text:
In scuba diving, are nitrogen narcosis and high pressure nervous syndrome the same thing?
In training for scuba diving, they tell you that when you're bellow 100 ft or so you have to watch out for changes in mental state that resemble drunkenness. The cause of these mental disturbances is called nitrogen narcosis, and it has something to do with the increased pressure on the nitrogen component of the gas that you're breathing out of your tank. I just read this article from the what-if section of XKCD (halfway down the page, under the header about Michael Phelps) that mentioned a very similar sounding disorder called high pressure nervous syndrome. Are nitrogen narcosis and high pressure nervous syndrome related, or are the effects of high pressure nitrogen and high pressure by itself separable?

what does the linked paper (by Hunger Jr and Bennet 1974) say?

These are different things.
Nitrogen Narcosis or more commonly Gas Narcosis is the narcotic effect of gasses like Oxygen and Nitrogen under pressure. The effects are most prominent under 30m and commercial/technical dives doing dives to 40/50m on air tend to experience the effects most. (Narcosis is managed by adding an inert gas - in most gases Helium - to air to form a mixture referred to as Trimix (Helium/Oxygen/Nitrogen) this then produces an effect as if the diver is diving to a shallower depth and is referred to as Equivalent Narcotic Depth, in some cases Heliox (Helium & Oxygen) was also used)
High Pressure Nervous Syndrome is an interesting aspect of deep diving and used to be called Helium Jitters/Tremors as the accepted standard was that it was caused by breathing Helium mixtures under 150m. Some people hold this to be true and others claim that it has nothing to do with Helium but rather the pressure disrupting the flow of electric signals thru the nervous system.
What is interesting is that they found that if you used Trimix (Helium/Nitrogen/Oxygen) rather than Heliox (Helium/Oxygen) the onset happened later or not as severe. And the slower your descent is the slower the onset of the symptoms.
Some Docs to Read:
Narcosis - Relatively simple document on Narcosis
Narcosis - "Narcosis is not unique to nitrogen; however, it can occur with many of the so-called “noble” or inert gases, with the exception of helium. Add to this the fact that other inert gases each have their own brand of narcotic effects at depth, and you have a complicated picture for technical and commercial divers. One of these rare gases, argon, for example, has about twice the narcotic potency of nitrogen, but helium has very weak narcotic properties and is less soluble than nitrogen in body tissues."
HPNS - Relatively Simple doc on HPNS
HPNS - Very technical discussion on gasses, from a HPNS and Narcosis view point.
References:
Bennett, P.B. 1982b. The high pressure nervous syndrome in man. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 262-296.
Bennett, P.B. 1990. Inert gas narcosis and HPNS. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.).W.B. Saunders Company, Philadelphia. pp. 69-81.
Bennett, P.B, R. Coggin, and J. Roby. 1981. Control of HPNS in humans during rapid compression with trimix to 650 m (2132 ft). Undersea Biomed. Res., 8(2): 85-100.


text:
How many humans have been in my lineage? Is it almost the same for every human currently living?
If I were to count my father, my grandfather, my great-grandfather, and so on up till, say chimps, or the most common ancestor, or whatever that suits the more accurate answer, how many humans would there have been in my direct lineage?
And would it be almost the same for every human being currently living?

Closely related question: Initial population when i count backwards?

Note that when pedigrees collapse, there are not necessarily the same number of generations on each leg. So even for an individual there isn't a single number which is "the number of generations back to the last human/chimp common ancestor" since the number depends which route you take, although you could for example take the minimum. Consider for example Prince William (Windsor) whose parents were 7th cousins once removed (http://users.uniserve.com/~canyon/ancestor.htm) as well as other relationships. This isn't specifically aristocratic inbreeding, they're just better at keeping records :-)

@SteveJessop: I think when you only consider male ancestors, there's only one route, which bypasses that issue

@MooingDuck Whether you consider female ancestors or not is irrelevant if you are looking for a common ancestor, because the amount of time between each generation differs at each link in the chain.  Hence the "once removed" part can occur where these differences added up to a whole generation.

@Michael: Ah right.  I was pointing out that each person only has a single chain, thus pedigree collapse and "depends on which route you take" are incorrect.  However, you raise a good point that not all people's chains are the same length.

A quick back-of-the-envelope answer to the number of generations that have passed since the estimated human-chimp split would be to divide the the split, approximately 7 million years ago (Langergraber et al. 2012), by the human generation time. The human generation time can be tricky to estimate, but 20 years is often used. However, the average number is likely to be higher. Research has shown that the great apes (chimps, gorilla, orangutan) have generation times comparatble to humans, in the range of 18-29 years (Langergraber et al. 2012).
Using 7 million years and 20 years yields an estimated 350000 ancestral generations for each living human. A more conservative estimate, using an average generation time of 28, would result in 250000 generations. However, some have argued that the human-chimp split is closer to 13 million years old, which would mean that approximately 650000 generations have passed (using a generation time of 20 years).
The exact number of ancestral generations for each human will naturally differ a bit, and some populations might have higher or lower numbers on average due to chance events or historical reasons (colonizations patterns etc). However, due to the law of large numbers my guess would be that discrepancies are likely to have averaged out. In any case, the current estimates of the human-chimp split and average historical generation times are so uncertain, so that they will swamp any other effects when trying to calculate the number of ancestoral generations.
However, this is only answering the number of ancestral generations. The number of ancestors in your full pedigree is something completely different. Since every ancestor has 2 parents, the number of ancestors will grow exponentially. Theoretically, the full pedigree of ancestors can be calculated using:
$$N_\text{ancestors} = \sum_{i=1}^t 2^i \hspace{1em} \text{or} \hspace{1em} 2^{t+1}-2$$
where t is the number of generations. However, this will yield an unreasonably large number of ancestors (~$2.3*10^{105}$ over just 350 generations), since it assumes that all of your ancestors are unrelated. Basically, you run into something called pedigree collapse, which means that your pedigree will have many overlaps (due to inbreeding, overlapping generations etc), so all of your ancestors cannot be seen as unrelated. In practice, this means that the number of ancestors in successive generations will stop doubling for each generation you go back, and will eventually start shrinking, which will drastically reduce the number of unique ancestors. For more on this, see answers to the question Initial population when i count backwards?. That question is basically asking about the same issue, but less specifically. There might be studies that have tried to calculate the average number of ancestors to living humans, but I haven't seen any. Therefore, I cannot say anything more specific about the average number of unique ancestors for a living human individual.

This estimation is the number of generations, not ancestors. Ancestors should double after every generation, since a human has a father and a mother. Thus, the number of ancestors in 350000 generations should be 350000^2 = 122500 million humans. (Sorry, deleted previous comment for it being not really precise. My mistake there)

I have a question about this answer. I know the OP specified males, but... (if it were only male lineage) wouldn't it look more like a tree with the single trunk pointing to him, since he has two grandfathers, and they each have two grandfathers, so 2 + 4 + 8 + 16 + 32 + 64... for x generations of grandfathers?

@ederbf As I've added, I read the Q as asking for the number of "direct" ancestors. I agree that the full pedigree is something completely different, and have added a section on this, with a link to a related Q asking specifically about the full family tree.

@ederbf Doubeling in every generation is 2^350000, not 350000^2.  Exponetial, not polynomial.  So the actual number would have been about 10^115000 - Except for the pedigree collapse that fileunderwater describes.

@Taemyr, That is true. I rushed too much writing, editing and such...

Did a major rewrite of my answer, since I'm unclear about exactly what the poster is asking (full family tree, "direct" ancestors etc). This is not a full answer, but could work as a starting point.

I would argue that the total number of ancestors would vary significantly between people, due to your last point about how pedigree tend to overlap over time.  decreases in pedigree due to shared ancestors.  To give an extreme example imagine someone who's parent's were brother and sister.  They have only 2 grandparents instead of the standard 4, their total number of ancestors is in theory half that of someone produced from a non incesterous relationship.  That also implies people from areas with smaller breeding pools, like island nations, japan etc, would have fewer ancestors.

Everyone on earth shares a single most common recent ancestor around 3500 years ago (source), and given the vast depth of time between this ancestor and the human/chimp split it seems reasonable to assume that the number of ancestors derived via this route vastly outweighs all other ancestors so it makes sense to conclude that the difference in number of ancestors between people is a small proportion of the total number.
As for estimating how large that number is, I'm really not sure how you'd do it.

Are you claiming that two people from the native populations of Australia and South America share a common ancestor 3500 years ago?

@JackAidley: http://en.wikipedia.org/wiki/Most_recent_common_ancestor "the human MRCA may have lived 2,000 to 4,000 years ago. This estimate is based on a non-genetic, mathematical model that assumes random mating and does not take into account important aspects of human population substructure such as assortative mating and historical geographical constraints on interbreeding."

@MooingDuck: Perhaps you'd like to read the link I gave.

@Joe: It's not my claim. It's the number given in the primary literature source I linked to. Other estimates exist but even then they only push it back to around 8000 years ago, still a small period of time in comparison to the time since the human/chimp split.

The link you gave says almost exactly the same thing, that their model "ignores essential aspects of population substructure, such as ... the relative isolation of geographically separated groups."

@Joe: It's a model. Any model will be, by it's nature, limited. The limitations are discussed in the paper, as is there potential impacts on the resulting number.

@Joe: You misread the abstract.  "the random mating model ignores essential aspects like...geographically separated groups.  Here we show that recent common ancestors also emerge from two models incorporating substantial population substructure." http://www.nature.com/nature/journal/v431/n7008/fig_tab/nature02842_ft.html shows that they do indeed take into account geographic seperation and migration.

Another factor not mentioned is that the number of generations will be a range even when accurately calculated for one individual. If, for example, my dad's dad's dad's etc generation was 25 years on average and my mum's mum's mum's etc generation was 20 years then you don't have to go back very far to have for them to be different. In the example 100 years ago in my dad's side is 4 generations and on my mum's side it's 5 generations.

We could try to cut the answer out:

the Population Reference Bureau estimates that about 107 billion
people have ever lived
today's population is about 7.6 billion
only 0-14 of them which are in your direct linage (parents up to grand-grand parents) are alive
world population of year 1500, when exponential growth started, is estimated to about 425 million
(https://www.wolframalpha.com/input/?i=world+population+1500). This
is about 25 generations ago. Almost all of them are not your
ancestors (by integration you should get a number of about 20 billion
people which are NOT your ancestors, while about 500.000 are)
world population 8000 b.c. is estimated to about 5 million, and 10000 b.c. to about 1 million.
majority of people before 10000 b.c. might be your ancestors. This could well be more than 10 billion people (much insecurity and definition problems here)

.. which means, we "only" need an estimation of 10000 b.c. to 1500 a.c. After playing around with Excel, I believe, it should be in the ballpark of 1 billion.
hence my best estimate would be 11 billion (10 billion before 10000 b.c. and 1 billion after).

mixed people should have more ancestors. My bet is that Children of mixed Mexicans and Chinese have most ancestors.

at some point back in history, more than 2 children on average (per parent couple) go into your ancestor tree. This is why additions shrink further back in time.

billions of people died throughout mankind history without having siblings living today.

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DNA from Egyptian Mummies Evolution vs Human of Today
Comment: I ask my biological questions from the point of view of mathematical proportions. I am not a biologist.
Are there significant differences in DNA from Egyptian Mummies vs. those available from humans today (5K years aprox)?
Related to this question, I found this answer https://biology.stackexchange.com/a/20301/13003, but just because of lactase tolerance it takes around 7K years!!! which for me is very slow! (without taking into consideration that tolerance probably is only adaptation or this change is detectable at DNA level?)
To get back to Homo Sapiens (300K years) we would have to revert in 60 (300K/5K) similar time ratios.
I found this question Are there differences in DNA between humans of today and humans from 2000 years ago?
Obviously the changes are not homogeneous, perhaps some occurred faster than others, however, the fact that such changes have not been detected in 5K years exerts pressure for the changes to occur almost immediately; that is to say, the Homo Sapiens species appears and immediately there must be changes at the DNA level.
Not only the immediacy of the change, but also the amount of accumulated changes between Homo Sapiens and modern man (ie, simultaneous DNA changes between a subject and his great-great-grandparents).
If changes in climate, environment and food are determining factors, it implies an instability of the DNA (few generations to present a change).
Personally, the fact that no change in DNA has been found for at least 5K years casts doubt on whether we came from Homo Sapiens.
Same calculation could be derived from Homo Sapiens. 66M years after the destruction of the meteorite. 300K years for changes in the DNA of Homo Sapiens and the Human of Today. That produces 220 time ratios (66M/300K).
Comment: I personally think we would need more time ratios to get from a species after the destruction of the Meteorite to Homo Sapiens 300K years ago
What other considerations should I take into account for a more biologically appropriate analysis?

For this to be an answerable and appropriate question on this site you would need to: 1) define what you mean by "significant", 2) make this clearly focused on a single question, 3) remove nonsensical statements like "Personally, the fact that no change in DNA has been found for at least 5K years casts doubt on whether we came from Homo Sapiens.", and 4) provide a clear explanation of any of the numerous assertions you've made that you think are essential to your question. Please take the [tour] and consult the [help] starting with [ask] for details.

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Biological basis of the science fiction story "The Dipteroid phenomenon"
The science fiction novelette by Poul Anderson The Dipteroid Phenomenon describes a plot in which

 the protagonist Evalyth is one of the members of a space-faring civilisation which is rediscovering atavistic humans stranded on other planets following the fall of human civilisation from an interplanetary war in the past.

The husband of the protagonist is murdered and cannibalised by the savage guiding him through the jungle, and she finds and captures the savage's whole family in revenge, intending to execute the savage. While doing so, she discovers that all of the humans on the planet, including the civilised city-dwellers, have a tradition of cannibalising humans. The savages hunt each other for cannibalism, while the city-dwellers hunt down the savages, which they then keep as slaves for consumption.

In the end of the story, it is revealed that:

 all of the male humans on the planet are unable to sexually mature normally due to a genetic mutation in their Y-chromosome, which results in them having to consume male genitals in order to reach sexual maturity.

The novel then further states that the phenomenon of having to consume males in order to mature is also found in terrestrial Diptera flies.

'Hence a dipteroid phenomenon may have appeared in man on this planet. Such a thing is unknown
  among higher animals elsewhere, but it is conceivable. A modification of the Y chromosome would
  produce it. The test for that modification, and thus the test of the hypothesis, is easily made.'
  The voice stopped. Evalyth heard the blood slugging in her veins. 'What are you talking about?'
  "The phenomenon is found among lower animals on lower worlds,' the computer told her. 'It is
  uncommon and so is not widely known. The name derives from the Diptera, a type of dung fly on Old
  Earth.'

Is this "dipteroid phenomenon" a real biological phenomenon observed in Diptera dung flies on Earth? I was unable to find a scientific paper describing this rather interesting phenomenon.

After some research, it appears that the phenomenon being discussed was the consumption of Diptera flies by the dung fly, Scatophaga stercoraria. This paper describes their inability to sexually mature without consuming prey (for which Musca domestica flies were provided).

Male  Scatophaga  stercoraria must prey on other Diptera before they
  display sexual behavior, develop  the  accessory cells  of  their  ejaculatory ducts, and
  achieve  full elongation of  the testes. The corpus allatum also becomes enlarged
  after predation and is  necessary for  the onset of sexual behavior and development
  of reproductive organs. The complex diet consumed  during predation apparently
  cactivates the corpus allatum, and the hormone released acts  independently on
  organ growth and sexual behavior.

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Why do PCR manufacturers recommend assembling the reaction mix on ice?
Many PCR manufacturers recommend preparing the reaction mix for the reaction on ice. For example, here is NEB's recommendation for their Q5 polymerase. Other manufacturers also include similar steps:

We recommend assembling all reaction components on ice and quickly
  transferring the reactions to a thermocycler preheated to the
  denaturation temperature (98°C).

However, I can't think of a good rationale for this. This ResearchGate thread describes a few reasons, but they don't seem to make much sense.
Primer mispriming onto bacterial gDNA - Highly unlikely, since the initial melting step would melt away these misprimed primers and allow them to prime the correct sites.
Polymerase is proofreading (3'-5' exonuclease) - Proofreading activity should not affect any of the components, since the primer oligos are present in very large quantities, and the template should not be significantly affected by any proofreading, since they already have the correct sequence.
RNA is degraded by the polymerase - An extremely ridiculous answer, since PCR does not use RNA as a template, and RT-qPCR uses reverse-transcribed cDNA as the template. Whether the RNA is stable or not has no bearing on the activity of a DNA-only PCR once the RNA has been reverse-transcribed.
Polymerase is thermolabile - This is probably the most ridiculous answer to the question. The whole point of using polymerases like Taq, Pfu and Q5 is that they are from thermophile organisms, and they are highly thermostable to withstand the high temperatures during PCR.
What, then, is the reason PCR reactions are recommended to be assembled on ice?

As I was told as an undergrad, polymerase is thermostable but it could also activate on room temperature. As you are carefully going to cycle between temperatures, you don't want the reaction to start early on room temperature.

Actually I do not care the temp much. But, primer mispriming could happen, that's why hot start method is developed. Polymerase is proofreading (3'-5' exonuclease) can disturb your PCR. Primers are excess as you mention, but truncated primers may miss-anneal to unexpected regions and once PCR reactions occur in these regions, primers anneal, 3'-5' exonuclease adjust the sequences and PCR reactions occur again. In addition, having various length of primers in a reaction tube is not good in general.

I agree with skymingen but Taq's activity at RT is low. However all this may matter much only for real-time PCR. As with primer mispriming- all misprimed primers would dissociate during the heating annealing step. IMO, keeping in ice is just a long followed lab practice and it is better making mix at RT if you are not fast enough.


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Do plants produce any heat?
Many plants (e.g. roses, palms) can be protected from frost during the winter if shielded with an appropriate coat that can be bought in garden shops. Do plants produce any heat that can be kept inside with these "clothes"?

Some produce quite a lot, like Skunk Cabbage and the Voodoo Lily. The latter can even sustain temperatures over 15 degrees celsius above its surroundings. This is a fairly good article on exothermic plants

The senator tree in Florida produced heat. It burned to the ground from internal combustion.

Cellular respiration in plants is slightly different than in other eukaryotes because the electron transport chain contains an additional enzyme called Alternative Oxidase (AOX). AOX takes some electrons out of the pathway prematurely - basically the energy is used to generate heat instead of ATP.
The exact purpose of AOX in plants is still unclear. Plants will make more AOX in response to cold, wounding, and oxidative stress. We know of at least one plant (skunk cabbage) that exploits this pathway to generate enough heat to melt snow. This link gives a pretty good overview.

(AOX is dear to my heart, since my first 3 years working in a laboratory were spent studying this gene <3)

This is interesting @Amy. Why do you say that the exact purpose of AOX is unclear? Do you mean it is unclear what AOX does, or it is unclear why it does it?

@Amy The melting snow part is really fascinating, +1

@poshpaws what AOX does is pretty well understood, but the "why" isn't completely clear. When the electron transport chain converts energy into heat, it's "lost" rather than doing something useful - making ATP. It may be because since plants can't run away from their problems (temperature, wounding from bugs, and other things that lead to reactive oxygen species) they need an additional way to deal with oxidative stress that other organisms never developed.

I always thought the purpose of AOX (apart from heating) was as an electron sink to help decrease photoinhibition, in the same way that photorespiration is.

Plants will be respiring continuously, which is an exothermic process. Therefore the plants will be producing a small amount of heat. The protection from frost may be more a result of the vastly smaller convection current of the coat compared to the atmosphere rather than by reducing any conduction away of heat produced by the plant, however.
Keeping the plant out of the wind by 'dressing it' will reduce the rate of transpiration when the stomata are open.  I would very tentatively suggest that, as water has a very high specific heat capacity, having a greater volume of water within the plant would help to retain any heat that was produced by respiration.  However this is entirely speculation on my part.

Snow is also a good insulator, and these "coats" may mirror that effect. See here for some measurements of the temperature difference: http://snailstales.blogspot.com/2010/02/temperature-under-snow-part-3.html

Some plants have mitochondrial pathways that produce heat. That's why skunk cabbage can be seen poking outing of the snow in late winter/early spring. Here's a review:  http://onlinelibrary.wiley.com/doi/10.1111/j.1744-7909.2010.01004.x/pdf

These and other plants make use of the cyanide-resistant pathway. This is a short-cut in the electron transport chain that allows the plant to produce extra heat at the expense of not using those electrons to manufacture ATP. (It is called the cyanide-resistant pathway because it provides an alternate pathway for the electrons to take. Rather than killing the cell quickly via free-radical production, it is slowly starved via lack of ATP.)

Yes, respiration is exothermic and plants (like all living things) respire.
I think the effect of covering the plant has to more to do with reducing sensible heat loss , e.g. direct transfer of heat from plant to air) rather than latent heat loss (through evaporation).
The cover is effectively reducing the mixing of the air near the plant (and closer to the temperature of the surface of the earth) with the free atmosphere (closer to the temperature reported by the weatherman)


text:
How fast animals habituate to wearing shoes
You probably have seen hilarious videos of dogs wearing shoes for the first time. Animals usually very uncomfortable and try to "shake it off", as they seem to consider shoes be some sort of sticky dirt.
I could only find short clips of dogs wearing shoes for the first time, but I would like to know, how fast dogs, or other animals, will learn that shoes are an integral part of their feet and continue with normal stride?

From AllDogBoots, it seems that teaching dog to walk in shoes will take up to 4 days and a lot of treats.

It probably is the same as making you wear socks full of dry peas and walking, added with dog reasoning whereby they don't know if they will be able to get the socks off. If you put some floppy socks on a yanomami/ a forest tribesperson, so they can walk in the forst with socks, they would take 4 days to get used to it too.


text:
What is the difference between sequence, reads, and contigs of genetic material?
Can someone explain the differences between sequence, reads, and contigs of genetic material such as DNA, if possible with an example?
I am new to bioinformatics, and I have not found any conclusive answers for all these concepts on the web.

Welcome to Biology! Is this question with regard to a specific research area such as DNA?

yes, I think so. Regard to DNA, DNA sequence

My understanding of those three words as follows:

sequence is a generic name describing order of biological letters (DNA/RNA or amino acids). Both contigs and reads are DNA/RNA or aa sequences
reads are just a short hand for sequenced reads. Usually sequenced reads refer to somewhat digital information obtained from the sequencing machine (for example Illumina MySeq) and stored in the fastq file with quality scores per base. Reads are usually short. However "short" changes rapidly. Right now MySeq produces reads anywhere between 50-150 base pairs long (bp). From a single run (it will really depends on the run) you can get millions of reads, where each read will be set bp size e.g 100bp long. All reads are stored in a single fastq file per replicate, where all reads in that file are usually of uniform size e.g all 5 million reads are 100bp long.

As a bioinformatician your first job is to identify where about those reads come from. Depending on the experimental goal and on what sort of sequencing you were doing e.g DNA-seq or RNA-seq you may or may not encounter contigs.

contigs are simply reads that have been assembled together. For example if you are doing de novo transcriptomics. Then you would:

purify your transcript from a tissue and send it off for sequencing
get your fastq files with sequenced reads, that are all short reads
(e.g 100 bp)
assemble those 100bp reads into a longer contig that hopefully will resemble your individual transcript

@vvilp no probs. as an aside here is a cool pdf I found somewhere on internet http://helix.biology.mcmaster.ca/3S03.pdf. it might help you with your bioinformatics learning

I have taken a look at PDF. Nice tutorial! Thank you

@vvilp I'm glad it helped. by the way here is the link http://biology.stackexchange.com/questions/31546/book-source-for-learning-bioinformatics-focused-on-genomics where I found that pdf file. There might be some more useful info for your bioinfo

I'm going to say the same thing as @Serine but in a slightly different context. Let's take an example where you want to compare smoking persons against non-smokers.
In this context, you'd want to take a DNA sequence of smoking persons.  However, due to technology limitation you won't get a single DNA sequence from the sequencing machine. You'll get millions of short overlapping DNA sequences known as reads.
We need an assembler to "map" the reads and compare them with a reference genome. In this example, the reference genome could have been the human HG38.
The assembler would need to merge the overlapping-reads into a set of non-overalapping regions, known as contigs.

Usual aligners do not assemble reads.

Sorry, I meant mapping.

Thank you Student T. Now I know the mainly difference between reads and contigs


text:
Aloe species identification
I am trying to find out which species these are.  Someone claimed they were Aloe Vera, but I am skeptical as I have never seen Aloe Vera with that kind of growth. These look more like Aloe Juvenna to me.
What do you think?

Definitely not Aloe vera.

Try here: http://www.succulentguide.com/cactus/?genus=Aloe

Also please update if they decide to flower :)


text:
Do non-enzyme catalysed reaction pathways exist?
Can their be a kind of chemical reaction pathway in a cell, that is catalyzed or regulated but NOT necessarily by enzymes? I could not find anything on Google.
I have almost no background in biology, and am only studying certain topics from a mathematical perspective.

If by enzyme you mean "protein" aka polypeptide, than there are such things as catalitic RNAs. Those are molecules of RNA that facilitate chemical reactions but don't change themselves (definition of catalyst). I think that, based on the discovery of such RNAs, it is now believed that life might have started from or with the help of catalytic RNAs (please forgive the speculative tone, see self-replicating RNAs).
You might find this article interesting: The Road to Non-Enzymatic Molecular Networks, which describes non-enzymatic networks. The problem with searching this topic is that most current publications, seem to me, to concentrate on way to transfer enzymatic reactions into inorganic catalysis systems--because those systems can be more clean and easy to expand--than purifying enzymes for biotech.

This should rather be a comment than a full answer in my opinion. You make good points, but i think this needs to be elaborated.

in what way? also, RNAs are only example of pure non-protein catalysts I can think of. Others involve coenzymes, e.g. vitamins while they are part of proteins. There is not much surface metal catalysis in cellular biology (Pt)

Well, in my mind I was thinking of enzymes which help in metabolism, regulate intracellular reactions and such..

@aandreev - In a way that you describe what catalitc RNAs or ribozymes are, how do they work, what reactions do they play roles in. Also some peer-reviewed article on the topic would be nice. I too use wikipedia as source for explaining basic things in my answers but for the main topic I think peer reviewed literature is more suitable.

@jablesauce Well, that is not very common, after all cellular biology is protein-centered. I wish someone with more insight will answer.

The article you linked is is non-free and might not provide much help as I think it is inaccessible to most users. Also posting google scholar search results does not show too much effort.

@poka.nandor I try to avoid answering in comments, even if there might no be much to say on topic. But I think that ribozymes are too googleable to expand on definitions/functions. In it I follow this meta@bio discussion: http://meta.biology.stackexchange.com/questions/552/comments-with-answers

That is fine, but then take time and put effort in it to be nice elaborate answer. It's better for everyone.

-1 for not putting real effort in answering the question.


text:
Why do genes with closely related functions often reside on different chromosomes?
Why do genes with closely related products are so often positioned on different chromosomes?
To illustrate what I mean, here is an example from immunology:

the invariant region of MHC is on chromosome 5
the variant region of MHC is on chromosome 6
β2-microglobulin is on chromosome 15

These three gene products associate into a single protein-complex to present antigens. Why are these genes situated on different chromosomes? Wouldn't it make more sense to keep them associated into a localized region onto a single chromosome so that their transcription can be jointly regulated?
It is just an example; I get the impression that many multiprotein complexes are formed with products from different chromosomes.

I don't understand your question - you mean why associated gene products are located on different chromosomes?

probably, because it creates more variability, through random mutations and crosses you can enhance parts of same pathway independently. Chromosomes are mixed up during sexual reproduction as an additional mechanism of variability (together with crossing-over) during meiosis.

@AliceD Yes. Please edit my question if you think it needs clarification! My English is far from perfect.

Perhaps something like this?

Simply because it can (happen). Natural selection does not yield processes that are designed because there are no designers involved. Barring non-terrestrial involvement (cf. the pan-spermian hypothesis), as Stephen Jay Gould was fond of pointing out, natural selection can only work on what has come before. In other words, the raw material consists of what is currently available (for better or worse). All that matters is having more offspring than other individuals have in the next generation. That is what gets selected. It doesn't matter what we think about comparative efficiency.

The thing we must remember is that during evolution, there occurs many events that may result in genomic reshuffling.
Considering your example of MHC, when we look into the evolution of the complexes

The classical human MHC contains 224 genes, .... Antibody and T cell mediated immune responses against invading pathogens are initiated through MHC class I and class II molecules. These main components are not only missing from invertebrates, but are also not present in primitive jawless fish, such as hagfish and lamprey. MHC class I and II molecules do, however, exist in all jawed vertebrates, including the cartilaginous fish.

Now that tells us something in itself. If you observe the universal evolutionary tree, we can conclude that the hagfish and lamprey are most ancestral, especially compared to telostii. This is crucial when speaking in terms of evolution, as

this demonstrates that the separation of the MHC class I and class II loci is characteristic of teleost fish, which represent half of all vertebrates. Since the genes of the immune system were present in the common ancestor of tetrapods and teleosts, the differences in their genomic organisation may be the result of lineage-specific chromosomal events such as duplications, inversions, deletions and translocations.

You can read more about the MHCs here:
Sambrook, Jennifer G., Felipe Figueroa, and Stephan Beck. "A genome-wide survey of Major Histocompatibility Complex (MHC) genes and their paralogues in zebrafish." BMC genomics 6.1 (2005): 152.
And thats usually the reason for the major changes you see. Often other changes occur, due to transposons, which cause pseudogenes to form and/or neofunctionaliation to occur. You can read about them here:
Feschotte, Cédric, and Ellen J. Pritham. "DNA transposons and the evolution of eukaryotic genomes." Annual review of genetics 41 (2007): 331.
I am fairly certain, that this applies practically to majority of the genes, that are not linked strongly genetically (http://learn.genetics.utah.edu/content/pigeons/geneticlinkage/).

Can you give me some link about how this duplications, inversions, deletions and translocations affect the regulation of such genes? Are they activated by the same stimulus? I guess so, because they are duplicates at the beginning of separation.

Would you prefer me to answer here or in a different question? as you are asking more about functional divergence, and the evolutionary fate of diverged genes, and in the original question here you asked about linkage and genome wide chromosomal events

If you think it does worth a new question, then ofc. I can write a new one.

@inf3rno its upto you really. You can look up subfunctionalisation here (http://en.wikipedia.org/wiki/Subfunctionalization)

Thx, I'll read about it.


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Why humans didn't evolve to safely consume rotten food?
I'm not a biology person at all so please forgive me if my question is silly.
I was just wondering that why didn't evolution cause us to digest, without issues  decomposed food?

What evolutionary advantage would that give us? "Rotten" by definition means that some or all of the usable nutrients have decomposed, so what is the point?

Well imo animals eat half decomposed things.

I understand that is what spices were originally used for ; to mask bad flavors in food that is "turning" ( bad).

There's really no "why" answer here, any more than you can say "why" cows eat grass, or blue whales eat krill.  Evolution doesn't have a purpose or goal.  The only answer is "because our ancestors survived without eating rotten food".

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4519257/ it doesnt give us a significant survival advantage... food rots very fast in some climates, but while fruit and leaves are alive, the are very abundant.

You could argue that we have the ability to eat certain "rotten" foods, those that have fermented.

Yes, there are animals called carrion eaters that will preferentially consume rotting food, because they have either enzymes or commensal microbiota that aid in digesting it and obtaining energy/nutrients from it. However, we and most other animals don't have that ability because of biochemical trade-offs.

@Bryan Krause: Then there's cheese.  Or various sauces made from rotten fish, from Roman garum & liquamen to southeast Asian things like the Vietnamese nuoc mam.

@jamesqf I believe those are also fermented (besides cheese).

Food is considered "rotten" when it has a large population of micororganisms like bacteria and fungus eating it. Some of these microorganisms have evolved to produce toxins that harm animals that would otherwise eat the food. Animals could evolve to tolerate these toxins, and some have. However, bacteria have a large advantage over animals in an evolutionary arms race due to their short generation time and large population number. So competing with bacteria over carrion is a specialized niche, avoiding it has been selected for in most animal lineages.


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Why are the bodies of the Risso's dolphin covered in scratches?
Risso's dolphin in wild population seem to obtain scratches with aging. What is causing them and what do they mean?

[ From Jefferson et al. 2015, Marine Mammals of the World, 2nd edition, p 212: "At sea, the best identification characteristic is the coloration and scarring. Adult Risso's dolphins range from dark gray to nearly white, but are typically covered with white scratches, spots, and blotches. Many of these are thought to result from the beacks and suckers of squid, their major prey, but others may be caused by the teeth of other Risso's dolphins. If fact, this species is the most heavily-scarred of all the dolphins." ]

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support for your claims. Unsupported posts come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!

Although little is known about these animals, they seem to obtain these scars from scratching in fights with their prey, giant squid, and from the teeth of other Risso's dolphin.
https://uk.whales.org/species-guide/rissos-dolphin

Most of the linear scars are thought to be caused by intraspecific interactions, e.g. scratches from each others teeth, though some more circular or oval scars are thought to come from squid.  Cookie cutter scars are not commonly described for Risso's dolphins though they are common in other whales and dolphins.
Encyclopedia of Marine Mammals.  2002. W.F. Perrin, B. Wursig, J.G.M Thewissin.  Academic Press: New York.

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support for your claims. Unsupported posts come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!

As others have said, most of these marks come from intraspecies interactions. However, what makes Risso's different is that they more or less keep their marks for a long period of time.
For example, here is a blog from Morigenos (Slovenian Marine Mammal society) explaining how they use rake marks to help them identify different bottlenose dolphins from year to year. That the marks can fade or change as new marks are added.  Noting these scars is a common tactic when using photo-identification to mark individuals when studying a dolphin population. However, because rake marks and other scaring can fade, it is far more common to use the back edge of the dorsal fin to identify different individuals (Clabby, American Scientist).
Risso's dolphins, however, loose pigmentation in their skin while their wounds are healing (MacLeod, 1998), meaning that their scars last for a longer time period. So much so, that individuals within a population can be recognized up to 3 years based on their scars alone (Mariani et al.,2016).
Why is this? Likely due to male on male competition. Younger Risso's have a faster scar recovery rate, indicating that the more scars you have, the beefier you are and the more combats you have survived, making you a better mate. However, the skin pigmentation alteration is present in both females and males.
The Mariani paper really does a great job of summarizing what is known about Risso's dolphin marks, and how long they last.  It's freely available online, so it is 100% worth the read.
Monica Mariani, Angelo Miragliuolo, Barbara Mussi, Giovanni F. Russo, Giandomenico Ardizzone, Daniela S. Pace, Analysis of the natural markings of Risso’s dolphins (Grampus griseus) in the central Mediterranean Sea, Journal of Mammalogy, Volume 97, Issue 6, 5 December 2016, Pages 1512–1524, https://doi.org/10.1093/jmammal/gyw109


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Alder Tree Root Nodule Origins?
I recently found out that alder trees have root nodules which contain nitrogen-fixing bacteria and that alders are primary colonizers in primary succession. That leads me to this question: since there are really no fungi in the soil and since the alder is a colonizing species, where does the fungi come from? Or is my assumption that there are no fungi in the soil incorrect?

Welcome to Biology S.E.! If you need any assistance, please visit The Help Center.

Where did you hear that alder trees are primary colonizers? Primary colonizers tend to be organisms such as mosses and bryophytes. I don't know for sure, but I would be willing to bet good money that the fungi make it there long before the alder trees do

Any soil microbiology textbook will tell you that there are a great number of fungi in most soils. I believe there are 12 or 13 species of non-legumes capable of fixing atmospheric nitrogen. Podocarpus is one of them. Look at the roots of podocarpus and you will see nodules all along the roots.


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Surface Power Density of Fluorescing Reaction
I am looking to find out what is the ballpark power density of a fluorescing PCR reaction using a SYBR Green or Taq Man dye might be. Is it on the order of $E_e=1mW/cm^2$, less or more? Any help of data would be useful.

shouldn't amount of light you detect depend on the excitation power? and total volume, and geometry of reaction volume?...

@aandreev Yes it would, I'm sure things like the amounts of reactants would also play into this. With that said, is there any ballpark for any currently used devices on the market?


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What is the reasoning behind the Drake Equation?
I've read a bunch on how the Drake Equation is constructed, but I'm not able to understand some of the reasoning behind it.
$$
N = R_* \cdot f_p \cdot n_e \cdot f_l \cdot f_i \cdot f_c \cdot L \cdot f_d
$$
Why does $f_c$ represent the fraction of intelligent life able to communicate? Isn't communication (in some form) part of what defines intelligent life itself? Or is this term included just to break the number down further?
I'm asking this here and not elsewhere because I'm wondering specifically about this term and not the entire equation.

Geez this so called "equation" is about us being able to get signal from them - fc is for telecommunication, not speech.

This question is not off topic because it is about astrobiology.

The second half of that sentence on Wikipedia says it all: "the fraction of these civilizations that have developed communications, fc, i.e., technologies that release detectable signs into space"

Humanity has had roughly the same level of intelligence for tens of thousands of years, and as the Drake Equation estimates the number of civilizations capable of extrasolar communication - we only met that criteria ourselves within the last century.


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Reason behind using inducible promoter for heterologous expression
Protocols often seem to use regulatable promoters when expressing a heterologous gene in a host like yeast where they add something like IPTG to induce expression from (say) the lac promoter.
Is there a reason to do this as opposed to using a constitutive promoter? i.e. Is there reason to think that regulatable (inducible) promoters have higher expression levels than constitutive promoters?
In other words, what utility is there in having an external "switch", i.e. the IPTG to turn on expression on-demand rather than just boost the default expression level using a promoter not requiring induction?
The goal here is small biomolecule synthesis by industrial fermentation of a transgenic yeast.
Example Protocol:
L21 Star™ (DE3) E. coli cells (Invitrogen) were co-transformed with the plasmids pACYCDuet-4506 and Ct94-pETDuet and transformed cells were selected on carbenicillin (50 μg/ml) chloramphenicol (34 μg/ml) LB-agarose plates. Single colonies were used to inoculate 5 mL LB medium with 50 μg/ml carbenicilin and 34 μg/ml chloramphenicol. The culture was incubated overnight at 37° C. The next day 2 mL of TB medium supplemented with the same antibiotics were inoculated with 0.2 mL of the overnight culture. After 6 hours incubation at 37° C., the culture was cooled down to 28° C. and 1 mM IPTG, 2 mg/mL mevalonate (prepared by dissolving mevalonolactone (Sigma) in 0.5N NaOH at a concentration of 1 g/mL and incubating the solution for 30 minutes at 37° C.) and 0.2 mL decane were added to each tube. The cultures were incubated for 48 hours at 28° C. The cultures were then extracted twice with 2 volumes of ethyl acetate, the organic phase was concentrated to 500 μL and analyzed by GC-MS as described above in Example 3. In these conditions sesquiterpene production above 200 mg/L was routinely achieved. Beta-santalene was produced.

This sounds an awful lot like a homework or quiz question. As such you need to show your effort to answer the question. Please refer to Biology S.E help center for information and policies on asking questions on the site. These links, http://biology.stackexchange.com/help/how-to-ask , http://biology.stackexchange.com/help/on-topic , and http://biology.stackexchange.com/help/dont-ask are particularly helpful.

@AMR I'm not sure why you think this is a Homework question & I'm also not sure how to convince you that it is not. In any case, if it helps I am working on a feasibility study to industrially manufacture a 250 MW secondary metabolite which is currently only available as a plant extract. The wild type gene responsible has been sequenced. The native expression is low, <50 mg/L mostly because of bottlenecks in making FPP the precursor & FPP-sinks via Squalene.

Inducible promotors are a useful tool especially in experiments where the inserted/altered gene may needs to be suppressed at first. Consider an experiment where one wishes to investigate a putative Alzheimer-inducing gene in a model of old age. When you insert the exogeneous/altered gene, you may wish to suppress expression up until the point where your animals reach a sufficiently old age to mimick geriatric patients developing Alzheimer symptoms. Another example is where one uses genes that are lethal or induce gross developmental changes in utero when expressed during development.

@Christiaan Makes sense. I was just wondering about my industrial fermentation use-case where all I want to do is maximize the yield of a secondary metabolite.

Heterologous promoters often express genes that are toxic to the organism when expressed in too high quantities. When the genes are expressed constitutively, the organism will either grow slowly or die before they reach a high density suitable for production of the protein.
As such, it is not about expressing the genes all the time, but expressing the maximum amount of gene product over the shortest period of time. It doesn't make sense for the cells to express the gene product all the time, if they can't reach sufficient densities first. More product will be made if the cells are allowed to grow to a relatively high density, then inducing expression on all of them. This would allow relatively large production levels in a short period of time.

Perfect! This explanation makes a lot of sense. This is exactly the part I was missing in my understanding. This totally justifies using induction.


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Stop codons and exons?
If we had a hypotheical gene called gene exampleGene and this gene had 5 exons, labeled A, B, C, D, and E in that order on the chromosome, could it be the case that the stop codon for this gene be on exon D and the exon E still being a exon that would be transcribed in? I can not see this to be true, since If I  remember correctly, transcription stops BEFORE the stop codon, and when stopped, the pre-mRNA is then further processed, but everything after that stop would not be a part of the exampleGene ?
My lazy diagram of how I think of the supposed exampleGene to be:
---A-----B---C---------D(stop codon)-------E---
After transcription via RNA polymerase:
A-----B---C---------D

Take a look at this schematic of a mature mRNA.

[source]
The coding region (ie the part that is translated) is between the start and stop codons, but the 5' and 3' untranslated regions (UTRs) are also transcribed by RNA polymerase; these are part of the first and last exons, respectively. The transcription start site is labelled right in front of the 5' UTR. For the purpose of this answer, transcription termination can be said to occur at the poly(A) signal (the poly(A) tail is added post-transcriptionally, as is the 5' cap).
To be clear, the point I'm hopefully making is that transcription does not involve codons. RNA polymerase does not stop at the stop codon nor does it start at the start codon. In fact, it doesn't even "know" what codons are.

Thank you, this makes alot more sense now, but when you say RNA polymerase does not "stop at the stop codon" , could you detail that more?  What I do not get is how RNA polymerase is initiated then. From what i remember various protein complexes initiate it, and then I assume various protein complexes end it.

@RoSiv In eukaryotes, the mechanism behind transcription termination is somewhat unclear. After the poly(A) sequence (AAUAAA) is transcribed, proteins recognize it and cleave the mRNA, after which it is polyadenylated. However, RNA polymerase continues to transcribe past the signal sequence. It is thought that, after cleavage,  either RNAP is modified to become less processive and eventually falls off or an exonuclease begins degrading the second RNA until it catches up to RNAP and pulls the transcript out.

You mix up translation and transcription. Transcription creates mRNA from DNA template. Transcription also includes splicing, that is excision of introns so that mature mRNA contains only exons. In your example it goes like that:
DNA (chromosome): ---A----B--...--Dstop---E---
premature mRNA: A----B---...---Dstop--E---polyA
mature mRNA: AB..DstopE-polyA
Translation is the creation of polypeptide from template mature mRNA.
If codons in exon A correspond to polypeptide sequence a and so on for other exons, your polypeptide translated from mature mRNA will look something like that:
$NH_2$-ab..d-$COOH$
Stop codon stops translation. mRNA might still contain a lot of information after the stop codon, for example, for targeting mRNA to compartment of the cell (e.g. presynaptic site).

@anndreev       Yea i made a typo but will leave it in so your post is in context, thank you. But What I dont understand is for the E exon, how is that transcribed? Is that not the role of RNA polyemerase, to transcribe until it hits the point before a stop codon? How then, would that E be included into the premature mRNA, when it would be past the stop codon? And also, my chemistry is poor, but the NH2 would be the amino group, and the COOH  the carboxyl  group, which generlizes the form of a long polypeptide chain right?

proteins are produces by ribosome from N to C end (yes, one is amino-, other is carboxyl-terminus); 2) RNA polymerase stops at the terminator sequence, it has nothing to do with codons, some RNAs are not even coding a protein! 3) Since exon E is before terminator, it will be processed via RNA polymerase. As I said, RNA after stop codon might be very useful for e.g. localization


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Question about epinephrine
In my class we were told that adrenaline (or epinephrine) causes vasoconstriction.
My question was I had always thought that people took this via an EpiPen when they were having an allergic reaction.
So I thought it would make sense, that it would dilate vessels, because this will allow more air through. Or does the constriction help because it tightens the vessels in the throat allowing a reduction of swelling?

An allergic reaction requiring an epipen can be caused by swelling in the throat and/or bronchoconstriction (spasms decreasing the diameter of bronchioles). Bronchoconstriction can occur in the absence of soft tissue swelling in the lips, tongue and throat, and vs. versa.
Epinephrine reduces pharyngeal edema (swelling) because it is a potent vasoconstrictor in small arterioles and precapillary sphincters in most body organ systems. This is effected through alpha-1 adrenergic receptor activation. While the blood pressure and heart rate increase (due to beta-1 adrenergic effects), the permeability at the capillary level is decreased, relieving swelling.
At the same time, epinephrine relaxes bronchial muscle. It has a powerful bronchodilator action when bronchial muscle is contracted because it is a powerful beta2 adrenergic agonist.
Finally, epinephrine inhibits antigen-induced release of inflammatory mediators from mast cells, and to a lesser extent from diminution of bronchial secretions and congestion within the mucosa. Inhibition of mast cell secretion is mediated by beta2 adrenergic receptors.

Adapted from Simons. Kemp et al. World Allergy Organization Journal 2008 1(Suppl 2):S18-S26   doi:10.1186/1939-4551-1-S2-S18
Epinephrine: The Drug of Choice for Anaphylaxis--A Statement of the World Allergy Organization


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Why did the Brain develop in the front in most organisms?
I was wondering: why most, well, pretty much all organism with a brain have it right in front of their bodies or at the top.

I believe the general argument goes like this: it's expected that the sense organs appear toward the anterior end of the organism (you want to see, smell, hear what's in front of you). For the ease and efficiency of processing inputs, it makes sense that nerve bundles appear close the sense organs. These nerve bundles eventually became brains.

I agree with @p.s.w.g.

@p.s.w.g - while your explanation makes sense, it doesn't hold true, especially in insects (butterflies 'taste' with their feet, etc.). It does hold true for eyes, though. Optic lobes are a large part of insect brains. Interesting to contemplate.

@anongoodnurse - humans feel touch, heat and pain in their limbs. Fact stands that neuronal cell bodies congregate in the anterior parts in humans and insects alike. I think that's the PO's question - why is the brain (i.e., ganglions in insects) situated in the head region?

The wiki article on cephalization may help.

everyone is talking about eyes and ignoring the mouth :0

I was wondering: why most, well, pretty much all organism with a brain have it right in front of their bodies or at the top.

I believe you're confounding origins. Complex brains -- like those in us and other mammals -- are situated in the position that has been the best-protected over millions of years of evolution.
Evolution did not decide where the front of the animal should be and then put the brain there. Rather, evolutionary pressures resulted in the brain being an excellent survival tool, and the species that could protect it best kept its benefits. It just so happened that, since complex brains require an enormous amount of resources and are quite fragile, wherever the organism could best protect the brain became its "front".
In mammals that became a skull. In some insects it's in the thorax or abdomen. In sea slugs... well, there really isn't a complex brain in sea-slugs... so the difference between their front-end and back-end is pretty minimal. Same with worms and other very simple creatures.
So think of it like this:
Brain = Good for Survival, but Fragile --> Brain Needs Protection --> Wherever Protection is Best = Where the "head"/"front" has evolved

I thought about it too, but isn't such an argument mixes cause and effect? Fly shouldn't care where to have its brain, abdomen works as well for protection. I would expect to skull evolve around brain, rather than brain evolve around skull. Otherwise brain should be located throughout insides of thick bones, as protection is best there.

@aandreev -- They co-evolved. As brains became more complex and bigger, there needed to be a better place to store them. Thick bones aren't very spacious. Hollow bones aren't very protective. The compromise for organisms evolving a larger brain was the skull: A hollow, encapsulating bone that can also be very dense (especially among goats, bovines, etc.). It's also a design that means there's only one area to protect instead of every single thick bone in your body.

TL;DR Visual and auditory systems are crucial for survival, especially in higher animals. Also, visual/auditory systems have great number of cells. For processing to be effective, it should be performed closer to data acquisition (eyes).
First of all, for example, in mouse or human, central nervous system includes brain and spinal cord. Since spinal cord is extremely important at regulating different physiological processes as well as in performing complicated motor tasks, it would be unjust to not think about CNS as a whole.
If you talk only about brain part of CNS, it makes sense to locate important processing pathways near sensitive organs for two reasons. First, it saves material on running long axons from many sensory cells. Secondly, longer axons deliver information slower. If there is a sense that is important for survival, than information in that modality must be delivered and processes as quick as possible.
In comments to the question @anongoodnurse mentioned that "butterflies 'taste' with their feet". I would argue that a) taste in butterflies is not vital for immediate survival and b) number of taste buds is very limited, whereas retinal cells are count up to more than thousand per eye.
But what about humans? We also able to "taste with our feet", e.g. feel temperature. For survival it is crucial to be able to escape hot surface as fast as we can. And we do, thanks to a direct reflex arc going from sensory cells to spinal cord and motor neurons. Which brings back point about CNS as a whole system. Crucial information and immediate decisions are made closer to sensitive organs.


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What happens to a human body once a sugary snack is consumed?
I'm looking to understand the effects of sugary snacks and/or drinks on a human body. I'm particularly interested in the timing of the ingestion versus various hormonal levels that may be circadian in nature. Is the release of insulin circadian in nature?
Scenario 1:
A person eats 50 grams of trail mix- raisins, sugared pineapple, sugared mango.
What happens in the next couple hours?
Which hormones get released and for how long?
Does the timing of ingestion produce different effects (ex: consumed at 11AM vs 3PM vs 8 PM?) on the body?
Scenario 2:
A person eats 100 grams of trail mix and drinks a can of sugary nectar (48 grams of sugar dissolved in water).
Will this cause the sugar "crash"?
Is there some grams per kilogram of weight guideline on how much refined sugar or corn syrup a human body can handle at once?
Thank you for your response or any keywords that may help me search for this information!

The human/animal digestive tract breaks down food chemically (with low pH/acid), enzymatically (like proteases and glycolytic enaymes which break down protein and sugars respectively), as well as symbiotically (bacteria participates in the breakdown of some compounds in the gut).  The results are released into the blood stream for the most of the body to assimilate.
With foods with complex carbohydrates (scenario 1), the results can be only a modest change in the glucose level in the serum.  This depends upon the specific food which you can understand better by researching the 'glycemic index'.  Highly glycemic foods result in rather short term release of simple carbohydrates glucose/sucrose into the blood.  Lower glycimic food contain complex carbohydrates (which are elaborate chains of sugars) which need to be broken up into simple carbohydrates before they are metabolized the the cells.
Foods which contain a lot of simple carbohydrates change the sugar levels in the blood nearly immediately and it can go quite high.  simple carbohydrates are monomers or dimers of sugars.  BTW complex carbohydrates have few pictures on the web, but you can imagine them as chains and networks of many many simple carbohydrates linked together.
Not all simple carbohydrates are used by human beings for energy.  For instance the glycosamine in 'joint juice' is the sort that makes cartilidge, which just to show you how different some complex carbohydrates can be. BTW i don't recommend joint juice, just trying to give a familiar example.  Its unlikely that the glucosamine you drink will be directly used for your joints!
So glucose is the energy currency in the blood.  when the glucose level goes up insulin is secreted by the pancreas which tells the cells to take up the glucose for glycogen (internal cell energy storage in a complex carbohydrate) or to be metabolized directly.  Diabetes results when insulin is not produced (type I) or when the cells stop responding to insulin (type II).
Human tolerance to glucose in the blood is estimated to be up to about 100 mg/dl long term. higher than this on the average is not healthy and can go up to several hundreds and cause lots of degeneration in the kidney, liver, and eyes, and more.  Exercise and fasting increase insulin sensitivity and athletes have blood glucose that is quite low even if they have a sugary beverage.
hope this helps - many keywords embedded within...
One last note.  Fructose, which is about 45-60% of high fructose corn syrup (the rest is sucrose) is almost entirely metabolized in the liver.  This is why fructose can be harmful to people who drink too much sweetened beverages.  With the liver taking in the vast majority of fructose, it tends to make fat out of it, sort of overdosing it to make it fatter than the rest of you relatively quickly.  Fatty liver is a marginally disfunctional liver and can cause health problems down the way.  Abdominal body fat (not on your love handles, but amongst your chest cavity and internal organs) is particularly harmful as it interferes with all sorts of organ function.  Probably something everyone should be aware of.

@AlexStone you're welcome :)


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How do duplicate brain regions (ex: left/right amygdaloid body) operate together?
I frequently hear talk about parts of the brain like "Amygdala" or "Hypothalamus", so I looked them up in an app called "essential anatomy". What I see is that there's mirror symmetry, and most of these glands/nuclei are actually mirrored in two halves of the brain.
I'm trying to understand how two halves of nuclei like amygdala work together. For example, it is frequently said that Amygdala processes fear response. If it was a single nucleus, it is conceptually easy to comprehend, but what about a "multi core" nuclei with two halves? Which half would process the fear response?
Additional questions to help clarify this question:

Are duplicate nuclei connected through some nerves, making up a single organ?
Is there a dominant/non-dominant relationship between halves (like dominant hand)?
Or do nuclei fulfill identical role within different brain halves (right half gets scared, then left half gets scared)?

Here's an image that prompted my curiocity - it is a 3D model of nuclei that sit on top of brain stem and under white matter.

Regarding to amygdala, I have read somewhere that they have slightly different functions like processing negative and/or positive emotions. So maybe they are not have to be in communication? I am not sure tho. I hope somebody explain and we can learn it.

The two symmetrical counterparts of a brain compartment can interact with each other through connections in the corpus callosum. The purpose behind two regions of the same kind differs. For example, often it is to handle inputs from the two sides of the body respectively. Check out http://en.wikipedia.org/wiki/Lateralization_of_brain_function to get started.


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Are there anyother method under research for curing rabies?
Why is rabies incurable after onset of symptoms? Although we administer HRIG (lyssa virus antibody) to the patient, why doesn't it work after onset of symptoms? And are there any other successful treatments for rabies like that of Milwaukee protocol which are under research? I also want to know how successful  is Milwaukee protocol so far?

Antibody wont cross blood brain barrier. Rabies virus infects the hippocampus.


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What is the explanation for the smaller number of tRNA than codons?

Translation, or decoding, of the four-nucleotide language of DNA and
  mRNA into the 20–amino acid language of proteins requires tRNAs and
  enzymes called aminoacyl-tRNA synthetases. To participate in protein
  synthesis, a tRNA molecule must become chemically linked to a
  particular amino acid via a high-energy bond, forming an
  aminoacyl-tRNA; the anticodon in the tRNA then base-pairs with a codon
  in mRNA so that the activated amino acid can be added to the growing
  polypeptide chain.
Some 30–40 different tRNAs have been identified in bacterial cells
  and as many as 50–100 in animal and plant cells. Thus the number of
  tRNAs in most cells is more than the number of amino acids used in
  protein synthesis (20) and also differs from the number of amino acid
  codons in the genetic code (61). Consequently, many amino acids have
  more than one tRNA to which they can attach ; in addition, many tRNAs
  can pair with more than one codon.

If perfect Watson-Crick base pairing were demanded between codons and anticodons, cells would have to contain exactly 61 different tRNA species, one for each codon that specifies an amino acid. As noted above, however, many cells contain fewer than 61 tRNAs.
What is the explanation for the smaller number of tRNA than  codons codons?

Th reason for this is that for the third base of the tRNA non-Watson-Crick pairing is allowed. This phenomenon is called "Wobble base pairing". See the figure (from here) for illustration (from here):

If you have a look at the codon table for amino acids, than the variation in the code for one amino acid mostly happens on the third position (from here):

This allows a smaller number of tRNA than 64, as there is some flexibility. The third base can be represented like this (taken from this answer):

In the table Cricks predictions are compared to the pairings found in experiments.

Mostly this, but there's also post-transcriptional tRNA modification so instead of U you can have e.g. cmo5U in the wobble position to pair with all 4 canonical bases..

I would add that the genetic code is degenerate, which in this context means that there is more than one way to "spell" some of the "words" in the "message." Since there are only 20 different words (the amino acids), and since the "alphabet" for this code only contains 4 different letters (the nucleotide bases), if we add the limitation that all of the words in our message are the same length, then 3 bases per a.a. is the most efficient or economical code (4 x 4 x 4 = 64 possible combinations). By removing the 3 termination codons in the code there are 61 codons that need to spell 20 a.a.

The table shown is that of Crick’s original wobble predictions. These did not all turn out to be correct, specifically that U in the anticodon only pairs with A or G in the codon. An updated table can be found in the answer to another question.

@David Good point, thanks. I updated the answer.

Watson-Crick base pairing can be violated by wobble base pairing.
The 5' of the anticodon has more freedom in binding, that is why, for many amino acids, the last part of the codon has more possible characters.


text:
Can someone link me to resources on the efficiency of sticky end ligation?
I really would like to know if sticky end ligation could potentially be performed with very high efficiency, and which factors influence that.  However, I can't find any papers on the subject, even though I'm sure they exist.  I was hoping someone would know of some literature.

What exactly do you want to know?

I want to know if there is literature that shows that sticky end ligations occurs without indels and that sticky end ligation can be done with around 80%+ efficiency.

The best resource for troubleshooting ligations I found (and use frequently) is this NEB page.  That is assuming you've already referred to the instructions provided with the enzyme you're using.   In my case it's T4 Ligase, again from NEB.   It's helpful to check the FAQs and the references listed on that page.    Also, you can make use of their Molar Calculator tool on Ligation setting (see more from first link).
Good luck with high efficiency!

To measure the frequency of indels at the ligation site you can use a vector with a unique restriction site in the lacZ gene. With a colorimetric assay you can count the number of white cfu. Perfect ligation in-frame yields blue cfu

Welcome to Bio.SE and thanks for sharing your answer. Please avoid using acronyms and unintelligible jargon. I have a biochemical background (ages ago since last using it admittedly) and frankly I don't understand this answer.

Yes, this is entirely understandable.

Altought it it is could be more digested, I think that the response is not unanderstandable: it refers to the prototypical "blue-white assay" using the LacZ gene, which encodes beta galactosidase and this digests X-gal making bacterial colonies blue.(the word "cfu" stands for colony forming unit)

He is poposing to digest with restriction enzime this gene and check after ligation the % of blue/white colonies (of course after restriction and ligation E.col are transformed).If all ligation process happened without introducing any indel, the gene should be functional and the colonies blue, and the % of blue colonies serves as a readout of efficiency

I guess I want to know what the maximum possible efficiency of religation is.

The enzymatic reaction requires adenosine triphosphate as a co-factor, and Mg++ (as well as a dilute buffer). The substrate is double-stranded fragments of DNA possessing 5' phosphates. Blunt ended DNA fragments can be ligated to each other, and this reaction is enhanced by adding polyethylene glycol. However DNA with complementary overhangs are ligated much more efficiently. The reaction is at least trimolecular (2 DNA ends + 1 protein) so the reaction volume affects the concentration and therefore the rate. So how long do you want to let the reaction proceed?


text:
Why is an increase in the amount of oxygen in the atmosphere favorable for life?
I have followed the David Attenborough series on 'First life' and heard, that an increase in the amount of oxygen in the atmosphere, as it took place just before the Cambrium, is generally favorable for life and also enables the evolution of larger organisms.
Why is that so? Is it because aerobic respiration had a better conversion rate to energy?

I think you are right - O2 allows more energy to be released from fuels in less time, allowing warm-blooded animals to develop and thrive in colder climates. However, this was only possible through large-scale adaptations to eliminate oxygen radicals in the body. Oxygen is about the most reactive compound around and therefore potentially lethal. Hence 'generally favorable form life' seems to be an invalid statement. In fact, you could envision the abudance of plant life killing life instead of supporting it.

@AliceD Indeed, see https://en.wikipedia.org/wiki/Great_Oxygenation_Event.

Because it's favorable for the process of aerobic respiration which requires O2 to produce ATP, which is the little power storage unit.
With a bigger concentration of O2, it was possible to produce more ATP, should you evolve in that direction and you needed that constraint to be removed.


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What is the minimum eye?
What is the minimum eye which confers some evolutionary advantage?
By minimum I mean anything less than this has no advantage whatsoever and therefore is not favored by natural selection.
By eye, I mean not just a light sensor but also infrastructure which converts the light stimulus into an advantageous response.
Ideally would like a clear unambiguous before/after case especially on the infrastructure between the mutated protein and the cell's response mechanism which translates this into a survival advantage.
(I assume Opsin proteins floating around the cytoplasm by themselves confers no advantage without some kind of other infrastructure)
please also provide an estimate of the number of coordinated DNA base pairs which needed to change to confer this advantage so that a proper probability estimate can be done.

An opsin protein attached at the membrane of cells exposed to light with a standard biochemical cascade allowing for example to regulate the expression of a gene will potentially be beneficial. Would this answer your question?

@Remi.b wouldn't this need a custom cocktail of chemical cascade to convert the light impulse to something useful (we are after all talking about a cell without an eye). The details of this cascade is really my question. which includesalso the details of how the impulse would be converted to something advantageous

@Remi.b will check out these links. thanks. looks complicated. wish there was something which addresses this specific question.

I moved my comments into an answer. I think that all the links directly address your specific question. Or I may not understand your question. Maybe the last link on the structure and function of the opsin gene is the information that you're specifically seeking for. I am not sure.

I think "eye" needs to be quite strictly defined before answering is possible.

@ChrisStronks I agree. Not knowing what the OP is meaning by "eye" made the answer difficult to write and make it quite generalist and approximative. But I am not sure what the question is anyway. I think the OP struggles with how an opsin protein works.

@Remi.b yes agreed totally. I upvoted your answer as I agree that your description is the simplest *light sensor *, however, an opsin system alone may not be categorized as an eye.

@ChrisStronks right. you'd need other infrastructure converting it to an sight sensation/reaction which is really what this question is about

Is this question inspired by that Darwin quote that creationists seem to love?  Because if so that was totally taken out of context, see here.

@augurar no it was my own thought. can be applied to the emergence of all new information. not just the eye

I think that you are expecting for some complicated system while such things are not necessarily involved. You basically just need a protein that is light-sensitive and some cascade of signal transduction. A light-sensitive protein is just a protein which conformation is changed in the presence of photons of a given wavelength. This cascade of signal transduction can be very standard. It doesn't need to be anything extraordinary.
Consider a mutation that turns a given protein into a light-sensitive protein. Such mutant protein could easily still activate the same cascade (and eventually regulate the expression of the same gene) and may eventually be beneficial. A visual signal (presence/absence of photons of a given wavelength) directly affect the conformation of the protein which in result can activate a whole cascade. The cascade doesn't need to have evolved after the protein had acquired the ability to response to photons. You may want to dive into the details of how the structure and function of the opsin proteins.
This article describes how an ancestral non-light sensitive protein (coded in GPCR gene. The proteins are also called serpentine) evolved into a light-sensitive protein (opsin). The article also link to other articles that discuss this transition.
There are several types of light-senstive proteins in different kingdom, including plants and bacteria that don't have nerves.
You can learn more about the cascade of transduction on wikipedia (here or here for example). You may want to learn more about opsin proteins and learn more about light-sensitive proteins.
Wikipedia page: Evolution of eyes > Early Eyes will probably interest you as well. Depending on the definition you use for "eye" (note, "eyes" have evolved independently 50 to 100 times), Planarian might be a good example of a species that have a primitive eye.

thank you but I am looking for an actual working example. either way, thanks for the links

Are you looking for a species that has a very primitive form of "eye" (eye taken in the strict sense of animal eye I suppose)?

no i am looking to understand what is involved in jumping from no eye to minimum eye

Do the sentences (in my answer) not answer your question? Consider a mutation that turns a given protein into a light-sensitive protein. Such mutant protein could easily still activate the same cascade (and eventually regulate the expression of the same gene) and may eventually be beneficial.

There is now a small paragraph (the second paragraph) about how a single mutation that offers the ability to sense light might be beneficial. Let me know if it still doesn't answer the question.

if you could provide a detailed example yes. but merely stating this does not. need something unambiguous. something scientific which can be put to the test

I linked an article that describe a specific example (see edited answer). Does it answer your question?

will need to research all these links. thanks. ideally would like a clear unambiguous before/after case

If I may say something that has nothing to do with the subject of the discussion; it sounds like you don't need this info for research purpose or whatever (otherwise the question would have been much clearer from the beginning) but that you arrived on this site almost ready to refuse any explanation one could give you. People who does that often end up protecting their first opinions toward any explanation by digging always further a possible way to refute the evidences even going to the philosophy of knowledge (or of logic). I'd advice not to make the mistake to be "primarily opinion based".

Enjoy the readings!

I have a hard time to understand what you would call a "clear before/after scenario". I think you either expect a an observation with a methodology that one with very little knowledge in biology can understand (in which case, we could sum up this point of view to "I don't trust your answer because I am not able to understand your answer") or an observation where the mutation would naturally occur behind our eyes, which is of course extremely unlikely to ever happen. But in the second case, I don't really understand what difference that would make.

I don't see how this answers the question. I agree that it is possible for one protein to mutate into another. What I am asking is about the other infrastructure which translates the light's effect on the protein into a minimal sight response. regarding what you wrote that the existing cascade could be reused, can you provide details or better yet empirical evidence for this? ex an experiment where a microorganism without any kind of sight had opsin proteins injected or mutated in its cell menbrane and this offered minimal sight. without this your answer is useless to me. but thank you anyways

i also dont see how this answers the question. the OP is asking for a minimum eye with the minimum accompanying infrastructure. maybe this should be a comment.

@user813801 On one hand the OP is asking for the minimal number of changes for an "eye" to be beneficial. I showed that very few changes can lead to sensitive abilities. Now if the OP were not to consider the thing I described as being an eye (but he seems to not complain about that), the thing I described would still makes sense in order to describe the adaptive valley that the OP assumed to exist between having no eyes and having an eye. I would agree though that the absence of definition of what is an eye make the question confusing

if you dont understand the question, then clarify before giving a bunch of links to peripheral issues

@user813801 Criticisms about the sense of the questions have been made below the question and there are currently 4 lose votes. I prefer avoid editing the post myself to clarify it as I am afraid the OP would feel like I change the sense of its post. I just thought I would do my best and give an answer to a somehow unclear question.

the OP made changes to the question to address all those points

A mutation that lets a non-light-sensitve protein be light-sensitive would already have all the necessary infrastructure, since it would still have whatever cascade the original, non-light-sensitive protein used.  Generally speaking, no additional infrastructure would be needed.

the article you reference says: "the origin of phototransduction in animals MAY have involved the alteration of only a single component...Taken together, these data support a view that the origination of animal phototransduction, and by extension of animal vision itself, involved the evolution of an existing CNG-based cascade into a functionally new cascade, founded by a novel opsin lineage of light-sensitive G-protein-coupled receptors." how much change is this? please give as much details as possible. thanks

Please continue this discussion in chat.

Comments are not for extended discussion; this conversation has been moved to chat.

A relatively simple proto-eye is the pineal gland. It has been considered to be the third eye and it is involved in circadian rhythms in man, it is involved in thermo regulation, and in reptiles and amfibians it is in fact directly light-sensitive.
However, it is not an eye as such, because the pineal does not convey topographical information about the environment to the brain. It is more of a light sensor in reptiles and amfibians. However, it is a sensor embedded in the central nervous system of higher organisms including humans. As such, it is not just a light sensor, but an endocrinic organ involved in the light-based entrain of endogenous circadian clocks present in various organs. It has been implicated to be an integral part of the visual system in early life:

hypothetic four-eyed protovertebrate. Source: Vigh et al., 2002
The hypothetical system in the picture is not so much different from the lancet fish today, a 'living fossil'. In early life, and reptiles and amfibians today, the pineal is directly light-sensitive and thereby entrains the circadian clock directly via endocrinic functions. Synchronizing the circadian clock helps organisms to adapt to the environmental light periods, in other words prepare diurnal creatures to wake up in the morning and get ready to hunt etc. Hence it aids survival of various species in different biotopes (Vigh et al., 2002). In humans and other mammals with a dense, solid skull light-sensng is taken over by the retina, as the skull prevents admission of light. Here the pineal has only an endocrinic function receiving afferent input from the eye.
Reference
Vigh et al., Histol Histopathol 2002;17:555-90

thank you. can this structure be useful if it were simpler? if yes, then it is not a minimum eye.

It is useful in organisms living today, such as for synchronizing day/night cycles or for either moving towards areas that are likely to have food or moving away from areas that are likely to have predators.

@RayS. - the pineal gland is the most simple structure I know that has been called an eye, but is far more rudimentary than the eyes that re-construct the visual environment. To me, it is more than a molecular light sensor (it is an organ), but its light-sensing capabilities are not such that it generates conscious perceptions of the environment.


text:
What plant is it?
Do you know what plant is it? I found it in France

Why was this downvoted?

@MarchHo possibly because there is no mention of size/scale, what the overall plant looks like, where/when it was found (mountain, valley, seaside, plains, dry, wet, hot, cold, summer, winter, etc.).

That looks like a magnolia tree, those pods should bloom into an impressive white flower. https://en.wikipedia.org/wiki/Magnolia. While I can tell as much as that, I'm not familiar with identifying these any further.

I dont think it is a Magnolia tree because of the its size its huge!!!

That's a magnolia tree. They are grown around the world for ornament, wood, and foliage.
The seedpods are a bit further along than my nice, unripe one, but as they ripen and dry, all those "scales" (see the line up the middle of each one?) open up and let a ripe seed into the world.

Note the shiny, thick (evergreen) pointed oblong leaves with brown fuzzy undersides.

I would guess by the seedpod and the shape of the leaves that it's a Magnolia grandiflora. Magnolias are an ancient tree, like the Ginko.

Magnolia is one of the most ancient angiosperm (flowering plant) genera, with fossil specimens dated at 20 million years old, and fossils of plants belonging to the Magnoliaceae family dating to 95 million years ago. The genus appears to have evolved before bees appeared, so the floral structure developed to encourage pollination by beetles...
Eight species of Magnolia are native to the southeastern U.S., where they have become a popular symbol of southern culture, used in myriad place names and in literature, music (including magnolia-titled songs by the Grateful Dead, Beck, and JJ Cale), movies, and art. Magnolia is the state tree of Mississippi, and M. grandiflora (southern magnolia or sweet bay) is the state flower of both Mississippi and Louisiana.


text:
What happened to the gypsy moth epidemics in the Northeast US?
I remember that back in the 1980s, 1980-1984, gypsy moths were a veritable plague in the Northeast United States. They were literally everywhere. Sidewalks were covered with their squashed bodies (of the caterpillar). You would drive through areas and every single tree would have dozens of nests. Every summer would be gypsy-moth-a-geddon.
By the late 1980s this completely ended for some reason. I sometimes see a gypsy moth caterpillar here or there, but it is a rarity.
What happened? Did a predator proliferate? Was there a pathogen or disease that wiped them out?

It appears that the gypsy moths were controlled by pesticide spraying by the US Forestry Service.
The defoliation areas measured peaked at 12 million acres in 1981 and again at 7 million acres in 1990.

In response, there was significant spraying of various insecticides starting from 1982 through 1996, peaking in 1990. This spraying managed to keep gypsy moth defoliation areas under 2 million acres since 1993.


text:
What is this bug?
I recorded a video of this bug:

https://youtu.be/0eoWfHLEo7A
I counted 8 legs, the front legs are a little curved. The drawing on the flat back is dark and looks like the image of Jesus with some light from behind, hahahaha. I found it on the curtain of my bedroom. I believe it belongs to some tree where it can use its camouflage. Can anyone identify it?
Location: Valencia, Spain.

Where (geographically speaking) was it found?

Grao de Gandia, Valencia, Spain.

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I think it looks a lot like a European Pigeon Tick (Argas reflexus).

They infest pigeons and they die when infesting humans, which they only do if they are very hungry (yours looks hungry though).
May also transmit diseases.
Edit:
It could also be an Blyborough Tick (Argas vespertilionis). They infest bats and are a little rounder in shape but look otherwise similar.

Thank you very much! I'm glad I killed it in time. Although it went inside a hole and I had to stick something to kill it.

By the way, we live close to a park full of bats and some have tried getting in. So, it is highly likely to be an Argas vespertilionis

My best guess is a soft-bodied tick, perhaps of the Ornithodoros genus, although the determination of the species is a little more difficult. Though, if it's O. erraticus they're known for causing african swine fever in Spain and Portugal (1).
Ornithodoros
In response to the comments, here's a link from Texas A&M which notes the ticks pump waste+water back out into the host, and this is why they transmit so many infections.

That wiki page says "The opening between the midgut and hindgut has been lost, making the ticks unable to pass digestive waste products out of their bodies", so do these ticks just fill up with waste?

If that is true, no doubt why they carry diseases and viruses.

@user137 I've updated the answer to respond to your comment. The ticks pump the waste back into the host.

@Kendall That makes these ticks even worse.