What are some of the immediate challenges to break through before finding a cure for mad cow disease?

The main problem is that Mad Cow disease is not caused by a "normal" pathogen but by a prion, a protein.

Traditionally, disease causing agents can be classified into viruses, bacteria, fungi, and parasites. Bacteria, fungi and parasites are all living organisms, alive in the traditional sense. It is, therefore, possible to design drugs that kill them.

Viruses are trickier, while not really alive in the traditional sense, they still have to make copies of their genetic material (DNA, or RNA in the case of many viruses) in order to cause infection. Therefore, drugs like ganciclovir that stop the formation of viral DNA can be an effective treatment.

Prion based diseases such as Mad Cow disease, Creutzfeldt–Jakob disease and Kuru, are not caused by a classical infectious agent but by a simple protein, a prion. Prions are misfolded versions of proteins already present in the host's body. When a prion interacts with the host protein, it causes this protein to adopt the same, misfolded, state as the prion. Protein function depends directly on the protein's structure, the way it is folded in three dimensional space. Therefore, the misfolded protein can no longer carry out its physiological role and disease symptoms occur.

Now, since the prion is just a protein, one single molecule, there is no essential life process that we can disrupt. We have to attack them using chemical agents that target the prion while not affecting the healthy, correctly folded, host protein. This is very hard to do.

The blood-brain barrier mentioned by Larry_Parnell is another problem. Briefly, the BBB, is a kind of fence that only allows certain of the various items circulating in the blood stream to enter the organism's brain. This is a wonderful defensive feature but it makes it much harder to design drugs that can enter the brain and target pathogens found there.


Why is the pressure pulse bigger after exercise?

I would guess that pulse pressure increases after exercise. As I understand it,

Systolic pressure is simply resistance against the pressure wave of the ejected blood. Since the stroke volume is increased in exercise to deliver more blood, systolic pressure will be definitely be increased.
During diastole, the major resistance to flow is due to peripheral resistance (major arteries now assist flow by releasing stored energy), and this is reduced in exercise due to vasodilation. Although there is more flow, since the resistance is markedly reduced, diastolic pressure may drop.

Hence, pulse pressure should increase.


Wikipedia actually covers this:

  Most bilateral animals, including all the vertebrates, are coelomates.

Now, some coelomates have subsequently lost their coelom but primates (actually, I believe, all vertebrates) are not among them. In humans, the coelom forms, amongst others, the pleural cavity.

So, yes: humans do have a coelom that partitions into different, unconnected body cavities during development.


Do ants really dispose of their own dead, and how/why?

Eating the dead makes far more likely you will catch whatever killed them. They transport and dispose of the dead for the same reasons we do, to reduce disease vectors. They dispose of their garbage for much the same reason, in fact they often dispose of both in the same place even if they separate the two in distinct piles. Hygiene is very important is colonial insects because you are constantly surrounded by other ants which makes disease transfer very easy. Fungal infections are particularly problematic. They also have specialized toilet sites for the same reason.

Note only some ants transport the dead outside, other put them is special chambers far from normal traffic and reserved for that purpose and refuse disposal. In either case they are moving them away from casual contact.

Source

Source 2


I think this is just
Tegenaria domestica. I am from Czech republic and this is really big and kinde everywhere. Specialy in garages.


How does translational immunotherapy work?

Tumors are commonly infiltrated with lymphocytes, including T cells, macs, DCs and B cells. The crux of the paper is that their attenuated virus secretes TLR ligands (Toll-like receptor) that resulted in an activation of tumor-suppressive M1 macrophages, a concomitant reduction in immune-suppressive M2 macrophage activity, and an influx of immune infiltrate to the tumor.

So M1 macs are activated typically by IFN-y and LPS stimulation, which is typically through TLR4. Their salmonella is attenuated and causes no disease, check one. It's gram-negative and thus has LPS, check two. It's engineered to secrete bacterial flagellin, a TLR5 agonist, check three.

M1 macs secrete IL12, important for polarizing T cells to TH1/TC1 phenotypes that are oncolytic, and IL10 which can elicit anti-tumor immunity though it's reputation is that of an immunosuppressant. M1 macs can also kill tumors of their own accord by producing nitric oxide which is cytotoxic to tumor cells. TLR4 agonsim on it's own accord also activates T cells in an NF-kB-dependent manner.

Whats also interesting is the inflammatory signal actuated by the macrophages actually tells other immune cells "hey come check this out," and potentially makes for a more robust anti-tumor response. The idea is that inflamed tissues secrete signalling or chemotactic molecules called chemokines which are picked up by chemokine receptors on leukocytes, telling them to enter the zone of infection (and thus the malignancy).

You'll also find, however, that despite immunological advances, modulating cells is a challenge due to the nature of each type of cancer's TME (tumor microenvironment). And so in your paper they tested it in a murine system in bladder cancer, but will it work in a human melanoma must be qualified, for example.


Would intravenous insulin + glucose significantly accelerate glycogen synthesis?

Concluding from this 1991 PubMed article, intravenous (or subcutaneous) insulin may not stimulate glycogen synthesis more than naturally secreted insulin.

  Experiments carried out in man have suggested that insulin may play
  only a permissive role in the determination of splanchnic glucose
  uptake. In a study by DeFronzo et al. (5), in which the plasma glucose
  and insulin levels were raised via peripheral intravenous infusion to
  223 mg/dl and 55 μU/ml, respectively, net splanchnic glucose
  uptake was 1.0 mg/kg per min. The rate of glucose uptake did not
  change appreciably when the arterial insulin level was raised further
  to 191 μU/ml.

So, at insulin level 191 μU/ml, there was no greater hepatic glucose uptake than at 55 μU/ml and hence no further stimulation of glycogen synthesis.

According to Emedicine, insulin levels can increase to 276 μU/ml 1 hour after glucose administration.

Which means that even naturally secreted insulin can reach levels that no longer stimulate glycogen synthesis and there is no point to give insulin by injection to stimulate it.


Why are there no Nissl bodies in the axon?

Molecularly, Nissl bodies are the densely clustered ribosomes on the ER. The basophilia is due to the RNA in the ribosomes. The question you have raised is a very significant one. For perspective, I quote a book Fundamental Neuroscience, 2002 (2002 is pretty old for neuroscience!)

The hillock is a region where materials either are committed to the axon (cytoskeletal elements, synaptic vesicle precursors, mitochondria, etc.) or are excluded from the axon (RER and free polysomes, dendritic microtubule-associated proteins). The molecular basis for this sorting is not understood. Cytoplasm in the axon hillock does not appear to contain a physical "sizing" barrier (like a filter) because large organelles such as mitochondria readily enter the axon, whereas only a small number of essentially excluded structures such as polysomes are occasionally seen only in the initial segment of the axon and not in the axon proper.

But a recent paper GG Farias et al. 2015, proposed the presence of a special area in the axon hillock known as the Pre Axonal Exclusion Zone (PAEZ) that tries to explain this polarized sorting by differential binding of microtubule motors.

Although the paper mainly talks of the sorting of axonal and somatodendritic vesicles as seen in the picture, they also seem to apply for the RER which actually are the basis for Nissl's granules.

This structure excludes not only somatodendritic vesicles but also larger organelles, such as the Golgi complex and the rough ER, in effect constituting the cytoplasmic boundary for the somatodendritic and axonal domains..... The exclusion of the rough ER and Golgi complex, in addition to somatodendritic vesicles, at the PAEZ suggests that a common restriction mechanism may operate for all of these organelles.

Well, as you might have understood by now, it's not a matter of the size of the axon/ dendrite since same sized vesicles are being diverted in either direction and as previously mentioned, even mitochondria enter the axon.


What prevents the human intestine from 'exploding' as a consequence of bacteria growth?

Bacteria can't create mass, even when they divide. During division, you go from one "big" bacterium to two "little" bacteria, which then have to accumulate nutrients and grow bigger before they can divide again.

When nutrients are plentiful, this can happen rapidly, and you do see exponential growth. But the exponential growth phase is only valid when there is an excess of food in the environment. Bacterial growth curves follow a typical lag/log/stationary/death profile. The log (exponential) phase only applies when nutrients are in excess. Whenever some nutrient becomes limiting (because it's already incorporated into another bacterium, for example) the bacteria switch to stationary phase growth, and reduce replication or stop it completely.

So you would never get an "explosion" of intestinal bacteria - the bacterial mass is strictly limited to the amount of mass (food) input into the system. Once that's all (or mostly) converted, the bacteria will stop growing and start dying.

If you kept accumulating mass in your intestine, you're correct that eventually it would "explode". However, most people regularly (pun intended) eliminate excess intestinal contents. (Which, as bpedit mentions in their answer, contains a high proportion of bacterial cells.) This limits the total mass contained in the intestine, and keeps it from "exploding".


Does long term use of antibiotics in humans actually lead to a greater risk of infection?

does long term use of antibiotics breed these strains in the bodies of antibiotic users[,] and increase the risk of various bodily infections?

Yes to the first question (although I would use the words select for). No, not usually for the second question in the individual(*), yes in the population.

This should be looked at as a problem in populations of both people/animals and bacterial populations in general. Given time, any living organism will be favored if a mutation involving a selective pressure (like an antibiotic) is introduced, not only in those towards which the antibiotic is directed but also among the normal microbiota. The longer the selective pressure (antibiotic treatment), the greater the probability that a resistant strain of one bacteria or another will develop.

That's why there's a push (in studies) to limit the number of days of antibiotic use necessary to the least number needed which still proves efficient in eradicating an infection. (The trend is towards kill 'em quick and kill 'em all - higher doses for shorter periods, or make it strong and only long enough to cause the extinction of the illness-causing bacteria and not long enough for selection of resistance mutations.)

It is quite normal to have potentially pathogenic bacteria as part of one's microbiome. Usually other beneficial bacteria and conditions keep these in check. But antibiotic resistance, once selected for, can persist for longer periods of time than previously recognized (up to four years in one study). This gives even a small population of resistant bacteria to genetically transfer resistance to others.

Short-term use is less likely to select for resistance in one individual, but, in terms of populations of people, antibiotics are used so ubiquitously that resistant strains will be selected for in shorter treatment intervals by sheer numbers of people being treated.

  When resistant and susceptible organisms compete to colonize or infect hosts, and use of an antibiotic has a greater impact on the transmission of susceptible bacteria than resistant ones, then increasing use of the antibiotic will result in an increase in frequency of organisms resistant to that drug in the population, even if the risk for treated patients is modest. Antimicrobial use and patient-to-patient transmission are not independent pathways for promoting of antimicrobial resistance, rather they are inextricably linked.

"Long term use" in one individual is relatively uncommon and unnecessary, but if necessary, usually does more good than harm to that individual. Almost all (if not all) of the population of the bacteria you're trying to eliminate from one site will be susceptible to the antibiotic and will die, leaving, in a few cases, a few resistant ones that your body can handle naturally, or that can repopulate to "normal" levels without causing illness. But they are then there, the resistant ones, to spread within a population of the individual's microbiome, and the population of people. The next person with a problem, who might have picked up that resistant strain, will not respond well to the same antibiotic. Nor will the patient who was initially treated, if the problem recurs with an antibiotic resistant strain. So, as I said, yes and no.

That's why people (doctors, vets, and - with help - patients) should consider a risk-to-benefit-ratio whenever using an antibiotic. From that standpoint, it is always unethical to use an antibiotic for what is probably a virus, because the benefit to a patient is very small, but the risk - to that patient, who might suffer complications from its use, and to the population if a resistant strain is selected for - is relatively high. Better to wait it out to see if it is bacterial (if one can't test for it directly), and treat it if it does turn out to be. Of course, the risk of not treating in certain populations must also be considered: the elderly, the immunosuppressed, infants, and people with other illnesses or predispositions to infection.

It's not just use of antibiotics in patients/humans that causes problems; its use in any situation can lead to selection for resistance. This is well documented to occur in the meat industry, where a grower often tries to minimize the effect of cost-efficient but insalubrious growing conditions by giving antibiotics to the entire population of meat-animals (beef or poultry) to cut the monetary losses associated with potential illnesses.

It's a multifactorial, and often monetarily driven, problem. Doctors share the blame, but so do patients who demand antibiotics thinking they know better than the doctor, and who will doctor-shop until they find one who will do their bidding, or make a stink for the doctor who refuses. Some doctors still refuse, but they pay a heavy (non-monetary and sometimes monetary) price for doing so.

In the meat industry, it's always a monetarily driven process.

  This review focuses on agricultural antimicrobial drug use as a major driver of antimicrobial resistance worldwide for four reasons: It is the largest use of antimicrobials worldwide; much of the use of antimicrobials in agriculture results in subtherapeutic exposures of bacteria; drugs of every important clinical class are utilized in agriculture; and human populations are exposed to antimicrobial-resistant pathogens via consumption of animal products as well as through widespread release into the environment.

What YOU can do:
Do not take an antibiotic for a viral infection like a cold or the flu.
Do not save some of your antibiotic for the next time you get sick.
Take an antibiotic exactly as the healthcare provider tells you. Complete the prescribed course of treatment even if you are feeling better. If treatment stops too soon, some bacteria may survive and re-infect.
Do not take antibiotics prescribed for someone else.
If your healthcare provider determines that you do not have a bacterial infection, ask about ways to help relieve your symptoms. Do not pressure your provider to prescribe an antibiotic.

Antibiotic resistance: delaying the inevitable
Get Smart: Know When Antibiotics Work
Short-Term Antibiotic Treatment Has Differing Long-Term Impacts on the Human Throat and Gut Microbiome
Antimicrobial Use and Antimicrobial Resistance: A Population Perspective
Comparison of 8 vs 15 Days of Antibiotic Therapy for Ventilator-Associated Pneumonia in AdultsA Randomized Trial
Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria
Industrial Food Animal Production, Antimicrobial Resistance, and Human Health


How does one experimentally obtain a hemoglobin-oxygen dissociation curve?

There are existing instruments commercially available to measure hemoglobin-oxygen saturation curves. Whole blood or lysed blood can be used; I would expect the instrumentation to come with specific directions for sample preparation because it may depend on the exact equipment.

These devices use a spectrophotometer to measure saturation, taking advantage of the same color difference between arterial and venous blood that is visible to the human eye.

To collect a curve, you start with the sample saturated in room air or oxygen, and the instrument gradually introduces nitrogen to replace the oxygen, while also monitoring oxygen concentrations using a Clarke electrode.

Here is an example paper that uses one of these devices. Their precise methods may or may not be appropriate to your research approach.

References

Head, C. A., Brugnara, C., Martinez-Ruiz, R., Kacmarek, R. M., Bridges, K. R., Kuter, D., ... & Zapol, W. M. (1997). Low concentrations of nitric oxide increase oxygen affinity of sickle erythrocytes in vitro and in vivo. Journal of Clinical Investigation, 100(5), 1193.


As far as I remember the pathology course from medical school, chronic long-lasting inflammation often leads to proliferation of connective tussie and ultimately to fibrosis.

The actual mechanism here is the lack of oxygen which is used-up by different immune system cells to produce peroxydes and superoxydes.


Which turtle species was on board the Iranian Space Agency launch in 2010?

Sorry, too big for comment!
It's actually hard to tell, as there is no official claim on this one.

Photo Link: http://youtu.be/nZoNdf6hlII?t=17s
Al I guess is, it can be:

Native breed of Iran like, Spur-Thighed Tortoise (Testudo graeca)

or something like this

(source: deserttortoise.org)
Trachemys scripta elegans


Is there any disadvantage to having a really low adipocyte count in our times?

You mentioned something odd in the tittle "adipocyte count", this was likely a mistake, but I will address it anyway. I recall something about liposuction not being preventative for
   diabetes:

You can have more adipocytes with less lipids in each cell, or fewer
   adipocytes with more lipid in each cell. Hypertrophy vs hyperplasia, just like in the question you asked on muscles elsewhere on this forum. Anyway, when a patient gets liposuction they decrease the number of
   adipocytes. Then if s/he gains the weight back the size of their
   individual adipocytes will be larger than it was before the
   liposuction. Somehow this was bad, and it increased insulin resistance. in a way, decreased "adipocyte count" is dangerous.

here is the other, obvious stuff on endocrine function of adipose tissue that you surely already know since your profile is very endocrine based, but anyway, here goes:

Adipose tissue has hormonal functions, secreting horomones (leptin, adiponectin, and resisting... these modify appetite as well as insulin resistance) and modifying them (converting testosterone to estrogen vi the enzyme aromatase).

The adipose-derived hormones are quite mysterious to me, I don't know much about them. The effects of the aromatase in adipose tissue are more obvious:

men will have increased estrogen levels (for example leading to gynecomastia aka man boobs, as a chubby guy I know this all to well)
women will have higher estrogen which will stimulate LH secretion from the pituitary stimulating theca intern cells in the ovary which will increase testosterone levels. The condition in women is known as PCOS.

In a person with little adipose tissues, there will be less conversion of testosterone to estrogen, so men will have less estrogen. Women will also have less estrogen, and less testosterone, aka they will not have PCOS in those women that already have PCOS, but thats not saying much :)

I may be wrong on some of this information, anyone please correct me.


Are gene variants at different loci also called alleles?

EDIT:
Short answer : Yes: "allele" is a synonym for "gene variant", irrespective of location (locus).

Background
Original answer: From About Education I found this definition for an allele:

  An allele is an alternative form of a gene (one member of a pair) that is located at a specific position on a specific chromosome.

EDIT:
Hence, two alleles are located at the same locus, but are situated on a different chromosome.

ADDITION EDIT: Given the many high-quality comments (and the downvote) I erased the concluding sentence of my first attempt and I will elaborate below:

Feero et al. (2010) gives the following more elaborate definition of "allele" (text relevant to the question is bolded out):

  Specific locations in the human genome where differences between individual people
  are found are generally referred to as variations, and the term “normal” or “wild type” is often used to refer to the most common variant at a location in a given population group. In its simplest form, the variation has two different spellings, referred to as “alleles.” If the frequency of the minor allele is greater than 1%, such variants are called polymorphisms. The word “mutation” is generally reserved for changes in DNA that are believed or known to be pathologic [...] or for changes that are [very] recent (e.g., not inherited DNA changes).

Hence, from my understanding, the original quoted definition from About Education still stands.

As to the critical comments placed by the PO, @fileunderwater and @WYSIWYG:

(1) [...] what is a copy or a variant of a gene at a different locus on the same chromosome? - That is a very interesting question, and I think Feero et al. (2010) deals with that simply by saying

  In its simplest form, the variation has two different spellings, referred to as “alleles.”

In other words - perhaps the gene duplication is a step too far for this terminology. And in fact, although I regret having to cite wikipedia here, it does provide a very enlightening sentence:

  [...] [A]t the gene locus for the ABO blood type [...] classical genetics recognizes three alleles, IA, IB, and i, that determine compatibility of blood transfusions. Any individual has one of six possible genotypes (IAIA, IAi, IBIB, IBi, IAIB, and ii) that produce one of four possible phenotypes [...].

Hence, what this implicitly tells us is that an allele is, as Feero et al. (2010) also says, simply a gene variation.

This means that it basically boils down to what is a "chromosome locus"?

An article by Proulx & Phillips, 2006 entitled "ALLELIC DIVERGENCE PRECEDES AND PROMOTES GENE DUPLICATION" mentions:

  [...] [H]eterozygotes at a single locus are broken up by segregation, whereas for duplicate loci an individual can carry copies of alternative alleles at separate
  loci.

Hence, what the authors implicitly say is that an allele is a gene variation and that a locus is a fixed position on a chromosome. Hence, a gene duplication means 2 loci that can carry the same or a different allele. This should answer

(2) Are the alleles at the two duplicated loci then named differently, even if their DNA sequences are identical (as well as the protein they might be coding for), namely no, an allele has a name (e.g. IA) that remains unchanged when duplicated. The locus is then different for the duplicate, but the name of the allele stays the same (as an allele is, by definition, simply a gene variant wherever on the chromosome).

(3a) [...] two versions of a gene at two different loci are alleles (not paralogs)?: yes

(3b) What about the same identical version at two different loci: same allele or not? yes, same allele, allele has nothing to do with locus. Just a gene variant. Where ever.

Reference
Feero et al. N Engl J Med 2010;362:2001-11
Proulx & Phillips. Evolution 2006;60:881-892


Pores don't change size; that is, the diameter of pore does not increase or decrease in hot or cold environments. Your skin, where pores are located, is not muscle but an organ so the pores don't contract or expand.

Pores can become clogged with dirt, oil, and debris (make up). When pores are clogged, you are more inclined to notice which would cause the illusion that the pore is bigger.

  It's important to know that you can't actually "shrink" your pores. They're nothing but small openings in the skin -- because they don't have muscles, they can't open or close. So although you can't physically change the structure of your pores by making them smaller, there are things that you can do to minimize their appearance$^1$.


Measuring transgenic gene expression with a microplate reader

Spectophotometry

Does the photometer allow using different wavelengths of light? Perhaps using a spectrophotometer might give you a control and your desired value, i.e. blue light may be absorbed by your sample, but red might not? The absorbance spectrum of the molybdenum-blue complex is very specific and you could use this to your advantage using spectral photometry.

Photometry + correcting for absorbance due to cell growth

Another approach is to quantify over time how your bacteria affect absorbance as a function of time and then subtract this from your experimental values.  For example, in a wellplate, place the following adjacently: use a (i) well without cells, and only arsenite in solution, (ii) cells without arsenite, and (iii) cells with arsenite. This should allow you to quantify quite accurately how much the arsenite, the cells, and how much both affect absorbance.

Of course as you say there may be an interaction between the cells and the arsenite slowing or speeding up cell growth, so that would be a pickle to disentangle. You could try, perhaps in the wellplates (this would be best!), to find out what effect arsenite has on growth and correct your final data this way.

Periodically sampling the solution; removing bacteria from the measurement

Another idea would be to culture your cells in arsenite, and take samples to obtain time-points. For each sample, you filter using small syringe filters (these are cheap and are typically used for sterilizing solutions, i.e. getting rid of bacteria but keeping the solution, given their pore size of ~.1 microns) and then perform photometry for the molybdenum-blue complex. This is typical practice in microbiology.

PCR? An idea.

Last but not least, it's good to remember this is an indirect readout of transgenic gene expression. Similarly, you could use quantitative PCR to quantify the expression of any transgenes - here, you use housekeeping genes as controls for cell number, and the mRNA expression of your transgene as the readout. You would be reading out the expression of mRNA, but I personally don't think it would be more 'indirect' than measuring arsenate concentrations in solution, especially when there are confounding factors and awkwardness in getting a clean measurement. The PCR approach would be quite accurate and likely more reliable.

These are just some initial thoughts - perhaps you could add a comment or we could chat about this if you think it could spark up some concrete ideas!


The nature of time has been discussed for millenia. We don't know exactly why or where time perception exists, but we do have some information on how it is perceived.

The circadian rhythm is basically in place to help us sleep, wake and perform tasks in a 24 hour cycle of light. Robbed of light, and the melatonin it's absence produces, the rhythm shifts considerably.

Vision is a powerful cue for the passage of time. Bees have an extremely sophisticated ability to predict the sun's location at a given moment (they can count the moments). While I doubt the same is true for humans, our eyes give us a great deal of information about the passage of time: the time in a 24 hour period (the position of the sun, moon, stars, shadows, etc), and the time in a year, the time in a lifetime. Witnessing the passage of time, according to physicist Paul Davies, we observe how the “later states of the world differ from earlier states that we still remember.”

Besides the important input from our eyes and memories, we also have internal timekeepers.  A study decades ago on short order cooks (I can't seem to find it) found that an experienced cook can keep internal time to the second, and can keep multiple "stopwatches" going in his head: the scrambled eggs, the toast, the pancakes, the grilled cheese sandwiches all take a certain amount of time, and short order cooks can tell when that time has passed with extraordinary precision.

The fact that the fluids flow at different rates tells us that we perceive time differently under different circumstances. Time perception is surprisingly prone to measurable distortions and illusions.

  The importance of our temporal experiences for daily living is strikingly documented in individual neurological cases where patients report of an accelerated progression of time and, consequently, have troubles in adequately interacting with the environment, i.e. driving a car. Psychological research has shown that cognitive functions such as attention, working memory as well as long-term memory determine our temporal judgements. Moreover, drive states, moods and emotions, as well as factors of personality influence duration estimates. For example, time intervals are judged to be longer when we pay more attention to time and when the load of varying experiences stored in memory is higher. Our subjective well-being also strongly influences how time is experienced. Time speeds up when we are involved in pleasant activities, but it drags during periods of boredom. Thus, our sense of time is a function of the intricate interplay between specific cognitive functions and of our momentary mood states.[1]

Where exactly time is perceived by the brain is unknown, but several areas keep appearing, most prominently, the cerebellum, the right posterior parietal cortex, the right prefrontal cortex, as well as fronto-striatal circuits. All have been implicated as the neural substrates of a potential timekeeping mechanism. The inner experience of time[1] gives a broad overview. The conclusion is worth reading.

To further support that the where is not known, consider the following:

  Studies done in humans also support the hypothesis that striatum and its afferents are involved in interval timing. Recent fMRI data showed that timing network could involve cortico-striatal loops, including premotor and supplementary motor areas, frontal operculum and dorsolateral prefrontal cortex, and temporal and parietal cortices, as well as the putamen. Imaging studies in humans, lesion studies in humans and rodents, and drug studies in rodents all point towards a central role of the basal ganglia in interval timing. The anatomy of the basal ganglia suggests that information is proceeded through cortico-striato-thalamic loops. Severe deficiencies in reproducing temporal intervals were also found in Parkinson’s patients, therefore, further supporting the hypothesis of basal ganglia involvement in interval timing. There are also lesions data suggesting that the timing network is much widely distributed. Lesions of the nucleus basalis magnocellularis, a cholinergic nucleus in the basal forebrain with projections to the frontal cortex, induced a progressive, proportional, delay in peak time response (memory pattern). This effect is believed to be related to altered temporal memories [42,43] due to change in acetylcholine (ACh) level. Lesions of the frontal cortex produce similar memory patterns, whereas lesions of the hippocampus or fimbria fornix, a basal forebrain cholinergic nucleus with projections to the hippocampus, result in memory effects translated into an advance of the peak time response. These experimental findings undoubtedly support the hypothesis of a distributed interval timing neural network.[2]

For a fun but non-scientific look at time, the NYT has written an understandable article.[3]

The final answer is that no one knows for sure.

The Experience and Perception of Time
1 The inner experience of time
2 Why noise is useful in functional and neural mechanisms of interval timing?
3 Where Did the Time Go? Do Not Ask the Brain
 Time and the Brain: How Subjective Time Relates to Neural Time
Human time perception and its illusions


The energy used to catalyze the peptidyl transferase reaction is from the breakage of the bond between the amino acid in question, and the aminoacyl-tRNA it's attached to. The two reactions are coupled by the ribosome. The ribosome can then lower the entropy by positioning of the molecules (including water) in the active site as described here.

So we have our reaction ΔG = ΔH - TΔS

Your ΔG is positive because your reaction is endergonic, and the ΔH is positive because the peptide bond is the system, and you're absorbing energy to form it. The entropy is decreasing as such (removing enerygy = removing heat from outside the system), and the actual reaction for the formation of a peptide bond is unfavorable. As I mention above, this unfavorable reaction is coupled to a favorable reaction in the hydrolysis of an aminoacyl-tRNA to make it possible. What I forgot to mention above is that the ribosome is making this more favorable as well by decreasing the activation entropy for the reaction, and that's what they describe in the linked journal.


No, it's not. There are common plants that can only reproduce asexually.

It's likely you can buy produce from several plants which are unable to do so at your local supermarket. The most famous example is, of course, the banana which is a sterile mutant and all bananas of a particular variety are clones, but some seedless varieties of grapes and oranges would also count (although most seedless fruit you find in the supermarket are actually produced with hormonal treatments rather than being asexual varieties).

These plants are examples of artificial selection but there are also examples of plants that have lost the ability to sexually reproduce in the wild. The evening primrose is a good example, with some 30% of species in the genus Oenothera having evolved to be asexual (Hollister et al, 2015), but this is not the only example. It is likely that, just as in animal species, asexuality has short (on an evolutionary timescale) term advantages but results in lower fitness in the longer term.


Kidney failure → Inhibition of Na+/K+ pump → Heart failure

Hyperkalemia (too much blood K+) caused by kidney failure is because the kidney is not clearing excess K+, and most K+ excretion is by the kidneys. Usually kidney failure alone isn't sufficient to cause hyperkalemia (Lehnhardt and Kemper,
 2011), and note that kidney failure can cause problems via many other mechanisms besides hyperkalemia.

The reason that hyperkalemia causes problems with heart and other muscle function isn't directly because of the Na+/K+ pump, but because of how the electrical potential of cells controls contraction. Cardiac myocytes, like most cells, have a negative resting potential, with high K+ inside and low Na+ and Ca2+ inside, and a resting conductance that is higher for K+ than the other ions. When the cell is depolarized to around -40mV, a rush of Na+ and Ca2+ comes in that further depolarizes the cell and also causes the muscle contraction.

Normally, this "action potential" is terminated by opening K+-channels, which returns the cell to a hyperpolarized/resting state by letting K+ ions flow out, ready to fire another action potential and contract again. However, the resting potential is determined by the Goldman equation and depends on the concentration of each ion both inside and outside the cell. The reversal potential for K+ depends on there being a lot of K+ inside the cell, and very little K+ outside the cell. Therefore, it takes a large negative potential to keep K+ in equilibrium. As the K+ concentration outside the cells increases, the equilibrium potential for K+ gets closer to 0 mV. Eventually, cells can't repolarize after contraction and effectively stay in "contraction mode" without relaxing.

Although the Na+/K+ pump is somewhat dependent on the concentrations of Na+/K+, the typical role for that pump is to push K+ ions into cells and pull Na+ ions out. If blood K+ is high, that will not do anything to prevent the Na+/K+ pump from operating, so suppression of that pump is not having any mediating role in this process.

As a side note, KCl is used in lethal injection in the United States as the final drug administered, which stops the heart by causing immediate hyperkalemia.


Why do frogs and toads only appear when it is dark outside?

I see them,( or their ripples after they jump into the water ) during the day; I have 2 small ponds in the yard. I see tree frogs in my patio plants during the day but they are sleeping. The frogs/toads certainly make more noise when it rains ,has rained, or is going to rain. even during the day. They are certainly more active at night . I expect more bugs around then . I only see the geckos at night ,near the lights.


Why do home-grown fruits tend to taste better than mass-produced consumer fruits?

"Industrial" fruits and vegetables are not grown as much for flavor as for convenience, pest resistance, appearance, resistance to peel problems, resistance to bruising, etc. etc. Profitability is the main consideration.

There are many varieties of apple grown in orchards that taste wonderful (better than my grandmother's gnarly green apples) but don't hold up to shipping and storage well.

Finally, please don't get your information from fantasy tales. There are so many good sites for attaining information.


Why do antidepressants have a delayed onset of action?

Short answer
The mechanism of action of serotonin-specific reuptake inhibitors, a commonly-prescribed class of antidepressants, is a downregulation of 5HT1A receptors through negative feedback. This downregulation of receptors takes time.

Background
Serotonin-specific reuptake inhibitors (SSRIs) are a class of antidepressants commonly prescribed to treat depression. Their therapeuric effects may need weeks of treatment (Celada, 2004), which can be explained by their action on 5HT1A receptors in the dendritic region of the serotoninergic neurons in the raphe nucleus. By blocking serotonin (5HT) reuptake, negative feedback mechanisms cause the 5HT1A receptors to downregulate. This downregulation of the presynaptic modulatory 5HT1A receptors changes the firing pattern of the serotonergic neuron into a more fluttering mode, so that it releases more 5HT (Duman, 2007). More 5HT makes you feel better. That is how it fits into the monoaminergic hypothesis. To have the 5HT1A receptors respond this way takes time, as it is an adaptive response that downregulates of 5HT1A receptors, i.e., less receptors are present on the cell's membrane.

This is only an expanation of delayed action of SSRIs, a specific subclass of antidepressants. For example, there are newer classes of antidepressants that seem to work faster (5HT4 action) (Duman, 2007).

References
- Celada et al., J Psychiatry Neurosci (2004); 29(4): 252–65
- Duman, Neuron (2007); 55(5): 712-25


Does a tubular sodium reabsorption cause a stimulation of β2-adrenergic receptors?

You've got it backwards. "norepinephrine-induced tubular sodium reabsorption" is the whole process. The β2-adrenergic receptors respond to norepinephrine (this is the "norepinephrine-induced" bit). The receptors then suppress WNK4 in the distal tube ("tubular"), which causes the Na-Cl cotransporter to activate, which in turn causes sodium reabsorption.

This was probably a poorly phrased sentence on the part of the writers, but the sentence follows the same logic as "According to the First Law of Thermodynamics, energy cannot be created or destroyed". The description of the process is just complicated by multiple clauses.


What would classify those findings of the University of Sheffield experiment as aliens?

I wouldn't say that there is an established protocol - claims of alien life are not commonly testable or even legitimate - but if something were discovered and deemed "alive," a fairly good sign it was alien would be if its genetic makeup were based on something other than DNA or RNA.  That would be a dead giveaway the organism had side-stepped every known organism on Earth and while that doesn't prove alien-ness, it would certainly hint strongly of a non-Terran genesis.  There are arguments for and against carbon/CHNOPS-based life but that is nowhere near as definitive.

Also, there's another really good technique.  I don't like to resort to ad hominem attacks, but ideally the discovery should be by someone who has not already made verifiable false claims on the same topic.


Are there tools for automatically parsing glycan names into tree structures?

Edit: C# Functions used in our system, slightly paired down for to simplfy

using Microsoft.VisualBasic;
using System;
using System.Collections;
using System.Collections.Generic;
using System.Data;
using System.Diagnostics;
using System.Web;
using System.Net;
using System.IO;
using System.Text.RegularExpressions;

public class KEGGCaller
{
    public object ReturnKEGGgif(string GlycanMonoCode, System.Web.HttpServerUtility HTTPUtilityHolder)
    {

        string CallURL = "http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=";
        string GlycanURL = HTTPUtilityHolder.HtmlEncode(GlycanMonoCode);
        WebClient wc = new WebClient();
        System.Drawing.Image GlycanGif = default(System.Drawing.Image);
        CallURL += GlycanURL + "&mode=bfind&max_hit=1";
        StreamReader reader = new StreamReader(wc.OpenRead(CallURL));
        string Gcode = FetchGcode(reader.ReadToEnd());
        if (Gcode == "Failed") {
            return 0;
        } else {
            System.Net.HttpWebRequest Request = default(System.Net.HttpWebRequest);
            System.Net.HttpWebResponse Response = default(System.Net.HttpWebResponse);
            Request = System.Net.WebRequest.Create("http://www.genome.jp/dbget-bin/www_bget?gl:" + Gcode + ".gif");
            Response = (System.Net.WebResponse)Request.GetResponse;
            if (Request.HaveResponse) {
                if (Response.StatusCode == HttpStatusCode.OK) {
                    GlycanGif = System.Drawing.Image.FromStream(Response.GetResponseStream);
                    return GlycanGif;
                } else {
                    return 2;
                }
            } else {
                return 1;
            }

        }

    }
    public object FetchGcode(string PageBlock)
    {
        string MatchURLString = "?gl:G\d\d\d\d\d";
        Match URLMatch = Regex.Match(PageBlock, MatchURLString);
        if (URLMatch.Success) {
            return Strings.Right(URLMatch.Value, 6);
        } else {
            return "Failed";
        }
    }

}

Remainder of the Answer

Biomodels.Net is a great resource to begin with and familiarize yourself with the field and get ideas of how to tackle your qualification needs.  We used it when we were doing drug screens.

More specifically for glycans, you're going to be looking at KEGG.  Then use KEGG draw for your visual application.  If you actually just want to parse them, here is the table on the monosaccharides used (most places).

Here's a better link right to the download in case you didn't find it.  The script we wrote was pretty simple, here is the basic logic.

Start with the monosaccharide code.

Call a single return of DBGET to GenomeNet pulling from KEGG Glycan.  For example:
(GlcNAc)6 (Man)3 (Asn)1
would be called:

 http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=%28GlcNAc%296+%28Man%293+%28Asn%291&mode=bfind&max_hit=1

Where http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords= and &mode=bfind&max_hit=1 are going to be constant and the middle part is going to be your search.

You need to change your monosaccharide to standard URL ASCII Reference, concatenating each monosaccharide with a "+".  Thus (GlcNAc)6 (Man)3 (Asn)1 becomes %28GlcNAc%296+%28Man%293+%28Asn%291.

That will give you one hit with the link to your exact match if there is one.  There will be one link on the returned page in the format of http://www.genome.jp/dbget-bin/www_bget?gl:G#####, where G##### is your glycan number (in our example G00021).

Once you have the glycan number you're good to go.  All of the structure images can be found at:
http://www.genome.jp/Fig/glycan/G#####.gif

And then you just download your GIF.  The way we did our batches was to do each step for all the hits then move to the next step.

Hope that helps more.


How do you call "pocoya" bird in English?

I have done some reading based on your descriptors of the bird and your examples, the bird in question is a nightjar and I think they are referring to the Common Paruaque. All nightjars fit your first 2 points, the 3rd point is the only clue we can use to determine what species of nightjar you are describing. There are 11 species of nightjar is Nicaragua.

It seems the Common Pauraque (Nyctidromus albicollis) is commonly known as the "Pocoyo" in spanish, but the spelling may not been certain. Here's a quote from page 9 of an article on the birds of Nicaragua from 1957:

"The species is known in Nicaragua as “Pocoyo” (exact spelling uncertain)".
Reference.

The other bird you describe, the Ocellated Poorwill (Nyctiphrynus ocellatus) is referred to as the "Pocoyo ocelado".

The only other nightjar that might be called Pocoya is the Common Nighthawk (Chordeiles minor), but it is referred to as "Anapero".

I believe when referring to "Pocoya" it is most likely the Common Pauraque as the Ocellated Poorwill would have another descriptive word in it's name in spanish.


Why do oranges in the US have a small separate part?

This is specific to navel oranges, which have a conjoined twin fruit.

This blog gives an account of this.


Why do humans seem to be the only mammals that like spicy food?

I think like many things spicy food became something that we used as a tool. Used mostly for preserving food, those countries where it gets very hot due to a tropical climate you'll find the food tends to be much spicer in areas where parasitic flies and other pathogens would contaminate the food faster. The spicier it is, the longer your food stocks would last. Over generations they developed a higher and higher tolerance.


Animals and especially female animals might not "want" to reproduce when circumstances are bad for babies.  Pregnancy and rearing of infants is a big commitment of resources for female mammals.  If a female is under stress, or sick she might avoid having sex even though she could get pregnant because evolutionarily that was a winning strategy for her ancestors - committing the physical and nutritional resources to a pregnancy and fetus unlikely to survive current circumstances puts the mother and subsequent pregnancies at risk.

A more extreme example is the Bruce Effect.  Pregnant females exposed to the pheromones of a strange new male "decide" not to reproduce - their bodies resorb the fetuses.  Presumably this is because the new male is a risk to the fetus and they would do better calling off the doomed project, and possibly having a new litter with the new male if he shows up.

Weirder is the circumstance of parents that kill and sometimes eat their young.  That happens in mammals, birds, fish and others.  It is hard to see how this sort of thing advances genetic fitness - it seems like a crossed wire or misfire of some sort.  Certain animals, however, seem to do it all the time; hamsters come to mind.  Maybe stress causes weird behavior?  In any case this too would seem like a case of deciding not to reproduce.


I don't think this will work. Grafting will usually work between the same species and sometimes between the same genus. You're talking about grafting Philodendron cordatum to Quercus robur. The former is a tree from Europe, the latter a flowering plant from Brazil. They aren't compatible in the slightest. The graft will never take.

One possible route you might want to consider that may be more successful, but a lot more difficult, is using agrobacterium tumefaciens to infect a mix of cells from the two species. If you have a homogeneous mix of individual cells in culture, infect it with A. tumefaciens, the resulting gall will contain cells from both (incompatible) species. How they grow from there is unknown.


Troubleshooting for Agarose Gel Electrophoresis

I haven't found a manual for this machine, but my guess is that you exceed the maximum current which the power supply can provide. This is something I have experienced myself for electrophoresis.

Usually power supplies then switch into the constant current mode at the maximum current they can deliver, which I think is what happens here. If the voltage you choose is lower, you do not run into this limitation, thats why it is working without problems.

So you can either run your gels at constant current, which makes them run faster but also produces more heat, which can make your gel blurry. Or you live with a slightly smaller constant voltage, have your gels run a bit slower, but probably have a bit better resolution. I have to say that I have never had any problems with the resolution, even when I ran my gels really fast.


When did mouth pipetting stop becoming a way to handle liquids in a lab?

Mouth pipetting, while almost unheard of in modern laboratories in developed countries, is still very much a current protocol in many parts of the world.

For example, this paper analyses the proportion of clinical labs in Pakistan and found evidence of poor biosafety practices (emphasis mine):

  Results: A total of 1,647 (92.4%) males and 135 (7.6%) females
  participated in the study, with over half (59.7%) having more than
  five years of work experience. Results showed that 28.4% of the
  laboratory technicians from Punjab, 35.7% from Sindh, 32% from
  Balochistan and 38.4% from Khyber Pakhtoon Khawa (KPK) did not use any
  personal protective equipment. Almost 46% of the respondents (34.2%
  from Punjab, 61.9% from Sindh, 25.2% from Balochistan and 85% from
  KPK) said they reused syringes either occasionally or regularly.
  Furthermore, 30.7% of the respondents said they discard used syringes
  directly into municipal dustbins. The majority (66.7%) claimed there
  are no separate bins for sharps, so they throw these in municipal
  dustbins. Mouth pipetting was reported by 28.3% technicians.

Additionally, a Google Scholar search for papers published in the past 5 years involving mouth pipetting turned up 670 hits out of 284000 total hits, a proportion of 0.23%. This is further evidence that this dangerous technique has not been fully eradicated from labs.


If the haploid prothallium of a fern fertilizes itself into a diploid sporophyte, does this make all ferns clones?

No, it would not be accurate to label them clones, and the organism still goes through sexual reproduction even if they are selfed. Selfed offspring would get two copies of the "same" chromosome (when selfed within the same prothallus), when the parent might have two chromosomes of different origins, and there will also be recombination during meiosis (during spore production in the sporangia), which will alter the chromosomes. And even if all selfed offspring from the same prothallus will carry that same chromosomes, different prothalli from the same parent will carry different chromosomes, which means that all offspring will not be identical. So to label selfed ferns as clones wouldn't be accurate, since the offspring wouldn't be genetically identical to their parents and offspring from different prothalli would also not be genetically identical. The situation is similar to e.g. monoecious plants that lack self-incompatibility (especially those pollinated by wind), where selfing will be common. The difference in ferns is that all gametes on the same prothallus will carry the same chromosomes.

Also note that some ferns have mechanisms to avoid self-fertilization, and that many species have a mixed mating strategy that allow both selfing and outcrossing, usually with higher fitness in outcrossed individuals.


Thickness / size / volume of a macrophage

BioNumbers is a good database for different values (numbers) in biological systems. From BioNumbers*:

Volume of an alveolar macrophage ( Homo sapiens ) = 4990 (±174) µm3

Diameter of an alveolar macrophage ( Homo sapiens ) = 21.2 (±0.3)  µm

So, your thickness should be (assuming a circular shape of the cell):

Volume/(pi×(0.5×diameter)2) = 14.15 (±1.52) µm

Apparently, the size of the alveolar macrophages varies a lot between different species.

  The AM from humans were significantly larger (p < 0.05) than those
  from all other species studied, corresponding to a 4-fold larger cell
  volume of human AM (4990 +/- 174 microns 3) compared to hamster (1328
  +/- 123 microns 3) and rat (1166 +/- 42 microns 3) AM

*
The paper that BioNumber refers to is this:
Krombach, Fritz, et al. "Cell size of alveolar macrophages: an interspecies comparison." Environmental health perspectives 105.Suppl 5 (1997): 1261.


How does allele dominance work in polyploid organisms?

Dominance works in the same way.

However, polyploids have complex inheritance patterns!

1. Punnett square for polyploid inheritance

  One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.

The table you mentioned in this case should be the Punnett square. And its two dimensions correspond to two types of gametes that fuses in sexual reproduction. So even if you want to utilize Punnett square to work with tetraploids, hexaploids, or even octoploids, you still use a two-dimensional table because there are only two types of gametes involved. The fundamental difference is that you have to assign combinations of alleles to the first row and first column of the table instead of a single allele as you would do with a monohybrid cross.

However, deciding what combinations are allowed will be really intricate in this case, depending on two different factors: pairing behavior during meiosis and the resulting chromosome segregation. Variations in those aspects make general rules for polyploid inheritance impossible. In extreme cases, we can consider the organism to be either fully autopolyploid or allopolyploid.

An autopolyploid has more than two complete copies of the genome of a single ancestral species, and in the extreme case we consider the chromosomes have multivalent formation during meiosis and undergo unbiased segregation.

An allopolyploid has more than two complete copies of the genome derived more or less complete from different species, and in the extreme case we consider the allopolyploid has strictly bivalent formation between the chromosomes of a common origin.

This is a monohybrid cross, and it seems familiar and boring, right?

The following pictures depict how to use Punnett square with a tetraploid with two different alleles at a certain locus, and they are really captivating...

In this final picture you may find that the cross has "degenerated" into a monohybrid cross. If we try to depict something more complex, like a tetraploid with four different alleles at a single locus, we will obtain resultsvery different from normal crosses for diploids.

2. Dominance in polyploids

  One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.

This is true based on the definition of dominance:

  Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus.

3. Recessive traits in polyploids

  One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.

For this one, you cannot simply assume it because as I've said above, the inheritance patterns for polyploids, including octoploids, can be really complex and dependent on the particular species and the multivalent formation at the particular gene locus you wish to investigate. Thus, it's difficult to predict the the portion of individuals with a recessive phenotype in a population. There are so many intermediate patterns between two extremities of autopolyploidy and allopolyploidy that geneticists have to rely on sophisticated computational models to help them explain the data collected from experiments!

Source:

Rieger, R.; Michaelis, A.; Green, M.M. (1968). A glossary of genetics and cytogenetics: Classical and molecular. New York: Springer-Verlag.
Soltis, Pamela & Soltis, Douglas. (2012). Polyploidy and Genome Evolution. 10.1007/978-3-642-31442-1.


Text/resource with information on all skeletal muscles and their motor units

You can try Biomechanical models used in software frameworks such as OpenSim.

Here is an example of a combined upper and lower body model in XML: ULB_Project.


Can Naegleria fowleri enter through your ear?

Ears? No. The tympanic membrane (eardrum) is a watertight barrier between the outer ear and middle ear.

  Exposure to the organism is extremely common due to its wide distribution in nature, but thus far lacks the ability to infect the body through any method other than direct contact with the olfactory nerve, which is exposed only at the extreme vertical terminus of the paranasal sinuses; the contaminated water must be deeply insufflated into the sinus cavities for transmission to occur.

In short: Don't huff warm lake water too deeply through your nose, and you'll probably never get it.

You shouldn't find it in your stool. Other amoebic infections can be found in your stool, as they can attack the lining of your intestines, but Naegleria, specifically, will reside in your sinuses and brain until you die or receive treatment.


How does the embryo inside a shelled egg get oxygen?

The key point in both cases is that the eggshell and membrane are permeable to oxygen, as you thought. There are subtleties - for instance, the oxygen-permeability of avian (hard-shelled) eggshells changes during development.

In the case of eggs laid underground, as in sea turtle eggs, the leathery shell is still permeable to oxygen. The sand restricts oxygen flow, but turtles seem to take care to not bury their eggs too deep for oxygen to diffuse to their developing nest.


Peach pits with two seeds: Are the seeds identical twins?

Polyembryony occurs when a single fertilized egg produces more than 1 embryo. This is the process that produces genetically identical twins.

Although polyembryony is common in some plants, I found limited information about polyembryony in peaches. I decided to broaden my search into drupes more generally. Drupes or "stone fruits" are the fruits with a fleshy outside (exocarp and mesocarp) and a hard inner shell (endocarp) around typically a single seed. Peaches are part of this category, as are almonds (the almond itself is the inner seed), cherries, and coffee.

The best citations I found reach back into history a bit.

From Webber, J. M. (1940). Polyembryony. The Botanical Review, 6(11), 575-598.:

  Cases of the first class of false polyembryony
  commonly occur in such drupes as almonds, plums and peaches.
  Although these drupes normally have a single seed within the hard
  seed-like endocarp, sometimes two or even three are found. ' During
  formation, each of the plural seeds develops from a separate
  ovule, provided with a separate funiculus and micropyle. Similar
  cases of such false polyembryony have recently been reported in
  Coffea (63) and Sandoricum (47, 49).

This passage would suggest that most likely what you are observing is false polyembryony. Immediately prior to this passage, the "first class" refers to:

  those in which more than one ovule develops in a normally 1-ovulate seed-like structure or locule

as contrasted with the second type:

  occasionally two of the developing ovules unite to form what appears to be a single composite ovule.

Another source, Zdruikovskaya-Rikhter, A. I. (1970). The phenomenon of polyembryony in the peach. Tr. Nikitsk. botan. sad, 46, 173-177. is in Russian and only available to me in abstract form in English. The abstract reads:

  In a number of varieties, two and sometimes three megaspores were functional, giving rise to several embryo sacs. On fertilization, embryos develop in these, causing the phenomenon of pseudopolyembryony.

Therefore this source seems to agree with the first.

However, a more recent paper Martínez-Gómez, P., & Gradziel, T. M. (2003). Sexual polyembryony in almond. Sexual plant reproduction, 16(3), 135-139., focused on almonds, suggests that certain almond cultivars are prone to true polyembryony, though it seems like the additional seeds are often a bit stunted and have high mortality. They also reference a paper purporting to mention polyembryony in peach, Toyama, T. K. (1974). Haploidy in peach. HortScience, 9, 187-188., though I cannot find this article in anything but Japanese - the title, however, suggests that these may be haploid polyembryos, which also occur with the almonds - these are indeed from division of the same embryo, but because they are haploid they would not actually be genetically identical, since each is taking half of the diploid chromosomes.

With only these limited descriptions to go by, which seem to be mostly observational rather than backed by any systematic study, I would hesitantly conclude that most likely what you are seeing is a fruit in which two separate ovules developed together, and therefore could be as genetically different as any two different peaches from the same tree. True polyembryos seem to be possible in stone fruits, but as a mostly rare occurrence that is only common in particular strains - when it does occur, it may be via haploidy, which means the seeds will still be genetically distinct.


What is the role of gills in terrestrial Crustaceans?

Short answer
Gills in terrestrial crabs serve a role in water storage and ion homeostasis.

Background
Crustaceans are a huge group of species within the phylum of arthropods, including crabs, lobsters, crayfish, shrimp, krill and barnacles. Because of the huge variety of species within the crustaceans, I'll focus this answer on terrestrial crabs.

Air-breathing crabs have universally retained gills, but have also developed accessory breathing organs, usually lungs formed from the inner lining of the gill chamber. Aquatic crabs generally have large gills with very thin closely packed lamellae. Land crabs feature lungs that are well vascularized, have short blood-gas diffusion distances and often have adaptations to increase surface area, all of which greatly increase the diffusing capacity of the respiratory
system (Farreley & Greenaway, 1994).

In contrast, the gills in land crabs  are reduced in size and in surface area. The epithelium is usually modified for ion transport as indicated by the presence of densely packed mitochondria and relatively long blood/gas diffusion distances. Hence, the gills in land crabs are thought to primarily serve an osmoregulatory role, rather than a gas-exchange function (Farreley & Greenaway, 1994). The gills are thought to be involved in salt and water uptake. Their spongy structure is thought to aid in their function as water storage areas in periods of molting (Edney, 1977).  However, the gills in many species are still capable of gas exchange, although less efficiently than the lungs (Farreley & Greenaway, 1994).

References
- Edney, Water Balance in Land Arthropods, Zoophys & Ecology, Springer, New York (1977); 9
- Farreley & Greenaway, J Exp Biol (1994); 187: 113–30


How are 6 "fixed" CO2 molecules joined toegther as glucose?

It's not really possible to break it down this way. The CO2 fixated by the RUBISCO enzyme generates two phosphoglycerate (2 x 3C) molecules from one ribulose bisphophate molecule (5C), while the rest of the Calvin cycle serves to regenerate 3 ribulose bisphophate from 5 phosphoglycerate. Hence, one 3-carbon sugar (glyceraldehyde phosphate or dihydroxyacetone phosphate) can exit the cycle for every 3 CO3 captured. The regeneration of ribulose bisphosphate involves several enzymes, and the stoichiometry is rather complicated; it would take an entire essay to describe it all. I suggest you look the calvin cycle in the metacyc database, it's a nice interactive resource where you can explore all the details of the reactions. Wikipedia also provides some details on these reactions.

The glyceraldehyde phosphate produced by the Calvin cycle is then converted to glucose and other sugars by the enzymes of gluconeogenesis. The key enzyme is fructose diphosphate aldolase (or simply "aldolase") which condenses glyceraldehyde phosphate and dihydroxyacetone phosphate to one fructose-1,6-diphosphate. A chart of the pathway leading to other sugars is found here.


They are vital if not incredibly useful in many other mammals but not humans. People have tried to look for a role and seen that they activate in times of stress or anxiety. However this probably only serves to heighten both stress and anxiety as you now also don't smell that great either. There is no identifiable role in humans apart from causing a variety of disorders such as an abcess.

When physically examining a patient with a very painful condition, doing something that greatly provokes symptoms will often cause the anal glands to secrete. As a doctor, I interpret it as a clear warning that the patient is in distress, and that I need to exercise greater caution. I don't know of any science supporting this, but the function seems self-evident.


Can a person really die quickly from biting their tongue?

I know of an ER doctor who had a patient who removed (by biting and pulling) every last part of her tongue, she survived that (although, her ability to speak was probably shot). The stump of her tongue clotted before she could even go into shock (at least where it was really serious).

Here is a quote from the book Angels in the ER  (this is a paramedic speaking with the doc):

  "Every bit of it. Gone. And the funny thing, Doc, is it didn't even
  bleed very much."
  The doctor then asked his patient to open her
  mouth... "it was gone!"

It would certainly be possible to commit suicide doing this if one was a hemophiliac or continued to remove the clot from the hole(s) in their tongue (although the latter could be a potentially painful and I have a feeling that it would take a very, very long time!).


Can't identify this fish caught off NC coast

i think this is a frogfish. there is multiple types of this fish. i think this is an Ocellated frogfish. frogfishes related to anglerfishes. memorizing animals by classification eventually helps with identification. little google search and using fishbase site about information helps. this sites very helpful about finding fishes.

fisbase frogfishes

frogfish site

this link says it can be found on North Carolina


What is the second phase of photosynthesis?

Here's an overview of both the Light and Dark cycles of photosynthesis, which looked particularly useful to me as it shows that the energy-carriers ATP and NADPH2 generated through solar energy are used in the dark cycle to generate sugars.

.

Here is another one that shows more details on the precursors involved in the Calvin cycle:

As commented by others, googling 'dark cycle' or its synonyms will give thousands of optional images to choose from if these don't suffice. The first one is taken from tutorvista.com the second one from users.rcn.com.


How to understand Aposematism and Batesian mimicry

I could be misreading your question, but it doesn't sound very specific. Rather, it sounds like you're asking "How can I make sense of all the various color schemes employed by venomous species?" So I'll take a stab at it...

Animal coloration is a very complex phenomenon, with a number of overlapping physiological traits, evolutionary strategies, etc.

Consider the famous relationship between the monarch and viceroy butterflies, which bear a striking similarity. The viceroy was long regarded as a harmless insect that predators avoided because it resembled the monarch, which many predators find non-appetizing.

More recently, it was proposed that the viceroy is also unpalatable. Thus, the similar color patterns may simply reinforce each other. (Mutual Mimicry: Viceroy and Monarch)

But that's just one isolated example of a bewildering spectrum of color schemes. Some animals apparently use bright colors as a warning - "I'm toxic!" - while other venomous species may be dull colored for whatever reason. A dull-colored species may use its venom to capture prey, which it captures in ambush; thus, it has evolved camouflage, rather than conspicuous colors.

Coloration is also about more than warning. Coloration can serve as a means of communication. It can help a member of a species recognize fellow members. Bright colors are very popular in mating rituals.

So you have all these overlapping traits and countless unique evolutionary experiments interwoven into a can of worms.

One example that comes to mind is venomous snakes native to the United States. The rattlesnake and cottonmouth are pretty drab-colored and generally well camouflaged. Of course, rattlesnakes warn potential enemies with their famous rattles. I think the cottonmouth can be considered fairly drab colored as well.

However, the coral snake has a very vivid and distinctive color pattern. And there are snakes that bear a remarkably resemblance to coral snakes (see some examples).


How do biologists infect cells with viruses within a lab setting?

You'll probably want to consider whether HeLa cells are the optimal cell line for acheiving your objectives. This paper shows minimal change in cell viability of HeLa cells innoculated with SARS-CoV and SARS-CoV2, but it's probably a good resource for how cell-culture infections are performed. This paper claims that VeroE6 is the standard cell line for producing viral stocks of SARS CoV-2.

Best of luck with your proposal.


Bootstrapping (symmetry breaking) in evolution

I found a paper which gives four conditions that have to be met:

Condition 1: A rule should be enforced that individuals
must meet some minimal criterion (MC) before they
can reproduce, and that criterion must be nontrivial
Condition 2: The evolution of new individuals should
create novel opportunities for satisfying the MC
Condition 3: Decisions about how and where individuals
interact with the world should be made by the individuals
themselves
Condition 4: The potential size and complexity of
the individuals’ phenotypes should be (in principle) unbounded

Source: Soros, Stanley (2014): Identifying Necessary Conditions for Open-Ended Evolution through the Artificial Life World of Chromaria

Chromaria is "an experimental platform that allows the exploration of evolutionary theories in an intuitive and visually engaging way" from EPLEX, the Evolutionary Complexity Research Group at the University of Central Florida (UCF)


Is there a reliable source for storage and stability of reducing agents like DTT?

Thiol-Based Reducing Agents

The instability of thiol-based reducing agents in solution is due to their propensity to form disulfide bonds by the following half reaction:

$$\ce{2RSH -> RSSR + 2H+ + 2e-}$$

It is clear that disulfide formation requires:

Deprotonation of the thiols to form thiolates (RS-).
An electron acceptor.

Therefore, solutions of thiol-based reducing agents would be most stable when:

The pH is buffered to where the thiol form predominates. The pKa of the thiol in β-mercaptoethanol is 9.5 and in dithiothreitol are 9.2 and 10.1  (Whitesides et al., 1977). Buffering the pH lower than this should increase stability.
Electron acceptors are removed. In aqueous solution, the electron acceptor is molecular oxygen. Degassing the buffer and storing the solutions under an inert gas such as argon should increase stability.
Reaction catalysts are removed. Divalent metal cations, especially copper (II) (Cu2+), catalyze oxygen dependent disulfide formation, even in trace amounts (Smith et al., 1994). Therefore a chelator such as EDTA should increase stability.
Temperature is low. As with most chemical reactions, rate increases with temperature.

The stabilities of the thiol-based reducing agents β-mercaptoethanol (β-ME), dithiothreitol (DTT) and glutathione (GSH) have been determined in solution as a function of pH at 20°C (Stevens et al., 1983):

...and temperature at pH 8.5:

...as well as in the presence of copper (II) and EDTA at pH 8.5 and 20°C:

Below is the tabulated raw data (this is the actual data from the paper which I used to create the above graphs, but take note that I found it difficult to plot “>100”):

                               Half-life (h)
pH    Temp (°C)    Additive    β-ME    DTT    GSH
6.5   20           -           >100    40     16
7.5   20           -           10      10     9
8.5   20           -           4.0     1.4    1.3
8.5   0            -           21      11     8
8.5   40           -           1.0     0.2    0.2
8.5   20           Cu(II)      0.6     0.6    1.2
8.5   20           EDTA        >100    4      70

As expected, stability decreased with increasing pH and temperature, and also with the addition of copper. Stability increased with the addition of EDTA.

Non-Thiol-Based Reducing Agents

Han and Han (1994) studied the effect of pH and buffer composition on the solution stability of tris(2-carboxyethyl)phosphine (TCEP). Though this is not a thiol-based reducing agent, it is still subject to oxidation. However, it is quite stable in solution:

pH    Solute/Buffer     % TCEP Oxidized After 3 Weeks
7.5   Tris-HCl          18.7 ± 0.6
8.5   Tris-HCl          16.8 ± 0.5
9.5   Tris-HCl          14.5 ± 0.5
8.2   borate             6.6 ± 0.2
10.2  borate             5.3 ± 0.1
6.8   HEPES             14.8 ± 0.4
8.2   HEPES             13.6 ± 0.3
9.7   CAPS               9.8 ± 0.3
11.1  CAPS               4.3 ± 0.1

Stability increased with increasing pH, though the effect was not large. Interestingly, the buffer composition had a larger effect on stability which was especially pronounced with phosphate:

        % TCEP Oxidized After 72 Hours
 pH     0.15 M phosphate    0.35 M phosphate
 6.0    not determined      11.2 ± 0.3
 6.8     8.1 ± 0.4          56.8 ± 2.3
 7.0    23.5 ± 0.9           100
 7.2    33.4 ± 1.0           100
 7.4    56.5 ± 1.4           100
 7.6    56.8 ± 2.1           100
 7.8    48.9 ± 2.5           100
 8.0    36.6 ± 1.7           100
10.6    not determined      11.7 ± 0.5
11.6    not determined       9.1 ± 0.4

References

Han JC, Han GY. 1994. A Procedure for Quantitative Determination of Tris(2-Carboxyethyl)phosphine, an Odorless Reducing Agent More Stable and Effective Than Dithiothreitol. Anal Biochem 220(1):5-10.

Smith RC, Reed VD, Hill WE. 1994. Oxidation Of Thiols By Copper(II). Phosphorus Sulfur Silicon Relat Elem 90(1-4):147-154.

Stevens R, Stevens L, Price NC. 1983. The stabilities of various thiol compounds used in protein purifications. Biochemical Education 11(2):70.

Whitesides GM, Lilburn JE, Szajewski RP. 1977. Rates of thiol-disulfide interchange reactions between mono- and dithiols and Ellman's reagent. J Org Chem 42(2):332-338.


How much time do the different mechanisms of gene regulation need to take effect?

People often imprecisely say that type of regulation takes place on the order of many minutes to hours, and that may be as precise as you can get given the variable kinetics of any given pathway.

Also, all genes in eukaryotes require general transcription factors, but basically all of them also require activators to act first to recruit the GTFs and histone modifying components (which allow GTFs and their friend RNA polymerase to access genes). So, they are generally downstream of activators and their recruitment is part of what contributes to the kinetics in euakryotes.

For RNAi, the kinetics of knockdown in RNAi could largely depend on the rate of degradation of the protein (which is HIGHLY variable). Even if you take away the mRNA, the protein is still there until it's degraded. If it's normally degraded fast, the kinetics of mRNA degradation will be limiting. If it's slow, then you have to wait for the protein to be degraded by its natural mechanisms (https://en.wikipedia.org/wiki/Proteasome).

Sigma is saying RNAi effects can be seen in around 24 hours

http://www.sigmaaldrich.com/life-science/functional-genomics-and-rnai/sirna/learning-center/mission-sup-reg0/experimental-design0.html#s3

Thermo is implying something similar by saying RNAi effects can be seen for 5-7 days post-transfection (i.e. they imply that it can be seen after a day).

https://www.thermofisher.com/ca/en/home/references/ambion-tech-support/rnai-sirna/tech-notes/duration-of-sirna-induced-silencing.html


Why do dozens of preys run away from a clearly outnumbered predator? (e.g. zebras and lion)

Why run?

To some extent, selfishness. Remember that natural selection acts within species.

Combat is dangerous. Very dangerous. Even if you are not immediately killed and successfully fend off a predator, wounds can weaken you, damage your senses, and/or kill over time with infection.

If you are a zebra, or a sheep, and you are in a group of other conspecifics, the safest action for you may be to not be the individual that is attacked. Sometimes, you might achieve this by simply advertising being a tough target. Other times, your best bet is to run away. This concept is sometimes humorously discussed in the context of humans and bears: you don't have to be faster than the bear, you have to be faster than the slowest person with you. This is called selfish herd behavior.

Fleeing predation is likely to be the default behavior

If you imagine an allele that changes an animal's behavior to combat an attacking predator (when other conspecifics predominantly run from predators), it is difficult for this allele to grow in the population. Individuals with the allele will get in fights, and although they may reduce predation of the herd as a whole, they will individually be selected against.

Similarly, imagine an allele that changes an animal's behavior to run from an attacking predator (when other conspecifics predominantly attack predators). Individuals with this allele will avoid fights, stay healthier, and breed better than their conspecifics that are getting beaten up, and eventually the herd will be mostly escapers.

Exceptions to the default

However, as pointed out in a comment by gardenhead, not all prey try to escape.

To avoid the 'default' escape behavior, there must be some other motivation: fighting back has to be special some how. In the context of group selection, fighting back may be selected for if it means improved survival of related conspecifics. This behavior is often seen in defense of offspring, but can expand to larger related groups. However, even defense of offspring can be risky, and it is not uncommon in nature for mothers to abandon offspring they cannot defend. It may be safer and more productive in the long run to survive and produce new offspring next year.

Another alternative would be some sort of social/sexual selection, where strong individuals who defend the group (likely males) have increased likelihood to mate.

References

Fischhoff, I. R., Dushoff, J., Sundaresan, S. R., Cordingley, J. E., & Rubenstein, D. I. (2009). Reproductive status influences group size and persistence of bonds in male plains zebra (Equus burchelli). Behavioral Ecology and Sociobiology, 63(7), 1035-1043.

Hamilton, W. D. (1971). Geometry for the selfish herd. Journal of theoretical Biology, 31(2), 295-311.

King, A. J., Wilson, A. M., Wilshin, S. D., Lowe, J., Haddadi, H., Hailes, S., & Morton, A. J. (2012). Selfish-herd behaviour of sheep under threat. Current Biology, 22(14), R561-R562.

Sjare, B., & Stirling, I. (1996). The breeding behavior of Atlantic walruses, Odobenus rosmarus rosmarus, in the Canadian High Arctic. Canadian Journal of Zoology, 74(5), 897-911.

Smith, W. P. (1987). Maternal defense in Columbian white-tailed deer: when is it worth it?. The American Naturalist, 130(2), 310-316.

Wood, A. J., & Ackland, G. J. (2007). Evolving the selfish herd: emergence of distinct aggregating strategies in an individual-based model. Proceedings of the Royal Society of London B: Biological Sciences, 274(1618), 1637-1642.


Why do the two sexes have different reproductive costs and capabilities?

I may have misunderstood your question, but there is no theory why usually reproductive costs are on the female, as this is a fact. Females have usually larger (and fewer) reproductive cells (gametes), they frequently have to carry the embryo until birth, and sometimes they have to attend to the offspring during the first stages of their lives. To put it very simple, females are stuck with their offspring from the moment of conception until they are born - sometimes even longer - while males generally can mate with many females in a short period of time, potentially having much more offspring.
A consequence of this is that, usually, females are choosy (they want good mates), whereas males just try to mate as much as possible. Female choosiness generates sexual competition, as females prefer to mate with males having certain characteristics that hint to a superior genotypes/phenotype that may be passed to their prole (e.g. beautiful plumage, social status, size of the wallet). Sometimes the costs of attending offspring after birth are higher than the costs associated with reproduction alone. In some of these cases, we may observe unusual behaviors, e.g. male-only parental care and choosy males.
This is a very broad and complex topic and a short answer here cannot cover all of it. John Maynard Smith developed the game theory approach most commonly used to investigate the consequences of different pay-offs for the two sexes and to explore how these can influence the behavior of the parents. Moreover, this topic is also covered in many behavioral biology textbooks. I have had very positive experiences with Krebs & Davis Behavioural Ecology (ISBN-13: 978-0865427310), which I would recommend.
Hope to have clarified some of your doubts.
Cheers,
Emilio


Wintercreeper, Euonymus fortunei

Given that you're just over in Illinois, here's the page from our Plant Finder database.

In regards to your second question, this factsheet from UMich mentions (and gives citations) for its use as a medicine. Given that, I'd avoid eating it if I were you, but there's not mention of it being especially toxic.


Literature that demonstrates organisms have a competitive advantage in numbers

I have found these papers:
http://www.sciencedirect.com/science/article/pii/S0169534713002322

http://www.sciencedirect.com/science/article/pii/S0040580912001360

http://www.ncbi.nlm.nih.gov/pubmed/19416834

http://www.ncbi.nlm.nih.gov/pubmed/21930936

The last two argue that larger groups have better "problem solving" capability, and this is a clear advantage in competition.


How can computer predictions of protein folding be verified computationally?

Overview

Modelling has come on leaps and bounds over the last decade or so and in many cases has acted as a sometimes viable, and inexpensive substitute for experimental structures.

  How do you know when you get it right?

Ultimately, one still needs experimental evidence to know when a model generated in silico is right. But there are ways of scoring a model for how likely it is to be right.

  Is there some way of verifying, in silico, that you have found a legitimate/correct structure for a protein?

There are lots of ways to score and verify your models. Each method tells you something slightly different about the merits, or lack thereof, of your structural model. Some are designed to weed out the obviously awful models and some allow you to detect exactly where your model looks to be accurate or inaccurate.

MODELLER Homology modelling output verification on the fly.

I am most familiar with modeller for homology modelling. Other softwares are available and they are each evaluated by CASP every two years since 1994.

In homology modelling there are 3 common scoring systems that can be used to assess the biochemical viability of a model. This email covers when to use each one. My answer expands and explains a bit more.

molpdf is the Modeller objective function.
GA341, discussed here is derived from  Z-score (calculated with a statistical potential
function), which is a target-template sequence identity, and a
measure of structural compactness.
DOPE is a more up to date method, first published in 2006, and is more true to "biological viability". From the publication:

  DOPE is based on an improved reference
  state that corresponds to noninteracting atoms in a homogeneous sphere with the radius dependent on
  a sample native structure; it thus accounts for the finite and spherical shape of the native structures.

Which to use depends on what you want to do with the model, but of those three scores, DOPE is the most reliable at separating native-like models from "decoys".  DOPE is usually the starting place for figuring out which models might be right and which models are just plain rubbish.

Note:  If you use Rosetta then there will be equivalents to these, or you can run your generated models through these techniques. If you are using SWISS MODEL that comes with it's own somewhat black box verification techniques but you can still export the model for further verification.

General model check against experimental data.

A further validation of homology modelling methods or other structural models is ProSA. ProSA provides a great visual representation of where the z-score lies amongst actual crystal and NMR structures. There are probably others that do similar functions, but this is my personal go-to to get an idea of where my structure lies among experimentally gathered structures.

Sensitive residue by residue verification.

Although the aforementioned methods examine each residue, they usually output an overall score. Residue by residue scores are also available and require a lot of careful interpretation. For example, if you are analysing catalytic activity, a surface looping region that scores poorly might not be an issue, but a core catalytic residue that scores poorly renders the model useless. This means that just because your model has a good (lower) overall DOPE score than another model, doesn't mean it is necessarily a more accurate model for what you are interested in.

There are plenty of sensitive modelling scoring systems. Some of which are XdVal, MTZdump, the famous albeit old-school Ramachandran Plotting method, pdbU, pdbSNAFU, PROCHECK, Verify3D, and ERRAT to name a few. Each has a place when checking how correct your model is.


Cutting dna using restriction endonuclease

Welcome to Biology.SE. I think this question would be better on-topic on math.SE.

Assuming the chromosome is either 4 bases long or infinitely long, then the answer is simply $\left(\frac{1}{4}\right)^4$. However, chromosomes are not infinitely long so the result should be (negligibly) lower than $\left(\frac{1}{4}\right)^4$. If chromosomes are only 3 nucleotide long, then of course, the probability will be $0$. If it is 4 bases long the probability is $\left(\frac{1}{4}\right)^4$. If it is 5 bases long the probability is $\frac{2}{4^5} = \frac{1}{2}\left(\frac{1}{4}\right)^4$.

Consider this numerical approximation, to ensure the result is correct with this simple one liner in R

n = 1e7
length(gregexpr('abcd', paste(letters[sample(1:4,n,replace=TRUE)], collapse=""), perl=TRUE)[[1]])/n
[1] 0.0039041

which is really close to $\left(\frac{1}{4}\right)^4 ≈ 0.00390625$.

So, in a genome of 3 giga bases, that represents an expected $\frac{3\cdot 10^9}{4^4} = 11,718,750$ (or ~11 millions) such locations where Alu 1 can cut.


Is the sex of siblings mutually independent?

There is at least one paper that claims this:

  A test for heritability of the sex ratio in human genealogical data is reported here, with the finding that there is significant heritability of the parental sex ratio by male, but not female offspring.

--Trends in Population Sex Ratios May be Explained by Changes in the Frequencies of Polymorphic Alleles of a Sex Ratio Gene. Corry Gellatly, Evolutionary Biology 36:190-200, 2009 DOI: 10.1007/s11692-008-9046-3.

In other words (simplistically) some families are more prone to have male offspring, which implies that the probability of male offspring is not independent.  However, this is a hypothesis, not a proven fact, and I think it's not a very strong hypothesis.

A non-scholarly, but apparently careful, discussion is here:

  The odds of having a girl seem decrease after having each boy, but only very slightly. Even after 3 boys, you are only 6.4% more likely to have a 4th boy than a girl.

What are the odds of having another boy or girl?


Why would a mammalian vector plasmid require an antibacterial resistance gene?

I think the assumption you are making is that the ampicillin resistance gene would save a purpose in the mammalian cells.
It does not.

As you said, it is only use during the cloning process to select the bacteria to replicate and produce more of it.

There is a resistance gene on the vector you posted which affect mammalian cells: neomycin. In this case, once transfected into mammalian cells, you could select only the cells with the plasmid by adding neomycin the cell culture medium.

Note: neomycin selection can take some time (4-5 days) and higher dose than for example puromycin. Hope this helps!


Relationship of RNA-binding proteins to peptidyl-prolyl cis-trans isomerase

Without seeing the sequence of the RNA-binding protein it is impossible to be sure, but the obvious conclusion is:

  The RNA-binding protein is a peptidyl-prolyl cis-trans isomerase.

It has been known since 1989 that peptidyl-prolyl cis-trans isomerase is a multiple-function protein, also exhibiting properties of the cyclophilins, proteins which bind cyclosporin A. The post raised the possibility that it may have other activities and a literature search reveals several more recent papers that indicate cylcophilin A can bind certain RNAs. I list some of the titles:

A nuclear RNA-binding cyclophilin in human T cells (1996) FEBS Letters 398 201–205

Molecular cloning, structure and expression of a novel nuclear RNA-binding cyclophilin-like gene (PPIL4) from human fetal brain (2001) Cytogenet Cell Genet 95 43–47

Cyclophilin A Binds to the Viral RNA and Replication Proteins, Resulting in Inhibition of Tombusviral Replicase Assembly (2013) J. Virol. 87 13330–13342

Structure of RNA-interacting Cyclophilin A-like protein from Piriformospora indica that provides salinity-stress tolerance in plants (2013) Scientific Reports 3 : 3001, DOI: 10.1038/srep03001


Yes, it is.

Gerardo Furtado has already provided a short answer in the comments, but allow me to explain why.

The 4^3 = 64 if all bases can be chosen freely comes down to 4*4*4=64, because you can choose from 4 options for each of the 3 bases.

If you restrict the possibilities of one of the bases, e.g. there are only 2 options for the third base (as in your example), the formula changes to 4*4*2=32, as you can choose from 4 options each for the first 2 bases and from 2 options for the 3rd base.

Edit:
If the 2 'N's from 'NNK' have to be the same, you can choose the first base freely (4 options), the second base is already defined (it has to be the same as the first base, 1 option) and there are 2 options for the 3rd base as described above. Thus, we get 4*1*2=8 possible codons

I hope I could clear this up.


Overdiagnosis and overtreatment are intertwined. There is debate about how to best describe the problem, but narrowly defined, overdiagnosis occurs when increasingly sensitive tests - or changing definitions - identify abnormalities that are minor, non-progressive, or likely to resolve on their own, and that, if left untreated, will not cause symptoms or shorten an individual's life. Having a diagnosis makes well-persons think they're ill (overdiagnosis). If they are then treated for this diagnosis, they are overtreated.

An example involving changing definitions pertains to diabetes. When the official definition of diabetes changed from having a fasting blood sugar (FBS) of "X" or greater to an FBS of "X-y" or greater, 1.6 million new diabetics were instantly diagnosed, some of whom are not likely to develop symptoms and complications and are not likely to benefit from treatment. This is overdiagnosis.

If one goes on to put such a patient (let's say, on the lower end, "X-y+1" on a blood sugar (BS) lowering agent, and they pass out because their BS drops too low, then they are overtreated. If they happened to be driving when they pass out, and get into a fatal accident, they literally die from overtreatment, if it can't be shown that they would have suffered from a marginally elevated FBS. (If it can be shown to be dangerous to have an FBS of X-y+1, then this is a risk of treatment, not overtreatment.)

For an example of increased sensitivity of tests, say a new test is available, a blood test called a "D-dimer", which will reveal with 100% accuracy the presence of a dangerous pulmonary embolism (it's very sensitive). However, it is also known to be positive when there is no pulmonary embolism as well, but it's not known how often (so it's not specific). But it's an exciting new test!

A patient goes into the Emergency room for one of the following: atypical chest pain, dizziness, shortness of breath, leg pain consistent with a blood clot in the calf, or loss of consciousness. In addition to an EKG, chest x-ray (CXR) and a few other tests, a D-dimer is ordered. The EKG, CXR and other tests are negative, but the D-Dimer is positive. The tentative diagnosis is pulmonary embolism (PE).

Because the D-dimer indicates that a dangerous condition may be present, a spiral CAT Scan with contrast is ordered on all those people. Some will have a life-threatening PE (appropriately diagnosed*). A large number will have a negative CAT Scan. (diagnosis excluded) But a significant number will have a very small PE. Because this is relatively new and surprising, and it's not known whether they should be treated (maybe nothing will happen if they don't treat? Maybe this happens in normal people and we just never knew it?), the doctors, who are accustomed to treating all PE's will put the patients on blood thinners. This is overdiagnosis of PE, and treating it is overtreatment, because some treated people will have "bleeds" - a stroke, GI bleeding, other. It is now known that these tiny PE's are often seen in patients who suffer no harm at all from them, therefore in order to stem overdiagnosis (and subsequent overtreatment), the D-dimer test is ordered less frequently.

  ...[We] are in the midst of an epidemic of diagnosis. Conventional wisdom tells us that finding problems early saves lives because we have the opportunity to fix the problems early. [Conventional wisdom tells us that} There is no risk in finding things early. The truth is that early diagnosis is a double-edged sword; while it has the potential to help some, it has a potential to harm us. Such overdiagnosis leads to overtreatment when these “pseudo-diseases” are conventionally managed and treated as if they were real abnormalities; because these findings have a benign prognosis, treatment can only do harm.

Overdiagnosed: Making People Sick in the Pursuit of Health
Overdiagnosis
Using Evidence to Combat Overdiagnosis and Overtreatment: Evaluating Treatments, Tests, and Disease Definitions in the Time of Too Much


Has a beneficial mutation ever been documented?

The answer depends on what you mean by "observed".

Bacteria acquire antibiotic resistance genes all the time, for example. This happens 'in the wild', but you can see in the lab that bacteria can become resistant overnight - I'd call that 'observed'.

There are many papers about the emergence of antibiotic resistance (not that I'm suggesting this is the only observable beneficial mutation).

In this paper, for example, several spontaneous mutations are induced in H. pylori in the lab in a short space of time:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90364/

In this paper, estimation of mutation rates are attempted in the emergence of resistance:
http://aac.asm.org/content/44/7/1771.full

It should be pointed out however that the timeframes can vary wildly. If a bacteria acquires a resistance gene by horizontal transfer, for example, this could be considered virtually instantaneous. Spontaneous mutations may take longer to emerge, and might only do so in the presence of steadily increased selection pressure, by contrast.


What is meant by Remote Diuretics & Remote Vomiting?

"Remote" can mean distant/far away, often in space but also in time (as in, the "remote past"). In just the search results you included in your question it is fairly clear that these sources are using the word "remote" to mean (relatively)"far away in time" or simply "not recent."

For example:

  associated with remote diuretic use, therefore, diuretic effects were already washed off

Referring to diuretic use in the past, so there is not current diuretic effect but the secondary consequences are still present.

Note that these terms are quite uncommon in the literature, I get 21 results in Google Scholar for "remote diuretic" and 16 for "remote vomiting" and nearly all seem to be related to the specific context of hypokalemia.