Does the energy from ATP hydrolysis vary among different cells? I know that when ATP is hydrolyzed into ADP it gives 7.3 kcal/mol. The question is, does this value vary among different types of cells?

Yes, the energy from ATP hydrolysis can vary between different cell types and condition, because it depends on several factors. Hence, you will find different values in various textbooks.

First, like any chemical reaction, the free energy $\Delta G$ of ATP hydrolysis depends on the concentrations of the reactants. You can explore different values of $\Delta G$ with this calculation tool. Typical values are [ATP] = 10 mM, [ADP] = 1 mM and [P$_i$] = 20 mM, which gives $\Delta G$ = 42 kJ/mol (10 kcal/mol). But all these concentrations can vary between cells, and there is not much data available on intracellular concentrations in specific cell types. Many textbooks give free energy values denoted $\Delta G^{\circ}{'}$ which are calculated at concentrations of 1M, which is of course completely unphysiological.

In addition, the $\Delta G$ is strongly affected by the concentration of Mg$^{2+}$, because this ion associates with phosphate groups and alters their free energy. It also depends on pH, since the phosphate groups can take up/release protons. If you are interested, an in depth analysis is found here.


Can disease resistance from vaccination be inherited? If a person has taken a vaccine against a particular disease and is resistant to that disease, will his/her children will be resistant to that disease??

Not usually. I say usually because there's a fairly new (~15 years old) branch of genetics known as epigentics which has been shown to allow for inheritance of acquired traits. So it's possible that if the way in which a vaccine worked was altering your epigenome or genome, that it could be passed down to your children. However, that's just a hypothetical since none of the vaccines that I know of currently work in that way, but maybe something in the future will.

As of now, vaccines generally give you immunity by introducing some portion of the virus you're vaccinating against and "sensitizing" your immune system against it. This could be the viral envelope, it could be viral DNA/RNA, could be a viral protein, etc. However, in all of these cases, your immune cells are carrying out a fairly complex process in which they make antibodies with an almost random pattern constantly, and when one is produced that binds to this virus, it tells the B cell that produced that antibody to start making more. In this way, it "confirms" that this B cell is onto something.

Having said that, the B cells themselves are not passed on from parent to child, so a child would not be permanently immune to a virus even if the parent was. BUT, some antibodies can be passed from mother to child through the umbilical cord. These antibodies have a finite life and since they're not cells, they don't replicate and device. So the child would be immune to whatever a given antibody works against as long as that antibody remains in their system (usually on the order of weeks to months). Once the antibody is degraded, they no longer have any immunity, just as their parents did not have immunity before being vaccinated.


New GO terms after TopGO enrichment? I ran an enrichment analysis with custom annotations using TopGO and surprisingly I obtained new GO terms inside the significant GO terms.

Is that  possible? The only reason I can imagine this is possible is because TopGO adds new GO terms based on the input GO terms, since GO ontology is structured hierarchically.

Please let me know if you need more details about the experiment.

Code:

https://drive.google.com/file/d/0B8-ZAuZe8jldbjNuTHhNeXRVX00/edit?usp=sharing

TopGO output:

https://drive.google.com/file/d/0B8-ZAuZe8jldZnlYUzlxZ3psMWc/edit?usp=sharing

Thanks, Bernardo

These new GO terms seem to be the parents of the already GO terms present in my original dataset.


Determination of gene direction I have one sequence that composed of sequences of three genes. I should determine the direction of each gene, but two of these genes are disrupted, and I can't determine the initial codon. Does anyone knows how I can determine the direction of genes?

I'd first try translating it and looking to see if there are big regions that jump out at you that do not have stop codons in them.  I normally use this tool for quick and dirty translations, it gives you all 6 reading frames.  Also, you could just try BLASTXing your sequence if it is short enough.  BLASTX translates your DNA in all 6 reading frames and will search the protein database for matching proteins.  Most anything will have a hit in there, and if you get a hit it will show you the DNA sequence and reading frame that got translated.  If your sequence is too big, break it down into smaller chunks until BLASTX works.  One of your chunks will have your gene in it, and it will get a protein hit.  You'll also need to break it up if you have two genes in one chunk, but you only get results for one of them because its longer and gives better hits.


What does characterization mean in a genomics context? "The resulting libraries of gene sequences allow CDC and other
  laboratories to compare the genes of currently circulating influenza
  viruses with the genes of older influenza viruses and viruses used in
  vaccines. Through this process of comparing genetic sequences, called
  genetic characterization, CDC can make informed assumptions regarding.."

I'm unsure what genetic characterization means. What do the researchers actually here?

There's no technical definition for "genetic characterization". It is simply a phrase used by authors based on the normal meaning of the words: (1) having to do with genes and heredity, and (2) describing the essential character.  Of course the bounds of the genetics and the essence of their nature are entirely in the eye of the author and reader, so no particular definition applies across all papers in genomics (or in other fields).


Why is tRNA called an adaptor molecule? All I know about adaptor is that it is a device that converts attributes of one electrical device or system to those of an otherwise incompatible device or system.
Thank you.

RNA and proteins are not electrical systems, but the idea of translating a signal between incompatible systems can be applied here.

Proteins are made through a process called Translation, where instructions stored in a piece of mRNA are used by the Ribosome to make protein.

tRNAs adapt the mRNA nucleotide sequence into a protein's peptide sequence by acting as an intermediary. A tRNA is charged by attaching an amino acid to one end, it then binds the ribosome mRNA complex at the position defined by a codon. A codon is a sequence of 3 nucleotides that codes for an amino acid.

You could think of the tRNA being like a SD Card to USB adaptor to get information from one device to another.


Gene knockdown vs gene knockout vs knocksideways? How are the techniques: Knock-sideways, knockout & knock-down different?

Hello and welcome Adil Amchi.
In genetics and molecular biology there are differences between the terms knock-out, knock-down and (the lesser known term) knock-sideways.
Knock-sideways: Inactivates proteins. Could be done using small molecule inhibitors.
Knock-out: Gene removal, no gene expression. Could be done using CRISPR.
Knock-down: Gene expression is reduced. Could be done using interference RNA.
(Another reference for Knock-sideways:

"Importantly, the rapidity of the “knock-sideways” system allowed the researchers to observe a phenotype distinct from siRNA-mediated knockdown of the same protein...")


What does the human body use oxygen for besides the final electron acceptor in the electron transport chain? My biology teachers never explained why animals need to breathe oxygen, just that we organisms die if we don't get oxygen for too long. Maybe one of them happened to mention that its used to make ATP. Now in my AP Biology class we finally learned the specifics of how oxygen is used in the electron transport chain due to its high electronegativity. But I assume this probably isn't the only reason we need oxygen.

What other purposes does the oxygen we take in through respiration serve? Does oxygen deprivation result in death just due to the halting of ATP production, or is there some other reason as well? What percentage of the oxygen we take in through respiration is expelled later through the breath as carbon dioxide?

Superoxide, O2− is created by the immune system in phagocytes (including neutrophils, monocytes, macrophages, dendritic cells, and mast cells) which use NADPH oxidase to produce it from O2 for use against invading microorganisms. However, under normal conditions, the mitochondrial electron transport chain is a major source of O2−, converting up to perhaps 5% of O2 to superoxide. [1]
As a side note, there are two sides to this coin.  While this is a useful tool against microorganisms, the formation of the reactive oxygen species has been incriminated in autoimmune reactions and diabetes (type 1). [2]

[1] Packer L, Ed. Methods in Enzymology, Volume 349. San Diego, Calif: Academic Press; 2002
[2] Thayer TC, Delano M, et al. (2011) Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes,60(8), 2144-51.


Which ant/wasp species is that? Anybody knows which species (or genus, family...) of ant/wasp is that?

It's from Brazilian Amazon (Upper Negro River, Amazonas state). About 2-3 cm long (about one inch), maybe. It was walking on the sandy road around noon. Don't know the month of the year.

Given the presence of a petiole and postpetiole, this is most likely a winged ant (drone or queen), such as this similar one here:
https://bugguide.net/node/view/57281


Does a fully-resolved phylogenetic tree have to be dichotomous? I read that wherever there is polytomy there is an unresolved pattern of divergence. I don't understand why this is so.

When divergence takes place, is it necessary that there will be division into only 2 paths? Can't there be more than 2 paths with all the paths being equally related to each other (that is, no 2 paths being related more to each other than to a third path)?

In other words, does a fully-resolved phylogenetic tree have to be dichotomous?

In theory, yes, every tree has to be dichotomous. You can understand a trichotomy in a tree as the summatory of two dichotomies that had happened so close in time that you cannot know wich was first.

Given a certain population, assume that some individuals colonize a new environment, got reproductively isolated and form a new specie. This is the typical speciation process. In this case, the two species, share a common ancestor. If you go back in time, all the individuals of the new specie will descend of only one individual. The same goes for the original specie. If you go back further, this individuals will share an ancestor, too. This is the conceptual meaning of the dichotomy, but normally it is impossible to determinate wich was exactly the common ancestor.

Now imagine that the original population formed not one, but two new species. And that this process happened about the same time as the one described before. It is conceptually possible that a set of three brothers were the origin of three different species (wich will be a true trichotomy), but not only it's very unlikely, but it's virtually impossible to prove. Since two close dichotomies are far more probable than a trichotomy, it's assumed that every tree has to be dichotomous, and that a trichotomy is in fact due to lack of resolution.


Do twins "run in the family"? My wife and I recently found out that we are going to have twins and so nearly everyone asks if we have a family history of twins.  Now I know that the answer for me is that it doesn't matter—as a man, I have no influence on my wife's tendency to hyper-ovulate.  And, of course, if we turn out to have monozygotic twins (we don't know yet), genetics plays no part.

Therefore the question only matters on my wife's side and only if dizygotic twins are known in her heritage. As it happens, we don't know of any twins on her side.  Given that many factors besides genetics are relevant to twins being born and we only know her family history for a half-dozen generations with any confidence, what are the odds that we would observe twins in her family history if she is genetically predisposed to having them?

Or, to put in another way, can I respond that nutrition and other factors were probably more important than genetics?

The propensity for heterozygotic twins seems to be driven primarily by genetics, with additional factors playing a role (http://152.98.160.29/contents/p/staff/CV162Lewis_UQ_Copy.pdf', info site):

hormones ("Mothers of fraternal twins tend to be taller, and have earlier and shorter menstrual cycles")
ethnic background (which is really genetic) - African women are more likely than Caucasian women to have them, and Caucasian women are more likely than Asian women to have fraternal twins
mother's age
nutrition
previous births
fertility drugs

I also found a link to a genetic study published in Nature that claims to have linked a DNA region to dyzotic twins, but the Nature website seems to be down - maybe it will work later: A region on chromosome 3 is linked to dizygotic twinning - Nature.

Note that the father does not contribute to the chance of having heterozygotic twins, but a male offspring could pass the gene to daughter.


Largest direct ancestor of humans Going back the genealogical lineage from present humans to the beginning of life, what was the biggest - in terms of body size or mass - animal in this sequence?

More generally, what would a time vs. size graph look like? Obviously the first ones were tiny microbes, but do we have "deep valleys" and high peaks one after the other? I know that our ancestors at the time of the dinosaurs were very small rodents. Were there some even smaller ones earlier (not referring to the microbes)?

We can't really say for sure, because we have insufficient information about this. We can't trace every step of evolution through fossils. We can make educated guesses for most stages of evolutionary history, but they remain guesses.

Please note: Most of what we find in the fossil record are species that are not directly our ancestors, but rather branched off our evolutionary line and then went extinct. Those fossils can still give a good indication as to what the morphological features of our common ancestor were. And a lot of this is guesswork with some evidence behind it.

Going "down" the timeline of humans, we roughly encounter these steps:

Homo

The genus Homo: appeared roughly three million years ago, includes species such as Homo erectus and Homo habilis. Fossils of Homo habilis point to a height of around 100 to 135 centimeters, fossils of Homo erectus are closer in size to modern humans with 145 to 185 centimeters. The rest of the Homo genus was smaller than modern humans (Homo heidelbergensis/rudolfensis/neanderthalis)

Australopithecus

The fossils from Australopithecus are around 3 to 4 million years old, the most famous is probably "Lucy", a member of Australopithecus afarensis. Since members of all Australopithecus species appear to be smaller than humans (afarensis: 100-150 centimeters, africanus: 115 to 140 centimeters, etc.), it is likely that our common ancestor was smaller than modern humans. (Our ancestors likely were Australopithecus, we just don't know which species)

Apes

The split between the line leading to modern humans and the line leading to modern chimpanzees occured somewhere around 4 to 7 million years ago. The clade is called Hominini. The split between those and the line leading to modern gorillas occured around 8 to 19 million years ago (yes, the dates are getting fuzzier). A fossil coming close to this ancestor may be Nakalipithecus nakayamai, however, we only have a fossil jaw from that species.

Going back, we get to the split between modern-day humans/chimpanzees/gorillas and modern-day orang-utans. This is the "ape" family, Hominidae. The largest ape that we know of, Gigantopithecus, that grew to about 3 meters, is classified as an orang-utan. Note that this is not a direct ancestor of humans. Even if our ancestors were larger than modern humans at this point it's unlikely that we are talking about anything larger than a big gorilla.

Primates

Going a bit in the reverse order here: The first true primates evolved around 55 million years ago. Fossils from that time are about the size of squirrels. Humans are "old world monkeys" who first appeared around 40 million years ago - the fossils from that clade we know, for example Apidium or Aegyptopithecus are a bit larger, some as large as a dog.

Primate-like mammals

The first primate-like mammals, called Plesiadapiformes appeared around 60 million years ago. We don't know all that much about them, but the most famous Purgatorius was the size of a rat or mouse.

Mammals / placenta mammals

Going back even further, things become even murkier, but early mammals were small. Placentalia, placental mammals appeared around 90 million years ago. They were small, arboreal (tree-dwelling) animals. Early mammals appeared around 160 million years ago and fossils we have from that time place them around the size of a shrew.

Now, is it possible that there were larger mammals in there somewhere, that then "shrunk" again? Sure. Just unlikely.

Therapsid

Therapsis are mammals and their ancestors, evolved around 275 million years ago. The most well-known fossils from around then are Tetraceratops insignis. All we have from it is a skull of about 9 centimeters size.

Synapsid

Synapsis are making things complicated. As you mentioned in a comment, there were some really big synapsids. According to the Tree of Life project:

  Early synapsids were moderately large (body length between 50 cm and 3 m)

Tetrapods

Tetrapods is the name for the clade that encompasses what we now call amphibians, reptiles and mammals - those animals appeared around 380 million years ago. An example of an early fossil from that time is Dendrerpeton, which was up to 1 meter in length.

Vertebrata

Synapsids are vertebrates. Vertebrates first appeared more than 450 million years ago. The time period following that, the Silurian, is called the "age of fishes".  Those fish could get really large, some of their jaws being over one meter wide. That's really all the information I could find.

Chordates

Taking another big step back, vertebrates are chordates, a group that first appeared in the Cambrian, somewhere around 550 million years ago. Early fossils are mostly small, for example Pikaia is about 5 centimeters large. Yannanozoon lividum is around 3 centimeters.

Before chordates

Before chordates, we really don't know all that much, the fossil record is poor because the structures that usually fossilize hadn't even evolved yet. For example, Hiemalora is around 3 centimeters in diameter. Whether it is our ancestor, we have no idea.

And before that come the first multicellular animals, the first animals, the first eukyrotes, and the archae,...

In summary

In summary, while we can only make guesses, the history of animal size from unicellular organisms to us probably wasn't spectacular. We go from very small (pre-Cambrian), to small (Cambrian), large or small (fish and synapsids), around 1 meter-ish (tetrapods), smaller again (early mammals, mammals), a bit larger (primates), again a bit larger (apes), and then to "human-sized".


Would some dinosaur egg be the most massive cell that ever existed? Are dinosaur egg relatively small compared to eggs of modern birds? The egg of a large modern bird is a very large cell, not the largest possible biological cell since there are very long nerves in squid, but it's likely the most massive modern cell.

But, what about the cells of prehistory? Many dinosaurs were far larger than modern birds, but I had trouble finding information on just how large their eggs could be. I was also surprised that the eggs were not bigger than those of modern birds. It seems the ratio of egg size to dinosaur size was much smaller... or has that even been studied?

Maybe the large eggs were all destroyed?

The biggest known egg was laid by Aepyornis, the so-called Madagascan "elephant bird." See this short video. Of course, the eggs of most dinosaurs are unknown, so there could be something more massive waiting to be discovered. But the eggs of species much bigger than Aepyornis have been discovered, and the eggs just don't measure up to Madagascar's champion.

I'm not an expert on dinosaur eggs, but if you're looking for information, try searching for Protoceratops and Maiasaura peeblesorum. Protoceratops is a ceratopsian, ancestral to the more familiar Triceratops, whose remains are abundant in Mongolia. I believe many Protoceratops eggs have been discovered. (See At Last, A True Protoceratops Nest)

Maiasaura is a duck-billed dinosaur (hadrosaur) that left numerous fossils in what is now Montana. The fossils include some fabulous remains of nurseries (e.g. Egg Mountain). (See Maiasaura)

These links may not feature any information about egg size, but they should at least give you some background information. I'm sure Dr. John Horner has commented on the size of Maiasaura eggs somewhere. He's written on a wide variety of topics, including dinosaur growth rates, physiology, etc.

P.S. Here's a cool link. There's a photo of a fossilized Maiasaura embryo emerging from its egg (#4, I think). Another page (8?) claims that no dinosaur egg could be more than two feet in diameter.


Did the Britons 100 years ago have different intestinal flora and fauna? Note: this is not a question about history, but about human digestive system over time :)

I know a lot of colleagues who traveled for business trips to India. All of them caught  terrible diarrhea there, in spite of keeping all the rules related to use of reboiled or canned water only, eating only peeled fruits, not eating the street food etc.

My question is: how did the millions (or hundred thousands, I am not sure with the amount) of Britons survived in India during the time of the British Raj 1858-1947?

Did they have to keep the same safety dietary rules as the contemporary Westerners all the time? (I cannot see this as technically possible...)

Were our intestinal flora and fauna different one hundred years ago?

Was the hygiene level and quality of water much lower in Europe then so coming to India was not such a biological shock? (Well, I would believe this in the 1800s but not in the 1900s...)

Or did just some of them die and the rest got accustomed?

EDIT:

I am aware that there is an initial shock for your body when travelling to a very different area generally. However, the Indians (and other Asians) can easily drink the tap water in most of the EU countries and eat the street food, which is not valid vice-versa. So there must be some difference.

Who said they did not have the same problems? I'm sure they did and I'm sure most of them had horrible diarrhea.

A quick google search brought up Man and Microbes: Disease and Plagues in History and Modern Times, by Arno Karlen which states that

  In 1817, when the first cholera pandemic began [...]. In Calcutta and Jessore, cholera killed 5,000 British soldiers within weeks

However, those who survived would get used to it eventually. Cholera is much more serious than simple dysentery of course but its main symptom is also diarrhea.

The locals of wherever you happen to be are used to the pathogens that are common in the drinking water. If I am not from a place and drink water with new pathogens, I will be sick. I will also, however, eventually get over it and my body will be used to them. Depending on the details, either because I have developed an immunity or because I have developed the necessary intestinal fauna to deal with it.

So while the intestinal fauna may indeed have changed over time, this has absolutely nothing to do with what you're asking. First because your assumption is wrong (the British were subjected to the same health issues as modern Europeans visiting Asia) and second because people adapt.


Differences in the action of Scopolamine and Atropine Both Scopolamine and Atropine are muscarinic antagonists, having essentially the same action: blocking parasympathetic nerve receptors.

The action on the brain by muscarinic antagonists is presumed to be caused by dilation of blood vessels, thus we might expect the effect on the brain by the two compounds to be similar.

However, in actuality the action of the two compounds on the brain is somewhat different. Scopolamine begins causing strong psychotropic effects even in very small doses before it has any effects on the skeletal nervous system. Conversely, atropine begins having effects on the muscular system long before it begins having psychotropic effects and in fact, potentially toxic doses of atropine have to be administered before significant psychotropic effects begin manifesting.

If the apparent biochemical action of the two compounds is similar, why do we see this difference in the effects between the two with regards to the brain?

It seems that the reason for the different effect of Atropine and Scopolamine on the brain is related to the structural difference between them.
From the chemical structures below it is evident that the two molecules are almost identical, save for an epoxide group that is found in Scopolamine but not in Atropine.

According to Brody's Human Pharmacology: Molecular to Clinical, 5th edition, 2010, pp. 113-115, this epoxide reduces Scopolamine's base strength and enables it to penetrate into the brain more readily than Atropine.
Faster penetration into the brain = earlier appearance of psychotropic effects.


What is this wood-infesting insect? I have these insects in a very old wooden floor. I would like to know whether they are possibly termites, and if not, what they are.

They are about 4 mm in length (and I've had difficulty taking a picture with a standard camera, I may be able to get a better one in a couple of days). This one is dead and may have been crushed a little. Another sign of their presence is little heaps of wood dust appearing with a periodicity of 24-48 hrs, which are about 1 cm in diameter.

Following the indications of @usr137, I think it's rather an ant, indeed it has a slender mid-portion of the body, corresponding to detail (4) in this termite/ant comparative:

But they are much smaller than the ranges I find for carpenter ants (6—19 mm).

To close this, we're now reasonnably sure that they were carpenter ants or a close relative. One more clue is that they infested the wood close to a window receiving sunshine and were much more active when it was warm there. Thanks to @user137.


Consequence of Plants as Incomplete Protein Source Some years ago, in a 1000~ level biology course we learned that the DNA essentially encodes formulas for creating proteins from amino acids. While the human body can synthesize many many amino acids, some we are unable to synthesize and we dub these as essential amino acids because we must obtain them from our diet. However, surely something must be capable of synthesizing the amino acids, otherwise they would not make it up the food chain to us, which opens the door to the possibility that animals may have varying capabilities in regards to amino acid synthesis. Presumably, this is why cats have to obtain a high protein diet, as they have high need for protein but a poor ability to synthesize them?

Moreover, in doing basic research into nutrition to plan a regular workout schedule there is some need to distinguish protein sources as not all protein sources are considered to be complete proteins because they do not provide all amino acids, or otherwise do not provide them in the right balance.  Particularly, many fruits and vegetables tend to be poor sources of protein.

For plants which are incomplete protein sources, they would seem to lack the ability to synthesize some amino acids. They also would not be able to obtain these through diet, as they're plants. Consequently, does this mean that some plants may not encode for a specific amino acid throughout their entire DNA?

With a few exceptions among some bacteria, all species on the planet make protein from the same 21 amino acids, and the relative abundances of amino acids is very similar in proteins from plants, animals, fungi and even prokaryotes. See for example this article (available as PDF here). So protein from pretty much any food provides the same amino acids.

The idea that plant proteins are "incomplete" and lack some amino acids seems to be a myth: see for example this correspondence in the American Heart Association's journal Circulation. Plants generally contain less protein than meats per weight, but there is nothing wrong with the protein they contain. Most people in the world obtain the majority of their protein from plants. There are probably some specific parts of some plants that are not nutritionally optimal --- if you for example lived exclusively on peanuts for a year, you might experience some problems ... But any commonsense, varied plant diet will provide all amino acids. A detailed report (and some mythbusting) is here.

Regarding essential amino acids, as mentioned in comments this is a species-specific concept. Humans and most animals can synthesize about half of the 21 amino acids, while the remaining are essential. There are some species differences --- arginine is essential for cats, for example, but not for adult humans. In contrast, plants can synthesize all amino acids. But their protein composition is similar in the end.


Explanation of the meaning of high-throughput Almost all of the papers about bioinformatics, I faced with the high-throughput word, but I could not find any explanation about it (I think it is so easy to understand and that's why anyone explains it but I could not do it ) . Is there anyone who can explain me what do they mean by high-throughput ? Thanks in advance.

High-throughput sequencing specifically refers to sequencing techniques like Illumina that allow you to sequence massive amounts of DNA at once (hundreds of thousands of strands), as opposed to older techniques such as cloning the cDNA in plasmids, followed by sequencing.


ratio between heat transfer coefficient and thermal conductivity Consider the Robin boundary condition for the diffusion/heat equation $\mathrm{u_t=a(t)u_{xx}+f(x,t)}$:

$$\mathrm{-k(t)u_x(0,t)=h(t)u(0,t)}$$

or

$$\mathrm{u_x(0,t)+\frac{h(t)}{k(t)}u(0,t)=0}$$

where $\mathrm{k(t)}$ thermal conductivity and $\mathrm{h(t)}$ heat tranfer coefficient.

My Question: Is it possible that the ratio $\mathrm{h(t)/k(t)}$ to be constant? Could anyone please help me? I have really no idea.

Most likely, you can't assume that $h/k$ might be constant. Reason is that those parameters are characteristics of two very separate systems.

Thermal conductivity shows how fast heat can be propagated through material. That is, it answers question: if block of metal has $T_0$ temperature on its surface A, and you apply temperature $T_1$ (higher) to opposite surface B, how long it will take for whole block to get to temperature $T_1$.

Heat transfer coefficient is a characteristic of a system. For example, when you have coolant on one side of metal plate, and heated air on the other. Question is how efficiently heat will be transferred from one side to the other. For more you can check this link. As you can see, transfer coefficient $U$ is a function of conductivity of the metal plate $k$. Hence, generally, relationship is non-linear.


Why does the side of the mebrane of a neuron with a high concentration of positive ions become electrically negative? I am having a real hard time understanding why the side with a high concentration of positive ions becomes the negative side of the membrane (in a neuron). This website http://www.st-andrews.ac.uk/~wjh/neurotut/mempot.html says its because "...the positive ions flow away from the high concentration side". But I still don't get it. Wouldn't it make more sense to then say that the high concentration site (more positive ions) has more positive voltage?

Q. “Wouldn’t it make more sense to then say that the high concentration site (more positive ions) has more positive voltage?”

A. No.

I know little about electrophysiology, but looking at the graphics and explanation that precede the screen from which the sentence you quote is taken the statement is justified. Where are you going wrong?

Your argument implies that the side with the high concentration should be positive because it has more positive (K+) ions. But it has (initially) an equal number of negative ions (Cl–) so it is initially electrically neutral. (The graphic indicates this by having no charge on the K — not a very satisfactory idea in my opinion.)

The important thing to note is the premise — that the membrane is permeable to K+ ions, but not to Cl– ions. So, even though there is a concentration gradient, only the K+ ions can move across the membrane (the graphic shows those moving with a +ve charge). As they do so each leaves its ‘partner’ Cl– ion behind, so a negative charge builds up at the high concentration side. At equilibrium there may be a high concentration of K+ ions at the ‘left’ of the diagram, but there is an even higher concentration of Cl– ions!

Good luck with your further reading of these pages! It looks as if it gets much more complex as it goes on.


How do poikilotherms thrive in a wide range of core temperatures? What is it about the metabolism of a poikilotherm that enables them to adapt to the surrounding temperature?

I'm not an expert in this topic but I have read a reasonable amount on animal thermal regulation, especially in insects, so maybe I can give some insight into your question.
First of all, an important thing I learned is that one must differentiate poikilotherms from homeotherms and endotherms from ectotherms.
According to Randall et al (1997):

Endotherms are animals which generate their own body heat through metabolism, while ectotherms have a hard time generating enough body heat to maintain their physiological functions, as they have low metabolic rates.
Homeotherms are animals which are able to maintan their body temperature at a more or less constant rate, while in poikilotherms body temperature fluctuates more or less with the environmental temperature.

This a somewhat troubling classification. Insects, for example, are considered ectotherms/poikilotherms, but they may show a condition called heterothermy: they are (most of the time) ectotherms, but they may be able to generate heat through some metabolic activity, and in this situation, they are showing endothermy. This happens quite often in winged insects, which may raise their body temperatures by flapping their thoracic muscles which move their wings. They may also ventilate themselves using their wings, lowering their body temperature, which (I'm not sure about this) may be considered an endothermic behaviour, as they are lowering their temperature in spite of the ambient temperature. Bees and wasps are even able to control their nest temperatures when the whole colony uses their wings to heat or cool their nest. So classifying animals in one of these categories is not so straightforward, but I'm just pointing this out because this is important. I don't think this invalidates your question, so I will talk about poikilotherms/ectotherms for now on.

One important thing to know about these animals is (Randall et al 1997):

  Often, ectotherms have low rates of metabolic heat production and high
  thermal conductances-that is, they are poorly insulated. As a result,
  heat derived from metabolic processes is quickly lost to cooler
  surroundings. Accordingly, heat exchange with the environment is much
  more important than metabolic heat production in determining an
  ectotherm's body temperature. On the other hand, the high thermal
  conductance allows ectotherms to absorb heat readily from their
  surroundings.

As for how they control their temperatures...well, there are lots of mechanisms. I'll state some of them.

As Remi.b stated, behaviour is an important mechanism of temperature regulation in poikilotherms/ectotherms. This happens with basking/avoiding sunlight (as previously said), but also happens in the example of wing flapping I mentioned. Another interesting behaviour mechanism for temperature control is microhabitat selection: desert ants, for example, may face soil temperatures as high as 70° C when searching for food. They lower the harmful effects of such a high temperature by standing high on their legs and/or climbing onto small grasses or rocks which they find through their way. This may seem useless to us, but it plays a big difference between life or death for them (Marsh 1985).
Some animals have antifreeze substances in their blood which prevents them from freezing to death (see Randall et al 1997). This is common in arthropods.
Colour may play an important part in temperature regulation, as lighter body colours make the animal absorb heat less quickly than darker colours.
Some bumblebees may heat up by producing heat at the cost of ATP (a clearly endothermic characteristic) (May 1979).
Body size plays a huge part in body temperature regulation, not only in endotherms, but in ectotherms too. Lighton et al (1994) demonstrate that bigger workers from a species of ant called Veromessor pergandei can withstand dessication from higher temperatures for longer than smaller workers (and they show only a few milimeters difference in their sizes).

Well, as you may see, I don't think there is a straightforward answer. The way I look at it is that, as almost anything in biology, different organisms may show different strategies of coping with thermoregulation. I suggest you take a look at the following book if you want to know more or if I haven't quite answered your question (and the articles I have cited are the ones below):

Book: Randall et al. 1994. Eckert Animal Physiology: Mechanisms and Adaptations. W. H. Freeman  and Company.

Journal articles:
May, M. 1979. Insect thermoregulation. Annual Review of Entomology.

Lighton et al. 1994. Is bigger better? Water balance in the polymorphic desert harvester ant Messor pergandei.
(The name of the ant above changed, that's why I called it Veromessor pergandei)

Marsh, A. C. Microclimatic factors influencing foraging patterns and sucess of the thermophilic desert ant, Ocymyrmex barbiger. Insectex sociaux.


Did the construction of the Panama Canal lead to a huge change in the local marine ecology? Before the Panama Canal opened in 1914, its two ends were only 77 km apart over land, but the closest sea route was 32,000 km long (around the entirety of South America) and passed through much colder waters near Cape Horn. Therefore, I suspect that the Atlantic and Pacific marine ecosystems were more or less completely isolated from each other and contained very different species before the Canal opened. It also seems plausible that once the canal opened and a 77-km marine route opened up, these two ecosystems very quickly came into contact and may have reached a new, drastically different equilibrium. Is this correct? I could imagine the ecological effects being equivalent to the sudden creation of a 77-km bridge connecting the ecosystems of, say, the United States and Kenya.

The panama canal is not just a long contiguous connection between the two oceans as you might think. It operates under a system of locks of varying height because the surrounding region is actually fairly mountainous, so a ship has to enter a lock, let it fill until equilibration with the next lock whilst the boat rises, the barriers open, the boat moves into the next section and the process repeats. It is fairly unlikely much wildlife would be able to pass through this system thus not causing the vast ecological effects you might imagine. https://www.youtube.com/watch?v=hoQ7RHyG-EA this link visualises it for you :)


Does increased physical activity increase the rate of cell division? Ever since learning that the shortening of telomeres is linked to aging I've tried to figure out what causes cells to divide, and if it's possible to slow down the rate of cell division through life style changes.

How would, for example, increased or decreased metabolism affect the cell cycle? If we exercise a lot, would it tear on the cells in any way, forcing faster cell division?

My understanding is that telomeres are linked to cell senescence, which is not necessarily the same thing as organism senescence. So even if you could track down a method to slow cell division, it would more likely mess with organ function now rather than extend life.

Here's a nice summary of cell senescence: http://www.ncbi.nlm.nih.gov/books/NBK26877/#A3266

I did look into cell division in muscle, and new muscle cells come from satellite cells, rather than from mitotic division of currently active muscle cells.

Caloric restriction was the hot new way to live longer for a while, but studies in primates found that a sensible diet and good genetics have a bigger effect. Which is pretty much the T-shirt in medical science.

This question was asked last spring as well. Coincidence? Homework?


Do animals' facial expressions have similar meanings to humans'? In the following pictures, the dog seems to be smiling to the camera. People staring at these picture also tend to feel comfortable and relaxed, presumably because they think it's very happy playing with the swing.

However, my question is, is the dog really happy, or we are just (incorrectly) interpreting the dog's facial expression according to our experience used to read humans' facial expression?

I would say no, facial expressions in humans do not generally relate to facial expressions in other animals. Even though there are some cases (as described in the comments an previous answers) that refer to domesticated animals, I do not know of any convincing evidence that the facial expressions of humans are faithfully interpreted, or even mimicked, by other animals - at least outside the group of great apes. Further, the cases arguing that (domesticated) animals can do it are often anecdotal (I am not saying wrong!). Taking an evolutionary perspective, I would not even expect it to be happening (or rather by very close relatives only, i.e. other great apes) because facial expressions as behavioural signals are part of communication and therefore often rather species-specific.

But not only that ... there is emerging evidence that facial expressions are not even interpreted uniformly in all human populations: in this article by Crivelli et al. (2016) in Front. Psychol. the authors argue to include anthropological data to cognitive studies. According to their findings, not including a human evolutionary perspective might result in strong biases. They strengthen their point by giving an example of differential interpretation of facial expressions in a Melanesian society which is described in more biological terms in PNAS [Crivelli et al. (2016)]. What they found is that adolescents of this society interpret a facial expression (gasping face) that in other societies conveys fear as a threatening and angry expression.

Generalising this means that if there is divergence in signaling by facial expressions even among human populations, I would consider it unlikely that there is a general homologous system of facial expressions among mammals. There might, however, be a trend in domesticated animals to understand human expressions and adapt behaviour according to them. It still is an extraordinary claim to infer from this that they can actually mimic these expressions, and I have not yet seen convincing evidence for that.


Why isn't the insertion of a single nucleotide destructive for DNA? As far as I know proteins are built by sequentially reading triplets of nucleotides.
But if at a certain point a nucleotide is inserted in the sequence, the following sequence of triplets is completely different.

For example:

AATACGGTACCATTA ...

AAT ACG GTA CCA TTA ...

But inserting a nucleotide B at second place we get

ABA TAC GGT ACC ATT ...

Which is completely different.

However I know from theory that a single nucleotide insertion is not dangerous in most cases.

Could someone clarify my mind about this?

A single substitution can often be silent, or at least not impact the structure and function of the resulting protein in a significant way. But what you describe is a frameshift, and that is one of the most destructive mutations. It will completely change the sequence of the protein after this mutation and disrupt the function of those parts of the protein.

Insertions or deletions that result in a frameshift are absolutely destructive mutations.


Why people fear GMOs? Can't we map a plant composition? My main question is can we map what a fruit is made of? For instance apples are made of 0.0002% of protein X, 0.00001 of protein Y, 0.001% of amino acid Z... etc...

If we can, then my next question would be why do people fear eating GMOs?
I understand the argument that if you introduce a new compound to your body you don't know its effect on you, but if for instance you insert a new gene into the plant where it is resistant to drought- can we not simply analyze its product and if its composition haven't changed than everything is alright?

Thank you very much!

People are not always rational when it comes to what they eat, especially when the compounds that make up the food have long, arcane-sounding names.

It is indeed possible to analyse the amino acid composition of a food substance. However, this has no bearing whatsoever on the safety of the food product.

For example, the following are two truncated protein sequences. One of them is a fragment constituent of cobra venom, the other is a fragment of harmless DNA polymerase. Without looking up or otherwise referring to the PDB IDs, it is not obvious which is which, even to an experienced molecular biologist.

  3HRZ:A|PDBID|CHAIN|SEQUENCE
  ALYTLITPAVLRTDTEEQILVEAHGDSTPKQLDIFVHDFPRKQKTLFQTRVDMNPAGGMLVTPTIEIPAKEVSTDSRQNQ

  1KLN:A|PDBID|CHAIN|SEQUENCE
  VISYDNYVTILDEETLKAWIAKLEKAPVFAFATETDSLDNISANLVGLSFAIEPGVAAYIPVAHDYLDAPDQISRERALE

Furthermore, even if scientists can prove beyond reasonable doubt that the two products are chemically identical, people will still irrationally purchase them. A clear example is the different prices commanded by "natural" versus "artificial" flavourings, as seen in this Scientific American article.

  Consumers pay a lot for natural flavorings. But these are in fact no better in quality, nor are they safer, than their cost-effective artificial counterparts.


Does zygosity have meaning for mitochondrial variants? I am working on a system that annotates variants in human DNA sequences. One of the pieces of information reported is the zygosity of the variant. I noticed that mitochondrial variants are also shown to be either homo- or heterozygous.

How does that make sense? Does it make sense? As far as I know, the mitochondrial DNA is just a single, circular DNA molecule. So I can understand considering all mitochondrial variants heterozygous, by definition. I could also accept that one could think of them as homozygous by definition. I just don't see how some variants can be homo- and others heterozygous. Am I missing something or is the annotation system I'm using not making sense?

You abosolutely can have mixed populations of mitochondria in a cell (it is in fact very common). Therefore when you sequence the mtDNA you will get a completely variable percentace of reads containing a variant from close to 0% to 100% (there is a lower limit based on the quality and read depth of the sequencing data).

You can't consider the variants to be heterozygous or homozygous as conventional zygosity doesnt apply. Heteroplasmic and homoplasmic are the terms which are used.


What are the advantages and disadvantages of being ambidextrous? Most of us have one dominant hand. We find it nigh on impossible to do very delicate or dextrous activities with our other-hand. This seems like an apparent weakness, and a rather odd one when you first think about it.

Cursory internet searches revealed unexpected findings. One website said it has mostly negative effects on the brain. However I don't trust the source at all.

I'd be interested to know about the "story" about the good and bad of ambidextrous physiology. Particularly, I am interested in the neuroscience of ambidextrous people.

I think that the advantages of using both hands with equal ease is quite evident whether it be sports, at your work or while you are doing your household chores.

An obvious advantage is using both hands to write or draw with both at the same time.

I would be focusing on the disadvantages that may be faced.

  1) Ambidextrous people are more prone to suffer from Synaesthesia
  (reference)

  2) They are likely to possess (not necessarily) the LRRTM1 gene which
  is linked with Schizophrenia (reference).

  3) They score lesser in intelligence testing (reference).

  4) Mixed handed children are more likely to suffer from ADHD
  (reference).

  5) Mixed handedness is associated with greater age-related decline
  (reference)

  6) They are easier to anger and influence emotionally (reference).

There are quite a few studies that have pointed out that it may not be all that good a condition but Leonardo da Vinci who was probably the most diversely talented man who ever lived is said to have been ambidextrous. He apparently could draw with one hand and write with the other at the same time, so I would have to say that the positives of the condition are extremely good (reference).

edit:

This probably qualifies as a second question :-D but I just saw a thought by biogirl in the comments section on "whether our ancestors used both the hands and using just one hand is recently evolved" and she has a point there. From a study publlished in 1977 I quote.

  The predominance of the right hand over the left was also reported
  among Egyptian art forms 3,500 to 4,500 years old, where the ratio of
  left- to right-handers was 9:111 and 5:100, respectively. However,
  going further back using the "Draw-a-Man Test," found that ancient
  paleolithic man, from 1,750,000 to 8,000 years B.C., was probably
  either more ambidextrous or that there was a greater proportion of
  left-handers than there are now. (reference)

Also from a study titled "Evolutionary Back Grounds of Human Left Handedness", the authors concluded that

  For most manual tasks, especially those tasks involved in competitive
  activities, increasing performance by the specialization of one hand
  is certainly adaptive. Aggressive interactions are responsible for
  fundamental selection pressures acting during primate and human
  evolution. The higher prevalence of right-handedness might well be due
  to a previously existing cerebral bias. But the specialization of one
  forelimb leading to right or left-handedness is better viewed as the
  result of natural selection. (reference)


What is the lifecycle of hanging woody vines? In the first ten seconds of this video, you can see a vine that appears to have started its life 60 feet up in a tree and has now grown down almost close enough to touch the ground. I have seen similar vines that do make it to the ground and start curling around, but don't sink roots. Why do they create this long woody stem? Or do they start at the bottom, grow up the tree, and then release their roots somehow so they can swing free? They're sometimes not wrapped around the trunk at all, just hanging from the very upper branches, as if their seeds found purchase there and started stealing nutrients to grow. Is that possible?

I have swung from these in several locations in Wisconsin and Iowa. They're very tightly attached.

There are no epiphytic vines in the US. Most likely, if it's sturdy  enough that you can swing from it, it's the vine of a wild grape. (The vine in the video is classic wild grape.)

They grow like most other flowering plants: they start innocently enough with a seed that takes root in the ground. They are initially tender and small stemmed.

From there, they grow along the ground, sending out tendrils. If they find something growing vertically, they cling to it (a shrub, tree trunk, or a low hanging branch) and grow upwards towards the light. If they have enough light (they are shade intolerant), they continue to grow, branch, and elongate. because they can become quite heavy, they break canopy branches of their supporting tree and fall in long loops toward the ground.

If the loop breaks for some reason, you have one swinging vine. But if you diligently follow it back, you'll find either the continuation of the vine near the canopy (the part after the break) or the trunk growing from the ground alongside of a nearby tree.

Though cool-looking, they are very destructive, bringing down not only branches but often entire trees (plural. They intertwine different tree branches, and if they bring down one tree, others fall in a domino-effect.)

Imagine that SOB hanging onto your upper arms for support (not the guy, the grapevine).

Smaller vines (which can also be destructive) that climb up the sides of trees are Oriental Bittersweet, Poison Ivy, Virginia Creeper, etc. (Probably Kudzu as well, but we don't have that here yet.) But these aren't likely to become large or sturdy enough to swing from if they come loose from the tree.

This is a photo of two common offenders: a wild grape (dark shreddy bark, about 2.5 inches in diameter) being slowly strangled by an oriental bittersweet (lighter bark), both climbing this large oak. If you look carefully, the base (roots) of both these vines are behind the tree (about five feet), one on either side. (You might have to take my word for it...)

Wild Grape


What is this yellow-pink flower? Found in Pennsylvania, Philadelphia County

This is intentionally planted, not sure if it is indigenous to this region. Thank you for your expertise!

It resembles Lantana Camara, from the family of Verbenaceae that is native to American tropics according to Wikipedia.

They come in variety of different colors, and the one you have photographed is the Pink Caprice.

Image Source: Cindy Dyer's Blog


Would muscle fatigue still occur if aerobic conditions for a working muscle is maintained? Put another way if the muscle is given everything it needs to contract and do work will it ever get tired or have a reduction in energy efficiency?

As far as I understand muscles depend upon a blood supply delivering oxygen and nutrients (e.g. glucose and calcium) to effectively contract at its best level of performance. With the ability to work under anaerobic conditions if need be but producing lactic acid as a by-product which reduces the muscles ability to contract and therefore producing fatigue.

I also know that muscles are dependent upon temperature to work efficiently like the rest of the body. So, if the muscles temperature was able to be regulated well enough to maintain efficiency and aerobic conditions are met could fatigue be negated?

It seems that you are asking about activity significantly above basal metabolic rate. If aerobic conditions are maintained (and with appropriate training), muscles can operate more or less continuously for very long durations, days to weeks. In non-humans:

Godwits have been recorded flying over 7000 miles (>11000 km) without stopping for 9 days
Arctic terms migrate 44000 miles (>70000 km), albeit with stopovers
Humpback whales migrate 5000 miles (8000 km). Their muscles are probably operating close to continuously.
Many (most?) species of sharks swim continuously.

There are probably other examples as well (feel free to add). For humans, usually the limit to endurance is sleep. Two forms of racing push human endurance, but the longer races almost always require at least minimal sleep:

Ultramarathons, foot races of 50 mi (80 km), 100 mi (160 km) or more (e.g., 24 hours, multi-day).
Race Across America, Paris-Brest-Paris, and similar endurance bicycle races. The RAAM has a record time of 3107 mi (4971 km) in 8 days, 9 hours for a mean velocity of 15.4 mi/hr (24.6 km/hr).


What is this bird called? I've found this bird.

Does anyone know what is it?

It is White breasted Kingfisher also called White throated Kingfisher. Halcyon smyrnensis.

Why this is Halcyon smyrnensis?

Halcyon kingfishers are mostly large kingfishers with heavy bills.

According to wikipedia this genus has 11 species, some workers also include genera Pelargopsis, Syma and Todirhamphus.

Out of all the 11 species only two are comparable to H. smyrnensis; Halcyon badia and Halcyon coromanda.

Halcyon badia is an African resident.

Additional information:

They are “sit and wait” predators of small ground animals including large insects, rodents, snakes, and frogs, but some will also take fish.

The genus Halcyon in the current sense consists mainly of species resident in sub-Saharan Africa, with a couple of representatives in southern Asia, one of which, the white-throated kingfisher, occasionally reaches Europe. White-throated and Ruddy kingfishers (Halcyon coromanda) are at least partially migratory.


Can you be infected by two coronaviruses at once? E.g. could you be infected by COVID-19 as well as a different strand of coronaviruses (e.g. those that circulate in the population every flu season)?

Yes:

Coinfections involving multiple HCoVs were also detected (Table 2).
...

Human Coronaviruses HCoV-NL63 and HCoV-HKU1 in Hospitalized Children with Acute Respiratory Infections in Beijing, China, Advances in Virology (2011)


Get protein annotation from Uniprot out of protein mappings Having a file of for about 10k mapping identifiers how can I get the annotations of the proteins from Uniprot  ? As it is not possible to do It manually

My mappings are contained in a .csv file
They are from STRING database Example 9606.ENSP00000387699

This problem is discussed here. Apparently STRING IDs are in KEGG format but these can be mapped on to Uniprot IDs using information downloadable from here. I guess that it is either the protein.aliases data or the mapping_files data that you would need. The first link provides a Python script to extract useful info from the downloaded data. These are big downloads so I haven't actually tried this out myself.

Presumably once you have the STRING→Uniprot conversion done you can query Uniprot with the output as a batch request.

Good luck!


What's the name of the fibrous strands that hold the seeds in a pumpkin? If you cut open a pumpkin, the seeds are suspended inside the pumpkin by some fibrous, slimey strands. You can see them in the middle of this sliced-open pumpkin:

I'm writing a post for the Cooking.SE blog, and am trying to find out the proper botanical term. Someone suggested that might be called the endocarp, but I want to make sure and also see if there is a more specific term.

Edit

In "Morpho-Physiological Aspects of Productivity and Quality in Squash and Pumpkins (Cucurbita spp.)" §C.1, I see this:

  In the central portion of the fruit, a mass of tough fibers, together with vascular strands connected to the seeds, comprise the placental tissue. The endocarp is made up of small, thin-walled cells that form a membranous tissue that adheres to seed, becoming a transparent skin on dried seeds. (emphasis added)

Am I reading correctly that the name for this part of the pumpkin is "placental tissue", and that the endocarp is just a thin layer on the seeds themselves?

This part of the fruit is called "Endocarp". It does not become more specific as that, as far as I know.

http://en.wikipedia.org/wiki/Fruit_anatomy


Can Green color give Rest to Eyes? Is it correct that Green color gives rest to our eyes compare to other colors?

In our eyes, the dioptric difference between the dispersion of red versus blue light is approximately 2D.

Remembering that the human eye's peak spectral sensitivity lies at 550 nm (green), the human retina is deliberately placed such that it is in between the dispersion of white light, i.e., between red and blue. This optimizes the best level of focus specifically for its peak spectral sensitivity. The pupil and the nucleus of the lens also help to minimize chromatic aberration.

In short, the eye is constructed such that it is easiest to focus on green light, which is in the middle of the visible spectrum and has the strongest receptors.


In our solar system which other planet could have been in the "habitable zone" in the past? With changes in our solar system, such as planets moving away from the sun and the reduction in solar radiation, which other planets in our solar system could have been, in the past, in a suitable zone for life to originate?

This answer is also speculative, but according to the planetary habitable zone models proposed by "Habitable zone for Earth-like planets in the solar system" (Franck et al. 2000), a key finding was that:

  an Earth-like planet at Martian distance
  would have been habitable up to about 500 Ma ago while the position of Venus was always outside the habitable zone.

So, Mars could have been habitable, but as it is much smaller than Earth, it has a smaller gravitational field presumably a major factor in how it lost much of its atmosphere.


Does anyone know what insect is this? Living in Brasília, central Brazil; currently experiencing rainy warm/hot days.

This looks like it's a female Pelecinid parasitic wasp (see this page for an overview of the family in the western hemisphere); from your location the species is either Pelecinus polyturator or Pelecinus dichrous (all of BugGuide's images are of the former, that being the one also found in the United States).


Removing Sugars Bound to a Protein I recently purchased some Maltose Binding Protein and as the name suggests this protein binds to maltose. The problem I have is the protein arrive with maltose bound. I know this through native mass spectrometry analysis.

Is there a way of removing the maltose bound to my protein sample while also keeping the protein in its native state?

Examples of two states from the PDB can be seen here: Bound and unbound

It's not clear from the question what the biological source of the maltose binding protein (MBP) is. As you may know E. coli MBP is used as a fusion partner in an expression-purification system marketed by New England Biolabs (this becomes relevant below).
My initial thought upon reading your question was to suggest dialysis. However I found some hints online that this might be problematical and eventually found this on a FAQ at the New England Biolabs site. Looks like this may be your answer.

Question: In order to rebind MBP to the column, the maltose must be removed. Can this be done by dialysis?
Dialysis does not work very well to remove maltose from maltose-binding protein. This is a general phenomenon of binding protein/ligand interactions; after the free ligand is gone, ligand that is released from the binding site usually finds another binding site before it encounters the dialysis membrane (28). We have determined empirically that binding the fusion to a chromatography resin and then washing away the maltose is much more effective. We prefer standard chromatography (e.g. DEAE) as the separation step, since it can separate the Factor Xa and MBP from the protein of interest. In case MBP co-elutes with the protein of interest, we include a large volume washing step to remove the maltose before starting the salt gradient. This way, the mixture can be run over an amylose column afterward if necessary.

So, in summary they are suggesting that you bind the protein to an ion exchange column; wash with lots of buffer; then elute the cleaned-up protein (using salt or a change of pH  - you will have to know something about your protein's behaviour on the column to do this).


How are Genetic Circuits Modelled? I've read a recent Nature Methods paper by Moon T.S. et al, in which a synthetic genetic circuit consisting of layered logic gates was created. For example, the paper, a circuit is modelled in Figure 4a. How is this circuit computationally modelled? Can you refer me to any graduate level texts on the subject?

The following papers are a good starting point:

René Thomas, Boolean formalization of genetic control circuits, Journal of Theoretical Biology, Volume 42, Issue 3, December 1973, Pages 563-585 <= A classic paper in the field.
Thieffry D. Dynamical roles of biological regulatory circuits. Brief
Bioinform. 2007 Jul;8(4):220-5.
Remy E, Ruet P. From minimal signed circuits to the dynamics of Boolean
regulatory networks. Bioinformatics. 2008 Aug 15;24(16):i220-6

You can also have a look at Computational Methods in Systems Biology, International Conference CMSB 2007, Edinburgh, Scotland, September 20-21, 2007. Proceedings, specifically the chapter "Decision diagrams for the representation and analysis of logical models of genetic networks" by A. Naldi, D. Thieffry and C. Chaouiya,


Original paper about the all or none law for neurons I am looking for the original paper about the all or none law for neural activity.

I know that there is a very old article about the all or none law for mammalian heart muscle fibers, but I'm specifically interested in when this idea was first stated about neural activity.

In A logical calculus of the ideas immanent in nervous activity from 1943 this law is already mentioned like an established hypothesis, so it is probably quite old.

This probably goes back to Lucas (1909), Adrian (1912), and Bernstein (1912). But the idea might have started from Helmholtz (1850).

Lucas, K (1909). The ``all or none'' contraction of the amphibian skeletal muscle fibre. Journal of Physiology; 38: 113--133.
Adrian, ED (1912). On the conduction of subnormal disturbances in normal nerve. Journal of Physiology; 45: 389--412
Bernstein, J (1912). Electrobiologie. Braunschweig: Vieweg.

See also: Galvani's Spark: The Story of the Nerve Impulse and The great Era of English Electrophysiology:
from Francis Gotch to Hodgkin and Huxley


Pressure measurement blood flow During blood pressure measurement, when the flow within the arteries of the arm is interrupted, how is blood flow redistributed to the rest of the circulatory system? Is it possible that more blood enters the carotid arteries and therefore causes an increase in blood flow in the brain?

You have a point there, but it probably does not play a big role. First one arm is not such a big branch, and then the carotids contain the main pressure "sensors", so the heart might just beat a bit weaker/slower. Resistance is higher, but demand is less.

Compressions like that can happen all the time, through weight or muscle tension. If it is not both legs at once, this is only a problem for the blocked-off part, after a while.


Plant identification - variegated ivy-like What plant is this? It's in the UK, grown in a pot, and looks like a variegated ivy.

Leaves are about 2 cm in diameter, and the full plant about 50 cm.

Found an answer myself, so here it is.

This is Ceropegia linearis ssp. woodii, also known as hearts on a string or hearts entangled.

More information about the plant can be found at https://www.rhs.org.uk/plants/details?plantid=5862


What do we know about the Last Universal Common Ancestor (LUCA)? All life on Earth (bacteria, archaea, eukarya) is thought to have evolved from a common ancestor, or last universal common ancestor (LUCA). What do we know about the characteristics of LUCA based upon extant life?

Carl Woese has much to say on this subject, including:

  “The ancestor cannot have been a particular organism, a single
  organismal lineage. It was communal, a loosely knit, diverse
  conglomeration of primitive cells that evolved as a unit, and it
  eventually developed to a stage where it broke into several distinct
  communities, which in their turn become the three primary lines of
  descent [bacteria, archaea and eukaryotes].”

There is a 2000 Scientific American article by W.F. Doolittle that discusses much of Woese's (and others') work understanding this question.

Also, see a couple of Woese articles here and here.


No. of genes in chromosomes. phenotype Why do cells need all the genes of all the 22 pairs (excluding the 2 X- or Y-chromosomes) of autosomes in every somatic cell, when each and every cell which is specialised for its function does not manifest all the phenotypes that are encoded by the genes present? Aren't the genes other than those whose phenotypes (& hence some chromosomes) are expressed by that cell, redundant?

This may have to do with the fact that the cells require 'housekeeping genes', which are typically constitutive genes that are expressed in all cells of an organism under normal and patho-physiological conditions. Housekeeping and other essential genes are distributed uniformly across different chromosomes thereby making any chromosome indispensable.

"Housekeeping genes are genes that are required for the maintenance of basal cellular functions that are essential for the existence of a cell, regardless of its specific role in the tissue or organism. Thus, they are expected to be expressed in all cells of an organism under normal conditions, irrespective of tissue type, developmental stage, cell cycle state, or external signal."
http://www.cell.com/trends/genetics/pdf/S0168-9525(13)00089-9.pdf

Intriguingly, chromosome X lacks housekeeping genes. A recent study suggested a possible explanation for this, as follows: "In the end, we have found the answer to be quite simple. Whereas most chromosomes operate in pairs, meaning there are two copies of each gene in every cell, in contrast, we only have one active copy of the X chromosome. This means it is not sustainable for highly active genes to be on the X chromosome. Housekeeping genes tend also to be highly active – they just couldn't survive on the X.”
http://www.bath.ac.uk/news/2016/01/12/x-chromosome/

Gene expression is regulated through transcriptional and translational regulation of genes to generate tissue-specific mRNA. Moreover, through alternative splicing a gene can code for multiple types of proteins. Alternative pre-mRNA splicing is widely used by (higher) eukaryotes to generate different protein isoforms in specific cell or tissue types. This means that the same gene can have different gene products in different cell types.

"Alternative splicing is a mechanism for generating a versatile repertoire of functionally different proteins within individual cells. The significance of alternative splicing is clearly evident in highly specialized cells such as neurons. For example, all of the main neurotransmitter receptors contain subunits that are alternatively spliced, which influences their localization, as well as their ligand-binding, signal-transducing and electro-physiological properties."
http://www.nature.com/nrn/journal/v2/n1/full/nrn0101_043a.html
http://nar.oxfordjournals.org/content/30/17/3754.short
http://genomebiology.biomedcentral.com/articles/10.1186/gb-2004-5-10-r74

Protein-coding sequences account for only a very small fraction of the genome (approximately 1.5%), and the rest is associated with non-coding RNA molecules, regulatory DNA sequences, LINEs, SINEs, introns, and sequences for which as yet no function has been determined. Furthermore, gene expression is controlled by regulatory elements that can be located far away along the same chromosome or in some cases even on other chromosomes. Genes and these regulatory elements physically associate with each other resulting in complex genome-wide networks of chromosomal interactions.
https://en.wikipedia.org/wiki/Human_genome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653627/

The genome is very intricate and consists of elements that interact with each other to regulate gene expression and to carry out various functions. Loss of any of these elements may affect other elements and disrupt cellular homoeostasis, resulting in cellular dysfunction, death or cancer.

I hope this somewhat answers your question.


Help ID snake near Deming NM This snake is in our yard, south of Deming NM, in Luna County.
Approximate length is about 3 1/2 feet.
It moved slowly at the time, but was being picked on by a couple of medium-sized birds.
It is basically black with a black, narrow head.
The body and snout have pale yellowish markings.  On the body, the yellow is individual scales, so almost spotted.  And on the snout, more like lines or stripes.
I have some good photos, and even videos, but it says the files are too big - need to be under 2 giggleburps or something and I don't know how to do that.

Though a full body image would help a lot, I feel certain that it is the desert king snake scientifically known as Lampropeltis getula splendida. This species is seen in most parts of New Mexico and is not venomous. It primarily feeds on rodents, lizards, birds, snakes and eggs.
Here's a link to a website with more details on this species and other snake species of New Mexico: http://www.nmherpsociety.org/reptiles/snakes/lampropeltisgetulasplendida/index.html
Here's a variety of different photos of the desert king snake from different angles (but different ages, sizes and pattern varieties of the same species).


How did viruses learn to utilize the workings of a cell? This is my first post here, so excuse me for its simplicity.

Viruses can infiltrate a cell, overtake it and multiply. It has projecting fibers whose ends are shaped as kind of a "key" to a mobile sentry on the cells membrane so it can be permitted access into the cell. When it enters the endosome of a cell, a protein pump blows an acidic gas onto the virus to break it down, thinking it's a special nutrient. But the virus expects this of course, and when the protecting fibers break off (and so too the body of the virus) proteins are released that rips apart the skin of the endosome so the virus can escape.

These are just two of many things the virus does to compromise a cell. Its entire existence is for the sole purpose for infecting a cell, and it seems to know how to do that perfectly. How did the virus evolve to know how to do things like this?

It's a numbers game.  Viruses can produce thousands, millions, even billions of copies every day, and only one of them needs to be slightly better to get ahead.  Rhinoviruses make roughly one error every time the genome is replicated; over many, many replications a single change can arise giving an advantageous effect.  As another example, it's been said that HIV mutates every single spot on its genome every single day.  Evolution is simply a waiting game.

This article is a pretty cool write up detailing the process.  It says exactly what I said: large numbers, high mutation rate.  Besides, the virus only has to take advantage of cellular processes, not make new ones every time.  That's much more efficient.  It also details some specific changes that explain some differences between similar viruses.  It's amazing, but a single base change can mean a single protein is different which can mean a different receptor is used for binding, which can make all the difference.

And there's this cool quote:

  [T]here may well be more viruses in a single common cold infection than there have been primates in the entire history of life on Earth.


Why does the pET- expression vector contain a LacI gene additionally to the one in the genome? The pET plasmid is used for protein expression with T7 promotor in expression strains, such as E.coli BL21(DE3)

It contains a lacI gene which codes for the lac repressor protein, a protein of interest under the control of a T7 promoter for T7 RNA polymerase and a lac operator which can block transcription, directly behind the promotor. The lac operon is another control of transcription of the protein of interest.

Furthermore, T7 polymerase is located in the genome as well under the control of the lac operon.

When IPTG is added, the lac repressor is inactivated -> T7 polymerase and therefore the protein of interest will be expressed.

The Lac I gene is already present in the genome of the expression strain used, why is it also cloned into the pET vectors?

According to this article, a single lacI gene copy gives rise to about 10 copies of lacI protein per cell, and we can conclude, therefore, that this is the amount required to keep a single lac operon repressed.  The article also mentions the lacIQ mutation in the promoter of lacI that results in a ten-fold increase in the level of lacI protein.

If a lac expression construct is present at more than 100 copies per cell the result will be leaky repression, and this can result in selection for mutations in the gene of interest if it has deleterious effects on the host bacteria. The easiest way around this problem is to put a lacI (or lacIQ) gene on the expression plasmid so that repressor levels are commensurate with the number of copies of the lac operator, as in the pET vectors.


What species is this interestingly colored brown moth This fella fluttered into a kitchen at night, maybe from the vegetation in the yard, and I got lucky to trap it in a transparent plastic bag for a while (with enough room to move, which it started doing at about the same pace it had been flying before but sometimes sitting still) so I got a couple of close-up pictures.
I think the coloring and some other features are too far off the familiar plodia interpunctella to be the same species, also a number of other features seem different in appearance and behavior. (Wings not folded straight back and much wider, doesn't like sitting still on wall for extended period of time.)
Length is about 12-13 mm (wings included and folded). It also sat down wings spread out very wide where I first found it (no picture of that posture included).
Location: Southern part of Germany, city landscape with river/lake within half a mile
What species is this and what would it live and feed on (if the adult feeds at all in this species) ?
As it was examined bottom up, I noticed a contracting and expanding movement of the abdominal segments (roughly last 2 images). What is that movement?

It could be Pyralis farinalis, the meal moth. It is a cosmopolitan moth of the family Pyralidae. Its larvae are pests of certain stored foods, namely milled plant products. I don't think it's adults feed as they do not live long after mating.
Here is a link to its Wikipedia article:Pyralis farinalis


Reasons why this protein is not suitable as an immunogen? In a paper entitled "Progress and Prospects on Vaccine Development against SARS-CoV-2", the authors write the following in section 2.5:

"Compared with S, N, and M protein, E protein is not suitable for use as an immunogen. For one reason, it consists of 76–109 amino acids in different coronaviruses with channel activity, thus the immunogenicity is limited. Studies have shown that SARS-CoV E protein is an important virulence factor, and the secretion of inflammatory factors IL-1β, TNF, and IL-6 are significantly reduced after
knocking out E protein"

Question

Why does the fact it consists of 76–109 amino acids in different coronaviruses with channel activity imply its immunogenicity would be limited?

The article implies E proteins are quite different between the previous known strains - so a vaccine targeted against E protein may only affect a limited range of strains.

But when I do a BLAST search on CS079032.1 I find nearly all the protein sequences are identical (results below).


Can mold grow on copper pipes? Couple months ago noticed something was literally, for lack of a better term, eating paint off of lead pipes.  And I noticed joints in copper pipe seemed to be "leaking" flux. Now all the water in my house causes lips and tongue to feel as if they have cold sores or anesthesised.  taste could be rusty.

Copper inhibits growth of organisms. See " Antimicrobial properties of copper" in Wikipedia.


Can cerebrospinal fluid deliver nutrients/drugs to neurons during sleep? I'm looking at this article on the possible mechanism of detoxifying brain during sleep using cerebrospinal fluid. It states that at night, the space between neurons may allow better (up to 20x) circulation of cerebrospinal fluid within the brain to clean out metabolic by products of daytime activity.

My question is if this may also work in reverse and allow to deliver drugs within the fluid to the brain.  If a person ingests a drug or nutrient before sleep, would the increase in circulation of cerebrospinal fluid deliver the drug to deep regions of the brain? Or does the blood-brain barrier prevent drugs from entering cerebrospinal fluid?

Only certain drugs can cross the blood brain barrier (BBB). However, there exist techniques to deliver drugs to the brain that otherwise cannot permeate through the BBB.
One such technique is called intrathecal delivery that injects drugs directly into the cerebrospinal fluid, avoiding the BBB problem and allowing the drug to reach cells, including neurons, in the brain. It has been used for certain kinds of chemotherapy, pain management, treatment of spastic cerebral palsy, and more recently for enzyme replacement therapy.
However with intrathecal delivery there is a risk of infection.

Having said that, if a drug reaches the CSF then your hypothesis should be correct. There is no experimental evidence for it yet.


Drake's Law. What is the genome-wide mutation rate and what are the estimates? Drake's rule

Drake's rule states that the genome-wide mutation rate is more or less constant across all species — from E.coli to the house sparrow.

Data

From what I think being Drake's original paper (table 1, page 4) on the subject (see here) is at the order of $3\times 10^{-3}$. When I look at this paper, I see that the genome-wide mutation rate is roughly around 30 for human. When I look at this paper, they cite some other papers suggesting a genome-wide mutation rate in the order of 0.1 to 1 in multicellular eukaryotes and typically at the order of 1 for vertebrates. Finally, when I look at this speech (at the 60th minute), it seems however that the genome-wide mutation rate in human is 2.2.

What is going wrong?

Do I mix-up different concepts or are there some very contradicting estimates depending on the article we look at? Isn't the genome-wide mutation rate, $U$, which is just the number of de novo mutations transmitted to one offspring on average? What is a correct estimate of $U$ for human for example (1, 2.2 or 30)?

There are so many things that are implied in this paper, not explicitly said.

The mutation rate here detected seems to be the emergence of chain-terminating (CT) mutations, which truncate protein coding genes, usually just one gene in a bacterium or phage, which would be possible to observe from inspecting a plate to see which colonies die or survive.

This is only a specific kind of mutation, but Drake assumes that its frequency is related to the overall mutation rate.  Which is probably fine.  Mutations we infer from this work arise spontaneously from a similar mechanism in all organisms.  This is just ionizing radiation for the most part.  So at a first glance we still believe this.  That there are no specific mechanisms for mutation.  Since this is usually ionizing radiation we would expect that the rate would go up when there's more radiation around and it most certainly does.

There are lots of reasons that animals and humans would have a smaller rate.  Drake is including in the paper the involvement of DNA repair mechanisms in the experiment as they are intrinsic to the survival of the yeast and bacterial cases and the phage may also enjoy the benefit thereof.

In some organisms there is a lot more DNA repair possible.  So that would mitigate the mutation rate in some cases like Deinococcus radiodurans.

Metazoans and diploid organisms which undergo meiosis for sexual reproduction have other methods for reducing the number of mutations they pass on.  Meiosis and recombination will allow the removal of many mutations by competition in gametes.  Since there are two copies of each chromosome, mutations are constantly being competed against their unmutated versions as gametes.  Then eukaryotes have their own repair enzymes and conditions.  Then lastly recombining into diploids, they also show mutations less often.

For these reasons and others, the mutation rate being even across the genome does not mean that that the mutations accumulate evenly.  Mutations still tend to accumulate in regions where positive selection is operational.  Here is an excerpt from a recent genomic comparison of five strains of rice:

  Despite strong purifying selective pressures on most Oryza genes, we documented a large number of positively selected genes, especially those genes involved in flower development, reproduction, and resistance-related processes. These diversifying genes are expected to have played key roles in adaptations to their ecological niches in Asia, South America, Africa and Australia.


Anaerobic respiration choice in E. coli Under anaerobic conditions E. coli has two options to generate ATP: fermentation (substrate-level phosphorylation), and respiration (proton gradient, chemisomotic phosphorylation). Which is favored? What determines the choice? If availability of enzymes required for anaerobic respiration is decisive, what regulates them under anaerobic conditions?

I looked into the web but did not find the answer.

Let me first clarify the difference between anaerobic respiration and fermentation.
Literally respiration refers to breathing, but its definition has been extended to include cellular metabolism that leads to ATP generation.

Fermentation, as you said depends on substrate level phosphorylation. Anaerobic respiration on the other hand just means ATP synthesis in the absence of oxygen- in other words anoxic. This happens in several cases in which the terminal electron acceptor is not oxygen but some other chemical species such as $Fe^{3+}$ or fumarate.

E.coli can carry out ETC mediated ATP synthesis both in the presence and absence of oxygen. At high oxygen concentration it uses $O_2$ as electron acceptor, mediated by cytochrome-d. At low oxygen concentration other kinds of cytochromes accumulate and the cell uses fumarate or nitrate as the terminal electron acceptor with the help of fumarate reductase and nitrate reductase respectively. This is an old article but is still quite informative. Check it out.
Fumarate and nitrate reductases are regulated as a part of what is known as FNR regulon. FNR is an oxygen-sensitive transcription regulator. In the presence of oxygen it is inactivated. In the absence of oxygen it activates the fumarate and nitrate reductase genes.

Perhaps in the absence of these alternate electron acceptors, the bacterium totally depends on SLP.


What flower is this grown in Southern China It is grown in Tropical Southern China. It is not wild.

Google images sais that it's a mexican petunia, I think it's right due to the good focus of your image, and the different attributes of the photo.

http://www.gardenality.com/ImageViewer/?id=2116&IUID=3&RID=88#imageId=2116


Does Usnea (Old Mans Beard) have negative effects on the respiratory system? Being a fungus does it have negative effects similar to that of mold, especially on the respiratory system?

According to the Institute for Traditional Medicine and the Gale Encyclopedia of Alternative Medicine:

Usnea (aka Songluo or "Old Man's Beard") is a fruiticose lichen (not a fungus).
Used in traditional medicine worldwide, including historically in China, Europe and by native Americans, as well as globally today.

"Uses": topical antiseptic; therapuetic agent; medicinal herb; anti-cancer
It has traditionally been used in the treatment of bronchitis, in the treatment of tuberculosis, to ease coughing, to cleanse lungs and as an expectorant (i.e, to resolve phlegm).

Contains a secondary metabolite, usnic acid, which is claimed to be an effective inhibitor of gram positive bacteria-including tuberculosis, staphylococcus, streptococcus, and pneumococcus

So Usnea is often used for the lungs. In fact, today, supporters of traditional medicine still use it rather regularly as an expectorant. I could find no sources that claimed that this was unsafe or had any negative effects on the respiratory system. I would think that if you were to inhale any usnea, its effects would simply rid your body of any particulates during expectoration.

However, a number of sources (e.g., see Sanchez
et al., 2006, here , here and here) mention that usneic acid can cause liver damage (and failure).

Disclaimer: I did not find any reputable source acknowledging usnea to be effective at treating any of the aforementioned ailments. Use at your own risk.

Citations

Sanchez, W.T., Maple, T.J., Burgart, L.J. & Kamath, P.S. (2006). Usnic acidhepatotoxicity. Mayo Clinic Proceedings 81: 541-544


How is NAD+ used in lactic acid fermentation after it is oxidized from NADH? I am confused with the whole process of glycolysis and the fate of the products of this reaction. So, I understand that anaerobic glycolysis results in 2 pyruvate + 2 NADH and 2 net ATP. Is the whole anaerobic purpose of glycolysis to make the 2 net ATP? Then pyruvate and NADH are waste products? Also, pyruvate then reduces to lactic acid. What is the need for this? NADH is oxidized to NAD+. How is NAD+ used? Also, lactic acid is eventually converted back to pyruvate through Cori cycle. How is that pyruvate used?

Anaerobic Glycolysis

As this question refers to glycolysis in the context of lactic acid fermentation it clearly relates to anaerobic glycolysis, which is why I added that to the question.

I believe it is correct to regard the primary purpose of anaerobic glycolysis as being to generate ATP for the anaerobic organism or tissue.

To understand the roles of NAD and lactate in this process you need to consider the chemistry. The conversion of glucose to pyruvate is an oxidative process, with the oxidizing agent being NAD+, which itself is reduced to NADH. For glycolysis to continue the NADH must be reoxidized to regenerate NAD+. This is the primary purpose of the reduction of pyruvate to lactate and is summarized in my own diagram, below.

So, the answers to your (paraphrased) questions “what are NAD and lactic acid needed for?” and “are they waste products?” are:

NADH isn’t needed for anything — it’s the consequence of the oxidative function of NAD+. No, it is not a waste product — it has to be reoxidized otherwise glycolysis would stop for lack of oxidising power.
Lactate also is not needed for anything, as evidenced by the fact that other reduced products of pyruvate are produced in different organisms, most notably ethanol in yeasts. Ethanol can certainly be regarded as a waste product, although the carbon skeleton of lactate is salvaged in multicellular oxygen-breathing organisms.

The so-called cycle of Cori & Cori

In my opinion it is best to approach glycolysis as I have done above, without reference to the tissue or organism, so as to understand the essential features of the process.

In the specific case of mammals, some tissues perform glycolysis anaerobically, e.g. the red blood cell (which lacks mitochondria) or rapidly excercising muscle (where the blood supply and number of mitochondria are not sufficient to generate ATP for muscle contraction. The liver, in contrast, has a plentiful supply of oxygen and hence NAD+, and so can reoxidize lactate to pyruvate if the former is transported in the blood from the anaerobic tissue to the liver, salvaging the carbon skeleton.

Under conditions of low blood sugar (e.g. starvation) it is important that the pyruvate be reconverted into glucose in the liver by gluconeogenesis, rather than be converted to other products, and the glucose is released into the blood. In this case one goes full circle, this process is generally referred to as the Cori Cycle. I always avoided this term myself in teaching students as I found it caused confusion with cycles such as the tricarboxylic acid cycle and the urea cycle, where all the chemical interconversions take place in the same tissue.

Footnote: Glycolysis under aerobic conditions

Under aerobic conditions (e.g. in the liver after a carbohydrate meal) the purpose of glycolysis is not primarily to generate energy but to utilize the glucose, storing it as fat (after glycogen capacity is reached) or using it to synthesize intermediates. There are different fates for the pyruvate (acetyl-CoA is shown), but lactate is not one of them as the NADH can be reoxidized far more efficiently in the mitochondria, with molecular oxygen being the ultimate oxidizing agent.

Text References

Berg et al. Section. 16.1 covers glycolysis in great detail under aerobic conditions. The lactic dehydrogenase reaction is given little emphasis, but can be found in section 16.1.9.


How long can you effectively store a glycerol stock at -20 degrees Celsius? I know that glycerol stocks are typically kept in a -80 °C freezer, however there are some people who do not have access to such equipment. How long would you be able to keep a glycerol stock at around -20 °C (typical household freezer temperature). I would like to create a new stock before anything goes amiss.

While I believe that it is possible to keep a bacterial culture viable while frozen in glycerol stock at around -20 °C, as attested to by WYSIWYG, it is important to note that your "typical household freezer" may not be suitable for such a purpose.

This is because household freezers usually have an "auto-defrost" function. This makes it temporarily thaw out to remove the frost that condenses from atmospheric moisture. If storing sensitive materials such as bacterial/cell culture frozen stocks, this would lead to repeated freeze-thaw cycles which would damage the viability of the stocks.

For that reason, almost all laboratory freezers do not have that function, and instead need to be manually defrosted routinely.


Gene configuration : Divergent vs convergent I start reading a paper where they discuss the effect of the divergent promoter/gene and the convergent promoter/gene on the genetic expression of an organism.

So I want to know what is the difference between the two of them ?

RNA polymerase produces transcripts by scanning along DNA, linearly. Simplifying things, genes can thus be thought of as having a start (or 5' end) which is the main site where the polymerase begins to transcribe, and and end, where it stops. Divergent promoters are promoters oriented so that the polymerase transcribes in opposite directions, away from the two promoters (like so: <- -> ). Convergent promoters instead transcribe towards each other (like so -> <- ) . This means, for instance, that the polymerases coming from two convergent promoters could collide with one another.


Does the body have a gate control for pain I understand it is not the most accurate source but I recall a House episode where he claimed the body had a control mechanism for pain in which only the most painful thing was felt. Is that true? and if so how does the body control which injury we feel and could we use this to our advantage?

Pain receptors, more precisely pain signal propagation, can be inhibited in several ways. One is, for example, fine touch receptors (mechanoreceptor in illustration) inhibit propagation of pain signal in spinal cord (a lot of pain processing happens in spinal cord):

That is why humans often rub skin around or nearby injury, whether it is in joints or something more superficial. You should find more information about such control in any textbook on pain. See this page for short primer.

Next, pain propagation is modulated -- still in spinal cord -- by descending pathway from brain and brain stem. See this page for more, or address Kandel's textbook.

Now, I don't know whether or not it is identified how/where brain "selects" to what pain pay attention. My hypothesis is that it happens by competition, e.g. several signals compete by inhibiting each other via some mechanism, probably, related to stress-induced analgesia.


What is solitary flower? I am Just confused whether solitary means single flower in the whole plant or one flower on one branch of the plant?

Solitary flower means one flower at a specific position of a plant. It usually accompanies with another word either terminal or axillary.

Soliary terminal means a flower present at the apex of the main stem or its branches. e.g.  Trillium grandiflorum.

 Image taken from http://ohioplants.org/inflorescences/

Solitary axillary means a flower arising from the axil of a leaf. e.g. China
rose.

Image taken from https://commons.wikimedia.org/wiki/File:China_rose.JPG

 This is Sida rhombifolia. This picture is clearer.

No. It doesn't mean that a plant has a single flower.It speaks all about the position of the flower. Think of roses , they are solitary terminals and are in numbers in each plant, always growing at the apices of branches.

Source: My two years of learning Botany as an additional Undergraduate subject.


Why is rabies incurable? I'm still not sure about the mechanics that lead to rabies being incurable. I know that it can be treated before any symptoms show up, but why is it that once symptoms show the person is a dead man walking?

This is because rabies is a viral infection of nervous tissue that propagates through peripheral nerves into the brain and causes brain tissue inflammation (encephalitis).

As long as the virus is in the brain there is no way to get rid of it. The main trade-off here is that everything that would kill the virus will be as (or even more) aggressive against the brain tissue, and impairment of the latter will lead to really heavy deficits in vital functions like breathing and thermoregulation.

The first manifestations of rabies are those due to brain damage. This means, the virus is already there and the brain is already fatally damaged.


Identification of a larva Last week-end I was working in my parent's garden and when I dig a bit the ground, I found few larvas I never seen before. My father told me there are there every time when he's doing the garden springtime.

I took some pictures (I just put it on leaves for the picture to see better than on the ground).

One low-res:

And the gallery hi-resolution pictures

The location is in northern of Switzerland (Jura) at around 700 meters above the sea and the larvas were inside the ground in around 3-5 centimeters (1-2 inches) deep.

What you are seeing is a cocoon for a moth pupa.

Here is a link to a YouTube video of one hatching that is normal found in the soil.