How exactly does long-term tension (over months) build up in the ligaments, tendons, muscles?

Tension is not a quantifiable thing, rather an abstract concept to describe feelings of stress in muscles.  I think I see what you are getting at but I would separate it into two questions.

"Is massage provably beneficial to muscles under physically induced stress?"

Emphatically yes, however there are so many different types of massage, some are more medically viable than others.  Most massage stimulates muscles to encourage a release of tightening, much like exercise does, though I would assume that there's also a psychosomatic that plays a significant role as well due to human contact.

The other question, more the point "Are massage therapist's claims about relief true?"

Some are and some aren't.  Unless it's by a medical professional (prescribed physical therapy for instance) they can claim whatever they like.  "Reiki contributes to your body balance and wellness by attuning your energy"  This can not be proven, but not really disproven either, so they can claim it all they want though it's purely anecdotal (if not outright fabrication on the part of less ethical individuals.)

In summary: Massage has tangible benefits, but if the claims of the therapist sound too good to be true, they probably are.


What factors affect the rate of siderophore production by microbes?

I think that you are interested in how bacteria regulate the expression of genes that produce siderophores. For a technical reference you can see this paper studying Vibrio, or this paper studying Pseudomonas. For a more general review see here.

Note that this is a diverse piece of metabolism and therefore there are likely to be a diversity of mechanisms by which siderophore production occurs, though superficially it appears that there are some general principles you can draw. I recommend looking at those papers and trying to understand the commonalities.


What are these lentil like eggs? (Utah, United States)

They look just like katydid eggs.

Image for comparison from the Missouri Botanical Garden:


Does translation have a way of preventing mismatching between mRNA codons and tRNA anti-codons?

Summary

Non-cognate codon–anticodon interactions on the ribosome do occur, but do not normally result in misincorporation of amino acids into protein. This is because aminoacyl-tRNA binds the ribosomal A-site in an EF-1A–aminoacyl-tRNA–GTP complex, and hydrolysis of GTP must occur before the peptide bond can form. The non-cognate interaction appears to be unable to trigger this hydrolysis and dissociates from the ribosome.

More Detailed Explanation

The hydrogen bonding between the bases of the mRNA codon and the tRNA anticodon is the basis of the specificity of decoding. It is easy to see that a codon such as 5’-GGG-3’ would form nine hydrogen bonds with an anticodon 3’-CCC-5’, but none with an anticodon 3’-AAA-5’. However, as the question makes clear, the situation is not quite so simple if two of the codon bases form the correct hydrogen bonds. A more telling example is shown below (here with the same tRNA, but different codons), where the difference between a his-tRNA interacting with a His codon and a Gln codon is only the strength of a GU ‘wobble’ base pair, often reckoned to be that of a single hydrogen bond. Certainly there is a difference in energy of the two interactions, but not enough to prevent a significant extent of miscoding.

The answer to this conundrum turned out to be the solution to another long-standing puzzle — that of why GTP is required in the binding of aminoacyl-tRNA to the A-site of the ribosome, which is directed by EF-1A (originally known in bacteria as EF-Tu). The GTP is not required for peptide-bond formation — the energy for that is supplied by the ATP in the tRNA synthetase reaction. It transpires that the role of GTP is in maintaining the fidelity of translation. The hydrolysis of GTP only occurs when the correct tRNA is bound — presumably the conformation of the incorrect interaction does not allow this to occur — so the non-cognate tRNA will eventually dissociate from the ribosome.

It is interesting that the other elongation factor, EF-2 (EF-G), involved in translocation of the peptidyl-tRNA, binds to the same site on the ribosome in a complex with GTP, and that translocation and removal of the deacylated tRNA can only occur after hydrolysis of GTP. It is as if the requirement for GTP hydrolysis ensures that the system is in the correct conformation before the next step of the complex process proceeds.

References

Berg et al. provides a general account, freely available online. A more detailed structural consideration can be found in a review by Nilsson and Nissen, which requires library access.


Antihistamine's effect on insulin secretion and tiredness?

Thanks to studies on animal behavior and on histamine dection in the Central Nervous System, researchers found out the "histaminergic system".
It's thought that histamine-containing neurons regulate sleep-wake cyrcle, immunity, memory, body temperature, drinking, feeding rhythms. By the way, knockout rats who lack of histamine system don't show big defects in any function.

H1-Receptors for Histamine are distributed in the CNS and in the rest of the body. H1-antagonists (such as Promethazine, Chlorcyclizine, Loratadine...) have different effects on CNS, depending on dose. At conventional doses central depression appears and patients are sedated. They can even experience an antihistamine "hangover" in the morning, even if they take these drugs at bedtime. By the way, antihistamine overdose typically shows with convulsions.

The "non-sedating" H1-antagonists, or "second generation" have a lot less effects on CNS. They have polar chemical structure: they can not cross the blood-brain barrier.
By the way, a lot of typical and atypical anti-psychotic drugs have H1-antagonism effects on the brain (with H2 and H4 antagonism): their main goal is sedation to stop the patient from hurting himself (or others) during manic episodes.

So I think the last two sentences explain that sedation is almost a totally CNS-mediated side effect of antihistamine drugs.

H1-antagonists don't suppress gastic secretion, do not inhibit salivary, lacrimal or other exocrine secretions. Older H1-antagonists have an anti-colinergic effect on muscarinic receptors: they may reduce ACh-mediated secretions, typically in mouth and in the respiratory tree.

H2-antagonists are used to treat acid-peptic desease (as PPIs, proton pump inhibitors). CNS-related side effects are not commons, and include: confusion, delirium, hallucinations, slurred speech and headaches. These effects are mostly related with IV infusion of the H2-antagonist.

I just made a very small research on PubMed. I found this:
http://www.ncbi.nlm.nih.gov/pubmed/3529778
as you can see it is a study (on only 9 patients, in 1986), about insuline-glucose-Cpeptide and ranitidine (H2-antagonist) relations. Their conclusion is "Ranitidine significantly increased the area under concentration/time curves for glucose and insulin but not that of C-peptide. Our data indicate that ranitidine does not affect pancreatic insulin release nor peripheral glucose utilization and are consistent with the hypothesis that ranitidine influences the hepatic clearance of glucose and insulin both of which undergo high first-pass liver extraction."

I think that tiredness is a typical CNS-mediated side effects of H1-antagonists (anti-allergic) but is not a side effect of H2-antagonists (anti-acid). Maybe H2-antagonists affects insulin action via hepatic effects.

*I'm italian (sorry for any english mistake) and I am a last-year medicine college student.
I wrote trying to summarize some chapters (8, 32 and 45) of:
- "Goodman & Gilman's The Pharmacological Basis of Therapeutics" - L. Brunton, B. Chabner, B. Knollman - 12th edition; McGrawth Hill 2011


Statistically, why is the number of mutated genes in eggs treated with chemical mutagenesis one?

The expected number of mutation would not follow normal distribution (ND) as you speculated because a ND would have negative values too as it ranges from $(-\infty,\infty)$, as Remi has also pointed out. In many cases a ND can be approximated because the variance would be so less that you can practically find no negative values. However, it is a wrong assumption to consider all biological statistics as ND by default. Please see this post. Basically, ND approximations can be made on multiple measurements that follow the central limit theorem. Now, in your case of a ND centered at 1, I'll tell you how that is impossible. You can have 2 and more than 2 mutations but you cannot have less than 0 mutations. The distribution is not symmetric and is skewed towards right. You also cannot have fractional mutations and therefore the distribution has to be discrete and not continuous.

Mutagenesis itself can be modelled as a Poisson process. For more information on this please see this post. So the probability of $k$ mutations in a time window, $t$, can be represented by the following equation:

$$P(n=k)=\frac{(\lambda t)^ke^{-\lambda t}}{k!}$$

Where $\lambda$ is the rate of mutagenesis.

The mean number of mutations (and also the variance for a Poisson distribution) would be $\lambda t$.

Now, the rate of mutagenesis would be proportional to the concentration of the mutagen. I speculate that the relationship between them would follow a saturation kinetics (like Michaelis-Menten) but at lower concentrations it would be essentially linear.

Moreover, the rate of mutagenesis would also depend on the cell type.

Therefore, standardization is required and labs working in this area for a long time develop standardized protocols (with specific mutagen concentrations and treatment times) which would let them avoid multiple mutations. Even then, they have to screen a lot of individuals to filter out the non-mutants.

Basically, there is no magic number.


what is the biggest known functional distance between an enhancer and its target gene (TSS) in cis?

I haven't found 1.5 Mb, but 1 Megabase. This is the case for the shh gene in chicken, where the enhancer element is located 1 Mb upstream. The original article can be found here:

"A long-range Shh enhancer regulates expression in the developing
limb and fin and is associated with preaxial polydactyly."

There are two reviews which are also interesting in this context:

When needles look like hay: How to find tissue-specific enhancers in
model organism genomes
Remote control of gene expression.


What is meant by "heads" and "tails" in the context of gene orientation?

The heads and tails, in this paper, refer to the orientation of sgRNA binding sites. If there are two tandem sites in the same orientation then they are referred to as head-to-tail (end of the first site followed by the beginning of the second site). It is also apparent from the excerpt that you have included in your question.

Head-to-head and tail-to-tail refer to the site pairs that are placed in the opposite strands; the former (H2H) refers to a configuration in which the beginnings of the two sites are closer whereas the latter (T2T) refers to the case where the ends of the two sites are closer.

Regarding your question about the placement of sites within -10 to +30 bp of each other:

I think the point of the paper is that the two cuts by the nickases should be close enough and in the T2T orientation for a maximally disruptive double strand break. If the distance between the single stranded cuts (nicks) is increased then they effectively are just two single strand breaks which are repaired efficiently. The authors also conclude that using two nickases in this fashion produces has lower chances of mistargeting compared to that of a normal Cas9 (that makes double strand cuts).


How does the enzyme ATP Synthase use a proton concentration gradient to make ATP?

Image from wikipedia page on ATP synthase

In brief, the addition and release of protons to the structure cause a conformational change that leads to another conformational change.  This series of conformational changes occurs in such a way that it induces a rotational motion.

The rotation of the central axel that extends through both hemispheres of this large complex is driven by the proton gradient.  Specific residues in the c12 ring are protonated in order to drive this rotation.  A high concentration of protons (in this picture the high concentration is found above the complex) allows each of the subunits in the membrane to be constantly loaded with H+ ammunition, ready to fire when it comes to be their turn.

The function of this axel is to slightly but significantly change the shape of one subunit at at a time in the red part.

Changing the conformation of subunits in the red part is what allows for the three steps in ATP synthesis to occur: binding of ADP and Pi, catalysis of the formation of ATP, and release of ATP.

All of these changes occur at the molecular level.  The proton forms a bond with a single amino acid of the entire protein complex, but this is sufficient to cause a difference in the most stable 3-dimensional structure of the whole.  This could cause either a cascade of changes that result in a net rotation or it could cause a re-stabilization of the structure due to electrostatic forces.

According to Vinit K. Rastogi & Mark E. Girvin in their 1999 Nature paper on the subject, it's more like the former:

  Earlier models proposed simple rotational diffusion of a rigid c12 ring, possibly driven by electrostatic forces. The structural data on protonation-linked conformational changes in subunit c indicate that the process may be more mechanical, with local rotations within subunit c driving larger-scale rotations of the c12 oligomer as a whole, in a `wheels within wheels' type of mechanism.

The whole paper's a good read.  But this is as current as I am on the topic, and it's likely that a more detailed mechanism has been determined for the action of ATP synthase since 1999.


It is kind of confusing.  Here's the sequence, from the ncbi link

GGACATTTAAMGAGGTACGTG

So M is "A or C"

Its a missense mutation, the amino acid called for is either an N or a K.

GGACATTTAAAGAGGTACGTG = K amino acid

GGACATTTAACGAGGTACGTG = N amino acid

GGACATTTAAGGAGGTACGTG = K amino acid

GGACATTTAATGAGGTACGTG = N amino acid

When you blastx it, the top hits are all the K allele, across a few species.

When you blast the DNA, the non-human hits in nr all have a G, not an A or C.  So I guess that's why they are calling that the ancestral allele.  The human hits to nr all have A, so the K amino acid is conserved.


What exactly does the phrase "chimerical sharing" mean in this abstract?

This term — chimerical sharing seems to be used only in this study as a google search did not return any other results. So, it is not a standard term. I believe what they mean by this term is that the twins shared x% of the paternal genome but the sharing is not homogeneous for each cell. In other words each twin has some cells with genetic material from sperm-1 and the others with genetic material from sperm-2.

If the two sperms were genetically identical, then you would not see any chimerism. Let's now consider only one allele as a marker of paternal parentage. So, there will be two populations of cells for each allele.  If both populations are of the same size then you would have 50% chimerism in a single individual (i.e. the allele frequency). The percentage of chimerism may be different between the twins.

Now, there may be several genomic regions at which the paternal-genomes differ. Since the paternal chromosomes would not be symmetrically partitioned between the blastomeres, the different genetic markers (alleles) are likely to have different extents of chimerism.

In this study they measured the frequencies of a few SNPs that were informative for deducing the parentage.

  Analysis of SNPs from twin amniotic fluid and parental blood showed
  that 265,489 maternal and 179,205 paternal SNPs were informative for
  parent of origin.

They noted that ~78% of the paternal SNPs were found in both the twins.

  Of these, the twins shared 265,400 maternal and 139,155 paternal SNPs,
  which makes them 100% maternally identical and 77.7% paternally
  identical.

Note that this is just a qualitative test for the presence or absence of the alleles. This does not say anything about the extent of chimerism of different alleles. (There are some figures in the supplementary data for the frequencies of different SNP but they are not in a tabular form and hence difficult to deduce).


What is the frequency distribution of each base in a DNA sequence?

The frequency of the bases in the genome isn't equal to 0.25, the frequency depends on what kind of organism you mean. However let's take a look at some of them:

bacteria, most of the time we can see a bias towards some bases, this could be a GC bias, for example if the bacteria lives in extreme conditions, because GC can vorm three hydrogen bonds compared to AT which can only form two hydrogen bonds. So it's genome is more resistent to extreme temperature, less denaturation chance because the stronger bonds. In bacteria there are also some polymerases which have a bias towards bases, I won't discuss this in depth to keep it short, but from these two points we can already conclude the genome isn't random
Homo Sapien, for example we need CpG Island near our promotor region, to regulate transcription. Further we have higher GC% in gene coding regions to reduce mutation chance, because we don't want to mutate genes wich are needed for survival. Their are also some sequence which are very specific for example TATA box and Poly-A signal, if our genome would be random, so all base would have a frequency of 0.25 these specific sequence could occur at place where we don't want them or they wouldn't occur at places where we want them. We need a promotor (with TATA box) for RNA polymerase binding, if our genome was random we have a big chance we would have genes wihtout a TATA box so no transcription of these genes will occur

There are a lot  more properties of the genome we could discuss but I think this will give you enough insight why the bases in the genome don't have a equally alike frequence of 0.25

UPDATE:

in addition to your second question: I think the chance of finding a genome which has an equally alike distribution is very small. because almost all organisms have undergo evelution, and when we have evolution there is natural selection and natural selection relies on mutations. So (almost) all genomes have udergo mutation, however this sometimes can favor an equally distibution for example if our genome is AGAA and one A mutates to an G we will have an equally alike proportion. So to summarize: maybe you can take a look at NCBI and look for a gc 50% wich means 50% AT so 25% of each base. If you find a genome wich has exact 50% gc, you have found your answer


Talking about cells in general, the main problem about higher temperatures is the denaturation of proteins (when proteins lose their structure and then they don't work anymore), and every organism has a specific range of temperatures in which its proteins have evolved to work in that determined range.

The most common example of bacteria living at high temperatures is Thermus aquaticus (or others) which proteins are widely used in laboratories for their peculiarity to be able to work at more than 70 °C (e.g. polymerase chain reaction).

In humans the mean temperature is 37 °C, and it's not unusual during severe fevers to get it rising to 39-40 °C (so the assumption that over 39 °C occurs death is incorrect). Of course you can reach higher temperatures but reaching 43-44 °C leads to multi-organ damages. You can find out more in this review.

Another thing to take in consideration is that cells must contain water in liquid phase, so over the 100 °C limit (at atmospheric pressure, so the limit can increase alongside pressure) it's kind of impossible to find living cells.


At which step should I apply a detection filter when preprocessing microarray data? (Before/After normalization, batch effects removal)

My comment above still stands; provided your detection filter doesn't rely on your data being normalized, your detection filter can exist anywhere.

However, since it seems you know that you want to run a PCA, and know all the normalization's you'd like to try already, it is simplest to run all of your normalization first, that her than having to filter out high scoring vectors that appear to be caused by inter-sample variation.


Why is the skin of European bog bodies brown?

The anaerobic decomposition of moss produces tannins in the peat.

  The bog water interacts with the acids in the moss and produce tannin
  and other chemicals that preserve the bodies that fall or are cast
  into the bog; hence the numerous well-preserved bog bodies.
  http://www.digitalmedievalist.com/opinionated-celtic-faqs/bog-bodies/

The tannins tan the bodies just like tanning leather; the color of the bodies darken and the tanning action also preserves them.


The rate of mutation has been studied since the early 1900s, which is when your question was put to rest in a prescient paper by JBS Haldane (1949). Essentially the answer is that it varies a lot between organisms and environmental conditions, but for any given gene a mutation occurs once in about 50,000 sexual replications. That is equivalent to, in a human, several hundred new mutations in each person born. Impressively, Haldane's calculations have since been confirmed by a variety of other methods (e.g. Nachman & Crowell, 2000; Xue et al., 2009).

Faster rates of evolution have been recorded in other organisms, and there have been many, many studies looking at the rate of increase in sizes of the whole body or of particular organs of a wide variety of animals and plants.

For example, Azevedo et al. (2002) look at the rate of mutations affecting size (trying to select for decrease in body size) in C. elegans, and found mutations affecting size occured at a rate of ~0.0025 per haploid genome per generation.

In another example, with a result more definite regarding your question, Keightley (1998) investigated the rate of change in average body weight under conditions of selection for increased body size, over 50 generations in mice. They recorded an average increase of 0.23-0.57% body weight per generation from new mutations. That's pretty huge, and demonstrates how rapidly a complex trait can change by mutation under selection.

I wrote a small piece of python code to calculate the increase after x generations at the same rate (the formula is very simple)...

initial = 1
rate = 0.35
generations = 1000
result = initial * (1.0 + rate) ** generations
print result
>>>20.10655586861808

Thus if we assume that approximately the average rate found in the mouse study (0.35%) could be the rate at which giraffes' necks might increase under strong selection, after 1000 generations the mean neck length would be over 20 times the original length. A low estimate for wild giraffe longevity is around 20 years, thus for giraffe necks to increase around 20x might take 20,000 years. Of course this basic estimate is making a whole lot of assumptions, but the point is that rates of mutation are actually very high, easily enough to explain the diversity of traits we see in the world.

References

 Azevedo RBR, Keightley PD, Laurén-Määttä C, Vassilieva LL, Lynch M, Leroi AM. 2002. Spontaneous Mutational Variation for Body Size in Caenorhabditis Elegans. Genetics 162: 755–765.
 Haldane JBS. 1949. THE RATE OF MUTATION OF HUMAN GENES. Hereditas 35: 267–273.
 Keightley PD. 1998. Genetic Basis of Response to 50 Generations of Selection on Body Weight in Inbred Mice. Genetics 148: 1931–1939.
 Nachman MW, Crowell SL. 2000. Estimate of the Mutation Rate Per Nucleotide in Humans. Genetics 156: 297–304.
 Xue Y, Wang Q, Long Q, Ng BL, Swerdlow H, Burton J, Skuce C, Taylor R, Abdellah Z, Zhao Y, et al.. 2009. Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree. Current Biology 19: 1453–1457.


What is the purpose of ethanol in a DNA extraction experiment?

In the case you describe the ethanol is not there to do anything with the cells but to make the DNA precipitate out of solution. DNA is very poorly soluble in 50-70% ethanol and it will precipitate out as a white sticky pellet. It works even better if the alcohol is kept very cold.

Ethanol does kill cells by denaturing proteins and disturbing the lipid bilayers but after you have added the soap, most cells will already have been disrupted.


Similarity between a heart attack and a spasm

I was able to do some reading and research and I found some interesting information that was a). news to me. And b). the answer is yes... And no.

A spasm can be the cause of a heart attack by causing the coronary artery to contract. When that artery contracts, it causes a dramatic decrease in blood flow to the heart. When the heart looses access to oxygenated blood it can cause chest pain (angina) or even an MI (Myocardial Infarction a.k.a. a heart attack). This spasm is can be caused by exposure to extreme cold, smoking and the use of certain recreational drugs.

However, this type of spasm cannot be stopped with defibrillation. Treatment for these involves administering Nitroglycerin and then later treatment involving Statin drugs and such.

In the terms you are speaking of, I don't see that that would be quite accurate. The most common cause of sudden cardiac death is VF (Ventricular Fibrillation) which is essentially an uncontrollable quivering of the heart muscle. I've never heard this described as a spasm though. Google searches of spasm and heart spasm have all lead to definitions of the word spasm and the coronary artery spasm mentioned above.

However, within that, I think you have a valid point and a decent understanding of how things work, just perhaps not fitting under the definition of a spasm.

When a defibrillator is used, it delivers a measured electrical shock to the person's heart and hopefully stops the chaotic electrical rhythm. I'm not sure if this part is correct however, I do not think you should look at that as a stretching of the muscle though. It is an electrical intervention that interrupts the former rhythm and hopefully the heart "forgets" what it was doing and returns to a sinus rhythm.

So, to summarize: A heart attack can be caused by a spasm; however, defibrillation does not help that type of attack. A defibrillator does not 'stretch' the heart but rather interrupts it's former rhythm. Because an irregular heart beat is not considered a spasm, I find it difficult to believe that any form of EMP would help it; however, I would love to hear that it has!

For more information on Ventricular Fibrillation, CAS (Coronary Artery Spasm) and AED's (Automated External Defibrillator(s)). Please see the following:

MedlinePlus - on V-fib

The Mayo Clinic - on CAS

HeartSine - on AED's

I hope this was helpful for you!

Edits:

In the comments, we had discussed a variety of possible causes and treatments for spasms, as well as what - if any - connection there is between how a spasm in perhaps a leg would be caused as compared to how one in your heart could be caused.

From the reading and research I did, I was fairly inconclusive about the safety or desirability of a device to prevent heart attacks using an EMP device implanted in your brain or on your brain stem.

As far as how similar a spasm in your heart is to a spasm in any other muscle, they are not very similar. As seen here, a muscle spasm in most parts of the body can be caused by numerous things, such as dehydration, poor blood circulation, mineral deficiencies etc. Whereas a heart spasm (know as a CAS) can be caused by alcohol withdrawal, stimulant use, extreme cold... As seen here.


What is an apomorphy? What is a plesiomorphy? Can someone confirm these definitions?

That sounds pretty good. On this kind of things wikipaedia is very reliable.
You can also look at this very synthetic page:

https://www.enotes.com/homework-help/distinguish-between-synapomorphy-apomorphy-304128


How can DNA replication result in hair pin structures?

DNA Hairpins are formed when two regions in same single stranded DNA are complementary in nucleotide sequence but in the opposite directions (as represented in image below). These two sets of nucleotide sequences base-pair with each other by forming hydrogen bonds between adenine-thymine and guanine-cytosine respectively to form hairpin loop. Same structures can be seen in case of RNA.

(Figure via: https://brilliant.org/problems/dna-zipper/)

Single stranded binding (SSB) proteins bind to single DNA nucleotide sequences and prevent the breakdown of newly synthesized DNA because of nucleases and it also removes the secondary structure of the DNA  strands like hairpin loops so that other enzymes can bind to DNA strand and operate properly. As represented in figure below SSB bind to ssDNA through electrostatic interactions and prevent the bond formation within the nucleotides of single DNA strand, thus preventing formation of hairpin loops in DNA.

(Figure via: http://helicase.pbworks.com/w/page/17605582/Amanda-Kinney)

(via: https://proteopedia.org/wiki/index.php/Single_stranded_binding_protein)


What does x in "Miscanthus × giganteus" name stand for?

It means that the plant is a hybrid. Having it in the middle means that it is between species of the same genus, else the × (it's not the letter x but the multiplication symbol ×) would have been in front.

It is very commonly used in taxonomic nomenclature, namely every time you have a hybrid. This means you'll usually see it with plants, as animals very rarely interbreed.

Wikipedia says that your plant is a hybrid from Miscanthus sinensis and Miscanthus sacchariflorus. It is an easy place to look up most hybrids you might encounter.


Is it true that there is a spider that eats parasites from caterpillars

Oddly enough it is a bit difficult to find good field studies where the diet of spiders was studied.  I have a feeling it's a hard thing to get funding for.  Luckily some do exist.

Peucetia viridans has been shown to eat from the Chrysididae family and Lepidoptera order, but I didn't find an explicit statement that it ate the larvae out of the caterpillar.  Likewise Oxyopes globifer was found to have eaten from the Braconidae family and Lepidotera.

At this point you might be wondering why I'm looking for spiders that have been shown to eat both parasitoids (Chrysididae and Braconidae) and caterpillars (Lepidotera).  It my assumption that in the scenario you describe a spider that would normal eat ether the caterpillar or the larvae would be just as happy to eat them both if it was lucky enough to find them.

I could find one example where it seems wolf spiders under the right conditions might seek out larvae, and I found a fun photo of a wolf spider eating larvae (though not the kind in the study).

I never saw the video you were talking about, and I too could not find it.  It is not unreasonable to assume that an opportunistic spider wouldn't just take the opportunity to feed on both, or that it might find the larvae more tasty and just eat them.  I've not found a spider seeking caterpillar as of yet.


Where are the statistics for vaccine side effects?

(World Health Organisation, 2014. p. 2) shows the adverse effect (side-effect) rates for the MMR vaccine. For instance, fever  between the 7th to 12th day after vaccination occurs in 5 to 15% of vaccine recipients and rashes occur in 2-5% of vaccines, etc. Page 6 summarises the results in a table. As you point out, the adverse effects are variable in severity and dependent on the particular vaccine; an organisation like the WHO will take into account the risk and severity of these adverse effects before recommending the use of the vaccine. And as you point out, it is not believed by the scientific community at large that vaccines have links with autism.
References
World Health Organisation. (2014). Information sheet observed rate of vaccine reactions measles, mumps and rubella vaccines.


Why a striped baby is not the result of a white and a black parent?

The reason that there are no stripes when black and white people get babies is the fact that the number of pigment cells is the same for black and white people. What is different is the amount of pigment produced, and it will be different in the kids as well (lighter than the dark parent, darker than the light parent) See references 1 and 2 for details on the melanocyte density. Skin color is a multigenic trait, so the genetic background of both parents and their effects on pigmentation come into full play here.

Besides this effect, humans do have stripes, although they are mostly not visible. They are called Blaschko's lines and look like below:

These develop from the migration pattern of the melanocytes (and their precursor cells) in the developing embryo. They can get visible in some rare genetic conditions or by diseases. See reference 3 for a more popular explanation and reference 4 for a review on this field.

References:

The Regional Anatomy of the Human Integument with Special Reference
to the Distribution of Hair Follicles, Sweat Glands and Melanocytes
General Biology of Mammalian Pigmentation
Blaschko’s Lines
Lines of Blaschko.


What is the smallest known organism with a skeleton?

The smallest vertebrate (if that's what you mean; there are many invertebrates with endoskeletons that are not made of bone) is Paedophryne amanuensis, a Papua New Guinea frog that's about 7 mm long.


Genbank is a database of nucleotide sequences that are public.

NCBI stands for "National Center for Biotechnology Information" (in the US).

Entrez is NCBI's retrieval system.

You can find more information in this article

I don't know which kind of databases you are looking for, but there are hundreds of them!
In this wikipedia article there are some of them.


I agree with commenter Martin Klvana, but there are a couple things going on here I wanted to touch on:

I think that your second quote is making an error in saying that if prions cause immune responses that means they aren't "infectious" in the sense of propagating misfolding of homologous proteins. The standard understanding is that prions work biochemically by refolding prionogenic proteins to make more infection prion particles (see e.g. wikipedia), similar to your source 1 and your textbook. It's completely possible that these newly infectious prion particles lead to immune reactions in additional to the "infecting" particle. The key here is to separate the biochemical phenomenon (propagated misfolding of proteins) from the medical phenomenon (disease, immunological response).
To more directly answer the question: as far as I can tell from scanning a couple of articles (here, here), immune responses are not a prominent part of the best-known prion diseases, but I'm not an expert and could be wrong. I was unable to easily locate the 1997 Medical Hypotheses paper referenced by your source 2.
I haven't looked deeply into this, but that website appears to be run by an advocacy group and the "read full article" link is broken. So... I would put less stock in that source. Advocacy groups are fine and all but I don't think that their blog posts are good sources of biomedical science information.

Hope that helps.


Why do some grasshoppers have a black exoskeleton?

Field crickets are rather distinct from grasshoppers. Although both groups are in the Order Orthoptera, grasshoppers are insects of the suborder Caelifera and field crickets are in the family Gryllidae of the suborder Ensifera.

For a discussion on insect coloraiton, see here.

If you'd like a specific species ID, please provide more information as requested in the comments.

Generally, field crickets are black, red or brown in color.

However, some species of grasshoppers are likewise black:

For example: Romalea species such as R. microptera and dark nymphs and morphs of R. guttata

Finally, here is a simple checklist of some typical differences between grasshoppers and crickets.


Yes, sub- or satellite colonies are common in many species (see e.g. Hölldobler & Wilson, 1990; Debout et al. 2007), and these are then labelled as polydomous species. Subcolonies can either contain extra queens, but sometimes only contain foraging workers. The purpose can be both to expand foraging grounds or as a pre-stage for colony budding. The distance between colonies can differ dramatically between species, but there are cases of supercolonies (especially in the Argentine ant) streching over hundreds of square kilometers (Moffett 2012).

Satellite colonies are also common in e.g. Carpenter ants (Camponotus) and wood ants (e.g. Formica rufa), and when colonies are found inside a house there is often a primary colony somewhere outside the building (see e.g. Ants in the home).


How many Amperes to kill fruit flies and mosquitoes?

I am not an electrician and may not be the right person to answer this. But I recently read this paper (Keller et al., 2016) and maybe this helps ... Keller et al. (2016) have a look at laser induced mortality in mosquitoes. It might not be fully adaptable to your needs (there is not much context in your question, though; I have no idea what kind of trap you are trying to build ... if it's going to be a fancy laser trap, the cited paper will be your perfect guide through the building process - however, you have to figure out the automatic camera detection (they are planning that, too) for yourself as they have not published that, yet).

Now, giving a concrete answer: Keller et al., (2016) found that lasers with 0.5W to 4W are sufficient for efficient mosquito inactivation. If you are planning to use a plug bucket (230V) this would be (0.5W/230V=) 0.002A to (4W/230V=) 0.017A. You could also set this up with a 9V battery. With a 4W laser this would be (4W/9V=) 0.44A. Using a lithium-based battery this would last for about (1000mAh/(4W/9V=0.44A)=1Ah/0.44A=) 2.27h total laser time.

I do not know if this easily translates to electric current, though ...


Why do humans lose subcutaneous fat tissue with age?

Short answer
We do not loose fat (cells) as we age; on the contrary - we tend to gain fat by about 1 or 2% per decade. The place where it gets stored does change; instead of going into subcutaneous regions, it gets stored around the abdomen. A sex hormone imbalance might be the cause of this gain in visceral fat.

Background
What a coincidence! I just finished an article in the Sci Am May issue of this year (2018) on exactly this topic, literally just minutes ago.

In young folks, fat tends to accumulate under the skin, while in older folks this tends to shift to accumulation of fat around the abdominal viscera (the internal organs). Bottom line: we don't loose fat overall, we just store it elsewhere. What's more, as we age we store more fat as our base metabolic rates drop.

Why this happens is no known, but there are some interesting findings:

Sex hormones are involved; women in menopause (estrogen levels drop) gain more visceral and belly fat and loose it around the hips (they go from pear to apple);
However, a drop in estrogen is not the cause, as certain ailments lead to belly fat in young women with plenty of estrogen;
Androgen-using females (transgenders) gain more visceral fat.

These findings together have lead to the idea that a sex hormone imbalance might be the cause. However, some findings counter this idea:

Afro-Americans have less visceral fat, while Asians have more;
Blocking FSH results in less visceral fat, which may have other mechanisms of actions than estrogen.

Reference
- Wallis, Sci Am May issue 2018


How to increase the rate of absorption and assimilation of food?

The rate of absorption is controlled by two essential physical factors:

Contact surface between intestinal content and intestinal mucosa.
Time of contact.

There are many other factors including intestinal peristalsis, gastric, pancreatic and bile secretions that stimulate/help absorption.

So increasing or accelerating intestinal passage of food won't do any good (see diarrhea). Water will not be absorbed into the blood flow thus leading to dehydration and hypovolemia. Also the alimentary principles, vitamins, essential aminoacids won't be absorbed.

On the other hand, slowing down the passage has negative effects. It allows bacterial saprophytic flora to multiply so much that those microorganisms become pathogenic by producing toxins. And increased contact time equals increased absorption both of toxins and food principles.


What are the effects of sleep deprivation?

24 Hour Mark

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

36 Hours

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

48 Hours

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

72 Hours

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

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

.


Do repetitive movements on EEGs show up as discernible patterns?

Specific events, e.g. finger flexions, generate synchronized neuronal responses in the brain that can be measured on the scalp with EEG. However, a voltage response to a single event typically generates a low-amplitude response relative to the background EEG. One way to enhance the signal-to-noise ratio is to repeatedly record the EEG in response to the same event. By time-locking the event with the EEG and averaging the individual event-related EEGs, the random background noise will be reduced (stochastic noise) and the event-related potential (or ERP) can be extracted from the EEG (Woodman, 2010). An example of an ERP to repeated index finger flexions is shown in Fig. 1. Such a wave doesn't need 10,000 repeats. 25 may be sufficient.

If you characterize this ERP and determine specific features of it (duration, amplitude, latency after event etc.) you can generate algorithms that detect these features in the raw EEG, without the need to do repeated measures. In fact, thinking of a motor movement (e.g. grasp that coffee mug) generates very similar EEG activity as the factual act of grasping that mug. By recording the ERPs using events like think of grasping that coffee mug from a person missing a hand, and subsequently designing the necessary algorithms to detect that waveform near-realtime in the person's EEG, one can design brain-computer interfaces to control prosthetic limbs (Guger & Pfurtscheller, 2016).

Fig. 1. ERP to voluntary index finger flexions. Motor activity was recorded from the motor area. Source: Ball et al. (1999)

References
- Ball et al. NeuroImage (1999); 10: 682–94
- Guger & Pfurtscheller, AAATE 5th European Conference Advancement of Assistive Technology (2016)
- Woodman, Atten Percept Psychophys (2010); 72(8): 10.3758


Short answer
Proprioceptic receptors provide a feedback mechanism from the body to the brain, telling the brain what our limbs are doing and where they are with respect to the body without visual feedback being needed.

Background
Muscles, skin and joints contain proprioceptic receptors. They sense position and movement of our limbs and trunk, they register force as well as heaviness. Examples of such receptors are limb tendon organs and possibly also muscle spindles, which contribute to the senses of force and heaviness.

Proprioceptive sensations are influenced by visual input, but operate without it. The proprioceptive system is responsible for the ability to touch your nose with your eyes closed and the examples you have given related to catching a ball while not paying visual attention to the position of your hands.

Afferent signals from these receptors are combined and processed in the brain. Together they form information about limb position and movement. This information is mapped relative to a central body map to determine the location of the limbs in space.  The proprioceptive senses, particularly of limb position and movement, deteriorate with age and are associated with an increased risk of falls in the elderly.

Reference
Proske & Gandevia, Phys Rev 2012; 92:1651-97


How will changing the concentration of a Tris buffer affect amylase enzyme activity?

I realize I'm 4 years late, but wanted to give an answer to this. It appears that tris often has inhibitory effects on amylase activity. Adding more Tris will lead to competitive inhibition with the substrate and will skew the results.

Binding of Tris to Bacillus licheniformis alpha-amylase can affect its starch hydrolysis activity
https://www.ncbi.nlm.nih.gov/pubmed/18289113


Can experiments in ELISA kits be monitored via both fluorometry and photometry?

can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

This is essentially correct.

You can have the same ELISA work on different methods of detection. The most common ELISA is colorimetric, and works by binding a secondary antibody conjugated to some enzyme to your primary antibody. Fluorescent ELISA platforms are less-widespread but only because the colorimetric ELISA is reputed and "gold standard."

Horseradish peroxidase (hrp) is a common conjugate system utilized in sandwich ELISAs, and by adding TMB solution to the reaction wells, the resulting reaction produces a diimine that turns the liquid in the well blue, and does so in proportion to the amount of analyte captured. You stop the reaction by adding an acid, which turns the well yellow, and you read the OD at 450nm (they also recommend you subtract the OD at 510nm to account for the light scattering of the microplate).

Figure 1. R&D Systems Quantikine assays, HRP-streptavidin detection. https://www.rndsystems.com/products/quantikine-hs-colorimetric-sandwich-elisas-high-sensitivity

On the other hand, we know that we can also conjugate the antibody with a fluorescent molecule if we wanted to, like FITC or PE. All we need to do is excite the molecule with an appropriate light source or laser to get a fluorescent emission, and read with an appropriate system to read those signals. The fluorescent intensity would then be proportional to the captured analyte, based on a standard curve just like any ELISA.

So the real answer is we can use one, the other, or both, just not at the same time.

Just be cognizant that different platforms can yield different results, so you have to validate your two platforms, and correlate the two to ensure reproducibility. Most labs just try to stick with one or the other, though.


The exact mechanism is not known:

  Modafinil has wake-promoting actions similar to sympathomimetic agents like amphetamine and methylphenidate, although the pharmacologic profile is not identical to that of sympathomimetic amines. [...] Modafinil-induced wakefulness can be attenuated by the α1-adrenergic receptor antagonist prazosin; however, Modafinil is inactive in other in vitro assay systems known to be responsive to α-adrenergic agonists, such as the rat vas deferens preparation. [...] Modafinil is not a direct- or indirect-acting dopamine receptor agonist. However, in vitro, Modafinil binds to the dopamine transporter and inhibits dopamine reuptake. This activity has been associated in vivo with increased extracellular dopamine levels in some brain regions of animals [1].

A 2010 study has concluded that:

  Recent evidence suggests that modafinil may block the dopamine transporter (DAT) and that the dopamine D1 receptor (D1R) may contribute to modafinil effects [2].

Another one confirms modafinil's dopaminergic activity:

  These findings indicate that modafinil has a long duration of action, with alerting properties arising predominantly from dopaminergic activity [3].

It seems to be dependent on catecholaminergic signaling:

  It binds competitively to the cell-membrane dopamine (DA) transporter and is dependent on catecholaminergic (dopaminergic and adrenergic) signaling for its wake-promoting effects. [...] Modafinil is an exceptionally weak, but apparently very selective, DA transporter inhibitor. [...] The conformational constraints on the interaction of modafinil with the DA transporter - and probably, as a consequence, its effects on trace amine receptor signaling in the catecholaminergic cell - are unique among catecholaminergic agents [4].

References:

Drugs.com. Modafinil. Clinical Pharmacology. Available from http://www.drugs.com/pro/modafinil.html (accessed 29.07.2014)
Young JW, Geyer MA. Action of modafinil--increased motivation via the dopamine transporter inhibition and D1 receptors? Biol. Psychiatry. 2010 Apr 15;67(8):784-7. doi: 10.1016/j.biopsych.2009.12.015. PubMed PMID: 20132929.
Turner C, Belyavin A, Nicholson A. Duration of activity and mode of action of modafinil: Studies on sleep and wakefulness in humans. J. Psychopharmacol. (Oxford). 2013 Dec 3;28(7):643-654. doi: 10.1177/0269881113508173. PubMed PMID: 24306135.
Wisor J. Modafinil as a catecholaminergic agent: empirical evidence and unanswered questions. Front Neurol. 2013 Oct 7;4:139. doi: 10.3389/fneur.2013.00139. PubMed PMID: 24109471.


Whats the difference between voltage gated and ligand gated neurons?

There is no such thing as voltage gated or ligand gated NEURONS. I believe what you are refering to are what is known as voltage gated and ligand gated ion CHANNELS. Each neuron has both types of channels in their cell membrane.

Voltage gated ion channels open in response to voltage (i.e. when the cell gets depolarized) where as ligand gated channels open in response to a ligand (some chemical signal) binding to them.

Both types of channels are critical for proper activation of the post synaptic neuron. The pre synaptic neuron releases neurotransmitters into the synaptic cleft, these neurotransmitters then bind to the ligand gated channels, thus activating them. The ligand gated channels open up and allow the influx of sodium, which depolarizes the cell. This depolarization activates nearby voltage gated ion channels, which open up and let in even more sodium. Voltage gated sodium channels open up one region at a time, the previous region providing enough depolarization to activate the next regions voltage gated channels. This effectively allows the action potential to propagate through the cell.


How come that we "feel" it when someone's watching us

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


What term describes insects that must eat protein to reproduce?

The term I was looking for was anautogeny, or an anautogenous insect. I had slightly confused the definition, with the actual definition being; 'a gravid female insect that requires a blood meal before oviposition'.


Neurons are tetraploid in pathological situations like Alzheimer disease:

Neurons that duplicate their DNA are rarely observed to undergo mitosis, and they remain for long time as tetraploid cells, in accordance with the chronic course of the disease. We have recently shown that cell cycle re-entry and somatic tetraploidization occurs during normal development in a subpopulation of RGCs (retinal ganglion cells), giving rise to enlarged neurons with extensive dendritic trees. Tetraploization in these neurons occurs in response to the activation of the neurotrophin receptor p75NTR by an endogenous source of NGF (nerve growth factor).

Source: Frade JM, López-Sánchez N. A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR. Cell Cycle 2010; 9:1934 - 1941; PMID: 20436277; http://dx.doi.org/10.4161/cc.9.10.11582

These neurons are generated in response to nerve growth factor (NGF) acting through the neurotrophin receptor p75 (p75NTR), which induces E2F1 activity and cell cycle re-entry in migrating RGC neuroblasts lacking retinoblastoma (Rb) protein. We have also showed that brain-derived neurotrophic factor (BDNF) prevents G2/M transition in the tetraploid RGCs, thus being crucial for the maintenance of the tetraploid status as well as the survival of these neurons. The realization that tetraploid neurons can be readily observed in the vertebrate nervous system has important physiological consequences.
Several eukaryotes are known to undergo endoreduplicative cycles leading to somatic polyploidy, thus increasing cell size in specific tissues. Examples of polyploidy in neurons are known in some invertebrates.

Source: José María Frade. Somatic tetraploidy in vertebrate neurons - Implications in physiology and pathology. Commun Integr Biol. 2010 Mar-Apr; 3(2): 201–203. PMCID: PMC2889987


Biologically, does life and death matter?

We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore?

Fear of death is hard-wired into our nervous systems. A thirsty wildebeest will approach crocodile-infested water very, very reluctantly. The wildebeest isn't thinking about the selfish gene or the loss of his function in the world; he's hardwired to be afraid of the situation. The same is true for any prey animal: fawn, rabbit, gazelle, mouse. The difference (maybe; simplifying for convenience) is that we are rational, and like all of our primitive fears (e.g., of the dark, when there really were sharp-toothed predators with better night vision than ourselves), we try to rationalize them. We also rationalize our existence.

  Is the functionality of something the only thing that life cares?

Nature is red in tooth and claw. If you want to anthropomorphize Nature, then sure, we matter (we're destroying the earth at unprecedented speeds). If you believe in a spirit, we matter. But if you believe in none of it, the only purpose we serve is to propagate ourselves, and when the last of our species is gone, Nature will not care a whit. Just as it doesn't care that dinosaurs, wooly mammoths, passenger pigeons, tasmanian tigers or baiji river dolphin are gone.

It can be argued that in the grand scheme of things (and here I'm speaking of the entire Universe), biological life doesn't matter at all.


What plastic eating organisms are there to help with plastic in landfills problem?

I remember this link - about a high school student who's science fair project was a basic but effective selection experiment.  He cut up plastic and put it in a yeast medium (growth medium for microorganisms) for a few weeks.  It says he tweaked the temperature and other incubation conditions for a few weeks and got a significant degradation of the plastic in the media.  The microorganisms in the media were not characterized.

That article is great because the bloggers compiled a list of similar work.

There are a couple of links that point to styrene degradation by Pseudomonas putida variants.  Pseudomonas putida is a likely candidate from bacteriology - it was first isolated near chemical and petroleum spills - they can degrade petrochemicals and organotoxics, so researchers might tend to start with this bacteria or an isolate of it.

This paper identifies Phanerochaete chrysosporium, a white rot fungus as an organism that can degrade phenolic resins.  White rot fungi are found in wood rot and can degrade lignin which is derived from a poly-phenolic like biosynthesis pathway.  So this is also an interesting lead.  It doesn't always grow to industrial scale - I've known people working on this even in the early 80s.

So it seems despite the fact that plastic never seems to go away, there are organisms in the wild that will chew away at the plastic, and with a little bit of selection work you can pick them out pretty easily.  This survey of the plastic dump in the Pacific gyre found that there were marine microorgs that might be eating plastic there too.  They had a preliminary report:

  So far, the DNA sequences obtained by her lab show that almost 25% of the bacteria on one polyethylene surface were vibrios

A survey of the tropical rainforest also found a collection of fungi that can subsist on polyurethane. These included Pestalotiopsis microspora which seems to be have the so far unique property of anaerobic degradation of polyurethane.

Overall it seems that finding organisms in the wild is of ongoing interest.  This may be because biodegradation of plastic tends to be slow, which makes sense because if it were quick there would be no problem with dumping it into the dirt of into the ocean, but it would also rot over time in the back yard or in your boat.  While its possible that more fishing trips may find the perfect plastic eater, its also possible that industrial processes for the bioremediation of plastics may have to wait for some engineered organisms.


If there is such known "Mitochondrial Eve", does it means that all the mitochondrial dna in everyone's body is same?

The mitochondrial genome has a nonzero mutation rate, though estimates differ according to method. Estimates are approximately 10^-8 per bp per year on average, and the mt genome is ~20,000 bp. So we can do some math and expect that many (or most) people experience heteroplasmy, which is to say that they carry various different mitochondria (in the same person).
Note also that you inherit multiple mitochondria from your mother, not just one.
So- no, not everyone has exactly the same mitochondria, even if we can trace them all back to a single hypothetical human.


How would one determine whether a chemical will upregulate a certain class of proteins?

One way of examining this is by looking at the transcriptome as a whole before and after the introduction of the chemical. I would use microarray or next generation sequencing RNA-seq technology to look on the expression level of all the genes after the introduction of the chemical, some inert control and no treatment control.

Then, you can calculate the relative fold change in expression of all genes, under treatment vs. control. Next, you can do a GO term enrichment of the significantly upregulated genes, and see if the term "deacylases" shows significant enrichment in genes that are upregulated under treatment vs. control.


The cloaca, which is the common opening of the urinary, excretory, and reproductive systems, is present in birds as well as in non-avian reptiles (and thus presumably dinosaurs), amphibians, and monotremes (e.g., duck-billed platypus). To answer your first question, yes, this condition does seem to be universal for those groups mentioned above.

To answer your second question, evolutionary history is as good a reason as I can think of. The cloacal system has worked well enough for >350 million years (in the case of amphibians).


Are there animal species with sex of an offspring determined by sex of preceding offspring?

I can think of one (perhaps trivial) case where this happens. In insects with haplodiploid sex determination (like Hymenoptera) then almost all of a male's offspring will be female, as they will be diploid.


Hydrogen peroxide as a reactive oxygen species (ROS) is a highly problematic molecule for the processes inside of cells (it can spontaneously oxidize and damage cellular components). With Catalase, organisms have a very effective enzyme which degrades the peroxide into water and oxygen.

However, although the molecule is problematic, it is still produced by organisms in traces. For its production by the NADPH oxidase, first NADPH is oxidized and superoxide is formed. The reaction looks like the following:

$NADPH + O_2 \rightarrow NADP^+ + H^+ + O_2^-$

In a second step the superoxide dismutase uses two molecules of superoxide and H+ to generate H2O2, the total reaction (which is divided into several steps) looks like this:

$2O_2^- + 2 H^+ \rightarrow H_2O_2 + O_2$

H2O2 is then usually degraded by the catalase (or used in immunological processes like the respiratory burst).


I don't have enough rep yet to comment on your question, but I have read the whole of Kandel's Principles of Neural Science in 2nd year of med school (last year) and I thoroughly enjoyed all of it!

I would recommend Part II: Cell and Molecular Biology of the Neuron to you, as this is where most detailed discussion about the molecolular structure of membrane proteins etc. is happening. And that's only about 110 pages. It probably doesn't go as far as what you are looking for, but I found it a very good introduction to the field of ion channels and how they work. The rest of the book is very interesting if you are keen to get a thorough overview of the whole field of neural science, but you won't find too much detail on the biochemical level there. Part III: Synaptic Transmission with about 150 pages is also a very good read.

For a specific focus on biochemistry you'll have to look for another book, but quite likely you'll find good candidates in the Selected Readings at the end of each chapter, here is one example of those lists from chapter 7:


Best tip I can give you is buying a textbook or popular science book about ethology. That should give you an overview about research done in the past decades. Konrad Lorenz was a pioneer of ethology, so a book should summarize his work, e.g. this one

For more current stuff look up some journals in this field:

Animal Behaviour
Journal of Comparative Psychology

Animals having a small brain compared to mammals but nevertheless showing very intelligent and reflective behaviour like this rook are currently interesting research objects. This kind of research is not really tricky or expensive as you see, it just has to be done by a student :) But behaviorism as the leading paradigm in the middle of the 20th century has probably made a lot of more fruitful research approaches impossible.


Depending on the technique used, the short answer is yes.  For those of us who have been in the field for a long time, questions like this bring up memories of articles or seminars we have seen, but we really have to sift through a lot of non-digitized articles to find it. Although I will have to do some searching  to find it, there is a beautiful article using voltage clamping in very skilled fighter pilots where the author suggested (accurately IMO) a graphic representation of the formation of a thought. (I realize that without references, it is still hearsay, but perhaps someone else will recognize the details & be able to fill in the gaps more quickly.) But I will try to find the article and post the details.


What is the scientific name of this flying insect?

This insect is, indeed, related to dragonflies. This is a damselfly.

Damselflies are Odonata insects from the Suborder Zygoptera. Unlike dragonflies (Suborder Anisoptera), damselflies fold their wings when resting. This is the most noticeable difference between damselflies and dragonflies:

Regarding your specimen, I'd say that it is Caconeura ramburi, the indian blue bambootail. Here is an image for comparison:

The site where I found that image, conveniently called Odonata of India, is a good source of information.


Material on the analysis of (micro)array data

A good place to start would be Statistical Methods for Microarray Data Analysis. I'd also suggest papers from the labs of Terry Speed, Gary Churchill, John Quackenbush, and Gordon Smyth.

Also, I found some papers that specifically reflect on your exact issue: how to apply the methods developed for DNA microarrays to analyze protein arrays.

Eckel-Passow et al. Experimental design and analysis of antibody microarrays: applying methods from cDNA arrays. Cancer Res. 2005 Apr 15;65(8):2985-9.
Royce et al. Extrapolating traditional DNA microarray statistics to tiling and protein microarray technologies. Methods Enzymol. 2006;411:282-311.


Was it Pando? Pando is a single, massive 80,000 year old Populus tremuloides (quaking aspen) individual, that is assumed to have a single, massive root system covering 106 acres.


Not sure if generalized plasmid taxonomy is going to be relevant any longer. A lot of these old names were created before the exact sequence and function of the various DNA sequences were known. This is becoming especially true as synthetic biology allows us to mix and match parts of plasmids at will. If you want to dig through a lot of the old plasmid classification papers, a lot of them are published before 1980.

Back then I'd imagine conversations went more: "oh look, I found an R plasmid conferring ampicillin resistance", instead our more modern understanding: "oh, I have a plasmid conferring ampR via bla "

That being said, I think the more specific / specialized plasmid classifications will stick around for a while as they confer a lot of domain specific meaning.  Check out Ti and Ri plamids which have very specific meanings in plant pathogens and are used in the genetic engineering of them.  You'll notice that the classification for these plasmids comes from a lot more than a single gene.

There have been some modern attempts to classify plasmids, but rely a lot more on the structure / lineage of the plasmid rather than the payload genes (replication origin, size, etc.). Check out [1] for an example.

[1] Wang, et. al. 2009. Plasmid.


Cheapest way to measure S. aureus and Rhinoviruses density at home

For anyone getting ideas

S. aureus and Rhinovirus are risk class 2 infectious substances that should only be handled in a BSL or containment level 2 environment. Your only feasible step here is swab, seal, and send to a lab that can handle it.


E. Cpm to fmol/mg:  Enter the specific radioactivity as cpm/fmol, the number of cpm counted, and the protein content of the sample in mg. The result is the number of binding sites in fmol/mg protein.

here is a guide of conversions.

The measure is a relative measure, and it can't be very precise as a discrete measure without knowing the precise measurement conditions, i.e. is it mixed every 5 minutes or every 1 minute, is it dissolved in 1 liter or 100ml? CPM denotes the reactivity and not the weight. You are more likely to get a Mol/L rating associated with a CPM, and two vials with the same CPM rating can have different Mol/L and Mg/L depending on their reactivity.

So, if your paper gives you a comparative measurement, and if it gives you a specific measurement at some stage you should be able to multiply it and figure out the numbers for the various days.


Origin of the biochemical term, Pi (inorganic phosphate)

This terminology is at least as old as September 1944 when Enzymatic Synthesis of Acetyl Phosphate Journal of Biological Chemistry
155,  55-70 was published by Lipmann, which says:

Inorganic phosphate, referred to as Pi, was estimated
colorimetrically

See also the definition of "inorganic phosphate" and "orthophosphate" from this 1943 University of Wisconsin Thesis:

Compound:  Inorganic phosphate or orthophosphate
Definition: Phosphate whose calcium salt is insoluble in water-alcohol mixtures under the conditions to be described. E.G. NaH2PO4

In other words, "orthophosphate" was a generic term for mono, di, or tri basic phosphate.  It did not have the narrower meaning attributed in the OP.


How does a fetus retain a blood group different from its mother?

The maternal and fetal blood circulation systems are completely separate. The embryo's blood cells start developing at around week 5 gestational age (3 weeks after conception), the same way any other tissue is developed by the fetus itself. By around week 7 gestational age, a circulatory system has developed and the heart has started beating.

All nutrition goes through the placenta, which keeps the two circulatory systems separate by the so-called placental blood barrier.

Rhesus incompability is only a concern after the first birth (or miscarriage) because then the maternal and fetal blood had the opportunity to mix and lead to the mother developing antibodies.

Also, as AMR pointed out in the comments, blood group incompatibility is mediated through IgG antibodies - those don't start to be produced at all until birth and at higher levels not until six months to a year after birth. See also At what age do babies begin to synthesize their own antibodies?


Is it possible that a set of functionally related proteins in a pathway fulfill different functions?

If Y can be seen as the inverse or absence of X function, it sounds to me like an incoherent type 3 feed-forward loop, where
A activates B
B activates C
A inhibits/reverses C

example from literature, E.coli: fnr as A, and arcA as B, cydAB as C
source: http://www.pnas.org/content/100/21/11980.long


How does a smoker's finger or mustache get yellowish by nicotine?

Pure nicotine is a yellow colored liquid (although some sources say it's a clear liquid.) "Tar" is a complex sludge that is also yellow-brown. So it's difficult to distinguish 'nicotine stain' from a 'tar stain' based on visual inspection. Let's go to other considerations.

The concept of a 'stain' implies that simple hand washing doesn't remove the coloration. Since nicotine is water miscible, one would expect it's easily removed with soap and water. That implies that either a) a smoker's stain is not primarily nicotine, or b) the nicotine reacts with the skin to create the stain.

Nicotine is sufficiently functionalized that it could conceivably undergo some interesting chemical reactions with proteins, but I don't think that's what's happening. A simple observation is that transdermal nicotine patches do not contain a colored agent, and do not stain the skin. Score one point for the "mostly tar" explanation. Cigarette smoke contains far more tar than nicotine, and tar will deposit on most-any surface (at ambient temperatures), so it's parsimonious to proceed with the "mostly tar" explanation.

The picture shows that the stain occurs on both fingernails and skin. The most abundant protein that's common to those two tissues is keratin. Like other examples of protein staining, the mechanism is complicated and poorly understood, but the basic outline is that parts of keratin are greasy (the non-polar amino acids) that associate with other greasy things.  (EDIT: AliceD's answer also depicts the well-known staining of teeth, which are not keratinized, showing that the staining mechanism is likely a nonspecific adsorption of greasy things onto surfaces.)

The stain can be fixed through the involvement of free radicals and other reactive species in cigarette smoke, like formaldehyde. In this sense, reactive oxygen species are active participants. I don't think oxygen deprivation plays a role here. I don't think this can be described as a melanosis, as the skin isn't producing melanin in response to smoking but is simply being coated in tar.

Even if the stain was completely fixed, the coloring would fade away as the exterior skin cells are sloughed off, consistent with normal skin physiology. This is the explanation for the fading of any stained epidermis. The persistence of tar stains on teeth (which do not exfoliate) further evinces that the stain is removed through the replacement of skin cells.


How to convince suspension cells to adhere more tightly?

My main concern here is why you are using suspension-culture selected cells for an adherent cell-based assay? Is it possible to obtain a clone of adherent HT1080? Depending on what you are assaying with your protein of interest, the cell biology may be altered changing from suspension/adherent culture systems.

Here are my experiences using PC12 cells in culture, which are weakly adherent cells, with a preference to grow in clumps, rather than monolayers. I have found that these cells have a preference for specific tissue plastic; (without mentioning names), these cells will adhere on some poly-D-lysine coated plates while they won't adhere on others. I routinely perform immunofluorescence microscopy with these cells, and grow them on glass cover slips which I have skim-coated with rat tail type I collagen. This coating provides minor background in the green range and only when imaging close to the glass. With a bright fluorophore (e.g., AlexaFluor or cyanin dyes for fixed cell; enhanced GFP for live cells), this backgorund is not a problem for quantitative microscopy.

Lastly, for secretion assays we use high-glucose DMEM supplemented with 1% dialyzed FBS. If memory serves, this retains all serum components less than ~15 kDa, which includes various growth factors. I have observed these cells continue to live for up to one day (and maybe longer?) in supplemented medium, while they die after a few hours without. This may also help with non-specific binding you may be worried about with drug addition.


Which of the two chromosomes in a pair is expressed?

The majority of normal autosomal genes have biallelic expression, i.e. the alleles on both chromosomes are used to make protein. This is why mutations in a gene which cause non-function of the product can be silent if the mutation is heterozygous (only found on one of the alleles), because the effect is masked by the second, fully-functional, copy of the gene. In other cases heterozygous mutations may cause slight phenotypes, because half of the protein produced is non-functional.

A small minority of autosomal genes have monoallelic expression, through a process called imprinting. This is where one of the alleles of the gene is modified by methylation of the DNA, or of histones (the proteins which are used to package and condense DNA). This imprinting switches off the expression of that allele, so that protein is only made from the other allele of the gene. Usually in this case, which allele is switched off depends on which parent it came from.

Things are slightly more complicated in the case of genes on X or Y chromosomes. Men have only a single X chromosome, and a single Y chromosome. This means that any mutation on X or Y which causes a phenotype will always present itself, because there is no second copy to mask it.

In the case of women, who have two X chromosomes and no Y, something similar to imprinting happens, where one of the X chromosomes is chosen to be inactivated. This X-inactivation process occurs very early in development, and the inactive X chromosome is kept that way for the rest of that person's life. In this case, however, the choice of which chromosome is inactivated is not dependent on which parent the chromosome came from, and is entirely random.

Some further reading:

http://www.nature.com/scitable/topicpage/monoallelic-expression-8813275

http://www.nature.com/scitable/topicpage/genetic-imprinting-and-x-inactivation-1066


How credible is the Remenko's two-component color vision theory?

That era produced a lot of very questionable science from Russia; there is no good reason to doubt the three-component color vision theory, and it's also the basis of all RGB TVs and computer monitors. However, I can't read Russian so I don't have any idea what this two-component theory is.

Typical humans have three cone cells, which is the biological origin of having three components for color vision. Colorblind individuals who lack one of the three cones have color discrimination issues consistent with the three component model. I am not aware of any credible research that questions this.

The lack of further study into the theory you refer to probably puts it into the category of "not even wrong" - based on such flawed reasoning or premises that it isn't worth disputing.

Nathans, J., Merbs, S. L., Sung, C. H., Weitz, C. J., & Wang, Y. (1992). Molecular genetics of human visual pigments. Annual review of genetics, 26(1), 403-424.


What makes an E.coli an E.coli, genotype or phenotype?

The context for identifying E. coli is primarily clinical Microbiology, and in the clinical lab the identification is primarily phenotypic, based on various properties such as growth and morphology on selective media, Gram stain appearance, biochemical characteristics, etc - only under unusual circumstances is genetic testing done. The latter is problematic because of extreme genetic diversity within the species and some overlap with others (even other genera).

The problems with the notion of "species" in E. coli in the context of 16s sequencing, horizontal gene transfer, mobile genetic elements, plasmids, etc is discussed at some length in Quammen's recent book The Tangled Tree.

For now, phenotypic species identification is the norm, as illustrated by the "Nomenclature" guidance to authors of the Journal of Bacteriology, a publication of the American Society for Microbiology.


What is the difference between HPLC and FPLC and why is FPLC preferable for protein purification?

The only difference between FPLC and HPLC is the amount of pressure the pumps apply to the column. FPLC columns have a maximum pressure of about of 3-4 MPa, whereas HPLC columns can withstand or require much higher pressures. As a general rule, HPLC columns won't work with old FPLC equipment; FPLC columns can go on HPLCs as long as the pressure can be regulated.

Manufacturers have been marketing separate equipment to handle these different classes of columns, but the trend seems to be heading towards machines that can handle both types of columns without issue. A GE rep told me a few years ago that they've improved the pumps on the AKTAs to the point that "they're technically HPLCs now." The term "FPLC" is probably on its way out.


What is bilateral symmetry in "bilateria", an actual symmentry

You are missing that "bilateral symmetry" does not mean "the divisions are the same on some arbitrary plane" it means "the divisions are the same on one specific plane".

That specific plane for animals with bilateral symmetry is on the mid-saggittal plane that divides the body into left and right. You won't get symmetry if you bisect in any other plane. If you do get symmetry in a different plane, then you are no longer talking about bilateral symmetry but rather some other type of symmetry, such as radial symmetry, spherical symmetry, or biradial symmetry.

Note also that although many animals do not have perfect bilateral symmetry in their internal organs (humans, for one), they are still considered to be bilateral symmetrical, because the bilateral symmetry is the main organizing feature of the whole animal.


Can humans' ability to dive with only breathing modifications tell us anything about our evolution?

This is not a complete answer to your question, but your question prompted me to research the Mammalian Diving Reflex, which is used, according to the article, as a survival mechanism rather than assisting us in day to day functioning.

Looking at the evolution of the diving reflex, and how it appears in varying degrees in all mammals, suggest that it has been around for a long time, this article suggests for over 125 million years.


Is curling the fingers considered digit flexion?

In the vertical plane, bending of the fingers is indeed referred to as flexion, while straightening is called extension. In the horizontal plane, spreading the fingers is called abduction, and approximation is called adduction (Fig. 1).

Fig. 1. Finger movements and terminology. source: US Dept. of Veteran Affairs


Are there any arboreal mammals which eat leeches?

First I'd like to point out that there are over 500 species of leeches. Most of them live in fresh water (nearly 90%), and so most tree-living animals would not come into contact with these leeches. Because of this a leech's biggest predator would be fish.

According to The New World Encyclopaedia the predators of leeches are fish, crayfish, turtles, birds, frogs, dragonflies, and damselflies. It states that many of their predators have also been their prey. Ecospark also adds snails and other insects to the list. Biokids also points out that leeches will eat other leeches.

Britannica cautions humans about swimming and drinking water with leeches in it. They can attach to internal cavities - such as the nose and throat and then the leeches can drop into the lungs and cause suffocation. In Asia, it is common for a domesticated animal to die in this fashion.

According to Animals.mom.me monkeys and other omnivorous animals will eat leeches that live on land, but land leeches aren't very common. After over an hour of searching various websites and information about leeches, there is no other source stating that mammals eat leeches.

However, it is possible to eat leeches. They did it on a television show called Fear Factor (video of the leeches being eaten linked). Before you go eating leeches though, remember these people were monitored both during and after ingestion of the leeches.

Short answer: There are no recorded mammals as predators to leeches, but it is known that pets have eaten leeches (as well as breathed them in). And humans are also able to eat leeches. It's all about if the leech is within grabbing distance when the mammal is hungry.


Is there a database containing sequences of human cell lines?

As pointed out by @kmm (http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/) is an excellent database. Alternatively you can look at the broad institute page (http://www.broadinstitute.org/software/cprg/?q=data-resource) in the cancer cell line encyclopedia section, then go to the browse tab and select the cell line for a very comprehensive list of cell lines.


A second telomerase is not necessary, as the lagging strand is filled in by the DNA-Polymerase, see this figure:


How to Determine the Most Conserved Sequence from BLAST Result?

The "best" is the one with the highest ID score, lowest e-value and greatest length. There is no magic bullet, all of these are important. You should always look for the most similar sequence that matches as much as your query as possible with the lowest e-value possible.

Furthermore, it will depend on what you are looking at. If, for example, you are blasting a protein with a specific domain and are looking to find its homolog in another species, it is often more important that the domain be conserved than that the whole sequence be very identical. If you find a sequence with high identity but where the domain is not conserved, that is probably not what you are looking for.


I know that so much fats running in the bloodstream could deposit in arteries, harden forming a plaque and cause atherosclerosis. But what about veins (which are formed from same types of layers as arteries) and capillaries?

Wikipedia says this:

  Veins do not develop atheromata, because they are not subjected to the same haemodynamic pressure that arteries are,[8] unless surgically moved to function as an artery, as in bypass surgery.

The cited study isn't freely available, but seems to have tested in rabbits by surgically modifying their blood flow and giving them a high fat diet.

As for capillaries, they are continuously remodeled, so while they do become clogged for a variety of reasons, once flow stops they're disassembled and new capillaries formed if the tissue becomes hypoxic.


Why isn't the upper limit of pain lower in humans?

You are assuming that fighting back with a bad wound would be more useful than dropping to the ground. That is not always the case.

Dropping to the ground and ceasing activity is very adaptive in almost any situation involving potentially significant blood loss. Becoming prone or supine prevents loss of consciousness, the most critical aspect of survival. Decreased movement is also likely to decrease the rate of blood loss (though not in as significant a manner as consciousness).

Certainly with a significant abdominal wound, running would increase cardiac output, which would increase bleeding. Is running from a traumatic event advantageous if you pass out before escaping? On the other hand, lying prone and holding the wound (instinctive) may reduce bleeding and prolong consciousness and life.

What "cannot be helped" (like withdrawing a hand from a flame) is usually advantageous.

An infant's cry changes during circumcision (an involuntary reaction to pain). The cry in turn naturally produces a visceral reaction in nearby adults that compels action (causes a state of strong sympathetic nervous system activation.) The adult either avoids the cry by trying to distance themself, or responds by coming to the infant's cry.

The infant cannot help changing the intensity of the cry with intense pain. If a "certain level of pain" was as far as one could feel, the baby might not elicit the sense of urgency in adults which it does.

Newborn pain cries and vagal tone: parallel changes in response to circumcision.
ASSESSMENT OF INFANT CRY: ACOUSTIC CRY ANALYSIS AND PARENTAL PERCEPTION


simple explanation of a crispr screen vs pooled crispr screen?

In the context of pooled CRISPR screen, you first design a library of gRNAs against a certain set of targets (instead of just one target).

The library can have the size you want, most commonly it is either targeting the kinome, or the whole genome (genome-wide).
In this context, you would add the full library on your cell of interest in which you want to make the perturbations.

Depending on how the screen is set-up you try to select the perturbations which either allow you to pass a selection process (toxicity, fluorescent readout, etc). Usually an elegant way is to have either a label also code barcode which helps you to identify the gRNA which generated the surviving/selected phenotype. With the barcode/gRNA you can track back which gene was likely perturbed in the screening process.

Hope that helps and that answers you question, please don't hesitate to further refine it if this is not clear to you.


There is a common misconception that a selective process is needed to remove a feature from a population. However, the correct approach is quite the opposite: selective processes normally maintain a feature in a population: if a given feature stops promoting selective advantage, its corresponding genes start to "erode" and the feature disappears from the population (and that can happen in different rates, depending on several factors: have in mind that maladaptative features do exist).

That being said, the maintenance of wings in ostriches indicates us that there must be a reason for it.

It has been hypothesised that wings:

Improve balance when running;
Helps regulating temperature;
Serve as mating display.

(source: University of Washington)


There are literally millions of biomolecules.  Some of them we know the structures and chemical properties of others we know nothing about.   I'm going to focus on sugars.  It would be too broad a question probably even to list all biomolecules, much less describe how their chemical synthesis would be performed.

The good news is that industrial manufacturing of biomolecules is done for thousands of compounds and even available.  Certainly chemical synthesis of sugars is possible and even available but is very expensive and often produces side products compared to fermentation processes or extraction from plants say.

Sugars, for instance glucose are very similar, but if you look at this structure you will see that the four OH (alcohol) groups could point up or down.  Any manufacture of glucose would have to get each one of these bonds exactly right.  This is D-glucose, which is commonly available as extracted with water from sugar beets and sugar cane.  I can buy 10 pounds of it at the store for less than $10.

Compare with L-glucose, which is synthesized by a chemist.  Its available (though not really recommended for human consumption because its got impurities and doesn't necessarily pass FDA definitions of purity to be a food) at the cost of $87 per gram.

So the answer is probably best put like this: who would pay \$87,000 for a bag of sugar when they could pay $10?  Cases where one would have to pay a company to produce a biomolecule, its going to cost...


How are germ cells not reduced in number?

In case of gametogenesis (let us talk about spermatogenesis) gametes are formed from meiotic division of Primary spermatocytes.

In Primates Primary spermatocytes are cells that that are formed from mitotic division of B spermatogonia (which is another class of germ cells) which inturn are formed from mitosis of Ap spermatogonia which arise from mitotic division of Ad spermatogonia.  Ad spermatogonia are inturn formed from Primordial germ cells (see below for details).

Ad spermatogonia are dark A type spermatogonia, reserve stem cells  which occasionally divde to renew itself and Ap spermatogonia are pale A type spermatogonia, renewing stem cells.

  Why the testis doesn't run out of germ cells? (adaptation of your key question)

The reserved  Ad spermatogonia and renewal of both  Ad and  Ap spermatogonia are responsible for the continuous cycles of spermatogenesis.

  This process starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. (wikipedia)

The process of spermatogenesis in human:

In non-primates like mice it is little different, the following diagram should explain it:

Note:

Germ cells are cells that give rise to gametes ( present at any level of gametogenesis).
Primordial germ cells are embryonic cells that originate from a different location (outside the gonads) and migrate into the gonads during the course of embryonic development to divide into germ cells.
In females, oogenesis also involve production of germ cells (cells of primary follicles) from PGCs through mitosis but the primary follicles produced is fixed, doesn't increase after birth so at a definite age of 40-45 gametogenesis stops.

Further reading:

Stem Cells in Reproductive Medicine by  Carlos Simón, Antonio Pellicer, Renee Reijo Pera
A paper


Pregnancy from two parents with incompatible blood types, can it lead to complications?

The rhesus factor (the + / - part of the blood group) can cause complications with pregnancy under certain conditions and lead to the so called Rh disease:

If the mother is rhesus negative and the father, rhesus positive; then the birth of a child with Rh+ blood group (inherited from the father) can cause the mother to build antibodies against this blood group. Therefore, a second pregnancy with a child that also has Rh+ blood group can have complications if no precautions are taken at any other point.

If these specific conditions are not all met, then no complications should arise from the blood groups.


Definition of Haplotype

The concept of haplotype has the default to be subject to several definiton that differs mostly by their complexity to be understood and by their specificity but different definitions also sometimes differ slightly in their meaning.

In simple terms the concept is pretty easy. A haplotype is a porte-manteau word of haploid genotype and it refers to half the genotype.

What the question is asking

The question is asking is Here is half of the genotype of the child, what do you expect the other half to be?. Note however, that for the last two markers, the first haplotype is not indicated so they are just asking for the genotypes here which makes the question slightly poorly phrased IMO.

The answer key

The answer concern the father, which is silly as the question is about the child. So the answer you stated definitely does not answer the question.

The answer

We have to look marker per marker to answer the question and then consider them all together to reconstruct the haplotype. In absence of information on the subject, we are going to assume that the markers are completely independent (unlinked, eventually on different chromosomes). We will also assume no mutation (probably negligible anyway) and we assume no crazy kind of inheritance such as some selfish elements. You will note also that information about the first child tells nothing about the second child.

Marker A

The first allele inherited necessarily comes from the mother and therefore, the second allele must comes from the father. As a consequence the second allele is either 3 or 4 with equal probability.

Marker B

The first allele inherited necessarily comes from the father and therefore, the second allele must comes from the mother. As a consequence the second allele is either 1 or 4 with equal probability.

Marker C

The four possible genotype are [5,7], [5,11], [11,7] or [11,11], that all occur with equal probability. This means that for Marker C, at one haplotype, the probability of being 5 or 7 is $\frac{1}{4}$ and the probability of being 11 is $\frac{1}{2}$.

Marker D

The four possible genotype are [4,7], [4,8], [7,7] or [7,8], that all occur with equal probability. This means that for Marker D, at one haplotype, the probability of being 4 or 8 is $\frac{1}{4}$ and the probability of being 7 is $\frac{1}{2}$.

Whole Haplotype

From the above, you can compute all possible haplotypes and calculate the most likely to occur. However, there are some ties. The most likely genotypes are (3,1,11,7), (3,4,11,7), (4,1,11,7) and (4,4,11,7) that could occur with probability $\left(\frac{1}{2}\right)^4 = \frac{1}{16}$.


That is Himalayan balsam (Impatiens glandulifera).

  Tall, stems often reddish. Lvs opposite or in threes, with small red teeth. Fls large, pale to dark pink-purple, with short bent spur; July-Oct. Bare places, especially by streams.

The Wild Flowers of Britain and Northern Europe. Fitter, Fitter, Blamey. 1974. Collins, London.


If you feed bacteria 2-aminopurine then at some low rate it gets incorporated into into the DNA instead of adenine during DNA replication. In other words there will be a base pair between thymidine and 2-aminopurine.

Two things could happen:

DNA repair could detect the unusual base and attempt to correct. If the 2-aminopurine is excised then adenine will be inserted--no mutation. If, however the thymidine is excised then sometimes a cytidine will be inserted. This gets resolved below.
During the next cell division the replication machinery will sometimes incorporate a dC across from the 2-aminopurine. Then in the following cell-division a dG will be incorporated across from the C, so what used to be an A-T base pair has become a G-C base pair (eventually).


How did the activities of protocells become inheritable?

The sequence is believed to be opposite of that implied by the phrasing of the question: the inheritance of structures supporting inheritance came before protocells.  The important point is that you need a system of reproduction before building more complicated structures (such as a cell).  Without replication (reproduction), a cell would be little more than a soap bubble, and would disappear without a trace before long.

The initial (or very early) form of replication is thought to be based on a simple form of RNA. The reason for this is that (1) RNA does encode genetic information in a way that is replicatable, and (2) RNA can take on shapes and chemical structures that act as an enzyme (called a ribozyme) that catalyze chemical reactions.  The hypothesis is that an RNA molecule formed that catalyzed assembly of copies of RNA chains, including itself.

After such replication was established, probably some kind of enclosure like the cell membrane evolved to contain the chemicals, making the reactions more efficient.  After (or maybe before) this, RNA catalyzing assembly of simple protein-like molecules whose sequence was encoded by RNA sequences evolved, leading to protein-based cellular machinery.  This mechanism is still evident in life today in that protein assembly uses a ribozyme-based molecule assembly (the ribosome) to translate messenger-RNA into proteins.


Is one DNA molecule same as one chromosome

Considering the encyclopedic definition of a molecule...

  Molecules are held together by shared electron pairs, or covalent bonds.

...one DNA molecule is one DNA strand.

Put another way, one DNA molecule is a polymer of nucleotides connected by phosphodiester bonds. This means that one intact double-stranded chromosome is composed of two molecules of DNA interacting by hydrogen bonds.

In practice, however, one piece of double-stranded DNA is commonly called a DNA molecule.

All of the chromosomes in a cell constitute a single genome.

To further add to the confusion, identical chromatids may be said to compose a single chromosome, such that one replicated chromosome composed of two chromatids may comprise four DNA molecules, by the definition outlined above.

Note, the same encyclopedia lists ionic bonds as being on the same "continuum" as covalent bonds...

  Ionic and covalent bonding therefore can be regarded as constituting a continuum rather than as alternatives.

...so atoms held together in ionic interactions are also considered molecules, by this definition.