How does one measure the length of telomeres?

Again, not an expert, but I found this article seems to say it pretty well:

Telomere's are most commonly measured by qPCR of the repetitive regions with degenerate oligomer sequences such as "TTAGGG and CCCTAA repeats"  Although articles like this one appear to advance measurements in vertebrates, this reference from 2011 implies two techniques continue to be most common:

1) qPCR with the appropriate oligos and then running them on an agarose gel

2) Southern blot of a restriction digest that leaves the telomeres intact

Clearly sequencing techniques don't do well with repetitive sequences such as this, so in general this still seems like the most common method.

This would indeed be quite destructive, at least for the cells used, though a biopsy would be enough, though apparently micrograms of DNA are required.  Kind of a large amount.

The accuracy would then be limited to that of the gel or blot.  That would generally be a percentage of total length, I think 2% might be obtainable, but I'm not sure about that part.


How to find the age of a memory stored in the brain?

We are only barely beginning to understand how the brain works, including memory. We do know that it is a very complex thing. There are many different kinds of memory; many different processes are involved in creating and recalling memories. One factor that plays into a naïve concept of "how old a memory is" is that "remembering" does not seem to be a passive activity; instead, every time we remember a memory we re-create it.

Having said that I don't see a theoretical reason why there wouldn't be a way to determine the age of a memory... but we currently don't know it.

Consider that we don't magically know the ages of stones, plants, or animals. We learned to figure it out from studying those things, seeing how they change over time, and deducing ways to use that knowledge to guess their age. For example, people discovered that in many climates trees alternate a growing season and a dormant season, and this results in the trunk having "tree rings" for each year they've lived. They've also seen that animals have specific life cycles and look different (if only in size) depending on their ages, and they can use that to roughly estimate an animal's age. Obviously this depends completely on the animal in question; different animals grow in different ways and we can tell their ages in correspondingly different ways, and not always to great precision.

For most of human history we were completely unable to tell the age of stones. Only the discovery of radioactivity, and that the atoms inside stones transmute into other elements over the millennia and that this allows us to tell how long it has been since the stone crystallized (i.e. the atoms got stuck where they are), enabled radiometric dating.

Similarly with memory, it is completely plausible that once we understand very well what a memory is, what its exact correlates in the brain are, and how those correlates change over time, it will be possible to tell how old a memory is. But we aren't there yet (see some articles at the end for where we are).

And while it's plausible that we'll be able to know the age of a memory once we understand it well enough, it is by no means inevitable. To give a counter-example, there is absolutely no way to tell the age of, say, a water molecule. We understand water molecules extremely well. They form and can be destroyed, so for every water molecule there is a certain amount of time since it formed, i.e. it has an age. But a water molecule is just an oxygen atom linked to two hydrogen atoms; its properties are dictated by chemistry and don't depend on how long it has existed. There is no way to tell the age of a given water molecule just from looking at it. Similarly, computers give a timestamp to a file when they create it, but if they didn't do that I don't think we could tell how long a file had been on the disk just from examining the disk itself. So it is certainly theoretically possible that once we understand how memory works, we'll find that we can't, in fact, know the age of a memory.

Here are some papers on memory to give an idea of what neurobiologists are looking at these days:

The Regulation of Transcription in Memory Consolidation
http://cshperspectives.cshlp.org/content/7/1/a021741.short
This paper looks at the role of DNA transcription in the consolidation of long-term memory (as such consolidation apparently requires new proteins being created)

Structural Components of Synaptic Plasticity and Memory Consolidation
http://cshperspectives.cshlp.org/content/7/7/a021758.short
This paper (more or less the same authors) looks at the structural factors involved in consolidating memories by strenghtening synapses and creating new ones.

The many faces of working memory and short-term storage
https://link.springer.com/article/10.3758/s13423-016-1191-6
This recent (2017) paper discusses "Working memory" and how the field doesn't have a single, coherent definition of that concept yet.

Functional neuroimaging studies of encoding, priming, and explicit memory retrieval
http://www.pnas.org/content/95/3/891.short
This 1998 imaging study looks at what regions of the brain light up in various memory-related tasks, and suggests such imaging studies can be useful to investigate brain function. They were right, but notice how general the areas they see are, and how they only can guess at what might be going on there.

The Molecular Biology of Memory Storage:
A Dialog Between Genes and Synapses
http://teachline.ls.huji.ac.il/72336/sphira/Kandelnobellecture.pdf
This is a very long lecture from 2000 from one of the authors of the above papers, summarizing their life's research on the molecular and synapse-level mechanisms of memory. These paragraphs give a historical overview of how scientists have thought memory works:

  In his Croonian Lecture to the Royal Society of 1894, Santiago Ramo´n y Cajal
  proposed a theory of memory storage: memory is stored in the growth of new connections[16]. This prescient idea was neglected in good part for half a century as students of learning fought over newer competing ideas. First, Karl Lashley, Ross Adey, Wolfgang Köhler, and a number of Gestalt psychologists proposed that learning leads to changes in electric fields or chemical gradients, which they postulated surround neuronal populations and are produced by the aggregate activity of cells recruited by the learning process. Second, Alexander Forbes and Lorente de No proposed that memory is stored dynamically by a self-reexciting chain of neurons. This idea was later championed by Donald Hebb as a mechanism for short-term memory. Finally, Holger Hyden proposed that learning led to changes in the base composition of DNA or RNA. Even though there was much discussion about the merits of each of these ideas, there was no direct evidence to support any of them [reviewed in 17].

  We were now in a position to address these alternative ideas by confronting
  directly the question of how learning can occur in a circuit with fixed neuronal
  elements. Kupfermann, Castellucci, Carew, Hawkins, and I examined the neural
  circuit of the gill-withdrawal reflex while the animal underwent sensitization or habituation, a form of learning in which the animal learns to ignore an innocuous stimulus to siphon when given with monotonous repetition. (We later also extended these studies to an examination of classical conditioning [20].) Our studies provided clear evidence for Cajal’s idea: learning results from changes in the strength of the synaptic connections between precisely interconnected cells [6, 7]. Thus, while the organism’s developmental program assures that the connections between cells are invariant, it does not specify their precise strength. Rather, experience alters the strength and effectiveness of these pre-existing chemical connections. Seen in the perspective of these three forms of learning, synaptic plasticity emerged as a fundamental mechanism for information storage by the nervous system, a mechanism that is built into the very molecular architecture of chemical synapses [95]

Notice how twenty years ago, this person was saying we can finally begin to answer century-old questions of what form memory storage takes in the brain to begin with.

A Putative Biochemical Engram of Long-Term Memory
https://www.sciencedirect.com/science/article/pii/S0960982216311393
Exciting 2016 article: they've maybe found one place where one memory might be stored! First line of the abstract:

  How a transient experience creates an enduring yet dynamic memory remains an unresolved issue in studies of memory.

Same idea in the first line of the abstract of this 2016 article on associative memory:

Neural ensemble dynamics underlying a long-term associative memory
https://www.nature.com/articles/nature21682

  The brain’s ability to associate different stimuli is vital for long-term memory, but how neural ensembles encode associative memories is unknown.


Why do mutations in Drosophila dsx (double sex) affect both males and females?

Expression of the double-sex gene is rather unusual, so it is not surprising that you are having difficulty understand mutations in it. The simplified diagram below (adapted from Gilbert’s Developmental Biolgy — available on-line) should help clarify the matter.

The key concept is that although the double-sex gene (dsx) is expressed in both male and female flies, the gene products (DsxF add DsxM) are different in the two cases. This is achieved by alternative splicing of the RNA transcript, controlled ultimately by X and Y chromosome dosage. (If you are unfamiliar with alternative splicing, see e.g. this section of [Molecular Biology of the Cell (http://www.ncbi.nlm.nih.gov/books/NBK21558/).)

The second important concept (the details of which, I admit, I am less familiar with) is that sex is determined by both activating genes specific for the particular sex and inactivating genes for the opposite sex. Thus, the diagram shows that DsxF both activates expression of genes for female sex differentiation and represses expresses of genes for male sex differentiation. Likewise DsxM activates expression of genes for male sex differentiation and represses expresses of genes for female sex differentiation.

Thus, according to this schema, if dsx is completely knocked out there will be consequences in both male and female. In the female, in the absence of DsxF, the genes for female sex differentiation will not be activated, but those for male sex differentiation will not be repressed. This presumably results in the intersex phenotype. Likewise, in the male, the absence of DsxM prevents the expression of the genes for male sex differentiation, but does not repress those for female sex differentiation. Again, I presume this results in the intersex phenotype.


Ammonites are not strictly defined. One can reffer to ammonites as to the whole group of ammonoids (Ammonoidea, ammonites sensu latto). This is common, but not supported by most researchers. Researchers use the term "ammonoid" for paleozoic ammonoidea and "ammonite" for Jurassic and Cretaceous Ammonoidea (ammonites sensu stricto). Ammonites sensu stricto reffer to ammonoids with complex (ammonitic) sutures, which are typical for Jurassic and Cretaceous ages. However, complex ammonitic sutures are not exclusive for Jurassic and Cretaceous ammonoids. Ceratitic sutures are not exclusive for Triassic either and occur in Jurassic ammonoids, too.

  So caution must be exercised when using suture lines as a means of
  classification. To obviate some of the problems posed by this
  simplistic classification, Wedekind, in 1918, introduced the terms
  palaeo-, meso- and neoammo-noids to classify ammonoids better.

(PDF) Goniatites. Available from: https://www.researchgate.net/publication/262048294_Goniatites [accessed May 12 2019].


What is the energy source for adipocytes?

Adipocytes use glucose as an energy source. They express the insulin-responsive glucose transporter GLUT4 just like muscle cells so that when blood glucose levels rise they are primed to take the glucose up for fatty acid biosynthesis, but they also use glucose as a fuel molecule.


Mitochondria and plastids are the result of two ancient mergers. A kind of symbiotic relationship where one cell phogocytized another. Rather than being digested, the phagocytized cell, complete with its own DNA cooperated with the cell that "ate" it. This was part of the evolution of eukaryotes. This idea is called endosymbiosis, and was championed by Lynn Margulis in the late 1960s. Mitochondria and plastids come from Bacteria, and carry the traces of their original DNA. However, a complete genome was no longer required for the new function, so mitochondria lost many redundant genes. Mitochondrial genomes are much smaller. Plastid genomes are larger than mitochondrial genomes, but smaller than the genomes from which they originated.


What determines when twining plants twine?

Thigmotropism

This is a special case of tropism, called thigmotropism. In botany, tropism is a modified growth in response of an environmental stimulus. The most famous tropisms are:

Phototropism: plant growth in response to a light stimulus
Gravitropism: plant growth in response to gravity

In the case of thigmotropism, the growth is modified in response to touch (from the greek θιγμός). Curiously, this phenomenon was studied by Darwin in his late life: Darwin, C. (1865), On the Movements and Habits of Climbing Plants.. Journal of the Linnean Society of London, Botany, 9: 1–118. doi:10.1111/j.1095-8339.1865.tb00011.x

The mechanism of thigmotropism can be compared to that of phototropism: in phototropism, the shaded side of the stem apex has a higher concentration of auxins compared to the sunny side and, therefore, grows more quickly, and the result is that the plant grows towards the light source (positive phototropism).

In thigmotropism, there are mechanic receptors in the epidermis which detect touch (mechanoreceptors), possibly membrane proteins. Then, after detecting touch, there is a signal transduction somehow, which "informs" the cells opposite to the touching side about the stimulus, and those cells exhibit an increased rate of growth.

The mechanism may be similar to that of phototropism, also depending on auxins. According to Scorza et al. (2011):

  Ultrastructural studies revealed that most thigmotropic and thigmonastic movements are caused by differentially changing cell turgor within a given tissue. Auxin has emerged as a key molecule that modulates proton extrusion and thus causing changes in cell turgor by enhancing the activity of H+ATPase in cell membranes. (emphasis mine)

The actual details regarding the mechanism are not well understood, and they are way less understood than those of phototropism or gravitropism, for instance. The result, however, is that the touching side grows less that the opposite side:

If you combine thigmotropism and negative gravitropism (the growth against gravity), the result is that the climber grows up going around the support, in an upwards spiral:

A detailed explanation can be found here: Plant tropisms. 1st ed..

Sources:

Scorza, Livia Camilla Trevisan, and Marcelo Carnier Dornelas. “Plants on the Move:  Towards Common Mechanisms Governing Mechanically-Induced Plant Movements.” Plant Signaling & Behavior 6.12 (2011): 1979–1986. PMC. Web. 14 May 2017.
Gilroy, S. and Masson, P. (2008). Plant tropisms. 1st ed. Ames, Iowa: Blackwell Pub


Local warming of a patch of skin will cause vasodilation. However, after prolonged warming there is a 'die away' phenomenon, is which blood vessels slowly constrict back to their normal diameter.

  Johnson JM, Kellogg DL Jr. Local thermal control of the human
  cutaneous circulation. J Appl Physiol (1985). 2010;109(4):1229–1238.
  doi:10.1152/japplphysiol.00407.2010
  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2963328/


What are the main differences between tubers and taproots?

They are actually completely different plant parts: a taproot is the central root of a taproot-system plant while a tuber is an engorged modified underground stem called a rhizome.

A morphological and functional difference between rhizomes and roots are that rhizomes (being modified stems) have nodes, while roots never do.

Note: a node = the location on a plant stem where buds (leaves, flowers, stem branches) initiate

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001)1:

  Taproot. The main root axis from which smaller root branches arise; a root system with a main root axis and smaller branches...Figure 1273

  Root. The portion of the plant axis lacking nodes and leaves and usually found below ground.

Compared to...

  Tuber. The thickened portion of a rhizome bearing nodes and buds; underground stem modified for food storage. Figure 1366

  Rhizome. A horizontal underground stem. Figure 1052

See here for a photo of a potato plant showing a young tuber and an older tuber growing on the end of a rhizome.

According to here:

  Tubers-are swollen regions of stems that store food for subsequent growth. The potato is an example. It is a stem because it has many nodes called eyes with spaces between eyes known as internodes. Potato tubers develop at the end of swollen underground stem structures, rhizomes.

  Eyes of potatoes are really axillary buds which contain several small buds at each site. These buds can expand to form shoots which grow on to make whole plants.

You can explore histologic, anatomic, and physiologic differences of stems vs roots more generally to understand broader differences between the two plant parts.

Examples:

Proença & Sajo (2008)2 discuss root and rhizome anatomy in select bromeliads.
Figure 1 from Hernán et al. (2014) shows how the vascular and various tissue layers can differ quite a bit between roots and rhizomes on the same plant.

Notes:

Some structures characteristics of roots (e.g., casparian strips) can also occur in rhizomes. (E.g., see Lersten 19974.
Unlike potatoes (which are tubers), sweet potatoes (Ipomoea batatas) are actually a modified root called tuberous roots

Works Cited:

1 Harris, J.G. and Harris, M.W., 1994. Plant identification terminology: an illustrated glossary (No. QK9 H37 2001). Utah: Spring Lake Publishing.

2 Proença, S.L. and Sajo, M.D.G., 2008. Rhizome and root anatomy of 14 species of Bromeliaceae. Rodriguésia, 59(1), pp.113-128.

3 Hernán, G., Varela, B.G., Fortunato, R.H. and Wagner, M.L., 2014. Pharmacobotany of two Valeriana species (Valerianaceae) of Argentinian Patagonia known as “Ñancolahuen”. Lat Am J Pharm, 33(6), pp.891-6.

4 Lersten, N.R., 1997. Occurrence of endodermis with a casparian strip in stem and leaf. The Botanical Review, 63(3), pp.265-272.


Regarding the kingdom Animalia, which phylogenic tree is more common: Molecular Comparisons or Body-Plan Grades

Long story short, use sequence information if you can.

The long story long:
Sequence information and the trees generated from them are strictly more reliable than morphological characters. For instance: sharks are pretty much the same shape they were millions of years ago, but they've been accumulating genetic differences 'invisibly' that allows us to group the different kinds of shark accurately. Where genetic data is unavailable (paleontology as a rule, certain kinds of field taxonomy where it's cheaper to code the morphological features of each new beetle than sequence them all) morphological trees are still used. So in terms of which tree type is more common: It depends.

In terms of which tree type is more accepted, it's genetic data by a landslide. Genetic data by and large is much less affected by homologous structures and convergent evolution. In addition, it works on species that all look pretty much identical (imagine trying to code hundreds of bacterial species that are all closely related). Using highly conserved cellular machinery, trees for very distant species can be constructed. Using unconserved noncoding sequences trees for very closely related individuals trees can be constructed with a reasonable degree of accuracy.

Some examples: Mitochondrial Eve would be impossible to date with morphological characters. There's just not enough morphological variation between humans.
Opabinia is a really good example of how hard it is to classify things based on shape, especially when they're a weird shape.
Something you can do yourself: Human  and Thermodesulfator(seq) are about as morphologically distinct as two living things can be. One is you, and one eats carbon dioxide and breathes sulfate and hydrogen. It lives at the bottom of the sea and would be more at home in a cup of hot coffee than outside it. Nevertheless, the two species show ~50% sequence similarity using 16S, twice as much as would be expected by chance and easily enough to classify a third thing as more closely related to one or the other. Try it yourself if you like.


Will gene mutations give rise to a protein that is shorter than the full length protein?

It depends on the nature of the insertion or deletion.

Many mutations are point mutations, where one single nucleotide is changed:

ATGACTACGCTATTCAGT
M  T  T  L  F  S

ATGTCTACGCTATTCAGT
M  S  T  L  F  S

Notice that changing the fourth A to a T caused a T->S change in the final protein, and didn't change its length. However, an insertion/deletion is different. Starting with this sequence:

ATGTCTATTGACGCTATTCAG
M  S  I  D  A  I  Q

Let's have an insertion, an A after the A in position 7:

ATGTCTAATTGACGCTATTCAG
M  S  N  STOP

Notice we now have a stop codon (TGA). This means the protein will be truncated, and will be much smaller. That isn't always the case. Rather than adding an A at position 7, let's add it after position 9:

ATGTCTATTAGACGCTATTCA
M  S  I  R  R  Y  S

The protein is about the same length, but the AAs are completely different than the original version after the insertion:

M  S  I  D  A  I  Q
M  S  I  R  R  Y  S

This is called a frameshift mutation. Biologically, these mutations are harmful because they change all the amino acids after the mutation, the protein is often not functional and can end up being different sizes (if a stop codon is now in frame or out of frame) and the protein can even end up being unstable and rapidly degraded.

So, to answer your question about the length of the protein, it'll increase/decrease by one AA every time 3 nucleotides are added/removed, but can increase or decrease drastically if a stop codon is added or removed by a frameshift mutation.


How can we differentiate between respiration and breathing?

There are two uses of the term respiration: physiological respiration and cellular respiration

Physiological respiration involves the intake of outside oxygen and its distribution to the tissues of the body. Breathing is a part of physiological respiration and functions to bring oxygen into the lungs and expel carbon dioxide.

Cellular respiration is a chemical process by which energy is obtained within individual cells from biomolecules like glucose. In aerobic respiration, oxygen is used. Cells can also use fermentation and, for some, anaerobic respiration to obtain energy.


Bacterial cell lysis buffer used in proteomics procedures

I'm a HUGE fan of FASP (filter-aided sample preparation) which is an in-solution preparation/digestion. It is very fast, allows you to not worry about a protein precipitation step, and gets rid of all MS incompatible substances with the wash steps (so doesn't matter what lysis buffer you use). It requires very few, inexpensive materials (a pack of 100 centrifuge filter units is less than 250 USD from VWR) and has great recovery. This is the link to the Nature Methods paper that the linked protocol is based on (the linked protocol is an updated, faster version of the Nature Methods one).


"50% of the variance in antisocial phenotypes is the result of genetic factors" means what?

In a population the phenotypic variance can be caused by several underlying variance including the variance in the environment and the genetic variance (among others). The fraction of the phenotypic variance that is caused by the genetic variance is what we called the heritability in the broad sense. The fraction of the phenotypic variance that is caused by the additive genetic variance is what we called the heritability in the narrow sense.

So the sentence

  50% of the variance in antisocial phenotypes is the result of genetic factors.

can be rephrased as

  Antisocial phenotypes have a heritability of 0.5.

The concept of heritability is useful as it gives us an idea of how well selection can act on the changing the frequency of phenotypic traits in the population (see How to interpret the breeders equation?). Please have a look at Why is a heritability coefficient not an index of how “genetic” something is? for more information.


Identification of red, plum-like fruit (probably from Southern Russia)

Can't be certain from the picture, but they look a lot like Cornelian Cherry (Cornus mas: https://en.wikipedia.org/wiki/Cornus_mas ).  However, the ones in my garden (western US) don't ripen until late September/October.

Perhaps they could return to the market, and ask for the Russian name?


How fast do lipids on the inside and outside of a lipid bilayer exchange?

A cursory search seems to show at least a few papers using sum-frequency vibrational spectroscopy to measure rates of flip-flopping/transverse diffusion in lipid bilayers.
This paper in particular ("1,2-Diacyl-Phosphatidylcholine Flip-Flop Measured Directly by Sum-Frequency Vibrational Spectroscopy") cites an activation barrier of 79 kJ/mol which corresponds to a rate on the order of 10^-4/s.
There is also this review which seems to have more information on the topic: http://dx.doi.org/10.1021/acs.accounts.6b00435.


What is the speed of neurotransmitter release and receptor binding in a neuronal synapse?

It seems to depend on the size of the neurotransmitter. The bigger the neurotransmitter is the longer the neuron has to be stimulated to actually release the neurotransmitter. But in the case of Acetylcholine it seems to need only about 2ms after a presynaptic stimulus to generate a postsynaptic membrane potential and after about 5ms all the Acetylcholine in the synaptic gap is cleaved allowing the postsynaptic cell to repolarize. The example get described here.


When infected with malaria, how many parasites are within a human host?

The uninucleate sporozoites are injected by the mosquito into a human host. They mature in the liver parenchymal cells in schizonts. Each schizont releases into the blood flow 2,000 to 40,000 uninucleate merozoites. Each of them can infect a red blood cell. Here, a merozoite can release other 10 to 36 merozoites [1].

The numer of injected sporozites depends on the bite and the number of bites [2]. And it seems that a parasitemia greater than 5000/microliters which is usually achieved by 10 infective bites during a 28-day period triggers the signs and symptoms [3].

I couldn't find any data on the mosquito parasitemia. It has been found that the infected mosquito and the parasite mutually benefit each other and thereby promote transmission of the infection. The Plasmodium-infected mosquitoes have a better survival and show an increased rate of blood-feeding, particularly from an infected host [4].

References:

James M. Crutcher and Stephen L. Hoffman. Medical Microbiology. 4th edition. 1996, The University of Texas Medical Branch at Galveston.
Garrett-Jones C, Shidrawi GR. Malaria vectorial capacity of a population of Anopheles gambiae: an exercise in epidemiological entomology. Bull. World Health Organ. 1969 Apr;40(4):531-45. PubMed PMID: 5306719.
McElroy PD, Beier JC, Oster CN, Beadle C, Sherwood JA, Oloo AJ, Hoffman SL. Predicting outcome in malaria: correlation between rate of exposure to infected mosquitoes and level of Plasmodium falciparum parasitemia. Am. J. Trop. Med. Hyg. 1994 Nov;51(5):523-32. PubMed PMID: 7985743.
Dr. B.S. Kakkilaya's Malaria Web Site. Life Cycle of Malaria.


Why does a fetus drink and urinate into the amniotic fluid?

In utero, the growing little human is getting ready to be an independently functioning individual. While it is everything but that, it must be able to obtain fluids and nutrients through its mother's milk, and that from pretty much the first hour of its life.

To develop proper kidney function, the growing fetus needs to ingest fluids just as it will do post partum. Because a mini bar isn't available, it has to drink whatever is available, i.e., amniotic fluid and indeed, its own urine. Shortly after the kidneys start to produce urine, the fetal swallowing commences.

Amniotic fluid is 98% water and 2% salts and cells from the baby. Until the fetal kidneys start working during month four, amniotic fluid is made by the mother’s body. But after month 4, the fetus starts to make his contribution to the amniotic fluid by urinating into it (Penn Medicine). Production of amniotic fluid is then predominately accomplished by excretion of fetal urine (300 ml/kg fetal weight/day or 600 to 1200 ml/day near term) and the secretion of oral, nasal, tracheal, and pulmonary fluids (60 to 100 ml/kg fetal weight/day). Fetal breathing movements also contribute by efflux of lung fluid into the amniotic fluid. Removal of AF is predominately accomplished by fetal swallowing (200 to 250 ml/kg fetal weight/day) (Underwood et al., 2005).

The water in amniotic fluid originally comes from maternal plasma and passes through the fetal membranes. As the placenta develops, water and solutes from maternal plasma pass across the placenta to the fetus and then to the amniotic fluid (Underwood et al., 2005), see Fig. 1.

Swallowing its own urine is not only not dangerous, it is essential to proper development. A decrease in fetal urine production or excretion can result in a reduced amount of amniotic fluid (oligohydramnios). Oligohydramnios can result in fetal lung deformations (pulmonary hypoplasia) and increased risk of infection.  Fetal mortality rates as high as 80-90% have been reported with oligohydramnios diagnosed in the second trimester (Source: Patient Info).

If the fetus would have to prevent the production of urine in utero, the kidneys would have to remain nonfunctional during development, which would be disastrous once it is born. Renal failure is in fact pretty common in newborns, but can be fatal without proper treatment (Andreoli, 2004).

Fig. 1. After month 4, amniotic fluid is derived from maternal plasma that passes via the placenta, to the fetus and then to the amnionic fluid. Source: Underwood et al., (2005).

References
- Andreoli, Semin Perinatol (2004); 28(2): 112-23)
- Underwood et al., J Perinatol (2005); 25: 341–48


Why are there no fresh water osmoconformers?

There are virtually no freshwater osmoconformers but there are some exceptions like being both an osmoconformer and an osmoregulator based on the salinity of the environment.

Osmoconformers keep their internal fluids isotonic to their environment and they maintain an internal salinity similar to the surrounding water. The concentration of solutes in freshwater is very low and if any organism were to have that low concentration of solutes in its body, it would not have enough proteins, ions, etc. to effectively conduct the biochemistry of living.

Here is a rare example of a freshwater species Daphnia which can be both an osmoconformer and an osmoregulator:

  For freshwater osmoconformer species, most of the time there is a gradient between their internal
  osmotic concentration and that of the external environment; consequently, osmoconformers will
  vary in their cellular osmotic volume contents and as a result, some FW species (e.g. Daphnia),
  osmoregulate at low salinity levels but are osmoconformers at raised salinities. Some physiological
  processes, including reproduction and metabolic rate however, can be affected negatively by these
  changes (this group regulate their osmotic pressure actively) (Chen and Stillman, 2012).

  https://eprints.qut.edu.au/107457/1/Azam_Moshtaghi_Thesis.pdf

Additionally, there is the term euryhaline used for the aquatic organisms who are able to tolerate a wide range of salinity. There are fish species that can live in salt water, fresh water and brackish water. You can see a list in the Wikipedia/Euryhaline Article.


Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions?

According to the highly respected WORMATLAS: A Database of Behavioral and Structural Anatomy of Caenorhabditis elegans, the number is invariable in this animal, one of the most studied in the world.

  There are 302 neurons in the nervous system of C. elegans; this number is invariant between animals. Each neuron has a unique combination of properties, such as morphology, connectivity and position, so that every neuron may be given a unique label. Groups of neurons that differ from each other only in position have been assigned to classes. There are 118 classes that have been made using these criteria, the class sizes ranging from 1 to 13. Thus C. elegans has a rich variety of neuron types in spite of having only a small total complement of neurons. (Emphasis mine)

From the above, you might guess that the number of synapses are not, however.

  The full list of synapses for hermaphrodite (including larval stages) and adult male are currently being reviewed and revised for the Wormwiring Project. All data comes from re/analysis of the sections for the hermaphrodite N2U, N2T, N2W and JSE animals, and male N2Y and n930 animals. The total counts of both electrical and chemical synapses are likely to be substantially higher than what was reported in the Mind of a Worm.

Would I be surprised if someone found a different number in a particular  specimen? No more so than when people are born with four kidneys, a parasitized twin, etc.

Edited to Add:

An article, Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans has identified mutations with more or fewer neurons:

  Specifically, unc-83 and unc-84 mutations affect certain precursor cells that generate both neural and nonneural descendants; lin-22 and lin-26 mutants lead to the generation of supernumerary neural cells with a concomitant loss of nonneural cells; lin-4, lin-14, lin-28, and lin-29 mutants perturb global aspects of developmental timing, altering the time of appearance (or preventing the appearance) of both neural and nonneural cells...

However, access to the paper is restricted, and I don't know if these mutations were induced (most likely were.)

HT to @canadianer for the link that led to my link.


Yes, your understanding is correct.

That being said, it is standard to refer to population / species at specific points in time. Also, it is standard to refer to these ancestral populations relative to what they are the ancestors of. For example, we generally don't refer to the population 2-3 (as you named it) but we rather refer to the node/population/species 3 as the Most Recent Common Ancestor (MRCA) of Athropoda, Mollusca, Chordata and Echinodermata. The tree presented here is not complete but all Athropoda, Mollusca, Chordata and Echinodermata are Bilateria while Cnideria and Porifera aren't. Hence, you could say that the ancestor at node 3 is the MRCA of all Bilateria.

Related posts

This intro to phylogeny
If dinosaurs could have feathers, would they still be reptiles?


Roughly at least, how many types of cells comprise human blood?

I think any answer to this question will be subjective, depending on what you consider to be distinct cell types --- how detailed the classification should be.

As you mentioned, if you consider all immune cell populations that can be separated by surface antigens, that's already a pretty large number. In 2013, the Immunological Genome (Immgen) project reported characterization of 249 immune cell types, and I think they are still working on expanding their catalogue (see immgen.org). One can argue about which of these are really different enough to be called "cell types", but I think it gives a pretty good ballpark number.

At some level of resolution though, the notion of "cell type" itself becomes slippery. While previously it was thought that many cell types were terminally differentiated (unable to change back to more primitive forms), we now increasingly find that these "cell types" are more like temporary "cell states", or phenotypes, that can change over time. For immune cells, this phenomenon is often called "plasticity"; for more information, see for example this paper. The advent of single-cell genomics has further strengthened this view, demonstrating that individual cells can dynamically change their gene expression pattens. These issues makes it hard to uniquely define and count cell types, and it might be more useful to reason quantitatively in terms of the phenotypes and behavior we can measure --- expression patterns, signalling molecules, metabolism and so on.


A cnidocyte is a poison-loaded harpoon connected to a pressure plate, implemented at the microscale level in a cell. Something triggers the plate, the harpoon jets out. Simple enough.


The arithmetic of human sperm
A young, healthy man produces about 1000 sperms every second, which comes to about 90 million per day [1]. These sperms are stored in the epididymis and ductus deferens until ejaculation. With several days of storage, the number can easily become big enough to allow for multiple ejaculations on the same day.
The maturation period of 64 days does not matter here, because sperms form and mature asynchronously [1]. While one spermatogonium is on day 1 of its life, another is on day 2, another on day 3 and so on. Only those sperms that are mature are released from the testes (NOT directly in semen, but into the epididymis for storage).
Does semen normally contain sperm with abnormal morphology?
Yes. Even men in whom 96% of the ejaculated sperms have abnormal morphology can successfully conceive [2].
What happens on ejaculating repeatedly?
This has already been assessed in several studies [3–5]. Overall, the results have been that with repeated ejaculation in quick succession,

Semen volume decreases.
Sperm count decreases (pointing to sperm depletion) but not to zero.
The percentage of sperms with abnormal morphology remains unchanged.

Hope that answers your questions.
References

Mesiano S, Jones EE. The male reproductive system. In: Boron WF, Boulpaep EF, editors. Medical physiology. 3rd ed. Philadelphia: Elsevier; c2017. p 1092–1107.
Cooper TG, Noonan E, von Eckardstein S, et al. World Health Organization reference values for human semen characteristics. Human Reproduction Update. 2010 May–Jun;16(3):231–45. doi: 10.1093/humupd/dmp048
Oldereid NB, Gordeladze JO, Kirkhus B, Purvis K. Human sperm characteristics during frequent ejaculation. J Reprod Fertil. 1984 May;71(1):135–140. doi: 10.1530/jrf.0.0710135
Zvĕrina J, Pondĕlícková J. Changes in seminal parameters of ejaculates after repeated ejaculation. Andrologia. 1988 Jan–Feb;20(1):52–4. doi: 10.1111/j.1439-0272.1988.tb02363.x
Mayorga-Torres JM, Agarwal A, Roychoudhury S, et al. Can a short term of repeated ejaculations affect seminal parameters? J Reprod Infertil. 2016 Jul-Sep;17(3):177-83. http://www.jri.ir/article/674


How is it decided that one drug is better than others by X times?

In general, there is no universal way to quantify the effect of a drug; the quantification procedure depends crucially on what effect the drug is supposed to have. For example, if the drug is supposed to decrease blood thickness, then a measure of the drug's efficacy is a measurement of change in blood thickness upon application of a given concentration of drug. So I'll focus on the case of analgesics, since that's the context of your original question.

While I can't say for sure how this particular quantity was measured, it appears that the effect of analgesics like morphine or enkephalins is measured by direct measurements of pain under different administered concentrations of drug. This can be done in animal or human studies. In animal studies, varying concentrations of a drug are administered, and then the response of the animal to different pain stimuli is recorded. One common example of a pain measurement is a hot plate, where the animal's foot is placed on a hot plate and the time until it tries to remove its foot is measured.

These studies can also be done in humans. In this study (1), the effect of a particular drug was measured by different tests, including

electrical shocks of increasing intensity; maximum intensity of pain subject wanted to endure was measured.
pressure applied to the finger: maximum pressure subject wanted to endure was measured.
heat applied to the forearm (maximum tolerable temperature measured)
dominant hand immersed in ice water for up to 2 minutes. Subjects continually reported level of pain on a 0-10 scale, sum of all pain levels over course of experiment was used as measurement of total pain endured.
Tourniquet applied to cut off blood supply for up to 2 minutes, pain measured in same way as above.

If these pain measurements are recorded when the patient has different levels of the drug in their system, then comparing drug effects amounts to identifying the concentration of drug at which a particular pain response is achieved. In other words

  Drug A is X times more powerful than drug B if drug A causes the same effect on pain response (measured in some way like the ones measured before) as drug B at X times lower concentration.

As a side note, the initial thought I had was that this might be measured by quantifying the receptor-ligand affinity of the various drugs for the pain receptors (opioid receptors) in the nervous system. In that situation, saying that drug A was 200 times more powerful than drug B would amount to saying that A's affinity (or Kd) for a particular receptor was 200 times greater than B. Or something along those lines (see the Wikipedia article on receptor-ligand interactions). That would be a 'universal' way to measure drug efficacies, since a large number of drugs work by blocking certain receptors in the brain. But biology is too complicated to permit a straightforward relationship between binding affinity and perceived drug effect. At least, not yet!

References and Further Reading

(1): Luginbuhl M et al (2001). Comparison of Five Experimental Pain Tests to Measure Analgesic Effects of Alfentanil. Anesthesiology 95:22-29

(2): Jackson H. (1952) The effect of analgesic drugs on the sensation of thermal pain in man. Br. J. Pharmacol Chemother. 7(2): 204–214.

(3):Estrup Olesen A et al. (2012). Pharmacological Reviews 64(3):722-779 Extensive review of this subject.


If you want an actual number, well, it depends (of course).  First off, what is your definition of loci?  That term is broad, and can be construed to mean everything from large, megabase-length genes to every individual base.

That being said, it turns out there are some serious runs of homozygosity (ROH, meaning long regions of the genome that are homozygous) in human populations.  This of course will vary widely from population to population, and amongst outbred individuals.  This paper has some AMAZING figures that are worth checking out but are a little more involved.  Here is a table from this paper which is likewise quite excellent; also, check out figure 3.

EDIT

Your new/edited question is actually very difficult to answer.  For an extreme example, look at the Human leukocyte antigen; some have hundreds or thousands of alleles, but if you were homozygous for each it would be bad (disease susceptibility) but you'd be fine otherwise.

Again, it depends on what you consider an allele or locus.  Most studies look at single base changes (SNPs) because they are 1. easy and 2. useful.  It turns out that there are a lot of these single changes.  The Human HapMap project is hard at work on this and recently published a data set with 3.1 million of these SNPs, among 270 individuals from different populations, roughly one every kilobase.  In a similar vein, the 1000 genomes project recently published an enormous catalog of variation from almost 1,110 individuals in 14 populations.  Both projects focused on major variants.

The best answer I can give you from these studies is that, within a given population, any two DNA strands are around 80% identical, of which around 0.5% is by direct relation (table 5.  Those numbers vary hugely between populations, with Yoruba Nigerians being the most diverse, followed by Utah Whites and then Han Chinese and Tokyo Japanese.  This is just an average across the entire genome, as purported functional differences are comparably rare, with over 85% of protein-altering changes being very rare (<0.5% frequency).

In summary, almost every single site we know of has more than one version somewhere.  Most traits are very complex and are affected by many genes, so even similar appearances can come from very different genetics.  Individuals tend to be highly heterozygous, even if populations on a whole have limited heterozygosity.  A single pair of siblings mating can produce massive defects, showing just how necessary our heterozygosity is.  We each have dozens of large, lethal mutations (deletions, mostly) that don't usually matter thanks to heterozygosity.


What is the function of cystine, cysteine, and cysteine protease?

I'm not sure as to what level of detail I should answer this question, but I will try to give you as much information as I can that I think will be relevant to.. whatever it is you are doing.

Cysteine proteases

Are a class of enzymes that degrade proteins, and utilise cysteine-residues as part of their catalytic mechanism.

Cystine

Is, as you said, a cysteine-dimer.. Which basically means two cysteines stuck together.

These are often formed in the intermediate steps of a cysteine protease's catalytic mechanism.

But also, during protein degradation within the lysosome, cystine can be released as a free molecule. When this happens, it will be transported in to the cytoplasm, to be processed via anabolic pathways into various products, such as glutathione (an antioxidant).

So, basically, the function of your seven-transmembrane (7TM) transporter protein is:

To make accessible to the cell, the digested products of proteins (or, amino acids).

Cystine is an amino acid. Cysteine is also an amino acid. These can all be used by a cell to create new molecules, such as proteins, or antioxidants, or vitamins or cofactors, etc., so many things. And can indeed be broken down in to cysteine.

The function of the CTNS gene, is to provide the cell with the genetic information used to synthesise the 7TM-transporter protein.


Which inflammatory response with Cytomegalovirus infection?

According to this paper the virus triggers the innate immune system and induces inflammatory cytokines as well as interferon stimulated genes (which is a response to a viral infection).
It seems to be recognized by the cells via the Toll-like receptor 2 and CD14, which subsequently trigger the cytokine production. A schematic view comes from the second paper:

These two articles are interesting in this context, the first addresses CMV in special,
the second is a pretty recent review about how viruses are recognized and how cytokines are involved:

Human cytomegalovirus activates inflammatory cytokine responses via
CD14 and Toll-like receptor 2.
Learning from the messengers: innate sensing of viruses and cytokine
regulation of immunity - clues for treatments and vaccines.


You can blast for E.coli proteins only using Uniprot. Firstly, you restrict the search to the "target database" UniprotKB...Bacteria. After performing the blast search, you can further restrict your search results to include only hits for one "Popular organism", e.g. "Escherichia".


We don't get it from the sun, it's synthesized.

Humans can get it...

via nutrition.
via synthesis in the skin, which depends on UV radiation. Sun is the major source of it (the radiation, not the vitamin), and synthesis in the skin the major source of the vitamin. However, it needs further modification in the liver or kidney to become bioactive. UV radiation is necessary and directly causing the opening of a cyclic molecule structure, changing a cholesterol to a previtamin D3.

For more details see chapter 'Biosynthesis' at https://en.wikipedia.org/wiki/Vitamin_D


It looks like a Hesperiidae (Skipper), not a hawk moth (Sphingidae). There are more than 3500 species of skippers worldwide though, and I don't know what species this is. However, I'm sure that somebody who knows butterflies in Bangladesh could identify this to the genus level.

One suggestion/guess/starting point might be Baoris pagana, but this is merely based on a quick glance at skippers found in India.

(picture from http://www.ifoundbutterflies.org/)


What does 'proper' mean in the anatomical context?

This use of proper is simply using one of the normal English meanings of the adjective proper: "In the very strictest sense of the word or phrase".  Thus, while 'oral cavity' generally might be taken to include, in part, the space between the cheeks and the teeth, the term 'oral cavity proper' refers to a stricter definition which excludes that space.


I don't think there is a single "class of graph" that isn't used in biology.

In biology (just like in any other natural science), we have all kind of data types;

non-ordinal variables
boolean
ordinal categorical
numeric
tree data
other types of network data
pure functions (from statistical or theoretical models)
pictures
sounds
etc..

We make all kind of graphs out of these data;

scater plot
points or lines with eventually error bars
bar graphs with eventually error bars
kites
boxplot
images (colored shaped kind of things; e.g. density maps)
phase diagrams
multidimensional graphs
pie charts
function graphs
Venn diagrams
existential graphs
flow diagrams (incl. alluvial diagrams, spankey diagrams, ...)
trees
matching trees
other types of networks
schematic representations
pictures
spectrograms
videos
interactive graphs
etc...

One can really display any kind of data / information in anyway (s)he wants to.

Kite graphs are just simple graphs to compare frequencies variation along a continuous variable and among a categorical (ordinal or not) variable. It isn't the most common types of graphs but we see them. As a matter of fact, in a paper of mine that is currently under revision the figure 1 is a kite graph (with nested non-ordinal categorical variables).

Just look at random papers to find graphs. Go on google.scholar.com and search for any biology subject and you'll find papers with graphs.


Why does a lightsource postpone the time it takes for the leaves falling from a birch tree?

It's to do with the chemistry taking place in the system, and then in turn the balance of energy resources.

Leaves contain chlorophyll, a molecule that traps light energy. It is large molecule containing a long carbon chain and a magnesium atom surrounded by 4 nitrogen atoms. In terms of a plants energy resources it is an 'expensive' molecule, but it is worth it as it is important to the plant.

The conversion of light energy by plants, using chlorophyll, is called photosynthesis. The chemistry of photosynthesis using chlorophyll is complex, but essentially Carbon Dioxide (CO2) from the air is combined with Water (H2O) from the roots to produce sugar and oxygen. Excess sugar is transported to the roots and stored as starch, and some sugar is used to keep the living cells throughout the plant alive. They need energy and this gained through respiration. Again, the actual chemistry is quite complex, but simply put the cells take in Oxygen from the air and 'burn' the sugar to release energy, this gives off Carbon Dioxide and Water. (There is plenty of resources and explanation on the actual mechanism - search for "ATP and ADP in plants")

Notice that it starts with carbon dioxide and water and ends with carbon dioxide and water, the energy is held within the chemical bonds.

When there is plenty of light (and water) the rate of photosynthesis, and therefore the rate of energy production, is high. The plant is producing excess energy, and the leaves are 'worth' the energy needed to keep them alive and functioning. Note that temperature also has an influence. The warmer the temperature (to a point) the greater the rate of photosynthesis.

So, in temperate climates with markedly different day lengths and temperatures between the summer and winter seasons some plants have evolved to be deciduous and shed their leaves in the autumn. The point at which this will start to happen will be when the day length shortens, and the temperature drops, and so when the amount of energy that the leaves are able to produce starts to balance the amount of energy being used to maintain the leaf.

If a plant has an artificial light source then the leaves will continue to be able to produce more energy than they use and so will be retained for longer.


Certainly not cicada killers--those have yellow stripes on them, are considerably larger, and also have a very different shape of abdomen. Here's a good pic of one of those: https://bugguide.net/node/view/1721236/bgimage.
They certainly look to have a hymenopteran "waist" so that means they aren't termites, they are some kind of winged ant. Possibly carpenter ants due to the large size (for ants) and the reddish-brown color (like this one https://bugguide.net/node/view/1056576/bgimage).


Do animals other than humans have different blood types?

The answer to this question can be found by searching the Internet.

  For some blood types, evolution and environmental selective pressures
  are clearly important for their persistence. For example, the Duffy
  blood type includes a receptor that allows certain types of malarial
  parasites to enter the red cell. Thus, in some malarial areas of
  Africa, populations with Duffy-negative blood types have a distinct
  survival advantage because absence of the Duffy antigen provides a
  measure of protection against malaria. The percentage of people
  lacking the Duffy antigen is much higher in these locations than in
  areas not endemic for malaria.

more here http://www.scientificamerican.com/article/why-do-people-have-differ/

  Animals and bacteria have cell surface antigens referred to as a blood
  type. Antigens from the human ABO blood group system are also found in
  apes and old world monkeys, which have inherited the same system.
  Other animal blood sometimes agglutinates (to varying levels of
  intensity) with human blood group reagents, but the structure of the
  blood group antigens in animals is not always identical to those
  typically found in humans. The classification of most animal blood
  groups therefore uses different blood typing systems to those used for
  classification of human blood.

more here  http://en.wikipedia.org/wiki/Blood_type_%28non-human%29


What controls specific gene silencing during cell differentiation?

The cells differentiation during post fertilization period is govern by a set of regulatory genes called Homeotic genes.These are genes that "select" the identity of entire segments or structures in the bodies of developing organisms.
These gene encodes a transcription factor that is expressed in a specific region of the organism starting in its early development i.e. embryo stage. The transcription factors change the expression of target genes to enact the genetic “program” that's right for each segment.

The homeotic transcription factors shown in the diagram above[homology between Hox genes in mice and humans] contain a DNA-binding protein region called the homeodomain, which is encoded by a segment of DNA, called the homeobox.The animal genes containing homeobox sequences are specifically referred to as Hox genes. This family of genes is responsible for determining the general body plan, such as the number of body segments of an animal, the number and placement of appendages, and animal head-tail directionality.

In addition to this genes, the early developmental cascade include the following genes:

Maternal effects genes:These are genes whose mRNAs are placed in the egg cell by the mother before fertilization. Some of the mRNAs are “tied” to the head or tail end of the embryo and are responsible for setting up the head-tail polarity. The maternal effects genes encode regulators of transcription or translation that control each other as well as other genes.
Gap genes: They are activated through interactions between the protein products of the maternal effects genes, and they also regulate each other. They're responsible for defining large, multi-segment regions in many organisms.
Pair-rule genes: These are turned on by interactions between gap genes, and their expression patterns are refined by interactions with one another. They appear in multiple “stripes” along the embryo, similar in pattern to the segments of the adult organism.When a pair-rule gene is missing due to mutation, there is a loss of structures in the segment regions where the gene is normally expressed.

For further information you can refer this link:
-  Click here 1
- Click here 2
-  Click here 3


I've been trying to figure out something that works for some time.  I have recently tried 3 cheap protocols using commonly available lab reagents.  I was using buccal samples (0.2 ml of spit).

1) Boil the sample in Tris EDTA Buffer
2) NaOH Extraction
3) Direct N Lyse

I compared them to a genomic DNA extraction kit (FAST DNA Prep - MP Biomedicals).

I have heard lots of people use NaOH extraction to get DNA from tissue and cell preps, but none of the first three worked for me after 2-3 tries.  One of the people in my lab said that I could replace the bead beater with vortexing with glass beads.

I tried vortexing with beads with all four methods, including the kit and only the kit worked.  I got a PCR result from control primers.

When you look at the costs of getting all the ingredients for the buffers kits are not so expensive - $1-$2 per sample.

A lot of these kits can handle solid animal tissues, though the one I have doesn't specifically cite hair.  I would try it out.

I guess the point of my post was that there are lots of simple sounding published methods, but they don't always produce results without a bunch of debugging.  I know alkaline lysis has worked for several people I know and is the basis of the kits.  Its pretty simple.

That's my experience anyway.


What does the human body use oxygen for besides the final electron acceptor in the electron transport chain?

Superoxide, O2− is created by the immune system in phagocytes (including neutrophils, monocytes, macrophages, dendritic cells, and mast cells) which use NADPH oxidase to produce it from O2 for use against invading microorganisms. However, under normal conditions, the mitochondrial electron transport chain is a major source of O2−, converting up to perhaps 5% of O2 to superoxide. [1]
As a side note, there are two sides to this coin.  While this is a useful tool against microorganisms, the formation of the reactive oxygen species has been incriminated in autoimmune reactions and diabetes (type 1). [2]

[1] Packer L, Ed. Methods in Enzymology, Volume 349. San Diego, Calif: Academic Press; 2002
[2] Thayer TC, Delano M, et al. (2011) Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes,60(8), 2144-51.


Is new idea equivalent to forming new synaptic connection?

There is a lot of debate over what "thoughts" are in terms of consciousness, and this has been referred to as the "hard problem". However, it seems pretty clear that in some form patterns of brain activity are the "stuff" that underlies a thought/idea: if you change patterns of brain activity, you change the thought.
Therefore, I would describe a "new" idea as a "new pattern of brain activity" rather than connections. While the exact timescale of a "pattern" should be is unclear, perhaps a few hundred milliseconds is a good guess (see for example Luczak et al 2015, and the recent paper by Davis et al 2020). Brain activity is constantly shifting, of course, so really every moment experienced is a new thought of some sort.
There are too many studies to name all of them that show that some consistent pattern of brain activity is associated with some thought. The review by Harris, 2005 is a favorite of mine, but there are many levels of analysis to approach these questions. You might find some more compelling work among the studies of the biological basis of perception.
One particularly elegant paper is Liu et al, 2012. They used some molecular tricks to identify neurons in a rodent brain that are activated during a fearful context, and they cause long-term expression of a protein in those specific cells that they then use to reactivate those same cells at a later time. Reactivating those cells causes the fear behavior to return, effectively triggering the same ideas.
Connections between cells can also change pretty rapidly, but this would be better described as memory rather than an initial thought or idea. This can involve de novo creation of synapses, but more often is studied as a change in synaptic strength. Weak synapses can be strengthened with certain input patterns, and we call this long-term potentiation. The idea of connections between neurons as the stuff of memory goes back some 100 years to Ramón y Cajal.

Davis, Z. W., Muller, L., Martinez-Trujillo, J., Sejnowski, T., & Reynolds, J. H. (2020). Spontaneous travelling cortical waves gate perception in behaving primates. Nature, 1-5.
Harris, K. D. (2005). Neural signatures of cell assembly organization. Nature Reviews Neuroscience, 6(5), 399-407.
Liu, X., Ramirez, S., Pang, P. T., Puryear, C. B., Govindarajan, A., Deisseroth, K., & Tonegawa, S. (2012). Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature, 484(7394), 381-385.
Luczak, A., McNaughton, B. L., & Harris, K. D. (2015). Packet-based communication in the cortex. Nature Reviews Neuroscience, 16(12), 745-755.


What limits the maximum spacing of Nodes of Ranvier and which organisms tend to have the widest gaps?

This is best answered via something called cable theory.  Basically, as the action potential (AP) propagates along the membrane of the axon, it's tripping voltage gated channels that "renew" the flux of ions into the stream at the nodes. There are no ion channels under the sheathing (or they are there anatomically and inactive, but I don't remember), so the current is able to zip through that area.  There's no renewal of AP, but there's no loss due to leak of ions either.  Since there's no influx of ions from outside of the membrane until the next node, the capacitance and resistance of the membrane is exponentially decaying the voltage.  So, if the distance between the nodes was too long, the voltage would just die off and the AP wouldn't propagate.

I don't have any anatomical data about individual species, but know that only the smaller diameter axons require sheathing to compensate for the slower ion flow due to higher resistance (e.g., the squid giant axon(not to be confused with the "giant squid" axon) has no myelination due to its large diameter).


How can I reduce the background gradient in phase contrast microscopy?

If you're not already doing so, make sure you set up Kohler illumination every time you use the microscope -- see this tutorial by Steven Ruzin.

The lamp or the phase ring may be misaligned. There are usually small hexagonal set screws on the lamp housing and the condenser, respectively, to adjust these.

Imaging near the edge of a dish or well can lead to uneven illumination as the light is bent by the walls of the culture vessel. If this might be the cause, try re-doing the Kohler illumination before you take each image.

If you can't find the cause of the problem, there are several ways to correct for uneven background described here. Maybe one of them will work with your analysis.


Flaccidity in plant cells

  The failure to display turgidity especially as seen with plant cells.
  The suspension of cells from plants in isotonic solutions results in the state termed flaccidity. On a cellular level it represents a lack of pressure of the plasma membrane against the plant cell wall. A more extreme state, termed plasmolysis, is seen given suspension of cells in a hypertonic solution, i.e., as occurs with bacteria suspended in solutions containing high salt or sugar concentrations.

A flaccid cell is one which is in an isotonic solution, this means that the solution and the cell have an equal water conc.. Although there are always water molecules flowing into and out of the cell, they balance each other out. So a cell is referred to as flaccid when it is between being turgid and plasmolysed.

Plasmolysis in plant cells

  If a plant cell is placed in a hypertonic solution, the plant cell loses water and hence turgor pressure by plasmolysis: pressure decreases to the point where the protoplasm of the cell peels away from the cell wall, leaving gaps between the cell wall and the membrane and making the plant cell flaccid.

Sources:

http://www.biologyaspoetry.com/terms/flaccidity_cell_biology.html
http://study.com/academy/lesson/what-are-plasmolysis-deplasmolysis.html
https://en.wikipedia.org/wiki/Plasmolysis


Premise of life cycle synchronization between predator and prey

New Answer, based on first comment by user2686410 and subsequent edits to the question.

  I have interpreted "synchronizing their own generations to divisors..." to mean synchronizing the length of the life cycle. I am happy to hear of another interpretation.

First, the overall goal of Goles et al. (2001) does not seem to test hypotheses related to the evolution of life cycles in the cicadas per se. It seems their overall goal instead may have been to explore the generation of prime numbers from numerical theory, using biologically-based models. For example, from the abstract they state,

  The model marks an encounter of two seemingly unrelated disciplines: biology and number theory. A restriction to the latter, provides an evolutionary generator of arbitrarily large prime numbers.

and at the end of the discussion they write,

  Although there are traditional methods for prime number detection (see e.g., Ref. 23) that are faster than the methods presented here, it is remarkable that the generation of prime numbers can be performed using a biological model.

To more directly address your question and if I understand their models, Goles et al. (2001) do seem to allow the the life cycles of both predators and prey to co-evolve yet this is not always clear.

  We compare now a prey mutating to a cycle Y' with the resident prey (cycle length Y ) at constant X. Analogously, we compare mutant cycles X' with resident cycles X at constant Y (Goles et al. 2001, pg. 34; emphasis added).

Here, they seem to be saying that the life cycle of one (predator or prey) can change while other other remains constant (prey or predator). The life cycles don't coevolve.  Subsequent formulas and statements imply an interactive effect between the predator and prey life cycles. (Honestly, their writing is somewhat opague to me and they do not define all of their mathematical terms, making it difficult to follow the logic of their models.)

Regardless, the results of their initial models, shown in the figure below, shows the prey converging on a 17 year life cycle while the predators converge on a 4 year cycle. Somewhat more complex models tended to converge on 13 and 17 year cycles, although other primes like 11, 19 and 23, had similar probabilities of evolving.

Goles et al. (2001) admit at the outset of their paper that there is no evidence for predators with periodical cycles that align with the life cycles of cicadas. This would be consistent with general ecological observations. Most predators consume multiple prey items. Highly specialized predators would be more vulnerable to extinction if their prey source went extinct.

Another numerical model, developed by Tanaka et al. (2009) explicitly to explore life cycle evolution of cicadas, does not include predator life cycles at all. Their results still converge on 13 and 17 year life cycles although they restricted the possible range of life cycles to between 10 and 20 years. Thus, it does not appear to be necessary for predators to evolve a life cycle that coincides with prey life cycles for the predator satiation hypothesis to work. Of course, this is consistent with the real world observations that cicadas do not appear to have predators with concommitant life cycles.

Original answer, lightly edited

In the case of the cicadas, they are the prey, not the predators. They are not synchronizing their life cycles with the predators (if I am interpreting your entire question correctly). The argument is that cicadas have evolved synchronized life cycles to maximize survivorship.  By having a large number of individuals emerge within a very short period of time, the very high density means most individuals will live long enough to reproduce because the predators (birds, small rodents, etc.) will be satiated (see Williams and Simon 1995 for a review and pointers to early literature). Some predators of cicadas will be always present so the cicadas are not synchronizing to any specific predator.

Goles et al. (2001) used numerical models to argue that such life cycles will tend to converge on prime numbers. (As discussed in the update above)

Tanaka et al. (2009) recently argued, again using numerical models, that the prime number-based life cycles of cicadas evolved as a result of the Allee effect. The Allee effect basically states that there is a positive association between the fitness of individuals in the population and the population size or density. Below a certain size, a population is unable to sustain itself and is vulnerable to extinction. Tanaka et al. argue that the Allee effect results in prime-based life cycles under varying environmental parameters. They further argue that maintenance of alternate life cycles minimize hybridization between groups with different life cycle timings.

What seems to really remain to understand the evolution of cicada life cycles is to unravel the genetic mechanisms involved with timing.

Literature Cited

Goles, E. et al. 2001. Prime number selection of cycles in a predator-prey model. Complexity 6: 33-38.

Tanaka, Y. et al. 2009. Allee effect in the selection for prime-number cycles in periodical cicadas. Proceedings of the National Academy of Sciences USA 106: 8975-8979.

Williams, K.S. and C. Simon. 1995. The ecology, behavior, and evolution of periodical cicadas. Annual Reviews of Entomology 40: 269-295.


Do adjacent axons in a nerve influence each other?

Yes, activity in other cells can affect the surrounding electric field and thereby influence the behavior of nearby neurons. This phenomenon, known as ephatic coupling, can be important but is usually small.

For many cases, it is likely too small to be of physiological importance. Note that individual action potentials are quite transient and, especially in myelinated axons, the resulting currents are local and small. Therefore it's unlikely that a single neuron's activity will have a noticeable effect on nearby neurons.

However, in unmyelinated axon tracts and/or when a larger group of neurons is active, ephatic coupling is more likely. In particular, it seems to play a role in synchronizing cell populations during oscillations. For example, Anastassiou et al (2011) found that firing of cortical neurons could be entrained by the extracellular field and affected the intracellular membrane potential by about 0.5 mV.

Anastassiou, C.A., Perin, R., Markram, H., Koch, C., 2011. Ephaptic coupling of cortical neurons. Nature Neuroscience 14, 217–223.

Also, for reference:

Jefferys, J.G., 1995. Nonsynaptic modulation of neuronal activity in the brain: electric currents and extracellular ions. Physiol Rev 75, 689–723.

Buzsáki, G., Anastassiou, C.A., Koch, C., 2012. The origin of extracellular fields and currents — EEG, ECoG, LFP and spikes. Nature Reviews Neuroscience 13, 407–420. (see pages 411-412)

Edit:
For your particular case, action potential propagation in one axon is very unlikely to affect the other axons in any relevant way in a tract of myelinated axons. This is especially true because the initiation of action potentials does not occur along the axon itself, but where the axon is just branching from the cell body (the axon initial segment). Threshold is important at the initiation site, but is not really relevant in the tract itself, where the axon is just conducting the signal it receives from the initiation site.


Mitochondrial donation - why is the second woman needed?

It looks like the current techniques might better be described as "nuclear donation".  You take an ovum with healthy mitochondria, remove the nucleus, and insert the desired nucleus from the woman with bad mitochrondria.  So yes, currently, the mitochonrdria have to come from an ovum, and therefore a woman.


The answer is of interest not only in sleep but also the perceptions of patients under anesthesia, comatose states, etc.
Our senses aren't 'dimmed' in sleep. There is no effective way to turn off our senses. The best way to explain what happens in sleep is that at some point (the last point, actually), our cognitive processing of sensations changes. That is, our higher brain functions allow us to ignore certain sensory input. This effect has been most studied in sound perception.
In a sleep study involving sound and EEG/fMRI during all phases of (drug-free) sleep,

The first significant result of this study is that the pattern of brain activation associated with auditory stimulation was strikingly similar in wakefulness and sleep, suggesting that sensory processing occurred in both conditions. However, we found qualitative differences in brain activation associated with auditory processing during sleep compared to wakefulness. The reduced regional activity during sleep, compared to wakefulness, in the left parietal and, bilaterally, in the prefrontal cortex, thalamus, and cingulate gyrus (part of the limbic system) suggests that these areas may be involved in the further processing and perceptual integration of sensory inputs likely to occur during wakefulness only.[1]

Supporting this is evidence that some sounds awaken someone no matter at what stage they are in sleep, for example, young mothers are woken up by their infants' lightest movements[2], and the fact that we respond to our own names in a similar fashion in sleep and in wakefulness, but such responses are not shown for presentation of other first names.[3]

These results suggest that the sleeping brain, during SII and PS, elicits a differential cognitive response to the presentation of the subject's own name, comparable to that occurring during wakefulness, and therefore that the sleeping brain is able to detect and categorize some particular aspects of stimulus significance.[3]
Thus, the results suggest that when subjects were listening to their own name during sleep some brain regions were selectively more responsive than in any other condition. ...we have demonstrated that the sleeping brain is able to process auditory stimuli. In addition, we postulate the existence of a functional network capable of detecting and facilitating processing of emotionally relevant inputs during sleep.[1]
Our results support the view that PS is not a state of "sensory isolation"; failure to respond to external stimuli during this stage may depend upon mechanisms occurring only after the sensory input has undergone cognitive analysis.[4]

However, as you noted, odors are not good at waking people up.

Some suggest that the human olfactory system during sleep is sufficiently well tuned to ensure arousal to such threatening stimuli as odors associated with smoke from fire. Our results strongly suggest otherwise. The intensity, strength, and noxiousness of the pyridine stimulus elicited behavioral arousal or EEG activation on fewer than half of stage 2 trials, less than one third of REM-sleep trials, and virtually no stage-4- sleep trials. This is a nontrivial lack of response, since pyridine is a component of coal tar and is also used as a herbicide for firewood, and thus is a likely by-product of many real fires. In practical terms, therefore, olfactory awareness in humans is low to absent during sleep, and human olfaction appears insufficiently sensitive and reliable to act as a sentinel system. We further note that auditory arousal threshold is highest in young and sleep-deprived individuals, increasing the likelihood that olfactory processing is even worse for children and sleep-deprived adults.[5]

The methodology in the olfactory study varies quite significantly from the auditory study. Better studies may shed more evidence on why olfactory stimuli are processed differently from other stimuli.
As to what percent? That probably differs from person to person, and I did not search the literature for that.
[1] Auditory Processing across the Sleep-Wake Cycle: Simultaneous EEG and fMRI Monitoring in Humans
[2] Changes in sleep patterns of young women from late pregnancy to postpartum: relationships to their infants' movements
[3] A differential brain response to the subject's own name persist during sleep
[4] Brain Processing of Stimulus Deviance During Slow-Wave and Paradoxical Sleep: A Study of Human Auditory Evoked Responses Using the Oddball Paradigm.
[5] Minimal Olfactory Perception During Sleep: Why Odor Alarms Will Not Work for Humans


Why do soil bacteria produce nitrous oxide as a result of anhydrous ammonia fertilizer application?

Addressing the first part of your question:

  Is it common for most soil bacteria to make significant quantities of
  nitrous oxide after ammonia is added, or is there only a small subset
  of bacteria present in soil that might do this?

No, not all soil bacteria can oxidize ammonia. According to wiki:

  The oxidation of ammonia into nitrite is performed by two groups of
  organisms, ammonia-oxidizing bacteria (AOB) and ammonia-oxidizing
  archaea (AOA).

The role of archaea in the soil nitrogen cycle is not well-known yet, although it could be greater than that of bacteria. On the other hand, the role and metabolism of AOB are more or less studied.

The process of ammonia-oxidizing is also called nitrification and AOB sometimes referred as nitrifying bacteria. The most known bacteria genera from this group are Methylomonas, Nitrosococcus, Nitrosomonas and Nitrosospira. I think the most studied species is Nitrosomonas europaea Winogradsky 1892.

For reference see: Arp DJ, Sayavedra-Soto LA, Hommes NG. Molecular biology and biochemistry of ammonia oxidation by Nitrosomonas europaea. Arch. Microbiol. 178 (2002) 250-5.

The second part of the question:

  What is the metabolic pathway in this case?

Although, the metabolic pathways vary in different genera, let's look at ammonia metabolism in N. europea.

In the simplest case, it is a two-step process.
According to KEGG:

Step 1. The enzyme ammonia monooxygenase converts ammonia to hydroxylamine. The enzyme contains copper, iron and possibly zinc. It requires two electrons, which are derived indirectly from the quinone pool via a membrane-bound donor. The reaction is:

NH3 + a reduced acceptor + O2 = NH2OH + an acceptor + H2O

Step 2. The enzyme hydroxylamine dehydrogenase converts hydroxylamine to nitrite. This reaction requires specialized cytochrome as an acceptor of electrons. The reaction is:

NH2OH + H2O + 4 ferricytochrome c = NO2 + 4 ferrocytochrome c + 5 H+

While nitrite is the main product, the enzyme from N. europaea can produce nitric oxide as well. Therefore Step 2 can produce nitric oxide (NO). In this case, additional mechanisms of converting NO to NO2 are involved.

Further destiny of released nitrite can be different. In one process it could be oxidized by different microorganisms (bacteria, archaea) to nitrate (NO3) which could be consumed by plants or washed out to deeper horizons with water. In another case, nitrite, nitric oxide and nitrate could be involved in process of denitrification. During this process, a group of denitrifying organisms (bacteria, archaea and fungi) consume nitrogenous compounds and reduce them to nitrogen (N2), which can escape to the atmosphere. This process can occur through different metabolic pathways mainly with aid of reductases like nitric oxide reductase. One of the possible intermediate product of such pathways is a nitrous oxide (NO2). If N2O escapes from cells we can observe a resale of nitrous oxide from soil.

Let's return to your first question, and particularly to the part where you ask about significant amounts of nitrous oxide.

First of all, nitrification is a natural process and is a part of the nitrogen cycle. Some organisms fixate nitrogen and convert it to ammonia, some oxidize ammonia to nitrous compounds and some of them reduce it back to nitrogen. It occurs everywhere virtually in all terrestrial and water biocenoses. In a healthy ecosystem, the inflow of nitrogen is theoretically equal to the outflow (with temporal deposition in trophic chains). In such natural conditions, the release of nitrous oxide should be neglectable.

The situation changes significantly when we add an ammonia to soil artificially as a fertilizer. The main problem is that we break an equilibrium between nitrogen fixation, nitrification and denitrification. The second big problem is that an ammonia is toxic for most organisms, so we can alter microbiome. In such case, we can expect an excess of products of nitrification and improper denitrification with exaggerated levels of released nitrous oxide. The actual proportions vary significantly depending on both biotic and abiotic conditions, therefore it is difficult to predict real levels of nitrous oxide released without in situ examination.

P.S. sorry for possible bad writing.


It is neither living nor dead. It is simply not alive the way that any other collection of chemicals is not alive. Is salt alive or dead?

A cell's membrane consists of a collection of chemicals (mainly lipids and proteins). Individual chemicals can never be considered living or dead, any more than rocks or water can be living or dead. While the actual definition of life is tricky, everyone agrees that in order to be alive you need to (at the very least)

Somehow interact with your environment
Be able to make more copies of yourself

Therefore, the cells themselves are alive but the individual parts of the cells are not since they cannot make copies of themselves (this gets complicated when considering some organelles but never mind that here). Similarly, you are alive but your teeth are not. While you can make more of you (you can have children) your teeth cannot make more teeth.


Why bovine serum albumin is used in mass-spectroscopy and how to interpret such data?

Their LC-MS-MS data was only semi-quantitative as gathered, meaning they could compare relative levels of one protein to another in the same sample, but not necessarily between different samples with a high degree of confidence. So, they spiked known amounts of BSA, an extremely well-characterized protein frequently used in the lab, into their samples and created a standard curve across different concentrations that correlated pretty well with the input amounts. They could then use this curve to better quantify the other proteins in their samples among all the different sample types. This in turn allowed them to say with greater certainty that, for example, Protein X was expressed at three-fold higher levels in Sample A than in Sample B. Otherwise, they would only have been able to say that Sample A expression of Protein X was higher than Sample B.


A substrate is an underlying substance or layer, or less strictly, the medium within or upon which an organism grows. For instance, you can have a filamentous fungus grow on a solid medium (e.g. on an agar plate) or in liquid medium (e.g. in a shaken flask containing a solution) and its substrate would be the contents of the agar or solution. It's nothing more fancy than that.

For instance, you could design 4 growth conditions for a strain of fungus.

Case in point, a hypothetical table could look like this:

                        *Substrate*

                Wheat straw     Sugar beet pulp
                             |
          Liquid         1   |   2
                             |
*Medium*             -----------------
                             |
           Agar          3   |   4

Simple!


Anecdotally I have never observed a preference in lab mice, but we have never made a detailed study of it. Males do not seem to favor non-incestuous over incestuous breeding. Though inbreeding does tend to produce smaller litter sizes over generations and inbred strains of lab mice do tend to be less hearty. Though lab mice are a bit removed from the situation in the wild.


What is the strand specificity of a reference genome?

First of all, the reference genome strand specificity is referred to as sense (positive strand) or antisense (negative strand). Now let's consider to sequencing data or FASTQ files. When we align reads, a resulting SAM or BAM file has a column specifying strand information, we usually see a + or - strand.

For more background on the strand names here's a somewhat incorrect note from the wiki article under sense (molecular biology)

  The strand names actually depend on which direction you are writing
  the sequence that contains the information for proteins (the "sense"
  information), not on which strand is on the top or bottom (that is
  arbitrary). The only real biological information that is important for
  labeling strands is the location of the 5' phosphate group and the 3'
  hydroxyl group because these ends determine the direction of
  transcription and translation. A sequence 5' CGCTAT 3' is equivalent
  to a sequence written 3' TATCGC 5' as long as the 5' and 3' ends are
  noted. If the ends are not labeled, convention is to assume that the
  sequence is written in the 5' to 3' direction. Watson strand refers to
  5' to 3' top strand (5' → 3'), whereas Crick strand refers to 5' to 3'
  bottom strand (3' ← 5').[4] Both Watson and Crick strands can be
  either sense or antisense strands depending on the gene whose
  sequences are displayed in the genome sequence database. For example,
  YEL021W, an alias of URA3 gene used in NCBI database, defines that
  this gene is located on the 21st open reading frame (ORF) from the
  centromere of the left arm (L) of Yeast (Y) chromosome number V (E),
  and that the expression coding strand is Watson strand (W). YKL074C
  defines the 74th ORF to the left of the centromere of chromosome XI
  and denotes coding strand from the Crick strand (C). Another confusing
  term referring to "Plus" and "Minus" strand is also widely used.
  Whatever the strand is a sense (positive) or antisense (negative), the
  default query sequence in NCBI BLAST alignment is "Plus" strand.

Although it is correct when it says

Watson = Sense = Plus Strands
Crick = Antisense = Negative Strands

A satisfactory answer/convention is provided/suggested in this PMC article covering the terminology of the Watson and Crick strands

Below are some interesting excerpts from the publication:

  The earliest reference that we could find to the "Watson strand" and
  the "Crick strand" is somewhat tongue-in-cheek and comes from a pair
  of papers in 1967 by Wacław Szybalski and colleagues. They
  bound the two DNA strands of phage λ to the synthetic polynucleotide,
  poly(IG), which has an affinity to cytosine-rich regions. They then
  separated the two strands by density, which turned out to be
  determined by the amount of bound poly(IG). In a cesium-chloride
  density gradient, the strand with more bound poly(IG) was denser and
  heavier than its complement. Because the "dense" strand was
  cytosine-rich, Szybalski and colleagues called it the "C strand."
  Logically, thus, the complementary strand, which was guanine rich,
  should have been the "G strand." Instead, it was christened the "W
  strand."

So the authors note that the Strands started on their terminology journey with their roles reversed with the Crick strand specifying the heavy strand (with IG) and the Watson strand specifying the lighter one.

They also note that the present day terminology of the WC model is non-arbitratrily based on the current horizontal drawing convention where one strand is placed on top and the other at the bottom.

They also suggested a typical convention which is followed today. If it was due to their suggestion is a different matter altogether, but beyond the scope of this question.

  Given the amount of effort already spent on standardizing such
  databases, and their influence on other disciplines, we feel that the
  genomic definition of Watson and Crick strands has the most mass
  behind it. Specifically, we find that the unambiguous usage of the
  Saccharomyces Genome Database to be the most useful. Under the first
  part of our proposal, the centromere is a reference point that divides
  a chromosome into two arms of unequal length. The chromosome is
  oriented so that shorter arm is on the left and the longer arm on the
  right. Furthermore, the top strand has its 5'-end at the left
  (short-arm) telomere and its 3'-end at the right (long-arm) telomere.
  This strand is the Watson strand. Similarly, the bottom strand has its
  5'-end at the right telomere and its 3' at the left telomere and is
  the Crick strand. We further propose that "top", "forward", and "plus"
  be used as synonyms for the Watson strand and "bottom", "reverse", and
  "minus" for the Crick strand.

and later on...

  If it is ultimately impossible to distinguish Watson and Crick strands
  using biological properties, then we propose that Watson should refer
  to the stand arbitrarily used as a reference in a database (i.e. the
  "plus" stand) and the Crick strand should refer to its complement

But let's come back to sequencing data or FASTQ files. When we align reads, a resulting SAM or BAM file has a column specifying strand information, we usually see a + or - strand.

Which suggests that the product originated from either the Watson (positive) or the Crick (negative) strands. For example, a read is actually the reverse complement of the product, but since you do a PCR step during you library preparation, that particular bit of information is lost and therefore the downstream analysis protocols tend to consider the entire loci any single product aligns to.

The difference between strand specific sequencing and non-strand specific sequencing are covered here.


How does cerebrospinal fluid circulate in the central nervous system?

There are several points here.

Arachnoid granulations are not the only "sinks" for CSF.

Even though it is true that most of the CSF is eliminated from ventricular system and subarachnoid space through these granulations, there are also suggestions that there are also other potential mechanism of shunting CSF into the venous system:

Cranial nerves leaving CNS go through dura mater and these holes are not sealed, so it is suggested that some CSF can just go along the nerves and then accumulate in the lymphatic nodes in submucus.
Dura mater is mostly perforated at the area of lamina cribrosa, that basically separates the nasal holes and our brain. Leaking through multiple small holes here CSF is accumulated into the lymphatic submucusal nodes, found in abundance here. This way is considered to be primary CSF drainage way in newborns who don't have a well developed granularities in (sub)arachnoid space.
Spinal nerves, especially in the upper part of the spinal cord, also leave unsealed holes and the presence of lymphatic nodes adjacent to the places where these nerves leave the verterbral column also make them a potential place for CSF drainage.

Arachnoid granularitis do not only drain, they are capable of active CSF uptake.

CFS is not just "circulating" here going from the place of its origin in lateral ventricles to venous system. The granularities are here to actively resorb this fluid, meaning that they effectively take it up forming vacuoles and then excrete it to the venous system. Constant uptake leads to the pressure gradient (see also below!) that acts as a driving force for CSF.

Venous system has generally low pressure, thus sucking the CSF up to drainage points.

Speaking about drainage we also should consider the fact that the venous system has a pressure lower than the atmospheric pressure and much lower than pressure in any middle-sized arterial vessels. This is reached by having elastic walls and by transmitting the negative pressure from the mediastinum during the inhale, when the diaphragm and the thorax expand. This negative pressure propagates mostly to the connected vessels, including sinus system. Due to the elastic wall other parts of venous system can accommodate this negative pressure constrict their lumen, but not the sinus system which has a hard external framework formed by dura mater and bones. That is here we can measure the lowest pressure and this is the pressure that sucks CSF in into the venous system.

I hope that answers your question.


Why is the prefrontal cortex called such?

The prefrontal cortex (PFC) is a part of the frontal lobe (Fig. 1).

Lobe means

  [A part] demarcated from the rest of the organ by a fissure (crack), sulcus (groove), connective tissue or simply by its shape. For example, there are the frontal, parietal, temporal, and occipital lobes of the brain.

Cortex means

  The outer or superficial part of an organ or bodily structure (such as the kidney, adrenal gland, or cerebellum or a bone); especially: cerebral cortex

The frontal lobe is called as such, because... it's in the front of the brain.

The prefrontal cortex is called that way because it forms the frontmost part of the frontal cortex. Prefrontal means

  anterior to or involving the anterior part of a frontal structure

Anterior meaning

  situated before or toward the front

Indeed Siddiqui et al (2008) mention:

  The anterior part of the frontal lobe referred in the literature as ‘pre’-frontal lobe has been simultaneously referred to as ‘frontal granular cortex’ and ‘frontal association cortex.’ The anterior most portion of the frontal lobe is occupied by the PFC...

Reference
- Siddiqui et al., Indian J Psychiatry (2008); 50(3): 202–8

Fig. 1. The frontal lobe includes the prefrontal cortex (PFC). source: Socratic


Are homozygous carriers of the CCR5-Δ32 allele fully immune to all known strains of HIV?

I would say no.
Some HIV strains are X4-tropic and not R5 tropic. That means that the virus uses the CXCR4 coreceptor and not the CCR5 coreceptor for entry into the CD4-positive cell.


Can a tumor produce something not currently found in our own bodies?

If you look at a cancer textbook (eg. Robert A. Weinberg's The Biology of Cancer), you'll find that by definition, a tumor arises from tissues normally found in the patient's body. There's a great deal more to it than just that simple statement, but given the context of the question, I think that answer should suffice.

In writing, "...tumors growing a tooth, hair...", I think you're talking about teratomas. These contain "normal derivatives of all three germ layers". These arise naturally from cells "...typically found in the human body..."

Cancer is a process where mutations in a single cell transform that cell into something that is by definition not "typically found in the human body." But a human cell transformed by mutation into a tumor (benign or malignant) is never (to the best of my knowledge) going to magically become a cell from another species or a very distant ancestor (ie. something that is not "typically found in the human body.").


DNA gel extraction: chemical contaminants

Here are some possible reasons:

Your yield is very low, which you can infer from a low 260 absorbance. Either make sure your restriction digest is efficient or add more substrate to the digest reaction.
Carbohydrate contamination, which will cause high 230 absorbance. Wash the column one more time with buffer QG (the step is described in the Qiagen gel extraction manual; if you're already doing a wash with buffer QG, do an extra one).
You didn't dry the column enough and some ethanol from the wash remains in the sample. This can also cause high 230 absorbance and your sample with smell of ethanol. Place your column in an empty collection tube and spin it down for a long time (15-20 min). Don't worry, the DNA can withstand it.


Help Finding Specific BlaZ Gene Type Sequences on Genbank

You might have already tried this, but how about doing a BLAST search using one of the sequences you do have, and perhaps limiting the organism to Staph a.
More info:
The below article did a similar comparison and mentions types RN9 and FAR10, perhaps these are related (or  misspelled originally)  See below.
"Real-Time PCR Assay for Detection of blaZ Genes in Staphylococcus aureus Clinical Isolates" at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993521/
mentions:
"type A, PC1(pI254) and NCTC 9789; type B, 22260 and ST79/741; type C, 3804(pII3804), RN9(pII147), and V137; and type D, FAR10"
In any case I highly recommend going to your original article of interest, and use the "cited by" function to find more recent papers.


Run length means how far the mitochondria move, each time they move.
The article this references is:
"GSK3β Is Involved in the Relief of Mitochondria Pausing in a Tau-Dependent Manner".
This article has a figure showing the distances in micrometers, although I have trouble working out interpreting the error bars on the graph to see if the distances ("run length") are really different.


How do cancers eventually lead to death / other debilitating symptoms?

This is a very general answer to a very general question.

So, in general, cancer occurs when cells stop behaving as they are supposed to.
Your body is made by something like 200 different kinds of cells (epithelial cells, neuronal cells, blood cells and so on) working together to maintain the body's functions. If many of those cells stop doing what they are supposed to do then your body will start malfunctioning. Different kinds of malfunctioning will occur depending on what kind and on how many cancer cells will spread throughout your body. This can eventually cause system failures.
If your lung cells are malfunctioning, for example, you may expect respiration problems.
Often cancerous cells spread all around your body (metastasis) and several tissues and organs will be compromised simultaneously leading to a complex pattern of symptoms.
Fatigue, pain, inflammations, and bleeding are common symptoms in many advanced stages of cancer since tissues and organs start to get seriously damaged.