What does "radiographic progression" mean in cancer?

"Radiographic" refers to imaging modalities like x-rays, CT scans, MRI, etc.

"Progression" in medical terms is referring to progression of disease, where progression means advancing to the next stage, getting worse, etc.

Radiographic progression in the context of cancer would mean that based on X-rays, CT, MRI, etc, the cancer has gotten worse in some way. The exact meaning of progression has to be defined on some rating scale and will differ from study to study. Radiographic progression is not the only way to measure disease progression, other measures can also be used like symptoms experienced.


Is there any database with RNA classification?

Rfam is a database about RNA families, similar to Pfam (wich is for proteins). I think it's what you're looking for.
http://rfam.sanger.ac.uk/search

You could also enjoy miRbase, a database for micro RNAs: http://www.mirbase.org/
There are tRNA databases, too, like this one: http://trnadb.bioinf.uni-leipzig.de/
And this tool for predict RNA secondary structure (However, this kind of tools aren't as good as they proteinic counterpart): http://mfold.rna.albany.edu/?q=mfold/RNA-Folding-Form


Where can I find a picture of the inflorescence of Epipremnum aureum (golden pothos)?

Figure 4d on page 6 of (Hung, 2016) shows a flower the authors managed to induce in E. aureum (This is one of the papers that mgkrebbs cited in his answer).

Hung, 2016 - Chiu-Yueh Hung, Jie Qiu, et al., "Gibberellin deficiency is responsible for shy-flowering nature of Epipremnum aureum", Scientific Reports 27 June 2016, DOI: 10.1038/srep28598 Creative Commons Attribution 4.0


Identification of Bird feather, probably from a predatory bird

This is a Common Kestrel (Falco tinnunculus) primary wing feather, so it is indeed from a predatory bird. The orange hue suggests that this came from a juvenile and/or female individual. Featherbase provides a good reference here.
For future feather identification questions, you may wish to post them to the Found Feathers project on iNaturalist.


Lotka-Voltera predator prey model isocline?

I think your issue is mainly with the interpretation of the isoclines.

If you assume this standard predator-prey model:

$$\frac{dN_1}{dt} = rN_1-pN_1N_2$$
$$\frac{dN_2}{dt} = apN_1N_2-mN_2$$

you get the isoclines:
$$ N_2 = \frac{r}{p} $$
$$ N_1 = \frac{m}{ap}$$

with the first isocline referring to prey and the second to predators. These isoclines mean that the population growth rate of prey and predators (respectively) will be zero exactly at these isoclines (as well as at the point N1=N2=0). Since the isoclines, for this partuicular model, are fixed values and not functions of N1 and/or N2 they will be strait lines. Also, in a sense, you should view the isoclines as the borderline case where population growth rate shifts between a positive and a negative value (ie a growing or a decreasing population). The isoclines are not giving you the population size of the prey at a certain predator population size (which you seem to be implying with "...why we are getting variable prey population on isocline for same value of predator population"), but the locations in the plane where the population growth rate (for either prey or predators) is zero.

A graphical view of only the prey isocline (with some color coding) can be:

This means that the prey population (blue) is growing (arrows to the right) below the blue prey isocline, so there if a "flow" to the right there, while it is declining at predator population sizes above the isocline (arrows to the left). So basically, for all predator population sizes (N2) below isocline the prey population will grow, and for all N2 above the isocline the prey population will decline. In reality the rate of increase/decrease differs depending on how far from the isocline you are (so arrows should be of different lenghts), but to simplify the issue and to show the general principle I'm just showing the direction of flow here.

The same picture for the predator population is:

Here the predator population (orange) is declining to the left of the orange predator isocline (arrows down) because there is too little prey to sustain the population, and increasing to the right of the isocline (arrows up).

If you combine these you get this, with the black arrows showing the overall direction of the combined population trajectories:

I hope this clarifies the issue a bit. Otherwise, please comment and hightlight what parts you find unclear.

Also, the dynamics of this Lotka-Volterra model also means that populations that start exactly at the intersection of the isoclines (i.e. both N1 and N2 will lie at that point) will stay there, since that is an (unstable) equilibrium point. Populations that are started anywhere else in this plane (except for cases where N1 and/or N2 is zero), will follow an oscillating population trajectory, that will not change if there isn't any external pertubations (environmental changes, input/output through immigration/emmigration etc). Therefore, the combined trajectories of N1 and N2 will form an ellipse in the plane, until they are perturbed (by something outside the current model), when they will then settle at a new ellipsis. For examples of the ellipses, see this phase-plane graph from Wikipedia, with initial values as points:

However, also note that changing the model, i.e. to include a logistic component to the prey population, will completely change the population dynamics.


How accurate are Illumina microarray chips for genotyping?

23andme uses DNA microarrays ("chips") to perform genotyping. These methods only assay a set of previously known single nucleotide variants, so the probability of missing some specific variant (false negative) is high if that variant is not specifically assayed. It is not quite 100% as frequently known variants missing from the chip are closely associated with a variant that is on the chip, so you can sometimes impute missing data.

Sequencing-based methods will in theory pick up unanticipated variants, but they have their own foibles.

Generally both methods are quite good at single nucleotide variants (SNVs) but are bad to only ok at other kinds of variants. See for example (this paper (chosen somewhat at random, there are many similar papers) to see what the state of the art is for sequencing-based non-SNV calls.

Getting back to chips, these themselves depend somewhat on what version of the genotyping chip is used. For specific information on different versions of 23andme chips, I recommend this blog. For tech specs on the most recent Illumina chip used by 23andme, you can see their product sheet, and specifically Table 5. Their data claims that call rate among targeted variants is >99%, and among those the reproducibility is >99.9%. However things can be reproducibly wrong, so that's not exactly false positive that you requested.

Though it's somewhat old, this paper will give you a sense of both technologies in terms of variant ascertainment, claiming 89% sensitivity and 99.6% specificity (for European genotypes only) for either low coverage sequencing or a then-current chip.

To learn more about how these stats work for chips, specifically for false positives, this video may help.

Hope that helps.


How would a plant sprout and grow in a zero gravity environment?

There have been several experiments in growing plants in microgravity (strictly speaking, we do not achieve "zero-g" since astronauts remain in orbit about the Earth).

Changes in plant growth due to the influence of a gravity field is sometimes called gravimorphogenesis. More specifically, gravitropism is a differential growth response of plant organs to gravity. For example, roots grow downwards (positive gravitropism) and shoots grow upwards (negative gravitropism) on Earth.

Studies (e.g. 1) suggest that in micro-g, there is no preferred direction; roots may grow "up" and shoots "down".

It is thought that this growth response is due to the relative distribution of auxin in the plant. On Earth, auxin will preferentially move down into the root-tips due to the location of amyloplasts in the root-cap cells. In micro-g, amyloplasts do not settle at the "bottom" of the plant, therefore there is a more generalized distribution of auxin, and therefore there will be no preferred growth direction.

In addition, changes in plant gene expression as a response to micro-g environments are also being investigated (2) and suggest that auxin transport inhibitors may block the activation of the auxin responsive promoters in Nicotiana spp. (tabacco).

(1) Mechanisms in the Early Phases of plant Gravitropism CRC Crit Rev Plant Sci. 2000 ;19 (6):551-73  11806421  Cit:65

(2) Transcription Profiling of the Early Gravitropic Response in Arabidopsis Using High-Density Oligonucleotide Probe Microarrays, Plant Physiol. 2002 October; 130(2): 720–728.
doi:  10.1104/pp.009688


Why are sight and sound prerequisites for intelligence?

To answer your question, we must first ask the question What is defined as intelligence?

A googling will tell you that most people believe intelligence to be something related to apes or even more conservatively to humans. But, I find this to be a bit unpragmatic. The closest level of abstraction I find towards defining intelligence is this wiki on Animal Cognition. Having said so, I personally would define intelligence on a much more abstract level.

Intelligence can be broadly defined as a learned response towards an external stimulus, providing the organism with an increased fitness/survival within it's ecosystem.

So Intelligence can be broken down into two parts

Memory of a stimulus
A programmed response towards that stimulus

This is a very famous video showcasing intelligence in the animal world; Crow Intelligence test

But My objective is to state that sight and sound are are not at all prerequisites of intelligence.

This paper from way back in 2014 is I think the best that I can state

Memory and Fitness Optimization of Bacteria under Fluctuating Environments

In this particular paper the authors test the capacity of E coli to produce a response within fluctuating environments, and they find that as the generations progress the later generations take lesser time to produce a response towards the stimulus. They also note that what happens if the prior external environmental state is restored. In such a case later generations become optimised for that particular state.

This is a very good example of memory which is stored at the level of DNA, and a level of intelligence is manifested in a microbial system. So therefore, can you really state that "sight- and sound" are pre-requisites of intelligence. I would say No They are not, that would be an over-simplistic way of what intelligence really is.


Do muscles still hold glycogen reserves if there is no carbohydrate input

Most of it isn't but a little bit is.

When your body has very little glucose and a lot of fat(Which can be the case if an overweight or obese person goes on a low carb diet) the ketones and fatty acids and glucose produced by the liver are used almost exclusively to keep the body alive although a little is synthesized into glycogen.

Specifically when you don't eat anything gluconeogenesis alone supplies enough for 1 day. Then the fat metabolism accelerates because gluconeogenesis is not enough. This is when you get into a state of ketosis(this can also happen in bodybuilders since increased muscle = increased fat metabolism). This ketosis causes fast weight loss from not just water like a lot of other diets but also from fat. This fat then eventually depletes and it metabolizes protein exclusively(during all this time it does metabolise some protein). However that can't continue forever even if the amino acids get reused over and over again because some are used to produce ATP. Thus you eventually would die from starvation with obese people surviving longer than underweight people.

Anyway as far as exercise assuming that you start off obese, getting your body into a state of ketosis makes your performance even better than on just glucose alone after a while of adjusting to fat metabolism since 1 molecule of palmatic acid(16 carbon fatty acid) produces 106 ATP compared to 32 ATP for 1 glucose molecule so your muscles can go longer without being exhausted. Theoretically someone who is 50 pounds overweight could exercise 24/7 for several days if he/she is in a state of ketosis.

Here is a reference to the low glycogen and increased muscle performance:
http://www.bodybuilding.com/fun/glen12.htm

As to why it is 106 ATP it is because each NADH produces 2.5 ATP and each FADH2 produces 1.5 ATP and because of the activation step using 2 ATP just like how NADH transport from cytoplasm to mitochondria takes 2 ATP, 1 per NADH in glycolysis.


Erythrocytes are far more than inert "bags" of oxygen. They are complex, highly specialized cells and, like all cells, they require a number of basic processes to be maintained to work properly.

A good example (out of many) of why red blood cells need energy would be the active transport of ions across the membrane, a mechanism important for any type of human cell.

Quoting an article by Knight & Welt (J General Physio, 1974):

  The human red blood cell maintains a high intracellular potassium (K) and low sodium (Na) apparently by balancing passive movements of the ions with their active transport in the opposite direction. Thus the cell extrudes Na and accumulates K in a linked process (...). The component of Na-K transport (...) is dependent on adenosine triphosphate (ATP) in the cell.

A visual explanation of how export of sodium and import of potassium are linked to the consumption of ATP:

This means that to maintain correct gradients across the membrane (important to maintain osmotic level, and to provide a potential energy exploited in other import-export processes) the cell must continuously spend molecular energy.

Producing ATP in red blood cell is also important to maintain a pool of phosphate-donors for phosphorylation signals, involved in cell signaling for example.

Interestingly, it was also shown that releasing ATP is also a way for erythrocytes to communicate with their environment, possibly to stimulate microvessel dilatation and thereby allowing proper circulation of oxygen near the destination site (see Ellsworth et al, Acta Physiol 2016 for a detailed review).

All these processes require ATP, and therefore a continuous metabolic activity.


The hybridization situation you describe could be found in ring species, and is partially related to this concept.
For instance, the three species A, B and C could have partially overlapping distributions, such as:

In such a situation (assuming that the relative distributions have been stable over evolutionary time), A and C might be able to produce offspring, as well as B and C, while A and B might not produce viable offspring if they would meet.

Here is a picture from the wikipedia page for a similar situation, showing interbreeding between seven gull species in the genus Larus:

However, I also know that the ring species concept has been challanged, mainly by the fact that there are very few good empirical examples of ring species. See for instance the nice blog post "There are no ring species" by Jerry Coyne, which may also include a couple of examples of species groups that are relevant to your question.

Also, the hybridization patterns that you describe can be caused by other processes, for instance specific reproductive barriers between groups of species (molecular or behavioural). My answer is therefore merely mentioning one possible explanation for the hybridization patterns you ask for, but there are many other processes to consider.


How do chameleons signal cells to change color?

As said by @dblyons, there has not been a lot of research (biochemical) on chameleons. So, the exact part of mechanism that you're looking for is still not understood. However, we have recently caught the broad end of the stick. Chameleons don't have special cells for color, their complete skin has a layer of pigments (dermal iridophores) which helps them in changing color. See this (or this) article:

  Chameleon skin has a superficial layer which contains pigments, and under the layer are cells with guanine crystals. Chameleons change color by changing the space between the guanine crystals, which changes the wavelength of light reflected off the crystals which changes the color of the skin.

These guanine crystals are actually like colorless mirrors, but by changing the distance between these crystals, wavelength of light absorbed (and reflected) can be changed. It is quite similar to how the color of ozone changes from pale blue in gas to violet-black in solid form. However, how chameleons trigger this change in distance of crystals, is not yet known.

This is how these crystal lattice works:
sourcesource

This is what a guanine crystal looks like ((a) is guanine):

You can also see a nice real-time video of guanine crystals changing color of chameleon here.

The color changing portion of skin has 3 main layers:

superficial s-iridophores which help in changing color in visible region rapdily.
deep d-iridophores which reflect light in infrared refion and are thought to provide thermal protection to chameleon.
layer of melanin which is actually yellow in color, making chameleons naturally yellow(!) in color. When the guanine crystals come closer, they reflect the blue portion of visible spectrum. This blue light, along with the natural yellow color of melanin, becomes green which gives green color to chameleon. So, the actual color visible to us is a combination of color reflected by guanine crystal and yellow color of melanin.

As I said already, the exact biochemical signalling process behind this process is not known yet. It could be complex hormonal or neurotransmitter signals. However, hormones are considered as the main triggers because chameleons have been shown to change color due to changes in mood instead of environmental protection.

  Cephalopods such as the octopus have complex chromatophore organs controlled by muscles to achieve this, whereas vertebrates such as chameleons generate a similar effect by cell signalling. Such signals can be hormones or neurotransmitters and may be initiated by changes in mood, temperature, stress or visible changes in the local environment.


Sample suggestions for phase contrast microscopy

Any green, soft leaf from a non-toxic plant is a good start. Cut a thin slice from the leaf (either to look at the cross-section or the surface). Try different leafs with different colors - there might be colors in the cytosol and/or in chromoplasts.

Concrete example for dynamic structures:

Elodea leafs: they consist of only two cell layers and can be looked at under the microscope without further preparation. Keep the the leaf in water and cover it with a cover slide before looking at it under the microscope and add water when it starts drying out. The green chloroplasts in the plant cells are moving around as long as the cell lives.

You might find Elodea either in a pond or in a store selling aquarium fish and the like. You can keep Elodea alive and grow it in nutritious water at a sunny place.


What is the difference between pluripotent and totipotent cells?

Expending on Gerando Furtado link

Totipotent cells can differentiate into three germ layers (endoderm, mesoderm, or ectoderm), into cells of the cytotrophoblast layer or syncytiotrophoblast layer of the placenta.

Pluripotent cells can differentiate into the three germ layers (endoderm, mesoderm, or ectoderm).

So totipotent cells develop into the all the cells of the embryonic body and fetal side of the placenta. While pluripotent cells can only develop into cells of the embryonic body.


Transmembrane protein: does signal peptide always form a loop?

I think perhaps a picture might help, also see some lecture notes here, where I pulled the pictures from: in short, if you have an unbroken chain, you can't stick it through a hole except as a loop unless you start at the very end, and often you don't want to do that.

Signal sequences can be anywhere on the protein. That portion is the part of the peptide that binds to the translocator pore in the membrane. That portion has to stay bound for the process to continue: it isn't possible to just "feed through" the growing polypeptide without securing it somehow, and that's precisely what the signal sequence is doing by interacting with the translocon.

http://web.uconn.edu/mcb380/fig12-45a.GIF

http://web.uconn.edu/mcb380/fig12-45b.GIF

This process also allows for all sorts of arrangements: sending the whole protein through, or just the N- or C- end, or having multiple signal sequences to create multiple transmembrane domains. Especially in the latter case, there really isn't any other way to do it except by forming some loop someplace, unless you were to actually ligate separate polypeptides together, which would be quite messy and difficult and require additional specialized enzymes: much more complicated than a nice, tidy loop.


Do two compatible tRNA codons bond together?

Yes, tRNA can form dimers. For example it was shown that E. Coli tRNA GCC forms homodimers, i.e. two identical molecules interact with each other. In this case the dimerization occurs between the anti-codon loops (what was probably meant with UUU and AAA).

References:

Sequence and structure of naturally-occurring tRNA transcripts and site-directed variants are significant barriers to forming oligomers beyond dimers.
(Harold S. Bernhardt, Warren P. Tate, Advances in Bioscience and Biotechnology, 2013, 4, 1-16 ABB)
Anticodon-anticodon interaction induces conformational changes in tRNA: yeast tRNAAsp, a model for tRNA-mRNA recognition.(D Moras, A C Dock, P Dumas, E Westhof, P Romby, J P Ebel, and R Giegé, Proc Natl Acad Sci U S A. 1986 Feb;83(4):932-6)

A naturally occuring mutation, A3243G in human tRNA(Leu(UUR)), causes dimerization via a motif which is not in the anti-codon loop.

Reference:

Wittenhagen LM1, Kelley SO., Nat Struct Biol. 2002 Aug;9(8):586-90.,
Dimerization of a pathogenic human mitochondrial tRNA.


Plants have sulfate transporters which they use to assimilate sulfur. Since sulfate is the conjugate base of sulfuric acid, this could be construed as a "yes" for your question. Sulfuric acid would be present in its conjugate base form at physiological pH values.

However, it would be unwise to water your plants with sulfuric acid, as many plants have an optimal pH range which will quickly cause death when sulfuric acid lowers the pH of the soil below that range. As a result, areas afflicted by acid rain may require treatment with alkaline limestone to resolve this issue.


What is the functional difference between hemoglobin and ferritin?

Hemoglobin is the protein of erythrocytes (red blood cells) which has ferrous ions (Fe2+) bound in its subunits. These are able to keep oxygen bound which enables the cell to transport oxygen through the circulation. It's not really for storage of iron, it's for using it.

Ferritin is the actual storage protein, cells express it to store iron in case of deficiency and also to regulate the amount they have in the cell. According to this, it's mainly expressed in muscle, liver and kidney cells (but I'm not too sure about the details of that study so I might have got that wrong).

Edit: just found this in one of my old lectures; unfortunately it doesn't quote sources: ferritin stores iron in liver and heart. The total iron in the body is ~3.9g, of which 2.5g are in use in hemoglobin, 500mg in stores (an additional 250mg in the liver), 150mg in bone marrow, 300mg in myoglobin and 150mg in other enzymes. The remaining 5mg are bound to transferrin in the plasma.


Separate DNA fragments with very different size (oligo and lambda-DNA)

A spin column might work for your purposes since you can do multiple rounds of binding if your volume is too large to bind in a single pass, but for DNA of that size a lot will be irreversibly stuck to the column.  See for example the protocol for the Monarch® PCR & DNA Cleanup Kit.

Consequently I would recommend just doing an ethanol precipitation, which favors recovery of longer DNA molecules (see for example this protocol).


Klenow fragment does not seem to have 5->3 exonuclease activity, but it can still displace nucleotides in front of him - How?

Generally, the New England Biolabs website is a great resource for this sort of information.  Maybe you already know this: Klenow fragment is widely used in molecular biology today. The broad use of Klenow fragment is because it will remove 3' overhangs, thereby 'polishing' or 'blunting' the DNA.  See the famous cloning techniques manual for additional information.

It is a polymerase, though, and it does perform 5-->3' elongation in the presence of dNTPs.  (sidenote: Klenow was initially used in polymerase chain reaction (PCR) development, and later replaced with heat-stable Taq pol.)

The so-called 'strand displacement' activity of the enzyme allows the 5-->3 elongation of the new strand to occur even in the presence of an existing, annealed strand ahead of the advancing polymerase, as you say.  This may seem problematic at first glance, but the job of polymerase is to make a complete, templated copy of DNA -- that is why reseachers use it, and that is its job in nature too!  Stand displacement is really convenient for scientists when using random primers, for instance.  The DNA polymerization can continue unimpeded despite the presence of a 'downstream' barrier.  This is also why not having 5'-->3' exonuclease activity is helpful in this context.  (sidenote: pol I is not the main replicative polymerase in E. coli. and its discovery is one of the great stories of post-war biology).

I hope this addresses your question(s).


Your claim that "there is a lack of genetic diversity" in mitochondria is not correct. There is no connection between recombination and mutation rates per se. In fact, mitochondria have much higher mutation rates than nucleus and different types of mitochondrial DNA can even co-exist in one organism, a phenomenon called heteroplasmy (which is found at a frequency of ~90% in human).

But: there is a connection between mutation fixation rate and effective population size. Because mitochondria are normally inherited through maternal line, effective population size for their genome is smaller than that of the nuclear genome, and thus any mutations in the mitochondrial DNA reach fixation faster, but again this is counteracted by high mutation rates.

There is no problem with functionality: as always if something gets broken (and it is easy to break something in the mitochondrial genome, since genes are normally tightly packed in it) respective genotype is eliminated or reduced in frequency by natural selection. In the case of mitochondria this selection acts both upon the level of individual organisms (intra-individual somatic pool of mitochondria: positive and negative selection) and the level of populations (mostly purifying selection in humans). It is nevertheless true, that given the virtual lack of recombination, selection becomes the only force of purging deleterious mutations.


If re-boiling does not curdle the milk, can that be taken as an indicator that the milk hasn't developed the bacteria (and their toxins)?

Fresh milk does not separate when boiled. I use it in sauces and pan gravies and it always boils and never separates.

My suspicion is that you are separating it on purpose, for example to make cheese. In that case you have to add acid or rennet to separate it. If you then re-boil it to separate it again, you get very little solids. I have made cheese at home then tried to 'ricotta' the left over whey and all I get is a tiny bit of solids.


Are there any traces for evolution in modern humans over the last 100 years?

Spotting evolution over only 4 generations would be very difficult. You certainly wouldn't see an entire bone disappear in that timeframe, though it might be slightly smaller in average people today than it was several generations ago. Over the timescale you're describing, the only real option is epigenetic changes, which might not be permanent enough to "count" as evolution.


Artifacts are variations introduced by non-biological processes. Sequencing involves a lot of chemical reactions, and changes in nucleotides that can seem like mutations are really introduced somewhere in the processing of the sample. That's what we call "sequencing artifacts". Proper experiment design, with careful replication, should help you clarify which changes in nucleotides are biologically significant.


What is the smallest difference in light wavelength that the human eye can detect?

The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls.

As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly.  That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. wiki on the subject


Getting SNP data from FTP Site of NCBI SNP:

It's actually simple to download the data from the NCBI, if you follow the method given by FAQ( as given by @WYSIWYG).

Step 1:

Goto organism FTP: ftp://ftp.ncbi.nlm.nih.gov/snp/organisms/

Step 2

Open your required organism folder:

From here you can download any file you wanted. If you trying to study the whole organism please download any one of the whole folders(ASN.1, rs_fasta, XML(recommended)).

Now,

It's not about the downloading it's about understanding the files which are provided.

files types:

XML files
ASN.1 or Abstract Syntax Notation One
rs_fasta

All of them contents almost the same data, just in different format. It's up to you how your script(preferably Python or Perl) works to get out the import information.

Other way of Download from NCBI FTP:

You can always use filezilla:

Put Host as : ftp://ftp.ncbi.nlm.nih.gov/snp/organisms/
rest Username and Password, etc empty


Are Y spermatocytes faster but less resilient than X spermatocytes?

I searched and found a letter which clearly mentions about misinformation that sperm with Y chromosome swims faster than X carrying sperms.I think this link may help https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440662/

The letter says "The widely held idea that spermatozoa bearing the Y chromosome (Y sperm) swim faster than those bearing the X chromosome (X sperm) seems to have originated from Shettles's work in 1960, using phase-contrast microscopy.He claimed to have observed, “two distinct populations” of spermatozoa. After attempting to count the chromosomes, he concluded that the smaller heads contain the Y and the larger the X chromosome. There were no intermediate types.
The following year he reiterated these findings, adding that smaller headed spermatozoa can migrate more rapidly and fertilize the egg more often in the distal part of the tube.
Reading Shettles's reports in Nature and other peer-reviewed journals, many researchers thereafter believed that Y sperm swims faster than X sperm. The finding particularly influenced research on sperm separation.

Although several attempts have been made to correct this impression, it was not until the development of computer-assisted sperm analysis (CASA) that reliable observations could be made. So far, researchers have found no morphological differences between human X sperm and Y sperm.4 Neither mature sperm nor their precursors possess significant morphological differences between X and Y genotypes, and Y bull sperm does not swim faster than X sperm."

You can see the reference and read more
1. Shettles LB. Nuclear morphology of human spermatozoa. Nature 1960;186: 648-9. [PubMed]
2. Shettles LB. After office hours: conception and birth sex ratios: a review. Obstet Gynec 1961;18: 122-30.
3. Moruzzi JF, Wyrobek AJ, Mayall BH, Gledhill BL. Quantification and classification of human sperm morphology by computer-assisted image analysis. Fertil Steril 1988; 50: 142-52. [PubMed]
4. Hossain AM, Barik S, Kulkarni PM. Lack of significant morphological differences between human X and Y spermatozoa and their precursor cells (spermatids) exposed to different prehybridization treatments. J Androl 2001; 22: 119-23. [PubMed]
5. Penfold LM, Holt C, Holt WV, Welch DG, Cran DG, Johnson LA. Comparative motility of X and Y chromosome-bearing bovine sperm separated on the basis of DNA content by flow sorting. Mol Reprod Dev 1998;50: 323-7. [PubMed]

Hope this help!


Which enzyme catalyzes transcription and which translation?

Sorry, but you started on the right track. What you're looking for is called the central dogma of protein synthesis.

Genomic DNA is transcribed in the nucleus into messenger RNA (mRNA) by RNA polymerase. RNA polymerase is DNA-dependent; it needs a DNA template to make an RNA version of the message.

The messenger RNA moves into the cytoplasm where it gets translated by ribosomes into an a polypeptide (protein). Ribosomes are the enzyme that do the translating, and perhaps your confusion is because ribosomes are made up of both RNA molecules and proteins (a ribonucleotide complex).

Aminoacyl tRNA synthetases are the enzymes that make aminoacyl tRNAs (tRNA for short). These tRNA bring individual amino acids to the ribosome as the ribosome is extending the polypetide product of the mRNA message.


How do cis-regulatory elements and trans-regulatory elements behave differently?

I was thinking cis would be favored because the gene is close by

Your intuition is correct.  Cis-regulatory elements like enhancers are more efficient at enhancing transcription of genes in cis than genes in trans, but trans interactions of cis-regulatory elements do occur.  Take a look at figure 2B of this paper and the accompanying text:

  ... quantitative RT-PCR showed that relative levels of GFP transcripts from constructs inserted at 37B were similar to those from transgenes at 53F, with 1.7% [95% C.I., 1.6–1.8%] of total GFP transcript in eye discs where GMR acts in trans relative to those where activation is in cis ...

The interaction of alleles between homologous chromosomes is called transvection, and this can be realized as binding of the enhancer associated with one allele to the promoter of the other allele.  Figure 9 of this paper is a good explanatory graphic.


How to use Transect-based sampling to select sample trees

More detail on what your studying, the question you want to answer, and how you want to go about doing it would be very helpful. But I can answer this basic question of how to select tree's with a transect.

You will need:

Forms to fill out for data.
A compass.
A transect tape (really a very long tape measure, about 100 yards or meters).
A sampling design that fits your study. (I'm assuming you already have this, but if you want to talk more about it see above.)
A wooden meter stick.

Once you are in your 1st area and ready to select a random subset of trees.

Pick a random spot. (Usually done by throwing a stick or water bottle over the back of your head and going wherever it lands).
Pick a random number between 0-360. This will be the random direction you go in from your random spot. Find north on your compass, then which way your random number points. In your mind mark a way point in that distance you can walk to (a mountain peak, a distinct tree, anything).
Stick the beginning of your transect tape in the ground and start walking. The length that you walk should be predetermined from your study design.

Now you'll select trees to perform whatever measurement that you've decided on. But how? Most forests are not so dense that a straight transect tape will touch many of them. This is where the meter stick comes in. Walk back down the transect and choose any tree that comes within 1 meter of the tape on either side. Is the forest not dense enough to include enough trees that way? Then simply increase the length of your transect, or length that you measure out from the transect (ie. 2 meters, or 3 meters).

This is technically called a "belt transect". And it used in natural resources to measure things that are abundant, but not very dense. Such as trees in a forest or shrubs in the desert. It is essentially a giant quadrat.

Why all the randomness? Humans are naturally bias. Even if you think you are not being bias, you could subconsciously be choosing a starting point in a dense patch of trees, or a direction that will let you measure your favorite species. A rigorous study relies on a random sample of a population of interest, and small non-random decisions like this means it is not a random sample, but a bias sample.


What is the meaning of 'primary' and 'secondary' sympatric speciation in this paper?

TLDR
Sympatric speciation and allopatric speciation with later migration into the same habitat were historically diffucult to distinguish without looking at palaeo-biological data. The paper argues that while palaeo-genetics has made this easier, it is still difficult to distinguish pure sympatric speciation (which it calls primary) and sympatric speciation with a geneflow from an geographically separated (allopatrically speciated?) subpopulation (which it terms "secondary sympatric speciation" or "speciation with secondary gene flow", "...with secondary contact" etc.).
Speciation
Speciation is the divergence of one species (with one gene pool) into two different species (with different gene pools). It is obvious that this will happen if subpolulations are geographically separated and continue to adapt to their local conditions (allopatric speciation).
However, Mayr suggested (back in the 1940s) that there is another type of speciation that happens while the speciating populations share a habitat, and, consequently, while gene flow between these subpopulations is maintained until the speciation process is complete. This requires strong selection pressure towards two different ecological niches each with their associated adaptations.
Empirical examples have been discussed and called into question again. One cool and frequently discussed example is that of the apple maggot in North America that has developed from the hawthorn maggot after the introduction of apples in North America.
Debate
Unequivocal examples for pure sympatric speciation are rare, leading to some debate about the merits of the concept. Sympatric speciation models (following Maynard Smith's models from the 1960s) as well as the reasons for skepticism towards them are illustratively explained for instance in this article (Felsenstein 1980), page 133-135.
The debate continues, today with additional, newer findings from genetics, palaeo-genetics, etc. This is what the article in the OP (Foote, 2018) was about. The pdf of the article (Foote, 2018) without paywall can also be found here. While Foote suggests that what pure sympartic speciation and speciation with secondary gene flow may never be unequivocally distinguished (without additional palaeo-genetic information), others are more optimistic, e.g. Richards et al. 2019 (without paywall on biorxiv). Coincidentally, Richards et al. have a very nice illustration (their Figure 1) that illustrates the issue the OP was asking about.


DNA replication - how many times and when does it occur?

This sounds like a difference in perspective of when exactly cells "die". If you consider that, in a cell division, a mother cell "gives birth" to two daughter cells, you could argue that the mother cell has "died". It makes sense to think about cell division in this way because it puts both daughter cells in the same level, without one being "special" due to it being the mother cell itself while the other is considered the "new cell".

If you face cell division like this, any cell (eukaryote or procaryote) will only really duplicate their DNA once: they duplicate their DNA -> they split into daughter cells, in which they "die" -> (eventually) each daughter cell duplicate their DNA -> and so on.

Like I said this is just a particular POV we can adpot when we try to understand and describe cell cycle and cell division (although it is a common one for researchers in the field).


Does LSD "stay" in your fat storage and then "returns" back?

I've heard this rumor for years, both from pro- and anti-drug people, and it is not true. According to this review of LSD's pharmacology, its half-life in the body is about 5 hours, with it being completely cleared within about 15-28 hours. There is no evidence that it accumulates long-term in fat, cerebrospinal fluid (CSF), or anywhere else in any pharmacologically significant quantity.
Reference:
"The Pharmacology of Lysergic Acid Diethylamide: A Review" CNS Neurosci Ther. 2008 Winter; 14(4): 295–314. PMID: 19040555 DOI: 10.1111/j.1755-5949.2008.00059.x


Current human behavior as a genetic heritage

All phenotypic traits have some part of the variance which is explained by the environment and  some part that is explained by the genes. The heritability is then defined as:

$$H_N = \frac{V_{genetic}}{V_{phenotype}} = \frac{V_{genetic}}{V_{genetic}+V_{environment}+V_{interaction. gene.environment}}$$

where $V_{genetic}$ is the Variance in phenotypic traits due to genes, $V_{phenotype}$ is the total phenotypic variance, $V_{environment}$ is the variance due to environment and $V_{interaction. gene.environment}$ is the variance due to interaction between genes and environment.

So your question (if I understand it correctly) should rather be a list of phenotypic traits (behavior) and ask what is the heritability of each trait in the world-wide human population (or on a given subset of the human population).

I think, there is no objective manner of defining a given phenotypic trait. You should chose subjectively, some behavior, define it accurately and then ask the question what is it's heritability.

Moreover, it is quite hard to measure a behavior. It is much easier to estimate the heritability of height in humans.

There are several different methods in order to estimate heritability of a trait. See this wikipedia article

Some of these experiments are not feasible on humans for ethical reasons. Some others are quite limited and are quite expensive. I don't think we have many studies that quantify the heritability of behavioral traits in humans but I might be mistaken.

As said by @AlanBoyd, there is a field called evolutionary psychology that deal with this kind of question. To my knowledge this field is mostly a purely theoretical field and therefore, it does not quite allow to measure heritability.

A good start into this science would be the wikipedia article which seems quite complete.  I can give you some books but I haven't read most of them. Here and here are introductory books in the field. I think this book is a classic in the field. I read this book and it is quite interesting. There are actually many books in this field. The best think you can do is maybe to typewrite "evolutionary psychology" in amazon.

As a sidenote: If you enter in the field of evolutionary psychology you might as well be interested by memetic evolution (evolution of culture). Here is a classic book on the subject.

Be careful in these fields, I think that some ideas do not deserve to be considered as part of science while other do!


How does chest wall compliance affect functional residual capacity (FRC)?

As far as lung is concerned both inspiration and expiration are passive. Lung just responds to intrathoracic pressure by accommodating more air during inspiration and expelling air during expiration. The active processes in the lung as far as air flow is concerned are limited to the bronchial tree smooth muscles which can increase or decrease the resistance to air flow. The compliance of the lung parenchyma is a function of its anatomical composition.

During inspiration the thoracic volume is actively increased by:

Outward expansion of ribs by the intercostal muscles
Downward expansion of diaphragm

This increase in thoracic volume is refected in all intra thoracic organs:

Venous return increases due to the negative pull
Negative pleural pressure causes air to be pulled into the lungs

Normal expiration on the other hand is passive due to relaxation of the above mentioned muscles. Relaxation will cause a decrease in the thoracic volume which will push the excess air and blood out.

An increase in the compliance of the thoracic cavity would mean weakening of the fascia and bones of the thoracic cage. In other words, the structures that the muscles attach to will become weak. This will cause muscle action to cause excessive expansion of the thoracic cage during inspiration and during expiration due to weaker pull by the attached structures, even residual tone of the muscle may cause distortion of anatomy preventing adequate reduction in the thoracic volume causing increased residual volume. Thusb reducing the volume of the air expired.


Association of shorter telomeres with heart disease

This seems a bit like a hen and egg problem. Telomere length is both associated with age and with heart diseases, but heart disease is also associated with age. The question here is, is one really causing the other here (short telomeres heart problems) or do they occur simultaneously? The other problem with heart disease is that it is a multi-risk disease, with many risks accumulating with age. The figure below sums this up, it is from the first paper:

Have a look on these articles:

Telomere biology in heart failure
Aging, telomeres and heart failure.
Telomeres and Cardiovascular Disease


If you have an antibody that is directed against, for example, a bacterial surface protein, then by mixing the bacterial cells with the antibody at a suitable stoichiometry you could observe clumping of the cells as the antibody molecules essentially cross link the cells together. This would be an example of using an agglutination (clumping) assay with a particulate antigen. You can also probably see why it is important that each cell (particle) carries many copies of the antigen for cross linking to take place effectively.

If, however, the antibody of interest is directed against a soluble protein, then mixtures of antigen and antibody are less likely to form cross-linked complexes, although it can happen and can be used for example in the Ouchterlony technique. If you want to use an agglutination test (i.e clumping of particles) with a soluble antigen then you can achieve this by attaching multiple copies of the antigen to macroscopic particles. This is what is being described in the definition of Latex agglutination in your question.

I imagine that there are ways of attaching a soluble antigen to red blood cells (e.g. by chemical cross-linking to the red blood cell surface) in which case you could observe clumping of the red blood cells when you added your antibody.


What is this red little cocoon like creature here?

This looks like a lady beetle pupa.  Given the appearance and your description of it's size, my guess would be of Harmonia axyridis.
Here'a link, with a picture of another pupa about half way down the page: https://edis.ifas.ufl.edu/publication/in361. This species has a diversity of colorations, both on the adults and the pupa.
Here's an example of another pupa of what is most likely the same species (from https://bugguide.net/node/view/410817/bgimage):


What phenotypes can arise from gender-related aneuploidy?

Note that anyone with a Y chromosome is considered a genetic male. Also, aneuploidy is usually a result of nondisjunction (but can have other causes as well) and is usually not inherited.

47,XXX is called Triple X syndrome and occurs in approximately 1 in 1,000 female births. These individuals usually appear normal, but may have tall stature, a small head, and delayed development. According to this case report, the tall stature is possibly due to SHOX gene triplication, in some cases. The short stature homeobox gene (SHOX) gene is a gene on the X and Y chromosome and is associated with short stature if a copy of the gene is missing or mutated. The case report states, "The enhancing effect of SHOX gene triplication on growth was ascribed to the concomitant absence of gonadal steroids in cases of gonadal dysgenesis, allowing a prolonged period of growth."
47,XXY is called Klinefelter's syndrome. Here is an image/diagram of symptoms. These people may have gynecomastia (enlarged breasts), less muscle, less body hair, and hypogonadism (decreased testicular function, also resulting in smaller testicles and penis) due to lower testosterone production. These symptoms become more obvious after puberty, because individuals with Klinefelter's have less "masculinization" (for lack of a better word). Cognitive problems are usually present. It occurs in roughly 1 in 500 to 1 in 1,000 male births.
47,XYY is XYY syndrome and has an incidence of 1 in 1,000 male births. They appear normal but may be slightly taller than average. This study looked at the cognitive and motor phenotypes of boys with Klinefelter's and XYY syndromes. It found that both groups have generalized cognitive impairment, but XYY has more profound language impairment and Klinefelter's has more significant motor impairment. Their hypothesis is that "the more severe language-based cognitive phenotype in XYY versus KS is likely to be genetically determined on the basis of abnormal dosage of specific Y chromosome genes, but not abnormal levels of testosterone because XYY is not associated with testicular failure."

There's also 45, X0 (Turner syndrome), in which girls have a webbed neck,  broad chest, low-set ears, short stature, gonadal dysfunction, and often other conditions such as a bicuspid aortic valve, coarctation of the aorta, and vision problems. Image of symptoms. It occurs in 1 in 2,000 live births. Individuals usually have 1 X chromosome, but may also have 2 X chromosomes, with 1 of them being incomplete (source). The single copy of the SHOX gene (mentioned above) has been linked to the short stature in Turner syndrome.

Interestingly, people with 47,XYY and 47,XXX people often have normal fertility, but not in the other two cases. My uneducated guess is that the extra "normal" chromosome (for the person's sex) doesn't disrupt gonadal function.


Short answer
There is no dead end from the entrance of the auditory canal to the tympanic membrane. The diameter and shape of the object inserted rather determine whether it can reach deep enough.

Background
The above statement can be proved by following examples:

ENT doctors use an otoscope on a regular basis to directly examine the tympanic membrane (eardrum), meaning the emitted light entering the meatus from the otoscope, and the reflected light from the tympanic membrane exiting the auditory meatus are following straight paths.

Another practical example is the use of tympanic temperature to quickly measure core temperature. Again, the infrared light emitted by the tympanic membrane has to follow a straight path out of the meatus, otherwise it would be absorbed.

Lastly, see below picture that graphically shows the relative straightness of the meatus. There is some curvature, but certainly no dead end. A dead end, or hooked region with a sharp angle would be disastrous for hearing sensitivity, as it would block the passage of sound waves to the middle ear.

structures of the ear. source: WebMD.

The finger is simply too wide to enter the meatus to the tympanic membrane. In contrast, cotton buds do readily enter the meatus up until the tympanic membrane and ENT doctors sadly see quite a lot of cases where folks turn in with ruptured tympanic membranes due to excessively deep insertions of cotton buds.


Do artificial light sources cause enough fatalities in light-attracted insect species to cause eventual extinction?

Short answer:
Yes, it is highly likely that artificial light sources may cause such high mortality that insects become (locally) extinct.

Long answer:
As you will understand, it is almost impossible to perform an experiment where lights cause extinction of a species. However, we have a lot of 'circumstantial evidence'; cases where it is clear that lights have dramatically decreased species richness (which means local extinction). If lights can cause local extinction, they can also cause global extinction if, as in your question, their entire population would be exposed to light.

Percentage of insects attracted/killed by light
Why insects are attracted to light remains unanswered, but that they do is clear. Also, it is known that insects that are attracted suffer an increased mortality, due to the light itself and due to predators actively hunting the blinded and inactive insects. The reported estimates of the number of insects that are attracted and killed by a light source differ and depend on the light source (color mainly), the background lighting (moon!) and other factors. A fair estimate is that about a third of the insects that are attracted by a light source are killed
A third is a very high mortality, that is off course added onto the other (natural and man-made) mortality insects suffer from. It is very likely that this would cause insect populations to become extinct, especially those already at risk.

Based on observations
Eisenbeis&Hänel give a number of examples that show that insects populations dramatically decline when exposed to lights:
- the number of insects drawn to the lights of newly build fuel stations is high in the first years, than rapidly declines.
- the butterfly fauna in remote Austrian valleys declines after introduction of lighting (for tourism).
- The number of caddisflies drawn to lights exceeds that of the number found in a stream.


Consider this from the point of view of integrating whole body metabolism.

The body operates on a fuel economy built around glucose. Active muscle produces lactate (C3) which is exported to the liver through the bloodstream. Liver converts lactate to glucose (C6) which is then exported to the tissues.

What if muscle produced ethanol (C2)? Liver metabolises this to acetate. This could be converted to acetyl CoA and so on to fatty acids, but there is no way to achieve net synthesis of glucose from acetate. Muscle can of course use fatty acids, so you could conceive of an alternative system based upon this. It may be that this is less efficent from the point of view of energy useage - I haven't checked this because there is a more compelling argument against using ethanol.

According to this paper, lactate levels in the bloodstream can reach 15 - 25 mM during exercise. If muscle exported ethanol instead of lactate then blood alcohol content (BAC) would reach the same levels.

The middle of that range, 20 mM ethanol, is equivalent to a BAC of 0.076% which is just below the legal limit for driving in the USA and the UK, and above the legal limit in many European countries. This BAC is associated with effects upon reasoning, depth perception and peripheral vision. So, from an evolutionary position it really wouldn't make sense to have a metabolic system based around sending this much ethanol through the blood.


Are there organisms that have incorporated plastic into their lives?

Biodegradable waste is a type of waste which can be broken down, in a
  reasonable amount of time, into its base compounds by micro-organisms
  and other living things, regardless of what those compounds may be.

from wikipedia

So yes, there are microbes which are capable of biodegradating manmade plastic. It depends on plastic types.

If you meant creating new pathways to biodegradate non-biodegradable plastics, then I don't think so. My opinion that by some of those plastics there are theoretical barriers (e.g. energy barriers or toxic byproducts), and by some of them evolution might create a pathway in time (I don't think in our lifetime, but nothing is impossible).

There are microbes which build plastics to store energy. They are just polymers like starch or cellulose (sugar polymers), with different building stones... Afaik the first biodegradable plastics came from here, but so they were very expensive. Nowadays we don't need microbes in the polymerization process, e.g. we can create polylactic-acid without the presence of microbes.

edit:

I have found an interesting article in the topic.

  Now, for the first time, researchers have found detailed evidence that
  bacteria in an animal’s gut can safely biodegrade plastic and
  potentially help reduce the environmental impact of plastic in
  landfill and elsewhere. The animal in question? The humble mealworm –
  which turns out to be not so humble after all.

  Researchers led by Stanford University in US and Beihang University in
  China found that the mealworm – the larval form of the darkling beetle
  – can safely subsist on a diet of Styrofoam and other kinds of
  polystyrene, with bacteria in the worm’s gut biodegrading the plastic
  as part of its digestive process. The findings are significant because
  it was previously thought that these substances were non-biodegradable
  – meaning they ended up in landfill (or worse, our oceans, where
  they’d accumulate for decades).

ScienceAlert - Scientists find worms can safely eat the plastic in our garbage


This is a good question, because the answer to the overall question (is the information in DNA complete - yes) is not the same as the one to the more specific ones (would a cell survive if the DNA was swapped with that of another life form - no). Let me elaborate:

The information in the DNA of in any given organisms (except for a virus) IS complete. This means that the DNA has 'code' for all the molecules required to build and sustain this organism.

However, the DNA of an organism alone (or placed inside an unnatural environment like a completely different cell) is not sufficient to actually make or build that organism. The reason for this is that, while the DNA has all the necessary code, without the correct machinery to actually read that code nothing can or will happen. Eukaryotes and bacteria are so vastly different (which is to be expected after millions of years of evolution for both), basically all the different machineries are not compatible anymore: transcription binding sites are different, gene structure (exons/introns vs. operons) is different, Ribosomes are different, ... [btw this also means that just putting the gene of an eukaryote into a bacterium doesn't work, researchers have to modify it accordingly to work].
Even between different eukaryotes (and probably some bacteria but I'm not sure about that) exchanging the nuclear DNA would not produce viable cells (or at least not ones that could grow into an organism), since again the transcription machinery would not match up sufficiently.


Relative roles of ATP and NADPH in anabolic and other processes

Preamble

I don’t know where you read the statement “NADPH is... the main agent necessary for anabolic reactions”, but  out of context it is very misleading, and it is difficult to envisage circumstances in which it would be helpful for students of metabolism.

Put simply, NAPH is only used in anabolic pathways which involve chemical reduction.

You ask for a suitable book, but the book I’m going to quote from (Berg et al., Biochemistry) would overwhelm you (and any other student — it is grossly overweight). However an old edition is available on-line, and by citing specific sections you can read what is relevant (and spare me breaking up my answer with pirated diagrams).

ATP and NADPH: energetic similarities and differences

ATP and NADPH can both be regarded as ‘energy-rich’ in the sense that they can undergo reactions that have a high negative change in Gibbs Free Energy (which is what determines whether a reaction proceeds) and that this can be linked to certain other reactions with a positive free-energy change — including, but not exclusively, those in biosynthesis — to drive an overall reaction. (Incidentally both these compounds are synthesized in reactions powered by solar energy during photosynthesis.) However the nature of this linkage or coupling to other reactions differs between NADPH and ATP, and this difference determines the roles that they can play.

The oxidation of NADPH to NADP+ has a standard redox potential of +0.32V , which is an effective a negative standard free-energy change, but it can only occur in conjunction with another redox ‘half-reaction’ with a redox potential that will result in an overall negative free-energy change. Berg et al., section 18.2.1, presents a calculation to show how NADH (essentially similar to NADPH in this respect) can reduce pyruvate to lactate. The key point is that this overall reaction is a chemical reduction, so that the ‘energy’ of NADPH is only of use in reductive synthesis.

The ‘energy’ of ATP (more properly its group transfer potential) is in fact the negative free energy of the hydrolysis of ATP to ADP (and orthophosphate), or to AMP (and pyrophosphate). If an enzyme can couple this reaction to another with positive free energy of hydrolysis then it can drive the second reaction. This important point is dealt with in Berg et al. section 14.1.3 and it is also worth reading the preceding section. ATP is not a reducing agent so is not limited to oxido-reduction reactions. (The hydrolysis of ATP can also be used to provide e.g. mechanical or electrical or light energy, which is why Berg et al refer to it in section 14.1.2 as “…the Universal Currency of Free Energy in Biological Systems”.)  In synthetic processes ATP (or other nucleotide triphosphates derived from it) is often used in reactions forming bonds (C–C, peptide, glycosidic, phophodiester). In some of these cases the hydrolysis of the ATP is used to generate an activated form of the basic component, which allows it to form the bond in a subsequent reaction.

Example of a synthetic pathway using both NADPH and ATP

In Fatty acid synthesis NADPH is used for two reduction reactions — ketone to alcohol, unsaturated C=C to saturated C–C bond — whereas ATP hydrolysis is coupled to the formation of the C–C bond of the condensing unit, malonyl CoA. This is shown in Figure 22.22 of Berg et al..

Example of synthetic pathways using ATP but not NADPH

The synthesis of the peptide bonds of proteins requires condensation of the carboxylic acid group of one amino acid with the amino group of another. This is not a reductive process and NADPH is not involved. ATP hydrolysis ‘activates’ each amino acid by attaching it to the ribose of a transfer-RNA in a bond that has a high enough free energy of hydrolysis to ‘drive’ peptide bond formation to the growing polypeptide chain at the peptidyl transferase centre of the ribosome.

Melanin synthesis?

This is an area in which I am profoundly ignorant, but from Googling it would appear that the first phase of melanin synthesis is the conversion of tyrosine to DOPA and then to indoles. These reactions are oxidative (using molecular oxygen) rather than reductive, so do not use NADPH, and the bond formation is cyclization to form the pyrole ring. This seems to proceed without ATP — presumably it is energetically favourable overall. There is a Wikipedia entry for the key tyrosinase oxidation reaction.

I suppose the anabolic phase is the polymerization of the aromatic units to form the crosslinked polymeric structure of melanin. This appears to be poorly understood, but there is certainly no indication that NADPH is involved, and it would appear to depend on chemical features of the environment of the melanosome, rather than on ATP. (There is a recent short review in this area by VJ Hearing).

You mention the role of sunlight in this process. Although sunlight in itself can provide the energy for one stage of the synthesis of Vitamin D in the skin, this is a ring-splitting step. A direct role in the polymerization of melanin doesn’t seem to be suggested.


Do physicians/biologists not know all the different types of viruses out there?

No, Biologists don't know all the viruses that exist out there. There's a lot! We do know many of the ones infecting humans, though, especially the ones leading to the most common diseases.

  The fact that the doctor didn't know what type of virus she has bothers me.

Without knowing any symptoms, your girlfriend likely had was some kind of influenza (flu), rhinovirus (cold), norovirus (diarrhea, etc) or respiratory syncytial virus (strong). That's just the most common virus infections. Identifying those is possible (see lab tests for norovirus or influenza), but it's unnecessary in most cases.

The thing is, no matter which of these she has, the medical advice will stay the same - rest and fluids. So identifying them is just going to add time and money.

There are some cases where viral identification is done even for these diseases. For example, before giving an antiviral like Tamiflu, which is for example given to pregnant women with the flu. Before giving an antiviral, it should be established that she is indeed infected with the influenza virus. These tests are also done in patients who are hospitalized. In some countries and years, all influenza cases are screened to later know what strains of the virus infected how many people and how it spread.

As an example, if the result of the test doesn't change the treatment, the influenza test is recommended against by the CDC. With a gastrointestinal issue where norovirus is suspected, nobody is going to make an identification for a straightforward case.


Is the cell cycle applicable to meiosis as well, or just mitosis?

The cell cycle is only associated with mitosis. The cell cycle is the normal process of cell division with which cells can indefinitely increase their number by cyclically repeating the process.  When a cell goes through the cycle, the result is two cells that are genetically identical.
Meiosis is a special type of cell division (which can occur only in eukaryotes) that produces cells that are not genetically identical to the initiating cell.  The number of chromosomes in each of the resulting cells is half the number that were in the initial cell.  (These haploid cells can later participate in fertilization, producing a cell with the original number of chromosomes.)  Many of the steps of meiosis are similar to the steps involved in mitosis, but overall the process is more complex. Since meiosis reduces the number of chromosomes, it cannot be repeated and so does not take part in a cell division cycle.


The dura mater is formed by the mesoderm. The mesoderm is the middle layer of the early trilaminar embryo. The three germ layers are the ectoderm, mesoderm and endoderm, formed by gastrulation. The middle germ layer forms connective tissues and muscle throughout the body, with the exception of the head region, where some of these structures have a neural crest (ectoderm) origin. Connective tissues include cartilage, bone, blood, blood vessel endothelium and dermis, but also the dura mater. The muscles include cardiac, skeletal and smooth muscle (fig. 1).

Fig. 1. Germ layers. Source: UNSW

Source
- UNSW


Let's compare ATP, glucose and fatty acids in terms of energy storage.

ATP has a molecular weight of 507 Da
Glucose has a molecular weight of 180 Da, and contains the same amount of energy as 31 ATP molecules
Fatty acids vary in size, but a gram of fat contains about twice as much energy as a gram of glucose (or glycogen)

The difference in energy density is huge, you would need enormous amounts of ATP to replace glucose/glycogen as energy storage mechanism, not to speak of fat. You can't put an arbitrary amount of ATP molecules into a cell, you 'll get into problems due to the osmotic pressure lots of molecules inside the cell would cause. Glucose is stored as glycogen in cells due to this effect, which makes one large glycogen molecule out of lots of glucose molecules.

The energy density difference is even larger if you take into account that ATP and glucose bind water, while fat is stored without surrounding water. The actual difference in energy density of glycogen and fat is around 6 times.

ATP is also not as stable as fat, it can get hydrolized in water. This would be a problem for long-term storage of energy.

You'll find some more details in Albert's "Molecular Biology of the Cell"


Various factors from different sources:

-- Diseases like Anther Smut Disease (reference).

-- Rampant use of herbicides.

-- Invasion of exotic pest species (reference).

-- Spatiotemporal variation in the pollination of Silene virginica by the ruby-throat hummingbird which is its principal pollinator (reference).


Why would a python go after such large prey?

It's hard to answer your question directly. But one might start by noting that pythons are hardly alone - snakes in general have evolved the ability to swallow prey that is much larger than themselves. It's probably not unusual for opportunistic carnivores to stumble across gorged snakes and make a meal out of them.

But there's a flip side: Consider an animal that has to feed daily. If it doesn't gorge itself snake-style, then it will never be in such a vulnerable state. But it still has to venture out of its shelter or hiding spot to feed EVERY DAY, putting itself at risk each time.

If a snake eats just once a week, then it can spend six entire days hiding from predators.

In summary, it would appear to be a numbers game, and the statistics obviously favor snakes, which have been around for millions of years.


It seems there're no ids for a mature sequence. You better search for a parent sequence ids. You could check, but it also seems that HGNC ids are -miR-30E- part.
So you could try Ensemble search (you should input names in 'Filter'-'GENE' section) or use Genenames. As you see, it has API, and you could use it programmatically with HGNC ids.


Is there any relationship between the height of a tree and the number of branches emerging from the main stem?

The height is only one of a few factors; also the species and environment are more significant. A spruce growing in unshaded location may have branches to ground level while the same species in a dense woods will only have branches at the top. A southern pine ( in the US) is often 100 ft tall with all the branches in the top 30 ft ; these trees drop the lower branches because of limited light and because various vines climb into the lower branches ( until the branches die and fall).


During non-cyclic photophosphorylation, how does NADP+ become NADPH?

Specifically during non-cyclic photophosphorylation, I know that the chlorophyll already has preexisting NADP+ molecules, water is broken to release 2 hydrogen atoms and 1 oxygen atom (two water molecules break down to form gaseous oxygen that we breath), those 2 hydrogen atoms get sent down and along the Electron Transport Chain via solar energy and then I believe one goes to a protein called ATP synthase and the other goes to photostem 1. After photostem 1 that hydrogen binds to free floating NADP+ molecules to from charged NADPH. This should be the gist of it all but I would also recommend listening to someone else's input as well.


Are casein proteins in UHT milk digestable for infants or toddlers?

UHT treatment increases the digestibility of casein.

Ultra High Temperature Treatment, but Not Pasteurization, Affects the Postprandial Kinetics of Milk Proteins in Humans (Journal of Nutrition)

  Moreover, the UHT treatment of milk causes structural changes in its
  protein system. The main change is the denaturation of whey proteins
  and their interaction with casein micelles. Consequently, it was
  expected that the behavior of the UHT milk would be similar to that of
  casein micelles, as observed with native casein. However, it has been
  shown that the interaction between casein micelles and whey proteins
  is also accompanied by a large increase in number of very small,
  soluble particles resulting from the desegregation of casein micelles.
  Consequently, by weakening the interaction forces between caseins,
  heat treatment provokes both a loss of the micelle framework and the
  formation of small aggregates. Correlatively, an increase in the
  amount of nonsedimentable casein has been observed in UHT milk
  following high-speed centrifugation (33). Two effects of these changes
  on milk properties may be softer coagulation and a higher
  susceptibility to enzymatic hydrolysis due to loosening of the
  micellar structure and the presence of small aggregates that may be
  more accessible to enzymes.

In the stomach of adult or infant, gastric acid and the enzyme pepsin denaturate whey and casein proteins from either raw or heated milk Critical Reviews in Food Science and Nutrition). The denatured proteins are then nearly completely digested by the enzymes pepsin in the stomach and by trypsin, chymotrypsin and peptidases in the small intestine (Medical Libretexts.

Humans, including infants do not have the enzyme rennin (chymosin).

  Rennin, also called chymosin, protein-digesting enzyme that curdles milk by transforming caseinogen into insoluble casein; it is
  found only in the fourth stomach of cud-chewing animals, such as cows.
  Its action extends the period in which milk is retained in the stomach
  of the young animal. In animals that lack rennin, milk is coagulated
  by the action of pepsin as is the case in humans. A commercial form of
  rennin, rennet, is used in manufacturing cheese and preparing
  junket (Britannica).

  Chymosin is secreted in the neonatal stomach of ruminants (cattle,
  goats, camels), pigs, cats, and rats. Animals including humans,
  chimps, and horses have inactivating mutations in their chymosin gene
  and do not secrete the enzyme (vivo.colostate.edu).

There's one study that mentions the presence of chymosin in humans, but the evidence seems to be very weak as described in another Biology SE answer. Some articles, like this one mention chymosin in humans without proper references.


Is brain plasticity such that we can train ourself to see with our ears?

Short answer
Yes, we can see with our ears.

Background
Bach-y-Rita famously stated "We see with our brains, not our eyes". Bach-y-Rita worked for decades on sensory substitution. Sensory substitution approaches in general aim to replace for a lost sense by redirecting information normally captured by that sense to another still functional one.

Bach-y-Rita focused on substituting vision by tactile information. His Tactile Vision Substitution System (TVSS) captured camera images and translated them to tactile images projected onto the back of blind subjects. His decades of research eventually culminated in the commercially available BrainPort device (Stronks, 2016).

Vision-to-auditory substitution devices have also been developed, most notably the vOICe by Peter Meijer and the prosthesis-substituting-vision-by-audition (PSVA) device, among others. The vOICe translates images into sounds by re-mapping their x-axis into the time domain, and their y-axis into the frequency domain (Meijer, 1992). This “image-sweepline” technique has subsequently been deployed in the EyeMusic device for use in sensory substitution (Abboud et al., 2014). The PSVA makes use of a pixel-by-pixel acoustic frequency transformation,where vertical position is coded as pitch and horizontal position as binaural intensity and phase differences, and brightness into loudness (Capelle et al., 1998).

Peter Meijer refers to the vOICe as generating 'soundscapes', much like the approach you are describing. I seriously encourage you to contact him, he is a very nice guy and open to exchange.

Anyway, to come to your question - can we see with our ears? Yes we can. Several studies have indicated that sounds can successfully be used to perform visual tasks, including localization (De Volder et al., 1999), pattern recognition (Arno et al.,2001a, 2001b) and depth-perception (Renier and DeVolder, 2010).

Several studies have shown that the visually deprived brain is capable of re-routing auditory sensations into visual equivalents by re-routing this information to the de-afferented visual cortex in the blind (reviewed in, e.g., Poirier et al., 2007). This is referred to as cross-modal plasticity of the brain.

However, the learning curve is quite steep, in that a lot of practice is needed to obtain useful information from visual information coded through sound (Stronks et al, 2015). Further, what is probably the biggest issue in analyzing soundscapes is visual clutter. While the visual system is very well capable of filtering out image clutter and extract the useful information, soundscapes will inevitably turn every irrelevant object in the scene into a corresponding sound. Front-end visual processing techniques are likely to be key to turning an auditory visual substitution device into a practically feasible device for the blind, or the sighted for that matter.

The visual cortex is recruited for auditory tasks in the blind, but not in the sighted. However, I am inclined to believe it is practice, and not visual deprivation per se, that determines the performance with sensory substitution approaches in general (Stronks et al, 2015).

References
- Abboud et al., Rest Neurol Neurosci (2014); 32: 247–57
- Arno et al., Neuroimage (2001a); 13(4): 632–45
- Arno et al., App Cog Psych (2001b); 15(5): 509–19
- Capelle et al., IEEE Trans Biomed Eng (1998); 45(10): 1279 - 93
- De Volder et al., Brain Res (1999); 826(1): 128–34
- Meijer, IEEE Trans Biomed Eng (1992); 39: 112–21
- Poirier et al., Neurosci Biobehav Rev (2007); 31(7): 1064–70
- Renier and De Volder, J Integr Neurosci (2010); 4(4): 489
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Expert Rev Med Dev (2016); 13(10): 919-31


Why is therapeutic index a ratio instead of an interval?

Most drugs are measured by mass - they are then dissolved in some solution or incorporated with fillers into pill form.

If you are worried only about a difference, say from measuring out a volume to be given intravenously, then it would be trivial to solve that issue by dilution: you could take your drug that was dissolved in 1 mL, dilute it so that you are giving 50 mL instead, and make the difference unimportant. The ratio, however, stays the same, regardless of formulation.

A ratio is also much more likely to come up in clinical practice. Take your example, where the toxic dose is only 2X the effective dose. That means that an error where a drug is accidentally given twice could be a serious problem. It doesn't really matter if the volume delivered is small or large, just that someone doesn't realize the drug was already given.


Difference between thylakoids and lamellae in a chloroplast?

The answer above goes in depth so I will try go off that.
Firstly, lamella is the word used to describe plate-like structures. A thylakoid therefore, being a flattened vesicle, would fit this description, so a thylakoid is a type of lamella.
As mentioned earlier, a lamellar system consists of uniform thylakoids, the thylakoids being the individual lamella.

I have the same textbook as you, OCR A2 Biology, and I must admit I had the same confusion. What this textbook fails to mention is the fact that thylakoids are just one type of lamellae.

The textbook also states that the inner membrane of the chloroplast is "folded into lamellae (thin plates)". There are two types of lamellae in the chloroplast, thylakoids and intergranal lamellae, both are stacked, however only thylakoids appear as "piles of pennies" as it states. Intergranal lamellae look nothing like pennies, which is why the textbook is strongly misleading, they are big flattened bits of membrane that connect together different grana (stacks of thylakoids).

Note: my answer comes in 3 years late (I'm currently doing my A2), and the textbook in question will see its last use this year as the current A2 level syllabus is updated, I hope my answer still helps to clear up any confusion should OCR mess up again on this one


Dehydration Synthesis: Why does a monomer contribute a -H instead of an H atom?

The dash ("-") does not represent a negative charge or an electron.  It simply indicates that the group of atoms ( -OH or -H ) are attached (covalently bonded) to other atoms in a molecule.  So they are saying one monomer (molecule) contributes OH to the reaction and the other H.  (A charge is indicated by a trailing superscript minus sign.)


Different components of the ECM can be stained differently but since you asked about hyaluronic acid (HA) I'll limit my answer to its staining.

See this paper. They use Hyaluran Binding Protein (HABP) as a specific probe for HA.

  Because HA has a very simple, conserved composition and is
  ubiquitously expressed in all animals that have a developed immune
  response, HA is not immunogenic. Therefore, there are no antibodies
  that specifically recognize HA, and traditional immunohistochemical
  methods of detection of HA are not possible. Fortunately, a very
  specific and tightly binding protein, the hyaluronan binding protein
  (HABP), which is composed of the HA binding domain with the link
  module from aggrecan, was isolated (Hascall and Heinegård 1974;
  Tengblad 1979) and adapted as an HA probe (Ripellino et al. 1985).
  HABP is now widely employed for specific detection of HA.

Biotin tagged HABP can be used for IHC based visualization procedures.


Google for sublithic or hypolithic.

You'll find lots of things like (https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-11274-4_767) with further references and links


What is the best way to orally administer a water insoluble powdered drug to macaque monkeys?

If it is not water-soluble (lipophobic or hydrophilic), the only other alternative would be that it is fat-soluble (lipophilic or hydrophobic). Consider adding the powder to fatty solids or liquids which can be absorbed from the GI tract into the vascular system, if that is where you'd like the drug to go to be distributed throughout the body. Ideally, you would need to look up the target concentration of the drug within the blood in order to be effective, its volume of distribution, its bioavailability, its half-life, mechanism of metabolism, and calculate from there how much you would really need in order to last the full 2 weeks.


What is this growth on a Rosa rugosa stem?

This looks like a gall. At first I thought that it was the common rose bedeguar gall, also known as Robin's pincushion gall which is caused by Diplolepsis rosae, a small wasp. However, there is a related wasp, the spiny rose stem gall wasp Diplolepsis spinosa, which attacks Rosa rugosa so I imagine this is what you have here.

Incidentally, you are probably wondering what bedeguar might mean. According to the OED it derives from a French word bédégar which in turn comes from the Persian bād-āwar ('wind-brought’).


What measures are commonly used for the complexity of an organism?

This is a very interesting question. Not sure if there is any way to answer without specifying a definition for complexity.

It is clear that everything is made of only the same few elements, so complexity must involve more than that. Do the number and position of identical molecules matter? If so, size matters and we would label a large jelly-fish as more complex than a cat and the air in a large hot-air ballon as more complex than any single living organism (assuming it is bigger).

I think it is clear that this is not what is meant by biological complexity. Molecules acting identically should not count multiple times; the number of different molecules matters more than the mere number of molecules. But are immune cells really more complex simply because of a relatively minor difference that allows them to generate a wide variety of genetic variants?

What about the variable coat color of a calico cat. Does the complex and non-repeatable (even with cloning) pattern mean it is complex, or does the fact that a simple genetic process underlies it mean it is simple.

The difference in complexity of different representation of the same thing is a classic problem in information theory (see Kolmogorov complexity). The ratio of the circumference of a circle to its diameter requires an infinite number of decimal digits to describe, but it is just a single geometric concept and it can be represented with one or two characters, as pi or π. This applies to the problem of using phenotypes to measure complexity -- the language and definitions we use to describe or to differentiate phenotypes determines what is complex and what is simple.

Moving beyond a simple static snapshot case, biological complexity involves time-dependent evolution. The "game of life" demonstrates how simple rules + initial conditions yield apparent complex behaviors, and the beauty of fractals arises the same way. Many apparently complex organisms grow from small seeds plus time-evolved exposure to simple things like water and light and CO2. Are trees only as complex as the seed they grow from?

Finally, what about higher order complexity? One human brain is very similar in general makeup to another, but the concepts and memories stored seem complex and very different. Comparing the complexity of stored information between two people is the whole complexity problem over again.

It seems to me that complexity can only be cleanly measured within a specific context, and then only relatively. One can measure the relative genomic complexity of two organism as the edit distance between the alphabetic sequences representing their genomes. The relative regulatory complexity can be measured as mentioned above by @user1682. Each of these says something about an organisms complexity. But what if organism A has higher genomic complexity and organism B has higher regulatory complexity? It might be possible to derive something like a principle component "basis set" from several of these kinds of measurements using a training set and a list of organisms with predefined complexity values. Applying this "standard" scoring metric to another organism would allow ranking it on a "standard" scale, but it would be difficult to generate and obtain consensus on the initial "expert" ranked organism scale. Such a standard might have some value, but is not really theoretically satisfying in that it describe an organisms complexity in the same way that the average of a small sample describes the distribution of a large population.


What advantage does the pseudostratified epithelial structure type provide over squamous, cuboidal, and columnar?

Why not have ciliated columnar tissue?

The respiratory epithelium in the trachea is columnar. The three classifications you bring up in your question: cuboidal, columnar, and squamous, describe the shape of individual cells. The trachea, as you saw in your trachea sample, has columnar epithelial cells (when healthy). The cells are longer along the axis perpendicular to the basement membrane than they are along the axis parallel to it.

You can also classify epithelium according to the number of cell layers between the basement membrane and the free surface of the epithelium. The two possible classifications here are simple (one cell layer) and stratified (more than one cell layer).

The classification pseudostratified means it looks like it's stratified, but it is actually simple. As with any other histological classification, this classification describes structure rather than function. The epithelium in the trachea is simple columnar because all the cells touch the basement membrane, but without knowing that (just by looking at a cross section) it would appear to be stratified because the nuclei of all the different cells do not line up. That is why it is called pseudostratified. The difficulty in distinguishing pseudostratified and stratified from an ordinary cross section of a trachea may be difficult to appreciate without an image. It is not obvious that there is only one cell layer above the basement membrane here, but there is:

As with other simple columnar epithelial tissues, the trachea is specialized for both secretion and barrier formation.

You could speculate on the possible strengths and weaknesses of the pseudostratified structure, but it just happens to be the case that a certain cell population that has nuclei that are closer to the basement membrane (here labeled BC), and a certain cell population has nuclei that are further from the basement membrane (here labeled CC). Those cells with the lower lying nuclei are sometimes called basal cells, and are not terminally differentiated. They provide a reserve for cell replacement in response to normal loss of cells and/or pathophysiological processes like infection and inflammation.

Now, other simple cuboidal epithelial structures, e.g., in the intestine, do not have a pseudostratified structure. If you look at a healthy section of large intestine, the nuclei of the epithelium clearly line up, and it's not hard to see that the structure is a simple epithelium. For those unfamiliar, the epithelium here is only the outer layer. The seemingly disorganized mass of cells deep to the epithelial basement membrane are connective tissue (labeled CT). Look for a thin pink line in each of these slides to help orient yourself to the epithelial tissue. That's the basement membrane.

This simple cuboidal epithelium is also renewed in response to normal loss of cells and pathophysiological processes like infection and inflammation, but doesn't have a pseudostratified structure. This means, clearly, you don't need a pseudostratified structure in order to renew an epithelial surface. So I would caution you not to expect structure and function to be so neatly tied together in histology. It's a descriptive science. You can learn and understand what these structures do, but it's not necessarily a good idea to try to shoehorn the structures into logical rules. The usual answer to "why" in histology, is "because that's what it looks like".

You can read the details in Ross Histology, Chs. 5 (for general classifications and the general concept of pseudostratified epithelium), 19 (for respiratory epithelium and the details on pseudostratified epithelium), and 17 (if you want to compare the respiratory structures to the epithelial structures in the GI tract). Images are from Ross Ch. 5.


What is the biological function of nose, underarm, and pubic hair?

From this article I quote

  Hair in the nose is one of the body's first lines of defense against
  harmful environmental pathogens such as germs, fungus, and spores.

  Another purpose for nose hair is to provide additional humidity to the
  inhaled air. As the air passes through the nasal passages, the mucus
  and hair provide heat and moisture. Humidity is an important factor
  for the rest of the respiratory system, such as the larynx and lungs.

  Hair in the form of tiny cilia also draw solid particles towards the
  interface between the nose and throat. Harmful debris is generally
  directed towards the back of the throat and esophagus for swallowing,
  while the filtered air continues towards the larynx and lungs.

If you look on an evolutionary perspective, the arm pit hair follicles as well as pubic hair have a type of sweat gland associated with them, called an apocrine gland, that begins to function at puberty and is widely associated with scent-communication via chemicals known as pheromones (reference).

Some other functions that are associated with pubic hair are:

Keeping the genitals warm.
Drawing attention to the genitalia.
It also decreases friction during intercourse (reference).

The nose hair is definitely not vestigial. As long as the armpit hair (between the body and arm in certain heavyset individuals) and pubic hair serve to reduce friction and male sweat serves to increase female hormones, I wouldn't call them vestigial (reference).


Fighting of harmful microbes (and not antigens per se, although specific antigenic recognition is important), involves a lot of processes which require several lignad-binding molecules and ligands on the WBC surface. While the whole array of these proteins and their functions is very complex, we can take the case of a neutrophil trying to defend the body against microbes in a local wound, the so-called acute local inflammation response.

1. Adhesion to the endothelium

Here is where several selectins play a role. The simple broad idea is that in presence of microorganisms, as sensed by the local immune cells (tissue macrophages, blood cells in case of a vessel breach etc), there is an upregulation of chemokines in the local environment which causes the endothelium to increase the expression of certain adhesion molecules (ligands with receptors on WBC and vice versa) as well as other hemodynamic changes causing the neutrophil to come in close contact with these in the vicinity of the wound and bind to the endothelium. This is ften subdivided into three processes, margination, rolling and adhesion. L-selectin is one of these adhesion mediators, along with other selectins and integrins.

2. Migration through the endothelium into the tissues (diapedesis)

3. Chemotaxis towards microbes

4. Action on the microbes

Points 2,3 and 4 have their own mediators (see CD31, chemokines - AA, C5a, leukotrienes).

Reference:
Robbins and Cortran: Pathologic Basis of Disease, 9e

Other sources:
Wikipedia page


How do drugs tests check so many substances?

There are a lot of different methods to test samples for drugs. The most common for a "screening" test, like one might encounter before being hired for a job, are based on immunoassays. These use antibodies to detect certain substances in the sample. These are good for testing for a few drugs or categories of drugs (like THC, benzodiazepines, opiates, amphetamines, etc.), however they can't test for a large number of drugs at once, and often won't tell you the specific drug (e.g. it'll say "positive for benzodiazepines", not "positive for alprazolam"). If someone tests positive on one of these screening tests, then the samples can be re-submitted for further testing to clarify what is causing the positive result.

Drug testing for elite athletes is a whole different story. The World Anti-Doping Agency has established protocols for the Athlete Biological Passport, which uses standard methods to test samples and record various biological parameters over time, to ensure that athletes aren't manipulating their bodies artificially.

The exact details of how this is done is pretty complex, but they don't need to divide samples into a bunch of separate samples and test each one for a single drug. These standardized kits are able to be run on one urine sample (divided in two) and a couple of tubes of blood, the same size you'd get drawn at a doctor (just 3-5 mL each).

One way they test for many different substances using a single tube is through gas-chromatography mass-spectoscopy (GC-MS), which is a combined method to separate apart substances in the blood and identify them by their molecular weight. By comparing athlete's blood and urine samples to known patterns produced by banned substances, they're able to test for many different compounds using a single sample.


What is the name of the critter depicted in the attached image?

That is the larva of a carpet beetle.

  Larvae feed on natural fibers and can damage carpets, furniture, clothing and insect collections.

"Anthrenus verbasci - larva side (aka)" by André Karwath aka Aka on Wikimedia

Related question: What kind of caterpillar is this?, though I think that the larva photographed in that example is either of a different species or at a different time period within the larval stage.


What causes people to smell one persistent smell during Covid-19 infection?

At this time any hypothesis regarding the parosmia seems to be untested.  Speculative sentences in lay and technical sources point toward the olfactory bulb.  (I have seen indications regarding the cilia of the olfactory neurons, the bulb itself, and the blood supply, but this seems to stray from our topic)
When we look in more detail, the olfactory bulb consists largely of glomeruli (balls of neuropil about 0.1-0.2 mm in size), which receive input from specific kinds of olfactory neurons that receive from specific odorant receptors (ORs).  See this figure for the situation in mice.  The dorsal region of the olfactory bulb is mostly one type of these, Class I ORs, and the ventral part is all Class II. (more)  If you are following this research you might want to try to figure out if the odors people report are mostly Class I (more hydrophilic) or Class II (more hydrophobic), which might allow you to hypothesize something about the relative strengths of signals from these regions in the model you develop.  Reading anecdotes is scientifically useless, but fascinating - this man describes citrus as tasting "extremely oxidized", which certainly fuels a speculation along that line.
Answering the question in any good way would seem to demand good human olfactory tissue from people who catch Covid, suffer ongoing parosmia, die from something else, and then donate their brains to science.  I'm not sure we're going to see a definitive answer that way soon.  It would be worth keeping an eye out for fMRI data.  I suspect that well-focused high-frequency terahertz might be used to image or even stimulate olfactory glomeruli (phones with 'smell-o-vision') but for now that's science fiction.


Book recommendation: Modern Synthetic theory

There is no modern book of evolutionary biology that is not about the modern synthesis. So what you are looking for is just an introductory book to evolutionary biology.

I think the 2 most common introductory textbook to evolutionary biology are:

"Evolution: Making Sense of Life" by Carl Zimmer
"Evolution" by Futuyma

Note by the way that one can find recommendation on population genetics (subfield of evolution) here.