Is there any case in which excitability increases with lowering the RMP?

A typical voltage-gated sodium channel has 3 gating states: open, closed, and inactivated. The third category is the important one here.

Open channels are open: they let ions through.

Closed channels are closed: they don't let ions through, however, they are available to open and their probability of opening increases as the membrane voltage rises from negative towards positive.

Inactivated channels don't pass ions, but it also cannot be opened by depolarized voltage. Instead, it needs a negative membrane voltage to pass back to the Closed state.

When a sodium channel opens, it only stays that way briefly before going to an inactivated state. Recovery from inactivated back to "closed but openable" requires the

If you depolarize a cell gradually, this will open sodium channels, but it will also increase the number of channels stuck in this "inactivated" state. That means there are fewer channels available to flip from closed to open.

When a cell is hyperpolarized, there are fewer channels stuck in the inactivated state, and so the threshold potential can actually become more negative: it takes a smaller voltage step to open enough channels to trigger an action potential, because there are more channels available to open. You can describe this situation as being "more excitable" despite the hyperpolarized potential.

Some cells, including cardiac cells and other types of pacemaker neurons, will actually depolarize spontaneously from this hyperpolarized potential and reach threshold all on their own without external input.


Regional circulation and Cardiac output?

It might be as simple as 'point of view'.


No, not that I have ever seen. Classically, the Enzyme Commission (E.C.) identifiers are the only way to be certain that two (or more) abbreviations or acronyms are all referring to the same enzyme activity. Sometimes, when the situation becomes very complicated interested parties will co-author a proposed new naming convention within their subfield. Some journals may require specific abbreviations, but otherwise authors are free to use whatever nomenclature they like.


Spider with brown zig zags on abdomen and black head

As far as I know you've found a male steatoda triangulosa or triangulate cobweb (weaver) spider

More info:
https://en.m.wikipedia.org/wiki/Triangulate_cobweb_spider
http://lancaster.unl.edu/pest/resources/triangulatespider.shtml


This is acaena magellanica which is also called "Buzzy Burr" or "Greater Burnett". See these images for comparision (from here and here):


Concentration calculation of Factor VIII for Elisa

My answer: 4.79 µg/ml

(All values below are µg/ml)

Calibration data

Determine the mean of the four absorbance values at each dilution.

The calibration curve is then a plot of concentration (x-axis) against mean absorbance. Note that the actual concentration in the assay is (2123/2200)/dilution where dilution is 20, 40 or 80. If you chart this you will see that the data fit well to a straight line.

Use the Excel SLOPE and INTERCEPT functions to derive the parameters of the trendline. (I get SLOPE = 30.59; INTERCEPT = -0.8225)

The equation for converting an observed absorbance value to a concentration is:

concentration = (absorbance - INTERCEPT)/SLOPE

Sample data

For the sample measurements the only one that is valid is that for the 20x dilution because the other absorbances lie outside the range of the calibration data (see note below).

Using 0.406 as the absorbance value in the equation above gives a value of 0.01596 for the concentration in the assay well. This sample was diluted 20-fold for the assay, and the source for that dilution was derived from a 15-fold ‘pre-dilution’ so the original concentration of the sample is 300x the assay value which is 4.788 µg/ml.

Note

I don't know the nature of the discrepancy between your calculations and the target value, but if you try to incorporate the 40x and 80x dilutions for the sample you will get higher values for the sample concentration. Presumably the assay becomes non-linear at low concentrations.


Help with understanding XKCD's “How Vaccine Failure due to Viral Vector Immunity Works” Why is this response a failure exactly?

Yes, the cartoon is a description of immune action.
Traditionally shown is first exposure being a vaccine, and the second exposure being the bad virus being destroyed.
However, this cartoon is describing viral vector immunity.
The first exposure is a viral vaccine. This alerts and educates the immune system about not just the intended antigen, but also the (harmless) carrier virus which is represented by a horse.
The second exposure is a different viral vaccine.
The immune system immediately mounts a successful response against the vaccine because is recognises the carrier virus.
So the immune system doesn't get the chance to learn about the antigen associated with the second virus.
A example of viral vaccine failure would be useful - I will see if I can find one if no-one else does.


How are vaccines and inoculations different?

If you became infected before the advent of vaccination, you would either live or die. You would also probably die with really good odds. Being said, someone who lived a disease developed immunologic tolerance to the causative agent, that much you could begin to understand. To expose someone to smallpox was to really endanger their lives, so they found that a similar virus known as Vaccinia, which would normally cause cowpox, could be administered to a patient and they would catch cowpox, but now they were resistant to catching smallpox. You can read about all this on the wiki page for vaccination.

Inoculation generally differs because in the case of inoculaton, you could hope for a less virulent strain of a pathogen but you weren't guaranteed it. You ended up with vaccination methods that increased the safety of the process: On one hand, you could infect someone with related pathogen that causes a milder disease for protection from a more dangerous, related pathogen. On the other, you could find a way to disable the agents pathogenicity, such as heat-killing.

Modern vaccinations are much more refined in that we know so much more. Attenuated strains, for example, you take a virus that grows well in human cells and infect monkey cells just as an example. After many generations the virus grows well in the monkey cells, but no longer the human cells. The strain should still retain it's antigens, however, so when you inject a human now, the virus doesn't cause a disease but you produce antibodies to the virus.

In short, you can protect a population from a disease that would normally devastate it with a dramatically improved efficacy.


All of your reasoning is correct - viruses are not motile (i.e. not self-propelled).

I don't understand why you think this would cause a difficulty in the case of bacteria.

Edit in response to comment @Remi.b

Some cursory research on estimating probabilities of collisions between particles engaged in random walks has revealed some very challenging maths. So I decided to simply look at some data.

Remarkably there is a fairly recent paper describing investigations of the kinetics of bacteriophage adsorption.

  Moldovan, et al. (2007) On Kinetics of Phage Adsorption. Biophysical Journal 93:303–315

I didn't realise it was still possible to publish papers like this, but in fact it is very interesting. For our current purposes we only need to consider the data presented in Figure 3, which show that when E. coli cells at a density of 108 cells ml-1 are mixed with bacteriophage λ at a density of 5 x 104 particles ml-1, then 90% of the phage have attached to a bacterial cell within less than 10 min.

Just to relate this to a real life situation, it is estimated that sea water contains bacteria at a density of 106 cells ml-1 and phage at 5 x 107 particles ml-1.


Originally the position had a G:C pair. After the mutation, there is an oxoG:C pair. Upon replication, the strand with C will pair to G and the original pair will be created as expected. However, since oxoG can also pair with A, the strand with oxoG may form an oxoG:A pair. Another round of replication gives the products T:A and oxoG:A. Thus the G in the original strand is replaced by T (ie it is a G$\ce{->}$T transversion).


What are the uses of centrioles and matrix of centrosomes?

THis was too long for a comment.
It would be helpful for you to indicate what exactly you mean by "cells can still function normally and grow".
There are a few observations related to your question about absence of centrioles (from your wiki page):

In Drosophila mitosis and development can occur to some extent in centriolar mutants, but "they die shortly after birth" due to flagellar and ciliar defects.

Some organisms do not have centrioles and use other mechanisms (e.g. angiosperms).

So, in the sections of your wiki page "Fertility", "Ciliogenesis", etc., those list the functional significance of centrioles.
If what you mean is "what is the role of centrioles in mitosis", then we of course have a separate question. You can find a lot of resources on this topic via google searches.
As for your last question, about the synthetic sphere, you will have to spell out the experiment in much more detail- for example, what do you mean by "synthetic sphere"? A sphere defined by a lipid bilayer with gamma-TuRC (for example) on its surface and no other features is not a cell and won't go through a cell cycle.


I don't know much (read: anything) about the .NET framework but a little search turned up Microsoft's .NET Bio:

  .NET Bio (formerly Microsoft Biology Foundation [MBF]) is a language-neutral bioinformatics toolkit built as an extension to the Microsoft .NET Framework—initially aimed at the area of Genomics research. Currently, it implements a range of parsers for common bioinformatics file formats; a range of algorithms for manipulating DNA, RNA, and protein sequences; and a set of connectors to biological web services such as NCBI BLAST.

Free (as in beer) and open source!  And from this it looks pretty cool.


X-recessive disorder pedigree confusing me

Remember: A and B are genetic markers that might be linked to the disease gene. Neither A nor B are actually the hemophilia disease mutation (or gene), A or B are proxies, or substitutes for the mutation in the disease gene.
Since it is an X-linked recessive, it is only the Mother's two X chromosomes that are candidates.  You can completely ignore the Father's copy of X that also happens to carry the A marker.
In the F1 generation every male who received the copy of the Mother's X marked with A died, and every male who received her X marked with B survived. Therefore her X marked with A is linked to the mutation.

Those other AA females are either heterozygotes, or outsiders who married into the family. The outsiders do not carry the mutation.

Perhaps your confusion is due in part to the fact that some key facts are not explicit in the pedigree diagram from your instructor's course materials? Try drawing the various genotypes out like this:


Yes, they are action-reaction pair.( Newton’s third law).
No, it won’t tear under normal circumstances. The filament withstands all that force because the attractive force between its constituents is far more than the force generated by myosin actin cycle.


What are the units of Phylogenetic Independent Contrasts (PICs)

From what I understand, the answer is; it depends. As you point out in the comment to Remi.b, contrasts are standardized by branch lengths (which are assumed to be proportional to "evolutionary time") before they are analysed (to obtain standardized independent contrasts). However, branch lengths can be come from a number of different sources (divergence times, genetic similarity etc), can be based on different evolutionary models, and can also be transformed (log etc). Therefore, you cannot say what the units of standardized independent contrasts are in general. They would probably not be dimensionless though, since branch lenghts are seldomly (if ever?) expressed in the same units as the raw contrasts. Units such as log(kg)/year or kg/log(year) are more likely. Ultimately, in the usual case, the point of standardizing is to assure that all contrasts receive equal weight in the the analysis, and the creation of suitable branch lengths can be a trial-and-error process, where you e.g. study the relationship between standardized contrasts and the standard deviation of contrasts to see if they have been adequately standardized.

I guess you could describe the process as:

calculate contrasts
calculate standardized contrasts (using branch lengths)
when the contrasts are appropriately standardized, you have obtained phylogenetically independent contrasts.

Here are a couple of relevant quotes from Garland et al., 1992:

  ...independent contrasts must be adequately standardized so that they will receive equal weighting in subsequent correlation or regression analyses.

also

  Second, the statistical adequacy of any proposed branch lengths should be viewed as an empirical issue (cf. Grafen, 1989, 1992; Harvey and Pagel, 1991; Pagel and Harvey, 1992). Third, different transformations -
  and indeed entirely different branch
  lengths, based on different information -
  can be used for different characters. The
  use of different branch lengths for different characters would be analogous to using different transformations for the two variables in an ordinary correlation or regression.

finally

  Standardized independent contrasts essentially indicate minimum average "rates" (or, in Bookstein's [1988] terminology, "reduced speeds") of character change occurring along two branches deriving from a
  common ancestor (Garland, 1992). Because
  they are standardized, they do not indicate
  absolute amounts of change. For example,
  a large contrast (absolute difference) between two species at the tips of a phylogeny may yield a small standardized contrast if the branch lengths of that contrast
  are long.


Is there any data on Neanderthal admixture in Western European Hunter Gatherers?

tldr; Neanderthal ancestry is roughly equally the same between the groups you mentioned.
It's almost certain that the major pulse of Neanderthal admixture into non-Africans occurred very soon after the primary out of Africa event (here I am referring to the out of Africa migration which contributed towards most of the ancestry of all non-Africans today - of course there were other out of Africa migrations which were effective dead ends).
This is well established from a) looking at the size distribution of Neanderthal fragments in the human genome (ref, ref) and b) the fact admixture occurred around 232–430 generations before the 45kya year old UstIshim individual was alive. So most lines of evidence suggest this admixture took place between 50-60kya.
This is much earlier than the diversification of West Eurasian populations into groups like Yamnaya, Anatolian farmers and Western Hunter Gatherers. Therefore, there is no reason to expect any one of these ancestral groups would have had higher amounts of Neanderthal ancestry than any others, since the admixture event occurred into the common ancestor of all these populations.
Indeed, from Haak 2014:

The ancient individuals had indistinguishable levels of Neanderthal
ancestry when compared to each other (∼2%) and to present-day
Eurasians (Supplementary Information section 6)

There are some ancient individuals such as Oase1 who carried substantially more Neanderthal ancestry than modern day samples (in fact this individual has very recent Neanderthal relative), but that they didn't contribute anything towards the ancestry of later groups.
Btw I know a lot of these reference are old - I will add some more recent estimates later, but they don't change the overall picture.


Where do most mutations come from, mitosis or meiosis?

@Remi.b I think we can do better than 1962. Let's fast-forward here to 2014, in the post-genomic era.  I think this paper provides some data relevant to your query: Possible mechanisms for Chromothripsis .


What factors affect the number of individuals in an animal group?

this depends on what you mean by group.

If you mean population then it is mostly environmental factors, although part of the environment can be other member of your species, some groups have a minimum functional size, such as passenger pigeons and breeding in groups behavior, or have density controls(if you are too spread out you might never run into another member of your species to breed with) , these internal factors are fairly rare however compared to basic resources availability, things like food, water, territory, shelter, nutrients, ect.

If you mean size of individual packs, herds, ect, then it is a mix of both, behavior which is almost always genetic is the main cause. However this behavior can be alter or triggered by environmental factors and its ultimate evolution is strongly affected by those factors as well. for instance large herd behavior will never evolve if the environment cannot support it, and if the environment changes the behavior may stop being beneficial.


In journal articles, they are doing many studies every year describing the state of the art tools and procedures for sequencing plant genomes.

by researching 5 minutes you have results of this kind:

http://www.pnas.org/content/95/16/9693.full

  Protocols involved commercially available kits (e.g., Qiagen’s RNeasy Plant Minikit), non-commercial RNA extraction lab protocols (e.g., CTAB, acid phenol) and hybrid methods that combined components of both commercial kits and lab protocols. The detailed protocols used for all isolations are available online in Appendix S1.
  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050226

  Tissue and organ samples for Northern blot analysis of gene expression patterns were taken during the growing season and frozen in liquid nitrogen, then stored at −80°C. Shoot-tip samples are the terminal 1–2 cm of succulent stem tissue from elongating branches and terminal leaders. Immature xylem was harvested with a vegetable peeler from the surface of woody stems after removal of the bark, and includes cells with primary cell walls derived from the cambial zone through the zone of radial cell expansion. Compression wood and side wood immature xylem RNAs were those used for preparation of the libraries, whereas vertical immature xylem denotes samples taken from stems of control trees growing vertically. The tissue described as “phloem” was collected from the inner surface of the bark of vertical stems and actually includes periderm and other tissues as well as active phloem. Planings were collected from the surface of vertical woody stems with a wood plane after immature xylem was harvested and includes cells that have formed secondary cell walls strong enough to resist harvesting by the vegetable peeler. Needle samples were partially expanded juvenile needles.

here are some more texts for you to check

http://www.pnas.org/content/106/31/12794.full

https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-7-214

From_field_to_film_Rapid_sequencing_methods_for_field-collected_plant_species

It took me 5 minutes to find these informations by searching articles for

  plant sequencing methods


Is an attraction to studying the philosophy of biology a good reason to pursue grad studies in the field?

In my opinion, yes and bioethics is a very interesting domain.
 First, there is a growing interest in ethics (which is a branch of philosophy) in the fast-growing field of synthetic biology ("next-generation" genetic engineering, the design of new organisms, genetic manipulations in humans etc.). In many publications (check out "synthetic biology" and "ethics" on google) and conferences, people are saying how far behind is bioethics, compared to synthetic biology. There are many burning questions such as: If we create new organisms, should we release them to the environment? Should we edit the human genome? To what extent? (Just curing illness, or maybe also to improve traits?) Should this ability be democratized?
Should a person's genetic information be used when looking for a job? Insurance? And so many more questions, not to mention the bioethics of the state healthcare (compulsory vaccinations etc.)
There are a lot of scientists that know nothing about philosophy and a lot of philosophy experts that know nothing about science. There are not enough people who know both and can help with these question.


Why can't certain nucleoside analogs be used to label bacterial RNA?

Meng et al. actually give their explanation in the first paragraph of their results section. The main reasons for their claim are that they did not detect any labeling with 4SU or EU and that both analogs suppress bacterial growth. Also they raise the issue with the naturally occurring 4SU in tRNAs.

Aiming to develop nucleoside analogs compatible with bacterial RNA labeling, we first set out to evaluate the two nucleoside analogs widely used in eukaryotic cells. E. coli cells were incubated with 4SU or EU at varied concentrations for 2 h, which resulted in no detectable labeling even at high concentrations (Supplementary Figure S1A, B). Moreover, severe suppression of bacterial growth was observed with both 4SU and EU (Supplementary Figure S1C, D), which was in agreement with previous observations that 4SU impaired cellular metabolism in E. coli (31). Cell viability was significantly impaired with 4SU at concentrations higher than 100 μM, while EU did not induce significant decrease in cell viability (Supplementary Figure S1E, F). In addition, tRNAs of bacteria contain endogenous 4SU generated via thiolation of uracil (32), which may interfere with metabolic labeling if exogenous 4SU would be used. Of note, although EU does not incorporate into DNA in mammalian cells (10), significant labeling of DNA was observed in EU-treated E. coli, presumably due to metabolic conversion of EU to EdUTP (Supplementary Figure S1G). Together, these results demonstrate that 4SU and EU are not applicable for bacteria.

This explanation is not necessarily incompatible with the results in the other references mostly because the strains and the test approaches are different.
In Favre et al. they use a different strain of E. coli,"an Escherichia coli
pyrD strain" that is optimized for 4SU incorporation :
In Material and Methods :

pyrD used to control the level of 4-thiouridine incorporation

and in Results :

a) growth of E. coli AB1157 sfiA pyrD in the presence of 4-thiouridine
Preliminary studies showed that the level of s4U incorporation into the rRNA of strains MRE 600 or K12 AB1157 grown in a standard glucose medium in the presence of 4-thiouridine remained at the detection limit. We therefore use AB1157 pyrD mutant deficient in the pyrimidine biosynthesis pathway. To our growth medium we systematically add 40 μg/ml uridine because it is  the minimal concentration required to supplement growth fully. The growth of the pyrD mutant was first examined at different temperatures and different exogeneous s4U concentrations from 40 μg/ml upwards in the conditions defined in Material and Methods, In Fig. 1 we report  the growth curves obtained for two s4U/U ratios,1 and 2.5, and four temperatures: 25°C, 28°C, 30°C, 35°C. When the ratio is 1 there is practically no growth inhibition. With  a ratio of 2.5 the  growth  inhibition becomes strongly dependent on temperature. The culture does not grow at all at 20°C, the  growth is linear between 25°C and 30°C and for temperatures above 30°C it escapes inhibition, becoming exponential. As will be described below significant s4U incorporation occurs in  conditions where growth is linear.

In Favre et al. as seen at the end of the paragraph above as well as in another publication (Bezerra and Favre, 1990) from the same lab shows that incorporation of 4SU depends on several factors.
Concerning the work of Blenkiron et al., it is harder to explain but they also use a different strain so that may impact the incorporation and they do not use the same approaches compared to Meng et al. to detect it. Confocal microscopy for Blenkiron et al. vs Dot blot and In-gel fluorescence for Meng et al..
Finally as far as the grant abstract is concerned, it's hard to conclude because the information is scarce but as Meng et al. they also observed an effect (although milder) of 5EU on bacterial growth and again, they used a different approach to observe the labeling based on fluorescence microscopy as Blenkiron et al..

References :

Meng L, Guo Y, Tang Q, Huang R, Xie Y, Chen X. Metabolic RNA labeling for probing RNA dynamics in bacteria. Nucleic Acids Res. 2020 Dec 16;48(22):12566-12576.
Favre A, Bezerra R, Hajnsdorf E, Lemaigre Dubreuil Y, Expert-Bezançon A. Substitution of uridine in vivo by the intrinsic photoactivable probe 4-thiouridine in Escherichia coli RNA. Its use for E. coli ribosome structural analysis. Eur J Biochem. 1986 Nov 3;160(3):441-9.
Blenkiron C, Simonov D, Muthukaruppan A, Tsai P, Dauros P, Green S, Hong J, Print CG, Swift S, Phillips AR. Uropathogenic Escherichia coli Releases Extracellular Vesicles That Are Associated with RNA. PLoS One. 2016 Aug 8;11(8):e0160440.
Bezerra R, Favre A. In vivo incorporation of the intrinsic photolabel 4-thiouridine into Escherichia coli RNAs. Biochemical and biophysical research communications. 1990 Jan 15;166(1):29-37.


According to this article polar bodies sometimes apoptose but sometimes are "capable of developing into complex, highly organized structures, or even enabling parthenogenesis". Despite their fate being far less than the oocyte.

It also states they're present not only in other animals, but also some plants.

"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo. These apparent “oddities” reveal the diverse mechanisms used during reproductive development and may even allude to the origins of meiotic strategies."

It looks like polar bodies are very important in humans, but not other organisms:

"Polar bodies may, however, give rise to human embryoids if fertilized and twins may even result when one spermatozoa fertilizes the ovum and a second sperm fertilizes its sister polar body (Bieber et al., 1981). No twin pairs resulting from fertilization of the second (haploid) polar body have been reported (Machin, 2009), but clearly polar bodies have cellular and developmental potentials beyond apoptosis, even in humans."

"But in many other organisms, polar bodies are not dispensable. They are not simply waste bins for three-quarters of the genetic material produced during oogenesis, and they do not disappear following meiosis."


Will a vasectomy prevent genetic engineering of a child?

From the wording of your question the 'genetic engineering' that you are envisaging will involve sperm. So the question is really, does vasectomy affect sperm production?

The answer is that it does, but it doesn't abolish it. For example:

  McVicar et al. (2005) Effects of vasectomy on spermatogenesis and fertility outcome after testicular sperm extraction combined with ICSI. Human Reproduction 20: 2795-2800

These authors found that sperm yield fell to about 35% > 5 years post-vasectomy.


Can one derive COVID-19 risk from a cheap consumer genetic test like 23andme?

I suppose the answer is 'theoretically yes, but don't trust the results much'.
The 23andme genotyping array is very useful for ancestry testing, but much less useful for clinical diagnostics. I have worked in the past for Genomics England (an arm of the NHS in the U.K. which performs genetic diagnostics for rare disease). There, the samples were sequenced to very high coverage and underwent extremely stringent quality control checks which were being constantly updated. If you want to interpret a variant in a clinical sense, you have to very sure that you get the right genotype.
I believe that the details of how 23andme performs its variant calling and quality control are proprietary and therefore I would never trust their variant calls for any kind of clinical diagnostics, and neither would any clinician I know. This doesn't mean 23andme results are invalid - they are very useful and pretty accurate for testing ancestry, but they are not valid for clinical diagnostics. If your risk calculations hinges upon a few SNPs of relatively large effect size (such as BRCA), then you want to be very sure you make the correct variant call. You simply do not get this assurance with 23andme.
Secondly, like you mention, many of the SNPs you refer to aren't covered by the 23andme array. The effect size of a particular SNP on a trait is calculated for that specific SNP only. Extrapolating the effect size for one SNP in a gene to another, nearby, SNP in the same gene is likely to give you innaccurate results. In fact, the same SNP in the same gene can have pretty different effects in different people (https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/febs.14080 caused by the environment, pleiotropy).


How do prions transmit their conformation to other proteins?

It is thought that infectious prions exist as clusters forming a crystalline structure. When a protein with the same primary structure is encountered but with a different tertiary structure, the normal protein undergoes a conformational change in order to integrate into the cluster. Presumably there are molecular forces involved that induce the conformational change.

http://www.rsc.org/chemistryworld/Issues/2005/October/prions.asp


After vasectomy, where does the sperm go?

A vasectomy [...] is a contraceptive procedure in men in which the vas deferens, or sperm duct, is cut and the cut ends are sealed in order to prevent the transportation of sperm. Sperm is still produced, but does not leave the body. Vasectomy is usually done as a means of sterilization and is sometimes reversible.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

When the vasectomy is complete, sperm cannot exit the body through the penis. Sperm are still produced by the testicles, but they are soon broken down and absorbed by the body. Much fluid content is absorbed by membranes in the epididymis, and much solid content is broken down by the responding macrophages and re-absorbed via the blood stream. Sperm is matured in the epididymis for about a month before leaving the testicles. After vasectomy, the membranes must increase in size to absorb and store more fluid; this triggering of the immune system causes more macrophages to be recruited to break down and re-absorb more solid content.
http://en.wikipedia.org/wiki/Vasectomy

A vasectomy only blocks sperm and does not affect your sexual drive, your ability to have an erection, orgasm or ejaculation or your ability to have and enjoy sex. Sperm is only a small fraction of the total liquid in your semen(almost 4-5 %). The amount of fluid, intensity – even color and texture – does not appear to change when sperm is absent.
...
The body absorbs unused sperm cells normally – whether or not you’ve had a vasectomy. After the procedure, the testicles will continue to produce sperm, but they will not leave the body in the semen. They dissolve and are simply and naturally absorbed by the body.
(from http://urology.med.miami.edu/specialties/male-urologic-health/vasectomy)

Sperm are produced in the testicles.  They are stored and reach maturation in the epididymis, a tightly coiled, muscular tube that is 15 to 18 feet long and leads into the vas deferens.   The muscle of the epididymis and the vasdeferens contract to propel the sperm through these structures and into the urethra at the base of the penis so the sperm eventually can fertilize an egg.
http://vasectomyreversalcenterofamerica.com/microsurgical-vasectomy-reversal/faqs/

Sperm are produced in the seminiferous tubules of the testes, and this does not change. A vasectomy does not affect the function of the testes. It is a physical separation of the vas deferens from each testis, so that the sperm cells cannot be ejaculated. However, the rest of the semen, which is made in the seminal vesicles behind the bladder and which is stored in the prostate, is ejaculated so the male reproductive experience will not change. He can still ejaculate, but there will be no sperm cells in the semen, so there can be no fertilization of an egg cell during intercourse.


Identification of this humpbacked, brown, clawed insect climbing up my wall?

That's the exoskeleton (shed outer shell) of a young cicada, left behind when it emerged as an adult and (we can imagine) flew off somewhere to sing, and find a mate.

This article on EarthSky has a nice description of the big cicada hatch this summer (2013), and also a great picture of an adult cicada emerging from the exoskeleton. However, this article and other recent news about cicadas mostly deals with the Eastern US genus Magicicada, and it's likely that in Arizona you're seeing a different genus (that is, a different type of cicada).

You'd probably have to find an adult in order to identify exactly what genus and species of cicada you've got. Alternatively, you could listen for their songs – this site has examples of calls from many Western US species, including the Apache Cicada Diceroprocta apache, which seems to be a common cicada in your area.


Power consumption of a ATP synthase in Watts

There are tons of mechanistic studies of ATP synthase so you may be able to get a better answer from finding one of those. But here's a rough estimate based on thermodynamics and enzyme kinetics.

The $\Delta G$ of ATP synthesis/hydrolysis is about -50 kJ/mol. The $V_{max}$ is in the low hundreds (here is an estimate of 350 $s^{-1}$ for E. coli ATP synthase), giving you something like 17 MW/mol or 30 aW (3e-17 W) /molecule.

I did look briefly at some mechanistic studies, and found this reference of 80 pN * nM for the torque generated. That translates to almost exactly the same 50 kJ/mol (ATP synthase is very efficient). But of course you still need the $V_{max}$ (number of rotations per second) to get the power.


Citing your source would help to answer.

In order to test an elastic modulus, you need to apply some non-zero strain. If the strain is infinitesimal, then compression and stretch modulus will be equal. But if it is finite, then there can be a difference due to the structure of the material.

In bone, I believe porosity will provide most of the dissymetry between compression and extension: at small scales, the material can rearrange using the pores without much deformation. Whereas in extension, there has to be some deformation of the osteons.

In other living tissue, the difference can be due to filamentous proteins: if you compress them, they buckle (form loops) without much resistance. If you exert extensive stress, once they are stretched tight they will resist any further extension. (Think of what a piece of string would do, it's very similar)


Your question conflates two separable events, a redox process and an acid-base dissociation.

The interconversion between disulfides and free sulfhydryls is a redox reaction, governed by the redox potential of the surroundings. The importance of redox potential to the -S-S- <> -SH equilibrium is illustrated by the difference between the cytosol and the lumen of the endoplasmic reticulum (ER). The cytosol is reducing and so free thiols are prevalent (there are usually no disulfide bonds in cytosolic proteins) whereas the ER lumen is oxidising, and the formation of disulfides in secreted proteins is promoted. The redox potentials of the two compartments is set primarily by the ratio between oxidised glutathione and reduced glutathione.

The thiol group in cysteine residues of proteins typically has a pKa of around 7, so it will indeed have some acidic character at slightly alkaline pH, dissociating to form a thiolate group. This doesn't however promote the reformation of disulfides, and in any case if it is important for a protein to have an undissociated thiol, then the environment of the specific cysteine residue can be adapted to raise its pKa. Note however that it is also possible that the thiolate form may be compatible with (or even required for) the function of the enzyme.


In general receptor-binding substances cause an "overflow" of your own already produced neurotransmitter. Your brain reacts by reducing the receptors. Also your own neurotransmitter production may be down-regulated by negative feedback. When you take away the "medication" afterwards, there are less receptors together with less neurotransmitter, causing withdrawal symptoms.

When you put in more substance in a control loop, there will always be some sort of "adaption" in order to reinstate a new balance (1). If you take in just enough drugs to balance the neurotransmitter-receptor system in a way, that the signal transduction in terms of nerve pulses remain the same, you have reached a tolerance stage, but not an effect stage. Still, medication is not "useless", since not all receptors will be dissipated. It is a matter of dose rate to increase the nerve pulses; once there is relatively more neurotransmitter (2) available than before medication, one should obtain a constant effect or an effectively altered control loop balance.

(1) https://books.google.at/books?id=z9TUch7m144C&pg=PA34&lpg=PA34&dq=receptor+regulation+up+down+neurotransmitter+drugs&source=bl&ots=2-4GRChqBi&sig=6e0YM-UrfgnMlw6e-rXR2Or7Qxc&hl=de&sa=X&ved=0ahUKEwixr_D25ZDMAhWB7RQKHcF9DqYQ6AEIHzAA#v=onepage&q=receptor%20regulation%20up%20down%20neurotransmitter%20drugs&f=false

(2) http://www.merckmanuals.com/professional/clinical-pharmacology/pharmacodynamics/drug-receptor-interactions


BAM is the current standard for sequence alignments, and can be used to store unaligned reads/sequences, but when used for unaligned sequences also contains unused alignment data that would bloat the file.

An alternative way to compress a DNA sequence file is via 2-bit (or 4-bit encoding) which can compress the sequence content by 75% (in 2-bit encoding, each nucleotide can be represented by 2-bits in the file eg A: 00, G: 01, C: 10, T: 11). I do not know of a generalizable tool that will compress/decompress aside from rolling your own. Further, the data must be de-compressed prior to streaming it into any alignment/sequence software. For general purpose compression algorithms, bzip2 can outperform (at least in compression) other algorithms (eg zip, gzip)


Between Cholera and Polio, which disease cannot be controlled by killing the vectors

Both of these diseases do not have vectors,
Cholera is a foodborne / waterborne disease and Poliomyelitis is spread through fecal-oral or oral-oral contact with an infected person.
They both only infect humans.

Thus, both cannot be controlled through killing any vector.

The best way to prevent Cholera is to avoid potentially contaminated food and water and follow proper sanitation practices.

The best way to prevent polio is through immunisation via vaccines.

For more information:

Cholera

Poliomyelitis


During mitosis the cellular organelles that have their own genetic information reproduce independently. Other organelles like the Golgi complex disintegrates and then form all over again in the daughter cells. Other organelles that are smaller and more numerous like ribosomes are divided between the two cells. Meiosis is the same thing only that there is crossing over in the nucleus of the cell.


What unicellular eukaryotes reproduce sexually?

This addresses your original question of "simplest" versus smallest. I'm not sure of sizes.

Investigate diplomonads: https://en.wikipedia.org/wiki/Diplomonad Most notable among them is Giardia: https://en.wikipedia.org/wiki/Giardia

These critters are primitive enough to lack Golgi and their version of "mitochondria" are substantially different enough (not synthesizing ATP) to be called by another name, mitosomes. Most have two nucleii and were not even thought to reproduce sexually  until relatively recently


If it is a good idea to use PacBio depends a lot on what you want to sequence and what you want to do with the data you get. In short: you get longer reads but about 15% error per base. This means, you will have to cope with those errors, there are possibilities to do that. How much coverage you will get of you sample I cannot tell you, as I do not know what kind of sample you want to sequence.

How much data you get out of one SMRTcell depends also on the chemistry, I think it currently is between 275 Mb and 375 Mb, depending on chemistry. They have a nice brochure you could look at.

Anyway, you probably will have to get some advice by a bioinformatician of you choice on how to design and analyse your sequencing experiment.


Does the human ear adapt to noise levels?

In  this instance, I would say your attention has been adjusted, not your ear's ability to perceive sound. Our ears don't have a control setting or a means of adjusting incoming sound levels (though I'm certain when an ambulance with loud siren drives by, we all wish we did).

What you are experiencing is a prioritization of the sound by your brain in relationship to other sounds.

You put the sound on before you go to sleep. Your brain accepts that incoming sound as non-vital, non-threatening sound. (Radio, meant to soothe, supposed to be there, relegate this sound to innocuous)
Come dawn, new and novel sounds appear. For our brains, the new and novel could indicate a threat, so your brain prioritizes that sound over the known and considered innocuous sound (your radio) which it has heard all night. Birds, tennis balls on courts are distinctive enough your brain would prioritize them even though you know in your conscious mind neither is an actual threat.
As you waken, your brain then reminds you there is still another sound in your environment which is not threatening and yet still prevalent (your radio) prompting you to decide if you want to do anything with the non-threatening sound.

Yes, this is an oversimplification of a very complex process of sound prioritization but most modern science bears this out. As a curiosity, our minds are predisposed to seek out information which may be vital to us, hence the reason conversations held by other people who are on the phone are so distracting because our brains dislike hearing things which may be necessary to our survival but only hearing half of the conversation.

EDIT:

As I was reminded there are some involuntary control elements built into the ear via:

the tensor tympani muscle whose role is to dampen sounds (mainly internal ones such as chewing)
and the stapedius muscle which dampens the ability of the stapes vibration and protects the inner ear from high noise levels, primarily the volume of your own voice.

You can thank the stapedius muscle for making your voice sound so strange to you when you hear it on a recording. You have never truly heard your voice until you hear an external recording and playback of it!


The prototypes for these proteins are:

the bacteriophage λ proteins Int and Xis, required for, respectively the integration and excision of prophages. They are, as mentioned by @WYSIWYG, recombinases.

Genetic map of bacteriophage λ (source of image)

the original Ihf (integrative/integration host factor) was identified as an E. coli protein required for prophage integration.

As you might expect Int and Xis proteins occur in many phage genomes, and in integrated prophages in bacterial genomes, and Ihf, because it is involved in bacterial DNA replication, is ubiquitous. I imagine the actual source of the proteins used by Life Technologies could be a trade secret.


Biological Neural Network Training for Babies

Biological neurons function in a very different way, as compared to the simplistic artificial neural networks of machine learning. For example, see how real neurons work and how they connect with each other. The types of neurons themselves are very varied:  "...neurons to take specialized forms such as unipolar,bipolar,  multipolar,  anaxonic,  pseudounipolar,  basket  cells, purkinje cells, Lugaro cells, spindle cells and more.".
As for the eyes, light passes through a large network of neurons before hitting the rod and cone cells. It's the opposite for the octopus retina. Animal babies are able to learn to walk much quicker than human babies. Also, have a look at videos of how blind children learn to walk.
So essentially, there's a lot lot lot more going on in the creation and working of the human body than just "neural network training". A really nice paper titled "facts and anomalies" gives perspective into this complexity.
Nobody fully understands how the system of cells and the equilibrium works. It's extremely complex and multi-dimensional. When you look at the complexity inside a single cell and the electron transport chain, you'll notice that there's a heck of a lot of things that are already pre-programmed and designed to make use of the molecular properties of nature to create structures and motors using the equilibrium of chemical properties. When such an equilibrium is created, evolution and adaptation can happen, but only in a very controlled manner. So I do not believe a baby's neural network is getting trained to walk or see. It's pre-trained from millions of years of evolution. The reason it may be taking some time to mature, is probably because the corresponding neurons in the brain are taking some time to get created, grow and find their way in the brain to form the right synapses.


Think this review from Nature can answer your question. A brief summary  ( with slight simplification):

The ascending activating system (that is responsible for wakefulness) has two branches:

The first one ascends to the thalamus and activates the thalamic relay neurons - these transmit information to the cortex. They get their main input form two acetylcholine producing group of cells:  the pedunculo-
pontine and laterodorsal tegmental nuclei (PPT/LDT). These two group of cells are also the source of main input for reticular nucleus of the thalamus.

  The neurons in the PPT/LDT fire most rapidly during wakefulness and rapid eye movement (REM) sleep, which is the stage accompanied by cortical
  activation, loss of muscle tone in the body and active dreams

The second branch, directly activates neurons in the hypothalamus, basal forebrain (BF) and cortex, bypassing the thalamus. This pathway has origins in monoaminergic neurons in the upper brainstem, caudal hypothalamus, as well as the noradrenergic locus coeruleus (LC), serotoninergic dorsal (DR) and median raphe nuclei, dopaminergic ventral periaqueductal grey matter and histaminergic tuberomammillary neurons. Input from this pathway to the cortex is extended /augmented by the lateral hypothalamic peptidergic neurons (that contain melanin-concentrating hormone (MCH) or orexin/hypocretin), and BF neurons(that produce acetylcholine or GABA).

Sleep is promoted by the so called VLPO (ventrolateral preoptic nucleus).
The VLPO send outputs to major group of cells of the arousal system in the hypothalamus and brainstem.

  The VLPO neurons are primarily active during sleep, and contain the inhibitory neurotransmitters, galanin and GABA.
  The VLPO also receives afferents from each of the major
  monoaminergic systems. Both noradrenaline and serotonin inhibit
  VLPO neurons. The latter do not have histamine receptors, but the
  tuberomammillary neurons also contain GABA, which is inhibitory
  to VLPO neurons, as well as several other potentially inhibitory pep
  tides, such as galanin and endomorphin. Therefore, the VLPO can
  be inhibited by the very arousal systems that it inhibits during sleep.

As you can see in the quote from the paper these two systems can mutually inhibit each other and basically work as a seesaw or 'flip-flop switch'. In this system activity in one  subsystem shuts down the inhibition from the other subsystem and disinhibits its own action (selfreinforcing loop). The transition from one state to the other is relatively fast. Orexin plays important role in stabilizing the switch in one position or the other.

Regulation pf sleep:

Homeostatic:
It is unclear how homeaostatic regulation of sleep work, yet it has been proposed, that adenosine accumulation in the brain may signal for 'need for sleep'. The extended wakefulness causes the exhaustion of brain glycogen reserves and depletion of ATP levels. As ATP is degraded to ADP, AMP and eventually adenosine, extracellular adenosine levels rise in some parts of the brain including the BF.

  In addition, adenosine might disinhibit the  VLPO via presynaptic A1 receptors by reducing inhibitory GABAergic inputs.

This implies that during sleep ATP and energy sources are regenerated and free adenosine levels drop, thus inhibition of VLPO might take place again.
Also it is important to note that the amount of sleep we need is proportional to the time we spend awake.

Circadian regulation:

It is known that humans have quite precise :circadian rhythm:

  The suprachiasmatic nucleus (SCN) serves as the brain’s ‘master
  clock’. Neurons in the SCN fire in a 24-hour cycle that is driven by a
  transcriptional–translational loop, which persists even when the neurons are dissociated in cell culture.

The SCN has moderate output to the VLPO or orexin neurons, but it has more important projections to the adjacent subparaventricular zone (SPZ) and the dorsomedial nucleus of the hypothalamus (DMH).

  The SPZ also has relatively limited projections to the VLPO, orexin
  neurons and other components of the wake-sleep-regulatory system. However, a major target is the DMH. This region receives inputs from many more neurons in the SPZ than the SCN, so the SPZ is in a position to amplify the output of the SCN. (...) The DMH is one of the largest sources of input to the VLPO and orexin neurons and is crucial for conveying SCN influence to the wake–sleep-regulatory system. The DMH projection to the VLPO comes largely from GABA-containing neurons (that is, those that promote wakefulness by inhibiting sleep), and the projection to the LHA originates from neurons containing glutamate and thyrotropin-releasing hormone (which should presumably be excitatory and promote wakefulness).

So as you can see our circadian rhythm as direct control over our sleep-wake cycle, and that the SCN can heavily promote awakening through SPZ and DMH.

Thorough review and details can be found in the article I linked at the beginning, I only tried to select key information to provide a (not so ) brief summary. We only sleep about 7-8 hours normally because this is enough for homeostatic regeneration and our circadian rhythm promotes wakefulness in the morning (this is quite simplified).

Based on their abstract these limited access papers might also be useful (unfortunately I do not have full access to them right now):

http://www.eurekaselect.com/87813/article
http://www.sciencedirect.com/science/article/pii/S0074774210930018
http://www.sciencedirect.com/science/article/pii/S0896627315001312


These are definitely some sort of aphid (small sap-sucking true bugs in the superfamily Aphidoidea).

Based on the coloration and shape of the pest and the host plant, my best guess is that you're looking at Hyalopterus pruni (or the Mealy Plum Aphid).

Note: the scientific name of this species has changed at least 21 times!

 Photo by Jack Kelly Clark

Looks like this person also found this species of aphids on a black cherry tree if you want to see more picture.

Description:

  Wingless adult aphids are pale green with three dark green longitudinal stripes on their backs. Their bodies are covered with a white, mealy wax. [source].

Host Plants:

Typically trees in the Prunus genus: cherries, plums, almonds, apricots, nectarines, and -- you guessed it --  peaches. [source].

Damage:

Plant can become stunted from high numbers of aphids, but the primary concern is the development of mold that grows on the aphid's honeydew. [source].

Management:

See this University of California Agriculture and Natural Resources site for management suggestions.

Suggestions:

Biological: lady beetles, lacewings, or soldier flies
Organic: biological control + sprays of neem oil
Pesticides (typically not needed): Phosmet, Diazinon, and others in the fall; neem oil, flonicamid and others in the spring.

Final Notes:

Just because an aphid shares a name with an individual plant (e.g., the green peach aphid mentioned in the comments) doesn't mean that the species is limited to just that plant or that any aphid found on said host is that species. Many aphids feed on a wide range of host plants, so limiting your host to an individual species doesn't necessarily rule out a wide range of pests. However, it is not uncommon for an aphid species to stick to a single genus, narrow set of genera, or narrow set of families of host plants.


Can DNA produce ribozyme-like structures?

There are no known natural DNA enzymes (deoxyribozymes), but there are various synthetic DNA enzymes. The first deoxyribozyme that has been reported (Breaker and Joyce, 1994) catalyzed the Pb2+-dependant cleavage of RNA.

Various deoxyribozymes have been synthesized, they can catalyze RNA cleavage, RNA ligation and many other reactions like DNA phosphorylation or Thymine dimer photoreversion, and even a Diels-Alder reaction (see Baum and Silverman, 2008 for a review).

DNA lacks the 2'-hydroxyl group that RNA posesses, but there is some evidence that this doesn't significantly decrease the potential of deoxyribozymes compared to ribozymes. In one experiment DNA and RNA enzymes that catalyze a Carbon-Carbon bond formation were compared and both achieved comparable catalytic rates (Chandra and Silverman, 2008).

For more information about DNA enzymes you can look at the publications from the Silverman lab, they're probably the most active research group in this field.

Baum, D. A. & Silverman, S. K. Deoxyribozymes: useful DNA catalysts in vitro and in vivo. Cell. Mol. Life Sci. 65, 2156-2174 (2008).
Breaker, R. R. & Joyce, G. F. A DNA enzyme that cleaves RNA. Chem. Biol. 1, 223-229 (1994).
Chandra, M. & Silverman, S. K. DNA and RNA Can Be Equally Efficient Catalysts for Carbon−Carbon Bond Formation. J. Am. Chem. Soc. 130, 2936-2937 (2008).


Can CRISPR-Cas9 make changes on a living organism?

Answer is yes, but it depends on which kind of phenotype you're going to restore/change. As you can imagine, using crispr cas9 on an high amount of cells require one condition: edited cells need to have a clear advantage in surviving besides the previous.

Here's an example of a crispr-cas9 protocol followed to restore a wildtype phenotype in adult mice.


HIV and effectiveness of inhibitor cocktail over single inhibitor

Your answer is correct. HIV-1 encodes a single homodimeric aspartic protease, with each monomer containing the classic Asp-Thr-Gly motif, and the dimer's active site being formed with the two monomeric active sites creating a cleft where the proteolysis takes place. In it, water acts as a nucleophile in conjunction with the aspartic acid residue to hydrolyze the peptide bond in the protein's target.

WikiMedia: Aspartyl protease mechanism.png

A number of HIV-1 proteins are synthesized as polyproteins, and protease is required to cleave them in the appropriate spot(s) so they can assume their mature forms. This is a very big deal, because without these cleavage events HIV-1 cannot complete its replication cycle, and so becomes non-infectious.

WikiMedia: HIV-replication-cycle.svg

Protease inhibitors act by "sticking" in the binding cleft, obscuring the aspartate and preventing binding of the target proteins. However, these small-molecule inhibitors are very specific to HIV-1 and the amino acid residues that compose the binding cleft, otherwise they could potentially inhibit one or more of the many aspartyl proteases our body makes naturally. While it is not very likely that a destructive mutation in the Asp-Thr-Gly motif would result in a replication-competent virus, other more conservative mutations may occur in the binding cleft that still allow the target to bind and be cleaved. However, depending on the exact protease inhibitor being used, a single mutation, even if it's conservative, may still be enough to dramatically decrease the inhibitor's binding efficiency and allow protease to maintain some or all of its functional capacity. This is why cocktails of inhibitors are used: they each depend on different amino acids for their binding, so if mutations arise at some point that do affect the activity of one inhibitor, others may still be unaffected. Evolutionarily-speaking, the inhibitors put a tremendous selection pressure on the virus, which combined with HIV-1's naturally "sloppy" replication process, leads to mutants appearing in relatively short periods of time.

There are two kinds of epitopes in the adaptive immune system: those recognized by antibodies and B cells, and those recognized by T cells when presented in the context of MHC. Antibody epitopes are generally found on the surface of a pathogen or a pathogen-infected cell (when speaking in the context of infectious diseases), as proteins or other compounds capable of raising an immune response that are only located completely inside of the pathogen or infected cell are not available for binding. T cell epitopes, on the other hand, are linear peptide fragments (and sometimes other molecules, like glycolipids) generated by internal processing in the antigen-presenting cell, and are usually pretty representative of the complete contents of the cell, native and foreign. Native epitopes generally don't produce immune responses - when they do, autoimmunity occurs. Foreign epitopes are recognized by circulating T cells, and help prime an immune response against the infected cells. (As a side note, since HIV-1 infects a subset of T cells, it is a way for them to escape immune detection). Mutations in the protease protein may affect some of the epitopes it produces, but those mutations are just as likely to increase visibility to the immune system as decrease it, so overall there's no net gain or loss.


Molecularly, why can you straighten or perm hair?

For straightening hair with a flat iron:

This source provided by bobthejoe states that temporarily straightening hair involves the breaking of hydrogen bonds between keratin molecules within hair.

  One of the reasons hair is curly is because of hydrogen bonds between the proteins (keratin) that make up your hair [...]. Another way to alter hydrogen bonds is with heat; electric straighteners work because of this principle. The platters on electric straighteners are flat so that when your hair cools it takes the shape of "flat" as the hydrogen bonds reform. The same thing occurs with curling irons, but since the heating element is circular, the hair stays curled as it cools. The effect of heat, however, is temporary, over time the hydrogen bonds eventually return to their original form and the hairs goes back to the way they were. This rearrangement happens because moisture in the air hydrates the proteins.

This source provides a similar explanation.

  Running a flat iron through blown-dry hair breaks the hair’s hydrogen bonds. It flattens hair until water or water vapor (from humidity, drizzle or the shower) penetrates the hair fiber and allows the hydrogen bonds to revert to their natural positions.

Thus, the straightening of hair with an flat iron does not involve the breakage of disulfide bonds as I had originally hypothesized.

For perming hair:

This article suggests that perming involves the chemical treatment of hair with reducing agents to break the present disulfide bonds between cysteine amino acids, followed by the reformation of the disulfide bonds in the desired curled shape.

  In a standard “cold” perm, hair is put into curlers and the reducing agent ammonium thioglycolate is added. The disulfide bonds break and keratin molecules are now free to move around and adjust to the shape of the curl. Then a “neutralizer,” such as hydrogen peroxide, is added to reverse the effect of the reducing agent. New disulfide bonds form so the keratin molecules are locked into the shape of the curls.

This Wikipedia article also suggests that the chemical straightening of hair is obtained with the same process.


What is meant by “genes at the trunk of the evolutionary tree”?

I think the article is using a phylogenetic tree to explain the stages of how the tumor has evolved.

According to Nature.com >>

  All trees have a shared 'trunk', which represents the complement of
  mutations shared by all malignant cells within the cancer.

Or simplified by Britannica.com >>

  Phylogenetic tree, also called Dendrogram, a diagram showing the
  evolutionary interrelations of a group of organisms derived from a
  common ancestral form. The ancestor is in the tree “trunk”; organisms
  that have arisen from it are placed at the ends of tree “branches.”

For a visual representation, this is a phylogenetic tree for evolution of breast cancer >>

Image Source: Phylogenetic Cancer Trees


This paper found that these enzymes recognize RNA:DNA heteroduplexes. Such duplexes are unlikely to be encountered in vivo. They are present when DNA is primed for replication, but these duplexes are relatively short and thus are less likely to randomly contain a recognition sequence. Furthermore, if the recognition sequence is found in the primer, the gDNA will be methylated specifically to protect it from degradation. RNA:DNA duplexes are also found during transcription, but they are also short and the gDNA would be methylated. Additionally, the transcription bubble where the heteroduplex forms is protected by RNA polymerase, which subsequently displaces the transcript from the gDNA as it leaves the elongating complex.

It's also important to note that this paper found that these enzymes don't cleave RNA:DNA as well as they do DNA:DNA duplexes and these results occurred under experimental conditions with relatively high concentrations of enzyme and substrate. The lower catalytic efficiency is likely due to lower binding affinity, which could be caused by:

presence of uracil in RNA (this was explicitly mentioned in the paper)
2'-OH presenting a steric barrier
helix shape (RNA tends to adopt an A-form helix)


What is the context in which a species gets the name "elegans"

Since "meaningfulness" is not listed among the requirements for new names, any author is free in his choice of name derivation. [There are nevertheless some natural restrictions, such that new names are to be treated as Latin irrespective of the etymology and should follow Latin grammar (with botanical nomenclature being much more meticulous in this respect).]
There are indeed some cases when the name of the species may be meaningful for the purpose of the choice of type species (the "typicus/a/um" names and tautonomous names like "Glis glis"), but "elegans" doesn't belong here.

So, the high frequency of "elegans" has nothing to do with typification and reflects nothing else than the will of authors to reflect their emotions. One recurrent cause of "elegans"-names among paleontologists, for example, is good preservation of the respective fossil material. [By the way, there are even more emotionally loaded (but less frequent) names like "mirabilis/e" or "enigmatica/us/um".]

Since providing etymologies for names alongside formal descriptions of new species at a certain moment became an official recommendation, you can make your own collection of causes people provide to justify their choice of "elegans" as species names.

EDIT: I've just found this revelation: (Oxytomoides elegans, fossil bivalve) "Etymology. Elegans, Latin for choice or select, referring to what we regard as esthetically pleasing appearance of the species".


Modern views on the correspondence of moles

There are a lot of different types of moles out there, and while there are correlations in locations of some classes based on their nature, there is nothing like the correspondence described.

There is, however, a long history of attempting to attribute meanings and patterns to moles, however, since essentially random phenomena like this tend to engage our human biases for pattern-making.


Michaelis-Menten Kinetics: Does measuring apparent Km and Vmax take into account competing reactions?

Have you heard of something known as "Occam's Razor" ?

It says when you have multiple possible explanations/hypotheses then select the one which is simplest (i.e least number of assumptions)

Same with mathematical models. Chemical kinetics models usually assume first order unless there is some evidence against it. Similarly, for enzyme kinetics, as long as you don't think there is something anomalous going on, use Michaelis-Menten model.

  What if there are entire reactions going on that are consuming the
  product or substrate that are not known

Many physiological enzyme catalysed reaction are not Michaelis-Menten. If you happen to have an insight about it or if the simulations dont match the experimental data, you can revise the model.

However, Michaelis-Menten model for for competitive inhibition exists, as you yourself indicate in the link.


Glycosylation is a controlled process that involves a carbohydrate being attached to a hydroxyl or other functional group of another molecule. I think you meant to say glycation instead of glycosylation, and that is a random process that involves free sugars attaching to proteins.

https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation


Are 'homeothermic' and 'endothermic' synonymous?

Traditionally, the terms poikilotherm and homeotherm were used to refer to organisms that don't regulate their body temperature and that regulate their body temperature, respectively.

However, those terms are not the best ones, regarding their etymology. For instance, poikilos (Greek ποικίλος, "many-coloured") means "diverse", "varied", while homoios (Greek ὅμοιoς) means "similar", "resembling". But some fish, which we define as a poikilotherm, may have a lifetime body temperature variation of 1℃ or less, while some mammals like a squirrel, which we define as an homeotherm, may have a daily body temperature variation of more than 20℃.

Then the terms ectotherms and endotherms appeared, as a new and modern terminology. And they are indeed meant to be that.

The problem is that a lot of people simply thought that ectotherm was a new name for poikilotherm and that endotherm was a new name for homeotherm, as if they were synonyms. But they are not. Follow me:

(A word of caution before we proceed: unfortunately, there is no organisation that regulates the terms used in the various branches of biology, as IUPAC does for chemistry. Thus, the acceptance of a term depends largely on the consensus among the researchers and the book authors. My answer here describes the nomenclature used by Whithers, Comparative animal physiology, in my opinion the best book on comparative physiology.)

Thermoconforms and Thermoregulators

According to Withers (1992), animals can be classified in two groups, regarding the ability to regulate their body temperature:

Thermoconforms: animals that don't regulate their body temperatures. Their body temperature is pretty much the temperature of their surroundings.
Thermoregulators: animals that actively regulate their body temperature. Their body temperature, therefore, may differ from the temperature of their surroundings.

In Withers' words:

  Most animals are unable to control their body temperature, and Tb passively conforms to their thermal environment; these animals thermoconform [...] Some animals, in contrast, regulate their body temperature often against a substantial thermal gradient between their body and the environment; they thermoregulate.

By the way, this suffix pattern of _conform and _regulator is common along the book. For instance, Withers talks about osmoconforms and osmoregulators (capable or not of regulating their body osmolarity), and so on.

So, thermoconform and thermoregulator are terms that describe if the animal is capable or not of regulating its body temperature. But those terms do not describe the source of the thermal energy.

Endotherms and Ectotherms

Here comes endotherm and ectotherm. In short:

Endotherm: the main source of heat (thermal energy) is the organism itself.
Ectotherm: the main source of heat (thermal energy) is the environment.

According to Withers:

  The terms ectotherm and endotherm are perhaps the most useful for describing the thermal capabilities of animals because they have a mechanistic basis. An ectotherm is an animal whose thermal balance is predominated by external sources of heat, and its metabolic heat production is insignificant. [...] Endotherms are animals whose thermal balance is predominated by their endogenous metabolic heat production.

Now we can try to combine those terms, and that will led us to the comprehension that none of them is synonymous neither of poikilotherm nor homeotherm:

All thermoconforms are ectotherms, that's not problematic. But things become complicated when it come to thermoregulators: thermoregulators can be ectotherms or endotherms.

For instance, most reptiles are ectotherm thermoregulators, but some dinosaurian reptiles, such as the birds (and most probably all other Dinosauria), are endotherm thermoregulators.

This table (ibid) summarizes the possible combinations very well:

Conclusion

It's clear that the terms poikilotherm and homeotherm (or even worse, cold-blooded and warm-blooded) are outdated and inadequate.

But they should not be simply replaced by the pair ectotherm/endotherm. Ectotherm and endotherm are terms that refer only to the main source of heat. The most adequate terms for describing the ability to regulate the temperature are thermoconform and thermoregulator (which, by the way, are not synonymous with poikilotherm/homeotherm either).

Source:

Withers, P. (1992). Comparative animal physiology. Forth Worth: Saunders.


How does core-conductor model correspond to an actual neuron?

What may be confusing is that the myelin is wrapped around the membrane of the axon.

The easiest way to see this is in cross-section:

From here.

The axon is indicated by #1 in the diagram and the myelin sheath is #4

The intracellular space (as represented by the horizontal resistors in the case of your model of the axon) is the fluid, replete with ions, that is contained within the membrane of the axons.

At the nodes of Ranvier, there is a break in the myelin sheath, exposing the underlying membrane of the axon.  In membrane in those gaps of the sheath, there are sodium channels (voltage gated) and potassium channels that facilitate the influx and efflux of ions that "refresh" the action potential as it travels down the axon.  The extracellular space is simply the milieu of fluid in the space between the axon and any adjoining cells.  For the purposes of analyzing the currents of the neuron, the sodium and potassium ions (and the conductances of the channels) are all that you really need to be concerned with.

What is confusing about your diagram is that it represents the conductance -- the inverse of the resistance of the channels -- of the channels (inwards and outwards) as a single vertical resistor in between the horizontal resistors of the intracellular membrane. This oversimplification is handy when doing the cable theory-type analysis, but it betrays the actual physiology of the neuron.

From a model standpoint, I'm breaking all the rules here, but you can think of things like this:

where one "rung" of your resistor ladder has $r_m$ broken out into the 2 components and drawn differently.


Is there human Anatomy software that provides great detail?

My favorite is this one and it is quite detailed and interactive. It does not use virtual reality technology, but it is a good resource for anatomy students. Then there is this one, but it is more virtually animated and less real. Hope this helps!


Stay young by reinserting own DNA from years ago?

Lots of questions here. I recommend taking college level courses in Biochemistry, Molecular Biology, and Medical Physiology, and Geriatrics.

There are other issues than just DNA. Systemic failure is system-wide, and probably most of the issues are still yet undiscovered. Good news I guess if you want to be a researcher in this exciting field! As for DNA-ends, read up on Telomerase. As for DNA copying learn about PCR and sequencing methods. Generally speaking, reverse transcription can be dangerous. Please see many of diseases we are having a hard-time solving, which often use these pathways. Seriously avoid that one. Not everything in DNA is used by the organism at any given time, and some information is elsewhere. Moreover, what if we use DNA as DATA storage besides blueprint information? Hint: while the jury may be still out on Neurons, environmental factors may be passed as epigenetic traits by not just primary shape such as DNA methylation but by obstructing access via conformation and histone wrapping. Not even mentioning mitochondrial dna or prenatal development factors.

Instead: A good diet and exercise.


Why proximal muscle weakness is seen earlier than distal muscle weakness in Dermatomyositis?

Usefull links:
https://www.mda.org/disease/dermatomyositis/causes-inheritance
https://emedicine.medscape.com/article/332783-overview#a1

My hypothesis are

1) Since skin, is commonly involved in sunexposed areas, may be enviornmental factors do play a major role. So, Proximal Muscles are more used in day to day work, so are more favourable site for drugs, autoantibodies to act upon.

2)May be, in case of due to drugs or vaccines, proximal muscles may be are preferrential site of action of these, making these group of muscle more suceptible.

By the way correct answer would be: Its under research.


Different colors mean different wave lenght and energy, as displayed in the picture.

Using Planck's theory, the shorter the wave is, the more energy it carries.
On day light, all these wave lenghts are present, including UV from sun. With no sun-light, your eyes aren't hit by those, so there's no need of using higher energy waves (that's exactly how night mode on iPhone works, using only lower energy waves).


Sickle-cell trait : Why is only one type of beta chain found in any one hemoglobin molecule?

For one specific hemoglobin molecule, yes it's just one type of beta chain.  In the case of a heterozygote, this hemoglobin molecule could be expressing from the bS gene OR the normal beta gene.  Let's call it a 50/50 chance for each hemoglobin to be expressing bS.  Because RBCs have a ton of hemoglobin in them, this 50/50 or so expression of bS wouldn't be enough to cause RBC sickling and disease, and it also helps explain the heterozygote advantage vs malaria.


Why do athletes see a dip in performance in their thirties?

The decline in athletic performance is a result of senescence; the question then becomes "why do we senescence?"

A number of questions on this site have addressed this. These include Why does evolution not make our life longer?, Why do we age?, and any number of others that one can pull up with a search for senescence. It is key to distinguish between proximate (how, physiologically ) and ultimate (why, evolutionarily) explanations. It's not entirely clear to me from your question which of the two you are asking.


What is the difference between clinical and non-clinical depression, and is there a term for different severity of the bipolar disorder?

I think the main question here is:

  Is there a term…which describes a bipolar disorder of lesser severity[?]

Yes. There are a couple ways to think about this, but you’re clearly accustomed to differentiating the manic and depressive phases of bipolar disorder, so I’ll start with that.

There is mania (excerpted from DSM 5*):

  A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week and present most of the day, nearly every day...

  B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior:

  Inflated self-esteem or grandiosity.
  Decreased need for sleep
  More talkative than usual or pressure to keep talking.
  Flight of ideas or subjective experience that thoughts are racing.
  Distractibility
  Increase in goal-directed activity
  Excessive involvement in activities that have a high potential for painful consequences

  C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning....

And there is hypomania:

  A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day. ….

  B. [This criteria is the same as for mania.]
  ....
  E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization.

I have bolded the main differences between the two definitions. You can see that hypomania is the term for the less severe form of the manic phase of bipolar depression.

Neither mania nor hypomania is likely to occur in the absence of depressive symptoms, however. Thus, there are two basic phenotypes of bipolar disorder (summarized from DSM 5*):

Bipolar I disorder: Patient experiences mania; depressive periods may not qualify as Major Depressive Disorder.

Bipolar II disorder: Major Depressive episodes are required; manic phase may be hypomanic. (This is classically considered a less severe syndrome, but this notion has been challenged in recent years.)

And finally, one more term for you:

Cyclothymic disorder: patient experiences both hypomanic and depressive periods without ever fulfilling the criteria for an episode of mania, hypomania, or major depression.

(Your other question you seem to already know the answer to, but since it's in the title.....  Nonclinical depression refers to something on the spectrum of normal (i.e. not pathological), such as situational mood disturbance. A related concept, subclinical depression is a loose term to describe depressive symptoms that don't meet criteria for Major Depressive Disorder..)

*American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.


Why are there six reading frames if only one strand of DNA is referred to as the ‘coding strand’?

The coding strand refers to the DNA strand with the same base order as the RNA transcript for a particular gene. As one gene is always entirely present on a single DNA strand there are indeed 3 reading frames possible in this strand, with only 1 actually containing the correct codon sequence for this gene.

However when we view an entire genome it is entirely possible for one gene to be present on one strand with another gene present on the other,  meaning that the coding strand for one gene is the non-coding strand for the other. This is why there are 6 possible reading frames for the genome as a whole as both strands can (and do) contain genes.

As to the ORF, both definitions seem to be in use. In the context of trying to discover genes by looking for long ORFs the first definition is probably more helpful as following the second definition could lead to a lot of falsely predicted genes (for an extreme example a long stop codon free sequence that has no start codons either would be considered a possible gene even though that should be impossible).


The hoatzin has a digestive system that makes use of bacterial fermentation. Many other birds also consume grass, e.g. ostriches, ducks and geese.

There's also a large body of literature on how birds can digest cellulose.


How do biologists determine the parents of a child

Your description is not totally correct (or understandable). There is plenty of source of information online so, I won't repeat the whole thing here. In very short and very simplified, talking about humans...

Ploidy, meiosis and fecundation

Both parents are diploid (2N=46). Both parents have specific cells that are undergoing meiosis (in testis and in ovaries). After meiosis, the cells (spermatozoids and ovules) are haploid (1N = 23). The spermatozoid and the ovule fuse (fecundation) to make another diploid (2N = 46) individual. This diploid individual will grow for about 9 months in the mother's uterus before coming out!

Crossover

Now, during meiosis, cross-over occurs. It is a mechanism where the two chromosomes mix up their material. When the cross-over occurs in the father for example, it is the chromosome that the father receive from his father and the chromosome that he received from his mother that mix-up their genetic material.

Possible chromosomes

Let's say the maternally inherited chromosome of the dad is

AAAAAAAAAAAAAA

Let's say the paternally inherited chromosome of the dad is

BBBBBBBBBBBBBB

Then, in the meiosis (where spermatozoids are produced), the two chromosome might mix up and the haploid spermatzoid can end up with something like

BBBBBBBBBBBAAA

Now, on the mother's side, her two chromosomes are, say,

CCCCCCCCCCCCCC

and

DDDDDDDDDDDDDD

The mother might therefore transmit

DDDDDDDCCCCCCC

The (diploid) baby would then be

BBBBBBBBBBBAAA
DDDDDDDCCCCCCC

So of course, the chromosomes present in the baby are a bit different form the ones present in the parents but we can still recognize them. If there is doubt who the father is, a genetic analysis of another father might return the chromosomes

BBBBBBBBBBBBBB
FFFFFFFFFFFFFF

, then we would know this individual cannot be the father because he could have not transmitted the AAA part of the chromosome found in the kid.


How do two parents, recessive and dominant genes and two complimentary nucleotides end up in one DNA?

I think you really need to go back to the very basics and try to understand the DNA molecule, what a chromosome is, DNA replication and mitosis, what homologous chromosomes are, what non homologous chromosomes are, what sister chromatids are, what non sister chromatids are before you attempt to understand meioses. And I would definitely recommend you learn all of these things well before you attempt to understand molecular inheritance, but let me see if I can at least begin to clarify some of your misconceptions.

If you are having a hard time understanding the concepts as written, try looking up the articles on Simple English Wikipedia first. The try to make their articles easier for novices to understand.

There is no such concept as Dominant Nucleotide Bases. The two strands of the DNA double helix are complementary and antiparallel. Genes can reside on either strand.

You are also getting really mixed about recombination via crossing over in meiosis. The chromosomes that are being recombined in the mother are from her parents, so technically the chromosomes that are being recombined are the grandparents chromosomes.

The same is happening when the father produces gametes. The chromosomes from his parents are swapping pieces of DNA.

At the end of meiosis, each gamete has a random assortment of 23 chromosomes, either from the father or the mother of the adult male or the father or the mother of the adult female.

The 23 can be recombined meaning that the chromosome is part grandma and part grandpa, or it is a grandmother's chromosome that has not recombined or a grandfather's chromosome that has not recombined. Just looking at the possible ways that 23 chromosomes can randomly assort without taking into account recombination to produce a gamete, there are about 8 million combinations. Add recombination and it gives you a huge amount of genetic diversity.

So those are the haploid gametes. When fertilization occurs the sperm from the father donates its random assortment of 23 chromosomes and the ovum from the mother has 23 randomly assorted chromosomes of its own. This gives you at total of 46; 23 from the father, made up of a random assortment of chromosomes from his father and mother (or chromosomes recombined by crossing over to be part his mom and part his dad), and 23 from the mother with the same pattern of random assortment and recombination.

Also, the double helix doesn't dissociate (come apart) during crossing over [NOTE: for those who know, please do not jump on me for not explaining strand invasion here and the need for homologous sequences for crossing over]. One part of a grandparent's chromosome is exchanged for the exact same part of a chromosome from the other grandparent's chromosome, assuming normal cross over events. The alleles (versions) of the genes in that segment may vary, which is why you have a chromosome is part grandmother and part grandfather.

As for dominant autosomal genetic traits versus recessive genetic traits. A dominant trait means that a heterozygous child will express the phenotype even though they only have one copy of the dominant allele. If it is a disease, then we say the person is affected. If it is a recessive trait, then the heterozygous child will not express the phenotype, so they are not affected by the disease, but they carry the allele and can pass it on to their children. This person is said to be a carrier. If a person is homozygous for a recessive trait, then they will be affected by the disease and show the phenotype.

As for inheritance, you have to draw the punnet squares. This will show you the different patterns and probabilities of inheritance.

UPDATE

I think that you are getting confused by the idea that you inherit one set of 23 chromosomes from your mother and one set of 23 chromosomes from you father. While this is true, meiosis happens in their reproductive organs before fertilization (for the most part, but the important part happens there and then).

The example of the father is easier. He has two sets of chromosomes, one set that he inherited from his mother and one set he inherited from his father. At the beginning of meiosis all 46 chromosomes replicate. They make an exact copy of themselves and are joined at the centromeres. You have 2 sister chromatids on each of those chromosomes. Now the the homologous chromosomes will pair up, so one of the chromatids on the paternal chromosome (say chromosome 4 from Grandfather's set) will join with a non sister chromatid from the maternal chromosome (Grandmother's chromosome 4). So you have four chromatids from chromosome 4 lined up at the metaphase plate. The two non sister chromatids that are joined will recombine when the kinetochores move along the microtubules towards the poles of the spindle. At the end of all of this you have two cells that contain 23 chromosomes, each with a sister chromatid, however the sister chromatids are no longer identical because one of them recombined with the the non sister chromatid of its homologous chromosome. The thing you must remember is that each chromosome assorted independently of the other. For Chromosome 1 the maternal chromosome may have gone to the left cell while the paternal chromosome went to the right. Then for chromosome 2 you might have the maternal chromosome go right and the paternal chromosome go left. And so on and so forth. The number of possible combinations of how you can arrange two sets of 23 chromosomes is 2^23 or about 8 million different combinations.

During meiosis II the 23 chromosomes again line up at the metaphase plate and they are attached to the spindle by both sides of their centromere / kinetochore complex. When the migrate the two sister chromatids migrate towards opposite poles. Again it is completely random as to whether the recombined chromatid or the chromatid that did not undergo recombination will migrate to the right or the left. Again, there are 2^23 possible combinations for EACH cell.

So you end up with an incredible amount of genetic diversity on how chromosomes are assorted within the gametes. You will still only have four possible outcomes  in the copies of any single gene that you get. You will inherit either your paternal grandfather's copy or your paternal grandmother's copy and you will inherit either your maternal grandmother's copy or your maternal grandfather's copy. That is why if a genetic disease is caused by one gene, it depends on which copies you inherit.


I'm just going to outline the alternatives, I'll leave validating why choice C to you.

Choice A. If the new molecule acts in the same fashion as Hh, the results will be identical. If the new molecule bound to Pct but did not effect a response, that might work.

Choice D. Addition of Ci into the nucleus initiates transcription which seems to be the issue here.

Choice B. Best wrong answer! Can you inject enough stem cells to make a difference? Will the cells have some adverse effect? More importantly, the binding of messengers to receptors is a reversible process. The Hh will be able to detach from Ptc on the stem cells and eventually interact with Ptc on the native cells.

So, what effect will Hh have if the Smo in unable to respond?


Low-cost simple water testing for faecal contamination

The best and most common would be the "multiple fermentation tube” or “most probable number” technique. Rather than testing for all pathogenic bacteria, it uses indicator microorganisms to assess the potability of the water. You'll need a lab to do this but if you have access to one, I'm sure that all the needed materials are common there. Here's a copy of the method: https://www.who.int/water_sanitation_health/resourcesquality/wqmchap10.pdf


Yes.

  Evolutionary success of bacteria relies on the constant fine-tuning of
  their mutation rates, which optimizes their adaptability to constantly
  changing environmental conditions. When adaptation is limited by the
  mutation supply rate, under some conditions, natural selection favours
  increased mutation rates by acting on allelic variation of the genetic
  systems that control fidelity of DNA replication and repair. Mutator
  alleles are carried to high frequency through hitchhiking with the
  adaptive mutations they generate. However, when fitness gain no longer
  counterbalances the fitness loss due to continuous generation of
  deleterious mutations, natural selection favours reduction of mutation
  rates. Selection and counter-selection of high mutation rates depends
  on many factors: the number of mutations required for adaptation, the
  strength of mutator alleles, bacterial population size, competition
  with other strains, migration, and spatial and temporal environmental
  heterogeneity. Such modulations of mutation rates may also play a role
  in the evolution of antibiotic resistance.

https://www.ncbi.nlm.nih.gov/pubmed/16677295

Large differences in mutation rates can be found among viruses: 10^-3 mutations per nucleotide per replication in RNA bacteriophage Qβ versus 10^-8 mutations per nucleotide per replication in DNA Herpes simplex virus. Generally, RNA viruses have higher mutation rate because RNA-dependent RNA polymerases lack the proof-reading capacity present in DNA polymerases. However, both increasing and decreasing these typical mutation rates leads to reduced virulence of the virus population.

https://www.ncbi.nlm.nih.gov/pubmed/16220146

https://www.ncbi.nlm.nih.gov/pubmed/16327776


It is Giant Stomach Worm (Hirudinella Ventricosa).

It is a platyhelmith parasitic to Wahoo fish, feeding on its blood and found inside the stomach. It makes 98% of Wahoo's parasitic infections.

  It is a fleshy worm that varies in size and shape; with extended worms the size of a mans finger and contracted ones about the size of a walnut.

It requires two hosts to complete its lifecycle; a snail and a wahoo fish.

A picture from National Geographic Society

Source: lahaina news

Note: A youtube video shows this worm moving.


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

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

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


How can fruit flies and mice share the same gene that says to build an eye if they evolved separately?

Both fruit flies (Drosophila) and mice (Mus) are classified  under Bilateria.
The presence of such a highly conserved sequence in both species suggests that they share a urbilaterian ancestor who also used a similar gene to turn on eye formation (not create the whole eye, just start the process).

Even though the structure of insect and mammalian eyes diverged evolutionarily after the common ancestor, the switch that starts eye development worked so well there was little need to change it.  I suppose one could say that it remains backwards compatible.


Creatinine is formed irreversibly and non-enzymically from creatine and phosphocreatinine and is usually assumed to be metabolically inert in humans (Wyss & Rima Kaddurah-Daouk, 2000, Creatine and Creatinine Metabolism): no human enzyme is known to metabolize creatinine, and this compound is normally eliminated from the body via the kidneys

  In chronic liver failure, however, "a significant quantity of creatinine is excreted into the gut, as is true of urea and uric acid, and is metabolized by gut flora" (Jones & Burnett, 1974, Creatinine Metabolism in Humans with Decreased Renal Function: Creatinine Deficit.

This was 'news to me', and the observation about urea is also surprising, but it looks to be a very good paper.


How does soap affect membrane permeability? Which component of the membrane does it affect?

@mdperry answered well. If you need some diagrams to help with understanding, this article Should be helpful.

As you surmised, when you add detergent, it is lysing some cells of the beetroot that contain pigment.  That pigment then gets released into solution.  I've annotated the image below for the micelles that gets formed, except I spelled it wrong :/