Does biotin affect downstream experiments, such as RT-qPCR?

Having looked into this question, I came across this paper, where they mixed biotin labelled EGFR-mutant-specific oligonucleotide and isolated the target using streptavidin beads followed by real-time TaqMan PCR allowing a 40 fold increase in detection sensitivity of the mutant allele, suggesting that biotin does not effect nucleotides in PCR based experiments.

The life technologies webpage claims that Streptavidin-Coupled Dynabeads M-270 can be used in a PCR reaction as stated below although certain streptavidin-coupled beads can have an effect on the PCR reaction. Hence I do not think biotin itself would be a problem for an amplification reaction.

  beads can be used directly in PCR, as they do not inhibit enzymatic reaction. Slight PCR-inhibition has been seen when 75–100 µg of Dynabeads® M-280 Streptavidin was used in 50 µL PCR reaction, and a concentration over 100 µg per 50 µL reaction seems to inhibit PCR completely. Dynabeads® M-270 Streptavidin do not show any inhibitory effect on PCR at these concentrations.

In fact you can buy kits such as this where you can generate/incorporate biotin into your RNA of interest for any purpose. The use of biotin and its incorporation into nucleotides seems prevalent in the literature and there are even kits for this purpose hence you should be on the safe side with your biotin labelled RNA experiments. I think the biggest challenge in RNA work is to keep it from degradation, which as far as I know is achieved through maintenance at -80 oC.


How can I make sure my UV-purificator kills bacteria?

Not having the equipment needed to actually count bacteria, you can use things you know bacteria does to find out how much they were affected.

My approach would be thus:

Select a model bacteria. There are a few candidates, but probably the most readily available is lactobacilli, which can be found in yogurt and (loosely translating terms of art) is a Gram-stainable fermentor-sometimes-breather.
Infect the water with a known quantity of bacteria and a food source (lactobacilli eat lactose - ie from milk) and equally divide it into a control and experimental group...
You'll need to find an alternative way to estimate the bacterial content in the volume of water used compared to a control colony. Since lactobacilli produce lactic acid, you could use the pH value of the water (either with an indicator or a meter) to detect bacterial metabolism, compare that to the control's pH value.
Record the UV exposure time from the experimental group, and isolate the control group from any potential UV light source, such as the sun.

Even if you find that, for example, your particular strain of lactobacilli is not sensitive to your UV light source, that's a perfectly scientific result! How did you obtain it? The source likely knows what kind of bacteria it is. Perhaps the UV light merely interferes with bacterial metabolism, and doesn't kill it. Unanswered questions are wonderful, you may have provided a place for further research to take place. You could then use the two groups to infect a food source (ie milk) and compare post-exposure growth, depending on how much time is available.


Has anyone yet figured out how sensory signals for eyes and ears are encoded by our organ into electrical signals?

I think the encoding is quite well understood, and in fact there are artifical cochleas available for deaf people: https://en.wikipedia.org/wiki/Cochlear_implant
For retina replacements, I think the hurdle is establishing the connections from any device to the nerve.  There are roughly 120 million rods and 6 million cones in the human eye. (Per Wikipedia: https://en.wikipedia.org/wiki/Photoreceptor_cell )  These connect to about 1.2 million optic nerves, so making the proper connections would seem to be a non-trivial matter.


Is the Basic Reproduction Number in epidemiology dependent on population size?

From what I understand (as an ecologist/population modeller), $R_0$ in epidemiology is not dependent on host population size per se, at least not in its basic form. It is also not dependent on the number of susceptible individuals, since it is defined as the number of secondary infections in a fully susceptible population, see e.g. this section in Farrington et al (2001):

  The basic reproduction number of an infectious agent in a given population is the average number of secondary infections which one typical infected individual would generate if the population were completely susceptible.

This is also consistent with the Wikipedia description ("...in an otherwise uninfected population"). $R_0$ is however dependent on the environment (dispersal routes, host-host interactions etc), which also why it is used to evaluate and compare the effect of control measures. Host-host interactions is also dependent on population density, so $R_0$ is indirectly influenced by host population density, and this is partially why estimated $R_0$ values for the same disease will differ between countries and populations.

Fundamentally and conceptually, $R_0$ is the same thing as the Net reproductive rate (often also labelled $R_0$) in demography and population modelling, and it was originally borrowed from demography to epidemiology. As such, the net reproductive rate is often used in for instance pest control to evaluate the potential impact of pest species on agricultural crops, in direct analog to the basic reproduction number in epidemiology (see Emiljanowicz et al, 2014 for a randomly picked, recent example). Most commonly, $R_0$ (both in population dynamics and epidemiology) is calculated from static demographic rates, but nothing prevents you from considering stochastic effects, density dependence or e.g. ways that demographic rates are functions of host density or population size. This could lead to formulations where $R_0$ is an explicit function of host population  density, but that is not the standard use of $R_0$.

To me, it seems like you are asking for the effective reproduction number ($R(t)$), which can be defined by:

  ...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population."

This section is from a WHO paper on meases (Chiew et al, 2013). So basically, $R(t)$ is the average number of secondary cases per primary case at time $t$ (including the effects of immunity and/or control measures). As you can see, $R(t)$ is a function of time, and it can e.g. be used to describe the temporal dynamics of SIR-type models.


Needle-like crystals observed in wild-grape wine under microscope. Potentially harmful?

you are correct that these grapes have raphides. After doing some research, I found out that the grape raphides are twinned crystals. Raphides can cause much irritation for many herbivores (therefore, it is a protection mechanism) but less so for humans. In grapes, however, the irritation is much less than other raphide-containing species. This probably has to do eith the fact that it has a twinned structure (this is what I think, but I haven't found any research on this).

As a side note, what you have done is known as a whole mount, in which is entire organism specimen is placed on the slide, usually after crushing. It is a geeat way to examine the contents of the cell vacuole, which is where this raphides are commonly found.

References:

http://www.ncbi.nlm.nih.gov/pubmed/10648203
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091341


Can protein structure be determined by X-Ray Diffraction in a single image?

You cannot solve a structure with a single frame, even with perfect diffraction.

The reason you need images over a large swath of angles is because the diffraction pattern is also in three dimensions, in the so-called "reciprocal space".  At minimum, a 180° rotation of the crystal is needed to sweep the entire reciprocal space sphere with the plane of detection, though symmetry in the crystal structure can reduce this further (some of my proteins only required 90°, I think hexagonal unit cells with 6-fold symmetry can live with 30°).  Because crystals are real things (read: non-ideal, doubly so for protein crystals), the sweep is extended to gain some redundancy.


A mutation question from the Indian National Biology Olympiad

Now, one of them claimed that if the volume were to remain constant,
then mass is directly proportional to density hence the insertion
mutation should cause increase in mass corresponding to a similar
increase in density.

I don't think that's quite how it works.  You don't worry about the volumes being used.  In those experiments (I don't know that anyone does them anymore)  the DNA is in a solution of really salty water.  Larger molecules get pushed more to the bottom of the tube, so the mutant DNA is larger, since it was close to the bottom.
https://embryo.asu.edu/pages/equilibrium-density-gradient-centrifugation-cesium-chloride-solutions-developed-matthew#:~:text=Density%20gradient%20centrifugation%20enables%20scientists,molecules%20based%20on%20density%20alone.

Thus, centrifugal force pushes the larger components of a mixture
farther from the rotor and closer to the bottom of the tube.

Larger DNA means an insertion.  Point mutations are not detectable with this method.


Why are clementines easier to peel than oranges?

I think it all comes down to the thickness of the skin and how it's attached to the fruit itself.  For me, it depends on the variety of oranges and/or clementines, mandarins, etc. that I'm peeling.  Usually fruits with thick, hard skin are easier to peel whereas fruits with softer more delicate skin are harder to peel off in one piece.  Factors like growth climate and ripeness effect the skin quality.

If you roll the fruit on a hard surface under your palm before peeling, it makes the skin easier to peel off in one piece.


Is eye colour of Drosophila a polygenic trait or an X-linked trait?

Polygenic and X-linked are not mutually exclusive; a trait can be polygenic, X-linked, neither, or both.

Polygenic traits are those affected by many genes. According to Conner and Hartl, "Traits that are affected by many gene loci are often called polygenic traits." For example, childhood intelligence is affected by many genes throughout the genome. Monogenic traits are relatively rare, but are linked to some diseases, and occur when a single gene affects the trait; most traits are affected by multiple genes.

X-linked traits are affected by genes (only) situated on the X. If a trait is monogenic, it is very easy to describe it as being, or not being, X-linked. If the gene is on the X, it is X-linked. If it is on the Y, it is Y-linked. If it is in the autosomes, it is autosomally linked. If all of the genes affecting a trait are found on the X then that trait is X-linked. A gene on the X is X-linked, but I would only call a trait X-linked if all genes were on the X. If there was a mix of X-linked and autosomal genetic variation I would describe the trait as having some X-linked genes.

For polygenic traits it is less likely that the genes would be all X-linked, so it is less likely that the trait is X-linked. Imagine a trait affected by 10 genes, and those 10 genes are randomly spread across the genome. It is unlikely that all 10 would be on the X. However, if some were on the X, then we could describe the trait as having X-linked variation. Many highly polygenic traits will have some X-linked variation.

Having more genes affecting the trait further increases the probability that some genes will be on the sex chromosomes. For example, lifespan is expected to be a highly polygenic trait, and genetic variation in lifepsan can be attributed to the Y chromosome in Drosophila melanogaster, despite the Y carrying just a tiny fraction of the genes.

Many eye colour traits in Drosophila can be attributed to single genes, and White in the image below is X-linked. However, one can also produce a white-eyed fly using multiple genes; in this paper one of the lines used has white eyes as a result of combining genes (T(2;3) rdgC st pp bwD) which are on the autosomes.


Are there specific features of birds that cats/small predators are attracted to?

Not all cat predatory behavior is innate. Researchers found that cats predatory behavior for birds vs. mice depends to a significant degree on training by the mother: if the mother taught predatory behavior with birds, the kittens grew up to be better at catching birds than at catching mice and vice versa. Supportive data shows that aside from monkeys and other primates, cats are among the most adept at learning by observing the successes and failures of other animals attempting to complete tasks to obtain a reward. This might influence, therefore, a cat's response to and attraction for objects in the air or on the floor.

Blindfolded cats can hunt mice by vibration. Paul Leyhausen, a German animal behaviorist studied domestic cats (and related felines) from the 1950's through the 1970's, and much of what is known about their predatory behavior is thanks to him.

Although their vision is not especially keen, domestic cats see well in dim light and readily perceive motion. According to Leyhausen, prey movement and the direction of movement are the only factors which innately release crouching, stalking, and catching behaviors in cats. When presented with quail, cats were far more likely to go after active quail than those stilled by tonic immobility. Cats are also more likely to go after smaller prey (mice > rats) and mice were much more likely to elicit play pawing.

Leyhausen also demonstrated that rodents were probably the natural prey of cats.

Though there has been much study of cats and predation, little is available on detail of the kind you are interested in.  My best guess for a good toy for a cat would be a smaller object that moved along the floor.

More information can be obtained from Leyhausen's book, Cat Behavior: The Predatory and Social Behavior of Domestic and Wild Cats.

Effects of the mother, object play, and adult experience on predation in cats
 The effects of experience on the predatory patterns of cats
 Tonic immobility in Japanese quail can reduce the probability of sustained attack by cats
 The behavioral bases of prolonged suppression of predatory attack in cats


Is it possible to consume O2 via a pill form to inhibit the need to breathe?

The problem is volume and surface area for gas exchange.  The volume in a pill is puny compared to the amounts you pull in and out breathing.

But could you use something other than the lung for gas exchange?  The colon has a lot of surface area and the small intestine even more.  Maybe if you flooded your gut with an oxygenated fluid like that liquid fluorocarbon the mice breathe, or even oxygen saturated water you could get some of that out via your intestinal villi.  Dragonfly larvae do something like that, performing gas exchange with their rectums.  You would need to exchange the liquid at least as fast as you breathe, getting all the depleted liquid out and new oxygenated liquid in.

Some of those high colonic machines work like that, as I understand: fast in and fast out.  People might not notice you were holding your breath because they were distracted by the churning machine with the hose up your trouser leg.  Maybe you could pass out cards or wear a T-shirt explaining what was going on because you would still have to breathe to talk and that would ruin it.  If you do this would you please post video and link it up here?  Thanks.


Is there such thing as Animal non-verbal body language?

The closest reason that I know of for such behaviour is simple conditioning!

B. F. Skinner conducted some fairly famous experiments with pigeons, where he put hungry pigeons in cages, and randomly administered the food. The pigeons associated the foods arrival with whatever they happened to be doing at the time (be it looking to the right, or bobbing their heads). They would then keep trying this until more food came out (randomly), and the pigeons 'superstition' was confirmed. See the wiki.

I realize this is not concrete, but it seems to me that they are not 'communicating' as such, they are simply repeating what has worked before. It is your anthropomorphication that has meant this seems like deliberate communication in my opinion. Although I'm sure it could be argued that all communication is having been 'conditioned' to use words/gestures to get your meaning across.

Update (14.6.12)

Just read the abstract for this paper (published yesterday) that finds that experts in dog behaviour can interpret the ('socially relevant') posture of a dog in a similar way to that of a human. We can therefore interpret the body language of an animal (in this case, dog), if we are familiar (you do not even have to have owned a dog necessarily) with the kinds of postures adopted. So the dog does not have to consciously 'communicate' for us to interpret their emotional state (happy/sad/angry/...).

In terms of human-pet communication then, there seems to be more emphasis on the human interpretation of the natural postures adopted by animals, than the animals themselves. Pets may behave very differently to animals in the wild, but it comes back to what the specific human is used to. If you have had a lot of contact with pet dogs you are in a better position to associate the current behaviour of a pet dog with the correct emotional state. No doubt the animal with subconsciously adjust their behaviour to achieve the 'correct' human interpretation, and thus get fed, or whatever.


What would be the best design for spike-and-recovery and linearity-of-dilution validation experiments in one 96-well ELISA plate?

Background:

There are a lot of recipes to extract protein from human tissues out there, but all of them boil down to one thing; preserving the tissue proteins as much as possible while obtaining a reasonable yield for downstream applications, using extraction buffer, extra techniques, and by adding protease inhibitors
ELISA is one of the those downstream applications that you might be interested in, but one important question? is the sample matrix that you have already obtained valid for the ELISA assay? keep in mind, your sample is not serum, it is a mixture of tissue, extraction buffer, and protease inhibitors, and other things as well
Two known assays are usually performed to address the above question. These are, spike-and-recovery (SAR), and linearity-of-dilution (LOD), and these two assays are specific to the analyte that you want to measure in your samples, e.g., cytokines, factors, Igs, etc...and specific also to the tissue, and assay kit as well
Often times, you are interested in performing these two assays with minimum resources as much as possible, i.e., less time, less kit materials, and, most importantly, less sample material. This can be quite challenging and it depends on many issues that is out scope of this post to discuss them all
If you are interested in performing these two assays using only one 96-well ELISA plate and examine validity of different sample matrices, sample buffer (lysis buffer or sometimes called extraction buffer) for a certain analyte, say X, then this scheme below is for you:

Technical Notes:

In this scheme, recovery is examined in 3 types of solutions; assay buffer, sample buffer and samples. These are different in their complexity. Typically, the assay buffer is usually optimized to detect the standard protein provided with the commercial kit
The idea of spike-and-recovery is that you add a certain amount from standard stock solution into the wells containing the solution to be tested (e.g., sample buffer or samples) and measure them, to see whether you can recover that amount again, and how much you can recover from it in %. If, for any reason, you couldn't recover that amount in comparison with a control well, where that same amount was added into assay buffer, then this means that something in the test solution is not in favor of the assay. The specific amount you add into the wells is called spike, and it should be the same amount across all tested wells (try to be consistent). Make sure that the added amount when diluted in the well, its final concentration should still be measured by the assay and lie inside your standard curve. E.g., if your standard curve is from 4- 4500 pg/mL, and each well has 100µl of sample, if you want now to add spike into that sample well, you may add whatever amount you want that will still give you at the end a reading inside the standard curve, you may choose to add 10µl from the highest stock which is 500pg/mL, so you end up here with 1/10, that is 50pg/mL, which is fine as it lies inside the 4-500pg/mL range. Alternatively, you can add 50µl sample + 50µl spike (500pg/mL) and would end up with 1/2 dilution (which is the same in this scheme), that is 250pg/mL, which is also fine. So it is up to you to choose, keeping in mind the final concentration should lie inside your standard curve
For the linearity-of-dilution, it is obvious that you need a high concentration solution that you can make two-fold (or whatever fold you like) serial dilution from and its reading should still lie inside the standard curve. The best candidate for this is the high spiked wells. The LOD would tell you about the effect of different dilutions on the precision of the assay
For SAR and LOD you will get at the end an average percentage from 3 samples at least (calculation example will be provided later), I added a fourth sample, but this fourth can be a different sample type, say samples from tissue culture, so it is up to you to re-design this scheme and be innovative
Choosing the best dilution is not an easy task, it is not without compromises sometimes. For example, if you have a harsh sample buffer, you may not have good recovery at 1/2, 1/4, 1/8 dilutions of the sample buffer in assay buffer, whereas almost good recovery is achieved at 1/16, then this dilution factor is most probably the one you should go for in your assay. On the other hand, 1/16 might not be detected by your ELISA assay, which is limited by its sensitivity. Here, the E wells can give you a clue whether you detect something in these unspiked samples or not, that's why I recommend you include at least one sample of high expected value of the analyte in question (this is not easy sometimes to predict) in this scheme, here this is sample 3. One more thing, if you get good recovery at 1/16 DO NOT go to 1/32 or 1/64, as it is obvious that with these higher dilutions you are reducing the chance of the analyte's detectability as it is limited by your assay's sensitivity
In most of the cases, you will see that the dilution factor of good recovery of the sample buffer in columns 3 and 4, will coincide with that of the spiked samples in columns 5, 7, and 9. This will give you the assurance that you are in the right direction. If sample 4 is extracted by a different sample buffer, then it is clear that should not expect to end up with the same dilution factor (please, be more reasonable!)


Using catalase-test to determine if Staphylo- or Streptococcus

Generally yes: streptococci are catalase negative while staphylococci are catalase positive.

  The catalase test is important in distinguishing streptococci (catalase-negative) [from] staphylococci which are catalase positive.

  Unlike Staphylococcus, all streptococci lack the enzyme catalase.

However, there are exceptions to every rule:

Catalase negative Staphylococcus aureus.

Catalase positive Streptococcus sp.


Why are diabetic people often overweight?

How are diabetes and obesity connected in light of low lipase activity?
Short answer: There's more than one type of diabetes.  (And to complicate things, there's also more than one type of lipase.  It's unclear from the question which type were mentioned in what you read.)

Diabetes mellitus is usually divided into Type 1 (insulin-deficient) and Type 2 (insulin-resistant).  Obesity is a risk factor for Type 2 diabetes, but not all diabetics are overweight. In fact, people with Type 1 are often lean.

Decreased lipase activity is not a major symptom of diabetes.  However, these two articles suggest that plasma lipase activity may be lower in cases of Type 1 diabetes but not Type 2.
Junglee, D. et al., Low pancreatic lipase in insulin-dependent diabetics, 1983.
Dendona, P. et al., Exocrine pancreatic function in diabetes mellitus, 1984.


Computational/mathematical models for predicting phenotype from genotype

The Karr et al. paper attempts to capture most of the details in their model by combining features from the genome, transcriptome, proteome, and metabolome. This work heavily builds off of the coarse-grained models that you ask of especially on the work from Bernhard Palsson from which Markus Covert did his training. The answer to your question rests entirely on the type of question that you seek and what you want the model to do.

For the most part, most of your questions can be answered using COBRA, the COnstratins Based Reconstruction and Analysis Toolbox. You can get a good idea of what genotypes can be knocked out and see how it affects the phenotype as long as the phenotype is a known pathway that gets affected by that gene and you don't care about temporal and dynamic information.

There is also the E-Cell Project for E. coli. I personally don't know much about it but it has created some basic models for E. coli and that may be good enough.

If you want to build your own models, you should check out BiGG where all of the large-scale reconstructions exists. A good chunk of the code is stored at the Palsson lab website where you can attempt to use COBRA and start generating your own hypotheses.


Neurotransmitters were classically the most specific in terms of demands on experimental demonstration (thus, the so-called "classical neurotransmitter") but the chief role of neurotransmitter is direct neuron-to-neuron communication via the synaptic cleft in which the post-synaptic neuron has channels that readily engage the neurotransmitter.  Classical neurotransmitters also require inactivation and are stored in vesicles in the presynaptic terminal (while under the modern definition, these last two requirements aren't as strict, allowing peptides and gasses like NO to be considered a neurotransmitter).

Neuromodulators, are more of an extra-synaptic application... a bath in the extracellular medium that modulates the excitability of a population of cells.  In this regard,neurotransmitters can be considered neuromodulators when their action is on channels outside of the synaptic cleft.

I have never heard the term neuromediator before, but looking at the results on Google suggest that it is the result of translation from Easterm European languages (Polish and Romanian) and seems to be synonymous with neurotransmitter.


Why does inbreed produce a higher percentage of abnormal babies?

Many disease/abnormality causing alleles of a genes are maintained in populations through their recessive nature. That is to say, in order for the disease to manifest itself in offspring they must in have TWO copies of the disease causing allele - they must be homozygous for the disease causing allele. Inbreeding leads to a far greater chance of being homozygous at a disease locus if a recent common ancestor of the parents was affected or a carrier. The likelihood of this occurring is measured by the Inbreeding Coefficient.


What is the point of a runny nose during a cold?

Edited by request for clarity

The biological purpose of a runny nose is to clear pathogens and allergens trapped in the mucus out of the nasal cavity and sinuses as a result of rhinitis or sinusitis.

Mucus is considered to be part of the innate immune system and provides mechanical and chemical defenses against pathogens.

Mucus acts as a barrier protection that is difficult for pathogens to breach.
Mucus is capable of trapping pathogens in it and when that mucus is swept out of your upper respiratory track through your nose or down your esophagus, the pathogens are removed from those areas as well.
Defensive proteins called Mucins, Lysozymes, and Immunoglobulins are secreted into the mucus and provide additional protection, as they can lyse or opsonize pathogens.

Mucus keeps epithelial cells moist so that they do not dehydrate as air passes over them. This in turn keeps epithelial cells healthy so that they maintain a tight cell layer in order to protect the underlying tissue.

As part of the mechanical defenses against pathogens, epithelial cells are ciliated and they rhythmically sweep mucus from the sinuses and nasal cavity mainly into your esophagus and digestive system, but can also move mucus into your nose. Most of the time we aren't even aware this clearance of mucus is happening and it travels down our esophagus into our stomach's and intestines where it can be excreted from the body. This is the case when you do not have an infection and your mucus is not viscous.

When you have an infection the inflammatory response is triggered by cytokines from macrophages. Those cytokines induce cells in the area to do many things. One is to increase mucus production. This may cause epithelial cells in your nostrils and nasal cavity and sinuses to secrete more mucus as well, and this will be swept away through your nose, where you will notice it as a runny nose.

Usually your nose is runnier with rhinovirus infections or with allergens than it is when you have a bacterial infection where mucous tends to be thicker and more viscous. The ciliated epithelial cells have an easier time moving the thinner mucous of a viral infection or allergy than the thicker mucus of a bacterial infection, so you notice a runny nose more when you have a cold or hay fever.

So in short, the biological purpose of a runny nose is that it is part of the immune response to clear pathogens away and protect your uninfected epithelial cells from being infected. It also clears out much of the debris and inflammatory proteins that are found at the site of the infection so that they do not remain in the area to further inflame tissue that is trying to heal. When you have allergies your immune system reacts inappropriately to a benign substance, and if the allergen finds its way into your nasal cavity, it will generate rhinitis and cause your nose to run.


Potential to destroy viruses using prions?

Prions are misfolded "versions" of proteins already present in the genome. These tend to bind to their properly folded counterparts and catalyze their misfolding into prions. Although unlikely, it is not impossible to imagine that they might interact with other macromolecules. That being said, injecting a human with prionic particles for any reason (especially in a clinical trial for the common cold) is EXTREMELY unlikely. Even if you prove that it works in animal models, injecting a person would be considered too risky. Additionally, the "benefit" of that would be marginal - curing the common cold, from which > 99% of people recover even without any medication. Given that there is great risk and very little benefit, we will most likely never know for sure how feasible this is (at least for the common cold). As a concept, it could work, but would be extremely difficult to get right.


In the notch signaling pathway, what is Fringe activating?

Usually, in such depictions where a species is pointing to a reaction or an interaction, the arrows mean that the species affects that reaction (for example, catalysis by an enzyme ). Generally pointy arrow heads denote positive effect (enhancing the reaction, for example an enzyme) and flat heads denote a negative interaction (repression). An arrow from one molecule to another can be used to depict a conversion (like glucose converting to glucose 6 phosphate).

There are no real standards on how to depict a pathway. So, it can be confusing.

In this case, Fringe actually alters Notch signalling (see below). So the arrow makes sense. However, the figure also has an arrow from Delta to Notch which can be interpreted as Delta getting converted to Notch. They also show an arrow from Notch to NICD which actually means a conversion. I would say that the depictions in this figure are inconsistent.

From NCBI Gene entry on Human homolog of Fringe, LFNG:

  This gene is a member of the glycosyltransferase 31 gene family.
  Members of this gene family, which also includes the MFNG (GeneID:
  4242) and RFNG (GeneID: 5986) genes, encode evolutionarily conserved
  glycosyltransferases that act in the Notch signaling pathway to define
  boundaries during embryonic development. While their genomic structure
  is distinct from other glycosyltransferases, these proteins have a
  fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that
  leads to elongation of O-linked fucose residues on Notch, which alters
  Notch signaling. The protein encoded by this gene is predicted to be a
  single-pass type II Golgi membrane protein but it may also be secreted
  and proteolytically processed like the related proteins in mouse and
  Drosophila (PMID: 9187150). Mutations in this gene have been
  associated with autosomal recessive spondylocostal dysostosis 3.
  [provided by RefSeq, May 2018]

From Shao et al (2002):

  Recent studies have demonstrated that O-fucose modifications play an
  essential role in Notch function. Reduction of O-fucosyltransferase
  expression in Drosophila using RNAi (11) or in mice by gene ablation2
  causes Notch-like phenotypes, suggesting that O-fucose modifications
  are essential for Notch function. In addition, we and others have
  shown that Notch activation is modulated by extension of O-fucose on
  Notch with the fucose-specific β1,3-N-acetylglucosaminyltransferase
  Fringe (for recent reviews, see Refs. 12 and 13). Fringe was first
  identified in Drosophila and shown to inhibit Notch's ability to
  respond to Serrate but to potentiate its ability to respond to Delta
  (14). Three Drosophila Fringe homologues have been identified in
  mammals: Lunatic fringe (Lfng), Manic fringe (Mfng), and Radical
  fringe (Rfng) (15). The β1,3-N-acetylglucosaminyltransferase activity
  of Fringe proteins is essential for their biological activity in
  Drosophila (16-18) and in cell-based Notch signaling assays (19), and
  the O-fucose residues are required for Fringe to modulate Notch
  activity (16, 19). Thus, Fringe mediates its effects on Notch
  signaling by the addition of GlcNAc to O-fucose moieties. Nonetheless,
  neither the specific role ofO-fucose in Notch function nor the
  mechanism of how a change in sugar structure alters Notch function is
  known.


Trying to understand the big picture behind DNA sequencing, alignment and searching

Here's a quick summary of a few mis-hits in your otherwise good analysis:

Not many bioinformatics applications use Hadoop, Apache Spark or Apache Flink. In fact, I have never heard of the Apache Spark and Flink tools, and I've seen only 2 people use Hadoop to process alignment files.

Reads are not "converted" real, physical DNA. They are representations of the signals from the molecules making up the DNA, as read by sequencing machines.
A,T,C,G are molecules making up DNA. N refers to "any of A,T,C,G", which translates to either unknown or ambiguous.
Reads are stored in FASTQ files. Sequences are stored in FASTA files. Reads include sequence as well as quality information, so, FASTA+QUAL=FASTQ
Re-ordering is a crude but approximate way to think about it. Remember, this process involves overlaps while reordering seldom does. Overlaps are crucial to the process of assembly/alignment. You are correct about the alignment to reference sequence and de novo assembly parts.
This is correct, though statistical models are applied to account for differences that are not necessarily significant variants (such as for sequencing errors)
Yes, variants, which include SNPs, can be correlated to differences in phenotype (traits). Emotional tendencies is something a bit too advanced, think of something more basic like diabetes or eye color.

The picture you have here is of a regular NGS analysis pipeline. This involves alignment/assembly, variant calling and biological analysis with relevant hypotheses. The assembly/alignment is the most computationally expensive part, and we use either HPC clusters or scalable cloud services such as AWS to get this done.

You should definitely talk to a biologist that has some computational experience to gain insight into the reason behind our analyses. Once you understand the motivations, your contribution will be more relevant and helpful to the community.


Original Answer (posted originally as a Comment)

It is now accepted that high cholesterol causes atherosclerosis. Cholesterol a major component of the plaques that block arteries. 'Good' and 'bad' cholesterol refer to the way cholesterol is transported in the bloodstream.

'Bad' cholesterol is cholesterol in the form of low density lipoproteins or LDL, and 'good' cholesterol is in the form of high-density lipoproteins or HDL.

Or at least that is how it used to be. It is still accepted that high concentrations of LDL in blood promote atherosclerosis, that is high levels of LDL may still be considered 'bad', but drugs that specifically raise the levels of HDL have had serious adverse effects.

Check out this great article: Cholesterol and Controversy: Past, present and Future by  Jeanne Garbarino, especially the section on "Deconstructing Cholesterol: “Bad” is still bad, but is “good” still good?". It is hard to know what the current position is. And check out the work of Brown and Goldstein.

Edit

Goldstein, in his Nobel lecture, famously said (see here)

  Cholesterol is a Janus-faced molecule. The very property that makes it useful in cell membranes, namely its absolute insolubility in water, also makes it lethal. For when cholesterol accumulates in the wrong place, for example within the wall of an artery, it cannot be readily mobilized, and its presence eventually leads to the development of an atherosclerotic plaque.

Cholesterol may be synthesized in the body, or obtained from the diet.  The site of biosynthesis is mainly the liver. Cholesterol and fats (triacylglycerols) are transported in the bloodstream as lipoprotein particles, which may be roughly described as a lipid core surrounded by a protein coat, and may be viewed as a mechanism for transporting insoluble fat molecules (by 'coating' them with a soluble protein exterior).

There are five main classes of lipoprotein particles (see, for example, Berg): chylomicrons, very low density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)

Cholesterol (and fats) are transported from the liver to other tissues in the form of low-density lipoproteins (LDL).  High-density lipoproteins, on the other hand, pick up cholesterol and fats in the blood and from specialized cells and transport them to the liver. Hence the names 'bad' and 'good' cholesterol.  (In reality, of course, things are more complex than this simple scenario: for a very readable account, see Berg).

The ratio of 'bad' to 'good' cholesterol, ie the ratio of LDL to HDL may be used diagnostically, and a healthy LDL/HDL ratio is about 3.5 (see Berg), but in view of the studies cited by Garbarino a low ratio due to high concentrations of HDL (rather than low LDL) might not be so great either. In fact, if LDL is in check, there may be no benefit to raising HDL (Garbarino article).  But I suppose the physicians will always find a way to waffle (and to charge for the privilege).

It is a common misconception that plants do not contain cholesterol. (My original answer to this question attempted to promulgate this nonsense). In particular, plant membranes do contain cholesterol. However, the amount of cholesterol in plants is low compared to that found in animals (Behrman & Gopalan, 2005).  But it is certainly not zero. The nucleus of maize shoots contain significant amounts of cholesterol, for example (Kemp & Mercer, 1968).

This great reference, Cholesterol in Plants, by Behrman & Gopalan (2005) suggests that the following paragraph should be inserted into biochemistry texts.

  More than 250 steroids have been described in plants.
  Of these,  perhaps  sitosterol,  which  differs  from  cholesterol by an ethyl substituent at position 24, is the most
  common.  But  plants  also  contain  cholesterol  both  free
  and esterified. Cholesterol occurs as a component of plant
  membranes  and  as  part  of  the  surface  lipids  of  leaves
  where it is sometimes the major sterol. The quantity of
  cholesterol is generally small when expressed as percent
  of  total  lipid.  While  cholesterol  averages  perhaps  50
  mg/kg total lipid in plants, it can be as high as 5g/kg
  (or more) in animals.

A great generalization is the following (Behrman & Gopalan, 2005)

  Prokaryotes do not contain cholesterol

These authors also suggest that one of the reasons for the common misconception that plants do not contain cholesterol is "legalities of food labeling that allow small quantities of cholesterol in foods to be called zero".

I suppose we should not be too surprised that plants can make cholesterol. They can of course, make steroids, the Mexican yam being the original source of a precursor of a particularly important one.

A key enzyme in the biosynthesis of cholesterol is HMG-CoA reductase, which is the target for statins, and these drugs  may be used to lower serum cholesterol levels (but there may be side-effects).

One interesting thing about the biosynthesis of cholesterol is that the final cyclization step requires oxygen which has lead to much philosophical and evolutionary debate (see, for example, here).

Finally, another quote from Goldstein

  Cholesterol is the most highly decorated small molecule in biology. Thirteen
  Nobel Prizes have been awarded to scientists who devoted major parts of their
  careers to cholesterol. Ever since it was first isolated from gallstones in
  1784, almost exactly 200 years ago, cholesterol has exerted a hypnotic fascination for scientists from the most diverse domains of science and medicine


"Other" classification for epitopes in the Immune Epitope Database (IEDB)

I presume that these epitopes represent peptides that have been eluted from MHC molecules and then sequenced by mass spec.  You can then compare these peptide sequences to a reference genome (more specifically to the proteins predicted to arise from the reference genome).  If the peptide matches perfectly to a predicted protein, then you assign it that identify.

But many peptides will not align to the predicted proteins, and so they can't be unambiguously assigned a gene of origin.

There are many reasons why MHC-derived peptides may not match the proteome.  Most obviously, the reference genomes are typically from a single individual, so if the sequenced peptide has a SNP, or other allelic variation, it won't line up.  As well, a significant number of peptides undergo some form of modification during antigen processing, such as deglycosylation changing Asn to Asp, proteasome-mediated cleavage and re-annealing, and so on.  These modified peptides also won't line up to the predicted proteome.


While the heart is affected during septic shock, it is the result of the chain of events that occur as a result of a systemic release of the pro-inflammatory cytokine Tumor Necrosis Factor alpha (TNF-$\alpha$) that leads to the "collapse of the circulatory and respiratory system." (Janeway's Immunobiology, 8th Edition) See also Tumor necrosis factor signaling.
When leukocytes, mainly macrophages encounter a pathogen or the antigenic product of a pathogen, pathogen-associated molecular patterns (PAMPs) such as endotoxins or exotoxins, their pattern recognition receptors (PRRs), such as the toll-like receptors, are bound and signaling occurs which stimulates the production and release of pro-inflammatory cytokines. In a localized infection, this is a beneficial response, however when the response is systemic, it will lead to a catastrophic cascade that leads to septic shock and often death.
Under "normal" conditions, TNF-$\alpha$ is an inducer of local inflammatory response. When an endotoxin such as lipopolysaccharide (LPS) is detected by TLR-4 on macrophages in the local microenvironment of an infection, the macrophages are stimulated to secrete TNF-$\alpha$. TNF-$\alpha$ produces the following physiological effects:

Activates the vascular endothelium

The endothelial cells will begin expressing a different assortment of receptors that recruit leukocytes out of the blood and into the tissue
This also allows for increased platelet adhesion to the activated endothelial vessels

Increases vascular permeability

Increased entry of Immunoglobulin G into the infected tissue
Increases entry of Complement proteins from the plasma to the tissue
Increased access to leukocytes and activated lymphocytes for extravasation into the infection microenvironment

Increased fluid drainage to lymph nodes

- Janeway's Immunobiology, 8th Edition; p 101
One of the mechanisms that is beneficial to the local inflammatory response, namely platelet adhesion will become problematic in the systemic response and will lead to multi-organ failure. In the local environment, however, it helps to prevent the spread of infection and shunts fluid flow away from the bloodstream and to the lymphatic system where it will be encountered by the components of the adaptive immune system. Locally:

Another important action of TNF-$\alpha$ is to stimulate endothelial cells to express proteins that trigger blood clotting in the local small vessels, occluding them and cutting off blood flow. This can be important in preventing the pathogen from entering the bloodstream and spreading through the blood to organs all over the body. Instead, the fluid that has leaked into the tissue in the early phases of an infection carries the pathogen, usually enclosed in dendritic cells, via the lymph to the regional lymph nodes, where an adaptive immune response can be initiated.
- Janeway's Immunobiology, 8th Edition; pp 107-108

You can begin to see where the inflammatory response triggered by TNF-$\alpha$ may become a catastrophic problem if it is secreted systemically.

Once an infection spreads to the bloodstream, however, the same mechanisms by which TNF-$\alpha$ so effectively contains local infection instead become catastrophic. Although produced as a membrane associated cytokine, TNF-$\alpha$ can be cleaved by a specific protease TACE (TNF-$\alpha$-converting enzyme, formerly called ADAM17) and released from the membrane as a soluble cytokine. The presence of infection in the bloodstream, or sepsis, is accompanied by a massive release of TNF-$\alpha$ by macrophages in the liver, spleen, and other sites throughout the body. The systemic release of TNF-$\alpha$ into the bloodstream causes vasodilation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually shock, known in this case as septic shock because the underlying cause is a bacterial infection. The TNF-$\alpha$ release in septic shock also triggers blood clotting in small vessels throughout the body--known as disseminated intravascular coagulation--which leads to the massive consumption of clotting proteins, so that the patient’s blood cannot clot appropriately. Disseminating intravascular coagulation frequently leads to the failure of vital organs such as the kidneys, liver, heart, and lungs, which are quickly compromised by the failure of normal perfusion; consequently, septic shock has a high mortality rate.
- Janeway's Immunobiology, 8th Edition; pp 108-109

So, as you can see, it is the effect of the depletion of clotting factor, the loss of plasma volume and blood pressure, and the alteration of the blood's ability to clot which likely is leading to the arrhythmic effects that you have observed in the heart.
The figure below summarizes both the localized and systemic effects of TNF-$\alpha$ release.
$\alpha$ can have damaging effects when released systemically" />
- Janeway's Immunobiology, 5th Edition; Figure 2.37
Effects of TNF-$\alpha$ on the heart
There is research from the 1990s and early 2000s that deals with the effects of TNF-$\alpha$ both on the heart and expression of the cytokine in failing heart tissue. Below is a brief selection of those articles. The final reference discusses the link between Toll-like receptor 4 activation and the promotion of cardiac arrhythmias:
From Cardiac-specific overexpression of tumor necrosis factor-alpha causes lethal myocarditis in transgenic mice. Kubota, et.al. J Card Fail. 1997 Jun;3(2):117-24.

Tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine with negative inotropic effects, can be detected in myocardium with end-stage heart failure, after endotoxin administration, and during transplant rejection. Various studies suggest that TNF-alpha participates in the pathogenesis of cardiac dysfunction.
Overexpression of TNF-alpha in the heart leads to severe myocarditis and cardiomegaly. These results support the hypothesis that myocardial expression of TNF-alpha can contribute to the pathogenesis of cardiac dysfunction.

From Dilated Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Tumor Necrosis Factor-$\alpha$. Kubota, et.al.
Circulation Research.1997; 81: 627-635; doi: 10.1161/01.RES.81.4.627

That end-stage congestive heart failure is associated with a marked increase in circulating TNF-$\alpha$ levels has been reported by numerous investigators. Furthermore, there appears to be a direct relationship between disease severity and circulating levels of TNF-$\alpha$.
In the present study, we demonstrate that chronic overexpression of TNF-$\alpha$ results in the development of a dilated cardiomyopathy that shows (1) ventricular hypertrophy, (2) ventricular dilatation, (3) interstitial infiltrates, (4) interstitial fibrosis, (5) rare myocyte apoptosis, (6) a diminished ejection fraction, (7) attenuation of $\beta$1-adrenergic responsiveness, and (8) expression of atrial natriuretic factor in the ventricle. Additionally, mice overexpressing the TNF-α transgene had a marked increase in mortality. More than half of the mice that died spontaneously presented with exceptional dilatation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure.

From The role of tumor necrosis factor in the pathophysiology of heart failure Feldman, et.al. Journal of the American College of Cardiology
Volume 35, Issue 3, 1 March 2000, Pages 537–544

In summary, both basic and clinical studies strongly support the hypothesis that myocardial expression of TNF alpha is an important step in the pathophysiologic pathway leading to progressive cardiac dilatation and failure.

From Toll-like receptor 4 activation promotes cardiac arrhythmias by decreasing the transient outward potassium current (Ito) through an IRF3-dependent and MyD88-independent pathway. Monnerat-Cahli, et. al. J Mol Cell Cardiol. 2014 Nov;76:116-25. doi: 10.1016/j.yjmcc.2014.08.012. Epub 2014 Aug 25.

Abstract
Cardiac arrhythmias are one of the main causes of death worldwide. Several studies have shown that inflammation plays a key role in different cardiac diseases and Toll-like receptors (TLRs) seem to be involved in cardiac complications. In the present study, we investigated whether the activation of TLR4 induces cardiac electrical remodeling and arrhythmias, and the signaling pathway involved in these effects. Membrane potential was recorded in Wistar rat ventricle. Ca(2+) transients, as well as the L-type Ca(2+) current (ICaL) and the transient outward K(+) current (Ito), were recorded in isolated myocytes after 24 h exposure to the TLR4 agonist, lipopolysaccharide (LPS, 1 μg/ml). TLR4 stimulation in vitro promoted a cardiac electrical remodeling that leads to action potential prolongation associated with arrhythmic events, such as delayed afterdepolarization and triggered activity. After 24 h LPS incubation, Ito amplitude, as well as Kv4.3 and KChIP2 mRNA levels were reduced. The Ito decrease by LPS was prevented by inhibition of interferon regulatory factor 3 (IRF3), but not by inhibition of interleukin-1 receptor-associated kinase 4 (IRAK4) or nuclear factor kappa B (NF-κB). Extrasystolic activity was present in 25% of the cells, but apart from that, Ca(2+) transients and ICaL were not affected by LPS; however, Na(+)/Ca(2+) exchanger (NCX) activity was apparently increased. We conclude that TLR4 activation decreased Ito, which increased AP duration via a MyD88-independent, IRF3-dependent pathway. The longer action potential, associated with enhanced Ca(2+) efflux via NCX, could explain the presence of arrhythmias in the LPS group.


What is the purpose of the outer mitochondrial membrane?

Structure origins

Originally the mitochondrial outer membrane (MOM) was likely the result of a bacteria that could survive in a vesicle formed of the plasma membrane.

This explains why the plasma membrane and the MOM are structurally similar, however, the proteins that are present in either mean that their functions are very different.The MOM has a specialised translocation complex for example.

Functional significance.

The MOM is actually much more complex than an evolutionary hangover and is essential to modern cells by regulating what that mitochondrial inner membrane is exposed to. The MOM plays this role using porins. Indeed, if the porins of the MOM are disrupted, the entire cell dies (Chipuk et al, 2006). Additionally, the MOM allows a physical association between the ER and the mitochondria called the mitochondria-associated ER membrane (MAM). The MAM is essential for $ {Ca}^{2+} $ transfer.

  The MAM thus integrates signal transduction with metabolic pathways to
  regulate the communication and functional interactions between the ER
  and mitochondrion. (Hayashi et al, 2009)

Answer: The MOM is essential in regulating what the MIM is exposed to, and allows signalling between the ER and mitochondria.


The key word you are missing is "relatively": I'm not clear what they mean "relatively" to based on where you cut off the passage, but they probably mean relative to the entire diameter of the vessel; the statement is probably not true for area but you would have to choose a particular artery and arteriole to compare, and both categories have a lot of variation in size within and between organisms.

Arterioles do have a "relatively" thicker muscle layer than the great arteries because they are the place where most of the contraction takes place that regulates the resistance of different vascular beds. Because of that, though, their lumen size varies quite a bit depending on the state of the muscle. When the smooth muscle in the vessel wall is relaxed, arterioles are much larger than when contracted. Even if the book is correct that according to whatever measure of "relative" they are using, arterioles have a wider lumen, I have a hard time believing this would be true over the entire range of contraction.


What is the effective relatedness of inbreeding?

In "The Selfish Gene" Dawkins claims a relatedness factor of 1/128 to be pretty much the same as the baseline chance for the rest of the population to have the same gene, so that would be a third cousin. (Or your great great great great great grandparents, though an incestuous relationship with them is quite unlikely I think.)

I'm not sure where he got that from though.


Batch convert miRNA names to Accession IDs?

If you want it all, download the mirRNA.xls.zip file from mirbase here:

ftp://mirbase.org/pub/mirbase/CURRENT/

its a spreadsheet that includes these data as columns and also more information besides - for the entire database.


Looking to study botany, some general advice

Have you checked out Botany classes at nearby community colleges?  You may have trouble finding an evening class, but I'm sure you'll find daytime classes opening up in the January.

If you need to study independently, can I suggest checking out the Tree Care Industry Association's store. www.tcia.org  They have various learning material to read and watch, leading towards a professional arborist certification.

Good luck in your endeavor.


Looks as if you'll have to do some reconstruction work building the full sequence from the information here and elsewhere in this paper:

  Nucleotide sequence accession numbers.The DDBJ/EMBL/GenBank accession numbers for the sequences reported in this paper are AB031076(the SalI-XhoI 3.0-kb fragment of pMG101), D84187(rDNA for strain S55), D86354 (rDNA for USDA 4362), D86355 (rDNA for USDA 4377), AB031077 (plasmid pMG103), and AB031078 (plasmid pMG105).

--Sequence Analysis of the Cryptic Plasmid pMG101 from Rhodopseudomonas palustris and Construction of Stable Cloning Vectors


Plasma Membrane Proteins and Cytoskeletal Attachment

a. Membrane proteins are responsible for both cell to cell recognition and cell anchoring and are stabilised by linking through to the microtubulele cytoskeletal ﬁbres.

Not entirely correct as you yourself pointed out that integrins attach to actin filaments.

  b. A protein that is enzymatically active and membrane-bound will function significantly differently to a protein that is enzymatically active and cytosolic.

Possible but not necessary.

  c. Membrane proteins are manufactured in the internal cavity (lumen) of the rough ER.

They are secreted in the ER and modified there too but not manufactured there.

  d. Damage to the smooth ER could alter the makeup of the molecules that are displayed at the cell surface.

Seems correct because the statement itself does not claim certainty. It says that the makeup of cell surface molecules (which could be lipids or proteins) could change in response to SER damage.


How does the counter-current multiplier work in the nephrons?

Countercurrent multiplication

What is flowing in the opposite direction to the glomerular filtrate for it to be called "counter-current"?

The filtrate is moving in the opposite direction of the filtrate. It's a loop. Filtrate moves in two directions relative to the nephron, down (from the cortex toward the papilla/through the medulla) and up (from the medulla to the cortex). We'll start with up, because that's where the active transport occurs

Up: as filtrate moves up the ascending limb, $Na^+$, $K^+$ and $Cl^-$ are actively pumped out of the filtrate and into the surrounding ECF. This limb, the ascending limb, is impermeable to water, so water doesn't follow the active transport of solutes and the fluid becomes more concentrated in the ECF than in the tubule lumen. So on the way up, the filtrate becomes more dilute.

Down: the descending limb is permeable to water and to ions along with it, so as filtrate moves down the descending limb, the osmolarity of the filtrate equilibrates with the concentrated ECF. This equilibration between descending limb filtrate and the ECF, makes the filtrate more concentrated, so on the way down, the filtrate becomes more concentrated.

By itself, the active transport of solutes out of the filtrate and into the ECF on the way up the ascending limb, (with dilution again by the water on the way down the descending limb) would seem to make only a small difference, but consider what happens as the filtrate continues to flow, while the ECF doesn't.
Consider this diagram from Constanzo Physiology, Chapter 6:

First, the active transport of solutes out of the ascending limb brings the ascending limb filtrate from 300 mOsm to 200, while the ECF becomes concentrated. The descending limb and ECF equilibrate, and you're left with an ECF and descending limb osmolarity that has gone from 300 mOsm to 400. This gives you the state represented in frame (1). The increase in ECF and descending limb filtrate osmolarity that is caused by active transport of solutes from the ascending limb is called the single effect.
When fluid moves, 300 mOsm filtrate flows in from the glomerulus, replacing the 400 mOsm filtrate at the beginning of the descending limb (which equilibrates with the ECF), but 400 mOsm filtrate from the end of the descending limb flows around the hairpin and continues along the ascending limb, giving you the state represented in frame (2). This new state is the result of the flow of fluid.
Now the single effect operates on this new state. At each point along the ascending limb, active transport of solutes dilutes the filtrate in the ascending limb and concentrates the ECF, which equilibrates with the filtrate in the descending limb, giving you the state represented in frame (3). Here you can start to see an up/down gradient establish. Continue these steps, and you can see how a substantial gradient can form.
Countercurrent exchange
After being presented with countercurrent multiplication, students will often ask how it is that solutes and water equilibrate horizontally in this diagram (i.e., between the descending limb and the ECF), but not vertically. This is a different question, and is where you start to need yet another compartment, the blood in the vasa recta. This mechanism is called countercurrent exchange, but is the answer to another question (how come the corticomedullary gradient doesn't dissipate?).
Original paper
In addition to physiology texts (e.g., Costanzo Chapter 6), you can read one of the most important original papers supporting this mechanism. Originally published in 1959, it was reprinted here in 1997 and available for download. See if you can follow the connection between the data and this mechanism.


Help me identify this spider from my garden

I believe it is a Garden Orb Weaver spider. The Australian garden orb weaver, Eriophora transmarina, has a strikingly similar body


Unidentified insect seen in southern UK, near North Downs

Though it might resemble a woolly aphid (https://dengarden.com/gardening/Woolly-Aphids-Whats-that-Fluffy-White-Stuff-on-my-Tree). I'm more certain that it is a mealy bug instead (https://puffycarrot.com/little-fuzzy-white-bugs/). the fact that it is not on a plant is what confuses me since both these species are usually living on plants which is where they grow.
here is some images i found that look almost identical to the photo you have and give other angles to the species, you can compare it with the images in the other links:
https://www.flickr.com/photos/unique127/2539022716/
https://www.ecosia.org/images?q=white+furry+insect#id=DDEE9FF71839419EF585778C7DA8F1E1545E98D1


Stem cell research and female egg synthesis

I suppose that there is no connection between producing egg from somatic cells and stem cell research. The thing that you have mentioned: "produce a female human egg from other female body cells" was already done in 1996 (!) in sheep. Technically, there is no reason that this procedure will not work in Human as well. So in term of years: this was possible 20 years ago ... :-)


It's just a variant of kale, part of the genus Brassica. I think you'd call this particular variant redbor or purple, bluntly, but you could go further because kale is often classified by the type of leaf. So in your picture, curly 'redbor' or 'purple' kale.

This is your specific name: Brassica oleracea Acephala Group.

(just sort of look at wikipedia)


Are there ways to genetically increase mutation rate of E.coli?

Mutations are caused by the insertion of the wrong bases during replication, or by chemical changes to bases, either by chemical agents or by radiation.

The rate of mutations could be increased by exchanging the E.coli polymerases with other polymerases displaying higher error rates (or with less proofreading capabilities). A lot of errors are quickly repaired via different mechanisms, knocking out all or a few of those mechanisms might result in an E.coli strain with an increased mutation rate (if they survive).
https://www.ncbi.nlm.nih.gov/books/NBK9900/

A more elaborate way would be to engineer E.coli to contain a pathway that synthesizes a mutagenic compound. The easiest way to to this would be 1 enzyme that generates reactive oxygen species, as those also cause DNA damage. You could also delete some of the catalases and other enzymes that remove reactive oxygen species instead.
https://www.ncbi.nlm.nih.gov/pubmed/16824196


In terms of differentiation, how many generations of asexual reproduction, will usually be equal to 1 of sexual?

Welcome to Biology.SE!
Clarification of the question
It is unclear what you mean by differentiation? I will assume that the question is

For what value of $n$. is the number of pairwise differences between any two siblings under sexual reproduction is equal to the number of pairwise differences between any two $n^{th}$ cousins under asexual reproduction?

Answer
The answer to this question mainly depend on (1) the mutation rate and (2) the amount of genetic variation present in the sexual population (which itself is a function of the mutation rate).
Assuming a panmictic population of constant size $N$, assuming equal sex-ratio and non-overlapping generation (and a few other assumptions), we can make some estimations. Let's assume that the sexual and asexual populations that we are comparing have the same mutation rate $\mu$.
Sexual population
Using coalescent theory, one can show that the expected number of pairwise difference between any two individual in a sexual population is $4 N \mu$. It would be off-topic to explain why this is true. I let you open a population genetics book and/or open a different post.
Asexual population
Assuming an infinite site model (just like coalescent theory does), the number of pairwise differences between $n^{th}$ cousins is $2 n \mu$.
Comparison
Let's set the equation
$$2 n \mu = 4 N \mu$$
and solve for $n$, we get
$$n = 2 N$$
In words, $2N$ cousins in asexual populations have the same number of pairwise differences (on average) than two sibling in a sexual population of size $N$.
Remarks
Please note that the conclusion is drawn from important (but common) assumptions. Note also that drawing conclusions from the above calculation such as "sex helps retain genetic diversity" would be wrong, as we are comparing sibling to $n^{th}$ cousins and not randomly chosen individuals in the population.


Can we change the direction of a neurological signal?

"Neurological signal", or as I would put it, action potential, or activity propagation can be modeled as current in an electrical circuit. Trick is that such a circuit contains a bunch of highly regulated and non-linear and non-static elements. Imaging bunch of potentiometers (variable resistances) in your circuit. And all of them behave depending on something else in the system. So certainly currents will go somewhere, but level of control and complexity is phenomenal.

An example that should let you appreciate possibility of rerouting is simple Pavlovian conditioning. Neutral stimulus (bell) that has no evident connection to stomach, after conditioning elicits response there. Even though circuitry is very complicated and signal propagation is hard to investigate, this is an evidence that changing path of signals is very possible in some way. (Of course, conditioning require changes in higher-than-stomach systems, some intermediate levels).

On more practical note, we can readout neuronal activity in region A (of brain, muscle or else) and rely it via electrical stimulation somewhere in brain or muscle or gland. Both parts of this are available technology. As of drugs, some people report "seeing" sounds while intoxicated, this might be an example of such temporary effects.


What is this thorny plant with cute leaves?

https://en.wikipedia.org/wiki/Dalbergia_melanoxylon

The Mpingo looks quite similar to this plant. However, more information is needed like the approximate size of the leaves and the number of leaves on a branch.


Is a "Fact" any theory for which there is overwhelming evidence in any field other than biology?

Your question really applies to any scientific theory, not just evolution.

The problem is that, outside of the scientific world, a theory is often thought as something unproven, an unproven guess if you wish. This is not true for scientific theories, which, instead are confirmed by experimental data.

The OED defines theory as:

  A scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena; a hypothesis that has been confirmed or established by observation or experiment, and is propounded or accepted as accounting for the known facts; a statement of what are held to be the general laws, principles, or causes of something known or observed.

and fact as:

  Something that has really occurred or is actually the case; something certainly known to be of this character; hence, a particular truth known by actual observation or authentic testimony, as opposed to what is merely inferred, or to a conjecture or fiction; a datum of experience, as distinguished from the conclusions that may be based upon it.

So, essentially we start with an unproven idea, we corroborate it with facts (=experimental data) and we define our theory accordingly to facts.

So, why don't we say that evolution is true or that it is a dogma or that it is a fact?

Well, that is not how science work. Evolution is a scientific theory, and it always will be. Maybe (hopefully, dare I say) in 50 years from now new evidence will have make us change the theory of evolution, at least some bits of it.
Luckily evolutionary biology is not stuck at the time of Darwin and genetics is not stuck at the time of Mendel. Many new pieces of evidence have made us improve the theories that they initially defined.

Does that mean they were bad scientist or that they experiments were faked? Not at all!  Simply as their knowledge was more restricted than ours, they could not formulate a more advanced theory. Mendel's experiments still hold true, but now we know that transmissions of characters is not as simple. He was just looking at a special case. And his experiments still fit in our current theory, and will have to fit in any future one.

A scientific theory is defined by its falsifiability, that is

  the trait of a statement, hypothesis, or theory whereby it could be shown to be false if some conceivable observation were true. In this sense, falsify is synonymous with nullify, meaning not "to commit fraud" but "show to be false".

The famous black swan example by Karl Popper (see e.g. Conjectures and refutations, 1963, chapter 11.6), can be exemplified by (source: Wikipedia):

  One notices a white swan. From this one can conclude:
      At least one swan is white.
  From this, one may wish to conjecture:
      All swans are white.
  It is impractical to observe all the swans in the world to verify that they are all white.

  Even so, the statement all swans are white is testable by being falsifiable. For, if in testing many swans, the researcher finds a single black swan, then the statement all swans are white would be falsified by the counterexample of the single black swan.

So, our theory of the white swan is accepted as "temporary true", as long as a black swan is not found. Obviously the more white swans we count (i.e. the more experimental evidence we have), the stronger our theory will be. But it will never be true.

I would like to finish quoting Richard Feynman:

  It is scientific only to say what is more likely and what less likely, and not to be proving all the time the possible and impossible.

and

  We never are right, we can only be sure we're wrong

I suggest to watch the full video of his fantastic lecture on scientific method on YouTube.


Is there any difference between fascia and skin ?Are both the different names of the same thing?

The superficial fascia is the lowermost layer of the skin found in nearly all parts of the body and it usually blends with the reticular region of the dermis. But that doesn't mean it's a part of the dermis. The subcutaneous tissue/hypodermis/superficial fascia is NOT part of the skin but lies beneath the  dermis of the skin. Therefore, it can't be used as an alternative name for the skin.


Are there genes in sex chromosomes that determine facial features?

Yes, having a Y chromosome does cause specific alterations to facial structure.

The Y chromosome doesn't contain much actual genetic information. Most of the information needed to activate the male developmental program (the female one is the default) is in just one gene 'SRT', the other genes on the Y chromosome aren't super important, such that you can get a normal looking (but infertile) man if this gene is transferred onto an X chromosome.

This SRT acts as a switch causing various changes, but one of the most important ones is the higher production of testosterone. Testosterone (and some other hormones called  'androgens' cause changes to a lot of things, and one of them is facial morphology. In fact weirdly, the bones in the face retain the capacity to grow in adults, so you can give someone hormone treatment and their facial structure will change (google this and you'll clearly see the difference in people's facial shape after hormone therapy for sex change procedures - especially around the jaw). There is also some correlation, in both sexes, between the amount of testosterone in someones blood and the 'manliness' of their face.

Your teenage friends are currently undergoing a natural process similar to artificial hormone treatment, and their faces will get more and more male looking as puberty goes on.


Calculation of Malthusian fertility and mortality from birth and death rates

If every member of the population breeds, the mean number of children born from a single individual during their whole life is $\beta$ times the duration of their life. The mean life duration is $1/\mu$. Hence the total fertility rate in the homogenous model you suggest is $$\frac\beta\mu$$ If only some proportion $p$ of the population can breed, the total fertility rate of each breeding individual is $$\frac\beta{p\mu}$$


Can viruses stabilize and increase the shelf life of wine and other foods?

There is at least one bacteriophage ("phage") that targets bacteria that spoil wine:

  The Gluconobacter phage GC1 is a novel member of the Tectiviridae family isolated from a juice sample collected during dry white wine making. The bacteriophage infects Gluconobacter cerinus, an acetic acid bacterium which represents a spoilage microorganism during wine making, mainly because it is able to produce ethyl alcohol and transform it into acetic acid.

This particular linked paper does not say anything about usage of bacteriophages as a food preservative or for food safety, but there is interest in using bacteriophages for this general application, as an alternative to the use of antibiotics in food production.

Phages are everywhere. Craig Venter went out on his yacht and scooped up a bunch for one of his papers. Phage therapy may end up augmenting or replacing antibiotics, which would be good for us humans as many disease-causing bacteria have developed or are developing resistance to them.


Cacao and products made from cacao contain a number of bioactive compounds. As far as the subjective sensation of a "buzz", there are three related alkaloids present in cacao that may account for this effect. Theobromine is present in the highest concentration, but is probably less potent of a stimulant. It's not well researched. Theophylline has a number of effects, and is well studied. It has CNS stimulant effects, with a similar mechanism of action to caffeine, as a competitive antagonist at adenosine receptors. Caffeine is also present in cacao. The stimulant effects of caffeine are known generally, but if you'd like to read more about the pharmacology this is a good review.


Does one parent transmit more DNA to the offspring than the other one?

SHORT ANSWER

The two parents transmit the same amount of genetic material to their offspring ....or almost

LONG ANSWER

Nuclear versus Cytoplasmic DNA

All Eukaryotes (everything that is neither a Bacteria nor an Archeabacteria) have nuclear and cytoplasmic DNA. Most of the DNA is nuclear DNA. As its name indicates, nuclear DNA is found in the nucleus. The cytoplasmic DNA is found in the cytoplasm, that is, outside of the nucleus. More specifically, in all eukaryotes, cytoplasmic DNA can be found in the mitochondrion. In plants (which are eukaryotes), you can find cytoplasmic DNA in the mitochondrion and in the plastids (including the chloroplasts (plastids active in photosynthesis)). See here for more information about the origin of the organelles (≈ organ of a cell) who carry DNA.

Nuclear and cytoplasmic DNA doesn't have the same mode of inheritance.

Inheritance of Nuclear Genes

In the diploid (see ploidy) phase (phase during which each individual carries two copies of each gene), an individual carries one copy from his/her mother and one from his/her father.

The above sentence assumes that a diploid phase exists (which is not the case of all species) and that genders (male vs female) exist which is by far not the case of each species. It also assumes that we are talking about autosomes (non-sexual chromosomes, see below for sexual chromosomes). These assumptions hold for humans for example. Note that the diploid phase is much longer in human than the haploid phase (spermatozoid, ovule). We say that humans are diplontic. Some species are haplontic (longer haploid phase) and some are haplo-diplontic. See life-cycle for more info.

In short: Inheritance of nuclear genes is bi-parental, each offspring necessarily carry one copy of a given gene from his/her father and the other copy from his/her mother.

Note: there are some exceptions to this perfect bi-parental transmission (see segregation distorter and intra-genomic conflict). Also, have a look at the short section on sexual chromosomes below.

Inheritance of Cytoplasmic Genes

There are many exceptions to what I am about to write...

Globally speaking, offspring inherit cytoplasmic DNA for their mothers only. That means that your mitochondrion is those of your mother only. Therefore, mothers transmit slightly more genes than fathers because of the concern of cytoplasmic genes.

To complete the picture...

Inheritance of Sexual Chromosomes (Nuclear DNA)

Not all sexual species have sex chromosomes but some do. In these species, it is not rare that one of the two sexual chromosomes is shorter than the other (In mammals, the $Y$ chromosome is shorter than the $X$ chromosome). In such a case, the male transmits slightly less DNA to their male offspring than to their female offspring. Also, in such case, fathers transmit less DNA to their male offspring than do mothers but males transmit as much DNA to their female offspring than do mothers.

The evolution of sex chromosomes is a very interesting subject as well and you will find tons of information on this website or on different sites.

Non-genetic inheritance

Nutrient in eggs

Not only genes are transmitted. Parents also transmit proteins and nutrients in the egg. Females transmit more nutrients to their offspring than males.

Epigenetic

Not only genes are transmitted. Parents also transmit modifications on the DNA that are not modifications in the DNA sequence per se. These modifications are called "epigenetic modifications". Not all species can produce epigenetic modifications. In species who can transmit epigenetic modifications, both males and females can produce them. It is possible that in some species mother have a higher variance in the modifications that they transmit than males (or vice-versa) but I am not aware of such things.

Environment and Cultural transmission

Not only genes are transmitted. Parents also offer an environment in which the offspring grow. Some species typically feed or protect their offsprings. Depending on the species males or females may have more influence on the environment experienced by the offsprings. Finally, in some species (human, chimps and orca for example) a set of traditions (culture) are transmitted to the offsprings from the parents. And depending on the species the father or the mother may have more influence in the culture transmitted to the offspring.

Length of chromosomes may differ between two randomly sampled individuals

Not all variants between two chromosomes in a population is caused by substitutions of one nucleotide by another. Some variation is due to deletions of nucleotides or insertions of nucleotides. You can even a very long piece of DNA who get inserted, duplicated or deleted. Therefore between two given individuals, the exact amount of DNA that is transmitted may also differ only because they happen to have different variants. However, this is not a systematic difference in the quantity of DNA that is transmitted by one sex or another unlike the other cases presented above.


Why are sea dwelling mammals less aggressive than land dwelling mammals?

More encounters on land

There are more land animals that meet humans walking around than there are sea animals that meet humans swimming around. If fewer attacks happen on humans in the sea environment, it might just be because there are fewer encounters with marine mammals than with land mammals.

Greater species diversity on land

In your list used as example, you cherry-picked a few aggressive(-ish) land mammals but the vast majority of land mammals are not aggressive toward humans. The fact that there are no marine mammal that are aggressive toward humans might just be because there are too few fewer marine mammal species.

Pseudoreplication and phylogenetic signal

I would argue that your sample size is not as large as you might think. There are only four lineages of mammals that evolve to live in the seas. There is therefore a phylogenetic signal and ignoring it would be a problem of pseudo replication.

For example, I could very well think of territorial behaviour (which is where a lot of aggressive behaviour comes from) as having a strong phylogenetic signal.

Why considering only humans?

Your post title talks about aggressiveness in general and the content of your post talks about attacks against humans. It sounds that considering only attacks against humans to be very unfair. Orcas, typically, are fierce and violent predators although no orcas have ever attacked a human in the wild.

Are they really that friendly to humans?

There has been a number of attacks in captivity (well known cases with orcas). Also, there have been a number of whales attacks against boats (according to this BBC article).

In short...

In short, I think your comparison is unfair. I think you are looking for an explanation for a pattern that does not really exist.


Off course you can! Here are career paths for you as per my limited knowledge:

BioStats

There are lot of applications in this domain. For example in Microarray Gene Expression or Proteomics analysis (for example, this paper).

Bioinformatics

Sequence alignments use common techniques like Dynamic Programming, Probabilistic or Heuristic methods, etc.

Computational Biology

There are lot of applications like Lagrangian and Eulerian Mechanics (Computational Anatomy), Computational Phylogenetics (Computational Evolutionary Biology), etc.

Systems Biology - In Systems Biology, you can have applications in:

1-) Probability and Hypothesis Testing - usually used to find associations between genes (Ref: S. Krawetz (ed.), Bioinformatics for Systems Biology, DOI 10.1007/978-1-59745-440-7_8, Chapter 8)

2-) Stochastic Modelling of Biological Patterns - ODEs,PDEs (applied to lot of problems), Markov Chains, HMM, PSSM are common mathematical implementations in this domain.

3-) Population Genetics - uses Statistical models (for example Genetic Distance), exponential equations (for example, Cumulative Effect of Mutation)

P.S: Here are some tools you might be interested in:

1-) Bioconductor - one of the main reasons why R is preferred language by BioStatisticians.

2-) BioPython

Wish you best of luck with your career!


What mammal or creature dropped this? (Warning: Gross Pictures)

You can see a similar pile of bird poop seen below a barn swallow nest:

 Source: deepmuckbigrake

Alternatively, if it really did appear overnight, perhaps a pile pf pigeon poop was pushed out of a nesting area in the soffit?

 Source: Scranton Times Tribune

If it's pigeon poop, you might want to be careful.


In situation A) there is no mention of growth, so there is no reason to assume something is cultured. If we assume that in A) a germ plant arises, it is no tissue culture but a regularly bred plant. It is no tissue culture, because a seed is typically formed after pollination, which involves the recombination of parent genes to form reproductive cells (pollen) and the fusion of these reproductive cells after pollination. Because the definition of plant tissue culture is:

  "... a form of cloning in which the plants are all genetically the same - similar to taking cuttings." (quoted from: Royal botanical gardens, NSW, australia).

it follows that seedlings are not clones of their parents.

Situation B) therefore meets the criterion of tissue culture, as new tissue grows out of a single progenitor cell.

So the answer is: they are not 2 examples of tissue culture, the difference being that A) is the result of a normal breeding and B) meets the criteria of tissue culture.


How to calculate the geometric mean titer (GMT) of titers from a haemagglutination assay (influenza)?

Typically "<10" is converted to a number that is below the limit of detection; often "9".  After that simply following the instructions you have yields a GMT of 77.9.  If you are using spreadsheet apps such as Excel or Google Sheets, they almost certainly offer "GEOMEAN" functions which will give the number directly.


Which algorithm to find the evolutionary relation of 5 sequences?

If you work with protein coding sequence and on the DNA level their to divergent, then it is better to use the amino acid sequence for alignment and phylogenetic reconstruction.

Better sampling can also help you, for this you can check the online databases with BLAST to find similar sequences that would fill the gap.

The problem with sequences with low sequence similarity is that it is difficult to identify homologous positions/characters and all alignment based methods rely on the assumption that the aligned positions are homologous.

Finally, there are alignment-free algorithms as well. (https://en.wikipedia.org/wiki/Alignment-free_sequence_analysis)

In general about algorithms for phylogenetics:

Nowadays, journals usually require you to run maximum likelihood (ML) analysis or Bayesian analysis. Both of these methods are referred to as model based. The most common programs used for these are RAxML (ML) and MrBayes (Bayesian). Another common software is MEGA (Molecular Evolutionary Genetics Analysis), which can run different tree building algorithms.

Usually, for quick reference maximum parsimony or neighbour-joining trees are good. For publication a maximum likelihood tree is very useful, since it returns a single best tree. While Bayesian analysis and maximum parsimony return a collection of trees.

It is also helpful different algorithms and if all return similar trees than you can be more sure about the relationships.


Why are there only 6 molecules of water produced in the synthesis of the fatty acid, palmitate?

I found the answer in Voet & Voet yesterday.

At the end of the biosynthesis, the palmitate is bonded with the Acyl-Carrier Protein (ACP) and it takes an hydrolysis to separate it, hence the missing H2O.


Realtime PCR uses a fluorescent dye which binds to double-stranded DNA and thus allows to measure the growing amount of DNA by each cycle. The DNA added to the reaction also binds the fluorescent dye and makes some part of the fluorescent background. When the PCR reaction starts, it takes a while until enough DNA is synthesized to go over the background and to be able to reliable distinguish the signal from the noise. I think this becomes clearer, when you look at the image below (from the NIH):

The Ct is the point where the signal can be distinguished from the background when it enters the exponential grwoth phase. The no template control stays below this threshold.


Where does the lactate produced by tumors go?

Most of the lactate produced by tumors probably enters the circulation and is taken up by other tissues (like the Cori cycle, correct). There are several studies like this one measuring glucose uptake and lactate release by tumors in vivo, and it is clear that a substantial amount of lactate is released into the veins draining the tumor site.

Oxidation of lactate by neighboring cells within tumors has been reported as well, but I don't know of any quantitative data on exactly how much lactate this process can consume. But it seems unlikely that this can remove a major fraction of lactate produced by glycolytic tumors, since glycolysis produces lactate at a much higher rate than respiration consumes it (per ATP generated).

It's also true that tumors can accumulate lactate. Some tumors are poorly perfused, with "disorganized" blood vessels and blood flow, and then waste products may not be cleared away efficiently.

So yes, all of the above :)  There are large differences between individual tumors in all these parameters, so there is no generally valid answer I think.


Is the mutation rate in pseudogenes higher than in coding regions?

It is important to distinguish between the rate of mutation, which is a biochemical process, and the rate of fixation, which is a population process whereby an allele with a particular mutation becomes fixed (present in all individuals) in the population. Relaxed purifying selection, such as that experienced by genes undergoing pseudogenisation, affects the fixation rate of mutations because new variants are not being filtered from the population by purifying selection. The mutation rate itself is probably constant, unless some other factor is at play.

In response to comments, I will say this: if functional constraints on the gene are relaxed to the point where all mutations are selectively neutral, then the process of mutation and substitution can be modelled by neutral theory and the expected rate of substitution (or fixation) is the same as the rate of mutation. This rate is dependent on several factors - lineage, life history, etc., and the difference between this rate and the fixation rate for a given coding region is dependent on the severity of functional constraint on that region.


Those appear to be Daddy Longleg spiders, and they are known for forming spider clusters, which is considered as gregarious behavior. Quoting Wikipedia:

  Many species of harvestmen easily tolerate members of their own species, with aggregations of many individuals often found at protected sites near water. These aggregations may number 200 individuals in the Laniatores, and more than 70,000 in certain Eupnoi. Gregarious behavior is likely a strategy against climatic odds, but also against predators, combining the effect of scent secretions, and reducing the probability of any particular individual being eaten.


What's the difference between the *types* of tissue dissociation enzymes?

It’s years since I looked at a Sigma catalogue (before it became Sigma-Aldrich) but as I remember, these designations are arbitrary proprietary ones used by Sigma to distinguish different sources — the key point being that Sigma didn’t generally manufacture all of these themselves, but obtained the from third parties.

The other point to note is that these enzyme preparations were/are generally impure,  but to differing extents, so the type designations allowed you to re-order a particular preparation that worked, and also to specify the actual grade you used when you published so that other people could repeat your work. More expensive grades would, no doubt, also work in the sort of crude application you describe, but they would be a waste of money.

I thought the catalogues used to give you some information (organism/tissue at least), but, as I said, it’s been a long time (although be careful with your “way back to the ’90s”, young man).


You could decide to just insert the new clade next to some "closest" one ("closest" being defined in a clever way that remains to be devised), but it is possible that the result will be different from what you would obtain by reconstructing the phylogeny from scratch. The reason is that the information that the character combination in the new clade brings may alter the relationships between the other groups present in the data in a newly optimized phylogeny.

An example of application is that one typically wants to add more taxa in a phylogeny in oder to prevent long branch attraction.

As an aside remark: When one speaks of a "clade", one usually thinks of a bunch of terminal taxa (leafs of the tree): do you want to insert an whole bunch of taxa forming a monophyletic group, whose internal topology is already known, or just one terminal taxon?


How is a portion of DNA selected and unwound from nucleosome?

This answer will be a very broad overview and is based largely on information from the textbook "Molecular Biology of the Gene" by Watson et al. (which I highly recommend).

Nucleosomes are dynamic structures.

The interactions between DNA and histones are non-specific and dynamic. Regions of DNA can be transiently unwrapped from the nucleosome and thus recognized by DNA binding proteins. In fact, because of the non-specific nature of the interaction, DNA can slide relative to the histone core and expose different sections of DNA. This can be facilitated by nucleosome remodelling complexes which can also catalyze complete ejection of histone octamers to expose even more DNA.

Nucleosomes can be positioned specifically.

The association of DNA binding proteins with specific sequences can prevent or control nucleosome formation at specific loci and leave tracts of exposed DNA accessible to the transcription machinery. Additionally, certain DNA sequences that form bent helices are preferentially bound by nucleosomes.

Chromatin compaction is highly regulated.

Two broad classes of chromatin are present in the interphase nucleus: highly condensed, transcriptionally inactive heterochromatin and less condensed, transcriptionally active euchromatin. Chromatin compaction is regulated by post-translational modification of histone tails, and modifications such as acetylation and phosphorylation, especially of the N-terminal tails, can prevent higher order, repressive chromatin compaction. The specific pattern of histone modification is referred to as the histone code and certain modifications are associated with gene expression. These modifications can be recognized by remodelling complexes and even transcription factors.

Further Reading:

Becker PB, Workman JL. 2013. Nucleosome Remodeling and Epigenetics. Cold Spring Harb Perspect Biol 5(9):a017905.


Short answer
I think the whitish color is due to the outer layer of nerve bundles: the epineurium. This surrounds all nerves, whether they contain myelinated fibers, unmyelinated fibers, or both.

Background
Nerves are bundles of axons (Fig. 1). Whether the axons are myelinated or not, the gross anatomy is similar; axons within a nerve are bundled into fascicles and surrounded by perineurium. Those fascicles are again bundled up and surrounded by epineurium. It is this epineurium that you probably are seeing and it has a whitish appearance (Fig. 2).

The surface of a nerve therefore does not contain myelin; myelin is present around individual axons and is not exposed. Hence, whether a nerve contains myelinated axons, unmyelinated ones, or both will not determine its outward appearance.

Fig. 1. Anatomy of a nerve bundle. source: EasyNoteCards

Macroscopic view of a nerve targeted for epineurial repair. source: wikipedia


Does pouring water on your skin affect the evaporation process and heat loss?

Drenching your head and face with cool water will both directly cool your skin (because cool water is colder than you) and contribute to evaporative cooling. Your skin doesn't care if the water that evaporates comes from sweat you made, the pool, a water bottle or a hose.

The Khan Academy video is a good review of the principle.


Is it possible to create DNA of a species that could be any animal

Suppose genome A generates organism oA and genome B generates organism oB. Their phenotypes pA and pB are quite different from each other.

Because genome A and B are not similar enough, organism oA and oB cannot sexually produce viable offspring.

Your question seems to boil down to: "Would it be possible to generate oA/pA and oB/pB from genome A, or a genome similar enough to genome A such that it can still sexually reproduce with genome A?"

So you basically ask whether any genome A could simultaneously produce pA and pB under different external conditions.

Answer: Possibly? The genes involved in the development of organisms typically don't respond to external stimuli but to genes which were active before them (in time). Various genes produce proteins which sense temperature, osmotic pressure or particular chemical species or ions. If those were factored into very early developmental programs, feeding into transcription factors to modify gene expression according to external factors, the same genome could produce drastically different organisms.

To speculate more about this yourself, it would probably help to go away from a code-based understanding of DNA and think more about what it is physically and biologically. Unlike computer programs, DNA "programs" can modify themselves and other programs or the functions they execute.

Biologically, DNA is an information carrier that is transcribed into RNA, which can have functions of its own and/or be translated into proteins. DNA interacts very tightly (physically) with a lot of RNA and protein components, and most things that happen in cells and tissues around them end up modifying the way DNA is handled in some way. Keywords that you could look up are "gene expression", "gene regulation" and "developmental biology".