Re-Plumping Dried Insects I have begun to display some of my soft bodied insects and as I am trying to rehydrate some of them that were plump in the abdomen, they appear to have shrunk and the bodies have sunk into themselves.  Does anyone know how to avoid this or what can be done to plump the bodies back up?

"Soft bodied" can come from a number of conditions, but generally, soft bodied insects are kept in ethanol. Adult insects should not need any kind of treatment before being pinned. Nymphs and immature insects should be in ethanol, and I suspect this is what you have. However, they can be freeze dried for a nice effect. One technique that works for females that are full of fatty eggs (such as Orthoptera) is to make an incision on the ventral side with an exacto-knife, and scrape out the contents of the abdomen. Then stuff with cotton, and close the incision. I think you likely have immatures, which should be in ethanol, but this technique would work if you are careful.


Damselfly identification Can somebody identify this damselfly? Found near a stream about 15 miles west of Boston.

It looks to me like a male Argia fumipennis violacea


Is the blastocyst a coeloblastula? A coeloblastula is that type of blastula which has a fluid-filled cavity. Since the blastocyst of mammals has a fluid-filled cavity too, can it be called a coeloblastula? My book however mentions the two as different, and it gives the frog as an example of animals having the coeloblastula and mammals as an example of having the blastocyst.

This is a bit tricky.

The blastocoel in e.g. amphibians separates ectoderm from endoderm and prevents cells of the blastocoel roof from inductive influence of vegetal cells. If you cut out the marginal zone and squish the roof onto vegetal cells, you will end up with mesoderm only:

Blastocoel is not homologous to blastocystic cavity. One could consider a tiny space between epiblast and hypoblast during gastrulation as a homologue of blastocoel, this however does not appear in mice. Blastocystic cavity forms at 32-cell stage thanks to Na+/K+ pumps as well as aquaporins. The inner cell mass is a mixture of cells expressing Gata6 and Nanog, which will form hypoblast and epiblast respectively.

But worry not, many people still call that cavity a blastocoel, in fact, I've seen it happen on Wikipedia. Anyway, I'd still recommend using separate terms for coeloblastula and blastocyst due to the non-homologous nature of blastocystic cavity and the blastocoel.

My sources:

https://kjcscientific.wordpress.com/project-excalibur/
Gilbert's Developmental Biology
Ćwiczenia z Biologii Rozwoju Zwierząt [Marek Maleszewski et al., University of Warsaw, Polish language publication]


Are these 2 procedures to fight cancer (cancer "vaccine", and cancer drugs which can attack all tumours) related? Last year appeared the new of a cancer "vaccine" (not a vaccine in the traditional sense) tested in animals for 4 types of cancer and which worked in 97% of the cases to eliminate already existent tumours.

Cancer Vaccine Trial

Now appeared the new of "cancer drugs which can attack all tumours" to be fast-tracked by NHS.

Game changing cancer drugs can attack tumours

I would like to know if both procedures are based in similar ideas (meaning the second one could have a similar effectiveness to the first one) or if they are completely unrelated.

The first source (Science Direct) says that the "vaccine" treatment stimulates T cells to attack cancer. In general, this treatment is intended for all tumors and has been very successful in studies in mice. Cancer.net and Cancerresearchuk describe cancer treatment vaccines in a bit more detail.

The second source (Telegraph.co.uk) mentions “tumor agnostic” or "tissue agnostic" drugs, which target tumors according to their genetic make-up, rather than the tissue from which they arise. This treatment is intended only for specific tumors with known genetic mutations. Examples of tissue-agnostic drugs are pembrolizumab and larotrectinib, which are approved by FDA for treatment of certain metastatic solid tumors.

So, these are two different ideas and most of these drugs are currently in a research phase.


How is the type of genetic manipulation determined in CRISPR-Cas9? I've been reading up a bit on the CRISPR-Cas9 system for gene manipulation. From what I read, it introduces double-strand breaks at specific points determined by the choice of sgRNA. But how do you get from double-strand breaks to editing genes in incredibly specific ways? As far as I read you can fix point mutations, insert whole genes or disable genes with CRISPR-Cas9. How do you specify which kind of repair mechanism is invoked?

But how do you get from double-strand breaks to editing genes in
  incredibly specific ways?

You should read the wikipedia page on CRISPR-Cas system. The target specificity is provided by the tracrRNA.

  How do you specify which kind of repair mechanism is invoked?

The repair can be done either by Non Homologous End Joining (NHEJ) or Homologous Recombination (HR). If you provide excessive DNA template by transfection then it is likely to increase the chance of HR and this can be used for trangenesis.

When no template is provided then DNA can be repaired by HR with sister chromatin or NHEJ. Depending on the stage of the cell cycle one of these mechanisms is preferred over the other. HR is shown to be the most active in S-phase and starts declining in G2-phase.

So when you want to make transgenics or specific edits then co-transfect CRISPR-Cas with transgene DNA (with flanks homologous to target DNA sequence) or a homologous DNA with point mutation(s), preferably in cells at S-phase. It is possible to synchronize the cells using nocodazole or other molecules that arrest cell cycle.


What is biological intuition? Whenever I read or learn about prediction tools or aligners or motif detectors, I also hear that they are lacking in something called biological intuition. But I haven't been able to find a solid definition of what that is. Can someone please explain?

This is how I understand it: Bioinformatics tools are amazing at answering questions. The more specific the question each individual module of a tool can answer, the better their quality.

However, what they cannot do is ask the right question. You can find motifs with scores attached to the hit, but you cannot predict the relevance of that find. Is it a motif for a transcription factor binding site that inhibits a promoter for a downstream gene thereby suppressing activity, or does it bind a different factor enhancing a gene further downstream?

These questions need knowledge of the domain and of the genomic context, and this knowledge base is constantly evolving. Tools are getting intelligent, but they cannot have this intuition because they are still designed my human beings and we are always ahead thanks to experience.


Filamentous algae - what exactly am I looking at? I have just taken some images with my light microscope at 400x of  (what I think is) some form of filamentous algae from a local pond.

Now, I think I am looking at a single cell (centre) with some sort of arrangement of chloroplasts. Is this correct? Can anyone give me some more information on these structures?

I also have included a higher-constrast image of the specimen.

It looks indeed like a Spirogyra, or at least a member of the Zygnematales.
And yes, the green things are the chloroplasts (or one long chloroplast?), and they are arranged in spiral.

The "empty" space in the middle is likely the nucleus, and the darker circles within the chloroplast(s) could be the starch accumulated at the periphery of pyrenoids.


Never seen a spider with this pattern before Found this spider at work in the Leicestershire area of the United Kingdom. Never seen one with this kind of pattern on its back before so was curious as to what it is. (Size: 2-2.5 inches)

The depicted spider appears to be a European garden spider Araneus diadematus. The mottling pattern that forms a cross shape is probably one of the more distinctive features, giving these the nickname cross spiders. The distribution for your locale makes sense, based on data collected on these spp: http://srs.britishspiders.org.uk/portal.php/p/summary/s/Araneus+diadematus


Boiling A frog in a sous vidè bath So if i were to use a sous vidè water bath and a frog and slowley raised the temperature say 1 to 2 degrees a day would they survive harsh boiling water through thermoregulation

No.

No higher order organism has enough proteins that are stable at 100 degrees C to survive. Proteins denature at higher temps and all cellular functions that depend on them cease.

Some thermophillic bacteria have evolved proteins that are stable above 100 degrees C over eons of evolution.


Hershey and Chase experiment http://www.youtube.com/watch?v=3QJ4CjFsflA

This is a link to Hershey and Chase experiment. According to this experiment, we conclude that DNA is the genetic material. But how do we conclude that DNA is the genetic material? They only proved that DNA of virus enters into the bacteria, not the protein coat of virus.

The DNA of the virus later destroys the bacteria because the virus reproduces inside them. Does this demonstrate that DNA is the genetic material?

It is a matter of deduction. We know that:

Viruses entering a cell are capable of making more copies of themselves.
The only part of a virus that actually enters the cell is its DNA (or RNA, depending on the virus in question).

Based on these two facts, we can conclude that the DNA ̣--since it is the only part of the virus to enter the cell-- somehow contains the information necessary to make new copies of the virus and is, therefore, the genetic material of the virus.


ChIP-seq for histone modification not in agreement with RNA-seq for expression I have ChIP-seq for H3K79me2 and H3K36me3 and RNA-seq data for treated and untreated samples. Those two histones mark active genes. Lets say, hypothetically, a peak caller finds differential sites at gene A for both of those histone modifications. However, when I run RNA-seq analysis tools (like edgeR or DESeq2) this gene is not marked as differentially expressed (well it has a FDR value of >0.05).

There might be several technical reasons for RNA-seq analysis methods not to find this gene as differentially expressed because

it is really not differentially expressed
or it is not differentially expressed enough for the tools to detect it

However, I am more interested in the biological aspect. If two histones mark gene A as active in treated samples, one would expect that it would be expressed in RNA-seq. What mechanism could lead to the result that however the genes is marked as active by histones, it will not be differentially expressed in RNA-seq?

It is difficult to draw any conclusion without further experimentation. There may be many other factors that prevent the expression of the gene including factors like post-transcriptional regulators. Some histone modifications like the ones you are mentioning are also a bit dicey and there can be bivalent modifications too. However, if there is a strong reason to speculate that these marks are associated with repression then you can try these:

You can verify how many genes are there whose expression is not in accordance with the histone marks. If this for a small number of genes then you can investigate them separately. Use a statistical test to verify the significance of your correlation between histone mark and expression. If the discordance is widespread, then I would suggest you to repeat the RNAseq (easier and cheaper than repeating ChIP-seq). BTW, how were the read qualities? Depending on that you can decide which experiment needs repetition. Repetition will help you to know if the observation is indeed correct (a biological replicate); possibly you may end also up concluding that these marks are actually dicey.
If a few genes show discordance, then just do Real-Time PCR for these genes. RT-PCR is more sensitive and another technique of quantification is anyways good. Use a few concordant genes also, in the experiment.


Are any arthropods poisonous to the touch? I'm particularly interested in whether any insects are poisonous to the touch.  Note that toxic-bristled caterpillars are actually venomous, since in all species I'm familiar with, the bristles puncture the skin.  If there are any arthropods poisonous to the touch, I'm also curious as to what the most dangerous one is, but that may be beyond the bounds of this site.

The blister beetle genus Meloe, also known as oil beetles, secrete an oily substance containing a poison called cantharadin which causes blistering and swelling of the skin.

Source: http://statebystategardening.com/state.php/articles/do_not_touch_these_backyard_bugs


Do mutagens ever increase the "rate of evolution"? There are a lot of sci-fi plots where mutagens, especially radiation, cause some organism to evolve at an accelerated rate. Obviously evolution does not occur within a single organism and most of the authors behind these works are more concerned with finding a justification for a desired plot rather than adhering to known science. Nonetheless, I'm curious to know if there is any well-known case where such a scenario is true. (To get one obvious reply out of the way, all evolution that we've observed on Earth occurs in the presence of the background radiation experienced on Earth. Also, although mutagens by definition increase the rate of mutation, those mutations can of course be harmful, so the question is whether the effective "rate of evolution" can be increased rather than the rate of mutation.)

Is there any well-known case where introducing mutagens can increase the "rate of evolution" in an experimental evolution study?

By "rate of evolution", I'm informally referring to either the amount of time or the number of generations that pass before some beneficial mutation occurs and is selected for. For example, in the E. Coli strains from Lenski's E. coli evolution experiments, are there any known cases where a mutagen reduces the amount of time or the number of generations required for a non-citrate-metabolizing E. coli strain to acquire the ability to metabolize citrate?

Do mutagens ever increase the “rate of evolution”? [..] By "rate of evolution", I'm informally referring to either the amount of time or the number of generations that pass before some beneficial mutation occurs and is selected for

This is a very unusual definition of "rate of evolution" but I'm happy to consider it if you want.

If more mutations happen per generation, then it takes less time for a beneficial mutation to happen. So yes!

By rate of evolution, some people may like to refer to the rate at which neutral mutations fix (fixation=reaching a frequency of 1 in the population). If $\mu$ is the mutation rate, then $2N\mu$ mutations are produced each generation (assuming diploidy), and a fraction $\frac{1}{2N}$ of them fix (as they are neutral), this means that the rate of fixation is $\frac{2N\mu}{2N} = \mu$. So, again increasing the mutation rate increases the rate of fixation of neutral mutations. It is actually true also for deleterious and beneficial mutations but the computation is a little more complicated.

Note however, that there is a point after which the mutation rate is so high, that your population might be drawn to exctinction. This is called a mutational meltdown. Mutational meltdown is unlikely to happen unless the population size is already small to start with and/or the mutation rate is really really high.


Why does botulinum toxin seem to be more dangerous to humans than to other mammals? Various mammals seem to get away with eating parts of carcasses that we would prefer to not even touch, and that we assume will make us sick.
Because of that, I assume botulinum toxin is more dangerous to humans than many animals.

Is that right so far - can they handle more of some toxins compared to us?
Or are they better in avoiding harmful substances based on more suited olfactory sense?
Or are we just more afraid?

Assuming the differences exist - what is the cause for it?
Are there plausible explanations in terms of evolutionary pressure?

Because of that, I assume botulinum toxin is more dangerous to humans than many animals.

Couldn't find too many examples but, there are some things to consider (according to [1]):

there are seven distinct types of toxin with variable action among animals
different dose / effect intensity ratio between toxin types
toxins A, B, E and F cause disease in humans
toxin C and D are more common to birds, cattle, horses

And here are some numbers:

cattle median lethal dose: 0.388 ng /kg [2] of C type toxin
mouse median lethal dose ( 12.88 times more than cattle): 5 ng/kg [2] of C type toxin
human median lethal dose: 1 ng/kg [1] of A type toxin

When it comes to carcasses toxicity, there are some papers to consider:

Smith GR, Turner A. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type C. Epidemiol. Infect. 1987 Jun;98(3):345-51. PubMed PMID: 3297745. - Persistent toxicity at 20 and 37 degrees Celsius even for a long time. No toxicity at 16 degrees Celsius
Smith GR, Turner A, Till D. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type E. Epidemiol. Infect. 1988 Jun;100(3):399-405. PubMed PMID: 3288491. - Maximal toxicity at 30 degrees Celsius that is lost in time.

  are they better in avoiding harmful substances based on more suited olfactory sense?

Not if we are talking about nonproteolytic B, E and F type bacteria. Indeed, Clostridium botulinum, proteolytic type A, B and F types produce odor [3].

  Or are we just more afraid?

I don't see how fear could (significantly) influence pharmacodynamics and pharmacokinetics of the toxin.

References:

CIDRAP - Center for Infectious Disease Research and Policy. Botulism. Available from http://www.cidrap.umn.edu/infectious-disease-topics/botulism
Moeller RB, Puschner B, Walker RL, Rocke T, Galey FD, Cullor JS, Ardans AA. Determination of the median toxic dose of type C botulinum toxin in lactating dairy cows. J. Vet. Diagn. Invest. 2003 Nov;15(6):523-6. PubMed PMID: 14667014.
P. Kendall. Botulism. Colorado State University Extension. Available from http://www.ext.colostate.edu/pubs/foodnut/09305.html


Does sodium lower the harmful effect of potassium on kidneys? As far as I have read so far, it seems that potassium and sodium are trying to expel each other from the human body. A lot of documents on the web say too much sodium pressures the kidneys could cause a kidney failure. The same is also said for potassium.

If a person eats a lot of potassium-rich foods, does increasing sodium intake cancel out the harmful effect of potassium on the kidneys, or just double the harmful effect (he/she gets the harmful effect from both potassium AND sodium)?

Chemically speaking, sodium and potassium are very, very similar, and also pretty common, and our body needs both.

Due to their similar electrical properties in particular, they are used as kinds of 'counters' in some processes in the human body, as they can be distinguished to some extent by other processes, and the balance of the two is important.

What it is important to note, however, is that more potassium than sodium is needed, so an overly-high-potassium diet is rarely considered a health risk, even if only due to it being infrequent. People tend to be potassium-deficient rather than sodium-deficient.

Generally speaking, unless you are consuming way too much of both, having a potassium surplus is less problematic than a sodium surplus, and harmful effects certainly don't "stack", at least not trivially. Rather, extra potassium will tend to offset extra sodium, ameliorating rather than aggravating health effects.

Even so: All of this can vary wildly with general diet and other factors, so the prudent thing to do regarding ones sodium/potassium balance is to see one's doctor and have blood work done.


Why do the hormones FSH and LH decrease when the follicle is maturing and does size of follicle change during menstruation phase There are three phases in menstrual cycle. In follicular phase of menstrual cycle, the level of FSH and LH would rise because they would stimulate ovarian follicle to mature. However, when I check with diagram of menstrual cycle, I find FSH and LH hormones do actually decrease during day 4-14. Is that because of increase of oestrogen? However, by the time when FSH decreases, the follicle hasn't fully matured. Also, will follicle grow during menstruation, because in diagram, the size of follicle actually changes during Day 0-4, and FSH and LH hormones increases.

I find FSH and LH hormones do actually
  decrease during day 4-14. Is that because of increase of
  oestrogen？

You first need to note that during one ovarian cycle, multiple follicles are stimulated to grow at the same time by FSH. However, one follicle ends up being the dominant follicle, and it is the oocyte housed within this follicle that is released on day 14. The dominant follicle is the one whose cells express gonadotropin receptors the earliest and so have the greatest sensitivity to FSH. Its growth would outcompete the other developing follicles. During days 4–14, FSH begins to decline because the granulosa cells of the follicles secrete inhibin, which—just like in males—causes the release of FSH and LH from the pituitary to drop. Only the dominant follicle is capable of withstanding this FSH drop; the other developing follicles are thus eliminated.

  Also, another question is will follicle
  grow during menstruation, because on diagram,the size of follicle
  actually changes during Day 0-4, and FSH and LH hormones increases.

As user19099 explains, yes, follicles grow during menstruation. With the degeneration of the corpus luteum, the negative feedback effect of estrogen and progesterone (in combination) on the hypothalamus is relieved. Thus, GnRH levels increase, causing FSH and LH levels to increase (as reflected on the graph you included), and FSH will stimulate follicular development.

References

Marieb, Elaine Nicpon, and Katja Hoehn. Anatomy & Physiology. San Francisco, CA: Pearson/Benjamin Cummings, 2008. Print.


Why does chlorination still work? Chlorination has been used for over a century to disinfect water supplies. Why haven't microorganisms evolved immunity to this chlorine by now?

The reason chlorination still works is that it is aspecific, just as @AliceD mentioned.

The way chlorination works is mainly by oxidizing biological molecules. Chlorine, along with other halogens, is a strong oxidizing agent. It breaks down the phospholipid bilayer membrane, proteins and enzymes. There is no way organisms can overcome this, unless it uses none of the chemical molecules that react with chlorine, which is virtually none.

On the other hand, antibiotics inhibit particular enzymes and proteins in a particular way and by making one or two amino acids different in the protein, the microorganisms can easily overcome this.

Reference - http://www.sswm.info/sites/default/files/reference_attachments/TUE%202011%20The%20Chlorine%20Dilemma.pdf


Evolutionary explanation to why we have such large memory capacities? The scientific consensus is that no one ever fills up their memory capacity by learning facts and so on, even in the information age.  My question is therefore, is there an evolutionary reason as to why we have evolved to have such large memory capacities, when we never come close to filling it up?

We don't have large memory capacities.
If anything I would have asked the opposite, why is our memory so bad and unreliable considering how large our brains are. Even with this gigantic brain we struggle to remember a few phone numbers. Here's how our short term memory compares to monkeys: https://www.youtube.com/watch?v=zsXP8qeFF6A&ab_channel=BBCEarth . I have no explanation as to why humans are so bad at this, this amount of data should be nothing for a brain of our size.
As for long term memory, I'm not really convinced it is that large really, it seems to me people in general in ten years.. have forgotten pretty much everything. Occational glitch.. occational stuff, and even that is usually vague and full of wrongs.
And when people cram for exams.. take the best students ten years later and see how much they still remember, it will be just a tiny fraction.
What do you mean by "filling up their memory capacity"?
Are you expecting some sort of a state where the persons hard disk is full and nothing.. nothing new can be learned? That state doesn't make any sense, the brain is always deleting from memory plus it would make more sense to have the memory slowly deteriorate, rather than fall off a cliff into no functionality at all.
We don't remember anything. We always feel like we are going to remember the now for so long and all but we don't. And we have this bias because we don't remember what we don't remember, which is nearly everything.


How much fat can the body absorb? Implications for daily fat distribution This question is named analogous to this research: How much protein can the body use in a single meal for muscle-building? Implications for daily protein distribution http://ncbi.nlm.nih.gov/pmc/articles/PMC5828430

How many grams of lipids can the body absorb in one sitting? (I ask because a strict vegetarian or vegan diet is characteristically low in fat. Therefore, I consume extra virgin olive oil and nuts.)

Most of the research on pubmed.gov is about oral lipid drug administration/absorption. This work that seemed to come close is over my head and just doesn't seem to specify:

Intestinal Lipid Absorption and Transport by C T Phan 1 and P Tso

PMID: 11229876 DOI: 10.2741/phan

https://www.bioscience.org/2001/v6/af/A612/fulltext.htm

Image sources: Cronometer.com and Jackedonplants.co.uk

Indeed, lipid fecal loss remains below 5% (w/w) even in situation of
  high fat supply in healthy humans, [30].

All about those guts and bowls folks!

Niot, I., Poirier, H., Tran, T. T. T., & Besnard, P. (2009). Intestinal absorption of long-chain fatty acids: Evidence and uncertainties. Progress in Lipid Research, 48(2), 101–115. doi:10.1016/j.plipres.2009.01.001

https://sci-hub.tw/10.1016/j.plipres.2009.01.001

[30] Ross AC. Overview of retinoid metabolism. J Nutr 1993;123:346–50

The issue remaining is how Ross' work doesn't seem to say anything about lipids. Yet, it appears from the mice studies nearly all fat is absorbed (except for ones with special conditions).

Ross, A. C. (1993). Overview of Retinoid Metabolism. The Journal of Nutrition, 123(suppl_2), 346–350. doi:10.1093/jn/123.suppl_2.346

https://sci-hub.tw/https://doi.org/10.1093/jn/123.suppl_2.346


Is it possible to calculate the energy required to speak a word? I was discussing with a colleague whether speaking would require more energy than communicating via instant message (GTalk, etc..).

If this is possible, then I'm particularly interested in whether certain sounds may consume more energy that others, and consequently could one language be more efficient than another.

For animals to check the amount of energy used for a certain behavior you can use a RESPIROMETER. It basically calculates the oxygen consumption.

In your case you could calculate for writing a sentence vs speaking the same sentence.

Regarding your second question:
At least in birds more than the type of sound (the frequency modulation) what matters for energy consumption is the amplitude --> how loud is your sound.


What does irregular heartbeat mean in simple language? I bought a blood pressure monitor (A&D UA-851) which has the option to measure irregular heartbeat.  I do understand what 'irregular' means, but why do irregular heartbeats happen and what are it's implications short and long term?

The normal cardiac cycle is comprised of two distinct phases: the systolic phase in which the heart contracts, ejecting the blood, followed by the the diastolic phase when the cardiac muscle relaxes, refilling the heart with blood.

This cycle is assured by specialised cardiomyocytes (Cardiac muscle cells) that conduct electrical impulses through the heart. When there's interference in this electric activity, the cycle becomes irregular or arrhythmic.

Arrhythmias can be divided by their place of origin:

Atrial (atria are the upper chambers of the heart)
Ventricular (ventricles are lower chambers of the heart)
Junctional (the junction between the two)
Heart blocks (caused by a blockade in the conductivity of the electrical specialised cardiomyocytes)

Some arrhythmias are physiological, such as the Respiratory sinus arrhythmia, a naturally occurring variation in heart rate that occurs during a breathing cycle. Also, in healthy individuals, some extra sistoles might occur without being the translation of a subjacent heart condition and have benign prognosis in individuals without other conditions.

However, some arrhythmias can have a wide range of health implications, from asymptomatic, to a mild intolerance to exercise, to Cerebrovascular Accident (CVA or stroke) or even sudden death due to cardiac arrest.

Therapeutic varies with the underlying cause but can be medical (with drugs such as Na+, K+ and Ca+ channel blockers, beta-blockers and Digoxin) or surgical (ie: Artificial pacemaker).


How to distinguish between a genetic bottleneck and directional selection? Genetic bottlenecks and directional selection should have relatively similar genetic signals: reduced heterozygosity and greater genetic divergence (Fst?) in contemporary populations compared to the past

How would one be able to distinguish between these two evolutionary forces if their signals are so similar?

Population bottleneck will have genome-wide effect while directional selection will affect only the locus (and closely linked loci via a selective sweep).

You can typically screen through the genome and calculate Tajima's D. Under a bottleneck scenario, Tajima's D will be expected to be negative everywhere. Under a directional selection scenario, Tajima's D would be negative only at the locus (and closely linked loci) to the one that is under selection.

There are of course a whole lot series of technics but the above is probably the simplest and most straight-forward (it probably lacks in power though).


Can storing food in a de-pressurized container result in anaerobic bacteria growth? I was looking for a way to store for longer some products which go bad quickly. I found a stainless steel container made with a hermetic lid that you can remove air through (using a pump) so you create a vacuum of sorts (I don't know to what level can the internal air pressure be reduced). The issue is whether storing food which isn't specially sterilized, such as vegetables or spices, can result in the growth of pathogens such as Clostridium botulinum? What I originally looked to buy such a container for is soy lecithin, as I read these go bad very quickly even if stored in a cool, dry place as advised.

Any sealed container can become anaerobic relatively quickly if there are oxygen consuming organisms inside (which there probably are if it's not sterilized). So, growth of anaerobes should always be a concern when using a sealed container for food storage, and proper temperatures for such storage should be considered.

A container like the one you describe would probably be good for extending the shelf life of dry foods that are sensitive to oxidation (coffee, spices, or your soy lecithin powder), and might even help stave off aerobic spoilage organisms (like molds), but it probably won't do anything to prevent growth of anaerobes like C. bolulinum or C. perfringins.


Dorsal vs Posterior and Ventral vs Anterior From prior reading, I thought that Dorsal is the same as Posterior and Ventral is the same as Anterior. However, when I checked in google images for these anatomical terms for a horse (just to strengthen my concept), i found that Dorsal is not the same as Posterior and Ventral is not the same as Anterior.

How is this possible? I have checked many websites but all state that Dorsal is the same as Posterior and Ventral is the same as Anterior. Am I going wrong somewhere?

Short Answer
This page on wikipedia gives a good synopsis of these concepts.
The confusion lies in the fact that many websites on anatomy discuss/describe/define these terms in relation to humans. However, in quadrupeds and fish (and  birds), Anterior/Posterior lies orthogonal to Ventral/Dorsal and are instead synonymous with Cranial(Rostral)/Caudal. Examining the etymologies of the 4 terms in question will demonstrate why there seems to be an inconsistency in their usage:
Ventral -> "belly" side
Dorsal -> "back" side
Anterior -> "before" or "toward the front"
Posterior -> "after" or coming after (opposite to) the anterior

Based on the body orientation of the organism (often associated with forms of locomotion), these terms can sometimes overlap (as in bipedal humans) but often lie perpendicular to each other (as in quadrupeds, fish and most birds).

A note about quadrupedalism (as summarized on Wikipedia [my emphasis added]):

Although the words quadruped and tetrapod are both derived from terms meaning "four-footed", they have distinct meanings. A tetrapod is any member of the taxonomic unit Tetrapoda (which is defined by descent from a specific four-limbed ancestor) whereas a quadruped actually uses four limbs for locomotion.

 Long Answer
Think of ventral (Latin venter = "belly") as being associated with the belly side (with belly referring to "swelling" or "inflating") -- or typically the side of the organism containing the digestive and respiratory organs. Dorsal (from Latin dorsum meaning "back") refers to the body region/"side" opposite that of ventral (and typically called the "back").
Anterior (from Latin ante meaning "before" or "in front of") refers to the "front" of the organism (i.e., the part of the organism you'd encounter 1st or before other body regions). Posterior (from Latin, comparative of posterus ("following") from post- meaning "after") is the opposite and refers to the part of the organism encountered "after" (or opposite) the anterior side.
Depending on the orientation of the organism, these terms may be synonymous in some instances but be orthogonal in other instances).

Sometimes anterior/posterior would be synonymous with ventral/dorsal, as is the case in humans or other bipedal organisms.
In other instances (e.g., in quadrupeds, fish or birds), posterior/anterior lies relatively orthogonal to the dorsal/ventral orientation. In these cases, dorsal/ventral is instead synonymous with superior (from Latin superior, comparative of superus "that is above," from super "above") and inferior (from Latin inferus meaning "low" or "below").

Often in these cases, anterior/posterior are instead associated with caudal/cranial (common alternatives for cranial  include cephalic or rostral).  Caudal (from Latin cauda meaning "tail") refers to the tail side of the organism (i.e., the side associated with coccygeal vertebrae or sometimes simply the side of the organism where waste is excreted). Conversely, cranial (Greek kranion = "skull") or  cephalic (from Latin cephalicus, from Greek kephalikos, from kephalē meaning "head") refer to the side of the organism containing the head. Rostral (referring to rostrum from Latin meaning "beak") is another synonym for cranial and refers to being "situated or occurring near the front end of the body, especially in the region of the nose and mouth or (in an embryo) near the hypophyseal region."

Some notes:

This English.SE question addresses etymology of the suffix "-erior."

You can find a pretty good list of anatomical etymologies here, here, here, or by simply searching "[word of interest]  etymology" in Google.

Also, this Bio.SE post addresses anatomical terminology usage in plants and body organs.

More generally, a frontal plane always divides an organism into ventral/dorsal.

Although these terms differ between shapes/orientations of organisms, using such terms for more specific body parts (e.g., heads or feet) are not always as inconsistent.

For example, anatomical positional terminology for brains is consistent across organisms.

One final note:
This approach to anatomical positional terminology only works with bilaterally symmetrical organisms. See here for terminology usage for other organisms.


How is pain induced by blunt and sharp objects? Normally, when something touch you, you won't feel pain. With a great force "touching" you, you will feel pain. However, if something that is spiky makes contact with you, you will feel pain. So, how much force should be exerted by a smooth/blunt object to make you feel pain? When and how does a spiky object make you feel pain?

It is a simple matter of biology and physics actually:

Firstly, pain is caused by the simulation of cutaneous nociceptors in the body, beneath the skin and are activated when the sensation crosses a threshold.

  Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system,[1] and, therefore, the ability of a body to sense potential harm. It is the afferent activity in the peripheral and central nervous systems produced by stimulation of specialized free nerve endings called nociceptors or "pain receptors" that only respond to tissue damage caused by intense chemical (e.g., chilli powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat and cold) stimulation.[2][3] Once stimulated, a nociceptor sends a signal along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of autonomic responses and may also result in a subjective experience of pain in sentient beings.[3] Nociceptive neurons generate trains of action potentials in response to intense stimuli, and the frequency of firing determines the intensity of the pain.[4]

From the wiki: https://en.wikipedia.org/wiki/Nociception

Now when you consider a knife, the surface area of the knife is small enough that it can cause damage. It's akin to holding a plastic sheet stretched tight and then piercing the sheet with the point of a knife. That is because the force is being transferred on a small point and hence easily extends the pain threshold.

However, when you consider a hammer, when the hammer touches you (lightly) you don't feel the pain because the force is spread over the larger surface area of the hammer and hence doesn't meet the threshold. However, if you hammer your finger in with force, the force being transferred is enough to shatter your bones, and in that case not only the cutaneous pain receptors activate, but the somatic receptors also activate, causing the feeling of pain.

TLDR: Knife has short surface area, and hence force transfer is over a small area, subsequently causing hurt. A hammer has a larger surface area, and hence unless more force is applied, the pain receptor threshold is not met and hence no pain.


Why do we absorb vitamins better from whole foods than from pills? We can't rely on pills to provide us our nutrients because we don't absorb the nutrients from the pills as effectively. Presumably this is because pills are lacking components that are required for certain reactions to take place.

Why can't we just create a pill that does have all the necessary components?

Why can't we just create a pill that does have all the necessary components?

I'm assuming you mean micronutrients (vitamins & minerals). A day's worth of macronutrients (energy and building-block providing chemicals - proteins, fats, sugars) are already very abundant and dense - a pill containing a day's worth would be the size of an egg.

Otherwise, we do. There are vitamin/mineral pills which have a very high absorbancy rate (usually those chelated or chemically bonded to various amino acids [words ending in -nate on the label]).

The big problem is that while the vitamins and minerals may satisfy your bare biochemical needs, that is all they do. They will not satisfy a hunger instinct (proteins and fats do that), and there are untold millions of compounds in the untold thousands of plants and products humans can pick up from the market. These compounds usually do not do much, but some are beneficial to our health.

So while multivitamins exist which provide you with a very efficient method of absorbing most of your vitamins and minerals, it's always recommended to get them directly from food since food will provide macronutrients (thus satisfying your hunger), the micronutrients you're curious about, and many potential beneficial compounds which are not necessary.

If you are still interested, Soylent Shakes are an attempt to provide all the micro- and macronutrients the body needs in an easier-to-consume form without all the messy cooking or multivitamin pills. Keep in mind the long-term effects of sticking to such a diet are more or less unknown, but it's as close as we can likely get to an "all-in-one" meal.


Can a brain be transplanted? Is it possible to transplant a brain and would it keep the memory? If not, what would be the prerequisite to transplant one?

"Is it possible" has a carefully conditional "yes".  Do we have the expertise or technology to do it now? No.  One of the biggest difficulties is that nerve tissues (the connections between brain and rest of body) will take time to heal... time during which the brain cannot sufficiently give commands to the rest of the body to keep autonomic functions running.

Head transplants, however, have been "successfully" completed using monkeys.  The monkey lived for sometime after the transplant, but eventually died.  China has also been known to do a similar procedure with dogs.

Caution, this may be too explicit for some; I'm not sure ethics boards would allow it nowadays:
Monkey Head Transplant


Do snRNAs exit the nucleus or not? In Molecular Biology of The Cell (Alberts, et al., 2015), it lists the various RNAs that are trafficked through the Nuclear Pore Complex (NPC) into the cytoplasm.

The list includes snRNAs, but I have seen it stated elsewhere that snRNAs don't leave the nucleus, that they are made there and perform their function there.

Is MBOC's version correct and snRNAs leave the nucleus, or are the other sources correct and the snRNAs are made, remain, and function in the nucleus?

After transcription of some UsnRNAs, the RNAs leave nuclei first. After assembly of various proteins and modification on the RNAs in cytosol, the RNAs come back to nuclei. In addition, it has been shown that mature U6snRNP shuttles between nuclear and cytosolic fractions in yeasts, if I remember correctly.

http://openi.nlm.nih.gov/detailedresult.php?img=2582628_gkn658f1&req=4


protocol for pulldown of DNA breakpoints? Is there any method to do pulldown enrichment of DNA breakpoints from a cell? I have found this paper reporting a method to enrich for the DNA single-strand breakpoints from meiotic recombination events:
 Khil PP, Smagulova F, Brick KM, Camerini-Otero RD, Petukhova GV. 2012. Sensitive mapping of recombination hotspots using sequencing-based detection of ssDNA. Genome research 22: 957–65.

I would like to know if there is something like that which will work on any status of the cell cycle, not only meiosis.

The paper you cite says that the break points are single stranded DNA which have specific proteins bound to them.

I'm not an expert here, but if thats the cause of meitotic break points there are some interesting possibilities for detecting them:

you could detect them with a tiling array.  - that's an micro array which has an oligomer every 40 bp or so of the genome.  The array could be used in a CHP experiment that detects the same proteins as in this paper.

Its possible that the array could possibly hybridize the single stranded DNA from the genome too if the conditions were right.  This sounds noisy though.

On the cheap side it might be possible to use PCR to copy the single stranded DNA from a chromosomal DNA prep.  if the oligos you use are labelled with streptavidin say, you could isolate it , re amplify it and sequence cheaply.

any of these sound like a good bit of work :)


Evolution of hunting behavior of parasitoid wasps Wasps in the genus Pepsis lay their eggs in a specific region on a species of tarantula and their larvae eat the tarantula organs in a specific sequence to keep it alive as long as possible.

How could this process have evolved, considering that a mistake at any stage results in death?

This is the description of the egg laying behaviour:

Upon finding a tarantula, the wasp locks its mandibles onto a foreleg and brings its stinger into position so as to paralyze it.

During this process, the tarantula tries unsuccessfully to dislodge the wasp, but the wasp ultimately locates the right part of the tarantula in which to insert its stinger.

Upon inserting it, the wasp injects a venom that paralyzes the tarantula. Note that the tarantula is ten times the weight of the wasp, so the wasp takes very big risk in trying to attack such a tarantula.

The wasp then drags the tarantula into a hole that it has already dug. It pulls the tarantula down into the  hole, attaches its egg to a specific part of the tarantula's body and then covers up the hole so that predators won't find it.

When the egg hatches, the larva eats the organs of the tarantula in a specific sequence so as to keep the tarantula alive for several weeks. Eating in the wrong sequence results in the death of the tarantula, and its subsequent putrefaction, which means the death of the wasp larva.

When the larva successfully eats in the right sequence, it is able to obtain enough nourishment to prepare for metamorphosis, ultimately resulting in a full-grown wasp, which then exits the hole and becomes a predatory wasp.

These wasps are solitary, which means there are no conspecifics to teach the new wasp how to do all this.
Thus, the entire behavioral program described above must be encoded in the wasp's genome.

The description above is based on:

Punzo, F. (2005). Experience affects hunting behavior of the wasp, Pepsis mildei Stål (Hymenoptera: Pompilidae). Entomologica Americana, 113(3), 222-229.

Petrunkevitch, A. (1952). The spider and the wasp. Scientific American, 187(2), 20-23.

Context is everything. Lets start by working back to front.

  larvae eat the tarantula organs in a specific sequence to keep it
  alive as long as possible.

Most of the time if the larva eat the organs in the wrong order they don't die, they just end up with less food. It is pretty easy to see how this could evolve to be better, larva that eat in the correct sequence end up with more food thus have an advantage, larva that eat in hte absolute wrong sequence don't survive.

  on a [specific] species of tarantula

Again easy many wasps are not as picky they will lay their eggs in/on a wide variety of hosts, but specialization is favored a lot in evolution as it helps your lineage exploit a resource better and better, you only have to deal with the defenses of a single species as opposed to many different ones which might have mutually exclusive solutions.

  lay their eggs in a specific region.

again failing to do this does not necessarily mean their larva die, it just means they are worse off becasue they don't get to eat as much. Again easy to see how this evolves, a wasp that picks its target end up with more well fed offspring. Many don't even lay their eggs inside the host but outside and let them eat the host from the outside in, this is what this species does.

  Upon finding a tarantula, the wasp locks its mandibles onto a foreleg and brings its stinger into position so as to paralyze it.

Again not every parasitic wasp does this many don't paralyse their host, but they jab them with the ovipositor relying in brute force to injure, paralyse, or kill the host. Others just lay their eggs on them and fly away. Others simply kill the host jam it in a hole and lay their eggs on it. But wasps that paralyse the host are less likely to get attacked. but even if they kill the host instead the larva still get a meal. hunting always tends to be risky, but as long as the reward outweighs the risk it can evolve. Additionally many wasps do not target adults but larva and eggs that can't fight back. venomous Stinging is actually fairly rare in wasps occuring only in the ones that attack the most dangerous hosts. Of course once a wasp lineage gets good ant not killing its host then there is little reason for the larva to be able to eat more putrid remains of the host, as such adaptations are costly so you can see how after they stop killing the prey the larva might lose the ability to keep eating dead hosts.

  The wasp then drags the tarantula into a hole that it has already dug.

Again not every species does this, some just lay their eggs on a host, without doing anything else, but this carries more risk of your larva getting dislodged or injured, but insects are not people if there is a parasite on their back there is not a lot they can do about it.

  These wasps are solitary, which means there are no conspecifics to
  teach the new wasp how to do all this. Thus, the entire behavioral
  program described above must be encoded in the wasp's genome.

Even your own source disagrees with this, it shows wasps get better at subduing the host the more often they do it, laying eggs in NOT a once in lifetime thing they may do it many many times, so not being perfect can still work.

Once you see the huge variety in parasitic wasp behavior it is much easier to the step by step sequence that can happen to get to each one. You are not even at the most extreme, there are wasps that go even further, like having viral mutualists, larva that can't poop so as not to contaminate a host they live inside, and even leaving chemical markers to keep other wasps from laying eggs in/on the same host. Parasitic wasps are rather well studied I invite you to look more into them, they are really good models of evolution.


What happens when I pop my ears? What happens when my ears are popped?

I understand it increases the air inside there which makes my volume louder, what happens after that, do my ears gradually readjust back to the air pressure that they were before?

What causes ears to (need to) be pressurized/depressurized?

The outer ear canal ends at the eardrum, and beyond that is the middle ear.  The middle ear is normally a closed chamber, but can be connected to the outside world by flexing the jaw or muscles related to.  The flexing opens the Eustachian tube, which runs from the middle ear to the back of the nose and mouth.

Hearing is best when the air pressure in the middle ear is the same as the pressure of the outside air.  If it is different, the ear drum is forced to bend outwards or inwards depending on whether the pressure is higher or lower in the middle ear.  In either case the ears senses less sound, and the volume is reduced more for some frequencies than others.

When you pop your ears, the Eustachian tubes open enough to allow your middle ears to equalize pressure with the outside world.  This restores the ear drum to its normal position and your hearing returns to your normal, optimal state which is louder and more balanced than the previous condition.  As time passes, your brain adapts to the new sound sensing state and you no longer notice any unusual loudness. The pressure in the middle ear doesn't change as your Eustachian tubes usually remain closed, and so the ear continues to hear well (as long as the outside air pressure remains little changed).


What is the function of Xylem parenchyma? why xylem need parenchyma cells ihave read these cells are connected with xylem by plasmodesma i know that plasmodesma is to connect between cytoplasm of two cells and xylem is dead so what is the need of xylem parenchyma ?

I would like to aswer your question. First definition, function is from this web:

  The xylem parenchyma is comprised of parenchyma cells. Parenchyma cells are the only living cells in the xylem. They have thin cell walls, large vacuoles, prominent nucleus, and protoplasts. They have differing shapes although they are usually cylindrical and lobed in form. In the trunks of woody plants, the xylem parenchyma cells are colourless and are believed to be involved chiefly in storing starch, oils, and other ergastic substances. The inclusions in xylem parenchyma cells may contain tanninferous compounds.

And from this article:

  Xylem parenchyma cells in contact with xylem conduits are assumed to simultaneously generate the energy gradient (deposition of solutes in the form of sugars, ions or a combination of both) that allows water to flow into empty vessels/tracheids, and supply water for refilling (Zwieniecki & Holbrook, 2009). Regarding the first task, the initial research focus has been on finding the source of osmoticum through analysis of carbohydrates in the parenchyma cells and the role of phloem in the delivery of sugars to sustain refilling. Both enzymatic analysis and visualization techniques have demonstrated that starch levels in living parenchyma cells adjacent to xylem vessels decrease on a timescale coincident with embolism refilling (Bucci et al., 2003, Nardini et al., 2011a, Sakr et al., 2003, Salleo et al., 2009, Secchi & Zwieniecki, 2011).


Basis of enzyme nomenclature — pyruvate dehydrogenase In the formation of AcetylCoA from pyruvate, why is the enzyme called “pyruvate dehydrogenase (complex)” when it involves the decarboxylation of pyruvate or the replacement of a carbonyl group by coenzyme A?

The pyruvate dehydrogenase complex catalyses the oxidative decarboxylation of pyruvate. A description of this is easy to find on the web (e.g. Wikipedia), but I would recommend the section in Berg et al. Biochemistry (online), as it is an authoritative book with a high reputation.

Pyruvate + CoA + NAD+ → acetylCoA + CO2 + NADH

In the overall reaction, shown above, pyruvate is being oxidized (hydrogen removed) by NAD+, which is reduced to NADH. Hence there is nothing surprising in the enzyme having acquired the description, dehydrogenase.
Before asking questions about enzyme nomenclature, one should consider the historical and scientific context in which names arose. This was general scientific ignorance of the overall metabolic pathways in which they occurred or even the direction in which the reaction normally proceeded. There is also the question of focus — here on oxidation of carbohydrates. The working names that arise — trivial names, as they are called — tend to stick: they are in the literature and everyone in the field knows what you are talking about. Eventually, when the dust has settled, scientific commissions assign systematic nomenclature. In this case there are three enzymes involved, so that each has its own systematic name:

Pyruvate dehydrogenase (acetyl-transferring) — EC 1.2.4.1
Dihydrolipoyl transacetylase — EC 2.3.1.12
Dihydrolipoamide dehydrogenase — EC 1.8.1.4

It can be seen that even the systematic name for enzyme E1 (which catalyses the decarboxylation) does not refer to the decarboxylation, but to the transfer of the acetyl group (to thiamine pyrophosphate and then to lipoamide), which is of more interest mechanistically.
Details of the reactions and alternative names corresponding to the EC numbers  (Enzyme Commission numbers) can be found either on the Queen Mary University site or Expasy.


Do invasive species cause long-term damage to ecosystems they invade? Growing up in the U.S., I was warned at various times of the dire consequences of a variety of introduced pests (usually insects).

Japanese beetles, gypsy moths, and most recently the brown marmorated stink bug are all introduced pests that, at various times, were described as serious threats to our ecology.

These threats aren't confined to arthropods, either.  The giant African land snail is causing a stir in Florida (indeed, Florida seems to suffer from an excessive variety of introduced species.

"Lack of native predators" is frequently cited as the primary reason many invasive species are considered such a risk to the ecology.

I understand that these introduced species can place tremendous pressure on native species that fill similar ecological niches, and may even push these species out of the region due to competition for food and habitat.  However, do the overall ecologies that these species are introduced to adjust over long periods of time?

The numbers of Japanese beetles and gypsy moths don't seem anywhere as high as when I was a child.  Has the ecosystem adjusted, or has the overpopulation self-corrected as the species ran low on food through over-consumption?  Or are the populations still just as problematic now as they were 30 years ago, and I just am not seeing the bigger picture?

What is the long-term impact that we've seen from invasive, introduced species?  Is there a significant difference on the long-term impact between introduced flora, arthropods, or mammals?

The answer really depends on how you think of invasive.  One extreme answer is to say that all things are relative, and that the concepts of local and invasive are all relative.  This matters to a certain extent because ecologists draw a fuzzy line between invasive and naturalized.  You could start with some basic species that we all think of as either good, local, or neutral.  Take the earthworm.  Most people think of it as a common native species, but the earthworm is actually an invasive species that has radically changed much of North America that came over with the Europeans.  Similarly, brown trout are also invasive, coming to the US in the 1800's.

As far as why invasive species succeed, it's still an open question.  What you reference is the enemy release hypothesis, but there are others such as disturbance, diversity of the new community, and just the traits.  Here's a good review of biological invasions and a second one.

To answer your question about adapting, I wouldn't trust your memory. It's important to keep in mind that most likely your memory is flawed, and you are only observing a very limited number samples with an incomplete sampling methodology.  For instance gypsy moths undergo wild population fluctuations, and have for over 100 years.  How well do ecosystems bounce back from invasions depends on lots of factors.  Often time the ecosystem can survive, but the some species won't.  An easy example would be Norther Hardwood forests.  Chestnuts (extirpated by an invasive fungus)are mostly gone from the wild, but the forest persists, as well as many of the species that rely on them.  So in part the answer to your question depends on scale.  The forest survived, but an individual species was nearly destroyed.

Ecological economists have tried to put a value on the destruction that invasive species have caused too.


Why are particular laser-related skin products not recommended for darker skin tones? This is about products such as:

The "Theradome" laser helmet (this claims to stimulate hair growth through lasers)

  Theradome™, a biomedical engineering company based in the Silicon Valley, is the proud designer, developer and manufacturer of the Theradome™ LH80 PRO, the first and most powerful FDA cleared OTC wearable laser hair helmet for laser hair growth treatment. At last, millions of people suffering hair loss can enjoy clinically effective laser hair restoration treatments at home, at an affordable price, with a simple push of a button.

Silk'n Flash&Go Hair Removal Device (claims to remove hair using lasers)

  Silk'n Flash&Go™ is a revolutionary light-based system for permanent results at home. Now you can remove unwanted hair forever on your body and face – all with gentle pulses of light that disable hair growth. It's the safe way to get smooth, beautiful skin.

From the information on the website, it would appear that the products are safe for all; however, both products seem to be not recommended for the two darkest skin colors on the Fitzpatrick Skin Tone Classification Scale on a variety of different product feedback websites. What is the reasoning behind this?

The reason for laser hair removal/growth products not being safe for darker skin tones is the ability for darker skin tones to absorb more light from the laser than lighter skin does BEFORE the light is able to reach the depth at which the hair follicle is located. Light from lasers must pass through the epidermis where melanocytes are located before they reach the hair follicle.

More melanin means increased ability to absorb wavelengths as seen in the curve below. Laser products such as Theradome (678nm) and Silk'N (475-1200 nm) have shorter wavelengths, which are highly absorbed by melanin, and therefore can damage skin in darker skin tone patients. Safer products like Nd:YAG are those that have higher wavelengths at 1064nm and can penetrate the skin without over-absorption by melanin.

Disclosures: I own no stock in any of these companies.

References:

http://www.theradome.com/press-release/
http://www.amazon.com/Silkn-Flash-Removal-Device-Cartridge/dp/B0093BOR4W
http://www.nature.com/jid/journal/v122/n2/full/5602198a.html


Why won't this spray kill this bug (household insecticide); could it be so selective? I have a can of bug spray. The label is in another language which I can not even type in order to do an online translation, but the ingredients are in romanized writing:

Metofluthrin  0.012% w/w
Phenothrin    0.100%
Cyphenothrin  0.100%

Wikipedia: Metofluthrin, Phenothrin, Cyphenothrin

I've been seeing small (3~4mm) dark flying bugs that seem to be able to take a direct hit. They may be grounded, but after a minute or two walking around and cleaning their wings, they fly away.

The spray worked very effectively on the cockroach I bought it for; this kind of thing happened about 90 seconds after a direct hit. Here they don't really infest as much as just wander in off the street and can't find their way out again.

I assume if I get rid of any residual sources of food or water the little flying things should die off. But I was really shocked to see them fly away undaunted after some serious aerosol action.

Here are some snapshots I took of the small bug trying to eat my spicy noodles. It's actually not so dark. Please please tell me it's not a tiny baby cockroach!

It's a tiny baby cockroach.  Sorry.

http://animalia-life.club/other/german-cockroach-nymph.html

I looked up your chemicals; the first (metofluthrin) is mosquito repellant and the others are for fleas and mosquitoes.  The combo makes me think that this is something intended for spraying on the body or on animals.  It is not strong enough.

You need to get a bigger boat.  Get a spray made for roaches.


Why is the frog genome so much larger than a fish's? As we have heard in the summaries of the human ENCODE project, 80 per cent of junk DNA appears to have an essential function. Many fish have a genome with only one tenth the size of a usual vertebrate genome. Why can fish have 1/10th of junk DNA and be still fully functional? What has a frog more than a fish has? I'm especially interested if we can see the difference somewhere, complexity of physiology or anatomy, or such.

Jap. puffer fish genome: 390 Megabases, 47,800-49,000 genes (UniProt)

Medaka genome: 690 Megabases, 24,600 genes

Clawed frog: 1,500 Megabases, 23,500 genes

Genome size is a poor indicator of an organism's complexity (already an ill-defined term). We cannot assume by any means that a larger genome corresponds to a more "complex" organism. There are some plants whose genomes are larger than most mammals, and indeed the largest eukaryotic genome (at least as of 2010) is the plant Paris japonica, weighing in at 1C = 152.23 pg (compared to Homo sapiens at 1C = 3 pg). Anecdotally, in my previous research lab I discussed with a colleague a fungal species whose genome size differed by orders of magnitude between different individuals of that species.

It should never surprise you to see an organism with a larger genome size than what you may consider to be a more complex organism.


DNA replication Okazaki fragments I understand multiple origin bubbles; DNA polymerase only synthesizes DNA from 5' to 3' and all that. But what I don't understand is why it has to be in fragments. Yes, DNA is anti parallel, and so the DNA elongates in opposite directions, since DNA polymerase can only go one way. But why not go on just like the leading strand? Why not continue happily along the DNA template continuously but in fragments?

I think you may have been misled by graphic representations of the process: The actual replication fork is very small as, like Rex Kerr mentions, it costs a lot of energy to keep DNA single stranded.

Have a watch of https://www.youtube.com/watch?v=yqESR7E4b_8 at minute 1:45, it contains a relatively realistic representation of the replication fork. Of course you have to imagine all of the space around the molecules in this video to be filled with other DNA, RNA, proteins and small molecules zipping about.

On top of this, we like to think of DNA as a lone double strand where occasionally a protein might attach and do something. Realistically however, most of the DNA is constantly being manipulated by all sorts of proteins (mostly histones for compression, but also transcription factors, methylating and demethylating enzymes, DNA repair enzymes,...). DNA replication has to minimise the interruption it causes to all the mechanisms going on around it, and the most effective way to do this is by replicating the lagging strands in fragments which can be zipped up quickly and left to whatever other proteins might do to it.


Umbrella term for "parts of the brain" I am looking for an umbrella term for general "parts of the brain", esp. for (somehow arbitrary) "subsets of neurons".

For the tree of life there is an umbrella term for all kinds of taxonomic groups all down the tree. They are called taxa.

Domains, kingdoms, phylums all down to families, genus, and species are taxa:

In brain sciences there seems to be no such umbrella term which is generally agreed upon.

Which term would best include all of the following?

brain hemispheres
coarse brain subdivisions (cerebellum, cerebrum, ...)
cerebral lobes (frontal, parietal, ...)
the thalamus („a large mass of gray matter“)
nuclei (thalamic, ...)
Brodman areas
cortical layers
cortical columns
the limbic system
regions of interest (in fMRI)

All of these immediate suggestions don't fit perfectly:

(brain) region
(brain) division
(brain) area
(brain) volume
(neural) group
(functional) system

When you just want to list the components of the brain, that is to say what the brain consists of from the gross anatomy perspective, you can say that the main parts of the brain are:

cerebrum
cerebellum
brainstem

You can also say that the parts of the brain are some smaller, but anatomically well defined components, such as the pineal gland and pituitary gland.

When you intend to describe the functions of anatomically well defined brain areas, you can say that the brain structures are cerebral lobes, thalamus, hypothalamus, hypocampus, amygdala, putamen, corpus callosum, cyngulate gyrus, etc.

A part is "a portion or division of a whole that is separate or distinct; piece. A structure is "mode of building, construction, or organization; arrangement of parts, elements, or constituents." So, it's not about what "it is," but about how you look at it. A thalamus is a part of brain and is a structure made of several nuclei...

You can see these terms used very differently in various texts, but a short overview of brain anatomy by Mayfield clinic use them in the same way as I did. These terms are not a part of any official classification in neurology.


Do people of the same height walk at the same speed? I'm working on a project that concerns movement and the human body. Before I begin to experiment, I need an answer to a question I'm sure has an answer, but doesn't Google well.

What I need to know is firstly whether I can assume that if people have the same height, they will also have the same leg length?

Secondly, if two different people have an identical height, will they take the same amount of time to cover the same distance when running at the same speed, regardless of their unique technique for running?

An Example:

Say I'm with a friend, we're both 6 feet tall exactly, we both get on to treadmills side-by-side and set it to a speed of 7.5km/hour.

Will we be moving exactly the same body parts at the same time - will our feet land on the treadmill at the same time?

Is there a possibility that people of the same height do not have the same leg length? If so, how likely is it on average?

People of the same height can easily have different leg lengths. Think western women models - currently they are typically women with relatively long legs while ordinary people can easily have shorter legs for the same total height. There's even leg-to-body ration section in Body proportions Wikipedia article.

This is why pedometers always require calibration - the procedure in which you have to walk a known distance and count steps and then know how much steps you need per mile. There're no tables that would assist by assuming certain steps-per-mile ration for known height.


What is the adjective for PHAGE? if the adjective of the noun BACTERIUM is 'bacterial' and that of VIRUS is 'viral', what is the adjective for (BACTERIO)PHAGE? Is 'phagial' accepted?
Thank you

In the literature, it's most common to see hyphenated compound adjectives, like "phage-mediated," "phage-dependent," or "phage-encoded" where "bacterial" or "viral" might be analogous. For example, "Phage‐mediated selection and the evolution and maintenance of restriction‐modification."
Sometimes "phage" seems to be used as a standalone adjective, like in "Phage antibodies: filamentous phage displaying antibody variable domains." Although I'm not sure that it would be correct to use "bacterial antibodies" or "viral antibodies" in this case, so maybe that one is an anomaly.
I would suggest following one of these trends, unless you want to do a lot of explaining to reviewers.


What method would you use to genotype SNPs in low quality samples? What method would you use to genotype SNPs in low quality samples? I ideally want to genotype hundreds of SNPs in hundreds of scat samples (very low amount of target DNA, potentially degraded and highly contaminated by other DNA).

I agree with @gchadwick that more infor would help.

However, based on my understanding of what you are trying to do (SNP genotyping on several genes), I suggest.
1) Enrich your DNA with DNA from the organism you want
2) Enrich your DNA with DNA in the desired regions (if any).

Solution: Target enrichment. You are probably aware that companies such as agilent, nimblegen and illumina offer target enrichment kist for next generation sequencing.
However, if your DNA is soooo bad, I suggest performing target selection with PCR.


What is the name of this about 10cm high, grey, "flat hat" fungus? I found this fungus on Corsica (France). Can you please help me to identify it?

Based on the dark lamellae and the ring around the foot, I would bet on something in the Agaricus genus. The French Wikipedia gives quite some details about common species in this genus: https://fr.wikipedia.org/wiki/Agaric


What determines the sex of hybrid offspring? I'm aware of the usual definition of Haldane's rule, which says that, if the offspring of inter-specific hybrid offspring are sterile, then the sterile offspring will be of the heterogametic sex. That is, for example, females in birds, and males in mammals. But I'm a bit confused. This implies that non-sterile hybrids are also produced, which rarely happens.

So, I have two questions, please:
 1. Does Haldane's Rule really mean that only offspring of the heterogametic sex are produced?

And 2. If so, please account for the exceptions. Crosses between Golden Pheasants and Lady Amherst's Pheasants regularly produce female as well as male offspring, as do crosses between Ring-necked Doves and Barbary Doves. Thanks!

I am detecting a bit of confusion in you wording of Haldane's rule.
Haldane's rule makes predictions on the fertility of offspring from an inter-specific cross, not the sex-ratio of the offspring from the cross.

"if inter-specific hybrid offspring are sterile, then the sterile offspring will be of the heterogametic sex."

In inter-specific crosses there is not an effect on sex-ratio of the resulting offspring, but a effect on the ability of the F1 offspring to reproduce.
For the offspring, those of the heterogametic sex, males in mammals (XY) and females in birds (ZW) will be sterile while the homogametic offspring will not be affected by hybrid sterility.


Can any gas other than nitrogen cause decompression sickness (the bends)? I know that our bodies use most of the oxygen we breathe in during a dive but, wouldn't our tissues, under pressure, absorb more oxygen than we need?  For instance, in normal circumstances, we don't use all the oxygen in each breath and we exhale some (this is what 'rebreathers' are for, right?)
Couldn't any gas we breathe in under pressure cause decompression sickness when we decompress?
Read this, from NASA:

"Astronauts put on their spacesuits several hours before a spacewalk.
The suits are pressurized. This means that the suits are filled with
oxygen.
Once in their suits, astronauts breathe pure oxygen for a few hours.
Breathing only oxygen gets rid of all the nitrogen in an astronaut's
body. If they didn't get rid of the nitrogen, the astronauts might get
gas bubbles in their body when they walked in space. These gas bubbles
can cause astronauts to feel pain in their shoulders, elbows, wrists
and knees. This pain is called getting "the bends" because it affects
the places where the body bends. Scuba divers can also get "the
bends."

Yes, it is possible to get decompression sickness with other gasses, such as the "oxygen bends" or oxygen decompression.  For instance, in this study, they demonstrated that oxygen decompression sickness in mice.  Another study demonstrates a more common non-nitrogen decompression sickness - helium bends.
Undoubtedly you will be wondering at this point why breathing pure oxygen would diminish (or, in certain circumstances, completely remove) the risk of bends as compared with nitrogen.  The reason is simply that oxygen, unlike nitrogen gas, is constantly being metabolized by the body tissues.  Consequently, even if the oxygen levels in your body fluids become elevated, they would have to be way higher than normal levels (like in the first study linked) before you would start to have it accumulating enough to form bubbles.
The body is designed for the shipping and handling of oxygen (think haemoglobin & myoglobin).  Nitrogen, on the other hand, is relatively incidentally present - so long as atmospheric pressure remains relatively constant (which it did until we devised technology allowing us to radically change it), it's present in low levels in all the body tissues without causing any trouble.


Why is coconut oil healthier when it has so much saturated fat? I noticed that coconut oil has ~96% saturated fat, and I was under the assumption that saturated fats = bad for health.

Why is it that coconut oil is healthier to alternatives with much less saturated fat?

coconut oil is composed mainly of medium-chain triglycerides, 1)it is smaller than other long-chain triglycerides so that it can be digested easily, 2)the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system, 3) liver prefer use medium-chain triglycerides as the fuel sources 4) medium-chain triglycerides will convert to monoglyceride and medium-chain fatty acid which have strong antibacterial


How is transport of glucose into prokaryotic cells different from transport into eukaryotic cells? I was reading page 92 of Fundamentals of Microbiology, 4th edition, which states

  In facilitated diffusion, the substance (glucose, for example) to be transported combines with a plasma membrane protein called a transporter.

The section of text that says this is in a section describing prokaryotic cell anatomy. As far as I understand human biology, (just to use one example) that facilitated diffusion is regulated by insulin, which, to use less than perfect language simply to streamline my question, uses insulin to "unlock" the plasma membrane proteins.

What's the difference when prokaryotic cells aren't dependent upon insulin to get glucose in?

In prokaryotes the glucose transporter is always present in the cell membrane; in cells whose glucose uptake is insulin-regulated the transporter is only present in the plama membrane when hormone levels are high.

GLUT4 is the isulin-regulated glucose transporter found in muscle and adipose tissue. When insulin levels are low the GLUT4 protein is in the membrane of small vesicles inside the cell. The appearance of insulin signals the fusion of these vesicles with the plasma membrane. In this way the number of GLUT4 molecules in the plasma membrane is increased, raising the capacity of the cell for glucose transport. GLUT4 transports glucose into the cell by facilitated diffusion.

More information about the GLUT family of glucose transporters can be found here.


Is it possible for neurons themselves to manifest cancerous behavior? From what I understand, one form of cancer is a faulty gene responsible for the programmed death of a cell.

Not long ago, popular wisdom used to say neurons don't regenerate. However that is no longer believed to be true, if I am to believe what the internet says. For me, this begs the question: can neurogenesis result in faulty death genes which in turn result in overgrowth of the number of neurons? Would those neurons be functional? And if so, if theoretically such a brain could be artificially sustained without a body, would its growth be beneficial (in terms of intelligence)?

Yes, but rarely.

Other types of brain cells are much more likely to form tumors. Oligodendrocytes, astrocytes, and more generally glial cells all form tumors with some regularity.

Nerve sheaths can also form benign growths.

Nerves themselves can even manifest cancerous behavior, even though they are nearly always benign and very slow growing. Unfortunately, they tend to cause seizures, increased intercranial pressure, and decreased neurological function in affected areas.


what kind of dinucleotides can be considered important from a mutational point of view other than CpG islands? CpG islands are regions with an high frequency of CpG (Cytosine-phosphate-Guanine) sites. The usual formal definition is that of a region with at least 200 bp, a GC percentage greater than 50% and an observed to expected ratio grater than 60%. In colorectal cancer, these regions have been found drastically methylated with respect to the normal mucosa tissues surrounding the tumor (Illingworth et al. 2010). This brought to speculate a role in the cancer onset. My question is: are there any other kind of dinucleotide rich regions that represent important cases of study in literature?If yes, can you suggest me some papers and references?Than you
Illingworth RS, Gruenewald-Schneider U, Webb S, Kerr AR, James KD, Turner DJ, Smith C, Harrison DJ, Andrews R, Bird AP (2010). "Orphan CpG islands identify numerous conserved promoters in the mammalian genome". PLOS Genet. 6 (9): e1001134. doi:10.1371/journal.pgen.1001134. PMC 2944787. PMID 20885785.

In some types of cancers like breast cancer, APOBEC3 cytidine deaminases can become upregulated and enhance mutagenesis. As shown in this mutational signature from cancer tissue data the enzymes prefer TC motifs.

Source: https://cancer.sanger.ac.uk/cosmic/signatures/SBS/index.tt


Is there any definition of life which makes viruses undeterminable? There are many different definitions of life (RNA, something that comes through evolution) but not one I have seen which could not determine wheter viruses are living things (even though there are many definitions both for YES and NO). Are there any such definitions (I'm looking for cases where it's really fundamental debate, not only struggling for the correct dictionary definition)?

Thank you.

Your last sentence is the key: defining life really is just finding a dictionary definition that we can agree upon. Biology is something that defies discrete definitions at times: "What is it to be alive?" "What is a species?" maybe even "What is the wild type allele of a gene?"
I would recommend not looking at viruses as a challenge to determine if they are alive or not so much as an excellent opportunity to discuss what we think are important characteristics of life.
Life can alternately be described as:
"Comprised of self-replicating cells" (a paraphrase of the "Cell Theory of Life"
or
As things that embody at least most of the following characteristics:
1. Self-Replicating
2. Metabolizing
3. Growing
4. Showing signs of adaptation
5. Being organized
6. Respond to their environment
7. Being comprised of cells

I like to think that we should focus on extraterrestrial forms when we define life. i.e. what would we want to see in an extraterrestrial in order to call it 'life'? While some are troubled by calling viruses alive here on earth, the same people might be willing to say that we have found extraterrestrial life on another planet if it was similar (granted, it's hard to imagine this kind of life existing without a host...)

as an aside: You might also ask whether this question is fit for this stack as it can not be supported by literature references (at least none that would actually support a conclusion). So should this be posted as 'Biology' or 'Philosophy'?


How many protons are pumped out per pair of electrons from NADH in oxidative phosphorylation? I have searched the web and found that 10 protons are suppose to get pumped out during the electron cycle, but i'm a bit confused.

I'm trying to count, for every complex(1/3/4), the number of protons that are reduced in the matrix versus the number of protons added to the intermembrane space. The numbers don't add up.

my calculations:

complex 1: 4 protons reduced, 4 protons added.
complex 3: 2 protons reduced, 4 protons added.
complex 4: 2 protons reduced(not counting the ones that condens to H2O), 2 protons added.

It seems like the mistake is in complex III. Look at this image from here:

It clearly shows the number of protons reduced in (and taken from) matrix and number of protons pumped into inter-membrane space. So the data becomes:

Complex I:

matrix: 2H+ reduced (from NADH + H+) + 2H+ pumped out

IMS: 4H+ pumped in

Complex II:

matrix: 2H+ reduced (from succinate)

IMS: 0H+ pumped in

Complex III:

matrix: 2H+ pumped out (when not considering complex II, you'd count 4H+ here)

IMS: 4H+ pumped in (2 from complex II)

Complex IV:

matrix: 2H+ reduced (to H2O, we won't consider it as you said) + 2H+ pumped out

IMS: 2H+ pumped in

TOTAL:

matrix: 10H+ subtracted/pumped out (with 2H+ to water, total 12H+)

IMS: 10H+ pumped in

This satisfies your statement that "10 protons are supposed to get pumped out during the electron cycle". I Hope this helps ;)

IMS = inter-membrane space


How does MEME compute the background frequency of nucleotides? I am trying to calculate a log-odds matrix for MAST input, from a position-specific probability matrix for the motif in which I am interested.

I would like to know how MEME estimates the background frequency of nucleotides, as it does the conversion from position-specific probability matrices to log-odds matrices when you choose to run MAST on MEME output.  Is it simply counting frequencies in the sequences supplied, or is there some sort of modeling going on to correct for sample size and whatnot?

EDIT: Another possibility that occurred to me is that MAST is capable of converting position-specific matrices to log-odds matrices.  I'd appreciate it if someone could clarify this point for me (and I'm still interested in how the background frequencies are calculated).  Also, I am specifically looking for answers with links to supporting documentation.

EDIT 2 (05/07/13): Alexander has answered the original question.  Does anyone have an answer to the first edit (re: MAST)?

EDIT 3: MAST doesn't like PSPMs; it will accept the job but crash.

At the MEME server page, there's a link to upload a customized background markov model (using the command line interface, this is the -bfile option).  From there, there's a link to the MEME Man Page.  Under "Objective Function", it specifies:

    The background model is an n-order Markov model. By default, it is a 0-order model consisting of the frequencies of the letters in the training set.

So yes, it's basically the simplest possible correction: no accounting for pairwise frequencies, complements, motif width, etc.  I expect this is because MEME can be applied to essentially any dataset, such as phage display bindings from a "truly" random set of short oligos. In which case making higher order assumptions about the pairwise independence would be detrimental.

Below that, I think it answers your question about the total log-odds calculation:

    The E-value reported by MEME is actually an approximation of the E-value of the log likelihood ratio. (An approximation is used because it is far more efficient to compute.) The approximation is based on the fact that the log likelihood ratio of a motif is the sum of the log likelihood ratios of each column of the motif. Instead of computing the statistical significance of this sum (its p-value), MEME computes the p-value of each column and then computes the significance of their product. Although not identical to the significance of the log likelihood ratio, this easier to compute objective function works very similarly in practice.


How come that we "feel" it when someone's watching us The question is relatively easy (the answer however..). We all know this feeling "being watched" and more often than not this is a real thing. If someone is staring at us from the side or from the back we sort-of "feel" it and we evenf eel the direction where it's coming from.

I can't seem to find a plausible answer for this though:

We actually see the people staring from the corner of our eyes - false, I tested this thoroughly and it also happens when your eyes are closed or someone's behind you.
Eyes don't send out energy (or "beams") as far as I know. They "receive" light but don't send any out, except for reflection.

So, what causes this strange phenomenon?

To quote the University of Sidney site:

  People often think that other people are staring at them even when
  they aren't research led by the University of Sydney has found.

  When in doubt, the human brain is more likely to tell its owner that
  they're under the gaze of another person, researchers from the
  University of Sydney and The Vision Centre reveal in a recent article
  in Current Biology.

Also, from the scientific paper:

  We presented participants with synthetic faces viewed under high and
  low levels of uncertainty and manipulated the faces by adding noise to
  the eyes. Then, we asked the participants to judge relative gaze
  directions. We found that all participants systematically perceived
  the noisy gaze as being directed more toward them. This suggests that
  the adult nervous system internally represents a prior for gaze and
  highlights the importance of experience in developing our
  interpretation of another’s gaze.

So you, and I, overestimate how often people is staring at us.

For details, see: http://sydney.edu.au/news/84.html?newsstoryid=11335 and https://www.cell.com/current-biology/retrieve/pii/S0960982213003321


Role of dam methylase in bacteria In bacteria, an enzyme called dam methylase (Deoxyadenosine methylase)  methylates adenines (A) in the sequence GATC in the new strand formed after replication.
What role does this methylation play?
I read that it has something to do with proofreading. If this is so, then how?

The dam methylase has three different functions:

Correction replication errors, since the new DNA molecule
is only hemimethylated (the old strand is methylated, the newly
synthesized is not). Since the proof-reading only takes place on the
new strand, errors introduced during replication can be corrected.
Regulation of replication: The ori of the chromosome is methylated to ensure that is only replicated once.
Regulation of transcription: Methylation of GATC sequences promote the transcription of genes.

For further details see the references.

References:

The great GATC: DNA methylation in E. coli
The dam and dcm strains of Escherichia coli--a review.
Dam methylation: coordinating cellular processes.


Cancer cells and their ability to avoid the immune system Since cancer cell retain their ability to trigger the immune system from their pre-cancerous state and any condition that causes an auto-immune reaction in a specific area of the body will attack any cells in that area then could an auto-immune reaction actually attack any cancer cells in that area also?

Noting that regular human cells are not able to avoid 'attacks' by an auto-immune response so the normal cells can not pass on any 'strategies' for avoiding an auto-immune disease attack to any cancerous cells they 'turn into'.. Is all this possible?

There are several types of cancer immune evasion.
Such as releasing immunesupressive cytokines, downregulation of MCH and comprising mutiations which are not immunogenic.
If the cancer at a tissue is evading immune system by immunosupressive cytokines it may not be affected from auto-immune attack.
However if the cancer is not attacked by the immune system just because it is not "different" enough from the nearby healthy tissues, then at this time auto-immune attack to the tissue may technnically attack the cancer also.


Get "DNA" of one parent based on its children I'm no biology expert so bear with me, but I've been given a task to estimate alleles of an animal based on the animal's children and the children's other parents.
I've looked up Mendel's laws but I'm not sure I can possibly determine the correct result - better show an example:
Let us say that we want to get alleles of a mother. We know the following:
Child 1 has alleles: AG, the father of the child has alleles: AG
Child 2 has alleles: GG, the father of the child has alleles: GG
Child 3 has alleles: GG, the father of the child has alleles: GG
According to Mendel's laws and the example above it would seem that
For the first child x father pair - the mother would have alleles AG
For the second and third child x father pair - the mother would have alleles either GG or it could have AG, CG or TG.
How can I determine which anwser is correct?
If needed I can provide more examples.

EDIT: More examples / clarification

I have a database of animals (cows/bulls). Each animal has ~50 000 SNPs, each SNP has 2 alleles.
However, some of the animals data are missing, for instance I do not have SNPs for a certain bull, but I do have SNPs of the bull's children and their mothers.
Now I need to figure out an algorithm that based on the SNPs of said children and the SNPs of their mothers tries to compute the SNPs of the bull.
Additional example: (each row represents a child - mother pair)
SNP                                 | Child alleles | Mother alleles | Possible father alleles
ARS-BFGL-BAC-19454  | GG               | AG                   | AG, GG
ARS-BFGL-BAC-19454  | AA                | AG                   | AG, AA

From the table above it is clear that the bull can only have AG.
However I do not know how to handle the following case:
SNP                                 | Child alleles | Mother alleles | Possible father alleles
ARS-BFGL-BAC-14220  | AG               | AG                   | AA, AG, GG
ARS-BFGL-BAC-14220  | GG               | GG                   | GG, AG, CG, TG
From the table above it looks like the bull can have either AG or GG - how do I figure out whether the father's value is AG or GG?

Ok, I think I can answer somewhat usefully with the update.
It's helpful in this case to think in terms of sampling alleles. It's true that the cases that you give are not 100% unambiguous, but it is not true that we can't give a somewhat confident estimate. We can still make a statistical prediction of the most probable genotype.
The first thing to note is that you are working with pedigrees. That is, you have parents and multiple children. Pedigrees are great because they allow you to pool information across individuals.
The next thing to note is that your alleles are almost certainly not of uniform frequency in the population. In other words, If I sample a random cow from the herd, the probability of allele $A$ at some arbitrary locus is almost certainly not the same as the probability of allele $G$. You can use that information in inferring the most likely allele. Moreover, you can put a precise number on the probability of any given allele.
The simplest method I can think of is to use genotype likelihoods, to account for pedigree information, and to incorporate the background allele frequency as a prior probability (h/t Vadim for the Bayesian approach).
A likelihood is the probability of some dataset given a specific hypothesis. In other words, your data is your offspring genotypes and your hypothesis would be the different offspring.
In your first example, we can logically rule out alleles other than $AG$. (That's actually not true; you should account for the possibility of genotyping error, but we'll ignore that for now.)
In your second example, we can't logically rule out all but one genotype. But we can say some things nonetheless:

you have said that there are only 2 alleles per locus (i.e. $A$ and $G$ are the only possible alleles).
$A$ and $G$ have distinct frequencies in the population.
we now at least one paternal allele ($G$).

Let's take a simple case of the likelihood application, in which we say that frequency of $Pr(A) = 0.9$ and $Pr(G) = 0.1$ (I am making these numbers up). Now in the ambiguous case:
$$Pr(paternal=GG | offspring\_genotypes=GG,AG) = \\
Pr(offspring\_genotypes = GG,AG|paternal=GG) * Pr(paternal=GG) = \\
Pr(offspring=GG | paternal=GG, maternal=GG) \\
* Pr(offspring=AG | paternal=GG, maternal=AG) * Pr(paternal=GG)
$$
and
$$Pr(paternal=AG | offspring\_genotypes=GG,AG) = \\
Pr(offspring\_genotypes = GG,AG | paternal=AG) * Pr(paternal=AG) = \\
Pr(offspring=GG | paternal=AG, maternal=GG) \\
* Pr(offspring AG | paternal=AG, maternal=AG) * Pr(paternal=AG)
$$
Which evaluate to:
$Pr(paternal GG) = 1.0 * (0.5 * 0.5 + 0.5 * 0.5) * (0.1 * 0.1) = 0.005$
and
$Pr(paternal AG) = (1.0 * 0.5) * (0.5 * 0.5 + 0.5 * 0.5) * (0.5 * 0.1) = 0.0125$
You can see that there are multiple ways for the offspring to get genotypes in the paternal $AG$ case, which is what leads to the terms with addition. Note also that the $Pr(paternal genotype)$ at the end handles the genotype frequency, as all the other terms are conditioned on the parental genotypes.
So in this highly artificial example, we prefer genotype of $AG$ somewhat (note that these likelihoods do not sum to 1.0). But, if we were to alter the genotype frequencies to 50% frequency of each allele, we would get:
$Pr(paternal GG) = 1.0 * (0.5 * 0.5 + 0.5 * 0.5) * (0.5 * 0.5) = 0.125$
and
$Pr(paternal AG) = (1.0 * 0.5) * (0.5 * 0.5 + 0.5 * 0.5) * (0.5 * 0.5) = 0.0625$
and you would come to the opposite conclusion!
So it really matters what the background frequency is, if you choose to consider that term.
You could also think about genotyping error or whatever as part of these calculations.
I am certain that there is a more sophisticated way to do this, that takes better advantage of available information, etc. Maybe I've even made a mistake in the computation- but this is an approach that you might use to infer paternal genotypes.


Is breathing a reflex action or is it an intrinsic process? The process of breathing is controlled by respiratory centers in the brain stem. Do these centers have an innate activity, i.e., just send out signals to breathing muscles intrinsically, and have the rate and manner in which they do so modified by various regulatory factors?

Or are they driven by imbalances (in levels of oxygen, carbon dioxide, hydrogen ions) like a reflex? Let's say that hypothetically these levels remain static in an acceptable state such that this reflex is no longer needed, would breathing stop since there's no longer a driving motive or would it continue because the respiratory centers have an intrinsic activity?

While the ultimate purpose of breathing could be considered to be the maintainance of a balance of the substances you are referring to (such as blood oxygen, carbon dioxide, and hydrogen ions), the blood levels of these substances do not directly control the production of action potentials within the motor neurons that promote the contraction of the diaphragm and intercostal muscles.

The propagation of these action potentials is initiated by signals from the medullary respiratory center, specifically the neurons in the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). In the VRG, a complex of neurons known pre-Bötzinger complex is responsible for generating the signals that cause the rhythmic muscle contractions involved in breathing:

  The respiratory rhythm generator is located in the pre-Bötzinger complex of neurons in the upper part of the VRG. This rhythm generator appears to be composed of pacemaker cells and a complex neural network that, acting together, set the basal respiratory rate.

Vanders Physiology, p473, 15th ed.

So breathing is indeed, as you mention, a process that is controlled by innate neuronal activity but regulated by the concentrations of PO2, PCO2, and H+ concentrations. I recommend you read pages 473 to 477 of Vanders Physiology, which explains these controls in detail, some of which do involve reflexes, say, if O2 concentration in the blood strays too low.

Interestingly, expiration, which is typically a result of actions potentials ceasing and respiratory muscles relaxing, can be controlled by a reflex, known as the Hering-Breuer reflex, during strenuous exercise when the lung is inflated by a large tidal volume. Stretch receptors in the airway in this case are activated, causing the inhibition of inspiratory neurons in the DRG.

Source: Vanders Physiology, 15th ed, section 13.9: "Control of Respiration"