How do white Caladiums perform enough photosynthesis to support their mass?

There are many different kinds of plants that have independently evolved this sort of variegation (non-green areas) in the leaves. However, the mechanisms by which they effect this vary between species.

Some have little or no chlorophyll in the non-green areas, but many others have changed the architecture of their leaf cell layers in the non-green areas, creating refraction effects that make the leaves appear white, but don't significantly change their photosynthetic efficiency (Sheue et al.) In fact, Arum italicum white areas actually have higher efficiency in certain light conditions! (La Rocca et al.)

I can't find any information on which type of variegation Caladium shows. The genus Caladium is related to the Arum I mentioned above which uses the "architecture" method, but it's also related to Epipremnum, which seems to use the "no-cholorophyl" method.

Sheue et al. mention that with some species that use the architecture method, using transmitted light instead of reflected light reveals that the white spots are actually green; while in no-chlorophyll plants the spots remain white. If you have a Caladium around, you could try holding its leaf up to a bright light, and see!

So, to answer your question: if Caladium is an 'architecture-variegation' plant, its white areas perform photosynthesis at or near the efficiency of the green areas of the leaf. If it's a 'no-chlorophyll-variegation' plant, it would have reduced efficiency, but might make up for this with strategies including:

Having a larger total leaf area (La Rocca et al. and also see this question)
Only developing large white areas if there's plenty of light as they grow (Garland et al.)
Increasing the mitochondrial activity in its white areas, which could lead to other energy efficiencies (Toshoji et al.)
Using Homo sapiens to help it reproduce and provide plenty of light for it. Many of these extreme variegation patterns are found in horticulturally bred varieties!
Just using its green areas for photosynthesis, and "accepting" the fact that the white areas are not producing energy. In natural populations, you often don't find varieties as completely white as in that picture: they usually show white spots and plenty of green. This is true of Caladium species in the wild, which may use the variegation to mimic and to prevent herbivory: potential pests think the leaves are already infested, and avoid them (Soltau et al.). In other words, even if the white patches represent decreased photosynthesis efficiency, it could be a trade-off in order to achieve less herbivory.

Garland KF, Burnett SE, Stack LB, Zhang D. 2010. Minimum Daily Light Integral for Growing High-quality Coleus. HortTechnology 20: 929–933.
 La Rocca NN, Rascio NN, Pupillo PP. 2011. Variegation in Arum italicum leaves. A structural-functional study. Plant Physiol Biochem 49: 1392–1398.
 Sheue C-RC, Pao S-HS, Chien L-FL, Chesson PP, Peng C-IC. 2012. Natural foliar variegation without costs? The case of Begonia. Ann Bot 109: 1065–1074.
 Soltau U, Dötterl S, Liede-Schumann S. 2009. Leaf variegation in Caladium steudneriifolium (Araceae): a case of mimicry? Evolutionary Ecology 23: 503–512.
 Toshoji HH, Katsumata TT, Takusagawa MM, Yusa YY, Sakai AA. 2012. Effects of chloroplast dysfunction on mitochondria: white sectors in variegated leaves have higher mitochondrial DNA levels and lower dark respiration rates than green sectors. Protoplasma 249: 805–817.


Nomenclature for mutations at specific nucleotide positions

As 'c.' stands for 'coding' sequence (instead of 'g.' for 'genomic'), according the HGVS guidelines it denotes the A to T substitution at nucleotide -35 of an intron (in the coding DNA positioned between nucleotides 1842 and 1843).


What is it about the housekeeping genes that makes them almost immune to gene regulation?

Housekeeping genes aren't clustered on a single chromosome. It is perhaps not that 'housekeeping' genes - broadly expressed genes - are 'above the laws of regulation'; rather that their regulation is merely more straight-forward than that of specialised genes.
I can think of 2 factors that could be relevant:

Abundance of methylation sites (CpG sites)
Promoter sequences and hence the transcription factors regulating expression of housekeeping genes are distinct from those controlling specialisation

I think the second (promoter sequences) is the better explanation, since housekeeping genes are abundant in CpG islands; but I'll explain a bit about both.
tl;dr: Housekeeping genes have simpler promoter and enhancer regions that are not bound by particular complexes which act to inactivate regions of the genome in a hierarchical manner during differentiation (according to the transcriptional program). http://genomebiology.com/2007/8/7/R140
Preamble
In forming tissues during development, cells must differentiate from embryonic stem cells, which have very wide potential to express many genes and give rise to all cell types; to partially specialised stem cells e.g. hematopoietic stem cells (HSCs) which are limited to give rise to all blood cells but not, say, neurons or pancreas or skin. Completely differentiated cells have a much more restricted domain of possible expression, and are more-or-less condemned to their fate.
Waddington's developmental landscape is a nice metaphor for how cells specialise:

DNA Methylation
A major mechanism behind this one-way narrowing of potential is methylation of DNA, which suppresses transcription. As the ball rolls down the landscape it acquires new stretches of methylation on its DNA, rendering it inactive which (for our purposes) is permanent and irreversible.
DNA methylation consolidates its chromatin inactivating function by acting as a signal for proteins which chemically modify histones (around which DNA is wrapped in chromatin) with further signals to condense chromatin, which occludes the transcriptional machinery from doing what it does best. (There are also activating histone modifications, and we imagine chromatin being, roughly, in OPEN and CLOSED states regarding the possibility of RNA polymerase gaining access to the DNA.) Since histones are ubiquitous & regularly spaced over the genome, there aren't "non-regulatable" regions - chromatin is opened or closed by the interactions of various DNA binding proteins, some reading and writing signals on to the chromatin.
So one plausible hypothesis is that housekeeping genes are relatively devoid of CpG sites (where methylation occurs). However I think this is not true. Many human genes have regions abundant in CpG (called 'islands') around their promoters, and in particular virtually all housekeeping genes. When genes are active, these CpG islands are unmethylated - hence in most tissues housekeeping genes have unmethylated CpG islands, something else is keeping them unmethylated.
Specialised cells, through a hierarchical transcriptional program of 'master regulators', successively close unneeded regions of their chromatin during differentiation, and keep open regions containing housekeeping genes, and the 'specialised genes' that relate to its specialism - these regulators are transcription factors which recognise the regions they act upon by binding promotor or enhancer sequences.
Housekeeping promoters and transcription factors
Transcription factors bind to enhancer or promoter sequences and open or close the chromatin for RNA polymerase, usually as part of a co-operative complex of many factors, including proteins that modify the histones or methylate DNA.
A good hypothesis is that the promoter/enhancer regions of housekeeping genes differ from those of specialised genes which are inactivated in many tissues. The transcriptional programs in differentiation must call forth factors that bind and inactivate specialised genes but keep active things like actin, ribosomal genes, etc.
This paper finds that upstream regions of housekeeping genes are less conserved, and a particular set of promoter motifs are over-represented. This suggests that housekeeping genes have relatively simple regulation by a few transcription factors; they lack binding sites for those transcription factors with important specialised roles in development.
To summarise, I think the following is likely: Housekeeping genes' promoter and enhancer regions exempt them from the complex transcriptional programs of hierarchical inactivation responsible for cell differentiation that many other genes are subject to. Housekeeping genes simply lack the relevant binding sites for these specialised transcription factors; they have instead more simple 'core' promoter elements. All the DNA methylation and opening/closing of the chromatin is a consequence of the transcriptional program.

http://en.wikipedia.org/wiki/CpG_site
http://en.wikipedia.org/wiki/Embryonic_stem_cell
http://en.wikipedia.org/wiki/Hematopoietic_stem_cell
http://www.nature.com/scitable/topicpage/the-role-of-methylation-in-gene-expression-1070
http://en.wikipedia.org/wiki/Histone
http://genesdev.cshlp.org/content/25/10/1010.full
http://genomebiology.com/2007/8/7/R140   < most relevant thing to read, and the basis of my own conclusion


Is there any way the food industry can benefit from biofilms?

inf3rno's comment provides a great example, in the production of vinegar (Food Safety Magazine):

  In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient.

This paper, Biofilms in the Food Environment (Czaczyk & Myszka, 2014) also provides examples of biofilm use in industrial food production (on page 75, 14th page in the linked PDF):

  Bioreactors
  with biofilms (biofilms represent a natural form of cell immobilization) are used to obtain acetic acid, citric acid, ethanol, and polysaccharides.

You can also check out Chapter 7 of this book of the same name, Biofilms in the Food Environment, for more information, if you're interested. It's not available for free online but you may be able to find it in a library.


DNA is charged negative. Where is all the positive charge in my body?

DNA in the body is not available as a free molecule, it is organized around DNA binding proteins, mostly the histone octamers. These proteins carry positive charges (mostly from lysine side chains) which interact with the phosphate backbone of the DNA. It is like in the figure below, the charges play an important role in the tight packaging. See here for more details.

The charge (or the temporary neutralization at some points of the DNA) is also important for the regulation of the DNA. Acetylation neutralizes the histone tail and loosens the DNA-protein structure (see here for more information).

Positively charged ions don't play a role in neutralizing the DNA charge in living cells (this is different for precipitations), as both are solubilized and split into ions. The concentration of positively charged ions like sodium and potassium are tightly controlled by the cells, as they are important for the function of transporters (for example the sodium-glucose transporters and others) or for keeping up membrane potentials. Moving the ions, which have to neutralize the DNA charge around would lead to a polarized nucleus.


The habit of burying food in modern dogs is an instinct that came from the grey wolf (Canis lupus) long ago, and originates from a phenomenon called surplus killing, where a carnivore would kill more than it could eat, and often use it at a later time.

  Many, if not all, carnivores possess behaviour patterns which allow utilization of a kill at a later time, or allow other members of the same social unit or offspring to use the food.

When the prey is small enough to transport, and there are pups, it is often returned to the den.

  Pups will usually remain in their den for the first three or four weeks of their lives before mother allows them to venture forth into the light. During this time the mother is quite dependant on her mate and other pack members to bring her food in the form of meat that is often regurgitated for her.

It is then fed on by the litter, and the excess buried for later use.

This is called 'caching', and is still seen today in the domestic dog (Canis familiaris).


Generally, all diploid species pass through a haploid phase in their life. This is called the alternation of generations and the cycle may be presented like this:

Commonly we see organisms that spend most of their life in the diploid phase, with greatly reduced haploid phase (e.g. humans "live" in haploid state only as gametes). However, this is not the only way possible. There are organisms, which spend similar amount of time in each phase, which change ploidy depending on the conditions of the environment and, of course, organisms which spend most of their lives as haploids, with only a short diploid stage.

As a rule, lower plants, fungi and protozoa may exibit this behaviour. Some examples:

Saccharomyces cerevisiae (yes, baker's yeast) will undergo meiosis and form haploid spores in unfavourable conditions, which then can grow as haploid colonies until they encounter a colony of opposite "sex"
Mosses commonly grow larger gametophytes (haploid) than sporophytes (diploid)
Some brown algae grow sporophytes and gametophytes that are indistinguishable form each other
Ferns often grow large sporophytes and small, but self-sufficient gametophytes.

Next question should be "why only lower plants and fungi?" And the shortest answer is that a diploid organism is usually more robust, it can survive more potentially lethal mutations than a haploid.


Are humans evolving since their first appearance?

The idea of first appearance suggest an important misunderstanding. There is no such as a first appearance of humans (or any other species) that would not be arbitrary. The Homo lineage evolves and keep evolving but don't think of humans as being created at some point and then eventually evolving. Life came to existence 4.6 billions years ago and it is evolving and diversifying ever since but no species has ever been created anew.

  Is the evolution a very prolonged progress

The only, non-arbitrary definition of evolution is a change of allele (=gene variant) frequency in a population over time. Such change occurs several times every second in humans. So evolution is constantly occurring. It really does not take much time. However, I realize that when layman ask "How much time does it take for evolution to occur" they mean something of the kind "How much time does it take for a previously absent phenotypic trait to come to existence in a population?". The problem is that the answer very much depend on what phenotypic trait and what are the selection pressures on this trait.

  are we going to witness further evolution of the human spieces?

Yes, we had, we are and we will. Humans are still evolving and you might want to have a look at the post Human Evolution in Modern Times.

  If so, in which direction?

In plenty of directions in the same time. Each phenotypic trait will evolve (not completely independent of each other though). There is no single direction for a whole species. You should therefore specify the trait of interest for the question to make sense. Again I think that the post Human Evolution in Modern Times will help you.

Want to have a basic understanding of what evolution is?

Understanding Evolution (UC Berkeley) is a free online very introductory course to evolutionary biology. It will help you to very quickly raise you level of knowledge of evolutionary processes.


why do we tighten out muscles against cold?

Consider most animals instinctively recoil from unpleasant sensations. Resisting this often involves tightening the muscles. Think about the last time you had to get a shot or pull a splinter out of the skin, you often tighten the muscles in an attempt to resist your own instinctual reaction. Even non-physical reactions like resisting fear or disgust often have similar responses, the mind and body do affect each other. Physical actions can effect mental states. Tensing muscles has been shown to have a direct effect on our willpower.


How does fluid pass through the glial limitans into the subarachnoid space?

Excellent question. This is an active area of research.

The glia limitans defines the external most layer of brain parenchyma. Previously thought to primarily be a barrier against migration and growth of neural cells out of the brain parenchyma during development, recent work has characterized its involvement in regulating the immune environment of the CNS. A 2017 JCI paper demonstrated that the tight junctions of the glia limitans are inducible in mouse in response to inflammatory cues. You may find the associated editorial helpful. In addition to demonstrating a dynamic role for the barrier function, you can see that tight junctions are not the standard state, and the typical state allows passive diffusion as well as active transport of small molecules between the CSF and brain ISF, but the question is not fully resolved.

Importantly, this is mouse data, and mouse data in particular cannot fully resolve questions about human astrocytes.


Where to obtain metabolic pathway datasets

KEGG is definitely your choice!

It is possible to get the whole list(s) of pathways: http://rest.kegg.jp/list/pathway (reference pathways) or http://rest.kegg.jp/list/pathway/hsa (for human).

Then you can use these IDs to retrieve information about individual pathways: http://rest.kegg.jp/get/hsa00053 (GeneBank-like format), http://rest.kegg.jp/get/hsa00053/image (image), http://rest.kegg.jp/get/hsa00053/kgml (KEGG xml). It will take a while, of course, and I'd recommend not to overload their server and make delays between queries. With the GeneBank-like format batch querying is also possible: http://rest.kegg.jp/get/hsa00053+hsa00061

This should likely be a one-time or at least rare operation, because of the load on their server (and I don't think they make big changes very often). You can retrieve info for new pathways, once they appear in http://rest.kegg.jp/list/pathway/...


What are the response frequencies of sensory neurons?

The auditory brainstem shows "phase-locking" typically up to 1-3Khz at most; 3000Hz is an incredibly high firing rate for a single neuron, but this phase-locking is achieved not by individual cells firing in-phase with an auditory stimulus, but rather with a population of cells that tend to fire in-phase, such that if you average across the population you get a phase-locked population volley.

In some cases, in some animals, this phase locking can even get to the higher frequencies (see here for example).

However, this phase locking seems primarily important for sound localization via interaural time differences. Frequency itself is encoded by which population of hair cells is activated, according to the properties of the basilar membrane. Firing rates of individual spiral ganglion cells are only faster than 100 Hz at very high stimulus intensities.

Similar to the spiral ganglion cells, retinal ganglion cells primary encode intensity information in their firing rates.

However, in both cases, it's important to recognize how crucial adaptation is in sensory systems. RGCs in particular fire primarily to transients, so it is typical to use light flashes, drifting gratings, or other dynamic stimuli. The response to a "medium long, medium strong signal of some fixed (wavelength)" is going to be brief, followed by silence, not a constant response like you imply.


The Fish-Tetrapod Transition, evolution of the "elbow" in Stem Tetrapods

The current research doesn't venture many details on the elbows/radius/ulna and locomotion biomechanics.
For the moment they just say the elbow was "slightly flexible" and that the bones were transitioning towards a round shape.
You can research deep into the resources and will perhaps find more.
Here are a resource which give context, found via "locomotor performance in stem tetrapods"
https://www.researchgate.net/publication/236460049_Historical_Perspectives_on_the_Evolution_of_Tetrapodomorph_Movement
There's also a 3D study of the legs here: https://www.researchgate.net/publication/227857349_Three-dimensional_limb_joint_mobility_in_the_early_tetrapod_Ichthyostega
https://sandykawano.weebly.com/locomotor-biomechanics-for-moving-onto-land.html


So an easy way to convert a cell from F+ to F- is to divide it without correctly replicating the plasmid and transferring it to a daughter cell, leaving you with one F+ and one F-. The cells that are F- now have a selective pressure advantage over the F+ cells, as they now don't require the energy to produce a plasmid when they divide. If that advantage is enough to overcome the frequency of conjugation, you'll end up having a population of F- cells.


Ion-exchange vs Gel Permeation Chromatography for proteins

Since lysozyme is so well studied, your best bet is to search the literature and see what methods other people use. See this paper, for example. They report that lysozyme can be affinity purified on Sephadex, but they also reference other methods in the introduction that you could take a look at.

Both of the methods you described sound reasonable. The only way to know which is best is to try them and see. In fact, the best approach, depending on your application, would likely be to use both methods for optimal purity. Even when I affinity purity a protein, I will still often perform ion-exchange as a polishing step.


Does cooking or ripening reduce the concentration of solanine in nightshade?

If you ask Dr. Duke's phytochemical database, by far the most solanine is found in green potatoe fruits (their skin), with much less in leaves and tissues. Similar values are seen in green tomatoes, with dozens of mg per 100g fruit. There is no value for Solanum dulcamara (doesn't mean there is nothing in it) but it appears to have small quantities of atropine. Furthermore, Wikipedia gives for solanine a minimum toxically effective dose for humans of 200 mg---that's where dizzyness and dispnoe starts---, and gives for children a lethal amount of S. dulcamara of 30-40 unripe berries or less. The amount of solanine increases (in potato) when temperature goes up, because it is produced by plants as an antifungal against rot. Ripening in S. dulcamara and, as we know all ourselves, potato and tomato, destroys solanine, so fully ripe berries seem to be okay. Solanine does not degrade when cooked but is lost with the cooking water. For an account of solanine poisoning from potatoes see e.g. this free paper. Newer potato varieties have much less solanine than those from former times.

http://www.ars-grin.gov/duke/

http://de.wikipedia.org/wiki/Solanin

Know your databases!


What is the human species divergence time

The erectus line that gives rise to antecessor is your best bet, at about 1.2 MYA. http://www.nature.com/nature/journal/v485/n7396/full/485033a.html
part of the problem is you are hitting the limit of where the term species is useful, once you get really close to the speciation event the term breaks down becasue everything is a ring species once time is included. Erectus includes both our ancestors and populations wholly isolated from us. Its like trying to draw a line between yellow and orange on a spectrum.


Should I consider one or two DNA chains to find how many nucleotides are in a gene?

Counting both strands is admirably correct, but most people will multiply the number of amino acids by three, not six.  For example, nucleotide positions in a reference sequence will increase by 3 for each amino acid in the presumptive coding sequence.  Besides, if you want to be that pedantic, you should say zero, since the DNA contains nucleotide residues, not individual nucleotides, as they have undergone dehydration synthesis.  I think in biology the right answer will almost never be marked correct by a machine. :)
The answer you come up with will also be influenced by whether you would like to include a stop codon (+3) to avoid nonsense-mediated degradation, and a transcriptional start site and polyadenylation sequence (in eukaryotes).  The ''gene'' itself, in the genetic sense, will include enhancer elements over a much longer region of the chromosome and regulatory 3'-untranslated regions.  And then there's alternative splicing to consider...


Behaviour of neuron when membrane potential is maintained at threshold potential or more

Before I start, I should point out that in order to change the membrane potential (known as the Vm) of a neuron you really need an internal electrode - so that you can pump current in to it, so increasing the potential above the resting membrane potential (RMP). The RMP is simply the Vm of a neuron at rest, without any external meddling by pesky scientists (or synaptic inputs).

When you depolarise a neuron - in other words, make it less negatively charged, it will fire an action potential once it crosses the spike threshold. This value is different for different neurons, but -50mV is usually not enough to trigger an action potential - normally it's more in the range between -30 and -40. But let's say it does, as it doesn't change the thrust of the question.

The major part of what happens during an action potential is that sodium channels open, allowing the spike to fire. Once closed, these channels have a 'refractory period' - essentially a time out, during which they are less likely to open again. So even though your neuron is still above spike threshold, it can't fire because the channels can't open. (For the aficionados, you can actually think of this as the spike threshold becoming temporarily more positive - going up to, say, -20mV).

So your neuron doesn't fire again for, say, 10ms, until the sodium channels reactivate. Then it does. So you get a train of regularly spaced action potentials at a certain frequency. The more you depolarise the neuron, the faster this frequency becomes until a point where the channels just become totally inactivated and the neuron stops firing. If you hold the cell at this voltage for more than a few seconds, in general it will die.


Long story short: Absolutely.

Short story long:

While your intuition that growing a lot of cells can increase the risk of damage that might cause cancer is spot on, your specifics are a little off. It's not the telomeres themselves that are the problem, but broad spectrum DNA damage and transcriptional changes. The condition of the telomeres doesn't directly affect the likelihood of a cell growth becoming more cancer-like. A cell with perfect telomeres fresh from a telomerase-expressing stem cell and cell with shortened telomeres have an equal chance of becoming cancerous. Cell populations with longer telomeres have 'more time' or more chances to develop mutations and cell expression damage, however. You're more likely to get in a car crash if you go to the store across town  than the neighborhood convenience store, even though it's not intrinsically more dangerous per mile driven.

The sunburn example can be a little misleading. It's not cell regrowth that's the key carcinogenic factor, but instead the direct DNA damage UV radiation can cause. In a particularly bad sunburn your skin cells may be killed or commit suicide(apoptosis) because of the DNA damage they've sustained. If the cells are damaged but do not die, they're likely to recover. Over time and repeated sun exposure, the skin cells that are most resistant to orders from the body to stop growing or die stick around and may grow and divide. Freckles are when this happens to a population of skin cells that ignore orders about how much brown pigment to be, but still listen to the orders that instruct them on how to be skin. When they stop listening to the skin orders, they officially become precancerous.

The acid reflux example is excellent. There are populations of stem cells throughout the adult body that produce skin cells and hair follicles and blood cells and all the other kinds of cells that are more or less expendable. Generally speaking these stem cells don't have do very much work replenishing esophagus cells, so when they are taxed by something killing off the esophagus lining regularly, they can 'break down' and lose control of their own replication.

It seems like you're both pretty interested in cellular mechanisms of cancer and a little shaky on current theories of cancer formation(there are a few), so if there's a section of this answer that needs to be more detailed or followup questions please let me know.


The answer is more like "It depends on the protein, and the renaturation (or refolding) process." There are a lot of factors that contribute to an individual protein's ability to refold, including size, sequence, secondary structure, amount and type of inter-amino acid links like disulfide bonds, number of subunits, the presence of chaperones/heat shock proteins, and, yes, how it was denatured in the first place (sorry, I couldn't resist). Smaller proteins will refold more easily than larger ones. Hydrophilic proteins tend to refold better than more hydrophobic ones, especially membrane-bound proteins. Multi-subunit proteins/complexes tend to need some help to properly reassemble. Adding in chaperones/heat shock proteins will almost certainly help the process along for all but the smallest and hardiest samples, and will give you better results than just dialyzing all the salts/detergents/chaotropic agents away into PBS. Finally, if you denature by boiling in Laemmli buffer, you're going to have a very difficult time refolding most things, while going from Guanidine HCl to PBS isn't always that bad, depending on what you're looking at.

So, unfortunately the answer is "it depends." You have to remember that the intracellular environment is very complex, and is designed to correctly fold proteins after they're made, and break down misfolded proteins before they can aggregate or cause other damage. There are hundreds of thousands of proteins just in humans, so it is rather difficult to make blanket statements, but for the sake of resistance to damage, many smaller, single-subunit proteins can likely be at least partly to mostly refolded and regain some or all of their original activity. As complexity grows, however, the likelihood of successfully regaining function decreases.


Are humans capable of both anaerobic respiration, and lactic acid fermentation?

Humans have no anaerobic respiration, if we define this as oxidation of a substrate with an external electron acceptor other than oxygen. In humans, the terminal electron acceptor in respiration is always oxygen, which is reduced at complex IV in the respiratory chain. Alternative electron acceptors are mostly found in bacteria and archaea.

I would call the anaerobic metabolism of glucose to lactate in humans a fermentation process. It consists of glycolysis, which converts glucose to pyruvate, which in turn is converted to lactate by lactate dehydrogenase. There is no terminal electron acceptor in this case; instead, energy is extracted from glucose by rearranging the molecular structure of the sugar into a more favorable ("low energy") configuration, without any net donation of electrons.

Note: this is how I use the terms, and I believe this is the most common usage in biochemistry today. But I am sure you can find other sources that define them differently. This is rather common in biology and biochemistry, and these terms are very old and fraught with all sorts of historical connotations. But names are not crucial; understanding the biochemical processes is. The important distinction here is that conversion of glucose to lactate does not oxidize the substrate and therefore needs no external electron acceptor; in this way it is fundamentally different from oxidative metabolism.


A mechanical stimulus can act on a tissue with elastic and viscoelastic properties in two ways [1, 2]:

distort the cellular membrane which leads to opening of ion channels.
create tension on the extracellular matrix or cytoskeleton, to which a ion channel is bound, thus leading to opening of the channel.

Stretch-activated ion channels opening leads to the formation of an action potential, if there is enough ionic flow to trigger depolarization [1, 3].

References:

Wikipedia contributors, "Stretch-activated ion channel," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stretch-activated_ion_channel&oldid=606349902 (accessed July 12, 2014).
Grigg P. Biophysical studies of mechanoreceptors. J. Appl. Physiol. 1986 Apr;60(4):1107-15. PubMed PMID: 2422151.
Wikipedia contributors, "Mechanotransduction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mechanotransduction&oldid=593605473 (accessed July 12, 2014).


Wobble pairing is just a phenomenon and not a hard and fast rule. There are some justifications for why it should exist and that is why it is still called a hypothesis. And this statement is not true:"the base on the third position of the codon and that on the anticodon need not be complementary". The anticodon residue corresponding to the third residue of codon can be a promiscuous base which can pair with two or many different bases.  The tRNA for Phenylalanine has an anticodon - GAA which can pair with both UUU and UUC but not UUA.

So the statement of wobble hypothesis is that the first base of the anticodon (often is a modified/atypical nucleobase) can show promiscuity of binding.


Can DNA be considered as a fractal antenna?

I looked at the original paper, Blank and Goodman "DNA is a fractal antenna in electromagnetic fields" Int J Radiation Biology, 87:4, 409-415, DOI:10.3109/09553002.2011.538130.

To be honest I can't give concrete reasons to doubt it, but here are a few things that raise my suspicions:

it is a review article that relies heavily on self-citation (15/50 citations are authored or co-authored by the two authors of this paper, including most of the primary experimental references)
in my judgement "responding to many different frequencies" and "having structures on several different scales" (Table 1) is not particularly strong evidence to support the conjecture that DNA acts as a fractal antenna; I would be much more convinced by an analysis based on physics rather than analogy (this comment on the paper by Foster reviews the physics of fractal antennas and its application to DNA and concludes that "Loose and implausible conjectures about DNA as a fractal antenna do not substitute for careful discussion of these matters"; I don't find the authors' rebuttal particularly convincing)
the authors cite epidemiological evidence that non-ionizing/low-frequency radiation causes cancer: according to the US NIH's National Cancer Institute, this evidence is weak. (However, one of the authors of this paper is a contrarian on this subject and believes that the mainstream view is wrong, for a variety of reasons.) (See Are low-intensity radio-waves carcinogenic? for more discussion on Biology.SE.)
the paper uses very disparate lines of evidence (not necessarily a bad thing, but in this case it feels haphazard): in particular, the authors discuss both low-frequency and ionizing radiation (this is part of their "DNA is sensitive to many different frequencies" argument, but ionizing radiation operates in a very different way)
it is highly speculative in places (e.g. "EMF is believed to have been an important driving force in evolution", p. 413, no reference; the authors go on to attribute the faster evolution of eukaryotes to the fact that their DNA structures are more fractal)
at least one of the references cited (de Pomerai et al. Nature 2000) was retracted in 2006 (5 years before the current paper was published)

What I can say in favor of the authors is that exploring the mechanisms by which low-frequency electromagnetic fields/radiation (ELF) affect cellular biology is indeed interesting; many of the epidemiological studies, while finding very weak effects, have also downplayed risk because so little is known about mechanisms of operation. If we could come up with a rigorous mechanistic understanding of ELF effects, that would be scientifically worthwhile.


conservation of C-peptide sequence in the guinea pig

The NCBI Nucleotide database can be used to search for coding sequences (mRNA and translated protein) of genes. You need to enter the name of the gene (INS) or protein (insulin) and then species (use either the common name, "guinea pig" or the scientific name, "Cavla porcellus").

Filter the results to show you only mRNA coding sequences (sometimes abbreviated as "complete CDS"). These entries are annotated with the regions that account for the signal peptide, mature peptide(s) and prodomain(s). In your case, the full proinsulin is annotated as mature peptide and the B and A chains. The C peptide connects the A and B chains, located between the only two dibasic sites (R55R56 and K88R89).

Another useful database is the UniProt Protein Knowledge Base which presents similar information in a slightly more graphical presentation. Here is guinea pig insulin in this database.

If you happen to compile a whole list of C-peptide domains from other mammals, then you can use an alignment tool like ClustalOmega to align the peptide sequences to look for commonalities.

As for guinea pigs, there is only a single insulin gene (like most mammals). Only mice and rats have a two gene insulin system, Ins1 and Ins2. Generally speaking, there is poor conservation of the C peptide domain across mammals, in part because it only serves to link the A and B chains together to form the necessary disulfide bridges.

If you are wondering whether an anti-guinea pig antibody will cross react with another species' epitope, that information is listed on the antibody specification sheet under species cross-reactivity. Some antibodies are more cross-reactive than others, and you will need to refer to the specific manufacturer's information to be sure.

Wang S, Wei W, Zheng Y, Hou J, Dou Y, et al. (2012) The Role of Insulin C-Peptide in the Coevolution Analyses of the Insulin Signaling Pathway: A Hint for Its Functions. PLoS ONE 7(12): e52847. doi:10.1371/journal.pone.0052847 A note on this paper, I would not take the conclusions that C-peptide has a physiological role in intracellular or endocrine signalling because it is still quite a controversial issue. I used this article because it was open access and to demonstrate in Figure 1 the variability of the C-peptide domain across selected mammals.


What are the constraints when growing an artificial brain?

The comments above are quite relevant -- we are years / decades away from growing functional brains in the lab, so there are probably innumerable constraints that we have likely not even thought of yet.

That being said, you might find this paper interesting: "Adaptive flight control with living neuronal networks on microelectrode arrays" [1]. The authors are able to succesfully culture rat neurons and electrically interface with them in order to control pitch and yaw in the XPlane flight simulation software.  It's a very crude system compared to an actual brain, but it's able to successfully use cells as rudimentary living neural networks. If you consider this to be a successful "artificial brain," then your constraints are all the ones associated with culturing neurons.

[1] DeMarse, et. al 2005


Cimbi-5 or 25i (25I-NBOMe) is a class 2C psychedelic drug.(wiki site.)

Lethal dose or LD50 of "Cimbi-5" is still unknown.

Though you can predict approximate the LD50 by structure computationally.


How is the enzyme glycogen synthase regulated?

The answer to this question can easily be found in standard biochemistry texts, e.g. one available online (albeit an old edition): http://www.ncbi.nlm.nih.gov/books/NBK22444/. Presumably this is why this question has not been answered previously. However I think it worth providing a summary answer in order to stress something that I feel perhaps does not receive enough emphasis in texts, and is ignored in the question.

This is that the regulation of glycogen metabolism (and indeed other aspects of carbohydrate metabolism) differs in different tissues because of the different situations in which its synthesis and breakdown is appropriate in relation to the integrated metabolism of the organism. If we just consider skeletal muscle and liver, the muscle stores glycogen to use itself when it needs to generate ATP to power contraction, whereas the liver stores glycogen so that it can provide other tissues with glucose when they require it either for work (e.g. the skeletal muscle) or in starvation (e.g. erythrocytes and brain).

The appropriate integration is provided in the first instance by the hormones mentioned (so-called first messengers), and the presence or absence of receptors in the tissues so that they will respond to these hormones or be refractory towards them, as appropriate.

Both liver and skeletal muscle have receptors for epinephrine (adrenaline) which is secreted as a stress response. This results in the breakdown of glycogen — used internally by the skeletal muscle and released as glucose by the liver, as already mentioned.

Liver also has receptors for glucagon, the hormone which is secreted in starvation or fasting, and also causes the breakdown of glycogen. The skeletal muscle does not have glucagon receptors because the nutritional state is irrelevant to its energy requirements.

Both liver and skeletal muscle have receptors for insulin, the hormone of the fed state, and respond to this by increasing the synthesis of glycogen to build up supplies to be available when needed.

How do these hormones work?

Glucagon and epinephrine (adrenaline) both work by activating adenyl cyclase (a so-called second messenger) in a G-protein-coupled manner to generate cyclic-AMP. This acts by a phosphorylation cascade to activate glycogen phosphorylase and inhibit glycogen synthase as described in any standard text. (Protein phosphatase 1 is also involved.) Glycogen breakdown is this enhanced.

Insulin acts differently. Binding to its receptor activates the protein's intrinsic tyrosine kinase, and there is a chain of subsequent protein self-phosphorylations culminating in the phosphorylation of protein phosphatase 1. This causes it to dephosphorylate both glycogen synthase and glycogen phosphorylase leading to the activation of the former and the inactivation of the latter. Glycogen synthesis is thus enhanced.

It is important to understand the molecular mechanisms of metabolic control, but it is also important to see them in the context of integrated tissue metabolism. So I will end with a question for the reader. The brain (which is absolutely dependent on glucose for part of its metabolism) stores a small amount of glycogen. How would you expect the brain to respond to the three hormones mentioned, and what would you expect to be the fate of the product of glycogen breakdown? If you have understood the principles above for liver and muscle you should be able to make rational predictions for brain (even should the facts turn out to be more complex).


How does waking up from an alarm clock work?

The brain does not "shut down" during sleep. While not everything about sleeping is understood, we do know that certain areas in the brain remain active during sleep. There is a good overview on sleep on the website of the National Institute of Neurological Disorders and Stroke.

  Until the 1950s, most people thought of sleep as a passive, dormant part of our daily lives. We now know that our brains are very active during sleep. Moreover, sleep affects our daily functioning and our physical and mental health in many ways that we are just beginning to understand

As for hearing, that part of the brain doesn't shut down during sleep - and for good reasons. Sudden, loud noises for example may be a sign of immediate danger. Any animal that just stops hearing a third of the day would be at a huge disadvantage.

The brain even processes the sounds we receive during sleep and doesn't wake on every loud noise. You might find the following article interesting: How do we hear while we sleep?

  Using electrodes implanted directly on the human cortex, a Johns Hopkins University undergraduate has located the part of the brain that appears to process sounds while people sleep. This site, in the frontal lobe, may be part of a vigilance system that, for instance, rouses a mother when her baby cries but lets the woman sleep when a truck rumbles by.

Alarm clocks are usually designed to just get louder and louder until we do wake up. Even despite that, some people actually do manage to sleep "through" the sounds, for example of they were very tired and haven't yet had enough sleep. This is speculation, but maybe in that instance the brain prioritizes sleep.

Other articles on the subject are for example Odd Sound Processing in the Sleeping Brain and Auditory information processing during human sleep as revealed by event-related brain potentials, but the main point is that we don't stop processing what happens around us just because we are asleep.


What are the differences between isozymes, allozymes and isoforms?

You have the basic idea:

Isozymes come from different genes but carry out the same enzymatic reaction.

Allozymes come from the same gene - i.e., the gene at a particular point on the chromosome; but chromosomes come in pairs, and the allozymes come from the 2 different chromosomes in the pair.

Isoform proteins ["protein variants"] are from the same gene, but they can have the same or different functions, depending on how they are spliced = which exons are included, and in what order. There's a nice picture in the Wikipedia article "protein isoform."

Here are Wikipedia links:

Isozyme - Wikipedia
https://en.wikipedia.org/wiki/Isozyme
Isozymes (also known as isoenzymes or more generally as multiple forms of enzymes) are enzymes that differ in amino acid sequence but catalyze the same chemical reaction.

Alloenzyme - Wikipedia
https://en.wikipedia.org/wiki/Alloenzyme
Alloenzymes (or also called allozymes) are variant forms of an enzyme which differ structurally but not functionally from other allozymes coded for by different alleles at the same locus.  ...These are opposed to isozymes, which are enzymes that perform the same function, but which are coded by genes located at different loci.

Protein isoform - Wikipedia
https://en.wikipedia.org/wiki/Protein_isoform
A protein isoform, or "protein variant" is a member of a set of highly similar proteins that originate from a single gene or gene family and are the result of genetic differences. While many perform the same or similar biological roles, some isoforms have unique functions.


Aren't antibiotic resistant probiotics dangerous?

Usually, resistance genes are located on plasmids---additional DNA rings in the bacterium that are part of the genome. These plasmids cause their own exchange with other bacteria, even from other species.

B. clausii, the probiotics organism in question here, appears to be special, though, in that it has no plasmids. His resistance genes come with the primary ring-shaped genome and should not be transferred via plasmid exchange to other bacteria. This doesn't rule out other means of gene transfer like phages or conjugation, however. In one study, it was unsuccessfully tried to transfer a macrolide resistance gene to other bacteria. They conclude

  A potential hazard is transfer of resistance to microorganisms
  pathogenic for humans. The risk that this event will occur and the
  consequences in terms of morbidity and mortality have not been
  evaluated. Parameters required for risk assessment include studies on
  the nature and mobility of the resistance genes of probiotics.

The only other paper on a B.clausii resistance gene didn't look at its transferability. That clearly shows we don't know enough.

B. Bozdogan, S. Galopin, R. Leclercq: Characterization of a new erm-related macrolide resistance gene present in probiotic strains of Bacillus clausii. In: Applied and environmental microbiology. Band 70, Nummer 1, Januar 2004, S. 280–284, {{ISSN|0099-2240}}. PMID 14711653. PMC 321311.


Endogenous just means that it is naturally occurring in the organism:

http://www.dictionary.com/browse/endogenous

endogenous cytoplasmic defense gene is a general description of a gene that is cytoplasmic and whose function is defending the organism. There isn't THE Endogenous cytoplasmic defense gene. There are many endogenous cytoplasmic defense genes. Note that it is the protein coded in the gene that is cytoplasmic, not the gene itself. It should say 'gene for endogenous cytoplasmic defense protein'.


Can controlled dose of Codeine improve brain's functionality?

the first time you take them you will feel better, think sharper, and
  act better

You are probably thinking of amphetamines, not opiates. Militaries have used amphetamines for just that purpose for decades, particularly for situations where long periods of attention are necessary. The problems are addiction, adaptation (lessening effects over time), withdrawal, side effects, etc.

Caffeine has very different cellular effects, but is also a stimulant, albeit a much weaker one. People around the globe use caffeine to achieve much of what you are suggesting on a daily basis. I actually think caffeine is a great example of what you are proposing, because (at least for people who tolerate it well and don't have any other conditions) it is safe, effective, and has less serious withdrawal symptoms and is somewhat less addictive than many other drugs. That said, among people who use caffeine regularly, some of the benefits begin to wane, and people start needing caffeine to maintain their normal level of alertness.

People with ADHD (and some others without, particularly students) also take amphetamines to help with attention (Adderall is an amphetamine; Ritalin/methylphenidate is closely related). There is a bit of controversy over whether that's a good idea or not. All of these things have side effects, including potential for changes in personality, anxiety, and various peripheral side effects, as well as the risks of dependency and symptoms of withdrawal.

Codeine and other opiates, on the other hand, are primarily useful for blocking pain. They are often associated with euphoria, but their other psychological effects are mostly depressant: drowsiness, respiratory depression, suppression of gut motility leading to constipation, etc. I'm not aware of any cognitive enhancement from codeine, unless the cognitive task you are trying to perform is sleep.


Why are fifth order Markov Models, the ones most often used for gene prediction?

The problem with increasingly complex HMMs is that their parameter space tends to explode with the nth-order of the HMMs. Higher number of parameters is often not great because it reduces the possible number of observations that go into training each parameter and can increase overfitting of the model.

From the information that you are providing it is possible that the 5th order model reaches the sweet spot of having great performance with a reasonably contained parameter space.

It is not clear how your model also works.

Is each state a single nucleotide or a single KMER?

Is it a generalized HMM with separate states for exons and introns with the KMERs being observations?

Work by the Bier lab has shown that 5-mers are very good at telling apart enhancers from background using a SVM model for classification. In your context it seems pretty reasonable to use 6-mers to find genes given this finding.

For more details please check "Biological Sequence Analysis" by Sean Eddy and the work of Dr. Michael Brent @ Washington University in Saint Louis (his lab has done a lot of research on HMMs for gene finding).

It'd be useful to have one or few paper references behind your question.


How close are we to having phages take over the role of infection control from antibiotics? What developments need to occur?

This is a very interesting topic. Indeed, historically, it might seem that "phage therapy" research is in a dormant state. But there are some groups actively doing theoretical research on the synergy between phage treatments and the immune system, as well as research on how the appearance of antibiotic resistance could be attenuated by the use of phages.

Nevertheless, this research is not what the field is trending towards, since there is still hope to find new antibiotics (for which, then, we will see other types of resistance evolving), and most of the funding agencies are still privileging this instead of the alternatives.

A colleage of mine is working on this very same theme. Here is one of his recent research papers on a specific type of infection.

Cheers,

Pedro


What medical and commercial proteins are made using genetically modified animals?

ATryn is a human antithrombin produced in the milk of transgenic goats by GTC Biotherapeutics. It has FDA approval and I believe that it is available for prescription in the USA.

Added later, after the emphasis of the question changed somewhat.

Proteins produced in a mammalian system are more likely to have post-translational modifications that are much closer to those found on the human protein. Antithrombin, for example, has four disulphide bonds and four glycosylation sites. Although it is reasonable to assume that the disulphide bonds would be correctly formed in a eukaryotic microorganism, the same isn't true of the glycosylation: microbial glycans differ from mammalian glycans, and these differences could affect the stability of the protein in the mammalian bloodstream, or the response of the mammalian immune system to the protein. Mammalian cells in culture could be used but are, of course, quite fastidious. So the holy grail of recombinant protein production has always been to get the protein secreted into an animal's milk, allowing the use of very cheap feedstocks and the easy harvest of the protein over a period of years, notwithstanding @shigeta's remarks.


There are two types of nucleic acids: 1) DNA --> which is double-stranded, so it's made of only two polynucleotides 2) RNA --> which is single-stranded so it's made of only one polynucleotide. So if we get back to my original question "Is a single polynucleotide necessarily and always a nucleic acid?" --> the answer is no, for DNA is a nucleic acid and it is made of two polynucleotides.


What is the distance between the sciatic nerve and the colon at the closest point?

Short answer
Sciatic nerve pain cannot be caused by a full colon.

background
The sciatic nerve runs at the back of the pelvis down the the leg. The sciatic nerve exits the spine from the lumbar spine to S3 in the sacrum (Fig. 1).

Fig.1. Left: sciatic nerve overview. Right: Sacral plexus. Source: Manchester Bedford Clinic

Hence the sciatic nerve does not come into contact with the bowel and intestines located ventrally in the abdominal cavity (Fig. 2).

Fig.2. Left: sciatic nerve in detail showing dorsal location. Right: Intestines ventrally situated in abdominal cavity. Source: Manchester Bedford Clinic and University of Maryland

Pain in the sciatic nerve (sciatica) is often caused by compression or entrapment by muscles, tendons, and other soft tissues along the nerve path Manchester Bedford Clinic.


Will lipid molecules 'flip-flop' over a membrane without the use of an enzyme?

Bilayer components will 'flip-flop' at measurable rates, but these are very different for different lipid classes. Here are the results of an experiment using fluorescently-labelled analogues.

  Bai, JN and Pagano, RE (1997) Measurement of spontaneous transfer and transbilayer movement of BODIPY-labeled lipids in lipid vesicles. Biochemistry 36:8840-8848 DOI: 10.1021/bi970145r

The authors followed the transbilayer (flip-flop) and interbilayer movement of fluorescently-labelled analogues of various membrane lipids: sphingomyelin (C-5-DMB-SM), ceramide (C-5-DMB-Cer), phosphatidylcholine (C-5-DMB-PC) and diacylglycerol (C-5-DMB-DAG) in a system of unilamellar vesicles consisting of 1-palmitoyl-2-oleoyl phosphatidylcholine.

The results were analysed in terms of a model in which the labelled molecules could move between vesicles and between the two monolayers of the bilayer.

half times:
            interbilayer    transbilayer (flip-flop)
C-5-DMB-SM  >21 s           3.3 h
C-5-DMB-Cer 350 s           22 min
C-5-DMB-PC  400 s           7.5 h
C-5-DMB-DAG 100 h           70 ms

So, for the phospholipid tested the half-time for flip-flop was 7.5 hours.


What is this insect? And does it eat aphids on plants?

Based on the head morphology and the upper limb visible on the first picture, I would say it looks like a mantis. The length of the abdomen also confirms the same.

The internet is also full of several non-scientific sources that seem to confirm they eat aphids. Animals will normally learn to avoid bitterness in food as it's a sign of toxicity. I haven't found a lot of information about how bitter are aphids, however mantis are sit-and-wait predators, so they will try most things that crawl their way. Judging by the following pictures (and the article linked at the end), I would say it's very likely:

  Indeed, catching every prey would be a beneficial strategy because of uncertainty in encountering another prey due to a sit-and-wait strategy. By holding prey with its forelegs and gradually eating the prey by chipping away at it, the mantis has enough time to find edible parts of prey and reject unpalatable parts/prey (Reitze and Nentwig 1991).

Sources:

https://en.wikipedia.org/wiki/Mantis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5882761/
https://praying-mantis.org/what-do-praying-mantis-eat/


Core Biological concepts explained to a Computer Scientist?

Evolution

Evolution is the accumulation of genetic mutations that results in phenotypic variation (physical characteristics) where surviving variations are more suited to the environment the organism lives in, thus allowing it to survive better and -- critically -- reproduce as-good-as or better-than its competing organisms.

In terms of computer science this would be like a starting with basic CPU design with all the absolute necessities. Now, let's pretend every generation of CPU after your first is going to be randomly designed by something called "Pressure OS". Pressure OS doesn't care if the CPUs it designs match the needs of the consumer. PrOS is unfeeling. An OS of pure logic. ALL it will do is make a bunch of random ones, note which ones sell the best, and make the best-selling ones to be the template for its next round of random designs.

  Selection and Variation

Selection is the process by which environmental pressures (low moisture, high heat, high altitude, available food, extreme pressures at the bottom of oceanic trenches, etc.) dictate how well each successive generation of organisms survive.

In our analogy, the Pressure OS is the cause of Selection. Some CPU designs aren't going to meet the needs of consumers (first-gen Atoms which could barely operate a toaster). Those ones won't be produced again. Others will be very successful (like the Pentium-4 Series which lasted for years) and will quickly outnumber the inferior ones.

Some designs, as odd as they are, will find success in areas outside enthusiast desktops or workstations. Like ARM designs which were never part of the desktop market, but found lots of success in phones and business devices.

Market requirements/environments, as met by the random variations produced by Pressure OS, created Variation in the types of CPUs available.

ARM Snapdragons could never, ever compete in the desktop enthusiast market. That's the realm of Sandy Bridges, Haswells, Semprons, and Phenoms. Then again, they're dramatically different designs -- which stem from common designs decades ago that have been heavily modified over the years -- that don't need to compete. Snapdragons and Semprons can co-exist because they fill different niches.

Now, when consumer needs change again -- if everybody gets tired of mobile phones, tablets, and desktops in favor of cone-shaped personal assistants which go in your ear -- then designs will change again under that new pressure. Eventually CPU one design will become the standard for that particular piece of hardware, and you could say that CPU variation had evolved to get there via selective pressure from consumers.

Biology operates in the exact same way, except the selection process is instigated by environmental pressures to produce organism variations that can successfully reproduce. It's also been going on for >3 Billion Years.


Cockroach-like insect identification (India)

It's a longhorn beetle (Cerambycidae).
Most likely, it's a Red-spotted longhorn beetle (Batocera rufomaculata), also known as a mango tree borer, mango stem-borer and tropical fig borer.
See this SE question pertaining to the same insect.

From Biolib:

Country check-list: China, India, Israel, Jordan, Laos, Lebanon, Madagascar, Malaysia, Mauritius, Myanmar, Pakistan, Puerto Rico, Sri Lanka, Syria, Thailand, Virgin Islands  [Might Not be complete]
Food: Ficus carica L. (Fig), Carica papaya L. (Papaya), Mangifera indica L. (Mango), Shorea robusta Gaertner f. (Sal Tree)

It might also be B. parryi, which, similar to B. rufomaculata, is common in SE Asia (but which is absent from Western Asia or Africa where B. rufomaculata is also found). Since you live in India, both are possible. I will look for a key to determine how to differentiate the 2 species.
Meanwhile, here is a list  of related species in the Lamiinae subfamily for further reference.
Also, a great resource (including keys) for wood boring beetles of the world!


What is the difference between multiple allelism and polymorphism?

The term polymorphism is broad and can have different meanings. Here are your definitions

Multiple Allelism: The existence of more than two alleles of the same gene within a population.
Polymorphism: the occurrence of more than two distinct phenotypes of a trait in a population.

Considering your definitions only, then multiple allelism has to do with genetics while polymorphism has to do with the phenotype.
Most loci (=position in the genome) that contain more than one allele (=genetic variant) have no effect on the phenotype. So multiple allelism does not necessarily yield to phenotypic polymorphism.
On the other hand, plenty of phenotypic variation in a population is due to environmental variation (including what an individual eats) and not to genetic variation. So phenotypic polymorphism is not necessarily caused by a case of multiple allelism.


cerebral edema and blood pressure, pulse

In cerebral oedema the observations (blood pressure, pulse, respiratory rate etc.) can be all over the place. They can depend on the cause e.g. infectious more likely to have raised pulse (tachycardia) with lower blood pressure (shock) but with the anxiety there might be raised blood pressure. Then with the vomiting, a symptom of cerebral oedema, this could lead to dehydration which leads to lower blood pressure or movement of fluid from the blood to the brain because it is oedematous could also drop the blood pressure. With the cerebral oedema affecting different structures, particularly the brain stem in coning (brain swells, pushes brain out through the big hole at the bottom where all the nerves come out particularly affecting respiratory rate) the respiratory rate could be low. It could also be high due to structures getting less oxygen causing the body to push the sympathetic nervous system to increase heart rate and respiratory rate.

In conclusion, things can be completely over the place but usually blood pressure is low and there's reflex tachycardia for the reasons explained above. For these reasons, to diagnose cerebral oedema we usually use the characteristic symptoms of nausea, vomiting, faintness and other features in a patient we know is at risk because of the signs and symptoms of the original disease or cause of the cerebral oedema e.g. the cancer, trauma or infection.


If you look at Fig. 2 in the paper, the bottom jaw has the split maxillary bone. Do you see how it says "MX" with two lines, instead of "MX" with 1 line on the top skull from Fig. 2? Each of those lines go to part of the split maxilla, with the joint being where it is pinched off (between teeth 5 and 6 on the drawing). There is also a CT image of the skull somewhere online that I've run across a few times (actually saw your question while looking for that image now).

I would also amend your statement a little in that it is not "as what is the point of 1/2 of jaw", it is that you can't have 1/2 of the joint(or split bone) existing. Either the maxilla is 1 piece or it is 2, but you cannot gradually go from 1 bone to 2 (similarly, either the cartilage of the joint exists or it doesn't. There can be a gradual change in how much cartilage there is, but if it's there or not is a binary question).

I hope that helps, off to look for the CT scan!


Example of well understood/modeled biological mechanism

I would point out that, assuming (as the other commenter noted) you are interested in analytic rather than statistical modelling (which seems a little unlikely to me given your area), most mathematical models are derived from first principles (often from physics) or other assumptions.
This suggests (to me) that looking at models of totally unrelated systems is not so useful; the whole idea of such models is to formalize your domain knowledge!

But I'll give some examples anyway.

For example, consider
 biophysical models of neurons or continuum mechanical models of cardiac tissue, both of which have rich histories of mathematical models developed over decades of work, based on both theoretical and empirical considerations (albeit largely from physics).
Perhaps slightly more related (or at least empirically driven) are the advances in systems biology, which tend to derive from some underlying laws of chemical kinetics, but utilize enormous amounts of (multivariate, temporal) data in fitting (often non-linear stochastic) systems of differential equations. Methods for computational protein structure prediction tend to use a mix of ad hoc rules (for computational time-cost reasons) and physics-based considerations in their models.
Evolutionary biology and population dynamics also have wonderful models (see the book from the commenter above).

My guess, given that your question does not have much detail, is that you would prefer statistical, i.e. probabilistic graphical or stochastic process, models instead.

Let's suppose you have a bunch of variables over time (e.g. the actions or status of a person) but you want to estimate an unobservable quantity (e.g. say, the degree to which they are insane [not my field, sorry]).
One simple probabilistic model is the hidden Markov model.
It has many examples of applications in sequence biology.
It also lets you figure out, in a way, which variables are important, and let's you tune certain parameters (e.g. it's order, which here describes how much the person's state at time $t$ affects their state at time $t+\Delta t$).
In terms of predictive modelling power, though, the state of the art is in deep learning models for time series.

Anyway, I'd consider what your goal is more carefully. If you indeed have a strong idea of an analytic model (motivated by some theory you know), then by all means formalize it. However, if you want the data itself to suggest a model for you, then use a statistical approach.

Note: apologies if this answer was too trivial, I was not sure what you did and did not know.


X inactivation is mediated by several epigenetic marks on DNA that cause condensation into heterochromatin. These include DNA methylation and histone modifications:
https://en.wikipedia.org/wiki/X-inactivation#Silencing

As you suggested, a newly copied DNA strand would be free of the epigenetic marks that mediate heterochromatin condensation. Yet epigenetic modifications are inherited, along with DNA molecules, by the daughter cells during cell division. That is, cells have ways of copying these modifications from the old DNA strands to the new ones. These mechanisms are not all known, and are the subject of much research.

In this fashion, each cell division produces two cells that inherit the X-inactivation status (i.e. heterochromatic state) of the parental cell.

This cycle of epigenetic inheritance only ends when the chromosomes are reactivated in primordial germ cells before meiosis and the production of eggs or sperm. The embryo of the animal's offspring can then make that initial, random X chromosome inactivation that is inherited by all of the cells in its body.


Does isolation have any effect upon mouse behavior?

Yeah, it's not good:

  Social isolation (SI) rearing in rodents causes a variety of behavioral changes, including hyperlocomotion, anxiety, impulsivity, aggression, and learning and memory deficits. These behavioral abnormalities in rodents may be related to the symptoms in patients with neuropsychiatric disorders, such as attention-deficit hyperactivity disorder, obsessive-compulsive disorder, autism, schizophrenia and depression...

Also:

  Our findings suggest that [social isolation]-induced behavioral abnormality is a psychobehavioral complex relevant to various clinical symptoms observed in neuropsychiatric disorders, including ADHD, schizophrenia and depression, and that SI-reared mice are a useful animal model to study the pathophysiology/pathogenesis of these diseases.

There's this:

  In contrast, long-term social isolation is a model to study the behavioral and neurochemical consequences of depriving rodents of social interaction. Many of the symptoms caused by long-term isolation resemble those seen in depression and anxiety disorders. Furthermore, long-term isolation of male mice is known to induce offensive and aggressive behavior, such as attacks.

And this:

  These data suggest that long-term isolation may induce functional changes in the sensitivity of alpha 2 receptor in the noradrenergic system...

And this:

  In the present study, we found that social isolation elevated the anxiety levels of mice...

Emphasis all my own.

There's a lot more meat in those studies, and especially the paper they cite in their introductions.  Some of them, as well as others also explore the effect of isolation in addition to other substances.  It can absolutely affect your studies, in particular behavioral or expression-based studies.  Your mouse house is good to change their practices.


What type of fish is this and why is it so big?

That is a Queensland Grouper (common name).


How do we know that dinosaurs were related to lizards and/or birds?

In general the answer is always the same: you construct a phylogenetic tree. In order to locate different species on this tree in relation to each other, you use various features to compare which species are more similar to each other than others.

The best way of doing this is by comparing their DNA sequence, especially orthologous genes (i.e. genes common to the species compared).

Unfortunately, genetic sequences usually aren’t available for extinct species. You can still compare homologous features though. For instance, the class of mammals are all characterised by the possession of mammary glands. Similarly, all vertebrates have a vertebral column and all aves are feathered, warm-blooded, egg-laying vertebrates.

The collection of many such features from fossile records allows the creation of more or less detailed phylogenies. The Wikipedia explanation mentions several transitional fossil forms which trace the evolution from dinosaurs to modern birds via several intermediates. All of the inferences are based on anatomical resemblance.

This may sound weak evidence but in fact anatomical homology has proved to be sufficiently accurate in constructing other phylogenies, where we have been able to verify the correctness using genome comparison data. So while there is much uncertainty about the precise branching point of birds from dinosaurs (or maybe archosaurs), there is near-certainty that the common ancestor of birds and dinosaurs was, in fact, an archosaur.


When differences between prokaryotes and eukaryotes are taught in an introductory biology course, a generic prokaryotic cell and a generic eukaryotic cell are typically compared. Cells in a complex multicellular organism, like a human, are quite diverse. Human red blood cells are one example of a highly specialized cell with a mature form that is quite different from the typical eukaryotic cell. Keratinocytes in the epidermis are another example (see Ross Histology, Ch. 15). In both cases, these cells produce large amounts of a single protein, eventually, at their most mature stage, stopping protein synthesis, extruding their nuclei and most other organelles.

The absence of a nucleus or other organelles, however, does not necessarily make either of these cells more susceptible to antibacterial antibiotics. Antibiotics are targeted toward things that bacteria have (positive differences), rather than the absence of typical eukaryotic structures. Almost all antibacterial antibiotics have one of three targets (see Goodman and Gilman Chs. 48, 52-55):

The bacterial cell wall or membrane
protein synthetic machinery
specialized metabolites required by bacteria

There is (almost) no overlap between these structures in bacteria  and structures in any of the diverse array of human cells. The one partial exception is a similarity between the mitochondrial and bacterial ribosome, that may, for example, be responsible for some of the toxicity of chloramphenicol (G&G Ch. 55).


What causes midcycle FSH surge in the menstrual cycle?

The LH surge is began by a impressive rise of estradiol produced by the preovulatory follicle and results in subsequent ovulation.
The LH surge stimulates luteinization of the granulosa cells and stimulates the synthesis of progesterone responsible for the midcycle FSH surge.


This product brochure seems to give a reasonable explanation:

  The following conditions help to form mould on sealants:

  High air humidity with little movement of air, eg: in bathrooms, showers, kitchens etc.
  Warmth
  Nutrients in the form of organic deposits. e.g. residues from body care materials
  such as soap, shower gel etc.

  Since elastic silicone joints have low thermal conductivity they are the warmest part of a tiled surface and where mould thrives best, in combination with organic residues and moisture.


I agree with Vance, we need a little more detail to better answer your question. From what I can tell, you are asking whether a single nucleotide polymorphism (SNP) that results in the addition of a cytosine base to your sequence is of concern when examining the methylation signature of that sequence.

I would first determine whether the polymorphism is common in the population using NCBI. The more common the polymorphism, the less likely it is to have a serious effect. However, that is not to say that it doesn't have any effect.

I would then examine how much the methylation of that one site varies compared to samples without the additional cytosine base.

Finally I would determine the importance of the location of the SNP. Is it located in a CpG island? Or is it located on the shores, shelves or 'open sea'? (see work by Sandoval et al.)

Without knowing all the above it is hard to make a call on how important/unimportant the SNP is in your methylation analysis.


The difficulty is in the semantic. In the sentence

  Selection acts on the genotype because that is what is inherited

it is unclear what is meant by "acts on". The point that the author(s) of this misconception were probably trying to make is that what define the reproductive success of an individual is the phenotype of an individual. In other words, it is the expression of those genes that affect the probability of the genes to be passed on but it is not the actual genetic sequence itself (or at least less directly so).

Let's assume a haploid case where at a given gene, allele A means 'tall' and allele B means 'short' and let's assume that size matters in defining fitness. It is ultimately not whether an individual carry the allele A or B that matters but whether the individual is tall or short. If by some fantastically random event there is an individual with allele B that is tall then this individual will rather have the same fitness as the tall individuals and not the same fitness as the B carrier individuals.


Is it impossible to increase skeletal bone mass, as opposed to just bone density?

If you search for
 - bone growth training
 - bone hypertrophy athletics,
 - bone diameter increase,
 - bone strengh hunter gatherer,
on google, you will find more articles than I could possibly summarise:

stimulation of longitudinal bone growth and widening of the joint space (cartilage hypertrophy) occur. The possibility of bony hypertrophy as a result of athletic training, especially with regard to increases in of bone density and bone diameter, should lead to incorporation of sports medical considerations into the prophylaxis and therapy of osteoporosis.

https://www.ncbi.nlm.nih.gov/pubmed/7856798

https://www.ncbi.nlm.nih.gov/pubmed/7478507

I have slender bones and it was the gain of muscle which helped me to balance my physique.


Is every part of a virus important for replication?

Unless you have a specific virus in mind, I can speak generally about viruses. It seems that the viral genome is reduced to just essential genes. Many viruses segregate their genome into periods of expression: early, mid and late. The early proteins are so-called because they encode for proteins that help their entry into cells (what is called infection). Middle and late genes tend to help the virus co-opt cellular machinery to aid in viral replication. Late genes are then useful for final stages of viral assembly and ultimtely their exit from the cell (lysis) and the newly made viral particles can go on and infect more cells. When viewed in this manner, it follows that removing even one coding region from the viral genome would inhibit the overall infection/reproduction/assembly process. In fact, if you remove the gene encoding for a viral envelope protein, purified virus added to cells in culture are able to infect cells, but not produce complete and functional viral particles. In this sense, they are infection-competent, but reproduction-incompetent.


The devil is in the details, and therefore we cannot just state that we have understood X% of the DNA. We know e.g. that 2% of the human DNA encode proteins. And for a good number of proteins we know what they do. So you might know that a particular codon AGT encodes a serine residue in a protein, which could have a catalytic activity. Or it has a structural activity. Or we are not sure what it does. Sometimes protein-coding and regulatory sequences overlap. So even if we first understood the protein-coding function, there was still the regulatory function to be discovered.

The upshot is that there are multiple levels of understanding, and big controversies of what they actually imply (see e.g. the ENCODE saga).


What is the maximum electric potential that can occur in the human body?

To the best of my knowledge, the potential difference across the hair cells in the inner ear (cochlea) (Fig. 1) is the highest in the (human) body. It is about 120 mV, mainly due to the exceptionally high positive potential of the scala media as provided by the stria vascularis, referred to as the endocochlear potential. This potential is mainly built up by the high amount of K+ pumped into the scala media by ion pumps located in the marginal cells and basal cells (Salt et al, 1987) in the stria vascularis. Adding the potential difference of -40 mV of the hair cell it yields a total difference of 120 mV (Fig. 2).

References
- Morrill & He, J Otology (2017); 12: 151-64
- Salt et al., Laryngoscope (1987); 97(8 Pt 1): 984-91

Fig. 1. The cochlea. source: Morrill & He (2017)

Fig. 2. The potential difference across the hair cells is 120 mV, due to the endocochlear potential of +80 mV in the scala media. source: University of Minnesota Dulluth


Does eating hard food really cause wisdom teeth to erupt properly?

Yes

The relative size and robustness of the jaw does appear to be strongly affected by diet, significantly more so than other parts of the skull. This is not that surprising many developmental pathways interact with physical activity. Bones in particular often rely on a certain amount of stress to develop properly. It is not all that different from low scale bone atrophy.

Size of the jaw of course effects how much space there is for wisdom teeth. As for the evolutionary effect, consider we have only had access to soft processed food on any scale in the last few generation, that is not much time evolutionarily.

Source


Scars are fibrous tissue that is left after an injury. The body does its best to fix a body part after an injury and scars are their best attempt at doing so. It would be pleasant to think we could have Wolverine type of healing capacities but we don't and the best we can do are those scars.

The ability to completely regenerate the damaged tissue depends upon the specific tissue. Also, some species are better of than others at regenerating their tissues. Such differences relate to the concept of cellular specialization.

For more information you should have a look at the wikipedia articles

Wikipedia > scars
Wikipedia > Regeneration
Wikipedia > cellular specialization

and the Biology.SE posts

Can a lizard shed a regrown tail again?
Can the regeneration mechanism of lizards be used in humans?


Ferredoxins and variants such as fladidoxins and rubredoxins are simply electron carrying protein that need to be regenerated, like the more energetic NADPH.
The key thing to remember is that redox balance is key. You cannot have electron pair accumulate so there has to be a terminal acceptor. In the case of aerobic resipration it is oxygen, in the case of iron or sulfur dissimilation it is iron(III) or sulfate, in the case of fermentation it is a small highly oxidised carbon (e.g. methanol, ethanol, butanediol, formate, acetate, propionate, lactate, succinate, fumarate). Carbon fixation requires electron pairs, which come from somewhere. The mechanism of how the carbon dioxide is assimilated can be via the Calvin cycle (plants and cyanobacteria), the Wood-Ljungdahl pathway or from the 3-hydroxypropionic cycle Prof. Fuchs described in Chloroflexi and Sulfolobus. In all three electrons come from somewhere (generally water, carbon monoxide and sulfur respectively).
The reason why there are both ferredoxins and NADPH is a tad harder to explain, but has to do with redox control and the fact that not always ferredoxin is regenerated by a NADPH reductase (also: NADH = catabolic, NADPH anabolic), but could be a fumarate reductase or similar.


Interesting!  I haven't seen anyone able to do this deliberately.

Goose bumps are caused by the tiny muscles at the base of hair follicles contracting, and the hair stands up.  The skin around it puckers.  It's mediated by the sympathetic nervous system (the "fight-or-flight" aspect of the system).  This is how animals' fur stands up when afraid or upset (think of a scared cat).

It's called the pilomotor reflex.  It also helps them keep warm (fur insulates) - so it happens when we're cold too.  But since we have so few hairs, it's not very useful to us. It's more of a vestigial reflex than anything.

It happens for other reasons too.  See the wikipedia article, it's a good place to start.  For more info, look at this article or a medical textbook.

If you can do it at will, you likely are in tune fairly well with your sympathetic nervous system.  That's excellent.  You may be able to make minor alterations in your pulse and blood pressure through breathing regulation - check out the concept of biofeedback.  It is a way to help manage stress, keep yourself calm in terrible situations, manage anxiety or panic disorders, anger management.....

Being able to use physical self-awareness to affect physiological changes takes practice to develop as a skill.  You've got a great start!


It would depend of the plasmid, the genes it contains and the promotors those genes have. Basically, regulation of extrachromosomal genes follow the same patterns of the rest. Bacteria, Archaea and some other organisms that can have plasmids will express the genes if the promotors of those genes are constitutive, or if they trigger by conditions that are present in a given moment. The degree of expression would be a function of the characteristics of the promoter and the number of copies of the plasmid. Finally, the number of copies of the plasmid would depend of its size and the characteristics of its replication origin.

Organisms can loss the plasmids if doing so don't suposse a negative effect (this is a big problem in industrial microbiology, since the recombinant strains may be unstable and reduce its productivity). In laboratory, a plasmid containing resistance genes towards an specific antibiotic would remain stable as long as this antibiotic is present in the media. The characteristics of its replication origin also play a big role determining the stabilty of plasmids. You can even select for the loss of plasmids, take the example of URA3 in Saccaromyces (not a bacteria, but the mechanisms are the same), wich can be used as a negative selection factor if the media contains 5-fluoroorotic acid.

So there's no particular advantage in expressing plasmidic genes all the time. When that happens, actually there exist an evolutionary pressure against the presence of the plasmid, and thus it trends to dissapear. Bacteria can survive without plasmids (with the exception of some that carry megaplasmids that acts more than little chromosomes. In some of this cases, the plasmid may contain genes for important methabolic pathways and other key elements of the cell, thought if the genes they carry are very importants, like polymerases or ribosomal RNAs, the term minichromosome is prefered). However, plasmids may contain genes that confer an important advantage to the population (like in presence of an antibiotic), and if so the plasmid spread. If at some point the ecological pressure cease, the plasmid would turn unstable again. Note that it's not impossible to have horizontal genes transfer between plasmid and chromosomes, and plasmids (alongside viruses and foreign transformed DNA) are important sources of new genetic material.


Do you know what type of insect this is?

There are 900 different species of Crickets but I would say it is a Camel Cricket based on the info provided.


While poison affects not every organism equally, plants did develop some poisons to avoid being eaten. However, if you look at the great multitude of so-called secondary metabolites, most of them are poisonous to either viruses, bacteria, fungi or other microorganisms, or insects, or even other plants. Plant evolution just hasn't had time to adapt to humans.

So, if some substance from plants is a poison to us, it's accidentally so, and the target was another organism. Examples: nicotine is first and foremost an insecticide, nematistat, and herbicide; aconitine, atropine, caffeine are insecticides; many essential oils (causing allergies in human) are antimicrobial and so on.

This has also to do with the fact that nerve cell physiology has not much changed since they developed in the first multi-celled animals, and poisons for insect nerves have at least some effect on human nerves.


Some bacteriophages adsorb on the pili. So the individuals carrying the F-element will be susceptible to these.
F-plasmid encoded membrane protein PifA is responsible for the T7 resistance [See here]. The exact mechanism is not known

If you see the list of references in the textbook chapter you will be able to trace the reference for a certain quoted fact


I couldn't really be completely sure by this picture alone so I did some searching around and turns out it is a Autographa Gamma(Silver Y)


What labs/companies provide comparative genomic analysis?

Earlham Institute have the expertise for this work.  They primarily work in public-funded research but they carried out private-sector work in the past.


The textbooks represent the synapses that way for didactic reasons. But, in fact, there are several protein complexes that keep the membranes (pre and post synaptic) attached. The most famous are the puncta adherentia junctions.

In these structures, several different proteins, like nectins and cadherins, promove cellular adhesion:

(source of the image: http://cshperspectives.cshlp.org/content/1/4/a003079)

These molecules are important not only for cellular adhesion, but for synaptic plasticity as well.

Source: Adherens Junctions: from Molecular Mechanisms to Tissue Development and Disease


Number of serotonergic neurons in mouse/rat DRN

The mouse and rat dorsal raphe nuclei contain about 9000 and about 11.500 serotonergic neurons, respectively. It turns out the corresponding 1988 and 1982 references are widely cited - directly as well as indirectly. I could not find any newer data/evaluations.


Is there an evolutionary basis for why women mature faster than men?

Reproduction is kind of the definition of biological success. Logically, it works because it works because it works. Provided that the mother is responsible and healthy, there's a good chance the offspring will survive and reproduce. And since health and age are like opposing forces, the sooner a female develops and develops responsibility, the more likely they will be to reproduce and supply viable offspring to the population.

Similarly, males remain verile for many years past their prime. Since it doesn't matter (as much) whether the father survives child birth, his health is less important. More important (genetically) is the spread of his DNA. The more time a male has to do that the more his DNA will spread. So why not start earlier? Reproducing for an extra ten or twenty years will cause the spread of a much greater amount of DNA than 1 or 2 years early on, and (plausibly) since the male often has a dangerous occupation, males that develop(ed) later (when their size/strength was greater), probably help(ed) ensure the males' survival.

And there is something to say about sexual preference. It is likely that the males' disposition toward healthy females and a females' dispositon toward successful males is genetic... much like a bird who sings the best song. Why? Because it is/was a successful cascade of events.


Would non-human carnivores be able to survive on farmed foods?

The foods people in the developed world typically feed their carnivorous pets (including dogs and cats) are not made primarily from meat.  Instead, they are made from plants, specifically grains, such as corn, rice and wheat.

In order to get our pets to eat foods that are so different from the meat-rich diets of their ancestors, we add flavors to the food.

Check out this episode on the making of pet foods from the television series "How Its Made", http://www.youtube.com/watch?v=220PSFJWHao.

So, to answer your question directly-- yes, in places like the USA, domestic dogs and cats are already living on a diet that is almost entirely plant-based.


How do colds and flu not infinitely recur?

Short answer:
Because your immune system adapts to the virus causing the flu or the common cold and, thus, you become immune to it.

Longer answer:
When B cells first encounter an antigen (usually a protein on the surface of a pathogen), the antigen attaches to a receptor, stimulating the B cells. Some B cells change into memory cells, which remember that specific antigen, and others change into plasma cells. Plasma cells produce antibodies that are specific to the antigen that stimulated their production.
After the first encounter with an antigen, production of enough of the specific antibody takes several days. Thus, the primary immune response is slow and that's the reason you experience the symptoms of the disease.
But thereafter, whenever B cells encounter the antigen again, memory B cells very rapidly recognize the antigen, multiply, change into plasma cells, and produce antibodies. This response is quick and very effective.
This means that, theoretically, you shouldn't be able to become sick twice by the same virus.
However,
virus are very prone to mutations. If these mutations occur in the genes that code for antibody-binding sites, the antibodies produced by B Cells become less effective. This is called Antigenic drift and the reason you might catch the Flu every year (because, with enough time, the virus antigens become different enough to "fool" your immune system).

Also, there are a few explanations why the flu has a seasonal pattern, with a peak usually at winter. One of the theories postulates that in cold weather, people tend to stay indoor, favoring virus transmission.
Recently, an interesting article was published that found that:

transmission of influenza B viruses is enhanced at colder
temperatures, providing an explanation for the seasonality of
influenza epidemics in temperate climates

source


Appropriate statistical test for a student lab?

To choose the right statistical method (it is more than just saying "use the t-test") you need to think about your experiment. A good starting point is this figure from Bitesizebio:

There are two relevant articles on that website:

Let’s Talk About Stats: Comparing Two Sets of Data
Let’s Talk About Stats: Comparing Multiple Datasets

Probably also interesting is the definition of statistical terms:

Let’s Talk About Stats: Understanding the Lingo


If you have no medical background at all, you will need a general text that teaches more than just digestive physiology. That is because you need to understand the function of other systems that have an influence over the digestive system (for example, the peripheral nervous system).

Here are a few good general references to get you started:

Physiology by Linda Costanzo, arguably the most synthetic. Extremely good, but I am unsure of its value for someone who has no medical background.
Vander's Human Physiology, arguably the simplest, used in first year of medical school.
Medical Physiology by  Walter F. Boron, arguably the most complex, I would not recommend it as a first try.

You can start by trying to read the digestive physiology chapters, and look up the knowledge you lack in other chapters.


Was the mitochondrion or chloroplast first?

Mitochondria evolved before chloroplasts.

We know this because Mitochondria form a monophyletic group: e.g. all life with mitochondria traces back to a single common ancestor (source). Since the group with chloroplasts groups within this clade, it must be the case that either (a) chloroplasts were obtained by an organism that already had mitochondria or (b) chloroplasts were independently lost by multiple lineages within the Eukaryotic clade and then many of these lineages re-acquired chloroplasts by secondary endosymbiosis. Since (a) is a (much) more parsimonious explanation it is the one it makes sense to accept.


How do Benzodiazepines induce Rewarding (Euphoric) effects?

Okay, I read the question wrong.

Benzodiazepines do not bind to GABAA receptors universally. Thus the presumption that it inhibits the mesolimbic dopamine pathway may be wrong. They may not interact directly with said pathway at all.

Many subtypes for the GABAA receptor exist. The receptor consists of 5 subunits. The following subunits are known to exist: α1-6, β1-3 and γ1-3. The most common combination has two α, two β and one γ. You find ones with distinct compositions at distinct locations in the brain. All have two bindingsites for GABA, but only a subset has an additional binding site for benzodiazepines.

The benzodiazepine binding site is at the interface of an α and a γ subunit, so receptors without this structure will show no affinity for benzodiazepines. Additionally the α subunit must contain a histidine residue, which is only true for α1, α2, α3 and α5. That is paraphrased from wikipedia, where you can find the sources as well.

I still think you need to consider the idea that benzodiazepines may not interact directly with the dopaminergic reward pathway, like opiates and cocaine does. I attribute the euphoria to be an indirect effect, resulting from the muscle relaxation (which will feel like you had a good massage), and the calmness of the mind.


Why is GTP, not ATP, produced in Gluconeogenesis & TCA Cycle?

Nice question. Beginning with Krebs cycle, there is actually no specific answer as both GTP and ATP are produced. First, see this article for why GTP is the more frequent product:

  It may be that at the beginning, both GTP and ATP were equally available for energy and that the succinyl CoA synthetase reaction happened to choose GTP and that reaction is still with us today, billions of years later, even though we run the TCA cycle clockwise (forward) instead of backwards.

So, actually both ATP and GTP can be produced. And indeed both are produced, depending upon the organism. See this article:

  A step with significant variability is the conversion of succinyl-CoA to succinate. Most organisms utilize EC 6.2.1.5, succinate–CoA ligase (ADP-forming) (despite its name, the enzyme operates in the pathway in the direction of ATP formation). In mammals a GTP-forming enzyme, succinate–CoA ligase (GDP-forming) (EC 6.2.1.4) also operates. The level of utilization of each isoform is tissue dependent. In some acetate-producing bacteria, such as Acetobacter aceti, an entirely different enzyme catalyzes this conversion – EC 2.8.3.18, succinyl-CoA:acetate CoA-transferase. This specialized enzyme links the TCA cycle with acetate metabolism in these organisms. Some bacteria, such as Helicobacter pylori, employ yet another enzyme for this conversion – succinyl-CoA:acetoacetate CoA-transferase (EC 2.8.3.5).

So, there is no strict rule that only GTP will be produced instead of ATP at that step. And, afterall, it does not matter much as both of them carry equal energy.

Now coming to Gluconeogenesis, GTP is hydrolyzed by the enzyme Phosphoenolpyruvate Carboxykinase or PEPCK. This enzyme can also work with both ATP and GTP, depending on the sepcific type of enzyme. See this article (links added separately):

  It is classified under EC number 4.1.1. There are three main types, distinguished by the source of the energy to drive the reaction:

  4.1.1.32 - GTP (PCK1, PCK2)
  4.1.1.38 - diphosphate
  4.1.1.49 - ATP

Thus, there is no strict protocol for using specific energy carrier in the process, both ATP and GTP can be used in the reaction. Its just because GTP is more frequently used that it is mentioned instead of GTP/ATP in the reaction.