What is the biological mechanism linking temperature and probability to be infected with a virus? It is common knowledge that when you're cold you could get a cold.

What is the mechanism linking temperature and viral infection?

It is common knowledge that when you're cold you could get a cold.

This may be a nice illustration why we need to be wary of “common knowledge”.

  What is the mechanism linking temperature and viral infection?

This isn’t clear. There are a few proposed mechanisms but a likely explanation is: “there is no mechanism” – and the assumed correlation between cold temperature and catching a cold might be nothing more than an illusion – a form of confirmation bias.

In fact, we don’t even know for sure that the cold season coincides with cold temperatures.

On the other hand, a 2007 review [1] found that

  … most of the available evidence from laboratory and clinical studies suggests that inhaled cold air, cooling of the body surface and cold stress induced by lowering the core body temperature cause pathophysiological responses such as vasoconstriction in the respiratory tract mucosa and suppression of immune responses, which are responsible for increased susceptibility to infections.
   [emphasis mine]

So according to their results, potential mechanisms which link temperatures and viral infection are indirect:

The lowered core body temperature would imply, in my interpretation, that the body has to expend more energy to maintain its temperature, and hence less energy to power its immune system (which is expensive).
Lack of respiratory tract mucosa removes an important physical barrier between the environment and the body, and allows pathogens to enter the body with much less resistance.

[1] Mourtzoukou & Falagas: Exposure to Cold and respiratory tract infections, in Int J Tuberc Lung Dis. (2007), pp 938–943


Can anyone id this flower I took this photo on Madeira, in a botanical garden.

This is Kleinia, a genus from Asteraceae family. It is a succulent  native to  Africa.

I found a number of possible candidates, there may be more:

Kleinia abyssinica

Kleinia fulgens
Kleinia stapeliiformis
Kleinia pendula

P.S. There's not much free information from authoritative sources online about this genus. There are similarities in the blossoms' colour across  the Genus and also differences within a single species so to do a species level ID more information about the plant is needed.


How to separate peptide on SDS PAGE? I want to separate 1600 Da peptide on SDS PAGE, on 20% GEL I didn't get any band, How can I separate on PAGE? Can I use 25% SDS PAGE?

Image is of an 18% Tris-tricine small-peptide SDS-polyacrylamide gel stained with coomassie blue dye [source].

Your peptide is 1.6 kDa; it would not run off in 20% gel if you don't run it for a long time. Also, try to prevent heating up of the gel (you can run it in a cold room or in front of an A/C vent).  However, it is better to use other techniques such as chromatography. You can also try dialysis if other unwanted peptides are much larger.
Protocol for Tris-Tricine SDS-PAGE.


Can you use a microscope without an eyepiece? Can you use a microscope without an eyepiece?

Yes, you can. I have a microscope where the data can be transferred to a screen on a computer instead of going to the eyepiece. This microscope has both an eyepiece and the option to redirect the image to a screen. However, I also have a microscope with a screen only. So, I suppose you can have a microscope without an eyepiece.

I have never come across a microscope that has neither an eyepiece nor a camera but I don't know whether it's possible or not.


Why shouldn't I clean microscope slides with a paper towel? I've recently bought a microscope and been looking at a lot of bacteria and such, and have quickly run out of clean slides. I've seen videos and articles saying how you shouldn't clean microscope slides with a paper towel and to use an ultrasonic cleaner instead. I don't have access to an ultrasonic cleaner, so I am wondering what is wrong with cleaning them with a paper towel?

Also if anyone knows of any good liquid solutions for cleaning slides that information would much be appreciated.

The main reason to avoid paper towels, tissues, and etc. is that they shed lint (paper fibers) which will be left behind on your slide and eventually interfere with your prep. They look small to the naked eye, but they are not small compared to the prep on your slide.

The other issue with paper towels and etc. is that there might be some particulate matter in the paper that's hard enough to scratch glass or optical coatings. This is more of an issue for optics - especially coated ones - than for cheap microscope slides, but it's something to consider.

If you're not mounting permanent preps then ultrasonic cleaning is probably a bit of overkill - although I have a surplus sonicator and it does a great job on a lot of tasks. It's generally sufficient to rinse the slide with distilled or deionized water and then follow up with (clean) alcohol. Optical purists will say spectroscopy grade methanol, but for home use any reasonably pure MeOH, EtOH or iPrOH will probably do. The main concern, again, is leaving behind particulates or residues. You can allow the slides to air dry if you're using pure alcohol, or use a piece of lens tissue (lint free paper tissue) to help them dry faster. I've also used Kimwipes in a pinch, but they're not truly lint free so not ideal. They're still much better than a tissue or paper towel.


What is the difference between "lineage restriction" and "differentiated" in terms of stem cell biology Is there a subtle difference between these two concepts or are they basically the same thing? When I mean differentiated, I don't mean terminally differentiated.

When you look at the development of the embryo, at the beginning all cells are totipotent, meaning they can develop into any cell type of the body. This changes relatively fast by differentiation, which means that the totipotent cells develop into more specialized cell types, which then can not give rise to all cell types. So the different germ layers (meso, ecto- and endoderm) develop and from these all the cell types in our body. See the first figure for clarification (from here):

Lineage restriction means that you have a differentiated cell line, which can only further develop into cells of this line. So hematipoietic stem cells can only further develop into cells of the hematopietic line (lymphocytes, erythrocytes, basophiles and so on), like shown in the figure below (taken from here):


Why do cats like enclosed spaces (e.g. boxes) so much? A recent article doesn't reach a firm conclusion, but offers two possible explanations.

  Hiding is a behavioral strategy of the species to cope with
  environmental changes and stressors.

It keeps the cat at a comfortable temperature.

"Cats like boxes because they are cryptic animals; they like to hide,"And a box gives them a place of safety and security."
While inside a box, cats feel that they cannot be snuck up on from behind or the side — anything that wants to approach them must come directly into their field of vision. In effect, such hiding spaces allow them to watch the world around them without being seen.

And if something interesting passes in front of the cat — be it prey or a toy — it can dash out to get the object, and then quickly return to its safety spot.

Boxes also provide cats with a cozy, safe place to sleep, which is very important given that the felines sleep for up to 20 hours a day.


Linkage distance calculation What is the map unit distance between L and S allele ?

My working : If we take the normal ratio :9:3:3:1 , first one should be 9/16 = 0.5625
and then subtract 0.51 from it, we get 0.0525, similarly working we get 0.0525 difference for all 4 and so the distance is 0.0525 X 4 X 100 = 21

Is my working correct ?

With the heterozygous genotype $LlSs$, there are two kinds of linkages possible.
1. Cis=$LS.ls$
2. Trans=$Ls.lS$

All the possible gametes ($LS,lS,Ls,ls$) in both cases are same, but their frequency differs based on the strength of linkage and hence, the distance on the chromosome map. In either case, the frequency of $LS$ and $ls$ will be same, and $Ls$ and $lS$ will be same. This is because, in the Cis linkage, the former pair will constitute the parental linkage and the latter will be the recombinants, but both the gametes within the pair are equally likely to be formed. The same is the case for Trans linkage where the former pair acts as the recombinants.

According to the given table, frequency of $llss$ is $0.01$. $llss$ can only be formed by the combination of two $ls$ gametes. Therefore the probability of an $ls$ gamete will be $\sqrt{(0.01)}=0.1$.
The probability of getting an $ls$ gamete is $0.1$. Therefore, the probability of $LS$ is $0.1$, $lS$ is $0.4$ and $Ls$ is $0.4$.

As $Ls$ and $lS$ are more probable, they are more likely to be linked, and hence the genotype will be in Trans linkage. Then the frequency of recombinants($LS,ls$) is $0.2$. The chromosomal distance is $20 \text{ cM}$ or $20\text{ map units}$.

I am not sure whether my line of arguments are true. If you do find any flaw, please let me know.


Single Nucleotide Polymorphisms and diseases I am writing a report on how Single Nucleotide Polymorphisms occurring in each of these regions:

Transcription factor (TF) binding sites
Epigentic signals
Splicing variants
MicroRNA binding sites
Coding regions

can cause diseases.   Related literature suggestion from you or just informations that you know would be grateful

SNPs in all these regions will modify the DNA sequence. Effects will depend on where exactly the SNP is. I'll summarize the conditions in which effects can be maximum

Transcription Factors (TFs) binding sites: SNP in the nucleotide positions that bind to the recognition amino acids in the TF
Epigentic signals: C->X [x: A,G,T] SNPs can disrupt DNA methylation hotspots
Splicing variants: SNPs at splice donor/acceptor sites can cause intron retention
microRNA binding sites: SNP in seed region can abolish miRNA targeting
Coding regions: certain SNPs can create premature stop codons for e.g. CAG (Gln) -> UAG (stop)

there is a lot of work on SNPs. If you search in pubmed for all these categories, you'll get many research articles as well as reviews.


How does this diagram illustrate carbon cycling in lakes? Could someone please explain the following process to me:

This process refers to carbon cycling in lakes and is described in the context of $CO_2$ flux from lakes into the atmosphere. GPP is gross primary production, $CO_2$ is carbon dioxide, R is respiration, and OM is organic matter. I realize that this question may be rather simplistic to some but my basic knowledge of any biological/ecological processes is rather limited. So, basically what I am asking is

have I written this process correctly?
how can this process be described?

This shows the major biological transformations of carbon in any system (not just lakes).

On the Left Side:

$GPP$ (Gross Primary Production) is the total amount of $C$ from atmospheric $CO_2$† that is reduced into organic molecules during the calvin cycle of photosynthesis.  This is the process performed by photosynthetic organisms like green plants and algae.

† atmospheric $CO_2$ diffuses into water and develops into several species of inorganic carbon molecules that plants and algae can use but in general you can think of this carbon as being very closely related to atmospheric $CO_2$

$OM$ is a pool of organic matter, which is a general term for reduced carbon molecules.  $OM$ can be living organism tissues (e.g., a fish), dead tissues (e.g., senescent leaves) or biologically generated organic molecules (e.g., sugar that leached from a plant).  $OM$ is the principle pool of energy and raw materials for all living things on Earth so this is a really important pool of stuff.

Since $GPP$ is taking $CO_2$ and converting it to $OM$ as the left side progresses, the amount of $CO_2$ in the atmosphere goes down and the amount of $OM$ in the biosphere goes up.

On the Right Side:

$R$ (respiration) is the oxidation of reduced carbon-containing molecules for the purpose of extracting usable energy.  This may be familiar as "cellular respiration" but there are other metabolic pathways that accomplish the same goal.  In the end when the $C$ in the $OM$ is oxidized and the energy released the $C$ that was in the $OM$ gets converted into $CO_2$.

Note that this is the opposite of the Left Side, so as this occurs, the amount of $OM$ in the biosphere goes down and the amount of $CO_2$ in the atmosphere goes up.

If the Left and Right sides are balanced, then there is no net change in the size of the $OM$ pool or the amount of $CO_2$ in the atmosphere.  However, note that over relatively short time scales these can be very out of balance.  Any time plants or algae are growing (i.e., gaining mass as $OM$) the Left Side > the Right Side or $GPP$ > $R$.  Once those plants die, they accumulate in the system as dead $OM$.  The decomposition of accumulated dead $OM$ by microbes will generally make the Right Side > Left Side or $R$ > $GPP$.

This picture from Wikicommons shows the same cycle in a more realistic setting.


Does stress physically age our body? Going by the assumption that stress eventually triggers a flight/fight response, and the subsequent realization that flight/fight puts the body in a system of readiness to use it's available resources (mental, physical).

Does it make sense to think that stress physically ages a person? I am specifically referring to characteristics identified with aging such as  bleached hair, telomere shortening, wrinkles around the eyes, etc.

The fight/flight situation, through activation of the sympathetic part of the autonomous nerve system, leads to secretion of catechol amines, i.e. adrenaline and noradrenaline. The effects of these hormones, if excreted continously or without real resting time, are thought to be bad for your health. If you recall the possible effects of those two substances (which are both similar to amphetamine, by the way), and look at what big studies have found about the impact of high blood pressure then you know the most important negative effect of stress, IMHO.

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


By what mechanism does penicillin resistance usually develop in Streptococcus pneumoniae? There are three mechanisms:

  prevention of the interaction between antibiotic and the target PBP;
  modification of the binding of the antibiotic to the PBP;
  hydrolysis of the antibiotic by a beta-lactamase.

  Medical Microbiology, 6e, p. 200, Murray

PBP: penicillin-binding protein

It may be the case that the most common mechanism is not known.
It is just one of these three depending on the situation.

What is the most common mechanism by which penicillin resistance develops in S. pneumoniae?

I think your guess is quite spot-on. According to this scientific article I found online, They did a whole genome sequencing on penicillin-resistant Streptococcus pneumoniae and their conclusion was

  ....is mediated by a mosaic of genes encoding altered
  penicillin-binding proteins (PBPs). Nonetheless, S. pneumoniae has
  also developed non-PBP mechanisms implicated in penicillin resistance.

In clinical medical laboratory point of view, S. pneumoniae's AST is done with oxacillin instead of Penicillin because OXA gives better cut-off between Susceptible, Intermediate and Resistance. You may see a big zone of inhibition when you used PEN disk but that doesn't mean the isolate is susceptible to PEN. This may suggests that "hydrolysis of the antibiotic by a beta-lactamase" is less likely to be the main mechanism?


Do variant callers miss rare variants in reference? Generally variant calling programs (such as GATK-UnifiedGenotyper) look for differences between reference genome and submitted sequence. However, we all know that reference genome consist rare variants in various positions. If submitted sequence has this rare form of that variant, variant call doesn't see it and doesn't report at all. However, that variant could be very precious for analysis.

So, how can I solve this problem? What should I do to not miss that rare variants even they are in reference genome?

If the reference sequence is associated with a disease or increased susceptibility to some phenotype, the the population you're using to compare against (with a variant) will show protection to it. So either way you're going to find an association, this will just change the sign of the coefficient.


Average dimensions of the human back (anthropometry) I am wondering if anyone can point me to (a scientific source that provides) the estimates of the dimensions (length x width) of the human back?

I am specifically interested in the dimensions (length * width, or surface) of the lower back of the average adult, and in specific the region between the 7th thoracic and 4th lumbar vertebra - i.e., the region between T7 - L4 in the image below:

Ideally a distinction is made between males and females and perhaps kids as well. The area of research dealing with this matter is anthropometry.

Please mention the source to any information provided. I have access to some not-scientifically based sources (clothing companies for example). Although additional such sources are welcomed, scientifically-based answers are preferred.

This doesn't really answer the question and I only post it at the asker's request.

NASA has measured the dimensions of the back in 40 year old American males and 40 year old Japanese females in the year 2000 at 1G. Of course gravity matters to NASA…

From figure 3.3.1.3-1 (American male). All data in centimetres:

921 Waist back

5th percentile: 43.7
50th percentile: 47.6
95th percentile: 51.6

506 Interscye

5th percentile: 32.9
50th percentile: 39.2
95th percentile: 45.4


Questions regarding ELISA I have recently peformed an ELISA (Enzyme-linked immunosorbent assay), but I still have some questions, let me first outline what I did:

We had a number (20) of tubes containing fake 'bodily fluids' , namely saliva. One of these tubes contained the Epstein-Barr virus, which on its turn causes Pfeiffer's disease, aka the 'kissing disease' (so we basically conducted an experiment to see how fast the virus would spread within a class if everybody started kissing each other, if you don't mind the crudity).
Everybody mixed their saliva with the saliva of 3 other people, so at the end everybody had a tube with the saliva of 4 different people in it.
Since we worked in pairs of 2, every duo got a microtiter plate with 12 wells in it: 3 wells for a positive control, 3 wells for a negative control, 3 wells for the fluids of 1 of the duo and 3 wells for the fluids of the other one. You pippete in (is that correct?) the fluids accordingly.
After a while you rinse and clean the wells with wash buffer.
Then you pippete in the primary antibody in each well.
After a while you rinse and clean the wells with wash buffer.
Following this you pippete in the secondary antibody (conjugated with the enzyme HRP).
After a while you rinse and clean the wells with wash buffer.
Finally, you add the enzyme substrate (TMB) to each well. This causes a blue color if when in contact with HRP. The positive controls must come out blue, the negative must come out colorless, and the other wells can go either way, depending if you have the virus.

I hope this is not to crudely explained, again. These are my questions concerning the experiment:

What do the components of the acronym 'ELISA' actually stand for? Does immunosorbent refer to the binding of the antigens to the wells? My English isn't too good, and these acronyms and abbreviations often seem foreign to me (nevermind that they are foreign since I'm not English, you get the point I hope).
When you pippete in the saliva in the wells, what actually sticks to the wells? All of the antigens in your saliva? Because it's hard to believe that they make special microtiter plates for every single antigen seperately. I assume it is only the antigens, since the primary antibodies attach to the antigens only, so there is no need for the microtiter plate itself to bind to antibodies.
How would we get the primary and secondary antibody? This is my assumption: The primary antibody we get is by injecting some antigens of the Epstein-Barr Virus into a human and then taking a serum. The secondary antibody could be gotten by injecting a random human primary antibody into ANY animal, irrelevant which anyimal, and then taking a serum. After that you conjugate an enzyme to the secondary antibody. Is this correct?

ELISA is Enzyme-Linked ImmunoSorbent Assay (capitalisation to point out source of acronym).

You can read about the various ways to do an ELISA here.

In your case this was probably an indirect ELISA. All ELISA techniques make use of the fact that proteins stick to plastic. In your case the protein components of the saliva, including the virus (the viral coat is proteinaceous) will stick to the wells. After rinsing out the sample the wells are treated with another protein (usually bovine serum albumin (BSA)) to completely block all available protein binding sites. At this stage these wells will no longer bind protein non-specifically, but will bind anti-EBV Ig because of the presence of the EBV particles bound to the plastic. This bound anti-EBV can then be detected with a secondary antibody. The protein complexes will build as follows:

plastic/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate

It would also be possible to do this experiment as a sandwich ELISA. In this format the wells would have been pretreated with anti-EBV serum (or purified anti-EBV IgG) then blocked with BSA. At this stage these wells will no longer bind protein non-specifically, but will bind EBV because of the presence of the EBV-specific antibody. Once samples have been incubated in these wells (so that any EBV can bind to the antibody coating the wells) another antibody (raised in a different animal) is added, and this will bind to the EBV that has been captured by the original antibody that coats the wells. This latter antibody is then detected with a conjugate. The protein complexes will build as follows:

plastic/mouse anti-EBV/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate

Your description of how to get the antibodies is basically correct, except that the primary antibody will probably have been raised in rabbits or mice, and certainly not in humans.

Added later: I didn't read the first question carefully enough. An ELISA is an assay because it measures something. It is based on a binding reaction mediated by an antibody-antigen interaction (immunosorbent). It is enzyme-linked because the secondary antibody is present as an antibody-enzyme conjugate. It is the amount of this conjugate that remains bound at the final step which is what is measured - the assay is set up so that the amount of this enzyme is a measure of the amount of the original molecule that is being assayed.


Modeling yeast biochemical pathway using enzyme kinetics I need enzyme concentration and metabolites concentration values to en-corporate these values in my model and do some simulation.

I searched through some database

yeast metabolome database http://www.ymdb.ca/
brenda and other enzyme databases for enzmye conc
and also did some literature search

but couldn't find much of data

where possibly i can get these data ??
is there any other way to do simulation without data.

You should take a look at SGD (the Saccharomyces Genome Database), and in particular YeastCyc. Some protein information pages at SGD give estimates of molecules per cell taken from this Nature paper.

Added later in response to some comments:

The question asks about levels of metabolites and of enzymes, not of transcripts. Microarray data can be, at best, only a guide to levels of proteins. Estimating the levels of metabolites from microarray data is a complete non-starter since there are entire layers of regulation that will be ignored. Just to give one example of a pitfall in this approach: you could have high levels of transcript from which you could you could infer high levels of enzyme, but that enzyme could be inactivated by a post-translational modification.


Is it possible to produce bread using only microorganisms? I am wondering if it is theoretically possible to produce bread using only microorganisms. If one lists all the chemical components, proteins fermentation time, etc., is it then doable to combine the needed (engineered) microorganisms in one bio-reactor, let them do their thing and produce the wanted product (bread in this case)? Maybe there is a review paper on this topic but I haven't found it yet.

My background: Molecular biology, I know too little about microbiology and bio-reactors, etc.

It looks like that yeast has been engineered to produce starch.

First of all, the authors had to knock out the genes responsible for the glycogen metabolism pathway (both glycolysis and gluconeogenesis). Then they introduced eight genes known to belong to the amylopectin biosynthetic pathway. The authors succeeded in having starch granules in yeast.

You could start with this yeast strain to produce your bread. You'll probably need to at least dry them in order to reduce them to some sort of flour (probably a hard one, since the yeast would be rich in proteins); otherwise, some means to purify starch grains from yeast should be devised. Then you'd mix them with water and regular baker yeast and maybe you could obtain a bread-like food!


Why can't we propose a solid theory regarding origin of life? What  information is greatly lacking which does not allow us to propose a  solid theory for origin of life ?

First of all, we do have some solid theories to explain the origin of life. That said, the main thing missing in order to be able to accept one of these theories with a decent amount of certainty is the ability to run a planetary scale experiment for a few billion years.

The theories are fine, the problem is that we cannot really test them. In order to test a theory that describes the origin of life, we will have to recreate the original conditions (think of a test tube the size of the Earth) and then pump energy into the system and watch what happens over the next few billions of years. This is not really feasible, for obvious reasons. I really doubt you will be able to get funding for an experiment that will run that long.


What is this thing? It is hairy mostly a cocoon, and i saw a white worm pop out of it. It is spreading rapidly I suspect it is originating from the mud. This has some plastic bits with it. They are spreading all over my walls. I think it is some  kind of cocoon for worm. Should it's rapid growth in terms of number be a matter of concern? found in Bangalore, India,

Bagworms?
https://en.wikipedia.org/wiki/Bagworm_moth
I don't know how destructive individual species are. They probably aren't more than an aesthetic concern.


changing DNA of an organism is it possible at least theoretically to change the DNA of an organism ?

so we take for example an organism with multiple cells then we change its DNA without killing this organism

to correct genetic defects or to improve it

Erm. Sort of. Kind of depends on your definition. It hasn't been done for multicellular organisms though.

Craig Venter et al did this exact experiment a few years ago with a completely synthetic Mycoplasma genome.

http://www.jcvi.org/cms/press/press-releases/full-text/article/first-minimal-synthetic-bacterial-cell-designed-and-constructed-by-scientists-at-venter-institute-an/

If you just want to change small segments of DNA that's where cloning and gene therapy come in, and we do that A LOT.


How does a bacterium age without cell division? If somehow a bacterium, let's say E. coli, is engineered in such a way that it loses the formation of ftsZ ring (or other ways that inhibit cell division), and if other conditions are optimal for bacterial growth, then will the bacterium grow without cell division? If so, how long will it live? And how will it age?

First of all, the growth of a bacterium is associated with an increase in cell biomass.So if a bacterium is restricted from replicating it does not grow. Coming to your later parts of the questions about how long will it live and will it age;
Yes, a bacterium would age irrespective of its ability to replicate.According to The Free radical hypothesis, all organisms age due to random deleterious events, oxidative damage by ROS produced during normal metabolism. It has also been found that cells undergo irreparable damage which can also lead to cell death eventually.

A complete review on bacterial ageing:
http://www.ias.ac.in/article/fulltext/reso/017/04/0347-0364


What factors affect the likelihood of auditory stimuli causing arousal during sleep? I've noticed that the sound of water drops makes me wake up from sleep but other more strong sounds don't make me wake up. I can't find anything about this. The only reason I can think of is maybe because the sound of drops is continuous. Is there any research about the qualitative aspects of certain noises that affect the likelihood of causing arousal  from sleep?

The other day I was reading "Sleep soundly every night,feeling fantastic everyday" by Robert S. Rosenberg.
Somewhere in the books it was written as:
"Sound: You need your bedroom to not only be cool and dark, but also quiet. If a dripping faucet or the barking of a neighbor’s dog is interfering with your sleep, try earplugs, earphones, or generating white or pink noise to even the sound field so your ears won’t focus on the background contrast of environmental sounds. There are machines available to do so, but for some the sound of a fan will do the trick. If your partner’s snoring is keeping you awake, you should encourage him or her to be checked by a doctor for sleep apnea. Treatment can improve your sleep and also might save his or her life."

by searching more I found out that the difference between the range of frequencies from moment to moment is a more important factor than a sudden loud noise.

The idea behind white or pink noise or the natural ones like the sound of fan is that they produce a broad range of frequencies at the same level.And by doing so they can reduce or at least mask the disruption.


How many abdominal sclerites would be there in a cockroach? Every tegmina of a cockroach has sclerites which are analogous to the bones of humans.

Every abdominal segment of cockroach consists of two lateral sclerite plates called pleura along with a dorsal terga and a ventral sterna. But what will be the case with the last body segment where 10th sternum is absent?

I mean will, there be any pleuron in the tenth segment because, following our textbook, pleura serve for articulation among sterna and terga and also spiracles are present in the first eight abdominal segments but the 10th sternum is absent in Periplaneta americana.

Actually there is no evidence of the presence of any pleurons in the last segment in our text book.

Moreover, there are no abdominal spiracles in the 9th and 10th segments so there is no particular reason to say that pleura are present in the 9th and 10th segments as well.

Tergal plates:

There are ten tergal plates. The $8^{th}$ tergum in the male and both $8^{th}$ and $9^{th}$ terga in the female are not visible  as they are overlapped by the $7^{th}$ tergum.

The $10^{th}$ tergum extends beyond the posterior end of the body and has a deep groove in the middle of its free end.

Sternal plates:

Only nine sterna are present as the $10^{th}$ sternum is absent.
In the male, nine sterna are visible whereas in the female, only seven sterna are visible.

In females, the $7^{th}$, $8^{th}$ and $9^{th}$ sterna together forma brood pouch. The brood pouch has two parts: the anterior – genital chamber or gynatrium  and the posterior – gothecal chamber.

(source: lander.edu)

(source: lander.edu)

Sources:

http://www.slideshare.net/prof_aarif/animal-types-cockroach
https://learnzoology.wordpress.com/category/periplaneta-americana/page/15/
http://zoologybaburao.in/pdfs/7.%20Unit%20VII.pdf (Best)
http://www.eskool.com/files/subject/ppt/103_11_07_04_01.pdf
http://www.sakshieducation.com/(S(clpea355rwddux55iuci1cer))/Inter(New)/Material/IstYearEM/Zoology/07_01_ARTHROPODA_COCKROACH_UPTO_LOCOMOTION.pdf

Update:

Youtube links for Cockroach dissection:

https://youtube.com/watch?v=ZwvG69ICnps
https://youtube.com/watch?v=wF7ew2w24as


Cellular Immunity Response What response of cellular immunity would appear after complementary protein activation to keep pathogenic bacteria away from our body?

Notes: I do appreciate your explanation. Though I am facing multiple choices:

(a) wrapping the bacteria cell (b) immobilize the bacteria cell (c)    destroying the bacteria cell by enzyme (d) creating pores on the bacteria cell

The key answer is (c) but then I do not know what enzymes make this happens. Any Idea?

As you can simply find on Wikipedia, the cellular immunity, or Cell-mediated immunity,

  is an immune response that does not involve antibodies, but rather
  involves the activation of phagocytes, antigen-specific cytotoxic
  T-lymphocytes, and the release of various cytokines in response to an
  antigen.

The answer (c) (destroying the bacteria cell by enzyme) refers to the phagocytes, cells that contain many enzymes, like lysozymes. Those funny enzyme can destroy the bacteria cell's wall.

Actually, I think that the answer (d) could be right, but it's not complete. In fact not every enzymes works on the cell's wall!


What kinds of animals does insular dwarfism affect and how large does an island need to be to escape it? 3
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I've been wondering about insular dwarfism, and would like to know if it only affects certain animals (Since some animals grow larger upon colonizing an island, often due to the absence of predators.) Do only big animals get smaller, and if so, how big is "big"? Are there any taxonomic groups that are more or less prone to insular dwarfism?

The second thing that I'd like to know is the minimum size of an island without insular dwarfism could be. Also, I'm not sure if resources, biodiversity or climate affects it too (Considering Bergman's rule, the increased competition in jungles, etc.) This may sound like a lot of questions, but the main components of an answer I'd like are shown in the title - who and where.

There are no general rules. We have just observed repetitively that organisms living on small pieces of lands tend to be particularly large (insular gigantism) or particularly small (insular dwarfism) compared to the main land counterparts.

There are several possible reasons for these changes and those reasons vary among species. Dwarfism is most definitely not always a consequence and there is no hard coded minimal island size for such change to happen or not happen.


How to determine the primary Uniprot accession number from a list of accession numbers? Given a list of UniProt IDs that are linked to an Ensembl ID, is there a way to systematically determine which is the primary accession number with no other information?

According to ExPasy

  Researchers who wish to cite entries in their publications should always cite the first accession number. This is commonly referred to as the 'primary accession number'. 'Secondary accession numbers' are sorted alphanumerically.

But what if the order has been jumbled or compiled from a different source and resorted.

For example:

Ensembl:

ENSMUSG00000035642

Uniprot:

Q8R0P4, Q8CF11, D6RJK8, D6RJJ4, D3Z442, D3Z1Q3, D3YZD8, D3YY39, D3YX09, D3YWY5

This question is cross listed on the Bioinformatics stack-exchange.

I think there is an issue with the terminology. The "primary" accession number, is the first accession number in cases where an entry has more than one accession number, as described in http://www.uniprot.org/help/accession_numbers:

  Entries can have more than one accession number. This can be due to
  two distinct mechanisms:

a) When two or more entries are merged, the accession numbers from all entries are kept. The first accession number is referred to as the

  ‘Primary (citable) accession number’, while the others are referred to
  as ‘Secondary accession numbers’. These are listed in alphanumerical
  order.

b) If an existing entry is split into two or more entries (‘demerged’), new ‘primary’ accession numbers are attributed to all

  the split entries while all original accession numbers are retained as
  ‘secondary’ accession numbers.

  Example: P29358 which has been ‘demerged’ into P68250 and P68251.

Both reviewed and unreviewed entries can have primary accession numbers.

What you probably mean, as previous posters understood, are accession numbers of reviewed entries as opposed to unreviewed ones.

In that case, you can indeed add "reviewed:yes" to your query, e.g. when you are using the UniProt ID mapping, http://www.uniprot.org/help/uploadlists


Finding confidence level of miRNA disease associations I'm an undergraduate computer engineering student, and I have a project about bioinformatics. In this manner, I need to find prediction( or association I'm not sure the correct terminology) confidence of miRNA disease relationships. Let me make more clear my question with an example. For instance, in one of the bioinformatics related databases( HMDD) it is said that, miRNA X is related with disease Y. I want to find that what is the confidence. I mean  you're 100% sure about such releationship? Do you know any database for that purpose? In HMDD I can only find miRNA - disease name couples it does not give any statistics.

You can start off by studying how an miRNA regulates the functioning of a gene. it basically binds to the 3'UTR and 5'UTR of an mRNA and restricts its translation. There will be genes associated with the disease of your interest,  find out the miRNA's related to those genes. You can use micro array data to find out the up-regulated genes. Target scan human, miRDB, are various databases for retrieving the miRNA's related with the genes.
The confidence level for finding out the association of certain miRNA's with the disease can never be 100%. but a relationship can be established by simply viewing the complementarity between the miRNA and the mRNA expressed during the diseased state.


What happen if we inject restriction enzyme into the blood Just a curious question, if we extract restriction enzyme and inject it to our body, what happen?

Does antibody recognize and block it?
Can restriction enzyme pass over cell membrane and destroy the DNA of a living cell ?

The appearance of any foreign antigens (e.g., proteins like restriction enzymes fall n this category) in the circulatory system should trigger an immune response.

There are actually two membrane barriers that the enzymes have to traverse to gain access to the nuclear genome: the cell membrane, and the nuclear membrane.  Proteins are typically too large and too charged to cross a lipid bilayer membrane--unless there is a pore (like on the nuclear membrane) or receptor for the protein on the cell surface.

When cells are engineered to express foreign restriction enzymes using transgenes, then yes, if the protein can enter the nucleus then the enzyme will start to digest all of its recognition sites.

Jasper Rine demonstrated this for the Baker's Yeast S. cerevisiae in 1986.


Where does the fate map of a human embryo end? I'm confused about the fate map of a human embryo. Is it just a particular part of the embryo development or does it include everything, from the conception (germinal stage) to the day the baby is born?

In the developing embryo you have the three germ layers: Endoderm, mesoderm and ectoderm. From these layers all cell lineages of the body develop and can be traced back through their differentiation and migration to this three layers.
Have a look on the image below, which illustrates this pretty nicely:

The figure is part of this PhD thesis, which also seems worth reading when you are interested in this topic.


Do all humans experience flatus regardless of their diet? Flatus frequency is affected by diet, so I was wondering if flatus production solely depends on the food eaten, meaning that some people never ever release flatus because they don't eat any flatus-producing food. I guess if they say they don't, they're probably in denial...

Eventhough food contributes the most to flatulance, it can also be caused by swallowing air when you chew gum or smoke. It can also be caused by health conditions like coeliac disease and gastroenteritis (reference). So it is indeed hard to believe when people claim that they never fart.


Which factors besides the thermodynamic stability are important for the hairpin in intrinsic transcription termination? Intrinsic termination (rho-independent) relies on a stable hairpin with a subsequent uridine repeat. The common explanation on how these sequences cause the termination of the transcription are based on the thermodynamic stability of the sequence. The GC-rich stable hairpin together with the destabilizing U-repeat supposedly destabilize the binding of the polymerase enough to cause it to disassociate from the template.

What I'm looking for are specific requirements on the termination sequences that are not based on thermodynamics.

Are there any specific requirements on the hairpin sequence beyond a certain thermodynamic stability.
Are there any loop variants that are known to reduce the termination efficiency?
Does the shape of the hairpin, e.g. any kinks or bulges in it, have an influence on termination efficiency?

The typical requirements I read are 5-14bp and GC-rich, and I'd like to know if there are any more specific requirements, especially ones related to the structure and not the stability of the hairpin.

The RNA hairpin transcription terminator in prokaryotes is terminated by the GC rich hairpin followed by 4+ uracil bases as you describe it.

The original reference describing the hairpin, described the sequence requirements as being for the thermodynamic stability of the hairpin, but the protein nusA has also been found to stimulate termination.

You might think that there would be some protein that would precisely bind this motif and mediate the termination, but at least as far as I can find, it appears that the hairpin clogs up the polymerase itself, causing termination.  This review linked here has some nice pictures of the RNAP bindig pocket model.


Can any plant regenerate missing tissue? I have not yet found a plant that, when an insect eats a hole in one of its leaves, it can regenerate the lost tissue. Many plants will grow a new stem if the old one is cut, but it is not a perfect regeneration, and has no likeness in form to the previous stem. Are there any plants that can, even to a degree, regenerate missing tissue?

In general, plant cells only undergo differentiation at special regions in the plant known as meristems. Two of the primary types of meristem are the root apical meristem (at the tips of roots) and the shoot apical meristem (at shoot tips)^. Within the shoot apical meristem the plant cells divide and begin to differentiate into different cell types (such as different cells of the leaf, or vascular cells). Later growth (of, say, a leaf) is largely a result of cell expansion (although cell division does still occur, but drops off as the leaf expands). Therefore, if you punch a hole in a leaf, it probably won't be filled in because the cells in that leaf have finished growing and dividing.

However, as a shoot grows, more meristems are created. These are found in the axillary buds, just above where the leaf meets the stem. The meristems in the axillary buds can grow to form branches. Different plants obviously make different numbers of branches, but there is a common control mechanism known as apical dominance, where the meristem at the tip of the shoot suppresses the growth of the lower axillary buds. This is why a shoot with no branches can be made to grow branches by cutting off the tip (gardeners often do this to make "leggy" plants more bushy).

All of that was a long explanation to say, no, a plant doesn't normally^^ regenerate in the sense of filling in cells that have gone missing. However, if you cut off a shoot, the next remaining bud might begin to grow and, in a sense, replace the part that was lost. In that case, an existing bud is recruited to form a new branch and replace lost functionality, but I wouldn't say that qualifies as regenerating missing tissue.

^There are other types of meristem as well.

^^If you torture plant cells enough you can force them to become "stem cells" and thereby make an entirely new plant, but this is rare in nature.


Is there a reproductive barrier between Khoisan and other humans? I have heard in an ethnology lecture that more or less all human ethnicities interbreed without a barrier (rate of reproduction of fertile offspring) except the Khoisan + any other human ethnicities, where fertile offspring is less likely than when other humans interbreed (as a an anecdotic side note, there are rumors about Zulu men who prefer Khoisan women as second or third spouse in order not to produce too many kids). My question is if some can confirm or falsify this (any literature coverage)?

Check the book "Genetic Nature/Culture: Anthropology and Science Beyond the Two-Culture Divide" edited by Alan H. Goodman, Deborah Heath, M. Susan Lindee. Page 205 states that that is a myth started by geneticist F Lenz of Gottingen that has been disproven.


NMR spectroscopy detection methods for proteins I've stumbled upon a table comparing the sensitivities of different detection methods in NMR spectroscopy: "Direct", "DEPT" and "Inverse", where "Inverse" seems to be the most sensitive.

What exactly are those different methods are and how do they differ?

In most cases when you perform NMR experiments on proteins you detect the signal on the protons. Even if you're looking at other nuclei, in the end you transfer the magnetization to a proton and detect that signal. This is simply the most sensitive method due to the high gyromagnetic ratio of 1H, and this is the method that is labeled "inverse" in your figure. This is pretty much the default way to measure heteronuclear spectra.

Direct detection means that you directly observe the less sensitive nucleus like 13C. This has certain advantages especially for large proteins where you often have to deuterate the protons to be able to measure anything useful.

DEPT is a type of experiment where magnetization is transferred from the directly attached protons to the heteronucleus. This increases the sensitivity and allows to distinguish CH and CH3 groups from CH2 groups


What is the difference between muscle fascicle and muscle bundle? In the photo above (given by Bio teacher), the muscle bundle is shown to be as a bundle of fascicles, but in most web definitions I've seen, the two terms are used interchangeably. What is the correct name for the part labeled "muscle bundle" if there are in fact no distinctions between bundle and fascicle?

Short answer
Muscle fascicles are the building blocks of skeletal muscle.

Background
Skeletal muscle, or striated muscle is composed of many units called muscle fascicles. The fascicles are bound together by a type of connective tissue called fascia.

Fascicles in skeletal muscle are composed of muscle cells, called mycocytes. These cells are referred to as muscle fibers in skeletal muscle. Myocytes contain small strands called myofibrils, which are the contractile elements in the muscle cells. The myofibrils move as skeletal muscle contracts.

Putting it all back together, myofibrils are the contractile elements in muscle cells (muscle fibers); muscle fibers make-up muscle fascicles; and muscle fascicles are bound together by fascia to compose the skeletal muscle.

Hence the part labeled 'muscle bundle' is a muscle, made out of a bundle of fascicles.

Source: Penn Medicine


How does the dopamine spike from drugs compare quantitatively to pleasurable non-drug activities? I did find this popular press article that quotes a researcher offering the following quantification: "in lab experiments done on animals, sex causes dopamine levels to jump from 100 to 200 units, and cocaine causes them to spike to 350 units. '[With] methamphetamine you get a release from the base level to about 1,250 units...'" [1]

However, I haven't found any research study supporting this claim or providing any details?

[1] http://www.pbs.org/wgbh/pages/frontline/meth/body/

This review article [1] gives dopamine responses for rats (similar to the BBC article above) and includes references to the underlying studies:

Sex/Food:  150% - 300%
Alcohol/Ethanol:  190%  (1g/kg) *
Morphine: 200% (1mg/kg) *
Nicotine:  220%   (0.6mg/kg) *
Cocaine:  350%  (5mg/kg)
Methamphetamine:  1000%  (1mg/kg)

These are percentages of the baseline dopamine level (not percentage increases), so 100% would be no effect.  They correspond to dopamine levels in the Nucleus Accumbens, which is a brain region involved in processing reward.

Also, the drug effects are dose dependent, so the above values show the dosage with the largest effect among the dosages tested in this study [2], which was referenced from the review article.  The values marked with asterisks were estimated visually from the graphs.

[1] Allerton M, Blake W. The "Party Drug" Crystal Methamphetamine: Risk Factor for the Acquisition of HIV. Perm J. 2008;12(1):56–58.
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042341/

[2] Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci U S A. 1988;85(14):5274–5278.
 https://www.ncbi.nlm.nih.gov/pubmed/2899326


Sexual Differentiation in Monoecious plants with unisexual flowers In monoecious plants having unisexual flowers (eg Zea Mays, Ricinus Communis etc), there must be some mechanism as to produce two sexually distinct flowers from the same genotype. Since both the type of flowers are placed on the same plant, the genetic constitution of the cells of both the type of flowers will be similar. What is the mechanism by which the development of two sexually distinct flowers is carried out in such plants?

Is the mechanism similar to the mechanism for differential gene expression in case of embryonic development (Homeobox genes)? And moreover, is the genetic constitution of the pollen produced by the male flower similar to that of the egg produced by the female flower, with respect to the composition of autosomes and allosomes (if any)?

I will be able to answer only a part of the question.

Sex determination in Zea Mays

Initially, all the flowers in the plant are perfect, ie they have both the male and the female
flowers. This is followed by abortion of stamen or pistil resulting in unisexual flowers.

Which part of the flower undergoes abortion is determined according to the location of the flower. The florets in the tassel undergo the suppression of the pistil primordia resulting in staminate flowers, while the florets in the ear undergo suppression of stamen primordia resulting in female flowers.

The hormone Gibberelic Acid seems to play a role in sex determination.

Source and other useful links :

Sex determination in Plants by CC Ainsworth.
Sex chromsomes in flowering plants
Sex determination in monoecious and dioecious plants
The sex determination process in maize


Choice of Molecular markers to carry out molecular phylogenetics For evolutionary analysis of different individuals within a population, the preferable molecular markers are non-coding regions of mitochondrial DNA. My question is that why they are used what is the logic behind that and why specifically mitochondrial non-coding region is taken for evolutionary analysis between them?

The molecular markers need have an appropriate amount of divergence to resolve the phylogeny at the desired scale. If the markers are too conserved, there will not be enough characters differing between taxa. On the contrary, if the markers are too divergent, the sequences may be somewhat randomized, there may be misleading convergences between distant taxa...

Non-coding regions are usually less constrained than coding regions, so they can accumulate more mutations. This makes them more suitable for studies at small evolutionary scale.


Speed of electric signal vs chemical diffusion I'm currently reading the book, "An Introduction to Nervous Systems" by Ralph J. Greenspan.
On page 20, there is a sentence that confused me. It was, "Electrical signaling has the advantage of being able to cover large distances very quickly, much more quickly than chemical diffusion". It is in the context of the primitive signaling mechanism in Paramecium.
My doubt was, isn't the electrical signal caused by the movement of ions? Then how is it any different from chemical diffusion? And again, it's not a electrical signal that travels, but a changing potential, right? Then how does it move at a faster pace than diffusion?

Membrane potential is a directed force, while diffusion is a random walk

Your confusion is entirely justified, as you're correct that both diffusion and depolarization rely on the speed of ion travel. Where they differ is that depolarization is a directed force, occuring only in one direction along the membrane, whereas diffusion is subject to the stochastic walk of ions in water.

When membranes depolarize, the whole membrane begins with a certain amount of "pressure" built up behind it. As the signal propagates, a small area of this pressure is released at a time and triggers the next section to trip. That next section is essentially identical to the previous one, with the same amount of pressure behind it initially. In this way, you can imagine membranes "conserving" the initial concentration, so that the signal strength isn't dependent on the distance from the signal itself.

Diffusion, on the other hand, is stronger initially and decays over distance because of its stochastic nature. It's a probabilistic force, and so depends in general on something like the square root of the distance. If you imagine a thousand ions taking a step forward in one moment, in the next it's equally likely that five hundred take a step backward even as an equal amount moves forward. So the signal degrades over time and distance from the source.

If that was confusing, the following metaphor may help. Depolarization acts like a line of dominos, while diffusion acts like a complex dance. Check out this video of the largest human mattress dominos: the speed they're falling over is pretty constant when they're not turning. Compare that to two dancing humans who are equally likely to move forward and backward, and hopefully you can see that the mattress dominos is the faster way to go, even though each one is theoretically limited by how fast a human could move.


where can I find estimated costs of laboratory equipment? Often when I am curious about purchasing new laboratory equipment I cannot find a ballpark figure for the price.  Companies that sell expensive lab equipment prefer if you contact their customer service or sales teams to inquire about prices.  I don't want to go through all of that hassle, as well as exposing myself to  potential marketing emails.  Is there any website that lists ballpark figures for lab equipment?  The type of equipment I am talking about are things like PCR thermal cyclers, Flow cytometers, nucleofection devices, centrifuges, etc.

Thanks in advance.

The best way (if you're buying new) is to contact the manufacturer/distributor. Sales people get inquiries like this all the time, and are generally more than happy to accommodate you (because they get commission on any sales they make). Most items have customized pricing depending on the customer, their order history, the number of items being ordered, add-ons like maintenance contracts, reagents, etc. Many complex instruments like flow cytometers have many customization options, including the number and type of lasers, different types of filter sets, tube vs. plate-based acquisition, type of computer, licenses for software, etc. Sales people know their company's product lines the best, and are willing to talk to you to figure out your needs and then recommend the product that works best for you, which may not necessarily be the one you were originally thinking of.

You can always ask to not be added to any email lists, and if you are added, commercial emails (in the United States, at least) are required to have an unsubscribe link in every email. Check out the CAN-SPAM Act of 2003 for details.


What is my pet tortoise' species? I got this tortoise from my uncle. He said that it wandered into his yard. Found in Khon Kaen, Thailand during the summer.

It is a Burmese brown mountain tortoise - Manouria Emys Emys
 I differentiated it from a burmese black mountain turtle by this method.


Why doesn't chloride cause high blood pressure? Assuming osmotic pressure is the (main?) culprit, why isn't the chlorine ion loose in your body after eating salt considered equally responsible for hypertension?

I have searched Google and Wikipedia, and cannot find an answer.

I have looked here at Stack Exchange, too.

Why is it that you always hear about how bad 'sodium' is for your diet, but every sodium cation comes with a chloride....

Could someone point me to an article, at least?

Osmotic pressure is not the main mechanism of sodium-induced high blood pressure.

  high dietary salt raises cerebrospinal fluid [Na(+)]. This leads, via the Na(+)-sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction

How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.


Backbone hydrogen bonds between adjacent amino acids in a protein? Is it possible for two adjacent amino acids in a peptide to form hydrogen bonds between the backbone NH and CO?

Are there any examples of such situations in proteins and how common are they?

If such bonds are rare, why is this so?

The situation you ask about was originally part of the 27 ribbon and 2.27 helix structures considered as possibilities by protein chemists (Linus Pauling?) in the 50s or 60s. The diagram below, showing the ribbon, is from the classic text (long out of print) The Structure and Action of Proteins by Dickerson and Geis.

This turns out to be very rare in proteins. To understand why, one must remind oneself of the conditions for forming hydrogen bonds in proteins. For hydrogen bonds between peptide bonds these would be:

Correct distance between hydrogen of the NH and the O of the CO (too far apart — bond weak, too close — repulsion).
Near(ish) linear angle of the NH and OC.
Lack of steric repulsion of other atoms in the structure

Calculations indicated that a 2.27 helix would be less strained than the 27 ribbon:

Playing with polyglycine in Bosco Ho’s Ramachandran Plot Explorer (Rama) indicates steric repulsion still exists in this structure (white striped connectors):

I could only find one report of this structure, and that was in the artificial peptide Ac-(∆ELeu)5-NHMe, with a model using dihedral angles Φ,Ψ approx. –60°, 30° (as in the Rama simulation) shown below:

It should be noted that this position of the Ramachandran plot is at the margins of stability, and I would expect the bonding only to occur in proteins where it was stabilized by other interactions (as in this artificial peptide) and no lower energy structure were possible.


Earth overshoot day: is it a sound concept? Today, August 8th, is Earth Overshoot Day (EOD) for 2016, the day when humanity supposedly has consumed the natural resources available from the planet for the year 2016; we're now running a deficit, somehow. At least if your believe the calculations of the Global Footprint Network (GFN), the think tank behind this concept. EOD is well reported by media every year, and perhaps it does some good as an ecology awareness thing. But is the idea scientifically sound?

EOD is based on the ecological footprint concept. The ecological footprint of a person (measured in hectares) is the area of the earth required to extract the natural resources needed to sustain that person: to grow crops, keep farm animals, obtain natural resources for consumables, etc. It's a very complex thing to calculate, and of course people argue about what the correct formula should be. One article by Willis Eschenbach (2010) goes into some depth and argues that the formula used by GFN vastly overestimates the footprint. I don't know who is right, but it does seem like the footprint is very difficult to estimate, so we should probably be careful with drawing strong conclusions.

But I have a more fundamental problem with EOD. Regardless of how it's calculated, the claim that we have today "overshot" our yearly earth-budget, at 8 months out of 12, means that we are consuming about 1.5 of the available food and natural resources available; or that the footprint of humanity is 1.5 Earths. This is not some kind of parable: GFN really claims that we have exhausted our natural resources, by a wide margin, and that this has been going on since the 1970's.

My question is, what are we all living on then?

As of today there should be no more food around, or any other natural-derived product for that matter. If GFNs estimate is correct, shouldn't humanity be long dead? Shouldn't we expect 1/3 of the earth's "surplus" population to die off pretty quickly? Doesn't the fact that we're not dead prove that EOD is wrong? Isn't it physically impossible for our total footprint to exceed 1 Earth?

EDIT: Nice to see that this question stirred a lot of debate! :) I think several answers bring up one key point that resolves the problem: GFN defines the footprint not as the actual area required for production at present (which must be < 1 Earth), but the area required for sustainable production (which is larger). Exactly how the sustainable area is defined is still mysterious to me, but I guess it is at least theoretically possible.

TL;DR: it's a simplified measure of sustainability, but accurate enough to be useful for public engagement

EOD is hosted and calculated by Global Footprint Network (GFN), an international think tank. The GFN estimates national and global net supply and demand for renewable resources, specifically:

food and fiber products,
livestock and fish products,
timber and other forest products,
space for urban infrastructure, and
carbon sequestration.

From the website:

  Global Footprint Network measures a population’s demand for and
  ecosystems’ supply of resources and services. These calculations then
  serve as the foundation for calculating Earth Overshoot Day.

  On the supply side, a city, state, or nation’s biocapacity represents
  its biologically productive land and sea area, including forest lands,
  grazing lands, cropland, fishing grounds, and built-up land.

  On the demand side, the Ecological Footprint measures a population’s
  demand for plant-based food and fiber products, livestock and fish
  products, timber and other forest products, space for urban
  infrastructure, and forest to absorb its carbon dioxide emissions from
  fossil fuels.

The results are reported in 'global hectares', the area which would be required using global average productivity, to aid intercomparability.

The methodology was published in 2013 (Borucke &al 2013).

So, to answer the question in your title ("Earth overshoot day: is it a sound concept?"), data quality may be an issue (I haven't pored over the paper in detail) but the basic methodology is arguably appropriate for the question they're asking. The only issue I might have is that they effectively consider land and sea use to be interchangeable, but I'm not sure the alternative would be an improvement.

To answer the second part of your question ("what are we all living on then?"), it is possible to harvest more from a system than it can sustainably produce. Exceeding this harms the future productivity of the system. To take the specific examples named for EOD:

Overharvesting plant-based food and fibre products can result in soil acidification, soil erosion, and/or soil salinification;
Overharvesting livestock and fish products can result in overgrazing and/or overfishing;
Overharvesting timber and other forest products results in deforestation;
Using more space for urban infrastructure reduces the availability of land for the other examples on this list;
Producing more carbon emissions than can be absorbed by its forest leads to an increase in atmospheric carbon, resulting in climate change.

Ultimately, while 'Earth Overshoot Day' is a public engagement activity, there is a reasonably robust and transparent methodology behind it which is good enough for the job. Remember: all models are wrong, some models are useful.


How does regurgitated food go to the 3rd stomach chamber instead of going to the 1st? Ruminants are known for their regurgitation of food; the food goes through the 1st and 2nd stomach chambers, then returns to the oral cavity in cuds. The cuds then come back into the stomach, but this time they go through the 3rd and 4th chambers, instead of going to the 1st and 2nd again.

How is it ensured that the regurgitated food doesn't go through the 1st and 2nd chamber by a mistake?

Your question supposes a very linear version of the flow of stomach contents of:

1->2->mouth->3->4

In reality, it is not so linear. Firstly some background: The rumen and reticulum form the first two parts of the four, and are in fact a single chamber/organ (collectively known as the reticulorumen). They have different wall structures, and perform initial digestion of different particles (mostly heavier particles in the rumen such as grain and more digested hay). This reticulorumen chamber is where the initial microbial fermentation of the feed occurs. Matter passes from rumen to reticulum and back regularly by means of two distinct muscle contractions.

To aid in the breakdown of the feed, the cud is regularly regurgitated, chewed and then re-ingested. The re-ingested cud returns to the reticulorumen. From there, in order to advance down into the later stages of the digestive tract, it must pass through the reticulorumen orifice into the third compartment - the omasum. The orifice allows particles up to 4mm in size in cattle.

The omasum chamber removes water and some nutrients. The contractions of the omasum remove water and move solids through the system, and the contractions are speculated to filter out any larger particles and return them to the reticulorumen. Matter that has been processed by the omasum is passed along to the fourth chamber, the abomasum.

So to answer your question in brief, after mastication the cud returns to chambers one and two, potentially going round this loop several times until it is sufficiently broken down by chewing, saliva and bacterial action, and then it can proceed from there to the third chamber.

The "digesta circulation and reticulo rumen motility in the ruminent" paper (C. Poncet, C.H. Malbert, R. Baumont) has this to say:

  The outflow of digesta, allowed by the opening of the ROO [reticulorumen orifice] during the second phase of the reticular contraction, is highly selective. The effluent does not contain particles greater than 2mm in sheep and 4mm in cattle. This is due to the buoyancy of the large particles in the reticulum, to the self filtration of the digesta during the passage through the ROO and perhaps to backflows from the omasum to the reticulum.

You may find it useful to get a copy of this collection of papers (quote from p.366): http://books.google.co.uk/books?id=Bcsa8Z4u-E4C&printsec=frontcover#v=onepage&q&f=false


Which cultivated plants produce most nectar for pollinators? Pollinators are important for many crop types (e.g. wikipedia list), but I am wondering how important the crops are to feed the pollinator. Obviously, some of the crop plants provide much more food than others, and the plants that depend on pollinators for their reproduction will be likely to attract the pollinators with pollen, nectar, or both. But I am not sure that I can use the dependance on pollinator as an accurate estmator of the quantity of nectar that is actually available for pollinator.

I can think of the rapeseed as being very rich in nectar, but are there other "nectar rich" flowers ? For instance, what about sunflower, potatoes, peas ,sugar beet, mustard, flax, lucern, clover, maize, wheat...

To sum up, I would like to have a list of the most common European cultivated plants that produce a reasonalble amount of nectar accessible to insect pollinators. (rem : I've asked a similar question about pollen, and maybe the answer is the same, but as far as I understood some plants have more pollen and some plants have more nectar.)

Lacy phacelia or purple tansy (Phacelia tanacetifolia), which can be
planted any time of year due to its short growing season. After
flowering, it is plowed into the ground to enrich the soil with
humus
All types of clovers: excellent nectar plants that plowed after
flowering and enrich the soil with nitrogen, or scythe them and use
as feed for animals
Sunflowers: after flowering, they greatly enhance the structure of
soil and enrich it with hummus
Rapeseed and poppy
Buckwheat: planted it in summer and when it fades, the seeds and
ground into flour

Scroll to page 13 (Appendix II). Here you will find a list of all significant nectar-producing plants in Europe

Scroll to page 21 for average nectar production (mg sugar/day/flower) of important agricultural crop flowers

Melliferous potential of twenty-seven plant families determined from the N data sets recorded in thirty-eight papers ranked by decreasing median values - scroll to page 5 under Table 1)

The google keywords you are looking for are along the lines of: "melliferous potential of agricultural crops in europe" and variants of this


Are there any air-plants with parts that are edible for humans? Are any air plants (Tillansia sp.) safe for humans to eat? I haven't been able to find whether or not there are. Pineapple is in the same family (Bromeliaceae), but isn't an air plant.

Monstera deliciosa seems to fit the bill. From Wikipedia:

  This member of the arum family Araceae is an epiphyte with aerial roots...

  Wild seedlings grow towards the darkest area they can find until they find a tree trunk, then start to grow up towards the light, creeping up the tree.[6][dead reference link]

  Fruit

  The fruit of Monstera deliciosa is up to 25 cm long and 3–4 cm diameter, looking like a green ear of maize covered with hexagonal scales.

  Fruits of plants of the Araceae (Arum family) often contain Raphides and Trichosclereids – needle-like structures of calcium oxalate.

  The fruit may be ripened by cutting it when the first scales begin to lift up and it begins to exude a pungent odor. It is wrapped in a paper bag and set aside until the scales begin popping off. The scales are then brushed off or fall away to reveal the edible flesh underneath. The flesh, which is similar to pineapple in texture, can be cut away from the core and eaten. It has a fruity taste similar to jackfruit and pineapple. The unripe green fruits can irritate the throat and the latex of the leaves and vines can create rashes in the skin, because both contain potassium oxalate: that is the reason why the fruits have to be consumed when the scales lift up.[9]

  Plants grown indoors in temperate regions occasionally produce flowers and fruit.

  In Mexico, a leaf or root infusion is drunk daily to relieve arthritis.[6][dead reference link]

  In Martinique the root is used to make a remedy for snakebite.[6][dead reference link]

Here's a picture of the fruit by Bruno Navez:

Dragonfruit (Hylocereus undatus) is also hemiepiphytic. You may also be interested in this page about epiphytic cactus fruits and this post on Yahoo! Groups where I found M. deliciosa. The author claims:

  I have eaten the fruits off my Acanthostachys strobilacea, an epiphytic bromeliad, and they are reminiscent of the related terrestrial pineapple just slightly more acidic but still very palatable (to me at least). [Hyperlink added.]


Why are so few foods blue? Although blue foods exist, they're rare enough compared to other foods for food preparers to use blue plasters as a convention. The natural colour of a given food is due to pigments that have some biological origin. Is there any evolutionary reason why these are rarely blue?

Short answer
Blue color is not only rare in edible organisms - Blue color is rare in both the animal and plant Kingdoms in general. In animals, blue coloring is generated through structural optic light effects, and not through colored pigments. In the few blue-colored plants, the blue color is generated by blue pigment, namely anthocyanins. The reason for the scarcity of blue pigments remains unknown as far as I know.

Background
The vast majority of animals are incapable of making blue pigments, but the reason appears to be unknown, according to NPR. In fact, not one vertebrate is known to be able to. Even brilliantly blue peacock feathers or a blue eye, for example, don't contain blue pigment. Instead, they all rely on structural colors to appear blue. Structural colors are brought about by the physical properties of delicately arranged micro- and nanostructures.

Blue morpho butterflies are a great example of a brilliant blue color brought about by structural colors. Morphos have a 6-inch wingspan — one side a dull brown and the other a vibrant, reflective blue. The butterflies have tiny transparent structures on the surface of their wings that scatter light in just the right way to make them appear a vibrant blue. But if you grind up the wings, the dust — robbed of its reflective prism structures — would just look gray or brown.

Similarly, the poison dart frog is blue because of the iridiphores in its skin, which contain no pigment but instead feature mirror-like plates that scatter and reflect blue light (source: By Bio).

Morpho and poison dart frog. sources: Wikipedia & LJN Herpetology

Similarly, in the Kingdom of plants less than 10 percent of the 280,000 species of flowering plants produce blue flowers. In fact, there is no true blue pigment in plants and blue is even more rare in foliage than it is in flowers. Blue hues in plants are also generated by floral trickery with the common red anthocyanin pigments. Plants tweak, or modify, the red anthocyanin pigments to make blue flowers, including pH shifts and mixing of pigments, molecules and ions. These complicated alterations, combined with reflected light through the pigments, create the blue hue (source: Mother Nature Network).

But why the blue pigments are so scarce, seems to be unknown as far as I know (MNN, NPR, Science blogs)

Sources
- MNN
- NPR
- Photobiology


Is it possible to use microalgae to produce food and live on it? I know microalgae have not less protein and starch, grow quickly, require less. So, is it possible to use them for producing food (replace rice and wheat) and live on it?

Currently, I only saw people eat it as an extra-nutrition.

I don't see why microalgae couldn't be a main food source (putting aside the taste factor).

It contains many different lipids, carbohydrates, proteins and other essential nutrients that are digestible and would be beneficial to humans. I do know that microalgae has a very high lipid content (hence why they're often harvested for biofuels), but it can nonetheless provide nutritional value (ie. feed a starving man).

However, not how this is completely different from living solely off of microalgae. This likely wouldn't be possible, as us humans cannot synthesize all nutrients that we need from scratch. These nutrients are deemed essential nutrients. This problem usually arises when your diet is too restricted to certain types of food. So whether it's microalgae or any other type of consumable, you wouldn't be able to live by only eating that thing.

Another related problem is that growing microalgae is more difficult than it would seem, as is once again usually encountered in second-generation biofuel manufacturing. Temperature, light, cell density, nutrients, and much more must be precisely managed to obtain a increasingly growing population of microalgae. The pros and cons of farming microalgae for billion of hungry people would have to be contrasted with other current agricultures, like corn, soy and rice.


STRING ID - allelic differences and splice variants STRING has protein (amino acid sequences) mapped to a single gene ID.
I have these doubts with respect to STRING ID.
I find that

1.All alleles of a single gene share the same STRING ID and
2.Especially in Eukaryotes, splice variants of the single gene(which might translate to different proteins) share the same STRING ID.

Does STRING take into account these two things like UniProt and have different IDs based on allelic differences and splice variants?If so,how?

STRING does not distinguish between different products of the same gene. E.g. for human, the protein identifier you see (ENSP...) corresponds to the longest splice form for each gene (ENSG...). Therefore, STRING won't help you if you need to distinguish between splice forms.

Splice forms are merged because for most sources of evidence, there is little data for the interactions of individual splice forms.


What are the biological and nutritional benefits of having numerous smaller meals a day? I have heard here and there that instead of consuming 3 largish meals (the traditional 3 meals a day), that consuming several smaller meals throughout the day is beneficial for health (and weight loss).

How true is this statement?  What are the biological advantages, if any, of such a diet?

One rationale is that smaller meals will cause less insulin secretion compared to a larger meal. With less circulating insulin over the time, insulin will be under the threshold required to activate the adipogenic program in the white adipose tissue. So, you will burn ingested carbohydrates instead of converting them in fat despite the same caloric intake. See for instance Munster and Saris, Plos One 2012.


How do you culture Cutibacterium acnes? I've been thinking of culturing Cutibacterium acnes (old name is Propionibacterium acnes) for a thesis topic of mine on the comparison of the efficacy of local antibacterial topical skin care products but I have no idea how to culture it. I haven't encountered any definite instructions on the process in culturing it aside from it being an aerotolerant anaerobe and requring an anaerobic incubator.

Douglas & Gunter (1946) The Taxonomic Position of Corynebacterium acnes. J Bacteriol 52: 15-23.

This is the paper, in which Corynebacterium acnes was proposed to be transferred to the genus Propionibacterium as Propionibacterium acnes, and it contains a detailed description of the cultivation procedure.


Synthetic life creation - status of attempts First I apologize for my incorrect English and for lack of modern knowledge regarding the subject (I studied biology a long time ago).

I'm interested to find out:

if there were successful attempts of life creation from conditions that we suppose were dominant on early Earth
if there were not, are such attempts still being conducted?

To clarify, by "life creation" I mean the accidental creation of entire organism in conditions of organic compounds, water, electricity, radiation etc. being present (Abiogenesis).

If this is already answered here, I'm sorry for asking, I have researched this, this, this and this question with no luck.

There have been lot's of attempts, no success so far, a few groups are still working on. However, many steps forward have been done in the last decades.

Starting from the Miller experiment which demonstrated that the building blocks of life chemistry can be obtained starting from fairly simple chemical compounds. Following, Luisi and Szostak showed that 1) nucleic acids can polymerize without the help of enzymes and 2) autocatalytic micelles form spontaneously in many different conditions. It is also important to remember the work of Otto that showed how different molecules can self-replicates.

There are many more examples reported in the literature, still, the complete "creation" of life from matter has not been yet accomplished. However, the results from the experimental work done so far suggest that it is only matter of time and lots of combinatorial work. Unfortunately, there are little to no investments in this field. It's very hard to get the funds needed to start an international cooperation (like the one made to sequence the human genome or to build the CERN's Large Hadron Collider) with the goal of actually making life in the lab. I think that the work of a few (uncoordinated) groups will not get to the goal in the next few years.


What is the top speed of muscle contraction? Currently I am looking into what muscles groups are most used during a football kick. I have a hypothesis that the quadriceps are not as used as most people think because the momentum the swing creates makes the knee extend to fast for the quadriceps to contract.

To prove this I need to know the speed the knee extends during a football kick and the time it takes for the quadriceps to contract. I know how fast the knee extends through my own research.

Does anyone have any information on the speed of muscle contraction?
Quadriceps contraction time would be optimal, but any information relevant would be very helpful

Your question is a good one. The velocity of muscle contraction depends on the:

Initial length of the muscle
The Load on the muscle

Source: Medical Physiology : a cellular and molecular approach by Walter F. Boron, Emile L. Boulpaep - 2nd ed. Page 248

From the above picture we can see that:

The velocity of muscle contraction is not constant. Initially it is zero and then it accelerates to reach a peak
The maximum velocity of muscle contraction is constant at any different initial muscle length
The lower the load the steeper the rise of velocity

So the velocity of muscle contraction should be calculated on a case by case basis.

What can be calculated

What can be calculated is the displacement and frequency of actin myosin cross-bridging.

Under microscopically isotonic conditions, the quantal displacement of a single cross-bridge is ~11 nm.

The frequency of actin-myosin cross-bridging depends on atleast:

ATP concentration
Temperature

At an ATP concentration of 1 µM the frequency is 3.8 ± 0.4 M-1s-1

At 170C the mean time for single displacement was 15±20 ms. While at 250C the mean was 6.4±3.6 ms.

Source: Characterization of Single Actin-Myosin Interactions by Jeffrey T. Finer, Amit D. Mehta and James A. Spudich.
Biophysical Journal, Volume 68, April 1995, p.291s-297s

Concerning your actual question regarding the quadriceps velocity and the velocity of the swing, you should keep the following in mind while calculating:

Quadriceps acts over a second order lever: The Knee is the fulcrum, the effort is put over the tibial tuberosity where the quadriceps is inserted and the load is the foot and whatever it hits/lifts...
The contraction of the quadriceps is calculated as linear velocity while the kicking action is circular - so what you actually observe is the angular velocity. So appropriate angular velocity to linear velocity conversion should be made.

All the best!


Tissue fluid water potential just a quick question. Is the tissue fluid the same water potential as the cells it surrounds? I am a bit confused because if it was lower it would cause water to leave the cell and if it was higher water would enter the cell and both aren't really good for the cell. I believe tissue fluid is isotonic, am I correct?

Yes, cell membranes are highly permeable for water. While diffusion through the membrane is possible (description, and some science), it is most effective through water channel proteins (aquaporins). The different expression levels of aquaporins in different cell types result in differences in the permeability.

And yes, the tissue fluid has to be isotonic to the cell interior. The water balance in the body is therefore highly regulated. If not enough water is available, the blood osmolarity (ratio between solubles and water) increases. This is sensed in the hypothalamus (an area in the brain which is a major player in hormone regulation) and results in production of the hormone vasopressin. This will not only increase your thirst (and therefore add more water to the system) but also regulate aquaporin expression, improving reabsorbtion of water in the kidney (nicely shown here, actual science here). Urine production is of course also important in the response to drinking too much, which can be harmful as well..

If tonicity is deregulated, this has serious consequences for the body (some more science). For example, mutations in vasopressin or kindney aquaporins can result in very similar phenotypes, characterized by dehydration because water levels cannot be properly regulated (even more science).

edited for more explanation, because people complain when I give short answers to short questions ;)


Why were wisdom teeth not eliminated by evolution? Supposedly evolution was very efficient and evolved many human proteins over a few thousand generations. Yet obvious detrimental traits like wisdom teeth remained. Why?

Reductions in the size of our lower jaw that result in wisdom teeth sometimes becoming impacted result from changes in our diet, and are not the direct result of the evolution of a smaller jaw. This means that natural selection has had at most 8000 years to act on the phenomenon, which occurs in people in their mid to late 20s (who, historically, probably would have already reproduced if they were going to), and so the selective advantage of lacking wisdom teeth has not had enough time or been strong enough to cause the no-wisdom-teeth phenotype to spread throughout the human population.

Global human mandibular variation reflects differences in agricultural and hunter-gatherer subsistence strategies - Cramon-Taubadel, PNAS (2011)

Before Agriculture, Human Jaws Were a Perfect Fit for Human Teeth - Smithsonian.com (2015)

Incongruity between Affinity Patterns Based on Mandibular and Lower Dental Dimensions following the Transition to Agriculture in the Near East, Anatolia and Europe - PLOS One (2015)


Mapping a mutation to known SNP, 3' UTR, miR I've parsed out a very large TCGA cancer ssm (single mutation file) file to give me the essential information.

The ssm is in the following format:

['Gene name', 'Ensembl Gene ID', 'Chromosome', 'Chromosome start', 'Cancer Type']
['NTRK1', 'ENSG00000198400', '1','156849827', 'Prostate Adenocarcinoma (TCGA, US)']

From there I would like to grab each mutation and :

Map the chromosomal position to a known SNP (rs something output).
See if this snp is found in a 3'UTR
See if this snp is found in a miRNA
Missense or sense mutation
Any relevant genbank etc.. ids

I'd like to do this Python (I think BioPython is suited for this) for downstream applications.

In order:

Unfortunately, there's no easy way to batch query with only location. You could look up SNPs within genes here.  (You could find the gene a SNP is located in by searching an annotated human genome file for the position.)
You can figure out whether it's in 3'UTR by comparing to a list of human 3' UTRs. The UCSC genome browser page here will help: change the region to "genome", output format to "BED", click "get output", and then filter for 3' UTRs.
You can figure out if it's in a miRNA by comparing chr/start positions to the database available here.
You could use the chromosomal locations and compare to the human genome sequence.  There is probably a better way to do this, but the FASTA for each chromosome is available here.
You could use the SNP IDs to map to Genbank accessions, as per the instructions here.

You don't need BioPython for the first three steps, since it's just parsing each line and comparing values. BioPython is useful for working with FASTA files (so part 4).  All in all, this is mostly reduced to a programming question with all of these resources (basically, you need split each string to get the appropriate numbers/IDs and then compare).


Is this arthropod non-intrusive and recommended to be left alive? I am in Portugal (Lisbon) at the moment, and when leaving my room late at night (12 pm ~ 04 am) I usually face about 4 of these arthropods in the corridors:

(For reference, the "line" in the image is a standard separation on the floor. This particular example of the animal is a little smaller than a nail.) They seem to have quite variable sizes and walk primarily on ground. Also, as implicit above, they seem to be active primarily during the late night. (I don't see them much often, if at all, during the morning/afternoon.) They can be quite fast, but if left unharmed do not move much. They also appear to take shelter inside the walls.

From what I searched, it seems possible that they are centipedes. I've seen sites saying that they are useful to keep other less pleasant animals at bay. My questions are: What are those animals, and should I leave them be or not?

This appears to be a silverfish, a very common household "pest" in the Lepismatidae family of insects.

 Photo Credit: Dong-Hwan Choe. Source: UC IPM

Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].

According to Wikipedia, you can find them all arround the world:

  Silverfish are a cosmopolitan species, found in Africa, the Americas, Australia, Eurasia, and other parts of the Pacific.[8] They inhabit moist areas, requiring a relative humidity between 75% and 95%.[9] In urban areas, they can be found in attics, basements, bathtubs, sinks, kitchens, old books, classrooms, and showers.[3]

They are relatively harmless due to their weak jaws [source], and their presence is typically a larger nuisance than the damage or disruption that they cause.

We have a number of posts already identifying silverfish and asking about management advice. Try yping "silverfish" into the Search bar at the top of the page to search for more information.


Mutation-drift equilibrium and among loci variance in heterozygosity At mutation-drift balance, the increased heterozygosity brought by new mutations is exactly equal to the loss of heterozygosity due to genetic drift. At equilibrium, the expected heterozygosity for a given locus is:

$$\hat h = \frac{4Nu}{1+4Nu}$$

The expected heterozygosity is only the first moment of the whole distribution of locus specific heterozygosity. What is the (among loci) variance in heterozygosity?

In The Distribution of Gene Frequencies in Populations, Sewall Wrights derivates a continuous approximation to the probability distribution for the frequency of an allele in a panmictic population under the pressure of drift and mutation on a bi-allelic locus. In his paper, he reports several version of the same equation. Below is one of them, where $\phi(q)$ is the probability density of the one specified allele to be at frequency $q$.

$$\phi(q) = C q^{4N\nu -1}(1-q)^{4N\mu -1}$$

, where $C=\frac{\Gamma(4N\mu+4N\nu)}{\Gamma (4N\mu) \cdot \Gamma (4N\nu)}$ is a constant, $\mu$ and $\nu$ and the forward and backward mutation rate The heterozygosity is then a simple one-to-one function of the allele frequency.


By What Mechanism can Felines Reverse Diabetes? To my knowledge house cats (and likely other felines) are the only animal able to go into remission after onset of Type 2 diabetes mellitus. I don't have a reference, this has been by peers in my research institution and by a veterinarian. Has this mechanism been studied, and if so, what is it?

I spent a couple of years working in a diabetes research institute.  And you did hear right.

Cats dogs monkeys all can be susceptible to diabetes, although rats and mice don't seem to have diabetes that behaves the same way as humans - I don't think a mouse has ever been observed to get diabetes without specific gene knockouts.  One could argue that mice simply do not get diabetes the way people do.

There are two causes of type 2 diabetes in the research world.  The first happens because the animal may have a genetic susceptibility and environmental conditions induce the disease (like most people).  The second happens because of mutations in one specific gene or another pretty much cause it to happen when the animal gets to a mature age (google term: mature onset diabetes in the young (MODY)).  MODY genes have not proven to be a great model for type 2 diabetes treatment in most people (about 1% of diabetics have a MODY diabetes though).

Cats and dogs have been animals of interest as models of diabetes because their symptoms are human like and have shorter reproductive cycles.  Some cats (like Burmese) clearly have a greater genetic predisposition to diabetes, but cats who are obese, have high glycemic diets, or who get little or no physical activity are more likely to develop diabetes.

As with humans, the condition leads to the insulin secreting cells of of the pancreas to slowly degrade and if these cells are gone, there is no recovery from type 2 diabetes. All this given its likely that cats get diabetes that is similar to the human condition.

In treating cats its been shown that such diabetes can be reversed.  The most important thing to do - common to all treatments - is to change the cat's diet - restrict calories if the cat is obese and change high glycemic food.  Additionally, insulin or drug treatments that reduce insulin resistance (such as are given to humans) can restart the islet cells that secrete insulin if the animal is lucky and don't always have to be lifetime prescriptions.

The reference I have does not give remission statistics, but it must work a reasonable amount of the time.

But I wouldn't want to leave you with the impression that cats are special.  It turns out that human diabetes type 2 is often reversible.  This reference estimates 80% of the time. This study mostly focuses on the same treatments - change of diet and some fasting, but no exercise regimin as the cats.

There's probably nothing magical about cat diabetes 2... ;)


Where are all the dead cockroaches? Major North American cities are full of large cockroaches. Given their numbers and relatively short lifespan, there must be staggering quantities of cockroaches dying in a city every day. However, I never seem to encounter their carcasses in cities.

I notice a fair number of dead roaches indoors, which actually surprises me since you would think that there is more thorough cleaning and pest control indoors vs. city streets. The number of dead roaches I see indoors seems about consistent with the number of live ones.

However, outdoors I see a lot of live roaches, and hardly any dead ones. Most carcasses I notice are mechanically damaged and near heavy traffic areas, so most likely stepped on by someone who was walking by. But what about roaches dying of natural causes (or disease/poison)? Are there animals that scavenge the carcasses very efficiently (ants? birds?)? Do the roaches like to run away and die in isolation? Do they just not die naturally very often, and usually get hunted by a predator?

Note that I am asking specifically about city cockroaches, in mostly concrete areas.

In the big cities of North America (e.g N.Y), the big piles of dirt and moisture attract many hostile animals such as the ones you mentioned: the cockroaches. You should also consider that in the north there is a very common factor that attracts collonies of cockroaches: the low to mediocre temperatures. Moreover, you should reconsider the cleanliness of the sewers. The sewer and the leftovers that exist there are highly nutritional for the cockroaches. That's why you don't see many dead ones on the streets. And where is the start of the sewers? The sewers start from every house. That's why you notice more roaches in the houses than outdoors. They need a place that might provide them the sewer's environment such as the bathrooms, or an other place in the house that has moisture and is mostly dark. Cockroaches live and die to the same place and don't go somewhere else to die. The decay rate outdoors is higher of course, than indoors because every house is cleaner than the roads. With the process of cleaning many factors, such as mites are swept away to the environment.

For the second part of your question:

Outdoors there are many  scavengers and natural predators for the cockroaches. Some of them are: toads, frogs, beetles, geckos, iguanas and birds.  Entomopathogenic fungi have also been identified as lethal to roaches, as their spores attach to insects and kill them within weeks. Cockroaches affected by fungi then pass the parasite on to other cockroaches, and the cycle continues.

Ants prey on some cockroach species, but other roachess actually live with ants in their colonies. These are called myrmecophiles, meaning lovers of ants. They don't seem to offer their hosts anything in return for living with them, and are usually tiny and unobtrusive. Other species - termitophiles - live in similar fashion with termites.

And yes ants are the major factor of dicomposion in nature, because they devour almost anything.

I hope this answered your question, becaused I used very extended research :)