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What in fast food fries have that regular fries don't?
Why is it that a french fry from a fast food restaurant doesn't seem to spoil the same way as one that one would cook at home?
PS: If given enough time will fast food french fries eventually decompose; if so, how long?

Why did you tag this "neuroscience"? Your question seems to be about preservatives in food. You might be able to get answers if you edit your title and body to make that more clear.

I suspect you are asking why a fast food fry doesn't spoil?  Water availability...  Read my answer to this post:  https://biology.stackexchange.com/a/57877/19432

I went through a longer winded explanation here:  https://biology.stackexchange.com/a/57877/19432.
In brief, food spoils if water is bio-available to micro-organisms.  In the case of a french fry from say, McDonalds. This fry has a very small volume to surface area ratio, and hence is able to dry out what little water is left after the frying process before micro-organisms can proliferate enough to visibly "spoil" the fry.
If, in your own kitchen, you were take a fresh potato, cut it into fries, and cook them in oil long enough to nearly dehydrate the fry, it would not spoil either in a dry environment.
Take either of those items that had been allowed to cool down and pick up micro-organisms (yeast and bacteria) from the air and place into a sealed ziplock bag with a little water and they would both spoil.
For your last question, in a dry environment, once something has become desiccated, decomposition stops and your fry would only decompose if the environment became more humid.  Think about naturally preserved mummies in an arid environment.
Edit: Light also can break bonds...and lend to further decomposition in the absence of micro-organisms. As can physical abrasion from wind, sand etc... So naturally mummified remains of great age would also have been protected from light and abrasion as well.


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List of amino acid frequency of different foods?
I'm trying to write a little application calculating the biological value of protein content of different meals using the amino acid frequency of different foods.
The idea is that the user can choose amount and type of different ingredients and finally obtains the biological value index for the meal.
For this calculation I'd need a list of amino acid frequencies of the different foods.
Any idea how I could obtain this?
My first idea was to just use the DNA of the different plants to extrapolate the proteins synthesized and then obtain the amino acid frequency from there but I know that genome and proteome is not correlating.
Any ideas / thoughts?

try the US FDA's website - it's a vetted website that has this database information - it is listed in this questions as well that appears to be a duplicate... biology.stackexchange.com/q/41844/16299

A reasonable starting place could be the Food and Agriculture Organization of the United Nations:
http://www.fao.org/docrep/005/AC854T/AC854T03.htm#chI.I
This source looks by no means complete or easy to parse, but some simple web scraping may help you wrangle the data into a database.

try the US FDA's website - it is listed in this questions as well that appears to be a duplicate... http://biology.stackexchange.com/q/41844/16299

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Do "shooting" animals exist?
The well-known cartoon imagery of porcupines shooting their quills at opponents in a fight is just that: a silly cartoon concept that isn't real.  But it makes me wonder, does that mechanism exist elsewhere in nature?
Are there any animals whose bodies produce solid projectiles that are used as launched/thrown weapons?  (Not looking for liquid ranged weapons such as skunk spray, bombardier beetles, etc.)

Clarity please. Are you excluding humans? Does this "production" exclude use of tools? Would you include the poo projectiles produced by primates?

@tyersome Yes, when I say "animals whose bodies produce solid projectiles," I mean produced biologically by the body, not produced externally by the use of tools.

Tarantulas can eject lots of bristle at potential predators. They often kick the bristles off with their legs, and I was told that they can eject them by tensioning their skin, but that's probably false, so I won't write a reply, here's a pic: https://www.youtube.com/watch?v=1cPxqjSG6HU

I don't know if it counts as shooting, horned lizard can "shoot jets of blood from their eyes for distances of up to five feet", according to an xkcd "what if" which points to Wikipedia page about horned lizard.

While not a solid produced by their body, pistol shrimp shoot "cavitation bubbles" to stun and even kill small fish! https://en.m.wikipedia.org/wiki/Alpheidae

Not projectile, but bonkers. Horned Lizards can shoot blood from their eyes when endangered: https://biology.stackexchange.com/questions/19794/how-did-the-horned-lizard-evolve

There's also the mantis shrimp, which has two appendages that can be fired at a target so quickly that they boil the water around them: https://en.wikipedia.org/wiki/Mantis_shrimp - however those are permanent appendages, not projectiles.

Many species of caterpillars eject their poop in pellet form at high speed.  It has been theorized that they do this to avoid drawing the attention of predators, so I suppose you could argue that this is a defensive mechanism; but it's not really a weapon.

https://en.wikipedia.org/wiki/Urticating_hair - "Urticating hairs or urticating bristles are one of the primary defense mechanisms used by numerous plants, almost all New World tarantulas, and various lepidopteran caterpillars. ... Many tarantula species eject bristles from their abdomens, directing them toward potential attackers"

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A good exemple should be the “harpoon” in cone snails (Conidae), which is created from a modified tooth inside their proboscis.

(Cone snail with proboscis, from KQED.org)
The harpoon is launched at prey at close distance, and is used to poison and stun prey, and later to pull them in. According to high-speed camera capture the harpoon is launched in just 200 microseconds, with an acceleration similar to a gun. The “harpoon“ structure is also very similar to a human made harpoon (see picture below)

(from KQED.org, Courtesy Manuel Jimenez Tenorio, Universidad de Cádiz)

(from KQED.org, Courtesy Joseph Schulz, Occidental College)
These harpoons are not re-used, and a cone snail can have up to 20 harpoons at different stages of development (see Cone snail toxicity).
It is also worth noting that the harpoon and its venom is a potent defence weapon also against humans. One cone snail can contain poison to kill about 700 people, and people stung by cone snails can get severely injured or even die (fatality reported to 15-75% according to Kapil et al, see below).
If you would include use of tools, in projectile use/shooting animals, apes and elephants are known to use stones as throwing weapons (see wiki-page linked below).
Sources:
https://www.kqed.org/science/1923898/watch-these-snails-stab-fish-and-swallow-them-whole
wikipedia: projectile use by non-human organisms  (with other examples of projectile use)
Kapil S, Hendriksen S, Cooper JS. Cone Snail Toxicity. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. www.ncbi.nlm.nih.gov

An excellent example (unless you consider this a tool) of a weapon using animal would be the "web casting spiders" which are a diverse group of spiders known as the Deinopidae. These spiders create a special elastic web that they hold between their fore-feet, and then dangling down from a surface, they expand and push the web onto their prey.
There is an excellent video from the BBC of this happening here

@JiminyCricket. Coincidence indeed. Yet, I know almost nothing about these creatures. I was just going to provide a link to a drive for you - so feel free to delete any personal details. regenerative eye paper

Although not a hard projectile the Archerfish shoots water
https://en.wikipedia.org/wiki/Archerfish

@user253751 - If you search for spitting world records you may be surprised

"Not looking for liquid ranged weapons"

Can't find it at the moment, but I remember lizards shooting blood from their eyes, most likely from What if? blog by xkcd.

@valisstillwithMonica Here ya go.  It's a defense mechanism

+1 because it's still the physical effects of the projectile that the fish is going for, not like skunk spray which is basically chemical (odour), not impact or making a bug's wings wet.

Spitting spiders will shoot their strands of web (extremely quickly) toward prey:
https://www.youtube.com/watch?v=DFozCr_tj8I

It is a common notion that porcupines can shoots spines but in reality, they can't. But there are some animals that can shoot/throw projectiles at the target as a result of either offensive or defensive mechanism. The projectile can be anything ranging from spikes or thorn to big objects like rocks, sticks, nuts or even faeces. You can find the details in the Wikipedia article.
The Wikipedia article mentions tarantulas that have a dense covering of hairs called urticating hairs on the abdomen that they sometimes use as protection against enemies. They can kick these hairs off by flicking them into the air at a target using their back pairs of legs. These fine hairs are barbed and designed to irritate and can be lethal to small animals such as rodents as well as humans.
Sea cucumber can expel its internal organs through its anus which can be sticky and sometimes contain a toxic chemical that can kill predators.

There is a plant called Sphagnum that disperses its seeds through an explosion that functions similar to that of a cap gun. It's pretty sick.
here it is in action

OP wants to know shooting "animals" not plants.

@NilayGhosh the question text wonders "does that mechanism exist elsewhere in nature?" so plants would be included there. Possibly the title only mentions "animals" as the questioner hadn't considered plants as a possibility - however this appears to be a seed dispersal tactic rather than a weapon

@MartinSmith I would think so but again in 2nd para, it is written "Are there any animals whose bodies ...". If OP were to consider both animals and plants, then the question would be too broad. Also, the other answers involved animals. So, this is an odd-one out.

Fieldfares guard their nests by attacking predators with their poop. Arguably feces is undigested material, but it does contain some secretions made in the body. Admittedly, fieldfare poop is more of a paste than a solid.
https://www.youtube.com/watch?v=Fdrl__ggV9k

I think it would be well argued that bird poop is a liquid generally - there are seabirds that projectile vomit to protect chicks, which would be also considered a liquid. I think the main criterion to the question is created and solid.

No, there are not animals which produce solid projectiles to shoot/launch/throw for defence or hunting. I think these criteria mean "aimed and detached".
There are tethered projectiles like cnidocyst in Cnidaria, but they don't detach (Wikipedia/cnidocyte). Harpoon-like organ in cone snails which is mentioned by @fileunderwater doesn't detach from the body (albeit detaches internally) and it must work in this way in order for the snail to hold and draw its prey (Wikipedia/cone snail). Spitting spider which is mentioned by @JimN doesn't store solid silk to shoot, it sprays the materials (Wikipedia/spider silk). It seems that the nearest thing is the urticating hairs in tarantula which is mentioned by @NilayGhosh; but tarantula doesn't shoot, it detaches hairs to make them airborne (Wikipedia/urticating hair). As the question has those criteria, these don't count.
There is a similar question on the possibility of that ability in worldbuilding.stackexchange (link) which you can review.

You should remove the first line of your post, as other posts have proved it false. "Never say never."

@LevelRiverSt What other answers prove this one false? serekani already specifically mentions some of them and says why they don't meet the criteria in the question (a solid projectile shot by an animal). The question doesn't disallow tethered projectiles, so you could argue that's an unnecessary limitation, but I think it's an interesting point to bring up.

@kwc 1. sea snail harpoon - complies with question, shoots, does not detach in use, but "is not re-used" so it must detach afterwards. 2. Of the spider answers, the spitting spider web is clearly projected & detaches in use (at least some parts) and works because it is toxic and sticky. (Watch the video.) It may not be hard, but it's not a liquid or a gas, most definitely a solid. This post then almost contradicts itself because it mentions urticating hairs, which are clearly produced by the animal's body and are solid (though having watched a video they are perhaps not really a projectile.)

@kwc the sea cucumber internal organs and pufferfish look like examples that fit the criteria, but following your comment I haven't been able to substantiate that they actually detach (all I've seen shows them remaining attached.) Equally, its pretty much impossible to substantiate a claim that there is no animal in existence that produces solid projectiles that shoot and detach, which is why I think it is unwise to say it. Consider how many species there are out there still to be discovered.

I know and admire that stackexchange community is passionate in and enjoy learning, researching and exchanging knowledge, and these are the most important things beside providing an answer. But there should be an answer at the end if possible. When and if OP tweaks the question a little bit, one or some of these animals are the answer.

@LevelRiverSt I understand the point:"Never say never." But it isn't necessary or customary to add "as long as we know" to every statement. If one asks if there are any fish species which lay egg on ice, the answer is no. Of course the question can be edited numerous times to try to fit the question to an answer, but this can make asking a question meaningless from the very beginning most of the time.

@serenaki your post has a box above it saying Want to improve this post? Add citations from reputable sources by editing the post. Posts with unsourced content may be edited or deleted which drew my eye to it. I would upvote it if you removed that first line, because I don't believe it's definitely true (and having watched some spitting spider videos I think it's false.) If you changed it to say you don't know of any such animal, that would not be overstating the case. The rest of the answer is good and interesting.

So if you would be shot by a human-made whale harpoon, you wouldn't consider this a death by a "...solid projectile(s) that are used as [a] launched/thrown weapon..."? In that case you are using a pretty limiting definition of launched projectile weapon. Especially considering that wire-guided missiles were common anti-tank weapons up to the 70s.

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Would a colony with only one male and female collapse?
This is a thought experiment:
If we form a population with only a single founder pair, can this population survive? What would happen? Would this inbreeding cause the population to go extinct? Could such a population continue to exist indefinitely?

There is only a probabilistic answer to this question. However, if you exclude external factors such as environmental stochasticity, predation pressure etc., and only care about the genetic component, there should be formulae to estimate this probability. You would still have to make some assumptions, e.g. the degree of heterozygosity of the initial pair...

If we're talking about lab mice, this is routinely done, since pure strains of lab mice are all genetically identical (barring the low level of spontaneous mutation).  If we're speaking more generally, inbreeding is generally bad and may well lead to extinction, but it's not inevitable; the presence of introduced species on e.g. islands originally populated with only a handful of individuals shows that it can be overcome.

Populations founded by a single pair are quite common in the lab
The Drosophila Genetic Reference Panel, one such example of high artificial inbreeding, is a series of inbred lines where the researchers mated brother and sister flies for 20 generations to form the lines, which means they will be highly inbred. When you do these though you often lose many of the initial lines because of inbreeding depression. Inbreeding depression is reduced fitness as a result of increased homozygosity in the lines - deleterious mutations are more frequently expressed. I have tried to find the number of initial pairs they used to make the ~200 DGRP lines but come up unsuccessful, but I've heard it was around 1500 pairs, although that may be well off the mark*.
What would happen to your mice?
Just like the DGRP lines, there is a high risk that the population would collapse. However, if they do get through a few generations of inbreeding, and are kept in steady conditions (i.e. selection doesn't change once the lines are formed), then they have an ok chance of persisting. If you started with multiple founder pairs then there's a better chance you will still have some (very inbred) mice in a few generations. The success rate will depend on the frequency of deleterious mutations and strength of their effects.
What is inbreeding?
Inbreeding is increased homozygosity in the population than would be expected under random mating. For example, if the frequency of two alleles ($A_1$ and $A_2$) at a gene are $p = 0.1$ and $q = 0.9$ respectively, the expected frequency of $A_1A_1$ homozygotes is
$p^2 = 0.1^2 = 0.01$
the expected frequency of $A_2A_2$ homozygotes is
$q^2 = 0.9^2 = 0.81$
and the expected frequency of heterozygotes is
$A_1A_2$ is $2pq = 2 \times 0.1 \times 0.9 = 0.18$
If the true frequency of heterozygotes ($A_1A_2$) is less than 0.18, then there is inbreeding.
Is there a benefit to inbreeding?
Well inbreeding can be a good thing. Imagine all of those lines that did not collapse. It is possible that a population formed out of those would have higher fitness than the original population, because deleterious mutations may have been purged (lines carrying deleterious mutations are more likely to collapse). So a highly inbred population can prosper. However, that population would also have lower genetic variance. Genetic variance places limits on the potential for adaptation, low genetic variance means low potential to respond to selection. So, if selection is not constant, then inbred populations are more likely to go extinct as they are unable to adapt to novel scenarios.
Inbreeding in nature
One classical example of high inbreeding in nature is in cheetahs, where it is beleived they went through a strong genetic bottleneck ~10,000 years ago. The problems faced by cheetahs today really highlights the problems of high inbreeding because they are struggling to adapt. Genetic bottlenecking is a  serious long-term problem for many species including the Javan rhino, the Kakapo, Mountain Gorillas, and others; even if we can stop poaching and habitat loss wiping out these species in the short-term, they will struggle to adapt to changes in the climate etc..

"As a species, cheetahs have famously low levels of genetic
  variation. This can probably be attributed to a population bottleneck
  they experienced around 10,000 years ago, barely avoiding extinction
  at the end of the last ice age. However, the situation has worsened in
  modern times. Habitat encroachment and poaching have further reduce
  cheetah numbers, consequently snuffing out even more genetic variation
  and leaving cheetahs even more vulnerable to extinction."

* Supporting material from the DGRP paper would suggest that it was indeed formed from 1500 isofemale lines.

There have been several studies with similar structure and background as your experiment, such as  "Inbreeding Effects on Reproductive Outcome: A Study Based on a Large Sample from the Endogamous Vadde of Kolleru Lake, Andhra Pradesh, India" from 1992.
It was an experiment to investigate this hypothesis:

Sanghvi's hypothesis on long term effects of inbreeding was tested in Kotas. Kota is a numerically small tribal population in the Nilgiri district, Tamil Nadu State, India. Consanguineous marriages are common in this tribe. A total of 95 couples were taken for this study and necessary data were collected on a set proforma. Of the 95 couples, 28 (29.5%) were consanguineously related. The inbreeding coefficient for autosomal genes is 0.022 and for sex-linked genes is 0.03. Inbreeding effects on reproductive losses were examined through an exponential regression model. Although the regression coefficient B values are positive, they are insignificant, suggesting no consistent relationship between degree of consanguinity and the reproductive losses. The estimates of genetic load is 1.8 lethal equivalents per gamete and the average B/A ratio is 5. These findings empirically support the Sanghvi's contention.

The abstract of the experiment from 1992:

Inbreeding effects on reproductive outcome vis-à-vis fertility, prenatal loss and prereproductive mortality, and secondary sex ratio of live and dead children were examined in a large sample of 2078 women of the Vadde fishing population of Kolleru Lake in Andhra Pradesh, India. Demographically, this population is a single endogamous unit. By using an exponential regression model with the proportion of offspring survival as a dependent variable and the inbreeding coefficient as an independent variable, I further examined the inbreeding effects. The results were compared with results from other fishing groups and other southern Indian and non-Indian populations. The results among the Vadde were consistent with those found for other groups of Telugu-speaking fishermen and several other southern Indian populations in that the effects were neither perceptible nor significant. The average B value and the number of lethal equivalents found for the highly inbred southern Indian populations in general and for the Vadde in particular were much smaller than those from other parts of the world, providing empirical support to Sanghvi's hypothesis on long-term effects of inbreeding.

The hypothesis was also supported by another investigation, looking at The effect of inbreeding on mortality and morbidity among Telugu-speaking populations of Kharagpur, West Bengal, India.

Increased mortality and morbidity including congenital malformations among the offspring of consanguineous marriages have been widely reported in human populations from different parts of the world. However, there are few studies on the effect of the intensity of inbreeding and different degrees of inbreeding on mortality and morbidity. The present study is an attempt to examine the effects of inbreeding on mortality and morbidity including congenital disorders in different levels of inbreeding among Telugu-speaking populations of Kharagpur, West Bengal, India, based on data collected through extensive pedigrees. The study reveals that the frequency of spontaneous abortions and stillbirths is higher in the offspring of consanguineous marriages than in that of non-consanguineous marriages. A similar effect is also observed in the infant mortality rate, which is known to have a genetic component, but is not seen in the mortality rate of children and juveniles. The rate of morbidity is consistently higher in the offspring of consanguineous marriages with a sex bias in favour of inbred females. The increased morbidity rates in inbred individuals tend to be inversely correlated with the increase in average autosomal inbreeding coefficient. This appears to strengthen Sanghvi's hypothesis of a decline in the frequency of deleterious genes with intensification of inbreeding through generations. The present study also confirms an increase in genetic disorders with an increase in inbreeding in almost all populations.

Sources & Further Reading:

http://www.jstor.org/stable/41465109?seq=1#page_scan_tab_contents
http://www.popline.org/node/184635
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080450/
http://www.ncbi.nlm.nih.gov/pubmed/1398609
http://www.newworldencyclopedia.org/entry/Exogamy_and_endogamy

It's generally best to write up an answer in your own words. By quickly scanning the pasted excerpts, I can't find an answer to the question.

What is "Sanghvi's hypothesis on long term effects of inbreeding"? This post doesn't answer the question at all well and simply pasting text from a paper is generally not a good approach

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What is the difference between eugenics and evolution by natural selection?
So with the working definition of Eugenics: "the aim to improve the human gene pool". What are key features that distinguish Eugenics from evolution by natural selection?  I mean, besides that natural selection occurs naturally.

With that definition, the major difference is that eugenics is artificial. Additionally, natural selection has no aim.

Natural selection is a descriptive theory that aims to explain the diversity of life. Eugenics was a political/ideological project for "improving the human gene pool." Obviously, these are completely different.

Eugenics is selective breeding to artificially promote certain 'desirable' genetic traits. Natural selection occurs without human interference and is due solely to the challenges of nature.

Selection is a mechanism of evolution which favours specific forms of traits over others, this can cause the spread of beneficial mutations through a population.
Natural selection is the spread of beneficial traits/genes through populations as a result of the natural variance in their effect on reproductive output (a function of life history traits like lifespan aging and reproductive rates). A classic example is that of Darwin's finches, where different variants of bill length and shape have evolved in populations based on what food resources (types of seed) are available to them and their ability to utilise those resources.
Artificial selection is selection imposed on a population by humans to deliberately affect specific traits. Examples of this would be milk yield in cattle (we want more efficient production and better quality milk), dog breeds (selection on a whole host of traits like colour, beardedness, height, length) and crops like wheat and barley (selected for higher efficiency and  quality output).
Eugenics, coming from the greek for "well-born" or "good" race, is the application of artificial selection principles to humans. Just as with cattle or crops, there is an aim, it may be to increase height, remove genetic diseases, or promote a certain set of traits like blonde hair and blue eyes. Historically we can associate with a number of radical political ideologies, such as Nazism. Even here in Sweden (people tend to think of it as a very progressive and equality driven country) there was a program of eugenics until very recently, achieved by forcibly sterilising or coercing people in to it, for various reasons (racial purity, health, and antisocial behaviour). Here's an interesting example of a girl designated as being genetically inferior because her family had a history of alcoholism (that page gives a good history of eugenics too). The social and ethical problems of eugenics are obvious.
Under normal conditions a persons reproductive output is largely determined by their own choices and actions whereas under eugenics that choice is taken away and made by someone else and specifically with the aim of "improving" the quality of the population.
So in summary:

natural selection is the result of natural variance in fitness linked to traits
artificial selection leads to a change in traits, in a specifically targeted direction, decided and imposed by another organism (usually humans, I know of no other species which does this)
eugenics is practice of artificial selection on humans enacted by humans with the specific aim of improving quality: often for social, economic, or political reasons and is generally accepted as being against human rights these days.

First, you need to recognise the difference between Natural selection and Artificial selection. As a basic definition, you can say that in natural selection, selection is done on fitness (overall, long-term success of reproduction) and is determined by the complete living environment of the species. In artificial selection, selection is done by humans on a plant or animal species for specific attributes that are desired (see any Evolutionary textbook for more on the difference). So the two processes generally try to optimize completely different things, and artificial selection has a goal which is not the case for natural selection.
Generally, Eugenics can be likened to artificial selection, done by humans on humans. The methods used (selective breeding, culling, trunkated selection, sterilization etc.) are potentially the same. The difference between eugenics and articifial selection on plants and animals other than humans is purely moral and political (and therefore off-topic for Bio-SE).
However, eugenics has also often been misguided in practice (if you ignore for a moment the usually horrible morals behind it). First, it relies on desired and undesired genotypes and phenotypes. Most people would not regard these as valid concepts, and even so, what will be desired/undesired will clearly differ between societies and over time. Second, eugenics does not appreciate the value of genetic diversity for the long-term success of a population (it will rather result in lower diversity). Third, eugenics is usually aimed for obvious physical traits and diseases, without much regard for their genetic background (e.g. heterozygious recessive carriers of disease). Fourth, eugenics usually devolve into a hunt for "weaker" groups of people, even if this has nothing to do with the gene pool of the population (for instance, many birth defects and the prevalence of Down's syndrome has almost nothing to do with the genetics of the population).
I guess you could argue that ongoing selection in humans is a form of eugenics since it is to a large extent determined by human interactions and choices (see e.g. Courtiol et al 2012 & Geary et al. 2004). However, this is definitely not a standard definition, and big difference compared to "normal" eugenics is that it is not guided by a common and explicit goal. I also know that some people label the collective outcome of individual decisions as a form of eugenics, which might be relevant for how you view Preimplantation genetic diagnosis (PGD) and prenatal screening.

In principle, eugenics is just like selective breeding of animals and plants. For example, dogs have been bred for a variety of traits to fit into several niches, and corn has been bred to produce large yields in several climates. Eugenics would attempt to do the same for humans. However, no one agrees on how to "improve" the human gene pool, and far too often eugenecists have sought to remove criminals, the disabled, the jews, or whoever they feel is inferior. And the methods used to bring about their genetic utopia include forced sterilization and/or death camps. There is no moral way to implement eugenics, and I don't think humans should be in the business of deciding which people are superior or inferior and who is allowed to reproduce, it's always dangerous.

what about PGD and using it to prevent the birth of a child who would otherwise lead a life of suffering? or inevitable death?

@user125535 Preimplantation genetic diagnosis (PGD) is not done with the purpose to improve the human gene pool (which is the case for Eugenics), so I think there is a big difference. As you say, they are done with the purpose to relieve potential suffering or for the sake of the parents. However, the same methods could theoretically be used by an eugenics programme.

authors: ميخائيل مينا


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Why does ampicillin in solution turn yellow?
I have a universal tube with 10 mg mL-1 ampicillin. When I got it, it was supposed to be sterile. It was opened for approximately 20 minutes for an experiment and has since been standing around sealed for a good month now.
Within the last couple weeks, it has gradually turned yellow. Right now the colour is faint, with a green-ish tint.
Why would it turn yellow? I know NADH is yellow, so that was my first guess. But I couldn't exaplain why ampicillin would cause NADH to accumulate, so I discarded that.
Side info: Ampicillin acts on bacterial cell walls, maybe that might help.

I assume you know that, but ampicillin solution should be stored at -20°C in aliquots, it's not the most stable molecule.

Ah, I never thought it could just be an unstable molecule. I'm going to read up a bit more about the ampicillin itself then; I thought it had something to do with contamination.

Just take a look at the structure, does that four-membered ring look strained to you? ;-)

Oh wow I didn't even know that was possible. So could the colour come from the Phe-like member when it breaks off?

Why is NADH the first thing to come to mind? Time for some physical chemistry.
Beta-lactams has a shorter ring structure which give it a different absorbance (around 322 nm apparently (source needed)) which gives it a blueish hue. Typically Penicillin and Ampicillin start off as an off-white. As hinted by @Mad Scientist, the beta-lactam rings are unstable and will undergo acid-catalyzed hydrolysis which breaks the 4-membered ring.
The Penicillin core also near a ketone which can attack the ketone in the lactam (I'm pretty sure this qualifies as enol chemistry but it has been awhile). The cyclization will form a 5-membered oxazole ring. Based on my experience, unsaturated 5-membered rings will absorb at a higher wavelength tending to result in a yellowish color (570-590 nM) so I am going to suggest that is the source of your color.

Ampicillin degradation

Cheers, very informative. NADH was just because that's the only yellow compound our classes have dealt with until now.


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Is local equilibrium a reasonable assumption for evolutionary processes?
Whenever I look at discussions of fitness landscapes (in particular, Kauffman's NK model) the questions tend to resemble:

The population is at a local equilibrium, but another equilibrium of higher fitness exists, how will the population cross the fitness valley between these equilibria?

These sort of statements assume that the population has reached a local equilibrium. Although, the local equilibria must exist, why do the people working in this field believe that they can be found before environmental (or other external events) change the fitness function? Are the timescales required to go from a random initial population to one that is at a local equilibrium compatible with the typical time-scales on which a fixed fitness landscape is an appropriate approximation?
If we switch to the polar opposite model of complete frequency-dependent selection (say replicator dynamics in evolutionary game theory) then limit-cycles (think rock-paper scissors game) and chaotic-attractors are common and it is possible for the population genetics to be constantly changing and never at equilibrium.
In an experimental setting, it also seems like although beneficial point-mutations are much more rare than deleterious, they do exist. This would suggest that experimentally, organisms are not at a local equilibrium. Do model organisms tend to be at local fitness equilibria?
In general, is the local equilibrium assumption in fitness landscapes research a reasonable assumption?

Nothing is at a genome-wide local equilibrium. Graham Bell wrote fairly extensively on this (IIRC).
Some loci

will be at what are likely global optimums (e.g. Cytochrome oxidase)
will be at local but not global optimums (e.g. low-fitness malaria resistance vs. high fitness malaria resistance: for the extremely cool story check out this page)
will not be at any optima because the environment shifts too quickly (e.g. loci clearly under frequency-dependent selection, such as MHC).

So, in general, it depends what you are trying to model. If you want to model a specific kind of evolutionary change, then model that kind of evolutionary change. If you want to model a different kind of change, then model that kind of evolutionary change. Natural populations will likely follow any model some of the time, but will probably never follow any model all of the time.

You mean Graham Bell?

Yup. That's the one. You'd think I could look six inches above my screen to the binding of a book to check the spelling of his name, wouldn't you?

I looked through Bell's publications, and I can't see a paper that suggests that he has been looking at this. Can you give an example?

In his book "Selection: the mechanism of evolution" he talks extensively on the dynamics of selection : i.e. how selection is changing over time, in different environments, etc. In particular I am recall some claims that evolution cannot be modelled as a markov-process because the state space is too large and impossible to characterize. My memory of this is quite vague, so I could be remembering a different author, and I can't find the relevant passage in this book right now.

You are right - overall the environment, which is always subject to change puts individuals in dynamic equilibrium. See the Red Queen hypothesis.  The genome itself is never completely at equilibrium either.

I think the jury is out on this one, there are examples of evidence both for and against reachability of local equilibrium and even these examples can be interpreted in many ways. I present three pieces of evidence and some interpretations. In general, my feeling after reading about this is that the assumption of equilibrium is ingrained in mathematical models for convenience and historic reasons not because there is solid evidence for it. (I expand more on this in this blog post).
Evidence against: vestigial features and macroevolutionary change
From a genome-wide perspective, it seems that equilibrium is at odds with the intuition of naturalists. Consider for example vestigial features of your own body like your appendix, goose bumps, tonsils, wisdom teeth, third eyelid, or the second joint in the middle of your foot made immobile by a tightened ligament (see video below). Wouldn't it be more efficient (and thus produce marginally higher fitness) if you didn't spend the energy to construct these features? Of course, this naturalist argument is not convincing since we don’t know if there are any small mutations that could remove these vestigial features from our development, I could just be describing a different local optimum that lays on the other side of a fitness valley from my current vertex.
The other tempting naturalist example of macroevolutionary changes like speciation is also not convincing for static fitness landscapes. The usual retort is that on these timescales the environment is not constant and depends on the organisms through mechanisms like niche-construction or frequency-dependence. This defense of local equilibria is actually a central part of the punctuated equilibrium theory of evolution; the environment changes (either through an external effect like meteor or internal effect like migration or niche-construction) and the wild-type becomes not locally optimal, but adaptation quickly carries the species to a new nearby local optimum where it remains for a long period of time until the next environmental change. Naturalistic observations are insufficient to settle this question, so we need to turn to experiments.
Evidence for: affinity maturation
The length of evolutionary process leading to affinity maturation is very short, typically a local equilibrium is found after only 6-8 nucleotide changes in CDR (Crews et al., 1981; Tonegawa, 1983; Clark et al., 1985), so you need only a few point mutations to quickly develop a drastically better tuned antibody -- an adaptive process that happens on the order of days. There are two reservations to keep in mind:
First, the adapted B-cells were not experimentally isolated and all of their point-mutations were not checked to guarantee that a fitness peak was reached. In both theoretical and experimental treatments of evolution, it is known that fitness increases tend to show a pattern of geometrically diminishing returns (Lenski & Travisano 1994; Orr, 1998; Cooper & Lenski, 2000) which means that after a few generations the fitness change will be so small that the fixation time in the large population of B-cells will be longer than the presence of the pathogen causing the immune response. We might not be seeing more steps because the next steps might have a fitness increase too small to fixate before the environment (and thus, fitness landscape) changes again.
Second, as can be seen from the AID protein (and other mechanisms) increasing the rate of mutation by a factor of $10^6$ along the gene encoding antibody proteins, this is a fitness landscape that has been shaped by previous evolution of the human immune system to find fit mutants as quickly as possible. This biases the phenomenon towards landscapes where local maxima would be easier to find than usual, and thus makes it not a good candidate for considering evolution under more typical conditions.
Evidence against: long-term evolution experiment
A more typical setting might be the evolution of E. coli in a static fitness landscape. Here, biologists have run long-term experiments tracking a population for over 50,000 generations (Lenski & Travisano 1994; Cooper & Lenski, 2000; Blount et al. 2012) and continue to still find adaptations and marginal increases in fitness. This suggests that a local optimum is not quickly found, even though the environment is static. However, it is difficult to estimate the number of adaptive mutations that fixed in this population, and Lenski (2003) estimated that as few as 100 adaptive point-mutations fixated in the first 20,000 generations. It is also hard to argue that the population doesn't traverse small fitness valleys between measurements, which could be used to suggest that the colony is hopping from one easy-to-find local equilibrium to the next.
References
Blount, Z. D., J. E. Barrick, C. J. Davidson, and R. E. Lenski. (2012). Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489: 513-518.
Clark, S.H., Huppi, K., Ruezinsky, D., Staudt, L., Gerhard, W., & Weigert, M. (1985). Inter- and intraclonal diversity in the antibody response to influenza hemagglutin. J. Exp. Med. 161: 687.
Cooper, V.S., & Lenski, R.E. (2000). The population genetics of ecological specialization in evolving Escherichia coli populations. Nature 407: 736-739.
Crews, S., Griffin, J., Huang, H., Calame, K., & Hood, L. (1981). A single V gene segment encodes the immune response to phosphorylcholine: somatic mutation is correlated with the class of the antibody. Cell 25: 59.
Kauffman, S.A., & Weinberger E.D. (1989). The NK model of rugged fitness landscapes and its application to maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245.
Lenski, Richard E. (2003). "Phenotypic and Genomic Evolution during a 20,000-Generation Experiment with the Bacterium Escherichia coli". In Janick, Jules. Plant Breeding Reviews (New York: Wiley) 24(2): 225–65.
Orr, H.A. (1998). The population genetics of adaptation: the distribution of factors fixed during adaptive evolution. Evolution 52: 935-949.
Tonegawa, S. (1983). Somatic generation of antibody diversity. Nature 302: 575.

authors: Дмитрий Шитиков


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More general usage of the term 'congener'
In taxonomy the term 'congener' refers to two species within the same genus. In more colloquial usage, it can refer to any two objects within the same category. Is there a way to refer to related species that is not specific to a particular taxonomic rank--as in, in the same order or family but not necessarily the same genus?
Update: I guess the term 'relative' works, but I still wonder if there's a better term.

Confamiliar is used sometimes (just google it). At lower taxonomic levels, such a term somehow loses its meaning, doesn't it?

Can you give us an example sentence where you'd like to use this term? I'm finding it hard to understand why you wouldn't just use the family or order name itself (i.e., "Tigers, like other big cats, ..." instead of "tigers, like their confamiliars, ...")

authors: Даниел Игнатов


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Exon skipping in mammals
I've heard from several sources that the predominant form of alternative splicing (at least in mammals) is exon skipping. However, my personal evidence is only anecdotal: I've heard it and read it, but have not seen references to literature. Is there a seminal paper or set of papers establishing this finding that I can cite?

You can see this review.

There are several different types of alternative splicing (AS) events,
  which can be classified into four main subgroups. The first type is
  exon skipping, in which a type of exon known as a cassette exon is
  spliced out of the transcript together with its flanking introns (see
  the figure, part a). Exon skipping accounts for nearly 40% of AS
  events in higher eukaryotes [17, 111] but is extremely rare in lower
  eukaryotes.


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Genome-wide methylation analysis: sources of technical error?
We are doing a genome-wide analysis of methylation via bisulfite sequencing for an insect species. Previous experimental techniques have suggested the presence of methylation in this organism, including an AFLP analysis using methylation-sensitive restriction enzymes and a differential expression analysis using a methylation inhibitor.
Our bisulfite sequencing data, however, is giving us essentially no evidence of methylation. If this finding is true, it will be a pretty big deal. But before we go down that path, we want to make sure we've counted out all sources of technical error.

First, we wondered if the bisulfite treatment failed, but quickly determined that this would not explain the result. If the C --> T conversion had failed at an extremely high rate, you would expect to see methylation all over the place. That's the opposite of what we're seeing, which is essentially no methylation.
Second, we wondered if there was some kind of "overexposure" issue in the bisulfite treatment that caused even methylated Cs to convert to Ts. We found a paper describing this phenomenon[1], but reports we can find suggest this happens at a low (<10%) rate, which cannot explain our data.
Third, we wondered if perhaps there was an issue with the reads mapping to the genome, we got at least 70% mapping efficiency for each BS-seq sample, so that can't be it either.

Are there any other sources of technical error we should consider and check for before believing this result?

Genereux DP, Johnson WC, Burden AF, Stöger R, Laird CD (2008) Errors in the bisulfite conversion of DNA: modulating inappropriate- and failed-conversion frequencies. Nucleic Acids Research, 36(22):e150, doi:10.1093/nar/gkn691.

This sounds very interesting. Could you provide a link to the paper that found methylation? "Previous experimental techniques have suggested the presence of methylation in this organism,"


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What is this tiny thing on the branch
I noticed a tiny spot with weird shape on the shoot of a plant (Variegata), and there are many others on other branches. I wonder what is it, this is a cropped picture of it, Thank you!

This is a female of yet another scale insect (Coccoidea). We have discussed one recently.
I guess we can identify this one rather precisely as Ceroplastes sinensis or its close relative. Species of this group are of South American origin, but Ceroplastes sinensis has today an extremely broad distribution. So, if you found this plant ("Variegata" is a specific epithet, by the way: it would be of some help if you provided the generic name as well) in Europe or Asia it's likely sinensis itself.

thank you very much for your answer, Very instructive,  I am not a botanist, I don't know the naming techniques, I just searched by leaf colors and I found Variegata as the closest plant, I think it's a Ficus benjamina 'Variegata'


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What could cause spiral tree growth?
While hiking through one of the areas burned in the 1988 Yellowstone fires, I noticed that some of the trees appeared to have grown in spiral patterns.
Most downed trees have crack patterns that imply straight growth, but some look like the one in the picture.  The direction shown in the picture seems to be more common, but it's not universal, and it doesn't appear to be related to location -- another picture I took shows two adjacent logs that spiral in opposite directions.

The two commonly put-forward explanations for spiral growth of tree trunks related to stress-loading and damage-tolerance.
The stress-loading explanation states that spiral-grained trees flex more than straight-grained trees before they break. Flexibility under stress-loading is useful in areas with heavy snowfall (as the tree can flex until the snow falls off) and in areas with heavy wind (as the tree can flex in response to wind-buffeting instead of breaking).
The damage-tolerance explanation states that in trees with straight grain, the leaves (or needles, etc) have water delivered to them, via the xylem, from the roots on the same side of the trunk. In spiral-grained trees with several years of growth, water and nutrients from a given root can be transported to branches on all sides of the trunk. Therefore in spiral-grained trees, if one section of the tree's root system is damaged, it does not necessarily mean that a corresponding part of the canopy will have to die off.
Kubler (1991) discusses both the stress-loading and damage-tolerance explanations in much more detail, if you're interested in further reading.

Is this essentially to imply that trees spontaneously express this growth pattern in response to specific environmental conditions during their development?

From Kubler (1991; linked in answer): "One cannot, however, expect a strict causal relationship between environmental conditions and fiber directions, because spiral grain is "under a considerable degree of genetic control in many species;" only in some species the genetic control of spirality appears to be negligible (Harris 1989, p 159)".
So, mostly no, but some species may develop spirally in response to environmental conditions.

Thanks; sorry, I had just assumed it would be paywalled and didn't even make it to the abstract in this case.


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Is there an advantage to antibacterial soap?
There are plenty of different hand soaps out there, as well as hand sanitizers. Is there an advantage to soaps that claim that they're antibacterial vs soaps that just say soap?
In particular I'm looking at Softsoap who offers normal soap and antibacterial soap.
Examples:
Normal:

Antibacterial:

Short answer: There is no benefit for their use in households.
Long answer: These soaps (see here for the complete list) contain the so called quaternary ammonium compounds Benzalkonium chloride and Cetrimonium chloride which indeed have antimicrobial properties.
While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.
There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.
This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.
References:

Use of germicides in the home and the healthcare setting: is there a
relationship between germicide use and antibiotic resistance?
Plain soap as effective as antibacterial but without the risk
Consumer antibacterial soaps: effective or just risky?
Effect of antibacterial home cleaning and handwashing products on
infectious disease symptoms: a randomized, double-blind trial.
The Burning Question: Is It Safe to Use Antibacterial Soap?

Thanks for the link, updated my answer to discuss other members of the Softsoap antibacterial series.

If there is no difference between the normal soap and "antibacterial" ones, what benefits do hospitals get by using it?

@zaftcoAgeiha They make no sense in households. I clarified the answer. The thing is different in hospitals with people which have systematically learned how to disinfect their hands.

Chris has correctly identified the antibacterial agent in the hand soap depicted in the image in the question, and therefore his answer is superior as a direct answer.
Nevertheless, other members of the Softsoap series of hand soap uses triclosan, 0.15% as their antibacterial agent, as seen in an image of their ingredient list on the reverse of the bottle.
(click for enlarged image)

Triclosan has been shown to be effective by Webster et al (1992) in reducing the incidence of MRSA infection as well as being milder to the skin as compared to chlorhexidine gluconate in a neonatal ward.

The average number of new cases of MRSA per week was reduced from 3·4 to 0·14 (P < 0·0001) in the experimental ward whilst no significant changes occurred in the control ward.

Triclosan has also been shown by Jones et al (2000) to be effective on a large variety of different bacterial, viral and fungal strains.

Therefore, the usage of triclosan is effective as an antibacterial agent, and would likely result in less bacteria on the hands after washing.

The depicted softsoap product do not contain triclosan but beanzalkonium chloride. See here (you have to scroll down).

@Chris but most antibacterial soaps, these days contain triclosan. Tertiary ammonium salts are a bit harsh.

@WYSIWYG Still they are used in some products.

I'd note that less bacteria on your hands is not necessarily a good thing. The natural microbiome on your hands has noticeable protective effects.

@Jack Aidley Although your comment cannot answer the question, I think it's the best viewpoint that we can have with repect to the matter.

Using triclosane is a very bad idea. Microbes become resistant to it, and there is cross-resistance between triclosane and some antibiotics e.g. chloramphenicol and tetracycline. Here is a summary in the topic: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295542/ Afaik. most MRSA is already resistant to it and they grow much better with triclosane, because the antibiotics kills competing species. So I think your answer and your references are outdated, a lot of things happened in the last decades...

The sources you cite show triclosan has antibacterial properties.  But this implies neither that it is effective in the context of domestic liquid soap, nor that using hand soap with triclosan confers an actual health advantage.

@augurar At no point did I say that it is effective as hand soap nor that it confers a health advantage, just that it would likely result in there being less bacteria, ceteris paribus, due to the bacteriocidal action.

You may be interested to look into the Old friends hypothesis, since this is related to how the human immune system may respond to reduced biodiversity in the microbiota. The basic idea is that the human immune system is developed by exposture to the microbiota, and without exposture to organisms from our evolutionary past, immune system regulation might fail. This can then lead to poorly regulated inflammatory responses and
maybe allergies or other chronic inflammatory diseases. Since the exposture to our evolutionary Old friends is lower in developed countries and urban areas, this hypothesis might potentially (partially) explain the increased prevalence of allergies in developed countries. Even though it is somewhat tangential to your question, and does not directly answer the question of the pros and cons of antibacterial soap, it should still be relevant for a more general case.
Two good starting points are Rook (2013) and Hanski et al (2012). Rook (2013) is a general overview of the theory with many good references to empirical studies that relate to the hypothesis, by one of the main proponents of the theory. Hanski et al (2012) is an interesting epidemiological paper, where they relate the allergic disposition of individuals to both the general biodiversity in their larger living environment as well as the generic diversity of their skin microbiota. In the paper, they find a positive relationship in healthy individuals between immune responses and the abundance of the gammaproteobacterial genus Acinetobacter on the skin, but they do not find the same pattern in atopic individuals. The study also finds a negative relationship between the environmental biodiversity close to the homes of study subjects and the frequency of atopy (so high biodiversity -> lower levels of atopy).
To be clear, this is still a hypothesis that needs further testing and support. However, there are many interesting case studies that can lend support to it, and indicate plausible mechanisms.
References:

Rook. 2013. Regulation of the immune system by biodiversity from the natural environment: An ecosystem service essential to health. PNAS 110(46)
Hanski et al. 2012. Environmental biodiversity, human microbiota, and allergy are interrelated. PNAS 109(21)
Rook. 2013. Microbial ‘Old Friends’, immunoregulation and stress resilience. Evolution, Medicine, and Public Health
2013(1)

Related - https://en.wikipedia.org/wiki/Hygiene_hypothesis

Probably, it is worth to add some historic (and ironic) "perspective" to this question. It will probably explain that even without scientific research the answer to this question is probably "no" and that real use of bacterial soap should probably be reduced to hospital settings and not expanded to households as suggest promotions and commercials.
The historic perspective I wanted to add relates to the book "The Hermit in the Garden" by Gordon Campbell. Here live hermits are described (there were non-alive as well, this is why I call these "live"). Campbell cites another book -  "Sir William Gell's A Tour in the Lakes Made in 1797":
"the hermit is never to leave the place, or hold conversation with anyone for seven years during which he is neither to wash himself or cleanse himself in any way whatever, but is to let his hair and nails both on hands and feet, grow as long as nature will permit them."
From this "work" description we can speculate that "dangerous" infections were not expected during such a long period of soapless live. This is why we could assume that any soap is probably of limited "antibacterial" value for otherwise healthy person.
(Remark: This "exclamation" not trying to answer the question in a scientific way, but just to add some "color" to the question and the answers posted. I hope, it is worth to place it here instead of a comment).

Remember though, that they are living in isolation, they won't come in contact with as many bacteria or viruses as the general population. It's not like they will come in contact with sick people if they are living more or less in isolation. Besides, what viruses and bacteria are there they will adapt to especially if they are healthy individuals. However, I do appreciate the insite.

@SolarLunix They lived in gardens, their isolation from sick people were not absolute and contact with all the mosquitoes, flies, worms, dogs etc had to increase the exposure to multiple pathogens. I suppose it is interesting point to start with.

Human immune defense response is primed by cell damage products as it does not have prior knowledge about bacterial or viral "malware".
The whole purpose of disinfectant substances is damaging cells and potential organic disease carriers.  As those substances are not discriminating, frequent use of them will prime your immune defense against benign organic matter as well.  In combination with solvents that remove protective layers of fat and thus increase the permeation of this kind of cell waste into top skin layers, this sounds like a recipe for allergies and neurodermitic reactions in the long run.
There is a high correlation of countries (and eras) with high standards of living including household hygiene and autoimmune response problems.  Finding actual causations is work in progress.
While that is still the case, it is my gut feeling that contact with disinfectants should be reserved to cases of tangible risk.

Interesting answer. Can you please add some references to it?

Apart from references, I found your answer a little hard to read, could you please try to add a summery such as "Antibacterial soap doesn't help because..." ?

This is an interesting answer, but this kind of stuff will get you a lot of downvotes. The thing to remember about this site (and it is aggravating, and not very well stated) is that "it is not a forum." Answers are supposed to be very definite with reasons spelled out in detail, and supposition and comments about the question are suppoosed to go in the short comments.

That being said, I was unable to find any studies showing that Benzalkonium chloride caused over-sensitivity of the immune system to benign agents. I think you have generally the right idea, but most of your facts seem to be unfounded theories(?). Like others said, these things need references or clear statements that they're guesswork (in which case they're probably inappropriate for empirical discussions like this).


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The mystery of coconut tree
Could anyone please explain to me, why the nail which is nailed in a coconut tree is not raised from ground level, when the tree is growing up?

Could you please expand the informat

Could you please make me understand what you are asking?

Thanks, it's clear from the answer. I just wasn't sure which "rising" you mean.

First it needs to be said that coconut trees are not true trees, but palms, whose trunks are made of stems which grow in a cross woven pattern.
That being said - its true for any plant that no plant grows from the bottom up.  If you make a mark on any plant that mark will not rise much as the plant grows.
Plants grow from buds at the end of their stems.  As the plant grows taller  its because the tissue adds from the ends of its branches/stems.

In this illustration you can see the terminal bud, which is where the plant is growing up and also out into branches.  The palm is more like a bundle of grass stems, so the terminal bud is not obvious, but the leading edge of the grass will grow here.
A tightly wound core of stems in the crown of the palm, called the Heart of Palm is where the palm grows (see "growth point" in picture below).  It is also a terminal bud, but it is not as exposed and is not as obvious.

(figure from The Food and Agriculture Organization of the UN, fao.org)

"if you make a mark on any plant that mark will not rise much as the plant grows". This is not the case for plants with intercalary meristems, e.g. grasses (including bamboo). It should be true for woody plants though, as well as relatively large, established palms (I'm not sure about the growth patterns of palm saplings).


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What are anagenesis and cladogenesis?
Are they two types of speciation?
I have read wikipedia but can't figure out if they are really two types of speciation

Reading Wikipedia, it seems both give rise to new species and hence result in speciation. https://en.m.wikipedia.org/wiki/Cladogenesis. Just go through the link. 'New species' has been mentioned for both.

From Wikipedia:

Anagenesis, also known as "phyletic transformation", is when the new morphospecies is a result of rapid evolution in the ancestral form without speciation taking place, such that there are no remaining other populations of the ancestor species and the species can be considered extinct. [...] Anagenesis is in contrast to the branching speciation known as cladogenesis.

and

Cladogenesis is an evolutionary splitting event where a parent species splits into two distinct species, forming a clade. [...] Cladogenesis is in contrast to anagenesis, in which an ancestral species gradually accumulates change, and eventually, when enough is accumulated, the species is sufficiently distinct and different enough from its original starting form that it can be labeled as a new form - a new species.

So Cladogeneis is speciation by evolutionary splitting of a lineage and Anagenesis is designation of a morphospecies without splitting (gradual change).
This figure from Columbia University is useful to show the difference (http://rainbow.ldeo.columbia.edu/courses/v1001/anaclad.html):

Note that Anagenesis is most often used in Paleontology, and the possibility to distinguish between the two types depends on the resolution of the paleontological data. Whether to name a "speciation event" as one or the other, or how to use the terms generally, is also a matter of debate (see e.g. Aze et al. 2013. Identifying anagenesis and cladogenesis in the fossil record. PNAS).


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Is there software or a website where I can browse extinct species?
Is there any software/website where I can browse for extinct species? It must be based on real animals that are now extinct. It may be in animated versions.

What research have you done so far?

In your next post please start sentences with a capital letter, and use a capital for 'I'. I have corrected this for you.

fileunderwater's answer is probably the most accurate. I just wanted to add that, depending on your needs wikipedia > lists of extinct species can be a decent source of information.

You can search for species that are "Extinct" or "Extinct in the wild" at the IUCN red list website (International Union for Conservation of Nature and Natural Resources). That list currently includes 903 species, but some of the assessments might be obsolete (see annotations). From that list, you can click and get some basic information about each species.
Also note that many countries have regional Red Lists, where you can find information about regionally extinct species (i.e. species that have gone extinct in a particular country). For instance, 209 species are labelled "reginally extinct" in Sweden (http://artfakta.artdatabanken.se/, site only in Swedish), most of them insects, while still being present in other parts of the world.


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"structural and regulatory elements of genes"
Can anyone please explain a little about these two elements of genes? My main problem is with "which ‘switch on’ instructions".

genes have structural elements (which code for a particular protein) and regulatory elements (which ‘switch on’ instructions)

Welcome to Biology. Perhaps a visit to the help center may be recommended or read http://blog.stackoverflow.com/2010/09/good-subjective-bad-subjective/. We need to know what you need to know. "Explain a little" is too vague. I can explain a little, e.g., upstream regulatory elements may enhance or suppress gene expression by binding of transcription factors, but is this what you are after? Be specific! I vote to close because it is unclear what you are after. Questions should be in the form of "I don't understand element Y of X because of Z", and not in the form of "please explain X".

You need to explain more of your thinking. Also, where is the quote taken from?

The expression of protein coding genes happens by the process of transcription. So promoters facilitate access of the RNA polymerase complex to DNA to begin transcribing a locus on the genome. The promoter of a gene often contains sequences that bind proteins called transcription factors, which play a role in various parts of the transcriptional process as well as components of RNA polymerase themselves (Such as a Pribnow box in prokaryotes, or a TATA box or an initiator element in animals).
So whether a gene is turned on and if so, how much it is turned on, is a property of how many transcription factor binding sites exist in the promoter, the nature of the transcription factors themselves in terms of their influence on transcription, and in eukaryotes and some archaea, epigenetic processes that control the access of transcriptional machinery to the locus being transcribed.
So when you think about the two elements in a gene, think of a light (the bit of a gene that codes for proteins) and a dimmer (which controls how much RNA is made by the protein-coding bit)

A structural element is that part of the gene that is giving the code to specify an amino acid that's going to be translated into a protein. A lot of the rest of the code may say "start reading here" "stop reading" "ribosome bind here" etc.


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Is Asteraceae and Compositae the same family?
I'm wondering what taxonomic family sunflowers (Helianthus) belong to. Although it's mentioned it belongs to family Asteraceae it is also a composite flower. So it belongs to Asteraceae or Compositae or both?
And do they refer to the same family or to different families?

https://en.wikipedia.org/wiki/Asteraceae#Etymology not the most scientific source, but they seem to be synonyms.

There are a number of plant families that, for historical reasons, have two accepted family names. In addition to Asteraceae/Compositae, there's also Fabaceae/Leguminosae, Poaceae/Gramineae, and others.

They are either treated or even declared to be synonyms in all the texts using both of the terms that I have ever read.
Just one reference: the nearest Flora on my desk, G. Marconi, F. Corbetta, Flora della Pianura Padana e dell'Appennino Settentrionale, uses the notation Compositae = Asteraceae.
It is worth to note that Compositae, 'composite ones' in Latin, refers to the their typical capitulum inflorescence, while Asteraceae comes from Aster, a genus belonging to the family, meaning 'star' in Latin, which represents an allusion to the shape of the inflorescence of Aster, and of many other species, which is supposed to look like a star whose rays are represented by the ligules of the ligulate tiny flowers of the capitulum. Nevertheless, there also are species of the family having no ligulate flowers, for ex. Tanacetum vulgare.


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How to find the location of a gene, starting with the gene name and the DNA sequence of nucleotides?
I'm not a professional biologist, I'm just trying to analyze some actual data. Where should I look up the location of a gene and nucleotides it consist of? How can I find it in DNA? Is there an algorithm that can be used?

This is not clear. You have a gene and its sequence? You have a gene name and a genome sequence that could or could not have this gene? What type of "gene name" do you have? There are different identifiers for genes. If it is a standardised one, yes, you can get the gene sequence for example from Genbank and you can align the gene to a genome. But please try to make the question more specific and add more research.

To find the genomic location of a gene when you start with a gene name;
Use the UCSC Genome browser. This has a number of advantages. There are a number of species to choose from. It provides a representative image of the gene and regulatory elements that surround it. It can display a lot of extra information if you want to see it. The disadvantage ot the UCSC Genome browser is that the information density may overload non-professional users.
To find the genomic location of a gene when you start with a DNA sequence;
Use the search tool that links to the UCSC browser.
The alternative option is to search for your gene ID or sequence in NCBI Gene.
To search for a DNA nucleotide sequence using the link above, select Reference genomic sequences (refseq_genomic) from the pull-down tab in the Database field. Limiting the search to a species using the Organism field is also wise.
Both of these sites provide the information you are after. Taking time to read the help instructions will be useful.


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Cousin Marriage from genetics point of view
In most societies marriages between cousin are viewed negatively, due to a fear of "bad genes".
But lets say I am a girl and I marry the son of my mother's brother (i.e. my uncle), than there is no gene similarity.
Then I have two X-chromosomes, where one came from my father and the other one from my mother. My cousin (the son of my uncle) will have one Y-chromosome from his father and one X-chromosome from his mother (wh o is unrelated to me). My mother will also not be a carrier of my cousins Y-chromosome (since she is a female).
Does this all mean that this particular cousin marriage is unproblematic, and no different than a marriage between completely unrelated people?

I tried to clarify your question, so that there are no confusion. If I have misunderstood you, please feel free to roll-back the edit. Your question is however based on a misunderstanding of human genetics (autosomal vs sex chromosomes), which @mattDMo has explained clearly.

I think I am confused with X and Y chromosome and how gene overlap happen, according to my understanding X and Y has completely different genes , which is wrong

It depends on the physical fitness of the parents. A village in italy has been studied because all 400 of its inhabitants descend from the same two people, and it has very low disease results and high longevity, whereas on average, places like SA and Pakistan have above median levels of club foot and genetic disorders from cousin marriage. pak has 55 percent marriage between cousins and 10-15 percent genetic recessive disorders more than non cousin marraiges. 4.4 percent higher mortality rates also from cousin marriages, which is on par with mothers over the age of 40.

The problem is that humans have 22 other pairs of chromosomes than just the sex chromosomes X and Y. Reproducing with your cousin (the son of your mother's brother is the son of your uncle which means your cousin) is generally looked down upon because of inbreeding.
Here's how it breaks down. Your mother and her brother (your uncle) each received 50% of their genes from your grandmother, and 50% from your grandfather. You received 50% of your genes from your mother and the other 50% from your father, who presumably is unrelated to the family. Therefore, you received 25% (50% of 50%) of your genes from your grandmother, and 25% from your grandfather. The same is true of your cousin - 25% from grandmother, and 25% from grandfather. The chances of some of your 25% and his 25% overlapping are rather high (for any one allele of a gene, it has a 1 in 4 chance of being the same as the cousin's). Combine that with 19-20,000-something genes, and that's a lot of overlap.
The problem with overlap/inbreeding is that any "hidden" (recessive) alleles may become homozygous. This may not be a problem for some genes, but a rather big problem for others (see my previous answer about Hunter Syndrome for an example.) There is a real potential of serious genetic diseases in any children resulting from such a relationship, which of course isn't fair to them.

Simply put, if first cousins have children, there is an increased risk of birth defects in those children (as compared to children of unrelated couples).  This has been shown by studies such as this one reported in a major medical journal.
There is a genetic basis for this, which is known as inbreeding depression. Basically, everybody has some genetic defects, but they generally occur in different places among the genes.  However, in two closely related people, such as cousins, the defects are more likely to fall in the same genes because those people share some genes from the same source (e.g. the common grandparents).
It's true that certain kinds of cousins do not share either X or Y genes from a recent ancestor, but that has only a small impact.  That's because almost all genes are on chromosomes other than X or Y, and are inherited by all descendents regardless of the sexes of the people involved.  Therefore, the problem of birth defects (and miscarriages) occur for all kinds of first cousins.

Welcome to Biology.SE!

In most of society cousins marriage [..]

Who cares about marriage in biology? We only care about reproduction. Marriage is a social construct that is mainly irrelevant here.

[..] is seen bad due to fear of bad genes

The term "bad" is poorly used for 2 reasons. 1. There are no bad genes but only a selective differential between two alleles of this gene (or at any other sequence for that matter). 2. It relationship of dominance and epistasis that causes inbreeding depression and not bad alleles.

I have "X" and "X" chromosome, X came from my father and X from mother son of my mothers brother will have Y chromosome and X from his mother which is not family and since my mother has nothing to do with "Y" chromosome.

That's one long sentence :) Who is "mother son of my mothers brother"? You might have a typo here.
Why do you talk only about "X | Y" chromosomes? "X | Y" is one of the 23 pairs of chromosomes we have (not mentioning mtDNA).

Does this all mean that this marriage is as good as between unrelated people?

Yes.
The whole question is to know whether the two parents are related (in biological terms). What I mean by related is not is they know each or if their respective siblings got a baby together but if they share a common grandmother for example. If you draw the genealogical tree of each parent and you see a recent shared ancestor between the two parents, then inbreeding depression can be an issue. Otherwise, it is fine. The reproduction events occurring between their respective siblings is irrelevant.
However, be careful if you intend to jump into societal consequence. Science will not tell you what is acceptable or not in a society. It won't tell you what is good and what is bad. Knowing that a couple have no risk of inbreeding depression may affect your view about this couple but it does not mean that science has demonstrated that the marriage should or should not be allowed (assuming the society has anything to say on that matter).

The OP seems to be asking if a marriage between cousins (or rather, reproduction) could be problematic from a genetic point of view (restated: what if I would marry the son of by mother's brother? see: "...marry son of my mother's brother...[...] Does this all mean that this marriage is as good as between unrelated people?"). Therefore, your second to last paragraph is misleading or can cause confusion.

@fileunderwater i think you got my question, but answer I am not clear?

@fileunderwater Can you please expand to why it is unclear. I edited it but I don't quite understand what may have been unclear to the OP. Feel free to edit yourself as well. Thanks

@remi.b The question is asking whether reproduction between cousins (the "this marriage" part you are quoting refers to a cousin marriage), and the two persons are therefore definitely biologically related. Your initial answer was saying that this wasn't a problem - probably due to misunderstandings caused by unclear language in the question - which is incorrect.


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Genomic distribution of tRNAs in eukaryotes
The title says it all. I'm doing a literature search trying to see what is widely known and/or well established. I've found a couple of mentions that tRNAs are dispersed throughout the entire nuclear genome. Does this mean they are isolated from each other? Or do they occur in clusters? Is this true across eukaryotes? Or is any of this even well studied?

The positions are annotated but I don't think anyone did a comparison.  Surprisingly, the gencode GTF does not have the tRNA annotations!! Have a look at this database of tRNAs.

In Drosophila, at least, some are clustered (e.g. these), but there are many tRNA genes in eukaryotes, so overall they are dispersed. You might find the Genomic tRNA Database useful, and the paper describing it.


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Can PCR duplicates have complementary sequences?
It is common when analyzing paired-end whole-genome shotgun sequencing data to check for and eliminate PCR duplicates. The reasoning is that the probability of sampling a fragment of the genome of the same exact length from the same exact position in the genome multiple times is extremely low. Therefore, if you see multiple read pairs with the same exact sequence in both pairs, these don't represent independent events but are multiple copies of the same event.
My question is whether PCR duplicates can be reverse complements of each other. All the PCR duplicates I've observed myself have been exactly the same sequence on exactly the same strand. Is there a technical reason why this is the case, or is it possible that PCR duplicates could not be on the same strand as each other?

Depends exactly where the PCR step is in your library prep.  Usually, there is one that is done after adapters are added, to amplify fragments with intact primers on both sides.  These will of course all be the same orientation.

The standard directional Illumina library prep protocols that are used at the facility in my building follow the schematic below:

So, I guess this provides a potential technical explanation for your stranded duplicates, with the broad simple answer being it depends on the protocol used to make the libraries.


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Why does scar tissue change color?
I was wondering why, when you are cold, scar tissue turns bluish or purple while original skin stays the same color.
The only thing I can think of, is that maybe scar tissue gets less circulation than regular skin, so when it gets cold it restricts circulation.

The main mechanism behind the scar changing its color is the dilation of blood vessels within the scar tissue. The dilated vessels lead to the congestion of blood flow. The red blood cells moving more slowly leave more oxygen due to its diffusion to the tissue and the hemoglobin -- the oxygen holding protein -- changes its color from scarlet (bound to oxygen) to cyan (released/bound to CO2). Since scars are not covered by skin, the blood vessels are clearly visible here and you see this characteristic color.
The triggering mechanism here is cold that increases the energy barrier for many biochemical reactions, first of all those required for smooth muscle contraction.
Cold-induced vessel dilation (that can be seen, for example, on cheeks and extremities) with mild circulatory disturbances ultimately undergoes into so-called cold vessel paralysis when smooth muscles of blood vessel walls completely loose their ability to contract and are maximally dilated. The cyan color of the scar is usually seen at the very last stage, that can occur unexpectedly quickly because scars do not have any warmth insulation layer compared to the regions covered by skin.

Why does dilation of blood vessels cause congestion of blood flow? Should not a bigger cross section ease the blood flow? This seems contradictory to me.


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What is lack in sense of smell called?
People who lack the sense of hearing, vision and speaking are called Deaf, Blind and Mute.
But what is the person called if he/she lacks the sense of smell? Is there any case like that?

This condition is called 'anosmia', see these two links: Wikipedia and from the british National Health Service. They include a definition and reasons for anosmia.

the person would be called 'anosmic'. See https://en.wiktionary.org/wiki/anosmic


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Are there any bacterial lineages which are particularly well adapted to becoming endosymbionts?
Is there any particular bacterial lineages which contain a large number of endosymbiotic species and that inhabit a large range of eukaryotic hosts? To me, this would seem to suggest that they are particularly well adapted to becoming endosymbionts.

Can you give some more background? Which endosymbiotic bacterial linages do you know of from before, and are you interested in any specific types of endosymbiosis in particular?

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0027909

Members of the genus Xenorhabdus are entomopathogenic bacteria that associate with nematodes. The nematode-bacteria pair infects and kills insects, with both partners contributing to insect pathogenesis and the bacteria providing nutrition to the nematode from available insect-derived nutrients. The nematode provides the bacteria with protection from predators, access to nutrients, and a mechanism of dispersal. Members of the bacterial genus Photorhabdus also associate with nematodes to kill insects, and both genera of bacteria provide similar services to their different nematode hosts through unique physiological and metabolic mechanisms.

While that's definitely an interesting example of symbiosis, I think the question was more focused on whether there are bacterial lines that are more prone to forming endosymbiotic relationships with diverse species.


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Small yellow bug with black head and three black stripes on the back
Can anyone help me to find the name of this small yellow bug with black head and three black stripes on the back. It was found in Jura, France:

It looks like a yellower version of the brown marmorated stink bug (halyomorpha halys) nymphs I've seen in my garden in the US (west Texas). They change colors throughout their life span, so perhaps that's an older nymph that's begun changing to brown. They're prevalent in the US, Europe, and Asia, according to Wikipedia (https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug).
I have no research experience with this insect, and I am not a biologist -- all of my research on this consisted of google searches for variations on "small red beetle three black lines."

it looks like very similar indeed. A friend biologist said it could also be a Troilus luridus. To compare both: https://en.wikipedia.org/wiki/Troilus_luridus and https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug

Following doc http://www.northeastipm.org/neipm/assets/File/BMSB%20Resources/BMSB-IWG-Jun-2013/Invasion-of-BMSB-in-Europe-Haye.pdf explains that the halyomorpha halys was first recorded in Europe during the 90s, starting from Switzerland. And the place we found the bug is very near from Switzerland.

Very hard to determine the exact species without specifics like which plant/habitat it was found in,...
But one thing is for sure, this is a nymph of the Pentatomidae family.
Given the location this one is found, its size and the most likely encounter due to abundancy I'd say it's an early stage nymph of the Tritomegas bicolor (Pied Shieldbug).

1st instar nymph
https://c1.staticflickr.com/3/2915/14211267059_516d33c90f_b.jpg

Adult specimen
https://www.britishbugs.org.uk/heteroptera/Cydnidae/Cydnidae_images/tritomegas-bicolor_2.jpg
This species is found across North Africa, Europe and Central Asia, although in the British Isles, it becomes rarer towards the north, and is absent from Scotland and Ireland.
(source: Wikipedia Pied Shield Bug)
The adults are 5 to 7 mm in length. Their colour is mainly black with white irregular spots. You'll most likely find them on the ground (as they are burrowing bugs or burrower bugs), but occasionally or during nymph stage you'll find them on dead nettles (Lamium).
Hard to distinguish from T. sexmaculatus.
Extra information:
https://www.britishbugs.org.uk/heteroptera/Cydnidae/tritomegas_bicolor.html
useful classifying guide:
https://www.britishbugs.org.uk/heteroptera/idcards/life_stages.html

After your addition of locale I think Spined Citrus Bug isn't a possible candidate, from web results there is no sighting of it in France but your insect is of related taxon under the Suborder Heteroptera.

Unfit identification:
It appears a nymph of Spined Citrus Bug, Biprorulus bibax.

Although native to Australia, Biprorulus bibax is considered a pest because it feeds on the fruits of lemons, mandarins and oranges, causing drying and brown staining of the fruit segments, gumming on the skin and premature fruit drop.
Their native host is the desert lime, Eremocitrus glauca.
Late-stage nymphs (IV to V) are mainly green with black markings.
Adults are green, 15–20 mm long, and have a pair of prominent spines on the shoulder of the thorax.
When overwintering tight clusters of up to 50 adult bugs can be found in a single tree. A male-produced aggregation pheromone is responsible for the clustering. The pheromone is attractive to males and females, both reproductive and non-reproductive.

SOURCE: saveourwaterwaysnow, Originally from PRIMEFACT 217, SPINED CITRUS BUG 3, New South Wales Department
of Primary Industries ISSN 1832-6668
I couldn't find any credible source with description of the early instars but the picture of the late instar on the linked website surely shows resemblance with your bug and I think yours is an early instar (any instar below IV).

The egg is 1mm across, almost globular and pearly white when first laid. Red, yellow and black markings develop as the embryo matures.
The first instar is almost oval, 1.5 to 2 mm long, with a short rostrum.

Source: Heteroptera of Economic Importance
This website dedicated to the Biodiversity of Australia has recorded sightings of Biprorulus bibax eggs and hatchlings and the latter strongly resembles your insect.