text:
Why do heterozygous individuals have increased resistance to malaria?
I am aware that there is such a thing called heterozygous advantage, which is due to the presence of a certain single allele, and that an example of this could be with "sickle-cell anemia".  I am quite curious as to how exactly this heterozygous advantage is created.
Could the increased resistance against malaria be due to natural resistance or natural selection?

The heterozygous advantage generally lowers natural selection against the carriers of mutated alele, because it helps them to survive some specific conditions (which have to have some major impact on the survival rate). This means these individuals have bigger chances of reproducing, which means spread of the alele.
Sickle cell anaemia is one good example in countries with big incidence of malaria (caused by a protista plasmodium falciparum). This parasite reproduces itself in human Red Blood Cells (RBCs), destroys the cells and releases its sporozoits (which can infect other RBCs and the cycle continues). This massive destruction of RBCs is called haemolytic anaemia. Without enough RBCs and haemoglobin, the organism isn't able to function properly (falls ill in malaria).
Individuals which are heterozygous for HbS alele (which in homozygous state causes sickle-cell anaemia) can catch the parasite, but the chances are bigger, that the infected cells will be phagocytized by macrophages and the parasite will be unable to reproduce in them. Illustration Therefore the chances are bigger that they will survive the infection by plasmodium, therefore they can pass their genes (containing HbS gene to the next generation. (The whole process is a bit more complicated by presence of other genes, some details can be found here, but this mechanism seems to be the most important one.)
In general, many homozygots for "normal" Hb alele die as a result of malaria infection, most homozygots for HbS alele die for sickle-cell anaemia. So the winner is heterozygous conformation, which is saved from both. This influences the frequency of HbS alele (it makes it higher until this effect gets balanced with the effect of selection against HbS alele because of too many homozygous individuals with sickle-cell anaemia)
Another good examples in European population are heterozygozity for CFTR mutated alele, which helps during epidemics of cholera. Vibrio cholerae which causes this disease modifies the effects of G protein pathway for release of some ions (and water) into the lumen of intestine, which causes massive diarrhea. Specific mutations in CFTR gene deplete its function (the transport of Cl-) which in heterozygous conformation lowers the loss of water, which is the main cause of death in cholera, therefore helps the individuals to survive. Homozygous conformation however results in cystic fibrosis.
Hope this helps. :)

The heterozygous advantage generally lowers natural selection against the carriers of mutated alele,  sounds a little weird. "Heterozygote advantage" refers to the situation where  the heterozygote has a higher fitness than any homozygote. "Natural selection" refers to a differential in fitness between genotypes. Btw, allele takes two "l".

yes, I think that could be more understandable, thanks. But I hope the principle is clear from my comment.

Very interesting explanation has been proposed by Ferreira A. et al. 2011. Briefly, red blood cells of individuals carrying homozygous point mutation in haemoglobin beta-chain tend to be more prone to disruption.
Red blood cells are full of haemoglobin, so once their membrane is damaged, they release free haemoglobin and heme to the plasma. This is called intravascular haemolysis. Too high level of free heme is toxic and you can read about its consequences, for example here.
In the plasma of individuals with heterozygous mutation also there is an increased concentration of free heme, but definitely below harmful level.
However, it is enough to trigger mechanism that protects us from toxic effects of free heme. Heme oxygenase-1 (HO-1)catalyses heme to biliverdin, iron and carbon monoxide (CO). CO makes the vascular environment very unfavourable for Plasmodium.sp and probably protects from infection.
The study was performed in the mouse model.


text:
What kind of viruses can be found in sperm?
It is well known that the HIV virus can contaminate other people via sperm. But is this the only virus that sperm successfully could contain, or could for example rhinoviruses also be part of sperm?
What causes the difference if there is one?

Those are some viruses that can exist in sperm :

Zika : Zika and Sexual Transmission
Ebola : How Long Does the Ebola Virus Survive in Semen?
Hepatitis C : Hepatitis C virus detection in the semen of infected patients
Human papillomavirus infection (HPV) : Correlation between HPV sperm infection and male infertility
Herpes simplex : Detection of herpes simplex virus DNA in semen of men with genital HSV-2 infection
Hepatitis B : Effects of hepatitis B virus on human semen parameters and sperm DNA integrity

Do you know if there is a special cause for there present in sperm or is it just a matter of getting dropped by the bloodstream in the region of the organs involved by producing sperm no matter what kind of virus?

@Marijn, I think they will be within the DNA that sperm contains.

It almost looks like your children going to be a kind of virus than ?

Of course the virus normally will be inside their cells.

When I think of a virus I think it as a whole structure including membrane etc. But when it is in the DNA it is only a part of the virus. Because isn't a cell after multiple copies making of the virus exploding whereby all the viruses including membrane etc are loosed in the blood and other plasma's?

In most of the cases the explosion doesn't happen in sperm, honestly I don't know why.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What can pass through the intestinal membranes?
As I understand it, most substances need help to pass through the walls of the intestines.
For example, in hepatic recirculation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781307/) bile salts are grabbed and transported across the intestinal membranes by particular polypeptides.
Is there a summary of the sorts of things that can be transported across intestinal membranes? For example, hormones, stearates, lipids, etc. What general classes of molecules can pass the membrane and what cannot?
I am not looking for an exact answer, but a general characterization of major classes of organic molecules and their ability to pass through intestinal membranes into the body.

Your title says abdominal wall, which to me suggests outer muscular layers and/or parietal peritoneam, but your question seems to relate more to the inner epithelial gut tube lining or maybe the visceral peritoneal layers. Could you clarify what layer(s) you specifically are interested in.

Virtually all nutrients from food can be absorbed into blood through the lining of small intestine and colon.
What can be absorbed in the small intestine:

Water
Simple sugars (monosaccharides): glucose, fructose, galactose...
Amino acids and small peptides (dipeptides, tripeptides)
Free fatty acids, monoglycerides and cholesterol
Minerals: sodium, potassium, iron, etc.
Vitamins
Nucleic acids
Alcohol
Various other substances from food (polyphenols, sulfate, oxalate, caffeine, preservatives...)
Bile acids
Steroid hormones, such as cortisol, aldosterone and sex hormones (JCEM)
Drugs
Various toxins

What can be absorbed in the colon:

Water
Short-chain fatty acids (from bacterial fermentation of dietary fiber and sugar alcohols)
Sodium, potassium and some other electrolytes

What cannot be absorbed in the intestine:

Polysaccharides (such as starch), oligosaccharides, disaccharides
Dietary fiber (soluble fiber can be fermented and the resulting substances can be absorbed in the colon)
Whole proteins and big peptides
Triglycerides, diglycerides
Peptide hormones, such as insulin, glucagon, calcitonin, prolactin, growth hormone and parathyroid hormone (Cambridge Core)

Sources:

Lumenlearning (type of transport for all main nutrients)
Best Practice & Research: Clinical Gastroenterology (detailed description with carriers involved)

This table from Ganong's medical physiology will help you get your answer.

I hope it helps.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What animal's lower eye lid moves to upper one when closing eyes?
I know cock's lower eye lids moves to meet the upper one when it closes its eye.  What other animals does this?  BTW, "cock-eyed" can mean upside down, I think.

Nictitating membrane (inner eyelid) of sharks can cover sharks eye as it moves from the upper to the lower eye lid (http://en.wikipedia.org/wiki/Nictitating_membrane).

Actaully there are quite a few animals which actually moves there lower eyelids:

Most of the birds
Reptiles(Except Snake)
Amphibians

Are you sure? https://www.youtube.com/watch?v=dgh6ABfdlAU shows a hawk's nictitating membrane moving from sidewise.


text:
With an excess supply of nutrients, in how much time will the number of algae cells double in full sun?
I am growing algae in a container in my roof. It gets sunlight for the whole day as there are no clouds nowadays in my area. There is no lack of nutrients as I am constantly adding water mixed with organic waste. The dirt visible in the photos is from manure, which I added as fertilizer.
The water has become green and algae is deposited on top covering almost all of the surface area. There are no threads, so it is not filamentous.
Since there are probably several species of algae in it which I don't know, please tell me the doubling time of most common species.
Also, is there anything I can do to hasten the production of cells?
Below are pictures of the culture, as asked for.

I think it is possible to answer this question.

Please go through the articles http://www.marine.csiro.au/microalgae/methods/Growth%20rate.htm and http://eprints.cmfri.org.in/400/1/Article_09.pdf

I am presuming this a Blue Green Algae(BGA) Identify your algae
Growth rate for N1, N2 biomass at t1 and t2 time respectively, can be give as,
Growth rate:   $K'$ = $\ln \frac{(N_2 / N_1)}{(t_2 - t_1)}$

(source: csiro.au)
So, by this equation it is easy to calculate the doubling time of your algae.

For BGA normal doubling time is 6-8 hours.$^2$
Source:

http://www.marine.csiro.au/microalgae/methods/Growth%20rate.htm
https://sites.google.com/site/biomonstaaar/algae

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is it possible to trace of the ancestry of a person by only using his/her genetic information?
Is it possible to trace the descent of a person only using his/her genome sequence?

I edited your question to make it more clear. You mean the genetic information, the sequencing of the genome, right?

In short, yes, it is possible. There are companies that sequence part of your genome and then can trace it back to your ancestors. All human family trees can be traced back to their African origin 200 000 years ago, but the companies that sequence your genes do not do that. For example, 23andMe sequences only 1 million of your base pairs (single nucleotide polymorphisms (SNPs)). They trace your most recent heritage, which could lead to Europe, Africa, or Asia. They can basically trace which part of your chromosomes (and thus your ancestry) came from your mom or your dad:

Unlike the sex chromosomes and the mitochondrial DNA, which are inherited as blocks, the 22 biparental chromosomes, known as autosomes, are scrambled during reproduction. Through a process known as recombination, each parent pulls his or her paired set of 22 autosomes into chunks, then reassembles a new single set using half the material from each pair. The two single sets of chromomes from each parent are combined into a new paired set when a sperm fertilizes an egg.

You can read more about 23andMe here. There are other companies that are specialized in tracing your ancestry: Genetic Genealogy, DNA Tribes, and Heirlines.

Back when I was doing my PhD, there was a group in the same department as me working on an interesting project exploring the extent to which surnames (generally paternally inherited, at least in the modern west) and Y chromosomes (always paternally inherited) shared their descent.
The answers are always complicated, especially for more common surnames which have multiple origins. There are also confounding factors, such as the rate of non-paternity (which can be surprisingly high, often around 1-2%). It is, however, striking just how much you can tell about a person's heritage, just from a relatively small amount of genetic information.
For more info about the surnames work, see (1) and (2).


text:
Are mosquitoes repelled by high frequency sound?
I am totally confused whether ask this question to physics or biology stackexchange.
I downloaded a mobile application which claims to repel mosquitoes. This application basically produces sound from 16kHz to 22kHz (I doubt that it even produces more than 20kHz because we can't hear more than 20kHz naturally).
I totally doubt this application. Do mosquitoes go away in higher frequency of sound?

Try to ask one question per post. As is often the case with UPDATE titles, what follows should be its own question.

Have you heard of the proposed Bioacoustics Stack Exchange? It seems like you might be a valuable member of that community. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

After seeing your question, I decided to do a bit of research on the topic.

First Source: EurekAlert!

http://www.eurekalert.org/pub_releases/2007-04/jws-mrt041607.php

"Mosquito repellents that emit high-pitched sounds don't prevent
  bites"

Some key-points from the webpage:

A Cochrane Systematic Review of the use of electronic mosquito repellents (EMRs) failed to find any evidence that they work.

  To test these claims a team of Cochrane Researchers conducted a systematic review looking for trials conducted with EMRs. They located ten field trials that had been carried out in various parts of the world. None of these trials showed any evidence that EMRs work.

  All ten studies found that there was no difference in the number of mosquitoes found on the bare body parts of the human participants with or without an EMR

Second Source: Wikipedia

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

These electronic devices have been shown to have no effect as a mosquito repellent by studies done by the EPA and many universities.

Third Source: CBCnews

http://www.cbc.ca/news/story/2007/04/18/mosquito-repellent.html
Key points from the article:

"There was no evidence in the field studies to support any repelling effects of EMRs, hence >no evidence to support their promotion or use"

  -Ahmadali Enayati, researcher

This is a major point as well:

The study also said that in 12 of the 15 experiments, the landing rates of mosquitoes on subjects was in fact higher than in control groups.

The article also points out that female mosquitoes can't hear very well- Which supports the idea that high-frequency repellents are ineffective; Much more than you probably think. Why? Well, it's pretty simple:
Female Mosquitoes are the only Gender that Bite.

Overall, when you consider the countless studies and research put in to the effects of high-frequency sounds on mosquitoes, it's pretty obvious that:
No.High Frequency Sounds do NOT repel mosquitoes

All three sources reference the same study, and it's unfortunate that the details of the study haven't been made available for peer review.

Ok, so the results were published (http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD005434.pub2/full), but access to the article is not provided with the basic Wiley subscription package that (I assume) is available through most universities.

@DanielStandage http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD005434.pub2/abstract is the abstract where the relevant information is written: "All 10 studies found that there was no difference in the number of mosquitoes caught from the bare body parts of the human participants with or without an EMR".

The paper is now available without dealing with a pay-wall.
By the way, Wiley's website has this to say about the publication the paper was published in: "The Cochrane Library is a collection of databases that contain high-quality, independent evidence to inform healthcare decision making. Cochrane Reviews represent the highest level of evidence on which to base clinical treatment decisions. "

Ultrasound emitting devices are used to repel mosquitoes. We tested
  the repelling properties of a commercially available ultrasound device
  in a domestic setting in Gabon. Devices emitting three different block
  frequencies ranging from 3 to 11 kHz were tested in a paired,
  cross-over blinded and placebo controlled trial during eighteen nights
  in nine pairs of houses. A total of 7485 mosquitoes (10% Anopheles,
  62% Culex, 27% Mansonia and 1% Aedes) were caught, 23 per house per
  night. There was no significant difference in landing rate between the
  houses with ultrasound device and the houses with placebo for any
  species of mosquito. Thus the ultrasound device used was not effective
  against mosquitoes in this strictly controlled trial.

Sylla el-H K, Lell B, Kremsner PG. A blinded, controlled trial of an ultrasound device as mosquito repellent. Wiener Klinische Wochenschrift. 2000 May;112(10) 448-450. PubMed PMID: 10890136.

A bibliographic review about the use of electroacoustic devices with a
  supposed repellent action on the females of different species of
  hematophagous mosquitoes  is presented. 15 direct references and 2
  indirect ones are given, in which it is  concluded that these devices
  do not protect those who have them from the stings of mosquitoes. The
  names of 9 of the tested devices as well as of 16 of the main  species
  of mosquitoes present in the field tests are mentioned. These tests
  have  been carried out in very different ecological conditions from
  Alaska to Equatorial Africa. It is also stressed that the high
  intensity ultrasonic frequencies emitted by these devices produces a
  potentially harmful effect on man.

Rev Cubana Med Trop. 1998;50(2):89-92.
[Electronic repellents against mosquitoes: the propaganda and the reality].
[Article in Spanish]
Coro F(1), Suárez S.
Author information:
(1)Facultad de Biología, Universidad de La Habana, Ciudad de La Habana, Cuba.
PMID: 10349423  [PubMed - indexed for MEDLINE]

Answers are supposed to be written by yourself and not only consist of a citation.

@Chris I am not an expert in the field, what do I need to add to an abstract? I think it is self explanatory, doesn't it?


text:
What is the largest perennial herbaceous plant?
What is the largest perennial herbaceous plant? My guess would be some kind of banana or bamboo.

This sounds like another homework question.

Is the [tag:taxonomy] tag appropriate here?

It is not homework. Question about facts aren't necessarily homework. Please don't be biased.

The tallest banana species is Musa Ingens (15m) which grows in the forest of Papua New Guinea and Indonesia. It also claimed as the the world's largest herbaceous plant. http://www.thestatworld.com/2015/12/musa-ingens-the-tallest-banana-plant-in-world.html

As mentioned above, the largest perennial herbaceous plant is indeed the banana.  Whilst the main reference to this ("Yes, we have more bananas" - an article in the Royal Horticultural Society Journal from May 2002) has been removed from their website it would be I'm sure possible to order should you need to.
This summary of the banana mentions that the pseudo-stem of the banana plant grows to 6-7.6m in height - I haven't found anything taller when looking around so it doesn't generate any reason to doubt the removed article.
Regarding the comments on Bamboo, there are 7 genera containing bamboo species.  All of these (Arthrostylidium Rupr, Bambusa Schreb, Chusquea Kunth, Dendrocalamus Nees, Phyllostachys Siebold & Zucc., Pseudosasa Makino and Sasa Makino & Shibata) are described as having persistent woody stems so don't meet your herbaceous requirement.

So what happens with bamboo? Doesn't it grow a lot taller than 6 meters sometimes? It's also perennial and herbaceous, right?

Not all bamboo species are herbaceous, some are woody. I'll dig into the relative sizes of the two variants some more tomorrow =)

@Problemaniac I've done the research and it seems I was mistaken last night.  All genera with common name bamboo in ITIS are woody as shown in my now revised answer =)

So was it a common misunderstanding that "a bamboo forest is/can be just one big tall grass of a kind"?

It would seem to be - I would imagine that confusion stems (no pun intended) from all bamboo species being contained within the Family  Poaceae, which has a common name of 'grasses'.  However the distinction between herbaceous and woody happens lower down at Genus.

It's not a misunderstanding or confusion - all bamboos are grasses.  Grasses are defined as the graminoids, which includes Poaceae (the true grasses, including bamboo), plus the Cyperaceae (sedges) and Juncaceae (rushes). So it is perfectly accurate to call a bamboo forest a forest of tall grass.

@RoryM: the link to 'summary of the banana' is dead now.


text:
Substitute 25mM dNTPs mix with 10mM dNTPs
I need to make a solution of multiple compounds, one of them is dNTPs. The recipe calls for 20 μl 25 mM dNTPs in a 1250 μL master mix. Unfortunately I do not have it available at that concentration, can I substitute 25mM dNTP mix with 10mM mix?
TECHNICAL DETAILS

$dATP: C_{10}H_{13}N_5O_{12}P_3Na_3 - MW=557.2$
$dCTP: C_9H_{13}N_3O_{13}P_3Na_3 - MW=533.1$
$dGTP: C_{10}H_{13}N_5O_{13}P_3Na_3-MW=573.2$
$dTTP: C_{10}H_{14}N_2O_{14}P_3Na_3-MW=548.1$

Would it be 50μL of 10mM dNTPs to substitute the 20μL of 25mM dNTPs?

Yes, you can do this. As long as the final mix has the proper concentrations of everything, its fine. Just make sure you compensate the by adding 30 uL (the extra volume) less of water to the master mix.


text:
Online Molecular and Cellular Biology Video Lectures?
I am looking for video lectures to go through to guide my reading in intro molecular and cellular biology. I've had intro bio and I study evolutionary theory, but my molecule- and cell-level knowledge is weak.
I'm finding it impossible to know where to look in a big book like Alberts, or to read Lodish without a guide, so I really need lectures to help me out. I've tried the MIT OCW assignments and a few other similar sites, but I can't seem to find a course that includes lectures. Does anyone know of any? Ideally they'd follow Watson et al. for molecular and Lodish for cellular, but I can find other textbooks too.

MIT's OCW is weak when it comes to biology videos.
UC Berkeley has some good video content for molecular and cell biology.

See, for example, this playlist:
http://www.youtube.com/playlist?list=59C08AE05E752758
And explore the main UC Berkeley video lectures website here: http://webcast.berkeley.edu/

UCSD, if I recall correctly, has had some pretty good life science lectures available online to the public, as well.  Possibly also UCLA.
iTunes U is your friend here. Unfortunately, to really take advantage of it, you need to download iTunes -- but it's worth it.  The last time I looked, there was more there than I could possibly watch, and that was 4 years ago.

MIT OpenCourseWare provides very interesting material, and not only on biology.
You may be interested in seeing the video lectures from some of the Introductory biology courses, such as this one, this one or this other one.
There is, however, much more, check out the index of the available material for biology.

These are some of my favorite biology learning resources:
iBioSeminars
Academic Earth - Biology
Others include: Khan Academy - Biology, HHMI BioInteractive video collections, Wellcome Trust education resources.

This one is not precisely molecular and cell biology, but rather systems biology. It might help you as some kind of introduction, though:
Systems biology lecture 1
Also, if you are really really new to the subject, you can probably use "Molecular and Cell Biology for Dummies".

The Journal of Visualized Experiments (jove.com) is excellent but based on experimental protocols.
ItunesU also has great resources. Stay away from youtube - a lot of people there don't know what they are talking about.


text:
How can I measure bacterial alkaline phosphatase activity?
I want to measure alkaline phosphatase activity using PNPP in my mutant bacteria strains, but all the protocols I found involve purification of the phosphatase (which I have no need of).
Does anyone know a good protocol which involves using only the supernatant, without purification of the enzyme? What is the preferred buffer for the reaction?

I found this kit that appears to be compatible with biological samples.  Rather than buying the kit you may also be able to imitate / modify their protocol to do the assay with your super natant.

Thank you, but I don't think I can imitate the kit - they don't share the components of the buffers. It did give me some idea of how the protocol is done, so thank you.

There's a paper from 1973 describing a very simple protocol:
 Wolf PL, Von der Muehll E, Praisler K. 1973. A test for bacterial alkaline phosphatase: use in rapid identification of Serratia organisms. Clinical chemistry 19: 1248–9.


text:
Is there a correlation between muscle fibers and body types?
I have been told the number of muscle fibers a particular muscle has varies from person to person. Unfortunately, the person who told me this did not know much more than this. Initial searching on the web did not reveal much detail on this; some random sources suggested there was a correlation but they weren't referenced.
Is there a general correlation between the number of muscle fibers and body type (mesomorph, endomorph, ectomorph)?
What about a correlation between muscle fiber type (Type I/Type IIa/Type IIx/Type IIb) and body type?

Don't know about fibre numbers, but there is a correlation between fibre types and athletic ability, in that the ratio of type I to II (slow-twitch vs fast-twitch) determines whether a person would be naturally good at sprinting vs endurance activities. If you google for something like "striated muscle fibre twitch endurance" you should find quite a bit on that. I would imagine that your somatotypes would be quite influenced by fibre type ratio...

Body type is something about your constitution. I would probably formulate the question differently to ask for correlation between muscle types and physical strength/endurance, for there is some known correlations here (as @Amanda mentioned in her comment).

A recent paper called 'Genetic Influences in Sport and Physical Performance'[1] states:

"Muscle fibre type determination is complex. Whilst initial composition is likely to be strongly influenced by genetic factors, training has significant effects on fibre shifts."

They also go onto say that:

"However, the role of genetic variation in determining psychological state and responses remains poorly understood; only recently have specific genes been implicated in motivational behaviour and maintenance of exercise."

Finally:

"With the current state of knowledge, the field of genetic influences on sports performance remains in its infancy, despite over a decade of research."

An older paper which also examined fiber types stated that:

"These results reveal the existence of large interindividual variability and gender differences in the most common characteristics of the human skeletal muscle."[4].

Another study hypothesises that there may be racial differences in muscle fibre types.[2]. It's also said that a large variation in fiber composition of skeletal muscle within subgroups of athletic ability. This suggests that factors other than fiber-type composition contribute to performance.[3].
A small study carried out in the Croatian Navy found that ectomorphs had a better ability to sprint than endomorphs.[5]. They also found a positive correlation between calf girth and sprinting ability.
The information is a bit disjointed and sparse. However, to finally come around to the question at hand, it seems that although there may be differences according to body type initially (which obviously also has a genetic basis), training and physical activity contributes significantly to what number and types of fibres individuals possess.
There are lots of sport-specific research papers examining individuals' performance and suitability on body types.
A note on somatotyping: I guess it might also be handy note that somatotyping (endomorph, ectomorph and mesomorph) is just one theory on measuring an individual and it does have critics. The theory was initially developed in an attempt to link body type to behaviour.
It's been suggested that measurements like BMI are much more objective and useful.[6]. Another point made was that bodies change according to a number of environmental variables, nutrition etc.[7]. For example, one study suggested that intense labour during adolescence may affect somatotype (there are a few similar studies).[8]. So perhaps while using somatotypes to identify a person at one point in time is useful, it has limits in use as a long term classification.
This point probably has more relevance to the question at hand since with training and physical activity, a person can potentially change their somatotype at least to some extent; and also the number and types of muscle fibers (which evidence supports).

Puthucheary Z, et al. Genetic influences in sport and physical performance. Sports Med. 2011. 41:845-59.
Nielsen J. Glucose intolerance in the West African Diaspora: a skeletal muscle fibre type distribution hypothesis. Acta Physiol. 2011. 202(4):605-16.
DeLee: DeLee and Drez's Orthopaedic Sports Medicine. 3rd ed. Saunders.
Simoneau, et al. Human variation in skeletal muscle fiber-type proportion and enzyme activities. AJP - Endo. 1989. 257(4):567-572.
Sporis G. Impact of body composition on performance in fitness tests among personnel of the Croatian navy. Coll Antropol. 2011. 35(2):335-9.
Maddan, et al. The BMI as a somatotypic measure of physique: A rejoinder to Jeremy E.C. Genovese. The Social Science Journal. 2009. 46:394–401.
Parnell. Simplified somatotypes Original Research Article. Journal of Psychosomatic Research. 1964. 8(3):311-315.
Ozener, et al. The effect of labour on somatotype of males during the adolescent growth period. Homo. 2008. 59(2):161-72.

Awesome, I will look into all those papers for sure :)


text:
Is it possible to add a new sequence to a blast database without recreating it from scratch?
I have a new sequence and I want to add it to a pre-constructed BLAST database containing other sequences. The makeblastdb help does not give any hint on this regard.

You can use blastdbcmd to extract FASTA sequences from the BLAST database. Then you can append your extra sequence to the newly created FASTA file, and remake the BLAST DB using makeblastdb. Assuming you have a protein BLAST database in the current working directory, and a sequence you want to add to it in new.fa:
$ blastdbcmd -db proteindb -dbtype prot -out db.fa -entry all
    $ cat new.fa >> db.fa
$ makeblastdb -in db.fa -out newproteindb -dbtype prot

(Replace prot with nucl if you have a nucleotide database)

You may create a new database with the new sequences and create an alias linking the old and new databases with blastdb_aliastool


text:
How does translational coupling work in prokaryotes?
Today I heard about a phenomenon called "translational coupling", where the translation of one protein influences the translation of another protein. The messenger RNA levels don't seem influenced. How does this work? Do they need to be in the same operon?

Here is a relevant reference: Tian & Salis, A predictive biophysical model of translational coupling to coordinate and control protein expression in bacterial operons. Nucleic Acids Research. 2015
https://www.ncbi.nlm.nih.gov/pubmed/26117546/ HTH

Translational coupling describes in how some cases an mRNA will code from more than one protein (i.e. will be polycistronic).  Translational coupling is thought to be mostly used as a way to make a set of genes are translated at roughly the same amount in the cell.
Translational coupling is very common in prokaryotes and nearly half of e coli genes are found in a polycistronic operon.  What we know about them is revealing.  There are some fancy mechanisms to adjust the ratios of these adjacent genes, which are still coupled, but with ratios that are not just 1:1.  Its shown that the later genes are often translated at somewhat lower frequency because the first genes are available more quickly before the mRNA degrades.
Eric Alm @ MIT wrote this great paper on how operons evolve.
I've only been able to find this reference to a eukaryotic case of "translational coupling" which is very rare, but does exist.  The most common cases of translationally coupled genes in eukaryotes are RNA viruses which usually contain only a single full length mRNA which codes for all the genes in the virus.  The selective pressures to keep the viral genome small and constrain the ratios of these genes, will cause these genes to even overlap, starting the next one before the current gene finishes.

The above answer isn't entirely accurate. It's true that polycistronic mRNAs (i.e. operons) are very common in bacteria. But this isn't what is meant by translationally coupled.
Translational coupling happens when the second gene of two adjacent genes in an operon, doesn't have it's own ribosome binding site. Instead, the ribosome ends translation at a stop codon at the first gene, and then steps back slighly, and starts translating the from the start codon of the second gene. This happens when the coding regions of the two genes overlap:
E.g.
XXXXXXXXXATGAXXXXXXXXX
-the first series of Xs is the end of gene 1
- the TGA is the stop codon for gene 1
- the ribosome slides back one nucleotide and translates form ATG
- the second series of XXXX is the second genes coding region
The two genes are said to be translationally coupled because distrupting translation of the first gene would abolish translation of the second.

Can you please add some references?

I think this is right to be an answer, and furthermore Matt is correct. Translational coupling isn't the same as polycistronic transcription - but I agree a reference or two wouldn't hurt.

Vance, it's not a comment. The original answer is 100% incorrect.


text:
Gel electrophoresis after RNAse treatment

I do not understand how to solve this question. I know that RNAse will cut smaller pieces of RNA.
The answer given is A

The question is a bit vague in some important parts, so I'll have to make a few assumptions about what the authors likely meant.
RNAses are enzymes that degrade RNA. There are a few different ones that lead to different kinds of degradation. The type that you would use in an experiment like this is an RNAse that completely degrades RNA. The purpose of this is to be able to distinguish RNA from DNA. So whatever is left after the RNAse treatment is DNA, and the bands that vanished are RNA.
If you isolate nucleic acids from liver, the major DNA part would be genomic DNA. The major RNA components would be mRNA and rRNA. Genomic DNA is huge compared to mRNA and rRNA. In gel electrophoresis of nucleic acids, the bands that move further are smaller nucleic acids, and the bands that move less far are larger nucleic acids. So the band on the left in your example is likely genomic DNA, and the band to the right is mRNA or rRNA. After RNAse digestion only the left band should remain, which is answer A.

RNA can fold and will therefore migrate faster than DNA. So it shows up as the band which is towards the positive front. After RNAse treatment you'll lose that band. So the answer is A

Adding to that: A lot of RNAs are relatively small and migrate faster than a genomic DNA prep.


text:
How do I clean phenol contaminated RNA without losing any of the sample?
I recently extracted RNA from developing plant leaves for the first time, as part of a very long and intensive experiment. The samples were extremely precious because of the amount of effort that went into obtaining them (harvesting thousands of miniscule leaves, one from each plant, to get the required mass).
I extracted the RNA with TRIzol and chloroform. Nanodrop showed excellent yield as you would expect for actively growing young tissue, but some of the samples had really low 260/230 ratios. I know this suggests phenol or salt contamination, but what can I do to clean the samples without losing any of the precious RNA? And how can I avoid the contamination in the future?

You can clean up phenol by washing with choloroform, and then doing an isopropanol precipitation followed by a 75% EtOH wash (let me know if you'd like an exact protocol).
To avoid contamination (and sample loss), you have to be meticulous in your pipetting (which you'll get better with practice). You can always use those phase-lock tubes which basically jams a solid gel between the aqueous and organic phases so it's a lot easier to pipette.

Which bit of pipetting is the crucial part? Is it the removal of the clear upper phase after centrifugation? If so - do most people leave a bit of the upper phase behind so as to avoid contamination? I was trying to get every last drop!

@RichardSmith Yeah the pipetting of the organic/aqueous phase is crucial. It depends on (1) how good you are at pipetting, and (2) how "precious" your samples are. Of course, if you're more meticulous about getting as much sample you can get, there's a tradeoff between yield vs. purity. If I can spare some sample, I usually leave just a tiny bit to spare myself from touching the junk in the interphase between the two layers.

I must not be as good at pipetting as I thought! Thanks very much for your answer. I'll make sure I get better at pipetting and in the meantime I'll leave a safe amount of the aqueous phase behind.

@RichardSmith It might've not been completely your fault. The standard procedure is to clean up the RNA with isopropanol and Ethanol, which it didn't seem like you did. Once you do that, you should get super clean RNA even if there was a bump in your pipetting.

I did clean with isopropanol and Ethanol, and then Nanodropped afterwards. I take full responsibility!

@jp89, From what I understand the IPA and Ethanol cleans only effectively take care of the salts. The Phenol Choloroform extraction does a much better job with the removal of proteins. Possibly you could take some of the interphase and clean again. The phenol will affect your columns and affect your yields.

Also to get rid of all traces of phenol, try extracting with ether.

An ethanol precipitation should work. But I have had great success using the Qiagen RNA cleanup columns, which are in my opinion easier.  Here is a URL to see the RNA cleanup columns Qiagen offers:  http://www.qiagen.com/products/rnacleanupconcentration/default.aspx
Also in the future you should consider using PhaseLock tubes:
http://www.5prime.com/products/nucleic-acid-purification/organic-nucleic-acid-extraction/phase-lock-gel-.aspx
That saved me from having your exact problem many times over.

Thanks very much for the answer and the links. I'll keep the PhaseLock tubes in mind - I take it with the PhaseLock I don't need the cleanup kit?

Oh, and welcome to biology.SE :)

Thanks. Just started on the Home Brewing.SE and saw there was a biology one as well. Seems like a good idea. ;-)


text:
In what ways, if any, does administration of rapamycin *not* mimic calorie restriction?
Numerous sources like this say that rapamycin increases lifespan. And mTOR antagonism appears to be a large part of this (mTOR antagonism also appears to be a large part of calorie restriction's mechanism too).
Is the effect of calorie restriction equal to that of rapamycin treatment or are there differences?

I included the actual question in the main text, as it was not immediately clear what was the point of the question (I had to go back and re-read the title and then I understood).

Rapamycin specifically inhibits the mTOR pathway (mTOR = mammalian target of rapamycin), which has numerous downstream functions including protein biogenesis, regulation of cell cycle, immune function and apoptosis. The upstream effectors of mTOR include growth factors and amino acid availability, so you can certainly see that the lifespan enhancing effects of caloric restriction will be (at least in part) mediated by the mTOR pathway.
But there are key differences. mTOR also receives signals relating to DNA damage and inflammatory changes (to name just 2) that are essential for healthy survival. So any direct inhibition of this pathway will affect all the functions - I can't find the reference now, but I have definitel read in one of the numerous rodent studies that rapamycin treated mice have reduced immune function (i.e. the lifespan increased effects can only be seen in a controlled lab environment - in the wild mTOR-inhibition to this degree would be a disadvantage).
I think therefore it is fair to say that the effects of caloric restriction on longevity are mediated by mTOR, but administration of rapamycin is not an equivalent treatment.

Update
Really great review came out last month (http://www.ncbi.nlm.nih.gov/pubmed/22500797) - I recommend you give that a skim if you want detail!

Please add some sources...

@inquilinekea - It is important to note that 'caloric restriction' is not actually a single process - there are different types (e.g. 'diluted' food, or alternatively eating every other day) that are mediated by distinct molecular mechanisms - some of which are mTOR, others may be IGF/insulin signaling (these effects are additive!) [Greer et al (2009) Different dietary restriction regimens extend lifespan by both independent and overlapping genetic pathways in C. elegans]


text:
Can I compare Shannon indices of metagenome gene data?
I'm comparing 12 Metagenomes. I'm using HMM counts of a number of proteins known to exists as groups within certain operons. I have grouped the HMM counts for each type of operon and calculated the Shannon-Weaver index for each Metagenome.
My question is: Can I compare these Indices? Is there a better test to use than Mann Whitney U test? I would like to do this on the ungrouped data, but I have many zeroes for some fields?

Coincidence? Or is this your cross posting? http://stats.stackexchange.com/questions/29542/estimating-diversity-of-operon-types-using-hmms-across-metagenomes-mann-whitney

It is... Thought it was more of a statistical problem, hence the cross posting, and elaborate explanation.

FYI: http://johncarlosbaez.wordpress.com/2012/06/01/information-geometry-part-9/

I'm not an expert on Shannon-Weaver Index, but according to wikipedia it is the same as exponentially transformed Renyi entropy. If it is the case, you can compare them since they are scale invariant summary statistics. If you want error bars, you can always try resampling methods such as bootstrapping. Hypothesis testing can also be done with bootstrapping, although the power of the statistical test may not be very strong and fail to reject the null.

It is fairly simple to normalize this measure by the number of observations, so you can have values in the 0-1 range at the end, which are way easier to compare.


text:
If body temperature is 37°C (98.6°F), why are most people more comfortable at around 21°C (70°F)?
It may be different for other people, but for me, anything above 32°C (90°F) is very uncomfortable, and my body is inclined to seek cooler temperatures.  But I would think that at 32°C, the body would have less work to do to get itself to 37°C.  So why is it not comfortable in those temperatures?
My theory is this, but I don't know if it's right:
The body's abilities for warming itself are much more sophisticated than its abilities for cooling itself (which are non-existent, possibly?). So it likes to be in an environment 20-30 degrees below optimal because it can easily handle that.  But up in the 32's and we're dangerously close to going over the optimal, and the body doesn't know how to get it back down after that, so we are inclined to seek safer temperatures.
Is it something like that?

not all animals require this body temperature - mammals have made some good business of assuming their bodies will all be at the same temperature and then warming themselves up to the right temperature.  as the others note there are biological warmers, but no biological refrigerators, so choosing a temperature above most weather conditions was a useful part of the strategy of being warm blooded ...

I refer you to the quora answer: http://www.quora.com/Temperature/Why-do-air-temperatures-in-the-low-70s-Fahrenheits-feel-comfortable-to-humans

I added more details. Check out!

@reopen The question also asks the reason why the skin temperature is lower than the core temperature. This is not dealt with in the linked question

The body can never stop working. If the body stops working, you die.
And while the body is working it cannot avoid generating heat.
Being in an environment somewhat colder than the body makes getting rid of this excess heat easier, and is thus more comfortable.
The body's abilities for warming itself are much more sophisticated than
its abilities for cooling itself (which are non-existent, possibly?).

The body can cool itself down by sweating.

Although in general this answer seems reasonable, I would like to see some references. What is the amount of heat generated by the body, say, when you're sleeping? Does it change during the day? Depending on the season? Is it actually that non-negligible (we are talking about a 16° difference here...)

It is quite a substantial amount of heat, and it is more when we are active so therefore more during the day. I don't have the resources available nor how to calculate those amounts.

Thermodynamically, your BMR goes nearly completely towards heat, as you do no work on the environment. I have a BMR of about 1800 kCal, so I need to lose all of that heat through my 2 square meters of skin every day. Some of that is insensible perspiration, and some of it is just conduction.

As a rule of thumb, a human produces roughly the same heat as a 100-watt light bulb.

@RussellBorogove that is, slightly less than 100 watts?

This is due to the fact that skin is the interface where heat is lost.
Our body due to constant functioning, produces heat constantly as a by-product (due to exothermic reaction of ATP break mainly). The excess heat needs to be conducted away from the body, or it will cause a decrease in the body metabolism to prevent temperature rise.
Heat is lost mainly through the skin by:

Sweating - Through evaporation
Radiation - As heat waves (IR rays - That's why IR camera captures people at night)
Conduction - Directly through objects that touch skin
Convection - Through air circulation

When the ambient temperature rises, the heat lost through radiation, conduction, and convection drastically decreases. And often when the temperature is high, there is a accompanying rise in the relative humidity which decreases the heat loss through sweating (as the amount of water vapor is high in the atmosphere, the sweat does not evaporate, so no heat is lost).
So the heat which is not lost is felt as the "hot sensation". It relieves by stopping any activity, seeking shade or a cool place, etc... all of which increases the heat lost or decreases the heat produced.

You have to note that the temperature of skin is lower than the body temperature.

The Skin temperature is lower than the core body temperature for two reasons:

The skin acts as a medium through which the external temperature is measured - as such the skin temperature is at equilibrium with the external temperature. The brain regulates the core-body temperature in response to temperature measured through skin. If a person is exposed suddenly to cold environment, skin looses much of its heat in the form of radiation (radiation is direclty proportional to the temperature difference) this will cause perception of cold and the body starts shivering even though no actual heat loss has occured from the core body thermal load (only skin looses heat, not the body core). The brain anticipates that the core will loose its heat when exposed to such low temperature for prolonged periods and starts the warming mechanism before the actual cooling occurs such that the cooling is either prevented or minimized. This is called Anticipatory control and the temperature of skin being close to the ambient temperature within physiological limits is needed for this.
Skin is the medium (almost the only medium) through which the excessive heat produced by the body core during activity is expelled. The skin temperature is lower so that a constant gradient can be created between the body core and body surface to maintain the flow of heat. (Heat losses through urine and feces is minimal)

For more details see this question. All the answers in this question are good and will increase your understanding of what actually happens.

This answer was merged from a different question, which was removed, hence why it does not seem to be fully cogent @user75673

Your body requires energy to function.  Just like in a powerplant, the energy comes from oxidizing fuel (food, instead of coal or gas).  The efficiency Of conversion is rather low, and results in excess heat, which must be rejected to the environment.  When it's cool, the heat is easily convected to the surrounding air.  When it's warmer, or you're producing more waste heat than can be rejected through simple convection, your body relies on evaporative cooling, i.e. sweating.
When it's very cold, the normal waste heat is not sufficient to keep you warm enough for normal bodily functions, so you shiver.  This is physical activity which your body performs solely to create waste heat, which warms you up.
There's an article about muscle efficiency on Wikipedia, indicating that the human body is about 25% efficient.  This means that about 75% of the energy consumed must be rejected as heat.

It may be different for other people, but for me, anything above 32°C
  (90°F) is very uncomfortable, and my body is inclined to seek cooler
  temperatures

I think you've rather nailed the key point here. I'm going to deduce from your question that you live in a temperate country? Every year, foreign students from India come over to my university in Leicester, UK. Even when the temperature is, to us, unpleasantly hot they will be shivering in their coats and complaining it's too cold. Similarly, were I to go over to India I'd be suffering in the heat while they're thinking it's a lovely comfortable temperature.
So, I believe, the answer is nothing to do with the ability of the body to maintain certain temperatures - you'd need to go considerably above 32°C or below 21°C to reach temperatures the body can't cope with - but rather a question of acclimatisation. You find 21°C comfortable and 32°C comfortable because that is the temperature that you've become used to. You can probably even recognise this from your own experience: I'm sure you've experienced days in spring feeling delightfully warm when days of the same actual temperature in autumn feel unpleasantly cold.


text:
If DNA has a half life of about 500 years, how can old seeds be planted?
According to this article, DNA has a half life of 512 years
Wikipedia claims that there are seeds planted as old as 31000 years
Doing the basic math $100 / (2^{30000/512})$ we get that only about
$2.2989191*10^{-16}%$ of the DNA would be left
So how do these plants still grow when replanted?

That half-life was for temperatures of 13.1ºC. In more ideal conditions, such as for temperature of −5 ºC or drier conditions, the half-life would be longer. The Wikpedia article in fact states that the seeds that were 31,000 years old were frozen under permafrost.
The original article estimates that the half-life at −5 ºC (for a 30 bp fragment of mtDNA from bone) would be 158,000 years. I'm not sure how well this data can be extrapolated to seeds.

For completeness, so flowing my math there would be 87.66% DNA reaming in the seed

The source paper for the article is this one: The half-life of DNA in bone: measuring decay kinetics in 158 dated fossils (available for free). The crux of their methodology is given in the abstract "By analysing mitochondrial DNA (mtDNA) from 158 radiocarbon-dated bones of the extinct New Zealand moa..."
So the article you linked is talking about DNA survival after cell death in fossilised bones. Seeds have not undergone cell death; they're still a small collection of living cells designed to survive in a state of near inactivity until the conditions are suitable for them to germinate. It's therefore not at all clear that we should expect the results from this experiment to generalise to seeds. Doubly so given that, as pointed out by Jonathan, the fossils were effectively held at around 13.1ºC whereas the seeds in the study you mention were found in the permafrost.
Finally, the seeds weren't viable on their own. It was only with significant intervention that scientists were able to get the embryos contained within the seeds to grow.

+1 for showing that the Materials and Methods section of an article is as important (if not more) than its Results section.

authors: Максим Караваев


text:
Which plants live for more than one year and less than two years?
What kinds of plants live for more than one year and less than two years? Are there any categorical or taxonomical names for such plants?

Are these homework questions? If so you should be tagging it as homework.  But please keep in mind that stackexchange sites aren't here to do your homework for you.

Hi @Problemaniac - welcome to the community.  As mentioned above please use the homework tag where possible.  Also, from a formatting standpoint the Q1/2/3 isn't necessary =)  Regarding the close motion on this question, I do agree that this is perhaps too localised.

@TimN I'm limited as to how many characters I can place in the edit approve reason box - I think that it should be up to the OP to remove the examples part of the question when and if the community closes it as too localised.  Without the removal of the middle point then the edit would meet the too minor category so unfortunately I couldn't approve it - please do keep submitting edits to other questions however =)

This is not from homework actually. I've found answers (see edit).

@Problemaniac finding answers yourself is absolutely fine =D  It might be a better idea to post them as answers rather than editing them into your question though, as this may be clearer to future people who may find this question by google for example.

The plants are called Biennial plants.
Examples would be carrots or dandelions.


text:
How long will a vegetable live for after being harvested?
I understand this might depend on the types of vegetables, but is there an average or studied specifics? Does it die immediately? Is there a way to precisely diagnose death in plants? If so, what are the conditions for it?

Great question :-)

The short answer is that as long as the vegetable/fruit is fresh looking - i.e. the cells have not disintegrated - they will be respiring, many cells will be functioning quite normally, and the plant is still technically alive. In cases where the part of the plant we treat as a vegetable is a part intended for reproduction (e.g. a seed, or a tuber like a potato) the plant will keep growing.
The point at which the plant dies is not clearly defined like it is in animals, but generally if you can still eat it, it's still alive.
Death in plants is quite different from that in animals - we refer to it as senescence. The key difference is that it happens to tissues and organs which can die and separate from the organism. Individual leaves can die without the plant's health being affected. Once this has happened to all the parts, the organism is considered dead, but if there is any respiring tissue left, it's still alive.

Thank you for the answer. As a followup question: when you say " the cells have not disintegrated - they will be respiring, many cells will be functioning quite normally, and the plant is still technically alive", how dos this differ from animals? Is it the case that supplies for plants are distributed to cells in a different way, in such a way that if the animal's death occur, no nutrients will reach the cells and therefore they will all die together with the animal?

@Hector That's exactly right: animals generally rely on the coordination of their processes by a central system, involving for example the nervous system and the circulatory system. Those systems are vulnerable to interruption, and that's what we call death in animals. Plants on the other hand do not have their essential processes coordinated centrally; they are controlled by environmental forces (gravity, thermodynamics, etc.) which generally are not subject to sudden termination.

To continue..  Because plants grow iteratively, by repeatedly generating similar parts, there is no individual organ which is essential to the functioning of the rest. Contrast that with the determined growth of animals, where there is one head and if the head is removed, nothing else can happen. The growth pattern and the control system are interrelated.

Very interesting. Thank you again for answering.

@Richard Smith, that is a very good answer, and I would vote it up, but unfortunately, I used all of my votes for today. Is the fleshy part of fruit alive?

@jmusser thanks! Yes, the fleshy part is alive, i.e. respiring until it starts to look necrotic or rotten.


text:
How does Golgi's neural histological stain work?
What is known about the targets of Golgi staining of neurons? Are larger neurons more likely to be stained? Are specific cell types more susceptible than others?
The current wikipedia article says the mechanism is still not fully understood. What is preventing us from using the advanced molecular biology techniques to understand the process?

Some background information.
First of all one should notice, that Golgi staining belongs to so-called morphological types of stainings in neuroscience, where the actual anatomy of different neurons is revealed (compared to other techniques, like Ca-imaging or potential imaging).
Second, Golgi staining is a type of silver staining, there the sedimentation of silver or its salts (here: silver chromate) reveals the morphological traits of the cels.
And, third, Golgi staining is applied to fixed preparation. This means that the tissue (normally a brain slice) is pre-treated (here: with formol) to kill all cells and arrest every biological process.
What is known about the targets.
The common description of the target is quoted as "a limited number of cells at random in their entirety". This is the essence of Golgi staining:

Only single cells are stained, therefore there is no impediment from adjacent cell staining while deriving the morphological structure of the cells (very important for light microscopy where you have integrated input from different depths).
The cells are stained randomly, there is no known preference among neuronal cells for Golgi staining and I haven't seen any other types of cells in CNS stained with Golgi, therefore it is quite specific for neuronal cells (and leaving macro- and microglia, astrocytes etc. intact).
The cells are stained in their entirety, meaning that the complete cell is stained very nicely, showing detailed arborisation of dendritic tree, that was very important in studying of Purkinje cells in cerebellum.

Are larger neurons more likely to be stained? Are specific cell types more susceptible than others?
Golgi staining is used mostly for brain slices (I have never seen or heard its application for other tissues). Traditionally one of the biggest cells here are pyramid neurons (NA, ACh-ergic) and one of the smallest are interneurons (often GABA-ergic) -- both are amenable to Golgi staining (reference) and there is no seemingly clusterization of stained cells by their size or transmitter type.
What is preventing us from using the advanced molecular biology techniques to understand the process?
I can name several reasons for this:

Since Golgi staining is applied to fixed preparation the tissue is already "damaged" (formol leads to dessication of cells and shrumping), therefore it is difficult to use some fine mollecular biology methods to investigate these tissues.
There is no way to tell which cells get stained beforehand. And as long as  the microcrystallisation of silver chromate is started it can't be (easily) stopped and reversed. Therefore it is difficult to look at what caused the staining afterwards, then the whole cell is impregnated with silver.
I think there were no real attempts to crack the mistery of this staining: how intersting it might be, this seems to be an interdisciplinary question on the brink between biology and chemistry. So, maybe one day somebody will look into it and explain everything.

Nice answer, but I'd take issue with the statement that Golgi stain is neuron specific.  Golgi method does stain glia, e.g. Ramon y Cajal's retinal drawings often include Muller glia: http://webvision.med.utah.edu/imageswv/CajalMuller.jpeg


text:
intravenous (IV) in the tail vein of an anaesthetized mouse
I trained myself to do intravenous injection on live mice. However, on anaesthetized mice you don't see the flux of your product showing that your injection was successful. In the same way, on live mouse a slight back pressure can be used to pull blood into the syringe to confirm proper placement in the vessel before injecting. On anaesthetized mice, I really have difficulty to obtain blood. All my following experiments rely on this injection, so I really need to be sure that the injection was successful and I have no choice that to do the injection on an anaesthetized mouse. Of course I warm the animals before injection to dilate the veins but I don't know how much I can warm an anaestethized mouse.
I thought to put a catheter before anesthetization the mouse but I don't know if it will stay in place until the mouse is anaestetized.
Do you have any tips?

@Rory M: I am not so sure zoology really is the best tag, but definitely I am puzzled by the cardiology tag.

@nico zoology was a simple replace of animals as it didn't exist.  Cardiology is just going on the tag-wiki description - "The study of the physiology and pathology of the cardiovascular system".  I agree that they aren't fully right yet though, any suggestions? =S

@RoryM: ok for zoology, but here we are speaking of a technique for injecting an animal, I do not see it so related to cardiovascular system... maybe a "techniques" tag?

I'm definitely supportive of a techniques/procedure tag, I think it's a helpful classifier

Cleaning the tail with ethanol is of some help and also, as you said, warming the tail. We sometimes put one of those flexible lamps (such as this) to heat up only the tail.
When anesthesized (ketamine/xylazine or isoflurane) we keep our mice on a heated pad anyways.
Cannulation in the tail does not sound like a good idea to me, especially if you are going to have the animal wake up afterwards. If you're going to cannulate then go for the jugular, but be aware that doing it on a mouse requires quite a bit of experience and it's definitely way longer than a tail injection.
It really depends on your experiment


text:
Has there ever been an attempt to create nutritionally tailored food for adult human consumption?
For all domestic animals, and for all animals kept in laboratory, complete and precise composition of perfect food is figured out (cat food, dog food, cattle, rats, laboratory monkeys and apes) -- which contains precise composition of carbs, fats, proteins, aminoacids, minerals and vitamins. Everything is known. Convenient dry cat/dog food contains exactly that. Animals are healthy on this food.
The composition is also known for human babies. This is manufactured as "baby formula". Everything baby's organism needs to be healthy (and to grow).
How let's take human adults.
Was ever attempt made to create "dry human 'dog-food'"? This sounds stupid, but there are emergency situation in which such food can come very useful.
So my question is, is there anything special in human biology that prevents creation of complete "dry human food" that contains everything our organism needs to be healthy ?
Or it was created but tasted so disgusting that nobody would eat it ?
Or it actually exist somewhere ? Just curious.

Why would it have to taste disgusting? Dog/cat/rat/etc. food does not seem to taste disgusting to dogs/cats/rats/etc. Anyway, soldiers have rations and astronauts too!

The Monkey Chow Diaries may be a relevant, if not entirely scientific, experiment.

Military must have tried to develop such things. What about military energy bar type rations?

@Memming: see links in my comment

Military has meals ready to eat (MRE) that come in a variety of flavors, but are quite far from the granule type dog food that you are thinking of

I think "monkey chow" is the answer. Note that in real labs and zoos, monkeys get a lot of their calories from monkey chow, but are still fed fresh vegetables to provide fiber, obscure phytonutrients, and entertainment.

I know this post is quite old, but more recently Huel appeared. This claims to be a complete food for humans.

Yes.  Rob Rhinehart has developed what he refers to as "a food substitute intended to supply all of a human body's daily nutritional needs, made from powdered starch, rice protein, olive oil, and raw chemical powders" which he calls Soylent.
It was developed and tested largely in 2013, crowdfunded late 2013, and is expected to start shipping in 2014. Tests of at least 30 days with no other food intake have been performed, though this is being marketed as a food and not a medical aid of any sort, so does not require FDA testing.
Even if this didn't exist, there are numerous "complete" human diet foods meant for medical use.  These are mentioned in an article about soylent:

Jay Mirtallo is a professor of pharmacy at Ohio State and the immediate past president of American Society for Parental Enteral Nutrition, which focuses on the science and practice of providing food to patients through both intravenous injections and feeding tubes. His main concern with Rhinehart's plan is that he's making the concoction himself, rather than buying it from reputable suppliers.
"He basically made medical food," Mirtallo says. "If he wanted to switch to a liquid diet, those are already available."
Indeed they are. Companies like Abbott Nutrition and NestléHealthScience sell dozens of medical food products, intended to be used by patients under medical supervision and administered intravenously, orally, or through an incision in the stomach.
"They’re very complex products, in terms of making sure you get them in a form that’s palatable but that stays in a form that’s bioavailable to the body," Mirtallo says. "Some of the products are very difficult to get into a liquid form and may lose their potency when they do that, or could interact with other substances that keep them from being absorbed completely."

Rob appears to be attempting to make a consumer version, and so far reports are positive.
But even if you don't trust Rob's mixture, there are countless medically complete nutritional foods that are FDA approved, though not generally available at the supermarket.

I'd like to know the difference in price between Soylent and the proper medical food from "reputable suppliers."

Shortest answer: there's nothing special in human biology, you could totally make it
Short answer: Bachelor chow!

I would totally buy this stuff if they made it. The closest I have now to bland, flavorless, zero thought/effort food is Wheaties.
longer answer:
Seriously though, dogfood for humans wouldn't be that hard to make. If you just took everything from the RDI guidelines (the Recommended Daily Intake from which they calculate the percentages you find on food labels) and mashed it all together into a thick brown paste you would get all of the macro and micro nutrients that you theoretically require. Precise proportions are irrelevant because:
a) everyone is a little different, and
b) to some extent, our bodies are able to fine tune our digestive tracts to fit our specific diets (presumably this tuning would occur even faster if you ate the exact same thing for every meal). You're a mammalian omnivore. Enjoy it!
You probably shouldn't try to live on something like this for the rest of your life, since there's plenty of research suggesting that there are other micronutrients, such as phytocompounds (i.e. plant stuffs), that are poorly understood but may be beneficial to humans. One thing to note here is that any health claims about any antioxidant that is not on the list of essential vitamins (vitamin C is an antioxidant on the list) are almost certainly bunk and/or hokum.
The upshot is that you would only need, at most, utterly minuscule quantities of these miscellaneous micronutrients. You would be fine(ish) for at least a few months. For related reasons, your statement:

The composition is also known for human babies. This is manufactured as "baby formula". Everything baby's organism needs to be healthy (and to grow).

is largely correct but somewhat flawed. While it is true that many babies are raised solely on formula and subsequently turn out just fine, there are some things that you can only get from mother's milk. For example, the mother passes on components of her own immune system to her baby through her milk, which then help to strengthen the baby's own immune system. These are the kind of subtle but useful compounds which are encountered in a "natural" diet but which could never realistically be included in people chow.

I think you do not cover the aspect of whether such thing would be bearable -- by taste.

@Andrei By asking about the "bearability" of the taste you're veering away from biology and towards psychology. Here's how I think about it: I don't know if you've ever owned a dog before, but they like people food. A lot. And the more devious members of the species will scheme quite a bit to get at it. In general, though, their only two options are dogfood or starvation. Under those conditions I'm sure that most people would also grow acclimated to the taste.

@Andrei Getting into the psychology side of it, the current consensus among researchers these days is that it takes about two months of daily repetition for a human to establish a behavior as a habit. At that point, even if the behavior is somewhat arduous/painful, it becomes more natural for the person to continue with it than to cease.

@tel: related (unanswered so far) question: http://skeptics.stackexchange.com/questions/7985/does-it-take-21-days-to-form-a-habit

According to @Ilmari Karonen's comment and link, I have the answer. Such food does exist. However a person who tried to eat it and nothing else could bear it for only 7 days. He had cravings for "normal" food. The link was http://www.angryman.ca/monkey.html. Apparently the guy had weak will, but that's normal.

there are of course foods for bodybuilders and for weightgainers and losers, never seen just one food containing all (and I activly searched for it) but you can create your own mix if you buy some protein suplements (that are usaly made from whey and other byproducts that have a good ratio of the various essencial aminoacids) or just soyabeans that also have good aminoacid ratios and is cheaper; some carb rich foods and those complete vitamin/mineral suplements + essencial fattyacids (ie: cods liver oil). only problem is finding a trully complete vitamin/mineral supplement. I've searched in vain thus far.

It's absolutely doable. Humans aren't magic and their nutritional needs aren't unknowable. Taste would be an issue at the first generation, but that wouldn't be a issue going forward anymore than it was for early immigrants leaving old foods behind and learn to love the foods their new environment offered. Legal issues would inevitable arise when statistically significant variations among different groups eating different formulations are found, i.e. formulation 1 eaters have more arthritis than formulation 2 eaters while formulation 2 eaters live slightly shorter arthritis free lives. You get the idea. Ultimately, it will be the only way to sustainably support our ever increasing population. And, just like some pregnant women eat clay, man will occasionally add other nutrients to their own diet. It's important to understand humans don't have the most complex nutritional needs compared to our entire bionomy. We just have the ability to create the most diverse tastes to meet our completely normal needs.

Welcome. Can you add sources to your claims? It looks more of a personal opinion than a scientific answer.


text:
Descendants of dinosaurs
It is commonly accepted that birds are descendants of dinosaurs. It is nice that not all dinosaurs died out.
Are there other animals, descendants of dinosaurs,
 that survived ? (Maybe not till our time, but survived the time when most dinosaurs died).
By the way, what made flying dinosaurs survive and not die like other dinosaurs?

The fact that you do not limit answers to extant decendents makes this very hard to answer.  The taxonomic group "dinosaur" was on the earth for millions of years, so the answer will depend on where you start counting decendents.

Looks like Aves are the only ones that survived to the modern day. https://en.wikipedia.org/wiki/Dinosaur_classification

It is very hard to answer your second question since we still don't know for certain what made most of the dinosaurs/reptiles disappear.

Are you trying to understand if reptiles like lizards are descended from dinosaurs?

No. No other group found in the fossil record after the K-T boundary (the extinction "event") descends from dinosaurs.
It is likely that the extinction event was not itself instantaneous so if you wanted to be extremely picky you could argue that small numbers of individuals survived the K-T boundary but, apart from birds, none of these survivors went on to form long lasting lineages.
Non-avian dinosaurs that survived the extinction event are referred to as "palaeocene dinosaurs", there are some links on Wikipedia that might interest you.
You can see a diagram linking vertebrate groups here, similar diagrams can be found in most evolution texts.

Do you have good standard reference on dinosaur extinction at hand to back this up, e.g. a review paper (I'm not doubting it, just curious to read myself)?


text:
Why would diffusion be faster across a non-specialised tissue?
The standard protocol for a person experiencing chest pains is to chew a 300mg aspirin tablet, the argument being that chewing rather than swallowing the tablet results in the aspirin entering the blood stream faster.
From a biological standpoint, why is this the case?  Given that the stomach and GI tract are specialised tissues to allow for maximum diffusion, why would it be faster to pass aspirin across the gums (bucaal administration?) tongue and cheeks which are not specialised for this purpose?
It is not just a special case for aspirin either, as HypostopTM/GlucogelTM (acute treatment for hypoglycaemic shock, essentially concentrated sugar) is applied directly to the gums or cheek with a similar argument that in critical situations it is faster.
The only suggestion I could find was  very vague from the "Merck Manual":

The stomach has a relatively large epithelial surface, but its thick mucous layer and short transit time limit absorption
  Which I assume could mean that it is the reduced absorption rate in the stomach that makes the oral membranes faster, yet it also says that the delay in the stomach is brief.

I'd be really interested to know the biology behind this!

I don't have time to write a complete answer now. I will write one out later if no one beats me to it but note that the stomach is not specialized for absorption.  Only very limited absorption occurs upstream of the small intestine.  The key is that chewing greatly increases the surface area of the tablet, which speeds its dissolution and absorption across the mucosa.

Substances absorbed in intestine have to pass through the liver, maybe this cause the delay. See Wikipedia: Hepatic portal system

I had not even considered the mechanical action of chewing - how ridiculous!  However, it doesn't fully explain the difference as Hypostop is a gel and still preferentially applied directly into the mouth rather than being swallowed.

why would you by a pound of chopped ice rather than a single 1 pound cube of ice?

I think surface area is by far the dominant factor: the medical recommendation doesn't say you shouldn't swallow the tablet, only that you should chew it first. A well chewed anything is digested faster than an unchewed anything.

There are several issues here:
1) Any mucous membrane is a specialized tissue for absorption.
Mucous membranes are indeed not so good for passive diffusion, that makes them absolutely perfect tools for active absorption of certain substances, almost independently from the membrane type. To provide some examples: many drugs like cocaine are inhaled and absorbed in nasal cavities, whereas the rectum is also known and favorite delivery way for medicines.
Generally the absorption force of the mucous membrane is dependent upon how well it is vasculated, for after going through the basal membrane the substance directly enters the blood flow and quickly travels away, thus the concentration gradient on both sides of the basal membrane -- the main barrier in mucosa -- remains relatively high.
See  Bhat P. 1995. The limiting role of mucus in drug absorption: Drug permeation through mucus solution for an experimental model for this statement.
2) Mouth mucosa can absorb many substances.
There is a special term called "oral absorption" to describe the rapid drug absorption into blood flow from the mouth cavity. The mucous membrane is not specialized here, but small molecules are able to permeate here through all barriers.
3) Advantages of oral absorption.
There are some:

The mucous membrane in the mouth cavity is very highly vascularized. The whole mouth can be seen as a bundle of skeletal muscles and every muscle requires a lot of energy and oxygen, therefore they have one of the highest vascularity rates, having much less distance between single capillaries.
Blood flow is higher in the mouth cavity walls than in other inner organs. This is mostly because muscle contractions (during chewing) lead to increased propulsion of blood through capillaries and small vessels here.
Any substance that enters blood flow here bypasses the hepatic-portal system. This means that the substance does not have to wait until it is filtered by our liver, it is immediately distributed through the whole body.
There are special reflexes from oral mucosa to inner organs. Even not so important in case of aspirin, this is very important for some placebo drugs like methyl valerate (known as "Validol" in many countries) used a lot for treating angina pectoris whose only action is to activate the cold receptors in mouth and thereby leading to reflectory dilating of cardiac vessels.

This is why many drugs, like for example loperamid, are administered only as sub-lingual tablets. And this also explains why in emergency medicine many remedies are injected directly into the tongue.

"And this also explains why in emergency medicine many remedies are injected directly into the tongue." Ahhhh!

It would also be logical to note that a chewed tablet increases its surface-area-to-volume ratio for absorption relative to an intact tablet, for any absorptive tissue.

From an engineering point of view, if you chew it the surface area will be enlarged. For example, you take 2 containers with water and 2 tablets which will dissolve in this water. If you crumble one tablet, the take up rate (flux) will be much higher due to the enlarged surface area of the tablet. If you add mixing to the concept, the flux will increase even more. Therefore, in the same amount of stomach fluid there will be a higher concentration of medicine which can be taken up by the body.


text:
Have there been any experiments that duplicate chromosome copies from 23*2 to 23*3 or 23*4?
Deinococcus radiodurans is an amazing bacterium with a fantastic survival rate. It can survive to high doses of radiation, in a complete vacuum and in hydrochloric acid.
How does this bacterium manage to restore damaged chromosome?
It is polyploid with 4 to 10 copies of the genome which are packed in a highly ordered manner.
Does this imply that creating multiple copies of the genome or inceasing DNA base repair activity would increase life span?
Is that even conceivable on bigger life forms?

Could you please try to clarify your question, I have a hard time understanding what exactly you are trying to ask.

I have tried to edit your question. I still can't understand what you are asking. Do you believe that simply increasing ploidity will boost life span?

Upon reading the article: yes seems rigid packaging, no less important than the number of copies of the genome. Over time, the chromosomes are scattered and pile

Polyploidy works out in certain lineages, most famously in plants, but mammals aren't one of them. https://en.wikipedia.org/wiki/Polyploid#Animals

It's an idea that doesn't hold much promise.
Individuals who show diploid/tetraploid mosaicism present "failure to thrive and multiple minor anomalies." according to:

Alonso L et al (2002) Tetraploid/diploid mosaicism: case report and review of the literature. Annales de Genetique 45 177-180

On the other hand, complete tetraploidy is apparently lethal:

Nakamura, Y. et al. (2003) A Tetraploid Liveborn Neonate: Cytogenetic and Autopsy Findings. Archives of Pathology & Laboratory Medicine 127:1612-1614.
Abstract
Cytogenetic and autopsy findings of a nonmosaic tetraploid male neonate, alive until shortly after birth at 37 weeks' gestation, are described. Oligohydramnios, intrauterine growth retardation, cranial abnormalities, and Dandy-Walker malformation were noted prenatally. Autopsy findings included cleft lip and palate; overlapping fingers; low-set ears; simian creases; hypoplastic external genitalia with undescended testes; Dandy-Walker malformation; slightly dilated lateral and third ventricles; hypoplasia of the cerebrum, pons, medulla, pituitary gland, thymus, lung, adrenal gland, and kidney; large ventricular septal defect; and enteric cyst behind the urinary bladder. The placenta was hypoplastic and showed no remarkable abnormalities, except for mild syncytial knots. Chromosome analyses of amniotic fluid cells at 31 weeks' gestation and the umbilical cord blood cells at delivery revealed a 92,XXYY karyotype. G-, C-, Q-, and N-banding heteromorphic studies demonstrated duplication of paternal chromosomes 1, 3, and 15, and maternal chromosome 22. In addition, the results of an analysis with 16 CA repeat polymorphic markers were consistent with duplicated inheritance of 1 paternal and 1 maternal haploid sets to the tetraploid patient. Therefore, it is most likely that the tetraploidy was caused by a cytoplasmic cleavage failure at the first mitotic division.

full text available here.


text:
Why don't flies avoid the motorway?
Flies have a short lifespan, therefore evolution should technically happen over a shorter period of time (years).
Flies die all the time from getting hit by cars on the motorway.
Those flies that don't go near the motorways have a greater chance of reproducing.
If this was an advantage (motorway avoidance = not dying), shouldn't more and more flies be avoiding the motorway?
Cars have been around since, roughly ~1950. That's 60 years.
Why don't flies avoid the motorway?

Again, this kind of question is down-voted? As with this question there is an answer! In fact this is a semi-duplicate?

I agree and upvoted, though it might be nice if we had an FAQ as this sort of question pops up regularly...  evolution and biology is hard to get an entree.

"in the long run we're all dead men" - John Keynes
First is the fact that flies have adapted their way around cars long long ago by giving up longevity for faster breeding; flies are cheap and they just don't care if they get hit by a car.  The average flying insect lays large clutches of eggs - hundreds at a go is common.  See this reference on butterflies as an example.  In table 2 the potential fecundity (FEC) is I believe the number of eggs laid in a lifetime.  The smallest number is 53, the largest is 1500, the average is hundreds.  As long as one or two fly from each lifetime of breeding survives, the species holds on just fine, more and there is a population explosion.
Another side of the question is:

It would still be an advantage to be smart and stay off the road wouldn't it?  If they adapt so quickly why doesn't a mutant braniac fly come along that can see the cars and in short order all flies would have this trait... its just selection too, right?

The answer there is that not everything is available to adaption.   Flies could become that smart, heck maybe even smarter than us, but they have lots of pressure on them from many things they could do well, and their system is already doing many things very well enough for them to survive as they are without making such a large change that might require some short term disadvantages that prevent them from becoming entirely different animals.  The essay "why pigs don't have wings" is a pretty good reading for a longer more detailed answer.
Where I live its temperate and there is a good amount of water- lots of food and hospitable for all kinds of plants and animals can thrive here. On the hillsides where updraft currents blow flying insects.  The spiders 'figured this out' and the bushes and trees are often covered with cobwebs on this side of a house.  The flies don't avoid the wind just because so many of them are eaten - they would not themselves be able to mate or eat.
Note that the spiders haven't become 'smart' - just lucky to have landed in that area.  But then there are many many spiders there that they probably don't get a lot more food than a spider living on the other side of the house who has the only web for a space of several cubic feet.
Everything balances itself out in a competitive landscape because there are so many other living things ready to take advantage of a break like this.  Cars just aren't enough to budge the other things the flies have to watch out for. For more reading about how competition affects evolution read about the Red Queen and the Tangled bank.

i just saw this article.  moths are starting to avoid light.  it only took them about 120 years of electricity!  https://www.nytimes.com/2024/04/19/science/moths-light-attracted.html

Flies can and do evolve quickly thanks to a short generational time. However, your question seems to stem from a misunderstanding of what evolution entails.
Evolution occurs when the genome mutates. Why it mutates isn't particularly relevant, but a gene (or genes) mutates and as a result of that mutation a characteristic of the organism changes. It doesn't have to be a big change. Maybe a single protein somewhere operates 2% less efficiently, giving practically no outward signs of evolution. Sometimes it can be big - changes in coloration, changes in sensory perception, lifespan, etc.
In order for mutations (beneficial or detrimental) to have a significant effect across an entire population, the population itself has to be fairly small or the mutation has to give a large advantage over the old version.
Flies are not avoiding motorways because a mutation that specifically codes "AVOID CARS" is going to be very unlikely given that it would you would first have to encode what a "CAR" is in order to avoid it. That probably won't happen because on the time scale that evolution usually acts over very large populations (which flies have) we won't be driving cars by the time necessary for deaths due to cars has a serious effect.
Flies have huge populations and breed extremely quickly, so even if a few million are killed by cars, it doesn't put a dent in their population numbers. There's no reason for the change to occur. Combined with the extreme difficulty of actually encoding a gene specific to cars, the odds are it just won't happen in any realistic time-frame.

Wouldn't it be possible for the genome to mutate so flies avoid darker areas (i.e. black roads (not straight away but darker through generations)). These flies would be more successful. But I agree with your second point even if a few million are killed by cars, it doesn't put a dent in their population numbers

Sure, it's possible for the genome to mutate that way, but if you're just avoiding 'dark areas' then you're also avoiding natural 'dark areas' and not avoiding all of the light-colored roads made of concrete.
What's possible isn't so much the crux - there are very complex occurrences in the genome, but unless there's a big impact it's just not favored.

I second @Blundell here. There is no need for a concept of CAR in order to have a behavioural change that results in CAR AVOIDANCE. I think this is a misunderstanding of how evolution works (which I encounter in laymen very often) and downvoted this answer.

@luispedro: the essence of the answer does not change. You may not need to encode car, you may not need to encode car avoidance... the fact is: being smashed by cars is not really a big problem for flies, as the proportion of flies that dies like that is most probably very small. Actually, encoding for "avoid big objects that move" may even be negative, because, for instance, flies love to go on wild stinky animals... :)

@nico: Yes, the "irrelevancy" argument might be sufficient. That does not justify using a very wrong argument about how evolution could not generate a CAR AVOIDANCE behaviour. If that paragraph is removed, I will remove the downvote.

I also got an answer via email that I think is worth sharing.
Mrs Price:
I'm not answering officially as I’m probably wrong but…
The main point mentioned is that because flies have such a short
lifespan, so they should evolve faster than elephants or other slow
growing species.  While this is true, and there are many examples of r
(ruderal) species evolving rapidly* evolution is not a predictable or
sensible process, and there are many other factors that contribute to
evolution other than a short generation time.
One main question to consider is… how many flies are there?  And how
much of that population is affected by the road fatalities?  Whilst
there are over 23,000 insect species in the UK, your question
specifically concerned flies so… An average fly lives for around 35
days and can lay roughly 750 eggs in her lifetime, so fly numbers are
bloody huge!  Although a small proportion of flies may be killed by a
car, the proportion will be so small as to make no impact to the
overall population; therefore the driver for evolution is not strong
enough to have an impact on the species as a whole.
Another reason why motorway deaths may not have a significant impact
on the fly population is due to when the flies breed.  Even if
motorways killed 90% of all flies, the fact that many insects breed
hours after hatching from their egg means that the population is still
able to reproduce.  Killing something after it has bred is again not a
driver for evolution, it would have to be a very strong force that
kills a high number of individuals before they have chance to breed.
In summary, motorway deaths affect such a small amount of individuals
that it does not have a significant impact upon their populations, I
imagine that many many more of them get killed in spider webs each
day, however the idiots are still flying into those too!
Hope this helps :)

*The peppered moth changed colour from mottled to black due to the
population from the industrial revolution and then to white once the
air pollution had cleared as the ones that stood out had such a high
predation rate
*in the last 50 years some fish species have evolved a much smaller
body size due to the advantage of escaping through a net and being
able to carry on breeding


text:
Do dolphins really sleep?
I have always wondered, if dolphins sleep with one eye opened, do they really sleep at all?
According to this article dolphins indeed shut down their brains.
I already googled it. No help from wikipedia or other articles and publications found.

Of course we should note that our brain does not "shut down" (whatever that means) when we sleep.

I'd say that unihemispheric sleep and adaptations like it really are sleep - the brain activity on one side of the brain gives a characteristic sleep pattern.  It certainly must satisfy the needs of an aquatic mammal like a dolphin or a whale since they have to be partially conscious to breathe by surfacing regularly.
It does seem to affect the brain physiology, but is there a reason you would not call it sleep?

I suppose that it depends on how sleep is defined. If we define it a a mechanism by which the brain repairs itself in an altered state, then, yes they do indeed sleep. Just not with all of their brain at once.


text:
Why are plant cells rectangular and animal cells spherical shaped?
Is that because the plant cells have cell walls and animal cells don't, or is there a function performed by the different shapes? Perhaps round shapes assist the movement of cells?

Quite a few, perhaps even the majority, of animal cells are not round/spherical.  For extreme examples, consider neurons & astrocytes, muscle cells, etc.  Even blood cells aren't spherical, but disk-shaped.

@jamesqf - That is the basis for a good answer.

Animal cells
Generally all (animal) cells have different shapes because they do different things. Each cell type has a specific role which it has to play in order to assist the body in working efficiently and functionally. Thus their shape supports them to carry out these roles effectively.
Look at (animal cells):

Neurones
Photoreceptors
Immune Cells

Plant cells
They are often square shaped/rectangular because it is easier to build a "brick wall" (cell wall) out of rectangular bricks.  Any structure that minimises interstitial space will hence allow more "life", thus possibly making it stronger.
This is also due to:

Plant cells are not necessarily square, but they due tend to have distinct edges and be somewhat rectangular. This structure is caused by the cell wall which is very rigid and therefore forces the cell to have a defined shape.

However there is one exception I could think of, and those are pavement cells, they're neither round nor somewhat spherically shaped. Pavement cells are a cell type found in the outermost epidermal layer of plants.

Sources:

Beckett, B. S. Biology: A Modern Introduction. Oxford: Oxford UP, 1976. Print.
http://www.academia.edu/3786570/Plant_Cell
Rappaport, R. Cytokinesis in Animal Cells. Cambridge: Cambridge UP, 2005. Print.
http://biology.about.com/od/cellbiology/ss/plant-cell.htm
https://www.msu.edu/~whymerky/CellS&Funitplan.htm


text:
Blood clumping in mosquitos
Will a mosquito die due to blood clumping if it sucks blood from two people who have different blood groups? What will happen in its gut? Is there any mechanism to avoid clumping? Or do mosquitoes know what group it should suck?

Mosquitoes are not affected by blood clumping as they have to digest blood (cells, proteins, etc.) to assimilate them.

Female mosquitoes need blood for laying their eggs. This actually means that they need a source of rich protein and iron for their kids and hence, prey on us.
It is worthwhile for us to pause here and ponder over the difference between clumping and clotting before proceeding to the actual answer.
Agglutination tests as you may have come across are essentially antigen antibody reactions visible to the naked eye. Antibodies and antigens (on the RBCs) bind leading to the clumping that you talk of.
Clotting on the other hand is a complex set of reactions involving the thrombins and the platelets.
When a person is transfused of a wrong blood type, as in blood of another group is injected into his blood, something very bad is ought to happen. The clumping is extensive (an immune reaction) which leads to a clotting reaction, leading to a condition called DIC (Disseminated Intravascular Coagulation). This is an emergency situation since there can even be Acute Kidney failure.
Coming to the mosquito,

In the human case, we injected into the blood. Here it gets into the gut. The gut has enzymes which breaks down the proteins. Theres no antibody no antigen left out there!! Proteolytic enzymes start right from the very beginning.
Even if some clumping occurs, it doesn't actually matter. It mattered in the human case since it was a transfusion and the sequelae mattered.
Another important thing to keep in mind is we are talking only of clumping and not clotting. The mosquito takes care of clotting by secreting anticoagulants into the blood stream right when it is ready to have it meal. Clumping on the other hand, per se, doesn't turn the blood into a clot. If you have seen blood clumping in agglutination test, its not such a dramatic thing to occur. The blood still stays in liquidy. So clumping wouldn't pose much of a problem.

Hope this helps! Sorry but the climax wasn't that dramatic :)

interesting answer... do you have some citations/preferred sources so users can read more?

Maybe I could add that mosquitoes digest the blood before biting again, assuming they got all they needed in the first place