Attempt at an answer

I think it is a water strider. There are 1700 species of water strider. Some of them are easy to eliminate (the marine ones typically) but I am not really able to give you more info from your picture.

To make sure, it is a water strider, can you please tell us
- How long are the legs (hard to tell form the picture)?
- If it was alive, was it standing on water? What can you tell us about its behaviour?

What insects live in the water?

If it is a stream insect, it could be...

a mosquito larvea
a mayfly larvea
a odonate (dragonfly or damselfly) larvea
a water strider

Here are my thoughts for each of them

a mosquito larvea

No, mosquito larvea don't any limbs

a mayfly larvea

I can't see the long cerci

a odonate (dragonfly or damselfly) larvea

Again I can't see the cerci
Also, although, it is often hard to see, it does not appear to have a fancy detachable mouth piece.

a water strider

We can't tell the length of the limbs from the picture. Were they really long?
If it was alive, was it standing on the water?


The classification usually applies to the experimental conditions. Are the experimental conditions applied to an organism, or to a less than whole organism (cells culture --> all the way to test tube chemistry reactions)?

This is somewhat subjective, but in your case, since the experimental conditions are drying time of the pretty much whole organism (the tomato), I would call it an in-vivo experiment.

Think of it this way, if you treat animals with X and examine Y, this is an in-vivo experiment regardless of whether you are isolating proteins, DNA, RNA etc... to examine afterward to characterize the change in Y.

Now if you isolated cells first from mice and plated them to grow in cell-culture, and then treated with X to examine the same endpoint, this has become more ex-vivo.

In-vitro would be to isolate a single enzyme from mouse cells, put into a test tube, and examine its ability to reduce some substrate after X treatment.

In your case, if you isolated enzymes from tomatoes and then used them in a test-tube to reduce some agent and measure activity before and after a given treatment, this would be more ex-vivo and have gone all the way to in-vitro.

EDITED: Matt pointed out I had confused in-vitro and ex-vivo on my continuum and he was correct.


Does body fat percentage effect storage of fat soluble compounds?

Generally, yes.

Phenytoin, an anti-seizure drug, provides a good and well studied example.  The key issue here is that, for phenytoin, plasma half-life is proportional to the apparent volume of distribution of the drug.

(Apparent) volume of distribution is a pharmacokinetic property of a drug. It is the volume a drug would need to be dissolved in in order to achieve the concentration of the drug in plasma. For fat soluble compounds, this can be quite large, as the drug is primarily partitioned into fatty tissues, leaving a low concentration in plasma. Empirically, phenytoin's volume of distribution is higher for more obese patients, and (by the same reference), the half-life is proportionally longer.

As is often the case, though, it depends on the drug. For some lipid soluble drugs, an increased rate of metabolism by the liver in obesity compensates for the increased volume of distribution; for others, obesity doesn't have that much of an impact on volume of distribution in the first place.


What do you call clearly different sub-groups within a species?

In eusocial insects, especially ants and bees, these groups are called "castes" (see e.g. Hölldobler & Wilson, 1990. This is the same term that is used for social stratifications in some human societies e.g. in India.

One definition of caste is:

  ...the physical or the behavioural/physiological phenotype of a eusocial individual, or both.

(from Hölldobler & Wilson, see also antwiki.org)

Some division of labour as well as collective rearing of young can occur in prosocial animals as well, but there the term caste is not used.


Adult butterflies don't eat! I mean.... not in the sense of chewing on food. They rather drink. They get their nutrients via ingestion of liquid substances. Their mouth consists of a long tube called a proboscis that acts as a straw.

What do butterflies feed on?

The vast majority of butterflies eat nectar from flowers. Many species are quite specialized and feed on the nectar of a few species only.

There are a few exceptions though. Some species feed on tree sap, dung, mud (see mud-puddling), pollen, or rotting fruit. Butterflies are attracted to sodium and may as well try to feed on human sweat but I doubt there exist any species would get a non-negligible source of nutrients from human sweat. Coming to exceptions, you should definitely consider reading @DmitryGrigoryev's answer as well.

What do caterpillars feed on?

Of course, you are probably aware that butterflies have a complex (-ish) life cycle. The larva is called a caterpillar, while the adult is called a butterfly. So what do caterpillars eat?

Caterpillars have mandibles, so they can chew tissues and not just drink. Most caterpillars eat leaves and other plants parts. Again, many species are specialized to only a few plant species.

There are of course exceptions. For example in the Phengaris genus, (such as the famous large blue (Phengaris arion), caterpillars live in ant colonies and mimic the larvae of these ants. Some of them are able to trick the ants into feeding them as though they were ant larvae (e.g. Phengaris alcon, Phengaris rebeli). Others (e.g. the aforementioned Phengaris arion) will act as predators and eat the real ant larvae!

When the butterflies emerge from their cocoons after metamorphosis, the ants finally figure out the trickery and start attacking the butterfly. The butterfly has therefore very little time to try to fly away from the colony before getting killed. It is a critical life stage for individuals of this species.

How to feed a butterfly?

This section exists thanks to @Rodrigo's recommendation.

As a substitute of nectar one can simply use sugar water. The optimal sugar concentration (in mass-mass) is around 35% (Kim et al. 2011) although it likely varies among species.

Kim et al. 2011 explains that what limits optimal sugar concentration for insects is the viscosity of the solution. Too much sugar renders the solution too viscous and difficult to forage on. Interestingly, the ability to drink viscous solutions depends upon the drinking technic (active suction, capillary suction or viscous dipping) which vary, not among butterflies but among insects. The article is interesting.


Can you be infected by two coronaviruses at once?

Yes:

Coinfections involving multiple HCoVs were also detected (Table 2).
...

Human Coronaviruses HCoV-NL63 and HCoV-HKU1 in Hospitalized Children with Acute Respiratory Infections in Beijing, China, Advances in Virology (2011)


Why does getting certain chemicals in cuts hurt?

Shampoo contains surfactants, chemicals which cause lipids to emulsify. The cell membrane is composed primarily of phospholipids, which are vulnerable to action by surfactants. In fact, sodium dodecyl sulphate (SDS, often labelled SLS on shampoo bottles), an integral component of many shampoos is also used in the lab (albeit at substantially higher concentration) to achieve cell lysis.

The outer layer of skin is composed largely of a very tough type of cells called keratinocytes, which form an impenetrable barrier to potentially harmful chemicals like surfactants. Once the skin is ruptured, the surfactant can act on cells that don't have the protection of keratin, causing damage to cell membranes, and perhaps even cell death. This will obviously lead to an immune response and inflammation, which is likely to be the source of the burning sensation/pain that one feels.

The inflammatory process involves various immune system-related mediators such as bradykinin and prostaglandins, which act to increase the sensitivity of neurons to pain.

With other chemicals that cause a burning sensation, the mechanism of cell injury might be different, but ultimately, the immune mechanisms kick in, causing inflammation and pain.

Kid & Urban (2001) reviews the processes that cause inflammatory pain in great detail (full text is available for free).


Why are certain cells more likely to be attacked in autoimmune conditions?

Autoimmune reactions each have their target antigens. They'll "attack" wherever those antigens are expressed. In the case of Type 1 diabetes, many specific antigens have been identified, and they all correspond to regions on the surface of pancreatic islet β cells. Ultimately, however, the immune reaction is targeting proinsulin and its processed product insulin, which are produced by solely by β cells. This is an interesting review covering the topic.


Why is the blood thick in Wet Cupping / Hijama

We had a demonstration of blood coagulation/clotting in a biology lesson with the school nurse. She just took half a test-tube of blood sample from a class pupil and we waited a moment, and the blood became a solid lump inside the test-tube.
The process is there to protect you from leaking blood if you cut yourself, the process uses fibers and platelets and complex proteins.
https://www.youtube.com/results?search_query=blood+clotting
wiki: Coagulation
Blood letting is a very ancient practice that used all sorts of methods like annelids/leeches, which has not been proven to have any benefits. The blood in your body does not seperate into good blood and bad blood by sitting in a jar.


Modern understanding Darwin's "correlation of variation"

One must not confound a phenotypic variance-covariance matrix (usually called $P$) and a genetic variance-covariance matrix (usually called $G$) for a set of phenotypes. The mutational variance-covariance matrix is also a common concept (usually called $M$). There are a lot of papers on the evolution of the G-matrix (and related matrices).

In the abstract of Roff (2000), you can find the equuation

$$\Delta\bar z = GP^{-1}-S$$

, where $\Delta\bar z$ is the vector of mean responses, $G$ (often just called the G matrix) is the matrix of additive genetic variances and covariances, $P$ is the matrix of phenotypic variances and covariances and $S$ is the vector of selection differentials.

You will find much more by just googling "evolution of G-matrix"


Can an organism exist as a single cell but come together as multi-cellular during certain times?

Welcome to Biology StackExchange.

  Am I remembering this incorrectly?

No, you're remembering it correctly.

I think you're talking about slime molds. You'll find more information on the wiki page

Is this the video you saw? These images are pretty cool.

  Is this even possible?

Yes (given that it exists). There is no way to correctly answer this question as it really is an open-ended question. But here are a few words that may push you writing further posts.

Just a few words on the evolution of altruism

The main interest behind this life-cycle is that not all individuals reproduce. Some individuals form the stalk while others go through meiosis (see below on the life-cycle).

How unfair does it seem to those who form the stalk! Why would those individuals forming the stalk spend energy to help other individuals to reproduce?

Kin selection

Let's think about us, vertebrates, "real multicellular" organisms. The cell that is in your eye is never going to reproduce. Although it is spending all its energy into helping your ovules/spermatozoids to fuse. Why would this cell in the eye make such an effort? The genes in the spermatozoids/ovules are essentially the same as those in the "eye cell". Therefore, by helping your spermatozoids/ovules the eye cell is actually contributing to spreading copies of the genes that it is carrying. This is referred to as kin selection.

Slime molds and altruism

Now, the story is not exactly the same for the slime molds. The cells in the stalk can be quite different from those that are undergoing meiosis. Altruism can exist in a variety of different mechanisms and it would take several books to go over the literature about the evolution of altruism. Without knowing the literature specific to the slime molds reproduction, I just want to notice that the cell in the stalk will die anyway, whether or not it spend energy helping other cells reproducing. There is, therefore, no fitness cost into construction a stalk. Little population structure (causing higher relatedness within deme than among demes) could be enough to allow this behaviour to evolve.

Just a paper (that I haven't read) on the subject

Hudson et al. 2002

Genetics of the fruiting body

Interestingly, similar genes are being used in Dictyostelium discoideum (slime mold) to create this fruiting body than what is used in multicellular eukaryotes (ref.). Thanks to @Tim Cutts for this info.


What happens to the language processing brain part if no language is ever learned?

Although this specific experiment wouldn't be done, similar experiments have been done in experiments in animal models where a sensory input is removed/altered. These experiments show that if you remove some sort of sensory input, the parts of the brain originally responding to that input will take on other tasks. There have been many studies that show this, but the canonical reference is often this one, where the part of the brain previously responding to sensory input to a finger instead responds to stimulation of another finger after the original finger is amputated:

Merzenich, M. M., Nelson, R. J., Stryker, M. P., Cynader, M. S., Schoppmann, A., & Zook, J. M. (1984). Somatosensory cortical map changes following digit amputation in adult monkeys. Journal of comparative neurology, 224(4), 591-605.

There have also been studies of humans with sensory deficits like blindness or deafness that show similar reorganization, depending on the age the deficit is acquired. For examples, see:

Finney, E. M., Fine, I., & Dobkins, K. R. (2001). Visual stimuli activate auditory cortex in the deaf. Nature neuroscience, 4(12), 1171-1173.

Kujala, T., Huotilainen, M., Sinkkonen, J., Ahonen, A. I., Alho, K., Hämälä, M. S., ... & Salonen, O. (1995). Visual cortex activation in blind humans during sound discrimination. Neuroscience letters, 183(1), 143-146.

In summary, the result is that the neocortex is a very flexible, adaptable structure, and if inputs of a certain type are impoverished, that region of the cortex is used for other purposes. Essentially, neighboring functions creep in to that space.

Language processing in humans includes both auditory areas that respond to the sounds made by language, and premotor processing areas that seem to be important both for understanding the semantic content of language and for producing verbal output. None of these areas are truly language-unique, though, they are just regions that are active more than other areas when language-based tasks are occurring. In a person not exposed to a language, it's likely they would develop some rudimentary language-based skills anyways unless they were truly raised in some sort of sensory deprivation context - at this point an answer would get too far into speculation. Besides that, those areas would probably be re-purposed for other types of sensory processing and other types of motor planning.


Here's an article I found that seems to attempt to address this question, using a kind of machine-learning approach involving "Long Short-Term Memory" (LSTM)-Recurrent Neural Networks (RNN), to classify EEG from participants who were watching either "easy" or "difficult" online lectures - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620019/ .

It's not a complete account of their process, but the manuscript suggests that gamma-1 frequency bands in the frontal lobe (using a single EEG electrode) were the most valuable feature for distinguishing between trials in which participants were thrown into the middle of a challenging lecture, vs. trials in which participants were viewing the introductory background material at the beginning of the lecture. I'm interested in the same question as the one you proposed, so I hope to see more responses to your post!


Can mRNA be used by ribosomes more than once?

There are a few cases in translation that I can think of where an mRNA is translated more than once: the closed loop model of mRNA translation, translation reinitiation, and translation by polysomes.

Closed-loop model

Here's an interesting paper to get you started: ncbi

Essentially, the theory is that mRNA can form a closed loop with the 3' end held to the 5' end by various factors. The ribosome assembles near the start, runs through the mRNA, translating the polypeptide sequence, then dissociates at the STOP codon. Since the "end" of the mRNA is near the "start" of the mRNA, the ribosome can reassemble soon after dissociation.

Translation reinitiation

See this.

The ribosome dissociates incompletely at the STOP codon, the small subunit keeps moving on the mRNA, then the large subunit reattaches at a downstream start site. This happens when the mRNA has multiple ORFs.

Polysomes

(See the wikipedia article on Polysomes for more details)

This basically means that you have a ribosome train moving along an mRNA. The same protein is being translated multiple times, but by different ribosomes. One really cool thing about this is that it's actually been observed by electron microscopy!

(source: bioninja.com.au)

To answer the 2nd part of your question...
wikipedia

mRNA gets degraded in a process called RNA interference (RNAi). Small interfering RNAs (siRNAs) are also transcribed that are incorporated into a ribonucleoprotein complex (RISC) that has an mRNA cleaving activity. The siRNAs are complementary to segments of mRNAs in order to give specificity to RISC.


The human skin is indeed made off a number of different layers, the three most important are epidermis, dermis and hypodermis (also called subcutaneous fat), see the figure (from here) for details:

All three layers can be subcategorized further, I'll only give a few details here. More can be found for example in the Wikipedia article on skin.

Epidermis: Top layer of our skin, is covered with the stratum corneum, which consists of several layers of dead cells, which protect the layers below. New cells of the epidermis are made at the border between dermis and epidermis and travel upwards (actually the top layers are worn off). The epidermis is the place where the pigmentation takes place due to melanocytes embedded in the keratinocytes of the epidermis.

Dermis: The next layer is the dermis where a lot of important functions on the skin happen. Sweat and oil are produced in the dermis. The feeling of the skin is also mediated in the dermis where the ends of the nerves are embedded. The hair roots of the hairs of the skin are also located here as well as the blood capillaries which supply the skin.

Hypodermis or Subcutaneous fat: The last layer is the hypodermis. It attaches the dermis to the underlaying muscles and bones and houses bigger blood vessels and nerves which go up into the dermis. The fat layer is also important for controlling the body temperature and storing fat reserves.


Where in the nervous system are synapses chemical, and where are they electrical?

Synapses are almost all chemical, the electrical synapses are more of a "special case".

The speed of transmission across limbs, etc, has very little to do with the speed of the actual synapse. The signal itself is conducted electrically inside a given cell (this is an "action potential"), aided in many cases by insulating myelination. The synapse is just the endpoint.

Some places where electrical synapses/gap junctions are present are:

Between cardiomyocytes, to synchronize heart contraction
Between certain networks of inhibitory interneurons in the CNS
In some (but not nearly all) reflex circuits


Do leaves grow larger by adding cells at the centre or at the edge?

Plant leaves develop from leaf primordium or meristem tissue (this tissue has special properties that allow it to continue dividing to make more more cells, i.e. stem cells - not stem cells like cells in the stem but the technical term 'stem cells). Because of the hormone balances to maintain this division property the meristem tissue will remain close to the stem or branch of the plant at the base of the leaf whilst the new cells added to the leaf slowly move outwards.
https://www.sciencedirect.com/science/article/pii/S1369526616300929


Is urban beekeeeping harmful or are there good practices to follow?

Beekeeping in urban areas often require that beekeepers supplement their colonies with feed since urban areas have, on average, very little forage available to sustain a colony year-round. There are usually very little in terms of wildlife (or wild pollinators) when it comes to urban settings. In contrast, suburban areas would have more to offer as there are often backyard gardens and unmanicured lawns that could provide food throughout the season.
The wild pollinators within suburban to rural areas are probably under the biggest threat from managed colonies, but the impact is also usually very difficult to assess. Even with the limited range of managed colonies forage (around 5km), there's usually not enough of the colonies stretched out across a wide area in such big numbers that it would out-compete with other wild pollinators. The wild pollinators are often solitary, with much greater foraging capacity. As such, they would just move away from any competing resource if they're unable to defend it themselves until the threat subsides.
Regardless of the location (urban, suburban or rural), best practices still include protecting your colonies against diseases and pests. If you don't you may end up losing your colony, or spreading diseases to other colonies or wild pollinators. Probably the most significant threat nowadays globally (except for Australia) would be Varroa Destructor. So, best practices here would include keeping on top of these mite loads to avoid it from spreading and/or overrunning your colony.
As reference, here is a visual capture of the article:


Short answer would be yes. There are very simple examples such as responses to sudden bright lights controlled in the Trigeminal nerve bundle to constrict pupils. Visual reflexes are interesting because it can frequently involve a neuron crossover in the nerve bundle. This would be an inappropriate reflex due to a stimuli. The most common being suddenly being exposed to a bright light causing you to sneeze like pepper was thrown in your face. Also interestingly this is an autosomal dominant trait so one of your parents will have to have the same response for you to inherite it.
Photic sneeze response


Interchromosomic vs Intrachromosomic Recombinations

The prefix inter- means "between two or more", and the prefix intra- means "within one".

So interchromosomal recombination means recombination between two different chromosomes (for example, it normally and often occurs between each homologous paternal and maternal chromosome pair during the Prophase I stage of meiosis).

Intrachromosomal recombination would mean recombination within a single chromosome.


There are two common ways to generate a scale bar:

Measure it.  You can take a picture of an object with known spacing such as a grid target and then measure the size of each pixel.
Compute it.  If you know the magnification of your objective, and the magnification of any relay optics after the object but before your camera, you can compute the total optical magnification.  Then using the pixel size on your camera, you can get the actual pixel size.  For example, suppose you have a camera with 7.4 micron pixels, a 20x objective, and a 0.5x adapter lens before your camera, then you would have a pixel size in your image of 7.4/20/0.5 = 0.74 microns.


It is a Lepisma saccharina or silverfish.

It is rather common and yes, it's harmless.


How is deviated nasal septum related to cold

Nasal septum deviation is a condition where the cartilage which divides the nasal cavity into two nasal passages isn't centrally aligned, making one of the nostrils smaller and thus obstructed. Now, in our nose we have something called mucociliary clearance and that is the mechanism getting rid of unwanted particles and pathogens that get into contact with the mucous membranes in the nose.

Studies show that in individuals with a deviated septum the nasal mucociliary clearance time is slower than in individuals whose nasal passages are symmetrical. From this information one can conclude that the particles and pathogens that you inhale are getting to spend more time inside your nasal passages, thus giving the pathogens a better chance at striving and giving you sinusitis.

By looking at the information above you could think that the connection between nasal septum deviation and chronic sinusitis is clear. This literary review however states that the correlation between a deviated nasal septum and having chronic sinusitis is still unclear.


What does 'direction' mean in the statement "mutations are non-directional"?

(I give an explanation to the statements, please understand that almost all  evolutionary changes are mutational in the basis).

Let's say the greater height is advantageous in one area, while in other area the smaller height is advantageous. In the former area, the direction of phenotypic changes will be to the individual with higher height, while in the latter the direction will be to smallest one. The evolution "seeks" example to follow, so you "can" find which one was an example to move towards to (who is the reference point).

In the case of mutations the is no apparent direction. These chaotic changes can be advantageous, or may be not - one cannot find a particular direction towards some "example" / reference model.


What really causes the toxicity of wrongly-thawed meat?

This is a really fascinating question and got me reading stuff all through the night. If my response seems tl;dr, then please skip to the fourth paragraph.

From what I've found in literature, it may be the case that prolonged exposition to certain temperature ranges may prove lethal to some pathogens. Shortening this time or shifting the temperature may cause suboptimal death rate of microbes. El-Kest et al. have found that Listeria monocytogenes would be most effectively killed by 5 to 6 freeze-thaw cycles with 35 degrees C as the thawing temperature and -18 degrees as the freezing temperature. Freezing at -198 degrees proved way less successful in killing the bacteria. This suggests that not only the thawing temperature and rate have the influence on microbial diversity in meat but also the actual temperature of storage!
Here is the link to the publication by El-Kest et al.: http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-55.8.639?code=fopr-site

Freezing rate also has a significant influence. If freezing occurs slowly, ice crystals will mostly appear mainly outside cells with rapid freezing having the exact opposite effect. It is quite logical why it happens: spots within the food that are freezing will slowly make the unfrozen surroundings rich in ions and osmotically active substances, the water will gradually seep out from bacterial cells to the surroundings and subsequently freeze up. (https://books.google.pl/books?id=o6kJCAAAQBAJ&pg=PA25&lpg=PA25&dq=Inactivation+by+cold.+In+Inhibition+and+Inactivation+o+f+Vegetative+Microbes.&source=bl&ots=zlH-dMFiqo&sig=AfglM7piuvMnjI3q3JV0ovHy-FE&hl=pl&sa=X&ved=0ahUKEwjS-6fAypTYAhWiJJoKHe-gDJAQ6AEIQTAE#v=onepage&q=Inactivation%20by%20cold.%20In%20Inhibition%20and%20Inactivation%20o%20f%20Vegetative%20Microbes.&f=false)
From that perspective slow freezing is more likely to get microorganisms killed, as there is no cold-shock response and the cells do not become desiccated prior to freezing.

Now, let's look at the big question: why can't we use warm water to thaw meat. As one of the commenters pointed out, there is something called "danger zone" in frozen food safety, in fact USDA keeps talking about it all the time. This might be counterintuitive but by rapidly increasing the temperature in outer layers of meat, you will quickly provide microbes with ideal conditions for cellular division. As time progresses each next layer will be infested by bacteria from the outer layer as well as those that will just start undergoing cellular division, and so on, and so on, until you reach the very center. You end up with a pretty nice bunch of bacteria throughout your meal, though you shouldn't probably worry to much about it, unless you like your meat half-raw.

What happens during cold-water thaw or refrigerator thaw is different because you essentially increase the temperature of each consecutive layer but without providing enough thermal energy to give microbes a near-optimal temperature for intensive cellular division. Sure, they will start dividing anyway but to a much lesser degree. The temperature increase is not rapid therefore there is no abrupt resumption of life-cycles of microbes. Think of it as waking up on a cold winter day vs. warm, pleasant summer morning.

Still, you can use hot-water thaw safely if you're dealing with thin cuts of meat, if fact USDA approves it: http://onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2010.02037.x/full

Further reading:

https://www.fsis.usda.gov/shared/PDF/Big_Thaw.pdf
https://link.springer.com/content/pdf/10.1007/978-1-4615-5975-7_10.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662152/

Now, regarding your second question, I'll mostly answer from my own experience. We used to test meat in our microbiology lab during studies and we tested different kinds of meat. Teachers who teach the subject for 10+ years, when asked, admitted that there is generally a pattern of how many bacteria and what types of bacteria populate different kinds of meat, so there is no safe way to say that there is a single major pathogen that is responsible for food poisoning from meat in general. I'd say what's most dangerous are exotoxins produced by those bacteria, e.g. botulinum toxin is the most potent toxin known to mankind and Clostridium botulinum loves to populate meat stored at room temperature. Listeria is a popular example because of its great survivability in cold temperatures. But it really depends on the kind of meat and even on the specific batch of meat. You simply never know what you'll get with it.

Either way, you were not just overanalyzing the topic. There are really many factors to the quality of food preparation safety, especially when it comes to meat. To summarize:

Hot-water thaw can be used for thin slices of meat (I still use it for bigger slices as well, but only if I'm certain I'll fry the meat very thoroughly)
Cold-water thaw is better due to lower probability of serious bacterial infestation, especially recommended for thicker slices of meat
Freezing as well as thawing rate both influence meat quality
Freezing temperature cannot be too low, nor too high to ensure optimal death count of certain species of bacteria
Meat toxicity is generally caused by pathogenic bacteria that multiplied within or were previously present (e.g. due to improper meat handling by the producer), in most cases due to the toxins produced by the bacteria

Hope I helped a bit :)

[EDIT]
There was a request in the comments to include some more info about the toxins produced by food-borne pathogens. There's a good review here:
https://www.ncbi.nlm.nih.gov/pubmed/8750662 (not sure if paywalled though, I'm using library internet right now). You could group those toxins into 4 arbitrarily defined groups:

heat-liable enterotoxins – these generally can be destroyed in the process of cooking or frying; produced by Salmonella spp., E. coli, Campylobacter spp., Vibrio cholerae (yes, this one causes cholera)
heat-stable enterotoxins – these cannot be efficiently removed by heat preparation of food; produced by Yersinia enterolytica and some strains of E. coli
Shiga-Like toxins – they resemble verotoxin of Shiga spp.; produced by E. coli O157:H7 (this strain is very pesky, as it induces hemorrhagic diarrhea and kidney failure)
Unique toxins – some bacteria produce unique toxins, e.g. Bacillus cereus, Clostridium botulinum, Clostridium perfringens

Generally E. coli strains have many subtypes of heat-stable as well as heat-liable enterotoxins and some strains have other types of toxins like the O157:H7. The name "enterotoxins" refers to toxins that are secreted by microorganisms targeting intestines and generally they are cytotoxic, which essentially means they cause cell lysis of the host. Mechanisms of action are varying, e.g. cholera toxin triggers a cascade of reactions that overdrive CFTR channels (chloride ion transporters) and alters osmotic balance, which macroscopically manifests itself by a production of characteristic watery stool.

Worth noticing: some of those pathogens require other factors to cause disease, e.g. Vibrio cholerae requires a toxin-coregulated pilus to be pathogenic and some even do not produce any toxins directly (for instance Listeria monocytogenes overdrives lysosomes and doesn't let them take the bacterium apart, then it spreads from cell to cell by the means of actin filaments).

In the context of detox diets, there is a large dispute going on about their effectiveness whatsoever. I'd recommend confronting these two articles, which, to me are well written:
https://link.springer.com/chapter/10.1007/978-3-319-49929-1_33
http://onlinelibrary.wiley.com/doi/10.1111/jhn.12286/full
Some animal models have indeed shown some anti-toxic effects of certain foods, other researchers argue that most of the toxins eventually get to the liver and get broken down. The liver does its job pretty well, so running for two weeks on a "kale juice" would be a bad idea. People seem to forget that usually the dose is the poison: if you ingest highly diluted cyanide, it won't harm you, while drinking 7-8 liters of water at once could kill. Switching to an unbalanced, monotonous diet could be actually detrimental to health a lot more than those minuscule amounts of food-borne toxins ingested. The best way to live a healthy life is still: move, eat well and diverse, follow food safety guidelines, take care of your physical and mental health.


Is there a name for the use of sunlight in metabolic processes?

Photometabolism or photocatalysis would be apt terms and the former would specifically refer to biochemical reactions.

Photometabolism is also used in the context of the light dependent conversion of 7-dehydrocholesterol to Vitamin-D.

A google scholar search with photometabolism returns many peer-reviewed articles that have used this term. Some examples:

Photometabolism of 7-dehydrocholesterol to previtamin D3 in skin.
The photometabolism of glucose by an hydrogen-adapted alga
Photometabolism of Heterocyclic Aromatic Compounds by Rhodopseudomonas palustris OU 11.


What is the biological basis for tiredness after eating?

High carbohydrate meals will undoubtedly increase the relative levels of insulin, increase the shuttling of glucose from the blood to the cells, and leave you fatigued in wake of that. See reactive hypoglycemia. Reducing carbohydrate consumption should, to some level, reduce this effect. Caffeine should just as likely increase blood glucose levels by increasing glycogenolysis through PKA activation.

As Chris Stronks pointed out, eating can cause low blood pressure via redistribution of blood.


That is a moth, (Lepidoptera), in the family Pterophoridae. It looks very much like Stenodacma wahlbergi.  https://en.wikipedia.org/wiki/Stenodacma_wahlbergi


Range of dry matter yield per kg CO2 of different plant species

A plant contains about 50% of it's mass absorbed from the air, from CO2 which it converts with 45% efficiency. 40-45% CO2 fixation/respiration seems to be optimal for all plants, it's the balance of how much their cells need aerobic respiration day and night, compared to photosynthesis. That 50% absorbed from the air is fixed with H2O which provides most of the other 50%, and the rest is ashes.

According to this research:
The CO2 captured by plants is the result of the differences between
atmospheric CO2 absorbed during the process of photosynthesis and the CO2
released by the atmosphere during respiration. This difference is converted into
biomass and tends to fluctuate between 45 and 50% of the plant’s dry weight.
(the research states dry weight C measurements, they don't seem to measure CO2 absorption directly)

So it's better to search for "photosynthesis respiration ratio" to find research that measures the efficiency of the CO2 absorption:

the ratio of respiration and photosynthesis (R : P) was relatively constant, 0·40–0·45, and independent of temperature. This was consistent with earlier work by Ryle et al. (1976) [...] Some mechanistic understanding of the constancy of R : P was provided by Atkin et al. (2005), who found that respiration and photosynthesis in most examined plant species acclimated similarly after temperature change. More recently, Atkin et al. (2007) confirmed homeostasis of R : P, in Plantago spp., but this was not maintained when plants were subjected to higher temperatures than usually experienced in their habitats. Differences between photosynthetic and respiratory acclimation to temperature have been reported by Campbell et al. (2007) and Hartley et al. (2006). Cheng et al. (2000) found that the R : P of sunflower was also insensitive to changes in atmospheric CO2 concentration. Overall, the research confirms Monteith's (1981) assessment that the ratio may vary over short time periods but is constant over periods of weeks and longer.

That document has lots of research references and technical words and concepts to follow up.

It's good also to see google images for R P ratio graphs and tests.
https://www.researchgate.net/publication/263676467/figure/fig1/AS:278855131648023@1443495652845/Figure-3-Bottom-curve-simulated-10-d-running-average-leaf-respirationphotosynthesis.png

The conversion ratio is visible here, day is white, respiration is black.
https://www.researchgate.net/profile/James_Bunce/publication/43291524/figure/fig1/AS:273738792960009@1442275822297/Figure-4-The-ratio-of-average-night-time-respiration-rate-R-to-average-day-time.png


The explanation one of my tutors offered was this:

In cell recognition, it is very common for interactions between proteins to be based on weak interactions, but a certain degree of binding can trigger a (conformational) change which will instead establish a very strong interaction between the proteins involved.

In other words, if the contact is specific enough to 'count as a recognised pathogen', the interactions will immediately change to strong forces and the pathogen will not be able to move away.


What animal classes has also "Like Humans" XY Chromosomes for Males and XX for Females?

In mammals, Y chromosome determines the sex. SRY gene present on Y chromosome is responsible for sex determination. And, in absence of this gene results in female sex. Non-human mammals use several genes on the Y chromosome.

Platypus and Drosophila also uses XY sex determination system, but in different way. Like in platypus, combination of genes present on XY chromosome are used to determine sex characteristics. And in drosophila, two X chromosome gives female characteristics, and Y chromosome determines maleness.

Reference:
https://en.wikipedia.org/wiki/XY_sex-determination_system


Short answer
Valerian preparations contain many compounds, but it is not known which may be responsible for its sedative effects. It is likely that there is no single active compound and that valerian's effects result from multiple constituents acting independently or synergistically (source: NIH). Overall, I think it is safe to say that valerian's sedative properties are related to its GABAergic properties (Yuan, 2004).

Background
The constituents of the volatile oil obtained from the rhizomes (underground stems), and stolons (horizontal stems) of Valeriana spec are variable due to  the variability in genetic make-up and environmental factors impinging on the batch of plants used (source: NIH).

The major constituents include the monoterpene bornyl acetate and a variety of sesquiterpenes including valerenic acid.

Some of the sesquiterpenes have been shown to have a direct action on the amygdala, which is a brain structure in the limbic system. The amygdala is responsible for feelings of fear and anxiety. Valerenic acid has been shown to inhibit the breakdown of GABA in the brain, resulting in sedation. GABA is the principal inhibitory neurotransmitter in the nervous system.

The non-volatile monoterpenes known as valepotriates possess sedative activity, but their mode of action is not clearly known. The valepotriates themselves act as prodrugs, and are transformed into homobaldrinal which has sedative properties.

Extracts of valerian roots contain substantial amounts of GABA which could directly cause sedation. However, whether GABA reaches the central nervous system is debated.

Another compound present in extracts is a lignan, hydroxypinoresinol, and it binds to benzodiazepine receptors, which are GABAA receptors and the target of benzodiazepines, i.e. tranquilizers and sedatives (Houghton, 1999).

References
- Houghton, J Pharm Pharmacol (1999); 51: 505-12
- Yuan et al., Anesth Analg (2004); 98(2): 353-8


When you look at a certain mass of cells (in a petri dish, a tumor, whatever) which are in principle viable, growth can go in both directions. It can be poitive which means that the number of cells is growing over time.

It can also be negative, which results in a declining number of cells over time. We see this effect in cell growth assays, when we analyze the effect of certain treatments to our cells. Since we want to "kill" our cells with the treatment, a positive growth would indicate an unsuccessful treatment, a negative cell growth a positive treatment effect.


is left brachiochephalic vein and left pulmonary artery is same?

No, they are not the same.  The left brachiocephalic vein receives de-oxygenated blood from the left subclavian vein (draining the left arm) and the left internal jugular vein (draining the brain and parts of the face).  The brachiocephalic vein then joins with the superior vena cava which flows into the right atrium.

The left pulmonary artery carries the deoxygenated blood that has just passed through the right atrium and ventricle, through the pulmonary trunk to the left lung for oxygenation.

In the foetal circulation, the ductus arteroisus (before it closes into the ligamentum arteriosum) allows blood to bypass the lungs, which are not oxygenated in the uterus!

Please see this diagram (which shows the foetal circulation including PDA for you).  The left brachiocephalic vein is circled in yellow, whilst the left pulmonary artery is circled in green.

Image from public domain edition of Gray's.


The sequences you have posted seem to be (protein) amino acid sequences. The stop codon are present in DNA sequences and in mRNA sequences.

In DNA, the bases are A, G, C and T; stop codons are TAG, TGA and TAA.
In RNA, the bases are A, G, C and U; stop codons are UAG, UGA and UAA.
In DNA and RNA, other letters are used to specify degeneracy.

What you have here looks like protein sequences. So, there are no stop codons in sequences you have posted.


Why is it difficult to bend the waist while keeping the knees straight?

First off, I would be careful generalizing people's experiences with this exercise (..."Try it...You'll have trouble long before you reach 90 degrees"...):

Source: Yoga Tune Up

The muscles you are feeling at 90o, and the lady pictured above perhaps not even at 180o are the hamstrings. They run along the back of your thigh, attaching at both the hip and the knee. They flex the knee and extend (straighten) the hips.

Source: Precision Nutrition

When you do the exercise you are describing, the pelvis starts pulling on the hamstrings from the top because your knees are staying in place. Bending the knees releases the stretch.


Difference between inbreeding and interbreeding

You are basically correct. Most common usage in my experience:

Inbreeding refers to sexual reproduction between genetically closely related individuals, within a species. Inbreeding will increase the relatedness between individuals in a population.

Interbreeding refers to reproduction with another species (or race), and is often used as a synonym to crossbreeding or hybridization (when referring to hybrid offspring from two different species/races/breeds, not DNA hybridization). This is also how 'Interbreeding' is defined in the Oxford English Dictionary. However, 'Interbreeding' is sometimes used just to signify that two individuals can breed and have viable offspring ("...these two individuals can interbreed..."), and under this usage this can also include/overlap with inbreeding.

The latter usage can be seen in the Species article in Encyclopædia Britannica, online:

  Species, in biology, classification comprising related organisms that share common characteristics and are capable of interbreeding.
  ...
  Interbreeding only within the species is of great importance for evolution in that individuals of one species share a common gene pool that members of other species do not.


How much tissue is required to do RNA-seq analysis on a single organism?

Our DNA core wants 1.5 ug of RNA.  I find that I can obtain that amount from a standard Trizol prep from about 1 mg of Arabidopsis floral tissue.  I usually double or triple what I harvest to account for random variation in yield.


How is the effective dose calculated when only part of the body is irradiated?

Not sure that I understood your question correctly.

The concept of "effective dose" was specially introduced to provide a mechanism for assessing the radiation detriment from partial body irradiations in terms of data derived from whole body irradiations. The effective dose is the mean absorbed dose from a uniform whole-body irradiation that results in the same total radiation detriment as from the nonuniform, partial-body irradiation in question.

What is probably misleading you is the sum of the weighting factors to be 1. This is because we try to liken the partial body irradiation and the whole-body irradiation and the weighting factors represent the relative tissue sensitivity and susceptibility to the radiation. Your radiation should not go over all possible tissues and organs, you just assume the irradiation to be zero at them that cancels their summands so that they can be ignored in the final calculation. In other words, it is absolutely fine (and it is even so "by design") to have only some of the WT*HT factors in your formula.


What does ΔC and ΔN mean with regards to a protein sequence?

The Frat/GBP (frequently rearranged in T-cell lymphomas/GSK-3-binding protein) protein is a proto-oncogene that regulates the Wnt signalling pathway. (van Amerongen et al., 2004)
The cited paper (Franca-Koh, 2002) noted a correlation between some forms of Frat and GSK3 cellular localization. Without Frat, GSK3 is cytoplasmic. In the presence of Frat, the heterodimer Frat-GSK3 translocates to the nucleus. As Frat is phosphorylated, it was unclear then what mechanism(s) was(were) involved. To investigate the role of Frat, the authors hypothesized that a region of Frat may be involved, not necessarily the whole protein.
They engineered deletion constructs and added an N-terminal FLAG tag for easy affinity purification. They used the symbol delta (Δ) for deletion. The N-terminal region of residues 1 – 129 encompassing Domain 1, i.e. deletion of the C-terminal region is called ΔC; likewise, the C-terminal region of residues 129-274 encompassing Domain 2, i.e. deletion of the N-terminus is called ΔN. They also engineered a green fluorescent protein (GFP) tag fusion protein variant. Here are their constructs as illustrated on Figure 1 of their paper:

Human ortholog
I aligned the residue sequence of the murine Frat with the human orthologs: it has 79% identity to human Frat1 and 68% identity to human Frat2. mFrat residues 1 – 129 (ΔC) and 129 – 274 (ΔN) correspond to hFrat1 residues 1 – 132 and 132 – 279, respectively.
Added Note
Here is a co-crystal structure of GSK3β (N-terminal lobe in orange and C-terminal lobe in cyan) complexed with Frat1 peptide 197-226 (forest green) and an inhibitor (N-(6-(3,4-dihydroxyphenyl)-1H-pyrazolo[3,4-b]pyridin-3-yl)acetamide) (green) as deposited with RCSB as entry 5OY4.pdb . The presence of the inhibitor helps locate the active site in the image of the GSK3b protein kinase.

References
Franca-Koh, J., Yeo, M., Fraser, E., Young, N. and Dale, T.C. (2002) J. Biol. Chem. 277:43844-43848.
Van Amerongen, R., van der Gulfen, H., Bleeker, F., Jonkers, J. and Berns, A. (2004) J. Biol. Chem. 279:26967-26974.


Are the sympathetic and parasympathetic nervous systems exact opposites?

The Autonomic Nervous System is composed of the sympathetic and parasympathetic nervous systems. Each are dominant under different conditions - both are always active but one is dominant.
An important way to understand the the autonomic nervous system is in considering the effects of pharmaceutical drugs.
Sympathomimetic drugs enhance adrenergic function.
Sympatholytic drugs interrupt adrenergic function.
Parasympathomimetic drugs enhance cholinergic effects.
Anticholinergic drugs inhibit cholinergic effects.
For example:
Muscarinic antagonists are parasympatholytic (Anticholinergic) drugs - which reduce the effects of parasympathetic system.
But it is not that simple. They also increase sympathetic tone.
But again it is not always that simple. E.g. for sympathomimetic drugs (enhance adrenergic function) - there is no parasympathetic nervous system effect.
To answer your question, the sympathetic and parasympathetic nervous systems oppose each other sometimes. It depends on which receptors are activated and where.
(E.g.Alpha 1 receptors, Alpha 2 receptors, Beta 1 receptors & Beta 2 receptors).
Source & further reading on pharmaceutical interventions
Source & further reading on receptors


I found this review from 1999.  From the abstract:

  It is concluded that DNA-DNA interactions cannot bridge the distances between homologous chromosomes in the nucleus, and it is suggested that protein chains are formed between homologous segments. These attach to homologous chains emanating from homologous sequences in other chromosomes, and the chains move along each other until the homologous DNA sequences meet.

For more recent publications, you can search the citing articles here.


Is breathing a reflex action or is it an intrinsic process?

While the ultimate purpose of breathing could be considered to be the maintainance of a balance of the substances you are referring to (such as blood oxygen, carbon dioxide, and hydrogen ions), the blood levels of these substances do not directly control the production of action potentials within the motor neurons that promote the contraction of the diaphragm and intercostal muscles.

The propagation of these action potentials is initiated by signals from the medullary respiratory center, specifically the neurons in the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). In the VRG, a complex of neurons known pre-Bötzinger complex is responsible for generating the signals that cause the rhythmic muscle contractions involved in breathing:

  The respiratory rhythm generator is located in the pre-Bötzinger complex of neurons in the upper part of the VRG. This rhythm generator appears to be composed of pacemaker cells and a complex neural network that, acting together, set the basal respiratory rate.

Vanders Physiology, p473, 15th ed.

So breathing is indeed, as you mention, a process that is controlled by innate neuronal activity but regulated by the concentrations of PO2, PCO2, and H+ concentrations. I recommend you read pages 473 to 477 of Vanders Physiology, which explains these controls in detail, some of which do involve reflexes, say, if O2 concentration in the blood strays too low.

Interestingly, expiration, which is typically a result of actions potentials ceasing and respiratory muscles relaxing, can be controlled by a reflex, known as the Hering-Breuer reflex, during strenuous exercise when the lung is inflated by a large tidal volume. Stretch receptors in the airway in this case are activated, causing the inhibition of inspiratory neurons in the DRG.

Source: Vanders Physiology, 15th ed, section 13.9: "Control of Respiration"


Why are superantigens not "MHC-restricted", and what's the significance?

Normal, "non-super" antigens activate T-cells in the following manner: they are first engulfed and processed by a professional antigen presenting cell (APC), e.g., a macrophage. The processed antigen is then presented along with an MHC class II molecule on the surface of this cell. The T-cell's T Cell Receptor (TCR) then binds this complex; it must be able to recognize both the MHC class II and the antigen, and in addition to this "main signal" other co-simulatory signals are also needed. The important thing to remember is that a T-cell will only react to a specific antigen it's specific with when it's present with an MHC class II molecule it can recognize. This is known as MHC restriction

A person has 3 genes (each having 2 alleles,for a total of 6 alleles) for MHC class I: HLA A, B and C, and 3 genes for MHC class II: HLA DR, DQ and DP. These alleles are highly polymorphic, i.e., varied, with each of these 6 genes having hundreds or thousands of different alleles, and the combination of alleles differs from individual to individual; it's very unlikely that two people who aren't identical twins would have the same combination of HLA alleles.

MHC molecules can only bind peptides, and in addition, they cant bind ALL peptides; of all the peptides that can possibly be bound by an MHC molecule, a particular MHC molecule can only bind a select number of those peptides. Different MHC molecular forms, be they class I or II, can bind, and thus present, a different set of peptides. Having different HLA alleles at your immune system's disposal means there's a larger pool of possible peptides your APCs can present with the different MHC class II isoforms they have, allowing defense against a larger pool of antigens.

A normal antigen has 2 "restrictions" on its ability to activate a T-cell clone: it must be presented by an MHC class II isoform that can bind it, and it must be recognized by a T-cell with a compatible TCR.

Superantigens activate T-cells in an unconventional manner: They have a domain that binds to the TCR, though not at the usual antigen binding site, and a domain that binds to the MHC class II molecule, but not in the usual peptide-binding site these molecules possess. Since it binds outside of these regions that are specific to particular molecules, they're not restricted by the antigen specificity of the TCR nor are they restricted by the MHC class II isoform they're utilizing. Hence why, even if they do need MHC class II-positive cells to be able to activate a T-cell clone, they're not MHC-restricted.

Readings:

Immunobiology by Charles Janeway, Sections 5-13, 5-15 and 5-16.


Why AZT is selective towards HIV and doesn't impair human DNA replication?

Retroviruses depend on being able to convert their RNA genome into a DNA copy, and have a reverse transcriptase enzyme to do that. This unique activity is not found in human cells, allowing for potential antiviral therapy if a drug can be used to inhibit the reverse transcriptase while not affecting the human enzymes.

AZT is one such drug, by mimicking the nucleotide thymidine, it can it can act as a substrate for nucleotide kinases and become 5' phosphorylated. AZT is phosphorylated by host cell enzymes, specifically thymidine kinase, this means that the levels of AZT phosphates are similar between HIV infected and non-infected cells. Once the 5' triphosphate is formed, the drug is a substrate for the viral reverse transcriptase. If an AZT is incorporated into the DNA backbone, it terminates the DNA because the 3' OH is not available for further polymerization.

However, at high enough doses AZT can be toxic to healthy cells. One mechanism for toxicity is the depletion of thymidine, because AZT competes with thymidine for the kinase enzymes, but is phosphorylated at a slower rate. At high doses, >1mM, AZT can act as a substrate for human DNA polymerases. Thankfully, AZT is about 100 fold more selective for HIV reverse transcriptase than human DNA polymerase.

The mitochondrial DNA polymerase seems to be a little more sensitive to AZT than other human DNA polymerases. This can lead to toxicity in the heart, skeletal muscles, hepatocytes, or other cells that use a lot of mitochondria. This toxicity is generally reversible if doses are reduced.

For more information, read about other nucleotide analogs, such as acyclovir, ganciclovir, and others which work through similar mechanisms.


Are neurotransmitters part of the endocrine system?

Short answer
Synaptic signaling can be seen as a type of paracrine signaling, and is hence not an example of an endocrine system.

Background
Khan Academy has a nice accessible overview on this confusing topic:

Paracrine signaling
Signalling between nearby cells that are near one another van occur through the release of chemical messengers that diffuse through the intercellular space. This relatively short-distance communication is called paracrine signaling. Notable paracrine signaling occurs during development, where growth-hormone gradients regulate the differentiation of the various tissues.

Synaptic signaling
A unique type of paracrine signaling occurs between neuronal cells, namely synaptic signaling.

Autocrine signaling
Autocrine signaling refers to cell signaling to itself. Like paracrine signaling, autocrine signaling is important during development, but also in tumor metastasis.

Endocrine signaling
Communication over longer distances often occurs through the circulatory system is called endocrine signaling. Often it occurs through the release of hormones into the bloodstream. Hormones are produced and released by specialized cells and target cells in distant parts of the body. Endocrine glands include the thyroid, hypothalamus, and the pituitary, among others. For example, the pituitary in the brain releases growth hormone that affects growth and other functions throughout the body.

Juxtracrine signaling
Cells can also interact via direct contact. For instance, gap junctions in animals and plasmodesmata in plants allow for a direct communication between cells by forming tiny channels, allowing small compounds and ions to cross the cell's membrane to a neighboring cell. It occurs for instance in the brain.


Find the concentration of free receptors in a solution of 90% free ligand and 10% receptor-ligand complex, knowing only the value of kD

One big thing you're missing is units: Concentrations here must have concentration units - they can't be dimensionless numbers or percentages.

So one of the things you need to figure out is how to convert the percentages into concentration units. In this case, it's difficult to do directly, but we can apply a bit of algebra to figure it out. We're talking about 90% and 10% of the ligand in different forms, but we don't know anything about the total amount of ligand - that's alright, we'll just represent the total concentration of the ligand as $\ce{x mol \cdot l^{-1}}$. Therefore, we can now state that:

$$ \ce{ [L] = (0.9x) mol \cdot l^{-1}}$$
$$ \ce{ [RL] = (0.1x) mol \cdot l^{-1}}$$

Now the other bit of information we have is the equation for Kd:

$$\ce{ K_d = \frac{[R][L]}{[RL]} }$$

So we're looking for $\ce{[R]}$ (with associated concentration units!), and we know $\ce{ K_d }$, $\ce{[L]}$ and $\ce{[RL]}$ - or at least up to the unknown of $\ce{x}$. But, if you substitute the values you do know (including the factor of $\ce{x}$) into the equation and do some algebraic manipulation, I believe you'll find it doesn't actually matter what the value of $\ce{x}$ is - it should cancel out.

Note: If the value of $\ce{x}$ doesn't matter, why did I bother with the whole rigmarole of including it? Why didn't I just substitute 0.9 and 0.1 directly?

Well, the answer to that is my lead sentence - the concentrations in the equation should have (compatible) concentration units. If you don't have concentrations, you're using the equations incorrectly. (Look into the concept of dimensional analysis for a valuable way to help make sure you're doing many (but not all) calculations like this correctly.)

While for this specific problem things worked out nicely if you substitute the fractions/percentages directly, that's not a general solution. Depending on the exact setup of the problem, the $\ce{x}$s may or may not cancel cleanly. You may have to use some other equation/knowledge to put additional constraints on the value of $\ce{x}$. The only way to know that is to properly account for them from the start.


Is there a word for the length of time an animal stays with parents before going off on their own?

As you talk about bird, most of the terminology I am suggesting below comes from the ornithology literature.

Fledging period

Defined on wikipedia:

  Fledging is the stage in a volant animal's life between hatching or parturition and flight.

Nestling period

Defined in Kouba et al. (2015):

  In altricial birds, the nestling period is an important part of the breeding phase because the juveniles may spend quite a long time in the nest, with associated high energy costs for the parents.

Rearing period

See its usage in for examples Yuan et al. (1994) and Brickell et al. (2009)

Juvenile

While the term juvenile does not refer to a period of time, you can refer to this concept as the period while children are still juvenile. From dictionary.com

  a young bird in the stage when it has fledged, if altricial, or has replaced down of hatching, if precocial.


It's important to note that not all symbiotic relationships must be expressed in terms of a positive-negative (parasitism) or a positive-positive (mutualism) framework. I would guess that most tree epiphytes exist in a commensal framework with their host trees. That is, the epiphyte has a positive interaction (it gets somewhere to grow), and the host species has neither positive nor negative effects.


Sex (depending on how you define it), evolved very early (more than a billion years ago). Even species like yeast have a type of "sex" (see below).

Also, this doesn't mean there is necessarily a big difference between the two sexes.

The yeast Saccharomyces cerevisiae, for example, also has two "sexes", called mating types. One is called alpha and the other is called a. They can only mate if they have different mating types, so it is analogous in a way to mammalian sex. However, the genetic difference between these two types is tiny. There's a specific location in the genome that's called the MAT locus. This location can have either an alpha sequence or an a sequence, an that will determine the sex. The rest of the genome will be the same between sexes.

So it really doesn't seem like it is a huge evolutionary step to go from no sex to some simple version of sex.

See more details about yeast mating here.

Also see this wikipedia article on the evolution of sexual reproduction.


Contact Inhibition of Cell Division: Signaling Pathway

How does the mitotic entry machinery roughly respond to cell volume?

This is a broad question but luckily there is one article that addresses this precise question in detail. However, it is very likely that more discoveries are made on this topic in future.

Neurohr et al. (2019) have extensively studied the effect of cell volume on mitotic re-entry and cell cycle progression. They used Saccharamyces cerevesiae with temperature sensitive alleles of CDC28 to arrest the cells in G1 phase. At this stage high glucose concentration (2%) led to increase in cell volume compared to that of starved (0.1% glucose) or protein synthesis inhibited (2% glucose + cycloheximide) cells. Using this model they find that cytoplasmic dilution causes impairment of transcriptional regulation during cell cycle progression. This is because the transcription factors do not scale with cell size.

Read the paper for more details.

  What's a relatively straightforward downstream pathway (core
  elements), starting at the adherens junctions, that illustrates how
  cell-cell signalling gets the STOP signal to the mitotic entry
  machinery?

This is again a broad question if you expect all details. However, google scholar search on "contact inhibition pathway" suggests that the main downstream pathway is the Hippo signalling pathway.

Top hits on this topic:

Zeng, Qi, and Wanjin Hong. "The emerging role of the hippo pathway in cell contact inhibition, organ size control, and cancer development in mammals." Cancer cell 13.3 (2008): 188-192.
Kim, Nam-Gyun, et al. "E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components." PNAS 108.29 (2011): 11930-11935.
Gumbiner, Barry M., and Nam-Gyun Kim. "The Hippo-YAP signaling pathway and contact inhibition of growth." J Cell Sci 127.4 (2014): 709-717.


Bird Identification: New Delhi, April 2018

It looks like you're on the right track.  Here's a photo of a Jungle Babbler (Turdoides striata).  They are found on the Indian subcontinent.

Source: https://en.wikipedia.org/wiki/Jungle_babbler


Which organism built this 2 cm long sandy tube?

This is the nest of a Mud dauber, also known as Mud wasp. This was possibly made by a Black and Yellow Mud dauber based on the following information.

The nest of the black and yellow mud dauber is a simple, one-cell, urn-shaped nest. 1*

As for expecting something coming out of it? I doubt it, as the nests are sealed after depositing an egg.

After building a cell of the nest, the female wasp captures several spiders. The captured prey are stung and paralyzed before being placed in the nest (usually 6-15 per cell), and then a single egg is deposited on the prey within each cell. The wasp then seals the cell with a thick mud plug. 2*
Eventually, the hatching larva will eat the prey and emerge from the nest.


The spores (microspores or megaspores) in gymnosperms are haploid. The microspores came from the microsporocytes which are diploids cells of the sporophyte, divided via meiosis. So the haploid microspores do mitosis and form the male gametophytes (pollen grains), containing two male gametes (sperm cell) and a generative cell which will form the pollen tube.
The process conducting to female gametes in the ovule is very similar. A megasporocyte (diploid cell of the sporophyte) via two meiosis form four megaspores (haploid). Only one megaspore is functional (the others will degenerate) and do 3 consecutive mitosis to form eight nucleus with different functions, one of them is the egg cell (female gamete).
So the meiosis happens before the formation of the spores (actually it forms the spores) so they are haploid.
Source: R. F. Evert & S. E. Eichhorn "Raven Biology of Plants"


What do "e" "-" "C" and "E" mean in this output?

CCCEEE etc. are the secondary structural elements. In this case, the C refers to non-strand and non-helix regions i.e loop regions rather than a coiled region. The C or E usually refers to whether the residue is coiled (C) or part of a strand (E). H would be used to denote a helix, however, in the question, it appears that there are no helices. These letters are often different in different software: it's merely a point of semantics between different software.

e or - refers to if the amino acid at that position is exposed or not (- = buried).

For the method, here is the COBEpro paper, although it does seem very technical. The help page has more easily accessible information on the output.


What is the exact principle of capillary isotachophoresis?

Many of us are using isotachophoresis all the time without even realising it. The explanation that follows may not be exact, but I hope that it helps.

Firstly, think about a simple electrophoresis set-up - in agarose electrophoresis of DNA we have a uniformly distributed buffer such as Tris-borate. The current is carried by the borate ions and the DNA molecules run through the homogeneous electric field towards the anode. They separate by size because of the sieving effect of the agarose matrix.

Now let's think about what is happening in an SDS-PAGE separation (a Laemmli gel). Just to remind you:

The running (or reservoir)  buffer is Tris-glycine pH 8.3
The stacking gel is in Tris.HCl pH 6.8
The separating gel is in Tris.HCl pH 8.8

When the power supply is turned on, the glycinate ion in the top reservoir begins to move into the stacking gel. When it hits the zone of pH = 6.8 it is much closer to its pKa and so is now only weakly charged. Consequently it slows down. Meanwhile the chloride ions in the stacking gel have begun to move rapidly down through the stacking gel (towards the anode). This creates a discontinuous electric field: the chloride zone has a lower resistance than the glycinate zone so the field strength in the chloride zone is weaker than the field strength in the glycinate zone. This is a stable situation because the ions cannot stray into each other's zones: if a glycinate ion happens to diffuse forwards into the chloride zone it will experience a weaker field and slow down, whereas if a chloride ion diffuses back into the glycinate zone it will hit the stronger field and quickly move ahead again.

What about the SDS-protein complexes that were in the well? (I'll just refer to these as proteins from now on.) Their ionic properties lie between the glycinate and the chloride, and so they eventually end up moving through the stacking gel between the trailing zone of glycinate and the leading zone of chloride. Any protein that finds itself in the glycinate zone will move quickly forward (due to the higher field strength) and any protein that moves ahead by chance into the chloride zone will slow down due to the weak field strength, falling back into the protein zone. And in this way these zones move in a procession through the stacking gel, with the proteins being focussed into a very narrow region in the middle. The glycinate, the proteins and the chloride are all moving at the same speed, and so this is an example of isotachophoresis (isotacho- = "same speed"). The polyacrylamide gel matrix in the stacking gel has no separating function - its role is simply to stabilise against convective effects. The proteins can reach very high local concentrations in the stacking gel, and if you look carefully you will often see refractive effects as your sample runs through the stacking gel. In this way the protein sample is "applied" to the separating gel in a very tight band, perfect for achieving high resolution separation (bands broaden by diffusion in the separating gel so the tighter the bands ar eat the point of loading, the better the final result.)

Once the sample hits the separating gel, all of this breaks down: the pH is now 8.8 so the glycinate becomes strongly charged and zooms off ahead with the chloride through the gel, leaving the proteins to move more slowly due to the sieving effect of the polyacrylamide matrix.

It is possible to set up an isotachophoresis as described above in isolation. Individual proteins will have slightly different ionic properties and will line up in the region between the two buffer ions, allowing for their separation.


Is there any checked case of "involution"?

"Exactly the same" probably doesn't fly, just because there is so much possible variation, but for a fairly obvious example, consider birds.  Their ancestors evolved flight: some modern-day birds (ostriches, emus, kiwis, &c) have lost that ability, though their vestigal wings haven't re-evolved into legs.  But consider the evolutionary link between birds and theropod dinosaurs, and how many of those (e.g. T. rex) had vestigal forelimbs.

Another example would be dolphins and ichthyosaurs, which both independently "involved" from land-dwelling creatures back to a form that's similar to the ancestral fish.

But of course neither of these are really "involution" in the sense of reversing an evolutionary path.  They are cases of organisms exploring new evolutionary paths, where the environmental pressures (such as need for streamlining to move efficiently in water) cause them to resemble some ancestral form.


Do different people have the same number of mitochondria in comparable cell types?

".... The number and shape of mitochondria vary dramatically in different cell
types and can change in the same cell type under different physiological conditions, ranging from multiple spherical or cylindrically shaped organelles to a single organelle with a branched structure (a reticulum). The arrangement is controlled by the relative rates of mitochondrial division and fusion, which are regulated by dedicated GTPases that reside on mitochondrial membranes' In addition, the total organelle mass per cell can be regulated according to need.
For example, a large increase in mitochondria (as much as 5-10-fold) occurs
when a resting skeletal muscle is repeatedly stimulated to contract for a prolonged period."

Alberts, Bruce; Alexander Johnson; Julian Lewis; Martin Raff; Keith Roberts; Peter Walter, Molecular Biology of the Cell, 5th Edition.

As the Paragraph above explains, it can be assumed that due to different metabolism in different people, a specific number of mitochondria in the same cell types for different people may not be assumed.


He defines lineage selection as selection for traits which increase the fitness of a group of plasmids, rather than an individual plasmid with in a cell or a particular cell containing plasmids. He says that the unit of selection are "plasmid-host clades" : in other words the unit of selection is the group of closely related plasmids in separate cells. It is an example of a kin-selection though I haven't seen the specific terminology in widespread use. He likely doesn't use kin selection because the plasmids don't have well defined offspring, so he uses a broader term for kin--lineage. I might have preferred clade selection, but this term has its own baggage. I'm not sure (and neither is Paulsson) that kin selection is need to explain 'spitefully low loss' rates, since intra-cellular and inter-cellular selection both favor lower loss rates.


When did CRISPR/Cas9 evolve and what is the likelihood that a superior system for live cell genome editing has already evolved on earth since then?

Lots of interesting questions! Let me try to address a few of them as I don't think I am qualified to answer them all but hopefully I can get this thread started. I am a graduate student in the biophysical chemistry field and have been following a little bit of the Crispr Cas9 craze in the last couple of years. So I am not an expert on Cas9 by any means but I do find it interesting.

Many speculate that as long as their have been cellular life, viruses or some obligate parasites have existed as well. This stems from the idea that viruses perhaps are not "non-self" but rather are parts of the host that happen to become inanimate particles that escape the cell and then find another suitable host. Some viruses have co-evolved with the host, perhaps to prevent other viruses from invading its "home/birth mother". Again, much of this paragraph is just speculation, but it is likely that CRISPR systems, or an adaptive immune systems like it have existed as long as viruses/obligate parasites have.

Error rates, you can look at some of the papers that have come out recently but the idea is that there are a lot of error rates, especially if the RNA is constitutively transcribed from a plasmid. Some people have suggested delivering, not the plasmids for the guide RNAs and the Cas9 protein, but instead, the Cas9 protein complexed to the RNA itself. Other ways to control the amount you deliver to a cell include delivering the RNA for the Cas9 protein so it is eventually degraded. This avoids the complication of delivering DNA which can be transcribed multiple times potentially flooding your cell with cas9 protein or guide RNAs, increasing the likelihood of off target effects. Or you can have the cas9 protein and the guide RNA plasmids under inducible promoters, so you only get expression say if you introduce a small molecule to your cultured organism and limit the amount you deliver of it.

As to if there are other systems "superior" to it, and by superior you mean more efficient, and has less off targeting effects? Sure those things may very well exist, since we haven't sequenced the entire planet yet! All joking aside, maybe start looking around at research groups that do adaptive immunity in prokaryotes, you might find some interesting ideas...

VDJ is a very cool system that I know only a little about but this review might be worth checking out:

"Mechanism and Control of V(D)J Recombination versus ClassSwitch Recombination: Similarities and Differences", which can be found here.

Also recombination in meiotic versus mitotic replication is covered in this review: "Meiotic versus Mitotic Recombination: Two Different Routes for Double-Strand Break Repair", which is available here.

So to answer your question, I will have to defer to someone else!

My question to you is what is "advanced"? Life as we understand it has been evolving for about 3-4 billion years. "Advanced" suggests that one organism has evolved better or faster. I don't know if I would call anything more advanced per se, but maybe more complicated and more capable of rapidly adapting to new environmental pressures? Bacteria have us trumped if there were rapid changes to the environment, global warming, asteroids careening into the planet etc.

Estimating this probability requires knowing how large the entire sequence space of the Earth is, some have estimated 5-50 million eukaryotic species but depends on what metric you would use to define a new species. It is unknown for prokaryotes. My guess is that you have 100's of millions of different organisms that are capable of having some type of adaptive immune system that may be inherently different from CRISPR/Cas9 system but still use some similar elements, like nucleic acid complementation, as a mode of defending against obligate parasites. Then the questions are how many of those organisms have we sequenced and how many proteins do we have any idea how they function based on sequence similarities to other proteins? Or if we have directly characterized their 3D structure based on Cryogenic Transmission Electron Microscopy (Cryo EM), NMR or X-ray crystallography. So, I imagine we have just hit the tip of the iceberg in finding natural enzymes that can function as gene editing and gene locating tools. Plus, we may start designing our own enzymes like what Professor David Baker at UW works on. Huge ocean to go exploring, bring a molecular fishing pole :-)


How is color information transmitted from the eye to the brain?

Short answer
Color vision is mediated by spike rate modulation (frequency modulation if you like), as well as ganglion-cell specific stimulation.

Background
Ganglion cells exist that transmit opponent colors. The color opponency model predicts that we cannot perceive a greenish-red or yellowish blue, which is quite right. We can, however, see mixtures of the two channels, such as red and yellow (orange), and red and blue (purple).

Then opponent model predicts the existence of ganglion cells that are sensitive to red/green opponency and blue/yellow opponency (in trichromats like humans):

Indeed, it has been shown that these ganglion cells exist, i.e. cells that increase their firing in response to short-wavelength-sensitive (S+) and decrease their firing to middle-wavelength-sensitive (M-) and vice versa (Yin et al., 2009). Hence, it is not so that the frequency of light is represented in firing rate per se, but the frequencies of light are translated in spike rates, because spike rate is the only means in which neurons can transmit graded responses. In other words, every type of graded information is translated into spike rate eventually, including pressure differences, acoustic loudness etc.

Hence, as ganglion cells are sensitive to opponent pairs of colors, they do respond to particular colors. However, a "purple ganglion cell" does not exist, it is the combination of red and blue activations that lets us see colors due to synthetic processes in higher neural centers.

One ganglion cell can send different signals to the brain as it is basically an analogue converter of the red/green and yellow/blue opponent colors.

These inputs are sent to the thalamus (lateral geniculate nucleus) and higher visual cortices, where color-selective cells pick up the signals and integrate them for further processing. Here color mixtures are made to present the full gamut of colors as we know it:

Source: Dot-Color

Reference
- Yin et al. J Neurosci 2009;29:2706-24

Further reading
- Advantage of opponent color?


Breeding mosquitoes at lower temperature

Check "breeding temperature" and similar obscure phrases for the search.

There's a study on physical aspect of mosquitos bred in cold, they perhaps didn't note any significant metabolism change, you can read the articles, they mostly cover wing length scales and follicles.

There's a study on lave development speed which passes over breeding temps, it may however cover "egg temperature".


Why increasing the vector concentration does not increase the effeciency of bacterial transformation?

According to the Hanahan transformation protocol (one of the highest competencies published), a transformation of 200µl will contain $1×10^8 - 1.7×10^8$ cells.

Assuming that the pBR322 plasmid is used, 1ng of plasmid will convert to 0.36fmol of plasmid, or $6×10^8$ plasmid copies.

As we can clearly see, even at very low quantities of DNA used, there are multiple plasmids per cell. Since transformation is thought to be mediated by DNA channels, massively increasing the quantities of DNA would not equally increase transformation efficiency once all of these channels are saturated.

The example from NEB Turbo DH5α cells seems to show this quite well, that once DNA quantities exceed 1ng, the transformation efficiency drops precipitously.

This being said, if the amount of plasmids available is very large, there is no reason to avoid adding more than 1ng of DNA, as they would not reduce the total number of transformation colonies, but only the efficiency.


Difficulty in developing certain vaccines

Not an easy question, especially since the reasons for both pathogens are different.

For HIV the problems are manyfold:

Insufficient knowledge about required immunity

Its not known, which parameters are really important to raise an adequate immunity.

Variation in HIV strains

HIV has a very high mutation rate, which results in many different subtypes. This makes the virus extremely successful, but also causes problems for making vaccines. We have a similiar problem with vaccines for the flu, but there the number of subtypes is known and not very high. Still we need a new vaccine for each season based on the current viruses. For HIV there are no knwon proteins against which immunity can directed like in the case of the flu.
HIV also recombines very fast, so new variants can come up pretty fast.

HIV targets the immune system

The HI virus targets cells of the human immune system (namely CD4 T-cells) which are important for developing a proper response to a vaccination. These cells need to be stimulated, but on the other hand are destroyed and specially targeted by the virus.

Lack of an effective animal model

To develop and test good vaccines, scientists need good animal models to test the pathogen and see the effect of a treatment.
Chimpanzees show some response to HIV infections, but they are expensive to keep as laboratory animals and also rare to get. The problem is, that HIV is pretty good adapted to its human host.

Human subjects trials

This is more an ethic problem, but still needs to be adressed. To test the efficiency of new drugs, double-blinded placebo controlled test are done. Afterwards you can compare the placebo group to the treatment group and analyze the outcome. How do you do this with a deadly disease?
More information can be found on this webpage from the NIH.

For malaria some of the problems are similiar, others are different. he greatest problem was for years, that not enough money was available for research, which has been overcome only quite recently:

Plasmodium goes through different stages

The parasite causing malaria goes through three different stages in its development in the human body. With each step it hides again from the immune system. The different stages are also present in different cell types, see this image from JCI ("Advances and challenges in malaria vaccine development"):

antigen

Its not clear, against which antigens such a vaccine shoud be directed. This is due to the problem with the different stages and hasn't been found yet.

different pathogens

There are four forms of plasmodium which definitely cause malaria - : Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale and Plasmodium malariae. Newer results suggest, that Plasmodium knowlesi is also a pathogen for humans.

lack of animal models

More information can be found here.


Do the genes encoded by the nucleus for mitochondrial proteins have introns?

Nuclear genes for proteins destined for the mitochondrion can have
  introns…

…to the extent that other nuclear genes for that organism have introns.

For certain insects there is a database of such genes entitled MitoDrome, and if you click on D. melanogaster in the side panel on the home page of that site you get to a list of such genes for the eponymous fruit fly. You can inspect each one with the ‘view’ option, and the first few I looked at all had introns. Here is an example for one of the subunits of NADH-ubiquinone oxidoreductase, ND-18:

The subunits of this enzyme complex can be examined in other species, from which one can find that in Homo sapiens these nuclear genes also have introns. A related human gene is NDUFS4. Mutations in this gene have been described, at least one of which results in a genetic desease — Leigh syndrome. One of these mutations involves abberant splicing of the five exons of the gene (Lamont et al. Am J Med Genet Part A 173A:596–600).

The homologous gene in Saccharomyces cerevisiae, NDI1, does not have introns, like most other yeast genes.


Do all sources supply all sinks on a plant?

What you think about phloem is not correct, actually there are a lot of phloem which transport the photosynthetic. Although the overall pattern of transport in the phloem can be stated simply as source-to-sink movement, the specific pathways involved are often more complex. Not all sources supply all sinks on a plant; rather, certain sources preferentially supply specific sinks. In the case of herbaceous plants, such as sugar beet and soybean, the following generalizations can be made.

Proximity. The proximity of the source to the sink is a significant factor. The upper mature leaves on a plant usually provide photosynthetic to the growing shoot tip and young, immature leaves; the lower leaves supply predominantly the root system. Intermediate leaves export in both directions, bypassing the intervening mature leaves.
Development. The importance of various sinks may shift during plant development. Whereas the root and shoot
apices are usually the major sinks during vegetative growth, fruits generally become the dominant sinks during
reproductive development, particularly for adjacent and other nearby leaves.
Vascular connections. Source leaves preferentially supply sinks with which they have direct vascular connections. In the shoot system, for example, a given leaf is generally connected via the vascular system to other leaves directly above or below it on the stem. Such a vertical row of leaves is called an orthostichy. The number of internodes between leaves on the same orthostichy varies with the species.
Modification of translocation pathways. Interference with a translocation pathway by wounding or pruning can alter the patterns established by proximity and vascular connections that have been outlined here. In the absence of direct connections between source and sink, vascular interconnections, called anastomoses (singular anastomosis), can provide an alternative pathway. In sugar beet, for example, removing source leaves from one side of the plant can bring about cross-transfer of photosynthetic to young leaves (sink leaves) on the pruned side. Removal of the lower source leaves on a plant can force the upper source leaves to translocate materials to the roots, and removal of the upper source leaves can force lower source leaves to translocate materials to the upper parts of the plant.


The process is called endochondral ossification.

It is important to point out that not all bone is derived from cartilage. For example, when a bone is fractured and is healing, the new bone does not always come from cartilage, rather intramembranous ossification occurs. There are therefore multiple mechanisms at a microscopic level by which bone may form. Additionally, bone formation in the long bones is different to that in, for example, the flat bones of the skull.


How do penicillin resistant bacteria grow slower in the presence of penicillin?

Your hypothesis is incorrect.

You must be assuming that lactamase destroys the antibiotic with perfect efficiency. This is incorrect.

You must be assuming that the population will remain genetically stable. This is doubly incorrect. Firstly the penicillin will select highly resistant bacteria which suffer a greater fitness burden from expressing the lactamase. Second, in absence of penicillin, spontaneously arising mutants which suppress the lactamase are free to proliferate.

You must be assuming that carrying capacity is identical for Pen+ and Pen- media. Trivially, you claim your experiment disproves this, but the assumption is also baseless since this need not be the case.

Furthermore, your results are inconclusive. You lack crucial controls, such as putting the bacteria from the Pen+ into Pen- and vice versa to see if the growth difference is intrinsic. You have not only failed to provide the error of your measurements, but have failed to provide the quantitative measurements themselves, so we do not even know if the difference is statistically significant.

Lastly, there are several basic things which you could rightfully expect us to assume, but have nevertheless failed to provide. For instance, you do not say if the populations are clonal.


Can an enzyme be activated without allosteric inhibition or activation?

Apart from what Phototroph mentioned in their answer (competitive and non-competitive inhibition), an enzyme can be activated/inhibited via covalent modification of the protein (post-translational modification) such as phosphorylation by protein kinases (phosphorylation is the most common modification).


Clarifying distinction between genetic recombination , translocation. and transposition

Translocation is a mutation . Others are not necessarily .
By the way do not confuse those 3 terms with transversion and transition mutations.
Translocation refers to 2 concepts :

In protein localizing during/after transcription

wikipedia
article

A type of mutation in a chromosome

Chromosomal Translocation
(this is about the latter)

Translocation describes the relocation of a chromosomal segment to a
different position in the genome.

To some extent yes. Also It is a type of mutation . It does not happen normally and it is a result of malfunctioning proteins, mutagens etc. More importantly Translocation happens

a) between two nonhomologous chromosomes
b) between one chromosome and itself (it moves to a different locus
of the same chromosome)

See : Campbell biology 9th.ed.2011 Chapter 15 figure 15-14
you can say that
Translocation of DNA segments between homologous chromosomes has a specific name ("duplication"). Keep in mind that most of the times we do not consider a movement of DNA to a homologous DNA a "translocation" as noted above.
Recombination is a new combination of 2 DNA . Two DNA s become one. I believe the difference between Translocation and Recombination is that Translocation usually involves a huge amount of DNA (a lot of genes) compared to Recombintation ( probably not more than 10 genes or so)
I also agree with your statements on recombination. Here's more :

it usually describes a non-pathological process

Recombination happens in several ways. We have recombination resulted from DNA repair, recombination from Cross-over during meiosis, artificial lab DNA recombination (in vitro) and also recombination by some viruses during infection ( Recall Lysogenic cycles and retroviruses) or other vectors.
Therefore recombination CAN happen in pathologic and non-pathologic procedures.
See: Molecular Cell Biology Lodish et al 8th ed Section 5.6 "DNA repair and Recombination"
See T. L. Orr-Weaver and J. W. Szostak, 1985, Microbiol. Rev. 49:33.

Transposition:
essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements

Correct. Still I'm quite sure that we DO NOT use the term "Translocation" but instead "Recombination" for transposition.
a special case of Recombination which occurs as a result of transposase enzymes acting on mobile genetic elements.
Transposition involoves 2 or 3 genes and also it is not a type of mutation. So it is not a translocation.
See: Molecular Cell Biology Lodish et al 8th ed Section 8.3 "Transposable (Mobile) DNA Elements"


If by "simplest" you mean smallest genome, then according to Brock's Biology of Microrganisms (13th ed, p 319) the smallest autotroph is Aquifex aeolicus, a chemolithotroph bacterium. It's genome is 1.5M bases, about 1/3 of that of E.Coli, and was sequenced in 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9537320).

The genome is densely packed though and still carries some 1,500 open reading frames. The authors of the genome sequencing paper states that "metabolic flexibility seems to be reduced as a result of the limited genome size", which I guess is some evidence of "simplicity".


If hands are folded with both index fingers parallel, they will come closer and touch eventually?

The easy way to explai the first phenomenon is that at rest, your fingers - all of them - curl. Relax on your bed on your back. No matter what direction your hands face, they will curl inward as if loosely holding an egg. That's the anatominal position of the hands at rest, because the finger flexors are stronger than the extendors. So once you set the finfers up, you'll tire of keeping them extended, they'll start  to relax, and in doing so, will tough.

If I'm understanding the second example, that's because the flexor tendons for your fingers are actually in your forearm. Squeeze them and it shortens the tendons causing flexion.


Why do hair on head not get pilo-erected?

Piloerection of head hair does happen as often as it occurs elsewhere on the body, but head hair length tends to make it difficult to see. Close observation, especially with short hair, should make it visible.

Piloerection of head hair is something more commonly felt by the person it is happening to rather than seen by others (or in mirrors); when you get that "goose-bump" sensation across your scalp, that will be due to pilo-erection.

(PS added) I haven't provided citations - this is not a phenomena that has had much specific academic research and I have not found any stating it occurs - or stating it does not occur (except in association with balness) despite looking, but is almost universally experienced, often without close examination or reflection about what specifically happens.

Citing references for baldness resulting in absence of piloerection on the scalp is not quite the same as a reference specifically stating it happens, but ... Professor Rodney Sinclair, head of dermatology at the University of Melbourne says - “You can’t get goose bumps on the scalp when you go bald and you can’t regrow hairs either because the follicles can’t regenerate.” ( https://www.futurity.org/goose-bump-muscle-1324242-2/ ) ( https://link.springer.com/article/10.1007%2Fs12565-016-0359-5 )


Where does craniocaudal closure of anterior neuropore start?

Where is this second craniocaudal wave originating?

It begins in the prosencephalic region adjacent to the chiasmatic plate.

  Where is the final point of meeting (I suspect linea terminalis or anterior commissure) ?

Cranial linea terminalis represents the zone of closure of cranial neuropore.

  Could anyone post a picture or a reference to understand this visually (both waves of neurulation)?

Sources:

1: https://www.ncbi.nlm.nih.gov/pubmed/11948562

2: https://goo.gl/RLmQcj


What kind of owl does this moth look like?

First of all what a nice foto!

I think this is Antheraea polyphemus. According to Wikipedia, the moth has an average of 15 cm (6 in).

The purplish eyespots on hind wings give its name - from the Greek myth of the Cyclops Polyphemus.

And about the defence strategy it's quite interesting. As a green caterpillar, it is camouflaged by its color. However, if it's noticed then it starts to do pose like Sfinx to look less like a caterpillar, if it's still attacked by threat then it is started to make a clicking noise with its mandibles - sometimes as a prelude to or accompanied by defensive regurgitation of distasteful fluids.

When threatened, adult Polyphemus flip the front wings forward and also often flap the wings exposing the large hind wing eyespots - possibly to startle potential predators. The eyespots are possibly to protect an adult from Blue Jay.

The pattern on the hind wings of the polyphemus moth resembles that on the head of the great horned owl (Bubo virginianus).


Bug Identification: Is this small tubular, black bug a bed bug?

I'm going to suggest it is the larvae of a carpet beetle. Initially I thought possibly the Varied carpet beetle because of the lighter patches near the posterior end similar to this picture from the wiki page on this species:

Having said that the geographical range might not be correct so it could be a similar species so I've dug a bit deeper. There are some 120 species in North America, from this link I'd say that the Buffalo carpet beetle is a contender.

Carpet beetles are classified as a pest species:

  "larvae feed on natural fibers and can damage carpets, furniture, clothing and insect collections"

Not all bad though, the larvae are also known as wooly bears, how nice.