Interpretation of the Question
The question asks how the G-protein α- and βγ-subunits move, but does not state the context or circumstances of the movement. I assume that the question is, in fact:

How do the G-protein α- and βγ-subunits move apart and migrate
from receptor to target enzyme when their interaction is prevented by
the binding of GTP to the α-subunit?

False premise in the question
The problem envisaged in the question is that as the α- and γ-subunits have lipid moieties covalently bound to their amino acid chains, they are somehow part of the lipid cell membrane. This non sequitur may arise from a misunderstanding of lipid chemistry: the cell membrane is a bilayer the main constituent of which is individual molecules of phopholipids containing two long fatty acid chains and one polar organic phosphate (e.g. phosphatidyl choline) attached to a glycerol backbone. Other hydrophobic molecules (cholesterol, proteins with hydrophobic amino acids on their surfaces) can interact with these phospholipids.

The lipid moieties attached to the G-protein subunits are, in contrast, single palmitoyl or myristoyl fatty acid chains (in the case of the α-subunit) or farnesyl or geranyl (substituted fatty acid) chains (in the case of the γ-subunit). So the idea that they are somehow equivalent to the membrane phospholipids is incorrect.
How do they move?
As the lipid bilayer is fluid, its constituents can move within it, like ships on the sea. A review by Wedegaertner discussing G-protein trafficking illustrates this as shown below:

When the interaction between the subunits is prevented by GTP, they are free to drift apart in the membrane, like a boat cut loose from a ship at sea. The illustration shows them attached to the membrane by a single line representing the lipid group, but also considers evidence that they may move away from the membrane, presumably because the interaction is weakened on dissociation. Their movement is presumably random thermal motion in each case, as is that which leads to their reassociation after the GTP is hydrolysed.
However, as @BryanKrause mentions in his comment, it should be emphasized that the ability of the subunits to ‘float’ through the membrane (rather than ‘sink’ into the cytoplasm) facilitates their mode of action. They must first associate with the hormone/agonist receptor to receive the initial signal (or first messenger) and then move to interact with the target enzyme/protein which transmits the signal within the cell (e.g. through the second messenger cyclic AMP produced by the enzyme adenyl cyclase). See, for example, this Nature Scitable article.


Is arachnophobia connected to lower immunity against spider toxins?

This is an interesting question and may stem from the fact that spider phobias tend to run in families and thus have a genetic link - assuming susceptibility to toxin levels can be passed from parent to offspring.  However, instead a study found that the fear of spiders was caused by social learning of disgust reactions.

Source: https://www.psychologytoday.com/blog/why-we-worry/201407/why-are-we-afraid-spiders

Directly from source:

  In relation to the first question, it has been known for many years
  that spider phobia tends to run in families. It has often been assumed
  that this may represent a biological predisposition caused by the
  transmission of genes between parents and offspring. However, we found
  that this relationship was considerably more complex and indirect. We
  found that the only significant predictor of a child’s spider fear was
  not the level of spider fear in the parents, but their levels of
  disgust sensitivity. One interpretation of this finding is that spider
  fear may be transmitted within families as the result of social
  learning of the nature and intensity of disgust reactions–including
  disgust reactions to spiders.

Link to study abstract: http://www.sciencedirect.com/science/article/pii/000579679390041R


Are there animal species in which the females expend more energy attracting males than in their offspring?

The reason why, in most species, males are competing to access females and females are choosy is due to Bateman's principle.

  Bateman suggested that, since males are capable of producing millions of sperm cells with little effort, while females invest much higher levels of energy in order to nurture a relatively small number of eggs, the female plays a significantly larger role in their offspring's reproductive success. Bateman’s paradigm thus views females as the limiting factor of parental investment, over which males will compete in order to copulate successfully.

But there are exceptions to this general rule.

Fish

In many fish species (e.g. pipefish, scissortail sergeant and seahorses), males are choosy and females are competing. In these species, females deposit their eggs in a special brooding pouch that the male possesses. The male then has the energy cost of raising the offspring, while the female does not provide any parental care. As a result, males in these species must choose among competiting females for mates( Vincent et al., 1992)

Birds

In many bird species, there is bi-parental care, leading to competition among mates in both species. See the interesting case of Jacana jacana (Emlen and Wrege, 2004).

Frogs

In poison-arrow frogs (Dendrobates auratus), the male spend more energy for raising the offspring than the females and the males are therefore choosy (Wells, 1978).

Related: Why are female not competitive for reproduction like males?


What is the female equivalent of the morning erection that some men experience?

Women have erections too! These erections are called clitoral erection. Clitoral erections are usually accompanied with vaginal lubrification.

Just like men (see here), the absence of norepinephrine during the REM phase of the sleep causes erections. In women, this phenomenon is called Nocturnal clitoral tumescence while it is called Nocturnal penile tumescence in men. In women, not only the clitoris get engorged with blood but the vagina too.


That was surprisingly buried.

I found this in a paper describing genome build 3 - See "Materials and Methods".  I imagine that this is consistent through to the current build.  In any case it should get you started.

"Sequencing templates were made from P1, BAC and WGS DNA libraries using the D. melanogaster strain yellow (y1); cinnabar (cn1) brown (bw1) speck (sp1)."


Essentially that's what I remember, but there can be a lot more steps between A and C, i.e. more pathways interacting in different systems to produce an associative memory. Pavlov's dogs is the classic example:

1: Pavlov rings bell, dogs hear bell

2: Pavlov feeds dogs, (dogs rewarded)

3: Repeat 1 and 2 for a few days.

4: Ring bell, dogs will salivate and expect food, even if no food is on the way.

So, in the skull, the dogs are making a link between hearing a bell and a reward.

Dopamine is released at dopaminergic synapses, the limbic system is probably the best understood part of the memory/reward system, particularly the mesolimbic pathway for reward.

Neurons get triggered by presynaptic neurotransmitters, some require convergence of signals to reach threshold and trigger an action potential. Connections are strengthened by long-term potentiation, which has been argued to be the basis for memories, but that's a massive topic I'm not qualified to discuss.

I haven't heard of the "error prediction signal" before, might be a new discovery/thinking that I'm a bit behind on.


Possible calculations with temperature, humidity, images and VIS spectrum of a plant in an Integrating sphere

With the images you could, perhaps, assess growth rate of the plant which can be plotted against spectral content of light to investigate effects of light quality on growth. Using moist and water and temperature the same can be done. Multivariate analysis can help to implement all the values, while ANCOVA may may help to correct for covariance.

A detailed experimental set up may help to answer this question. Not specifically the hardware, but how the effect of water stress is measured. E.g., are multiple plants tested under different watering conditions? In that case all the other measures (temperature, light) are probably used to check whether everything is constant across all specimens except water availability. This may limit the usefulness of analysis of these additional measures. I think the other parameters (light, water, temperature) may be not so interesting other than covariates for water stress as they are either not controlled or deliberately kept constant. Moreover, probably their effects on plants are pretty obvious too.


What does it mean to say that the sympathetic nervous system is organized for diffuse activity?

"Mobilize" in this context means to:

  to release (something stored in the organism) for bodily use

Merriam-Webster

"Diffuse" means "spread out": it doesn't say anything about whether the effect is "major" or "minor" and I don't think it's useful to think in those terms. Instead you should just appreciate that there is no specific target affected by sympathetic activation, rather it is a whole body response: almost every organ system is involved.

Sympathetic nervous system activation occurs when an organism needs to be ready to act immediately (such as in a 'flight or fight' response), which includes more metabolism in the muscles and increased sensory sensitivity. It also includes compensating by reducing metabolism in the gut: even though digestion is a source of energy, it is slow rather than immediate and costs a lot of energy in the short term through the processes of digestion.


That is a butterfly known as a "Mapwing". It is in the family Nymphalidae. I'm pretty sure it is Cyrestis maenalis. https://wikivividly.com/wiki/Cyrestis_maenalis


Identify this thin and strangely-shaped dragonfly, and understand why the shape looks so weird

This dragonfly damselfly is from the species Pseudocopera ciliata. Dragon fly anatomy changes between species and there is not definitive answer for why it looks like that, the best guess i can give is that it may assist the female as she tries to find the hookup point for mating.
General Information
More Information(Pay-wall)
This is in Chinese but confirms presence in Taiwan: http://gaga.biodiv.tw/new23/s3-37.htm


Absorption rate of Infrequently eating animals?

I'll take a stab at this.

What fraction of your food is absorbed and what fraction is expelled is a function of what kind and how much indigestible material there is in the food, and not related to how often the animal eats.

How often an animal eats is a function of its metabolic demands(how many calories it needs) and how many calories it can get in one meal. Reptiles, as ectotherms, have a lower metabolic demand than endotherms. In addition, snakes can swallow huge amounts(relative to body weight) of high-calorie food in one sitting. As a result, snakes eat infrequently. Pet snakes are fed weekly or biweekly, depending on a number of factors. A reticulated python can swallow and digest something up to its own body weight. Ten weeks of digestion gives 1.4% of its own body weight daily, even without fasting.

Elephants are a migratory large mammal and eat about 4% of their body weight each day, more or less. This takes about 12-18 hours to collect, according to these people.

Elephants eat high-fiber, low-calorie foods, and as a result about 20% of their food mass is turned directly into poop. They feed often, and don't absorb much. Hummingbirds eat constantly, consuming their own body weight in food each day, but poop almost not at all. Their feces contains the indigestible parts of their food, just as the elephant feces does. The different is that large parts of elephant diet is indigestible fiber, while a tiny part of the hummingbird diet is indigestible insect exoskeletons.

All creatures absorb as much nutrition from their food as they can, and expel the remainder. How much remainder there is depends on what kind of food they eat.

Growth rates versus digestion rates and mass intake is a totally different and much more complicated question. Generally speaking, the growth-limiting factor is DNA replication or an essential acid or mineral deficiency and not a raw mass problem.


What are the small lumps in the mouth of the fish, and what is its function?

Yes those are teeth and some have them and some do not for the same reason some have sharp teeth wile others have flat scrapper teeth, it depends on their diet.

this kind of teeth are called molariform, and are used for crushing shellfish more than anything else. This slide show will help you, https://www.ru.ac.za/media/rhodesuniversity/content/ichthyology/documents/Anatomy%20Lecture%207.pdf


Why are Lymphatic trunks part of the Cardiovascular system?

The definition of "vascular" is as follows:-

  of, relating to, affecting, or consisting of a vessel or vessels, esp.
  those that carry blood:

By this defninition, the cardio-vascular system doesn't need to include only the blood vessels and the heart. It includes all conducting and distributing vessel elements including those which carry the lymph-Lymphatic vessels. The cardiovascular system stands for the "circulatory system"+ the heart tissues and since lymph is an essential part  of the circulation (of nutrients, hormones, wastes etc), the cardiovascular system must include the lymphatic system.

Lymphoid system is a completely different entity which includes spleen, the lymphoid tissue (MALT), the lymph nodes and the lymph vessels. Hence the lymphatic vessels belong to both, the cardiovascular system and the lymphatic system, but the MALT and Spleen (arguable and disputed) are only a part of the lymphatic system and not of the cardiovascular system.

MALT= Mucosal Associated Lymphoid TIssue


How many species did Carl Linnaeus classify?

More than 13,000.

Plants: >9,000 names.
In Systema Naturae 10th edition, commonly taken as the starting point of modern taxonomy, Linnaeus is reported to have published around 6,000 plant names (I haven't counted, but Müller-Wille gives 5,900 and Stearn says "almost 6,000". The Wikipedia figure of 7,700 may come from a different edition of Systema Naturae).

However, that's just SN10. Luckily, a wonderful source has compiled the names from all of Linnaeus's work:
The Linnaean Plant Name Typification Project of the Natural History Museum says that Linnaeus published more than 9,000 valid plant names in his life (names that are still valid under current nomenclatural conventions), and they have many of them in a searchable database with references to where Linnaeus published them.

Animals: >4,200 names.
For SN10, different authors give 4,236 or 4,378 animal names. Stearn says "nearly 4,400", so perhaps he too was unsure. The total number Linnaues described in his life is probably higher, as he did write separate zoological publications like Fauna Svevica, but I couldn't find a source like the project bringing together all of his animal names.

 Müller-Wille S. 2006. Linnaeus' herbarium cabinet: a piece of furniture and its function. Endeavour 30: 60–64.
Stearn WT. 1959. The Background of Linnaeus's Contributions to the Nomenclature and Methods of Systematic Biology.)


Why do same type of fruits come in different sizes?

Phenotypic variance

This variance in the appearance of living things is called phenotypic variance. There are a number of reasons for the existence of such phenotypic variance. In other words there are a number of underlying variances that can explain phenotypic variances.

Primary source of phenotypic variance

The two most obvious source of phenotypic variance are

genetic variance
environmental variance

Genetic variance is caused by individuals having different genetic predisposition in the population. Environmental variance is caused by the fact that different individuals experience different environments (both macro and micro - environmental differences).

Monozygotic twins look alike because, among them, they have no genetic variance. Even if raised in the same home, they still experience slightly different environments. If raised separately (which sometimes happen) then twins will differ a little more as they experience very different environments.

Other source of phenotypic variance

The other sources of phenotypic variances include
- epistatic variance
- developmental noise variance
- all covariances between all of these causal factors.

  Are there any articles or research about this?

Well yes! Your question is underlying an entire field of knowledge which is called quantitative genetics.

More information

For more information, I recommend having a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


How can the organic mercury compound Thiomersal be not dangerously toxic?

Thiomersal is broken down into two compounds, thiosalicylate and ethylmercury (Ensink 2015).  The thiosalicylate it is relatively non-toxic, and there is even some evidence that this compound could counteract some of the effects of mercury poisoining (Asadi et al 2010), though the mechanism of this inhibition has yet to be elucidated.
Although they have similar names, methylmercury and ethylmercury have very different levels of toxicity.  Methylmercury has long been known to be highly toxic, producing high levels of cell death in the brain, particularly in the cerebellum and the visual cortex (Ceccatelli et al 2010).
Unlike methylmercury, ethylmercury appears unable to cross the blood-brain barrier as fast as it is eliminated in the stool.  Consequently, small quantities of ethylmercury have been shown to be non-toxic, resulting in the relative non-toxicity of thiomersal (Pichichero et al 2002).

Sources:

Asadi S, Zhang B, Weng Z, Angelidou A, Kempuraj D, Alysandratos KD, Theoharides TC. 2010. Luteolin and thiosalicylate inhibit HgCl(2) and thimerosal-induced VEGF release from human mast cells. Int J Immunopathol Pharmacol 23(4): 1015-1020.

Ceccatelli S, Daré E, Moors M. 2010. Methylmercury-induced neurotoxicity and apoptosis. Chemico-Biological Interactions 188(2): 301-308. doi:10.1016/j.cbi.2010.04.007

Ensink E. 2015. Preservative or poison? The science behind Thimerosal. The Substrate (online): http://substrate.asbmb.org/2015/05/15/preservative-or-poison-the-science-behind-thimerosal/

Pichichero ME, Cernichiari E, Lopreiato J, Treanor J. 2002. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. The Lanclet 360(9347): 1737-1741. doi:10.1016/S0140-6736(02)11682-5


Measuring Gross Primary Productivity (GPP) using Light and Dark Bottle methods: Sample Question

The dynamics are:

Light bottle: GPP - Ra = 0.15
Dark bottle : Ra = 0.08

Then GPP = 0.15 + 0.08.

The amount of O2 used in the respiration is 0.08 mg O2 / L, not -0.08 mg O2 / L.


Confusion about the brain regions - temporal cortex, hippocampus and and white matter

"Lobe" refers to a section of the cerebral cortex, which is the outer part of the cerebrum. The cerebrum contains several structures, but the one that most people care about is the cerebral cortex, which is the 2-4 mm thick layer on the surface of the cerebrum. The cerebral cortex (or "cortex") is divided into several lobes, e.g. temporal lobe, occipital lobe. So, cortex and lobe are not the same thing, as the lobes subdivisions of the cortex as a whole. (See https://en.wikipedia.org/wiki/Cerebral_cortex)
The hippocampus is a region of the cortex in the temporal lobe. Therefore, it consists of gray matter. However, it is connected to several other structures by white matter (e.g. the fornix), and these structures are related to the hippocampus. (See https://en.wikipedia.org/wiki/Hippocampus#Anatomy)
Forebrain refers to the cerebrum as well as other structures, such as the thalamus and hypothalamus. The forebrain is defined as the telencephalon (which is basically the cerebrum) and the diencephalon (which contains the thalamus and hypothalamus). (See https://en.wikipedia.org/wiki/Forebrain and https://en.wikipedia.org/wiki/Diencephalon)
I don't know what you mean by the temporal cortex having "the long side of it outside the temporal lobe", but the temporal cortex and temporal lobe are basically the same thing.


It is related to Eustachian tube. It links the back of throat and the middle ear and allows air pressure to equalize in the middle ear. When you yawn air pressure goes up in this and it bends the ear drum and causes impair hearing (notice, just impair and not stop).
Yawning also helps to open Eustachian tube.


Can boiling water without high temperatures kill bacteria?

No, you do need to reach high temperates to kill the bacteria.

It's not about the evaporation, or the pressure that kills bacteria, rather it is the temperature that does. Higher temperatures have drastic effects on the molecular structures that occur within the bacteria, such as the denaturing of various proteins present inside the cell. As a result, if you wish to boil water to kill it, it must be done at an elevated temperature.

Wikipedia mentions that the optimum temperature for killing microbes is around 70°C,

  Boiling water is used as a method of making it potable by killing microbes that may be present. The sensitivity of different micro-organisms to heat varies, but if water is held at 70°C (158°F) for ten minutes, many organisms are killed, but some are more resistant to heat and require one minute at the boiling point of water.


The "proximate cause" would be a differential rate of growth on the different sides of the individual bananas. If the cells on the underside of the banana are dividing faster than those on the top, that will cause the upward curvature.

As to what causes the differential growth: I'm not a banana biologist, but I would suspect that a growth hormone of some sort finds itself more highly expressed in the part of the fruit that starts out closest to the stem.

Why that hormone might have decided to start doing that, and what selective advantage it might have given the early wild bananas, I have no idea. But our modern cultivated bananas have probably been strongly encouraged to do it, for compactness of shipping, if nothing else!


Such genome transplantation was performed between two Mycoplasma species in Craig Venter institute Genome transplantation in bacteria: changing one species to another. They found that the donor genome completely changes the recipient cell to accept the identity of the original donor cell.

Note of caution: the above experiment was conducted between two highly similar species, and as of yet it is unclear what is going to happen if the exchange is performed between two distantly related bacteria species.

As for eukaryotes -- the transplants may be not viable at all, because naked DNA is going to lack epigenetic information (histone modifications, DNA methylation) that is preset during gametogenesis.


Why mosquito bite is confined to a certain shape?

What you're referring to as a mosquito bite is actually the "wheal" (red swollen bump in the skin) that forms from an immune system reaction to antigens (foreign molecules) in the saliva of the mosquito that it leaves behind inside the bite.  It's not technically a toxin, just something that causes an immune reaction.

It's also not an infection, it's inflammation.  Infection might set in if the skin is scratched open and bacteria move in.

The reason it's red is that immune cells release cytokines (like histamine and that cause cause edema that leads to swelling, heat, itching, etc - and recruit other cells to do the same.

The cytokines that act locally have a range of effect, especially histamine.  The degree of immune reaction determines the size of the wheal and how long it lasts.  Scratching it contributes to irritation and can prolong resolution.  Scratching it open can lead to infection.


Why does influenza sometimes cause GI symptoms?

Article: How influenza virus infection might lead to gastrointestinal symptoms Source study: Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell-dependent inflammation.

The idea is that Influenza virus infection originates in the respiratory tract. In response, the body produces these CCR9+CD4+ Th cells denoted Th17 in the lungs. Gut epithelial cells produce CCL25, a chemokine made to attract cells expressing CCR9 chemokine receptor. Th17 cells are a subset of T-helper cells that produce interleukin-17, more about that here. So what they found, is that the Th17 cells produced by influenza infection in the lungs migrate to the gut through this CCR9/CCL25 interaction, and they secrete cytokines that are meant to defend against infection. Of course, mucosal immunity at the gut epithelium is always active, because there are commensal bacteria there that out-compete pathogens among other roles.

Down in a section titled "Lung-derived CD4+ T cells destroy microbiota homeostasis and promote resident Th17 cell polarization" their conclusion is that IFN-gamma secreted by the lung-derived Th17 cells destroys the homeostasis of the gut microbiota, and cause other Th17 cells to become polarized in a way that they end up producing the specific set of cytokines causing the trouble in the first place. You also have to understand that the other cytokines the Th17 cells are secreting are causing tissue damage, leading to symptoms of intestinal disease concomitantly with what we've been discussing above.

I think that the process is just recently being illuminated so it may not be completely understood, either.

  How are the lung-derived Th17 cells getting to the gut?

Generally, leukocytes in the lymphatics enter the blood through the left subclavian vein. Once there, they traffic to vascular endothelium expressing chemokine attractant molecules and utilize a number of adhesion molecules in concert to extravasate into the tissue expressing the attractant. This could mean multiple tissues given the right circumstances. The important thing to remember when i mentioned mucosal immunity is lots of effector cells are already there due to the presence of microbiota at all times, unlike the systemic response where effectors must be generated.

Here's a figure about extravasation, and another about mucosal immunity, and if you look here you can see that the Th17 lineage is under investigation due to it's inflammatory characteristics in autoimmune disease.


How can E. coli affect C. elegans expression?

Yes, as bizarre as it may seem, that is what happens. The E. coli express a double-stranded RNA hairpin (under the regulation of an inducible promoter), and the RNA contains a sequence derived from a C. elegans gene.  When the worms eat the bacteria they grind them up in their pharynx, and release the cell contents (including the induced RNA) into the worms' gut. The gut cells are able to absorb the dsRNA  and transport it to other cells as well. The RNAi pathway processes the inhibitory RNAs to down regulate the target gene.


Will ants arriving with travel luggage form a new colony?

An ant colony is started by a queen ant (reference). Worker ants are sterile, and cannot start a new colony (reference). The ants in your luggage are worker ants (unless you have a colony in there :) ). The original queen ant never leaves her colony, but during a nuptial flight, new queen ants will land in (hopefully) good nesting sites.  (reference) These ants can be told by their wings, which are non-existent in worker ants.

The worker ants have an average life span of 45-60 days (reference), so the ants in your luggage won't be around for very long.

Also see:

  If a worker ant gets separated from its colony, it's doomed. No other colony will take it in, and it can't start its own colony--only queens can do that. It might be able to live for a while, but generally not that long--a lost worker is generally more concerned with hunting for its colony than with feeding itself, and its energy reserves are fairly small (depending on the ant species--some have workers that are adapted to taking long foraging trips). A few ant species, however, have "supercolonies," where neighboring colonies are established by queens directly related to one another. When queens are close relatives, their workers tend to have similar chemical profiles, meaning they can move from colony to colony without triggering the usual colony defenses against intruders. (Intruders are recognized by their chemical profile--their odor--and not by appearance, ID card, etc.) In such cases, workers routinely transfer between colonies, so a worker may end up working for its grandmother or, forgive me, its aunt. (From this page)


Organism with the greatest amount of gold as percentage of body mass

Acidothiobacillus ferrooxidans can gain metabolic energy by utilizing gold thiosulphate complexes (Reith et al., 2007); Micrococcus luteus can oxidize methane to methanol using gold-containing enzyme (Levchenko et al., 2002).

However, for most organisms, gold is toxic (Wietkiewicz & Shaw, 1981); some bacteria actively detoxify gold: Cupriavidus (Ralstonia, Wautersia) metallidurans, Desulfotomaculum sp., Desulfovibrio sp., Hyphomonas adhaerens, Plectonema boryanum, Pseudomonas aeruginosa Salmonella enterica,  Shewanella algae, Spirulina platensis (Reith et al., 2007).

Reith F, Lengke MF, Falconer D, Craw D, Southam G (2007) The geomicrobiology of gold. ISME J. 1: 567-584.

Levchenko LA, Sadkov AP, Lariontseva NV, Koldasheva EM, Shilova AK, Shilov AE. (2002) Gold helps bacteria to oxidize methane. J Inorg Biochem 88: 251-253.

Witkiewicz  PL &  Shaw CF III (1981) Oxidative cleavage of peptide and protein disulphide bonds by gold(III): a mechanism for gold toxicity. J Chem Soc Chem Commun 21: 1111–1114.


Does Cholestyramine (CSM) raise Tyramine levels?

I'm not sure why "tyramine" is in the name "cholestyramine", but the molecular structure of tyramine is not present as part of the molecular structure of cholestyramine. Specifically, in tyramine the amino group is on the beta-carbon from the ring, and in cholestyramine the ammonium group is on the alpha-carbon (note the different number of points between the ring and the nitrogen in the line structures provided). I find it highly doubtful any reasonable metabolic reactions by the body could generate tyramine from cholestyramine.

Cholestyramine molecular structure

Tyramine molecular structure


How does injecting low doses of allergens cure allergies?

But are there ways to tell the body that this allergy is safe and there is no need to amount a response to it?

Yes, that's what allergy shots (Exposure Therapy) does. Exposure Therapy is an effective, albeit sometimes imperfect, method of letting the body know that a substance is common and that it shouldn't mount a response to it. Over time the body re-calibrates itself to accept the allergen, although in some cases it's never fully accepted.

A complete "cure" can be attained via allergy shots, but the extent of the therapy's success will rely almost exclusively on the individual's immune system. Some people can be cured completely, others will never be cured.

  If not, why not?

There will probably not be a general "allergy" cure anytime soon because we're still not 100% sure why the body responds in such an overprotective matter sometimes and not others. Even if we fully understood at some point, there are many ways which the immune system can go awry that result in allergies.

There isn't a single, double, or triple point of failure along the line - just about any immune cell, whether Mast, Eisonophile, T-Cell, T-Reg, B-Cell, etc. can misidentify a substance and contribute to an allergic reaction (although some are more likely candidates than others). More than that, just about any substance can become an allergen for people. There's a well-studied case of a woman who became allergic to Copper because of repeated exposure via an early version of IUD that she had implanted.

So with nearly every immune cell capable of mounting a response, and nearly anything in the world capable of provoking a response, the best route - at least thus far - has been repeated, increasing exposures to teach the body what is "OK" and what isn't. The absolute best way to avoid allergies later in life is to simply promote outdoor playtime and a widely variable diet to children while the immune system is operating at peak efficiency and learning capability.


Does neural oscillation happen at the same frequency in all parts of the brain simultaneously?

Neural oscillations occur on both a cellular level and on a macroscale level, the latter usually referred to as brain waves.

Looking at macroscale brain activity and particularly brain waves is often done via EEG, which has poor resolution and suffers from attenuation. EEG activation is really due to huge numbers of neurons. Hence, it represents a very coarse, averaged view of the current activity. So, even when the EEG shows nice smooth variation, the individual neurons are far from it! Of course, more recently, using other methods (e.g. fMRI) has become more common.

  My question is are all parts of the brain firing off at the same frequency at any given time or are some parts for example operating at a delta frequency and others operating at alpha frequency? Do different types of brainwave occur simultaneously or is always all of the brain operating at one frequency?

No, as I said, most studies look at the cortical areas specifically. But even within the cortex, the brain activity is very complicated, and certainly not subscribing to any one frequency. (In fact, when this hyper-synchronization happens, it is called an epileptic seizure! e.g. see Garcia-Hernandez et al, Understanding synchronization and hyper-synchronization in the the septo-hippocampal system).

In any case, imagine brain activity being measured over time. We then look at the frequency components (e.g. via Fourier analysis). See e.g. Gross, Analytical methods and experimental approaches for electrophysiological studies of brain oscillations for details. Notice these methods usually give the "strength" of the activity across the frequency spectrum. When there are brain waves, we are merely saying that activity is concentrated in a specific frequency band. It is often smeared across the band, and activity usually exists throughout the spectrum.

It also depends on spatial resolution of the frequency analysis. Some studies look at, say, just the Hippocampus. So yes, it is quite possible for some of the brain to operate at one frequency, while others operate at another. Or one could average over the whole cortex. It depends on the study!

So pretty much in all cases, everything is more heterogeneous than you might think.

Some literature to read:

Breakspear, Dynamic Models of Large-Scale Brain Activity
Varela et al, The Brainweb: Phase Synchronization and Large-Scale Integration
Salinas et al, Correlated Neural Activity and the Flow of Neural Information


What were the first neural systems like?

This question can be answered by taking a look back evolutionary and see how other organisms have utilized neurology. The prime example, because it was one of the first real models of the neurological system, is the squid. It has neurons with singularly long axons to send electrical pulses long distance. This method of electric pulse transfer has been evolutionary updated, essentially, but we can get an idea of how these cells came to be. If we look back at squid predecessors, like the jellyfish, we see that it also developed electrical impulse cells to aide in defense and movement. Back further, we see the sponge has no neurons, but has something similar. This gives us potential insight into the development of the cell. It has protein clusters that act similar to post-synaptic signaling. So it is likely the electrical impulses were developed based on the function of these protein clusters, and bam! Electrical pulses became a must faster way to communicate to different regions of a system than simply trying to protein signal across cells.

Of course, looking at this question evolutionary is tricky since the question of divergent evolution comes into play, and we can't know if the sponge protein clusters offer a potential answer to neuronal development. But, is interesting evidence and makes an interesting debate!

Source= Sakarya O, Armstrong KA, Adamska M; et al. (2007). Vosshall, Leslie, ed. "A post-synaptic scaffold at the origin of the animal kingdom". PLoS ONE


How are the gene sequences of individual sperm and egg cells "randomized"?

Meiosis is the type of cell division responsible for the diversification of genetic material among egg and sperm cells. The diversity comes primarily from crossing over (Prophase I) and the cell divisions (Telophase I & II) later on in the process.

  Meiosis begins with one diploid cell containing two copies of each
  chromosome—one from the organism's mother and one from its father—and
  produces four haploid cells containing one copy of each chromosome.
  Each of the resulting chromosomes in the gamete cells is a unique
  mixture of maternal and paternal DNA, ensuring that offspring are
  genetically distinct from either parent. This gives rise to genetic
  diversity in sexually reproducing populations, which provides the
  variation of physical and behavioural attributes (phenotypes) upon
  which natural selection acts.

Further detail of the precise phases can be found in the Wikipeida article.

[picture from wikipedia]


Cognate means of common origin.

In molecular biology, cognate is used to refer to known interacting pairs of functional entities. For example, cognate receptor of a ligand means the primary (default) receptor with which this ligand interacts. Similarly, cognate sites (which also includes enhancer) of a transcription factor (TF) refers to the well known and validated binding sites of the TF.

Also see this post.


How do asexually reproductive organisms mutate?

It is not necessary that no mutation occurs in the system where no gene recombination or "contaminant" takes place. There are mutations (which are sudden abrupt inheritable changes)

There can be errors in genome which can cause mutations.

Take example of replication of DNA-:

There are many enzymes linked with it : DNA polymerases ( I, II,III) in prokaryotes where asexual reproduction occurs which add nucleotides to make replicas of DNA of parent ( you can check the complete process at wikipedia)

Come to the point : DNA polymerase III, after synthesising dna chains has ability of proof reading. It can correct the mismatches ( hope you know that adenine bonds with thymine and cytosine with guanine, they are nitrogen bases of dna)

DNA polymerase III can correct the mismatches but it is not error proof- it can't distinguish between thymine and uracil (another nitrogen base ; thymine is methylated uracil)

This is only one possible error, there can be many such hence asexual reproduction isn't error proof


I highly suggest you actually look at studies that analyze this and there should be a good number since amylase is a well defined enzyme. (Bailey K, Hopkins RH, Dolby DE)

Not only that but applying this type of logic to any problem results in bad conclusions and therefore is bad science. (Berkeley)

The process of proving something scientifically is something that follows a somewhat predictable route. I only say that because not everything follows this exact path.

There is usually a nicer looking picture though I cannot seem to find it.

(Source)

So to answer bluntly, no. You cannot make that conclusion with any stretch of the imagination.

Being that amylases are so well studied you may have your answer after a few google searches, but the case remains that it took many years of research to reliably say so.


In the glomerulus of the nephron we have filtration occuring. The subsequent formation of an ultra-filtrate travels down the tubulus from Bowmans space; during this journey, the filtrate will be exposed to various transporters and forces such as solvent drags and diffusion gradients, which leads to the (re)absorption of this filtrate. Reabsorption occurs also in medullary tubules and later collecting ducts, until the filtrate (by now urine) reaches the calyces. (Note that secretion - that tubular cells permit the transportation of various electrolytes for instance to the tubulary lumen - also occurs in the nephron, giving it three ways to manipulate the its luminal contents: filtration, reabsorption and secretion)


Need Help Identifying this Critter (Insect?)

It looks like an adult Dobsonfly (Corydalidae), where the adult males have huge pincher-like jaws. Apparently, the jaws are the result of sexual selection and, even though they look scary, males cannot use them to bite.

I'm only vaguely familiar with the group though, and cannot say what species this is.

(Picture from bugguide.net)


Can sperm cells penetrate the cell membrane of non-ovum cells?

It is very possible that the specific enzymes that penetrate the cells can be used to lyse other cells or at least manipulate the plasma membrane. That being said, I don't think that sperm cells can be used to do that because the acrosomal reactions that you discuss are only activated by the presence of the zona pelliculada of the egg cell. Since that doesn't exist in any other type of cell a sperm cell can't be used for Acrosomal enzyme delivery for somatic cells, for example.
If you want to read more, the Wikipedia page about the Acrosome reaction is pretty good.


Does dairy negatively affect the voice for singing?

As it turns out, dairy products do not produce phlegm in the majority of people (the exception is the tiny group of people who are allergic to casein, the protein in some types of milk). Instead, the high fat content in dairy products thickens the mucous that is already present in a person’s airway, making it seem like there is more phlegm to deal with. Of course, having thicker phlegm can be just as problematic as having more phlegm. Luckily, this thickening sensation can be diminished simply by eating dairy products that have a lower fat content.

(https://www.operapulse.com/refine-your-craft/guide-to-opera-training/the-rules-of-singing-mythbusters-edition/)

Regarding the above quote, there is no medical evidence that states milk consumption causes phlegm production even for casein allergic individuals.

The study cited at the end shows that there is a correlation between milk consumption and thicker phlegm. However correlation is not causation. The authors explain that the allergy-like effects of milk are produced only when tissues are actively inflamed and exorphins (peptides produced when milk is broken down) stimulate mucus production from gut glands. The thicker phlegm effect is shown in only a segment of the studied population. Unless you're one of the few with inflamed tissues, you should be ok with drinking milk before a performance.

(http://www.researchgate.net/profile/Jim_Bartley/publication/40026300_Does_milk_increase_mucus_production/links/0fcfd5138d5212ef80000000.pdf)


Which of these components has C-H and COOH groups

Answer A is wrong because triglycerides are esters not carboxylic acids so they have -COOR group, not -COOH. Amino acids and fatty acids have -COOH groups and proteins too - on C-termini and in side chains.


Orangish-coloured insect living in wood chips

That is the pupa of a unicorn beetle, Dynastes tityus. https://arthurevans.wordpress.com/2010/09/15/453/


The insects you have found must be of a species of thrips. This excerpt from Wikipedia fits your description well:

  Thrips (order Thysanoptera) are minute (1 mm long or less), slender insects with fringed wings and unique asymmetrical mouthparts. Different thrips species feed, mostly on plants although a few are predators, by puncturing and sucking up the contents. Approximately 6,000 species have been described.

I won't try to identify the exact species, but here is a photo of a yellowish-orange thrip I have found:

Image source:

https://6legs2many.files.wordpress.com/2012/04/thysanoptera_thrips_fringe_wings.jpg


Can a blood type O be born from AB and A parents?

The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, IA, and IB. The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. [1]
So from this standpoint, normal Mendelian genetics cannot explain the blood-group 0 offspring, given the AB parent.
However, besides errors in testing, the (pseudo?) 0-bloodgroup could be explained by the Bombay phenotype. I don't know the incidence rate in your region, so I can't comment on the likelihood.
To give theoretical background, this would be considered a pseudo 0-phenotype, as the individual genetically does not need to be ii. Instead, the individual lacks another effective enzyme that is required for the A or B alleles to be effective; the blood-type specific sugars (N-Acetylgalactosamin|Galactose) cannot be attached to the red blood-cell membrane, as the anchor of these sugars (called H-substance) is not present.
Finally, to address your hypothesis of a gene-duplication followed by a gene knock-out: There is no need for a preceding duplication. The more probable cause is a single point mutation (or multiple) near the active center of the inherited A/B enzyme, or a nucleotide insertion/deletion in its coding region, causing a frame-shift. A completely (not partially!) inactivated A/B enzyme would effectively represent a novel 0-genotype.


Would a human survive eating only living ants?

This study in 1984 suggests it's a bad idea and other sites have said eating ants is for weight loss.

The abstract says that it goes into detail about the problems associated with eating ants as well as their low nutritional value.

So I believe the answer is no. You could not survive long term on a diet of only ants.


Difference between the P4 and P5 subtypes of P-type ATPases in plants

There are numerous differences between the various subtypes of P-type ATPases, simply because they have different amino acid sequences. Three important differences between P4 and P5 subtypes of P-type ATPases are the following:

Structurally, P4 ATPases have their supporting structural domain (S) in the C-terminus, while P5 ATPases have the S domain divided over the N and C termini. Figure 1 shows the basic structure of P-type ATPases.
Structurally, P4-ATPAses require a beta-subunit for proper function (Poulsen et al., 2008). As the substrate for P5-ATPases is unknown, it could not yet be tested if they also require a beta-subunit.
Functionally, P4-ATPases are putative lipid flippases, while P5-ATPase pumps have so far (per the 2011 report cited) no assigned substrate specificity.

Schematic outline of P-type ATPases. Source: Palmgren & Poul Nissen (2011)

References
- Palmgren & Poul Nissen, Annu Rev Biophys (2011); 40: 243–66
- Poulsen et al., Plant Cell (2008); 20: 658–76


Why do people feel extreme cold at different temperatures compared to other people of same body structure?

First of all, this observation is the norm across human perception. While humans react in roughly the same way to similar stimuli (e.g. both a cranberry and a tomato are seen as red, the destruction of tissue is felt as painful), the intensity tends to be different. Also, many stimuli elicit not just a knowledge of the state of the world or one's body, but also a reaction (e.g. shivering when cold, or emotions like fear when physical pain is felt), and these reactions differ between humans too. So, on a very general level, it can be answered with "Because that's how human perception works".

I know that this is a very unsatisfactory answer, so here are some factors off the top of my head. For any given case, one or more of them will cause the difference, and you cannot tell which ones from casual observation.

Your observation of "similar clothing" could have been incorrect. For example, an acrylic sweater can look exactly like a sheep wool sweater, but warms much less. Or, slightly shorter sleeves can cause much cooling if they leave the wrist exposed. Layering is also very important, and we generally only notice the uppermost clothing layer.
Your observation of "similar body structure" could have been not precise enough. People who have the same appearance can have different amounts and distributions of body fat. Maybe one person is simply better insulated than another one.
The state of their circulatory system was different. Vasoconstriction and vasodilation will change the skin temperature, which is sensed by peripheral thermoreceptors.
Estrogen is involved in thermal perception. The gender of the person and the current point in the menstrual cycle (or pregnancy) in women will make a difference.
The circadian cycle of the two people is probably not perfectly synchronised. Core body temperature varies during the cycle, and thermoperception depends on core body temperature too, not just skin temperature.
A different metabolism will cause one person to create more body heat than another
Other hormones (beyond estrogen and the ones ruling the circadian cycle and metabolism) probably have an effect on thermoperception, but I can't tell you details here. Temperature is regulated in the hypothalamic-pituitary-adrenal axis, so the hormones from it are likely to have an influence.
Normal variations in the two people's neural networks will change the intensity of signal perception. People are born with very unconnected neurons, and build unique connections depending on the environment they encounter while growing up. As a result, each person's brain functions slightly differently when given the same input.
Differences in neurotransmitter sensitivity can account for the difference in intensity of perception. People sometimes react differently to the same level of neurotransmitter, or also their brains secrete different amounts of neurotransmitter as a response to the same stimulus. These differences exist on an average level (e.g. glutamate can potentially "do" more for me than for you) but are also affected by drugs and illness.
Attention is a major part of perception. The CNS can suppress information from sensory organs at a very low level if the brain is focusing elsewhere.
Habit: people can intentionally or unintentionally learn to disregard or misinterpret their body sensations.
Psychological stress increases the core body temperature
The above reasons all assumed differences between a pair of healthy individuals. Some conditions, for example running a fever, but also neurological disorders anywhere along the complex pathways from sensors to cortex (and the other way round!) or diseases which for some reason alter thermoregulation, will all change the feeling of hot or cold.

This list is probably incomplete. Also, some of the factors I listed will overlap to some extent (e.g. vasodilation is frequently mediated through hormones, and ingrained habits are reflected in neural network connections). But the take away point is: Human perception is an active process, very far removed from simple "reporting" of the state of the environment. It is unrealistic to expect two individuals to have the same perception when exposed to the same stimuli.

For an in-depth description of how thermoperception and thermoregulation work physiologically, see this summarizing paper.


Why are Oxyuranus snake species named Taipan?

An answer is found at the Wikipedia page for Taipan:

  The common name, taipan, was coined by anthropologist Donald Thomson after the word used by the Wik-Mungkan Aboriginal people of central Cape York Peninsula, Queensland, Australia.

This passage is citing Sutton. 1995. Wik Ngathan Dictionary as support. I cannot evaluate the truth in this statement though.

For another reference see McKnight. 1981. The Wik-mungkan concept Nganwi: a study of mystical power and sickness in an Australian tribe. Bijdragen tot de Taal-, Land- en Volkenkunde 137, which refers to Taipan as the Rainbow serpent (an Aboriginal mythical creature) of the Wik-Mungkan tribe.

Even more folklore is found in McNamee. 2000. The Serpent's Tale: Snakes in Folklore and Literature in "Taipan the snake and the blue-tongued lizard".


Are domesticated animals really "more intelligent," or is that a myth/misunderstanding?

Domestication has little, if anything, to do with intelligence.  From biologist Jared Diamond, the 6 criteria for domestication are as follows:

  Flexible diet – Creatures that are willing to consume a wide variety of food sources and can live off less cumulative food from the food pyramid (such as corn or wheat), particularly food that is not utilized by humans (such as grass and forage) are less expensive to keep in captivity. Carnivores by definition feed primarily or only on flesh, which requires the expenditure of many animals, though they may exploit sources of meat not utilized by humans, such as scraps and vermin.
  Reasonably fast growth rate – Fast maturity rate compared to the human life span allows breeding intervention and makes the animal useful within an acceptable duration of caretaking. Some large animals require many years before they reach a useful size.
  Ability to be bred in captivity – Creatures that are reluctant to breed when kept in captivity do not produce useful offspring, and instead are limited to capture in their wild state. Creatures such as the panda, antelope and giant forest hog are territorial when breeding and cannot be maintained in crowded enclosures in captivity.
  Pleasant disposition – Large creatures that are aggressive toward humans are dangerous to keep in captivity. The African buffalo has an unpredictable nature and is highly dangerous to humans; similarly, although the American bison is raised in enclosed ranges in the Western United States, it is much too dangerous to be regarded as truly domesticated. Although similar to the domesticated pig in many ways, Africa's warthog and bushpig are also dangerous in captivity.
  Temperament which makes it unlikely to panic – A creature with a nervous disposition is difficult to keep in captivity as it may attempt to flee whenever startled. The gazelle is very flighty and it has a powerful leap that allows it to escape an enclosed pen. Some animals, such as the domestic sheep, still have a strong tendency to panic when their flight zone is encroached upon. However, most sheep also show a flocking instinct, whereby they stay close together when pressed. Livestock with such an instinct may be herded by people and dogs.
  Modifiable social hierarchy – Social creatures whose herds occupy overlapping ranges and recognize a hierarchy of dominance can be raised to recognize a human as the pack leader.

From his Pulitzer prize-winning book.

We (as a species) domesticated animals (and plants) by selecting traits we sought, and then breeding to keep alive/emphasize these traits. In hunting animals (retrievers, for example), intelligence may be one of those traits. Others might include obedience, speed, agility, even dark-colored coats for camouflage.

It's not really correct to say "more evolved" as @MarchHo explains in his comment. Rather, you might say "more docile", or "less aggressive".

Keep in mind that less aggressive, domesticated animals are not necessarily more intelligent than their wild counterparts.

status-myth


This is Common purslane, Portulaca oleracea. It is used in salads, although it contains oxalic acid and there are poisenous plants resembling Purslane, see comment below.
https://en.m.wikipedia.org/wiki/Portulaca_oleracea


The emergence of life out of matter is a very rare event.
The chance of having such event occurring more than once in a small time-frame is very little.

If the time-frame is large enough, then "New Life" could emerge again. However, in that case, the new emerging living organisms would be extremely disadvantaged by the presence of the "Old Life", already evolved to efficiently compete for energy sources etc.

Any new, barely functional, primordial life form cannot outperform the already existing ones, thus it would undergo extinction pretty soon. And that is why we ended up with a single tree of life on this planet.

Some links for further reading:

http://www.science20.com/stars_planets_life/calculating_odds_life_could_begin_chance

http://www.science20.com/news_releases/the_mathematical_probability_of_life_on_other_earth_like_planets

https://www.sciencedaily.com/releases/2018/01/180108090109.htm

https://www.scientificamerican.com/article/universal-common-ancestor/

https://www.nature.com/articles/nature09014

https://link.springer.com/article/10.1007%2Fs00239-010-9407-2

https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2896%2900631-X

https://www.sciencedirect.com/science/article/pii/S0022519318300419?via%3Dihub


Why do we use different micropipette tips for different volumes?

The short answer is yes, the accuracy is affected.

Automatic pipettes are most accurate in the middle of their range. The average error on a pipettes is already about 2%, but this is worse at the top end or bottom end of the pipettes minimal and maximal volume.

More subtly, have you ever tried to pipette 1 uL with a 1 mL pipette? Or even 5 uL. The bore of the pipette is too wide for starters, and the expulsion force/pressure to eject the fluid wouldn’t work very well.

On top of that, the surface tension would seriously hamper any ability to actually manipulate the fluid.


Is one of the terms preferred over the other?

Absolutely: "vascular plants" is the preferred one. "Higher plants" should be avoided. Here is a long explanation:

The Great Chain of Being

This term "higher plants", together with the term "higher animals", is just a remnant of a completely wrong concept that has (or shouldn't have) no place in the world after 1859: the Great Chain of Being, or scala naturae  in Latin.

This is the typical medieval representation of the scala naturae:

The Latin text on the ladder says: stone, fire, plant, beast, man, heaven, angel, god.

And here a more "modern" version of it (but equally wrong):

Unfortunately, this absurdity survived until the late twentieth century, and can be seen even today in some books/sites/lectures.

Linnaean Taxonomy

To understand the use of "higher plants" (and "higher animals") in biology, we have to go back a little in time.

When Linnaeus published his Systema Naturae, he divided the nature (Imperium Naturae) in 3 Kingdoms:

Regnum Animale: the animals;
Regnum Vegetabile: the plants;
Regnum Lapideum: the minerals (you read it right).

Note that, in this classification, "animals" correspond to what nowadays we call animals and protozoans, and "plants" correspond to what nowadays we call plants, algae, fungi and bacteria.

You have to keep in mind that this book was first published in 1735, well before the evolutionary biology being proposed in the XIX century and established in the XX century. Therefore, it is a book published when fixism was the current paradigm, full of mentions to the scala naturae.

So, the plants (as well as the animals) showed a continuum of species, going to the lower plants (the bacteria) to the higher plants (the flowering ones). It's worth mentioning again that, by that time, bacteria were plants: Phylum Schyzophyta, to be more precise.

Thus, we have "lower plants" and "higher plants", "lower animals" and "higher animals", as well as "lower minerals" and "higher minerals"!

Unfortunately, this terminology is so embedded in the biological sciences that even today, as I mentioned, we struggle to get rid of it.

Just drop "higher plants", whatever it means

As your Wikipedia link says, "higher plants" is a synonym of vascular plants. However, there are a lot of problems here:

First, this is a remnant of the scala naturae and, just because of that, should be avoided. Think of it as a meaningless term, just like "more evolved organism".

Second, there is no clear and indisputable definition of what is a "higher" plant. Some authors used to define the "higher plants" as the Angiosperms only, or the seed plants (Angiosperms + Gymnosperms), or the vascular plants (Angiosperms, Gymnosperms and Pteridophyta).

For instance, in lusophone biology books, it was very common a division in three groups:

lower plants: bacteria and algae;
intermediate plants: bryophytes and pteridophytes;
higher plants: gymnosperms and angiosperms.

In those books, "higher plants" doesn't mean vascular plants, but seed plants instead. One could argument that those books use an incorrect definition, but my point here is exactly that the definition of "higher plants" is imprecise and wrong by its very nature: there is no correct use.

In conclusion: the definition of "higher plant" is not precise, and because it's related to a completely wrong concept, its use should be avoided.


Could this Francobelgian comic book woman really have these 4 diseases at the same time?

Erythema multiforme (minor) can and does occur in a lot of people; while it is usually self-limited, it can recur, especially when the trigger is an unsuspected food.[1] How common is it? It is very common.

Necrobiosis Lipoidica is not uncommon in diabetics, less common but still found in non-diabetics. It can occur at any age, including the eighth decade. It also shows a sex predilection, being 3 times more common in women than in men.[2] How common is it? It is not rare.

Phlegmasia Alba and Cerulea Dolens[3] is serious and associated with deep vein thrombosis, which is an acute event. It is not uncommon, but it's not chronic. (More than 600,000 cases of venous thromboembolism are estimated to occur each year in the United States, all of which can lead to Phlegmasia Alba and Cerulea Dolens. How common is it? Luckily, not very. If the author is referring to garden-variety thrombophlebitis, though, that's a chronic problem, and not uncommon in the elderly. Thrombophlebitis is chronic and common enough.

I'm not going to address Metropathia Haemorrhagica, because, as you have noted, it's found in menstruating women.

Diseases generally don't really interfere with each other; some diseases can't co-exist (you can't have hyperthyroidism and hypothyroidism at the same time, for example, or have an active pituitary gland tumor and empty sella syndrome at the same time), but diseases don't interfere with each other exactly. Some diseases have common underlying foundations, so can occur co-morbidly, for example collagen vascular diseases can manifest with skin, joint, and lung findings, which might not be diagnosed as several manifestations of one disorder if it's not obvious. A better example might be diabetes, where similar underlying pathologies cause, say, heart disease, skin disease, eye-problems and kidney disease together.

Whatever, the likelihood of a little old lady having all four of your diseases are nil. The first three all the time (assuming not garden variety thrombophlebitis) - nil. Once, not impossible once, but not chronically. Of the first two - not far fetched. The first - common as dirt (comes and goes, though.)

I hope this helped.

[1] Erythema Multiforme on Medscape
[2] Necrobiosis Lipoidica on Medscape
[3] Phlegmasia Alba and Cerulea Dolens on Medscape


This click beetle belongs to the species Chalcolepidius rugatus.

According to the original description, this species is clothed, dorsally with white pubescence, with the sides of pronotum and elytra marginated by yellow, and ventrally, with brown pubescence. source

source

source

Distribution

source


Thyroid hormone metabolism and excretion

I have partially answered this question by discovering that the metabolic pathway is called enterohepatic circulation. In this interaction bile salts are absorbed and transported out of ileal mucosal cells by binding to albumin.

However, it is still unkown to me exactly how it is that thyroxine and other hormones are moderated in this process and how it works. Does the albumin collect thyroxine as well as bile salts? How is the process moderated? In other words, bile salts are allowed to be excreted according to some moderated control mechanism. What is this mechanism?


Why do toenails grow much slower than fingernails?

Going on the abstract of a study by J.P. Pessan, et al., fluoride intake, as well as "the fact that toenails are less prone to environmental contamination," constitutes a lesser need for growth in toenails than that in fingernails. Also, fluorine being a crucial component in maintaining the solidity of bones, the body may redirect more fluorine that is ingested by various means, to the hands than to the feet, due to the arguably more necessary functions of the hands (in that they are used them for agile and precise motions that tend to influence our survival), meaning less growth in toenails as evidenced in the first citation.


What are the effects of removing CD4 receptors?

The CD4 receptor is vital for the proper functioning of the immune system. It is found not only on T-Lymphocytes, but also on macrophages and dendritic cells. Its function on T-cells is to stabilize the interaction between the T-Cell receptor and the MHC Class 2 (often known as HLA II in humans) antigen complex on antigen presenting cells and improves the affinity dramatically.

CD4 is also vital for the activation of Helper T-Cells (2). It is needed in the signaling which occurs in the thymus that selects for CD4+ T-Cells. If you were to delete CD4, you are, in effect destroying the adaptive immune system in humans, as there would be no CD4+ produced. In this situation, you would not get activation of B-Cells or Cytotoxic T-Cells, and the immune system would only be left with its innate defenses to protect it. This is found in diseases such as Severe Combined Immunodeficiency and can only be cured with early bone-marrow transplantation.

A better target would be the CCR5 receptor. This receptor acts as a coreceptor for the interaction between GP120, the receptor on the surface of the HIV capsid and the CD4 receptor. People who have a mutation in the CCR5 receptor are resistant to the most prevalent isoform of HIV, as the interaction is necessary for the capsid to fuse with the plasma membrane of the CD4+ cell.

See this article about the CCR5-∆32 mutation. HIV Resistant Mutation


Do the eggs for larger litters come from the same meiosis events, or different ones?

I'm not sure about the ubiquity of this but, in many animals, each primary oocyte that undergoes oogenesis only produces one mature egg. The other products of meiosis are polar bodies, which are not fertilised. These cells often degenerate but can sometimes play supportive roles in embryogenesis.

To answer your question, each mature egg is necessarily from a different meiosis event and so it is not guaranteed that all of the mother's chromosomes are represented in her offspring.


What made this tiny honeycomb-like structure?

Many insects lay eggs in tight clusters; because of the shape of the eggs (like honeycomb cells themselves), the cluster looks a bit like a honeycomb.  If you had a high quality macro shot, the eggs might be easier to identify definitively.

Newly hatched Beet Armyworms:

Wheel Bug (Arilus cristatus) Eggs:

  Wheel bugs are common in eastern North America, but are confirmed to occupy areas of Mexico and Guatemala.

With wheel bug for size:

My guess is that you found a cluster of Wheel Bug eggs.

  Females lay eggs at a low elevation on trees, bushes, twigs, and other objects.[5] Secreted glue serves as an adhesive which maintains the cluster formation of the eggs. - Wikipedia


Difference between "wash" and "rinse" in biotechnological procedure descriptions

This is a very interesting question and it's kind of strange there doesn't seem to be any literature on it. One would expect those to have been carefully studied by the designers of automated microtechnique equipment such as tissue processors and slide stainers.

I own a fair amount of literature on microtechnique, ranging from the end of the 19th century up to the 1980's. I went trough some of those briefly this morning, but I couldn't find a definition for "dip", "rinse" or "wash" or their German, French, Dutch equivalents (And there are a lot more of those, such as "drain", "agitate", "flood", ...).

The problem is even more complicated than it looks alread, as, very often those terms are acompanied by an adjective adding even more confusion, such as "quick/slow dip", "brief rinse", "thorough wash" etc.

I suppose (but that's only speculation on my part) those therms being undefined has to do with the fact that, in microtechique there are that many variables involved, that it's often next to impossible to achieve reasonable results without esoteric stuff such as "technicians experience" coming into play. That's defenitly the case in the field of for example staining technique, when "the classics", such as Masson, Mallory/Heidenhain's AZAN, Van Gieson etc... need to be used.

But not only in that field: If you do some reading in mailing lists such as the Histonet Listserver, you'll notice that messages, questions etc. on "inadequate processing schedule", "reprocessing inadequatly paraffin infiltrated brain/heart/liver/pancreas/... tissue", "bubelled nuclei and an unidentified artefact", "Feulgen stain doesn't work!" are fairly common occurences. Regardless of how expensive the equipment, regardless of however wel reviewed the protocols, regardless of however strict the quality control.

The only -brief- definition of "dip", "rinse" and "wash" I know of and I can remember, is in the book I have, but I can't find for the moment (you'll always see it...):

Smith, A., Bruton, J.: "A colour Atlas of Histological Staining Technique",
? th edition, 1977, ISBN: 07234 0721 5
Publisher: Wolfe Medical Publications Ltd, UK.

Perhaps you'll get any further, starting from there.

O, and while probably pointing out the obvious: dip is shorter than rinse is shorter than wash.


Where does reverse transcriptase come from?

I was about to write an answer saying that all reverse transcriptases are viral genes/proteins, but then wikipedia reminded that the telomerase is technically also a reverse transcriptase.

To answer your (main?) question:

  I can't figure out whether the viruses provide reverse transcriptase or their RNA has the code for it

Retroviruses have (almost by definition) the code for a reverse transcriptase in their genome. However, they also have the enzyme (or rather an inactive pro-enzyme) packaged into the viral capsid. The reverse transcriptase is a part of the Pol gene.
There are some other viruses that also use reverse transcription, but aren't retroviruses - in these cases I'm not sure, but I would guess that they also have an RT in their genome.

Now going back to the telomerase and retro-transposon elemnts:

These are ancient genes/elements in the eukaryotic genome, that basically do the same thing as viral reverse transcriptases: they make DNA from RNA.
Retro-transposons are generally believed to be viral additions to the genome, collected over the course of evolution. However, also the Telomerase enzyme probably has one common origin with viral reverse transcriptases (Nakamura 1998, take a loot at figure 2 at the end), (Witzany 2008). The thing about these evolutionary events is that they go way back, up the point were eukaroytes just started evolving from ... something. The sources I cited argue that many "eukaroytic" features (e.g. nucleus, RNA processing, vesicular transport) were originally taken from viruses.


Calling is a risky activity because it makes the frog conspicuous to predators. When calling in a group, the risk to any given individual is minimized to the point that the minimal risk is outweighed by the advantage of attracting a mate. However, a single frog calling on his own is assuming all of the predation risk. So, the frogs are playing a bit of game theory and when too few are calling simultaneously to make the risk worthwhile, they will all tend to stop.


How long can an octopus survive out of the water?

Short answer
Under ideal conditions, an octopus may survive several minutes on land.

Background
Octopuses have gills and hence are dependent on water for the exchange of oxygen and carbon dioxide. Gills collapse on land because of the lack of buoyancy (source: UC Santa Barbara). Octopuses have three hearts. Two of these are dedicated to move blood to the animal’s gills, emphasizing the animal's dependence on its gills for oxygen supply. The third heart keeps circulation flowing to the organs. This organ heart actually stops beating when the octopus swims, explaining the species’ tendency to crawl rather than swim (source: Smithsonian).

According to the Scientific American, crawling out of the water is not uncommon for species of octopus that live in intertidal waters or near the shore (Fig. 1). Because most species of octopus are nocturnal, we humans just don't see it often. Their boneless bodies are seemingly unfit for moving out of water, but it is thought to be food-motivated, e.g. shellfish and snails that can be found in tidal pools.

Octopuses depend on water to breathe, so in addition to being a cumbersome mode of transportation, the land crawl is also a gamble. When their skin stays moist, a limited amount of gas exchange can occur through passive diffusion. This allows the octopus to survive on land for short periods of time, because oxygen is absorbed through the skin, instead of the gills. In moist, coastal areas it is believed they can crawl on land for at least several minutes. Mostly they go from pool to pool, never staying out of the water for extended periods. If faced with a dry surface in the sun, they will not survive for long (source: Scientific American).

Fig. 1. Octopus on land. Source: BBC

Your sub questions; I think small octopuses may survive longer, since passive gas exchange is the mode of survival on land. In general, an increase in diameter causes the volume to increase with a third power, while surface increases with a power of two. Therefore, an increase in body size reduces the surface-to-volume ratio and leads to reduced gas exchange. Because passive gas exchange needs large surface-to-volume ratios, I am inclined to believe small octopuses may cope better with terrestrial environments. However, in hot, arid conditions it is likely a bigger one will have an advantage, because it can store more oxygen in its blood.

In terms of species, I have to say I couldn't find any sources going in so much detail on this. Likely, as said, smaller species may do better in cool, moist conditions, while larger specimens may be better off in dry environments.

Reference
- Harmon Courage, Sci Am; (November 2011)


Yes, something can be both a hormone and an enzyme. There are a group of hormones known as peptide hormones. These are proteins (such as enzymes) that act as hormones indirectly (and maybe directly too?). A hormone is a chemical secreted by a cell that has some effect on another cell elsewhere in the body. In this case, the chemical just happens to be an enzyme. You can read about them on Wikipedia

Renin is secreted by the kidney, but its involved in arterial vasoconstriction (outside of kidney cells), so it is a hormone. And its also a peptide/enzyme, so it is considered both a hormone and an enzyme


Hardy-Weinberg equilibrium generalized to add inbreeding (non-random mating)

You're confused because you're failing to distinguish between 'identical' and 'identical by descent'. Some pairs of alleles would still be identical even in the absence of inbreeding.

We model the inbreeding by classifying allele pairs as IDB - always homozygous - or not IDB -  distributed according to Hardy Weinberg. The frequency of a pair of alleles being A1,A2 (or A2,A1) is thus the frequency under H.W.E. (2pq) multiplied by the chance of them NOT being IBD (1-FI). And conversely, a pair can be homozygous and not IBD - at frequency p 2(1-FI), or because they are IBD - at frequency p F I.


The reason that cartilage rarely is able to regenerate is that it is poorly vascularized and innervated. It doesn't have its own blood supply to deliver signaling molecules that promote regeneration and repair after injury.

There has been some recent progress on getting the body to repair and replace cartilage with lab created biogels detailed here.


Blackgram leaves. SDS page. Phosphate buffer method

You should de-stain your gel longer. I can see at least one thick band at the top, but without de-staining longer you are probably missing other fainter bands.

Also, please explain what you mean by "proper bands". The top one looks fine to me. There might be others but we cannot see them.


Ill effects of urea and NH₃ on metabolism

The denaturing effect of Urea is mostly at very high concentrations.   (~Molar levels)!

Physiologically, urea, a product of the breakdown of retired amino acids, will build up rather quickly if it weren't secreted in the urine. Looking into this, it doesn't seem as there is a clear understanding of why this causes a disease, though the buildup of a waste product definitely is a unifying concept.

Uremia - kidney failure - causes a build up of urea in the blood as the kidney eliminates urea from the blood into the bladder.  The specific effects of Urea on cell metabolism are probably numerous as the symptoms:  anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. Other symptoms include fatigue, nausea, vomiting, cold, bone pain, itch, shortness of breath, and seizures.

Being a metabolic waste product, it certainly would interfere with and inhibit any enzyme that produced urea - the Urea cycle in particular.  Its clear that uremia is ultimately associated with cell death, oxidative stress, some cell signalling and proliferation.

I'm just googling around here, but I don't think there is any one single answer as to what goes wrong when the cells are exposed to too much urea.


Can I get 1% of my one of my great great grandparents genes?

The science behind "being X % from a certain place" based on genetic analyses is... approximative at best. It relies on the assumption that some genetic traits are only found in certain (narrow) regions of the planet - which for most of them, is not really true.

Additionally, did your test provide any confidence metric for this result? If not, it may mean that it may be derived from a statistically unsignificant number of traits (and the number could therefore mean anything) or maybe it's simply something like 1% with a confidence interval of several points, in which case the result could be a compatibe the mathematical truth. Genomes are large and have complex dynamics, it it probably difficult to get a precise estimate.

On a side note, there is more genetic diversity in native African populations than on any other continent (for reasons pertaining to Homo sapiens history) so "African" does not describe a homogeneous population.

Source: https://www.nature.com/articles/nature13997 doi:10.1038/nature13997


Finding confidence level of miRNA disease associations

You can start off by studying how an miRNA regulates the functioning of a gene. it basically binds to the 3'UTR and 5'UTR of an mRNA and restricts its translation. There will be genes associated with the disease of your interest,  find out the miRNA's related to those genes. You can use micro array data to find out the up-regulated genes. Target scan human, miRDB, are various databases for retrieving the miRNA's related with the genes.
The confidence level for finding out the association of certain miRNA's with the disease can never be 100%. but a relationship can be established by simply viewing the complementarity between the miRNA and the mRNA expressed during the diseased state.


Is complete linkage found in all four chromosomes or only Y-chromosome of Drosophila?

All chromosomes. There is no crossing over in males in Drosophila. Check out the related question Why doesn't recombination occur in male Drosophila? for sources and context.


Is bad tasting food more likely to cause harm?

tl;dr; If someone likes a food item, then even if it taste not so great to you, it will probably not harm you. If a food item taste awful to everybody (in particular bitter), then it would probably be best to avoid it.

Taste perception per se is not subjective, you either can detect or not a defined compound at a defined concentration. Food preference however is of course much more subjective.

The most established theory in the field is that we evolved both bitterness and sourness as a warning signal for poisonous compounds and inedible food. Bitterness is often the most referenced as most poisonous substances taste bitter to humans (e.g. strychnine, nicotine, ...) and are detected at very low concentrations (in the nM to $\mu$M range) (Meyerhof W, 2005). In comparison, the threshold for sweet taste perception is well above > 100mM (Park DC, 2015), or put otherwise, humans are at least 1000x more sensitive to bitterness compared to sweetness. As a result, we evolved to detect small quantities of bitter compounds and to dislike food items that are bitter as they could be poisonous.

Now for your question, you are probably misusing the word taste when you meant flavor, which is a combination of both taste and aroma (i.e. taste perception and olfaction combined, for example the "taste" of a banana). Food preference varies from people to people based on both genetic, physiological and more importantly environmental factors, in particular food habits. Typical examples are spiciness and saltiness where you can slowly adapt to tolerate higher and higher concentrations, meaning that your own food preferences can shift over your lifetime. Another illustration is the common shift in food preferences between childhood and adulthood. In other words, food preference is not an excellent predictor of a harmful food item.


If a non-mammal is starved of oxygen for some time, how long would it take the animal's neurons to die?

Medically, recovery of brain function after 3 minutes of oxygen deprivation at body temperature is rare.

Further down here in 1 it indicates that at lower temperatures the time can be much longer.  At 13C, the record is 80 minutes for people.  Animals cooled to 0C have a record of recovery of three hours!  Not sure how much like themselves they feel after that though...


Do animals with their eyes ~180 degrees apart have depth perception?

Many such creatures do overlap in part of their field of view. Some don't.   Presumably, the former still have some range sense. It's generally accepted that range judgment it's far more valuable to predators while herbivores focus on movement over a wide range. (at least in the sources I've read on this.)

That said:

Focal length can provide some amount of depth information, but not like comparing two angles. ("accommodation " in the wiki article on depth perception)

Parallax can provide some useful depth information. This is a function of basoc geometry. (In the same article, see "motion parallax", "occultation", and "perspective")

Theoretically, if a creature is precisely enough aware of its movement, it could pick up depth by rotating its head. This is because of the previously mentioned geometry. (https://en.wikipedia.org/wiki/Depth_perception#cite_note-5)

Not sure if any animals actually do this, but some birds seem to.

This answer is, fundamentally, just a summary of elementary information. The wiki entry on depth perception chops up the list of factors a lot more fine than I did off the top of my head.

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

https://en.wikipedia.org/wiki/Equine_vision#Visual_field


The first part of the question is interesting.

  Does an increased reproduction/mortality rate provide an evolutionary advantage?

The concept of evolutionary advantage for a species needs to be used with much cautious as different definition of evolutionary advantage may exist. You should typically have a look at game theory beforehand to understand the issue of definition.

A species that have shorter generation time tend to respond faster to new selection pressure (even more so in species that have short generation time and also have high population size).

  why has humanity not been enslaved by mouse¹ overlords with superior intelligence and adaptations to suit the environment perfectly?

You seem to be viewing intelligence and/or species competitive ability as end goal of natural selection which suggests important misunderstanding of how evolution works.

  One of the reasons these traits may be more harmful than helpful is that predators benefit from a population increase

You might want to have a look at the post What prevents predator overpopulation?


This is normal, and the effect is accentuated dramatically if you pretend to be holding an imaginary round object (somewhat smaller than a baseball, for instance.) The fingertips will all approximately point towards the very end of the thumb.

(See upper right image.) If the stone were smaller, the effect would be more visible.)

This orientation of the fingers makes the hand and fingers extremely versatile, being able to grasp and manipulate objects of a wide variety of shapes.

It also allows fine manipulation of thumb and fingers. Touching each fingertip to the tip of the thumb quickly shows the same effect - the fingertips approximately align with the thumb. If they didn't align this way, we would lose some of our very fine (as in requiring great precision, not as in quality) motor skills.

I'm not going to hypothesize on why the hand evolved the way it did; it's very efficient and that seems reason enough.


Here is the link to the 1000 Genomes project, all the data is available for download. They already have a comprehensive list of SNPs as well.
It is not the only project around but it is definitely the one with more accurate data on so many genomes right now.


Superoxide radicals , basically damage the lipid bilayers. affecting the efficient gradient.
for example H+ ion gradient across lipid bilayer in ETC is very important. this gradient is affected if superoxide radicals are present.


How does MEME compute the background frequency of nucleotides?

At the MEME server page, there's a link to upload a customized background markov model (using the command line interface, this is the -bfile option).  From there, there's a link to the MEME Man Page.  Under "Objective Function", it specifies:

    The background model is an n-order Markov model. By default, it is a 0-order model consisting of the frequencies of the letters in the training set.

So yes, it's basically the simplest possible correction: no accounting for pairwise frequencies, complements, motif width, etc.  I expect this is because MEME can be applied to essentially any dataset, such as phage display bindings from a "truly" random set of short oligos. In which case making higher order assumptions about the pairwise independence would be detrimental.

Below that, I think it answers your question about the total log-odds calculation:

    The E-value reported by MEME is actually an approximation of the E-value of the log likelihood ratio. (An approximation is used because it is far more efficient to compute.) The approximation is based on the fact that the log likelihood ratio of a motif is the sum of the log likelihood ratios of each column of the motif. Instead of computing the statistical significance of this sum (its p-value), MEME computes the p-value of each column and then computes the significance of their product. Although not identical to the significance of the log likelihood ratio, this easier to compute objective function works very similarly in practice.


What's the worst that can happen from too much sleep deprivation? Can you die?

The short answer is: Yes.

Fatal familial insomnia is a genetically passed down disease that at some random point in a carriers life will suddenly stop them from sleeping, ever, they die within 7 to 18 months

I know you did not ask about the disease, but it shows (even without illegal war tests) that it will kill you eventually, even in humans.

I believe in humans without the disease a complete lack of sleep may kill them within weeks, but who knows? maybe it was the drug.


Does a fully-resolved phylogenetic tree have to be dichotomous?

In theory, yes, every tree has to be dichotomous. You can understand a trichotomy in a tree as the summatory of two dichotomies that had happened so close in time that you cannot know wich was first.

Given a certain population, assume that some individuals colonize a new environment, got reproductively isolated and form a new specie. This is the typical speciation process. In this case, the two species, share a common ancestor. If you go back in time, all the individuals of the new specie will descend of only one individual. The same goes for the original specie. If you go back further, this individuals will share an ancestor, too. This is the conceptual meaning of the dichotomy, but normally it is impossible to determinate wich was exactly the common ancestor.

Now imagine that the original population formed not one, but two new species. And that this process happened about the same time as the one described before. It is conceptually possible that a set of three brothers were the origin of three different species (wich will be a true trichotomy), but not only it's very unlikely, but it's virtually impossible to prove. Since two close dichotomies are far more probable than a trichotomy, it's assumed that every tree has to be dichotomous, and that a trichotomy is in fact due to lack of resolution.


cloning and blue white screening in pet21a

pET21A doesn't encode the lacZ α-peptide necessary for blue-white screening by complementation. Since DH5α has the lacZΔM15 background, only the lacZ ω-peptide is produced and thus β-galactosidase is inactive.


epitope in immunomic microarray DNA microarrays measure one response
  value for each gene per sample; that is, mRNA concentration produced
  by the gene but a single epitope can generate different response
  values corresponding to different epitopes in peptide–MHC chips.

The excerpt looks grammatically incorrect and is therefore confusing. I guess what it tries to convey is — like there can be several probes for a single mRNA in a normal gene-expression microarray, there can be several antibodies binding to different epitopes in the same protein. Different antibodies will bind to their cognate epitopes with different affinities. This is what is referred to as "response value"

By quality I guess what the authors mean is that for the same epitope it is possible to quantify the binding interactions between that epitope and antibodies of different classes (but same antigen binding site).

Having looked at this excerpt, I would not recommend this book to anyone.

You can also have a look at these two articles:

From Functional Genomics to Functional Immunomics: New Challenges, Old Problems, Big Rewards
Prospects for the Future Using Genomics and Proteomics in Clinical Microbiology


Do pyrosomes reproduce by ways other than cloning?

Indeed pyrosomes use a very interesting form of reproduction. They actually use both sexual and asexual form of reproduction each time they reproduce. Pyrosomes, which are colonial tunicates, produce both egg and sperm. In each pyrosome of a colony, a single egg is fertilized and develops into a 4-staged animal. This form leaves the parent body and starts forming its own colony. It does so using the process called budding, which rapidly develops a new colony of pyrosomes. You can see here, here or here for more information.

source (in french though ;)


Why is the formation of an enzyme-substrate complex endergonic (induced fit model)?

Most reactions require an activation energy to cross an energy barrier (this you may already know) after which the reaction is downhill. Even though enzyme catalysed reactions have a relatively lower activation energy compared to that of an uncatalysed reaction, there is still a transition state that has a higher free energy compared to the products. This transition state corresponds to the enzyme-substrate complex.

              Image Source: https://en.wikibooks.org/wiki/Structural_Biochemistry/Enzyme/Activation_energy

Free energy has enthalpic and entropic components (ΔG=ΔH-TΔS). Even though formation of bonds may reduce the enthalpy, the locking of the substrate and enzyme in a conformation also decreases the entropy. This could lead to overall increase in free energy (See here. For more details you can refer to this book- The Enzymes: Mechanisms of Catalysis by Paul Sigman. ISBN: 0121227200).


Intro Bio question: dihybrid punnet square

Hah! You can relax. There's no difference between RyrY and RrYy, as there is no fundamental ordering of genes like that. That being said, the standard convention would be to write RrYy (or at least RryY), so if your grader is a pedantic hardass they might take off a couple of points, but probably not the whole 16.


Protein function and how it does not get affected with amino acid

The side chains of some amino acids are not reactive and therefore not involved in any covalent chemistry in enzyme active centers.

Isoleucine, an essential amino acid, is one of the three amino acids having branched hydrocarbon side chains. It is usually interchangeable with leucine and occasionally with valine in proteins.

Typical amino acids and their alternatives usually have similar physicochemical properties.

Amino acid replacement is a change from one amino acid to a different amino acid in a protein due to point mutation in the corresponding DNA sequence. It is caused by nonsynonymous missense mutation which changes the codon sequence to code for another amino acid instead of the original.

The effects of amino acid replacement may vary depending on how similar or dissimilar the replaced amino acids are, as well as on their position in the sequence or the structure.

References:

http://www.biology.arizona.edu/biochemistry/problem_sets/aa/Isoleusine.html
https://en.wikipedia.org/wiki/Amino_acid_replacement


Looking for books on How the limbic system works and it role in non-verbal behavior

not sure if you are still looking, but I have two recommendations for you.

"Limbic systems for emotion and for memory, but no single limbic system" is a really long, but really great article on the topic.  You can find that online here:  https://www.sciencedirect.com/science/article/pii/S0010945213003110?via%3Dihub
It's been a while since I've read this one, but the book Synaptic Self:  How Our Brains Become Who We Are is a good read on this subject.  It's about the brain as a whole, but focuses a lot on the limbic system and amygdala (it's author, Joseph LeDoux, did much of the pioneering work on the amygdala).  It is from 1996, so the science isn't super up to date, but I still think it's a good read if you're just curious about the brain and limbic system.


Is a part of the spinal cord from the mesoderm?

The caudalmost part of the neural tube is formed by the caudal eminence. Isn't this mesodermal?

No,the neural tube is not mesodermal at caudal end.

According to Gray's Anatomy:

  At the time of caudal neuropore closure, the caudal midline cells are generically termed the caudal eminence (O’Rahilly and Müller 2004). A specific population of mesenchymal cells, the caudoneural hinge or junction, shares the same molecular markers as the primitive node. These cells aggregate at the midline and undergo mesenchymal/ epithelial transformation, producing a cellular cylinder that is contiguous with the caudal end of the neural tube. Further elongation of the caudal neural tube involves cavitation of the neural cylinder.

So, the cells in the caudal eminence form a solid cylinder(medullary cord) which is made hollow by elongation of neural tube. Therefore, mesodermal cells of caudal eminence are not forming the caudal end of neural tube.

Let's see the process of neural tube elongation from the citation given in the Gray's textbook:

Abbreviation used can be seen here

Schematic diagram can be seen here


Neurophotonics refers to the use of light to study the brain, including measurement (i.e. microscopy, including the use of fluorescent molecules that allow measurement of ions or voltages in live tissue, but also including histological techniques) and manipulation (using light to activate, inactivate, modulate, etc neural activity).

Optogenetics refers to the use of genetically encoded (whether delivered via virus or in a transgenic animal) constructs that respond to light and are introduced into cells where they are not normally found, often neurons. Neurophotonics is a broad term that would include optogenetics.

In my personal opinion, optogenetics is a fairly specific term that is useful, though it certainly has some popular buzz around it. Neurophotonics is a new buzzword that encompasses a lot of techniques that have been around a long time, and while these techniques are constantly improved upon, the neurophotonics label isn't really necessary (but sounds fun).