How is AMP "recharged" to become ATP in a cell? I understand that after the translation stage of ribosomal protein synthesis, tRNA molecules are floating in the cytoplasm without attached amino acids until they find the correct aminoacyl tRNA synthetase enzyme which revitalizes them.

However, in this process the enzyme takes an ATP molecule and returns an AMP (not ADP) molecule. It's been my understanding that an ATP's energy is normally harnessed via removing a single phosphate group and leaving an ADP molecule. Processes like respiration and photosynthesis deal with the conversion of ATP to ADP and vice versa. I understand that in removing the extra phosphate group to get an AMP more energy is released, but that also means that more energy has to be used to convert the AMP to ATP.

Does the cell convert the AMP to ADP, which will ultimately become ATP in respiration, or does the cell use some retrofitted respiration/metabolism to revitalize the AMP?

I would expect the first option but it would take energy (most likely from an ATP) and I would expect the amount of energy released from an ATP becoming an ADP to be different from the amount of energy released from an ADP becoming an AMP (so an ATP becoming an ADP would take more or less energy than would be required to make an AMP become an ADP, leading to inefficiencies). The other possibility (that I can see) is that the AMP is just used as a nucleotide in DNA and RNA, but I don't think that the numbers add up there. I've looked around but I can't find an answer.

So how do cells convert AMP to ATP? Also I was told that the ATP to ADP conversion is the general power-conversion. Is that not the case, or is this just some rare occurrence when AMPs are involved in power conversions?

AMP is first converted to ADP in the reaction

AMP + ATP $\leftrightarrow$ 2 ADP

catalyzed by adenylate kinase. So one phophate group is transfered from ATP to AMP, resulting in two ADP molecules. The ADP formed is then used to synthesize ATP as usual, by the mitochondrial ATP synthase or by the glycolysis enzymes.

For other nucleotides and deoxynucleotides, the monophosphate form NMP are usually phosphorylated to NDP using ATP, catalyzed by various kinases. For example, UMP and CMP is handled by the enzyme CMPK. Note that this is essentially the same type of reaction as adenylate kinase.

Regarding the energetics, the above reaction is only slightly favorable (at equal reactant concentrations) with $\Delta G=-2.6$ kJ/mol. In most cells, ATP concentration is much higher than ADP though, which helps drive the adenylate kinase reaction forward. See this site where you can investigate the energetics more closely.


Is carbohydrate an important part of phospholipid? My professor tells us that carbohydrate is an important part of phospholipid, but phospholipid is composed of Choline, Phosphate, Glycerol and two Fattyacid, and I don't think even one of them is carbohydrate.

What's wrong with my statements?

Your thinking is correct based on typical carbohydrates, but glycerol, the backbone of the phospholipid, is a 3-carbon carbohydrate that is usually derived from glucose.  It is not a sugar, but it does fall into the general class of polyols (aka sugar alcohols) that are a type of carbohydrate.

A carbohydrate definitely is an important structural part of the phospholipid, but your instructor probably should have been more clear in describing why that is the case; I can definitely understand your confusion here.


How long does it take for E. coli to shift feedstocks? With our fermentations we're noticing that it takes an appreciable amount of time for E. coli (K12 variant) to change from being metabolically streamlined on amino acids to being metabolically streamlined to glucose.

How long does it take for such microorganisms to adjust to a new feedstock?

This must depend upon the conditions in question, but I think it would not be very long.
The length of a generation for e coli can be 12 minutes or 24 hours, so that gives some idea of a typical time.

I did find this interesting case in the literature. They found that even as you subject e coli to minimal nutrients they are expressing genes that prepare them for a richer nutrient mix.  The bacteria are primed for a flood of carbohydrates succinate or amino acids.

This study incubated the e coli overnight before taking their readings, so this puts an upper bound of about 12 hours.  The implication is that if you are moving the bacteria to rich media it might be just a short time before they are in log phase growth.

In practice moving from LB plates to log phase growth is usually just like 4 hours.  This paper interestingly shows that cold adapted E coli moving to other media react in a few hours, but can show behavioral changes days out.

I would say that 4 hours might be a typical expectation. 12 is typically used in the literature.


Can a person really die quickly from biting their tongue? A common trope in certain circles (like Eastern martial fiction), is someone committing quick suicide by biting his or her tongue.  But is this really possible?

The internet turns up millions of pages of speculation, but no Straight Dope.  People have been removing the tongues from mammals, and each other, throughout human history.  There has to be some scientific data on this somewhere.

Will an untreated, severe, lingual laceration, really result in bleed-out of an otherwise healthy human?

Or will lingual trauma facilitate swallowing the tongue sufficiently to cause asphyxiation?

What does the science say?
Thanks!

I know of an ER doctor who had a patient who removed (by biting and pulling) every last part of her tongue, she survived that (although, her ability to speak was probably shot). The stump of her tongue clotted before she could even go into shock (at least where it was really serious).

Here is a quote from the book Angels in the ER  (this is a paramedic speaking with the doc):

  "Every bit of it. Gone. And the funny thing, Doc, is it didn't even
  bleed very much."
  The doctor then asked his patient to open her
  mouth... "it was gone!"

It would certainly be possible to commit suicide doing this if one was a hemophiliac or continued to remove the clot from the hole(s) in their tongue (although the latter could be a potentially painful and I have a feeling that it would take a very, very long time!).


Is there any evidence that a virus can modify human evolution I was just reading Evolution of lactose tolerance, and in it one line says "But there was a time in human history when our diet and environment conspired to create conditions that mimicked those of a disease epidemic".

Something I've always wondered is rather than natural selection occurring and survival of the fittest and so on, is that a viral epidemic caused a mutation in the survivors, i.e. DNA was inserted from the virus that modified the survivors genome. There is some evidence that a significant percentage of the human genome comes from viruses. Probably a naive question - so is there any evidence that this has occurred? From my lay perspective this is what attempts at genetic engineering use, so it's possible nature already did this?

It's always seemed to me that natural selection and point mutations, and the chance meeting of two people with the same mutation would be too slow and viruses would be a more efficient method to evolve a large population at the same time. Things like punctuated evolution might support this? not really sure.

The simplest example, that I can recall are the flu pandemics. The 1918 pandemic is the first to be described because of its severity, but quite possibly not the first in human history (see for example the Black Death - Yersinia pestis is a bacterium, but in the 15th century in just a few years it covered almost all of Europe, sometimes killing up to 40% of population in a given area).

Influenza pandemics appeared quite regularly during the 20th century, usually every 20 years and killed suspiciously many people compared to yearly influenza strains. Additionally, a person who survived one pandemic, was unaffected or only mildly affected by the next pandemic.

All this suggests, that the pandemics "clear" the population from susceptible individuals, and regularity of pandemics (notice, that 20 years is more or less the time of one human generation!) assures that the new generations also go through this kind of selection. The surviving individuals are more resistant to all strains of influenza then those, who never suffered from a pandemic. Maybe the influenza didn't mutate our DNA, but it could be a major force of natural selection.

And one more note: did you notice the great noise in media every time a new potentially pandemic strain is discovered? Actually, it's not just hyperboly of the danger. Last pandemic was in the '70s, so it's high time for a new one. And, since the last one was  almost 40 years ago, the new one (when it happens) will probably be very severe.


Is there any disadvantage to having a really low adipocyte count in our times? The key feature of adipocytes seems to be energy storage. Today humans in Western countries don't have to hunger and have therefore less need to store energy in fat cells.

Do adipocytes have additional functions that still make them valuable?
Wikipedia lists 10–13% and 2-5% for men as essential body fat percentage for woman. What functions don't get fulfilled if the body fat percentage drops below that level?

You mentioned something odd in the tittle "adipocyte count", this was likely a mistake, but I will address it anyway. I recall something about liposuction not being preventative for
   diabetes:

You can have more adipocytes with less lipids in each cell, or fewer
   adipocytes with more lipid in each cell. Hypertrophy vs hyperplasia, just like in the question you asked on muscles elsewhere on this forum. Anyway, when a patient gets liposuction they decrease the number of
   adipocytes. Then if s/he gains the weight back the size of their
   individual adipocytes will be larger than it was before the
   liposuction. Somehow this was bad, and it increased insulin resistance. in a way, decreased "adipocyte count" is dangerous.

here is the other, obvious stuff on endocrine function of adipose tissue that you surely already know since your profile is very endocrine based, but anyway, here goes:

Adipose tissue has hormonal functions, secreting horomones (leptin, adiponectin, and resisting... these modify appetite as well as insulin resistance) and modifying them (converting testosterone to estrogen vi the enzyme aromatase).

The adipose-derived hormones are quite mysterious to me, I don't know much about them. The effects of the aromatase in adipose tissue are more obvious:

men will have increased estrogen levels (for example leading to gynecomastia aka man boobs, as a chubby guy I know this all to well)
women will have higher estrogen which will stimulate LH secretion from the pituitary stimulating theca intern cells in the ovary which will increase testosterone levels. The condition in women is known as PCOS.

In a person with little adipose tissues, there will be less conversion of testosterone to estrogen, so men will have less estrogen. Women will also have less estrogen, and less testosterone, aka they will not have PCOS in those women that already have PCOS, but thats not saying much :)

I may be wrong on some of this information, anyone please correct me.


How do B memory cells provide immunological memory? Do they differentiate into plasma cells? My text book doesn't say anything about how B memory cells actually ensure a faster response the second time the antigen is encountered. My guess is that they differentiate into plasma cells which produce antibodies, and release cytokines to cause clonal expansion of the correct T killer cells, but I'm not sure...

Thanks in advance for any responses ^_^

This 2005 review in the Annual Review of Immunology entitled "Antigen-specific memory B cell development" would be a great first resource in answering your question in great detail. Briefly, memory B cells (MBC), upon re-exposure to the same antigen, very rapidly expand and differentiate into antibody-producing plasma cells (PC), with the help of memory T helper cells (Th). However, more MBC are still produced by this reaction, so that a second challenge with antigen doesn't deplete the memory population.

PC are geared towards producing gobs of antibody, and not much else. Upon stimulation with antigen, MBC will produce some cytokines to attract the Th cells that are required for costimulation and regulation, but to my understanding it is the Th cells that manage the whole response, activating effector T cells ("killer" T cells), NK cells, dendritic cells, etc., and not the MBC themselves.


What is the relationship between complexity and organization in biology? Is there any relationship between what we can call complexity and what we can call organization in biology? And if there is, what is it? Can we define these terms independently of each other or would the definition of one of them always inescapably include the other and vice versa? If the second is the case, what can such a relationship tell (or, at least suggest) us about life?

Here's food for thought. Entropy is always considered to flow naturally in a direction of order, to disorder. That is, the higher entropy a system has, the greater degree of disorder it has, and the less amount of work it can perform.

Now, look at a cell. It is a biological system of organic molecules that are able to organise themselves in a way that outweighs the forces of entropy. To "fight" the natural tendency of the universe that moves toward a state of disorder requires a highly complex system. And, in the process of going against entropically favorable mechanisms, a cell is also able to produce its own energy (stored as potential energy, or ATP if you will).

I guess you could say, a more complex system is able to organise itself in a greater number of ways for the purpose (and I use this word very loosely, as nothing really has a purpose) of yielding entropic energy to do work.


Could a trans-female person ever become pregnant? I was told that a transgender person, which I will define as anyone assigned male or female at birth that identifies opposite to that assignment, could never become pregnant conceptually, due to the lack of hormonal pathways present in cis-male / trans-female person.

Are there modern medical methods that would allow for someone born male and is now trans-female to ever become pregnant or is it the case that medical science is not, nor ever will be capable of allowing for this?

Edit: I would say this is a different question than the suggested duplicate because someone who has AIS or CAIS would have a different anatomy than men assigned at birth, although not by much.

Medical science has reached the point where it is able to consider performing uterine transplants in genetically female (cis-female) patients born without a uterus.
In the MedlinePlus report, First Uterus Transplant Planned in U.S. doctors at The Cleveland Clinic have plans to perform the first uterus transplant in the US sometime in 2016.
The article does however go on to state that the women will need to have been born with ovaries. The same matching process of blood and tissue typing that goes along with any organ transplant would still be in effect for this surgery.
It is also unlikely that the procedure would be open to women that lost their uterus due to cancer, as the recipients would be required to be on immunosuppression medication, and the risk of cancer recurrence would be too great.
As for your question about transplantation into Male-to-Female transgender patients, it is unlikely, at least with present technology that the person would be able to receive the transplant. There is a complex cascade of hormone signaling required for implantation of the embryo.
There could also be implications as to the formation of the placenta and how the person's body react to that. We have many examples of surrogacy, so we know that a woman can carry the embryo formed from the egg of another woman, but how the transgender person's somatic cells would react, given that they all have y-chromosomes is unknown.
According to a Yahoo! news article that interviewed Dr. Karine Chung, director of the fertility preservation program at the University of Southern California’s Keck School of Medicine and Dr. Christine McGinn, a New Hope, Pa., plastic surgeon who performs transgender surgeries on men and women, they foresee possibilities that this could happen in the future, however they do not cite any research that has been performed to date.
One of the issues would be the differing pelvic vasculature that a cis-male has to a cis-female, and what would need to be done to provide an adequate blood supply to sustain not only the uterus but the growing fetus as well.

...biological women have a leg up on biological males when it comes to accepting and nurturing a transplanted uterus. Women already have: vasculature needed to feed the uterus with blood, pelvic ligaments designed to support a uterus, a vagina and cervix, and natural hormones that prepare the uterus for implantation and support the pregnancy.
Men have none of those support systems — naturally — but none are impossible to create. “Male and female anatomy is not that different,” says Chung. “Probably at some point, somebody will figure out how to make that work.” (2)

The article does go on to point out that

Hormone therapy can shut off testosterone and introduce progesterone and estrogen needed to prepare the uterus for pregnancy.

Even though males do not have uterine veins and arteries needed to nurture the womb, it’s possible to attach a branch of a large vessel, like the internal iliac, to the uterus. “It’s doable, it just hasn’t been done,” Chung says.

Although it’s preferable for a vagina to support the uterus, it’s possible to attach a transplanted uterus to other ligaments in the pelvis.


What does uniprot consider "unambiguous" evidence for the subcellular domain of a protein? Uniprot has annotation for subcellular location of protein domains. This topological domain information of proteins is under the TOPO_DOM flag.

In most cases the subcellular location is assigned by rigorous sequence analysis both for the experimentally verified and predicted subcellular locations. Sometimes more reliable information is available...

  ... when the experimental technique used allows the unambiguous
  assignment of the transmembrane boundary to a particular position
  (X-ray crystallography, etc.), the ‘Sequence analysis’ qualifier is
  not added in the topological domain annotation. In this case, the
  positions of the topological domains can be propagated ‘By
  similarity’.

What evidence is available that constitutes "unambiguous assignment" so that the by similarity qualifier can be used?

Following your question, we have updated the documentation for topological domains in UniProtKB:
http://www.uniprot.org/help/topo_dom

I hope you will find it more informative now. Please don't hesitate to contact the UniProt helpdesk if you have any additional questions (or, if you prefer to discuss here, a short note to the helpdesk would help us spot your posting more reliably, since we cannot closely monitor all forums as you may understand).


What is the relationship between DNA molecules and the chromosomes? Regarding the human genome, if the DNA molecule is two continuous strands, with each gene occupying a segment in it, and there are 46 chromosomes each with some genes, where is the physical boundary of each gene?

My understanding of a molecule is a collection of atoms bound together by covalent bonds thus giving the substance its properties.

My reading so far gives me the understanding that the nucleus of a cell contains DNA, whose molecule is that famous double helix. At the same time, I read that the genes are packed into 46 chromosomes. This got me confused. How is the DNA molecule split into 46 parts?

To cite @canadianer, I don't really understand what you're asking but the following may help you.

Genome composition

First of, in the genome of most eukaryote (incl. all plants, fungi and animals), in general, genes constitute only a small part of the genome. Typically, in humans genes occupy 26% of the genome (24.5 for introns and only 1.5 for exons).

What does a genome look like?

Introduction

You say

  Isn't DNA one molecule?

I think this question shows an important misunderstand you have. Note that I will only talk about the nuclei of eukaryotes below.

DNA is a type of molecule, which is constituted of two anti-parallel strands. In the human genome, we have 46 chromosomes, that is 46 independent DNA molecules. Now, these exact numbers vary depending on the moment in the cell cycle you want to consider but this is a story for another time.

A little more advanced

Below is a karyotype of a human allowing you to visualize the chromosomes. The 46 chromosomes we have go by pairs (pair of homologuous chromosomes) and on the image, they are numbered by pairs, the last pair being the sex chromosomes. By the way, can you identify the sex?

Note now that, depending on the moment in the cell cycle you want to consider, each homologuous chromosome may be constituted one 1 or 2 DNA molecule, each of them being called a chromatid. Chromatids are physically attached by the centromere. Two physically attached chromatids are called sister chromatids.

More information

For the moment, I threw some vocabulary at you but it was probably a bit hard to follow. You can get more information at the posts

Chromosome and chromatid numbers during cell cycle phases
The human has 46 double chromosomes or simple chromosomes?

or simply an intro course to genetics such as the following three courses by Khan Academy

Classical and molecular genetics
DNA as the genetic material
Central dogma (DNA to RNA to protein)


What's the difference between naive and memory B cells? I understand that when naive B cells are exposed to antigens, they become memory B cells, but what is the functional difference between the two? I've looked at the quite a few article on B cells, but none of them stated the difference clearly enough for me to understand.

The main difference is that memory B cells start an immune reaction much more effective and faster than naive B cells. The reaction is also specific towards the antigen.

The memory B cell has a specific membrane receptor for an antigen. It produces specific antibodies only when exposed to the antigen.

References:

Tangye SG, Avery DT, Deenick EK, Hodgkin PD. Intrinsic differences in the proliferation of naive and memory human B cells as a mechanism for enhanced secondary immune responses. J. Immunol. 2003 Jan 15;170(2):686-94. PubMed PMID: 12517929.
Wikipedia contributors, "B cell," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=B_cell&oldid=612990219 (accessed June 26, 2014).


What is the best method to check for differential gene expression in large dataset? I want to identify aging differentially expressed genes My data is RNAseq data and I want to know which all genes (which I am looking for) are differentially expressed with age. I have tried the Kruskal-Wallis test and fold change methods. Do you have any better suggestions?

A standard pipeline for DGE would be Salmon for (pseudo)mapping + DESeq2 for statistical analysis.
Salmon is one of a set of modern, fast and accurate mapping software. Requires a transcriptome to be defined.
DESeq2 is a mature R (Bioconductor) package which can handle reasonably complex designs, including time series, but not mixed models. The vignettes are pretty thorough. It can handle data from pseudomapping software as well as data generated using more traditional methods, e.g. Star + FeatureCounts.
Using a pre-made RNAseq statistical package is a much better idea than trying to do, e.g. a Poisson/Neg.bin GLM manually for each gene (even though ultimately this is what DESeq2 does).
(agree this question is a better fit for SE Bioinf)


Is amphibians being descended from fish reflected in the animalia taxonomy? I think it is common knowledge that amphibians are descended from fish. At some point there was a transition from sea to land.
But when I try to confirm this through the Animalia taxonomy, the scientific classification of fish goes

https://en.wikipedia.org/wiki/Fish
while the scientific classification of amphibians go

https://en.wikipedia.org/wiki/Amphibian
If we draw this as a tree of sorts, we end up with

it seems to be quite obvious that fish and amphibians belong to the same phylum but different clades, but I'm not sure how that proves that amphibians are directly descended from fish?
I'm interested in a tree that shows amphibians branching off of the fish lineage.

Fish are a paraphyletic group: that is, any clade containing all fish also contains the tetrapods, which are not fish. For this reason, groups such as the class Pisces seen in older reference works are no longer used in formal classifications.

You got something completely wrong. In evolution one can not say that one taxonomical group evolved from the other. We say that two taxonomical groups have common distant relative. With that said all vertebrates have common distant relatives. Important is to know when did the branching in speciation happened.
Proto-amphibians evolved in Devonian by further speciation from relative that was sarcopterygiian (fish). It was a fish with some properties of amphibians (lungs and bones in appendages).


Where does Taq polymerase migrate during electrophoresis? Assuming a 1% Agarose gel with TAE.

Follow up questions:

Is there a way to stain for it?
Could the polymerase be captured and reused?

Unlike in an SDS-PAGE, where the SDS adds negative charges to all proteins, in a standard agarose gel for nucleic acids all proteins should move according to their own charge.

You can get a rough idea in which direction Taq would move by getting the amino acid sequence and calculating the isoelectric point at the pH you are running your get at. It might be that the protein isn't even negatively charged at this pH, then it would move in the opposite direction of the DNA out of the gel.

An exact prediction is rather hard, as it depends on the shape and size of the protein, the pore size in the agarose gel and the exact charge. It is not as simple as for DNA. You would have to just try it out to get an accurate value.

You can use any common method of staining proteins like Coomassie.

I think reusing the Taq is very unrealistic. It is still pretty stable at higher temperatures, so it will probably survive the temperatures the gel is running at. I would guess that you lose so much during PCR, gel and purification that it would not be worth the effort. And you would need to purify it extremely well, unless you want to amplify the same DNA in all your future PCR reactions. Any DNA contamination left from your gel might interfere with your later reactions.

If you require a very large amount of Taq and want to cut costs, I'd rather try and produce and purify the enzyme yourself. That should save you a lot of money if you really use a lot of it, but it is likely not worth it on a small scale.


Where can I find the pMON7124 plasmid sequence? I need the map of the pMON7124 plasmid. As this is not easy to find, I welcome any hints.

It seems that no good map of this plasmid is around. Life technology uses it in some of its bacterial strains, the quote:

  E. coli also contain the helper plasmid, pMON7124 (13.2 kb), which
  encodes the transposase and confers resistance to tetracycline. The
  helper plasmid provides the Tn7 transposition function in trans.

They link to the original publication, but the image quality in there is pretty bad:

They give some information in the text, so I would recommend reading the paper (if you have no access, let me know, I can help here):

A broad-host-range shuttle system for gene insertion into the
chromosomes of gram-negative bacteria.

If this is not enough, you could still try to get a better version from the author Gerard F. Berry (you can find his Monsanto email adress by googling for it).


Amino acid profile of GPCRs You are studying cellular signalling through a newly identified GPCR.
   Specifically you’re working on a pair of newly identified GPCRs,
  GPCR-A and GPCR-B. Each binds the same small ligand, but activates different
  heterotrimeric G-proteins that act on adenylyl cyclase.
  Your grad student mentor explains that both the receptors and the
  Gα and Gβγ subunits of the heterotrimeric G-proteins are membrane associated.  You examine the sequences of the seven predicted
  transmembrane α-helices of GPCR-B. You’re surprised to find that there are
  hydrophilic amino acid residues in these helices. How can you explain this
  observation?

This was an MIT quiz question.I have my guesses. But I wanted to know the correct answer.

Well, since GPCRs are transmembrane proteins, normally the transmembrane helices have higher hydrophobic amino acids or only hydrophobic, non-polar aa . Here it says they saw some polar residues. Well my guess is that, since there are two GPCRs a and b that bind to the same ligand, it could be that one activates a stimulatory G protein and the other an inhibitory G protein Gi . So probably the polar amino acids which are in the transmembrane alpha helical segment of the stimulatory GPCR is slightly displaced and is in the intracellular region of the inhibitory GPCR (Gpcr that activates inhibitory G protein ). To be in the intracellular region, it has to be hydrophilic.
This is all I can think of.

Any help with this question is much appreciated. It is not a homework question for me. I don't go to MIT. I just wanted to reinforce my concepts.

Polar amino acids in this case stabilize the helical structure within the apolar milieu of the membrane by making intra- and inter-helical connections. Thus the side chains of polar amino acids turn to one another while apolars face the apolar membrane. This would be definitely supported if you could find alternating apolar - polar segments in the sequence of helices.


Features in individuals causing high population variation As I understand it, a population with high variation is something sought after, since it makes the population better equipped to face a dynamic environment.

Then, I guess features in an individual which causes it's population's variation to be high, should be selected for (high mutation rate, other features.. ?).

If so, does this manifest itself partly as individuals preferring to mate with individuals from another population? (With genetic difference within reason, perhaps a norm for a proffered genetic difference between individuals)

I believe there are evidences in both directions in terms of mechanisms to favor variation in a population: outbreeding and crossing within individuals that look alike. There is a fine line between the two. Outbreeding helps in keeping variation and mixing variants that appeared in different parts of the population, but too much outbreeding can generate inviable offspring. Too much inbreeding also reduces viability. Certain plants have features that are selected to favor outbreeding and make inbreeding incompatible by rejecting incompatible ("self") pollen (self-incompatibility mechanisms).


Interpretation of agarose gel electrophoresis of a plasmid I am performing agarose gel electrophoresis of plasmid which is 2.5-3 kb in size. I am getting more than 3 bands, after restriction I got single band at 3.5kb in size.
Electrophoresis conditions- 0.5X TBE, constant voltage 150V.
why am I getting more than 3 bands after agarose gel electrophoresis of plasmid?

The closed plasmid comes in three different forms: nicked-relaxed, supercoiled and circular single-stranded. All three forms have a different tertiary structure and thus they run differently on the gel. This should look like this (image from here, there you also find a more detailed explanation):

When you digest the vector you linearize all the forms and they all have the same tertiary form.


ATP yield of fermentation: study to cite? Everywhere I find the ATP yields of respiratory and fermentative metabolism of glycolysis. While that of oxidative phosphorilation I could find in Stryer to cite one study where this was addressed (Hinkle 1991 observed 30 ATP/glucose) I cannot find a study where the 2 ATP/glucose was observed and the textbooks I've searched do not provide a citation.

Can anyone please provide a link or citation to a paper where the ATP yield of fermentation (regardless of process) was quantified/estimated?

Thanks

For glycolysis this is really not so much of an issue, because the ATP yield is fixed by stoichiometry. The early biochemistry work by Embden, Meyerhof, Parnas and other that mapped out the reaction mechanisms of the glycolytic pathway shows that you always obtain exactly 2 ATP per glucose; this is simply the stoichiometry of those reactions. There are a number of primary papers documenting these reaction mechanisms, but it's a large undertaking to go through all of it; the glycolysis chapter of Stryer's Biochemistry is a good summary I think. A brief review of the historical development is described in: "A Fresh View of Glycolysis and Glucokinase Regulation: History and Current Status".

For respiration it's very different, since there is no fixed stoichiometry for chemiosmosis --- the ATP yield depends on the proton gradient across the inner mitochondrial membrane, which in turn depends on a number of factors. So in this case ATP yield will differ between cell types and conditions, and must be measured experimentally.


How does the specificity to bind to antibody differs between 'hot' and 'cold' antigen in radioimmunoassay? This question is in relation to radioimmunoassay. In this assay, the 'cold' antigen replaces the 'hot' antigen. Why is it so, if both the antigens are same and hence their specificity? Does the radioactive molecule change its specificity?

The specificity is the same, but protein-ligand binding is an equilibrium process. In other words, the antigen is constantly associating with and dissociating from the antibody. As a hot antigen dissociates, it is possible that a cold antigen can take its place, and vice-versa. As the ratio of cold to hot antigen increases, there is a greater probability that cold antigens will take the place of hot antigens.

You can read more on Wikipedia.


What kinds of bacteria live in water bottles? I've always heard not to re-use disposable plastic water bottles.

According to this Huffington Post article, the reason is because:

  everyday wear and tear from repeated washings and reuse can lead to physical breakdown of the plastic, such as visible thinning or cracks. Bacteria can harbor in the cracks, posing a health risk.

Also, a study from the Canadian Journal of Public Health found nearly two-thirds of bottles sampled had bacterial levels that exceeded drinking water guidelines. (See here).

So my question is: What kinds of bacteria (or other microorganisms) live in water bottles? In other words, which species should we worry about in these cases?

This Livestrong Article lists species found in the water itself, but I'm more curious about what organisms get introduced and grow through re-use of the bottle.

This is relevant because bottled water just became the most sold consumer beverage in the US.

In addition to the cracks providing a better place for bacteria to grow, all plastic bottles, when reused, are subjected to high levels of bacteria due to contact with hands and mouths. So your water bottle can potentially host a range of bacteria.
Your water bottle traps humidity inside and provides a perfect growing medium, especially near the threads of the mouthpiece and along/within cracks in the bottle which provide better bacteria accumulation.
Microorganisms that Grow

Overall, most sources I could find remained very vague (numerous News stories) or mentioned bacteria generally:

Staphylococcus and streptococcus species, [Source].

Norovirus [Source].

The seemingly most detailed studies I could find came from Watanabe et al. 2014 and Ohnishi et al. (2012) who examined microbial growth in numerous beverage types. However, I could only find their their abstracts online, which report:

microbial growth was detected in ~20% of poured samples, and in ~51% of drank samples.

225 bacterial strains, 27 mold strains, and 77 yeast strains were isolated

Bacteria: Streptococcus spp. (e.g., S. salivarius) and Staphylococcus spp. (e.g., S. aureus), made up the majority. Enterotoxin-producing S. aureus and Bacillus cereus were also isolated.

Molds: Cladosporium spp., Tramets spp., Bjerkandera spp., and Penicillium spp.

 [I Will hunt down these articles to get more details and will update accordingly when I find them...]
Microorganisms in the Water

Based on a study found here, brand new bottles of water can have fungus spores (typically harmless), but opened bottles can show signs of greater diversity (e.g., fungi, skin Staphylococcus, and yeast.

Igbeneghu & Lamikanra (2014) found Staphylococcus species (notably S aureus) and strains of Pseudomonas in bottled water available in Africa.

Your Livestrong article lists a number of non-human pathogens such as: Ralstonia Pickettii, Acidovorax Temperans, A. Delafieldii, Agrobacterium Rhizogenes, Burkholderia Glumae, and Bacillus Thermoglucosidasius.

Juvonen et al.'s  (2011) "Microbiological spoilage and safety
risks in non-beer beverages" provides a thorough list of organisms found worldwide in different bottled waters and other beverages.

Other Issues

According to Rose State microbiologist, Dr. Amy Hurst:

The plastic materials degrade into the water, so then you're drinking very small plastic molecules. [Source].

PET plastics tend to leach when exposed to realistic though extreme conditions, such as exposure to sunlight, heat and storage time. [See UF article]

Bisphenol-A (BPA) and phthalates present in the bottles can leach into the water and possibly cause harm to humans.

Rochester (2013) provides a good review of BPA effects in humans and other test organisms.

New research shows that BPA alternatives such as BPS aren't any safer either; in fact, in some cases they are considered more dangerous to humans. All bisphenols are capable of mimicking the body's sex hormones, says Robin Mesnage, research associate with King's College London.

Al-Saleh et al (2011) found that  76% of the bottled waters they tested in Saudi markets contained measurable amounts of phthalates.

So Reusable Plastic Bottles are Better Right?

Well, from a bacteria standpoint, this isn't necessarily true.  According to a small study  of 12 reusable bottles being used for a week:

Avg bacteria load: 300k CFUs (colony forming units). Ranged between 25 - 900k CFU/cm$^2$.

Notable types found: E.coli, salmonella, and various gram-positive cocci and gram negative rod bacteria.

They found that different bottle types harbored different amounts and kinds of bacteria.


can self-fertilization in flowers be called asexual reproduction? Suppose a flower having both male and female reproductive parts is self-fertilized then can this be called asexual reproduction...?I'm quite confused cause in this case the fusion of male and female gametes do take place but again the gametes are from the same parent....please help.

According to this article from Berkeley, asexual reproduction is:

  Any reproductive process that does not involve meiosis or syngamy

Using this definition of asexual reproduction and knowing self-fertilization involves meiosis and syngamy, it is not asexual.


Usage of "lineage" over "species" Remi.b has suggested here:

  The concept of species is poorly defined and is often misleading. The concept of lineage is much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.

Definition of lineage from Wikipedia:

  An evolutionary lineage is a temporal series of organisms, populations, cells, or genes connected by a continuous line of descent from ancestor to descendent. Lineages are subsets of the evolutionary tree of life

If we're talking about populations, how do we know if two individuals have the same lineage?

Lineages have many levels, it is like using the word groups in some ways, they are stacked inside each other like the worlds biggest branching Russian nesting doll. All vertebrates is a lineage, all birds is another lineage, as is chickens, as is just rhode island reds. Two individuals of any earth life will always share some lineages. Lineage is not the same as clade however since they do not have to be monophyletic and usually refers to a stem line leading to a group, because of how lineage is named, it can be confusing. For instance the gorilla/human lineage could refer to basically all the great apes minus orangutans or it could refer to the sequence organisms leading to their common ancestor, or it could refer to the genetic lines to their common ancestor and back to themselves. And easy way to think of it is the outer boundaries of a lineage is not well defined. What is used to denote the lineage will help with what it is referring too.

You have to look at context. In paleontology because it is assumed you never have a direct ancestor it is used more vaguely almost like a "stem clade", in microbiology however it will be a far more precise term referring to one or more genetic lines.

The concept of species is misleading because people are trying to use our instinctual categorical thinking to describe a continuous series. It is like trying to define a color any category we invent to split the spectrum up will have many problems because it is not something with discrete differences.


Can reptiles digest grains? As a caretaker of a turtle, I sometimes struggle understanding the logic behind the inclusion of corn, soybean, and wheat meals in reptile food, such ingredients seem truly aberrant from what a reptile would naturally be exposed to. Nevertheless I am aware of the biological and chemical similarity between most organisms, so I wonder whether that will help reptiles, especially omnivores with an eclectic digestive ability, to digest these compounds.

I'm looking for legitimate studies on reptile digestibility; anecdotal experience or advice is supplementary if present.

This is not a yes / no question. Many tortoise eat plants (veggies and fruits) while some turtles eat fish too. Snakes are basically predators and do not dwell on plants neither do most of the lizards. I think if a reptile is capable of digesting plant food in general, then it should be able to digest preprocessed grains as well.

Edit:  As for whole intact grains I'm unsure, as canadianer pointed out in comments section, intact grains are hard(er) to digest. /end of edit/
I found this article where scientist fed alligators with a mixed diet in various setup. The diet included corn too and the 'gators responded well in terms that they could use carbon-hydrates.

  Recently, we (3) have demonstrated that hatchling alligators benefit from and apparently do utilize some dietary carbohydrate.


Identify a small spider from southern Poland / eastern Europe Can anyone identify this spider that I have just found in my home?

Details:

location: Katowice, Upper Silesia, southern Poland, eastern Europe (46.42 N, 17.78 E),
size: ~3-3.5 cm (from tip of one leg to tip of opposite leg) / < 1 cm (corpse lenght),
date: July 23th, 2020 (summer, approx. 10:30 am).

It is a Barn Funnel Weaver (Tegenaria domestica), In Europe it is known as the domestic house spider.
Here's some photos of this species to prove the similarities:

What caught my eye in particular that made it more clear that it was this species was the color patterns on the abdomen and cephalothorax, the size you mentioned, the shape of the feelers as well as the location.
The slight difference in shade of color may be due to being a different variety of the species or simply because of the weather and habitat that the spider is in.


Assessing probability from a pedigree This isn't exactly homework but I'd like to treat it as such. I'm asked to find the probability that both (III: 2) and (III: 3) are carriers given that (II: 7) and (III: 1) exhibited the recessive trait (affected individuals are marked black in the pedigree below).

Denoting the affected individuals with $aa$ (and so the dominant allele is denoted $A$), I was able to determine the following:

Both (II: 1) and (II: 2) are carriers.
Both (I: 3) and (I: 4) are carriers.
At least one of (I: 1) and (I: 2) must be a carrier.
The probability that (II: 6) is a carrier is $\frac{2}{3}$.

The answer is supposed to be $\frac{1}{3}\times\frac{1}{4}=\frac{1}{12}$.

I'm mostly confused as to how to approach this one case at a time. Suppose (II: 6) is indeed a carrier. Then if (II: 5) is homozygous for $A$, then (III: 3) has a $\frac{1}{2}$ probability of being a carrier; if (II: 5) is also a carrier, then (III: 3) has a $\frac{2}{3}$ probability of being a carrier.

Since the event that (II: 5) is homozygous is mutually exclusive from the event that he is heterozygous, would I just add these probabilities (i.e. $\frac{1}{2}+\frac{2}{3}$)? Then multiply by the $\frac{2}{3}$ of (II: 6)? This would give $\frac{7}{9}$, which doesn't seem to get me any closer to the right answer.

A different approach I tried was multiplying the respective probabilities for the (II: 5) events above, which gives $\frac{1}{3}$ and thus one factor of the provided answer. If this is right, and it seems to be, I'm not sure how to apply this to the (III: 2) side of the pedigree.

II:6 has a $2/3$ probability of being a carrier Aa.
II:3 has a $1/2$ probability of being a carrier Aa.
Assuming, just like canadianer
suggested, that the recessive gene is rare, autosomal, and
non-x-linked, this means II:5 and II:4 are both homozygous (AA).

If parents of III:2 are therefore Aa and AA, this gives III:2 the probability of being a carrier of $1/2$. However, we must multiply this value by $1/2$, because III:2's father has a $1/2$ probability of being Aa. Therefore $\frac{1}{2}\frac{1}{2}= 1/4 =$ probability of III:2 being a carrier.

Similarly for III:3, if her parents are Aa and AA, this gives III:3 the probability of being a carrier of $1/2$. However, we must multiple this value by $2/3$, because III:3's mother has a $2/3$ probability of being Aa. Therefore $\frac{1}{2}\frac{2}{3}= 1/3 =$ probability of III:3 being a carrier.

The probability of both III:2 and III:3 being carriers is the product of both their probabilities: $\frac{1}{3}\frac{1}{4}= 1/12$.


What exactly makes red meat (probably) unhealthy? It seems generally agreed that (even fresh, unprocessed) red meat is at least somewhat bad for human health.  But why exactly is this the case?  It's difficult to find any attempt at an explanation, especially for anyone not too familiar with diving deep into the medical literature.
Is it because the myoglobin in red meat is carcinogenic or otherwise harmful? That would seem to be the most direct explanation, and there are a few studies on this, but they don't seem to be widely cited in discussions on health effects of red meat.  If that is true, would it mean that one should avoid dark, myoglobin-rich fish and poultry such as tuna and ostrich just as much as mammal meat?
Is it only because red meat tends to be more fatty?  In that case, would leaner cuts of red meat have the same health effects as white meat?
Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?  (I had wrongly assumed this was a strange idea, but acvill's answer gives a plausible explanation.)

The gut microbiome is partly to blame, at least for the associations of red meat consumption with heart disease.  Red meat has a high concentration of L-carnitine, which is metabolized by bacteria in the gut to produce trimethylamine, which is further metabolized by FMO3 in the liver to produce trimethylamine-N-oxide (TMAO). High blood levels of TMAO are associated with higher risk for both cardiovascular disease and early death from any cause.
Sources on the relationship between the gut microbiome, L-carnitine, and heart health:
New study links L-carnitine in red meat to heart disease
Red meat, TMAO, and your heart

Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?

The NIH gives the following values for the carnitine content of different foods:

Food
Milligrams (mg)

Beef steak, cooked, 4 ounces
56–162

Ground beef, cooked, 4 ounces
87–99

Milk, whole, 1 cup
8

Codfish, cooked, 4 ounces
4–7

Chicken breast, cooked, 4 ounces
3–5

Ice cream, ½ cup
3

Cheese, cheddar, 2 ounces
2

Whole–wheat bread, 2 slices
0.2

Asparagus, cooked, ½ cup
0.1


Which mRNAs enter P-bodies? Processing bodies (P-bodies) are distinct foci within the cytoplasm of the eukaryotic cell consisting of many enzymes involved in mRNA turnover (ref). They play a fundamental role in RNA silencing/interference, particularly as an antiviral response, since they are the key site for siRNA-bound RISCs (small interfering RNA-bound RNA-induced silencing complexes) to degrade mRNA with an exogenous origin. Some mRNAs entering P-bodies then leave and re-initiate translation, and the switching mechanism for this is currently poorly understood.

However, I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation. Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?

It seems rather odd if RNAi has evolved to give viruses two independent targets for evasion, but if the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated (and therefore postpone movement to the P-body)? I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.

The paper cited above says "The available evidence indicates that P bodies are sites where mRNAs that are not being translated accumulate, the information carried by associated proteins and regulatory RNAs is integrated, and their fate — either translation, silencing or decay — is decided", but this is from 2007 and I'm aware RNAi is a very fast-moving field.

I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.

To be clear, P-bodies are in the cytoplasm (ie they are not separated by a membrane). There is also dynamic exchange of components between the ribonucleoprotein complex and free cytoplasmic pool (1):

  Most P-body components are distributed diffusely throughout the cytoplasm as well as being localized in P bodies. Quantitative information regarding the fractionation of these proteins between the cytoplasm and P bodies is still lacking, but given the volume of P bodies relative to that of the cytoplasm, the diffuse cytoplasmic fraction could be significantly larger, although the concentration of mRNA-decay factors might be much higher in P bodies. Also, P-body components dynamically exchange with the cytoplasmic pool, which indicates that decay enzymes and co-activators are not confined to P bodies. So, it is probable that mRNA decay also occurs, and might even be initiated, in the diffuse cytoplasm, and that P bodies arise by association of mRNA-decay intermediates induced by interactions between decay enzymes and cofactors. The concentration of mRNA-decay intermediates and mRNA-decay enzymes in P bodies would be expected to increase the speed of degradation and, in turn, reduce any potential competition between these RNA fragments and normal mRNAs for limiting cellular proteins involved in mRNA regulation.

I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation.

mRNA can also be degraded by exosomes (1):

  In eukaryotic cells, degradation of bulk mRNA occurs by two alternative pathways, both of which are preceded by removal of the poly(A) tail by deadenylases. Following this first rate-limiting step, mRNAs can undergo 3'→5' exonucleolytic decay, which is catalysed by the exosome... Alternatively, after deadenylation, the cap structure is removed by the decapping enzyme DCP2, rendering the mRNA susceptible to 5'→3' digestion by XRN1 [a P-body associated protein].

Also see (2), and this image therein:

If the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated?

That is, in fact, not the requirement (3)

  Recruitment of mRNA to PBs is not an occurrence of non-translation, rather requires active silencing via miRNA or RNAi mechanisms.

They reference another paper (4):

  Recent studies with mammalian cells have shown that P-body integrity is not required for ARE-mediated mRNA decay or silencing mediated by fully or partially complementary exogenous, transfected small interfering RNAs (siRNAs). In this study, we investigated the requirement for P-body integrity in NMD, mRNA decay, and silencing mediated by miRNAs and long double-stranded RNAs (dsRNAs). We show that these pathways are unaffected in cells lacking detectable, wild-type P bodies. However, although P bodies are not required for silencing, active silencing pathways are required for P-body formation in Drosophila melanogaster cells, indicating that P bodies are not the cause but a consequence of silencing.

Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?

The RISC complex can be involved in initial recognition and cleavage of viral RNA and the resulting fragments are subsequently degraded by the exosome or P-body associated proteins. RNAi associated components have been observed to be localised with P-bodies (1):

  Endonucleolytic cleavage of siRNA or plant miRNA targets is catalysed by the C-terminal PIWI domain of Argonaute proteins... Following this endonucleolytic cleavage, the resulting mRNA fragments are handed over to the general mRNA-decay machinery. In D. melanogaster, 5' and 3' mRNA fragments that are generated by Argonaute-mediated endonucleolytic cleavage are degraded by the exosome... and by XRN1, respectively.

You can also consider the R-gene viral defence mechanism in plants which induces P-body formation and suppression of translation in an RNAi independent manner (5):

  Plant NB-LRR proteins [R-genes] confer resistance to multiple pathogens, including viruses. Although the recognition of viruses by NB-LRR proteins is highly specific, previous studies have suggested that NB-LRR activation results in a response that targets all viruses in the infected cell... NB-LRR signaling does not result in the degradation of viral transcripts, but rather prevents them from associating with ribosomes and translating their genetic material. This indicates that defense against viruses involves the repression of viral RNA translation... As a consequence..., NB-LRR responses induce a dramatic increase in the biogenesis of RNA processing bodies (PBs). We demonstrate that other pathways that induce translational repression, such as UV irradiation and RNAi, also induce PBs. However, by investigating the phosphorylation status of eIF2α and by using suppressors of RNAi we show that the mechanisms leading to PB induction by NB-LRR signaling are different from these stimuli, thus defining a distinct type of translational control and anti-viral mechanism in plants.

There are many articles discussing how viruses subvert and/or repurpose P-body mediated decay if you want some further reading (3), (6), (7).


What are these tiny, almost transparent, dots in my vision? Sometimes when I stare at a very bright thing such as the sky I see little dots. It's actually more of a circle with a little dot inside it. They are half-transparent and they move around a lot. When I first see them they tend to appear in a group out of nowhere. I have seen one that is gray and almost black. What is this?

You are probably seeing floaters.

  Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent. At a young age, the vitreous is transparent, but as one ages, imperfections gradually develop

You might as well be seeing Scheerer's phenomenon

  The blue field entoptic phenomenon or Scheerer's phenomenon [..] is the appearance of tiny bright dots (nicknamed blue-sky sprites) moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky.

Please have a look at the wikipedia article for more information.

I only now realize that your question is a duplicate of Seeing strange things in light


Epidermal layer and muscle wall of colon? First of all,I wanted to ask that whether epidermis is present in colon ? And if yes than how is muscle wall present with respect to epidermis. Can anyone give me a pic that has both the epidermis and muscle wall of colon.

Good question. The colon is lined by epithelial cells (as are all hollow organs). These particular epithelial cells are different from epidermal cells, which are another particular type of epithelial cells found in skin.

Epithelial cells are distinguished by the way they connect with each other using tight junctions to form a permeability layer between compartments.

In the colon, the purpose of the epithelial cells is to both to absorb water and to form a barrier between the luminal contents and the body.  They form the layer facing the lumen. The muscular layers of the colon, both the circular and the longitudinal, are further out from the lumen. You can see them in this histology slide:


Can anyone ID this microorganism? I found this microorganism in a wet moss sample taken from my backyard in Richmond, Virginia (USA). I took some pictures of it at 40x, 100x, and 250x. I'm not entirely sure what it is, but I think it's some kind of rotifer based on it's behavior. It anchors onto a piece of moss while hunting. It stretches out to catch food, and once it's caught something, it snaps back into itself.

Any ideas as to what this is?

Appears to be a ciliate protist called Vorticella.

 Image source: Wikimedia (Author: Frank fox, 2010)
Vorticella always stood out to me because of their long, narrow stalk they use for anchoring with ciliate-lined bell-shaped oral end.

 Image source: MicrobeWiki (originally from Haw River Program)
Fun fact from Wikipedia:

The stalk is made up of the spasmoneme [also called "myoneme" above], a contractile organelle, with rigid rod filaments, batonnets, surrounding it. The coiled spasmoneme and batonnets serve as a molecular spring, so that Vorticella can contract. The cell body can move hundreds of micrometers in milliseconds. The spasmoneme is said to have higher specific power than the engine of the average car.

You likely mistook this for the more-commonly known rotifer due to the beating cilia at the oral end and tendency to anchor down, which are also both characteristics seen in rotifers. See this SE post about rotifers I wrote a while back which includes some nice animations.
Also, you can quickly differentiate Vorticella (which are typically free-living) from closely-related and morphologically-similar Carchesium, which are colonial.
See this video ("Vorticella - Under the Microscope) by Nick Moore) for various videos and some more info.


Saltatory conduction of nerve impulses I am aware about some basics of saltatory conduction of nerve impulses. I know that the nerve impulses (ion flow and the depolarization) are transferred from node to node in myelinated nerve fibers. In non-myelinated fibers, the ion flow and depolarization are repeated along the entire length of the axon. Thus the saltatory conduction is faster.

Why is it so that myelinated nerve fibers require less energy of activation then the non-myelinated ones?

Also, my book says that a rise in temperature accelerates the conduction of nerve impulses. I would like to know the reason for this.

The overall energy expenditure of a myelinated axon is lower compared to a non-myelinated axon, because myelination causes the action potential to be conducted in a saltatory fashion, i.e. the action potential jumps from one node of Ranvier to the next (Fig. 1). Saltatory conduction depolarizes only a small fraction of the membrane (i.e., the cumulative exposed membrane surface in the nodes of Ranvier) when an action potential travels through the axon, as opposed to the whole membrane in an unmyelinated axon. Hence, less ions are transported across the membrane for any given action potential. Therefore less work is required from the sodium-potassium pump (a.k.a. the Na+,K+-ATPase) to restore the electrochemical gradient across the cell membrane after the action potential. Because the sodium potassium pump  uses ATP to pump Na+ out and K+ into the cell (Lodish, 2000), myelinated axons require less energy than unmyelinated axons for an action potential to be conducted.

Fig. 1. Saltatory nerve conduction. Source: Antranik.

Note that this is different from the activation energy of a neuron. For physiological action potential generation in neurons with chemical synapses, the activation threshold is generally expressed in terms of activation voltage change, i.e. the depolarization amplitude necessary to generate an action potential. This is likely very similar between myelinated and non-myelinated neurons.

In terms of temperature; the action potential is mediated by the opening and closure (i.e. the gating) of ion channels. When an action potential travels through an axon, the depolarizing potential opens sodium channels which result in further depolaization, opening up new channels etc (Fig. 2).

Fig. 2. Action potentials travel through axons by voltage gated opening of sodium and potassium channels. Source: Rice.

The voltage differences that are sensed by the ion channels are generated by current flow. Increasing the temperature will enhance diffusion of ions through the channels and it will enhance the response kinetics of the ion channels. However, most proteins are highly temperature sensitive and too much of a temperature increase will impair ion channel functioning and eventually even denature the protein.

Reference
- Lodish, Molecular Cell Biology. 4th ed. New York: W. H. Freeman; 2000


Why Doesn’t Hypercalcemia Cause Muscle Spasms? If you have more calcium in the cell, wouldn’t more attach to troponin and initiate muscle contraction? Why does hypercalcemia cause muscle weakness instead of spasms?

Hypercalcemia does indeed cause muscle spasm, but as someone else wrote, hypercalcemia indicates the calcium levels in blood and not in the sarcoplasmic reticuli.

One example where you can observe that increased calcium leads to increased contraction is when you take the cardiac glycoside, digoxin. Digoxin inhibits the Na+/K+ ATPase causing an increased concentration of intracellular sodium ions. Indirectly, the increased levels of sodium will disturb the sodium gradient (because of the accumulation of sodium ions inside the cell) and stop the Na+/Ca2+ exchanger. The consequence of the disturbance of the sodium/calcium exchanger will lead to the increased levels of calcium and the increased storage of calcium in the sarcoplasmic reticulum and thus cause positive inotropy of the myocytes.

You can read more about it here:
Gheorghiade, Mihai, Kirkwood F. Adams, and Wilson S. Colucci. "Digoxin in the management of cardiovascular disorders." Circulation 109.24 (2004): 2959-2964.


Do housekeeping genes vary between tissues I am working on an RNA-Seq project, and I am aware that some researchers use housekeeping genes as a method of normalization.  My project has several different tissues, and I was wondering if housekeeping gene expression is generally invariant across tissue type?

My experience is: Yes they can vary quite a lot (according to differences in the genetic profile of the cells) and you have to test this. As a primer I can recommend reading the articles listed below. These are mostly looking into this in the context of realtime PCR, but this should be valid for RNAseq as well. For some applications it is also a good idea to use more than one gene for normalization.

References:

Accurate normalization of real-time quantitative RT-PCR data by
geometric averaging of multiple internal control genes.
Selection of housekeeping genes for gene expression studies in human
reticulocytes using real-time PCR
Reference Genes / Housekeeping Genes
Gene Ontology Based Housekeeping Gene Selection for RNA-seq
Normalization


Does testosterone increase female sexual behavior? According to my lecture notes testosterone generally increases sexual behavior.
Given that it's generally thought to be the male hormone I'm not quite sure whether they mean that it also increases sexual behavior in females.

What is the effect of testosterone on female sexual behavior?

I'll point you to this article by A. Tuiten et al.

To quickly answer your question, yes,  testosterone does have an enhancing effect on the sexual behaviour of human healthy adult females.

The (admittedly small) study indicated that after an dose of testosterone was given to the women there was found:

a statistically significantly [sic] increase in genital responsiveness (P = .04)
a statistically significant association between the increase in genital arousal and subjective reports of "genital sensations" (P = .02) and "sexual lust" (P = .01)

A time lag was reported from the administering of the dose to effects being seen of approximately 4.5 hours.

References

 Tuiten A. 2000. Time Course of Effects of Testosterone Administration on Sexual Arousal in Women. Archives of General Psychiatry 57: 149–153.


Involuntary twitches and apnoea during early phases of sleep I assume most people either experienced or have seen people with the following phenomenon: in the early phases of sleep sometimes involuntary twitches occur that usually accompany the pause of breathing (I'm aware that there's a  chronic sleeping disorder called sleeping apnea but I think it's different because what I'm asking about now is acute). I wonder if the twitching is some sort of emergency signal, so that the person would wake up (to some level not necessarily full awake) and start breathing. Is there any data that these (the pause in breathing and the twitches) are connected or they are independent? Also I'm also interested why this acute pause of breathing occurs?

Edit:

I've researched myself on this topic and it seems that what I've described is more likely a form of Obstructive sleep apnea.

Jerk-like muscle contractions occurring while drifting off to sleep are normal and are referred to as "sleep starts" or sleep myoclonus (National Institute of Health - NINDS).

Sleep Education explains the symptoms:

  Sleep starts usually consist of one strong jerk that affects much of the body. The arms and legs are most likely to be affected.

So sleep starts may be quite vigorous, but may consist just of small lip movements too.

The American Sleep Association mentions that:

  Sleep myoclonus will rarely disturb the subject or any bed partner to the point of waking and disrupting sleep [...].

In fact, sleep starts are associated with tachypnea, i.e., an increased in breath rate (Vetrugno & Montagna, 2011)

Hence, your hypothesis that a myoclonus is a mechanism to wake a person up (for whatever reason) seems unsupported.

Reference
- Vetrugno & Montagna, Sleep Medicine 2011; 12: S11–S16


Gel electrophoresis and foam I've never seen this kind of thing happen. What might trigger this??

Gas bubbles are foamed by electrolysis of water, generating bubbles of hydrogen gas on the negative electrode and oxygen gas on the positive electrode.

As for the foam itself... I am guessing there is some form of detergent in the buffer. Some electrophoresis buffers do contain detergent.


What is the cannabinoid autoreceptor? "Is there a cannabinoid autoreceptor? And if so what is the cannabinoid autoreceptor?"

(i.e. is the cannabinoid autoreceptor CB1, CB2 or is it one of the G protein coupled receptors, GPR18, GPR55 or GPR119?)

Where:

An autoreceptor is a receptor located presynaptically that sends back negative feedback that inhibits the synthesis of the neurotransmitter to which the autoreceptor belongs and this negative feedback also inhibits the release of the neurotransmitter from storage vesicles into the synaptic cleft.
The CB1 and CB2 receptors are respectively called the first and second cannabinoid receptors and are a pair of G protein coupled receptors.
GPR18, GPR55 and GPR119 are G protein coupled receptors that are also activated by some lipid messengers including a few of the endocannabinoids and their related compounds.

CB1 and CB2 are indeed particular genes which are present in neurons, but also liver and other tissues.  The HGNC website is a good resource for questions like this - HGNC is the international organization that tries to unify and track gene names.

The official gene names are CNR1 and CNR2 respectively.  Gene names are a bit of a mess, since many genes have been found by different experiments and so have many names.

CNR1 has other aliases, I see:
CANN6, CB-R, CB1, CB1A, and CB1K5.

CNR2 has only the one alias: CB2.

I also searched the HGNC website for those alternate gene symbols and they appear to be different genes, although CB1 and CB2 are GPCR class receptors, humans have hundreds of these genes.  Most cell scientists would not be surprised if cannabinols bound other receptors - the fact is probably only that CB1 and CB2 bind strongest and were found first.  Often weak binding is important to specific pharma/neuro responses.

That is to say there shouldn't be any single Cannabinoid receptor in the animal repetoire.  CB1 and CB2 almost certainly have a primary function other than cannibinol binding.  Primates evolved in the old world and cannabis is thought to have originated in the Himalayan regions.  From an evolutionary standpoint, the activity of cannabinoids is as much coincidence as anything, so you would expect that a single receptor gene is unlikely.


How is the transcription direction of RNA polymerase determined? When transcription factors attach to the DNA strand - How do they know in which direction they have to initialize the transcription by rna polymerase? Is it always read in the same direction anyway? What about those 'promoters'? Do they influence the transcription direction?

Transcription always proceeds in the direction 5' (5-prime) to 3' (3-prime) on the coding strand of DNA. Binding of both transcription factors and RNA polymerase to DNA depends on sequence motifs in the DNA. Transcription always happens in the same direction with respect to the chemical structure of the coding DNA strand, while the transcription direction with respect to the structure of the chromosome depends on which strand the coding sequence is found on (and thus which strand is defined as the coding strand for that gene).


The oldest common ancesstor of all human beings Do all human beings have a single oldest ancestor (a man and a woman), or were there were many ancestors at the same time at different places on earth?
This article sheds some light. Is there another authoritative report released more recently?

You are talking about the mitochondrial eve and the chromosome Y adam.  At some point there must be just one pair, though historically the evidence can be lost if there is a near complete extinction event.  Current evidence for eve points to SE Africa.


What is the role of various immune cells in demylinating neuropathy? Is there a simple description or article of the life cycle of tcells and other immune cells and how they become programmed to attack the myelin of the nerves?

When I try to read through an article like this: http://m.neurology.org/content/56/1/74.full its pretty frustrating. I consider myself fairly technical but not versed in biological systems.

Hi I don't think there is a simple way of describing the way the immune system works. However I'll give it a rough go. The immune system can be broken into two major categories, The innate immune system which does not need to learn about what foreign bodies are and works via physical systems such as the skin and molecular structures on cells such as PAMP-receptors (Pathogen associated mollecular pattern receptors) on Phagocytic cells (such as macrophages, neutrophils, ...) which innately recognize the bad guys which have characteristic non human molecular structures.

The other half of the immune system is called the adaptive immune system in which specialized cells T-cells and B-cells, rearrange their own DNA to create new and varied receptors which are specific for foreign antibodies.
T and B cells work together to recognize different sides(epitopes) of foreign mollecules (foreign peptides) and have to agree that the mollecule is foreign. A process of clonal selection and deletion of T-cells and B-cells in the thymus and bone marrow respectively can sometimes go wrong and this leads to auto-immunity. For example some B-cells which recognize self antigens might escape clonal deletion during their maturation process, and become later (many years ?) activated by a T cell which recognizes an adjuvant (close by aggravating molecule, such as a viral surface molecule).
Once the B-cells matures they can secrete self anti bodies.

Finally the innate and adaptive immune systems work together and shouldn't be thought of as separate. For example the complement system is part of the innate immune system as a molecular cascade amplifying immune system signals and works with both the adaptive and innate systems.

It would help if you can describe the specific type of autoimmune condition that you are investigating as there may be several ways that the immune system can become directed towards self.

There is a great online course from UC IRVINE and whose videos/lectures on the immune system available on youtube, you'll need at least 27 hours of good concentration, the autoimmune lectures are towards the last ones.

https://www.youtube.com/watch?v=gVCfC8WW4eU&list=PLIHnZ4fK_IyJaH2WNHIk2cFsnR2UM4z7t

My understanding is still evolving, however I hope this helps.


Are there cannibalistic k-selectors? My understanding of r- and k-selectors does not go deeper than the wikipedia article. I understand k-selectors to be creatures that put tendentially more effort and energy into rearing their offspring, but produce tendentially less offspring.

With cannibalism I don't mean eating their own on rare occasions, like after a plane crash in the Andes, but exibiting cannibalism outside of extreme situations.

My gut feeling tells me that expanding much energy into raising an offspring and then eating her does not make much sense, but the world is big, there's lots of different species of animals and most of them are weird once look closely enough.

A good answer explains why one species is a rather to be seen as a k-selector, and in what contexts the cannibalism happens. Since we are talking about a sliding scale of behaviours, the question might as well be read as: What cannibal is the strongest k-selector?

My answer is messy and incomplete! I very welcome editing!

As soon as an individual is killed, on might as well eat the dead, but the act of killing might not be for the purpose of eating. We might even say that eating a dead might not only be for the purpose of getting energy and matter but only to clean the living place. And killing might appear in many circumstances. The best way to consider such issue is certainly by using the quite fundamental model of kin selection theory. It fits as much to species that gain energy by eating the dead or not. The difference imply just a minor change in the payoff matrix.

The decision of one (the actor) to kill (and eat) another individual (the recipient) depends on:

the relatedness of the actor to the recipient (note a relatedness is not necessarily symmetric)
The competition this recipient causes on the actor
The cost (energy cost, risk of being injured or killed) of killing

Many species (ants, wolves) might kill or injured individuals of the same species, when for example there is competition for reaching a status in the hierarchy.

I think that the definition of k-selected species is not very accurate. First because there are limit cases. But also because r and k can relate to the function that describes the population growth of a species or might describe the amount of energy the parents spend into one offspring which is not necessarily the same thing. If we think of the parental care, we can think of the lions. When a male win the right to access to the females of another male, he will kill the babies that might be potential competitors to his progeny (because they take energy from the females or because females are not fertile before having lost their babies).

Killing its own offsprings is certainly not less common in k-selected species. You might think it is such a big cost to kill one of its own offspring when one has few offspring but what is important is to think in percentage. Killing 50% of the progeny has the same cost of an r-selected species than for a k-selected species.

If one has a probability of 10% to be able to raise its offspring to adult age. But this probability raised to more than 20% if it accepts to kill an offspring to save energy for the next offspring, then it wins by doing so. THen we might ask: "so would one make an offspring if it intends to kill it?"

Well it does not necessarily intend to kill it. It might need to decide late in the season whether or not it has better to kill its own offspring.

Then, maybe offspring might be used as a reserve of energy and matter for its siblings or for its parents.


Is this a nest and which wasp species? A friend found this stuck to his insect screen today.
He said it felt like dust.
This wasp/bee was alive.
Location is Germany.
Is this a nest?

First look:

After peeling it open:

Looks like this is a European wool carder bee (Anthidium manicatum)
More precisely a female, judging by the round end of the abdomen.

Information regarding the nest it was found in:

These bees construct their nests in preexisting cavities, using the trichomes of wooly plants.
Females use their mandibles, which are sharply toothed, to remove trichomes from the stems and leaves of various plants. They then roll up the trichomes into a ball and bring them to a preexisting cavity. Inside the cavity, the bees fashion the trichome ball into cells, where they deposit an egg as well as a provisioning mass consisting of nectar and pollen. Once finished, she seals the entrance to the cavity with a terminal plug, which consists of inorganic and organic materials that she brings to the nest. Source


How are memories stored in the brain? I've been thinking about this for a while and I can't figure out how a memory can be stored in the brain.

I understand that important memories are favourably retained, such as a near death experience, the birth of your child or your wedding day. But I cannot comprehend how this can be stored biologically in the brain.

Firstly, I'd like to emphasize that the understanding of memories and learning as we know it is still in its very early stages. In fact, the mechanisms behind short-term memory are still under intense debate.

As for long-term memory, it is essentially caused by chemical changes in synapses between neurons in the brain. When you sense stimuli from your environment, action potentials follow a specific trail of afferent neurons towards the central nervous system, which then sends a message back through efferent neurons to initiate a response. The high frequency of these action potentials from the same stimuli of whichever sense allows for the strengthening of specific connections between neurons, which is called long-term potentiation. This phenomenon is one of the major components of synaptic plasticity, which also applies to the weakening of synaptic connections between neurons due to lack of transmission, as well as the change in the number of connections the neurons are receiving and making. Synaptic plasticity is also influenced by the change in quantities of neurotransmitters being expulsed into the synaptic cleft, and how cells react to these neurotransmitters, which is highly regulated by calcium levels. Ultimately, synaptic plasticity in accordance with learning is referred to as Hebbian theory.

We are still not exactly sure where memories are stored within the brain, but we do know that the hippocampus does play a big part. It definitely aids in the storing and structuring of memories in the form of these millions of synaptic changes. Finally, memory consolidation occurring in others regions of the brain over longer periods of time is likely, but still debated by some.


Is it feasible to eradicate a virus without vaccines? Although a vaccine for hepatitis C virus (HCV) remains elusive, new direct-acting antiviral (DAA) drugs can cure HCV effectively and conveniently. The latest DAA, Epclusa, can cure 95-99% of chronic hepatitis C regardless of genotype (e.g. see here). So if DAA drugs become universally available, will HCV be the first virus eradicated solely by drugs?

Is it feasible to eradicate a virus without vaccines?

It is possible? I would say yes. But feasible... I think not. Consider this, once vaccinated, a person is usually immune to the virus. And you only need the vaccine to take hold, for an individual to acquire life time immunity. However with drug treatment... even once the treatment succeeds, the person can be reinfected. And you will have come back with drug treatment again.

Given the difficult in vaccination campaigns (ie polio) to eradicate the last reserved of a virus... I think a similar drug based campaign would a lot more difficult. There is no herd immunity to prevent the virus from reinfecting the wider population when it leaves its strong holds.


Why do neurons die so quickly (relative to other cells) when deprived of oxygen? This question could be considered a follow-up question to Why is a lack of oxygen fatal to cells?, although the top answer there does not address why damage starts to pop in.

The answer says this:

  Neurons are also highly metabolically active, which means they
  generate more waste products. A buildup of nitrogenous waste products
  in the cell (and bloodstream) can be potentially fatal due to it's
  effects on pH (screws up enzymes and a whole slew of biochemical
  reactions)

But when the brain is deprived of oxygen, metabolism shuts down. So waste products aren't being generated anymore.

====

Basically I'm wondering - what causes neurons, in particular, to die so quickly (relative to other cells, like kidney cells) after they're depleted of energy?

There is a good review in the Journal of Experimental Biology (Bickler and Donohoe 2002, JEB 205, 3579–3585) I will just summarize for those that do not have access to the review.

Neurons use lot of energy to maintain their polarized state, this is not required to other cells. When O2 or blood flow is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.


How significant is the genetic component of homosexual behaviour? From some basic googling, I found that nobody has ever proven that people are born gay and that environment plays a great part in homosexuality.

I wish to know if there is a genetic component to homosexual behaviour. If so, how significant is that component (in some measure such as percentage contribution to the behaviour). What are other factors that play a role in homosexuality i.e. what constitutes environmental factors?

This is not an area I know well, but I'm familiar with a couple of studies that have tried to estimate the heritable (genetic) component of homosexuality in humans. A review paper by Rice  et al (2012) points out that:

  Pedigree and twin studies indicate that homosexuality has substantial heritability in both sexes, yet concordance between identical twins is low and molecular studies have failed to find associated DNA makers.

Here is a selection of papers that should be of interest to you:

Pillard & Bailey. 1998. Human sexual orientation has a heritable component. Hum. Biol.
Bailey et al. 2000. Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. J Pers Soc Psychol.
Kirk et al. 2000. Measurement models for sexual orientation in a community twin sample. Behav Genet
Rice et al. 2012. Homosexuality as a consequence of epigenetically canalized sexual development. Q Rev Biol.

Kirk et al (2000) find a rather strong heritable component (30-60%), which also differs between males and females (stronger in females).

  Abstract
  Multivariate structural equation modeling techniques have been applied to examine the causes of individual differences in responses to several items concerning sexual orientation. To minimize potential ascertainment and response biases, the study sample involved a large (N = 4901) community-based cohort of Australian twins aged 18-52 who answered an anonymous questionnaire on sexual behavior and attitudes. The statistical power of the analysis was increased by the availability of multiple measures of sexual orientation (behaviors, attitudes and feelings), providing stronger evidence for the existence of additive genetic influences on this phenotype than in a previous analysis (Bailey et al., 2000). Estimates of the heritability of homosexuality in this sample ranged between 50 and 60% in females but were significantly lower (heritability of approximately 30%) in males.

Note however that is it often difficult to separate genetic and environmental components in these types of epidemiological data, especially when twins have grown up in the same environment. I'm also not in a position to judge or comment on the quality or methods of these studies.


What is the Baculovirus and how does it help in research? I was reading up about Biotechnology and the use of insects, and came across an interesting article about Insect Cell culture Techniques that specifically talked about the usage of the Baculovirus. If I understand correctly does this virus help express certain genes when inserted into a cell?

Sorry if I am way off or did not use proper terminology, I am a high school IB Biology student who still has a a lot to learn

Thanks!

Baculoviruses are a a class of viruses which infect only a pretty small number of insects (or their cells in cell culture). To do so, the virus has to infect a cell, take it over to produce the own proteins and DNA to make new virus particles and finally set these new particles free. This is basically what is shown in the image below (from here):

From the proteins encoded by the viral genome, not all are essential, meaning removing them will not do harm to the virus or its function. And this is used in Biotech to produce proteins of choice. One of the non-essential proteins is replaced by the sequence of the protein you want to have produced by the cells. You then take insect cells in cell culture (these are single insect cells which live in a big vessel full of culture medium), infect these cells with the modified virus and eventually harvest the protein from the culture.

The advantage of Baculoviruses is that they only infect the insect cells on which they are specialized so they are a safe way of producing proteins for pharmaceutic applications. If you want to read some more about this, start here.


What reasons allow for women to outlive men? It is a well-known fact that women tend to outlive men.

I often hear people unscientifically stating that men generally generally die younger because of the higher stress encountered in their work lives. I would personally immediately rule this out, as who's to say that that women's (past) home lives just weren't as stressful? Also, shouldn't we see a narrowing of difference in age with the recent gender equality issues? Since the trend in question still occurs in virtually all countries of the world, I think it's safe to assume that the phenomenon is purely physiological.

I am curious as to the most sound scientific theories or known reasons for why women typically outlive men. Finally, I understand that aging in itself is not a process that's completely understood, and thus am not expecting a "complete list" of factors.

In a study on longevity in 121 countries, women tended to outlive men by about 5 years [1]. The suggested causes for this are numerous, some of which are temporally, geographically, or culturally specific.

On the terminology, sex tends to refer to the absolute biological differences, whereas gender relates more to differences in perception/lifestyle (for instance, socio-economic differences).

Evidence

In a study on Greek centenarians the authors found that women outnumbered men (1.68:1), with men having a higher likelihood of smoking, and thus are more at risk of smoking-related illness and mortality (historically this was more true than today) [2]. This is also true for alcohol consumption. The authors also report that having a first degree relative who was also a centenarian is associated with longevity (highlighting the importance of genetic factors in lifespan determination).

There is also evidence that the rate of telomere shortening (number of cell-divisions until cell-cycle arrest) is sex-specific [3].

rwst cites an interesting paper, that presents evidence that suggests male hormones may decrease lifespan [4]. This may be due to differential onset of atherosclerosis and cardiovascular disease, caused by exposure to different sex hormones [5].

In a review on the brain/behaviour specific aspects of differential ageing between the sexes, the authors discuss differences in brain anatomy and cognitive (and emotional) functionality between the sexes [6].

Remarks

This is by no means an exhaustive list of the reasons for differences in lifespan between the sexes in humans. There are likely to be many other causes, such as men tending to have more 'risky' behaviours, and possibly other unknown genetic effects, such as having 2 X chromosomes, vs. XY.

References

Møller, A. P., et al (2009). Why men have shorter lives than women: effects of resource availability, infectious disease, and senescence. American journal of human biology : the official journal of the Human Biology Council, 21(3), 357-64. doi:10.1002/ajhb.20879
Tigani, X., et al (2011). Gender differences in Greek centenarians. A cross-sectional nation-wide study, examining multiple socio-demographic and personality factors and health locus of control. BMC geriatrics, 11, 87. doi:10.1186/1471-2318-11-87
Barrett, E. L. B., & Richardson, D. S. (2011). Sex differences in telomeres and lifespan. Aging cell, 10(6), 913-21. doi:10.1111/j.1474-9726.2011.00741.x
Min, K.-J., et al (2012). The lifespan of Korean eunuchs. Current Biology, *22(18), R792-R793. doi:10.1016/j.cub.2012.06.036
Pérez-López, F. R., et al (2010). Gender differences in cardiovascular disease: hormonal and biochemical influences. Reproductive sciences (Thousand Oaks, Calif.), 17(6), 511-31. doi:10.1177/1933719110367829
Kryspin-Exner, I., et al (2011). Geropsychology: the gender gap in human aging--a mini-review. Gerontology, 57(6), 539-48. doi:10.1159/000323154

Update

Just been reading this interesting paper by Maklakov, et al (2013, BioEssays) titled "Evolution of sex differences in lifespan and aging: Causes and constraints", which presents a more evolutionary/genetic argument for the differences.

Abstract

Why do the two sexes have different lifespans and rates of aging? Two hypotheses based on asymmetric inheritance of sex chromosomes (“unguarded X”) or mitochondrial genomes (“mother's curse”) explain sex differences in lifespan as sex-specific maladaptation leading to increased mortality in the shorter-lived sex. While asymmetric inheritance hypotheses equate long life with high fitness, considerable empirical evidence suggests that sexes resolve the fundamental tradeoff between reproduction and survival differently resulting in sex-specific optima for lifespan. However, selection for sex-specific values in life-history traits is constrained by intersexual genetic correlations resulting in intra-locus sexual conflict over optimal lifespan. The available data suggest that the evolution of sexual dimorphism only partially resolves these conflicts. Sexual conflict over optimal trait values, which has been demonstrated in model organisms and in humans, is likely to play a key role in shaping the evolution of lifespan, as well as in maintaining genetic variation for sex-specific diseases.


Bacterial cell lysis buffer used in proteomics procedures What kinds of detergent-free bacterial lysis buffers exist? The proteins we're extracting will be later analyzed by LC-MS/MS, and we're looking for a lysis buffer that won't interfere with this downstream analysis.

I'm a HUGE fan of FASP (filter-aided sample preparation) which is an in-solution preparation/digestion. It is very fast, allows you to not worry about a protein precipitation step, and gets rid of all MS incompatible substances with the wash steps (so doesn't matter what lysis buffer you use). It requires very few, inexpensive materials (a pack of 100 centrifuge filter units is less than 250 USD from VWR) and has great recovery. This is the link to the Nature Methods paper that the linked protocol is based on (the linked protocol is an updated, faster version of the Nature Methods one).


How would a warm winter affect maple sap production? The past winter (2011-2012) was warmer than usual.

Trees are normally tapped in late February when the daily maximum temperature goes above freezing. However, assuming that there have been relatively few days with a maximum temperature below freezing, how would this affect the timing and quantity of sap flow?

This article has a clear explanation (backed up by good links) of the effects of climate change on maple sap production, including the following:

Maple trees produce the best sap on cool days preceded by freezing nights – the cold weather causes the sap in the tree to freeze, creating a low-pressure vacuum that draws more sap up from the roots. When temperatures rise the next day, the sap melts and oozes through the tree, making for easy collection. When temperatures stay abnormally warm, as they have been lately, this process does not occur.
Additionally, the warm weather causes the trees to begin to bud.  The hormones that trigger budding also decrease the sap’s sugar content and spoil its taste. This means that it takes much larger quantities of sap to boil down to a gallon of syrup.


Is a female spider, well-fed by sexual cannibalism, less likely to mate again? The Wikipedia page on sexual cannibalism (e.g. female spiders eating their mates) currently has a statement that sounds wrong to me, but I don't feel expert enough to edit it out:

  An additional benefit to cannibalization is the idea that a well-fed female is less likely to mate again.

I can't see why that would be the case. Why not continue to seek a second, better, mate? Unless perhaps being well-fed makes you a slower, larger target for predators, so hiding for a while is a better tactic.

The reference given is to

  Female hunger can explain variation in cannibalistic behavior despite male sacrifice in redback spiders. 9, 33–42 (1988)

A bit of searching suggests the author meant to include Behaviour Ecology as the journal name. I've only read the abstract, but it does not seem to support the statement. It suggests a well-fed female is less likely to consume her mate, which seems intuitive.

Am I right that this Wikipedia sentence is incorrect? If I am wrong, is there an explanation for the effect that I am missing?

It does appear that Wikipedia has not provided the most appropriate reference for that statement, but it is repeated in the article it refers to and that you link to, both in the abstract:

  Male sacrifice may be adaptive because cannibalized males increase their paternity relative to those that are not eaten

and in the  body of the introduction:

  Males that are cannibalized obtain paternity advantages compared to males that survive copulation

These statements do not necessarily contradict the other statement that a well-fed female is less likely to consume her mate, but there might be some nuance missing here in terms of mating versus mate consumption behaviors. However, the authors cite Andrade, 1996 (see below) for the second statement, and this seems like a more appropriate reference for the statement on Wikipedia:

Yes, a female spider who eats her mate is less likely to mate again. Andrade 1996 shows that males who are eaten during copulation mate longer, fertilize more eggs, and the females are more likely to not mate again after eating a mate.

Andrade, M. C. (1996). Sexual selection for male sacrifice in the Australian redback spider. Science, 271(5245), 70-72.