Why are haploid cancer cells not killed by immune system? I have seen haploid cancer cells (I think it was leukemia cells) in a lab.

Sperms and eggs are haploid but are not destroyed by the body because they are protected by other cells surrounding them.

My questions :

How are haploid and diploid cells differentiated by our immune system ?
Why are the haploid cancer cells not killed ? I know I could as well ask why any cancer cells are not killed but I want to know if there is anything specific about these cells ?
How are these cells generated ? (By meiosis ?!)

Now that I did some research on this, it seems to be a very rare condition of acute lymphoblastic leukemia (ALL), see this article:"Chromosomes and causation of human cancer and leukemia. XLVII. severe hypodiploidy and chromosome conglomerations in ALL.".
This article ("Origin of near-haploidy in malignant hematopoietic cells.") hypothesizes that this might happen through gradual chromosome loss during cancer formation and that in the end one clone with a lower than normal number of chromosomes.

This seems connected to a much worse outcome of the cancer than for hyperdiploidies (more chromosomes than normal). See the "Atlas of Genetics and Cytogenetics in Oncology and Haematology".
They also define why haploid (or near haploid means: Less than thirty chromosomes, down to 23 have been observed). This is not the normal haploidy found in germ cells. Se also "Isolation and Characterization of a Near-Haploid Human Cell Line".

Since these chromosomal changes occur inside the nucleus I think this is mostly invisible to the immune system - so there is probably no difference how these cells escape the immune system compared to other cancer cells. I think its possible that due to the chromosomal loss some proteins which control apoptosis are lost, so the cells escape this fate as well.
Regarding the immune question, you can either start with the following articles or simply go over to Pubmed and choose some articles. In this field there is a lot of research going on.

Does the immune system see tumor as foreign or self?
The tumor microenvironment and its role in promoting tumor growth
Tumor Evasion from T Cell Surveillance

If there are access problems, let me know.


How is in-vitro fertilization technically achieved? I failed searching on Google technical details about how in-vitro fertilization is achieved. I'm referring to the toolset and its use, rather than the chemical or biological aspects of the process. I often watch on TV how a needle penetrates into a human egg to fertilize it with sperm, but provided that a human egg sizes about 100 microns, I come up with the following questions:

Do there really exist needles so thin to penetrate a 100 micron cell? In such case, how are these needles manipulated without breaking or losing them in the lab?
How do technicians manipulate the needle with such micrometric precision?
How do technicians keep the human egg still so they can break into it with the needle without pushing the egg away?

Not sure if these questions sound naive, but I haven't been able to find any simple answer to them on the Internet.

After following user David's hints, I have collected some videos that answer the questions I posted:

Regarding to needle manufacturing, there exist machines able to create micropipettes (this is how the needles are actually called) by heating glass cilinders and pulling them to create very thin tubes (capillaries). Click for featuring video.
Regarding to the high-precision manipulation, technicians use mechanical devices able to convert macroscopic motion (eg: human manipulation) to microscopic motion (eg: using reduction gears). Click for featuring video.
Regarding to how they keep the egg still, technicians use another type of pipette that slightly "sucks" the egg in a vaccuum-cleaner style. For a full-feature video of how the egg and sperm are manipulated, check this video out.


Are trees the only source of large amounts of oxygen? Trees use carbon dioxide and produce oxygen in the presence of sunlight.

But is there any other source?

If yes, are trees the most important source of oxygen, or is there any other source which produce more than trees do?

71% of the earth's surface is taken up by water. Not surprisingly therefore, the seas are an important source of oxygen. National Geographic claims that photosynthesis by phytoplankton (mostly single-celled phototrophs, such as cyanobacteria, green algae and diatoms) account for half of the earth's oxygen production. The other half, they claim, is produced on land by trees, shrubs, grasses, and other plants.

The Ecology Global Network takes it a step further and claims that all marine plants (including phytoplankton) together produce 70 to 80 percent of the oxygen in the atmosphere.

Based on these reports, hence, marine phototrophs account for 50 - 80% of the earth's oxygen production.

With regard to terrestrial oxygen production, NASA reports that 30% of the land is covered by trees, and as much as 45 percent of the carbon stored on land is tied up in forests. So on land, trees are definitely large contributors to oxygen production.


Why do we weigh less in the morning? At first I thought it may be related to physics.  You know, in one half of the day, the gravity changes, and the scale shows a different weight than the other.  Then at night, gravity intensifies, and you become slightly heavier.

But I'm a bit skeptical about that. Is that true?  That it's somehow related to gravitational fields?

Veritasium created an excellent video just on this topic, which I would recommend watching, but will summarize here.

A common misconception is that we lose weight when we digest food or burn calories. Keep in mind that that broken down food and those calories* aren't "going anywhere", so technically you shouldn't loose any mass (unless you get rid of the molecules by going to the restroom).

However, in the "informal" tests done by Derek Muller, he lost about 250 grams each night. Since during the night you sweat (which evaporates or gets absorbed into the sheets and blankets), he estimated that about 150 grams was lost through perspiration and breathing out water vapor.

The more surprising loss of mass, was 0.012 grams of carbon lost with each breath when breathing in oxygen, and then breathing out carbon dioxide. Although this seems like a tiny loss, assuming you breathe in and out about 7,680 times each night, that tiny mass loss adds up to almost 100 grams of weight loss through breathing alone.

I guess health magazines should start running articles like "Top way to lose more weight? Researchers say breathe more!"


Why does BLAST reduce word size for short proteins? I'm using BLAST to identify a short protein (BLASTp). If I check the short query then the word size reduces from 3 to 2. However the search will then be less reliable right? Because reducing the word size increases the chance of finding matches? So my instinct would be to raise the word size to almost the whole length of the query, because with a short query you want to search really specific to reduce output results, so apparently I'm missing something.

So I hope someone can explain me why reducing the word size from 3 to 2 is better for short proteins while using BLASTp

No, the search won't be less reliable. It will only be more sensitive, more capable of finding matches. To understand this, you need to understand how the BLAST algorithm works, what the word size means.

When you use a word size of $N$, BLAST starts by looking for a match of length $N$ between your query and target sequences. If such a match is found, BLAST then attempts to extend the match as far as possible. So, for example, consider these two sequences:

> query
CRKKL
> target
CRAKL

As you can see, they are quite similar:

query           CRKKL
target          CRAKL
                ** **

Now, what happens if you try to find the target sequence with BLAST using the query sequence and a word size of 2 ($N=2$)? BLAST will take the first
$N$ characters of the query and try to match them against the target:

CR
CR
**

It will then try to extend:

CRK
CRA
**

It will find a gap and apply the gap penalty, but continue matching since the next characters match1, thereby increasing the overall score of the alignment:

CRKK
CRAK
** *

And so on and so forth. BLAST starts by matching the first $N$-sized word and then attempts to extend the alignment.

Now, what if we were using $N=3$?

CRK
CRA
**

Because the word size is now 3, we need at least three matching residues to match in order to attempt to extend the alignment. Since there is no 3-letter match, the target is missed.

So, decreasing the word size is better for finding small protein matches because it can use shorter matching sequences as an alignment seed.
As a general rule, playing with the word size is a question of finding the right balance between specificity and sensitivity. Decreasing the word size helps you find more matches (increases sensitivity) but it will also find more divergent sequences (decrease specificity). Increasing the word size will reduce the number of matches (decrease sensitivity) because you need a longer perfect match to start extending the alignment, but will increase specificity for the same reason.

If you raise the word size to something close to the size of the query, you will only find almost exact matches. That might be what you want to do and it is what algorithms like BLAT which are designed to find near exact matches (for example, mapping a sequence to the genome it came from) do. Usually, however, we want less than perfect matches since we are looking for homologous sequences and not the exact same query. In such cases, we will decrease the word size for smaller proteins to increase our chances of finding homologs.

1 This is a bit of a simplification. The rules for extending alignments are a more complex but it serves to illustrate the point.


When do 3 germ layers form in embryo? And why is there only one mature egg formed? During the process of pregnancy, when do the 3 germ layers form in embryo? Is it after formation of gastrula? Also, during oogenesis, why does only one mature egg form? Why don't use polar body egg instead? During oogenesis, is there a crossing over occurring? If yes, at which stage?

I'll bifurcate the question and answer each part one at a time.

Germ layer formation: Gastrulation is a phase early in the embryonic development of most animals, during which the single-layered blastula is reorganized into a trilaminar ("three-layered") structure known as the gastrula. These three germ layers are known as the ectoderm, mesoderm, and endoderm i.e. the layers are formed with gastrula, or simply gastrula is the structure which contains these 3 layers.1

Polar body egg: Polar bodies generally don't have the ability to get fertilized as they are just residual parts of oogenesis. They are formed just to maintain haploid number in oocyte, so they don't even get sufficient amount of cytoplasm to survive (most of the cytoplasm is given to oocyte to provide nourishment to embryo). So they apoptose and disappear, but in some cases (like this), they are considered important and can even lead to unusual phenomena like polar body twinning, in which twinning occurs when the egg cell and polar body are both fertilized by separate sperms.2.

Cross over: In oogenesis (or specifically, ootidogenesis), cross over occurs during the conversion of primary oocyte to secondary oocyte and first polar body. Meiosis I of ootidogenesis begins during embryonic development, but halts in the diplotene stage of prophase I until puberty. For those primary oocytes that continue to develop in each menstrual cycle, during puberty, synapsis occurs and tetrads form, enabling chromosomal crossover to occur. As a result of meiosis I, the primary oocyte develops into the secondary oocyte and the first polar body.3

(In mammals, the first polar body normally disintegrates before dividing, so only two polar bodies are produced.)

References:

https://en.wikipedia.org/wiki/Gastrulation
https://en.wikipedia.org/wiki/Polar_body
https://en.wikipedia.org/wiki/Oogenesis
Polar bodies—more a lack of understanding than a lack of respect
Rare Forms of Twinning


Why does human facial and head hair continue to grow? Many people can grow extremely long head hair and facial hair. Are there evolutionary theories as to why this is the case? It seems like having long hair could be a disadvantage, and extremely long hair seems to be rare in other mammals.

How humans evolved to have head / beard hair that continues to grow longer than other animals is a topic that many anthropologists & biologists are still not sure about & there is no general consensus as to "why" yet.

The three main views that I am aware of however are :

1) Evolution of the "Aquatic Ape." (Ingram, 2000: Morgan 1997; 1982)

Infants, in order to hold onto their mothers in the water, would latch onto her hair. Limiting separation from the mother & increasing chances of survivability
Longer hair meant that infants / small children would need to swim less in order to get to their mother
Believed to be supported even further when you consider that aquatic mammals are almost always hairless, indicating that at one point, humans were highly "aquatic" mammals.

2) No real benefit, but used as a tool for "mate selection." (Darwin, 1871; Cooper 1971)

The view held by many of the Darwin school of thought (I do not mean that as a derogatory), is that at first, "hairiness" was sexually attractive, but eventually "hairlessness" became more sexually attractive in most places (i.e. the face to see facial expressions & socialize better; Wong & Simmons 2001)
A sign of "virility" & "health" as can be seen in the mate-selection behavior of lions. Which is true even today as human diagnostic material for health (Klevay, 1972).

3) Practical evolutionary benefits for the human species specifically

A lot of body heat escapes from the head, probably the most important part of your body. Hair is a good insulator that can keep in heat. This increases survivability in colder climates. (Wong & Simmons 2001; Bubenick 2003). (A disputed but considered credible reason, especially when you compare hair length and types across different regions throughout history)
Protection against damaging UV rays (while still permitting adequate Vit.D3 to come through) & some protection from free-radicals or other harmful particles. Because we became bi-pedal, the head was the main area exposed to the sun (as well as some of our back). Extending hair's usefulness to even hot environments, while other body hair became less important with the development of sweat glands (Wheeler 1985).
Heightened "Situational Awareness" through "Touch sense." A concept that may seem silly at first but has some evidence to support the theory. Though the hair is not "alive," it is connected to the follicles & your nerves. In a nutshell, it may help to increase "sensory awareness" & "data gathering" of your environment, which would favor longer hair. This would be an asset in survivability (Kardong 2002; keratin.com 2010; Sabah 1974; washington.edu)
Though not a collegiate Journal article, if reasonably credible, this small article is an interesting case for supporting hair & "Touch sense" in "recent history" & in combat-survival : http://www.sott.net/article/234783-The-Truth-About-Hair-and-Why-Indians-Would-Keep-Their-Hair-Long.

I personally lean 90% "Evolutionary benefits" & 10% "Mate selection" as to reasons why humans' hair continues to grow longer than other animals. Beard & head.

Hope this info was a little helpful.
There are copious amounts of other respectable articles on each point, but I only referenced a few.


Do slime mold expand or multiply? After reading about slime mold I was wondering, do slime mold simply expand outwards or multiply?
e.g. if I put 100 grams of slime mold in 1 location, will it expand to say, 2 locations, and have the 1st location with 80 grams left, and 2nd location with 20 grams (i.e total 100 grams), or is it that they multiply; 1st location still 100 grams, and 2nd location with 20 grams?

The answer is that they will do either or both, depending on conditions: this is one of the things that has caused complex systems scientists to be so interested in things like using slime molds in modeling optimization problems.
In good nutritional conditions, the cells will happily multiply. At the same time, they will flow and reshape themselves to spread and migrate in search of food when nutrients are not uniform.


How and when did sex evolve? As I know evolution comes bit by bit mutation by mutation

How sex evolved which requires a major change in at least two individuals one to become male and one to become female ?

When that happened as we can see sex in all animals and most plants?

Sex (depending on how you define it), evolved very early (more than a billion years ago). Even species like yeast have a type of "sex" (see below).

Also, this doesn't mean there is necessarily a big difference between the two sexes.

The yeast Saccharomyces cerevisiae, for example, also has two "sexes", called mating types. One is called alpha and the other is called a. They can only mate if they have different mating types, so it is analogous in a way to mammalian sex. However, the genetic difference between these two types is tiny. There's a specific location in the genome that's called the MAT locus. This location can have either an alpha sequence or an a sequence, an that will determine the sex. The rest of the genome will be the same between sexes.

So it really doesn't seem like it is a huge evolutionary step to go from no sex to some simple version of sex.

See more details about yeast mating here.

Also see this wikipedia article on the evolution of sexual reproduction.


Why can bacteria resist topical antibiotics, but not compounds like Benzoyl Peroxide? I excerpt from p 2 of 4, but p 4 of 4 reviews the entire article by Debra Jaliman, MD on Apr 17 2014.

Usually, topical antibiotics aren't recommended alone as an acne treatment, as they can increase the risk for antibiotic resistance in skin bacteria. However, using benzoyl peroxide with a topical antibiotic may reduce the chances of developing antibiotic resistance.
[Source:] Substances that kill acne bacteria by inflammation, such as benzoyl peroxide, oil of cloves, and chlorhexidine gluconate. Bacteria don’t develop resistance to these treatments, but they don’t kill as many bacteria, either.

If topical antibiotics can cause antibiotic resistance, why can't compounds like benzyl peroxide? I ask in general about other bactericide, not just benzyl peroxide.

Antibiotics ARE compounds, and they kill or inhibit the growth of bacteria by specific mechanisms. Each class of antibiotics has specific mechanism of actions. Given enough exposure to these antibiotics compounds, bacteria can develop specific molecular mechanism to nullify their effect, and hence antibiotics resistance. Antibiotics resistance will eventually develop with enough exposure to drive the organism's evolution . Whereas there are combination therapy, there are multi-drug resistance; whereas there are wonder drug, there are super bug.

General disinfectant compounds such as benzoyl peroxide or sodium dodecyl sulfate (in soap and detergent) have no specific molecular target that would differentiate host and intruders and hence can harm bacteria as much as the host cells. They are safe to use only because you have skin to prevent their intake. Since there is no molecular target to mutate to develop resistance, the resistance to general disinfectant will simply take a very long time.

That is to say, who could ensure bacteria cannot develop resistance to benzoyl peroxide? Resistance to phenyl derivative has long been reported [1], and bacterial catalase can easily break down the damaging effect of peroxide.

[1] Heinz Berger and Orville Wyss. J of Bacteriology (1953) vol. 65 p.103


Can you say "screening for a" in English? I know this is not a "Correct Use of English Forum" but I'm afraid that people from outside the field won't be able to properly answer my question.

Would it be correct to say "screening for a long peptide capable of killing Gram-positive bacteria"? Or you just have to turn the word "screening" into a noun like: "preparing a screening for a long peptide capable of killing Gram-positive bacteria"?

The last one doesn't seem right to me at all, but I'm not sure since I'm not a native speaker :(

Thank you for your time!

"Screening" can be a verb here ("we screen for the long peptide") so your first sentence would be correct.

Even in this biological context this might still be a question better fit for the English/Learning English forums though.


can a bacterium cell become a cancer? I don't mean if a bacterium can be the cause of cancer inside a human. But can actually a bacterium changes in the way as normal cells change into tumor cells?
So gaining such characteristics of a tumor cell and if inside human body create a tumor mass?

You ask two questions:

If a bacteria can get the same characteristics as tumor cells.
If such "bacterial tumor cells" actually can form a "tumor" within the
human body.

I assume that your question is not if bacteria can change in such a way that the can be confused with eukaryotic cells. This they cannot do. Bacteria cannot form organelles. Because they have no organelles they are solely dependent on their membrane for energy production. Because the surface area to volume ratio decreases with cell size there is a physical possible maximum size for bacteria. Here is some more in depth info on the subject.

So what characteristics can bacteria then have that tumor cells also have?
Well, according to wikipedia, a tumor is a mass of abnormal and excessively grown tissue (neoplasm) which may or may not be malignant. According to this definition bacteria could be tumor-like if the could form tissue and if this tissue could then grow abnormally or excessive.

And guess what? If you define tissue as "an ensemble of similar cells and their extracellular matrix from the same origin that together carry out a specific function." like Wikipedia does. Then you could argue that the biofilms some bacteria form are quite tissue-like since biofilms also contain an extracellular matrix, the cells within have the same origin and (in some cases) the bacteria can have differentiated functions.

However, the fact that bacteria can form biofilms does not make them tumor like. For that comparison to work mutated bacteria should be able to outgrow the rest of the biofilm. And while mutation that cause noncooperative/cheating/abnormally growing bacteria in biofilm are known, this kind of mutations cause the biofilm as a whole to grow slower. (source) In this sense comparing a biofilm to a colony of ants may be more appropriate than comparing it to tissue.

So to answer your questions:

Bacteria can form tissue-like formations, but when members of this formation do not cooperate anymore this typically leads to less growth, instead of increased growth.
Biofilms do form within humans. For example the bacterium Pseudomonas aeruginosa is assosiated with cystic fibrosis. And while cheaters exist among these bacteria, biofilms with high ratios of cheaters have a lower fitness. see this paper Therefor you would expect most biofilm within humans to be more tissue-like and less tumor-like.


Can any animals photosynthesize? Plants and animals have the following distinct properties:

Plants live from solar energy by photosynthesis, they use solar energy to make sugar and oxygen out of carbon dioxide, which gives them energy. Animals live from the sugar and oxygen plants created and produce carbon dioxide for their energy.
Animals can move across the planet while plants are tied to the ground.

Clearly, animals have a harder time to survive with no plants within their reach than plants have without animals coming close. This is logical because solar energy is always there while plants are not.

So my question is: Are there animals that can do photosynthesis? It's obvious that an animal with plant-like stateliness would be non-beneficial since it relies on eating other plants for it's energy and there may not always be plants within reach from it's spot.

But animals using the sun and carbon dioxide for energy production does not sound so stupid.

Night animals could also gather energy in their sleep.
Much easier than plants, animals could make sure nothing blocks their sunlight.
Many animals go through periods of hunger because food is scarce, for some of them this period is paired with high sunlight levels. (the dry season f.e.) (EDIT: This is just an idea, of course photosynthesis requires water, which is absent in the dry season. But still, in warm period with enough water, there's sometimes too much animals to feed from the available vegeation.)

Some things I already took into consideration:

I know that plants, because they are small in mass (compared to the area with which they can collect sunlight) and static, don't need nearly as much energy as animals do. Is this the main reason?
I know that f.e. reptiles, but in fact all cold-blooded animals, already use the sun's energy. But they only use the heat from the sun to warm their bodies, they don't photosynthesize.

There are 5 answers, all "yes" (though the first one is disputable).

First: there exists at least one animal which can produce its own chlorophyll:

A green sea slug appears to be part animal, part plant. It's the first critter discovered to produce the plant pigment chlorophyll.
The sea slugs live in salt marshes in New England and Canada. In addition to burglarizing the genes needed to make the green pigment chlorophyll, the slugs also steal tiny cell parts called chloroplasts, which they use to conduct photosynthesis. The chloroplasts use the chlorophyl to convert sunlight into energy, just as plants do, eliminating the need to eat food to gain energy.

The slug in the article appears to be Elysia chlorotica.

Elysia chlorotica is one of the "solar-powered sea slugs", utilizing solar energy via chloroplasts from its algal food. It lives in a subcellular endosymbiotic relationship with chloroplasts of the marine heterokont alga Vaucheria litorea.

UPDATE: As per @Teige's comment, this finding is somewhat disputable.

Second, animals need not produce their own Chlorophyll, and instead symbiotically host organisms that use Photosynthetis - e.g.  algae and cyanobacteria. This approach is called Photosynthetic symbioses.

Overall, 27 (49%) of the 55 eukaryotic groups identified by Baldauf (2003) have representatives which possess photosynthetic symbionts or their derivatives, the plastids. These include the three major groups of multicellular eukaryotes: the plants, which are derivatives of the most ancient symbiosis between eukaryotes and cyanobacteria; the fungi, many of which are lichenized with algae or cyanobacteria; and the animals. We, the authors, and probably many readers were taught that animals do not photosynthesize. This statement is true in the sense that the lineage giving rise to animals did not possess plastids, but false in the wider sense: many animals photosynthesize through symbiosis with algae or cyanobacteria.

Please note that while most organisms known for this are fungi, and some rare invertebrates (corals, clams, jellyfish, sponges, sea anemones), there is at least one example of vertebrate like this - spotted salamander (Ambystoma maculatum)

Non-chlorophyll synthesis

A 2010 study by researchers at Tel Aviv University discovered that the Oriental hornet (Vespa orientalis) converts sunlight into electric power using a pigment called xanthopterin. This is the first scientific evidence of a member of the animal kingdom engaging in photosynthesis, according to Wikipedia.

Another discovery from 2010 is possibly a second piece of evidence:

University of Arizona biologists researcher Nancy Moran and Tyler Jarvik discovered that pea aphids can make their own carotenoids, like a plant. “What happened is a fungal gene got into an aphid and was copied,” said Moran in a press release.

Their research article is http://www.sciencemag.org/content/328/5978/624, and they did not consider it conclusive:

The team warns that more research will be needed before we can be sure that aphids truly have photosynthesis-like abilities.

Third, depending on how you understand Photosynthesis, you can include other chemical reactions converting sunlight energy.
If the answer is "usual 6H2O + 6CO2 ----------> C6H12O6+ 6O2 reaction done via chlorophyll", then see answers #1,#2.
But if you simply literally translate the term (synthesizing new molecules using light), then you can ALSO include the process of generating Vitamin D from exposure to sunlight that
humans do thanks to cholesterol (link)

Non-biological answer.

As a side bonus, Ophiocordyceps sinensis is referred to as half-animal half-plant (not very scientifically IMHO). But it doesn't do photosynthesis.


Why is dimethyltryptamine (DMT) being released during death? I'm not very well informed about all the things related to biology and the current achievements of science in this field so if I'm wrong in anything I say, please let me know.

Many times I've come across a theory that the meaning of life itself is procreation - we simply live in order to make our species exist as long as possible. In the light of this theory, units like homosexuals or infertile people are totally useless and there's no really reason for them to exist from biological point of view. Though it's pretty obvious that in order to make us want to reproduce, something like joy of having sexual intercourse and life in general has been created. That's why units who only lack in ability to reproduce do live and most of the time they're fine.

Evolution doing adjustments in us in order to make us feel happy during our life seems to be understandable, but what about death? I've read that during death, a larger amount of DMT substance is being released in the brain - compound which is known from it's psychedelic effects, which in most cases are euphoric. It looks like we're not meant to feel 'bad' while dying, which is nice, but my question is - is it known why? What could be the evolutionary reason to create this mechanism? The unit which is about to die is not going to be useful anymore, so why bother? I'd like to somehow understand logic behind this.

The issue I suspect you are struggling with is the anthropomorphization of the evolutionary process.  Evolution is an optimization process driven by random mechanisms...i.e. there is often not a "reason" for why certain things are the way they are.  Evolution is not a conscious "designer" that produces things with a specific goal in mind...it simply "picks" the best random alteration and enhances it.  If there is no "best mutation", then there is no selection pressure to drive change overtime.

For example, one can ask, "Why do humans have 5 fingers on each hand, instead of 6 or 4?"  There is no answer, because the question itself is nonsensical.  Humans have 5 fingers simply because there is no pressure to drive a change to 6 or fingers, and so it boils down to randomness.  There is no "reason" humans have 2 arms, as opposed to 4.  That particular trait just randomly happened to be the one which became dominant.

So, to return to your question of "Why does the brain release DMT when dying?", the answer is that there IS no answer.  There is no selection pressure for or against that trait, it just happens.  As to the mechanism itself, I suspect that there is just a global breakdown of function in the brain, leading to a dump of ALL neurotransmitters.  When the reuptake pumps fail, the neurons just dump their contents into the extracellular space.  The result is pleasant hallucinations, giving the impression that humans are not "meant" to feel pain when dying.  Imposing that kind of rationale, however, is simply creating meaning out of chaos.  If you watch TV static long enough, your mind will start to see patterns which aren't there, simply because the human mind is "wired" to find patterns in chaos in order to better understand the environment.

To wrap this up, I suppose the answer to your question is that the brain is finding meaning in meaninglessness, simply because that is what the brain does.  We look for patterns to make sense out of our environment, which sometimes leads to spurious conclusions.  There is no reason that the brain hallucinates when dying, but there IS a reason that this trait appears to be a built-in mechanism.

I hope I was able to shed some light on the issue.  Or at the very least, not confuse you further :D


Are human fetuses more likely to be male? Question: From a physiological point of view, when sex is determined in a human fetus, is it equally likely to be male or female?

Studies in this area typically measure age at birth, where the data would have already been biased.  There's a slight imbalance in the human sex ratio, in that there's an overall tendency towards males.  However, this could be accounted for in numerous ways, such as abortion.

Fisher's principle suggests there would be an evolutionary tendency towards 50:50 chance.

The Fisher's principle is not applicable to the fetuses because it has been formulated for parental expenditure and basically states that the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1.

There are several mechanisms that we can use and that are mentioned in the canonical paper by James (2007):

  (a) there are equal numbers of X and Y chromosomes in mammalian sperms
  (b) X and Y stand equal chance of achieving conception
  (c)
  therefore equal number of male and female zygotes are formed, and that
  (d) therefore any variation of sex ratio at birth is due to sex
  selection between conception and birth.

James brings much evidence that none of these conventional beliefs is true. Rather, they are dependent upon many factors: exposure to stress during pregnancy, glucose level etc. He reports that there is an excess of males at birth in almost all human populations, and the natural sex ratio at birth is usually between 1.02 and 1.08. However, the ratio may deviate significantly from this range for natural reasons. (I really recommend reading the paper I linked, it is available for free).

Branum et al (2009) analyze birth statistics in the US taking into account many factors like ethnicity, gestational age and plurality and show that the ratio can increase even more with growing gestational age and has different values among different races.

So, taking everything together, I can say thay YES, the chances for human fetuses to be male are indeed higher.


Is it safe to look indirectly at the Sun? I.e., is exposure of sunlight onto the peripheral vision less damaging than exposure onto the fovea?

Behar-Cohen et al. notes the periphery of the cornea has a focusing effect:

  UVR incident from the periphery is refracted into the eye, and due to the focusing effect of the cornea, UV radiation is on average 22-fold stronger at the nasal limbus, which is the typical site for pterygium and pinguecula. Moreover, UV radiation is on average eight times stronger at the nasal lens cortex, the typical site for cortical cataract.

Authors note this in further papers as peripheral light focusing. Essentially, the light is refracted from the periphery of the cornea into the anterior segment of the eye. By this notion, I'd say indirectly looking at the sun is no less damaging than directly looking at it (given there are no other restrictions, such as special lenses, etc.).


Can androgen-insensitive genetic-males get pregnant? According to the linked report, people with androgen insensitivity syndrome appear as male, but have both feminine and masculine outer genitalia.

However, I was not able to find out whether their internal reproductive system is functional, i.e., if these people have a functional uterus.

Is it possible for such a person to get pregnant?

Short answer
People with androgen insensitivity syndrome do not have a functional uterus and cannot bear a child.

Background
Androgen-insensitive genetic males may develop female genitalia and internal female reproductive organs. However, in both partial androgen insensitivity syndrome (PAIS) and complete androgen insensitivity syndrome (CAIS) the uterus is absent, or is present only in a rudimentary form.

The reason for the absence, or rudimentary form of the uterus is the fact that Mullerian inhibiting substance (MIS), produced by the Sertoli cells of the fetal testes is present. MIS controls the regression of the mullerian ducts, and in its absence in XX females, the mullerian system develops into the uterus, oviducts, and upper vagina. However, in XY individuals with CAIS (and likely also with PAIS), MIS is produced normally by the testes resulting in inhibition of the growth of the uterus and fallopian tubes (Oakes et al., 2008).

Reference
- Oakes et al., J Pediatr Adolesc Gynecol (2008); 21: 305-10


What did the ancestors of textile moths eat? These days I had to wrestle a lot with textile moths. From the Internet I got the impression that these moths don’t feed on naturally available furs in the wild, but have specialised on man made textiles(?). From the Wikipedia entry on textiles I gather humans started wearing textiles (not furs) about 6500 years ago.

Did the ancestors of textile moths (from the time of textile adoption) feed on furs and such, or were they akin to today’s kitchen moths, which eat food stuffs?

In the latter case, is not 8500 years a very small time for such a fundamental change in animal biology? Or must I take into account the short lifespan of insects, equating each human year to a dozen generations and each human generation to about 300 moth generations, so that the change moths can undergo in 6500 years is more akin to that humans can undergo in 250.000 years (which perhaps has to be increased even further due to moth simplicity and large population making non lethal mutation more common) ? For comparison, it appears Homo  Sapiens emerged some 200.000 years ago.

Modern textile moths actually eat a wide variety of material, including fur, feathers, shed exoskeletons, bran, and grain. humans just pay more attention to them when they eat textiles. They prefer human handled material because we tend to create larger concentrations than occur in nature.

if you are interested in changes in biology in response to humans you may want to look at starch digestion in dogs, nylon eating bacteria, and body lice.


Do humans secrete and detect pheremones? Many animal species are capapble of secreting and also detecting pheremones from members of the same species, which relay messages and signals such as indicating sexual readiness.

Do humans do the same thing? Are humans capable of communicating in this subconscious fashion?

Yes, humans can secrete and sense pheromones, e.g. female tears dampen male sexual arousal.

Science 2011, 331(6014), 226-230

But then on the other hand, a key gene in mouse sex specific behavior (TRPC2) is a pseudogene, i.e. it is inactive, in humans.

Nature 2007, 448, 1009-1014

If you look at the references in those papers you will probably find a lot more examples.


How does coffee cause calcium loss in our body? Recently on radio a doctor advices to reduce the consumption of coffee as it leads to calcium loss(as my mother described). My initial response was: How could such thing be possible? What kind of experiment have been done to assure that the coffee is the cause and not something else? But then I found this article on internet, though it doesn't go into depth of the topic. So I'm wondering :

How does coffee cause calcium loss?
What is the related chemical reaction?
Does it just happen in intestine or elsewhere in the body?
What amount of coffee consumption would make it severe?

Caffeine and coffee do not seem to have any significant adverse effect on calcium metabolism. The supposed mechanisms are inhibition of calcium absorption in the intestine and stimulation of calcium excretion in the kidneys.

Effects of caffeine on bone and the calcium economy (Food and Chemical Toxicology, Journal, 2002):

  Caffeine-containing beverage consumption has been reported to be
  associated with reduced bone mass and increased fracture risk in some,
  but not most, observational studies. Human physiological studies and
  controlled balance studies show a clear but only a very small
  depressant effect of caffeine itself on intestinal calcium absorption,
  and no effect on total 24-h urinary calcium excretion. The
  epidemiologic studies showing a negative effect may be explained in
  part by an inverse relationship between consumption of milk and
  caffeine-containing beverages. Low calcium intake is clearly linked
  to skeletal fragility, and it is likely that a high caffeine intake is
  often a marker for a low calcium intake. The negative effect of
  caffeine on calcium absorption is small enough to be fully offset by
  as little as 1-2 tablespoons of milk. All of the observations
  implicating caffeine-containing beverages as a risk factor for
  osteoporosis have been made in populations consuming substantially
  less than optimal calcium intakes. There is no evidence that
  caffeine has any harmful effect on bone status or on the calcium
  economy in individuals who ingest the currently recommended daily
  allowances of calcium.

The Association between Coffee Consumption and Bone Status in Young Adult Males according to Calcium Intake Level (Clinical Nutrition Research, 2016):

  This study analyzed and compared the BMD [bone mineral density] and
  bone metabolism markers according to coffee intake in Korean young
  adult men aged 19-26 years. No significant associations were found
  between current coffee consumption level in Korean young men, and bone
  status and metabolism according to the calcium intake levels.


How many proteins on PDB have unknown function? I was wondering how many of the files in the Protein Data Bank (PDB) have unknown function. The only paper I can find from an internet search is this one from 2012, which I assume might be outdated. I’d welcome suggestions of how to find this information for myself.

The article cited in the question indicates that the authors searched the PDB with the term “unknown function”. There is nothing special about this — you just type in the standard search field and hit ‘Go’. I conducted a search of this type myself:

http://www.rcsb.org/pdb/results/results.do?tabtoshow=Current&qrid=91CA3A5F

Which returned 4384 structures out of approx. 149,600 in the data bank.

Of course, it is evident from the first page of the results that the number of unique proteins is smaller than this because a single study may examine different forms of the same protein.

I admit that I was surprised to find that people had spent time and money determining the structure of so many proteins of unknown function, but it appears that there is at least one blanket initiative to determine the structures of bacterial proteins of unknown functions because of their roles as potential pathogens. The idea would seem to be that they even if their mechanism of pathogenicity is unknown they could still be targeted on the basis of their structure.


Is a gametophyte a spore? The male and female gametophytes are pollen and embryo sacs respectively. I wondered if they are spores as their brethren are meiospores.

No.
But close.  Very close.  Basically, a gametophyte is a spore that has / is undergoing mitotic division.  Therefore, it is still haploid, having not undergone fertilization yet, but it is no longer a dormant, unicellular spore; it's passed into the new phase of gametophyte.
The gametophyte produces sexual organs which produce the gametes that will actually be used in fertilization.  Two gametes fuse, at which point, a diploid cell is produced (called a zygote, just as in animals).

The meiospores are the spores you see in the picture on the far left: they are dormant, unicellular, haploid spores, which will turn into the gametophytes.  (meio + spores; spores that have undergone meiosis)

Sources:

Meiospore, Biology Online
Gametophyte, Wikipedia
Plant Life Cycles, Developmental Biology, 6th ed.
Spore, Wikipedia


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?

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


Who compared developmental biology to crystallography? I need to find out the name of a nineteenth century biologist who compared developmental biology to crystallography. His idea was that crystals are formed from 'cells' (defined molecular units) that bond together to form arrays. In living organisms cells are bound together but the rules that form the structures change as the organism grows, especially in animals, which is why we have different organs. In both cases you have units that coalesce undirected but according to rules to form structures. I remember finding out about this biologist from a documentary which also showed illustrations from the book he wrote on the subject. I can't find his name or that of his book using a web search because it's too obscure and that would only work with the correct terms. Does anyone know anything about this?

The idea to compare biologic cells and crystal is mostly related to a German physiologist Theodor Schwann (1810-1882):

His work "Microscopic researches on the Conformity in Structure and Growth Between Animals and Plants, 1839 relates to this idea.

  He believed that new cells form principally outside pre-existing
  cells, and wanted to draw an analogy to crystal formation.

another source:

  The cell is the unit of structure, physiology, and organization in
  living things. The cell retains a dual existence as a distinct entity
  and a building block in the construction of organisms. Cells form by
  free-cell formation, similar to the formation of crystals (spontaneous
  generation).

(other related scientists are Schleiden, Virchow, Muller).


Do rare earth metals actually repel sharks? Stroud claims that sharks are effectively repelled by the use of rare earth metals in the water. There has even been a patent issued by the same author for rare earth-wrapped fish hooks to reduce the shark by-catch.

Apparently these metals work by generating an electric current that repels sharks via the shark's electric sensing organ.

Is the repellent action of rare earth metals scientifically confirmed? And if so would it be effective even on the largest and aggressive white sharks?

Also if effective why haven't dive equipment manufacturers developed shark repellent devices for sport divers?

Short answer
Electropositive metals such as the Lanthanides generate electrical currents when they come in contact with (sea) water. This electrical activity may repel sharks by over-stimulating their lateral line organ. However, the effectiveness of lanthanides as shark repellent depends on many factors. For example, hungry sharks, or sharks engaged in a feeding frenzy may simply ignore the stimulus altogether.

Background
Rare earth metals are Lanthanides - metals with a low electronegativity. Metals with low electronegativity are called electropositive. Electropositive metals (EPMs) react vigorously with water when immersed and generate electrical potentials that are thought to overstimulate the sharks’ highly sensitive electroreceptors, the ampullae of Lorenzini.

Many electropositive metals fall in groups I and II of the periodic table and explosively react with water. Examples include sodium and lithium. The Lanthanides, on the other hand, contain some less reactive elements.

There is in fact a considerable body of primary literature on the use of EPMs to deter sharks, because the by-catch of sharks is a recognized problem of modern fishery. However, much of this literature shows very mixed results of EPMs, and therefore I have based my (second :-) answer attempt on a recent review article by Hart and Collin (2015), which is available on-line and cites some fifteen primary research articles on the topic:

EPMs are primarily intended as a mechanism to reduce shark bycatch and catch depredation in longline fisheries, without affecting the catch of non-electrosensitive target teleost fishes. As you indicate in the question, EPMs can be formed into shapes that are easily attached to a fishing line or hook.

Early tests in the laboratory with captive sharks showed that several EPMs (including magnesium and rare-earth lanthanide elements such as cerium, lanthanum, neodymium and praseodymium) were effective in repelling various shark species. However, more recently, several studies showed no such repellent effects other species of shark, and it was shown that aversive behavior was highly dependent on various factors such as duration of food deprivation prior to testing. Specifically, hungry sharks ignored the EPM, especially when feeding in groups (feeding frenzies).

The results of field trials with EPMs were also mixed, with some studies showing a reduction in the catch rate of various shark species, while other studies showed no such effect. The authors of the review article summarize a range of factors that may influence the efficacy of EPMs in repelling sharks, including the type of EPM used, the relative sensitivity of the electrosensory system, shark density and competition, hunger level, and differences in feeding ecology. Other impediments to large-scale adoption of EPM technology by commercial fisheries include the relatively high cost of the rare-earth metals (although magnesium may represent a cheaper alternative), potential toxicity to other marine animals, and the fact that they dissolve rapidly in seawater and, therefore, must be replaced frequently. The use of EPMs for personal shark deterrent devices is also hampered by the limited effective range (<85 cm) of the electrical field they generate.

Instead, for use in scuba dive gear a rechargeable battery-powered capacitor-discharge unit connected to two or four electrodes is sufficient as shark repellent. Also, electro-magnetic induction using permanent magnets may be a more suitable alternative (Hart and Collin, 2015).

Regarding the great white: this shark has a lateral line featuring ampullae of Lorenzini, so EPMs may repel it, theoretically.

Reference
- Hart & Collin. Integrative Zoology; 10(1): 38–64


Do individual mammal hairs absorb water? In my look into the world of shaving I've seen claims that it is better to shave after a shower because the hairs will absorb water and soften, making the shave easier. Likewise, I've seen it claimed that natural hair brushes (i.e. boar and badger hair brushes) should be soaked before use. My question is: do the hair fibers actually absorb water, presumably thickening in the process, or does the water just adsorb onto the surface (maybe lifting the scales in the cuticle) meaning you can wet hair in aggregate, but it doesn't soften when soaked? Especially, is there a side-by-side comparison of a single hair under a microscope before and after soaking showing what happens?

Researching this answer took me to some strange literature, but it appears to suggest a little bit of both (at least for human hair, which is porous, implying that some water can suffuse through the cuticle into the cortex). For example this paper looks at the impact of this effect on drug testing.

There's also a few papers in cosmetics science journals describing various elements and effects of increased hair porosity, but I was unable to find one primary citation which characterised the trait.


What species is this mammal? I saw a mammal that looked like a large squirrel. I haven't seen anything quite like it. Can you help me identify it?

Squirrel-like, "hunched over" posture.
It was too large to be an eastern squirrel—approximately 2.5 feet, from nose to tail.
It had a fluffy tail like an eastern squirrel, not short and rat-like like a ferret.
Black face with white nose, body was chestnut-brown.
I saw this on the ground, not in a tree.
I saw it in a pine forest in east-central Alabama.
At one point, it sat up on its hind legs.

It sounds pretty much like a fox squirrel (or better: as masked face fox squirrel which are found in Alabama).
They look like this (taken from this website):

There seems to be quite some variation in terms of fur color, some animals are more greyish:

Taken from here, this website also contains some additional information.


Glycerol 3-phosphate nomenclature Why is Glycerol 3-phosphate named in such way? Shouldn't it be named as Glycerol 1-phosphate by proper IUPAC- nomenclature?

You're right, according to standard rules of nomenclature it would be called glycerol 1-phosphate. It comes back to the outdated D/L configuration nomenclature. A more thorough explanation is quoted below.

  When the R/S system (sequence rule) is applied, substitution of one of the primary hydroxyl groups often leads to changes in the configurational prefix, thus obscuring chemical and biogenetical relationships; it is generally inapplicable to the steric description of such mixtures as occur in triacy1glycerols isolated from natural sources. The stereospecific numbering of glycerol and its derivatives as proposed by Hirschmann [9], described above and in 1, avoids these difficulties; it has proved useful and is widely accepted.

Source.


Why are both glucagon and cortisol released in hypoglycemia? Cortisol is released in response to prolonged stresses; one situation when cortisol is released is when blood glucose level is low. In this situation cortisol acts on adipose tissue promoting fatty acid mobilization, and also promotes gluconeogenesis by degrading muscle proteins and converting them into pyruvate. Cortisol also stimulates gluconeogenesis by increasing the expression of PEP Carboxykinase the enzyme of gluconeogenensis pathway promoting the TCA Cycle intermediates or Oxaloacetate to convert into Phosphoenolpyruvate and promoting gluconeogenesis to balance the blood glucose level.

These are the same effects produced by glucagon to increase the blood glucose level when it is low.

My question then is what is the need for release of Cortisol? Also, if its release is important to control other pathways I haven't mentioned here, then why does cortisol produce the same effects as glucagon? Why is glucagon alone not enough to maintain blood glucose level?

Since the ability to utilize glucose for energy is necessary for life (look at the effect of hypoglycemia on brain function, for example), it makes sense that the regulation of serum glucose concentration would have a number of pathways, that is, redundancy helps to ensure continued proper function should one of the regulatory mechanisms fail.

Glucagon is considered the main physiological response to hypoglycemia; however, epinephrine, growth hormone, and cortisol - in that order - and very probably other factors yet to be named/elucidated also help to increase plasma glucose when it drops.

This kind of redundancy is very common. Cortisol, epinephrine and growth hormone all have other effects on tissue unrelated to glucose as well.

Glucose Counterregulatory Responses to Hypoglycemia


What are good practices with reusing desalting columns At least according to a few sources Prozyme and Protocols-Online, it is possible to reuse desalting columns and since I'm cheap I would like to also.

Key things seem to be washing with several column volumes of your buffer of choice. Also certain columns like crosslinked desalting columns are not amenable to regeneration. I'm curious about other factors.

I'm mainly using Bio-Rad micro-spins

Regardless of what protocol you use, and what the advertised efficacy of that protocol might be, in any situation like this I think the important thing to consider is: what would happen if the material taken from a re-used column was contaminated by a previous application? Can you live with the consequences of such contamination?

If you are preparing DNA for further use (PCR and/or cloning and/or transformation) then you run the risk of propagating a contaminant through subsequent steps and getting into a real mess. I worked in a lab once where one postgrad ended up spending several weeks working with a cloned fragment that was actually derived from someone else's work in the same lab (although not due to re-use of a column as far as I remember).

If you are preparing protein samples then the risks are possibly reduced, but if the protein sample is going to be subjected to sensitive methods (blotting, MS) then again, could get messy.


How good are the hematologic parameters (e,g, IL6 or others) in predicting which patients will develop a severe COVID-19 disease? Clinical implications of the hematologic profile of COVID-19 patients including cytokine storm, coagulation profile and thrombophilic complications are starting to be recognized. Hypercoagulability could be the potential cause of death due to COVID-19:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585459/
How good is the hematologic profile, including hematologic markers (such as interleukins and others) in predicting if COVID-19 is severe, has mild manifestations or it is asymptomatic?

A recent pre-print has studied this by measuring 86 accredited diagnostic parameters and plasma proteomes at 687 sampling points, in a cohort of 139 patients during hospitalisation.

We identified 26 protein biomarkers and 14 routine diagnostic markers
(Fig. 4a, Supp. Fig. SF20) that correlate with the time between the
first sampling point and release from inpatient care. The proteomic
signature associated with longer duration of inpatient treatment and
hence more severe COVID-19 progression includes upregulated components
of the complement system (C1QA, C1QB, C1QC) and reflects altered
coagulation (KLKB1, PLG, SERPIND1) and inflammation (CD14, B2M,
SERPINA3, CRP, GPLD1, PGLYRP2, AHSG).

They used a learning classifier to then predict survival in critically ill patients:

In a last step, we established a machine learning model based on
parenclitic networks52,53 (Methods) to predict survival in critically
ill patients (WHO grade 7, n=49) from the proteome of the earliest
single time point sample at WHO grade 7 for a particular patient. On
the test subjects (the data of whom were excluded when training the
machine learning model), high prediction accuracy was achieved, with
AUC = 0.81 for the receiver-operating characteristic (ROC) curve. Of
note, the model correctly predicted survival or adverse outcome weeks
in advance (median time from prediction to outcome 39 days,
interquartile range 16 - 64 days).

The 'predictive power' can be captured (not in a perfect way) by the AUC value - a value of 0 has the worst power to separate patients and 1 has perfect power, so 0.81 is pretty good overall. I haven't read the paper fully, but from a brief scan it looks as though their methodology is at least reasonably sound.


Why pick just a single bacterial transformed colony So after bacteria have been transformed to perhaps grow up a plasmid of interest, why pick only a single bacterial colony from a selective plate for further expansion?

I understand that this is to ensure that you are only working with a single genetic makeup because each separate colony is derived from only a single bacterium. What I can't rationalize is that if I am trying to expand and isolate a plasmid of interest, all colony expansions on a selective antibiotic plate should contain my plasmid. So is it really necessary to take only a single colony, because all colonies I pick should  be useful to me.

This is a matter of pragmatism in the culture process.

Taking 100 colonies instead of 1 increases the inoculation volume by a factor of 100, which then saves you perhaps 2 hours of bacterial growth time before your culture reaches the OD you want.

However, mutations and loss of plasmid in culture, while unlikely, are possible, especially if the bacteria were not cloning strains with their recombinases knocked out. In such a case, you would risk the downstream experiments being contaminated with mutants, be that protein expression, retroviral plasmid production, or something else.

Worse still, the mixture of bacteria containing mutants is less likely to be detected, since had you picked a single mutant colony, there would be absolutely no result, but a contaminated culture would produce a low but still positive result. Therefore, you may end up wasting many days or weeks troubleshooting your downstream experiments.

Therefore, picking single colonies is simply a matter of "better safe than sorry".


How scientists can be confident that human embryo tail is really a tail? From Wikipedia:

  Human embryos have a tail that measures about one-sixth of the size of the embryo itself. As the embryo develops into a fetus, the tail is absorbed by the growing body.

How are we sure that it is a real tail and is not a superficial resemblance of something else?

I ask this because some creationist guy challenged me in this regard.

We can be sure it's a tail because it is an extension of the vertebrae, and we define "tail" as an extension of the vertebrae, among other things.

  tail

  tāl/

  noun: tail; plural noun: tails

  the hindmost part of an animal, especially when prolonged beyond the rest of the body, such as the flexible extension of the backbone in a vertebrate, the feathers at the hind end of a bird, or a terminal appendage in an insect.

Emphasis mine. Source: www.oxforddictionaries.com


(How) can a pink grasshopper exist? I saw this foto on Reddit recently:

Is this possible? How can a grasshopper become like this? Is this just natural genetic mutation?

Pink individuals of the katydid species Amblycorypha oblongifolia are a relatively uncommon but natural phenomenon with a long history of research.

It looks from popular press accounts (Science Friday, Scientific American) that the pink coloration may be caused by a dominant allele, and is only rare because of a high selection pressure against pink individuals (i.e. they're much less good at hiding among leaves, and are eaten before they can reproduce).

Photo by Richard Whitby, via flickr.com/blueboat2 (cc-by-sa 2.0)


What are the effects of sleep deprivation? Having recently pulled an "all-nighter" while trying to fix a fatal bug in our release code, I started thinking of any health risks that I might have.

What are the adverse effects of staying up for staying up for 42 hours, considering I took no caffeine or other stimulants, as well as no depressants such as alcohol?

Upon googling I found a lack of facts, what would be good is a list of effects and rough times that they start happening.  And any significant problems I would face, but moreover I would like to know what causes them?  Unfortunately I only studied Biology until GCSE (UK - SAT/TAKS Alternative) and might need some simplified explanations or links to help understand more complex tasks.

I'm not even sure if this question is grammatically correct, and my brain power has slowly dwindled, should I be worried?  I have read this and understand it to a vague extend.

24 Hour Mark

The consequences of sleep deprivation at 24 hours is comparable to the cognitive impairment of someone with a blood-alcohol content of 0.10 percent, according to a 2010 study in the International Journal of Occupational Medicine and Environmental Health.

36 Hours

Now your health begins to be at risk. High levels of inflammatory markers are in the bloodstream, said Cralle, which can eventually lead to cardiovascular disease and high blood pressure. Additionally, hormones are affected — your emotions can be all over the place.

48 Hours

After two days of no sleep, the body begins compensating by shutting down for microsleeps, episodes that last from half a second to half a minute and are usually followed by a period of disorientation. “The person experiencing a microsleep falls asleep regardless of the activity they are engaged in,” she said. Microsleeps are similar to blackouts, and a person experiencing them is not consciously aware that they're occurring.

72 Hours

Expect significant deficits in concentration, motivation, perception, and other higher mental processes after many sleepless hours, Cralle said. “Even simple conversations can be a chore,” noted Kelley. This is when the mind is ripe for hallucinations. Kelley recalled a time he was on guard duty and repeatedly saw someone standing with a rifle in the woods, ready to sneak into camp. Upon closer inspection, he determined he was actually looking at a branch and shadows.

Sleep: Why We Need It and What Happens Without It - SciShow from Humza Zaidi's comment

.


How does increased heat increase the rate of metabolism? I have heard that taking a hot shower helps

blood circulation
metabolism.

For (2) metabolism, I think that the rate is increased since kinetic energy is given to compound to bond with enzymes to react. Is this the only reason? In addition, why is (1) true?

I don't think a hot shower has any substantial effect on body temperature, since this is carefully regulated by several mechanism to remain around 37$^\circ$C. When you expose the body to heat, you induce a response where the body increases heat loss and possibly reduces internal heat production in order to maintain the core temperature.

It is true that heating the body will increase blood circulation in the skin; this is a way for the body to carry heat from the core to the surface, where it can dissipate (radiate away). As for metabolism, I think the response to heat is less well studied than the response to cold, but presumably metabolic rate (specifically, mitochondrial respiration) will decrease in order to reduce internal heat generation, in order to maintain body temperature. Again, these are homeostatic responses that occur before there is any marked change in body temperature. Here is a review article on these mechanisms.

If you would expose the body to enough heat so that these normal responses cannot compensate, the body temperature will actually rise. Beyond 2-3 degrees (a normal fever), this is very dangerous because it will disturb a number of cellular processes. Cellular metabolism would certainly be affected, but mostly  because some enzymes have narrow temperature ranges where they can function; I don't think the actual heat energy of metabolites is an important factor here, but I don't know of any study on this. A variety of other proteins and cellular structures will be similarly affected. This will eventually affect key functions in the nervous and circulatory systems, which is life threatening. The Wikipedia page on hyperthermia is a good starting point for more information on this.


Is it possible for a human to live forever if he/she didn't catch any diseases? Aging is not a disease, but it's the gradual weakening of the body, as the body gets weaker it gets more prone to diseases. So one doesn't die from aging but from diseases. So if one didn't catch any diseases, would it possible for him/her to live forever? Or just longer than the maximum life span?

No that is not possible ever. There is something called telomere which is present in the chromosomes of cell .These Telomere triggers the action of ageging and leads body towards death. When we are in growing age the amount of telemere is very less but as we get older and older the amount of telemere get increases .
The rate of increase of telemere increases with each succesive cell disivision. Hence death is sure no matter what ever you do.


Are the changes required to produce genetically manipulated organisms (GMOS) considered to be mutations By definition, are mutations required to be natural, or are synthetic lab-induced genetic changes considered mutations too? Furthermore, are genetically manipulated organisms (GMOs) considered forced mutants?

What is a mutation?

A mutation is any change to the DNA sequence. From wikipedia

  In biology, a mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

Whether a given alteration to the DNA sequence occurred in nature or in a lab changes nothing to the fact that we call this alteration a mutation.

How common are mutations?

Just so that you realize how common mutations are: In humans, a couple having a baby typically transmit about 40 new mutations to this baby. This mutation rate is not quite the same between women and men (see Kong et al.(2012)).

What is a GMO?

I have never seen the term "forced mutants" before but it sounds like you might have a misrepresentation of what GMOs are and esp. in your misrepresentation, you might think that there is such natural category which are GMOs and other that are non GMOs but the boundaries between the two is more than vague.

Consider for example that the vast majority of our food has been manipulated by humans through artificial selection. Check out the ancestor of modern-day corn (from Genetic Society of America; original source: teosinte.wisc.edu; thanks @John)

This evolutionary change occurred via artificial selection mainly and without using modern genetic tools.


How does a biologist decide when she has enough results to publish a paper? Biology is so exciting! Answering a question leads to  thousand more questions! There is no limit to how much one kind find out about a phenomena…

So I have always wondered how someone can decide that it is time to publish some fixed amount of research they have done. How do biologists decide when to publish a paper? How do biologists know that results are sufficient enough for a publication?

When you do science you start with a question or a hypothesis. How is Gene A regulated? Or "does hormone B have an effect on the immune system". Or whatever.

Then you start by thinking how you can prove or disprove your question/hypothesis with experiments. You then do your experiments and see if they are enough to prove your question. It often happens that you have to do additional experiments to cover side-questions which appear during the work or to exclude some side-effects which may also be important. If you have done all this (with replicates) and looked from different angles on your problem, then you can start writing an article.

This includes some introduction from the literature and a classification of your results into the things already known. If you make strong claims, then you will need a lot of arguments (=results) to prove your point. It is quite hard to argue against "common knowledge".

The question of how much research is enough is quite philosophical, since you usually don't "finish" a topic. You look only at certain aspects from a certain angle. This can be quite different for other researchers.


Measuring Bioluminescent Algae Intensity For a science project, I am required to measure the intensity of the light given off by the Algae, Pyrocystis lunula. Can a photometer with a range of 1-50000 lux be able to pick it up? If not, what are some tools to measure the intensity(without costing to much money.)?

As stated here:

The lunate cysts of Pyrocystis lunula have a bioluminescent emission spectrum with a peak intensity of 477.5 ± 1 nm.

So, almost any spectrophotometer should be able to detect it, it's just bluish visible light.


The relation of a schizophrenia drug side effect and caffeine intake I am listening to the book Surviving Schizophrenia and in the book, it is mentioned that drugs like Clozapine increases in blood level if the patient takes Caffeine, and can have side effects due to elevated levels. In case the patient takes Caffeine, can't just less amount of Clozapine work since it'll be significant enough to help the patient and cause less side effects too? I am not from a medical background, sorry if these things are pretty obvious in medical community

I used Google Scholar with the search terms of clozapine, caffeine.
I only found small scale studies, but they agree that it is likely that Clozapine levels are affected by caffeine intake.
To really understand the implications of this it would be necessary to research what the range of Clozapine levels actually are in patients and what the effective level is, as well as the levels that give side-effects.
Only then can the changes due to caffeine be seen to be significant or not
Example paper studying 12 volunteers below (full text available)
Hägg, S., Spigset, O., Mjörndal, T. and Dahlqvist, R. (2000), Effect of caffeine on clozapine pharmacokinetics in healthy volunteers. British Journal of Clinical Pharmacology, 49: 59-63.
https://doi.org/10.1046/j.1365-2125.2000.00111.x
Available at:
https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1046/j.1365-2125.2000.00111.x


What is 'calcium conductance'? What is the meaning of calcium conductance in ion channels. I encountered this in the following text:

  It was established that the µ and δ opioid receptors open potassium
  channels, which results in reduction of calcium conductance (Simon, 2005).

Also why should opening a potassium channel reduce calcium conductance. How are they related ?

Reference:

Simon, E. J. (2005). Opiates: Neurobiology. In J. H. Lowinson, P. Ruiz, R. B. Millman & J. G. Langrod (Eds.), Substance abuse : a comprehensive textbook (4th ed., pp. xxiv, 1421 p.). Philadelphia: Lippincott Williams & Wilkins.

Conductance is the inverse of resistance, and measures how much of a given substance flows throught a channel. In this context, it means how many calcium ions enter the cell in a period of time.

There are at least two ways potassium channels may prevent the calcium to enter in the cell.

1) Potassium intake by ion channels decrease the membrane potential, restoring it to its rest state. Since many calcium channels are voltage-dependent, a reduction of the membrane potential would close them, effectively decreasing the calcium conductance.

2) Potassium channels may be coupled to different signaling pathways (i.e. G proteins), wich may affect indirectly other calcium channels.

In the case of opioid receptors it seems to be the first mechanism. With potassium channels open, the neuron is less likely to be activated, because it needs higher stimulation to reach the action potential. Calcium channels open in neurons mainly during action potential events (althought they may exist other calcium channels that open in other conditions, i. e in response to hormones or neuromodulators).


Definition of general anesthesia To quote Goodman & Gilman :

  An alternative way of defining the anesthetic state is to consider it
  as a collection of “component” changes in behavior or perception. The
  components of the anesthetic state include:
  • amnesia
  • immobility in
  response to noxious stimulation
  • attenuation of autonomic responses
  to noxious stimulation
  • analgesia
  • unconsciousness

My question is, does not the state of Unconsciousness already imply other components of analgesia and amnesia? Analgesia is the absence of the perception of pain, which is granted if there is unconsciousness which would be the absence of all perceptions.

I am not certain if unconsciousness also entails amnesia, but it seems that remembering what happened when unconscious seems considerably unlikely.

Apart from a reductionist argument for minimizing the constraints required for classification as a general anesthetic, I am more interested in cases where unconsciousness would be achieved without analgesia or amnesia, which could be a likely rationale behind including the additional caveats in the definition.

A state of unconsciousness does not guarantee analgesia nor amnesia. Besides, a muscle relaxant is often paramount to prevent movements. The perfect general anesthetic would do all of this and have hypnotic, analgesic, amnesic and muscle relaxant properties. Such compounds do not exist, because each effect works on a different part of the brain or elsewhere.

In practice, therefore, multiple compounds are administered to obtain the desired effect. A cocktail anesthetic not only ensures all the desired physiological changes, it also reduces the chance of toxic side effects relative to giving one constituent in a large enough dose to encompass all the effects. And there lies an important point, namely anesthetic depth.

If anesthesia is deep enough, all effects may, perhaps, be reached to some degree with a single compound, but the dose likely becomes so high that the side effects become too large. An example in this realm is alcohol, which when consumed in copious amounts, may come close in reaching all desired effects at least to some degree. A related compound is ether. But even with ether, which has been used in early days of surgery, surgical stress caused patients to die intra-operatively due to cardiac hyperactivity. Surgical stress needs to be minimized and that's why an analgesic is needed in the cocktail.

Commonly applied anelgesics in the OR are opiates, such as fentanyl. Anelgesics are critical for invasice surgery, because the body reacts to trauma even when the brain cannot process the information to the degree necessary to turn it into a conscious experience.

For instance, a widely used cocktail is propofol-based anesthesia: A propofol injection might be used to start anesthesia, fentanyl (injectable) is used to blunt the stress response, midazolam (injectable) given to ensure amnesia, and sevoflurane (inhalant) during the procedure to maintain the effects.


Previously frozen papaya seeds sprouted. How will it affect the plants? I thought about asking this on Gardening SE, but it seems to me as a technical subject which requires biological expertise to answer. This is not something that usually occurs for gardeners, so I don't think anyone there would have experience with it.

A bunch of seeds from a papaya fruit were put in the refrigerator. They were taken straight out of the fruit, along with pieces of pulp, sarcotesta and all.

The seeds ended up below zero. Probably only by a few degrees, at worst. They would have been in that state only for a few hours, at most. However, ice crystals had formed on them, and the pouch had hardened a little bit. I then thawed them. All that happened on May 19.

Well, I decided to plant them, as an experiment. And a few days ago, they started sprouting.

I actually have more seeds from the same fruit, which have not been exposed to below zero temperatures.

Now my question is: If I let these plants become large trees, will they in any way be different from the normal seeds? (Assuming they get equal treatment.)

I thought the seeds would die, so I was surprised when they sprouted. But since this is a tropical plant, could the negative temperatures have damaged their DNA in any way? Or had some other detrimental effect on them? Or can I expect these plants to be exactly like the other group? (Except for individual variations unrelated to the freezing, of course.)

Seeds are generally made in order to stand dry/cold conditions.
I don't see any reason to believe that the DNA got damaged during freezing (that could cause mutation and phenotypic changes). So, if they have germinated, the plants should not be any different from the controls.


Solution based measurement of Solvent-Accessible Surface Area of macromolecules The Solvent-Accessible Surface Area (SASA) is a valuable metric for looking at protein folding and protein-protein interactions. However, this measurement is typically done by calculating the SASA from a solved (and generally static) structure.

Chemical probes like diazirine and hydroxyl radicals show some bias regarding where they tend to bind. I'm realizing while I'm writing this question that NMR is a perfectly valid method to determine a solution based structure and then calculate the SASA. Similar strategies has also been used to examine structured RNAs. I'm curious about the variety of these methods and how accurate they are.

I only know of one method, but here it is.  You create a sphere the diameter of the VdW radius of water, and then 'roll' it along the surface.  I know this as a Richards-Lee surface, wikipedia has another name for it.

This looks complicated, but its not.  you move the probe sphere along the surface of the molecule in the XY plane until it just touches the vdW radius of the protein, keeping the center of the sphere as the surface, all the way around the molecule.  If you like, you can color the surface by the charge of the position too, which is useful for discussing solvent interactions.

Then you translate along the z axis and do another contour until you run out of protein.  Apparently jmol and other packages will do this for you.

Wikipedia references a more mathematical method LCPO, which I am not so familiar with.

Is this accurate?  As usual with such calculations its more of a guess than an answer.  You can do the calculation on any structure or any ensemble of structures (like NMR gives).  It doesn't understand how the molecule might be flexible or dynamic.  If you read up on your physical chemistry you see that proteins breathe and can allow diffusion into the core rather readily.  If I recall right, you can get rather large molecules quenching heme flouresence in hemoglobin at room temperature.

If you are looking to dock 2 proteins, SAS might be more useful.  Its an important piece of information, but not an ultimate answer.  I'm afraid with proteins that doesn't happen so easily.

@bobthejoe asked about SAS for which no structure exists.
This is an extremely difficult thing to even guess at.  The non helpful answer is that the surface of the protein goes as the cube root of the molecular weight of the protein.

By getting a solution of the protein and shooting it in a syhcrotron, you can get a mean radius of gyration pretty easily which will give you an ellipsoidal volume (and surface area) for a protein.  Again most of the particulars would be lost and this could easily be off by 25% for an irregularly shaped protein.  For a regular globular protein it might give an answer similar to the power law above.

I have seen physical chemistry experiments that look for changes in osmotic pressure when the salt concentration in a solution of the protein changes substantially (Adrian Parsegian's work at NIH in the late 80s).

I doubt you will find any of these answers useful as their mean error is going to be very large (20-200%) and also assumes the protein is soluable and amenable to the experimental conditions.

Solvent probes can help too.  For instance exposing the protein to D20 then doing mass spectroscopy on the protein. This is still only going to give you a general idea of how much of the peptide is surface exposed.  Protein structure is still pretty necessary to getting any accurate measurement of SAS I think.


Do mitochondria contain the genes to specify themselves? My book says :
"Mitochondria contain their own genetic material so when a cell divides, the mitochondria replicate themselves under the control of the nucleus."
The book means that the mitochondria contain the genes which produce the mitochondria right  ?

The answer is a bit more complicated than that. Mitochondria contain their own genome called mitochondrial DNA (mtDNA), encoding 13 proteins that are part of respiratory complexes I, III, IV, and V, 22 transfer RNAs (tRNAs), and two ribosomal RNAs (rRNAs). The separate tRNAs and rRNAs are necessary because the mitochondrial genome uses a slightly different genetic code than the nuclear genome.

So, the mitochondria contain nearly all of the genes necessary to construct the respiratory chain, as well as the machinery to translate the mRNA into protein. However, it does not contain any of the genes necessary to actually replicate the mtDNA (DNA polymerases, etc.) or construct the mitochondrion itself - synthesize the components of the different membranes, arrange the membranes in their required conformation, chaperones to assemble the complexes of the respiratory chain, etc. - these are all encoded in the nuclear DNA.


Many spermatozoa, but just one ovulum Why do men produce so much spermatozoa, that will get discarded, but women, just one ovulum, which is a good one.
Couldn't men produce good spermatozoa as a limited edition?
Where is the evolutionary advantage of things being like they are?

I think the asymmetry allows for a stronger selection process.  Sperm competition is a powerful force in evolution.

This is useful since sperm vary wildly in quality - for healthy human males only 50% might not be normally motile. Other animals can have a higher percentage, but there are always a significant number of floaters... This means that the fertilization via sperm takes out a lot of the less functional sperm.  Since these are in many cases the same genes we use as diploid organisms later, sperm competition really tames a lot of problems which might be produced in meiosis.

Many animals have multiple mating events from multiple males at just about the same time - when the female is in heat.  This gives a larger role for sperm competition - literally different sires are competing as sperm to fertilize the egg.

In females it is a different process of choosing the cells.  Ova are mostly eliminated in women by the time they reach reproductive age.  I think that this is not well understood biologically... references are hard to find.

The differences in the morphology and roles of the gametes, which goes back to the most primitive of animals has a strong role in selection of healthy offspring through a diverse set of mechanical and biochemical conditions experienced during fertilization.

Added Note: I ran across this reference for how ova are selected for presentation by the ovaries.  Its not really a review, but maybe a lead reference on how selection works in the female reproductive system - its also picky:

  In mammals, ovarian folliculogenesis is a process regulated by complex networks composed of various endocrine, paracrine and autocrine factors that interact coordinately.

Its no cake walk to being an egg either...


Why is the quality range of fastq format so broad? Referring to fastq format, it is clear that in fastq format, there are 94 quality value for a sequenced Nucleic Acid of a DNA sequence read and they are:

!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}~

So, I have two questions:

Why is the quality value range so broad (94 levels)?
In a particular case of analyzing data, we saw, the frequency of I is so high, which is not a good quality. So, why would we accept such a poor quality in research?

Initially, there were several quality encodings that used to follow different ranges of ASCII characters to denote the quality of read. The range that you mention is a union of all those encoding formats. Nowadays, the most common encoding is Phred+33 (used by Illumina, Sanger, Ion Torrent and other popular sequencers) which uses these characters:

!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHI

Character I denotes a phred score of 40. Aligners, when they read fasta files, by default assign a score of 40 (I) to all positions. This might be one why reason you are seeing a lot of I.

Anyways, if your fastq follows the phred+33 format then 40 (I) is a pretty good score which denotes a good quality read. Or you could be aligning fasta files. It would be a bad score if your encoding is phred+64 which I guess, is not the case.

ADDITION

The file that you linked is a fastq file. This sequencing experiment has been done on 454 GS FLX Titanium machine. 454 machines use a different way of calculating quality scores compared to the traditional basecalling phred scores. From the manual:

  6.6 Phred-equivalent Base Quality Scores

  Quality scores for individual called bases are determined by a method developed in
  collaboration with the Broad Institute (Genome Research,18(5): 763-70,
  2008), whereby the methodology described by Ewing and Green (Genome
  Research, 8: 186-194, 1998) for the creation of quality scores as part
  of the Phred basecalling algorithm is applied to generating quality
  scores for 454 Sequencing reads. The quality scores computed for each
  called base are written to the CWF and SFF files (and optionally to a file paralleling the basecall FASTA file). Briefly, the method
  compares the properties of each base’s flowgram signals against
  properties that have been found to correlate with accurate and/or
  error-prone signal information, using training sets of read data. A
  multivariate analysis of those properties determines the sets of
  property values that best describe “bins” of basecalls, then assigns
  the training set accuracy rates of the basecalls in each bin as a
  quality score using the following scale:

  $$Q = -10\ \text{log}_{10}(\text{error rate})$$

Usually, you'll have two files for 454 experiments — one that holds the sequence and the other that holds the quality at each position. These files can be combined to generate a fastq. This file is encoded in the phred+33 (also called Sanger/Illumina 1.9) format which I mentioned above. Phred+33, I guess, is also the standard encoding format adopted by NCBI/ENA/DDBJ and all new sequencing runs are encoded in this format. If you do not know the encoding you can run fastqc on your fastq file and it reports the type of encoding.

In your case, I would denote a score of 40 (ASCII value - 33) which means an error rate of 10-4 i.e. the read is of good quality.

The below graph is obtained by a fastqc run on your file. The bars denote quality statistics at each position. Note that the mean quality drops towards the end of the read.

A fasta file does not indicate quality but when you map them to your target, the aligner (I know of Bowtie based ones) assigns a default score of 40 at each position, during the alignment (and in the output).


Are cerebellar basket and stellate neurons actually different cell types? The title more or less says it all, but to contextualise a bit:

Cerebellar molecular layer interneurons have been classified, probably since Cajal, into the basket cells, which synapse onto the soma and axon initial segment of Purkinje cells, and stellate cells, which synapse onto the dendrites. The types are distinguishable in tissue slices by positional and morphological differences, but it is at least arguable that the variation is continuous and the boundary somewhat arbitrary. Both types take basically the same inputs and deliver the same outputs, albeit in marginally different cellular locations.

As far as I'm aware -- and I would be incredibly happy to be told otherwise -- there is no known difference in protein expression that can be used to distinguish between these interneuron types, for instance in dissociated culture.

So, is there in fact some identifying marker? And if not, is it still useful to classify them as separate types?

You are completely right with your guess that is was Ramón y Cajal who first described these cells in his famous monograph "Histologie de systeme nerveux de l'homme et des vertebres." published in Paris Maloine in 1911.

Since the only method he had at his disposal was Golgi's staining which is a pure anatomical staining (there is no living cell left in the tissue after the treatment with  potassium dichromate and silver nitrate) with silver chromate filling completely single cells at random.

Using only this staining and his eyes Cajal did classify the neurons according to their size, location in the brain and their shape. This is why we have such names like basket, stellate, moss, pyramide etc. in neuron description. This classification is purely anatomical and does not reflect any intrinsic properties of these cell, as for example being motor neurons or interneurons.

When I was studying histology at my medical school I was always told that there is new "mollecular biology"-based classification of neurons is about to come and to replace the existing classification by Cajal, many cell types were supposed to be merged there, among others also different anatatomical groups of interneurons. (This was one of the major research topic of the research facility where I studied neurohistology).

As far as I can see, this classification is still not here...


Could someone Identify this Insect Hive on my Balcony Grill A smallish insect hive has been forming on the grill of my balcony in the last month or two, and I wanted to know should I be worried or can I just let it be. Its 13th floor in Singapore, if the height helps in ID. So far they have not been very aggressive, and have not bothered us even if we get within few feet of it, but want to know if that can change in horror movie style..

You can find the pictures below, both are pretty much the same, but with some flash tweaking. For a size estimate, they appear to be between half and 1 cm long, and the distance between the bars of the grill is about 12 cm or so. Are they some kind of bees? Would they leave eventually or is this a long term thing. Also, the length of the hive appears to be growing at ~ 1-2 cm per week.

(crop of larger picture found below)

These are certainly paper wasps (Vespidae) building their paper nest. Looks like a species of Ropalidia, which are known from Singapore.

I know little about Ropalidia, it seems to be rather small and probably harmless, but our larger European wasps can sting and bite and are sometimes quite aggressive (this refers first of all to Vespula germanica).


Why does oxidative phosphorylation require complexes 2 and 3? I am learning about oxidative phosphorylation in cellular respiration now and do not understand the roles of complexes 2 and 3 in the process. Specifically, my textbook says that 2 and 3 pump H+ out into the inter-membrane space, just like complex 1 does.

Complex 1 pumps out the H+ from NADH, and I suppose that 2 would be needed to pump out the H+ from FADH2, but then why do we need complex 3? All the H+ has been pumped out already--there's none left!

Also, if this understanding were correct, there would be no purpose for the chain that started with NADH to go through complex 2 at all (because it already went through 1, as opposed to the chain starting with FADH2).

Thanks in advance for any clarification you can give.

The numbering of the complexes in the respiratory chain is confusing, as it creates the impression that the chain is structured like

Complex I $\rightarrow$ Complex II $\rightarrow$ Complex III $\rightarrow$ Complex IV

... but this is wrong. There are in fact several ways of feeding electrons into the respiratory chain. They all begin with one enzyme E that oxidizes an electron carrier in the mitochondrial matrix, such as NADH, FADH2, or ETF (electron transfer flavoprotein) and transfers electrons to coenzyme Q, which is then processed by Complex III, after which electrons are handed on to Complex IV. Both complex III and IV pump protons. But there are several options for the first enzyme E:

Complex I (NADH dehydrogenase). This handles all electrons from NADH (from many sources in oxidative metabolism) and is typically the major source of electrons in the chain. It is the only enzyme E that also pumps protons itself.
Complex II (succinate dehydrogenase) accepts electrons from succinate (a step in the TCA cycle).
ETF dehydrogenase accepts electrons from reduced ETF, notably from fatty acid oxidation.
Glycerol-3-phosphate dehydrogenase accepts electrons from cytosolic NADH (from glycolysis) via the glycorol-3-phosphate shuttle.

There are more alternatives, but I think these are the most important ones. So you are absolutely correct that when NADH is the substrate, Complex II is not involved. There is in fact not one respiratory chain, but several possible chains with different starting points E,

E $\rightarrow$ Complex III $\rightarrow$ Complex IV

You might think of this as a "fan in" structure where the various enzymes E all converge on Complex III. (I don't have the energy to draw this :)

As for the proton pumping at Complex III, it is not the case that the H$^+$ pumped are exactly those derived from NADH --- the system is more complicated than that. The respiratory chain(s) convert chemical energy from the redox reactions into potential energy (a proton gradient), but most of the H$^+$ pumped are obtained from the mitochondrial matrix. The exact number of protons varies depending on the substrate: for example, the 2 electrons donated by NADH at Complex I is sufficient to pump up to 10 protons. Actually, the stoichiometry is not fully understood, and there isn't really an exact integer number of H+ pumped, because this pumping is an imperfect physical process --- there is leakage, protins slipping back into the matrix etc.


How to get smallest subtree containing a set of nodes from BioPhylo? I'm testing out various phylogenetic libraries in Python. I want to read in a Newick tree, then, given a list of taxa, generate the smallest tree that contains them all. This task is quite simple and efficient in dendropy and ete2:

newick = '((raccoon, bear),((sea_lion,seal),((monkey,cat), weasel)),dog);'
taxa = ['raccoon', 'sea_lion']

import ete2
tree = ete2.Tree(newick)
pruned = tree.prune(taxa)

import dendropy
tree = dendropy.Tree.get_from_string(newick, 'newick')
pruned = tree.prune_taxa_with_labels(taxa)

I'm trying but failing to find equivalent functionality in the Bio.Phylo package. Trees do have a "prune" method, but it prunes a single node from the tree.

The common_ancestor function should give you the result you want: it gives you the tree (I think) that is the most recent common ancestor of all the given targets.