What's the determinant of the male-biased birth sex ratio in humans?

There are a number of ways in which the true sex-ratio at birth (let's assume the 51:49 is well estimated and is the true ratio) could deviate from 50:50. This list is just an brief overview.

Sex, in humans, is determined by the sex chromosome present in the haploid sperm cell which fertilises the egg. If males produced more or less Y-bearing sperm than X-bearing sperm, then the birth sex ratio would be expected to deviate from 50:50. However, studies suggest that sperm production is not biased towards X or Y bearing in humans.
The probability of fertilisation may differ between X- and Y-bearing sperm. If Y-bearing sperm were more likely to succeed in fertilising the egg then there would be a male-bias in the birth sex ratio. I've seen it suggested that the small Y chromosome makes the sperm slightly smaller and therefore faster, but can't find those claims right now. Regardless, it appears that sex ratio at fertilisation is not sex-biased.
Bias in the birth sex ratio can come through sex-biases in the failure rate in fetuses. If female fetuses are more likely to miscarry than male fetuses, over the course of the gestation, then the sex ratio at birth will be male-biased. It appears that there is sex-bias in the failure rate of fetuses which can be male or female-biased throughout gestation, but the tendency is for female-biased failure rate during the second trimester to generate an overall male-bias birth sex ratio.


There have been many personal experiences documented where people have experienced relief from itching of mosquito bites on the application of their own saliva to the itchy spot (reference 1, reference 2) It helps to reduce the itching because saliva has been proven to speed up tissue repair and has antibacterial properties. It also provides a moisturising effect on the itchy spot (reference). Salt is also known to provide relief to itching (reference) and the slight salt content of saliva helps in that respect too.


What is the most detailed living-tissue scan available

I assume you are asking what is the most high-resolution in vivo imaging that science has performed to date?

I think the best way to answer such questions is to explain the nature of the question.

This depends a lot on what kind of sample you are interested in for the question to address. It also depends on whether we are talking about time (temporal) or space (spatial) resolution, because there is usually a trade-off for imaging methods. Some things we can image with femtosecond resolution, and other things we can with femtometer precision.

What property do you want to look at? Is it a certain staining, such as a fluorescent marker? The topography of a molecule sitting on a membrane? The force generated by a motor protein?

Do you consider a reconstructed image (in 3D) from 2D slices to be a fair comparison with techniques that aim to directly image in 3D? Microscopy and imaging are quite advanced fields and we're only beginning to scratch the surface.

Some more considerations for the questioner: is your sample moving? Are we talking about imaging insects hovering near flowers, or anesthetized flatworms? What scale of the sample is being imaged? What are the requirements for keeping it alive during imaging? For instance, perfusing nutrients or imaging a microbe growing on a substrate normally requires the modification of your microscope in such a way that may limit your optical resolution. Imaging some things necessarily requires long working distance objectives, while other specimen may be visualized at short working distances. These have tremendous impact on resolution!

As a case study: let's say we are interested in looking at the human brain with high resolution. You can do this with high temporal resolution (using EEG) or with high spatial resolution using magnetic resonance! Or are you interested in the resolution of real time activity of the brain, as measured via oxygen delivery to regions? This is not possible with either of the above; you have to rely on functional imaging, e.g. fMRI!


Do animals demonstrate target practice (i.e., playful accuracy behavior)?

One example that comes to mind is archer fish. There is evidence that they improve with practice, but they practice on targets that are food items, so I'm not sure whether that counts as practice with respect to your question. Interestingly, there's also some evidence that they can improve their accuracy simply by watching other archer fish succeed.


How long can you effectively store a glycerol stock at -20 degrees Celsius?

While I believe that it is possible to keep a bacterial culture viable while frozen in glycerol stock at around -20 °C, as attested to by WYSIWYG, it is important to note that your "typical household freezer" may not be suitable for such a purpose.

This is because household freezers usually have an "auto-defrost" function. This makes it temporarily thaw out to remove the frost that condenses from atmospheric moisture. If storing sensitive materials such as bacterial/cell culture frozen stocks, this would lead to repeated freeze-thaw cycles which would damage the viability of the stocks.

For that reason, almost all laboratory freezers do not have that function, and instead need to be manually defrosted routinely.


It works via the placebo effect which according to recent research, is not the sort of trivial effect as it was thought to be.


Finding DNA from Amino Acid sequence problem

Your approach to translate the AA sequence, codon by codon, was correct. This was a bit of a trick question because to recognize it, you had to read the sequence backwards.

UGG-CAA-GGT-CAC etc is read directly off of the 3'->5' strand of the circled answer, reading from right to left.

The bottom left is a red herring because it starts with a start codon, ATG, but reading beyond the start codon, the sequence wouldn't match.


Acknowledging differentiation of species, in historical times

The branch of science you are looking for is taxonomy, that is the science of identifying and naming species, and arranging them into a classification.

Modern taxonomy was born from the studies of the Swedish zoologist Carl Linnæus (1707-1778), who first introduced, in his books Systema Naturae (Systems of Nature) and Species Plantarum (Plants Species) the now common binomial nomenclature where each different species is given a Latin name composed by two parts: one identifying the genus and one identifying the species.

For instance, various species of mice are in the genus Mus: the common house mouse is Mus musculus, but in the West Mediterranean you have another type of mouse, called Mus spretus.

Although this rigorous type of classification is quite recent, taxonomy existed much earlier.

Shennong, Emperor of China somewhere around 4000BC apparently tasted hundred of plants to test their curative properties. He wrote his observations in a book called the Shennong Ben Cao Jing.

On a similar note the Ebers Papyrus, dating ~1550 BC contains description of the properties of many plants.

To more "recent" times, around 300BC Aristotle was the first who actually classified animals (e.g. vertebrates and invertebrates) and his student Theophrastus wrote a classification of plants in his Historia Plantarum (Hystory of the Plants).

Some 400 years later Plinius in the Naturalis Historia (Natural History) enumerated many plants and animals and gave some of the first binomial names to certain species.

As to the point of how did they distinguish species: well, with their eyes and ears, of course!
You can distinguish a mouse from a vole because it is skinnier and has a longer tail.
Even more similar species can be easily distinguished without needing special equipment.
A good birdwatcher can distinguish a chiffchaff from a willow warbler by listening to their songs, looking at how they behave how they fly, the subtly different tones of their feathers etc.
We can do that now, without any special equipment, so they could before the Renaissance!


The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset. Artificial supplementation can increase sleep quality and regularity related to some sleep disorders and is often administered as pills or patches.

Adenosine is an inhibitory neuromodulator, ie it inhibits neural activity. Neural activity can be either excitatory or inhibitory and adenosine more strongly inhibits the excitatory neural activity. Thus, increased adenosine levels should decrease excitatory effect of nervous stimuli and make you feel more relaxed & sleepy.

Other hormones & neural pathways may be involved (serotonin and the serotonergic neural pathways for example) as well as other stimuli like other people's behaviours (yawning, stretching etc.).

This page and the wiki entry on melatonin have much more information.

From sleepfoundation:

  Melatonin is a natural hormone made by your body's pineal gland - a
  pea-sized gland located just above the middle of the brain. During the
  day the pineal is inactive. When the sun goes down and darkness
  occurs, the pineal is "turned on" and begins to actively produce
  melatonin, which is released into the blood. Usually, this occurs
  around 9 p.m. As a result, melatonin levels in the blood rise sharply
  and you begin to feel less alert. Sleep becomes more inviting.
  Melatonin levels in the blood stay elevated for about 12 hours - all
  through the night - before the light of a new day when they fall back
  to low daytime levels by about 9 a.m. Daytime levels of melatonin are
  barely detectable.


Are there any websites offering graphs for the light absorption of different enzymes?

It is not typical to investigate spectral absorption of compounds that are not useful for light absorption qualities, such as the compounds you've listed. Enzymes in particular will have less information because of the changes in binding partners our physical conformation to be enzymatically active. If you think there should be known info then I would try Google Scholar, Pubmed and a google search, in that order.

Edit:
The intended meaning of the question is related to spectroscopy and quantification of protein concentration. There are two common ways to determine protein concentration using optical methods (spectroscopy). The methods use colorimetric assays (colour intensity is proportional to protein concentration) or light absorbance at a reference wavelength. Both methods rely on light absorbance at a specific wavelength, but the former relies on an reagent that changes colour in response to protein quantity, and the latter depends on direct UV light absorbance. Here's a quick breakdown of each.

For both of these assays, to determine the quantity of a specific protein, they require a source of purified protein.

Colorimetric Assays:

These are traditional biochemical assays, of which the most widely used are the: Bradford, BCA and Lowry protein assays. These assays rely on reduction-oxidation reactions between the key assay reagent (Bradford's reagent, bicinchonic acid, or Lowry's reagent) and protein. For example, the BCA reagent is reduced in the presence of protein, causing a chelated copper ion, Cu(II), to be reduced to Cu(I), and effecting a purple colour. This purple colour intensity, which read at a specific wavelength (~520 nm) will indicate the amount of protein.

Near-UV Absorbance:

This method relies on 280 nm (near-UV) absorbance. Usually absorbance at 260 nm is also used for a correction factor. Specifically, amino acids with aromatic rings (eg, tryptophan) cause absorption at 280 nm. Peptide bonds absorb at 200 nm, and various other bonds, pH, ionic conditions, all influence and absorb at various wavelengths.

These methods cannot be used with a protein sample alone, because there are a number of conditions that can affect readings. To correct for this, a protein standard is also used. A protein standard uses a series of known concentrations of a known protein. The common protein concentrations can range from 20-2000 µg/mL; the common protein standards are bovine serum albumin, chicken ovalbumin or purified IgG. The protein standard acts as a reference for protein concentrations that are valid for that experiment, under those specific conditions. A curve is fit to the readings of the protein standard, and the sample concentrations can be read off the standard curve by using the absorbance readings.


Are Richard Lynn's estimates of African IQ inherently innacurate on the basis that most Africans aren't mentally retarded?

IQ is just a measure of how good you are at taking IQ tests, that's it. Those tests are usually culturally biased towards middle income first world citizens (among other things). Think of it this way, questions about mortgages, supermarkets, airplanes, or such thing presuppose the person being questions knows a reasonable amount about those things, this is not a reasonable assumption in many places around the world.

The classic "a train leave chicago at 10:00..." is a perfect example since the reader needs to know what a trains is, that chicago is a place, and what 10:00 means additionally they need to be familiar with reading exact measures of time and velocity, that they have already been taught basic math, are familiar with abstract questions, and that they are experienced readers, these are all fine assumptions for the New York suburbs but pretty bad ones for sub saharan subsistence farmers.

People who try to write the questions for said cultures often run into the reverse problem, we think of travels as a steady rate but to people who travel by boat know allowances need to be given for things like the speed the stream is moving, or the paddler taking breaks for lunch, information the writer may wrongfully assume or not understand. I recall a question about two people traveling along the same road that was consistently wrong because people in that culture thought is was proper for the faster person to slow down to match the slower for the safety of both (the norm in said society) so they constantly calculated their speed as the same, something the writers never anticipated.

There are millions of these differences across cultures and these cultural differences quickly snowball in to large differences when taking identical tests. So you are not seeing a real difference in intelligence just an artifact of culturally biased testing.


Can formalin fixed tissue stored in absolute ethanol be used for histology?

Can they be used? Sure. How much distortion you get will depend on the tissue type and several other factors. How important that distortion is will depend on what you are trying to measure. "Too much distortion" is a relative term. You can't really know how bad it will be without trying it.

Should this ever be done intentionally? No - there is good reason for using the gradual dehydration steps. I would be really hesitant to do any quantitative analysis or draw any solid conclusions from tissue processed incorrectly, though.


Proteins that are strongly overproduced in E. coli and S. cerevisiae?

Heat shock proteins - HSP70 and HSP30.

You may also have ribosomal subunits as well.


Do other young mammals turn their backs to their parent when upset?

Other Primates
Sulking is the behavior you are refering to and it is seen in orangutan, Chimp and Bonobo. Likely in other primates but I am not aware of any published works. I have heard about it in baboons but have not read the papers myself.
Source
Source2
Source3
Source4
Also adult humans DO do this on occasion, it is just often more subtle.
It is amazing how many identical social behaviors are seen in our close relatives, especially the ones about conflict and conflict resolution.


Why can't complex multicellular organisms reproduce by regeneration?

I was doing some research on this myself and from what I had found, the body has hox genes that direct the formation of body parts. So now the obvious question is that if a body part contains stem cells and hox genes, shouldn't it be able to regenerate a new body? Well, perhaps. But the problem is that as organisms become more complex, the process of the creation of their bodies also becomes more complex. For example, in the fruitfly, if the labial gene function is not expressed, the mouth and head that develop outside the body do not get involuted and that prevents the salivary gland from forming.

So the answer about why multicellular organisms can't regenerate so easily simply seems to be because the process of creating a multicellular body has for some reason become an extremely complex, intertwined process where various body parts creation is dependent on other body parts creation. So in the evolutionary process it's entirely possible that the stem cells noted that there's no point trying to regenerate a body part, and therefore they just don't.

Here's an anomaly. There's a jellyfish that can reverse aging and go back to infant stage. I think it's able to do so because it has a simple body structure.

Another possible reason could possibly be the presence of unstructured proteins which are more abundant in multicellular organisms.


Are ion channels/resistancies in Rall's model voltage-independent or not?

If you are interested in passive diffusion and not just membrane potential generation in a dendritic compartment, then you need to look at the cable equation:

$$\frac{1}{r_l}\frac{\partial^2 V}{\partial X^2} = c_m\frac{\partial V}{\partial T}+\frac{V}{r_m}$$

Here, every compartment is connected in series with resistances $r_l$.

We define the length constant as
$$ \lambda = \sqrt{\frac{r_m}{r_l}}  $$

and the time constant as
$$ \tau = r_mc_m$$

Then the equation can be re-written as:

$$\lambda^2\frac{\partial^2 V}{\partial X^2} = \tau\frac{\partial V}{\partial T}+V$$

The reason $G_e, G_i$ are not mentioned when talking about diffusion along the dendrite is that they are only involved in the generation of voltage $V$ in the compartment.


neural genes expressed in nasopharyngeal specimens

This paper mentions using a cytology brush (not the usual NP swab) to obtain cells from the olfactory epithelium. They obtained and cultured neural precursor cells. Have a look.
Trends in molecular medicine.
"The Olfactory Neural Epithelium as a Tool in Neuroscience"
Joëlle Lavoie, Patricia Gassó Astorga, [...], and Koko Ishizuka
from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399677/


True or False: Dideoxynucleotide sequence analysis Question

It is false, because DNA synthesis occurs via DNA polymerase,5' to 3'

By hydrolyzing activated nucleotides together. This occurs by nucleophilic attack of 3'-OH, of the last nucleotide in sequence, on alpha phosphate of a corresponding nucleotide triphosphates.


How diverse are species in remote, isolated areas on Earth?

The concept that you hint at, has been studied at the example of the island of Australia, where marsupials often look quite similar as their counterparts in the same ecological niche, which live outside Australia and have a placenta, and are less related on the DNA level (e.g.: squirrel-like animals, wolf-like, and the now everywhere extinct saber-toothed tiger-like...).

If you are interested to learn more, I would highly recommend to read Jerry Coyne's "Why evolution is True" ( http://jerrycoyne.uchicago.edu/index.html )

The specific example of Europe and Americas (which does not fully capture the complexity of your question), also is quite interesting - although it is very short on an evolutionary time-scale. E.g.: American squirrels, which lack predators in Europe, and only arrived in Europe because of human journeys following the rediscovery of Americas, are partially outcompeting the beloved red squirrels ( https://en.wikipedia.org/wiki/Eastern_grey_squirrels_in_Europe )


Is there any independent non-DNA based information system in the cell

According to the comments, the question is about inheritance systems of cells. The "mainstream" information storage and inheritance system is of course DNA (and RNA in some cases). However, there are additional and parallel inheritance systems even within a single cell (not to mention in multicellular organisms). These form a subset of epigenetic inheritance methods and - as expected - are less precise than the information copying mechanisms of polynucleotide replication (in eukaryotes) and certainly more limited in the amount of information that can stably maintained throughout generations. This was explored in detail by Eva Jablonka and Marion Lamb (among others) in a few books and many papers:

Jablonka, E. & Lamb, M. J. 1995. Epigenetic inheritance and evolution: The Lamarckian dimension. Oxford University Press, 346 pp.
Jablonka, E. & Lamb, M. J. 2006. Evolution in four dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. MIT Press, 472 pp.
Jablonka, E. & Szathmáry, E. 1995 The evolution of information storage and heredity. Trends in Ecology and Evolution, 10, pp. 206-211.
Maynard Smith, J. 1990 Models of a dual inheritance system. Journal
of Theoretical Biology, 143, p. 41-53.

  “An epigenetic ineritance system (EIS) is a system that enables a
  particular functional state or structural element to be transmitted
  from one cell generation to the next, even when the stimulus that
  originally induced it is no longer present. In other words, EISs are
  the systems that enable the transmission of various phenotypic
  expressions of the genetic information in an individual.” (Jablonka & Lamb 1995, p. 80.)

Epigenetic inheritance methods include the following systems that could in theory code for information that is potentially inherited from parent to daughter. The list is far from being exhaustive.

DNA methylation: a methyl group added to a gene's promoter represses its transcription. Methylation is heritable: when DNA replicates, methylation carries over. There are other chromatin-marking methods that are inherited.
Steady-state inheritance system: "the inheritance of functional states through self-sustaining metabolic networks, maintained by positive feedback." (Jablonka & Szathmáry 1995 TREE) The cytoplasm itself is also inherited by the daughter cells, but any information "stored" in the cytoplasm cannot effectively be "replicated" from cell to cell.
Structural inheritance system: 3D structures of the cell provide the template for similar structures to assemble, e.g. "transmission of cytoskeletal organization and of cortical organization" (Jablonka & Szathmáry 1995 TREE).
Symbionts and parasites (bacteria, viruses, plasmids, etc.) that can replicate within the cell (so that when the host divides, both daughter lineages receive the partner). Note, however, that if the parasite is too virulent then it is expected that horizontal transfer is more emphasized than vertical "inheritance".
Prion proteins. Prions are proteins that may exist in several distinct conformations, and at least one of these conformations is capable of replication by forcing its alternate conformation (and therefore alternate function) on the normal physiological form of the protein (both having the same amino-acid sequence). See Shorter, J. & Lindquist, S. 2005. Prions as adaptive conduits of memory and inheritance. Nature Reviews Genetics 6, p. 435–450.
...


Comparion between machine vision & human vision

This is a potentially very very broad question, but I'll try to provide a simple answer that addresses the biggest misconceptions.

First of all, animal vision (and brains more generally) is massively parallel. There may be some serial processing steps, but these are also massively parallel. Computers need to digest information into stereotyped operations that can be executed on a CPU. The brain has separate dedicated machinery to each point in space for early vision, so there is no need to process individual "lines" or points in sequence: it all happens at once.

Photoreceptor inputs are converted into center-surround receptive fields in retinal ganglion cells, where light in the center excites and light in the surround suppresses (ON-center cells), or vice versa (OFF-center cells). These receptive fields are then transmitted to thalamus (the lateral geniculate nucleus), and from there to V1, primary visual cortex.

You can then combine many of these circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception

The cells in V1 that respond to these "edges" are called "simple cells"; there are also "complex cells" that have more complicated receptive fields, and other sensitivity like to motion and color. Some computer vision strategies end up producing receptive fields that look a lot like the ones found in early visual areas, the earliest ones built out of Gaussian-filtered sin waves.

From V1, there are higher order visual areas that respond to things like shapes, motion, optic flow, etc.

Basic neuroscience textbooks tend to contain a lot of information on the early visual system, Purves Neuroscience is a good example, any edition is fine:

Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.


The technique described here is called microarray. Your question has given me an opportunity to put forth one of my opinions about certain problems of gene expression studies.

Gene expression is a measure of the activity of any gene. If the gene performs its activity in the form of a protein, then its expression should be a measure of the protein. If a gene makes a non-coding RNA then its expression is a measure of the RNA concentration.

[You can omit the cases of post-translational modification because of signal transduction. They are highly expressed and transiently but frequently used. ]

Like your example there are many studies which use mRNA concentration as a proxy for protein activity. This proxy works in many cases because transcriptional gene regulation is more frequently used mechanism for imparting stable changes. But the best strategy would always be to measure the proteins also.

Apart from microarray there are several techniques to measure RNA concentration:

RNA sequencing (high throughput)
Real-Time PCR (medium throughput)
Northern Blotting (Low throughput, semi-quantitative)

Many techniques exist for measuring proteins also:

Mass spectrometry (high throughput)
ELISA (Low throughput, quantitative)
Western blotting (Low throughput, semi-quantitative)

Usually the "proxy method" is used because protein quantification is comparatively more difficult. Antibody based techniques like ELISA and Western blotting have problems of cross comparison of proteins because of the variability of the antibody binding efficiency.


about the direct intervention of a child's gender

Sperms can and are sorted using flow cytometry to attempt to separate sub-populations carrying X or Y chromosomes. The technique isn't perfect but it is undergoing "clinical trials" in the USA.


How much of a DNA difference is between Chicken of the Woods, and Hen of the Woods?

I will assume from your comment that your question is

  Is a chicken of the woods just a hen of the woods growing on the side of a tree?

, which is very similar to me to

  Is a chicken of the woods and a hen of the woods the same species?

No, they are not the same species. Chicken of the woods is the common name of a number of species of the genus Laetiporus. Hen of the woods is the common name of the species Grifola frondosa. In fact, Grifola and Laetiporus don't even belong to the same family but only to the same order (order Polyporales).

According to the wikipedia links posted above, Grifola frondosa is indeed usually found at the base of the tree while Laetiporus is generally found in the wound of trees (mainly oak trees).


Western Blot: Fischer ECL substrate 2:1 instead of 1:1?

Well usually in an ECL kit, one of the reagents is the substrate and the other one is hydrogen peroxide, which activates the substrate for breakdown using the HRP on your secondary antibody (Ab) so I genuinely doubt what you are seeing is the result of ratio difference. In order to make that conclusion you need to run your samples twice (on two separate membranes) and do a 1:1 and 2:1 ECL and if you observed such a difference then you are on firmer grounds.

I suspect what has happened in the above experiment is that you have done a 1:1 (with 1Ab and 2Ab not distributed equally on the membrane) then after perhaps not a very thorough wash, you have done another 1Ab and 2Ab incubation using the a 2:1 mix. I suspect what has happened is that in your 1:1 the left hand side has not received the Ab mixtures very well and when you did the 2:1 since the right hand still Ab attached to it (if you didn't strip the membrane) so the left hand side was "forced" to get the Abs hence again the Ab mixture and ECL not equally bound. It is obvious since one image is opposite the other so its the Ab incubation step that has gone wrong. Otherwise if you have done the second ECL incubation mixture straight after the first and didn't do a wash step, the same can result if the membrane did not receive the initial ECL mixture equally since you can get a blocking effect by the old ECL mixture and perhaps what has happened is that the H2O2 or the substrate was present in excess in the second incubation step hence amplifying the signal in the sections of the membrane that did not receive the ECL mixture very well in the first place, relative to the rest of the membrane, which still has ECL liquid on it from the last experiment (again if you haven't washed the membrane well as ECL can be active for up to 24 hours in some kits but after a few hours the activity usually reduces but can still be observed)

What you need to do is after ECL, wash the membrane with TBST for a few minutes followed by TBS, leave the membrane in the sun to dry so that the Ab slowly denature (although that doesn't always happen specially with high affinity Abs such as anti-tubulin and actin). After at least 24 hours, strip the membrane from Ab and redo the Ab incubation. The best thing to do is to do all the incubation steps in a sealed bag then make sure the membrane receives the ECL mixture equally and do the visualisation. I would say however since the membrane is unequally "contaminated" with the Abs then the best thing to do is to redo the experimental run and re-run the gel. Its a pain but you need to get to the button of this!


Are there official criteria for an experiment to be considered statistically robust for publication in a decent scientific journal?

There is no single measure for "robustness" and a lot of it boils down to the field. Usually physics has a very high degree of precision: p value close to 0. For instance, the Higgs boson was a confidence level of 5 sigma, while biology or psychology is going to usually have more leeway: maybe 2 sigma (Sigma).

However, there should be no (statistical significance) criterion to publish. The idea that only positive studies should be published has led to biases in available data in a number of fields (Fighting publication bias: introducing the Negative Results section). Negative results are very useful to us as robustness of a theory is often evaluated using meta-analyses. If a person fails to publish their results because it does not robustly justify their theory, then the data available to perform a meta-analysis is diminished.

Clearly, you want the study to be properly run and you want the method to be reasonable. A garbage study, regardless of the statistical significance measured, is going to be looked upon negatively.

That being said, if your topic is something that has been researched a number of times, a small study is not going to be looked at very well, as there is already "better" information available. The study should provide some kind of new insight into the topic.


Can NSAIDs impact negatively the healing of tendons?

I would suggest you contact your doctor if you are suffering from tendinitis.

NSAIDs are often used as part of treament for tendinitis, but like all medications they can have side effects. Therefore again if you have concerns about taking NSAIDs contact your doctor.

As for the mechinism of action of NSAIDs they don't constrict vessels but instead reduce the production of inflammatory mediators (prostoglandins) which act to dilate some vessels. These inflammatory mediators also make blood vessels more permeable so that nutrients and cells from the blood can pass through the vessel walls and carry out repairs to damage tissue. The problem however with the bodies inflammatory response is that it can be too severe, so that rather than providing healing it itself can cause damage and pain. For this reason (and many others) NSAIDs may be useful.

But again if you have concerns about taking NSAIDs or any medical condition these please consult your doctor. The internet is not an appropriate place for medical advice, your doctor is.


It is selective pressure that determines and limits the number of neutral/beneficial mutations that can take place. The more constrained a locus is under selection, the easier it is to generate deleterious mutations and the harder it is to generate beneficial ones; this can be reflected in low substitution rates at such loci in populations with time.

One widely used method to measure this is to compute the Ka/Ks ratio to infer if a locus is selectively constrained or not.


What does 'kinetically accessible' mean in protein folding?

At some point during protein folding, there may exist lower energy states from a thermodynamic perspective (lower ΔG free enegy) which are actually unreachable in a given environment, because the required activation energy is too high. These are kinetically inaccessible states, conversely accessible state are those that can be reached.

For example, that could mean a protein could reach a lower energy state by unfolding a bit, but exposing hydrophobic amino acid even temporarily would require too much energy. So the lower energy state is not kinetically accessible.

This is somewhat similar to the concept of kinetic and thermodynamic reaction products in chemistry.


What does the spectrum of Chlorophyll fluorescence look like?

I think for your purpose you should start, for example, with this link:
https://academic.oup.com/jxb/article/60/11/2987/533160

UPD:

Chlorophyllous tissues emit radiation of wavelengths approximately 680-760 nm. Source: Plant Physiological Ecolgy, Second edition, Hans Lambers, F.Stuart Chapin III and Thijs L. Pons, New York : Springer, c2008, p. 37, Box 2A.4 Chlorophyll Fluorescence


The fundamental way in which this works is by geography: signals triggered by different stimuli travel by different pathways to different regions of the brain that are specialised for dealing with the sorts of information they contain.

For example, visual signals from the retina pass down the optic nerve and (after a few interesting twists and turns that, inter alia, send the left and right halves of each visual field to different brain hemispheres) wind up in the visual cortex, which contains neuronal networks adapted for recognising different structures and regularities in the image. Whereas sound information from the ears, after an even more tortuous sequence of processing steps, winds up in the auditory cortex.

Along the way, the signals will typically be split up across many neurons and reintegrated into new signals that pick out different kinds of information. So a particular stimulus will result in a complex spatio-temporal pattern of action potentials firing across many regions of the brain.

Conceptually, the further along this process you go, the more abstracted the signal probably becomes, so that it stands for a collection of events and ideas and thoughts rather than for excited photoreceptors or vibrating hair cells. But exactly how this parsing of the sensory content eventually turns into perception and conscious recognition is essentially unknown.


I'd say you guessed correctly. This does appear to be the hooded crow (Corvus cornix).

In German, it's called Nebelkrähe (meaning "mist crow").

 A Hooded Crow Corvus cornix in the garden of Belvedere (Vienna). [Source].

Description: ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.

C cornix is a Eurasian species that would be present in Austria:

Similar but incorrect species:

The only other similarly grey crow species I know are the grey crow (Corvus tristis), which is only present in New Guinea, and the western jackdaw Corvus monedula. The jackdaw is present in europe, but it can be ruled out because of its grey eyes and because of the grey feathers that creep superiorly from the birds nape onto its head (unlike your specimen).

Note: I exhaustively checked all commonly recognized species of the Corvus genus


There have been many proposals over the years as to why human consciousness has emerged and how, or even what it is.

Most of us will not be surprised to know that there is no consensus about an answer here.  Its hard to draw a trend from a single example.

Here is a little survey of the one's I've heard.

We are intelligent because we have opposable thumbs and can use tools, which evolved our brains.  This is an old one - maybe as old as Darwin's time.  I think its mostly ignored now because so many animals - including pandas and other non primates have opposable thumbs or use tools or both.  (monkeys and chimps use tools, and recently crows have also been observed to use tools.)
brain size.  We do have a large brain to body size ratio.  There are other animals with similar ratios and they don't have internets.
We are 'self-aware'.  That is to say we recognize ourselves as an individual.  It was proven that other primates can recognize themselves in mirrors (putting a red dot on their forehead. when they see their reflection, they touch their own forehead).  So that's not exclusive either.  its not a bad idea, but so far it doesn't seem to make the
'We ate something' I once read a discussion of how humans might have ingested psychotropic plants or fungi.  As you can see, this was 2010.  Its not the worst idea, but its hard to prove.  Lots of experiments on cats since the '60s have not produced cat's who care to tell us if they are intelligent.  Maybe they are just too smart in the first place.

These theories, from when I was a student are so discounted now, you can't find too much record of anymore since they were pre-internet and also they seem so unlikely now.

More modern theories have locked onto social configurations of human societies which drive intelligent adaptations.  This is stemming from observations that human evolution (the rate at which genetic variants are retained in the gene pool) are accelerating since humans have become social.

These new theories while standing on some amazing evidence are still feeling around in the dark - stuff about how social interactions have created a preference for intelligence-like traits. There is probably something to that - once intelligence gets a toehold it is a clear advantage.  But how did it show up only once and why us? I think that's the hard part that science has, for the moment, given a rest.


Safety of using industrial water for hand washing

The water from taps labelled "Industrial Water, Do Not Drink" comes from the same potable water line as domestic taps. The line should be split somewhere in the building, with the industrial line containing multiple backflow inhibitors to prevent cross contamination of potable or domestic water. Based on that fact, the water should be safe for hand washing, however, should be tested in the case of objective concern.


How do muscle cells synthesize glycogen?

Hexokinase catalyze glucose to form G-6-P is only the first step of the glycogen synthesis, and then the G-6-P will continue to processing a series reaction and finally become glycogen. So once the G-6-P forms, it will keep reacting, which will not inhibit the activity of hexokinase.


When there's a wound, the end result is a thrombus or thrombosis?

Here are a couple of distinctions,

1) The thrombus is the actual blood clot

2) Thrombosis is the condition of having a clot form in the blood vessel.

3) If the thrombus breaks away and becomes capable of traveling to some distant site, we refer to that as an embolus.

4) If the embolus lodges somewhere disrupting blood flow, we call that embolism, or in the case of a thrombus, thromboembolism.

So referring here, a protein called tissue factor is expressed on the outside of blood vessels, and when ruptured, is exposed to the blood stream that carries Factor VII. This initiates the coagulation response, and through the action of these factors you get platelets sticking to the endothelium, thrombin cleaving fibrinogen to fibrin that sticks to the platelets, and the fibrin/platelet plug forming over the wound is like a gel and RBCs become mired in it. So really, the thrombus is stuck to the endothelial wall.


If red blood cells have no mitochondria how are they able to metabolize glucose?

In humans (and all mammals), red blood cells lack mitochondria and therefore has no functional TCA cycle. They metabolize glucose mainly via glycolysis, forming lactate which is released from the cells; this yields 2 ATP for each glucose molecule, much less than complete oxidation (ca 30 ATP), but enough to support the red blood cells' energy needs.

There is some oxidation of glucose to CO2 in red blood cells though. This occurs mainly in the pentose phosphate pathway or "shunt", where 1 carbon of glucose is released as CO2, and the energy extracted is used to reduce NADP to NADPH, which functions as an antioxidant. The resulting 5-carbon sugars (pentoses) are then rearranged to a 3-carbon sugar (glyceraldehyde phosphate) which enter glycolysis again. Hence the term "shunt": 5/6 of the glucose carbon that enter actually comes back to glycolysis again.

By varying flux through the PPP, cells can balance the use of glucose for ATP (energy) or NADPH (antioxidant). Studies estimate that in human red blood cells, 10--30% of hexokinase flux is diverted through the PPP, and the remainder through upper glycolysis (see this and this article). This corresponds to 2--5% of glucose carbon released as CO2, and the remainder metabolized to lactate.

Note that the above apply to mammalian red blood cells. Red cells of other vertebrates, including birds and fish, retain both their nucleus and mitochondria, and their metabolism is different.


Could the protein dystrophin be artificially synthesised?

Great question.

Yes, it is almost certainly possible to artificially synthesize just about any protein. There can be difficulties with certain proteins, but these are more engineering problems rather than true limits to artificial synthesis.

The problem is getting the protein where it needs to be to be functional!

A great comparison is insulin. Insulin is an important regulatory protein that floats around in the bloodstream. That makes insulin therapy a relatively straightforward solution to a problem of not enough insulin: all you have to do is make or isolate some insulin and inject it into the bloodstream.

Dystrophin, however, is a structural protein that acts inside cells. Proteins are really big, and they can't be simply taken up by cells. There's no mechanism to get an arbitrary protein inside: any proteins that can be taken up by cells need to do so via some specialized mechanism.

If you wanted to replace a defective allele for dystrophin, then, the most feasible approach would be gene therapy: getting a patient's own cells to produce a functional copy of the protein. Efforts to entirely or partially replace dystrophin via gene therapy are a current area of research, but there are still many challenges to gene therapy approaches in general.

References

Harper, S. Q., Hauser, M. A., DelloRusso, C., Duan, D., Crawford, R. W., Phelps, S. F., ... & Chamberlain, J. S. (2002). Modular flexibility of dystrophin: implications for gene therapy of Duchenne muscular dystrophy. Nature medicine, 8(3), 253.

McGreevy, J. W., Hakim, C. H., McIntosh, M. A., & Duan, D. (2015). Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy. Disease models & mechanisms, 8(3), 195-213.

Pichavant, C., Aartsma-Rus, A., Clemens, P. R., Davies, K. E., Dickson, G., Takeda, S. I., ... & Tremblay, J. P. (2011). Current status of pharmaceutical and genetic therapeutic approaches to treat DMD. Molecular Therapy, 19(5), 830-840.

Verhaart, I. E., & Aartsma-Rus, A. (2012). Gene therapy for Duchenne muscular dystrophy. Current opinion in neurology, 25(5), 588-596.


Why do we absorb vitamins better from whole foods than from pills?

Why can't we just create a pill that does have all the necessary components?

I'm assuming you mean micronutrients (vitamins & minerals). A day's worth of macronutrients (energy and building-block providing chemicals - proteins, fats, sugars) are already very abundant and dense - a pill containing a day's worth would be the size of an egg.

Otherwise, we do. There are vitamin/mineral pills which have a very high absorbancy rate (usually those chelated or chemically bonded to various amino acids [words ending in -nate on the label]).

The big problem is that while the vitamins and minerals may satisfy your bare biochemical needs, that is all they do. They will not satisfy a hunger instinct (proteins and fats do that), and there are untold millions of compounds in the untold thousands of plants and products humans can pick up from the market. These compounds usually do not do much, but some are beneficial to our health.

So while multivitamins exist which provide you with a very efficient method of absorbing most of your vitamins and minerals, it's always recommended to get them directly from food since food will provide macronutrients (thus satisfying your hunger), the micronutrients you're curious about, and many potential beneficial compounds which are not necessary.

If you are still interested, Soylent Shakes are an attempt to provide all the micro- and macronutrients the body needs in an easier-to-consume form without all the messy cooking or multivitamin pills. Keep in mind the long-term effects of sticking to such a diet are more or less unknown, but it's as close as we can likely get to an "all-in-one" meal.


Should I consider [H+] as substrate in MCT transport equation?

To include or exclude the H+ basically depends on the scope of your model. The H+ can be used as external parameters if you assume that both sides of the membrane are well buffered and the pH will not change. If you want to simulate a condition during which the pH changes, like for example strong exercise in muscle or ischemia, then you would need separate H+ for each side of the membrane.


why dna polymerase 3 requires a primer for replication

You are confused among DNA replication, DNA transcrption, and RNA translation.

First, DNA replication happens during cell division, it create two exactly same daughter DNA.

Second, DNA transcription transcribes DNA sequence into RNA sequence, this RNA sequence may be used to synthesize protein, or RNA itself as signal, etc.

Third, RNA translation is the RNA sequence (codon) recognized by tRNA, and then synthesize protein sequence.

AUG is a codon in the RNA, the is recognized by tRNA, and then start translation. And please remember, DNA use A, G, C, T, but RNA use A, G, C, U, there is no U in DNA.

For DNA synthesis, why does it need primer? I have another answer for solving your question: https://biology.stackexchange.com/a/40954/17473


How does the Platypus grow before it eats?

The video is quite old and they knew a lot less about the species then.  They probably had to make some guesses.  Any modern reference I find doesn't mention any waiting period before nursing.

It seems to me that were this the case it would be very explicitly studied by now as it would be a real oddity for a mammal.  And we love platypus oddities.

Interestingly, the platypus doesn't actually have teets to be suckled on.  Instead the milk is expressed through their skin and into grooves on the belly that the newborns can drink from.


What is the difference between intracardiac and extracardiac reflexes in cardiac regulation?

Rate is controlled outside the heart by the Vagus Nerve having parasympathetic activity on the sinoatrial nerve.

Stroke volume (taking contractility and Starling's law as one) are factors from the cardiac tissue itself - "intracardiac".


Does sleep in humans re-structure based on the expected sleep time?

I haven't heard of studies like the one you're proposing, but you can test this hypothesis on yourself with this app.

Knowing you need to sleep less than your usual amount will probably affect the quantity and quality of your sleep, but not because of an "internal clock". Most likely, whatever you need to wake up early for will cause you some anxiety, which will affect both sleep duration and quality.


I agree with other commenters that we are not necessarily living in a time of small body masses.
Here is a paper on a body mass distribution. It's quite mathematical, but the first author (Aaron Clauset) is good.
For individual body masses, you can look at Kleiber's law - this says that body mass and metabolism are related by a power law.


Here is a list of programs that could work:

E-mouse Lab: http://e-mouselab.com, seems like the best fit for your requirements.
ZooEasy: http://standalone.zooeasy.com/en/pedigree-software/breeding-mice/breeders/index.html, Cheaper, good for breeding and pedigrees.
LabGuru: http://www.labguru.com, seems very professional and great for mice specimens as well.
MouseHouseApp: http://www.mousehouseapp.com, This is an iPhone and iPad app, so this would be good in the lab, but it depends on whether or not you have an iOS device.

Also, from what I found, Jackson Labs actually offers free mouse colony management programs. It does seem like it is cumbersome, but also a great program.

I will add more when I get time.


NAD+ is important in this step, since it is co-factor for the glyceraldehyde-3-phosphate dehydrogenase (G3PDH), which acts as a acceptor for the hydrogen atom from the C1 (see below).

If you look at the reaction, the aldehyde from the C1 is oxidized to a carboxylic acid which in a second step is turned into a phosphoester. To do so, a cysteine from the active center of the G3PDH attacks the G3P and forms a hemiacetal. This is oxidized into a thioester, the hydride which is split off in this step is transfered to the NAD+ bound by the G3PDH. In the second step the thioester formed between the enzyme and the G3P is attacked by a molecule of inorganic phosphate to form 1,3-BPG. This step is only made possible by splitting the very energy rich thioester bond. So for this reaction to happen you need both steps, as the formation of an energy rich phosphate ester bond would otherwise not happen. See here for more details.

To go directly from G3P to 3-PG you would need an enzyme which oxidizes the aldehyde group in the G3P. And then you need again an acceptor for the hydrogen which is split off here.


How can grass-fed livestock generate fat?

Short answer
Plants typically store energy in the form of starch. Animals, including livestock and humans for that matter, can digest starch, metabolize it into acetyl-CoA and turn it into fat.

Background
Plants contain sugars, formed by photosynthesis. Plants generally do not store energy in the form of fats, but in the form of starch, a glucose polysaccharide*. Animals digest this starch through hydrolysis catalyzed by the enzyme amylase back into glucose (Fig. 1). Cellulose is another polysaccharide. In grass-fed cattle, it is mainly cellulose that forms their source of energy. Cellulose cannot be digested by ruminants (cattle, goats, sheep) as they are unable to synthesise the enzymes needed to digest cellulose and other plant compounds. Cellulose can be hydrolyzed by cellulase enzymes in e.g. Ruminococcus species present in the ruminant tract in the guts of these animals. The cellulase enzyme endoglycosidase cleaves the disaccharide cellobiose from cellulose, and another type of enzyme, β-glucosidase hydrolyzes cellobiose into glucose monomers (sources: Microbe Wiki, University of Waikato).

Glucose is then degraded to pyruvate by aerobic glycolysis in the cytoplasm of the cell. Pyruvate is then transported into the mitochondria, where pyruvate dehydrogenase oxidatively decarboxylates pyruvate, forming acetyl-CoA and other products (Fig. 2).

Acetyl CoA can then serve as a substrate for citrate synthesis. Citrate, in turn, can be transported out of the mitochondria to the cytoplasm. There it can be split to generate cytoplasmic acetyl-CoA for fatty acid synthesis under the influence of anabolic factors like insulin in times of plenty (Fig. 3), referred to as lipogenesis.

Fig. 1. Starch is hydrolyzed by amylase. source: Biotek

Fig. 2. Acetyl-CoA formation. source: University of Utah

Fig. 3. Lipogenesis. source: Sharing in Health

*: Although plants usually store their energy reserves in the form of starch, there are important exceptions to this. Most notably certain seed pods, like peanuts and walnuts, contain substantial amounts of fat. Further, cell membranes and other components will add traces of fatty substances even in grassy plants. With credits to Marzipanherz.


Examples of humans intentionally introducing non-native species where everything went well?

The best examples are for when non-native pest species arrive, and then a search for their natural enemies in their native countries is undertaken to bring them back and control the invaders. This is called "biocontrol", and there are many examples of it going well, under carefully controlled conditions. https://biocontrol.entomology.cornell.edu/success.php
However, you are right to note that it is very difficult to predict.


Looking to understand the difference between (Fibroblast Growth Factor) FGF-2 and FGF-5

I'd suggest looking at this article on the FGF family. You will find a lot of information there about comparative analysis of the different proteins therein. For example (FGFR = FGF receptor, which binds FGF to transmit signals):

FGF–FGFR binding specificity is regulated both by primary sequence differences between the 18 FGFs and the 7 main FGFRs (FGFR1b, FGFR1c, FGFR2b, FGFR2c, FGFR3b, FGFR3c and FGFR4) and by temporal and spatial expression patterns of FGFs, FGFRs and HSGAGs. The alternative splice isoforms of FGFRs are generally tissue specific: the b isoform is usually expressed in epithelial tissue, whereas the c isoform is usually expressed in mesenchymal tissue23. Ligands are produced in either epithelial or mesenchymal tissue and generally activate receptors of the opposite tissue specificity: in normal physiology, a ligand produced in the epithelium will activate a mesenchymal receptor and vice versa. Several ligands, including FGF1 in particular, pose an exception to this general understanding by promiscuously binding to both b and c isoforms of certain FGFRs. Pathological states can result from a breakdown in binding specificity, as is common in cancers in which FGFs are overexpressed24. Structural studies of FGF1, FGF2, FGF8 and FGF10 with their cognate FGFRs show that sequence diversity at FGF N termini, variation in β1 strand length (FIG. 1b) and the alternatively spliced regions in D3 dictate their binding specificities (FIG. 2b, c).

So it's rather complex. Differences in FGF function are at least in part due to small biochemical differences that may give them differential affinity for different FGFRs, which then go on to transmit the FGF signals down the line. But at the same time the FGFs/FGFRs are expressed in different tissues, meaning that they may have relatively narrow spheres of influence.
If you look here you will see that different FGFs actually have relatively low similarity at the amino acid sequence level, and in some cases quite significant differences in gene structure (though they don't talk about 2 and 5 specifically). One notable difference there:

Most FGFs (FGFs 3-8, 10, 15, 17-19, and 21-23) have amino-terminal signal peptides and are readily secreted from cells. FGFs 9, 16 and 20 lack an obvious amino-terminal signal peptide but are nevertheless secreted [25,26,27]. FGF1 and FGF2 also lack signal sequences, but, unlike FGF9, are not secreted; they can, however, be found on the cell surface and within the extracellular matrix.

For some work on this topic specifically targeted towards FGF2 and FGF5, you can see this paper, which has this table about the location of FGF expression in follicle cells, showing that they are expressed in different places:

apologies to people with screen readers, I didn't have the motivation to copy it out into text. Here is a summary figure that they give:


The higher the temperature the faster E. coli will grow, with a maximum growth rate around 37 Celsius.

If you grow E coli at lower temperature, the ecoli will grow slower.

At 37°C you will see colonies overnight (16hr).

At 30°C you will see colonies in about 1 and a half days.

At 25°C you will see colonies in about 3-4 days.

You can do experiments at room temperature, but you will be waiting for days for what you will normally see after a 37°C overnight incubation.

As for satellite colonies.. yes ampicilin does break down with time and water. You can solve that problem by increasing the amount of Amp you are using from 25ug/ml to 100ug/ml. Or use 75ug/ml Carbenicilin. Or change your selection markers and use a more stable antibiotic like Chloroamphenicol.


To elaborate on A random zoologist's answer, the problem is that the human digestive system does not contain any cellulase enzymes. Cellulases are a class of enzymes that break down cellulose, the chief structural component of plants.  You might be able to obtain a small amount of nutrition from grass or other cellulose-rich materials, but as the plant cell walls are made of cellulose, most of the plant material will be indigestible.


Based on morphology alone, what type of claw does the Tyrannosaur have?

unfortunately they have fairly generic claws, they are not specialized enough to point to a use. They are curved enough to be used to grasp something but that is true for their ancestral line too so there is no sign of a specific directional selection.


What is the mechanism by which passive immunity works?

I commented on this question, but the OP's response prompted me to think again. Here is the graph from the document that the OP linked to:

Clearly what is confusing is that the parameter referred to as 'antibody level' rises quickly, but not as a step. In terms of the x-axis, vaguely labelled as weeks, it looks as if the level of antibody continues to rise over several days at least. The OP attempts to read into this an effect whereby the injected antibodies somehow stimulate the immune response in the recipient.

My knowledge of immunology isn't extensive enough to rule that out completely, but I don't think that is what this sketch graph is illustrating since the levels of these antibodies is shown as falling to zero due to destruction and excretion. This indicates that what is being graphed is just the injected antibodies.

In the absence of some real data for the time-course, my explanation for the rising phase illustrated is that this is showing levels of antibodies in the blood. However the prophylactic use of injected antibodies will often involve an intramuscular injection near the site of an injury. Here for example is a quotation from a recent review on the use of recombinant immunoglobulins (RIG) against rabies:

  Because vaccination needs time to induce a humoral response, application of RIG immediately after exposure is important to inhibit viral spread, even when accelerated vaccination schedules are applied. As much of the RIG dose as anatomically feasible should be injected into the area around the wound, and the remaining volume then given intramuscularly at a site distant from rabies vaccine inoculation. Isotope-labelled HRIG, injected around simulated bite wounds, diffused readily into surrounding tissue and about 25% was still detectable around the injection site 24 h later.

Thus the level of antibodies in the blood will continue to rise as they slowly enter the circulation from the site of injection.


Insect identification - pantry moth vs clothes moth

Although the images are very grainy and oddly lit, the second two images look a lot like a pantry moth. Specifically, it reminds me of a very common pantry pest:

Plodia interpunctella (Indian-meal moth).

 Source: Urban & Structural Entomology, Texas A&M University, USA

Range: [source]

The Indian-meal moth can be found on all inhabited continents. Although it is primarily tropical, it can live in a range of habitats and is a very common nuisance pest in food storage facilities and people's pantries worldwide.

Description: [source]

7-10 mm long (wing span ~ 1-1.5 cm)
Wing color:
-Posterior 1/2 of wing red/brown/bronze
-Anterior 1/3 of wing is white/light gray / ochre-yellow

Separated by dark band

Body color: reddish-brown

Pest Info: [source]

Adults live 5-7 days
Females lay 60-300 eggs
Eggs hatch in 2 - 14 days
Larvae do all of the destruction

Can even eat through plastic to get to food! [source]
Common Foods: Cornmeal, flour, dried fruits, nuts, seeds, health foods, pet foods.


How can I search for and find specific biology topics in scientific journals?

There are two possibilities for searching for scientific articles:

The first one is to use PubMed, a database which has been set up by the National Institute of Health in the US. It contains about 25 Million journal articles. All articles in this database are coming from peer-reviewed journals.

The other one is to use Google Scholar, which is better when you are unsure about search terms. It will give you more results, but you have to be careful here, since not all hits are from peer-reviewed journals, sometimes you get some quite questionable sources.


Why are restriction sites palindromic in nature?

Not all restriction sites are palindromes : https://en.wikipedia.org/wiki/List_of_restriction_enzyme_cutting_sites:_E%E2%80%93F#Whole_list_navigation

EcoRI: GAATTC (note that this is not 'palindromic' in the usual sense (e.g.'anna', GAATTC read backwards actually gives CTTAAG), but only if given the G-C A-T binding)

The double strand of DNA is composed of one strand in direction 5'-3' and another into the other direction (3'-5'). Restriction enzymes tend to be homodimers, thus would bind to both sides of the double strand, expecting the same recognition sequence. But as one strand runs into the other direction, the strands need to be palindromic to form a double strand.


Simplified molecular-input line-entry system

A 3D model of a (bio)moelcule represents a physical 3-dimensions. For an experimental structure, each atom has a 3D coordinate (x, y, z) and, if determined by crystallography, an additional isotropic or aniosotropic B-factor (that models atom fluctuations).

A '1D' SMILES is not a physical 1-dimensional representation, and can be converted to a graph (mathematics) representing the chemical structure. The specification of SMILES CAN retain information about structural isomers, stereoisomers (cis/trans; D/L), but not conformers/rotomers, which, unlike smaller chemical structures, IS restricted to certain favorable regions for larger biomolecules.

By "linkage" if you mean chemical linkage such as a disulfide bond, then SMILES can retain such information. By "interactions", if you mean hydrogen-bonding, salt-bridges and even hydrophobic interactions etc., then SMILES does not code in such information, but neither does a 3D model explicitly -- they are implied from the 3D coordinates for each atom.

Thus, converting from a 3D model to SMILES, you would lose

Unusual bond length and bond angle: they are necessarily specified from the 3D coordinates, but in SMILES (or the subsequent graph), they are taken as 'ideal'.
B-factor or temperature factor
Rotomers: e.g. Proteins have favored dihedral angles in both backbone and side chains, which is not specified in SMILES.
"Interactions": certain intramolecular interaction that is inevitable (e.g. salicylaldehyde) is implied in both SMILES and a 3D model. Most others can only be inferred in the 3D model.


'Pro-' is a general Latin preposition and English prefix with many meanings, but often in biology, as in this case, it means "before".  A proacinar cell is not yet an acinar cell (a cell of the acinus) but will be.  A related usage occurs with peptides such as proinsulin.
In Latin, "acinus" means a cluster of grapes.  You can find 'acini' in many places, notably exocrine glands, but in this case the pancreas is discussed.  With the help of Ms. Elbakyan, they tell quite a beautiful story, but the answer to this question is mostly in the first sentence of the abstract:  the stem cells (multipotent pancreatic progenitor cells) can become pro-acinar cells (which become secretory tissue of the acini, producing the pancreatic digestive enzymes), or else are reserved as bipotent progenitors that create the ducts and the islets of Langerhans.


Which point mutations in proteins are OK, and which cause significant change?

There are twenty standard amino acids, and some of them are structurally/functionally similar to each other, such as aspartate and glutamate, or asparagine and glutamine, or glycine and alanine. In general, mutations that cause these amino acid switches don't change the function of the protein, but that's just a general rule - it also depends on where these amino acids are in the protein structure. These are called conservative mutations.


Formula for number of divisions required to form x number of cells (Mitosis and Meiosis)

For a male, one primary spermatocyte produces two secondary spermatocytes through meiosis I, which in turn produce two spermatids each through meiosis II. So one primary spermatocyte produces four spermatids. That means that $x$ spermatids are produced after $x/4$ meiotic divisions consisting of once meiosis I and twice meiosis II.

However, we don't count the first cell here because a primary spermatocyte is fundamentally different form a spermatid. So in meiosis, the first cell isn't counted, and four new cells are produced.

In mitosis, we do count the first cell. Note that there are two cells produced form one, so there is only one new cell. Hence we get the formula $x-1$.


Are mosquitoes repelled by high frequency sound?

After seeing your question, I decided to do a bit of research on the topic.

First Source: EurekAlert!

http://www.eurekalert.org/pub_releases/2007-04/jws-mrt041607.php

  "Mosquito repellents that emit high-pitched sounds don't prevent
  bites"

Some key-points from the webpage:

  A Cochrane Systematic Review of the use of electronic mosquito repellents (EMRs) failed to find any evidence that they work.

  To test these claims a team of Cochrane Researchers conducted a systematic review looking for trials conducted with EMRs. They located ten field trials that had been carried out in various parts of the world. None of these trials showed any evidence that EMRs work.

  All ten studies found that there was no difference in the number of mosquitoes found on the bare body parts of the human participants with or without an EMR

Second Source: Wikipedia

http://en.wikipedia.org/wiki/Insect_repellent

  These electronic devices have been shown to have no effect as a mosquito repellent by studies done by the EPA and many universities.

Third Source: CBCnews

http://www.cbc.ca/news/story/2007/04/18/mosquito-repellent.html
Key points from the article:

  "There was no evidence in the field studies to support any repelling effects of EMRs, hence >no evidence to support their promotion or use"

  -Ahmadali Enayati, researcher

This is a major point as well:

  The study also said that in 12 of the 15 experiments, the landing rates of mosquitoes on subjects was in fact higher than in control groups.

The article also points out that female mosquitoes can't hear very well- Which supports the idea that high-frequency repellents are ineffective; Much more than you probably think. Why? Well, it's pretty simple:

Female Mosquitoes are the only Gender that Bite.

Overall, when you consider the countless studies and research put in to the effects of high-frequency sounds on mosquitoes, it's pretty obvious that:
No.High Frequency Sounds do NOT repel mosquitoes


How many traits can a multivariate breeders equation handle?

Noting that the right hand side can also be written $\mathbf{G}\mathbf{P}^{-1}\mathbf{s}$, we see that the only theoretical limitation of the multivariate breeders equation is the invertibility of the matrix $\mathbf{P}$. This happens when the measures of two traits are the same for all individuals, making two columns of the matrix the same I.e. It becomes singular.

This theoretical concern can become a practical concern quite quickly when multiple traits are measured. The solution is to effectively consider two traits as one.

The 'power' of the equation, by which I assume you mean something like 'accuracy of prediction', actually improves with the number of traits measured. Indeed, a big concern with measuring only a few traits is that the response to selection on those traits is actually 'caused' by selection on some other correlated but unmeasured trait.


Correlation between morphology of neurons and neurotransmitters

Yes, at least for the neurotransmitters that a given cell releases.

As far as the neurotransmitters a cell responds to, you are really better off thinking in terms of receptor expression. Most neurons will express receptors for many different neurotransmitters. It's far too broad to go into them all in an answer here.

As far as the transmitters that cells release, morphological types of neurons are very often associated with release of particular neurotransmitters. In the cortex, for example, pyramidal cells principally release glutamate while there are potentially dozens of morphological types (again, depending on how you define them) that release GABA; in the cerebellum, Purkinje neurons release GABA whereas granule cells release glutamate.

However, be careful: some terms like "granule cell" don't really refer to a special morphological type. They are really just describing "small cells in close proximity": these can be completely different types in different brain regions. It really makes no sense to ask these types of questions for the brain as a whole, you have to study individual brain regions, each of which is organized quite differently from the others.


Thanks for the pictures! That's the European Garden Spider (Araneus diadematus)

They are most commonly seen from June to October, but they reach a peak around right now.  This species is all over UK, and is widespread in gardens, woodland, and meadows.  Here is another picture for reference:

Fun Fact: After laying their eggs in late autumn, the females die and only the eggs make it through winter.  Upon hatching, they look quite different from the adults:


It all depends upon how $m$ is defined and that might vary from a paper to another. The rest, I find, is very much just a question of logic.

In the infinite island model (the model from which Wright's approximation was computed), the total number of migrants is of course, infinite (if $m≠0$). With $d$ demes (or islands), the total number of migrants is $dNm$ if $m$ is defined as the migration rate between any two patches.

Under a linear stepping stone model with only 1 step (because there exist more complex stepping stones models), with $d$ demes (or stones), the total number of migrants is $dNm$ (minus small approximation for the extremities of the world) if $m$ is defined as the migration rate from one deme to an adjacent deme. Half of $dNm$ are migrating toward the left and half of them are migrating toward the right.

  I thought that may be the case. Was SimBit designed assuming NmNm or Nm2Nm2?

In SimBit, you can use multiple modes to enter migration information. You can specify the migration rate from any patch to any other patch (mode A).

You can use island where you specify the probability of not migrating (which might arguably be a little unintuitive). If the probability of not migrating is $x$, and there are $d$ demes, then the number of migrants from one deme which patch size is $N$ to a single other deme of interest is $\frac{N(1-x)}{d}$. The number of migrants from this deme to any other deme is $N(1-x)$ and the total number of migrants in the whole (meta)population is $dN(1-x)$.

The mode LSS (Linear Stepping Stone), is a little complex as it is very flexible. You can specify the migration rate from a focal patch to any other patch considering they are place in a linear order. SimBit LSS indeed allows for stepping several stones apart if you want. If for example you input LSS 3 0.1 0.8 0.1 2 it means that the probably to migrate from any patch to a given adjacent patch is 0.1. The probability of migrating is 0.2 and the probability of not migrating is 0.8. With such model, the number of individuals exiting a given patch is $0.2N$ ($0.1N$ on each side) for a patch of size $N$. Assuming all patches have the same size, the total number of migrants for a (meta)population of $d$ patches is $0.2dN$.

Of course, if you allow for patch size to vary with carrying capacity or for migration rate to be affected by population mean fitness, then this expected number of migrants will vary among generations.


Is there a biological or technical reason for a 40 Ct cutoff in nucleic acid detection assay?

This is done because at some point you start amplifying nonsense and not get a meaningful signal. If (and this is most often not the case) you have the ideal doubling of you DNA template in each cycle, you can calculate how little DNA you start with to detect it only around cycle 40 - or the other way round: What you will amplify and see as a "signal" by then.
If you have templates which always really come this late, I would use more DNA (and probably more RNA to start the rtPCR) until this comes at least 2-3 cycles earlier and then do serial dilutions of your template to see if this signal is real or not. If so, you should see a relation between Ct and dilution.
For doing this you need a negative control which stays really negative until your sample signal shows up - which is tricky on its own because at some point you will see some kind of primer self-amplification. If this occurs in the same range as your sample, your signal cannot be used. If no other primers can be used for technical reasons, sometimes nested PCR has to be considered.
And last but not least all your reagents degrade over time by cycling them 40 times through the PCR program (also the polymerase), which affects the efficiency of the reaction.


Why do the feet of the Gecko Lizard not stick to Teflon surfaces?

Gecko feet have been the focus of a lot of research over the past 10 years.

Their ability to walk up vertical or even hanging from ceilings is attributed to tiny branching hairs growing from the pads of their feet.  The hairs branch down to the size of 100s of nanometers and its believed that this gives them large surfaces at the molecular scale, giving them a strong van der Waals adhesion force.

Teflon, being hydrocarbon chains covered with 'hard' electronegative flourine atoms doesn't provide the same attraction to the hairs, as van der Waals forces rely on mutual polarizability of atoms in close contact. That is to say, electronically fluffy atoms can stick together more readily.


Why draw blood from veins rather than arteries?

Veins have several advantages over arteries. From a purely practical standpoint, veins are easier to access due to their superficial location compared to the arteries which are located deeper under the skin. They have thinner walls (much less smooth muscle surrounding them) than arteries, and have less innervation, so piercing them with a needle requires less force and doesn't hurt as much. Venous pressure is also lower than arterial pressure, so there is less of a chance of blood seeping back out through the puncture point before it heals. Because of their thinner walls, veins tend to be larger than the corresponding artery in the area, so they hold more blood, making collection easier and faster.

Finally, it is somewhat safer if a small embolism (bubble in the blood) is introduced into a vein rather than an artery. Blood flow in veins always goes to larger and larger vessels, so there is very little chance of a vessel being blocked by the embolism before the bubble reaches the heart/lungs and is hopefully destroyed. Blood flow in an artery, on the other hand, always moves into smaller and smaller vessels, eventually ending in capilllaries, and there is a chance that a bubble introduced by a blood draw (generally rare) or more commonly an intravenous line (IV) could block a small blood vessel, potentially leading to hypoxia in the affected tissues.


Distribution of fitness in wild populations

Long for a comment but consider this to be an extended comment and not an exact answer:

At least for Poisson I can say that the random variable should fit the three Poisson postulates. Poisson RV generally describe discrete events in continuous intervals. A fitness function doesn't seem to be such a type of RV; it is a property of a population rather than an event.

I would also not expect it to be exponentially distributed which would mean that probability is highest for the most fit (or most unfit) individual i.e the more fit are more frequent. I assume that it cannot be decided who is the most fit until selection happens. This may still be the case just after a selection event but not otherwise.

It seems that this function should be Gaussian: assuming that there is little variability between individuals and what exists is because of independent events of mutation, these should converge to Gaussian as per the central limit theorem.

But generally the term that best describes this RV is a performance function. Fitness would always be a conditional RV.

For e.g. I would very roughly define fitness like this:

$f(X) = P(m(X)\ |\ p(X),S)$

where $f(x)$ is the fitness of $X$, $m(X)$ is the survival probability of $X$, $p(X)$ is performance in different tasks and $S$ is selection event.


What is the name of the baboons that live in Saudi Arabia

These look like Hamadryas Baboons (Papio hamadryas). They also fit the geographical location.


What stops myosin during muscle relaxation?

Relaxation of vertebrate skeletal muscle is thought to occur in the absence of  ${Ca}^{2+}$ as a result of tropomyosin physically blocking the binding of myosin to actin. This steric blocking model of muscle relaxation predicts that myosin subfragment 1 (S-1) will not bind to actin under conditions where the acto-S-1 ATPase rate is inhibited.[1]
However, in a paper that questions this model, it is concluded that in the absence of ${Ca}^{2+}$, troponin-tropomyosin inhibits the ATPase activity by inhibiting a kinetic step in the cycle of ATP hydrolysis, perhaps $P_i$ release.[2]

That is the simple answer, but I think a little elaboration on the above paragraphs might help add some substance:[2]

Vertebrate skeletal muscle contraction is the result of a cyclic interaction of thick myosin filaments with the thin filaments, composed primarily of actin, troponin, and tropomyosin, causing these two sets of filaments to slide past each other. This cycling is driven by the hydrolysis of ATP by myosin in a reaction which is activated by actin.

When the sarcoplasmic reticulum lowers the free ${Ca}^{2+}$ concentration from $10^{-5}$ to $<10^{−7} m$, muscle contraction ceases and the associated actin-activated myosin ATPase activity is inhibited. The proteins troponin and tropomyosin are responsible for this effect of ${Ca}^{2+}$ on the interaction between myosin and actin.

At levels of ${Ca}^{2+}$ low enough to cause relaxation, tropomyosin is positioned away from the central groove of the F-actin filament where it appears that it might interfere with the binding of the myosin cross-bridge. This structural work formed the basis of the steric blocking hypothesis which suggests that relaxation occurs when tropomyosin, in the “relaxed” position, physically blocks the binding of the myosin cross-bridge to actin.

Three-dimensional reconstructions from electron micro-graphs have suggested that the myosin cross-bridge and the tropomyosin molecule may be in close contact with each other on the actin filament, a requirement for a steric blocking type model.

The steric blocking model predicts that in the absence of ${Ca}^{2+}$ the degree of association of S-11 should be much weaker with regulated actin than with unregulated actin. In fact, in the absence of ${Ca}^{2+}$, the binding of S-1·ADP to regulated actin is strongly inhibited in a cooperative manner.

At low levels of saturation of the actin filament with S-1·ADP, the binding of S-1·ADP to the regulated actin filament is about $10^3$ times  weaker than at high levels of saturation.

However, the fact that S-1·ADP binds weakly to regulated actin does not prove the steric blocking model since, in relaxed muscle, the cross-bridges normally exist with bound ATP (or ADP · Pi) and not bound ADP. Therefore, the steric blocking model predicts that troponin-tropomyosin should inhibit the binding of S-1·ADP·Pi as well as S-1·ADP to regulated actin in the absence of ${Ca}^{2+}$.

Using stopped flow turbidity measurements, we have previously measured the effect of ${Ca}^{2+}$ on the association of S-1 · ATP and S-1 · ADP · Pi with regulated actin. Surprisingly, in the absence of ${Ca}^{2+}$, the binding constant of S-1 · ATP or S-1 · ADP · Pi to regulated actin was only decreased to 56% of the value in the presence of ${Ca}^{2+}$ although the rate of ATP hydolysis under the same conditions was decreased to 6% of the rate with ${Ca}^{2+}$ present. These data suggest, in disagreement with the steric blocking model, that inhibition of the rate of ATP hydrolysis, in the absence of ${Ca}^{2+}$, is not the result of inhibition of the binding of S-1 to regulated actin.

1- https://pubmed.ncbi.nlm.nih.gov/27065174/
2- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1266292/#FN2


Microtiter Dish Biofilm Formation Assay- Pseudomonas and Crystal Violet

Using the Gram stain for differentiation between G- and + requires the addition of alcohol, the critical step in Gram staining. Actually the first step, simple staining, goes the same for all types of bacteria. All bacteria gain the stain, but addition of alcohol makes the lipid in bacteria like Pseudomonas to lose it.


What was the evolutionary advantage of having seeds so large that they could only be dispersed by megafauna?

There are a few advantages to megafauna:

they travel large distances and are hence are likely to be able to
spread your seeds widely.
They also eat large amounts, so can carry a lot of seeds and
distribute those around widely.
Large fruit capable of being eaten only by the largest fauna might have the seeds survive by not being eaten and destroyed by smaller animals
Large animals have large guts, so the more of the seeds might survive undamaged

Another significant factor is that a megafauna animal also produces mega-feces, literally a large pile of nice warm fertilizer for the new plants to grow in.


Does turbidometeric method count cell number or cell mass?

Your text says that scattering is proportional to cell number, which is correct. It is not inversely proportional, as you stated.


why does blood when oxidized over time become bluish green?

Apparently there is a rare condition, sulfhemoglobinemia in which sulphide ions or H2S combine with the haem group in haemoglobin, causing a greenish colour. This can be related to certain drugs being present in the blood.

See here for an example in which surgeons discovered dark green blood in their patient.


This sort of method is indeed quite useful and frequently used in synthetic biology: I've used a similar approach before to generate 5' insulators for promoters.
Calculating the exact theoretical likelihood of what you want, so far as I understand, is a complex combinatoric equation that I wasn't able to get a nice closed form on with a few minutes of work. For your purposes, however, I expect that a reasonable estimate will do as well, and that can be made much more easily by modeling the population of each combination as an independent series of biased coin flips, i.e., a binomial distribution.
Consider a situation with $n$ potential combinations that you attempt to cover with $k$ random mutants. If we focus on a particular combination, we can see that each random mutant has a $\frac{1}{n}$ chance of hitting that combination. The whole set of mutants is thus a series of $k$ biased coin flips, with a probability $p_0 = (1-\frac{1}{n})^k$ of getting no mutants that hit that combination. This means that the probability $p_c$ that the combination is covered is $p_c = 1-p_0$, expanding to: $$p_c = 1-(1-\frac{1}{n})^k$$
With a large number of potential combinations and a large number of mutants, we can make a reasonable approximate by treating each combination as independent. In this case, the probability that all combinations are covered is the product of the probabilities that each combination is covered independently. They aren't actually independent: each combination that gets covered slightly detracts from the ability of other combinations to be covered. An estimate using an independence assumption is thus an overestimate of the actual likelihood, and the higher that $k$ is the closer the estimate should be to the exact probability. In short:
$$p_{all} < (1-(1-\frac{1}{n})^k)^n$$
This smells like the sort of equation there ought to be a nice identity for, but I don't know the identity, so I'll just give a couple of examples of calculating with it:

NNK = 32 combinations, 50 mutants (n=32, k=50): $p_{all}$ < 0.07%
NNK = 32 combinations, 100 mutants (n=32, k=100): $p_{all}$ < 25.5%
NNK = 32 combinations, 200 mutants (n=32, k=200): $p_{all}$ < 94.6%

As you can see there's a sharp transition as the coverage count increases.
Important caveat: the theoretical value may not give you what you want. In the paper I linked above, we used two degenerate primers with 18 N bases to inject 36bp of random material, which means we had $4.7x10^{21}$ possible combinations and should never have seen a repeat --- except that sequencing showed that we did indeed get several repeats out of only a few hundred colonies. Thus, biases in the biology may lead your statistics to be skewed from what the theory suggests.


This is a good question. This type of behavior -- pecking at a branch, wiping the side of the beak on a branch, pulling off twigs and dropping them, or knocking off pieces of bark -- is quite common among many corvid species, particularly when they are interrupted by something or someone that they might consider a threat. This includes not only potential predators but also potentially hostile conspecifics.

It is typically considered to be a form of displacement behavior. The concept of displacement behavior, from classical ethology, posits that when an animal experiences two conflicting drives to do two different things, it doesn't know which to do and does a third thing instead to dissipate the drive or anxiety. For branch-pecking in crows, see E.g Kilham and Waltermire 1990 Ch. 12.

Referece: Kilham, L., & Waltermire, J. (1990). The American crow and the common raven. Texas A&M University Press.


How long does it take unused antibodies to clear the system?

I agree that this question may be broader than a simple half-life question in theory, however, I think that it is still basically a half-life question. For instance, does the presence of the virus (using the flu example) contribute to opsionization and clearance? Possibly, but this would be variable and difficult to generalize about.

The question has been asked in a number of ways (for endogenous / exogenous antibody). For simplicity, Mankarious et al examined transferred antibody in IVIG therapy and found, "For total IgG, the half-life found was 25.8 days; for IgG1 it was 29.7 days; for IgG2 it was 26.9 days; and for IgG3 it was 15.7 days." - an answer in line with that proposed by canadianer, above.


Your answer to your titular question, How was the origin of CTVT parasitic cancer determined? is that cytogenic studies were done on the tumors. It arose in dogs and was logically assumed to be of dog origin, and was first characterized in 1876. The tumor cells were/are characterized by a rearranged karyotype, which is similar in tumors from in different parts of the world. (1969) Thus it was postulated that that the transmissible agent causing the CTVT is the tumor cell itself and that all worldwide CTVT have a clonal origin. (1985)

Your later question states:

  What percentage / degree of genetic similarity is needed to identify something as belonging to a specific species?

When a tumor arises in an animal (say a dog), it is automatically assumed that the cancerous cells, regardless of their ploidy, arose from that animal (in this case, a dog), not a different animal. Not all animals have had their entire genome sequenced, so this question as stated isn't answerable (although the genome of the dog has been completely sequenced). And certainly, not all tumor cell lines have been completely sequenced. The assumption of origin is made by looking at certain genes (e.g. histocompatibility genes) and others known to be species specific.

Since there are relatively few transmissible cancers (that is, where the cancer itself acts as the infectious agent), this is still a safe assumption. While I'm fairly confident more transmissible cancers will be found, I'm also fairly confident that they will be species specific, because in order to escape detection, they will need to be recognized immunologically as "self", as they must survive in the host at least long enough to be transmitted.

This is the case with canine transmissible venereal tumor (CTVT). It is also the case with the contagious tumor Tasmanian Devil face tumor disease (DFTD). Just as with the canine infectious cancer, DFTD cells in different individuals have identical, complex chromosomal rearrangements and are genetically identical to each other but different to the host devil.

  Spread of such an infectious cell line between unrelated individuals should be prevented by major histocompatibility complex (MHC) Class I antigens on the surface of the tumour cell, as Class I molecules play a key role in self/non-self-recognition. The recent emergence of the tumor (transmitted by biting) in the endangered marsupial Tasmanian devil (Sarcophilus harrisii) is an unfortunate exception. In the Tasmanian devil, the tumor is very aggressive and kills the host.

In the case of canine transmissible venereal tumor (CTVT), it was shown about five decades ago to be the same dog tumor being spread from dog to dog. The earliest studies were based on histological studies and karyotyping. Paraffin-embedded tumor samples still exist. More recently, with genetic analysis, it is possible to perform much more sophisticated testing on the tumor DNA.

  The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype.

Your quote

  likely originated at least 250 years ago from a wolf or an "old" Asian dog breed such as a husky or Shih Tzu...

Has been disputed. Estimates vary widely, from 11,000 years to 250 years.

Canine TVT: Evolution of Somatic Tumour Cell as Transmissible Parasites
MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer
Clonal Origin and Evolution of a Transmissible Cancer


If you're looking at evolutionary timescales, then the only available source of information is the target organism's genome sequence. At least some of the methods of horizontal gene transfer you mention leave a distinctive signature in the genome. For example, retrovirus particles that have become incorporated into the human genome are easily identified by their local DNA sequence.

So in terms of an experiment, you would sequence your specific gene of interest as well as the surrounding local sequence (say, 10,000 base pairs downstream and upstream of your gene). In at least some cases you would be able to say for sure "this gene arose from retroviral incorporation", whereas in others it would be more ambiguous.

References:
Belshaw, R. et al. Long-term reinfection of the human genome by endogenous retroviruses. PNAS (2004)


use of antibiotics in selection of good plasmids

Short answer: selection protocols are designed to work
When choosing a selectable marker for a plasmid, one chooses a gene that is known to be absent in the host organism of interest. For example, standard lab strains of E. coli are free from extragenomic plasmids and are susceptible to the antibiotic ampicillin. As such, plasmids that confer resistance to ampicillin are commonly used to maintain plasmids in E. coli lab strains.
Other things worth noting:
1. Antibiotic resistance genes are not universal.
That is, a bacterial strain that has a gene imparting resistance to one antibiotic may still be susceptible to many other antibiotics.
2. Not all plasmids carry antibiotic resistance genes.
Many naturally occurring plasmids are selected for in the wild because they carry genes that enable the bacteria to perform new metabolic functions, or impart virulence genes that enable bacteria infect a host organism: (https://en.wikipedia.org/wiki/Plasmid#Properties_and_characteristics).
This is also true of recombinant plasmids. Many commonly used yeast plasmids are selected for by enabling the host strain to produce a necessary nutrient that is absent in the growth medium.


Assays for detecting RNA binding with protein

I would reccomend an electrophoretic mobility shift assay (EMSA), one procedure for which can be found here.


Photosynthetic Pigments vs. Chloroplasts

Photosynthetic pigments are the chemicals which take part in photosynthesis, in particular they are they ones which absorb photons and fluoresce (emit photons of a different wavelength) or emit electrons. Pigments are molecules, and chlorophyll is a key example. These pigments are required for photosynthesis to take place, as they generate the electrons which create the electrochemical gradients which power photosynthesis, thus all photosynthetic organisms will have photosynthetic pigments of some kind.

Chloroplasts are membrane-bound organelles in plant cells, made up of many hundreds of thousands of molecules including pigments. Plant photosynthesis takes place on their internal membrane, the thylakoid. Specifically, the thylakoid membrane of chloroplasts is the membrane across which the aforementioned electrochemical gradients are created in plants.

Chloroplasts originated from a free-living bacterium, probably a cyanobacterium, entering a eukaryotic cell. So prokaryotes don't have them because the chloroplast endosymbiosis event was one way in which plants diverged from their non-plant ancestors. So you can think of a cyanobacterium as a free-living chloroplast - they have their own internal membranes similar to the thylakoid across which electrochemical gradients are created for photosynthesis. Conversely, you can think of a chloroplast as a small cyanobacterium living symbiotically inside a plant cell.


Is it possible for a person to become "reinfected" with the same strain of a virus?

The nature of infectious agents is that they transmit between organisms. This means that they have reservoirs outside a single host, and hence of course encountering the exact same strain twice is possible if this strain leaves the body and at a later stage is carried back to it. This could typically happen for example with influenza or common cold viruses, spreading from one child to other children at school and later being carried back to the original child through them.

The reason why the child will not develop another illness when being exposed to the same virus again is the adaptive immune response: After the first infection, immune cells specific to a pathogen will proliferate and differentiate both into effector cells to destroy the pathogen, and into memory cells. These can mount a much stronger immune response much faster when they come in contact with the same (or a structurally very similar) pathogen, meaning that a secondary exposure usually does not result in a proper infection and illness. Of course, this mechanism doesn't work properly for anyone with a compromised immune system.

In most cases where a viral disease develops repeatedly, this is due to evasion mechanisms. For example in some viruses, those antigens which tend to be targeted by immune systems have high mutation rates. In this case the "same" virus is actually a mutated strain which causes the same illness, but "looks" different to the immune system, and so the memory cells don't respond. Again, influenza is a great example. The reason why we get flu again winter after winter, is because this virus tends to mutate over the year with relatively low infection prevalence. Then during the winter, when the conditions are favourable for flu infections, typically only a small number of strains cause epidemics - because we were maybe immune to last year's influenza, but this year's has mutated antigens which our immune systems do not recognise yet.