Is casein hydrolysate the same thing as casamino acids?

Roughly, yes they are similar, but there are processing differences- the real difference is filtering. A product containing simply casein hydrosylate will only be roughly filtered with lots of peptides (like body builder products). Whereas casamino acids should be primarily clean/free amino acids (like nutrients for bacteria).

The actual manufacturing methods will be proprietary for the manufacturer... but you can trust that they are basically doing whatever works best to obtain the individual amino acids and/or whatever is cheapest for obtaining a useable product.

I have used bodybuiling and several other grades of casein products for growing bacteria. I have found that although various products may get the job done there are some serious drawbacks to casein products not intended for growing bacteria.

Differences include clarity of media, cleaning of glassware/fermenter/bioreactor, sudzing of aerated media, and the microorganism. Some microorganisms won't grow very well, and generally, those that can may still not grow quite as well or as fast... so that extra 10% or 20% cfus may be important (or maybe not since the price for quality may be 10 times higher).

The quality-features vs price must be weighed by the grower. Personally, I sometimes autoclave a cheap casein product in one (easy to clean) vessel then rag-filter it into another (then autoclave it again) for growing bacteria... but that's because I have about a thousand pounds of rough casein hydrosylate, and only a kg or so of casamino acids (for particular studies). This method does not eliminate all of the problems but it does reduce some of them.


Defining: Evolutionary (quantitative) Genetics and Population Genetics

According to Hartl & Clark on population genetics:

  "Population genetics deals with Mendel's laws and other genetic
  principles as they apply to entire populations of organisms.... also
  includes the study of the various forces that result in evolutionary
  changes in species through time."

According to Conner & Hartl also on population genetics:

  "Population genetics is the study of naturally occurring genetic
  differences between organisms; these differences are called genetic
  variation. Genetic variation is important because it is the raw
  material for evolution... to understand the purview of population
  genetics, we need to have a better understanding of populations and
  genetic variation"

According to Conner & Hartl on quantitative genetics:

  "Most phenotypic traits do not fall in to distinct categories, but
  rather are continuously distributed... These traits are called
  quantitative or metric traits because they need to be measured not
  just scored."

According to Falconer & Mackay on quantitative genetics (my personal favourite book on quant gen, which spends the first 5 chapters going through population genetics):

  "Quantitative genetics is concerned with the inheritance of those
  differences between individuals that of degree rather than of kind,
  quantitative rather than qualitative.... It is nevertheless a basic
  premise of quantitative genetics that the inheritance of quantitative
  differences depends on genes subject to the same laws of transmission
  and having the same general properties as the genes whose transmission
  and properties are displayed by qualitative differences.
  Quantitative genetics is therefore an extension of Mendelian genetics, resting squarely on Mendelian principles as its
  foundation."

Personally I would say that evolution is inescapably a population genetics process and (virtually) no study of it can be done without some understanding of population genetic principles. Many evolutionary genetics problems can be best dealt with using quantitative methods, and quantitative genetics is an extension of population genetic principles. Population genetics relies on selection, drift, mutation and gene flow - these are all key quantitative genetics.

Population genetics study focuses then on the four basic principles above from a (simplified) Mendelian view, while quantitative genetics deals with more realistic evolutionary genetic phenomena by allowing for, and assessing, genetic variance from many loci influenced by additivity, dominance, and environmental factors. Both fields are studies of evolutionary genetics, population genetics can be studied whilst ignoring quantitative genetics, but quantitative genetics relies on population genetics principles so I would call it an extension of - but not sub-field - of population genetics.


Do similar adaptations result in similiar genetic code?

It can be the case but it is not necessarily the case. You sure can have the same mutation happening and raising in frequency in two independent lineages but you may well also have different mutations leading to similar adaptations in different lineages.

Example

As you talk about humans, let's take an example from humans. The ability to digest lactose (milk) at adult age has evolve several times independently. I just copy-pasted from this answer of mine

  Gene LCT

  Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.

  Expression of LCT

  In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.

  Today, the inability to digest lactose at all ages in humans is called lactose intolerance.

  Three independent mutations

  Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different [SNPs][6] (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.

In this example we can know that the ability to digest lactose at adult age evolved at least 3 times independently. It is quite hard to tell whether it had evolved more than three times. It is indeed possible that the mutation G/C-14010 had occurred in two independent lineage but it would be hard to disentangle them today if the two lineages are not clearly geographically isolated (and in humans, very few populations are really isolated from the others).


What are possible health risks to women having large numbers of children?

A common problem for any woman who has experienced pregnancy and childbirth is damage to the levator ani muscle, which comprises a portion of the "pelvic floor."

 from here

This can cause a number of symptoms, including urinary incontinence (due to an increase in pressure on the bladder from less effective muscular support), and possible prolapse of the bladder, uterus, or rectum into the vagina, again due to the weakening of the pelvic floor.


This is an interesting an useful question about host-pathogen interactions. For a general reference (for both hosts with and without a competent CD4+ T-cell response) see Cecil Medicine, Ch.332, and Murray Medical Microbiology, Ch. 28. There is also a decent review in Lancet Infectious Disease that discusses the pathophysiology in immunocompromised hosts.
Overview / tl;dr
Tuberculous mycobacteria may not secrete any toxins or replicate quickly, but they are clever and persistent. Without an effective immune response, they will eventually overwhelm the lungs, spread to other organs, and kill the host through organ failure and/or embolization.  In these cases, infection is universally fatal if not treated. This is what happens in HIV patients with a low CD4+ T-cell count.
In hosts with a competent CD4+ T-cell response, infection is sometimes fully resolved and sometimes held at bay for many years without major organ damage.  In other cases, the immune system's methods are too powerful for the infected organ. Tissue damage in these cases is the direct result of prolonged activation of large fused groups of macrophages. Importantly, this is not an overactive immune response, it just happens to be too much for the local organ. You cannot treat TB by shutting down this immune response. If you block TNF-$\alpha$, for example (a major player in the cross talk between CD4+ T cells and macrophages), you end up with disseminated TB. The solution here is elimination of the pathogen with direct anti-mycobacterial treatment.
Initial Infection
In either an immunocompetent or immunocompromised host, tuberculous mycobacteria enter, e.g., alveolar macrophages through phagocytosis and, initially, prevent fusion of the phagosome with lysosomes, while allowing fusion with other vesicles. This allows the bacilli to live, access nutrients, and replicate within the macrophage.
Immunocompetent host
In the immunocompetent host, the interaction between the infected macrophage and CD4+ helper T cells leads to formation of an activated macrophage and either elimination of the mycobacteria or compartmentalization of the infection. Either of these outcomes are generally good for the host. Clearance of a pathogenic bacteria is obviously good. Latency in a walled off compartment is a close second.
The typical disease syndrome of pulmonary tuberculosis involves a brief, often unremarkable respiratory infection, followed by a long period of clinical latency. In many cases where the primary infection isn't fully cleared, latency may be lifelong, only to be discovered incidentally at autopsy. The brief illness followed by clinical latency corresponds to the infection of alveolar macrophages with an immune response that successfully walls off the infection.
In a host with generally capable CD4+ T cell / macrophage cross talk, if disease develops, it typically occurs after years or even decades of latency, through reactivation. Reactivation may be the result of a temporary failure of the compartmentalization strategy, with short term or partial immunosuppression due to age, some other illness or drug. It is sometimes the result of re-exposure. In severe cases, the result is a massive and damaging, but relatively slow immune response. This is not toxic shock syndrome or gram-negative sepsis. It occurs over month to years, with night sweats and weight loss. Fever may or may not be present. Tb is a slow burn. The OP is correct here, that the tissue damage seen in these cases (caseous necrosis, cavitary lesions, sometimes followed by hemorrhage), as well as the night sweats and weight loss, are all caused by the immune response, not directly by any toxin produced by the mycobacterium.
This lung (image from wikimedia commons) was chewed up by giant, angry macrophages, spurred on by CD4+ T-cells:

Immunocompromised host
This lung (image from a public slide set through the University of Utah), on the other hand, was not chewed up by giant angry macrophages, but was lethally infected with M. tuberculosis all the same:

In an immunocompromised host, the clinical syndrome is different. For an HIV patient with a low CD4+ T cell count, alveolar macrophages are not sufficiently activated. There are no large cavitary lesions, but they are also unable to clear or quarantine the replicating bacilli. This results in disseminated tuberculosis, sometimes with spread through the bloodstream to the brain, kidney, and bone, and devastating illness that is universally fatal without treatment. Death may result from organ failure (e.g., of the lung), infectious or non-infectious embolism.
Interestingly, in an AIDS patient with disseminated TB, when you combine TB treatment with HAART (highly active antiretroviral therapy), you can sometimes see a paradoxical worsening of symptoms. This is called immune reconstitution inflammatory syndrome, or IRIS. It may look like worsening TB, with fever and worsening lung function. The solution for TB-IRIS is not immunosuppression, but supportive care and, again, direct treatment with antimycobacterial therapy. Here again, the problem isn't an overactive immune response, it is the pathogen.


At an approximation the active sites of enzymes can be considered as having two aspects. The first relates to the catalysis — in this case the breaking of the glycosidic linkage. The second relates to binding the substrate. This review of the α-amylases by MacGregor et al. shows that there is a range of a-amylases, differing in this latter respect — their substrate specificity. In general there are binding sites for a varying numbers of glucose residues at either side of the bond being cleaved. This is shown in Fig. 3 of that review:

The important difference in the structure of glycogen and starch (amylopectin) — seldom mentioned in general biochemical or biology texts — is their patten of branching:

As this previous answer of mine to a different question explains, this results in a globular structure for glycogen granules in which only the ends of the chains are accessible. (The image below, from Protopedia, illustrates this better, especially if you imagine it in three dimensions.)

Hence the substrate-binding site of α-amylase does not have access to the residues that need to bind for it to perform hydroysis of glycogen, and, indeed, the enzyme that breaks down glycogen — glycogen phosphorylase — is specific for these free ends.

The α-amylases that can hydrolyse both α-1,4 and α-1,6 glycosidic links are quite few compared with those with specificity to one or the other type of linkage (see Table 2 of the MacGregor review, if you can obtain access to it). The impression obtained from following up two of the examples there is that the enzymes involved can exist in alternative conformations, the correct one of which is triggered by the substrate. An example is the glycogen debranching enzyme, the studies of which in Sulfolobus solfataricus and Candida glabrata can be read freely on-line. Although somewhat less directly relevant, the example of a Thermoactinomyces vulgaris neopullulanase is another variation on this theme.


As the other answer has already stated, there are cases of heart cancer. Just to expand on that answer further, according to this article, the rate of heart tumors is a mere 1.38 in 100,000 people per year and of that only around 10% are malignant (truly cancerous tumors) in nature. Just to put this into perspective of how low of a rate this is, the overall rate of cancer in the U.S. for both men and women combined is 352.2 per 100,000.[source]
Doing some rudimentary calculations, if the rate of malignant tumors is one tenth of 1.38 in 100,000, that means the rate of heart cancer is around 0.14 per 100,000! Just to add to how rare this is, the Mayo Clinic on average only sees around one case of heart cancer per year.[source]
Also, to clarify your statement about what types of cells can have cancer, it is not only dividing cells that can have cancer (even though the majority of cancer originates from cells undergoing a lot of cell division such as the skin and GI tract). While cell division by its nature causes a vast number of the mutations which would potentially lead to cancer, other environmental factors such as toxins and radiation could cause also cause similar mutations in cells that might not even be dividing.


You don't need any external library, it's enough to query Uniprot and extract the data you want from the response.

Here an example in Python 3:

from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/" + id + ".txt").read().decode()
result = data.split('SQ   ')[-1] #here all the info you need
mw = int(result.split(';')[1].strip().split()[0]) #extract the molecular weigth
print(mw)

If you want to batch query a lot of sequences then I suggest to sleep(0.5) after each query to avoid problems with their server.

Update

As correctly pointed out by @Jerven (see comment below), you can query the mass directly.

In this case, the code is the following:

from urllib.request import urlopen

id = "P42212"
data = urlopen("http://www.uniprot.org/uniprot/?query=id:{}&format=tab&columns=id,mass".format(id)).read().decode()
result = data.split('\n')[1].replace(',','')
mw = int(result.split('\t')[-1])
print(mw)


What is the name of the property of viruses that can go dormant in the host for 30 years?

As far as I know dormancy in viruses like the above stated chicken pox virus is known as virus latency which wikipedia defines as:

  The ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle.


How did giant sauropods satisfy their daily energy needs, considering their relatively small mouths?

Unlike mammals, saurischian dinosaurs don't have to chew their food. Like birds they have a gizzard to do that instead.

Look at a modern ostriches: they have a very small head because the head is only used to gather food not process it. Mammals process food in the head (chewing) so the head has to be large to support the muscles, teeth, and other apparatus for this. On the other hand, birds and sauropods use stones in the gizzard to grind up their food, so all that space is taken up in the torso instead of the head.  Ornithischian dinosaurs, which do chew, have large heads just like mammals.

Additionally since the mouth is not occupied chewing the time that would be lost chewing can be spent feeding instead. This can be a lot of time a cow spends 8 hours a day just chewing.

Source


After a bit of Googling I think I found it. It’s a pale tussock moth caterpillar. https://butterfly-conservation.org/moths/pale-tussock
It says it irritates the skin and can cause a nasty rash so I’m staying away for now.
I might risk moving it with a trowel and small tub though.


www.allergicliving.com claims that the cause to such an allergy is not the grass but is actually mold:

  Often patients will have allergy symptoms with fresh cut grass...That's not grass pollen allergy, that may be mold allergy from the molds being stirred up.

The site also mentions that simply having the physical presence of lawn mower "dust" in one's nose may cause symptoms.

Source: www.allergicliving.com/2010/07/02/outdoor-allergy-grass-allergy-attack


Why are dreams sometimes remembered and sometimes forgotten?

Scientists say that people can have multiple dreams every night and the ones that are not very significant are easily forgotten. Only those experiences that elicit an emotional response (happy, frightened) seem to stick in memory. Suggestions have also been made that being anxious or depressed makes our dreams stick to memory too (reference). A study suggests that people woken up during REM sleep seem to recall their dreams more often (reference). Here is a link to some common questions about dreams.


Tiny white very hard cell bug! Please help to identify!

Definitely an arachnid and mite (subclass Acari), and very likely a member of the order Parasitiformes, of which there are more than 100,000 species!!

The body plan is not all too different from a tick (order Ixodida), but the movement of your specimen in the video doesn't seem to match that of typical tick. As such, I next began examining species in the related order Mesostigmata.

Unfortunately, according to here, a clear detailed shot is needed to ID this specimen confidently:

  In most cases identification of Mesostigmata to family or lower can be accomplished only if the specimen is an adult female. The easiest way to determine the stage and sex of your specimen is to look at the intercoxal region.  Adult females have a genital opening that is almost invariably in the intercoxal region (species of Metagynella are exceptions) and covered by a sclerotized shield which may be truncate posteriorly or continue onto the ventral region.

However....

Mites just always seem to be associated with birds in urban homes, so I thought I'd do some google sleuthing....and voilà! I've found a near and reasonable match!

Specifically, your specimen looks quite similar to mites in the genus Ornithonyssus of the parasitic family Macronyssidae -- these are bird mites (or possibly rat mites). According to here,

  The tropical rat mite, Ornithonyssus bacoti, is one of the most common house invading species. The tropical fowl mite, Ornithonyssus bursa, and northern fowl mite, Ornithonyssus sylviarum, are also frequently encountered in homes. The latter two species are found principally on domestic or wild birds. The house mouse mite, Liponyssoides sanguineus, may also be found in structures with house mouse infestations. The tropical rat mite is a parasite on rats. Although none of these species are truly parasitic on humans, they bite people readily, often producing dermatitis and itching.

As for knowing the specific species, citybugs.tamu.edu suggests:

  Distinguishing between different species of Ornithonyssus mites to determine whether birds or rodents are the likely source is difficult and requires special expertise.

You can read more about Ornithonyssus bacoti, Ornithonyssus bursa, and Ornithonyssus sylviarum on Wikipedia, and you can see videos of these mites crawling on people here and here.

According to here, Ornithonyssus bacoti can be found as far North as Iceland.

 See below for images:

 Rat mite (Ornithonyssus bacoti). <1 mm;  © Erling Ólafsson; Source: www.ni.is

 Ornithonyssus spp.; Copyright 2014 Tom Murray; Source: bugguide.net

Note: I do not know this group of organisms well, so my answer serves as an (educated) guess to get you on the path toward proper identification...


What is the current theory of sexual orientations in Biology?

It seems we have more hypothesis than theories.

There is a book called "The Moral Animal", by Robert Wright, where he cites some researches relating order of birth with sexual orientation (of course, not a 100% direct relationship). That's for the proximal cause. For the distal cause (evolutive) it makes sense to me that we are a sort of "eusocial" species, with homosexuality having evolved for the fitness it adds to the family: having lots of offspring, it's benefitial for the family if a few of them don't reproduce, investing instead in other fields of knowledge, like medical herbs, technology, weapons, etc. This may explain why this behavior evolved in first place, and why it's so widespread in virtually every known human culture, and almost all families.

Biologist Alfred Kinsey founded the Kinsey Institute (kinseyinstitute.org) for the study of human sexuality. His theory (that also appears in the movie Kinsey) was that there is a gradient from totally homosexual to totally heterosexual, with many intermediary degrees. Our religious culture tries to "erase" this diversity because of platonic ideals of "perfect male" and "perfect female", but in Amazon I saw that people are much more "plastic" than that, probably because of the lack of power of such religious traditions. Historians also talk about homosexuality as a "usual practice" in pre-Colombian America. And it is said that China have no problem with homosexuality before the arrival of monotheists. In India, homosexuality became a crime only 3 years after the british invasion (so it seems it was very common there, too).


What are the limitations to current nucleotide sequencing technologies?

It seems like you answered your own question,the signal from a few molecules running through an enzyme or a polymerase tend to fall out of synch after a few hundred bases.  If an enzyme for sequencing was more rigorously in time step that could help for instance.  The machines read traces in four channels with nice bumps for each base.  See this article for a nice example. You can see that if there are too many of the same base consecutively it gets hard to tell how many bases there are there.  Over time all four traces will start to smear out and you cant tell Adam from Thelma if you take my meaning.

But there are other bottlenecks.

The sequencers currently put out such a high volume of data that the analysis of the meaning of the output data can't be analyzed fast enough.  This follows the trend in biotech over the past 12 years or so - more sequence data, micro array data, more mutation data, more genomes than people who can actually use it to understand the biology.  There is a bit of an analysis bottleneck now.

So some of these sequencers have greater read lengths, which can make it easier to assemble a sequence.  These sequencers generally cost more.  For instance if you have a library to sequence a little fungal or algal genome - you will get the answer back in a day or less now.  In the form of 1 Tb of reads maybe 50 to 200 bp long.  It might take quite a bit of time to put that together into a novel genome sequence, still more to find the genes, build the gene networks from a template of pathways etc.  Just imagine a thousand sequencers pumping out day and night and you get the picture  I'm trying to paint here.

About cost.  Ion Torrent and the new oxford nanopore sequencers are really cheap - \$50k to perhaps \$900 for Oxford Nanopore's USB sequencer.  Most other systems cost hundreds of thousands of dollars.  Ion torrent and Nanopore have more disposables - you throw away a chip or even the entire sequencer - at a cost of hundreds of dollars a sample.


How many Endogenous Retroviruses do we share with other primates?

There are several papers that cover this. Briefly, humans share the vast majority of their ERVs with other primates, but not all; and this is mainly because other primates have acquired ERVs that humans have not (rather than humans acquiring new ERVs themselves).  The third link, in particular, seems to cover your proposed reconstruction and concluded that in general "these sequences gave trees that were consistent with the well established phylogeny of the old world primates".

Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees
The decline of human endogenous retroviruses: extinction and survival
Constructing primate phylogenies from ancient retrovirus sequences


Whether something is considered a topographic barrier for an organism depends on the species being considered and its ability to traverse the terrain from one side of the barrier to the other. There's no blanket classification of what is considered a topographic barrier and what isn't.

For example, a certain mountain range may be a topographic gradient to a salamander (due to limited food, extreme weather conditions, etc.), but these same mountains might not be for a brown bear.


I've pondered this question too.  It's very clear that when we sneeze, the expelled air comes mostly from our mouths.  However, at least as far as my own sneezes are concerned, some of the air comes from my nose as well.  I know that if I pinch my nose closed as I sneeze, my ears hurt and pop.  If my nose is sniffly, I usually notice mucus come out.  Our soft palate partially lowers and our tongue rises as we sneeze, in order to divert a portion of the air up into our noses.  That position of our tongue is why our sneezes make a CHHH sound. If people intentionally keep their mouths wide open as they sneeze, that could explain why nothing comes from their nose, as there's nothing to divert the air.


It simply means a two dissimilar viruses. If you read the paper Falk and Bruening, they are worried that if you place a viral gene in a plant (here we call that the transgenic gene), then natural viruses may "mix" it's genes with the transgenic genes and create a superior virus. The thought is, you are speeding up the evolution of the virus by taking a beneficial gene from a non related (non homologous virus), something that would probably take a long time.


It think this spider is a Tegenaria domestica also known as the barn funnel weaver in North America and the domestic house spider in Europe. See here or here (picture taken from the first link):

They are not poisonous and usually avoid confrontations, but can bite.


Those are the cotyledons (seed leaves) of spinach.

For comparison, here's a picture of what spinach sprouts look like:

Source: https://wimastergardener.org/article/spinach-spinacia-oleracea/


You are right but a small correction: P represents primary producers. So the answer is just dead plants or tissues such as broken branches.
Death, excretion because of turnover (which includes urine or other metabolites), tissue turnover (shedding of dead cells, molting etc)
Maintenance, locomotion, repair, immunity


How exactly do mosquitoes navigate directly on target?

Mosquitoes do not rely on a single cue to find its host. It is the combination of CO2, temperature and odor cues, that makes mosquito an efficient blood feeder.
 These two papers might help you in understanding how mosquitoes target their hosts.

Genetic analysis of mosquito detection of humans

Multimodal Integration of Carbon Dioxide and Other Sensory
Cues Drives Mosquito Attraction to Humans


What are the white dots on the tree in this photo?

I'm not 100% sure, but I think they look like scale insects (Coccoidea). In particular it looks at bit like a hermaphrodite cottony cushion scale insect (Icerya purchasi)...

The white fluffy thing underneath the insects is the ootheca (egg case). The mature insect migrates to the main trunk of its host tree and attaches to the bark. It then secretes the cottony sack between itself and the bark. Hundreds of eggs are laid into the case, which eventually hatches and the nymphs disperse to the tips of branches where they feed on leaves. As they get older they gradually move first to twigs, then to branches and finally back to the main trunk to breed again.


Software to calculate Fst from sequence data

If You are familiar with R, try package adegenet. It contains very nice tutorials explaining its usage, including the very R basics. If You require graphical interface, install RStudio - very nice front-end for R. There are more possibilities how to calculate Fst in R, but adegenet is one of the most powerful genetic packages there.


Genetics of Cystic fibrosis

Cystic fibrosis is caused by an autosomal recessive allele. We therefore know that the frequency of the homozygote recessive allele is $P_{aa} = \frac{1}{2500}$, where $a$ denotes the recessive allele and $A$ will denote the dominant allele.

Solving the problem

The probability of the second child (from a second husband) has cystic fibrosis is the probability that a second husband is heterozygous ($P_{aA}$) times the probability that this father will transmit the recessive allele $a$ ($\frac{1}{2}$) times the probability that the mother transits the recessive allele $a$ ($\frac{1}{2}$, note that we know the mother is heterozygous as she is healthy but already had a child that suffers from cystic fibrosis).

So the answer is $p_{Aa} \frac{1}{2} \frac{1}{2} = p_{Aa} \frac{1}{4}$, we only need to calculate $p_{Aa}$. Let $x$ denote the frequency of the recessive $a$ allele, then $P_{Aa} = 2 x (1-x)$ at Hardy Weinberg equilibrium. As we know $p_{aa}=\frac{1}{2500}=x^2$, it results that $x=\sqrt{\frac{1}{2500}} = \frac{1}{50}=0.02$. Therefore, $p_{Aa}=2 x (1-x) = 0.0392$. The final answer is  $p_{Aa} \frac{1}{4} = \frac{0.0392}{4} = 0.0098 ≈ \frac{1}{100}$.

What you did wrong

You were pretty close to the right answer. In your calculations you multiplied the frequency of the recessive allele $a$ (which I called $x$) by $\frac{1}{4}$ but you should have multiplied the frequency of heterozygote genotypes (which I called $p_{Aa}=2 x (1-x)$) by $\frac{1}{4}$.


How are limits determined for systotic and diastotic blood pressure?

120/80 are not upper limits on blood pressure - many people have blood pressures far in excess of those numbers. Instead, these are numbers beyond which studies have shown connections to negative health outcomes - heart disease, for example.

There is nothing magical about the numbers 120 or 80 besides their divisibility by 10; a blood pressure of 121/81 is no more risky than 120/80 than 122/82 is over 121/81. Because of this, drawing a hard line isn't possible - it's just a suggestion.

Typically, systolic pressures less than 130-135 aren't given any special consideration beyond normal advice to exercise and eat well, unless there are other conditions/risks. Guidelines from the American Heart Association and the UK's NHS are to consider treatment only for diastolic pressures above 140mmHg. There has been some disagreement about these precise limits, with some recommendations for lower targets, for example here. Some of the disagreement seems to be the types of interventions - the guidelines to treat diastolic hypertension only above 140mmHg are mostly considering medications, whereas the guidelines to treat prehypertension are aiming for improved lifestyle: diet, exercise, etc.


If a bacterium had a protein on its surface that humans also have, would it cause an autoimmune disease?

It's believed that many autoimmune cases are triggered by what you describe - pathogens or opportunist bacteria and viruses that contain proteins similar to human proteins.For example:

Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy
Translocation of a gut pathobiont drives autoimmunity in mice and humans
Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease

However, it's important to understand that although these cross-reacting proteins may be required in the process of autoimmunity, they aren't sufficient to cause autoimmunity alone (or else everyone would have autoimmunity all the time). Autoimmunity needs to have a whole bunch of steps, including several pieces of genetic susceptibility and environmental conditions, before the specific trigger will cause a problem (and it's likely that once the many other conditions are satisfied, there are multiple potential triggers that can set up the final cascade).


What type of genetic changes occurs when ovaries or uterus are removed from female body?

welcome to biology stackexchange!

In the classical way we think of the body, there won't be a lot of genetic changes if the ovaries, uterus (or the testes for that matter) are removed from the body.

The main effect would be that the sex hormones that are produced in these organs would no longer be present and this would have a profound effect. So the broad answer might be 'no genetic effects but large endocrine changes'.  Endocrinology is the study of glands and their function in the body. Growing cysts, tumors as well as other effects seem like reasonable effects to see for such a drastic change in the body as removing the reproductive organs.

If I were hard pressed though probably this might end up with some small genetic effects compared to an individual who had never had the organs removed.  Mutations happen frequently in many of our tissues and also they respond to the environment to methylate the genome and modify it in non-genetic ways ( known as epigenetic effects).  This is purely conjecture but its also found that nearly everything has some effect on the cells.

hope this helps.


Is there a biological environment that we can we assume glutamate exists as glutamic acid?

At typical physiological pHs glutamate does exist as glutamate.

Broadly the acidity in the digestive track is enough to reduce glutamate to glutamic acid. The stomach for example has a healthy pH of between 1.5 to 3.5.

Canadianer points out in the comments that the active site during catalysis are protonated. There are obviously a lot of examples of this and sensitive evaluation by looking at the isocontours and surface potential of the protein structure are needed to draw conclusions if this might be important.


RNA-Seq library construction challenges: the biases of RNA fragmentation vs cDNA fragmentation

Good question, a lot of this is still being figured out. Here's what's known so far:

Fragmentation methods based on restriction enzymes aren't random.

Reverse-transcription performed with poly dT-oligomers, which bind to the 3' poly-A tails, is strongly biased towards 3’ end of transcripts.

Reverse-transcription with random hexamers results in an under-representation of 3’ ends. This is from the reduced number of priming positions at which the reverse transcriptase enzyme can start cDNA synthesis.


How can we digest lactose even though it has Beta glycosidic linkages?

One simple  reason is physical interaction.
lactose is only composed of two sugars, while cellulose is giant network of interlocked sugars. Cellulose keeps the sugars tightly packed in three dimensions. even getting to the bonding site is difficult.
human and many other lactases are a huge molecules that would never be able to fit on to a cellulose chain, while cellulase of often a tiny molecule as enzymes go and the active site is not buried in the center. Compare the two enzymes.

lactase

two different cellulase enzymes
Note the big difference in size. Also look at cellulase in action.

Notice it has to peel up the cellulose strip by strip, while lactose is just floating free in solution. This even limits the speed of cellulose breakdown. which means organisms that breakdown cellulose have to spend a log time doing it, while humans have a relatively short and fast digestive timeframe, so even if we could we would not get much from it.
These functional limits also makes a cellulase enzyme harder to evolve, since it can't be too large or in organisms with fast digestive processes.  We often forget the physical necessities of enzyme function. there are plenty of other reasons enzymes do not function on multiple substrates, but this is why is basically impossible to for evolution to change lactase into a cellulose cleaving enzyme.


Grafting vegetables onto fruit-bearing trees

For grafting to "take", the the two plants' vasculatures have to be organized similarly. This is not possible for two such differently organized stems as a pepper and an apple.

This is a cross section of a young woody stem (such as an apple, though this example is a tilia):

This is a cross section of an herbaceous stem (such as a pepper):

You can see there is dissimilarity in organization. Furthermore, herbaceous plant stems die back in the winter.

Even if possible, grafting an herbaceous (non-woody) stem onto a woody stem (e.g. apple) would not confer any advantage for the green pepper, a tender annual, and would be disadvantageous to the woody stemmed tree (pruning for no reason, when the branch would otherwise have produced apples, and the leaves performed their useful functions.


How can a blood test give information about rickets?

From the Wikipedia article I linked to in your question:

  Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones.

There is also a rare genetic form of rickets called Vitamin D-resistant rickets or X-linked hypophosphatemia that can be diagnosed by DNA sequencing of cells collected by a blood draw.

It should be noted that, at least in the case of rickets, blood tests alone will not diagnose the disease. There are many other possible symptoms of the disease, so a patient presenting with one or more of these symptoms may also be subjected to a blood test to confirm the diagnosis, not just make it on its own.


I-3 can be either A'A' or AA'. In Huntington's disease or Achondroplasia, the father could still survive to adulthood and reproduce. If the father had a chromosomal disorder such as Kallman's syndrome, he would be unable to reproduce. However, this is not a simple mutation, and it is not heritable. You should ask your instructor to clearly define the problem.


How much energy does a small spider expend per day just waiting for its web to vibrate?

Short answer
Approximately 240 J on a daily basis.

Background
Ballesteros et al. (2018) modeled basal metabolic rates of insects. They reckoned that endotherms, like insects, basically use energy directly correlated to the number of cells, which is linearly correlated to their body mass. They checked their model with experimental data from Chown et al. (2007) (Fig. 1).

Acknowledging that arachnids aren't insects, but that both are arthropods, let's take an average-sized web making spider, like the black widow, weighing in at 1 g. This yields a basal metabolic rate of 10 J/h, or 240 J/day. However, and given the linear correlation between energy expenditure and mass, a dwarf spider weighing in at 1 mg expends 1000 times less, and a Goliath bird eater approaching 200 g will expend 200 times more.

To convert the unit for the Black widow to a Watt scale, we get 1 J/s that corresponds to 1 W, so 1 J/h corresponds to about 0.3 mW.

Fig. 1. Base metabolic rate for insects. Data from more than 300 species were extracted from Chown et al. (2007). source: Ballesteros et al (2007)

References
- Ballesteros et al., Sci Rep (2018)
- Chown et al., BES (2007); 21(2): 282-90


What are the environmental conditions for larval Haemonchus contortus to survive?

Lowest temperature
2, 3, 4 and 5 week beakers containing eggs and non-infective larvae in lamb faeces didn't develop into infective larvae (L3) when exposed to fluctuating temperatures ranging from -1 to 15°C:

[...] there were no signiﬁcant differences in the number of harvested larvae
at the different time points for the faeces incubated at 15°C.
However, at 5°C and -1 to 15°C no development of eggs occurred,
although it was found that a small proportion developed into infective
larvae when incubated at 25°C for an extra week.
(1)

Highest temperature

Temperature of 40ºC negatively correlated with the survival rates of
H. contortus L3. [...]
Decreased motility was observed on day 10 after heating. [...]
Heating of L3 at
higher temperatures (45ºC and 50ºC) caused 100% lethality as early on
hour 48 and 24 of exposure
(2)

Desiccation
When it comes to dessication, there are three main things to take into account:

whether the larvae are in exsheathed or ensheathed state matters
they can survive several dessication/rehydration cycles
it is best survived below freezing temperatures

The experiments on desiccation survival showed that, after a few hours
exposure to 47% R.H., all exsheathed larvae died and all ensheathed
larvae survived. (3)

Desiccation protected the larvae against death on storage at
temperatures below freezing, but it was harmful at temperatures above
freezing. (4)

Ruminant larvae were able to survive up to 7 desiccation/rehydration
cycles, and, during anhydrobiosis, metabolic activity was decreased
and survival of the larvae was prolonged both in the laboratory and in
the field. (5)

pH

The effects of temperature on survival and development of the
free-living stages of H. contortus have been studied both by faecal
and by agar-culture methods. [...] with a pH range from 6.5 to 8.5 (6)

How long?
As usual, depends on the current environmental variables and current state of the organism and so forth. Read above sections. The article by P. T. Iliev, A. Ivanov, P. Prelezov has a few tables that can give you a good idea of these times (at least for temperature and humidity).

(1) The development and overwintering
survival of free-living larvae of
Haemonchus contortus in Sweden,
K. Troell, P. Waller and J. Höglund
(2) Effects of temperature and dessication on survival rate of Haemonchus contortus infective larval stage, P. T. Iliev, A. Ivanov, P. Prelezov
(3) Desiccation Survival of the Infective Larva of Haemonchus Contortus,
C. ELLENBY
(4) Effect of dessication on the survival of infective Haemonchus contortus larvae under laboratory conditions,
Kenneth S. Todd, Jr., Norman D. Levine and Paul A. Boatman
(5) Anhydrobiosis increases survival of trichostrongyle nematodes (abstract only),
S E Lettini, Michael Sukhdeo
(6) Trends and Perspectives in Parasitology 2 (page 84),
B. A. Newton


Is it in principle possible to revive an extinct species having no living relatives?

This may absolutely be possible. Check this for some info. But really it appears that using somatic nuclear transfer, using the same principle used to generate Dolly, we may be able to recreate an extinct species by swapping in the genetic material into a new cell. One current problem that we face with this is that while the genetics should be fine in nuclear transfer, controlling proper epigenetic programming is difficult.


EDIT: Thanks a lot to @abukaj for pointing out the mistake in my answer (and to @paracetamol for asking such a beautiful question). I am rewriting my answer to incorporate the (hopefully) correct background knowledge this time.

NEW ANSWER: As @paracetamol and @AlanBoyd (in their answer) pointed out the lack of credible support for the claim that infants produce rennin/chymosin, the previous answer attributing the digestion of casein in infants to chymosin had to be corrected. So, lets now look at the other possible candidates for casein (or, more specifically, $\kappa$-casein) digestion in infants.

As Martin et. al. (2016) claim, milk casein has some bioactive roles, such as forming masses with calcium and phosphorus1. Also, infant milk formulas mostly have higher casein content than human breast milk, making the former harder to digest than the latter. Back to the digestion point, human breast milk is known to contain many proteases in itself, including anionic trypsin, elastase, plasmin, cathepsin and kallikrein, while prothrombin has also been identified in human colostrums2. In fact, Ferranti et. al. (2004) also identified fragments of casein created by plasmin cleavage3. However, Chatterton et. al. (2004) were able to detect $\beta$-casein after 1 hour of in vivo gastric digestion in 8 day old infants, but not in 28 day old infants, suggesting the increase of digestive capacity of the infants4. This increase can be attributed to the development of gastric acid production system in the infants. For the case of newborns, Nakai and Li-Chan (1987) suggested that Pepsin C, also called gastricsin, can hydrolyze casein at the pH range of 4-5 (the lowest pH newborns can reach)5. However, the buffering effect of human and bovine milk proteins does not allow the gastric pH to reach the optimum pH required for activity of pepsin A and pepsin C.

How, then, is casein digested by infants at all? This is summarized (to some extent) by Chatterton et. al. (2013), according to which, although gastric pH is unable to reach the optimum pH for pepsin activity, it is sufficient for minor initial digestion of human milk proteins. This causes the release of glycomacropeptide, the C-terminal portion of casein. The combination of this initial digestion and the gastric pH, close to the pI of caseins (~ pH 4.6) causes precipitation of caseins and slowing down of their digestion. The casein peptides, on the other hand, are absorbed into plasma where they show a number of biological activities, including inflammation modulation and blood pressure regulation6.

Thus, even though infants lack chymosin and a fully mature digestive system, this is compensated by a combination of proteases in breast milk and the slower digestion process until the digestive system of the infants develops completely.

source

References:

Martin CR, Ling PR, Blackburn GL. Review of Infant Feeding: Key Features of Breast Milk and Infant Formula. Nutrients. 2016;8(5):279. Published 2016 May 11. doi:10.3390/nu8050279
Dallas DC, Underwood MA, Zivkovic AM, German JB. Digestion of Protein in Premature and Term Infants. J Nutr Disord Ther. 2012;2(3):112. doi:10.4172/2161-0509.1000112
Ferranti, Pasquale & Vittoria Traisci, Maria & Picariello, Gianluca & Nasi, Antonella & Boschi, Velia & Siervo, Mario & Falconi, Claudio & Chianese, Lina & Addeo, Francesco. (2004). Casein proteolysis in human milk: Tracing the pattern of casein breakdown and the formation of potential bioactive peptides. The Journal of dairy research. 71. 74-87.
Chatterton DEW, Rasmussen JT, Heegaard CW, Sørensen ES, Petersen TE. In vitro digestion of novel milk protein ingredients for use in infant formulas: research on biological functions. Trends in Food Science & Technology. 2004;15:373–383
Nakai, S. and Li-Chan, E. (1987) "Effect of Clotting in Stomachs of Infants on Protein Digestibility of Milk," Food Structure: Vol. 6: No.
2, Article 8.
Chatterton, D. E. W., Nguyen, D. N., Bering, S. B., & Sangild, P. T. (2013). Anti-inflammatory mechanisms of bioactive milk proteins in the intestine of newborns. The International Journal of Biochemistry & Cell Biology, 45(8), 1730–1747


The Human metabolome database (HMDB) contains many MS/MS and NMR spectra for human metabolites. You can acquire the spectra from the downloads section. The HMDB includes external identifiers for each compound. This includes the PubChem Compound IDs that are given on the NCBI database. There are 2 265 compounds with LC-MS/MS spectra in the HMDB.

The excellent MS-DIAL software package also comes with extensive positive and negative ion mode LC-MS/MS and GC-MS/MS spectral libraries in flat text format; that's also worth a look.

A lot of the raw spectral data is restricted due to multi party agreements (NIST, chemspider).


Can a vaccine or antidote be administrated via gases or sprays?

There are a number of currently used aerosolized vaccines throughout the world. Generally, these are studied and administered in single individual doses. There are advocates for the use of larger, sealed exposure chambers for rapid administration of vaccines to large numbers of people, possibly in the field, for example in a tent like this figure from the earlier linked reference.

The primary barriers for a general release of a vaccine or other medication as, e.g., an aerosolized spray, would be ethical (difficult to get consent from all potential exposed individuals) and dose related (difficult to ensure a specific safe and effective dose).

The closest natural experiment I'm aware of would be the use of live attenuated Sabin oral poliovirus vaccine. Unlike other currently used vaccines, the Sabin vaccine is transmissible. In developing countries, vaccine is transmitted from vaccinated individuals to un-vaccinated individuals through the fecal contamination of food and water, using the same route that wild type poliovirus is transmitted. This can result in extending immunity beyond those who directly receive the vaccine. You could conceptualize this as blanketing a local population with vaccine. It's not without problems, though, because in cases where the overall initial vaccine coverage is low, circulation of the vaccine can eventually result in reversion of the reservoir of previously non-virulent (attenuated) vaccine to a virulent type. This is how you get vaccine derived polio outbreaks, and one of the reason not to use transmissible viruses as vaccines.


Why is Fast Fourier Transform applied to raw EEG data?

Fast-Fourier Transform (FFT) transforms a signal from the time domain into the frequency domain. Basically, any time-dependent signal can be broken down in a collection of sinusoids. In this way, lengthy and noisy EEG recordings can be conveniently plotted in a frequency power-spectrum. By doing so, hidden features can become apparent. By adding all the sinusoids up after FFT, the original signal can be restored, so no information is lost.

A notable application of FFT in EEG is shown in Fig. 1, which shows an EEG in an awake person (top blue trace) and an EEG in a propofol-sedated person (bottom red trace). The traces are different, but exactly how different? Scientists like to quantify stuff.

Now look in Fig. 2, which shows the same data but filtered in the delta band (low-pass filtered EEG with a cut-off frequency of 1.5 Hz, left panel). Here it already becomes more apparent what's going on, but what exactly is the difference between the two traces? That difference becomes readily apparent in the frequency domain by using FFT (Fig. 2, right panel); The frequency spectrum has a peak at 0.2 Hz in both traces, but that peak is about twice as big in the anesthetized state than in the normal state. In other words, the anesthetized brain reveals more low-frequency activity.

Fig. 1. Raw EEG of an awake person (blue) and propofol-anesthetized person (red). source: Wang et al (2014).

Fig. 2.  Filtered EEGs (<1.5 Hz) of an awake person (blue) and propofol-anesthetized person (red) (left panel) and corresponding FFT spectra (right). source: Wang et al (2014).

This is reminiscent of the drowsiness encountered in slow-wave sleep; which is yet another example of why FFT is useful; various stages of sleep are markedly different in their EEG. For example, early stages of sleep are characterized by slow-wave EEG, while REM sleep is characterized by high-frequency EEG activity. By using FFT, these differences in frequency content can be captured in simple, quantifiable data.

Another widely applied FFT-based application is filtering in the frequency domain. Look at the sleep EEG in Fig. 3. By splitting the raw signal up in frequency bands, the noise can be removed (high-frequency components), but even better, the k-complex (a characteristic hallmark of normal sleep) can be beautifully isolated from a messy EEG signal (bottom trace, 12-15 Hz).

Fig. 3. EEG FFT-based filtering. source: Neurology

Reference
- Wang et al., Front Syst Neurosci (2014); 00215


What does "This variant falls on 11 transcripts in 3 genes" mean in the output from GnomAD?

In this particular case, there is another unannotated gene at the same locus, running in the opposite direction as SAMD11.

http://grch37.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000268179;r=1:865499-865579;t=ENST00000598827


Gene silencing: relative or absolute number of methylated CpG sites?

Generally, robust silencing by DNA methylation requires that all or most CG sites be methylated and that there are a good number of CG sites to methylate.  (A 'good number' is relative to each species depending on CG content of the respective genome.)

A promoter with ~10% of its CG sites methylated would not likely be silenced.  However, the caveat with this is that one well-placed methylated CG can cause silencing or at least decreased promoter efficiency.  Also, many promoters are depleted for CG, which means they can be fully methylated, but still not have much absolute methylation.  These promoters can be active despite apparent 'hypermethylation' in the CG context.  Also, a caveat to this is that promoters with zero methylation can be silenced, even if they have CG sites.  Basically, if CG methylation is important in the regulation of a gene, it will have CG sites in functionally-important parts of the promoter.  The promoter will be well-methylated when the gene is silenced, but because placement of de novo CG methylation is not absolutely perfect, there is a high likelihood that there will be more methylation than is needed for silencing to be achieved.  A sort of overkill phenotype.

This paper from the Schubeler lab is a nice foray into the mammalian promoters, which they break into 3 different groups depending on CpG content, and then further analyze each group for CG methylation profiles.


To me it seems to be an Araniella Cucurbitina ,also called a cucumber spider. It grows upto 4mm to 6mm. This type is native to the UK and they have venom which is not considered dangerous to humans.


It reminds me of the smooth-barked Australian gum trees / eucalyptus, like a salmon gum, ghost gum, etc.

Although there are no squirrels in Australia :)

This photo of a Salmon Gum is from http://www.fpc.wa.gov.au/content_migration/plantations/species/arid/salmon_gum.aspx


See the Wikipedia entry for nuptual flight.

The ants that you see most often are (wingless) female workers. The winged ants that you see are male drones whose only role is to fly with young queens for mating. The drones follow a different developmental pathway, emerge from the pupa as winged ants, and then wait in the nest until conditions are right for the big event.


Osmosis is defined as the flow of water/solvent molecules through a semipermeable membrane from a region of low to high solute concentration, until equilibrium is established.
To counter osmotic flow, some pressure must be applied to the solution in order to prevent pure solvent from going through the semipermeable membrane separating the two liquids; this is known as the osmotic pressure.
The osmotic pressure is the pressure required to counter, not sustain, osmosis.
The osmotic pressure can be approximated by using the following formula: $\Pi = i M R T$ .
U- Tube showing osmotic pressure. On the left side of the U-tube is an aqueous solution, and on the right side is pure water. The pure water is trying to dilute the solution by travelling through the semipermeable membrane. Eventually the added weight of the extra water on the left causes enough pressure to stop osmosis.
Osmotic pressure is the pressure that needs to be applied to a solution to prevent the inward flow of water across a semipermeable membrane. Osmotic pressure can also be explained as the pressure necessary to nullify osmosis. One way to stop osmosis is to increase the hydrostatic pressure on the solution side of the membrane; this ultimately squeezes the solvent molecules closer together, increasing their “escaping tendency.” The escaping tendency of the solution can be raised until it eventually equals that of the molecules in the pure solvent; at this point, osmosis will cease. The osmotic pressure is the pressure required to achieve osmotic equilibrium.
Osmotic pressure. Osmotic pressure is the pressure required to stop osmosis.
The osmotic pressure (II) of an ideal solution can be approximated by the Morse equation:
$\Pi = i M R T$
Here, i is the van ‘t Hoff factor, M is the molarity of the solution, R is the gas constant, and T is the absolute temperature in Kelvin. We can see from this equation that the amount of solute present in the solution will directly affect the osmotic pressure of the system.
Example
What is the osmotic pressure of a 1.35 M solution of NaCl at 25 $^\circ$C?
First, fill in all of the necessary information, and then solve:
i = 2 (NaCl breaks into two particles)
M = 1.35 $\frac{moles}{L}$
R = 0.0821 $\frac{L\times atm}{K \times mol}$
T = 25 $^\circ$C + 273 = 298 K
$\Pi = 2 \times 1.35 \times 0.0821 \times 298$
$\Pi = 66.1\ atm$


Adding the Propionyl-CoA Pathway to E.coli

If I understand it correctly the pathway goes: Acetyl-CoA --> Propionate --> Proprionyl-CoA --> ... --> 3-HP

Not exactly. The first reaction is:
$propionate + acetyl\textrm-CoA \rightarrow propionyl\textrm-CoA + acetate$
The CoA group is transferred from acetate to propionate. The following reactions are an oxidation to acryloyl-CoA and a subsequent hydration to 3-HP-CoA. Lastly the CoA group is transferred back to acetate.

Propionate is a 3 carbon molecule and so is 3-HP. So stoechiometric coefficients of 1 seem logical.


Difference between fertilin and fertilizin

Welcome to Biology SE.
Coming to your question, Fertilin and Fertilizin are different.
Fertilin
Fertilin is a sperm surface protein with an essential role in fertilization. It is required for the migration of spermatozoa through the oviduct, for binding to the zona pellucida, and for efficient binding to the egg plasma membrane. Fertilin consists of two subunits, fertilin alpha and beta, both of which belong to the metalloprotease-disintegrin protein family (ADAMs). Fertilin alpha and beta are made as larger precursors that are processed proteolytically at different stages of sperm maturation in the testis and epididymis. Fertilin alpha is processed first, most likely by a pro-protein convertase in the secretory pathway of testicular cells. Fertilin beta is processed later, while spermatozoa are in transit through the epididymis.(taken from this reference 1) Thus this protein is present in Sperm.
Fertilizin
Fertilizin is sperm-agglutinating substance (glycoproteins) present on Zona pellucida layer of the egg surface. Antifertilizin-fertilizin complex play a key role in sperm penetration. (Have a look at reference 2 &3 ). Thus, Fertilizin is present on egg surface.
Now look back at the images you provided with your question. Role of Ferilizin and fertilin-beta are clearly given.
References:

https://pdfs.semanticscholar.org/0043/f4525b6158d91a00682b86b1b9b15f726125.pdf

https://www.nature.com/articles/169548a0

https://www.journals.uchicago.edu/doi/pdfplus/10.2307/1537786


What's the difference between protein and DNA behaviour during agarose gel electrophoresis?

There are two important properties that determine how a molecule will move during gel electrophoresis:

size and shape of the molecule
charge of the molecule

You're applying an electric field, and all molecules will move according to their charge. The gel itself hinders the movement of larger molecules. This means that small molecules will move further than large molecules.

Nucleic acids like RNA and DNA have a uniform negative charge from the phosphate backbone. This means that they will generally separate according to their size and shape (plasmids can be present in different forms like supercoiled, circular or linearized).

Proteins have different charges, some have a positive charge at the pH typically used for gel electrophoresis, some have a negative charge, and some have no charge at that pH. So if you would simply run proteins on a gel, some would move backwards, some forward and some not at all.

To make the proteins separate according to their size we use the detergent SDS to denature the proteins, and to give them a uniform charge (SDS is negatively charged). Proteins are also run on polyacrylamide gels and not agarose as the size of the pores in agarose is a bad fit for the typical sized of proteins.

While I've never seen anyone using agarose for proteins, it seems that it is possible and sometimes used for larger proteins. I found one paper describing a protocol, they used very high concentrations of agarose in the range of 4-5%. I suspect that they won't handle well, but you should try that out yourself. If the proteins you're examining are a bit larger, using agarose should be possible.


Will this strategy work for verifying successful cloning of a DNA fragment into a plasmid vector?

Yes, your strategy would work, with the caveats already mentioned by @Cell.
Depending on which restriction enzyme and PCR buffer you use, you might even be able to skip step 2. NEB has a good list over their restriction enzymes and their activities in some common PCR buffers. With some reasoning that information is often applicable also to restriction enzymes of other brands.
Depending on your primer availability, another quick strategy is to simply use a primer pair such that one primer binds inside your fragment, and the other binds to the backbone. This should result in a PCR product only if your cloning was successful, and also verifies correct direction (in case you used blunt-end or single-site cloning). Two possible problems with this approach is:

If you get no bands at all you may not know if what failed was your cloning or the PCR reaction. The latter can be easily controlled for with a well-thought positive PCR control.
You may detect cases in which more than one copy of your fragment have been inserted. Although such cases are rare, it sometimes happens that inverted repeats of 3, 5, 7, ... etc copies get inserted in tandem.


Can proteins from different viruses be gathered in one virus?

If I understand your question, you're asking if you can take a protein from Virus A, and make Virus B produce that protein. The answer is yes, you certainly can do that, although depending on the proteins and viruses there may be some constraints. There are many examples of this being done, and even more examples of making a virus produce proteins from humans or other species.

The actual process of inserting a new gene can be pretty trivial; you can pick up handy kits of viruses specifically designed to have new genes inserted into them.  If you're putting the gene into a virus of your interest, the design process can be a little trickier; you need to be sure that the inserted protein doesn't disrupt something essential for the recipient, isn't too large for its genome, and so on.

But in principle, it's pretty simple.


Are there anatomical differences between male and female mammal brains before action of hormones?

Yes. Dewing et al. (20030 found that gene expression in mouse brains differs between male and female mice about 10.5 days after the mice had sex. This occurs before hormonal contributions to brain development. They identified about 35 genes that were appeared to show preferential expression in the female brain and another 16 that appeared to be show preferential expression in the male brain. Most of the genes identified were transcriptional regulators, signaling molecules, or involved with cellular differentiation. Of these 51, three were verified as showing female bias, and two of these were located on the X chromosome. Four genes were verified showing male bias, and two of these were located on the Y chromosome.
Similar results were found by Xu et al. (2002). They identified several of the same genes as Dewing et al., plus others that were linked to the sex chromosomes. They identified a total of six genes on the X chromosome that showed strong female expression bias during brain development. At least three of the genes were homologous between the X and Y chromosomes but showed different expression patterns between male and female brains at different stages of development.
The differences in genetic expression may cause some microscopic anatomical differences during brain development that is not explained by hormones (Bocklandt and Vilain 2007). They reviewed several studies that found differences in neuron growth, and density of vasopressin fibers in the lateral septum were more likely to be due to genetic expression than to hormonal expression. Bocklandt and Vilain did not identify the specific ages of the mice that showed these apparently gene-regulated differences but it is reasonable to speculate that these differences begin to appear in association with the differential gene expression.  Bocklandt and Vilain did not identify macroscopic differences between male and female brains prior to hormonal expression.

Citations
Bockland, S. and E. Vilain. 2007. Sex differences in brain and behavior: Hormones versus genes. pgs 245-266. In: Genetics of sexual differentiation and sexually dimorphic behaviors (D. Yamamoto, ed.). Academic Press.
Dewing, P. et al. 2003. Sexually dimorphic gene expression in mouse brain precedes gonadal differentiation. Molecular Brain Research 118: 82-90.
Xu, J. et al. 2002. Sex differences in sex chromosome gene expression in mouse brain. Human Molecular Genetics 11: 1409-1419.


If you need to inoculate milk with a known number of Bacillus subtilis spores then you will have to go follow a "sporulation" protocol - (going by your question I am not 100% certain whether this is what you want to do).

However, please find a sporulation protocol, developed by the Universities of Bonn and Freiburg, below:

Sporulation

Overnight culture

Inoculate your culture of Bacillus subtilis in 4 ml LB-medium
Let them grow overnight at 37°C, 200 rpm

Exponential growth

Measure the OD600 of your overnight culture and dilute it in LB-medium to an
OD600 off around 0.1-0.2/ml in 10 ml LB
Let the cells grow to an OD600 of 0,8/ml (37°C, 200 rpm)

Sporulation

Centrifuge 10 ml of the cells at 13,000 x g for 1 minute
Wash the pellet with 1 x PBS
Re-suspend the pellet in 5 ml DSM (Difco Sporulation Medium)
Let the cells grow for 24 hours at 37°C (200 rpm)

Lysozyme treatment (additional for spore purification)

Treat the samples with lysozyme (15 mg/ml) at a dilution of 1:6
Incubate for 1 h at room temperature
Wash 6 times with 1 x PBS

Additional:

count spores using a Neubauer improved counting chamber and make aliquots
with a defined number of spores per aliquot (e.g. 100 Million spores per 500 μl)

(Note: always use fresh DSM since the FeSO4 is rusting when it is in dilution)

May I make special mention of the Bacillus subtilis Manual here which was put together by the iGEM team and has proved as an excellent resource. The protocol above was taken from it.

Once you have your spore counts you can then inoculate the milk to your liking. However, please be aware that milk, unless completely pasteurised prior to inoculation, is not a sterile product. This means that other organisms might grow on whatever agar you decide to plate out on.


Are there functional examples of parallel DNA double helices?

Surprisingly, a parallel DNA duplex has been reported! In a paper, Tchurikov et al have reported the presence of parallel complementary DNA in the non-coding region of alcohol dehydrogenase gene as well as between two Drosophila DNA sequences. The region, which is ~40 bp long, has 76% bases in same polarity along with complementarity. However, its presence in vivo and its significance are not known (they observed its existwnce in vitro).

Tchurikov et al, in another paper, have reported that parallel complementary RNA in E. coli plays some role in RNA interference and is indeed more effective than antisense RNA in silencing mRNA for gene expression regulation. They also propose the presence of such a system in vivo in E. coli cells. (Seemingly, this paper alone is enough to answer your question since it fulfills all your criteria).

In another paper, Szabat et al have shown that DNA, 2'-O-MeRNA and RNA oligonucleotides can adopt parallel duplex configuration at pH 5 and lower. Also, presence of LNA stabilizes parallel duplex configuration. This might seem helpful in processes such as RNA interference, though this study too was in vitro (obviously, in vivo LNA is not known).

Many such papers, like Westhof et al, Mohammadi et al, etc. have reported the presence of parallel duplex DNA.

References:

 1. Tchurikov NA, Chernov BK, Golova YB, Nechipurenko YD. Parallel DNA: generation of a duplex between two Drosophila sequences in vitro. FEBS letters. 1989;257(2):415–8. pmid:2479581

 2. Tchurikov, N. A., L. G. Chistyakova, G. B. Zavilgelsky, I. V. Manukhov, B. K. Chernov, and Y. B. Golova. 2000. Gene-specific silencing by expression of parallel complementary RNA in Escherichia coli. J. Biol. Chem. 275:26523–26529

 3. Szabat M, Pedzinski T, Czapik T, Kierzek E, Kierzek R (2015) Structural Aspects of the Antiparallel and Parallel Duplexes Formed by DNA, 2’-O-Methyl RNA and RNA Oligonucleotides. PLoS ONE 10(11): e0143354. doi:10.1371/journal.pone.0143354

 4. Westhof, E., and M. Sundaralingam. 1980. X-ray structure of a cytidylyl-3′,5′-adenosine-proflavine complex: a self-paired parallel-chain double helical dimer with an intercalated acridine dye. Proc. Natl. Acad. Sci. USA. 77:1852–1856.

 5. Mohammadi, S., R. Klement, A. K. Shchyolkina, J. Liquier, T. M. Jovin, and E. Taillandier. 1998. FTIR and UV spectroscopy of parallel-stranded DNAs with mixed A-T/G-C sequences and their A-T/I-C analogues. Biochemistry. 37:16529–16537.


Has it been confirmed yet that the DNA found in dinosaurs was really DNA?

Apparently it wasn't. According to Wikipedia, A study that reported Dinosaur DNA was,

  mitochondrial cytochrome b sequences that had apparently been
  extracted from dinosaur bones dating to over 80 million years ago
  (reference).

However, contamination was found in the reported study (reference). Don't expect too much because this is a close to impossible task (reference 1). Most researchers pinned their hopes on DNA surviving trapped in amber resin but even that is not possible (reference).

If interested in cloning a dinosaur, quickly go through this article (or not).


Can (or have) antiviral drugs created drug-resistant viruses?

Resistance to antiviral therapy is a problem in the treatment of many viral illnesses.

Influenza is particularly significant given the epidemiological characteristics of the disease. This Nature Medicine article gives a good overview of oseltamivir resistant pandemic H1N1, which is a useful example, since our assumption that resistant virus would not spread very effectively was (probably predictably) not valid.

HIV is an excellent case study as well, since antiretroviral resistance is such an important issue in the treatment of that particular infection, and demonstrates the challenges of outwitting a pathogen with such a high error rate. This became apparent quite soon after introduction of (initially successful) monotherapy with AZT. In fact, preventing the emergence of resistant virus within the population of virus in a given patient is typically the primary consideration in choosing a drug regimen.

With regard to the other examples of antiviral treatment you mentioned, HCV resistance is well reviewed here. HSV resistance is reviewed here. Resistance has been observed in both examples, though it is more often considered in the normal course of treatment for HCV than HSV. I'd note that Harvoni, which you mentioned, is a combination therapy (ledipasvir-sofosbuvir). Combination therapy is one common strategy for preventing the emergence of resistance


Do I have to chew for digestion to kick in?

If you had to chew to digest, then beverages like sugary sodas would never be digested or provide calories or nutrients, as you (generally) don't chew when you drink them. No, chewing is not required for digestion or nutrient absorption. Chewing is important when eating solid foods, as the chewing action breaks down and begins to solublize the food, and stimulates the production of saliva, which contains enzymes that begin to break down the food prior to digestion in the stomach and intestines.


Why don't rates of cancer increase generation to generation?

Species age

  However, it doesn't appear to be the case that cancer rates increase as a species ages

Species don't have an age. All lineages on earth are about 3.5 billions years old. No, lineage is younger or older than that. A lineage does not get its genetics magically reset when the lineage gets a new species name. For more information about the standard misunderstandings about the concept of species, please have a look at the post How could humans have interbred with Neanderthals if we're a different species?

In all cases, there is some equilibrium between the selection pressures brought about mutations that are linked to cancer (whether mutations on oncogenes or on tumor suppressor genes).

Individual age

Individual, do have an age though. Cells, within multicellular individual replicate in order to ensure the multicellular individual growth and maintenance. Those cell lineage can accumulate mutations that could be linked to cancer development. Within the individual, these mutations are not deleterious and are therefore not selected against. Actually, in case of a cancer, those mutations are, by definition, beneficial as cancerous cells proliferate (have a large fitness). As a result one should expect that old organisms are at greater risk of developing cancer than younger organisms. In humans, this correlation exists, however, the statistics are slightly more complex than that. Typically, different types of cancer seem to show different age associations. See this article from the NIH as a start for more information.


The exact causes of the discomfort relief  after the breath-hold breakpoint  is unknown yet.

It has been stated that breath "pacemaker" continue to work independently of voluntary breath holding. Thus, while breath holding, the breath center is trying to activate the diaphragm and the afferent feedback from the diaphragm normally causes the feeling of discomfort. Thus, upon starting breathing again, i.e. actual diaphragm movements, the discomfort will diminish and the subject will feel relief.

Breath-holding and its breakpoint. Experimental Physiology Volume 91, Issue 1, January 2006.

full text of cited article


This is for an animal, not a plant. But, when I was in school, the Peppered moth was used as an example of rapid evolution from the 19th century. Its white coat made it very noticeable against soot-stained surfaces so it had a rapid selection pressure to become black. If you can organise a trip with your kid to a natural history museum, you might be able to find some specimens.


Are cell biology and cytology the same science?

Your professors are probably using cytology to refer to cytopathology which isn't strictly incorrect, but is a bit confusing since cytology also has a broader meaning.

Overall, the distinction isn't scientifically that important. Biology is so interconnected that you can't really stick strictly within any one "type" of science, they are only soft distinctions. If you need to learn a term for a course, there isn't much point to argue with your professors. Literally, the word "cytology" should refer to the study of cells, so in my opinion the narrow definition doesn't make sense, but like other words it is important to interpret it in context.

In my personal experience, I have usually heard "cell biology" used rather than "cytology" to broadly mean study of cells. If you are at an institution that calls their cytopathology labs "cytology" it doesn't much matter if there are other meanings for the word.


Why is untreated trypanosomiasis invariably fatal in humans?

African trypanosomiasis, or sleeping sickness, is caused by the protozoan Trypanosoma brucei, a single-celled eukaryote.  Being eukaryotic, it has a cell nucleus and a larger genome than most bacteria; it also has a flagellum with which it can propel itself.  Infection with T. brucei occurs via the bite of a blood-sucking fly, one of several species of tsetse fly.

The mammalian immune system has a difficult time with T. brucei because of an effective set of adaptations.  The protozoan's surface maintains a dense coat of a particular glycoprotein on its surface which generally hide other necessary surface features such as chemical receptors and ion channels. Since it is this glycoprotein that the adaptive immune system will encounter, that molecule is the one which it will develop antibodies to recognize.

Within a few days the protozoans would be recognized and soon eliminated by the immune system except that T. brucei at random times changes the glycoprotein used as its surface coat.  The mechanism that does this is called a variant surface glycoprotein (VSG) expression system.  The organism has a repertoire of about 1500 different proteins to  select from to use for a new glycoprotein coat.  The overall effect is that by the time the immune system is able to flood the body with the antibody type it has developed, most of the T. brucei population is not recognizable by those antibodies. T. brucei devotes a significant portion of its genome and its protein production to this immune evasion system.


What is the difference between average and monoisotopic mass calculations of peptides?

The elements that typically make up peptides and proteins can be present in different isotopes. For example, carbon is present to 98.9% as $\ce{^12C}$, and to 1.1% as $\ce{^13C}$.

The monoisotopic mass assumes that every element is present in the most abundant isotope, the average mass uses the actual distribution of the isotopes in nature.

If you have sufficient resolution in your mass spectrum you can see multiple signals corresponding to different isotope compositions of your molecule.


Would boiling water kill microorganisms in clothing that had feces spilled on it?

Using boiling water alone will not destroy all the toxic compounds found within faeces. One example is skatole, this is found in faeces and is partially responsible for the foul smell faeces gives off. By laundry I assume you mean laundry detergent? If so, it would depend on the detergent being used.

I hope this answered your question :)


On the premise of crop rotation, is there similarly a plant or organism able to provide nutrients into its environment that exists in water biomes?

The question isn't worded very clearly. Scientifically you cannot talk about crop rotation for natural ecology. Ecology has mutualism, commencalism, companion plants that grow together, i.e. some lichen that have three organisms together, plant, mushroom and bacteria, in sponges growing on trees and on rocks.

Crop rotation is especially important on land because we do monocultures, and our sewage doesnt go back into the field, there is a net drain on the soil minerals. In forests and the sea, the situation is different, because plants adapted to the soil grow and build up nutrients over time by rotting with organisms, being fertilized by worms, snails, insects birds and so forth. In the sea, fish provide that function and there isn't the same net drain on a sea environment as there is in a crop.

If you study green life inside different pots of water, from river, tap, rain, and pond, from different sources and different geologies, you will learn some things about aquatic ecology and nutrients. It reacts  with different plants and at different speeds.

The sea is physically so different from land, that the matter falling from the top can be transported miles away, that little comparison is made between nitrogen fixing in soil and in seawater. Also, the zone with the most light also has the strongest currents, so less chance for exchange of nutrients in ecology micro-climates and biomes.

crop rotation is mostly for N P K fixation.

On land NPK availability is often due to the acidity of the geology, which is not quite the same in the sea, plants can live on basalt or chalk, but they have endless flowing water and a good detritus layer in either.

In the sea, NPK is mostly brought by algea and cyanobacteria, which fall and bring it to the phito-detritus layer.

There are not the same forest type ecosystems in the sea as on land, where forests create many meters of peat bogs and massive NPK reserves, as in jungles sometimes. Because forests are less complex in the sea, less green stuff exists on the sea bed, we can say that the situation for plants is less profitable than on land and that instead the biomass exists more in floating small algea, Coccolithophores and so forth, which account invisible for most of the algal biomass of the sea. I cant find if there is more phyto biomass in the land or in the sea. I figure it's on land.

In freshwater environmetns, lakes can have an over or under abundance of NPK, and can bloom more or less completely for a given Ph and environment, given specific adaptations that help them to cope with a particular Ph. it's a lot more variable that the sea with PH going from 4 to 10 and beyond, when the sea ph is about 7.5-8.4.


In most* scenarios you will probably want to look at a comparison of proteins following some additional matching that considers more than a single gene/protein. Luckily, this is a very common problem and one can often look up homologs through existing reference databases such as https://www.ncbi.nlm.nih.gov/homologene

Further, if genes are not present, their documentation will provide a good overview on ways to find homologs in other organisms.

*in some very special scenarios, gene sequences might be more suitable. For instance if one wanted to study similarity of non-coding regions of a gene. However these exceptions would seem beyond the general character of the question.


I'm assuming that you have a solution of bacteria in your buffer directly after growing them for some time, and without performing a lysis step yet. The 2% SDS step looks like it is for lysis of your cells.

In that case, centrifuging the bacteria and resuspending them in lysis buffer is a very common step in many protocols. Separating whole bacteria from medium or buffer by centrifugation is pretty easy and should just work. But if at any of your previous steps you already lysed your bacteria, this won't work because the cells aren't intact anymore.


Protein structure prediction using PSSM? Or not?

I think you are making PSSMs out to be much more sophisticated than they really are.

A PSSM is merely a scoring matrix — it gives position specific scores for each residue at a given location.

There is no explicit pairing of interacting residues though that does sound like an interesting approach ...

You can learn more about PSSMs from many sources on bioinformatics including NCBI.


regarding evolution of ears and sense organs

When you are asking about the evolution of organs, you are already five steps ahead of yourself. To have sensory organs, you need cells that react to some stimulus:

Hearing, Touch: Mechanical stimulus
Smell, some pain: Chemical stimulus
Sight: Optic stimulus
Other (non-human) organisms can also sense electric fields, magnetic fields, ...

As soon as you have those, having 'organs' that house a lot of those cells surrounded by tissues that aid in the reception of these stimuli, is relatively trivial.

But isn't a sensory cell totally complicated? It is. But: A simple neuron already is a sensory cell of sorts: It reacts to electrical and chemical imbalances.

But isn't then a neuron totally comlicated? It is. But: A simple non-neuronal cell already has a lot of the intricate machinery that a neuron does - a neuron mostly has some special parts and structures that make it a neuron. A simple cell also does react to chemical and other stimuli (this is why hormones work, and how little one-celled animals can orient themselves towards the light or food, or away from dangerous chemicals)

But isn't a run-of-the-mill cell totally complicated? It is. But it actually is just the workings of several archaic cells crammed into one (one of the more popular theories on Eukaryote evolution has them result from a very intense partnership of several more basic cells). And those archaic cells can also react to stimuli (they manage their metabolism according to the available food, for instance)

But isn't a basic cell totally complicated? It is. But is actually is just the interaction of several molecules that have some very interesting properties - DNA/RNA can function as an information storage, but are at the same time tools that can cowork with other DNA/RNA, and also interfaces/interferes with proteins in interesting ways.

But aren't big molecules totally complicated? They are. We still need supercomputers to reliably model all of the intricacies of any given Protein-Protein or Protein-RNA interaction. Many proteins behave differently in different environments (electromagnetic field strengths, chemical environment, temperature and mechanical factors (e.g. ultrasound)) - they could be said to 'react' to certain triggers. But they are actually just chains of repetitive elements (so called polymers of so called monomers).

But aren't those monomers totally complicated? Some are, but here we slowly get into the realm of 'mostly modellable on a hefty home computer'.

So we have systems of systems of systems... All of them very complicated.

But evolution is not a process that involves understanding ot planning. It is simply the result of coincidences and inheritance. You can see colors that many animals cannnot. You have the requisite molecules in your sensory cells in your eyes. Some people can see more colors than you, an inheritable trait. Some people can see less colors. Currently those people have no evolutionary profit from this - they reproduce and die with the same probability as the rest of us. Likewise there are a million (possibly billion?) such traits in every human. Traits that are different from the rest. Little things. Ineffective things (= having no net effect). But there might come a time where seeing one color or not seeing it (= not being distracted by it) will give a continuous net positive or net negative effect on the reproduction of those people carrying that trait. That is the time when that trait will start to  be present in a larger piece of the population (over many generations). The people carrying that trait will also be different from one another. And the ones carrying the traits with the most positive net effect will multiply the most, etc. Humans in some distant future then can eye-sense some X-factor we cannot even describe currently (try describing different colors to a blind person) and thus have, say, Xeyes.


Where do the Ca ions that causes neurotransmitter release from synaptic bouton, come from?

Short answer

Neurotransmitter release is triggered by an influx of calcium ions from the extracellular space into the cytosol through voltage-gated calcium channels in the plasma membrane.

Long answer

Typical synaptic vesicle release is triggered by calcium influx through T-type calcium channels. These are voltage-sensitive channels in the plasma membrane; calcium flows through these channels from the extracellular space and is bound by synaptotagmin, a type/family of proteins associated with the vesicle fusion machinery (the SNAP/SNARE complex) to trigger (or, more precisely, to increase probability of) vesicle release.

Like just about every important class of proteins, these channels can be regulated by various mechanisms: gene expression, trafficking/colocalization, subunit composition, phosphorylation, etc. See the Iftinca & Zamponi review.

Calcium from internal stores, released by various mechanisms (calcium-induced, IP3-induced, can also be important to neuron plasticity and homeostasis but does not need to travel from the soma (ER extends throughout the cell). In some special cases, these internal calcium stores can be involved in release (see for example Babai et al 2010), but this example is from in photoreceptors in the retina which use a different release mechanism than typical neurons (they don't fire spikes, they have graded potentials and graded release probability, etc). Internal stores can also influence spontaneous release probability and may modulate release probability (see for example the review by Collin et al) but are not the primary "trigger" for release.

For more on the basic synaptic machinery, I'd recommend any edition (though of course recent is always best) of the textbook "Neuroscience" by Purves and coauthors.

Babai, N., Morgans, C. W., & Thoreson, W. B. (2010). Calcium-induced calcium release contributes to synaptic release from mouse rod photoreceptors. Neuroscience, 165(4), 1447-1456.

Collin, T., Marty, A., & Llano, I. (2005). Presynaptic calcium stores and synaptic transmission. Current opinion in neurobiology, 15(3), 275-281.

Iftinca, M. C., & Zamponi, G. W. (2009). Regulation of neuronal T-type calcium channels. Trends in pharmacological sciences, 30(1), 32-40.

Dale Purves, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, Richard D. Mooney, Michael L. Platt, Leonard E. White. (eds) (2018). Neuroscience. New York: Oxford University Press.


Why are mammals not very often (never?) toxic?

Answering the first part of your question: The cuban solenodon has venomous saliva. It's a mammal -- rather shrewlike in appearance. But yes, venomous mammals are rare!


How would real-time blood glucose monitoring work?

If you browse the on-line patent data bases - either www.uspto.gov or www.freepatentsonline.com for "glucose monitor" you'll find there are at least half a dozen technologies that have been proposed including the most non-invasive technologies such as using light - similar to the pulse oximeters used in hospitals to measure the pulse and PaO2 through the skin to more invasive methods that periodically pump small samples of blood outside the body for chemical or optical analysis. But in terms of accuracy, the best way to measure BG is by some means that can analyze arterial blood in vivo.

Companies that are trying to develop these devices are shooting for accuracies better than 12 mg/dL, but that's very hard to do with the noninvasive methods. There is a very new technology that uses a contact lens as the sensor, measuring from the iris and transmitting to remote electronics for processing, but that's still probably year's away. I believe the best products that are available today may be those developed by Dexcom in San Diego, CA. See their website here: http://www.dexcom.com/

The journal Science just published its year end Breakthroughs and that includes an article that shows hope in restoring the B cells in the pancreas for type I diabetics see http://www.sciencemag.org/content/346/6216/1444.full . This of course is the best solution - a cure. I hold hope scientists are less than 5 years away from that goal.


When do the first neurons appear in humans?

Apparently, olfactory axons and GnRH producing neurons are among the first neurons that migrate from neural crest at around 39th day of gestation in humans (Cassoni et al., 2016).

  In rodents, early GnRH neurons migrate together with a heterogeneous
  coalescence of placode-derived and neural crest-derived migratory
  cells (Forni et al., 2011) and olfactory axons, collectively called
  the ‘migratory mass’ (MM) (Miller et al., 2010; Valverde et al.,
  1992). This cell migration precedes the targeting of olfactory sensory
  axons to the developing olfactory bulb (OB). The existence of a
  similar MM in the human embryo has not yet been described. We thus
  immunolabeled consecutive sagittal sections of a CS 16 embryo† for GnRH
  and doublecortin (DCX) (Fig. 1D,E,G), a marker of immature migratory
  neurons (Gleeson et al., 1999). We identified a very small number (50
  in total) of immature GnRH-expressing cells in the nasal mesenchyme,
  in the medial portion of the olfactory placode (Fig. 1C-E), adjacent
  to the basal lamina of the VNO, showing that the acquisition of cell
  identity occurs outside the VNO between GW 5 and 6. At this stage, we
  observed a mixed mass of immature GnRH neurons expressing DCX (Fig.
  1F,G) or βIII-tubulin (Fig. 1H-J), migrating across the nasal
  mesenchyme towards the telencephalon. As in rodents (Miller et al.,
  2010), GnRH neurons in humans only represented a small proportion of
  the MM (Fig. 1G). Furthermore, these pioneer neurons of the MM
  expressed the delta/notch-like EGF repeat containing (DNER) (Fig.
  1H-J), a transmembrane protein specifically localized in the dendrites
  and cell bodies of postmitotic neurons.

  †Carnegie stage (CS) 16 = ∼39th day of gestation