Which is harder to contract - HIV or AIDS?

Your question depends hugely on the factors at play.

The rate of transmission depends on the route of infection.  Wikipedia has a good breakdown showing the wide variability.  Are they getting a blood transfusion?  90%.  Mother-to-infant?  25%.  Male-to-female vaginal sex?  No higher than 0.3%.  Not to mention that the incidence varies massively between countries, as does the most common route of infection.
The rate of progression to AIDS also depends on a large number of factors including age, viral load, various genotypes, access to medical treatment, and, of course, long-term nonprogressor (LTNP) status.

The incidence of LTNPs is around 1 in 500, or 0.2%, which overlaps with but is at the low end of transmission rates for some routes of infection.


Remember, phages infect bacteria. It looks like he used something called pMXs-based retroviral vectors instead, which is based on the Moloney murine leukemia virus (MMLV).

I have never heard of that virus before, but I do know of others used in vivo to deliver genes, including Lentivirus, Adenovirus, and Adeno-associated virus. All have their strengths and weaknesses. Adenovirus is large so you can fit a big gene inside it, but it tends to illicit a high immune response. AAV, on the other hand, is very small but has a much more mild immune response. It can fit a gene about 4kb long inside or half that if you use a fast expressing form called self-complementary AAV. What is nice about AAV is one of the subtypes (technically callled serotype) can cross the blood brain barrier, so it has already been used in clinical trials to try and treat neurological diseases, including Parkinson’s.


To what extent is Ebola airborne? (aerosols)

Interesting question and hard to answer definitively. First of all: It seems still pretty clear that the major (and by far most important) infection route comes from direct contact with infected people or their body fluids and that aerosol transmission is of far less significance. Ebola is infecting cells of the immune system (mostly macrophages and dendritic cells) which are located in the skin which makes the route through the respiratory organs pretty uneffecient, but it is possible.

However, there are reports for Ebola transmissions (or at least unclear cases in which a direct contact could be excluded), which suggest that the aerosl transmission is possible. There are reports of Ebola infections which spread among experimental animals between infected and non-infected (and without direct contact) control groups. This has been observed between rhesus monkeys and pigs. It was also possible for the pigs to infect non-human primates (see references 1-4 for details).

This results should be seen with some caution: At least for pigs an Ebola infection seems to be pretty much different than one in humans. There it looks more like a respiratory disease with all what comes along with it: Extended sneezing and coughing - which makes a lot of aerosol droplets. See reference 3 for the original paper and 5 and 6 for a summary and a classification. I think it is also possible that anatomical differences to the humans make such an infection route easier or harder.

Finally there are some reports of infected people which had no direct contact to people (see reference 7). However, this is rare and mostly restricted to people which where involved in health care for infected persons. These people come in close contact to the infected people which raises their chance of getting infected by aerosols. This underlines the importance for health care workers to get the right protective equipment.

References:

Transmission of Ebola virus (Zaire strain) to uninfected control
monkeys in a biocontainment laboratory.
Replication, Pathogenicity, Shedding, and Transmission of Zaire
ebolavirus in Pigs
Transmission of Ebola virus from pigs to non-human primates
Aerosol exposure to Zaire ebolavirus in three nonhuman primate
species: differences in disease course and clinical pathology
Pig-to-monkey Ebola: is there something in the air?
New paper on Ebola–no primate-to-primate transmission seen
Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo,
1995: Risk Factors for Patients without a Reported Exposure


This temperature range would be a compromise between a very low temperature needed to limit natural decay or decay triggered by micro-organisms (the lower the temperature, the lesser the decay) and the formation of destructive ice crystals.

Only pure water freezes at 0°C (32°F) under atmospheric pressure. But the content of apple cells and cell walls is a rather complex aqueous solution, containing many natural cryoprotectants, among which the fruit's sugars. Therefore, the freezing point of apples might be as low as 30°F.


Why are Chloride Anions necessary for gastric acid functioning?

Mebrane divide basicly enviroment to two disimular sections. This sections differ in lots of chemical/ phycical properties. One of those is electrochemical potential which it can be in the very simple way describe as whole charge of disimular section divided by biomembrane.

So if cell  pariental cells pumped into stomach that section will have too much positive value of electrochemical potencial which can repulse pumping more hydrogen ions back to the pariental cell. This lead to freeze hydrogen pumping to  the stomach area. Than chloride aniont came to the scene basicly to reduse positive charge and enable to pump tremendous amount of hydrogen to the stomach.


I would strongly suggest to ask someone in your lab about this, they will have a better idea about the different waste disposal methods you have available.

In general you would dispose anything that contains organic solvents like methanol in a waste container for generic solvent waste. You should have something like that somewhere in the lab.

One thing you always have to keep in mind is to never put anything still reactive into your waste container. A popular example would be a strong oxidizing agent, putting that into a solvent waste container is dangerous and could e.g. ignite the waste. This is not an issue in this case, but you should always keep that in mind.

Another aspect is the pH of the waste, in many cases the waste disposal facility will only accept reasonably neutral waste, so you should neutralize your waste before putting it into a container. Neutralizing it inside the container can be much more annoying. This might not be necessary if you have a dedicated acidic waste, you'll have to ask someone in your lab about that. The Bradford reagent is strongly acidic, so you'll have to pay attention to this aspect.


Why do moths not die when they fly into a window?

Simply because their body mass is small. It's the same as if an ant falls off from the roof of a building. It will suffer no harm because the speed of its fall will be very slow, but try the same yourself and you will surely die.

More scientifically, it's a question of kinetic energy: $E_{kinetic}=\frac{1}{2}\times mv^2$
You can see from this formula that if mass is small, then kinetic energy will also be small.

The second reason is that although insects are small in size, the materials they are made of are extremely resistant comparatively to their size. Therefore, the bug will survive when it meets the window pane.

An interesting corollary is that the common saying "if an ant was the size of a human, it could carry a locomotive, because it can carry many times its weight" is totally wrong. If an ant the size of a man tried that, it would break its back just like you and me, because material resistance is not proportional to size.


What's the benefit of the average human body temperature?

It's a balance between preventing infection and not requiring excessive food intake. It is has also been claimed that this is the temperature at which the most essential enzymes are most reactive, without becoming damaged by excess temperature.

References:

"Mammalian Endothermy Optimally Restricts Fungi and Metabolic Costs", by Aviv Bergman and Arturo Casadevall, DOI: https://doi.org/10.1128/mBio.00212-10
"Fungal virulence, vertebrate endothermy, and dinosaur extinction: is there a connection?" (.PDF), by Arturo Casadevall, DOI: https://doi.org/10.1016/j.fgb.2004.11.008

  "The number of fungal species that can thrive and therefore infect an animal declines by 6 percent for every 1° C rise in temperature. This means that tens of thousands of fungal species infect reptiles, amphibians and other cold-blooded animals, but only a few hundred harm mammals.".

It is useful to refer to ectotherms (an organism in which internal physiological sources of heat are of negligible importance in controlling body temperature, which permits them to operate at very economical metabolic rates) as poikilotherms when applicable.

  "Poikilothermic animals include types of vertebrate animals, specifically some fish, amphibians, and reptiles, as well as a large number of invertebrate animals. The naked mole-rat is the only mammal that is currently thought to be poikilothermic.".

  "Poikilotherm animals must be able to function over a wider range of temperatures than homeotherms. The speed of most chemical reactions vary with temperature, and in order to function poikilotherms may have four to ten enzyme systems that operate at different temperatures for an important chemical reaction. As a result, poikilotherms often have larger, more complex genomes than homeotherms in the same ecological niche. Frogs are a notable example of this effect, though their complex development is also an important factor in their large genome.

  Because their metabolism is variable and generally below that of homeothermic animals, sustained high-energy activities like powered flight in large animals or maintaining a large brain is generally beyond poikilotherm animals. The metabolism of poikilotherms favors strategies such as sit-and-wait hunting over chasing prey for larger animals with high movement cost. As they do not use their metabolisms to heat or cool themselves, total energy requirement over time is low. For the same body weight, poikilotherms need only 5 to 10% of the energy of homeotherms.".

This update speaks to the theories on enzymes (solitary from metabolism), offered in other answers.

Articles and theories that are not discredited:

Enzyme assays by Hans Bisswanger:

That article is mostly concerned with the temperature used to conduct assays of enzymes.

  "The essential requirements for enzyme assays are described and frequently occurring errors and pitfalls as well as their avoidance are discussed. The main factors, which must be considered for assaying enzymes, are temperature, pH, ionic strength and the proper concentrations of the essential components like substrates and enzymes. Standardization of these parameters would be desirable, but the diversity of the features of different enzymes prevents unification of assay conditions. Nevertheless, many enzymes, especially those from mammalian sources, possess a pH optimum near the physiological pH of 7.5, and the body temperature of about 37 °C can serve as assay temperature, although because of experimental reasons frequently 25 °C is preferred. But in many cases the particular features of the individual enzyme dictate special assay conditions, which can deviate considerably from recommended conditions.".

  ...

  "Enzymes display their highest activity at their respective optimum conditions, deviations from the optimum cause a reduction of the activity, depending on the degree of the deviation. Moderate deviations produce only small activity decreases which can be tolerated (Figure 1), and so the physiological conditions prevailing in the cell may be taken as standards for at least of the mammalian enzymes. However, assay procedures are usually adapted directly to the features of the individual enzyme and not to obey general standards. Enzymes are sensitive substances present in small amounts and their activity in the cell can often be detected only at their optimum conditions.".

Royal Society of Chemistry - "Enzymes - Function and structure":

  "As the temperature rises, reacting molecules have more and more kinetic energy. This increases the chances of a successful collision and so the rate increases. There is a certain temperature at which an enzyme's catalytic activity is at its greatest (see graph). This optimal temperature is usually around human body temperature (37.5 °C) for the enzymes in human cells.

  Above this temperature the enzyme structure begins to break down (denature) since at higher temperatures intra- and intermolecular bonds are broken as the enzyme molecules gain even more kinetic energy.".

Note: Wikipedia: "Wilson's temperature syndrome":

  "The American Thyroid Association (ATA) describes Wilson's syndrome as at odds with established knowledge of thyroid function. The ATA described the diagnostic criteria for Wilson's syndrome as imprecise and non-specific, and raised concern that the proposed treatments were potentially harmful. Florida State Medical Board members described Wilson's syndrome as a "phony syndrome" and a scam during disciplinary action against Wilson."

  ...

  "The ATA stated in 2005 that a "thorough review of the biomedical literature has found no scientific evidence supporting the existence of 'Wilson's Temperature Syndrome'." The statement added that the mean temperature of normal persons in the AM on waking is 97.5 °F, not 98.5 °F, and that many of the symptoms described by Wilson are nonspecific and typical of depression, anxiety, and psychological and social stress. It also notes that a similar set of symptoms occurs in the alternative diagnoses of neurasthenia, chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, chronic Epstein-Barr virus syndrome, and chronic candidiasis. Finally, the Association notes that chronic supplementation with triiodothyronine (T3) is particularly difficult and problematic, since various tissues set their own cellular levels of this hormone by making it individually from thyroxine, and supplementation of T3 may overwhelm this normal regulatory mechanism in some of these tissue.".

Reference: Wilson's Temperature Syndrome

"Metabolism Dependent on Enzymes"
"Enzyme Function Dependent On Temperature":

  "... when an enzyme-dependent chemical reaction is monitored for how well it takes place at various temperatures, the lower the temperature, the slower the chemical reaction. As the temperature is increased, the reaction rate will go faster with each increase until it reaches its optimum reaction rate. If the temperature is increased too much, the rate of reaction will diminish due to denaturing or change in shape of the enzyme.".

The treatment suggested by Wilson is what was discredited, the fact that enzyme reactions proceed differently at different temperatures is still supported. Reference to his article was included due to the partial overlap with established knowledge.


SARS-CoV - relative size of the spike protein

I'm not going to give you the final answer, because this is still a class assignment, after all, but I'll give you some tips. What you are looking at is a Western blot of whole-cell extracts from a cell line called Vero, either on its own (vertical ane 9, from numbering across the bottom) or infected with various viruses carrying specific genes, as indicated. Lanes 1-7 are from Vero cells infected with the BHPIV3 viral vector (a live-attenuated virus that can carry genes from another organism). Lane 1 is just the viral vector itself, with its own proteins. Lanes 2-7 are from cells infected with the viral vector carry certain genes from the SARS coronavirus. Lane 8 is from cells infected with SARS-CoV itself (so it carries all the previous genes). The numbers along the far right side are molecular weights, in kilodaltons.
A Western blot is performed in three parts - 1) separating the protein samples (whole-cell extracts) by molecular weight (size) in an SDS-PAGE gel by using an electric field, 2) transferring the separated proteins to a membrane, also using an electric field, and 3) using some sort of probe (usually a specific antibody) to determine what is present and in what amount. In this case, two antibodies were used. The lower, narrow image shows the samples probed with an antibody that recognizes the HPIV3 F protein, which is present in all the BHPIV3-infected lanes, in relatively equal amounts. This can be determined because the size/intensity of the different bands in each vertical lane is directly proportional to the amount of that protein present in the original sample.
The upper part of the image shows the extracts probed with an antibody that evidently recognizes the SARS S, M, and N proteins, but apparently not the E protein (as Lane 6, with the SARS-E virus, is blank). Using this information, you can now determine which bands correspond to which protein.
Keeping in mind that Lane 8 contains all the proteins from the SARS-CoV virus, while the previous lanes just contain certain ones as labeled along the top, you should now be able to use ImageJ to answer the question. I will give you one hint - there is much more information present than you need to answer the question. You actually only need 4 (well, maybe 5) of the lanes. I'll leave it to you to figure out which ones.


Is there any genetic similarity that defy evolution theory?

Your question seems rather confused to me, I don't quite understand it. Below I try to explain some stuff, I am not quite sure it would help you finding the answer to your question. Let me know if it helps you and how I can improve this answer.

While natural selection selects for a given allele (gene variant), mutations create new variation. And because of this process of mutation there is genetic pattern in species D that would cannot be found in species B (assuming that we have the DNA of species D). But what is similar between B and D were probably also present in their common ancestor B. The exceptions are molecular convergent evolution and horizontal gene transfer (natural of artificial).

Because of common ancestry …

Humans have similarities with pigs

Example: endothermic amniotes

Humans have similarities with a bug

Example: bilaterial symmetry

Humans have similarities with jellyfish

Example: Heterotrophy

Humans have similarities with an oak tree

Example: We have mitochondrias

Humans have similarites with any living things on earth!

Example: Genetic information is hold into a DNA/RNA molecule.

If you might observe that D is genetically speaking more similar to C than to E… This can be due to:

Horizontal gene transfer (artifical or natural)
The mutation rate (or ability to fix mutations) in one lineage might be greater than in another lineage.

For example, if lineage E underwent many mutations, they might be genetically speaking have accumulated many difference compare to D, way more than the number of difference that D has with C.

The phylogeny might be wrong
There might have had some convergent evolution.

Think about fishes which opsins in the eyes need to be adapted to the amount of light which depends on the turbidity of the water. After the three lineages splitted, the change of envirronment might have occured the sequence AATGATCCT suddenly became beneficial. Only two lineages had the chance to produce the right mutation. Or maybe lineage E live at low depth and therefore it doesn't need this mutation because there is enough light at low depth anyway.

Therefore, one should not expect a common ancestor to be the arithmetic mean (supposing it means something) of the current species. And one should not expect that two closely related species on the tree of life should necessarily be more genetically similar to each other than any of the two to a third species.

Note that the phylogeny is constructed mostly based on genetic data. Which makes that two closely related species (on our tree which is not necessary the absolute tree of life) are (almost) necessarily more genetically similar (it is kind of a definition then).


Antibodies also known as immunoglobulins consists of two heavy chains and two light chains linked via disulfide bonds to form Y-shaped structure (as shown in figure below).
This Y-shaped structure bestows antibodies with two properties. Firstly, antigen-binding through the antigen binding fragment(Fab); and secondly, interaction with immune cells and proteins through fragment crystallizable region (Fc) to stimulate and regulate host immune defense mechanisms.
Fc and Fab portions of the antibody molecule are joined by flexible hinge region which enables antibodies to interact with the antibody-binding proteins and thus help in mediating immune effector mechanisms. So, this Y-shaped structure provide proper flexibility for binding to antigens and proteins/immune cells of immune system.

Reference
https://www.ncbi.nlm.nih.gov/books/NBK27144/
https://immense-immunology-insight.blogspot.com/2013/10/antibody-structure-simplified.html


How to map the Gene name to its Gene Symbol?

Unfortunately, protein and gene name mapping is one of the most annoying problems in modern computational biology. There is no surefire way of doing this. Especially from hopeless gene names as the one in the paper you cite. Here are a few services you can try though:

General, text search, useful if you have a gene description (as in the case described in your question):

NCBI Entrez,
UniProt search

Mapping servers, useful if you have an actual gene/protein symbol/name (e.g. P53_HUMAN, AF240684, NP_001119585 etc)

UniProt ID Mapping
DAVID Gene ID Conversion Tool


How does having spare receptors change ED50 in an irreversible agonist

Irreversible antagonism is like removing receptors.

If there are spare receptors, maximum effect, or any effect level, can be recovered with more ligand (because displacing the irreversible ligand is not necessary, when there are other sites to fill).

$$K_D = \frac{R*L}{RL}$$

A given effect level corresponds to a given $RL$, but with less receptor $R$ available, more ligand $L$ is needed. That is by definition a change in ED50.

If you have no spare receptor (or there is enough antagonist to prevent full effect even with spare receptors), then maximum effect cannot be recovered. There is a new Emax, lower than without antagonist; but without shifting the dose-response curve to the right.

Here is an example in Rang&Dale (8th ed., p. 12, fig 2.6). Curves are labelled with time of incubation with a given quantity of irreversible inhibitor, that is equivalent to varying concentration of irreversible inhibitor at steady state. First two show the situation with spare receptors, and last two show what happens when the original Emax cannot be reached because there are not enough receptors left to elicit maximum response.


What is name of the red eyed rabbit or hare, found in Himalayan region?

Perhaps a bit underwhelmingly, those are Himalayan Rabbits.
https://en.wikipedia.org/wiki/Himalayan_rabbit

The pure white fur and red eyes are usually a sign of albinos, but in this case it's actually a trait of the entire species.

  [They] can only produce eumelanin under a certain temperature and they cannot produce pheomelanin at all.


What does sympathetic and parasympathetic 'tone' mean?

Short answer
Parasympathetic tone is not necessarily mediated by tonic firing.

Background
Nice question! I think part of the confusion stems from terminology. Let's start with some definitions first.

'Tone' in sympathetic tone can be translated as mean activity level (Hayano & Yuda, 2019).
'Tonic' firing by neurons may be translated as a sustained response, which activates during the course of the stimulus (Wang et al., 2014), although some neurons have intrinsic tonic activity as well, like thalamocortical neurons. This opposes to phasic firing neurons.
'Phasic firing' refers to a transient response with one or few action potentials at the onset of stimulus followed by accommodation (Wang et al., 2014).

In your post you seem to assume that parasympathetic tone equals tonic firing activity. I'm not so sure about this. For example, I found a catching paper on the parasympathetic regulation of lung function in guinea pigs (which lacks sympathetic innervation altogether). The paper nicely illustrates (Fig. 1) that parasympathetic regulation of the bronchi in guinea pigs is mediated by both tonic and phasic (burst) stimulation (Myers, 2000):

  [P]hasic neurons in guinea pig bronchial parasympathetic ganglia
  respond to a prolonged suprathreshold stimulation with a
  high‐frequency burst of action potentials ..., whereas tonic neurons are nonaccommodating and will respond with relatively lower
  frequency action potentials...

Fig. 1. Phasic and tonic neurons in guinea pig bronchial parasympathetic ganglia. source: (Myers, 2000)

References
- Hayano & Yuda, J Physiol Anthropol (2019); 38(3) (2019)
- Myers, JCN (2000); 419(417): 439-50
- Wang et al., Channels (2014); 8(4): 298–307


Do humans secrete and detect pheremones?

Yes, humans can secrete and sense pheromones, e.g. female tears dampen male sexual arousal.

Science 2011, 331(6014), 226-230

But then on the other hand, a key gene in mouse sex specific behavior (TRPC2) is a pseudogene, i.e. it is inactive, in humans.

Nature 2007, 448, 1009-1014

If you look at the references in those papers you will probably find a lot more examples.


How can action potentials be generated through thoughts?

This paper addresses the question that you are asking. The study is based on conscious decision making in rats.

Performance of rats were assessed in the following task:

The rats have to poke their snout into a waiting port until a auditory signal (beep) is heard.
After first beep the rats can get a small reward (small amount of water) in the reward port. However if the rat waits for a second beep it gets to have a bigger reward.

So there were three behavioral outcomes in the experiment done with 37 individuals:

Short-poke trials: Those that didn't wait for the signal (8.3 ± 4.6%)
Impatient trials: Those that waited for the first beep but did not wait for the second beep (58.8 ± 3.9%)
Patient trials: Those who successfully got the bigger reward. (32.9 ± 1.4%)

The impatient ones did not usually quit immediately after the first beep. This was not a lethargic response to signal but a moment of conflict between two decisions. There was a distribution of waiting times. The patient ones immediately responded to the second beep and took their reward.

Neural activity was studied in the M2 (secondary motor) cortex of impatient rats during the tasks and two kinds of neural activity was observed:

Ramp-to-threshold: Firing rate kept increasing till the end of waiting time suggestive of a neural threshold to quit waiting. (Fig 1)
Steady-transient activity: Firing rate correlated with waiting time i.e. higher firing rate higher the waiting time. This could constitute the neurons that are making the rat wait. (Fig 2)

  Figure 1: Ramp-to-Threshold.  Reproduced from Murakami et al. (2014) Nature Neuroscience 17,1574–1582

  Figure 2: Transient activity.  Reproduced from Murakami et al. (2014) Nature Neuroscience 17,1574–1582

It was also observed that this activity is task specific. The neurons that showed a certain activity in the above tasks did not behave the same way in the same rats performing a slightly different task.

So action potential is generated in the brain by "thoughts". However these thoughts are not generated de-novo. Any conscious decision is based on memory of past events and similar events evoke those memories, which in cellular terms is generation of action potential. In this case the action potential is generated in response to the rats' sensory input in the form of a beep. Other kinds of responses are instinctive and the brain circuitry has evolved to generate these kinds of responses to certain stimuli such as fear. The above example is a study of conscious decision making based on an acquired memory.


Well, saliva (or the rate of production of saliva in your mouth) can tell you a lot about health, but the information you acquire is extremely general, so it won't really give you an entire health analysis in terms of diseases, sugar levels, body temperature, likewise.

As for what saliva does tell about your health, here is an extract from a source:

  "Dr. Stuart Froum, president of the American Academy of Periodontists, says: “If the eye is the window to the soul, the mouth is the window to the body.” Saliva in the mouth is one of the best indicators of health. If something is off, there is a good chance your saliva will change as a direct reflection.

  Saliva is produced around the clock and is affected not only by every bite of food you take, but also every other thing you put in your mouth. If you notice your saliva is too stringy or thick, your body might be having a hard time producing saliva. This could be because of the prescription and over-the-counter medication you are taking.

  Studies indicate that an imbalance of the ‘stress hormone’ cortisol in saliva points to emotional sensitivity to stressful situations...the measurement of cortisol in saliva is becoming increasingly acceptable as a screening test for hypercortisolism, such as depression, hypertension and diabetes.

Source: http://healthtoday.com/5-things-your-saliva-can-tell-you-about-your-health/
http://www.medicaldaily.com


What regulates production of first transcription factors during development?

The first transcription factors for the first transcription after fertilization are already present in the ovum (egg) before it is fertilized.

Generally, all the machinery needed for transcription, translation, and the rest of the many necessary cellular functions are already present in a cell before it divides and develops.  This chain of dependency goes back eons of time to the origin of cells and the very origin of life.


What happens when a human ingests a large meal, and after a short time follows it up with a large amount of indigestible carbs?

Indigestible carbs are known as dietary fiber. They slow down gastric emptying, which results in slower absorption of the absorbable nutrients in the small intestine.

  Early research regarding soluble fiber demonstrated delayed gastric
  emptying and decreased absorption of macronutrients, resulting in
  lower postprandial blood glucose and insulin levels [44]. This is
  most likely due to the viscosity of soluble fibers inside the GI
  tract. Interestingly, different types of soluble fiber had varying
  effects on viscosity and nutrient absorption. Guar had the highest
  viscosity as well as the greatest effect at decreasing postprandial
  blood glucose. Therefore, it would be assumed that an increased level
  of soluble fiber would be associated with a decreased risk of
  diabetes. However, several recent studies have demonstrated the
  opposite showing no correlation between soluble fiber and a reduced
  risk of diabetes (Nutrients, 2010).

So, dietary fiber can slow down the absorption of macronutrients (carbohydrates, proteins, fats), but does not reduce the amount of macronutrients absorbed (at least not significantly).

Dietary fiber can be soluble (for example, stachyose and raffinose in legumes) or insoluble (for example, cellulose in fruit skins or grain hulls) (Linus Pauling Institute).

They are microbes, mainly in the large intestine (not in the healthy small intestine), that ferment soluble, but not insoluble fiber. Fermentation of a large amount of soluble fiber produces a lot of gas (flatulence), which typically occurs several hours after a meal.

Insoluble fiber can stimulate intestinal motility and thus help in constipation, but large amounts can be laxative, which could result in decreased absorption of nutrients; soluble fiber can trap some bile secreted by the gallbladder and may thus reduce the synthesis of cholesterol (Linus Pauling Institute).

Dietary fiber probably does not interfere significantly with the absorption of minerals and vitamins (Nutrients Review).


Is it possible to induce protein activation via frequency-specific mechanical waves?

This should defentily be possible and most likely already exists in the form of touch or pain receptors.

In the case of mechanical nocireceptors, which sense pressure or other mechanical changes in the tissue to signal pain, it's quite likely that there are distinct channel proteins that can correspond to mechanical deformation/pressure/etc, but I couldn't find any specifically known protein.

Most touch receptors seem to be based on bigger structures made up by neurons, so I'm not sure if they have one specific protein that senses mechanical movement, but I also wouldn't exclude that option - especially since almost nothing is known about non-human/mammalian touch receptors.


Prevent biofilm formation on moist surfaces

You can use some antibiotics or germicide or alcohol...they prevent the formation by interfering with the attachment or adhesion and expansion of immature biofilms..


Therapeutic hypothermia certainly is an extremely useful short-term treatment for hypoxic and ischaemic injury to tissues (caused by loss of blood flow and/or oxygen) and is part of the protocol for treating people in intensive care who have had out of hospital cardiac or respiratory arrest as well as being used during heart surgery in cardiopulmonary bypass. In addition there is currently research into treating people who have just had heart attacks and strokes, both conditions where there is acute loss of blood flow due to a clot.

However, there is little evidence as regards use of chronic (long term) hypothermia to prevent aging. While severe hypothermia does suppress cellular respiration and slow down metabolism and bodily function, it also often causes other abnormalities such as:

Disturbances in cardiac conduction that can lead to cardiac arrest
Markedly reduced blood flow to skin and limbs which can lead to tissue death in fingers, toes, etc.
Clotting dysfunction (haemorrhage if there is any injury)
Pulmonary oedema - fluid in the lungs causing inability to oxygenate and/or ventilate the blood
Increase in infections

There is, however, quite a lot more evidence in regards to slowing down cell ageing from oxidative stress using diet energy restriction and this has been replicated in rodents.

In other words, there really isn't any good evidence at this stage in regards to long term hypothermia, but currently, given the high risks of cardiac dysfunction and death, without invasive monitoring and intervention (such as in an ICU) it is not feasible.


Why do the most structurally well-characterized bacterial RNA polymerases belong to thermophiles?

I think both of your suggestions have some merit: (1) it appears that Thermus RNAPs are more stable and easier to crystallize (2) RNAP is highly conserved and so it is not critical to crystallize it from every bacterial species.


Why reaginic antibodies are absent in these types of syphilis?

To make the diagnosis of syphilis, the most common tests fall in two categories :

Non-specific tests like VDRL test & Rapid Plasma Reagin (RPR) test : those detect antibodies against cardiolipin, present in the treponema but also in our cells.
Specific/treponemal tests like TPPA/TPHA & FTA-ABS : antibodies titers against antigen specific to T. pallidum are  measured.

Non-specific titers decrease when antigenic stimulation ceases : either when syphilis is cured (no more treponema), or in the late stage where the number of bacteria present in non-immune-privileged zone is low (treponema is almost eliminated except in the central nervous system, eyes, testis where it is protected from immune response).

Specific titers fall very slowly if at all, once they are acquired.

Thus in late stage syphilis we get the following : VDRL- TPHA+, a source of confusion since this can also indicate old/cured syphilis.


All classes of drugs react differently in the body. Some bind to receptors, some clean receptors, some drugs cause re-uptake inhibition in the brain, and others destroy viral and bacterial infections. Classifying drugs and how the human body would develop a tolerance to them in a post on this website would take pages upon pages to answer. When you say steroids, i'm assuming you are talking about anabolic steroids. That is the male sex hormone testosterone and its multitudes of derivatives. (DHT and non-DHT). Your body does not in fact develop a "dependance" on the drugs, rather it is a checks and balances system that your endocrine system establishes. Lets say you take a dosage of Testosterone Cypionate at 200mg a week for a 20 week interval from your G.P (common treatment for andropause). In laymans terms, your body senses the increase of testosterone and tells your Leydig Cells in the testes to stop signaling LH (responsible for testosterone production). Because it sees that there is already an abundance of the hormone. Now, once treatment stops, there are a series of protocols one could take to stimulate the natural production of testosterone again. Other forms of AAS are much harder on the HPTA than others however. (Trenbolone Acetate)


Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?

It seems that yes, it is possible to increase the tolerance for lactose over time, and it has to do with the adaptation of microbiota.

A simplistic explanation comes in the following article:
 Hertzler SR, Savaiano DA. 1996. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. The American journal of clinical nutrition 64: 232–6.

In which the authors claim the following:

"Colonic adaptation appears to reduce the symptomatic response to lactose via several mechanisms. (...)
(...) increased β-galactosidase activity after regular lactose ingestion indicates that colonic bacteria are able to ferment lactose more rapidly. (...)
(...) This metabolic shift is thought to result from the proliferation of lactose-fermenting, non-hydrogen producing organisms such as Bifidobacteria."

This article makes reference to another one which supposedly explains the microbiota adaptation:
Hill Mi. Bacterial adaptation to lactase deficiency. In: Delmont J, ed. 1983. Milk intolerances and rejection. New York: Karger: 22–6.

But unfortunately I could not find the full text. I hope you are luckier than me.


Finding out the best concentration for my plant extract to be used as drug for diabetes

You have to try to determine the best concentration.

Usually there are multiple clinical trials, first in animals, then in humans to

figure out the effective dose
look for side effects
compare the new drug's efficacy with existing drugs


Do the organisms within a lichen communicate with each other?

Communication definitely happens, but I don't know of any research into response to disease.

One example are molecules known as lectins that help the fungal partner recognize the correct photobiont (algal or cyanobacterial) symbiont.

Another example are the physical connections between fungal hyphae and photobiont known as haustoria that appear to help the fungus extract sugars from the photobiont.

You should find this review by Piercey-Normore & Athukorala 2017 a helpful place to begin learning more.

Ref: Piercey-Normore, M. D., & Athukorala, S. N. (2017). Interface between fungi and green algae in lichen associations. Botany, 95(10), 1005-1014.


Apart from one isolated group of birds in Australia (i.e., mound nesters found in Australia that use external heat for incubation - see link), all birds incubate their eggs (see link). All species that returned from land to sea have retained their reproductive cycle (marine mammals still give live birth and suckle their young) and still rely on air for oxygen intake. Extrapolating this mammalian evolution to birds would result in a creature that returns to sea, with all ties to land cut off, but that still has to incubate their eggs under water. As they would still rely on air, this is not very feasible as they would need to go up often to breath. This would leave the eggs vulnerable to predation. Even worse, it would leave the eggs at the mercy of a relatively cold ocean cooling them down quickly. Incubation means that the eggs are pretty much kept at body temperature which is difficult in the sea regardless of breathing parents. In all, while there may be certain benefits of underwater life for birds, it will require some drastic evolutionary changes in terms of the reproductive cycle. A more parsimonious way of colonizing the sea is to go back to land once and a while to lay eggs, incubate them, and raise the young until they are sea-worthy, like penguins do as @MattDMo mentioned.


There are several requirements for bacteria to grow.

A carbon source - Sugar
A nitrogen / amino acids source - Beef stock
Gelatin is there to hold everything in place, it doesn't provide any nutrients.


is the pseduoknot the alignment of these base pairs

I'm not exactly sure what is meant by alignment, but if you mean base pairing from the flanking RNA to the loop of the hairpin you have depicted, then you would have an H-type pseudoknot.

Since you are interested in predicting these structures, it's important to note that a nucleic acid sequence capable of forming the necessary base-pairs for a pseudoknot structure does not imply that the sequence indeed forms a pseudoknot. It's likely that the sequence has a minimum free energy (MFE) structure that is not pseudoknotted. So the base-pairing capability is necessary but not sufficient for predicting these structures.

Take a look at the following (full-text) articles on pseudoknot prediction for additional information:

Computational Analysis of Noncoding RNAs
DotKnot: pseudoknot prediction using the probability dot plot under a refined energy model
A fast and robust iterative algorithm for prediction of RNA pseudoknotted secondary structures
KnotSeeker: Heuristic pseudoknot detection in long RNA sequences


What is cross-immunoreactivity, and how does it impact vaccine development?

Cross-immunoreactivity is just as you stated where an antibody that is specific to one antigen may recognize another antigen. I don't think this term is widely used as I see cross-reactive or broadly reactive more often. With regards to vaccines against viruses, cross-reactive immune responses are very important to establish an immune response that is effective against varying strains. Using Influenza as an example, an antibody that recognizes the HA protein of the H3N2 strain and also recognizes the HA protein of the H1N1 strain would be cross-reactive. If we had a vaccine capable of this we would not have seasonal flu.

Epitopes are specific regions on the antigen that are recognized by T cells or antibodies. They are the specific area on the protein structure that is recognized. Thus, for a response to be cross-reactive that specific structure must be present on both antigens. Epitopes could be located in any region of the protein, viruses will often have a region that is highly antigenic and highly variable to trick the immune response into focusing on the highly variable region rather than the more conserved regions.

Antigenic convergence is related to the sequence space available to the virus. Since viruses have limited space  for genes the amount of possible variation is limited as a single point mutation can have a large effect on the virus. Taking this into account some predictions could be made on how the virus might evolve. If the virus is evolving in such a way that there might be conserved epitopes, those epitopes might be important for cross-reactivity. Here is a paper on antigenic convergence in Hepatitis C. http://www.nature.com/articles/srep00267

This is a paper focused on flu, but it outlines the ideas surrounding cross-reactive antibody responses.
http://www.ncbi.nlm.nih.gov/pubmed/26175732


How is the reflectance spectrum of solids measured?

As the name implies, reflectance spectra are measured from light reflected off an object. Any object with reflects light, such as any opaque object) will work for this technique; to me this seems like solids are ideally suited for reflectance spectrphotometry. You might be used to transmission or absorbance spectrophotometry, which measures the amount of light transmitted or lost after passing through a sample. These methods are typically used for liquids which allow passage of light to some extent.

The paper (1) cited by the review you mention says that they used a "RAMSES-ARC hyperspectral radiance sensor," which is probably just as awesome as it sounds. In principle reflection spectrophotometry works very similarly to transmission-based spectrophotometry: generate monochromatic light, shine it at the sample, and measure the intensity of light that comes back at that wavelength (or over a range of wavelengths)$^†$. If you do this for many different wavelengths of light, you have a reflectance spectrum. This link might have some useful information.

$^†$ Edit: Modern-day spectrophotometers use a more efficient method in which broad-band light is passed onto the sample and the response at a single wavelength can later be mathematically reconstructed. If you're interested in these types of details, refer to Fourier Transform spectroscopy.

(1): Doring TF, Anchetti M, Hardie J. (2009). Autumn leaves seen through herbivore eyes. Proc. R. Soc. B 282(1801): 121-127.


Is it possible to use PCR to test for Machado-Joseph disease?

This paper describes an allele-specific PCR protocol to detect CAG repeat expansion in MJD patients:
Maciel P, Costa MDC, Ferro A, et al. Improvement in the Molecular Diagnosis of Machado-Joseph Disease. Arch Neurol. 2001;58(11):1821–1827.


Can plants produce oxygen at night (without light)?

Short Answer: Any plant can produce oxygen at night, but plants cannot produce oxygen without light.

Longer Answer: It all comes down to spontaneity of a reaction i.e. whether a reaction can occur without input of energy or not.

Before we talk about spontaneity, I feel it better to first know about the process we're talking about here. In photosynthesis, the water-splitting reaction occurs in the oxygen-evolving complex through a process known as Joliot-Kok cycle (or simply, Kok cycle)1. Although, the complete mechanism of this process is not understood yet, the basic reaction can be depicted in a diagram as2:

(Pay attention that in the diagram, the time taken is in microseconds and even nanoseconds. So, at molecular level, oxygen evolution does not take minutes or even seconds! However, at larger scale, release of oxygen might take longer time since the formed oxygen has to pass through many fluids, like thylakoid membrane, stroma, chloroplast membrane, cytoplasm, etc. before finally coming out in atmosphere)

To know where the photons are required (since the above diagram doesn't talk about that), I'll let in another diagram involving the steps where photons come in (as depicted by Rutherford et al, 1989):

As you can see, Kok cycle does not get direct input of energy through photons. Rather, it is the high energy P680+ which oxidizes a redox active tyrosine (YZ), which drives the reaction forward (the actual process is much more complex, see another answer or Halverson et al, 2003 for details).

Now, talking about spontaneity of this reaction, oxidation of water into hydrogen and oxygen is an endothermic process i.e. it is non-spontaneous in nature. In fact, the process requires 475 kJ/mol energy for occurring (Wikipedia). This energy barrier is so large that in the Kok cycle too, 4 photons are required to bring about oxidation of 1 water molecule (generally, catalysts are used so that they bring down the energy barrier of a non-spontaneous reaction so that it can be performed under normal conditions). Nilsson et al, 1857 talks about free energy change ($\Delta G_0$) of the cycle. See the graph for free energy change:

As is clearly visible from the graph, a higher amount of energy is needed to oxidize water ($E_P^+, S_2 \rightarrow S_3$) and even higher for liberation of dioxygen from the complex ($S_4 \rightarrow S_0$) (though the free energy change is negative for the last step i.e. liberation of oxygen is spontaneous, still the overall energy is larger than that at S3). Thus, since the reaction requires overall energy input, plants cannot produce oxygen without light. Also, as you suspect already, the point here is the abundance of light from man-made sources which makes some plants able to produce oxygen at night.

BONUS: I'll add some details about the thermodynamics of the system (skip this part if you're not interested in maths). The basic equations I will use here are Gibbs Fundamental Equation ($\Delta G = \Delta H - T\Delta S$), Arrhenius Equation ($k = A \times e^{-E_a/RT}$) and Eyring Equation ($k = k_BT/h \times e^{-\Delta G^\ddagger/RT}$) and used data will be from Nilsson et al, 1857.

From $\Delta G = \Delta H - T\Delta S$, to make a reaction spontaneous ($\Delta G < 0$), either there should be release of heat ($\Delta H < 0$) or increase in entropy ($\Delta S > 0$). As we know now, the reaction is endothermic i.e. there is absorption of heat. So, there must be increase in overall entropy to drive the reaction forward. If you look at the graph for free energy change in different steps of reaction, it comes out to be like this:

In this, $\Delta G_0$ is overall energy change, $\Delta G_{in}$ is the required energy input (given by photons), $\Delta G_{ex}$ is final free energy change and $\Delta G^\ddagger$ is Gibbs energy of activation. Here, $\Delta G_{ex}$ (shown in blue) corresponds to only the entropy change when final products (oxygen and protons) are released from the system as there is no enthalpy change here.

In release intermediate stage, the mole fraction $x = 1$ for oxygen, whereas in dissociated product stage mole fraction for water $x_1 = 56 /( [O_2]_0 + 56)$ and for oxygen $x_2 = [O_2]_0 / ([O_2]_0 + 56)$ (assuming molarity of water = 56 M) since in the final stage, water or oxygen or both can remain binded to the active site.

For release of oxygen: $[O_2]_0 = 273~\mu M$ and $T = 298~K$

which gives $\Delta G_1 = -~T\Delta S_1 = -~314~meV$

For release of proton: $\Delta G_2 = -~T\Delta S_2 = -~516~meV$ (since there is no enthalpy change, $\Delta H$ is neglected)

Now, $\Delta G_{ex} = \Delta G_1 + \Delta G_2 = -~314 - 516 = -~830~meV$

Also $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$

Since $\Delta G_{ex} > \Delta G_0$ therefore $\Delta G_{in} > 0$ i.e. energy is supplied.

Now, for the reaction $~~P_{680}Y_Z^{ox}M_3 \rightarrow P_{680}Y_ZM_0 + O_2$ (for which we've made the above graph)

Time constant $\tau \approx 10^{-3}~s$

i.e. $1/k = 10^{-3}~s$

or $k = 10^3~s^{-1}$

Using Eyring equation $k = k_BT/h \times e^{-\Delta G^\ddagger /RT}$

We get $\Delta G^\ddagger = -~580~meV$

In other words $\Delta G_{in} \leq -~580~meV$

Again $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$

On solving, $\Delta G_0 \leq -~250~meV$

Again, from Eyring equation, we get $k \geq 10^4~s^{-1}$

The large rate constant shows that there is a strong driving force for release of oxygen from the system, which is very likely due to increased entropy of the final product.

Thus, the enzyme brings down the free energy of the reaction, but at the expense of an increased activation energy barrier. Coming back to the main point, since energy is supplied to the system for the reaction, the reaction is non-spontaneous. However, the last step of the reaction is spontaneous (as also seen in the first graph) because of increase in translational and rotational entropy of final products when they are released (in above calculations, we neglected rotational entropy because of lack of data). Also, the above calculations were only for the last step of reaction ($S_4 \rightarrow S_0$) to show its spontaneity. In all other steps, energy has to be supplied to the system to drive the reaction forward (as shown in both first and second graphs above), making the overall reaction endergonic. I hope this helps now.

References:

 1. Wikipedia contributors. "Oxygen-evolving complex." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 Jan. 2017. Web. 18 Apr. 2017.

 2. Oxygen Evolution - 1996, Antony Crofts, University of Illinois at Urbana-Champaign

 3. A.W. Rutherford, Photosystem II, the water-splitting enzyme, Trends in Biochemical Sciences, Volume 14, Issue 6, 1989, Pages 227-232, ISSN 0968-0004, http://dx.doi.org/10.1016/0968-0004(89)90032-7.

 4. Halverson, Kelly M., and Bridgette A. Barry. “Evidence for Spontaneous Structural Changes in a Dark-Adapted State of Photosystem II.” Biophysical Journal 85.4 (2003): 2581–2588. Print.

 5. Wikipedia contributors. "Heterogeneous water oxidation." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 18 Apr. 2017. Web. 18 Apr. 2017.

 6. Håkan Nilsson, Laurent Cournac, Fabrice Rappaport, Johannes Messinger, Jérôme Lavergne, Estimation of the driving force for dioxygen formation in photosynthesis, Biochimica et Biophysica Acta (BBA) - Bioenergetics, Volume 1857, Issue 1, January 2016, Pages 23-33, ISSN 0005-2728, http://doi.org/10.1016/j.bbabio.2015.09.011.


I think i have an answer it is this nice guy.

Latin name is Leptoglossus occidentalis.

Short description of Leptoglossus occidentalis:

  Western Conifer Seed Bug
  The Western Conifer Seed Bug Leptoglossus occidentalis is a large and conspicuous squashbug, reaching a length of 20mm when adult. It is easily distinguished from all other GB coreids by its reddish-brown body, transverse white zigzag line across the centre of its wings and characteristic leaf-like expansions on the hind tibiae.


How does the MMR vaccine affect lymph nodes in preventing measles?

Lets define viremia first: The primary viremia occurs in the cells which the virus enters first in the body. There it replicates to high titers before it leaves this cells, spreads through the body and infects other cells. This is then the second viremia.

For measles the primary viremia occurs in the respiratory epithelium and in the local lymph nodes. The second viremia then occurs in skin, conjunctiva, respiratory tract, and other distant organs. In this phase also the characteristic rash occurs due to a hypersensitivity reaction of the skin. For details see here and here.

The measles vaccine works like any other vaccine: By raising an immune response against the vaccination virus. This leads to a normal immune response which leads to the production of specific antibodies against the measles virus and also to immunologic memory. These antibodies are available to fight the virus when it enters the body of a vaccinated person. This also triggers the proliferation of virus specific memory B cells which then differentiate into plasma cells and produce vast amounts of protective antibodies. So there is no special mechanism involved here beyond immunologic memory.


Calculating Possible Combinations of Bases in a DNA Strand of a Given Length

At each base, you can have 4 different bases (A,T,C or G). Therefore for the first base there are 4 possibilities, namely

A
T
C
G

For the first two base pairs there are $4^2 = 16$ possible combinations

AA
AT
AC
AG
TA
TT
TC
TG
CA
CT
CC
CG
GA
GT
GC
GG

For the first three bases, there are $4^3$ possible combinations. For 8 base pairs, there are $4^8 = 65536$ possible combinations. $2^8$, $8!$ and $8! + 2^4$ are all wrong.


Why does the SARS-CoV2 virus not remain infectious forever? Or does it?

Would it help to think a little differently? Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually.

Soap works in part by dissolving the layer of fat that keeps the virus together. It also ends up surrounding dirt so that it doesn’t stick to your skin and can be washed away with water. (These mechanisms take some time to work so that’s why people are recommended to wash their hands for 20+ seconds.)

As for when a virus is just on a surface, logically we know that how long a virus remains viable depends on both the air and the surface because the science reports different numbers depending on what the humidity is and what the surface is like. One helpful source notes:

  Similar molecules appear to interact more strongly with each other than dissimilar ones. Wood, fabric and skin interact fairly strongly with viruses.

  Contrast this with steel, porcelain and at least some plastics, such as Teflon. The surface structure also matters. The flatter the surface, the less the virus will “stick” to the surface. Rougher surfaces can actually pull the virus apart.

  The surface of fibers or wood, for instance, can form a lot of hydrogen bonds with the virus.

  In contrast, steel, porcelain or Teflon do not form much of a hydrogen bond with the virus. So the virus is not strongly bound to those surfaces and is quite stable.


Explain to a layperson how cigarettes smoke might cause cancer

I encountered the following paragraph in the textbook Life: The Science of Biology:

  Some chemicals add groups to the bases. For instance, benzopyrene, a component of cigarette smoke, adds a
  large chemical group to guanine, making it unavailable for base
  pairing. When DNA polymerase reaches such a modified guanine, it
  inserts any one of the four bases at random. Three-fourths of the time
  the inserted base is not cytosine, and a mutation results.

After finding the following quote in Wikipedia's Benzo(a)pyrene page, I decided to explain specifically how BaP can cause cancer:

  BaP has since been identified as a prime carcinogen in cigarette
  smoke.

My explanation:

A protein molecule is a chain of amino acids. Proteins are hugely important, as they are responsible for most of the cellular functions.
A DNA molecule is a chain of nucleic acids. There are 4 types of nucleic acids in DNA: A,G,C,T.
Having intact DNA molecules is crucial, because they include the encoding of proteins, according to which cells synthesize proteins.
A mutation is an alteration of a DNA molecule.
A mutation might lead to our cells synthesizing a malfunctioning protein. If a protein that should regulate cell division is malfunctioning, then the result might be uncontrolled cell division - cancer.
When you smoke, the chemical BaP (which is found in cigarettes smoke) might alter a G nucleic acid in a DNA molecule in some cell in your body. Later, when this cell tries to divide, it makes a copy of each of its DNA molecules, but it won't be able to identify that G nucleic acid (that BaP altered), so it would put a random nucleic acid in the copied DNA molecule. Thus, there is a 3/4 chance for a mutation.


Is there a way to measure ATP usage in the brain similarly to fMRI?

I'm pretty sure this doesn't exist. If it did, that would be awesome.

The following is 100% pure speculation with nothing to back this up at all (as a disclaimer).

Phosphorus-31 (the stable isotope) is NMR active, which means that you could theoretically use an MRI machine to visualize phosphorus. A quick google search shows scientists attempting to use phosphorus MRI for visualizing bone structure.

I don't really know much about MRI, but I do know some about small molecule NMR, which is based on the same principles. This is a pretty cool paper showing phosphorus-31 NMR used to measure ATP synthesis.

Maybe in the distant future it could be possible to use phosphorus-31 MRI to visualize ATP/ADP ratios in various tissues, including the brain. But that would be some amazing sci-fi stuff.


How can really even draw a defined line of what life is?

It's easy, really: just make one.  In the answer I linked to I go into the reasons why viruses aren't alive (spoiler alert: no ribosomes) and what our current definition is, but the bigger question is why does it matter?  We can draw the line wherever we want to, but it's still an arbitrary construct placed onto the universe by humans so we can sleep at night.  It's similar to intelligence.  We draw arbitrary lines around primates and dolphins and elephants and pigs and what have you, because they're the smartest and most thinking, but that's only for our own (legal) convenience.  Intelligence and awareness is a spectrum, there needn't be a point beyond which you "count."  There's no reason life can't be the same way.

Edit 1.5 years later to add a short, somewhat fanciful video I just watched, it goes into some of the complexity and difficulty with defining life; viruses show up about half way through.  It waxes philosophical toward the end, but that's sort of my point.  Arbitrary delineations are just that.


Can the excessive consumption of mineral water lead to kidney stones or other health issues?

I suffer from calcium oxalate stones.  My doctor pointed me to this study:

http://www.ncbi.nlm.nih.gov/pubmed/9096270

tl;dr;  For calcium oxalate, drinking Mineral Water high in Calcium and Magnesium may reduce the risk of forming stones.


Why do some drugs require you to take them in an "upright position"?

Metamucil is taken as a drink. You're more likely to aspirate versus swallow when drinking supine if you're ill with impaired swallowing reflexes.

It's also recommended that you take bisphophonates standing up so that gravity, and a glass of water, make sure the drug passes into the stomach. It can be highly corrosive if it gets stuck in the esophagus.


Human eyes do not take 24 images per second. Refresh done in parallel, each pixel separately, and the rate depends on the rate of color changing.

So, the work of eye is closer to MPEG encoding than to uncompressed AVI.


Does the brain always think of an appropriate response when reacting to a stimulus?

Well, not always but most of the time; reacting to stimuli is what defines the nervous system and the part of the nervous system that includes the brain is called the 'central nervous system' or CNS. Reactions to stimuli (nerve impulses) don't always have to pass through the brain as the CNS consists of the brain and the spinal cord. This means that in the case of thinking, if what you see (or sense) is something harmful (a man with a knife, feel extreme heat) then you will react without the nerve impulse having to pass through your brain (instead it will simply pass through your spinal cord). This is because the body does not need nor want to waste time thinking about an obvious and protective response. This reaction that requires no conscious thinking is called a 'reflex reaction' or an 'automatic reaction'. If you want to know more about this you should probably look into the nervous system.


Using ion-exchange chromatography to purify DNA from a cell extract - Is DNA more negatively charged then RNA?

A longer or duplexed Nucleic acid will have more charge per mole of the molecule. But generally it is not the overall charge that matters in electrophoresis or MS or chromatography; it is the charge density and specific charge (z/m) that matters (charge density of a longer RNA will be almost same as smaller RNA. they will also have same specific charge)

The properties of stationary phase  is very important in controlling the separation process. Without knowing what resin is used, it will be difficult to comment about why RNA is not retained.
Sometimes the strong basicity of the stationary phase, such as in quaternary ammonium resins, degrades RNA by alkaline hydrolysis.

If yours is a commercial resin then you will have a tough time finding out what exactly it is made of. Unless of course you break the column open and do a molecular analysis of the resin :P


Identifying a spider very similar to a brown recluse

I think this a nice male Cheiracanthium inclusum, the familiar "yellow sac spider" (outdoors edition).  The abdomen is what you would expect, the very long first pair of legs, the obvious eyes at the front of the head (middle two of the top row).
I'd feel more comfortable if I could see the usual very dark 'face' and chelicerae, but the angle of the photo is such that it might be just hidden.  The carapace pattern looks interesting, but it may well be that the flash of the photo is giving us a different look there.

Here's the link to the Bug Guide page, with a representative photo of a similar male:

https://bugguide.net/node/view/80427


What is mold detection threshold in humans?

It depends on the mold. For example, humans can smell octenol in ppb concentrations[1], presumably long before any toxic effects of this or other compounds produced by molds. Octenol is produced by many molds, always through breakdown of linoleic acid (part of many triglycerides, i.e., fatty oils present in most food).

Update: another example of a non-toxic mold is that causing cork taint. The responsible substances (trichloroanisoles, TCA) can be tasted by humans in wine at 2-4ng (nanograms) per liter wine.[2]

[1] M. J. Saxby: Food Taints and Off-Flavours., 2. ed., Springer 1995, ISBN 978-0-7514-0263-6, S. 210–212.

[2] http://schaechter.asmblog.org/schaechter/2018/07/tainted.html


What is the biological principle of this "holotropic breathwork" technique?

I think this is mostly caused by hyperventilation. The excessive breathing disturbs the balance between CO$_{2}$ and oxygen in our lungs. This will cause respiratory alkalosis (the blood pH, which is normally strictly regulated, gets higher), which can cause dizziness, headaches and fainting.

The shift in pH can also disturb the eclectrolyte balance, especially the concentration of the free dissolved calcium, as it binds to negatively charged plasma proteins (which release protons into the blood due to the higher pH). This can lead to craps and spasms.
I would be very careful not playing around here, as this can have some severe consequences.


How do non-human apes cool their body temperature in warm climates?

First they have less cooling needs than us, shady forests are cooler than sunlit savannah, they also are not as active, especially the larger ones, at least not in the hottest parts of the day. keep in mind chimps are much smaller than us so they have an easier time cooling off. They cool themselves the same way we do, by sweating, its just not s effective as it is in us, but then it doesn't need to be. .


What causes skewed lanes in a DNA gel electrophoresis experiment?

These are sequencing gels (in the cases here even radioactive ones) - they are run a lot longer than ordinary agarose gels and they are made from polyacrylamide. Im my experience, the most likely cause for skewing of lanes (not only bands) are samples, which still contain too much salts from the PCR reactions. This can also happen to only a few bands as seen here. Overall these are still pretty nice and clean gels, I have seen much worse.

Other reasons which cause uneven gels are cases where the acrylamide is not mixed good enough (causing the gel to have different concentration and thus causing different running conditions), uneven warming (although this was usually preventing by the gel heating system) and leaky gels where the electric field was not completely even.


Does melanin protect against nuclear radiation?

The absorption of gamma and x-ray radiation by skin is negligible, so the amount of melanin present is irrelevant. Stopping high energy photons requires a lot of mass, not a few microns of melanin.


Could super-caffeinating somebody's bloodstream be dangerous?

In extreme doses, caffeine can - like almost any substance - cause death. Wikipedia has this to say on the subject:

  Extreme overdose can result in death.[59][60] The median lethal dose
  (LD50) given orally is 192 milligrams per kilogram in rats. The LD50
  of caffeine in humans is dependent on individual sensitivity, but is
  estimated to be about 150 to 200 milligrams per kilogram of body mass
  or roughly 80 to 100 cups of coffee for an average adult.[61] Though
  achieving lethal dose of caffeine would be difficult with regular
  coffee, it is easier to reach high doses with caffeine pills, and the
  lethal dose can be lower in individuals whose ability to metabolize
  caffeine is impaired.

You may wish to consult the references mentioned in the Wikipedia article for further details (As we all know, one should not trust Wikipedia too much). Note that caffeine administrated directly to the bloodstream will be more dangerous than the same amounted ingested.

Information on caffeine toxicity can also be found at Medscape. I you need concrete examples, Holmgreen, Norden-Petterson and Ahlner have published case reports on four recent cases of coffeine-related fatalities. (3)

To cover all bases, it should be said that none of the information mentioned should be used to estimate a safe level of caffeine intake.


Hummingbirds can give the impression by their small body size that they are very fast and of course they are. The Anna-Hummingbird, about ten centimeters in size, reach speeds of 385 body lengths per second (27. 3 m/s or 98 km/h).
So they can get acceleration values of about ten times the acceleration due to gravity.

To the comparison: Peregrine falcons come on speeds of up to 200 body lengths per second in the nosedive and fighter jets, like e. g. the MiG-25 (a Mach 3 fast interceptor), reach only the approximately by 40 times of its total length by one second.

They got this enormous achievement mostly by their biological construction.

For example: the heart of the hummingbird is very large in relation to the body and beats 400 to 500 times per minute, its respiratory rate is up to 250 strokes per minute, so  lots of oxygen gets into their wings and they can perform so strong. During sleep, many hummingbirds reduce their heart rate to save energy.


Unequivocally, YES.

Before DNA sequencing was used to deduce the sequence of cloned or reverse-transcribed RNA molecules, slower and more cumbersome direct sequencing of RNA was performed using the method of Sanger et al.  (Sanger, F., Brownlee, G. G. and Barrel B. G. (1965) J. Mol. Biol. 13, pp. 373–398). This used ribonucleases in a manner somewhat similar to pre-Edmann protein sequencing.

Because of its abundance and ease of purification ribosomal RNA was a suitable species for this approach, and Carbon et al reported the complete sequence of E. coli 16S rRNA in 1978 (Carbon P., Ehresmann C., Ehresmann, B. and Ebel J.P. (1978) FEBS Letters 94, pp. 152-156).

Sigh! How little do modern molecular biologists know about the history of their subject.


how do we prevent restriction enzyme of bacteria to cut and destroy our new recombinant?

You're essentially looking for a restriction modification system. You modify the restriction sites with methyl groups in a way that blocks restriction enzymes from accessing them. The DNA methylation should also be maintained through replication. So if you have an EcoRI site, you can use an EcoRI methylase to block the action of EcoRI.


How do I calulcate the amount of concentrated stock solution to add to get the correct dilution?

For any question regarding volume and concentration, you should consider the equation $C_1V_1=C_2V_2$. We can use it to derive a general equation for the addition of concentrated stock solutions. We want to find the volume of stock solution ($V_1$) to add so that its final concentration is 1X. Here's what we know:

The initial concentration of stock solution, $C_1=X$
The final concentration of the solution, $C_2=1$
The volume of solution we are diluting the stock into, $V_s$

So the equation becomes:

$$XV_1=V_2$$

We don't know $V_2$, but we do that $V_2=V_1+V_s$. Subbing that in:

$$XV_1=V_1+V_s$$

Solving for $V_1$:

$$XV_1-V_1=V_s$$
$$V_1(X-1)=V_s$$
$$V_1=\frac{V_s}{X-1}$$

Then you simply need to sub in your values:

$$V_1=\frac{25μL}{6-1}$$
$$V_1=5μL$$

So you should add 5 μL of your 6X loading buffer to the 25 μL solution to get a 1X final concentration.


What allows grass eaters to digest cellulose?

No there is something else missing besides bacteria

humans often already have the right bacteria but they don't digest most of the cellulose they ingest because digesting cellulose with bacteria is SLOW. Too slow to keep up with normal mammalian digestion. You need a specialized gut that  either has a large complex stomach to keep recycling the cellulose in the system (foregut fermenters) or has large storage chambers to keep the cellulose a long time and allow it to be digested slowly (hindgut fermentation).

humans have neither. To make matters worse Humans have huge caloric needs compared to other animals of the same size. Brains are calorie hogs and our brains are so large they consume 1/4 of all our calories. That is 3 pounds of our mass consumes a quarter of all the calories we eat. honestly without the advent of cooking (which drastically improves the caloric availability of food) human brains could never have reached the size they did.

Further reading

More further reading


What are the differences between how glucagon and cortisol work to increase blood sugar?

Glucagon and cortisol are VERY different types of hormones, though each of them can affect glucose metabolism and effectively can increase glucose concentrations in the blood (albeit through different mechanisms).

Glucagon, pictured above, is a 31 amino acid peptide hormone (i.e. PROTEIN) that is released from the alpha-cells within the pancreatic islets. Glucagon travels through the blood and acts predominately in the liver on glucagon receptors. The glucagon peptide binds to the glucagon receptor on the OUTSIDE of the cell and transmits a signal to the INSIDE of the cell. This occurs when the glucagon binds to the receptor, changing its conformation or "shape" on the inside of the cell, which then causes binding and activation of a G-protein inside the cell ($G_S$). This $G_S$ protein activates an enzyme within the cell (adenylyl cyclase) to increase the concentration of a substance called cyclic AMP (aka cAMP) that activates a number of enzymes that ultimately increase the amount of glucose released by the liver. These effects are IMMEDIATE effects, which is why we sometimes give glucagon injections to treat patients with hypoglycemia (i.e. dangerously low blood sugar concentration). However, sustained glucagon signaling likely has effects on the expression of the enzymes that cause the glucose to be released from the liver as well (though that is a discussion for another question).

Cortisol, pictured above, is a steroid hormone (i.e. LIPID) that is released from the adrenal glands, specifically the zona fasciulata, which is the middle of the three 'layers' of the adrenal gland. Cortisol is referred to as a glucocorticoid and exerts its major effects through changing gene transcription in a variety of cell types. The way that cortisol does this is by binding its cortisol receptor, which is generally thought to be in the cytoplasm inside the cell. Upon binding of cortisol to the cortisol receptor, that complex is then transported into the nucleus of the cell where it binds DNA and can increase or decrease the transcription or expression of target genes. In the case of cortisol, these genes are for the enzymes that increase glucose production of the liver, and thus increase the body's capacity to maintain or elevate blood glucose. There is also some evidence that cortisol has additional effects independent of gene transcription, but that is outside the scope of this question. Regardless, the effects of cortisol on glucose metabolism are not immediate, but rather they take >30 minutes to several hours to begin to take effect.

As mentioned in the question, both glucagon and cortisol affect glucose metabolism. Cortisol also affects the transcription of a number of genes involved in adipose tissue and lipid metabolism, as well as genes that are involved in protein metabolism and inflammation. Cortisol can be injected into a patient with an autoimmune "flare-up" in order to quell the inflammation, but those are different mechanisms of cortisol than its effects on glucose metabolism. A description of those effects is also outside the scope of this question, but could easily be read about in recent reviews on cortisol available on PubMed, e.g. Recent Cortisol and Fatty Liver Review.


How do I prepare and clone from E. coli DNA?

Yes, you must fragment the genome in order to insert it into a vector for cloning; you can't "insert" the whole 5 Mbp genome of E. coli into a vector.  It's difficult to transform cells with huge plasmids, 2-20 kbp is an optimal range.  In any case, if you want a clone of the whole genome, wait 30 minutes and the cell will happily oblige you.

Most procedures that isolate genomic DNA will fragment it in the first place, as it is much too large and fragile to stay together, and if it did it, the majority would be caught up in other cell debris and discarded.  Vortexing with glass beads is a typical first step to randomly fragment it.  After this, you can digest the DNA and your vector to place matching ends on it, ligate it, and transform host cells.

If you want a targeted approach (to extract a specific gene, a technique with which I am unfamiliar), you may be able to use PCR on your extracted, fragmented DNA, as there would hopefully be one intact segment spanning what you want.


Does cell phone radiation promote longevity?

If you read the discussion, and also the full contents of the PDF which include some reviewer comments, there is concern about the control group:

  The survival of the control group of male rats in the current study (28%) was relatively low
  compared to other recent NTP studies in Hsd:Sprague Dawley® SD® (Harlan) rats (average 47%, range 24-72%).

Specifically, the control group had an abnormally high mortality rate for that strain of rat. There is no increase in longevity if you compare to historical data.


How to identify whether something is in linkage disequilibrium?

As per the definition you gave, you check whether there is a statistical association between the two. If knowing when allele is present at a locus does not affect the probability of finding a given allele at the other locus, then they are independent (there is no association). Otherwise, there is an association and hence the two loci are in linkage disequilirium.

See wikipedia > Linakge disequilibrium for more info.


In most marsupials, only the females have a pouch. However, males of the water opossum and the extinct tasmanian tiger (or thylacine) also have a pouch.  The males of both the thylacine and water opposum used/use their pouch to keep their genitalia from getting entangled in vegetation.


What are the differences between a benign tumor and swelling?

The term tumor is used in the medical definition of inflammation. However it just denotes a temporary swelling that goes down once the inflammation subsides. This swelling is due to edema (accumulation of fluid). You have to understand that in practice no one uses the term tumor to denote an inflammatory swelling. So the term “tumor” denoting edematous swelling is of historical significance only.

In modern practice the term tumor is used only to indicate abnormal growth of any kind. Either benign or malignant.

In pathology an inflammation is classically described as having the following features:

Tumor : Swelling
Dolor : Pain
Calor : Warmth
Rubor : Redness


How much are phase-contrast and dark-field microscopy used in biological research?

I use phase contrast very often, as it is only a matter of switching a lens group from bright field. Instead of spending hours with staining, or, worse, immunostaining, I get the big picture (cell diameter) in a few seconds. I can even go back to the same cells next day. Switching to dark-field is also a matter of turning a dial or pushing a switch.

If you already use brightfield, there is not much to learn about them in terms of actually useful physics, or sample preparation. The things you could learn - say, that colors are altered in darkfield - will rarely be needed in practice. These methods are the sort of things you don't really need to know in depth unless your experiments require them. Even then, practice and elbow grease would be more helpful than advanced optics. Remember that in most cases, the scientific hypothesis is more important than the tools you can use to solve it.


In order to date the age of a tree, you have three solutions :

If you can cut the tree then you can simply count the number of rings. Note that for very old trees the central rings will have rotted and you will only have a lower bound on its age.

If some parts of the tree are dead, you can use radiocarbon dating to estimate the time of death with a relatively bad precision (the error is about 100 years which can be a lot for a tree)

You can estimate its growth rate (either using the width of the rings, or by doing multiple measurements for several years), and deduce the age from its size.


What is the probability of an offspring sharing identical HLA typing as one of their parents?

If you follow your math, you will definitely not find a 1/1,000,000 chance of two random people being an HLA match, so it seems clear that the independence and equal weighting of types is not a great assumption.

We can make a different set of back-of-envelope assumptions, and just say that the 1/1000000 number comes from having 6 combined matches. In that case, you would interpret 1/1000000 as due to 6 independent matchings of probability 1/10. In that case, with a parent you only have to randomly match the other three. 1/10^3 = 1/1000, much closer to the 1/200. Further non-independence, unequal frequencies, and homozygosity makes 1/200 seem reasonable in a whole population (though individuals with more rare HLA would be less likely to match a parent or a random individual), and I presume the 1/200 number comes from actual observed frequencies rather than theoretical calculations.

Perhaps someone with more HLA expertise (I have basically none) will provide a better answer based on more specifics, but I just meant this as a quick napkin calculation for whether the numbers given are plausible, and I think that they are.


Why was it so hard to decode the corn genome?

The short answer is that corn genome is large and has a huge amount of duplication events. Around 80% of the genome are repeated. It's hard to assemble genomes with large amount of duplications because our sequencing technology, practically, at best can give ~500 base pairs. Figuring out the ordering of duplicated regions relies on scaffold sequences or comparative assembly to rice genome.


Generally I would advise against making a home-brew electroporator: the voltage needed for electroporation is so high, that even with professional equipment you can easily get arc lightning. In an self-built device that would pose a serious fire hazard.

However even theoretically there are problems with the design you propose:

1) It is important that ALL bacterial cells in the cuvette get exposed to electrical field induced by the high voltage spike. If you use simple electrodes you will only affect the few cells directly between them, which will drastically reduce efficiency of the electroporation. For your design to work properly you would need electrodes that exactly match the dimensions of an eppendorf tube to make sure all bacteria will be squeezed between them.

2) With your device you can only do one electroporation, then you have to thoroughly clean the electrodes. This has to be done for two reasons: first you don't want any carry over bacteria (or as Chris pointed out DNA) from one batch to another. Secondly the electrodes need to be clean of any salts (or other molecules that increase conduction in a solution) to prevent arc lightning between them.


What kinds of arousal can a human brain experience?

Depends on what you mean by "addiction": defined, addiction usually requires both psychological and physiological dependence, but conversationally we sometimes only talk about psychological dependence (as in here, your muscles won't cramp up if you NEED a horror flick).

If a person enjoys horror movies, is it the suspense? Such a rush is caused by the well-known fight-or-flight catecholamine epinephrine (also known as adrenaline). This is the short-term stress response at play. Comfort foods are a whole other story, because it depends on the food as well. Carbohydrates can contribute to serotonin levels, yes, but I read a super-interesting study a couple years back about saturated fat causing a decrease in corticosteroid levels and this sought to explain why people eat fatty foods when they are stressed (I'll try to find this article for you). Tryptophan, an amino acid, is converted to serotonin, which is why turkey, milk, and other sources of trp can make one sleepy.

Awesome question! I'm going to try to learn more about this and find that article for you. Dopamine is the primary player in most conventional addiction-talk, as it's crucial to the reward circuitry that is usually discussed.


Is there an Exit site (E-site) on the eukaryotic ribosome?

Prelude: Thinking about protein synthesis

I remember the time when there were only two sites on the ribosome, and when it became clear there were more, I resented the need to make my lecture notes and my contribution to a venerable text book more complicated. So I am neither a devotee nor an expert on the exit site, but if asked to guess who was right (even if, or especially if, the student was supported by Campbell’s Biology as @CSharp informs us) I would put my money on the ‘professor’. Why? Because protein synthesis and the ribosome are so ancient that although there have been changes in eukaryotic proteins synthesis, something so fundamental as the sites for the fundamental process would not change.

Answer

Yes, Virginia, the eukaryotic ribosome does have an exit site.

The evidence

Although editions of the venerable text book no longer appear and my research no longer impinges on protein biosynthesis, I still collect papers on the subject with my bibliographic software. The latest relevant publication I have is by Khatter et al. from Nature in 2015, entitled Structure of the Human 80S Ribosome.

As not all list members have access to Nature, as a subscriber I have taken the liberty to reproduce a a section from the abstract (my emphasis) and a pertinent illustration:

  Here we report the near-atomic structure of the human ribosome derived
  from high-resolution single-particle cryo-electron microscopy and
  atomic model building. The structure has an average resolution of 3.6A
  ̊, reaching 2.9A ̊ resolution in the most stable regions. It provides
  unprecedented insights into ribosomal RNA entities and amino acid side
  chains, notably of the transfer RNA binding sites and specific
  molecular interactions with the exit site tRNA.

The cryo-EM map and atomic coordinates have been deposited in the EMDB and Protein Data Bank under accession codes EMD-2938 and 4ug0, respectively.

I admit I haven’t researched and rehearsed the evidence, but I think that would be another question.


What kind of spider is this and is it poisonous?

It's a Mygalomorph spider, of the sort which are usually called Tarantulas.  This is told by the two long, upcurved spinnerets and the large, dish-shaped carapace, with the eyes clustered in a clump - looking rather like the disk of the USS Enterprise from Star Trek, if the command bump was placed near the front edge.  I'm not sure which species it would be, but the good news is that like almost all spiders, it's pretty much harmless to humans.  These guys do have large fangs, though, so if you got bitten by one, you'd feel it.  As far as I'm aware, the venom of South American species is no big deal, so the feeling of being poked by a big needle is likely to be the worst effect.  Presumably they were entering your house to hunt for the small animals which share your home with you - large insects, small mammals and lizards, maybe.  I'd post an image, but I'm not sure which tarantula this would be (not really being a tarantula guy), and you could probably do as good a job of searching the internet as I could.  However, here is a resource I was able to turn up with a short search:

ttfnc.org/livingworld/index.php/lwj/article/download/479/462

As I said, I'm not really a tarantula guy, and so am not confident as to a specific ID of this spider.  However, having been pressed for an image, there are in this article some images of a spider which may or may not be yours.  The images are, however, tarantulas from Trinidad.  You will need to page through to the end of the article to see them:

http://sciencepress.mnhn.fr/sites/default/files/articles/pdf/z2017n2a5.pdf


Copied from my comment:

It just means a sound that starts at a low frequency and goes up to a higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.


What's the minimum distance of focus for the lens of a human eye to reach maximum flatness?

There are practical questions in ophthalmology and you've asked someone that has a common theoretical answer: 6 meters.

However, you should know that from the same theoretical point the far the object the less accommodation we need, so the second answer is - infinity.

What is the difference? From the practical point the accommodation between this two points is negligible and does not have to be taken into account when we correct the refraction error.

Small theory - to see an object placed at a distance of 1 meter we need 1D of accommodation power (1/1meter=1D), to see an object placed at a distance of 30cm we need 3D of accommodation power (1/0.3meter=3D), for an object at a distance of 10cm we need 10 diopters and finally for an object at the distance of a 6 meter we need accommodate 0.16 diopter.

Thus between 6 meter and infinity the accommodation is very low and this is why the distant visual acuity is checked at this distance. Consequently, the lens convexity difference between 6 meters gaze and infinity is negligible and this is why the answer to your question is between 6 meters and infinity (zero accommodation).

From this explanation you can calculate the dioptric add for any reading distance  and understand how the reading spectacles correct the loss of accommodative power (=presbyopia, the vision of older people).

If you want to know how much the crystalline lens changes its dimensions during accommodation, the answer is near 7% for diameter and near 10% for thickness, so the lens as was convex, stays convex and the visible changes are minimal.


Is it possible to identify a particular gene sequence from next gen sequencing techniques (especially RNA-seq )?

Okay, so you have RNASeq, but no reference genome for your fish?  Just transcript sequence from zebrafish?  Are you just trying to see if this gene is expressed, or you need to a more global view to compare it to?

If you just want to see if the gene is expressed, easy thing to do is to make a reference just made up of zebrafish transcripts, align to that.  If there are too many differences between your fish and zebrafish, that won't work.

In which case, the next thing you could try is de novo assembly of your RNAseq data, then use blast to compare the zebrafish trasncripts to your assembled transcripts.  Blast will make alignments where a short read aligner might not.


What are the pros & cons of site-directed mutagenesis? What are the alternatives?

SDM will be the perfect tool for this mission, unless the plasmid in question is very large (20+ kb).

When you have performed the SDM, digest the products with dpnI to remove the original plasmids, transform e.coli and use a selective media matching your plasmid. Only bacteria with the plasmid will then be able to survive and form colonies, pick several colonies and perform a miniprep for each and sequence the area of interest. You can use the rest of the miniprep with the correct plasmid for transformation and expression. So skip step 5.


Availability of a database containing the proteins of Vibrio cholerae and their corresponding gene sequences

You want to go to PATRIC > Data > Download Tool.

From the Taxonomy tree, find Vibrio cholerae, choose Type of annotation as either PATRIC/RefSeq or both, choose the type of file you want (gbk or faa) and download from there.


How does chromosome number get halved in meiosis I?

If you consider sister chromatids to each be a chromosome, meiosis I, rather than halving the chromosome count, separates the homologous chromosomes, which result from sexual reproduction, from one another. Meiosis II then separates the sister chromatids from one another resulting in the final halving of chromosomes.

On the other hand, many if not most biologists don't consider the sister chromatids to be individual chromosomes until they are segregated during meiosis II. In this sense, meiosis I does reduce the chromosome count to half.


Why are Arabidopsis plant seeds being sent to the moon and not other seeds?

Without speculating further about specific decision making processes, Arabidopsis is the standard model organism in plant biology, similar to the mouse for mammals, the fruit fly for insects, C. elegans for nematodes, etc.

It's the first plant to have its genome sequenced, it's commonly used in undergraduate laboratory experiments in part because it grows very fast, etc.

If you were going to choose a plant arbitrarily for a research project, it might as well be Arabidopsis, I'd say it would be the default against which other options would be considered.


Protein bands not visible after sds page coomassie dye stain

The problem here is concentration. Coomassie Blue stain can only detect protein band greater than or near to 50ng, in this case, the concentration of your protein is too low for detection. If you want to stick with Coomassie stain, you can try colloidal Coomasie stain instead because it has a much lower detection limit than Coomasie blue (between 10ng to 20ng).
In addition, I think what causes such low protein concentration is the poor solubility of yeast cell wall. One way to get around this is to increase solubility is through chemical hydrolysis, for example using diluted sulphuric acid1-3. This will partially solubilize mannas-protein outer layer of the cell wall and help you to obtain soluble yeast cell wall products.
References:

Theodoro, S. D. S., Putarov, T. C., Tiemi, C., Volpe, L. M., de Oliveira, C. A. F., Glória, M. B. D. A., & Carciofi, A. C. (2019). Effects of the solubility of yeast cell wall preparations on their potential prebiotic properties in dogs. Plos one, 14(11), e0225659.
OGAWA, K., & MATSUDA, K. (1994). Characterization of Manno-oligosaccharides Containing α (1→ 2)-and α-(1→ 6)-Linkages Obtained from Saccharomyces cerevisiae Mannan by Controlled Acid Hydrolysist. Journal of Applied Glycoscience, 41(4), 433-437.
Peat, S. (1961). Polysaccharides of baker's yeast. Part IV. Mannnan. J. chem. Soc., 61, 29-34.


Does GC content determine codon bias or does codon bias determine GC content

Think about it this way, the G-C content is averaged over the entire genome, and varies between different species.  Whether you are dealing with prokaryotes, with relatively compact genomes, or with eukaryotes, with lots of non-coding regions, the open reading frames will, in general, be influenced by the average G-C content across the genome. Therefore we would predict that in species with lower G-C their open reading frames would be biased to using the codons in the genetic code that are higher in A-T. N.B. this also means that their tRNAs should also favour anticodons higher in A-T. In contrast, we would predict that in species with high G-C content, the open reading frames would be biased, in general, to using codons that are higher in G-C.
That is all G-C bias in codons is; for some amino acids like Met and Trp, there is only a single codon, but for other amino acids there can be up to six codons that can each encode the same amino acid side chain. It is in these ones with a higher number of degenerate codons that you are going to see the effect of codon bias.


Do vitamin enriched foods preserve their value when exposed to higher temperatures?

Here's one estimation about how much vitamins or minerals can get lost due to various "food processing" (cooking, drying, freezing) methods:

According to NutritionData, cooking can result in a loss of vitamins:

Vitamin A: 25%
Vitamin C: 50 %
Vitamin B complex vitamins: 25-70%
Minerals: 25-70%; most important: potassium loss in cooking water. In this study with potatoes:

  Leaching alone did not significantly reduce levels of potassium or
  other minerals in tubers. Boiling tuber cubes and shredded tubers
  decreased potassium levels by 50% and 75%, respectively.

According to USDA retention factors, the following vitamins are most affected by food processing:

Vitamin C
Vitamin B1, B6, B12 and folate

Vitamin and mineral loss is related to both the temperature and time of cooking.

Mineral loss can be prevented by cooking in vapour (steaming) instead of cooking in water.

According to this source, the following can be loses after heat treatment at 70 °C and (90 °C):

Vitamin A: 10% (30-40%)
Vitamin D: 15% (35%)
Vitamin B1: 15% (50%)
Folic acid: 5-20% (45%)
Vitamin C: 40% (85%)


Reason behind formation of different shapes of cell

Cell shape is dictated by the cytoskeletal arrangement. There are both intrinsic and extrinsic factors that control cell shape.

Extrinsic factors consist of environmental factors such as extracellular matrix. Rho-GTPases relay the environmental signal to the cells to cause cytoskeletal rearrangement.

Intrinsic factors are basically the stable transcriptomic identity (a gene regulatory programme) which determine a cell shape. I personally don't have an idea about what genes give an intrinsic cell shape. For e.g. why does hela cell look different from HEK cell in the same type of cell culture plate under same conditions (even at low densities where there is no neighbor effect).