the following is true for humans, I dunno about other animals:
schwann cells in peripheral nervous system can rebuild a severed axon if the perineurium of the nerve fibers are sutured together ... the same is not true for oligodendrocytes in the central nervous system. Thus only peripheral nerves can regenerate and not nerves located in the central nervous system (ie. spinal cord or brain).

surgical nerve regeneration after a nerve is severed is not the only possible form of nerve regeneration, another example would be when the facial nerve is damaged by bells palsy and then it regenerates itself. so a fun example of what can go wrong is when some of the nerves switch when they regenerate, so your brain thinks it's doing one thing, but since the nerves switched when they regenerated, it does the other. The example would be "crocodile tears syndrome", it has nothing to do with crocodiles (thats just the name) but rather this is where the facial nerves salivation fibers get switched with the crying fibers... so when they eat they cry...

as for neuro-rehabilitation in people suffering paralysis, this is a broad question. As I understand it, if it's the spinal cord thats cut then it will never regenerate, but if its a nerve that left the spinal cord (a peripheral nerve) than it may possibly regenerate. Here are some specific conditions:

Also it could be a temporary thing like Guillain-Barré syndrome where the immune system (hyper sensitized by a previous campylobacter bacteria or CMV virus, or for some other reason) temporarily injures the peripheral nerves and then after about 2 weeks they recover)

also there is there are drugs and toxins which are temporary, so one your body metabolizes/excretes (bile or urine) it is gone: botulinum toxin (from bacteria Clostridium botulinum), curare (south american plant poison), the many chemically modified versions of curare produced by pharmaceutical used in surgery to relax the muscles, and the list goes on for drugs/toxins. Again, drugs/toxins are temporary.

Stroke, though in the central nervous system, might be able to be rehabilitated since maybe everything wasn't destroyed (even though what was destroyed was destroyed permanently), and the patient can salvage what is left and use their neuroplasticity to try and use their brains slightly differently to be able to recover.

ALS, affects the ventral horn of the spinal cord... this one is irreversible at least today.

there are many other causes of paralysis which may nbe reversible or irreversible

glossary

schwann cell= the fatty cell that wraps around an individual nerve in order to myelin ate it... myelination being the fatty insulating of axon so they send electric signals faster...

axon= a projection off of the cell body that sends an electrical impulse to the end of the nerve that ultimately communicates with the target nerve/muscle/gland/etc

perineurium= outside protective sheath composed of connective tissue covering many nerve fibers

oligodendrocytes= the equivalent of a schwann cell, but in the central nervous system, it myelinates many nerves, unlike the schwann cell which only myelinates 1 nerve.

nerve fibers= a collection of many nerves running together

facial nerve= facial nerve innervated the muscles of the face and there are 2 facial nerves, one for each side of the face. the facial nerve doesn't only do face muscles, but also taste, salivation, and tear formation

bell's palsy= when the facial nerve stops working and half the face gets droopy... there are a lot of possible causes, like virus bacteria, and many many noninfectious causes...


See, since it was a simple drilling followed by restoration or filling, that means the infection was superficial, not involving the pulp where the nerves and blood vessels are situated.
Ok, so now to remove the superficial infection the dentist might have used an airotor. It's an instrument which rotates at high speed, has a hole for water spray to cool the fictional heat generated while it removes the caries or the infection from the tooth.High speed handpieces
Now as you may be knowing the crown portion of tooth has three layers- enamel, dentin and pulp. Only the pulp portion is innervated.
Now when the instrument is drilled into the tooth the infected enamel and superficial infected dentin must have been removed.
The dentin has numerous tubules known as dentinal tubules. These contain a fluid called dentinal fluid. Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.Hydrodynamic theory
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
However the restoration placed, you should have specified which restoration- silver coloured (amalgam) or the tooth coloured. These again have chemicals. These chemicals can penetrate through the tubules to the pulp to elicit a painful response even after the treatment. To prevent this, a liquid known as varnish is applied which acts as an insulator. Also if the infection is deeper, a base or other material depending on the type of restoration is also applied to prevent other stimuli. Varnish and bases
So either there may be a failure in these insulating materials or your pulp may require some time to heal from the procedure. It may have got healed by third or fourth day, if it was due to procedural trauma. In either case you should contact your dentist.
Hope I have solved your question :)
References have been given in the parentheses


Advantages of gregarious vs solitary behaviour?

I will assume that you are talking about Mallards, although other wildfowl are likely to exhibit similar behaviors.

Mallards aren't actually solitary during the summer, instead they form breeding pairs.  They form groups (sords) in the winter to migrate and for protection while moulting.

https://sta.uwi.edu/fst/lifesciences/documents/Anas_platyrhynchos.pdf
http://thefarmatwalnutcreek.com/Ducks_Swans_Mallard-Duck.html


Is starch and glycogen digestion intra or extracellular?

The problem with your question is that, right now, you have three different questions:

Is the starch/glycogen digestion intra or extracellular?
Do humans have the enzyme for intracellular digestion of starch?
Do plants have the ability to digest glycogen?

Unfortunately, that goes against Bio SE rules: you have to pick one question, otherwise your post will be closed as too broad ("Avoid asking multiple distinct questions at once.").

That being said, I'll address only this question:

  Do humans have the enzyme for intracellular digestion of starch?

The answer is yes. Intracellular digestion in humans (as in any animal) is performed by lysosomes, organelles that contain hydrolytic enzymes.

Lysosomes can digest proteins, lipids, carbohydrates, nucleic acids etc. Regarding digestion of carbohydrates, this is a short list of enzymes (the complete list is way bigger) found in human lysosomes:

alpha-Galactosidase
alpha-L-Fucosidase beta-Galactosidase-1
beta-Glucuronidase Chitinase
Chondroitin B Lyase/Chondroitinase B
Chondroitinase
Cytosolic beta-Glucosidase
Galactosylceramidase
Heparanase
Hyaluronidase
Lysosomal alpha-Glucosidase
O-GlcNAcase
O-Glycosidase

Among the enzymes listed above, this is the one that answers your question:
 Lysosomal alpha-Glucosidase.

That enzyme, which is a α-1,4-glucosidase, breaks down starch (and glycogen) to glucose.

Source:

Lübke, T., Lobel, P. and Sleat, D. (2009). Proteomics of the lysosome. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1793(4), pp.625-635..


Many receptors have a natural constitutive, or "baseline", amount of response that they generate, they're not just an on-off switch. At baseline, many receptors will generate a partial response, which means that certain things binding to them can either increase or decrease their response.

A neutral antagonist is one that causes no change in the signaling response of the thing that it's binding to. It simply stays the same. Note that this can still be important, because a neutral antagonist can block the binding of other agonists, ones that would have generated a change in response, even if the antagonist itself doesn't cause a response.

An inverse agonist is something that decreases the response of the receptor from its baseline all by itself. Often, this is caused by stabilizing the receptor in it's "off" state. If the receptor has some degree of constitutive activity, an inverse agonist will decrease its activity.

See this graph from this wikipedia page for a good explanation:


Why does my gel have such poor resolution?

Although your tech is referring to your DNA samples, your ladder also indicates there is some room for improvement of your running technique. -20C for a week should not have impacted the quality of the DNA assuming that it was good quality going into the freezer. You can mitigate DNAase activity by adding EDTA to your storage buffer, which will pull metal ions out of solution. Just make sure to take that into account if you're doing a reaction later that requires metal ions (like PCR).

DNA

Focusing first on the DNA samples. There are a few things to check.

How much did you load? I see you stated 20uL, but what was the concentration? It it more important to know the amount of ng being used as the sample. Various stains have different concentrations they can detect (EtBr, SYBR, etc.) I would check the specifics of the stain you're using to make sure you're loading an appropriate amount of DNA.

Are these PCR products? If so, how many cycles was your PCR run? I have seen similar results from PCR if the samples are run for too many cycles. Non-specific products begin to be produced in later cycles, and will cause degradation of your specific products. I would also re-check your primers, the extension time, and the polymerase you're using. It is more difficult to do extensions of the 5.8kb and 6.8kb sizes you mentioned, but not impossible.

Are these restriction digests? Do you have a control well showing the undigested plasmid, or other source? Your source should have a clean band first to expect a clean band in the results. If your source is clean and bright, and the digest looks like the samples above, check your digest buffer and enzymes.

Electrophoresis

There are several things which can improve the quality of an agarose gel. Thermofisher provides a guide for their tips and tricks. Below are things that I have found useful in my own experience.

The time between casting the gel and running it. A common practice is to make gels and store them in TBE/TAE buffer until they're ready to be used. In my experience, the quality of the gel will degrade over time, yielding diffuse bands. The best results are achieved with a freshly poured and cast gel.
Loading technique. Carefully loading the samples into the wells so that they settle as closely to the bottom without mixing with the surrounding buffer is key. The best results are achieved by having your pipet tip touching the bottom of the well, and slowly pulling it out as you release your sample so the sample does not have to settle down into the well on its own.
Run immediately after loading, and image immediately after running. Diffusion will cause nice tight bands to become poor the longer the samples sit in the well.
Voltage, timing, and agarose concentration. Getting these right takes practice. You'll want to try to run your gel as quickly as possible. The more time it sits in the gel, the more diffusion will occur. However, have the voltage too high, and you risk melting your gel. Vary the concentration of agarose to target the size of DNA you're after. I have previously used anywhere between 0.5% and 1.5%.
Prestaining the gel or poststaining? I prefer prestaining for the stains that work well, as it reduces the time the samples will sit in the gel allowing diffusion to occur.
I am looking at your ladder, and the link to the provided standard, and it is difficult to tell which bands are which. The 3.0kb fragment should stand out as the brightest, however the bottom band in your gel is the brightest. Is this the 3.0kb band? Maybe. It's difficult to count the number of bands above it to confirm. If it's not, which might be indicated by the fact that none of your samples seem to have run to the end of the gel, then this would be the 0.5kb band. If it is the 0.5kb band, the ladder intensity doesn't match up with your expected intensity. Double check your ladder so you can know what sizes you're looking at.


Can a hormone be absorbed into the body digestively?

This entirely depends on the kind of hormone. Hormones can be chemically completely different things. For example, estrogen is a steroid hormone and is chemically very stable so that it can pass the stomach without being harmed by the acidic conditions (even without enteric coating. AFAIK enteric coating is only used in emergency contraceptives, not in regular ones. And for the emergency contraceptives it is used in order to reduce side effects such as vomiting). As such, estrogen in your food or drink will have an effect on your body and there are many studies suggesting that this is a reason for reduced fertility in men.

On the other hand, insulin is a peptide, which would be digested and its hormone function completely inactivated when swallowed.

There is even the notion, that the gas nitric oxide may have a hormone function. In that case, it could reach the blood stream even through inhalation.

In summary, whether or not a hormone can be active after ingestion entirely depends on the kind of hormone.


Short answer
In hippocampal neurons, endocytosis does occur in the axon, but only at the synapse and at varicosities.

Background
In cultured rat hippocampal neurons, Parton et al. (1992) showed that the cell body and dendritic regions are indeed capable of endyctosis. They used horse-radish peroxidase dissolved in an internalization medium. In the axon, endocytosis was only found to occur in the pre-synaptic region and in varicosities. Varicosities are points of synaptic release from the axon, outside the synapse proper.

Hence, axonal endocytosis is limited to regions where neurotransmitters are released. Presynaptic terminals often engage actively in neurotransmitter reuptake mechanisms to recycle released neurotransmitters.

Reference
- Parton et al., J Cell Biol (1992); 119(1): 123–37


How do prions cross the blood brain barrier?

I am not sure if a perfect answer is possible owing to the fact that Prion diseases are still incompletely understood, and are actively under research. On a preliminary search, I found some papers which address the issue (cited at the end).

Since $PrP^C$ is normally found in the body, its role and its transport is also relevant to the issue. It seems to undergo bidirectional transport across the BBB using a saturable mechanism, mostly a specific transporter (1). It is taken up peripherally, and by several regions of the brain with the possibility that it is involved in various brain functions including modulating the BBB itself. Amyloid Beta-protein, with several kinetic and dynamic similarities with $PrP^C$, is shown to have BBB altering effects. (2) How far do the pathological prions follow this is seemingly unknown.
Autonomic nerves seem to play a role in their transport.(3) When challenged with prions, sympathectomy delays or even prevents the disease, whereas sympathetic hyperinnervation accelerates prion pathogenesis. There have been studies to elucidate the transport via the nerves, such as (4) and (5).

There are several other studies on this issue, and following the cited references might help you find them.

Reference number 3 also has information on the immunological response to prions.

References:

Banks WA, Robinson SM, Diaz-Espinoza R, Urayama A, Soto C. Transport of prion protein across the blood–brain barrier. Experimental neurology. 2009 Jul 31;218(1):162-7.
Giri R, Shen Y, Stins M, Du Yan S, Schmidt AM, Stern D, Kim KS, Zlokovic B, Kalra VK: Am J Physiol Cell Physiol. 2000 Dec; 279(6):C1772-81.
Aguzzi A, Zhu C. Five questions on prion diseases. PLoS Pathog. 2012 May 3;8(5):e1002651.
McBride PA, Schulz-Schaeffer WJ, Donaldson M, Bruce M, Diringer H, Kretzschmar HA, Beekes M. Early spread of scrapie from the gastrointestinal tract to the central nervous system involves autonomic fibers of the splanchnic and vagus nerves. Journal of virology. 2001 Oct 1;75(19):9320-7.
Glatzel M, Heppner FL, Albers KM, Aguzzi A. Sympathetic innervation of lymphoreticular organs is rate limiting for prion neuroinvasion. Neuron. 2001 Jul 19;31(1):25-34.


Explain allelic complementation at molecular level

As Matej said, mutations in two different genes (or even a gene and a non-coding regulatory element) can lead to complementation and as they pointed out, the complementation test is designed to check if mutations are on separate genes or not.

Molecular mechanisms that may lead to complementation (apart from Matej's example):

The double mutation in two enzymes in a pathway basically that does not alter the metabolic flux. Lets assume the pathway is linear i.e. no branches. The net flux would be limited by the slowest enzyme in the pathway. If a mutation increases activity of the rate limiting enzyme-1 while another mutation reduces the activity of enzyme-2 then the net flux may not change.
If a regulatory gene acts on another gene by some kind of molecular recognition (protein-DNA, protein-RNA, RNA-DNA, RNA-RNA, protein-protein), then the effect of a mutation in the recognition domain in the regulator can be complemented by another mutation in the target such that the binding affinity is preserved. For e.g. a miRNA regulating a mRNA. If a mutation in miRNA, A→G, is compensated by a mutation, U→C, in the target, then there may be no change in the molecular phenotype. This logic also applies for two gene products that function as a heterodimer.

However, different mutations in the same gene may also lead to complementation like effect. I cannot cite an example but there is a theoretical possibility. Therefore this answer is speculative. There can be two cases here:

Two different mutations in the same allele
Two different mutations in two different alleles

For case-1 you can imagine a situation in which the activity of the gene product depends on intramolecular interactions (secondary and tertiary structures). Two mutations can preserve the intramolecular interaction in a manner similar to the case of intermolecular interactions discussed above.

For case-2 you can imagine a gene-product that functions as a homodimer. If the two mutations preserve the intermolecular interactions in the dimer then you would see complementation. Case-2 can also be observed in a situation when the mutations occur in two different functional domains of two different alleles such that finally the dimer is still capable of carrying out its activity.


How do researchers map root systems of plants?

You originally posted this question on the Garden and Landscaping Section - that's where I'm from, and though it was moved here instead, I'll answer it anyway:

That image you've shown isn't like a photograph, its an impression of what the roots are like. Usual method of working out root patterns on plants is to remove what's known as a monolith, or a block of soil where the plant is - the soil is then either carefully removed by hand, in the manner that archaeologists use, or air blasted, or soaked off in water to reveal as much of the roots as possible. For trees or plants with very large roots, newer methods include geophysical surveying by machine, or electric resistance surveying. Even this doesn't reveal everything - many roots may penetrate too far down, or run along cracks in rocks beneath the soil. The root length and distribution pattern vary according to local conditions, so its hard to be definite about where the roots of any particular plant are in a particular position in the landscape.

Reference and further reading:

Plant Physiological Ecology (ISBN 978-94-009-2221-1; Google books link)

Especially, check the Introduction on page No.367


Why do dragonflies lose all of their coloration once they die?

This is probably because the color in dragon fly wing is due to chitin crystal and which is protected by some secretion over the entire wing something like cuticle upon leaves and when dragon fly dies that secreted substance upon wing washes away when not maintained resulting in shredding off of the color from wing. Sorry I can't comment (<50 reputation) so I did answer even tho im not clear with it.
Try reading this you might find something useful maybe Insect Wing
Also this journal said that while studying the wing of dragonflies they killed and kept them in lab it didnt mention that wing lost color Mechanism of the wing colouration in the dragonfly Zenithoptera lanei (Odonata: Libellulidae) and its role in intraspecific communication
So it might be possible that the video shows dragonflies after some long time maybe a week after death and body is intact because of chitin layer but wings bleached away in sun or degraded in environment.
Also wings have supply of veins so something related with continuous production might be cause of that thing too.


Is it possible to guide animals to a new breeding ground?

The problem that you mention deals primarily with habitat fragmentation, which has a great impact on species conservation. A fragmented habitat will impair migration and can result in inbreeding depression. This has been dealt with wildlife crossing in various sites in the world.


Are there antibiotics for all bacteria somewhere in the earth?

The number of antibiotics that remain undiscovered is huge, but is estimated to be tens of thousands of compounds.

The number of bacteria that remain undiscovered is also huge, but is estimated to be perhaps millions of species.

Resistance to antibiotics is developed by bacteria in response to other bacteria and human antibiotic use, but in theory all antibiotics should work on previously unexposed bacteria. In practice there are resistance mechanisms that operate on whole classes of antibiotics at once(drug exporters, for instance). So there might be a bacterium that happens to be actively or passively resistant to every antibiotic on the planet, but it's a question of statistics. I think it's pretty unlikely but there are a lot of bacteria, so it's theoretically possible. (It wouldn't be a dangerous pathogen, that amount of drug-resistance genes would 'weigh down' the genome and make it slow to divide, and all those transporters would be great immune system targets. The human immune system would eat it for breakfast.)

What is true is for every bacteria, there are at least some antibiotics it's already resistant to. Furthermore, some antibiotics aren't useful because they aren't selective enough and they are simply poisons. (We use them for chemotherapy agents sometimes, but they're not useful antibiotics).

Some fun examples: Vancomycin-resistant S. aureus is completely immune to nearly every antibiotic, including the last line of defense(methicillin) and the toxic really really last line of defense (vancomycin). It's susceptible to trimethoprim-sulfamethoxazole, one of the oldest antibiotics out there(~80 years old). On the other hand, the organism that causes tularemia is naturally immune to trimethoprim-sulfamethoxazole and always has been. It, in turn, is susceptible to nearly all other antibiotics.


Does drinking alcohol having UTI may help to kill the bacteria?

To begin answering your question,

  Does drinking alcohol in reasonable amount by healthy individual (nonalcoholic) having UTI helps to kill bacteria in the urinary tract
  (in order to get rid of them quicker)?

We have to clarify that EtG detects ethyl glucuronide which is a byproduct of ethanol and remains in the urine for several day. The presence of ethyl alcohol in urine is significantly shorter somewhere between 8-12 hours (reference).

So what does this mean? Well, in order to "kill" the bacteria causing the UTI it must be exposed to a minimal inhibitory concentration of ethyl alcohol for a certain amount of time. Depending on the bacteria causing the infection this concentration and exposure time varies.

So if the concentration of ethyl alcohol was high enough and the flow of your urination and micturition long enough, maybe, but is unlikely to have much effect.


What's the name of this bug from Toronto, Canada?

It's a moth fly. They're cute fuzzy little things. Most people consider them pests.

  An annoying and troublesome pest that concerns numerous homeowners is the moth fly, also commonly known as the drain fly, filter fly, or sewage fly. Moth flies are frequently found indoors on windows, sinks and walls.

They're often found around sink drains because the eggs and larvae survive on the biofilm in your, well, drains.


Clonidine is an agonist on the α2 receptor... but then again norepinephrine is also an agonist on the α2 receptor. Then the physiologic ligand of the a2 receptor, norepinephrine is autocrine (meaning it is released from a cell then binds on a receptor on the same cell) causing negative feed back and it inhibits further release of norepinephrine from the neuron thus preventing overstimulation. Clonidine is quite specific to the α2 receptor and it doesn't really stimulate α1/β1/β2. Given a situation  where only the α2 receptor is stimulated and none of the other epinephrine receptors, you would have a net decrease of sympathetic effects since the amount of norepinephrine being released is begin decreased by the stimulation of the α2 receptor on the presynaptic membrane of the sympathetic neuron. Hence clonidine is an α2 agonist that is sympatholytic

I have no clue what the difference are between these

agonist vs mimetic
adreno vs sympatho


What are the potential dangers (if any) facing the twin girls recently born in China with their CCR5 gene modified?

Important notes:

  I am not going into the ethical aspects of editing/removing CCR5 in human embryos, neither will I discuss potential effects of introducing that mutation into the human population. Both of these are very important issues, but out of the scope for this answer.
  As of now I'm not aware of any reliable sources of what was actually done in this case, so I will also keep my answer general / hypothetical without going into any specifics of these particular girls.

That out of the way lets get into the potential problems that could be caused by removing the CCR5 gene from  human embryo using the CRISPR-cas9 system. These can mainly be grouped into two classes: off-target or side effects of the procedure itself and any effects of a non-existing/functional CCR5 by itself.
One additional point I want to mention is that removal of CCR5 does not make one completely immune to HIV, because some strains of the virus (can) use the CXCR4 as a co-receptor instead.

1. CRISPR-Cas9 off-target effects

The CRISPR-Cas9 system has become very popular with scientists in the last few years, because it allows genome editing in very many organism with previously unmatched efficiency and speed. However, people only recently  - when the potential medical use of the system was being considered - started to look into the specificity of the system. What they found was, that while CRISPR-Cas9 is supposed to be very sequence specific it often also induces mutations in genes that were not supposed to be targeted.
There is a quite a lot of ongoing research to reduce these off-target effects, one good example being to use two variant copies of the system that each only cut on strand of the DNA at neighbouring sites (instead of cutting both strands at one site as is normally done).
If such mutations occur while genome editing an embryo the possible effects are very hard to predict - it could be anything from completely harmless to cancer inducing. If one wants any reliable estimate for this, it would be necessary to check for any off-target mutations by sequencing the whole genome of the edited embryo. That however requires (even with very modern techniques) removing at least a single cell from the growing embryo before the IVF procedure can take place and might therefore reduce chances of the IVF being successful.

Main source: Extensive review to CRISPR off-target effects

2. Side-effects of CCR5 removal

Normally it would be very hard (read: basically impossible) to predict what potential side effects the removal of a specific gene would have, even if there are e.g. mice where this has already been done but only studied for specific medical aspects. In this particular case however, we are in luck because there is a naturally occurring mutation called CCR5-Δ32 that also renders the protein completely dysfunctional. We can therefore pretty safely assume that the CCR5 removal by CRISPR-Cas9 will have similar effects to this mutation.

Since CCR5 is a gene expressed by immune cells, it  - unsurprisingly - has influences on various immune functions, but mostly seems to be affect infectious diseases. As this review puts it:

  In summary, there are ample data to suggest that CCR5 is involved in both positive and negative regulation of immune functions that relate to the regulation of leukocyte trafficking during infectious and postinfectious diseases.

One particular risk that seems to correlate with non-functional CCR5 is both initial infection and disease progression by flaviviruses. It has been reported that the CCR5-Δ32 mutation increases the risk of being affected by both the Tickborne encephalitis (TBE) virus and West Nile Virus, both of which can affect the nervous system if the diseases progresses far.


How fast will cells lyse under hypotonic conditions?

In the case of red blood cells, hemolysis in pure water occurs at just over 1 minute, 30 seconds, according to this paper. (Osmotic Properties of the Erythrocyte, M.H. Jacobs and Arthur K. Parpart, The Biological Bulletin, 1932)


Biological meaning of Lotka-Volterra Jacobian matrices

The Jacobian tells how the system changes along different state variables (which can be, for instance, the concentrations of the predator and the prey).

The Jacobian matrix by itself doesn't give you a lot of intuitive information. However, the eigenvalues of the Jacobian matrix at the equilibrium point tell you the nature of the steady state. For example if all the eigenvalues are negative then the system is stable at that point and the equilibrium point is called a stable node. If some of them are positive and some are negative then the system is metastable at that point and the point is called a saddle point. If all eigenvalues are positive then the point is unstable. If the eigenvalues have an imaginary part then the system exhibits oscillations. All these properties are local i.e. they just tell you the behaviour of the system near the equilibrium point.

I hope I am clear. This is not in a strict sense, a biological question. If you want to know more then read a book on nonlinear dynamics. Non-linear dynamics and Chaos by Steven Strogatz is a good place to start.

EDIT

When the system is locally linear (linearized at a given point) then the system dynamics at that point can be described as
$$\frac{dx}{dt}=J.x$$

Where $x$ is the state vector (a vector of the variables in the system) and $J$ is the Jacobian matrix. In this situation, the signs will denote the effect of a variable on the other variable. However, I am not sure (I feel it is highly unlikely) if this can be used to make any inferences about the food web.


An over-simplified model of cell division and its relation to stem cells

You have a few misconceptions about stem cells, I will try to explain where they are.
First of all, cells are not independent. They influence each other with signals and secreted messenger substances. If you look at a human embryo the state of totipotency (where all cells can differentiate into each cell type of the body) ends after 3-4 days when the blastocyte has developed. This structure already has a differentiation into a inner cell mass (embryoblast) and a outer cell layer (tropoblast).
If all cells would simply divide on their own, this would rather look like bacteria dividing in culture media, but not as a forming, multicellular organism.

From these few cells in the beginning all cell types of the body have to develop (around 200, if I remember the number correctly). To reach this, the pluripotent stem cells need to proliferate and differentiate (develop into more specialized cell types) quite a lot. So embryonic stem cells do proliferate. Adult stem cells are not proliferating at the same rate a embryonic, but they still do. A good example are the melanocyte stem cells (which are already pretty specialized as they can only further differentiate into melanocytes) which replenish the melanocyte population of the hair bulb at the beginning of each hair cycle. Differentiated cells can divide as well, when necessary, think only about wound healing.

Question 2: Stem cells (especially adult stem cells) need very defined living conditions. This includes specific signalling molecules (Oct or nanog are examples for that) to stay stem cells. If this signalling is missing (and it does in the normal human body) then these cells either differentiate or (more likely) die.
The only stem cell transplant which takes place regulary is the transfer of hematopoietic stem cells to leukemia patients. There the problem is to keep the immune system from atacking these cells as foreign.


Does the body have a mechanism for cleaning plaque buildup in arteries?

Atherosclerosis can be reversed to some extent by certain diets and change in life style that result in decrease of excessive weight, blood pressure and cholesterol levels.

Studies

1) Dietary Intervention to Reverse Carotid Atherosclerosis (Circulation, 2010)

In a study in Israel, in 140 participants, who were mostly age 40-65 and overweight, they observed an average of 5% reduction of the the volume of the carotid artery wall, which reflects the reduction of the plaque.

  Two-year weight loss diets can induce a significant regression of
  measurable carotid VWV [vessel wall volume]. The effect is similar
  in low-fat, Mediterranean, or low-carbohydrate strategies and appears
  to be mediated mainly by the weight loss–induced decline in blood
  pressure.

2) Intensive Lifestyle Changes for Reversal of Coronary Heart Disease (JAMA, 1998)

Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.

  Experimental group patients (20 [71%] of 28 patients completed 5-year
  follow-up) made and maintained comprehensive lifestyle changes for 5
  years, whereas control group patients (15 [75%] of 20 patients
  completed 5-year follow-up) made more moderate changes. In the
  experimental group, the average percent diameter stenosis at
  baseline decreased 1.75 absolute percentage points after 1 year (a
  4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the
  average percent diameter stenosis in the control group increased by
  2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28
  experimental group patients vs 45 events in 20 control group patients
  during the 5-year follow-up (risk ratio for any event for the control
  group, 2.47 [95% confidence interval, 1.48-4.20]).

  The experimental group reduced LDL cholesterol levels by 40% at 1 year
  and by 20% after 5 years.

  When we began this study, we believed that the younger patients with
  milder disease would be more likely to show regression, but we did not
  find this to be true. Instead, we found that the primary determinant
  of change in percent diameter stenosis in the experimental group was
  neither age nor disease severity but adherence to the recommended
  changes in diet and lifestyle.

  those who gained weight were more likely to show progression of atherosclerosis.

  Experimental group patients had a 91% reduction in reported frequency
  of angina after 1 year and a 72% reduction after 5 years (Table 5). In
  contrast, control group patients had a 186% increase in reported
  frequency of angina after 1 year and a 36% decrease in frequency after
  5 years.

Mechanisms

Reversal of atherosclerotic plaques can be achieved by removing the causes. According to Atherosclerosis: Process, Indicators, Risk Factors and New Hopes, (Int J Prev Med, 2014), decreasing excessive body weight + exercise + cholesterol-lowering diet + cessation of smoking can result in:

Less damage to the arterial intima
Higher HDL/LDL ratio, meaning adequate removal of LDL (by HDL) from the blood into the liver and thus less deposition of cholesterol into the arteries
Less inflammation in the arterial intima


The most common and simplest normalization method for spikes is the Total Count Normalization. It's actually what you're doing here, so what you're doing here is correct. TCM is a useful algorithm for normalizing sequencing depth, that includes your spike amounts.

  https://academic.oup.com/bib/article-lookup/doi/10.1093/bib/bbs046

has reference on the TCM normalization.

  Gene counts are divided by the total number of mapped reads (or library size) associated with their lane and multiplied by the mean total count across all the samples of the dataset.

The paper doesn't talk about spike-in controls, but the idea is the same. We'd use the spike-in controls for estimating the difference in sequence depth (instead of the whole data set).


Plasmid in the nucleus and gene expression

If you transfect cells with plasmid then these plasmids need to go into the nucleus (otherwise they wouldn't be transcribed). Getting the plasmid either happens during cell division (when the nucleus is not present) or by adding a signal sequence to the plasmid which induces the import into the nucleus through nuclear pores. The SV40 sequence is an example of such a sequence.

If you have the right promoter present on the plasmid, you can basically express any protein in the cell (unless it's toxic). The promoter either needs to come from the organism from which the cells are or has to be something universally activated like the CMV promoter (from the cytomegalo virus).

A good example for this is the expression of green fluorescent protein (GFP) which originates from jellyfish and can be expressed in cells to make them glow green (from here):

Untransfected cells or cells transfected with an empty plasmid (without GFP) don't glow.

Targeting specific cells or control the specific activation of genes only in one cell type is possible. For both you need sequence (and cell specific) promoter sequences which either allow the nuclear import (see reference 1-3) or the expression from a cell type specific promoter (see reference 4).

This has been done in the liver of mice in which the ApoE has been knocked-out. The expression of the human ApoE gene with a specific promoter led to the correction of the hypercholesterolemia the mice were suffering from. This needs a lot of knowledge on the promoter as well as on the other transcriptional regulation elements in the specific gene (see reference 4).

References:

Cell-specific nuclear import of plasmid DNA.
Tissue-specific and transcription factor-mediated nuclear entry of
DNA.
Progress and prospects: nuclear import of nonviral vectors.
Sustained liver-specific transgene expression from the albumin
promoter in mice following hydrodynamic plasmid DNA delivery.


That is a Thrips, order Thysanoptera. Not harmful. Not a bedbug or a louse. You can read about them here.
https://en.wikipedia.org/wiki/Thrips
(by the way the singular form of "Thrips" is "Thrips": there is no such thing as a "Thrip")


It's a kind of assassin bug, specifically a Masked Hunter:

  The surface of an immature Masked Hunter is sticky and it attracts lint and dust which helps to camouflage this predator.

and

  The name refers to the fact that its nymph camouflages itself with dust.

Though they feed on small insects, they will bite defensively, and when they do, it's fairly painful.


What are the different ways an exon gets spliced?

There are several ways splicing can occur, which depends on the RNA molecule to be spliced and the catalyst that performs the splicing:

mRNA splicing is carried out by spliceosome, which consists of small nuclear RNAs. There are sequences at the end of the introns and branch sties which indicate the splice sites. The so called lariat structure is formed when the 2'OH group of an adenosine residue in the branch site attacks the 5' splice site.
self-splicing of ribosomal RNA precursor - it is performed with the absence of spliceosome.
tRNA splicing - it requires three enzymes and ATP hydrolysis.

References:

Biochemistry, L. Stryer, 5th eddition

J. Abelson. tRNA Splicing


Why is it that heterozygous loci appear as two separate bands during gel electrophoresis while homozygous loci appear as one band?

A heterozygous locus has two different alleles and therefore it is possible that their DNA sequence lengths are different. However, it is unlikely that they are so different so as to be clearly resolved in a gel electrophoresis. Agarose gels can at best resolve 20bp; polyacrylamide gels can resolve smaller differences but it is only done for small DNA fragments.

I think upto 50bp difference is possible between alleles. But such huge insertions/deletions are rare and the difference between the alleles is usually a point mutation or small insertions/deletions(indels). Big indels are possible when a transgene is inserted specifically in one chromosome; these cases are mostly experimental.

If you consider paralogs as alleles then they can be of different lengths and can be resolved in agarose gels— usually the difference is in the untranslated regions. If you are doing Southern blot and using a probe that can bind to both paralogs then you will end up getting two bands.

Having said that, it is possible to see a difference in gel bands even if there is no size difference. This is possible by a technique called RFLP. In this technique the DNA is digested using a restriction enzyme which basically cuts the DNA at a specific sequence (usually a hexamer). If a point mutation abolishes or creates a restriction site then the fragment length would be different between the alleles. This is detectable on the gel.

A similar technique is AFLP.


The obese gene (OB gene) secretes a protein that functions in the signaling pathway of adipose tissue and adipocytes (fat cells) produce the hormone leptin (reference).

  When the amount of fat in the body increases, the amount of leptin
  released into the blood also increases and signals to the brain that
  the body has enough to eat (reference). Inversely, studies in rodents suggest
  that a reduction in leptin level during weight loss signals to the brain
  to increase feeding and decrease energy expenditure (reference).

Other molecules have a role to play in the ratio of BMI to leptin like the ghrelin hormone (reference). The genetic and environmental factors other than overall adiposity may also regulate leptin concentrations (reference) which is why individuals with the same weight may have different leptin concentrations.

A study has reported finding a strong exponential relationship for leptin levels with body mass index (BMI) (reference). Hope that answers both your questions.


Why did the sensitive plant (Mimosa pudica) evolve its leaf-closing mechanism?

There are many reasons why Mimosa pudica (More commonly now referred to as the TickleMe Plant) may have evolved it's leave- closing mechanism. I have observed the movement when insects have landed on my plants. The insects apprear to be frightened by the movement as they do move on rather quickly when the plant collapses. The movement of the TickleMe Plant also occurs when the sun sets or if I place the plant in a dark room. This may be a way to reduce water loss by transpiration as the leaves fold down upon each other. Another reason for the leave movement may be to expose the few thorns found on adult plants. This could be another warning for herbivores to stay away. In cold weather TickleMe Plants will close their leaves as well, could this be a way to maintain its body temperature. All in all, this is the most amazing house plant and I am always learning new things about this plant and its beautiful cotton candy like TickleMe Plant pink flowers.


Many invertebrates possess myelin. It is a misconception that invertebrates lack myelin.

The world speed record for a traveling bioelectric signal is held by the myelinated axons in the abdomen of the Penaeus shrimp!

Please take a look at this website or this review to find a highly recommended comprehensive website about invertebrate myelin from about a decade ago. Here you will find a list of references and additional readings if you are so inclined.

As an additional note: invertebrates also possess and very often make use of ensheathing glial cells, such as is the case with sensory neurons in lepidopterans (moths and butterflies) as depicted below. I've labeled the sheathing cells in pink and red. Please understand that it is currently still unclear whether these cells secrete myelin, though they are thought in some way to insulate the neuron. What you are looking at is a hair-shaped sensillum that is innervated by one or several sensory neurons; these are the basic functional units for sensing movement, proprioception, smell and taste and they exist across all invertebrates, often lining the cuticle and across the entire body, e.g. on legs, on the antennae, in genital tracts, etc. They are best studied in hexapod insects.


Why are siblings unidentical? (Which chromosome of the pair do gametes have?)

The gamete doesn't "choose" one or the other.  Both are made and you get two gametes, one for each.

Also it's unlikely to be an "exact copy" due to recombination and random or independent assortment.  There are also smaller influences on genetic variation, and epigenetics, but at this level of question I think you should focus on those two.

Was this homework?  If so it should be tagged.


Is the amount of phosphoric acid added to colas enough to disrupt the function of the kidney over the long term?

The phosphoric acid in cola will contribute to dietary intake of phosphate. I may be missing something, but, since the transporter functions to reabsorb phosphate that has been filtered out at the glomerulus, excess phosphate will spill over into the urine.

According to Wikipedia the RDA for phosphorus is 700 mg and the tolerable upper intake level is 4000 mg. Coca cola contains 17 mg phosphorus (as phosphate) 100 ml-1 (which is 340 mg in 2 L)

According to this source,

  in the United States, an average person drinks 412 8-ounce drinks — or 3296 ounces — of Coke per year.

This works out at 9 oz per day = 266 ml = 45 mg phosphorus

For comparison (from here):

white flour contains 595 mg 100 g-1
one boiled egg contains 220 mg
canned salmon contains 240 mg 100 g-1


Why doesn't the sperm die if there is citric acid and acid phosphatases in the semen?

Citric acid is a weak acid so in the context of a buffered physiological medium (semen pH 7.7) it will not cause any significant acidification. Acid phosphatases are enzymes with a pH optimum below 7 (as distinct from alkaline pho sphatases). Their presence has no implications for the pH of semen, although it is interesting to speculate why an alkaline fluid would contain an acid phosphatase.


Mechanism behind negative conductance of ion channels

This is the figure OP talks about:

Negative Conductance Caused by Entry of Sodium and Cesium Ions into the Potassium Channels of Squid Axons, Francisco Bezanill, Clay M. Armstrong (1972).

Short answer is that in non-linear mode of ion channel operation other ions start passing through it (channel loses specificity). Cumulative effect (because of different concentrations of different ions) is negative total conductance, if you don't measure currents of specific ions.


No, no human (or any other eukaryote lineage) are able to "create bacteria". The story you were told is wrong.

However and interestingly, female parasitoid wasps seem to "create viruses" (Herniou et al. 2013). The viruses are part of the wasp genome (lysogenic phase) and detach (lytic phase) in the ovaries only. The viruses, then infect the caterpillar in which the mother lay its eggs. The viruses ensure to reduce the immune system of the caterpillar in order to protect the wasp egg (and later larvae) and ensure its development to adulthood.


RNA interference and the former Petunias experiment >

They introduced a foreign gene responsible for petunia leaf colour, with the intentions of up-regulating gene expression for this colour, which was purple. What was observed however was intriguing. Rather than an up-regulation of the purple colour, the leaves were all white instead. This finding showed that the RNAi system in plants recognised the foreign gene and degraded it. Not only that, but the RNAi system also identified the endogenous equivalent of the foreign gene and down-regulated this also thinking it was foreign. This is how they discovered this miraculous finding :)


How are human rotaviruses generally transmitted?

Faecal-oral transmission. Ref from https://en.wikipedia.org/wiki/Rotavirus


Yeah, basic principles of osmosis there, but let me see if I can make it clear.  For illustration's sake, I'll take glucose as a solute and water as a solvent, but recall that the principles are true (though they can have added complexity) for other solutes and solvents (see this post on chem.SE).
Background
The basic principle behind osmosis is that conjoined systems tend toward equal concentrations.  In other words, if you have a more concentrated solution (more particles of glucose per amount of water) on one side of a membrane than the other, the solution "wants" to become equal on both sides of the membrane.
If the membrane is permeable, there's no problem: glucose can flow freely and equilibrate on both sides of the membrane.  So the solution just moves around "mixing" until there's the same concentration everywhere of solutes (ie., glucose) in the solvent (ie., water).
On the other hand, suppose that the membrane is semi-permeable, meaning that the the water can pass through but the glucose cannot.  The system still "wants" to get to equilibrium; a state of equal concentrations on either side of the membrane, but it cannot get the solute across.  What happens instead is that water starts moving from the side which is less concentrated to the side which is more concentrated.  This results in the concentration of particles on less concentrated side going up and the concentration on the more concentrated side going down, effectively equilibrating them.

Now look at Picture 1.  Intuition from all this would tell you that the concentrations would be equal.  However, there's a twist.  Osmosis can only exert so much pressure on a system, and if it has to resist a pressure, it eventually stops, even if the concentrations are not equal.
The assumption in the picture is that the balloons have the same elasticity, meaning that the balloon on the left is more stretched, and is exerting more pressure on the solution than the balloon on the right.  Therefore, it will counteract some of the osmotic pressure and push some water back onto the right side of the system.
Now look at Picture 2. Again, intuition would tell you that the balloons will have equal concentrations at the end of the scenario, but again, the pressure that the balloon on the left is exerting messes things up a bit.  Even though the balloon on the right is pushing water into the balloon on the left, it is unable to push as much as it would like to, because the pressure of the left balloon's elasticity counteracts the osmotic pressure.

Taking it to the next level
They're basically laying the foundation work for reverse osmosis in this question.  In the case of reverse osmosis, we would be artificially applying pressure to the balloon on the left, resulting in water flowing forcibly into the right container.  This can be an advantage if you want to increase the concentration of a liquid - which has hundreds of industrial usages, such as in concentrating maple syrup in Canada and the northern States.


Black insect with antennas and large abdomen

What species is this insect from and what is the insect called?

This is a Meloe proscarabaeus, most commonly known as a black oil beetle. Looking at the antenna of the insect in your provided image, it's clearly a female.

M. proscarabaeus

Males have a "kink" in their antennas, females don't.

  What caused it to have such a large abdomen?

The primary reason/cause for the large abdomen is eating. Initially, the abdomen is much smaller, but after eating it will rapidly swell. Another cause for such an abdomen is pregnancy.


Does finite rate of increase depend on mortality of individuals in a population?

*It's been several years since I've worked with similar equations. The following reply is based on memory, and if anyone has a firmer grasp of the materials, please modify or answer as you see fit.

I would assume λ is under ideal conditions or as an average of whatever species you're working with. Your modified lifetime reproductive output still leaves out many variables which can affect λ. By your own words it leaves out mutations and daughter cells that are dead-on-arrival. There could also be predation or conditions where the Mother-cell produces more than one Daughter-cell, resulting in R = 3 instead of 2 and your subsequent λ also being 3. UCLA Bioengineers have actually observed up to 5 daughter cells in cancer lines.

I'm not sure what you mean by "... or it depends on the natural situation?", but ultimately reality is always more complicated than basic equations usually describe. Either B or D can increase or decrease, depending on the species, environment, and how you define t.

Your equation still produces a population increase, just at a slower rate than your ideal conditions. If you're asking if there's a specific definition for "λ" referenced in your equation, I'm not aware of any specific definition for "λ" - it's not a Constant.

Your title question - does the rate of increase depend on mortality - is ultimately "Yes." If mortality is higher than the birth rate, then you will see a decrease of the population until extinction is reached if there isn't an equilibrium or rebound.

However, most populations change at an Exponential rate - NOT Geometric. To that end, you might be interested in the r/K Selection Theory and how they operate within Exponential equations (which are similar to your Geometric equations). In short, r-Selection is the reproductive strategy of producing extraordinary amounts of offspring with a very, very low survival rate. However, because so many are produced you only need a small overall percentage of survival to maintain or increase populations. The tapeworm I mentioned above is one of the stereotypical examples. K-Selection represents species that invest additional resources into raising a few offspring, usually just a handful that are carefully watched over and raised by the parent(s) until they are capable of reproducing themselves. Humans, elephants, most birds, and larger animals in general are K-selected.

For r-Selection your B and D will both be very high, and for K-Selection both B and D will be low. However, both will result in a positive λ simply because it's all about the ratios.


I would agree with you on this one - looks like a female or young male Libellula depressa (the 'broad bodied chaser') to me. It has the characteristic broad, flattened abdomen and the distinctive brown-yellow abdomen with bright yellow patches and the dark wing bases are both visible (the latter only just, to be fair). The broad abdomen differentiates it from the other Chaser and Skimmer dragonflies while the colour is quite distinctive (the species is sexually dimorphic; mature males have a blue abdomen while females and young males have a yellow abdomen). Not sure what you friend is talking about regarding the size; 3in long is about right for L. depressa. It's in the right geographical region too.

(thanks to @RHA for pointing out to me that young males also have yellow abdomens!)

Citation from Wikimedia Commons: By No machine-readable author provided. Bogdan assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=754252


I think there is more than one possibility for this.

Plates bearing colonies are stored for too long in 4C(as @mdperry suggested). This causes the colonies to lose the plasmid over-time as the antibiotic in the plate gets degraded over-time. There is a study on this and I've shared the link. (http://homepages.bw.edu/~mbumbuli/biotech/colin/index.html).
The insert is toxic to cells and promoter is not strong enough. There is a leaky expression causing cells to die.
Check the competent cells and their storage condition as it would greatly affect the efficiency of transformation. Do a mock transformation with plain plasmid without insert and spread them on an antibiotic plate.


Measuring luminescence in a fluorescence plate reader

I am René Inckemann and  I am PhD student at the Max Planck Institute in Marburg, Germany. In my PhD I am using luminescence on a regular basis and I was also responsible to organize some of our Platereaders.
So therefore I can tell you that you need a Platereader which is able to measure luminescence and you can not simply take a fluorescence platereader. The hardware for measuring luminescence and fluorescence is different.
However many Platereader models in these days already come with both options for the hardware, which means that you can measure luminescence and fluorescence in the same device. You just have to check your platereader model if it is capable of measuring luminescence.So you don't need a seperate platereader just for luminescence, but you need one, which has the luminescence addon installed.
Regarding your idea for normalizing luminescence, I also have strong interest in that and we have already started working on that. Maybe we can exchange ideas at some point?


Rescue experiments are the gold-standard for confirming that an effect is due to the gene of interest.

Removing a gene may have off-target effects but if you can return function to 'normal' by supplementing the gene back into the cell-line/animal then this is strong evidence that the gene and its product are the cause of effects that are seen in the experiment.

Wild-type cells would normally be included to show what 'normal' response  is.


While "common disease" has obscure incidence and prevalence definitions, "Rare" or "orphan disease" is more defined.

In the US, the rare disease defined as a condition which affect one (or less) of 200,000 people in population. However, this definition can be different in other countries, p.e. in Japan 1:50,000 or less.

We can assume that "common" disease is much frequent than "rare" one, thus the incidence and prevalence are much greater than per "rare disease" definition. However, again, there is no agreement of clear cut of "common disease" incidence and prevalence.


At What Rate Do Ions Leak Out of a Plasma Membrane Segment That Has No Ion Channels?

I'm going to mostly skip over the title of your question and focus on the confusion in the body, because the question in the title is a bit of an XY problem. It doesn't make much biological sense to think about a membrane that is truly that resistive (that is, I am unaware of any example neuron, or even any other cell, that has that property).

If there were truly no channels of any sort, you could indeed consider the resistance to be very high, at least as high as one could measure in patch clamp. Additionally, what matters is not the resistance itself but the ratio of the transverse to axial resistance; relative to the axial resistance the transverse resistance is already very high.

  From what I understand, one of the primary "benefits" of myelin is that it aids in increasing the transverse resistance of an axon

Your understanding is not completely correct. The insulating benefit of myelin (ignoring other organizational benefits) is not only related to the transverse resistance, but importantly to a decrease of the capacitance of the membrane (see Moore et al 1978 or Richardson et al 2000 for some example simulations; also any reasonable neuroscience textbook will explain this). You can test this yourself in a simulation environment like NEURON.

Myelin decreases capacitance by effectively increasing the distance between the 'plates' of the membrane capacitor (see this answer).

In order to charge a long length of membrane with channels on only at short segments, you would need enough charges to come in within that short segment to charge the entire length of axon, and the potential would decay with distance.

Myelin does also affect resistance, but that's mostly important because the membrane does not consist only of a phospholipid bilayer and there is non-zero leak. For example, there are channels under the lipid bilayer that establish a resting potential (Chiu & Ritchie, 1984).

Chiu, S. Y., & Ritchie, J. M. (1984). On the physiological role of internodal potassium channels and the security of conduction in myelinated nerve fibres. Proceedings of the Royal society of London. Series B. Biological sciences, 220(1221), 415-422.

Moore, J. W., Joyner, R. W., Brill, M. H., Waxman, S. D., & Najar-Joa, M. (1978). Simulations of conduction in uniform myelinated fibers. Relative sensitivity to changes in nodal and internodal parameters. Biophysical journal, 21(2), 147-160.

Richardson, A. G., McIntyre, C. C., & Grill, W. M. (2000). Modelling the effects of electric fields on nerve fibres: influence of the myelin sheath. Medical and Biological Engineering and Computing, 38(4), 438-446.


The question does not cite the source of the poster’s information, but it might well be the Wikipedia article on ESTs. I suspect the reason that does not answer the first question (“What are ESTs”) is the confusion in how ESTs are generated from cDNAs implicit in the second question “Which part of cDNA is cut…”. I therefore start by dealing with the source of the confusion.

Clarification 1: A Sequence need not have been Sequenced

One source of confusion lies in the word ‘sequence’. One meaning of this (noun only) is “a specific linear contiguous fragment or region of nucleic acid”. When used in this way there is no implication that even the length of this is accurately known, never mind the identity and linear arrangement of the nucleotides. The second use of the word sequence (noun) is the identity and order of nucleotides in a (linear) nucleic acid, with the corresponding verb meaning to determine this. Because today it is so cheap and quick to determine the sequence of a nucleic acid fragment, the student may not realize what a relatively slow and expensive undertaking it was in the last century. I shall use DNA fragment or region instead of the first use of ‘sequence’ in the rest of this answer.

Clarification 2: There are cDNAs and then there are cDNA clones

The second source of confusion seems to be with the cDNA clones. The question does not use the word ‘clone’, but asks “which part of cDNA is cut…”. This implies the poster is thinking in terms of individual cDNA clones in which the inserted cDNA fragment has been characterized — restriction mapped, perhaps sequenced and the protein product even identified. This is the approach adopted when the scientific problem is to identify the mRNA or gene encoding a particular protein — actin, beta-globin, etc. This is not the case with ESTs. Here the only characterization performed on a cDNA clone is a single DNA sequence determined (historically by the Sanger method) from a primer position in the cloning vector. This is because the focus is on producing a bulk library of DNA sequences.

So, what are ESTs and how are they generated?

As an alternative to the standard definition, one might say:

  An EST is a single DNA sequence read derived from only part of a mRNA. Despite its uncharacterized nature, possible redundancy, limited size (perhaps 100-200 nt) and likelihood of errors it is useful in combination with many others from the same tissue as providing a reference to genes that are expressed in that tissue.

So, to reiterate, the answer to “what part of the cDNA is cut…” is “none”. One (presumably) just isolated total DNA from the recombinants in the M13 plaques and ran a single sequence determination from the primer site. And this was because one did not know which EST would be useful, but a collection or library of ESTs would likely contain some that would be useful.

The word ‘tag’ expresses the fact that they act as a handle or reference to the gene or mRNA, rather than being complete in themselves.

Why are/were ESTs important/useful?

The words the poster used originally were “Why are they so instrumental in genomic research?”, but I think that certainly exaggerates their current — if not their past — utility, so I have rephrased the question. Examples of the use of ESTs are given in the Wikipedia article already quoted, so I shall quote from Peter Goodfellow, writing in Nature in 1995.

  Only 3 per cent of the human genome codes for proteins… the most important
  part of the genome is the protein coding genes and that sequencing these
  will give the largest return of biological information…

After pointing out his own scepticism towards the approach he briefly mentioned one important historical issue:

  Given these disincentives, why have tens of millions
  of dollars been spent on ESTs? After a brief exploratory phase… a major driving force was the hope and the fear that ESTs could be used to patent any gene that had been tagged. Attempts to patent genes via ESTs raised the spectre of an international trade war and the echoes are still reverberating around courts in the United States.

No longer, I hope. Goodfellow then turned to the science:

  It was hoped that large-scale EST projects would define the broad limits
  on the number of genes and the types of genes in the genome and provide a
  snapshot of their expression patterns. It was also expected that enough sequence
  information would be generated to be able to recognize new members of gene
  families of biological and commercial interest.

Coda: Yesterday and Today

Currently the method most used to investigate expression of genes as mRNA is, of course, RNAseq, which is faster, cheaper and, unlike ESTs, comprehensive.


Tc and Th1 interaction and viral immune response

PlaysDice's answer:

Antigen presenting cells migrate from skin/mucosa to secondary lymphoid organs like lymph nodes/spleen/GALT and drive T cell activation and maturation.
T helper cells with CD8 and MHCII complex recognise the virus and kill it.

I think this is what is happening, for instance in HIV infection:

where

dendritic cell (ADCC) presentation of HIV infected CD4+ to MHCII and T helper cell
T helper cell activates cytokine release
Natural killer cells come and lyse the HIV infected CD4+ T lymphocyte


What does it mean for the signals for transcription and translation to be "conserved"?

I concur with @Bez but wish to elaborate on the meaning of 'conserved'. It is generally used in the context of evolution. A conserved characteristic or gene or protein means that it has 'survived' a long time without being altered. As @Bez mentions, certain parts of the protein machinery in eukaryotes is very different from prokaryotes, the latter being considered to have arisen much earlier in evolution. For example, some post-transcriptional processes (e.g. splicing and many more differences) only occur in eukaryotes. But there are many similarities as well, such as the basic use of mRNA etc (see book section). The latter are examples of conserved mechanisms.  In the context of your question, it means that when you take eukaryotic DNA to express eukaryotic proteins it doesn't really matter which cell or host organism you take as it will be transcribed and folded correctly. For example, yeast is often used to express DNA from higher organisms as its protein synthesis is much the same across various eukaryotic species. However, expressing eukaryotic DNA in prokaryotes likely ends up in misfolded proteins without proper post-transcriptional modification and should be avoided.

As to your follow-up question: Folding of proteins happens in the endoplasmatic reticulum (ER) in eukaryotes (wiki), a cell organelle absent in prokaryotes as they lack a nucleus and associated organelles. Again, expression of eukaryotic genes in a prokaryotic expression system will end up in mis-folded proteins.

To get back to your overall question - the 'signals': DNA transcription, splicing, protein synthesis, post translational modification and folding are all regulated by signals, such as specific DNA codons to start and stop transcription, RNA codes for splicing and start translation and protein tags that are placed on specific amino acid combinations. These signals are well conserved across eukaryotic species.


This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.

Without further evidence, it's hard to narrow down to a species.

One possibility:

Neoscona crucifera (Hentz orbweaver, spotted orbweaver or barn spider)

 Source: Will Cook 2001

 Source: Wikipedia

Description:

Relatively variable in color (and sometimes pattern), but is usually rusty-red or golden orange color.

This site suggests females are reddish-brown to brown and males are lighter brown with the sides of the carapace nearly black.

Dorsal abdomen is brown and hairy; abdomen underside = black, with two white spots
The epithet crucifera refers to the cross-like pattern on their back
Legs have alternating light and dark brown bands.

Size: females = 9.5-19 mm long; males = somewhat smaller
Web: very large (up to 0.61 m diameter) and often on buildings and other man-made structures
Range: Eastern/Central USA + Mexico

According to Will Cook,

  Several other species of Neoscona are confusingly similar...Other species usually have a bolder pattern.

We can rule out Neoscona domiciliorum because Illinois is west of its range and the colroation is different. [Source].


Are more molecules of ADP than inorganic phosphate returned to the light reaction in photosynthesis?

Not 6, but 9 molecules of Pi are formed in the Calvin cycle, from the conversion of 9 ATP to 9 ADP:

Source: Columbia University


I made a quick sketch on the basis of the information you gave (this is not to scale):

Aminoacid 5 (aa5) of the protein is on the outside, aa90 is inside the membrane. What we don't know here where the transmembrane part starts (directly with aa6 or later) and how it is organised (I indicated this as a transmembrane helix, but this can of course be different). Then we know that the border between the transmembrane part and the cytosolic part is somewhere between aa90 and aa100, that aa100 to aa200 seems to be some connecting part. The aa200 to aa400 is a globular domain which shields hydrophobic amino acids from the cytosol, so this part has to contain a high percentage of hydrophobic amino acids.

The part from 400 to 600 is again cytosolic but with no further information about the structure. After aa600 starts a second transmembrane part of the protein, but here we don't know how long it is. The maximum possibility would be until aa977, since we know the aa978 is outside of the membrane.


Pump to separate protein/DNA instead of electrophoresis?

If you tried to set up a system in which movement of DNA molecules through a gel matrix was driven by pumping buffer, the gel would become compressed. I am old enough to remember running vertical agarose gel electrophoresis overnight, and these gels would collapse under normal pressure to about 2/3rds of their initial height. A gel porous enough to give useful separation of DNA molecules just isn't strong enough to withstand pumping.


What is this animal? Reminds me of a crab because of the way it crawls but it looks like a plant.

It looks like a clump of seaweed to me. But I can pick out pairs of legs.

It is a species of "seaweed crab" or "decorator crab": a crab that camouflages itself with bits of seaweed it picks up, so its appearance can vary depending on its surroundings. Here's a video, and as you say, in the speed department, it's a bit lacking.

It is identified as Naxia tumida as opposed to the larger decorator crabs. The cephalothorax is that round brown bump in the middle, and in front of it (in the middle below the long axis) are the pincer legs. The second and third pairs of legs have quite a lot of seaweed attached (making up what I've described as the 'long axis'.)

Here is a screenshot from the video of a Naxia tumida.


Are two colors (red + blue) necessary for LED grow lights, or would either color be sufficient?

tl;dr: Sort of?

Logically, either red or blue light should be sufficient. Chlorophyll a and chlorophyll b preferentially activate different photosystems, and both photosystems are required in green plants.

Practically, we're in luck and someone has actually done the experiment.

As the original study reports, plants need a little blue light to grow into the right shape. Red-only plants produce oxygen and grow, but they take weird shapes. It seems like plants can grow on red light, but they use blue light to work out where light is. See here for a reasonably lengthy treatment on most of the obvious combinations.


How to identify Ag nanoparticles in a solution?

This paper says that silver nanoparticles enhance the enzymatic reaction that happens in a normal ELISA assay. You should be able to observe a significative shift in UV absorbance comparing your bacteria to a control.

Otherwise, I'd think simply of lysing the bacteria and centrifugating the lysate. I'd expect the pellet to contain nanoparticles and to be somehow different (in color?) from a control pellet.


How exactly are genes swapped during the process of recombination?

There is quite a few misunderstanding in your question. So, I'll shortly give you some (simplified) definitions and then point you to another post.

Definitions and Basic Concepts

A locus (plur. loci) is a position along a chromosome. A some loci, there are  genes. To make things easy a gene is any sequence which is transcribed into RNA and translated into proteins.

Now at any locus, you might see different individuals having different variants. For example an individual may have the sequence ATTCT while another individual may have the sequence ATTGT. Those different variants are called alleles. It is key to understand that there is genetic variation in populations. This genetic variation is a big part of the reason why people around you look different and why you ressemble more your siblings (if you have any) than a random person in the population.

How does recombination have any impact?

To understand the effect of recombination you necessarily have to picture a several loci model. As you now understand the above definitions you will find your answer at this post: Why do we need two markers to measure a recombination rate?

Further readings

The following posts will also be of interest to you:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Chromosome and chromatid numbers during cell cycle phases


Looking for Kelly Chibale's paper on Malaria cure

This may be the paper you are looking for:

Ongaroraa DSB, Gutb J, Rosenthalb PJ, Masimirembwac CM, Chibale K. 2012. Benzoheterocyclic amodiaquine analogues with potent antiplasmodial activity: Synthesis and pharmacological evaluation. Bioorganic & Medicinal Chemistry Letters, 22(15): 5046–5050, doi:10.1016/j.bmcl.2012.06.010.


Autosomal genes expression occurs from both alleles simultaneously

Definition of dominance and recessivity

By definition, an allele is dominant over another allele if the phenotype of the homozygotes for the dominant allele and the phenotype of the heterozygote are the same but not the ones of the homozygotes for the recessive allele. In other words, let $p_{ab}$, be the phenotype of an individual with alleles a and b, then

$p_{rr} = P_1$
$p_{rR} = P_2$
$p_{RR} = P_2$

, where $P_1$ and $P_2$ are two phenotypic describer.

Note btw, that very very few traits have their variance explained only by the genetic variance, even fewer are explained only by variance at a single locus and yet even fewer have a locus that show a simple dominance / recessivity pattern.

Expression

If needed, please check gene expression.

The fact that an allele is dominant over another does not mean that the other allele is not being expressed. In fact, it does not say anything about the molecular mechanism by which this dominance pattern is achieved. It is possible that in some cases, if the recessive allele was not expressed at all, then the resulting phenotype would be $P_3$. It just so happen that most of the time, both alleles are being expressed.

Imagine for example a case of a locus coding for a black pigment. Let's consider haplotypes that where the gene is missing (copy number variation). Let's refer to such haplotype with 0. 00 are white. 0r individuals are light grey. rr individuals are grey. The allele R causes the expression of a lot of pigments so that both rR and RR individual are indistinguishably black. The allele r is still being expressed in heterozygotes rR even the phenotypes of rR and RR individuals are the same.


What can pass through the intestinal membranes?

Virtually all nutrients from food can be absorbed into blood through the lining of small intestine and colon.

What can be absorbed in the small intestine:

Water
Simple sugars (monosaccharides): glucose, fructose, galactose...
Amino acids and small peptides (dipeptides, tripeptides)
Free fatty acids, monoglycerides and cholesterol
Minerals: sodium, potassium, iron, etc.
Vitamins
Nucleic acids
Alcohol
Various other substances from food (polyphenols, sulfate, oxalate, caffeine, preservatives...)
Bile acids
Steroid hormones, such as cortisol, aldosterone and sex hormones (JCEM)
Drugs
Various toxins

What can be absorbed in the colon:

Water
Short-chain fatty acids (from bacterial fermentation of dietary fiber and sugar alcohols)
Sodium, potassium and some other electrolytes

What cannot be absorbed in the intestine:

Polysaccharides (such as starch), oligosaccharides, disaccharides
Dietary fiber (soluble fiber can be fermented and the resulting substances can be absorbed in the colon)
Whole proteins and big peptides
Triglycerides, diglycerides
Peptide hormones, such as insulin, glucagon, calcitonin, prolactin, growth hormone and parathyroid hormone (Cambridge Core)

Sources:

Lumenlearning (type of transport for all main nutrients)
Best Practice & Research: Clinical Gastroenterology (detailed description with carriers involved)


Is Zika suspected of causing birth defects only if contracted during pregnancy?

As you mentioned, there is evidence that mother-child transmission of Zika virus causes congenital anomalies like microencephaly.
Now your question, if a cleared infection before the pregnancy could affect it? In principle, no. Once the virus is cleared, it should not reactivate, unless there is reinfection. Here's a quote from the Zika article from Uptodate.com:

  Women of childbearing potential — It is uncertain how long women of childbearing potential should wait between Zika virus exposure/infection and conception. Most pregnant women with Zika virus exposure give birth to normal infants [111]. Zika virus usually remains in the blood of an infected person for a few days to a week, and thus far there is no evidence that a fetus conceived after the virus has cleared from the blood would be at risk for Zika infection [94,112]. However, information regarding the persistence of Zika virus following infection is not known. It has been suggested that infection due to other flaviviruses such as West Nile virus may persist years after initial infection [113-115]; these data are controversial. Pending further study, healthcare providers should encourage women to make such decisions based on their individual circumstances, values, and preferences.

  Daniel J Sexton, MD
  Editor-in-Chief — Infectious Diseases Section
  Editor — Bacterial Infections
  Professor of Medicine
  Duke University Medical Center


Are mediterranean sharks shyer than ocean sharks?

It really boils down to the species and the conditions. You are only able to cover a limited area and shallow depth and limited amount of time as a diver. Many species of shark are likely to know you are there before you know they are there and sharks can be shy and avoid divers. However certain shark spots can be popular feeding grounds, sleeping grounds, or mating areas. While I think there is a lot more historical pressure from fishing sharks in the Mediterranean, I don’t think there is anything innate about the sea there that makes all shark species there shy. I have heard of shark spots in Lebanon: http://www.nisd-online.com/article-101506-talesanddivesinlebanon.htm, though I do know the Red Sea offers a lot more in terms of shark encounters. There simply is a lot that goes into a shark encounter and we do not know nearly as much as we would like on their behavior. I’ve been on many dives in different parts of the world to see hammerheads in the wild and it can be a shot in the dark. It takes many years of local knowledge of the species’s behavior and conditions (season, tides, current, temperature, time of day, moon phases, undersea typography, etc). They are out there, but my best advice is to speak to fisherman and local divers, and also get creative in how you approach them (think about boat sounds, consider beach entries only, go in small groups, try early morning, try different seasons, etc.) Many scientists doing research on certain species in a locale find talking to fisherman to be a huge source of knowledge too.


What is this bug found in a garden in Utah?

Based on the pattern of yellow spots it might be a Say Stink Bug.
Check out this list of common Utah stinkbugs

The 12 - 17 mm size is consistent with OP's description and the fact that this insect is often found on ornamental shrubbery is consistent with finding it in a garden.


To what extent do domestic animals understand language?

Yes, they can understand some words and even simple sentences.
Here is what Animal Planet says:

Studies show that the average dog can understand about 165 different words, in some cases more if you make a point of training them. This includes the basic commands such as "sit," "stay," and "go," as well as a range of other terms, assuming they're tangible words and not abstract ideas.

Here are some supporting studies:

Some domestic dogs learn to comprehend human words, although the nature and basis of this learning is unknown [1].
A female mongrel dog, Sofia, was initially trained to respond to action (point and fetch) and object (ball, key, stick, bottle and bear) terms which were then presented as simultaneous, combinatorial requests (e.g. ball fetch, stick point). Sofia successfully responded to object-action requests presented as single sentences, and was able to flexibly generalize her performance across different contexts [2].

References:

Tempelmann S, Kaminski J, Tomasello M (2014) Do Domestic Dogs Learn Words Based on Humans’ Referential Behaviour? PLoS ONE 9(3): e91014. doi:10.1371/journal.pone.0091014
Ramos D, Ades C (2012) Two-Item Sentence Comprehension by a Dog (Canis familiaris). PLoS ONE 7(2): e29689. doi:10.1371/journal.pone.0029689


What is this dark brown organism growing on a door frame?

Termites.
Photograph the insects and we will try to identify further. If the insects keep running, freeze some. This could be a big problem, so get good information soon.
Online I see this article that might help.
" An identification guide to the wood destroying termites of south India"
Journal of the Indian Academy of Wood Science
ISSN 0972-172X Volume 8 Number 2
J Indian Acad Wood Sci (2011) 8:148-151
DOI 10.1007/s13196-012-0028-9


My opinion as a physicist would be that yes, they do.

Assuming a sperm-like structure with a single flagellum at the centre of a long, thin cell of uniform density. They would rotate around the axis of travel.

However, for other cells, this could be mitigated in several ways:

If the cell was submersed in or floating on a liquid, it is likely that the effects of Archimede's Principal would be sufficient to keep it in a fixed orientation (this is how ships and submarines stay upright despite rotors that all go in the same direction - the least dense parts of a body always attempt to restore themselves to the highest position).
Fluid in the cytoplasm could act as ballast, providing a counterrotation force thanks to the gravitational effect on it.
If the cell happened to be particularily masseous in relation to the force the flaggela were providing, this would make any rotational force negligible.
If the flagella were located away from the axis of travel (through the centre of gravity - ie to the sides) the torque would have less of an effect.

As for the navigational aspect of your question, if these cells do auto-rotate, they will have done so throughout their evoloutionary histories and therefore in all likelihood will have evolved navigation methods capable of dealing with this.

I will however put a disclaimer on this, I am not a biologist and am weighing in from the point of view of a physicist.


Should the length of the electrodes in the electrophoresis chamber be proportional to chamber's size?

These instructions for building an electrophoresis chamber don't comment on the minimum length of wire, but on the other hand they suggest using something called Monel Seizing Wire (Ni/Cu alloy - £8.95 for 10 m in the UK) or 20-gauge copper wire, so if you follow their advice you probably don't need to worry about cost.

I imagine that alloy electrodes won't last as long, but they would be cheap to replace - in fact you would be looking for opportunities to use up all of your excess wire!


Definitely not Megaloptera. Looks like a lampyrid (firefly) larval or female form. Note especially what look like single tarsal claws (on the end of the feet). This is diagnostic for Lampyridae (Coleoptera).


dark bands between segments and long tails match:

Distribution matches:


When you say "new DNA that is incorporated into the genome", it suggests that you misunderstand what genetic recombination. You might to ensure you really understand this concept before going any further.

Mutation rate and recombination rate tend to covary throughout the genome (Lercher and Hurst 2002). So, yes processes leading to recombination events also tend to cause mutational events.


Yes. Trypsin cleaves proteins and can do so quite indiscriminately if left on for very long. Trypsin is primarily used to cleave the proteins that cells use to adhere to each other and the plate in culture. It can cleave other membrane bound proteins as well, including receptors.

https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-17-36


How is DNA testing used to differentiate between different species?

Statistics of divergence
You can compute various statistics of group divergence. Typically you could consider the pairwise number of differences between any pair of individuals. For example the following two sequences
ATATATCCTGTGTCA
AAATATCTTGTGTCA
has 2 differences.
Obvious or obscure grouping
Often, individuals really group together quite naturally (if you perform a principle component analysis you will see clearly defined groups) but sometimes the groups are quite blurry.
The definition of species is arbitrary
Whether the grouping is blurry or not, it is often quite arbitrary how much two groups need to be different in order to classify them in different populations, different subspecies or different species, different genera, etc...
The problem here is more a problem of definition than a technical problem. You should have a look at this post to understand the issue behind the definition of species.

My attempt at a high school level explanation
Explain what a phylogenetic tree is
First draw a phylogenetic tree. Explain what they mean:

A node is an common ancestor
A leaf is a extant species (if the leaf gets to the top of the tree)
All species are related but some are more related than others..
Introduce the concept of sister clade
Explain that every species in a sister clade is equally related to the all the species in the other sister clade by highlighting their common ancestor.
Explain that no extant species is the ancestor of another species as the ancestors are the nodes.

You can get a short introduction to phylogenetic trees here on Biology.SE or here on Understanding Evolution.
Methods to reconstruct a phylogenetic tree
Let them wonder how we could get to know what the true phylogenetic tree is.
Suggest using phenotypic data and make them realize and if you put all the yellow flowers together, or the flying organisms (insects, birds, bats, squirrels) it won't work very well. So phenotypic data can sometimes be misleading. So explain that we can use genetic data by counting the number of pairwise differences. Let's consider the three different sequences
species A: ATCTCTG
species B: ATCTCTT
species C: AGGCATT
It sounds like the first two sequences are more closely related than any of them are to the third sequence. You can draw the tree for these three species.
Molecular clock (optional)
Knowing the rate at which mutations occur, one can date since when two lineages diverged based on genetic data. You will probably have to learn a bit more about molecular clock for yourself. You may ask a for high school explanation in another post.
Within population diversity (optional)
Recognizing the existence of genetic diversity within population is key to all evolutionary processes so it is good to let them understand the existence of such diversity early on.
Of course there is genetic diversity within a species that renders everything a little bit more complicated. For example, some of you have blue eyes while others have brown eyes (assuming there is variation for eye color among your students), this is due to the fact that the DNA sequence within each of you is a little different. Not as different as it is between humans and chimpanzee but a little bit different.
Genetic data to group populations into species
Then, you can say that genetic data can allow us to tell groups apart. You can show a PCA type of plot (without really explaining what a PCA really is) with colors. Each color correspond to a population (insiste on term population and not species). Something like

and then argue informally that light-yellow, green and red populations are probably different species while all the other populations seem to belong to the same species.
Problem with the species definition
If you really want to bring the question of the how to use genetic data to tell species apart, then you will first have to destroy their concept of species! For that, you should first have a look at this post. You will have to

Introduce the biological concept of species
Explain why this concept does not work for asexual species (hopefully they know that many species are asexual).
Give an example of another issue such as the classical (yet rarely observed) example of ring species (see here on Biology.SE or here on wikipedia)

Then, get back to the PCA and ask, how different two populations must be for them to be called different species? And make them realize that this is rather arbitrary. We can tell they are different lineages but it is up to everyone to decide what we want to call a species. However, very often vague intuition about how different a species should be is good enough.


Evolution after the development of sexual reproduction

My understanding of evolution is that genetic mutation occurs in individual members of a species, and they become a new species.

  Isn't a definition of species a group of genetically similar organisms that are pretty much exclusive in breeding ability?

Well, no.

You are correct in that the origin for any new species lies in mutations which occur in individuals and are then passed down through DNA.

You are misunderstanding that simply because a mutation exists in an individual that they become a new species. Take Lactase Persistence as a widely studied example in humans. The majority of the world is lactose intolerant after they stop drinking their mother's milk, but a single point mutation results in the ability to consume dairy products into adulthood. It does not make people who are lactose tolerant a new species, but it does open up a potential new nutrient source, which benefits the people who have it and thus it was passed down successfully over other variations.

In addition to that example, the definition of "Species" is NOT exactly defined. There are many variations, including (but not limited to):

1) A group of organisms that cannot interbreed in the wild.
2) A group of organisms with significantly different phenotypes (appearances).
3) A group of organisms with sufficient* genetic divergence.

*There is absolutely no scientific consensus on how much genetic divergence is necessary to create a new species. We share >95% of our genetics with Chimpanzees, so it's not much - it could be as little as a few key genes out of the entire genome.

So where you define the boundaries of species is up for grabs to some extent, but the most common is what you delineated - when a member of one group cannot interbreed with another group.

  Wouldn't there have to be a male and female with the same genetic divergence at the same time to make a new species?  What is the popularly accepted mechanism for the splitting into a new species in organisms that require sexual reproduction?

Nope. Assuming everything necessary for the gametes to produce fertile offspring is present (aka - the chromosomes aren't significantly altered and the gametes are compatible) then a new species emerges through successive generations.

One mother or father gives their mutation to their children, which pass it on to their children, which pass it on to their children, etc. If the mutation is significantly advantageous it will allow the children with the mutation to better survive in the environment, and over time it could become the dominant phenotype that could lead to the creation of a new species as further mutations build in the new group - further differing the generations of the mother/father from the original group the mother/father were born into. Good examples are the HAR - Human Accelerated Regions which are sets of genes that are pretty much the same throughout all other vertebrates, but startlingly different in humans. The HAR did not create humans, but it's thought the mutations contributed greatly to our intelligence - which allowed other mutations to be taken advantage of (like the humble opposable thumb) as our lifestyle changed due to the increased intelligence.

Not all mutations need to be advantageous, though. There's lots of fuzzy areas. If a mutation isn't beneficial, but also isn't that detrimental, it can also stick around in a population. These mutations might not lead to the creation of new species, but can certainly contribute to genetic divergence.


where to buy DNA sample kit? why isn't it easy to find online?

Most people using these tools for research and diagnosis have long-established connections and providers of industry standard tools. Most companies that provide these tools need a steady, reliable source of income, and historically demand for those tools comes from facilities such as hospitals and labs, not DIY biotechnologists (who typically can not afford the tools), so they focus on getting their products to the population demanding them most. There is budding interest in providing research and development tools to the general public such as this startup's stated goal:
http://www.the-odin.com/about-us/

But generally you have to go to a company's website, select the product you desire, and request a quote based on how many kits you'd like to order. The process isn't as easy or accessible for DIYers simply because the demand has not been great enough until recent technological advances such as CRISPR and DNA sequencing technologies made it cheap enough to run these tests on home equipment. It's similar to how not every computer geek could afford a CPU of a certain speed 20 years ago, but now CPU's of that speed are wide spread.

Salimetrics has some swab kits available for under 100 USD here
http://store.salimetrics.com/saliva-collection-methods/

Oragene offers saliva collection kits and this link details some storage options.
http://blog.dnagenotek.com/blogdnagenotekcom/bid/40944/Best-Practices-for-Long-term-Storage-of-Oragene-DNA-Samples

A list containing price per sample of oragene sample kits can be found here:
http://genomics.pitt.edu/pricing/price/HSCRF%20Genomics%20Research%20Core%20Price%20List.pdf

Some issues with collecting a saliva sample for DNA testing are neutralizing the enzymes and materials present that will degrade the DNA, and then isolating, storing, and testing the DNA. These techniques are usually used by trained professionals, once again highlighting the reason companies do not focus on selling to individuals, but to professional organizations.

An overview of the process of saliva collection and links to a few providers of the tools required to acquire your sample can be found here:
http://www.the-scientist.com/?articles.view/articleNo/43347/title/Tools-for-Drools/

This is a handbook detailing some tips on techniques used for collection and storage:
https://www.salimetrics.com/assets/documents/Saliva_Collection_Handbook.pdf

I am not affiliated with any of the companies mentioned above but if linking them is a no-no here on Stack Exchange the links will be removed and I will mention the companies only as examples. Hope this helps!