How do members of cryptic species know who to mate with?

As both @Rory M and @Alexander Galkin suggest, there are various non-visual mating behaviors to allow these species to select mates and also allow taxonomists and researchers to identify these species. And they hit on the two major ones, courtship rituals (mating calls, throat bulging, dancing) and pheromones.

Let's have a look at some two examples:

The widespread amazonian frog Allobates femoralis is now being approached as a species complex, with mating differences between the biologically distinct species varying from mating call note differences to cephalic amplexus (head grabbing during mate selection) and other various behavioral differences.[1]
Some crickets mate preferentially based on their species-specific song. Though, there is probably some genetic mixing with those crickets.

I think it's important to note that the species are cryptic because we as humans have decided they're hard to tell apart. Now, that similar morphology is also potentially difficult for predators to tell apart, or may be used by one or both species to parasitize on the other, it may be kept similar by sexual selection, or it may just not have great selective pressures to change. But the important part is that "cryptic species" is a box that we've created to describe traits we see.

Cryptic species as a window on diversity and conservation is a decent overview paper. (it's avaliable here if you don't have journal access)


Can a constitutively active kinase be highly regulated?

I think you have answered your own question, but yes, the nomenclature is confusing. When they say it is a constitutively active kinase, you are right, it plainly means the enzyme can always phosphorylate other molecules/proteins.
The regulation part is what you have in the review paper you cited. If the kinase is always on but localized in a compartment where there is nothing to phosphorylate, it could be considered "regulated". The same logic applies to the other regulation methods listed.


When you travel to different time zones, your circadian clock will be off (incorrect). The reason your circadian clock will be off is because your body has adapted to the time zone you are from. When you enter a new time zone, your circadian clock will still be functioning on the old the time zone. If the time zone difference is $\pm 12$ hours, this is a huge adjustment.

However, your body takes inputs from the environment. That is, you may see it is day light when your body is under the impression it is evening. Your circadian clock is controlled by your master clock located in the hypothalamus. As you take in these external inputs that counter your circadian clock, a group of nerve cells called the suprachiasmagic nucleus will slowly make the master clock adjustment [1]. This resetting can take a few days.

NIH Jet Lag Prevention Guideline

Additionally, there has been a bit of research on exercise reducing jet lag. In a study, researchers test outdoor exercise with flight crew members and found that the group that exercised outdoors had a hastened re synchronization of their circadian clock [2].

Another interesting article is Jet Lag in Athletes.


How are proteins containing other elements encoded?

Let's use an example, a case in point: the best known and plentiful one would be hemoglobin. It is a protein formed through the association of alpha- and beta-globin peptides into dimers or tetramers. The shape is largely a result of the sequence (peptide folding is reproducible, especially with the help of chaperones which may aid the correct folding process) and they fulfill their function by making use of an iron atom which they capture allow for their oxygen-carrying capacity. The iron is not encoded (since it's not an amino acid) but the sequence certainly determines the ability for globins to come together and sequester iron. If you wish, you could mutate the sequence to produce globins which would have reduced (or a complete inability) to use iron at their cores! The organism would be anemic, and depending on the extent of the effect, would be impaired or die.
Quoting the beta-globin gene page:

More than 10 mutations in the HBB gene have been found to cause
methemoglobinemia, beta-globin type, which is a condition that alters
the hemoglobin within red blood cells. These mutations often affect
the region of the protein that binds to heme [iron].

Lastly, a quick note on exactly how iron fits into the picture... inorganic iron can't simply be sequestered by the hemoglobin protein. The iron atom must first be covalently bound to form an organic compound called a heme group (see picture 1 below) which then acts as a 'prosthetic group' for the hemoglobin protein. When both enzymatic protein and prosthetic group come together, we jointly call them a holoenzyme, the complete unit which performs the oxygen capturing, carrying and releasing function inside red blood cells (see picture 2 below).


Why do specifically bananas go brown quicker in the fridge?

What's interesting with this one is we don't really know very well the mechanism behind what's called chilling injury. It happens to a range of fruits, like bananas, peaches, avocado, or apples. The belief is that the chilling alters membrane permeability to storage vacuoles inside the plant cells. Try On Food and Cooking, pp.269, and Puig et al. (2015) for references here.

Now the membrane permeability to the storage vacuole changes (it gets leaky), and inside these vacuoles are phenolic compounds. In the cytoplasm of the plant cell, there's an active enzyme called polyphenol oxidase (PO). The reactions it catalyzes end up with a compound called melanin, a brown/black pigment:

Fig A. An overview of what a PO might do.

So the phenolic compounds leak out and PO goes to work catalyzing reactions that start building up the dark pigments associated with browning. Being said, I can't at this moment find a good paper that says "look, this is how the entire process happens," but I'll be attempting to read a little deeper into the matter.

Keywords: flesh browning, enzymatic browning, chilling injury, polyphenol oxidase, storage quality, storage conditions


From the posture, it looks like it can belong to Geometridae (Larentiinae). But I haven't been able to find a species that has that particular color.


Where do gut bacteria come from in different organisms

For technical information on the subject, perhaps start with "vertical transmission insect symbionts" on google, which will lead to you to a variety of info's. Studies for symbionts of lice, fruit flies, mosquitos, termites, isopods, stinkbugs, butterflies and planthoppers.

Insect Symbiosis Vol 3 page 145 states:

Insects have been shown to use transovarian, egg smearing, and coprophagy, transmission, else entirely from the environment at every generation. There is a list of summaries of different insects that use different methods.

this also has masses of information:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967712/

Samples for large insects are taken with tweezers, small insects can be dunked in alcohol and then microbes are extracted.
Microbia RNA can be checked for evidence if the symbionts come from the parents. You can probably figure out a variety of methods for transmitting your insects symbionts, simply applying the wanted gut bacteria to the substrate of new cultures. I expect it can work in between species. you can try smearing eggs too.


Good question!

The term mutation can be used with two different meanings. Each definition can further be split into two different more detailed definitions. The reason for this slight mess is mainly historical. In short, a mutation can refer to

An event

narrow sense
broad sense

An allele

definition based on ancestral/derived states
definition based on frequency

Before going into the details of these definitions, it is important to first define a few other terms.

A few other definitions

The terms I want to define here are Locus, polymorphic locus, allele, nucleotide and phenotype.

In short (simplified version), a phenotype is the way an individual look. The variations of phenotypes of the individuals in a population depends upon the variation of genotypes and the variation of environments that they encounter. This concept is very much related to the concept of heritability. You may want to read more about it here.

The DNA sequence is made of four nucleotides. It is the sequence of these nucleotides that affect the phenotype of an individual

A locus is refers to the position of a DNA sequence of arbitrary length. At a given locus different types of sequence can exist, such a coding or non-coding sequence, a gene or just an intron, only a few codons, etc..

An allele is one variant of a sequence (often a gene) at a given locus. If, in the population, more than one allele exists at a given locus, than the locus is said to be polymorphic. Most polymorphic loci have only two alleles. In such case we can talk about bi-allelic loci.

Mutation as an event

A mutation can refer to an event.

Narrow definition

A mutation may refer to the event of a spontaneous change in the nucleotide sequence of an individual such as typically an indel (insertion or deletion of one or few nucleotides) or a substitution (substitution of a nucleotide by another one). In other words, a mutation can refer to the event of changing allele (eventually making up a new one) at a given locus.

Broad definition

The broad definition is similar to the narrow one expect that it encompass more types of genetic changes. In the broad sense, a mutation may refer more globally to any genetic spontaneous change. For example a whole chromosome deletion or a full genome duplication are examples of mutations.

In my experience, most often when the term "mutation" is used, it is to refer to the broad definition of mutation.

Mutation as an allele

A mutation can refer to an allele. Note however that very often we prefer using the terms "mutant allele", "mutant state" or just "mutant" as synonym to refer to this allele. Pretty much the only circumstance in which we would use the term mutation here is in sentences of the kind "Individual A carries the mutation.".

Definition based one ancestral/derived states

A mutation can refer to the allele that is derived from a more ancestral allele. Consider for example, a given locus was NOT polymorphic in the past. A mutation (in the sense of "event") occurs and the locus is now polymorphic. The allele that has been created by the mutation (in the sense of "event") is sometimes called "mutation".

Definition based on frequency

A mutation can refer to the allele that is at the lowest frequency in the population. For example, consider a bi-allelic locus with two alleles A and B. If the frequency of the allele B is lower than $\frac{1}{2}$ (that is lower than the frequency of the allele A), then the allele B can be referred to as the mutation. The reason for calling "mutation" the allele that is at low frequency is that most mutations are deleterious and as a consequence the mutant allele is often at low frequency. As a consequence, using the Definition based on frequency and Definition based one ancestral/derived states is often not important.

To address your question specifically

It is a little hard to directly address your question as it seems to have several misunderstanding on the concept of mutation. In the same time however, it feels like you are turning around the realization that there are several definitions in use.

  Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation?

The term mutation (whichever definition you pick) is intrinsically related to the concept of variation in the population but not so much to variation within a single individual (homozygote vs heterozygote).

If an individual "has a mutation on both allele", refers to the term mutation as an allele (in the narrow sense probably) and not as an event. More specifically it refers to one allele at a polymorphic locus (probably a locus of only one nucleotide) within the allele considered at the larger polymorphic locus considered.

  Does a mutation mean that it changed during lifetime

A mutation (in the sense of event) is a change that if often view at the moment of reproduction but the mutation may have occurred anytime in the lineage of the germ cells. Note, one may consider also mutation that occurred (during the lifetime of the individual) but in the soma cells. Such mutation will NOT be transmitted to the offspring.

  Or is there really a kind of standard taken where deviations are considered to be mutations?

Well...yes! A deviation is a deviation to a reference. In other words, we can replace "deviation" by "one allele of a polymorphic locus" in your question. And yes, a mutation (in the sense of a given allele) can refers to one allele of a polymorphic locus.


High protein turnover rate and protease inhibitors?

Scientists are recently finding (or coming to accept the notion) that, at least in eukaryotes, mRNA expression is poorly correlated to protein expression. There are several factors influencing translation regulation, such as siRNA or microRNAs, sequestering mRNAs while they are transported to various cell compartments, and others.  Even after the protein is made, there can be factors interfering with your expression reporter.  And as you mention, it may be degraded faster than you expect.  Cells try to keep proteins at certain expression levels, so if IL-1b is promoting expression without inhibiting the degradation pathway, degradation might kick into overdrive to bring the levels back down to normal.

Trying some protease inhibitors is worth a shot, since it's pretty simple by itself.  It should also increase your protein expression regardless of whether protein degradation is your limiting factor. If this doesn't work, or if it's prohibitively expensive to be sacrificing mice while you're working out a protocol (and is usually is), then I would turn to cell cultures and try and discern where you're getting blocked.  That kind of information will generally make a decent PNAS paper by itself.


Is the size of the genome across species roughly the same?

Chart of C-values (the mass of DNA in a single haploid cell); there is no logical order to the groups:

[source]

Base pairs in haploid genome (some examples):

Escherichia coli (bacterium): ~4.5 million
Caenorhabditis elegans (nematode worm): ~100 million
Homo sapiens (we all know what these are): ~3 billion
Pinus taeda (coniferous tree): ~22 billion
Prorocentrum micans (single-celled algae): ~245 billion

From these data we can conclude:

Different species do not have the same genome size.
Genome size is not correlated with complexity. Organismal complexity can be hard to define but, qualitatively, I think we can all agree that a human is more complex than a single-celled alga. And yet, humans have a genome that is 80 times smaller. This is known as the C-value paradox. Note, however, that this paradox has been resolved after it was found that the genomes of most eukaryotes contain a large proportion of non-coding and repetitive DNA.

Further reading:

The C-value paradox, junk DNA and ENCODE by Eddy SR

Eukaryotic Genome Complexity by Pray L


Can gelatine digestion make blood more thick?

No, because gelatin is a mixture of collagen-derived peptides. When you eat them, they are first hydrolyzed by stomach acids into constituent amino acids. These amino acids are then absorbed from the small intestines as nutrients.


Why do we blow when we're out of breath?

Trying to rephrase the question

If I understand the question (and what you missunderstand) correctly, I think one could rephrase the post as

When one spends some time under water and come back to the surface, one usually breath out and then breath in. This is surprising to me because I would expect the person to be out of air and therefore wouldn't need to breath out before breathing in.

Let me know if I failed to understand your question and misunderstandings

Answer

We don't incorporate the air we breath in our lungs. We only use the molecules of oxygen $O_2$ from the air (which takes ~20% of the total volume). This molecule goes in the blood, reach the cells and react with sugar to produce energy. The waster of this reaction is another molecule $CO_2$ that needs to be exhaled through the lungs.

So, really the volume and of air that we have in our lungs doesn't vary much (It actually increase a little bit as we had some carbons). Only the composition of the air that we have in our lungs changes. After some time, we need to renew this air and for this purpose we first need to breath out the air that is contain a high density of $CO_2$ before breathing in.

This is why when sticking the head out of the water many people first breath out and then breath in. Note, however that one can breath out all its air underwater and then only has to breath in when back at the surface.

EDIT

Are you asking why do we contract our lips during sport?

If yes, I think it very much depend from one person to another. There is probably no physiological advantage/disadvantage at doing so and it probably is just a consequence of expressing pain on our face.


How can a plant resist glyphosate (Roundup) herbicide?

I found a paper investigating the mechanism of glyphosate resistance in Conyza canadensis. They used 31P NMR to investigate the fate of the glyphosate in vivo. What they found is that the resistant plants are able to transport glyphosate into the vacuole:

  The following view of horseweed resistance to glyphosate emerges from
  the data presented herein. Glyphosate enters the cytoplasm of both R
  and S plant variants at the same rate. Within hours, however,
  glyphosate begins to occupy the vacuole in the R but not the S
  biotype. The identical pH values of R and S vacuoles speak against the
  possibility of a pH-driven process. This, coupled with the
  preferential movement of glyphosate from the cytosol to the vacuole in
  R tissue but not in S, suggests the presence of a transporter for
  glyphosate either specific to R or at a substantially greater
  concentration in R than in S tissue.

Another paper titled "Two non-target mechanisms are involved in glyphosate-resistant horseweed (Conyza canadensis L. Cronq.) biotypes" found a different mechanism for glyphosate resistance in addition to the sequestration into the vacuole.

  Glyphosate was metabolized faster in the R (C004) biotype than in the
  S biotype. The herbicide disappeared completely from the R (C004)
  biotype by conversion into glyoxylate, sarcosine and
  aminomethylphosphonic acid within 96 HAT.

The resistant plants seem to be able to metabolize glyphosate more effectively.

It is of course not guarenteed that these are the only mechanisms for glyphosate resistance, there are likely more variations.


Why are there both stop and start codons?

Start and stop codons are instructions for the ribosome to start and stop protein synthesis, respectively.

The region between the start and stop codon (inclusive of them) is called ORF (open reading frame) or sometimes CDS (Coding sequence).

Why does ribosome need explicit instructions for start and stop?

Ribosome recognizes an RNA as a mRNA if it has certain features. In bacteria and other prokaryotes there is a region on the mRNA called the Ribosome Binding Site (RBS) that helps in initial recruitment of the ribosome. In eukaryotes there are Kozak consensus sequences that help in identification of a start site. When the ribosome encounters an AUG codon then the initiation reactions take place (there are some proteins called initiation factors that help in this process). The ribosome just keeps moving along the mRNA and producing a polypeptide unless it encounters a stop codon. When it does other proteins called release factors come into play and they dislodge the ribosome from the mRNA.

What about a second AUG codon?

If the ribosome encounters another AUG codon after the start then it would consider it as a codon for methionine. However there are situations when the second AUG can act as an alternative start site. You can see this paper for details.

Why is stop codon essential?

You can imagine a situation where ribosome just goes till the end of mRNA — why stop it? The reason for this is that the mRNA 3' terminus usually has regulatory regions and most importantly poly-A tails (in eukaryotes) that should not be translated. Moreover stop codon also signals the ribosome to dislodge from the mRNA. If such processes didn't exist then ribosome will remain attached to the RNA.

If I only had a stop codon, would that also imply the next codon was start?

No. Because stop codon works only when translation has already started. However it is not essential that the stop codon should be followed by the 3'UTR. Usually in bacteria a single mRNA codes for multiple proteins. There are many ORFs that are lined one after the other; such mRNAs are called polycistronic mRNAs. In these cases there is another start codon a few distance ahead of a previous stop codon.


Is it possible to get infected with HIV from old blood?

Yes, you can transmit HIV with infected needles/syringes. This is a quite common mechanism of transmission when drug addicts share and re-use needles and syringes and also in third world hospitals with poor hygiene standards.

A drop of blood is considered infectious at least until it has completely dried up (some research showed that it might be contagious for up to 5 days longer when the conditions are right, see reference 1 below). Mostly HIV is senstive against high temperatures (over 60°C), while it is stable at low temperatures. It is very sensitive against shifts in pH (below 7 or above 8) and also against desinfectants like bleach. Have a look at the references below, a lot of research has been done by Abdala et al. in this field. You can find his whole reference list here (it contains more articles in this field).

References:

Survival of HIV-1 activity after disinfection, temperature and pH
changes, or drying.
Survival of HIV-1 in syringes.
Survival of HIV-1 in syringes: effects of temperature during
storage.
Viability of HIV-1 in syringes: implications for interventions among
injection drug users.


Phyllanthus caroliniensis

Phyllanthus caroliniensis, the Carolina leaf-flower, is a flowering plant native to the Americas, from the southeastern United States1 all the way to Argentina.2 The flowers are small and located where the leaf meets the stem.2

Kingdom: Plantae
Subkingdom: Tracheobionta
Superdivision: Spermatophyta
Division: Magnoliophyta
Class: Magnoliopsida – Dicotyledons
Subclass: Rosidae
Order: Euphorbiales
Family: Euphorbiaceae – Spurge family
Genus: Phyllanthus L. – leafflower

Sources:

http://plants.usda.gov/core/profile?symbol=PHCA9
https://en.wikipedia.org/wiki/Phyllanthus_caroliniensis
http://www.easttennesseewildflowers.com/gallery/index.php/Summer-Roadsides-White/Seedleaf50001
http://sura.ots.ac.cr/florula4/find_sp3.php?key_species_code=LS001041&key_kingdom=&key_phylum=&key_class=&key_order=&key_family=&key_genus=&specie_name=caroliniensis


This controlled experiment of burger decomposition explains in detail why fast food burgers do not decompose easily. The same can be applied to fries, which are smaller and come dehydrated from the frying.

The main take-aways from this experiment are:

1: Dehydration is the main reason why fast food fries/burgers do not decompose easily. Placing the burgers in a ziplock bag, preventing dehydration, causes the burgers to decompose.

2: Since an unsalted, home-made burger did not decompose, preservatives, chemicals, saturated fats, and other components are unlikely to be the case of the fast food burgers not rotting.


What happens to tube nucleus of the pollen tube after fertilisation?

Short Answer: It disintegrates.

Background: Although I was unable to find any primary reference, there were many secondary references stating that the pollen tube does disintegrate. In very short, after the pollen tube reaches the female gametophyte, the pollen tube nucleus disintegrates. For the 'why', it disintegrates to let the two sperm cells pass through, and also since its function of controlling the growth of pollen tube has finished.

For citation, you can have a look at:

Fertilization - Wikipedia
Advanced Biology -
A new mainstream text for the new specifications
Advanced Science; Michael Kent, 2000
Sexual Reproduction in Angiosperms; Kimball's Biology Pages
BIOPL 2410 Introductory Botany; KNiklas, TSilva; Cornell University
The Structure and Functions of Flowers - LeavingBio.net (image source)


Is there any evolutionary reason for why some organisms (wrasse) change their sex in adult stage?

This is an interesting question.  This strategy is common among wrasses, but the Labridae is a rather huge family.  I found this article here that I think may help answer your questions:  http://faculty.sites.uci.edu/johncavise/files/2011/03/299-SexDev-herms.pdf


Why proteinase K doesn't degrade itself?

According to invitrogen proteinase K does undergo autolysis, but that some leftover fragments still have protease activity. The solution should be stored at -20C, this low temperature is probably the best way to prevent autolysis. If you're using the enzyme to digest protein at 37C, you'll just have to deal with losing the proteinase k during the reaction and make sure you add enough to destroy the target protein before the proteinase is depleted.


Identify the pink mold infecting refrigerated lemons

I checked citrus diseases on wikipedia, then "ctrl+f" and typed in "pink mold". The result was Gliocladium roseum which is really a pink mold, but it is hard to find any image of it, where it is on fruits... So this is just a guess. Btw. I think it is rarely possible to identify microorganisms just by checking an image of them.


This is not a very helpful passage, I agree.  Some proteins are cleaved by other proteins (a protein that cuts another protein is called a protease).  Other proteins cleave themselves.  Otherwise, proteins are quite stable and don't just fragment wily-nily.

In the case of the first group (proteases acting on other proteins) the coagulation cascade may be a good place to start for you.  Precursor proteins in this pathway are converted to active enzymes by a chain reaction of protein 'division' and other protein modification.  This page has other interesting cases of this process, such as in food digestion, which may be what you're looking for.

Some of the second group are self-cleaving such that an intervening sequence is removed, and the ends are pasted back together.  (This is analogous to how introns are spliced from messenger RNA and the exons are spliced together.)  Such intervening protein sequences are called 'inteins'; the removal of one intein can generate one functional protein, so this isn't protein division.    However, some viruses encode self-cleaving regions that will split the mother protein into two or more pieces.  A famous example of this process, now used widely in biotechnology, is the 2A peptide, which is used to 'split' a single transgenenically-expressed protein into 2 (For instance if you want to express a protein and a marker such as GFP simultaneously, you could employ the 2A peptide to link these together.)

The first group may be of more interest to you because of the known role of these proteases in human health.  Also, in your question it sounds like you also may be referring to random 'fragmentation' of proteins, which is not currently known to be an important contributor to protein breakdown in the human body, even in the stomach.  Enzymes such as pepsin are responsible for digesting proteins.


The main question can be answered in a very dumb way: because the lower part of the body also needs blood... and this configuration is the surest way of doing that because of reasons given below (among many others, I am sure).

If you want an anatomical reason, well the most pertinent one would be that embryologically, the heart and vascular system are derived from a single straight tube, that then begins contracting and folding over itself to form the heart chambers, the aorta, and the pulmonary trunk.
If you want a physiological explanation, the aorta curves slowly because it is a point of the circulatory system where pressure is high. Apart from the fact that sharp kinks would cause a massive and useless loss of kinetic energy on blood flow from shear stress over the aortic walls (and therefore more heart workload), the induced shear stress would also damage the aortic walls much more quickly than in the actual configuration.

The third reason is just theory on my part, but it seems the vascular system is designed by priorities: you could imagine a system with two aortas. One for the upper body going up, and a second going down. However, such a configuration makes it mechanically impossible to balance perfusion to the organs, and especially ensure brain perfusion. For example, how would the body compensate if the upper aorta got clogged while the other stayed wide open? The single aorta configuration allows the heart to adapt to such mechanical perturbation scenarii using, for example, left ventricular hypertrophy.

However to add to some elements of your question:

the reason of the aortic coiling has certainly very little to do with elasticity and the vessel compression chamber principle.
Higher elasticity means the aorta is less stiff, not more.
When the aorta gets stiff (elasticity decreases) as it is often the case with age and calcification of the aortic walls, it is correct that the heart will need to work more, that systolic pressure will get higher, and diastolic pressure lower. This gives the classical clinical symptom of "cannonball" or "gunshot" pulse


How do people who have lost both of their legs produce red blood cells?

Red blood cells are produced in the red marrow which...

  "is found mainly in the flat bones, such as the pelvis, sternum,
  cranium, ribs, vertebrae and scapulae, and in the cancellous
  ("spongy") material at the epiphyseal ends of long bones such as the
  femur and humerus." - Wikipedia

So you are partly right; the femur is associated with red blood cell production, or Erythropoiesis to give it it's technical name, but there are other bones within the human body that also do this job. The process of erythropoiesis is stimulated when the kidneys detect low levels of oxygen in the blood stream and stimulate production of the hormone erythropoietin. Further, the role of the tibia and femur in erythropoiesis also decreases with age whereas...

  "the vertebrae, sternum, pelvis and ribs, and cranial bones continue
  to produce red blood cells throughout life." - again from the wiki page

So I'd suggest it is unlikely that loss of the legs would have a major impact on the production of red blood cells in adults. I imagine that with the loss of legs comes some reduction in functionality of erythropoiesis but also a lower requirement of red blood cell production (less blood capacity = less blood cells needed = less blood cells need to be produced). I can't find any studies which explore the ability or needs of amputees and non-amputees with regards to red blood cell production.


When do 3 germ layers form in embryo? And why is there only one mature egg formed?

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

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

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

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

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

References:

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


Potassium cyanide is added to the cobalamins produced by bacteria to give rise to cyanocobalamin. CN is strongly bonded to Co and will not easily dissociate, thereby making this form of B12 inactive. Therefore, it has been argued that cyanocobalamin is not a good vitamin supplement and other variants such as hydroxycobalamin or methylcobalamin should be used. Displacement of CN from the complex would be energy expensive and even if the reaction is efficient the amount of cyanide released would not be in the toxic concentration. The CN-Co bond is so strong that hydroxycobalamin is used as an antidote for cyanide poisoning; it forms cyanocobalamin by displacing OH with CN.

 Source: Wikipedia and the cross references.


What are the physiological effects of wine?

It is undisputed that heavy alcohol consumption (of any variety) leads to many deleterious effects on health.

It has also been claimed, however, that low to moderate alcohol intake can in fact be protective against some medical conditions (in particular, cardiovascular and cerebrovascular events). That is, there is often said to be a 'j-shaped' curve relating alcohol consumption to mortality and morbidity: low to moderate intake actually slightly reduces risk of adverse events relative to people who abstain completely from alcohol, but the risk increases markedly as consumption becomes heavy. See Plunk et al (2014): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872245/

Sometimes the protective association is attributed to the alcohol content itself (i.e. the ethanol), and sometimes to non-alcohol compounds (often specifically those found in red wine). The existence of such a possible protective effect at moderate doses is not a controversial position but it is also not settled science as yet. You should make up your own mind by reading reviews and ideally meta-analyses in the area. As a starting point, this 2013 review by Chiva-Blanch et al. in the journal Alcohol & Alcoholism has been well-cited by other researchers and is available to read in full here: https://academic.oup.com/alcalc/article/48/3/270/244770


How are nutrients absorbed by a pitcher plant?

Carnivorous plants use a variety of enzymes, including proteases which digest proteins to provide the plant with nitrogen. You might think that the hard exoskeleton would not be digested but pitcher plants (at least some types) produce chitinases which dissolve chitin (i.e. the exoskeleton), so there should be nothing left of the prey. The enzymes are secreted by tiny glands inside the pitcher.

  The enzymes that have been detected in carnivorous plants include amylase, chitinase, esterase, lipase, peroxidase, phosphatase, protease, and ribonuclease.

From the Sarracenia faq.

Aside from the enzymes secreted by the plant, there are micro-organisms present in the pitcher which will dissolve organic matter.

In my experience of growing Nepenthes and Sarracenia it seems to take a long time for the prey to dissolve and there is always some material left. Which type of pitcher plant are you growing?

There's a good description of CP digestion from the ICPS.
A more technical explanation about chitinase.

I can't find any specific detail on how the plant absorbs the nutrients, though even non-carnivorous plants can absorb nutrients through the leaf surface.


There are a number of ways, which are briefly summarized here. I also recommend reading this nice Scitable article on thermoregulation. It is not too technical. Felines do pant when they get hot. Horses do sweat. Jackrabbits can enlarge the blood vessels in their large ears to eliminate excess heat. Bird use a process called gular flapping, which is similar to panting of dogs and cats.  Animals can move into shaded areas.  The possible mechanisms are many.


Is genetic drift necessarily deleterious?

Drift is a random element of evolution from one generation to the next, it is equally likely to spread a deleterious mutation as a beneficial one.

The reason the answer is D is because selection should remove a deleterious allele, while drift makes no distinction, and is therefore the only scenario where drift is expected to be a reasonable answer. However, it is possible for drift to contribute to all of those scenarios.


Are there any animal species other than humans & chimps that engage in tribal conflicts?

In the introduction of an article by Gavrilets and Fortunato, the authors give (with references) some examples of intra-specific group conflicts:

  Social organisms living in stable groups often engage in aggressive interactions with conspecifics from neighbouring groups over territory, mating opportunities and other resources... Examples include border patrols in chimpanzees, raiding parties in spider monkeys, clan wars in hyenas and between-group fights in lions, free-ranging dogs, meerkats, Capuchin monkeys, blue monkeys, black howler monkeys and ring-tail lemurs.

Whether these conflicts (or others, such as ant colony conflicts) meet your definition of "tribal conflicts" you will have to decide.


Insects absolutely can metabolize poisons. This is because plants are absolutely chock-full of them, precisely to avoid insect predation, and in return many insects have developed immunities to many of these poisons. Or as this paper "DETOXIFICATION OF PLANT TOXINS BY INSECTS", which looks like it would be the answer to your question if it were free to read says:

  It is estimated that all plants
  contain some type of defensive compound (Rhodes
  and Gates, 1976). However, plant defensive compounds
  are not universally toxic to insects (Janzen,
  1979). Since almost all plant species are attacked by
  some insects (Schoonhaven, 1972), it is obvious that
  phytophagous insects have been able to develop
  countermeasures which allow them to feed successfully
  (Jones, 1972).

There are three main ways for an organism to neutralize a toxin: sequestering it where it will not harm the rest of the organism (and conveniently, may make the organism itself toxic to its own predators), excreting it (i.e. getting it out of the body altogether) and metabolizing it, i.e. chemically converting it into safer compounds. Often you will actually get combinations of those.

The first page of the paper sadly does not get into details about the extent to which insects use the third strategy, but it clearly states that they do.

This picture from Wikipedia shows some of the digestive organs that contribute to metabolizing toxins:

Organs that appear to deal with neutralizing toxins include the midgut (13), the fat body (not pictured), the hemolymph (not really an organ, it's the blood-equivalent liquid that all the organs bathe in), and the Malpighian tubes (20), though the latter (the apparent equivalent to our kidneys) probably serve more to physically get rid of the toxins than to metabolize them. From the Wikipedia page :

  In insects which feed on plant material containing noxious allelochemicals, Malpighian tubules also serve to rapidly excrete such compounds from the hemolymph.

And from here:

  Some small organic molecules are also
  actively transported into the tubule
  lumen by the transcellular pathway,
  including alkaloids (plant compounds
  which may be toxic to the insect).

This PLoS One paper (so, free to read) studies the enzymes that insects use to metabolize some toxins and notes among other things that:

  One of the best studied examples is the CYP gene superfamily of Papilio butterflies (Papilionidae), which have adapted to furanocoumarins, the toxic components of their food plants [15], [16]. These toxins are degraded by inducible CYPs that are expressed in the midgut and also in the fat body [17], [18].

and

  For Tyria, senecionine N-oxygenase (SNO), a soluble enzyme located in the hemolymph, has been shown to convert the pro-toxic free base efficiently into its non-toxic N-oxide [22] (Figure 1).

(emphases mine)

Another paper, "Chemical detoxification vs mechanical removal of host plant toxins in Eucalyptus feeding sawfly larvae (Hymenoptera: Pergidae)" describes how some sawfly larvae have special mechanisms for getting rid of and sequestering toxic oils, but also says :

  The oil sequestration is, however, incomplete and chemical gut content analyses by gas-chromatography (GC) revealed that 1,8-cineole does enter the midgut and is metabolised to hydroxycineole.

Another paper studying a class of enzymes generally associated with detoxification (but note the paper itself is about how those enzymes have other roles as well):

  Insect monooxygenases can be detected in a wide range of tissues.
  Highest monooxygenase activities are usually associated with the midgut, fat bodies and Malpighian tubules [9], but again the expression of individual P450s can vary between these tissues [17].

Insofar as insects have an equivalent to our livers it would seem to be the fat body. Like the liver this organ has many functions, including fat storage, energy metabolism and regulation, but also metabolizing toxins. From "INSECT FAT BODY: ENERGY, METABOLISM, AND REGULATION" (free to read):

  Whereas many insect tissues have vertebrate analogs, the fat body is an organ unique to insects (77). The fat body is a relatively large organ distributed throughout the insect body, preferentially underneath the integument and surrounding the gut and reproductive organ (36). Unlike the solid structure of the liver, the insect fat body is a loose tissue.

and

  Most of the insect’s intermediary metabolism takes place in this organ, including lipid and carbohydrate metabolism, protein synthesis, and amino acid and nitrogen metabolism.

and

  In addition to its role related to storage and utilization of nutrients, the fat body is an endocrine organ (65), produces several antimicrobial peptides (44), and participates in detoxification of nitrogen metabolism (74).

And from the other link:

  As in vertebrates, the oxidative metabolism is mediated via the tricarboxylic acid (TCA) cycle and the electron transport enzyme systems. The fat body contains enzymes mediating the gluconeogenesis process as well as enzymatic systems with a detoxification role to manage harmful endogenous metabolites and toxic xenobiotic compounds. Detoxifying enzyme systems include microsomal mixed function oxi-dases, in which the cytochrome P450 is predominant, various hydro-lytic enzymes (esterases, phosphoesterases), and conjugating systems.


What is the surface area of the vitreous humour in contact with aqueous humour?

Area=πr², d≈2cm (less than maximal d) -> r≈1cm,  thus the area in question is roughly

3.14*1cm*1cm≈3.14cm²

UPD by request (ref):

The vitreous body base middle is at ora serrata (+-2mm), so we should calculate the area at this level. Here is the reference of the diameter:

from: Basic and Clinical Science Course, Section 02


That appears to be what is known as a bagworm:

According to the University of Maryland extension Home & Garden Information Center, they can cause significant damage to ornamental plants especially conifers.


This isn't a complete answer, but searching Google Scholar for "Fibrobacter succinogenes human" I found this paper:

The cellulose-degrading microbial community of the human gut
varies according to the presence or absence of methanogens

The abstract of which begins this way:

  Cellulose-degrading microorganisms involved in the breakdown of plant cell wall material in the human gut remain rather unexplored despite their role in intestinal fermentation. Microcrystalline cellulose-degrading bacteria were previously identified in faeces of methane-excreting individuals, whereas these microorganisms were undetectable in faecal samples from non-methane excretors. This suggested that the
  structure and activity of the cellulose-degrading community differ in methane- and non-methane-excreting individuals.

Note also in Table 1, Fibrobacter succinogenes is one of the strains that seem to have been detected, so that answers the part of your question that seems to ask if humans can incorporate those bacteria into their gut fauna: yes, some already do.

This suggests to me that:

some humans do have a limited ability to digest cellulose through their gut bacteria, though this ability is probably limited enough that "humans can't digest cellulose" can still be considered true in the large scheme of things,
the challenge in digesting cellulose isn't so much getting the gut bacteria in there, but providing them with an environment where they will thrive and digest a lot of cellulose. This is probably where the specialized gut structures of ruminants come in; it becomes not so much a matter of digesting cellulose, but of digesting it well enough that you can live off of it. I'm guessing this is also related to the differences the paper found between people who excrete methane and those who don't but I wasn't able to figure out what that was supposed to be related to (is it a cause or an effect of the presence of certain gut bacteria? is it related to diet, genes, something else? I couldn't find that information in the paper though I didn't read every word)
according to the paper there isn't much research done into this.
the paper gives no info as to how significant those cellulose-digesting bacteria are to the host's energy balance, which I imagine is what you're really interested in. Is it significant, is it too small to be noticeable, does the host even benefit at all calorie-wise? They don't address that question in the paper.


What is this white fluff growing in my basement?

Might as well make this an answer.

  ...it seems to collapse when I rub my foot on it.

As @tyersome stated, it appears to be salt, not mold. Salt crystals would definitely collapse easily underfoot, and should be mostly quite dry, whereas mold would be... maybe squishy (?) but likely unpleasant in some way. Mold also smells, which you haven't mentioned, whereas salt is odorless.

To test, scrape a bit up (salt crystals should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water; it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in.

If it dissolves and you're brave, you can taste a tiny bit then spit and rinse. While salt isn't toxic, I can't vouch for what was in the grout.

My guess is that there may be a low spot or two in your basement where salt water is entering through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates.

If you have a magnifying glass, you should see crystals in the undisturbed deposit. If instead it looks soft and hairy, it is mold. I can't think of a white mold off the top of my head (well, Candida albicans, but that smells yeasty and is definitely not crumbly). Mold/yeast needs a substrate (food) to grow on, and wet grout isn't very nutritious. Mildew, sure, but mot big fluffy mold.

 I don't like this reference because it's not scientific, but it explains efflorescence well.)


Why does UV radiation from the Sun cause skin cancer?

Rather than 'breaks' caused by high energy radiation, UV radiation causes chemical modifications of the bases ('letters') that make up DNA. There are four bases in the DNA alphabet abbreviated to A,T,G or C belonging to two classes. A & G are guanines while T & C are pyrimidines.
When you have pyrimidine bases next to each other on a DNA strand, they can react to form photoproducts or pyrimidine dimers. These block transcription and replication and need to be repaired by nucleotide excision enzymes (only route in mammals) or photolyase enzymes (plants, many other organisms). TT dimers are the most frequent but dimers with a C cause more trouble as they can be imperfectly repaired causing a transition mutation. If they don't get repaired in time they can cause stalled replication which causes all kinds of trouble and can result in mutations that lead to cancer. You can find more on the wiki page.


Is rabies virus infectious outside host?

First off all we need to be 100% sure what does be infectious mean. According cambridge dictionary meaning of the word infectious is be able to past from one host organism (multicellular/cellular) from another. So this is actually biggest hole in your question.

But i think you mean something else then word infectious. In my oppinion you wanted to know if rabbies can survived outside of its host. The rabbies virus as many other viruses cannot live outside of its host. Rabbies is exists in "public reservoir". This fact only confirm its variety of hosts such as bat, bears, dogs etc. (technicly all warm blood species) and its long incubation period (for example 1-3 months in humans.

According this site:

Rabies virus is transmitted through saliva and brain/nervous system tissue. Only these specific bodily excretions and tissues transmit rabies virus. If contact with either of these has occurred, the type of exposure should be evaluated to determine if postexposure prophylaxis is necessary.
Contact such as petting or handling an animal, or contact with blood, urine or feces does not constitute an exposure. No postexposure prophylaxis is needed in these situations.
Rabies virus becomes noninfectious when it dries out and when it is exposed to sunlight. Different environmental conditions affect the rate at which the virus becomes inactive, but in general, if the material containing the virus is dry, the virus can be considered noninfectious.

To sum this:
Rabbies viruses need to have contact with host, typicly by biting. It is possible to be infected by other contacts such as kissing, licking not dry saliva, but still the virus cannot live long outside of body. So long incubation and variaty of possible host (most infected is bats) makes the true killing combination.


Why do women mature (physically) earlier than men?

This is a question about Neoteny and Heterochrony.

The closest field of study which will have specialists of this kind of topic is the study of the late maturation of humans compared to other species, which has had some research: 5-7 years ago there were some papers measuring the different bone growth rates of humans compared to chimpanzees and exploring the notion of natural selection through preference of immature traits: being attracted to girls with child like faces, smaller nose, large eyes, small voice, babyish, with various causes for example allowing for later brain pruning and longer brain development.

If you research in google publications you can find some research on the topic, for example:

Heterochrony in human evolution: the case for neoteny reconsidered

Sexual selection, physical attractiveness, and facial neoteny: cross-cultural evidence and implications (1995)

The origins of sex differences in human behavior: Evolved dispositions versus social roles.

It's all about evolutionary selection due to survival fitness. A complex age dynamic is at work in human evolution due to our extended lifetime, memory and brain size, amidst heavily variable social patterns (mate selection, monogamy, tribe size, bride rights, patriarchal/matriarchal systems) in paleolithic humans.

Bonobos mature at roughly the same time: 9 years, and female bonobos have a baby at 11 to 13 years. I think that illustrates the flexibility of maturation age according to the role of the adults.

Human females can have babies in between 9 and 15 years for the most part, some of them at 7, so maturation age is an evolutionary trait rapidly changeable according to fitness of the resulting offspring, so it is entirely fine tuned by survival performance.

EDIT: I wrote this answer to be helpful, but apparently my lack of sources and "errors?" deserve a mark down. so here is an additional text:

"They found that Paleolithic girls arrived at menarche - the first occurrence of menstruation - between seven and 13 years. This is a similar age to modern girls, which suggests that this is the evolutionarily determined age of puberty in girls.

'This would have matched the degree of psychosocial maturation necessary to function as an adult in Paleolithic society based on small groups of hunter-gatherers,' they write.

Disease and poor nutrition became more common as humans settled, causing puberty to be delayed. Modern hygiene, nutrition and medicine have allowed the age of menarche to fall to its original range.

However, today there is a mismatch between sexual maturity and psychosocial maturity, with sexual maturity occurring much earlier. This mismatch is a result of society becoming vastly more complex, with psychosocial maturity therefore taking longer to reach."

Note that they are talking about female adult paleolithic maturity and tasks at that age. Females compete for mates by attractiveness and fitness, and some research suggests that males compete for females by other mechanisms, even force or threat.(ref)

There is clearly a reason for which men are available to make and care for their offspring later than females. Females prefer older males by at least a couple of years with moderate adult muscle mass(ref), and in our species males of 17 to 35 years are biologically the strongest and wisest. Nature would have it that 11 /13 year old fathers clearly are counter productive to the survival of their partner and child in an ordinary setting of hunter gatherers, because of the very long gestation and complexity of human survival tasks.

The human mental maturation range has a wide variety of deviation, and between the age of 8 and 25, we are pre-programmed to be in an intense task of learning and physical adventure. Physical coordination of the male can reach an optimal level as late as the age of 22, 3/4 years after his bones have finished growing and his muscles and reflexes have had time to increase and adapt to his new frame, which is why athletes are at their physical peak between the ages of 18-27, and the "mental pruning" article suggests that their mind continues to re-organize itself well beyond the age of 30. During that stage, a human male is programmed to learn a wide array of advanced skills: flint knapping, tool making, botanic knowledge, hunting skills, clothes making, landscape exploration, orientation, memorization of food places, wells, tree climbing, metal work, net weaving, pottery, pigments, weapons, blow darts, wild animal experience (game, lions, rhinos, birds, rodents, traps, stalking, poisons, frogs) etc... All that time based survival experience reinforces the notion that a male reaches his functional optimum as a provider and protector of his family well after his sexual maturation age.

Females have a less physically intensive role to play in human society. While they can learn all the hunting/survival skills of the male, their central role is to be nourished and provide for the child(ref). Their parenting tasks rely less on individual memory because they stay socially at home more (papua new gineans, africans, aborigines, yanomami). Their task can be less intense physically, require less physical training, and can be less intensive on memory and adventure (being nourished, childcare, craftwork, leadership of the group at home and less in exploration and precarious tasks). Both the human male and female memory has a very important role for guiding the group. A female can provide guidance up till the age of 50-90 in a natural setting.

Females are generally less expendable and adventurous than males, because a male can potentially have 3 offspring every day, he is limited by the number of females, and she can only have 1 offspring every 9 months, she is more precious to the multiplication of the group.

Add to that the function of memory, hunter gatherer fitness, and social acumen, absorption of mental and survival skills

Other great apes have gestation periods arount 8.5 months compared to our 9.

Because of the difficulty to assess the paleolithic social and environmental pressures that caused the sex age maturation difference, it's a question that theorists would be unwise to wade into to any great depth, in an academically competetive field. A good anthropologist should be able to list all the predominant selection factors.


Since the Michaelis-Menton constant Km is the concentration of substrate at 0.5Vmax, it is an inverse measure of its substrate affinity, because a lower Km indicates that less substrate is needed to reach a certain reaction speed. Hence, a low Km means a high substrate affinity.

Your statement

  "Maybe the maximum velocity (Vmax) of higher-Km enzymes is higher? Then of course Km can have a higher value."

is incorrect. Km characterizes how steep reaction speed increases with substrate availability; it does not determine maximum speed.

Lastly, to address your title question, comparing affinities can make a lot of sense. For example, consider the case where enzymes catalyzing similar reactions in different species of organisms are compared. Very low Km means optimal use of small substrate levels, while a high Vmax shows optimized reaction speeds. This in turn may tell you something about optimal habitats and evolutionary pressure.


The centre + surround do not cancel completely, as you can see from these mudpuppy recordings. [Image 1] (Werblin and Dowling, 1969, I believe)

One function of a centre-surround set-up is to highlight the contrast at borders.  Most of the useful visual information is from borders/outlines, so this is a method of ignoring redundant information.  The highlighting of contrast borders and ignoring of redundant information explains why the neural image appears different. [Image 2 - right].
Another function of centre-surround fields is to avoid saturation, but this is more complicated to explain. [Image 2 - left] (Diagrams from Cambridge MVST Part IB lecture series by Hugh Matthews)


What are Codominant vs Dominant Genetic Markers?

From wikipedia

  If the genetic pattern of homozygotes can be distinguished from that
  of heterozygotes, then a marker is said to be co-dominant.

This definition seems to be different from the one used to explain allelic effects. For example, as you would know a SNP is basically a feature of the DNA sequence. It is more of a genotype rather than a phenotype. Markers are supposed to be phenotypes (can be a molecular phenotype too for example a marker for stem cells etc). SNPs do create allelic variants but they may or may not contribute to different phenotypes. Consequently, the allelic variants may exhibit dominance or co-dominance with respect to each other. So, going by the definition used in classical genetics, you cannot call SNP as a "dominant"/"co-dominant" marker.

That is a weird usage of the terminology but people have done it so the deed cannot be undone. I would avoid future usage of such misleading terms. Having said that SNP would fit the definition of a "co-dominant marker" if it is observed by DNA sequencing .

Personally, I would consider RFLP a technique and not a marker per se. RFLP can be used to differentiate SNPs but sometimes it may not even resolve different strongly visible phenotypes (its efficacy basically depends on the polymorphism at restriction sites). Heterozygotes however, would have a different band pattern compared to homozygotes. So it should be a "co-dominant" marker.

AFLP, as far as I know is simply PCR amplification of restriction fragments. It would be "co-dominant" for the same reasons. However, just a PCR based screen would not differentiate between homozygotes and heterozygotes and would thus be a "dominant" marker. Now again, these are techniques and not, in a true sense, "markers" whereas SNPs and microsatellites are actual DNA features. So these cannot be even compared. A technique, depending on its resolution, can be "dominant" or "co-dominant" as per these definitions.

For general interest

I would want to reiterate that these definitions, for some reasons mentioned above, are quite flawed and are therefore misleading (they may have been okay at certain point of time but are obsolete now). Please avoid their usage in your papers and reports and if possible point these flaws out, so that they do not propagate.


Is there any mechanical digestion that occurs once food/chyme enters the small intestine?

I believe in small intestine peristalsis is sometimes counted as mechanical digestion as the food is moved along the digestive tract. Chemical digestion occurs with enzymes secreted from the pancreas.

https://www.smartlivingnetwork.com/digestive/b/mechanical-and-chemical-digestion/ - source


Why do veins undergo vasoconstriction during physical activity?

I believe that the answer is in the same cited source (BioSBCC).

Veins are considered a blood reservoir and undergo constriction to mobilize blood.

  [...] the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest. [...] When the body needs to mobilize more blood for physical activity, the sympathetic nervous system induces vasoconstriction of veins.

The result is an increase in circulating blood volume. This changes cardiac output and arterial blood pressure (CV Physiology: Blood Volume).

I also recommend reading on Biology.SE: Where does extra blood come from to fill your muscles during exercise?


Where does the gluteus medius attach to the greater trochanter compared to the gluteus minimus attachment?

{1} greatly answers the question.

Regarding the insertion location (lateral view):

Note that unlike the gluteus minimus insertion, the gluteus medius insertion can also be viewed anterolaterally:

Table 2 contains more detailed insertion location data:

Regarding the insertion area:

  Gluteus maximus: Average Area, mm^2 (95% CI): 473.4 (381.0, 565.8). Thick, muscular insertion along the posterior femur on the linea aspera
  Gluteus medius: Composed of 2 contiguous rectangular footprints, the lateral facet oriented in the sagittal plane and the superomedial facet primarily in the transverse plane:

  Lateral facet: Average Area, mm^2 (95% CI): 141.1 (117.7, 164.5).
  Superomedial facet: Average Area, mm^2 (95% CI): 501.5 (442.8, 560.2).

  Gluteus minimus: Average Area, mm^2 (95% CI):  280.9 (229.3, 332.5). Two morphologies noted: The majority (11/14) were long, thin, and crescent shaped and ran medial to lateral and concave facing inferiorly, while a few (3/14) were bowtie in shape.

Below are some actual pictures of the gluteus minimus insertion, the gluteus medius insertion to get another sense of their shape and location. Still  from {1}, this picture shows the gluteus medius (but not the gluteus minimus):

From {2}, this picture shows both the gluteus medius muscle and the gluteus minimus muscle:

I also find this picture good to give a better sense as to where the greater trochanter is located with respect to the human body (image source (mirror)):

References:

{1} Philippon, Marc J., Max P. Michalski, Kevin J. Campbell, Mary T. Goldsmith, Brian M. Devitt, Coen A. Wijdicks, and Robert F. LaPrade. "Surgically relevant bony and soft tissue anatomy of the proximal femur." Orthopaedic journal of sports medicine 2, no. 6 (2014): 2325967114535188. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Surgically+Relevant+Bony+and+Soft+Tissue+Anatomy+of+the+Proximal+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/26535335 ; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555602/ ; https://doi.org/10.1177/2325967114535188
{2} Woodley, Stephanie J., Susan R. Mercer, and Helen D. Nicholson. "Morphology of the bursae associated with the greater trochanter of the femur." JBJS 90, no. 2 (2008): 284-294. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Morphology+of+the+Bursae+Associated+with+the+Greater+Trochanter+of+the+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/18245587 ; https://doi.org/10.2106/JBJS.G.00257


Does the body prioritise the use of available sugar before fat?

In a very simplified explanation  - the body usually picks the process which is easiest/ fastest which would be to absorb the glucose  then the fat would be used for energy as this takes longer to digest and absorb because it is a relatively complex molecule which also requires bile to emulsify it.

Starchy/ high glucose products will already be broken down in the mouth by amylase and absorbed in the intestine + pancreatic amylase etc. which takes around 20 mins-1hr whereas soluble fats are digested primarily in the small intestine (by enzyme lipase) for (very approx.) 1-4 hours depending on the amount ingested. Insoluble fats are broken down into soluble fatty acids and glycerol which can be absorbed into the blood.

The amount of either you use for energy just depends on how much energy you expend.


Why do different pain killers have different effects on people?

Short answer: different people have different amount of active receptors.
In treatment, combination scores of Pharmacodynamics and Pharmacokinetics determine the final effect of the drug.
Receptors determine many effects of the drug in many pathways.
Different people also sense pains differently (Psychology).

Review answer

The purpose of treatment is to relieve pain and maintain function.
Your question is biased.
You cannot only concentrate on painkilling in maintaining health.
These both are the reasons for the complains of the patient, not only the pain.

For instance, in rheumatoid arthritis, response to therapy can be quantitated using many measures including American College of Rheumatology system values ACR20, ACR50 and ACR70, which denotes the percentage of patients showing an improvement of 20%, 50% or 70% in a global assessment of signs (maintaining function) and symptoms (pains).

Each patient has own health, different from one another.
Our body adapts to the environment and individual conditions of the body to maintain homeostasis.
Receptors adapt for instance.
They can be active or inactive - in short-run and long-run - again depending on the conditions at hand.

Painkillers i.e. analgesics have different properties:

anti-inflammatory effect - acute and chronic conditions (inflammation is the major mechanism under many pathologies) e.g. nonsteiroidal anti-inflammatory drugs (NSAIDs, please, see this answer about the particular mechanisms and how different people have different effects from NSAID painkillers) and glucocorticoids (most)
symptoms relieving specific drugs e.g. disease-modifying antirheumatic drugs (DMARDs)
anti-platelet effect - e.g. the older you get, the more platelets stick together.
anti-pyretic effect
...

which all can be toxic.
Note that many drugs alone or/and as combination can work as painkillers i.e. pain relievers.
Aspirin for instance has both anti-inflammatory and anti-platelet properties.
However, it is rarely anymore used as anti-inflammatory.
The anti-platelet property is dependent on the exact dosage of the administration.
Aspirin's mechanism of action is to inhibit platelet COX which antiplatelet effect lasts 8-10 days (life of the platelet).
In other tissues, synthesis of new COX replaces the inactivated enzyme so that ordinary doses have a duration of 6-12 hours.
Please, review any Pharmacology -textbook for more info about aspirin.

Each these drug has own Pharmacodynamics and Pharmacokinetics

Pharmacodynamics answers to the question What drug does to the body? It stimulates some receptors, activates some pathways, ...
Pharmacokinetics - What does body do to the drug? It metabolises it (enzymes, receptors). It distributes it. It excretes it (kidneys, feaces).

In treatment, you consider what is the target organ.
You need to think what is causing the dysfunction and the pain.
You try to restore the function and relieve pain.
The component of drug needs to reach the target tissue e.g. your pancreas' beta cells do no produce insulin so your blood glucose is high.
Complications of this are polyuria and eventually exodus if untreated.
Insulin is injected into the fatty tissue.
We do not have long-term acting insulin administered orally - our metabolism start to break the drug so it does not have wanted treatment.
If insulin administered to the muscle, the time of action is too times less, again because muscle is metabolising the insulin i.e. a chain of peptides (protein).

No all symptoms and diseases have painkillers.
For instance, prehemorrhoid and some types of itching related to  posthemorrhoids.
However, for both, there are some special salvas for proplylaxis but they are not complete.

Now, you can start to read something in SuperBest's answer about host's physiological variables and addiction/tolerance which alters the mechanisms (receptors) of pathways in Pharmacodynamics and Pharmacokinetics.

Sources

Basic and Clinical Pharmacology, 11th edition, 2009, Bertram Katzung.
My notes in Pharmacology classes during 2014.


What's the therapeutic index of Pethidine (Meperidine in the US)?

Closest I reached:

Source: Page 105, The Complete Recovery, By Anthea Hatfield Google Book


CDK3 1 simple coding mutation/missense mutations (S106N) glioma

Good question, if you check COSMIC and search for S106N, you'll find no hit with CDK3. So it isn't there (anymore?). One possibility is that it was present in 2014, when the paper was written, and the mutation is removed in the mean time by curation.

However, if you look at genecards and look for the variants, on top of the table you'll find a link to expasy. here they cite to a paper in Nature, and in the supplementary data of this paper you'll find your CDK3 S106N mutation.


The yellow color comes from the accumulation of Bilirubin in the body. Bilirubin is a breakdown product of hemoglobin (contained in erythrocytes, also known as red blood cells, and responsible for the oxygen transport in the body). (This is also the reason why bruises get colored, as the blood which was released into the skin gets removed.) As erythrocytes live only for around 120 days, the hemoglobin needs to be recycled at the end of the life cycle, as free hemoglobin is a pretty problematic substance.

The recycling of the erythrocytes happens in the liver, the iron is recycled, and the hemoglobin is split in the globin (which is further broken down into the amino acids) and the heme which is oxidized by the heme oxidase to biliverdin and further by the biliverdin reductase to bilirubin.

As bilirubin is not water soluble it is bound to albumin and released into the bloodstream for the transport to the liver. In the liver this process goes on further until the bilirubin is water soluble and can be released with the bile into the intestine where it is finally excreted. See the image (from here) for an illustration:

If your liver is not working properly (for example due to an infection) the break-down process of the albumin-bound bilirubin is reduced or doesn't work and the yellow bilirubin accumulates in the body until the skin gets yellow. So this indicates a liver malfunction and is usually nothing to take easy.


What is meant by "genes involved in the stress response"?

The comment by @fileunderwater is apt: stress-response-related genes are genes that are activated during stress, such as exposure to heat. In bacteria, for example, there are heat-shock proteins that are involved in keeping the tertiary structure of proteins (folding/3D shape) intact during periods of heat exposure. Genes encoding these heat shock proteins are then called to be upregulated, and you would find them back in a typical micro array experiment. Hope this helps.


Beautiful blue enigmatic insect (mantid?) in Kenya

I'm converting my numerous comments into an "answer" -- I don't currently know the exact species, but I can at least explain some of my thoughts more completely.
Your specimen looks a lot like Gonatista grisea, a tree mantis that mimics a lichen -- as you mention in your post. However, G. grisea, is native to the southeastern USA. I could find no evidence of any reports finding this species in Africa, so we will rule it out.
If we examine some other species of the Gonatista genus (e.g., G. jaiba, G. major, G. phryganoides, and G. reticulata) we find that they are all neotropical and not found in Africa. Therefore, let's look elsewhere.
So, I would recommend examining other close members in the same family that are found in Africa.

I originally recommended reviewing Patel et al (2016) because they provide a checklist of the global distribution of other members of the Liturgusidae family. Using this guide, we could examine known African genera.

They list Dactylopteryx, Majanga (Madagascar), Theopompella, and Zouza as African genera.

However, I had not realized that there had been some taxonomic rearrangements, and Gonatista is now in the family Epaphroditidae.

The other genus in the same subfamily as Gonotista, Gonatistella, is monotypic, and G. nigropicta is not your species.

The other genera in this family, Epaphrodita and Callimantis, (as well as the now-moved genus Brancsikia) also do not seem to contain any species I could find that are morphologically similar to yours.

So maybe we should look elsewhere in the previous Liturgusidae...

Subtribe Humbertiellina in the Gonypetidae  family are just one example of another group perhaps worth investigating because it too was once contained within the original Liturgusidae family along with Gonatista and because some online evidence suggests some members of this subtribe (e.g., Humbertiella and Theopompa) share some similar physical characteristics to Gonatista.

Some non-reputable sources (e.g., here for Humbertiella and here and here for Theopompa servillei) show specimens similar to yours with labels as one of these two genera. I couldn't find consistent imagery or reputable sources with imagery to support either one as correct...
(Also, Patel et al. (2016) suggest these genera are recognized as Asian genera, and so they may be geographically unlikely anyway like Gonatista).

However, perhaps trying to solve your unknown specimen using taxonomic and trait-similarity approaches could be misleading.

According to Rivera (2010): "Whereas the monophyly of Mantodea is well supported, the evolutionary relationships within the order are still contentious. Several classification systems for mantids have been proposed...However, the natural affinities among supraspecific taxa have been extremely difficult to discern due to the highly variable and derived morphology of these insects."

According to Schwarz & Roy (2019): "As already noticed by previous authors, external morphology is highly homoplastic and does not provide useful systematic tools above subfamily level."

Schwarz & Roy (2019) do suggest that the morphology of male external genitalia may be useful for relating individuals as these traits tend to be fairly congruent with more recent molecular phylogenies. You could start there for further research.

(I myself can't discern meaningful detail of the genitalia in your photos, nor am I any type of expert on mantises, so this route of inquiry might be too much in the weeds for me...)

If you find a good key for your region, you might want to check out Brannoch et al (2017) for a "Manual of praying mantis morphology, nomenclature, and practices" to help you with all the mantid jargon. [it appears to be a very thorough and excellent resource!].
I will update this post if I find anything more definitive for you...

Citations
 Brannoch, S.K., Wieland, F., Rivera, J., Klass, K.D., Béthoux, O. and Svenson, G.J., 2017. Manual of praying mantis morphology, nomenclature, and practices (Insecta, Mantodea). ZooKeys, (696), p.1.
 Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803.
 Rivera, J., 2010. A historical review of praying mantid taxonomy and systematics in the Neotropical Region: State of knowledge and recent advances (Insecta: Mantodea). Zootaxa, 2638(1), pp.44-64.
 Schwarz, C.J. and Roy, R., 2019, March. The systematics of Mantodea revisited: an updated classification incorporating multiple data sources (Insecta: Dictyoptera). In Annales de la Société entomologique de France (NS) (Vol. 55, No. 2, pp. 101-196). Taylor & Francis.


If you're looking for a strictly and directly DNA-DNA mediated effect (no histones, no transcription involved) I'd look for sequence effects on chromatin remodelling, modulating access of transcription factors (TFs) to their elements. Something about this might be in this paper:
Szerlong, H. J., & Hansen, J. C. (2011). Nucleosome distribution and linker DNA: connecting nuclear function to dynamic chromatin structure. Biochemistry and Cell Biology = Biochimie et Biologie Cellulaire, 89(1), 24–34. doi:10.1139/O10-139


Is "aggregate percentage" still a valid term in ecology?

The formula of "aggregate percentage" that you show is just the arithmetic mean of percentages, and I suspect that no special term is used in most studies that use mean percentages as a measure of e.g. prey composition in a certain predator (as seems to be the case in your example).

When searching for studies I think you will have more luck with using "mean prey percentages", "prey percentages" or "mean percentage composition". For instance, see Shoup & Lane (2015) which includes the text (with my emphasis):

  Results of regressions correlating Secchi depth (mm) with prey percentages by weight in the stomach contents of Largemouth Bass sampled from Boomer.

Also (Ahlbeck et al, 2012):

  For each of the 25 individuals in each size class, the diet composition was calculated as the mass percentages of different prey, and then the average mass percentages were calculated for the size class.
  [...]
  prey percentages were first calculated for each fish separately and then averaged over all individuals in the sample (Hyslop 1980).

Finally, Ledger & Hildrew (2008):

  Mean percentage composition (food category area as percentage total particle area) of faecal pellets of N. pictetii nymphs fed biofilm from four acid streams and four circumneutral streams.


Coefficient of Inbreeding - implementation issue

The $F_i$ term is the term that accounts for inbreeding of your common ancestor X. If that common ancestor is not inbred then the term is 0 and the calculation is a little easier. Using the example you have given:

 X ─┬─ Y
    │
 ┌──┴──┐
GGGF  GGM
 │     │
GGF    │
 │    GM
GF     │
 │     │
 F ─┬─ M
    │
   Mick

In this case, the common ancestors are not inbred so the $F_i$ terms go away ($1+F_i = 1$). There are two paths of common ancestry (via X and Y), therefore the calculation of the two paths from the father (F) and mother (M) to X and Y is:

$F_{Mick} = \frac12^{n_{F,X}+n_{M,X}+1}(1+F_X)+\frac12^{n_{F,Y}+n_{M,Y}+1}(1+F_Y) $

$F_{Mick} = \frac12^{4+3+1}(1+0)+\frac12^{4+3+1}(1+0) $

$F_{Mick} = \frac{1}{256} + \frac{1}{256} = 0.0078 = 0.78\% $

In a more complex case, such as where ancestor X was inbred, $F_i$ cannot be ignored. In the following example, X's parents were first cousins:

  U ─┬─ V
     │
  ┌──┴──┐
 XGF   XGM
  │     |
  XF─┬─XM
     │
     X ─┬─ Y
        │
     ┌──┴──┐
    GGGF  GGM
     │     │
    GGF    │
     │    GM
    GF     │
     │     │
     F ─┬─ M
        │
       Mick

For this, we must first calculate $F_X$ (i.e. how inbred X is):

$F_X = \frac12^{n_{XF,U}+n_{XM,U}+1}(1+F_U)+\frac12^{n_{XF,V}+n_{XM,V}+1}(1+F_V) $

$F_X = \frac12^{2+2+1}(1+0)+\frac12^{2+2+1}(1+0)$

$F_X = \frac{1}{32} + \frac{1}{32} = 0.0625 = 6.25\% $

Then we can input this $F_X$ into the same calculation as done before for the simple case:

$F_{Mick} = \frac12^{n_{F,X}+n_{M,X}+1}(1+F_X)+\frac12^{n_{F,Y}+n_{M,Y}+1}(1+F_Y) $

$F_{Mick} = \frac12^{4+3+1}(1+0.0625)+\frac12^{4+3+1}(1+0)$

$F_{Mick} = 0.00415 + \frac{1}{256} = 0.0081 = 0.81\% $

A good explanation of these calculations with further examples can be found here: The Coefficient of Inbreeding (F) and its applications. The calculations can get quite complicated even with relatively simple inbreeding.


The substances that bees consume do end up in honey. There was a high-profile case in Brooklyn in 2010 (The Mystery of the Red Bees of Red Hook) where bees from several hives began producing red honey after feeding on dyed maraschino cherry juice from a local factory.

A follow-up article from 2015 (How Bees Revealed a Pot Farm Beneath the Maraschino Cherries) claims that the substance they began producing was not honey but “red gunk”; however, that may have been editorial license.


That's correct. Alleles are alternate forms of a gene that occur at the same locus and arise by mutation.
Another example might be sickle cell anemia where a SNP (a single base change) is the cause of the disease.


First of all, let me clear out that these numbers are calculated, not observed (obviously, nobody has counted the number of neurons in any part of brain). So, take these with a grain of salt.

I was unable to find any report that collects and displays all numbers together (Bio Numbers too didn't yield significant information). So I will compile here all the numbers I have found so far (and keep adding as I find more):

|----------------------|------------------|------------------------|
|PART OF BRAIN         |NUMBER OF NEURONS |               REFERENCE|
|----------------------|------------------|------------------------|
|The human brain       | over 120 billion |  Herculano-Houzel, 2009|
|Telencephalon         |  12-15 billion   |           Shariff, 1953|
|Cerebellum            |   101 billion    |    Anderson et al, 1992|
|Cerebral cortex       |  21-26 billion   |      Pelvig et al, 2008|
|Amygdaloid complex    |    12 million    |    Schumann et al, 2005|
|Hippocampus (CA1)     |  11-24 million   |        West et al, 1990|
|Brainstem             |   < 1 billion    |  Herculano-Houzel, 2009|
|Visual cortex         |   140 million    |       Leuba et al, 1994|
|Auditory cortex       |    1 billion     |University of Washington|
|Corpus callosum       |   200 million    |          Healthline.com|
|Spinal cord           |    1 billion     |University of Washington|
|Cortical minicolumn   |      80-120      |               Wikipedia|
|Cortical hypercolumn  |   5,000-10,000   |               Wikipedia|
|----------------------|------------------|------------------------|

I will continue adding more numbers as I find them. Again, nobody will claim these numbers to be exact, these are just estimates from calculations. Even different sources show different numbers. For example, the Washington University page puts the number of neurons in visual cortex to 528 million. Thus, don't expect these numbers to be anywhere near exact.

References:

Herculano-Houzel, 2009
Shariff, 1953
Anderson et al, 1992
Pelvig et al, 2008
Schumann et al, 2005
West et al, 1990
Leuba et al 1994
University of Washington
Healthline.com
Wikipedia Cortical minicolumn
Wikipedia Cortical hypercolumn


Take a look at the biomaRt package. This package allows you to access some databases in R directly. Quote from the user's guide:

  The package enables retrieval of large amounts of data
  in a uniform way without the need to know the underlying database schemas
  or write complex SQL queries. Examples of BioMart databases are Ensembl,
  Uniprot  and  HapMap.   These  major  databases  give  biomaRt  users  direct
  access to a diverse set of data and enable a wide range of powerful online
  queries from R.

In the user's guide you will find anything you need, i.e. description and example tasks, for doing queries on HGNC symbols, GO terms, and more.


Its simple:

Mass = Density * Volume

= 10^3 (Kg/m3) * (10^-18 m3)

= 10^-15 Kg

which is equal to 10^-12 gram or 1pico gram


Are there any examples in nature of two polypeptides joining into a single, continuous, third polypeptide?

I am not aware of anything precisely corresponding to your diagram, but the somewhat related behaviour of inteins may be of interest in this respect. They are defined in Wikipedia as:

  An intein is a segment of a protein that is able to excise itself and join the remaining portions (the exteins) with a peptide bond in a process termed protein splicing.

So, unlike either ribosomal or non-ribosomal polypeptide (e.g. antibiotic) sythesis, they catalyse a peptide bond between peptides rather than an amino acid and a peptide. However these are already part of single polypeptide chain before the intein itself is spliced out.

[Modified from Intein_mech.png to fit page. — The mechanism of protein splicing involving inteins. In this scheme, the N-extein is shown in red, the intein in black, and the C-extein in blue. X represents either an oxygen or sulfur atom.]


What are the major causes of mutations in DNA?

Welcome to Biology.SE!

  can environmental factors play a role in the amount of mutations that occur?

Yes! The environmental factors that increase the mutation rate are called mutagens. You will definitely want to have a look in the wikipedia article. You may also want to read the wikipedia page on mutagenesis

Some chemicals increase the mutation rate, physical agents such as radiation also increase the mutation rate. There are viruses that are mutagens as well. Also, the number of mutations that an organism produce can also be phenotypically plastic. For example, plants have been shown to increase thee number of mutations they produced in response to stressing environment. The reason (or at least the commonly stated reason) is that they produce many mutations, "hoping" that at least one of the offsprings will carry a beneficial mutation and will be very fit even in this environment that is stressing for the parents. Many viruses and some bacteria also act as mutagens.

  Are these mutations purely random events that occur when DNA is being copied into a cell?

Mutations are random in the sense that it is impossible to predict with certitude that a given mutation will occur at a given locus (locus=position in the genome). As a consequence, it is also true that mutations are random in the sense that it is impossible to predict the effect on the phenotype (and on the fitness) of a future mutation. Mutation rate varies throughout the genome. Typically, repeated DNA sequence tend to have higher mutation rate. Also, transposons causes many mutations and regions in the vicinity of transposons have higher mutation rate. But again, you should have a close look to the wikipedia pages I linked above.

Note that a full answer would require going into the terminology of the term "random" which itself is a question of philosophy. When using the term random, it is always important to specify what is meant exactly (which is not done in the question) as one may argue that since the Big Bang happened everything has been deterministic.


Is there a medical condition in which you can't cut your hair?

Alopecia and balding, these individual experience hair loss, thus nothing to cut


Determining if a specific proline is cis or trans in the protein?

Sarkar et al.(2007) Proline cis-trans Isomerization Controls Autoinhibition of a Signaling Protein. Molecular Cell 25, 413–426 (DOI 10.1016/j.molcel.2007.01.004), available here.

The authors report on the interactions between two SH3 domains of the Crk adaptor protein. Basically they find that the linker which tethers these two domains contains a proline which interconverts between the cis and trans conformations, and that this interconversion determines the interaction between the two domains. They follow isomerisation by using NMR.

Cis-trans peptidyl-prolyl isomerization is a subtle change, and I don't think that you will find a way of following it in a specific protein that is simpler than this, unfortunately.


difference between ischemia and oxygen-glucose deprived medium

Ischemia leads to tissular hypoxia and glycopenia due to an insufficient blood flow (e.g. due to atherosclerosis or thromboembolic diseases). Ischemia always result in hypoxia.

Hypoxia can occur without ischemia (e.g. due to anemia).

Tissular glycopenia can occur without ischemia (e.g. due to hypoglicemia).

Ischemia is a shortage in blood supply. Depriving cells form oxygen and glucose isn't the same as cutting their blood supply.


Looks like it must be a male Dynastes tityus (Linnaeus, 1763).

There are photos for comparison, and a full description with maps and some interesting notes on habitat and behavior, on the University of Nebraska State Museum Generic Guide to New World Scarab Beetles


What is in the space between neurons in a brain?

Not so empty, actually.

The human brain has a mass of ~1.5kg, and volume ~1200cc (a little bigger for men, a little smaller for women). So is heavier than water by a good margin.

While it has Cerebrospinal fluid, that only occupies the subarachnoid space (the space below the skull and above the cortex, contained between two layers: pia matter and arachnoid membrane) and the ventricular system (several spaces inside the brain, remnants of the embryological development of the brain).

Neuron density may vary widely, depending mainly on the particular characteristics of neuron cell types and their interconnections. But besides neurons, there's a lot of infrastructure inside the brain. For example:

Astroglia: They are a type of glial cells which participate in the formation of the blood-brain barrier (supporting the endothelial cells), nourishing of neurons, maintenance of ion and neurotransmitter concentrations, among others. They also keep in place most of the tissue.
Microglia: Small cells with immune (phagocitic) functions inside the brain.
Radial glia: A more specialized precursor cell, that also participates in neuronal migration in the brain.
Oligodendrocites: Cells responsible for the insulation (myelination) of axons.
Neuroepithelial cells: The stem cells in the brain.

Neuroglia, which includes the first four cell types above, accounts for ~90% of tissue in human brain (http://classes.biology.ucsd.edu/bipn140.WI13/documents/Gliamorethanjustbrainglue.pdf).

Also, when you collect some billions of axons, they can be quite representative in terms of mass and volume. The ratio between white matter and gray matter is close to one for humans, but lower for smaller mammals (http://www.pnas.org/content/97/10/5621.full.pdf).

About the last part of your question, the synaptic cleft (the space between pre-synaptic and post-synaptic neurons) is a salty solution: water with high concentration of sodium and chloride ions (and also calcium ions, neurotransmitters and a lot more). These ion concentrations are fundamental to the generation of action potentials, neural signaling, and the general dynamics of the brain.


Is it feasible to eradicate a virus without vaccines?

It is possible? I would say yes. But feasible... I think not. Consider this, once vaccinated, a person is usually immune to the virus. And you only need the vaccine to take hold, for an individual to acquire life time immunity. However with drug treatment... even once the treatment succeeds, the person can be reinfected. And you will have come back with drug treatment again.

Given the difficult in vaccination campaigns (ie polio) to eradicate the last reserved of a virus... I think a similar drug based campaign would a lot more difficult. There is no herd immunity to prevent the virus from reinfecting the wider population when it leaves its strong holds.


A constitutive or "housekeeping" enzyme is usually defined as an enzyme whose expression level (amount of protein) is always constant, independent of any environmental factors. Hence, regulation of constitutive enzymes must be post-translational, for example allosteric regulation of the enzymatic activity by substrates or products.

Note that constitutive enzymes is mostly a theoretical concept. There are probably no enzymes whose expression is completely unaffected by any environmental factor.


Is RNA polymerase affected by proteins bound to the coding sequence of a gene?

Nice question!
First of all make sure that you have multiple transcription stop / terminator sequences at the end of your first gene . This is quite standard procedure. Also in your case the phenomenon called transcription interference (TI) comes handy. Here's a review on TI. In short:

  the term TI usually refers to the direct negative impact of one transcriptional activity on a second transcriptional activity in cis.

Although TI is mostly defined as two transcription events affecting each other, at the low level the basis of it is that two proteins bound to the DNA affect each other's activity. Now since LacI's function is to inhibit transcription, thus it is strongly bound to the DNA and I'd say even if a polymerase somehow slips through the polyA signals at the end of the first gene it is likely to be stopped by the LacI already bound at the second promoter.

Alternatively you could put a weak promoter opposing the first gene and drive its expression, so it would collide with the oncoming polymerase from the first gene thus stopping it before reaching the second gene. Also here is another article on TI, that proposes a gene regulation network based on TI.


I would highly recommend you to look into the detailed descriptions (or even papers) of how gene prediction and genome annotation is done.
This is a very complicated problem and you seem to missing knowledge of many details that need to be considered, but also there is a lot known about how to do this right, so you don't have to solve this by yourself.

A few very important details, that you either haven't stated or are misunderstanding:

The the ATG codon is the start site of translation, but not the start of a gene. A gene encompasses a promoter (which are very hard to define/predict), 5' & 3' UTRs (untranslated regions) in addition to the open reading frame, which is marked by start & stop codons.
In addition the genomic (i.e. DNA) sequence will contain introns, which are usually much larger than the exons coding for the proteins, and may contain any sequences, so you can not look for codons there.
If you are working with species for which the genome sequence is already known (which is a big number of species), at least a 'rudimentary' gene prediction has very likely already been done. You can find the annotation of all identified features (like genes) in the genome annotation files corresponding to the genome, however this gets very detailed and complicated very fast.
If you are working with a newly sequenced species, where this has not yet been done you need to be aware whether you have genome and/or transcriptome sequences (the latter are important to find gene locations with high quality).


Does the repellence of an insecticide affect its efficacy (measured in insect mortality)?

You have a good hypothesis: the decrease in mortality is mediated by an increase in repellence. It sounds like you have a measurement of increased repellence, and it's a plausible mechanism (if an insect isn't near an insecticide, it can't be killed by that insecticide). Now you should test it.

If you are measuring repellence using a different assay (e.g., a choice assay, where the insect can enter a chamber with the insecticide vs. one without), than you could use as the denominator insects that enter the chamber with the insecticide. Compare mortality of insects that enter the chamber with insecticide changes with increasing concentrations in this assay with the mortality in your no choice assay.


It is a Rove beetle of the Genus Paederus.

Why Paederus sp.?

They are brightly colored  rove beetles, Coleopterans with short elytra.
Have metallic blue or green-coloured elytra.
Have bright orange or red on the pronotum and basal segments of the abdomen.

There are widely spread on the planet and I found two species of Paederus sp. that are found in East of Africa, together they are called Nairobi flies.

The medical condition it causes is called Paederus dermatitis.

  According to Medical and Veterinary Entomology (2009) "At least 20 of the more than 600 species of Paederus beetles have been associated with Paederus dermatitis", even though Paederus beetles do not bite or sting.

  This skin irritation results from contact with pederin, a vesicant toxin in the hemolymph of many but not all females in the genus Paederus.

  The toxin is manufactured, not by the beetles themselves, but by endosymbiont bacteria, probably some species of Pseudomonas.

  Three different genera of rove beetles, all members of the same subtribe Paederina, can cause paederus dermatitis: Paederus, Paederidus, and Megalopaederus.

Pederin

  Pederin blocks mitosis at levels as low as 1 ng/ml, by inhibiting protein and DNA synthesis without affecting RNA synthesis, prevents cell division...

This makes it also a potent antitumour agent.

  The manufacture of pederin is largely confined to adult female beetles—larvae and males only store pederin acquired maternally (i.e., through eggs) or by ingestion.

  It is a contender of the title of most powerful animal toxin.

  It is among the most potent animal products known, more so than Latrodectus venom, which is 15 times more potent than cobra venom.

  Ingestion can cause severe internal damage and intravenous injection causes death ...

Further Reading:

1. Dermatitis Paederus: About 06 cases occurred in Bun
ia,
Democratic Republic of Congo

2. STUDIES ON THE MECHANISM OF ACTION OF PEDERINE, 1968

References:

 1. Paederus

2. Pederin

3. Paederus dermatitis

4. Encyclopedia of Entomology

5. The Role of Natural Products in Drug Discovery

6. ChEBI

Note: I found the picture in your question is the same as that of Wikipedia's picture of Paederus.