text:
Do we use 100% of our cerebral capacity?
I saw a movie yesterday called Lucy. In this movie, a girl called Lucy absorbs a large amount of CPH4, and her brain capacity slowly increases.
So that brings me to my question which is :
Do we humans use 100% of our cerebral capacity or do we just use 15%?

No: http://www.wired.com/2014/07/everything-you-need-to-know-about-the-10-brain-myth-explained-in-60-seconds/

First of all, no device can work 100% of the theoretical capacity. Regarding maximal realistic capacity of the brain: Most people project a vague picture of the nervous system as if it is a room with a lot of independently operating machines. It is not like that. To explain how nervous system works would be too broad for this site. Please start some basic reading on wikipedia.

If you roughly know how a neural network responds to continuous input. You can easily figure out some facts: 1. It is impossible to use 100 % of your brain at the same time, 2. It is nearly impossible to not use all of it over some time, 3. It is impossible to use non of it at any time.

"We only use 15% of our brains in the same way that we only use 33% of a traffic light."

The idea that we only use 10% of our brain capacity is a myth.  There is a great article at wired.com that discusses the myth and it's history.
There is really no reason to evolve an entire brain of which only 10% is used.  One great point that they make is that minor brain damage can cause devastating effects, not what you would expect if you had 90% spare capacity waiting around.
The entire brain is rarely firing all at once, and it is hard to average how much is being used because it changes with activity.

That doesn't take away the fact that massive brain damage can result in relatively minor effects on cognition due to the fact that the functions are re-distributed to other areas. Meaning, there is available space. For example, hemispherectomy may result in remarkably little cognitive deficits in young folks.

A quibble: that minor brain damage can cause devastating effects is also consistent with the mythical 10% view. If it always caused devastating effects, it isn't. I can have a 1 TB hard drive with almost all of it free, but if I somehow lose just the boot sector...

"One great point that they make is that minor brain damage can cause devastating effects" That's not a great point at all. I probably use less than 10% of my body when writing but injuries to a small part of my body (say, a broken finger) can have a devastating effect on my ability to write.

There are more potential neuronal connections in the brain than there are atoms in the known universe.

@PCARR: That's not saying much, "number of connections" tend to explode in size very fast.  There are also more ways to group 80 students into 20 different groups than there are atoms in the observable universe.

Yes, minor brain damage can cause devastating effects, but large lesions may cause remarkably little damage, dependent on the person and location of the lesion. -1

There is definite truth in the notion that we do not use the full capacity of our cortex. It is generally accepted that there is a reserve present in the brain that can act as a backup for cerebral damage. Brain reserve can be defined in terms of the amount of damage that can be sustained before reaching a threshold for clinical expression (Stern, 2002).
A notable example is the removal of nearly half of the cortex (referred to as a hemispherectomy) in children with intractable epilepsy. Although behavioral changes may occur and motor skills may become compromised (Van Empelen et al., 2004), these children generally recover remarkably well and overall intellectual performance may in fact improve as compared to before surgery. (Note, however, that the quality of life and brain function of these patients was severely compromised by their medical condition) (Pulsifier et al., 2004). Another example where the brain is shown to have a reserve is the fact that cognitively normal elders sometimes are diagnosed with advanced Alzheimer’s disease pathology in their brains at death (Stern, 2002). In other words, while their cortex was severely damaged by Alzheimer's, they showed no clinical signs of cognitive deficits.
In all, the brain has a remarkable amount of reserve, which may be interpreted as an incomplete use of total brain capacity.
While this reserve is critical for brain plasticity in response to injury and aging, it is questionable whether it is available to enhance cognition as depicted in the movie.
References
- Pulsifier et al, Epilepsia (2004); 45(3):243-45
- Stern, J International Neuropsychol Soc (2002); 8: 448–60
- Van Empelen, Brain (2004); 127: 2071–79
Note
The linked wire article in the accepted answer is popular science and I wouldn't base a conclusion on a '60-second-all-you-need-to-know' pseudo-scientific web link.

There is definite truth in the notion that we do not use the full capacity of our cortex. I think this is is not a meaningful statement. For me the problem here is that comparing the brain to a hard disk storage is very problematic. What exactly is capacity of my brain? The number of bits of information can I store before it is "full"? I don't think the brain can be full. Your examples are awesome, but IMO they show that the brain has an amazing plasticity and can adapt to various changes very well.

@cel,  I am not comparing anything to a hard disk. My examples show that 50% of the cortex can be removed and that, indeed, the brain is plastic and can reroute many functions to other parts. Hence, the remaining cortex can perform additional tasks and as such there is a reserve, and hence we do not use 100% capacity.

I guess I just don't like the term reserve here. It sounds as if there is some backup storage that is currently unused, but can be activated if necessary. IIRC, after a damaging event such as a stroke, restructuring often leads to the loss of skills, such as being able to speak a foreign language.
So for me it's not a reserve, but a severe restructuring. I think the problem of the question is that capacity in terms of the brain is ill defined.

@cel I definitely agree capacity might have needed more explanation. The term reserve is an accepted term as far as I can see in the scientific  literature, more so than "capacity", which is indeed ill-defined. I therefore have sticked to appropriate terminology, i.e. reserve.


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If dog's DNA and human's DNA are almost same then can it be said that dogs evolved from humans?
https://www.youtube.com/watch?v=IbY122CSC5w
In this video it is said our DNA matches almost the dog's then it can be also said that dogs evolved from humans. Is it?

What!!! this is just too absurd. Have you even tried to read about how evolution really happens?

@WYSIWYG... Wow, I completely agree with you... that may be a first.

I agree the question is very introductory and I might agree with the idea that the question might deserve being closed. However, I disagree with the tone used by @WYSIWYG. It never helps to receive "it is absurd" when you have interrogations.

I agree with @Remi.b - especially as a moderator you should be respectful. And the homework close reason is misplaced too.

@Remi.b and AliceD, while I tend to try and give people the benefit of the doubt, the question is absurd. If the OP had watched the posted video, they understood absolutely nothing from it, as it went over, quickly, the idea of splitting from a common ancestor and also that the percent homology figures are contextual and do not necessarily imply phenotypic or even genotypic sameness. You cannot draw the conclusion that is implied by the question if you watch it. Minute Videos are geared towards non experts. It is perfectly clear. There are times where you just have to call it like it is.

@AliceD and Remi.b If there was a question from that video it would be how are the researchers able to make a claim that the genomes are ~99% homologous between Chimpanzee and Human if they excluded nearly a third of the genomes from the tally? At least there is a question that implies that the person actually watched and thought about the video and its content. They could also have asked if any other researchers have looked at the parts of the genomes that were excluded and determined how similar those are. At least those are thinking about experimental design and trying to look beyond No.s

@AMR- admittedly, I didn't watch the video. Perhaps WYSIWYG did as well and that could explain his reaction. Nonetheless, even then a little less harsh tone would have sufficed to convey the message.

No, it means dog and human shares common ancestor. Read here for more detailed answer to such questions. See following phylogenetic tree which shows time of divergence

Image: Wikipedia

It might be important to highlight that the tree you show is not representing the whole sister group of the platypus. It focuses on humans and represents mostly species that are closely related to humans. It would also be good to include the reference as there were debates about the exact relationship of some groups. Tolweb referring to a paper of 1995 (obviously outdated today) is showing a big polytomy.

That's true however I used diagram and reference assuming person asking question has no (or little) idea about evolution (as it is obvious from his/her question). This is what I can find which is easy to understand + is scientific enough.

I was mainly scared that the OP could bare in mind the wrong feeling that in the goal of evolution by looking at a tree that display man (the common chimpanzee actually) at it's last tip.

Species A evolving from species B makes no sense for extant species
It makes no sense to say from two extant (living) species that one evolved from the other one. Two extant species share a common ancestor though. The most recent common ancestor (MRCA) might have existed a very long time ago (as it is the case between an oak tree and a Ostrich for example) or be relatively recent (as it is the case between a reindeer and a blue whale for example).
Humans and dogs - phylogenetic relationships
Humans and dogs are both mammals. Their MRCA is about 100 millions years old. They are therefore relatively closely related and therefore share a lot of DNA in common. In other words, dogs and humans were the same species during 3.5 billions years. About 100 millions years ago, their lineage split (speciation) into two. One lineage became dogs, bears, bats and other Carnivorans (through succesive speciation events). The other lineage became elephants, orang-outans, humans, pigs, horses, rhinoceros, sea cows and many other things according to (oneZoom.org who is often nicely updated).
You can explore the tree of life by yourself. Either go on tolweb.org (Here are the Eutheria) or on oneZoom.org. I think that oneZoom is more up-to-date than tolweb.
Introductory course to evolutionary biology
You probably want to follow an introductory course of evolutionary biology. The Understanding Evolution project at Berkeley would be a great introduction

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What is the function of E. coli bacteria in the human gut?
What is the function of the bacterium, E. coli, in the human gut?
I have tried to find the answer by searching the Internet (e.g. here), but have been unsuccesful.

Nonpathogenic E. coli strains are a component of the gut microbiome of humans and many other organisms.
They are commensals, meaning that when they remain in the areas they have evolved to live in, and when they do not acquire virulence factors, they are benign. They live in our digestive tract and basically do nothing to harm us.
In fact, commensal microorganisms like E. coli can be considered part of the innate immune systems of their multicellular hosts. They take up space on the surfaces of the intestines and prevent colonization by pathogens.
Along with the endothelial cells and mucous, commensals form the barrier defenses that are the first line of protection against pathogenic organisms. Basically they are the good neighbors that don't cause problems and they don't leave space for bad neighbors to move in.
Problems can occur if they gain access to areas that are normally sterile. If the intestine is perforated and E. coli gain access to the thoracic cavity, they can become an opportunistic pathogen, as they will not be interacting with the host in a way that can control their proliferation. They can also come in contact with cells that are not expressing the necessary proteins to protect them from E. coli.
You can also end up with the situation where a pathogenic bacteria or a bacteriophage carrying a virulence factor can transfer that virulence factor to the commensal E. coli, turning them pathogenic.
But, for the most part, E. coli are there to take up space that could otherwise be colonized by harmful bacteria.

Commensal bacteria can produce usable metabolites, but I was unclear as to whether or not E.coli specifically provided any symbiotic benefit to the host or if they were simple commensal, space filling organisms.

Some relevant research has been published in the time since this question was asked and initially answered.
The label "commensal E. coli" encompasses a diverse group of strains. Different strains of E. coli, each isolated from the microbiota of healthy mice, have been shown to elicit different immunopathological responses after gnotobiotic colonization.1 Generally, strain-level differences in pathogenic potential are attributed to the carriage and expression of virulence factors 2,3, many of which are mobilizable.4,5 However, I find classifications that rely on the presence/absence of genes to be oversimplified and anthropocentric, and I favor a presentation of E. coli as a genetically and metabolically versatile organism whose activity in the gut is a function of the evolutionary balancing of inter-species interactions with fitness in the intestinal niche.6,7,8

References

Kittana H, Gomes-Neto JC, Heck K, Geis AL, Segura Muñoz RR, Cody LA, Schmaltz RJ, Bindels LB, Sinha R, Hostetter JM, Benson AK, Ramer-Tait AE. Commensal Escherichia coli Strains Can Promote Intestinal Inflammation via Differential Interleukin-6 Production. Front Immunol. 2018 Oct 9;9:2318.
Stromberg ZR, Van Goor A, Redweik GAJ, Wymore Brand MJ, Wannemuehler MJ, Mellata M. Pathogenic and non-pathogenic Escherichia coli colonization and host inflammatory response in a defined microbiota mouse model. Dis Model Mech. 2018 Nov 16;11(11):dmm035063.
Sarowska J, Futoma-Koloch B, Jama-Kmiecik A, Frej-Madrzak M, Ksiazczyk M, Bugla-Ploskonska G, Choroszy-Krol I. Virulence factors, prevalence and potential transmission of extraintestinal pathogenic Escherichia coli isolated from different sources: recent reports. Gut Pathog. 2019 Feb 21;11:10.
Proença JT, Barral DC, Gordo I. Commensal-to-pathogen transition: One-single transposon insertion results in two pathoadaptive traits in Escherichia coli -macrophage interaction. Sci Rep. 2017 Jul 3;7(1):4504.
Desvaux M, Dalmasso G, Beyrouthy R, Barnich N, Delmas J, Bonnet R. Pathogenicity Factors of Genomic Islands in Intestinal and Extraintestinal Escherichia coli. Front Microbiol. 2020 Sep 25;11:2065.
Le Gall T, Clermont O, Gouriou S, Picard B, Nassif X, Denamur E, Tenaillon O. Extraintestinal virulence is a coincidental by-product of commensalism in B2 phylogenetic group Escherichia coli strains. Mol Biol Evol. 2007 Nov;24(11):2373-84.
Barroso-Batista J, Pedro MF, Sales-Dias J, Pinto CJG, Thompson JA, Pereira H, Demengeot J, Gordo I, Xavier KB. Specific Eco-evolutionary Contexts in the Mouse Gut Reveal Escherichia coli Metabolic Versatility. Curr Biol. 2020 Mar 23;30(6):1049-1062.e7.
Braz VS, Melchior K, Moreira CG. Escherichia coli as a Multifaceted Pathogenic and Versatile Bacterium. Front Cell Infect Microbiol. 2020 Dec 21;10:548492.

E. coli do not serve a human function but live inside our digestive system because our bodies can't prevent bacteria like them from living there.  They live there because they can prosper and reproduce there.  Most strains of E. coli do not cause problems for us, and by being part of the normal bacterial population in our gut they out-compete other, potentially more harmful bacteria and keep them suppressed.  E. coli mainly live in the large intestine, not the stomach.

This is partially incorrect. In addition to regulating the intestinal flora (out competing more harmful bacteria), E. coli play a symbiotic role in the metabolism of carbohydrates and vitamin K

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Birth control hormones in the water? Or not?
This prior question talks about natural estrogen (TL;DR: Months to years):
How quickly do estrogens break down in the environment?
Ref:
http://dx.doi.org/10.1038/485441a
A lot of media has said, "birth control hormones in the water!!!!"
Ethinyl estradiol (EE2), is a synthetic hormone
eg: www.livescience.com/20532-birth-control-water-pollution.html
Conversely, a birth control advocacy group, says, "Naw, it's a very small part of the total estrogen load in the environment."
eg: www.arhp.org/publications-and-resources/contraception-journal/august-2011
(can't post more than two links) :P
What I recall reading was that one of the types of birth control hormones got processed by the human body, looked like it was changed (in the urine, etc), and so they were fine with it not causing an issue - but when it got into the environment, it rapidly got changed back into the (estrogen?) it was originally - and thus caused problems.
I'd like a nice summary of what's thought to be going on, preferably from a more neutral source.

Have you tried checking the Environmental Protection Agency's site? It you are talking about the United States, that is likely a chemical that they keep track of and have data on. There is also a distinction between what is in the drinking supply and what is being released into the environment through treated waste water. One would be a concern to humans and one would be a concern to wildlife (fish, birds, etc). I think the issue is that the molecule is excreted but the current methods of treating waste water do not break down the hormone and it is released into waterways.

Hormones are powerful signaling molecules that affect gene expression, and do not just control pregnancy. Many tumors are estrogen or testosterone positive, so there is a legitimate concern of what these molecules could do to the ecosystem of waterways.

On a related (but possibly tangential note), also check out the USGS NAWQA. I don't think it covers birth control, but does look at other pollutants.


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What determines which strand of DNA is transcribed by RNA polymerase?
DNA has two strands. How does the machinery of RNA transcription determine which one to transcribe?

I'll keep this short and simple. The direction of transcription (which determines which strand is used as the template) is controlled by the promoter, which is a region of specific DNA motifs at the 5' end of a gene. RNA polymerase binds to the promoter, which orients it on the correct strand and in the correct direction, after which it can proceed to transcribe the gene.

That great little animation is from this website.

To add to canadianer's answer, in fact genes can be found on both strands of the DNA in most eukaryotic cells, in the sense that the sense and anti-sense strands are not always the same strand. The direction is therefore completely determined by the promoter. Furthermore, there are bidirectional promoters.

This is interesting +1!! Can you add a reference to the sense/anti-sense being not confined to a particular strand?

@AliceD I'm pretty sure that he/she is just referring to the fact that, along an entire chromosome (which has two strands), some genes will be found on one strand and some on the other. The terms sense and antisense are relative to a specific gene, not an entire chromosome. Sometimes, uncommonly, two genes will overlap on opposite strands at the same loci.

@AliceD that would be pretty much any genome paper or undergraduate text book, really.  For a visual overview, have a look at this. You'll see genes in both directions, so on both strands (the direction is given by the arrows in the lines representing the genes).

@terdon, gosh I feel kind of..  erm,... dumb, but I have struggled with this concept for years. Thanks!!

@AliceD good grief, when did not knowing something not directly related to your field become a reason to feel dumb? Did I miss a meeting? My PhD was on gene prediction and genome annotation, so this is my bread and butter. Just don't ask me to describe the Krebs cycle :)

@terdon I have a BSc in Biochemistry. I left the field a decade ago and went into neuroscience. Honestly, I have struggled with this since the first time I started learning about DNA. It all didn't make sense. I honestly thought there was one coding strand, and the other was just a backbone for chemical stability..:-/ This post has enlightened me for sure. It all fell in place. Just here.

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Can microorganisms (e.g. bacteria) be damaged or killed by 253,7 nm light?
The question arose in a hospital, where I saw these flyers advertising lamps that emit such light. It was claimed that they can clean the air of microorganisms up to an arbitrary degree.
Does anyone know if that is a thing? (If it is, doesn't it also kill the beneficent types of microorganisms?)
Online I found quite a bit on the matter, but only from other distributors of similar installations.

This is UV-C radiation and light of this wavelength (which is emitted by low pressure mecury lamps) can indeed be used for disinfection purposes. The nucleic acids (DNA and RNA) has an absorption maximum for UVC radiation at 265nm, causing DNA/RNA damage. The radiation of the mercury lamps is only a little below, making them still quite effective (see the image from here):

This is used in "Ultraviolett germicidal irradiation" for example in water disinfection systems or also for workplaces. The problem with this irradiation is that it causes severe sunburns (and very fast) and also causes plastic materials to decompose (like leaving them in sunlight but much faster). Since I know the precautions for using such devices at workplaces, I wouldn't consider them safe for home use.
The other problem is that you need a pretty clean area for the radiation to be effective. We have to clean our work benches for doing cell culture work entirely so that no shadows are cast in which the UV radiation wouldn't be working since the area is shielded. Imagine this for your home. Additionally I think the fear for germs at home is massively overrated and that there is not need for theses devices at home.

Wow, thank you very much for this fast and concise answer! I wasn't thinking about using it at home^^, just wondering if it was a scam.

@Grantwalzer I wouldn't call it scam, but mostly these are useless for the home use. And most user would probably buy it for this purpose.


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How is flagellar movement controlled?
How does a cell control the movement of flagella? Both the rotatory movements and sideways movements helps the cell to move. How are these flagellar movements controlled ? It is through the regulation of the proteins flagellin and tubulin? I want to know the mechanism for both prokaryotic and eukaryotic flagella ?

No its not a homework question I know the rules of homework questions

Can you expand a little bit: What do you mean by how are they controlled? Response to stimulus or the biomechanical aspects? Note that the bacterial flagella is different from the eukaryotic flagella. Please clarify which one you are interested in.


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Why do changes in preload not cause changes in end systolic pressure?
I am trying to understand why changes in preload do not cause concomitant changes in end systolic pressure. If you have preload enhancement than this should lead to an increase in cardiac output..increased cardiac output at a constant heart rate I would think would lead to increased end systolic pressure. Why doesn't this occur?

remember that blood pressure is not solely dependent on heart rate and stroke volume. Total peripheral vascular resistance is important too. If you increase your cardiac output, your body may have a transient increase in end systolic pressure (i.e. systolic blood pressure) - but this is going to be balanced and decrease total peripheral resistance to maintain what the body is perceiving as "normal" systolic blood pressure.

One more thing to keep in mind is when talking about increased preload, you should note which ventricle is concerned. The left ventricular preload would increase only if the pulmonary blood return increases. However, the pulmonary vasculature is extremely compliant and can accommodate vast amounts of blood without significantly affecting the preload to the LV. The blood pressure, on the other hand is measured in the systemic circualtion which might not be affected that much if the preload to the RV increases.

Preload is defined as the volume of blood that stretches the ventricle at the end of diastole. Therefore, when preload is increased, the end diastolic volume is increased. In simpler terms, there is more blood in the heart just prior to contraction. Even though there is more blood being ejected from the ventricle during systole (that is, there is an increased stroke volume), the increase in preload alone will not affect the end systole volume or pressure.
When preload is increased while afterload and inotropy are held constant, the cardiac muscle fibres will still shorten to the same length. This means that the end systolic volume is unchanged, therefore the end systolic pressure is unchanged. This is best visualized by a pressure-volume loop. On the first example on the diagram below, you can see that the end systolic pressure and volume at point 3 are unchanged with increased preload:

Since cardiac output is equal to the product of stroke volume and heart rate, with increased preload the cardiac output is increased due to the increase in stroke volume. The reason why the end systolic pressure is unchanged with the increased cardiac output is because the end diastolic volume is increased.


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Can animals like squirrels leave "gifts" or tribute for humans?
I've heard anecdotal reports of squirrels bringing up gifts to a person's house after that person left out food for them. Sounds bizzare and unbelievable, until I actually saw some kind of a nut right on the welcome mat in front of the door. I moved it and saw that it was eaten (shell fragments) a couple days later, telling me that it was actually a good nut.
This makes me ask - is this just a coincidence, or do some animals, like squirrels indeed offer gifts or tribute to humans?
I'm aware that cats frequently bring killed animals to human doorstep:

By leaving a dead animal on the back porch, your cat is acting out its
  natural role as mother and teacher. You, her loving owner, represent
  her surrogate family. And frankly, she knows you would never have been
  able to catch that delicious mouse on your own.

However, for squirrels there's no domesticated relationship, humans are not a part of their family. Why would this behavior take place?

Crows have been known to reciprocate.  You may be interested in the BBC news article "Girl Who Gets Gifts From Birds" http://www.bbc.co.uk/news/magazine-31604026

@PCARR John Marzluff's book Gifts of the Crow looks into this behavior even further from an ethologist's perspective.

@Corvus  Oh cool!  Crows are amazing, I'll check this out.

I am almost sure squirrels are simply not intelligent enough for this

I was wondering the same, because I have been putting out birdseed, which the squirrels eat. This morning there was a HUGE perfect pine cone in the middle of back door mat,(it's under a car port , so it did't just land there.) I know the squirrels eat pinecones. My husband is convinced it's some social behavior that's being demonstrated.

I believe a lot of these behaviours can fall under the umbrella term of reciprocity, or  reciprocal altruism.

In evolutionary biology, reciprocal altruism is a behaviour whereby an
  organism acts in a manner that temporarily reduces its fitness while
  increasing another organism's fitness, with the expectation that the
  other organism will act in a similar manner at a later time (...) The concept is close to the strategy of "tit for tat" used in game theory.

For example, red-winged blackbird males help defend neighbor's nests. There has been some discussion around the reasons for this behaviour, but it has been observed that males reduced the amount of defense given to neighbors when neighbor males also reduced defense for their nests. Since kin selection doesn't seem to be an important factor here, this would support a tit-for-tat strategy (animals help those who previously helped them).
Some primates do this frequently too:

A monkey will present its back to another monkey, who will pick out
  parasites; after a time the roles will be reversed. Such reciprocity
  will pay off, in evolutionary terms, as long as the costs of helping
  are less than the benefits of being helped and as long as animals will
  not gain in the long run by "cheating" – that is to say, by receiving
  favours without returning them.

The example with the crows, mentioned in the comment, can be interpreted under this light too. Those crows seem to give presents expecting something in return (albeit delayed!).
What's interesting though is that altruism, at first sight, would seem to go against reproductive success. Group Selection, however, is something Darwin was already talking about in Origin of the Species.
So, back to squirrels. I didn't find particular research about them in their relationship with humans (will keep looking), but analysing it under reciprocal altruism it could be justified that they give nuts expecting a potential future benefit for them or their group. There's much more to this complex dynamic, but reciprocity is definitely a strong candidate for explaining your kind gift-presenting squirrels.
Some quick references and materials:

The evolution of reciprocal sharing
The Gift, by Marcel Mauss (complete online book) --> From an anthropology point of view, Mauss was the first one to talk about recicprocity as economics. Absolutely recommended read.
Social semantics: altruism, cooperation, mutualism, strong
reciprocity and group selection

Look, I searched your question about the animals that bring to humans some "gifts" and the only thing I found, was only for the cats. So, if you are intrested check this :
Cats are, first and foremost, natural-born hunters, as recent studies of the effects that feral and indoor-outdoor cats have on bird and rodent populations have shown. Cats allegedly kill billions of small animals every year in the United States alone. But that doesn’t make them evil — just extremely well-adapted to a carnivorous lifestyle.
Though they were first domesticated nearly 10,000 years ago, cats retain the keen hunting instincts of their wild ancestors, as well as the simple gut that allows them to digest raw meat.
However, many cats don't eat their prey, and sometimes they don't even kill it. (If you've ever had to chase an injured squirrel out of your kitchen, then you've seen this behavior firsthand.) Spayed female cats are the most likely to bring gory gifts to their owners. But they have their reasons.
In the wild, cat mothers teach their young how to eat their food by bringing home dead or injured prey. Domestic cats are no different. But in this modern age of spayed domestic cats, many female felines have no young to whom they need to pass on their hunting wisdom.
So, if cats love their owners, they bring to him some kinds of "gifts" such as mice and birds.This is a way for the cats to say "thank you" for the care that him gives to them. Also, squerls do not give "gifts". They are simply hiding supplies for the winter near human residents.


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How can a polar molecule pass through polar channels of proteins in the cell membrane?
To transport a polar molecule through the nonpolar cell membrane, a protein with a polar channel is needed to allow it to diffuse. However, if the molecule is polar and the channel is polar, wouldn't the molecule just be attracted to the polar amino acids and "stick" on the inside of it?
I may be thinking of this totally incorrectly, so please bear with my ignorance!
Thanks in advance :)

The water on both sides of the membrane is also polar. So that would help the transported molecule diffuse away from the protein once it passed through.

The molecule won't "stick" to the polar amino-acids for at least three reasons :

The amino-acids might not all be on the same plan, so their is always a force pulling the molecules transiting trough the channel in one direction (in or out the cell)
When  a flux is established, the repulsion forces between the molecules will force them to go in a direction, meaning that a coming molecule will basically push the ones already engaged in the channel.
For an ion or a protein, the water molecules constituting the hydratation shell of the molecule can't always follow it into the channel, so the water molecules present at the end of the channel (entry and end being relative to the direction of the flux) will more or less pull it outside the channel, as it is thermodynamically more stable to have a shell.  The fact that water molecules are able or not to follow the molecule depends on the size of the channel.

It's worth noting that water is itself a polar molecule, and that it can selectively cross the membrane thanks to channels called aquaporins.

Do you have a reference? Also, the first bullet point is hard to read. Perhaps explain the "molecules ", like, exported  particles or something. As of now it's quite unclear.

@AliceD : thank you for your remark, I clarified the first point.
Here can be found a reference relative to my third point.

No worries. +1 for the answer


text:
Western blot extrange band
I performed a WB using plasma rats and monkeys samples with anti ubiquitin K-48 antibody. In every sample the antibody binds something and it appears a specific band that seems to be 71kDa. When I used anti-ubiquitin unspecific antibody(just to see if I get the same results) same bands appears. It cannot be ubiquitination because the molecular weight. How can I explain the both antibodies bind something that I dont know?
Thanks

I can not see the reason why you deny ubiquitination. In addition, Ubiquitin K-48 ligated products can be recognized by anti-ubiquitin antibody. But, usually you could get multiple bands from cells and as a result, a whole lane is stained and smeary.

thanks for your answer. I see it strange because I am using several plasma samples of different animals, and it appears exaclty the same in all of them with the same molecular weight. So I dont know what is it. Because if there is poly-ub as  you say it should appears smears, but no a clear band of specific molecular weight in all the animals right? I am a litle confuse.

Plasma contains cells but also lots of extracellular proteins such as albumin, immunoglobulin, etc., right?  So, signals from cells can be very weak.

Yes but Im using as a control cells which I know they accumulated poly-ub K48, so the control looks as smear, however, plasma cells it does not look like that, it looks as a clear band of specific molecular weight that it does not correspond with the weight of the ubiquitin but is not a smear either. I am still confuse :/


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What do HG and NA mean in Geuvadis project RNAseq sample labels?
I'm looking at RNASeq Data from Geuvadis website e.g. the file GD660.GeneQuantRPKM.txt.gz.
The samples are labeled by e.g. HG00105.1.M_120209_7 or NA20812.2.M_111216_6
What do HG and NA mean? Are they ethnic backgrounds?
If not, how can I look up the ethnic mapping to the samples?
Thanks!

If you google HG00105, among the first hits is geo accession GSM649517 with the title HG00105/NA12878.
Channel1:
Characteristics gender: Male
cell line: lymphoblast cell line HG00105
ethnicity: British from England and Scotland, UK (1000 Genomes codes: GBR)

Channel2:
gender: female
cell line: lymphoblast cell line NA12878
ethnicity: Northwest European American from Utah (HapMap code: CEU)

So no, they are not coding for the ethnic background but are part of the unique identifier of the sample.


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Making positive charged polyacrylamide
I am interested in positive charged polyacrylamide to electrophorese molecules I am interested in.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643323/
http://onlinelibrary.wiley.com/doi/10.1002/bip.360300309/pdf
The articles shown above use allyltriethylammonium bromide (ATAB), but I am not sure which chemical they mention.
Or is there any other chemical to add to acrylamide to get positive charged polyacrylamide copolymer?

I would say that this question is better suited for chemistry.se.

ATAB contains a quaternary amine and a terminal carbon-carbon double bond. The polyacrylamide reaction links acrylamide by their double bonds forming the polymer. The double bond on ATAB can be incorporated into the growing polymer chain, and the quaternary amine holds a positive charge, making a positively charged polymer.
The immobilines mentioned are probably just a weak acid or weak base group with a terminal double bond like ATAB or acrlyamide. They get trapped into the polymer and if you pour the gel with a pH gradient, they pick up charges according to the pH. I haven't found a good concrete immobiline example, I can't access that second article you linked.
I am away from my good computer and cannot make chemical structures right now.

Thank you. I sensed how it works when I read, but I was not able to find the commercial products so I was wondering why. Now I find it.


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Molecular weight of my 2-D gel
I am a little confuse when I try to figure out the molecular weight of the marker on my gel. I used NuPage Novex 4-12% bis-tris gel and Mark12™ Unstained Standard as a marker. Could please someone help me to figure out the molecular weight of the marker on my gel? I find different images in internet and I am confuse.

It looks you have everything except for insulin A and B chain. https://www.thermofisher.com/order/catalog/product/LC5677

Please don't change your question as it makes the answer incorrect. If you have a new question, post a new question.

This is what I think. Does it help? Let me know if you need more information.


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Can an electrocardiogram be recorded with a single electrode?
Is it possible to do an electrocardiogram with one electrode? Or is it neccesary to have multiple electrodes? I do not understand much about EKG, so I am sorry if this question sounds naive.

Short answer
Any electrophysiological recording of potentials, including the electrocardiogram (ECG or EKG), measures a potential difference. Hence, two or more electrodes are necessary.
Background
The ECG measures the rhythmic voltages changes generated by the heart muscle. Voltage is defined as a potential difference between two points. Therefore, a voltage is always measured across two or more points. For example, when
you measure voltage when holding one out of two recording electrodes to one of the two poles of a battery, nothing will be recorded. This, because no current will flow through the potentiometer by connecting just one pole of the battery. Likewise, electrophysiology needs at least two recording channels to determine the voltage differential between the two. One channel is typically called the active electrode, the other the reference. The configuration of active and reference determines the polarity of the recorded voltage. Often a ground electrode is added to remove background noise.

This might sound odd but I was wondering, is it possible to make something like voltage clamp with ECG?

@Dexter - Theoretically yes, by adding stimulation capabilities to the electrodes. However, ECG records muscle activity typically by surface electrodes, and to voltage clamp the heart large currents would need to be injected. That would be akin to a defibrillator :)

Actually, yes you can. But you will not be able to make use of what you're seeing. There are six leads which are unipolar: V1, V2, V3, V4, V5 and V6. Any of these can monitor electrical activity in the heart without a second lead being present. In this instance, V1 or V6 would probably be the best for rhythm identification and monitoring.


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What Effect Does Skin Redness Have On Underlying Tissue?
When someone applies a rubefacient ( something that increases blood flow to the skin, turning it red), what effect does this have on the underlying tissue? Is blood supply increased radially from where the rubefacient was applied and thereby increasing blood flow to underlying tissue (I'm thinking up to a few centimeters of muscle) or is blood supply essentially being stolen locally in order to bring it to the skin?

Rubefacients cause cutaneous vasodilation (hence the redness), but they are a very broad group of drugs, and have multiple modes of action. They have different effects and side effects (locally and/or systemically). You need to specify the drug. Whatever it is it probably won't be an effective way to improve muscular blood supply, and if this is a medical question you really should talk to a doctor before applying topicals willy-nilly.


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By What Mechanism Does Heat Cause Muscle Relaxation?
Heat is commonly used "loosen" muscles, but what exactly is happening to relax the muscle? It wouldn't make sense that increased blood flow alone would relax muscle.

Read this it was very helpful to me as a Reiki Practitioner who wants to know how the heat generated by my hands on therapy with my patients for Hospice brings such relaxation to them.
http://healthyliving.azcentral.com/effects-temperature-muscular-contraction-11504.html

Please add some more details to your answer. Your answer may become invalid if the link expires or gets broken.

There may not be one because it may not have any effect.
It appears to be a placebo effect. There is not a lot of clinical evidence heat does anything beneficial, in fact cold may actually be more effective. Evidence of an effect appears to be mostly anecdotal or unscientific "studies".


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How is it decided what type of food we want to eat?
How is it decided what type of food we want to eat? For example, sometimes you would like to eat some sweets but not a full meal, other times you'd like to eat some fruit, sometimes not and so on.
I have read somewhere that organism can detect whether we are hungry or not and it gives the effect so that we feel that we are actually hungry. But the question is: is there something that measures for example what is level of glucose or aminoacids or some fats in blood and specifies not only whether we are hungry or not but also what type of food we should eat to replenish lacking resources?

I'm no biologist but here are two answers to your multidimensional question. "How is it decided what type of food we want to eat?"
There is new research into neuroscience and microbiological science about a phenomena where bacteria in our gut that produce vitamins and digest things that we cannot digest, contribute to the choices we make for our diet. Don't ask me how, but from my understanding they must somehow communicate with the brain to release dopamine while stimulating neurons responsible for choosing a certain food to crave. "Is there something that measures for example what is level of glucose or amino-acids or some fats in blood...?" Well yes actually, let's take the pancreas for example. It knows when blood sugar is high from digested materials and will begin to produce insulin. I won't go much further because already there is a response based on the detection of sugars. Your entire digestive tract is based on these detective processes in order to appropriately digest and react to digested material. Are there processes that tell your brain what to eat next? Well besides the bacteria, there are plenty of hormones produced by your gastrointestinal tract such as Ghrelin which is the most common "hunger hormone" and is responsible for homeostasis aka energy regulation/distribution throughout your body.
It's better not to ask how but to ask why when researching topics similar to this, the how is almost always provided. I'm not entirely sure how those hormones communicate with the brain, my knowledge of the brain is less biochemical and more neurological (e.g. neuron formation).


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Refer to Ran-GEF as a coenzyme?
Ran-GEF facilitates an exchange of GDP for GTP in the formation of Ran-GTP in the nucleus as part of gated import of proteins. Would I be correct in calling Ran-GEF or Ran-GAP coenzymes?

coenzymes are factors that bind to the enzyme so that enzyme can show its activity. In this case conversion between Ran GTP and Ran GDP are caused by hydrolysis and phosphorylation reactions. Ran GEF and Ran GAP are not binding to Ran GTP or Ran GDP.

Cofactor perhaps?


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How do two parents, recessive and dominant genes and two complimentary nucleotides end up in one DNA?
In the basic school, I was taught that half of genome is received from father and another half comes from mother in the form of double-helix DNA, whose first helix consists of dominant nucleotide bases and second helix is a kinda inverted copy of the first helix. I feel like 3 different concepts are mixed here into one DNA spiral and I cannot sort them out. Can you explain exactly how is every concept (parent material, recessive genes and complemenrary nucleotides) are represented in the DNA? The professional and wikipedia explanations are too full and I cannot extract this basic information from too much detail.
For instance, mother and father could donate non-overlapping sections of the double helix, e.g. you inherit a head of DNA from father and tail from mother. I can also guess that first helix consists of primary nucleotides whereas second helix is complimentary. I also understand that despite it is natural think that primary = dominant whereas complimentary nucleotide stands for recessive, it is unlikely coz dominant is a full gene rather than a single nucleotide and dominant is independent and can differ from recessive whereas complemntary implies deterministic relationship between two. Furthermore, receiving dominant from parent1 and recessive from parent2 contradicts the fact that only one of the parent alleles enters the offspring DNA. Probably both are inherited and only one is expressed in phenotype but I am not sure and ask to clarify this. In other words, I would like to know how both parent1 and parent2 chromosomes live in the child DNA if not in the form for helix1 + helix2. Particularly, what are these two chromosomes, next to every person, if not two helix of one DNA

and where are they located? Are these just two DNAs which exist only during meiosis, during first moments of fertilization? How do you end up with only one DNA in the end?
I would also like to know if individual's eggs DNA is coming from his own DNA or is formed in parallel, from his parents' DNA? That is, when individual's eggs' DNA is produced: during fetation of the parent, during his lifetime from his DNA or during fetation of the child?

Welcome to Biology.SE. Your question is very broad and therefore the answers cannot be complete. Try to limit your post to one unique and accurately defined question. Note also that your last sentence is not finished (I would also like to know which parts of the offspring DNA are produced during ....)

I agree with @Remi.b,  it is quite a wordy question with a lot of buried subquestions.

I think you really need to go back to the very basics and try to understand the DNA molecule, what a chromosome is, DNA replication and mitosis, what homologous chromosomes are, what non homologous chromosomes are, what sister chromatids are, what non sister chromatids are before you attempt to understand meioses. And I would definitely recommend you learn all of these things well before you attempt to understand molecular inheritance, but let me see if I can at least begin to clarify some of your misconceptions.
If you are having a hard time understanding the concepts as written, try looking up the articles on Simple English Wikipedia first. The try to make their articles easier for novices to understand.
There is no such concept as Dominant Nucleotide Bases. The two strands of the DNA double helix are complementary and antiparallel. Genes can reside on either strand.
You are also getting really mixed about recombination via crossing over in meiosis. The chromosomes that are being recombined in the mother are from her parents, so technically the chromosomes that are being recombined are the grandparents chromosomes.
The same is happening when the father produces gametes. The chromosomes from his parents are swapping pieces of DNA.
At the end of meiosis, each gamete has a random assortment of 23 chromosomes, either from the father or the mother of the adult male or the father or the mother of the adult female.
The 23 can be recombined meaning that the chromosome is part grandma and part grandpa, or it is a grandmother's chromosome that has not recombined or a grandfather's chromosome that has not recombined. Just looking at the possible ways that 23 chromosomes can randomly assort without taking into account recombination to produce a gamete, there are about 8 million combinations. Add recombination and it gives you a huge amount of genetic diversity.
So those are the haploid gametes. When fertilization occurs the sperm from the father donates its random assortment of 23 chromosomes and the ovum from the mother has 23 randomly assorted chromosomes of its own. This gives you at total of 46; 23 from the father, made up of a random assortment of chromosomes from his father and mother (or chromosomes recombined by crossing over to be part his mom and part his dad), and 23 from the mother with the same pattern of random assortment and recombination.
Also, the double helix doesn't dissociate (come apart) during crossing over [NOTE: for those who know, please do not jump on me for not explaining strand invasion here and the need for homologous sequences for crossing over]. One part of a grandparent's chromosome is exchanged for the exact same part of a chromosome from the other grandparent's chromosome, assuming normal cross over events. The alleles (versions) of the genes in that segment may vary, which is why you have a chromosome is part grandmother and part grandfather.
As for dominant autosomal genetic traits versus recessive genetic traits. A dominant trait means that a heterozygous child will express the phenotype even though they only have one copy of the dominant allele. If it is a disease, then we say the person is affected. If it is a recessive trait, then the heterozygous child will not express the phenotype, so they are not affected by the disease, but they carry the allele and can pass it on to their children. This person is said to be a carrier. If a person is homozygous for a recessive trait, then they will be affected by the disease and show the phenotype.
As for inheritance, you have to draw the punnet squares. This will show you the different patterns and probabilities of inheritance.
UPDATE
I think that you are getting confused by the idea that you inherit one set of 23 chromosomes from your mother and one set of 23 chromosomes from you father. While this is true, meiosis happens in their reproductive organs before fertilization (for the most part, but the important part happens there and then).
The example of the father is easier. He has two sets of chromosomes, one set that he inherited from his mother and one set he inherited from his father. At the beginning of meiosis all 46 chromosomes replicate. They make an exact copy of themselves and are joined at the centromeres. You have 2 sister chromatids on each of those chromosomes. Now the the homologous chromosomes will pair up, so one of the chromatids on the paternal chromosome (say chromosome 4 from Grandfather's set) will join with a non sister chromatid from the maternal chromosome (Grandmother's chromosome 4). So you have four chromatids from chromosome 4 lined up at the metaphase plate. The two non sister chromatids that are joined will recombine when the kinetochores move along the microtubules towards the poles of the spindle. At the end of all of this you have two cells that contain 23 chromosomes, each with a sister chromatid, however the sister chromatids are no longer identical because one of them recombined with the the non sister chromatid of its homologous chromosome. The thing you must remember is that each chromosome assorted independently of the other. For Chromosome 1 the maternal chromosome may have gone to the left cell while the paternal chromosome went to the right. Then for chromosome 2 you might have the maternal chromosome go right and the paternal chromosome go left. And so on and so forth. The number of possible combinations of how you can arrange two sets of 23 chromosomes is 2^23 or about 8 million different combinations.
During meiosis II the 23 chromosomes again line up at the metaphase plate and they are attached to the spindle by both sides of their centromere / kinetochore complex. When the migrate the two sister chromatids migrate towards opposite poles. Again it is completely random as to whether the recombined chromatid or the chromatid that did not undergo recombination will migrate to the right or the left. Again, there are 2^23 possible combinations for EACH cell.
So you end up with an incredible amount of genetic diversity on how chromosomes are assorted within the gametes. You will still only have four possible outcomes  in the copies of any single gene that you get. You will inherit either your paternal grandfather's copy or your paternal grandmother's copy and you will inherit either your maternal grandmother's copy or your maternal grandfather's copy. That is why if a genetic disease is caused by one gene, it depends on which copies you inherit.

I do confuse crossover with recombination indeed. Here in IT, we have a simplified picture where you need crossover to combine features of two survivors and you achieve recombination through crossover. I use recombination with crossover, interchangably, as long as DNA is linear, for this reason.

You seem to say a very non-obvious, sensational thing that instead of combining the features of fittest individuals, nature combines genes of their parents. This is very sensational because the well-qualified features, that favor the mom-dad fitness and survival, may be due to crossover in their proper DNA rather than their parent qualities. It is therefore that nature discards the parent DNA and starts over. There are good chances that I become good painter if nature tested my parents but my chances are reduced if it will use DNA of my grand parents to recreate mix of genes of my parents.

@ValentinTihomirov Your post is really too broad (and it gets upvotes probably because it got 2 answers) but you should consider no extending your set of questions any further and rather open new post for new questions. If you want to ask what is the difference between crossover and recombination then you can do so in a new post (note however that a google search will probably answer your question).

I asked my question because I seen this statement A dominant trait means that a heterozygous child will express the phenotype even though they only have one copy of the dominant allele many times. I want to know where are those alleles stored in. I always pictured them as a section of DNA sequence, whose first helix represents dominant gene and antihelix represents a recessive gene. It seems attractive, despite wrong for explained reasons, because you always speak about dominant and recessive as they always come in pairs.

Genes are semi randomly dispersed along each chromosome. I say semi randomly because gene duplications can result in genes that are very close to one another. Also most genes are not found at the very end of chromosomes. The estimated is that humans have about 25,000 genes distributed over 23 chromosomes. That averages to about 1,000 per chromosome, though some have more and some have less. There really isn't any order to where they are in a chromosome or which chromosome they are found on. The just are where they are as a result of how each germline evolve.

@ValentinTihomirov  I am not sure what is non obvious or sensational about what I said. Independent assortment was understood by Mendel before we knew about DNA. While meiosis ensures that each gamete gets a single copy of each chromosome, how those 23 get distributed from the 92 possible chromatids is entirely random so long as one if each type of chromatid makes it into a gamete. The traits that get passed on are solely dependent on the chromosomes contained in the egg and the sperm that fuse.

"I want to know where are those alleles stored in. I always pictured them as a section of DNA sequence, whose first helix represents dominant gene and antihelix represents a recessive gene" @ValentinTihomirov. This is wrong. One copy of a gene is on the chromosome that you get from dad and the other gene is from mom's chromosome. Each chromosome is a separate molecule of double stranded DNA. Dominant just means having only one copy, say gene from dad's chromosome is enough to make you sick. Recessive means the gene you get from dad and mom have to be the same, otherwise you won't get sick.

I understand that water is wet. I am asking if I carry both dominant and recessive alleles or only dominant one enters my body?

@ValentinTihomirov Whether you have dominant or recessive alleles is a function of the trait you are looking at. Eye color is an easy example. Brown eyes are Dominant; Blue eyes are Recessive. In order to have Blue, you need to have both alleles be recessive to produce the blue phenotype. To have Brown, you only need one brown allele, as that will produce the brown phenotype. If you have a parent with blue eyes and a parent with brown eyes, then you will be heterozygous if you have brown eyes, One dominant and one recessive. If you have blue, then both are recessive.

@ValentinTihomirov If you have the case where one parent has Brown eyes and one parent has Blue eyes and you end up with Blue eyes, that means that your brown eyed parent was heterozygous and had a brown allele and a blue allele and you ended up inheriting their blue allele along with your other parent's blue allele. As the blue parent was homozygous for blue, you were always going to get one blue allele, so there was a 50% chance that you would get the blue allele from your heterozygous brown parent and have blue eyes and a 50% chance that you would inherit the brown allele and have brown.

I will talk about humans only and I will not talk about the special case of sexual chromosomes (and anomalies such as trisomy 21) from the answer just to keep things easy. There is a lot to say, so I am just making a very short overview of different subjects. Get some coffee first, read slowly and don't hesitate to click on the wikipedia links to further your knowledge.
Pairs of chromosomes
We all have 46 chromosomes. The chromosomes can be arranged in 23 pairs. By definition the 3rd pair of chromosomes is the 3rd longest pair of chromosomes as you can see on this karyotype

You'll note that the 23rd pair is the pair of sexual chromosomes but I won't talk about them. Note by the way that species that have chromosomes present in pairs are called diploid. Some species are haploids (not pairs), some are tetraploids (4 chromosomes of the same type together), etc... While the terms "diploids species" is often used to refer to mammals for example, it is actually more correct to talk diplontic species. Diplontic species, are those species who are diploid most of the time and haploid only for a short period. Our ovules and spermatozoids are indeed haploids.
Pairs of chromatids
Chromosome are more-or-less X-shaped. Each "vertical line" of the X is a double stranded (double helix) chromatids. Two chromatids of the same chromosome are called sister chromatids. Two chromosomes of the same pair are called homologous chromosomes. Note that chromosomes don't always look as they are represented here, it depends on the phase during the life cycle of the cell but this is a story for another time. As you said, one chromatid is made of two strands that are "anti-parallel". The point of the junction in the center (although it is note always in the center as you can see) of the X-shape is called the centromere.
Inheritence
In a pair of chromosomes, one chromosome is inherited by the father, the other one by the mother. Therefore we receive exactly the same amount of genetic information from each parent (but see this post). The egg actually receive 2 single chromatids (one from the ovule and one from the spermatozoid). At some stage of the life cycle each chromatid duplicate to make those X-shaped chromosomes. Therefore, two sister chromatids are exactly (except exceptions!) identical. However, because one chromosome come from the father and the other one from the mother, two homologous chromosomes are not exactly identical. Note that mutations occur during replication of DNA (especially during meiosis). Note also that at the moment of producing our gametes (=spermatozoids and ovules), chromatids from different chromosomes (within the same pair) can exchange DNA. This process is called crossing-over. Here is a schema of this process

Crossover is the process by which two chromatids from different homologous chromosomes exchange their DNA. Chromatids do not merge into one (as suggested in your below comment). Look at the above picture. Top left are the two homologous chromosomes. Top right are the two homologous chromosomes after crossover (a little pink piece is now attached to a blue chromatid and vice-versa). In the bottom are the four resulting gametes (the 4 independent chromatids) after meiosis.
While crossover refers to the mechanism, recombination refers to the statistical association between two loci. On the above picture there are two loci represented and both are heterozygotes (see below for definition) as at one locus are the alleles aA and at the other locus are the alleles bB. Of course, on the sister chromatids both alleles are the same given that the two chromatids are just copy of one another where one comes from one parent. Therefore, a is always with b and A is always with B on the same chromatids. In the absence of crossover, we say that they segregate non-independently. If the offspring get A, (s)he will necessarily get B as well. However, if crossover can occur in between the two loci, then some gametes can carry a and B and some others can carry A and b. The statistical association between two locus is referred to as recombination. the recombination rate between two loci indicates the rate with which a crossover will occur between these two loci.
DNA
When talking about DNA, we usually refer to one double helix (one chromatid). DNA, is made of different chemical compounds including the nucleotides. There are 4 types of nucleotides that we are reffering to by the first letter of their names, A, T, C and G. Every time there's a T on one strand there is a A, in the other strand (and vice-versa). Every time there's a G on one strand there is a C, in the other strand (and vice-versa). In consequence one strand is some kind of a negative (photography) of the other strand.

From gene to protein
You can refer to a position on a chromosome as a locus. At different loci are different types of sequences. Without going into the details, a gene is a type of sequence that is used to make a protein. In order to make a protein from a gene, the double helix has to open up over a short region, some proteins come, read the DNA and make up an RNA out of it. The RNA is some kind of negative of the DNA strand that has been read (except that the Ts are replaced by Us). From the RNA some other mechanism (ribosomes; ribosomes are actually made of other RNAs but this is also a story for another time) make a protein our of the RNA. Here is an extremely simplified schema of this process.

Effects of the genotype on the phenotype
As I said above, there are some differences between homologous chromosomes. Consider for example that in a population, at a given locus (let's assume this locus correspond to a gene for simplicity) different chromosomes carry different variants. These variants are called alleles. The words recessivity, additivity or dominance refer to the relationship between two different alleles at the same locus in terms of how the two alleles affect the phenotype. Referring from wikipedia A phenotype [..] is the composite of an organism's observable characteristics or traits, such as its morphology, development, biochemical or physiological properties, phenology, behavior [..].
Recessivity, additivity and dominance
Let's call one allele Aand the other allele a. Given that one individual has two chromosomes, this individual at the locus under consideration can be either aa, aA, Aa or AA. The difference between aA and Aa is that in one case the A allele comes from the mother while in the other case it comes from the father. It essentially makes no difference, so let's just call these two types aA. a and A are said additive if the phenotype aA is the average phenotypes between the phenotype of aa and AA. If the phenotype aA is closer to the phenotype AA than tow the phenotype aa, then A is said to be partially dominant and a is partially recessive (or vice-verse for the opposite scenario). In the extreme case where the phenotype of aA is exactly like the phenotype of AA, then A is said to be dominant and a is recessive (or vice-verse for the opposite scenario). Overdominance is a third type of relationship where the phenotype of aA lies outside the range of phenotypes of aa and AA. Such as for example individuals having both aa and AA genotypes are small while individuals being aA are big. Btw, AA and aa individuals are said to be homozygous while aA are said to be heterozygous regardless of the functional relationship between the two alleles.
Consider for example a disease that is expressed only in the aa genotypes. In such case a is recessive. If two AA individuals mate together there is no risque for the child to carry the disease. If one aA individuals mate with a AA individual the child is either aA (with probability 0.5) or AA (with probability 0.5). If two aA individuals aA mate together, than a child is aA (with probability 0.5), AA (with probability 0.25) or aa (with probability 0.25). In other words, if two heterozygotes individuals mate together, they have a probability 0.25 that a given child will carry the disease if the disease is recessive. This probability reaches 0.75 if the disease is dominant (but the two heterozygote parents would both express the disease as well).

You exaggerate the number of questions I have asked. Particularly, I did not ask anything about RNA-proteines. I also understand what does dominant and recessive means. I just asked where are they located. The fact that mom chromotide is paired with father chromotide and I carry both separately throughout my life is everything I wanted to know. This explains how dominant allele is homologously coupled with recessive one. I still wonder which crossover are you talking about if the chromotides exist independently? Crossover/recombination is a process of merging two chromatide into one, right?

Maybe I oversee the number of questions but that would just mean that the post is a little unclear instead of being too broad. But anyway, we might get to the answer you're looking for before the question get closed. Please see edit in the "inheritence" paragraph below the picture.

@ValentinTihomirov Recombination/crossover is when elements of sister chromatids are exchanged between the two chromatids, see this wikipedia page. They do not merge into one.


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Who was the first to coin the terms of soft and hard selection?
Soft and hard selection are sometimes used with different definitions. I have been told that at first place hard and soft selection has been defined in the following way:

soft selection: Each deme makes the same contribution to the next generation
hard selection: Different demes make different contribution to the next generation

Who first described these concepts? What was the first paper?

Wallace, B. 1968 "Polymorphism, population size,and genetic load"?

At least in his 1975 paper "Hard and Soft Selection Revisited," Wallace says that he was the first to introduce the terms hard and soft selection in his 1968 paper that I cite above.

@falsum I think you can make an answer from your comment. Thanks

I believe it's Wallace, B. 1968 "Polymorphism, population size,and genetic load" In R. C. Lewontin Population Biology and Evolution. Wallace also discusses his distinction between soft and hard selection in his 1975 paper "Hard and Soft Selection Revisited" (JSTOR link).

Note also Christiansen 1975 who is quite an early paper. Actually I was wondering between the who would be the first to talk about selection softness. Thank you +1


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What is the point of a runny nose during a cold?
What is the biological purpose of having a runny nose during a cold?
Note, this is a different question than "What causes a runny nose" and other similar questions. Those question are about the cause, what starts the nose running. This question is about why? What is the body trying to do by making the nose run.
For example a cough, I'm guessing, is to help remove or loosen gunk in the lungs. Tears seem to have a point of cleaning the eyes. Diarrhea seems to have a point of clearing the bowels. Fevers have a point of killing viruses. Vomiting seems to have a point of getting rid of bad things in the stomach. Sweating seems to have a point of cooling the body down.
During a cold though, while reasons like inflammation etc cause a runny nose, what's the point? Why did we evolve to have runny noses during colds? What's the body trying to achieve by giving us a runny nose, specifically during a cold.

Does it need to be evolved? Can it not just be a side effect of some inflammatory process?

I don't know. That's the question. Tears seem to have a point. Coughing seems to have a point. Diarrhea seems to have a point. Fevers have a point. Vomiting seems to have a point. So, the question is does a runny noes have a point or as you suggest, is it just an unlucky side effect.

possible duplicate of If a trait would be advantageous to an organism, why hasn't it evolved?

This question is a duplicate because not everything needs to "have a point" in evolution.

This question is not asking why something hasn't evolved but, rather, why something has evolved. There's clearly potential for a scientific answer. In addition to AMR's answer, there's this idea: http://cmr.asm.org/content/24/1/210.full

@canadianer So the viruses are outflanking us again... Cause us to overproduce mucus to possibly induce a lower respiratory bacterial infection so that they can better infect the upper respiratory tract... I believe Homer Simpson would say "D'Oh!"

@AMR It's disappointing being outsmarted by something that's not even alive.

@canadianer one of my professors used to say that our genome is mostly viral anyway. If you can't beat'em, join'em I suppose.

Edited by request for clarity
The biological purpose of a runny nose is to clear pathogens and allergens trapped in the mucus out of the nasal cavity and sinuses as a result of rhinitis or sinusitis.

Mucus is considered to be part of the innate immune system and provides mechanical and chemical defenses against pathogens.

Mucus acts as a barrier protection that is difficult for pathogens to breach.
Mucus is capable of trapping pathogens in it and when that mucus is swept out of your upper respiratory track through your nose or down your esophagus, the pathogens are removed from those areas as well.
Defensive proteins called Mucins, Lysozymes, and Immunoglobulins are secreted into the mucus and provide additional protection, as they can lyse or opsonize pathogens.

Mucus keeps epithelial cells moist so that they do not dehydrate as air passes over them. This in turn keeps epithelial cells healthy so that they maintain a tight cell layer in order to protect the underlying tissue.

As part of the mechanical defenses against pathogens, epithelial cells are ciliated and they rhythmically sweep mucus from the sinuses and nasal cavity mainly into your esophagus and digestive system, but can also move mucus into your nose. Most of the time we aren't even aware this clearance of mucus is happening and it travels down our esophagus into our stomach's and intestines where it can be excreted from the body. This is the case when you do not have an infection and your mucus is not viscous.
When you have an infection the inflammatory response is triggered by cytokines from macrophages. Those cytokines induce cells in the area to do many things. One is to increase mucus production. This may cause epithelial cells in your nostrils and nasal cavity and sinuses to secrete more mucus as well, and this will be swept away through your nose, where you will notice it as a runny nose.
Usually your nose is runnier with rhinovirus infections or with allergens than it is when you have a bacterial infection where mucous tends to be thicker and more viscous. The ciliated epithelial cells have an easier time moving the thinner mucous of a viral infection or allergy than the thicker mucus of a bacterial infection, so you notice a runny nose more when you have a cold or hay fever.
So in short, the biological purpose of a runny nose is that it is part of the immune response to clear pathogens away and protect your uninfected epithelial cells from being infected. It also clears out much of the debris and inflammatory proteins that are found at the site of the infection so that they do not remain in the area to further inflame tissue that is trying to heal. When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run.

I agree with your last paragraph, but don't really follow the first. Why are you singling out the sinuses (do you think the main effect of a runny nose is to prevent sinusitis?) If so, that could be made more clear; if not, that should be made more clear as well.

@anongoodnurse I basically say sinuses because the mucus in you trachea and bronchi get swept up into your esophagus without going through your nose. For the most part the mucus that exits through the nose is from the sinuses and nasal cavity.

@gman I will add that our interaction with and adaptations to pathogens are significant drivers to evolution of the species.

Is this known through some sort of study, or conjecture?  I ask because I've heard it said that some symptoms, such as sneezing, are not the body's way of fighting a virus, but instead an effect that the virus has evolved to induce in the body to aid in spreading itself more readily.  A runny nose could be similar.  I have no idea, but am curious whether anyone really knows the answer.

Janeway's Immunobiology - 8th Edition. Chapter 2.

@anongoodnurse rhinitis is typically local, e.g., at the site of infection by a rhinovirus. So this answer is correct to focus on nasal and sinus production.

"When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run." <- What's the purpose of reacting inappropriately in so many humans?


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What are the sizes of the cells that make up human hair?
The question is in the title, but I'll explain why the question arose. I'm curious about the rates that various cells in the body divide, and have found various information relating to this, but nowhere can I find how often the cells divide in hair follicles (only that hair grows about 1 cm per 28 days, and that hair matrix epithelial cells divide very rapidly, which results in chemo patients' hair falling out). I figure that I can calculate a back-of-the envelope answer if I know the average size of hair cells. For example if they are 10 $\mu$m, and hair grows 1 cm per 28 days, then I would estimate that the relevant cell turnover time in the follicle is on the order of 1.5 per hour, assuming that the cellular division leading to the outward growth of the hair proceeds in a serial fashion. This sounds like a roughly plausible estimate, since it is significantly faster than the turnover of other cells in the human body with a high turnover (like stomach or blood neutrophils) which have a turnover of a few days.
In any case I would appreciate any insight, whether the size of hair follicle matrix epithelial cells or the cellular turnover rate in the follicle during the anagen phase.

10uM sounds reasonable, thouhg perhaps a bit low for a keratinocyte when "flattened out". But 1.5 cell divisions / hour sounds way too high. The fastest dividing human cells I'm aware of are activated lymphocytes, which can reach about 10h doubling time. The fastest cancer cell lines are around 15h. Probably there is a larger dividing mass in the follice which then "thins out" into the hair, so that comparing hair growth rate to cell diameter underestimates the doubling time.


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Difficulty in finding protein inhibition drugs
I was reading an article on a recent identification of a PARP-14 protein in cancer cells that is responsible for production of additional glucose which keeps cancer cells from dying, and that a PARP-14 inhibiting drug is still a long way from becoming reality.
Would like to ask any medical researchers/anyone with adequate knowledge, what is the difficulty in producing drugs that inhibit production by a certain protein? Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it? As how other types of drugs are made? Please give some specific examples regarding this topic. Your help is much appreciated.

Can you please link to or cite the article?

Basically the problem is finding or designing compound that can either competitively bind to the active site of a protein or an allosteric regulatory site that does not also interfere with proteins necessary to maintain cells elsewhere in the body.

@canadianer I am not sure that the link to the article is necessary. The OP gives a specific example and then asks a more general question about developing chemotherapeutics that target proteins, not necessarily why it would be difficult to find one for PARP-14. No?

@AMR It's not necessary, but I'd like to read it.

@canadianer http://www.ncbi.nlm.nih.gov/pubmed?LinkName=gene_pubmed&from_uid=54625
Sounds like it makes some form of modification to histones in DNA damaged cells that rescues them and contributes to their survival.

@AMR Yes I read that, which is why I'd also like to read the paper that says it produces glucose.

@canadianer This one? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179111/

Drug production is very long, tedious and costly process. It generally takes more than 10 years to make entirely new drug. It has various iterative aspects. take a look at following cartoon showing various steps in drug design ( Taken from Anderson 2003 )

Now coming to your questions,

what is the difficulty in producing drugs that inhibit production by a certain protein?

First of all you need to know other effects of that protein which might be essential for normal cell function. For example, there are many genes overexpression patterns which have correlated with cancer. This suggest excess quantity of these proteins/factors leads to cancer. Now one would like to block these proteins with inhibitors. However if you block these proteins, they might also affect regular cellular function. For example, SHC1 overexpression is correlated with breast cancer. However that protein is very important in apoptosis regulation, EGFR pathway, Oxidative stress and many more functions. Now if you inhibit this protein, your normal cells will also get damaged.

Isn't it about analyzing the chemical makeup and structure of the protein and finding ways to neutralize it

It is not that simple, for this you need inhibitor which can specifically either bind (it can be competition also) specifically with given protein. Most of the time there are other problems like , there might be other proteins with that structure which can affect other protein's function. There will be other important problems like

Delivery of inhibitor
Specificity (Inhibitor need to act only on target cells)
Sensitivity (Inhibitor need to be sensitive enough to get full response in low concentration)
Side effects (There might be side effects of this inhibitor which should be minimized)
Cell resistance (Many times cell becomes resistant to inhibitor)

Above mentioned points are actually major issues in all cancer treatments like Chemotherapy  , Radiation therapy, Immunotherapy , Hormone therapy etc.

Nice, but whether the protein is important for normal cell function was not part of the question I think. One thing is to figure out how to specifically inhibit a given protein with a drug (which is hard enough in itself). Whether this is a good idea at all, given the various functions the protein might have in the body, is a separate problem.


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

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

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

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

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

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


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How to find the concentration of an enzyme?
I need to know the concentration of pectinase enzyme (sigma aldrich) which has stated 5KU, 5U/mg protein (lowry) and lot result 20U/mg protein in the label of the enzyme bottle. This is all it has mentioned. How do I calculate the concentration from this information?
hey everyone, sorry for not been straight forward with the question. I'm asking for U/ml.I think I can find it if the label has mentioned the total volume of enzyme solution. Then I know how much mg in 5KU which is 5000/5=1000mg which I can easily get mg/ml or U/ml which is more appropriate. But the question is pointless if it hasn't mentioned the total volume. Thanks for the replies.
PS My supervisor asked me to prepare a standard graph of enzyme concentration (U/ml) against absorbance(O.D value) for DNS assay instead of a Galacturonic acid standard/glucose standard.(galacturonic acid is not available so he thinks it is better to you this graph than a standard glucose graph)
PS I checked the bottle again.On the bottom side of the bottle it has stated 10 ml.

What kind of concentration do you need? A mg/ml number? For enzymes this is relatively meaningless, since the activity is more important here (you can have a lot of dead protein in your preparation which is of no use for the enzyme reaction). So usually you get a U/ml (or whatever) concentration and you have a definition for the unit.

Is it just me or anyone else find ironic that OP's name k.m and he/she is asking for enzyme concentration :P

Welcome to BioSE! Please include a bit more information on how you have tried to solve the problem yourself.

If you want to know the concentration in moles/litre then you need the molecular weight of the protein molecule--you did not provide this information. You would also need the volume of the solution in the bottle--you did not provide this information. moles = weight (in grams) / molecular weight.

The enzyme unit U is not a measure of enzyme concentration but its activity, defined as the conversion of 1 micro mole ($\mu$mol) of substrate per minute (under a specified condition such as pH and T)
Absorbance (O.D. at a specific wavelength) of the enzyme is a measure of enzyme concentration, regardless of its activity. Depending on the unit of the extinction coefficient, Absorbance can be converted directly by Beer's Law to enzyme concentration, typically in mg/mL or in the standard mM.
5U/mg is the specific activity of pectinase, and the bottle contains a total of 5 kilo U (KU), meaning that there is a equivalent of 1g of active enzyme inside (often in powder). If you assume all pectinase molecules inside the bottle are active, when dissolved in 10mL water, you have a pectinase concentration of 100mg/mL. If the molecular weight of pectinase is 31kDa (31000 g/mol), then 100mg/mL is the same as 3.2mM in concentration.
By the way, Lowry protein assay measures enzyme concentration, not activity in U while DNS assay measures activity (of enzyme that produces reducing sugars), not enzyme concentration.


text:
Invertase calculation?
If I wanted to make $500\mathrm{\mu g}/\mathrm{ml}$ of invertase, from Sigma's Invertase from Baker's yeast, which states is grade VII, and greater than or equal to $300 \mathrm{units}/\mathrm{ml}$, then would these following calculations be right if I wanted $10 \mathrm{ml}$ of $500 \mathrm{mg}/\mathrm{ml}$ concentration of enzyme solution?
\begin{align}
M_1\times V_1 & = M_2\times V_2 \\
(300 \mathrm{units} ??)\times V_1 & = 10 \mathrm{ml}\times(500 \mathrm{units} ??) \\
V_1 & = 16.6 \mathrm{ml}
\end{align}
Therefore I need $300 \mathrm{\mu g}$ of the powdered enzyme which is equal to $0.0003 \mathrm{g}$ and add up to $16.6 \mathrm{ml}$ of sodium acetate buffer, to get my desired concentration of $500 \mathrm{\mu g}/\mathrm{ml}$?
Aside: And also, would this solution be able to be made in a day in advance and stored cold or would the enzymes degrade too much?
EDIT:
After reading the comments, googling, and looking back at old protocols. Is the following calculation below right then?
I need $500\mathrm{\mu g}/\mathrm{ml}$ as my concentration, therefore if I want $10\mathrm{ml}$ of my solution:
$$
(500 \mathrm{\mu g}/1 \mathrm{ml})\times 10 \mathrm{ml} = 0.005 \mathrm{g}
$$
Therefore, $0.005 \mathrm{g}$ up to $10 \mathrm{ml}$ of buffer.

I cannot find on the website where Sigma states that the enzyme concentration is 300 mg/mL, which isn't surprising because it is sold as a dry powder. They do say that it is 300 units/mg. You could make a solution with specific mass concentration, though that wouldn't take into account impurities, such as salts remaining from lyophilization.

you have units all wrong. do you need grams/volume or units, or what?

ps. Units are usually defined by activity. Like, 1 unit of enzyme converts X moles of molecules in 1 hour. So, more pure, higher-quality stuff will have more units per gram or per mole

@canadianer     Yes. I misspoke it was 300units/mg. How from that can I get 500 ug/ml?

@aaaaaa        I need 500ug/ml as my concentration. So would 16.6ml of buffer with 300ug of powder get me that concentration? Or if not, how would  I do the calculations? Thanks.

If you want 10 mL of 500 ug/mL sample, you take 5 mg of powder and 10 mL of buffer

@canadianer      I just saw your comment as I was typing. thanks. I guess what I was confused about was the 300units/mg that they stated. I thought that had some bearing on my calculation.

ok, but are you sure you want ug/mL as final concentration, not units/mL? I would suggest double-checking

@aaaaaa.         Yes that is what I need, thanks.


text:
Why are multiple copies of the 35S enhancer used for overexpression in plants?
I know that the CaMV 35S promoter is widely used for transgenic plants, where it acts as an enhancer element for constitutive overexpression.
I noticed that it is always used as a tandemly repeated enhancer with 4 copies.
Why 4 copies? Why not 1, 2, 3, 5, or 10?

When the enhancer was first studied it was obviously in a single copy.
Later work found that tandem duplication (2 copies) increased expression levels greatly. This 2-copy construct was then used in some studies.
Here is a quote from a 2003 paper (Ma et al. 2003 Nature Reviews Plants):

The CaMV 35S promoter is now the most popular choice
in DICOTYLEDONOUS PLANTS (dicots). It is a strong constitutive
promoter that can be made even more active by duplicating the enhancer region.

By 2009 the 4X35S is showing up in publications but I have not had any luck tracking down its origin.
So in brief: the exact number is because of history. Earlier on they used fewer copies.
There are probably diminishing returns to enhancer strength with more copies, and fewer copies is not strong enough.


text:
Biological Evolution outside of Earth
What drives evolution forward? I heard that climate change drives species to evolve and adapt. Is there any other mechanism that is encoded in our DNA by which species can over abrupt changes, evolve and adapt?
Say for example Jupiter's moon Europa. If I find species of fishes here in Earth that could theoretically, barely survive on those oceans. If I come back in 5 million years will they look the same they did when I placed them there? or is the process of natural selection universal, and I would expect to see changes in the fishes due to their new environment which is not Earth. basically would foreign species also evolve and adapt.

The relationship and adaptations made to pathogens. As for your hypothetical situation, they would need a food source and a source of oxygen. It is hard to say whether they would even survive as they did not evolve there and we cannot be 100% sure that Europa will have all of the properties they need for survival. We see the effects on the astronauts who live at the space station. They experience bone density loss, develop vision problems, etc. all due to the fact that we did not evolve in free fall. It is difficult to make predictions about adaptation in places we did not evolve in.

You take a population of fish and put them in a new environment (another planet even). Will they evolve?
Yes they would evolve as long as they don't get extinct. It sounds very likely that they would very quickly get extinct though.
Note, however that they were already constantly evolving while being on earth whether or not their environment was stable or changing through time. Evolution is not a thing that occurs only when the environment is changing. Stabilizing selection, genetic drift and mutations affect the allele frequencies too, not only directional selection.
General comments on the post
I don't quite understand the relationship between the first paragraph and the second paragraph.
The first paragraph suggests a few misunderstanding of evolutionary processes. I recommend that you have a look at a free online introductory course of evolutionary biology such as Understanding Evolution by Berckeley University for example. Typically, if some concepts I used in the second paragraph above were unknown to you, then you definitely want to have a look at Understanding Evolution


text:
Membrane Permeability to Pyruvate
Pyruvate seems to pass easily through the outer membrane of the mitochondrion but has difficulty entering the inner membrane (and gets in by H+ symport). I have two questions: (1) what property of pyruvate disallows it from passing through the inner membrane? Is it its charge? and (2) what structural differences are there between the outer and inner membranes of the mitochondrion that create their disparate permeabilities to pyruvate?

Pyruvate is negatively charged and quite polar, which makes it unfavourable to diffuse directly through any membrane. The outer mitochondrial membrane contains porins, which allow small molecules, like pyruvate, to passively diffuse through. Specifically, pyruvate uses voltage dependent anion channels. The inner mitochondrial membrane lacks such channels and depends on active transport by the long anticipated but only recently discovered mitochondrial pyruvate carrier (Herzig et al. and Bricker et al., 2012).


text:
Does antidromic conduction occur in the brain under normal conditions?
So I am reading a book on neuroscience and they mentioned in passing that the action potential is capable of travelling in either direction along the axon (orthodromic vs antidromic), The wikipedia antidromic article states that the effect is often used to confirm connections in laboratory experiments.
What I'm now wondering is if the phenomenon has been observed with normally behaving neurons in situ (as normal as a neuron under experimental observation can be anyway) and therefore possibly needs to be factored in when modelling neurons in software or is it safe/justified to treat the information as only flowing in one direction (orthodromic)?

Under physiological conditions, action potentials are generally assumed to travel one-way. Action potentials are generated in the dendritic region, and travel from the soma to the axon terminal. Because voltage-gated sodium channels are inactivated after having been active during action potential generation, the action potential cannot travel backwards because the tail-end of the action potential is basically temporarily shut down (Fig. 1). The duration of inactivation of sodium channels determines how fast a neuron can fire, i.e., it determines the refractory period of neurons (Purves et al., 2001).

Fig. 1. Action potential conduction and refractoriness. Source: Zoology.
When neural tissue is artificially electrically stimulated, however, action potentials can be generated anywhere along the neuron. When an axon is activated somehwere in the middle with an electrical stimulus, an action potential will travel both ways, i.e. normally to the axon terminal, but also antiodromically to the cell body.
However, it has been noted in vivo that some neurons do show antidromic action potentials under physiological conditions (Jansen et al., 1996). For modeling purposes I would not bother too much about this, though, because antidromic action potentials are generally only observed under artificial conditions.
References
- Jansen et al., J Neurophysiol; 76(6): 4206-9
- Purves et al., ed. Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001

Any chance you could expand on/summarize the Jansen et al. article (It's behind a $20 pay wall)

@norlesh - what do you wish to know? The authors found antidromic responses in some neurons in an animal model, but they don't expand on how and where they were generated. If you can say what you are after I'm happy to elaborate.

Guess I'm wondering in the article what effect/outcome the antidromic signal had in the animal model? did it just fizzle out once it reached the hillock or was there some observable function/benefit?

@norlesh - It was merely observed. They just monitored this type of neuron and saw that some spikes were out of sync. By doing the math they figured they must have been antidromic. It's a short observatory report (4 pages only). Happy to email the pdf, grab me on chat


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How can mammalian red blood cells live without a nucleus?
Even though they have a shorter lifespan than other varieties of cells, I would think that 120 days without a nucleus is still quite a long time.

It depends on what you call "to live". RBCs cannot divide, for instance. They cannot synthesise proteins either, so they are decaying after their nucleus is expelled. But they produce ATP using anaerobic glycolysis (as they lack mitochondria), which you may take as a characteristic of "living".


text:
Why does hypergranulation prevent the epithelialization of a wound?
I recently read about how does a wound heals. I read that when the granulation tissue protrudes out of the wound bed (proud flesh), the epithelialization cannot occur because the protruding proud flesh is in the way.
But I don't really understand why. Keratinocytes migrate on the surface of the granulation tissue. Even if it bulges out they should follow the geometry of it, shouldn't they? Otherwise I think none of our wounds would heal...