Have there been any successful studies showing that it is possible to increase IQ?

When talking about increasing intelligence there are a few things you have to keep in mind. Can you increase your IQ score? Probably, yes. Just take the same test twice, or more realistically practice a lot of IQ-type problems. You will probably raise a few points.

But this is just a score. When experts are talking about raising intelligence, they are talking about raising the underlying ability that tests can only estimate. Raising your test score does not necessarily mean that you raised your intelligence. What you want is something that transfers over to some general ability.

Richard Haier, the editor-in-chief of the journal Intelligence, has written extensively on this topic. In his 2014 article Increased Intelligence Is A Myth (So Far) he writes about this very subject of increasing intelligence (Haier, 2014). You can probably guess what the conclusion is from the title of the paper. This topic is also a substantial portion of his book The Neuroscience of Intelligence (Haier, 2016).

Technically, when you ask whether there are any studies that purport to have found a way to increase intelligence, then the answer is definitely yes. There are many (hundreds, probably thousands). The correct question to ask is whether any of these ways consistently replicate. At the moment, the answer to this question appears to be no. One of the most infamous "ways of increasing intelligence" was the supposed Mozart Effect. The hypothesis was that listening to Mozart music would increase intelligence, and there were studies providing evidence for this. Fairly silly, yes. It was not until a meta-analysis came out of Mozart Effect studies that this hypothesis was finally laid to rest (Pietschnig et al, 2010). There is a history of many supposed ways of increasing intelligence being suggested, but typically the more scientific scrutiny they are put under they tend appear less and less impressive. Therefore, whenever a new way of increasing intelligence is suggested, it may be good to have some scepticism.

Given the current body of evidence, the most plausible way of raising intelligence is probably education (Ritchie & Tucker-Drob, 2017). However, it is unclear whether education really increases general intelligence or just specific skills (Ritchie, Bates & Deary, 2015).

The best  non-genetic way to get high intelligence is probably not to increase your intelligence per se, but just to avoid decreasing it. This means avoiding things like lead exposure, don't suffer from iodine deficiency (Qian et al, 2005), get decent nutrition and so on. Anything that realistically could interfere with the development of the brain may be implicated in intelligence.

See also my answer to a similar question on the Psychology & Neuroscience Stack Exchange, which is slightly more comprehensive.


How does hair grow and is it similar to how grass grows?

In hair and nail growth new cells are added to the bottom. These cells are produced at the follicle. There are three stages called:

Anagen : active growth
Catagen : end of active growth
Telogen : total stop of follicular growth

I don't know what you mean by like grass but both nails and hair have a first in first out order.

Feathers present a contrasting case: the outermost portion is the most recent. Feather growth is relatively more complex. This article is a nice read on feathers.


Be glad to answer your questions.
fish also sounds. The difference is that they are put in different positions by the body to sound.The sound of fish is about 20HZ. Difficult to discern the human ear. But you can rely on instruments to imitate and perceived. Of course, some fish also relies purely on action to exchange summarize a sound.Some fish by ultrasonic communication with dolphins is very similar (dolphins are not fish).

2 colors.
Some fish by changing the body color transfer information, are located in the tropical shallow water.

3 flow.
Some fish to pass through the water with their fins flapping shaped courtship information.

4 pheromone.
Release pheromone few fish, mostly deep-sea fish.。


How are logarithmic trendline equations used to determine antibody concentrations in ELISA?

If by ln you mean the natural logarithm, then no, you can't rearrange the equation in that way. Try this:

$$m\cdot \ln(x) - c = y\\
\ln(x) = y + c\\
\ln(x) = \frac{y+c}{m}\\
\exp(\ln(x)) = \exp\left(\frac{y+c}{m}\right)\\
x = \exp\left(\frac{y+c}{m}\right)
$$


Why did humans get rid of their tail in the evolution?

The tail serves a variety of complex balance tasks in locomotion, turning, jumping, aerial balance, hanging, and most mammals have a tail, save for other examples, i.e. rabbits, pigs, capibaras, manx cats, seals and bats, lemmings and hamsters have mini tails.

All the previous large apes related to humans lost their tail millions of years ago. The reason why that occured are multiple and mixed. Multiple good explanations have been suggested.

Gibbons are some of our most monkey-like ape cousins. If you see how they move, they run on two legs rather than 4. Monkeys with tails are less adapted to walking and their pelvis is angled differently. https://www.youtube.com/watch?v=b9Pt2qgSqJw

Large animals with small tails, such as caribou, hippos, elephants, deer, seem to keep some kind of tail, however with chimpanzee type animals, once the tail became small it didn't stay on as a mini-tail. So would it make sense for chimpanzees/humans to have small tails like hippos or very long ones? If a chimp can run on 2 legs, that leaves it two hands to catch the tail of another competing chimp.

The big apes move differently to small apes: big apes live on the ground more, they don't run in trees as much, they move differently, they are larger, they have completely different body ratios for arm and leg size, and there have been a wide variety of propositions for hundreds of years on this topic without a particularly clear reason being accepted for which great apes don't have a tail.


It depends on what is understood by speaking.
Anatomy  If by speaking one means producing sounds similar to those produced by humans, than the ability to speak is largely determined by the anatomy of the speech organs - whether they can produce the same type of sound as human does. There are very few animals capable of this (I will find the reference), and this notably excludes some rather close human relatives, such as the great apes.
Neurology  Language is a more complex phenomenon than speaking. The most notable difference between the animal and the human communication is that the former typically uses a set of signals with hard-coded meanings, whereas the humans can construct an infinite number of phrases coveying complex meaning. The study of language from this angle has been traditionally carried out by linguists and computer scientists rather than biologists, under the general name of universal grammar (but may also appear under such terms as transformational grammar, generative grammar, etc. ) However, these studies have a direct biological implication that humans possess a genetically coded set of rules for sentence/phrase structure, which is independent on their native language. This clearly requires certain degree of neural development, which the language-less animals do not necessarily possess.
Psychology  Finally, language requires significant psychological development - even in humans. Feral children often fail to acquire language competences. Similarly, the extensive studies on small chidlren in care homes (starting from the works by Anna Freud and Melanie Klein from more than a hundred years ago) demoinstrated that children deprieved of normal human contact have significantly diminished speaking abilities. Getting back to the OP - one can therefore question whether an animal could concievably be exposed to normal human environment to facilitae development of linguistic ability similar to that of a human.
See here and here for more background.


My favourite definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

You might want to have a look at What does fitness really mean?.
What I like about this definition
I personally went with this definition because it is short and clear cut and directly highlight the importance of mathematical statistics in the evolutionary biology literature.
What I don't like about this definition
This definition has the issue that it may be hard to be fully understood to a layman reader. Also, I think my definition lack a mention of the phenotype as being causal to the fitness differential. While such mention is not necessary, I think it would clarify in most minds what selection is really about.

Now, let's consider the definitions that we typically get when we google the question
Wikipedia
Here

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype

I am quite unhappy with this definition. While I like that it highlights the fact that fitness difference is caused via phenotypic difference, it completely lack the idea that for a change in allele frequency to happen, this variation must be correlated to genetic variation.
I would note that the rest of the introduction on the wikipedia article clarify my criticisms. I only attack the short version (one sentence) version of the  definition.
Dictionnary.com
Here

the process by which forms of life having traits that better enable them to adapt to specific environmental pressures, as predators, changes in climate, or competition for food or mates, will tend to survive and reproduce in greater numbers than others of their kind, thus ensuring the perpetuation of those favorable traits in succeeding generations.

There are a few things I don't like about this definition
..traits that better enable them to adapt..
It sounds like they are talking about evolvability. I would just say traits that are better adapted.
..too much emphasis on the role of the environment..
Also, I don't like that it is presented as if all selection pressures where environmental (predators, climate, competition for food, etc...) and completely ignore a very important source of selection which are simply related to the functioning of the body. A mutation that causes an individual to fail copying DNA anymore will obviously be lethal and under very strong purifying selection. Such the "outside-of-the-body environment" is important but it is definitely not the only thing.
It is kind of a common misconception about evolution that selection occurs when there is a climate change and not so necessarily in other case in most people's mind.
..ensuring the perpetuation of those favorable traits in succeeding generations..
Well.. it does not "ensure" that these traits will be kept. First because it only increases the probability of certains allele to be kept or to reach fixation, it does not ensure it. Also, because depending on the genetic framework, once the underlying QTL have reached a given frequency, depending on the actual genetic mechanism (epistasis, dominance and others), traits that are being express might differ quite a bit from those that have been selected for.
Overall, I think the definition lack any notion to genetics.
Biology-online
Here

A process in nature in which organisms possessing certain genotypic characteristics that make them better adjusted to an environment tend to survive, reproduce, increase in number or frequency, and therefore, are able to transmit and perpetuate their essential genotypic qualities to succeeding generations

I like this definition. The only issues in my opinion are very similar to my above opinions

too much emphasis on the environment as done before
it seems that they define more the consequence of natural selection than what it actually really is.

What Google gave me when I entered 'what is natural selection?'

the process whereby organisms better adapted to their environment tend to survive and produce more offspring.

Again there is IMO, too much emphasis on the environment and no mention of thee actual mechanism (fitness - genetics correlation).

Potential confusion
Some people might use the term "selection" to refer to the existence of phenotype - fitness correlation and the "response to selection" as being the effect of such correlation of the population genetics whenever there is a non-zero association between phenotype and genotype. This nomenclature would typically be inspired by the terminology used in the Breeder's equation (see How to interpret the breeders equation?).
However, none of the definitions I could find clearly suggested that selection was nothing but a phenotype - fitness correlation as all of them implied that selection has a long term impact on the population phenotype which such phenotype - fitness correlation would not have in absence of a phenotype - genotype correlation.

Lewontin recipe
I am not sure a recipe count as a definition but Lewontin recipe is a good way to understand the what is natural selection

Individuals in a population varies in terms of a given trait
This trait has some heritability.
The fitness varies (not necessarily linearly) as the trait varies.

The recipe hides the complexities behind the term heritability. You can learn about the math of heritability at Why is a heritability coefficient not an index of how “genetic” something is? .


Why would a bacterial population show initial growth when it is in unfavorable growth conditions?

E. faecalis is an aerotolerant anaerobe, while E. coli is a facultative anaerobe therefore if in a non-aerobic environment it can switch to anaerobic respiration. E.coli is also capable of fermentation.

Here is an article for on the various respiratory pathways of E.coli: http://www.sciencedirect.com/science/article/pii/S0005272897000340

One other reasons why cells may grow in a nutrient poor medium is that many types of bacteria have programmed cell death that ultimately is for the better of the entire bacterial population. When nutrients get low some cells commit "suicide" and release nutrients to surrounding bacteria. Just an extra thought.


Interesting!  The size, shape and posture, as well as the visible patterning on the body, are all reminiscent of Dolomedes tenebrosus, the common terrestrial fishing spider here in the east.  However, there are a couple of odd things here:
1.  Dolomedes is a genus only found (as far as I know) in the eastern half of the US,
2.  The abdominal color pattern is a bit off from what I would expect (dark flank marks at the front of the abdomen, especially), and
3.  That looks like an egg sac the spider is sitting on top of, as if it was guarding, but fishing spiders (as far as I know) do not make egg sacs like that - they make ball-shaped egg sacs which they carry around with them using their fangs to hold them.

The thing is, nothing else rings a bell with me - the only other large wandering hunter that would be anything like that in the Pacific NW, that I know of, is the Giant Crab Spider Olios giganteus, which doesn't look much like that, although it does make a silken retreat/egg sac protection.

I confess that I am stumped, although I can confidently say that it is not a Yellow Sac Spider.

However, I can suggest two good options for identification:
the Burke Museum: https://www.burkemuseum.org/collections-and-research/biology/arachnology-and-entomology/contact-form

and Bug Guide: https://bugguide.net/node/view/6/bgimage

both of which can often do identifications from photos alone (although with spiders, this can sometimes be tricky).
Good luck!


What physical traits are derived from the Neanderthal DNA in human DNA?

There was a very readable piece on this topic by Chris Stringer in Nature in 2012. At that time his general conclusion was:

  It is not yet clear whether the archaic DNA many of us carry is tied to any visible traits.

Although he added:

  More controversially, some of the known differences in coding DNA
  between Neanderthals and recent humans are associated with brain
  development and function

quoting the paper in Science (2010) in which the Neanderthal sequence was published. There may be more recent information of which I am not aware.

As to your question about Neanderthal DNA in different populations, it is not present in people of African origin, but is present in those of Europeans and Asian origin.


Reason behind selection of sites of administration of pituitary extracts?

Melatonin is an evolutionary highly conserved molecule that plays an important role in conveying the clock and calendar information to all living organisms, including man. The hormone is synthesized mainly by the pineal gland, and, to a lesser extent, by extrapineal tissues--such as the retina, Harderian gland, and gastrointestinal tract.

It is a standard slow acting hormone injection. Once the injection is in the animal, it just propagates throughout the animal's physiology and takes the normal melatonin chemical and physiological pathways that it does in vertebrates, it prompts the pituitary gland to produce a lot of different hormones including sex and serotonin.

It doesn't act instantaneously if you overdose (humans have tried), OD negative effects occur after 1-2 days and thereafter. It doesn't react as violently as some other hormones such as Adrenaline, which is absorbed fast and dissipates fast and can give you a heart attack. Melatonin has a physiological effect that is more extended, for example steroids for inflammation.

The aim of intramuscular injection of the fish is that it is effective and safe, If you read the guides, they are concerned with the safety of the fish, it's nerves and vital organs... The tail is mostly muscle and the injection is IM. Once the hormone is injected, its absorbed by the animal over an extended period. There have been many experiments of pineal injection in rodents so refer to them to know the time frame of absorption.


This looks like it's a female Pelecinid parasitic wasp (see this page for an overview of the family in the western hemisphere); from your location the species is either Pelecinus polyturator or Pelecinus dichrous (all of BugGuide's images are of the former, that being the one also found in the United States).


Brian Hayes wrote a very interesting article from a mathematical point of view:

http://www.americanscientist.org/issues/pub/the-invention-of-the-genetic-code

especially the "Reality intrudes" section. Basically people had created fancy mathematical reasons why it has to be exactly 20. Nature, being nature, does not follow the reasoning, but has its own ideas. In other words there was nothing especially special about 20. In fact there seems to be a slow grafting of a 21st amino acid, selenocysteine using the codon UGA. Also pyrrolysine is considered the 22nd. The last section suggests that the code was originally doublet, so coded for <16 amino acids. This can partly explain why the third base in each codon is not as discriminating.

So perhaps in the year 2002012 someone will be asking on biology.stackexchange why there are only 40 amino acids.


Two things...

Rapidly proliferating tissues (esp tumours) rewire their energy metabolism anyway to aerobic glycolysis where you have energy being produced by lactic acid fermentation even if oxygen is present. This is called the Warburg effect.Here's the thing about "low yield" though - glycolysis chucks out less ATP per reaction at the end, but you can crunch through a lot more ATP by just having more of it going on.

Secondly, hypoxia in a tumour is generally rate limiting, and therefore the shunting away of alpha-KG with the consequence of increased angiogenesis is good for the tumour.


Which species were first described by Charles Darwin?

I don't know if these are his earliest descriptions but Darwin did describe several species of Planaria, such as Planaria vaginuloides, P. oceania, plus a new genus, Diplanaria in 1844.

Darwin, C. R. 1844. Brief descriptions of several terrestrial planariæ, and of some remarkable marine species, with an account of their habits. Annals and Magazine of Natural History 14 (October): 241-251, 1 plate.

Perhaps his best known taxonomic work is on barnacles (Cirripedia). He described several species in his monograph first monograph on the group.

Darwin, C. R. 1851 [=1852]. A monograph of the sub-class Cirripedia, with figures of all the species. The Lepadidæ; or, pedunculated cirripedes.. London: The Ray Society. Volume 1

The first monograph was followed by three other monographs on living and fossil Cirripedia.

I believe that most of his writings after publication of On the Origin of Species focused on expanding his evolutionary ideas rather than on descriptions of new species.

You can read nearly all of Darwin's writings online at http://darwin-online.org.uk. With careful searching you can find all (or nearly all) species descriptions.


Is warmth/temperature sensed linearly or on a different scale?

The human sensation of warmth is not the measurement of static temperature.  Humans detect the rate at which heat is leaving (or entering) their body.  For instance, if you are sitting in your 0 degree car in the morning, your hand in the open air will feels warmer than your hand touching the steering wheel, despite them both being at 0 degrees.
The reason is that heat conduction from your hand to the steering wheel is much faster than convective heat transfer from the air.  So you feel "colder" touching the steering wheel, but it's really that you're losing heat faster.
Scholarpedia's article on temperature receptors:
http://www.scholarpedia.org/article/Thermal_touch#Temperature_receptors

...Cold receptors respond to decreases in skin temperature over a range
of 5-43 °C...
...In contrast, warm receptors signal that skin temperature has
increased...


Why hasn't life on Earth reached an evolutionary stable strategy?

Because the environment on earth is not stable on the long run.

Antarctica was on the tropics. However plate tectonics has moved the continent from that location to south pole. And in time the continues will leave the poles and move toward the tropics again.

So a perfectly evolved animal in tropical Antarctica 200 million years ago, would have to continue evolving or it would have gone extinct as Antarctica moved southwards. And the animals living on Antarctica today will have to evolve as the continues continues with its motions.

Also predator-prey relationships... are red queen type relationship. They may appear stable on the outside, but both parties are actually under selection pressure to evolve, to counter the advantages of the other party. They are in an arms races. Pressure to out run the predator. Pressure to outwit the prey. Pressure to better camouflage. Pressure to detect prey from multiple senses (sound, sight smell).

So on the long term, the strategy that a predator uses will change as its prey evolves. And vise versa for the prey.


How are testosterone levels distributed among men and women?

To the first question we can look at a paper such as "Estimating age-specific trends in circulating testosterone and sex hormone-binding globulin in males and females across the lifespan" from Handelsman et al.  The figures they provide are:

The top image is of females, the bottom of males.  We can see throughout a lifetime that the top 2.5% of females and bottom 2.5% of males seem to have approximately the same amounts of testosterone.  If we went to the top and bottom 1% there would likely be consistent overlap between the male and female distributions.

I believe you are interpreting the figures correct, although it is important to keep in mind these figures do not include any information on age and are a single point measurement.  To facts that may limit the depth of inference you can make about testosterone levels among the sexes.


Do trees have genes for stopping growth?

The answer I got from Jan Kolář of Charles University:

  Traits of trees like height and mass are a result of the genes and
  environment. The determinative factor for the studied plants and
  animals is a big amount of various genes. When we get to know all the
  functions of all the genes, we should be able to determine the most
  important ones but for now we know just that gibberelin and auxin are
  very important for the growth of the tree, so we'll be looking for those
  genes which control the level of those hormones.

  In case of trees, a big part of the height they can grow are utterly
  mechanical factors. The stem and the main branches have to be enough
  strong not to break with their own weight and the roots have to be
  enough firmly rooted in the soil. This limit is determined mainly by
  genes that control the grow of the cell walls, their mechanical
  resistance etc.


What is the definition of the life biologically ?

Could not fit in a comment..

The question is off-topic

Biology is the study of life. Without a good definition of life, Biology itself is poorly defined. It appears that there is no universally accepted definition of life and therefore Biology (just like Chemistry and Physics to cite other examples) is a poorly defined field of study. But it is not scientists job to decide whether their work should stand within one category or another, nor whether those categories are natural categories (see prototype theory) or not. It is the job of philosophers and therefore this question is about philosophy and is off-topic here.

Few notes about the definition of life

Most often, philosophers see a continuum from not living to living things and not a clear dichotomy (ref.).

Biologists, most often just assume that bacteria, archea and eukaryotes are living things while viruses, viroids and prions are not living things. This arbitrary dichotomy is based on the concept of metabolism. However, this dichotomy can lead to some limit cases. Typically, considering viruses as not being living things yields to intuitive issues when thinking about macroviruses such as Marseillovirus and Lausanevirus.

There are two questions in your post

Of course, the definition of what is dead is a total different question from the question of what is a living thing. A stone is not dead it is just not a living thing. Even then, the definition of death is of interest to philosophers, not to biologists. You should always try to limit your post to a single question.


Is there a specific mechanism for the delivery of pain medication?

Short answer
No, orally taken painkillers act systemically.

Background
Taking a painkiller orally results in the drug being taken up into the bloodstream by the digestive system. From there it can potentially reach all tissues.

In other words, a pain response does not act as a chaperone. A hypothetical drug that would home in on tissues with a pain response, while avoiding unaffected tissues would be the ultimate painkiller, if it existed.

EDIT: To emphasize that painkillers act systemically I will elaborate on aspirine's pharmacokinetics. Notably, aspirine's actions are not restricted to the pain centers in the brain, and I quote the following excerpt from Wiley's interactive Concepts in Biochemistry]1:

  Aspirin's analgesic and anti-inflammatory effects are due to the drug's ability to stop the production of prostaglandins that cause tissue swelling and pain.

Aspirin's antipyretic (fever-reducing) effect is due to its direct action on the hypothalamus gland, which results in vasodilation of peripheral blood vessels and sweating.

Prostaglandins are also the key mediators of platelet aggregation. By modifying the COX enzymes within platelets, aspirin causes platelets to lose the "stickiness" that is needed to stimulate blood clotting.

Hence, by these examples it can be seen that aspirine works in the periphery (wound swelling and pain), centrally (brain's hypothalamus) as well as in the bloodstream. Hence, aspirine (and other orally administered painkillers) do not target specific areas in the body, and most certainly not only the brain.

There are such targeted drugs, however. An interesting one is carbamezipine, an anti-epileptic that blocks Na+ channels. It blocks Na+ channels only when they are in an active conformation, however (i.e., engaged in action potential firing). Epileptic activity is basically paroxysmal (massive), synchronous over-activity in the brain that is accompanied by massive Na+ channel activity. Hence, epileptic activity will in effect trigger the drug into action.


Energy input during ATP Dephosphorylation?

It sounds like you are asking about the activation energy of the ATP hydrolysis reaction. This paper estimates the activation at 35--39 kcal / mol, depending on details of the reaction mechanism. So yes, energy is needed to break the phosphate bond; this ensures that ATP does break down spontaneously (which would make it a rather useless molecule for cells).

Note that this concerns ATP hydrolysis without enzymatic catalysis. Enzymes that break the phosphate bond of ATP to drive reactions lower this reaction energy substantially.


What is the reason behind high resting membrane potential of pacemaker cells?

The pacemaker potential is interesting (to a biologist) as it involves your typical Na/K channels, Ca channel, as well as a funny current (If) or alternatively called hyperpolarization-activated current.

  The funny current is a mixed sodium-potassium current that activates
  upon hyperpolarization at voltages in the diastolic range (normally
  from -60/-70 mV to -40 mV). When at the end of a SA potential the
  membrane repolarizes below the If threshold (about -40/-50 mV), the
  funny current is activated and supplies inward current, which is
  responsible for starting the diastolic depolarization phase (DD); by
  this mechanism, the funny current controls the rate of spontaneous
  activity of sinoatrial myocytes, hence the cardiac rate.

  Pacemaker activity (or spontaneous electrical activity) of the
  sino-atrial node is based on the presence of a special phase called
  the diastolic depolarization during the action potential, in which
  cells depolarize spontaneously towards the AP threshold. Animal
  studies (mostly conducted on rabbit heart) have identified that this
  net inward current during the diastolic depolarization phase is the
  result of a complex interaction of multiple inwardly and outwardly
  directed ion currents....

Verkerk, Arie O., Antoni CG van Ginneken, and Ronald Wilders. "Pacemaker activity of the human sinoatrial node: role of the hyperpolarization-activated current, I f." International journal of cardiology 132.3 (2009): 318-336.

Also this

  The SAN is a complex tissue with regional differences in morphological
  and electrical properties.Animal studies have revealed that
  pacemaking in SAN cells follows from diastolic depolarization driven
  by a net inward current, which results from an interaction of multiple
  ion currents. Inward currents are activated during diastole:
  hyperpolarization-activated pacemaker current (If), background Na+
  current (Ib,Na), sustained inward current (Ist), T- and L-type Ca2+
  currents (ICa,T and ICa,L, respectively), and Ca2+-release activated
  Na+–Ca2+ exchange current (INCX). Conversely, outward currents are
  deactivated: rapid delayed rectifier K+ current (IKr) and slow delayed
  rectifier K+ current (IKs). The relative contributions of these
  currents to diastolic depolarization are a matter of debate.

Verkerk, Arie O., et al. "Pacemaker current (If) in the human sinoatrial node." European heart journal 28.20 (2007): 2472-2478.

Might I suggest you read up on the papers mentioned above?

You might also be interested in this:

Noma, Akinori. "Ionic mechanisms of the cardiac pacemaker potential." Japanese heart journal 37.5 (1996): 673-682.


How is membrane capacitance related to the increased speed of saltatory conduction?

Very nice question! I'll go through your three questions sequentially.

Q1: Why does lower capacitance increase "the effectiveness of nearby nodes" or allow the depolarizing voltage to "travel not by ion diffusion, but as an electric field"?

A: Capacitance basically results in sequestering of charge of opposite polarities along the cell membrane, which basically results in a neutralization of charge differences. The effect of this is explained on the website of Amrita and I quote:

  [...] a higher capacitance results in a lower potential difference. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

What myelin does is insulating the neuron, thereby decreasing its capacitance. You could say that by increasing the thickness of the membrane, the negative insides of the cell do not attract positive charge outside the cell. It's a bit simplified, yet it effectively describes what myelin does (see cambridge web page on capacitance).

So in a myelinated axon, when Na+ enters the cell in a node of Ranvier, the positive charge entering the cell is not counterbalanced by outside negative charge and hence, the charge is not or at least less counterbalanced. This allows for the depolarizing potential to be transmitted by electric charge. If there were no myelin, the depolarizing potential would fade out pretty quickly along the axon by neutralizing charges outside the cell. Without myelin the opening of more sodium channels in the direct vicinity are necessary not only to transmit the action potential across the axon, but it is also necessary to amplify the signal to prevent it from dying out. In a myelinated axon, hence, the depolarizing potential reaches much farther and in answer to your next question:

Q2:This allows us to say that λ, or the rate of spatial decay of potential, increases, decreasing the effective length of the neuron. Why should its decrease help faster conduction?)

One could say that myelination effectively decreases the length of the axon (the lamba parameter) as the depolaring potential reaches further along the axon.

The fact that the depolarizing potential reaches further means that voltage-operated sodium channels can be activated at larger distances from a certain depolaring potential. Hence, adjacent nodes of Ranvier can be spaced by as much as 1.5 mm. Due to the fact that the next node is activated by passive spread of an electric field, which is pretty much instant, it skips the intervening distance with about light speed, greatly enhancing conduction velocity.

Q3: And another question is, how would reduced density of sodium voltage gated channels cause a decreased capacitance?

Basically there are no ion channels below a myelin sheath as they are totally useless there. It is the myelin that decreases capacitance and there happen to be no channels underneath.


What chemical or biochemical agents do plants use to inhibit each other's growth?

As with the massive variety of compounds that serve to protect plants against insect and animals, resulting in a wide range of poisons, antibiotics and other natural insecticides, allelopathic compounds are highly varied with different methods of action: some merely prevent germination while others are effectively herbicides.

One example is Alliolaria petiolata. In that species the allelopathic substance is not known, but is thought to ahve a fungicidal effect that impedes mycorrhizal development, which would seriously affect the development of many species.


Why does a frog's oxygen intake through the skin and lungs vary throughout the year?

Cutaneous respiration is based, as every type of respiration, on diffusion of gases from a higher concentration (in water or air) to a lower one (in capillaries).

Citing from Johnson, Peter H. Raven, George B. (2002). "Respiration". Biology (6th ed.). Boston: McGraw-Hill. pp. 1053–1070:

In general, the rate of diffusion between two regions is governed by a relationship known as Fick’s Law of Diffusion:

R = D - A x ∆p/d

In this equation,

R = the rate of diffusion; the amount of oxygen or carbon dioxide diffusing per unit of time;
D = the diffusion constant;
A = the area over which diffusion takes place;
∆p = the difference in concentration (for gases, the difference in their partial pressures) between the interior of the organism and the external environment; and
d = the distance across which diffusion takes place.

As you can see, the rate of diffusion R can be increased:

By increasing A, the diffusion area;
By increasing ∆p, the difference in concentration;
By decreasing d, the diffusion distance.

In cutaneous respiration, nr.2 is not really an option; yes, capillaries can be optimised to bring blood rich in carbon dioxide and poor in oxygen really close to skin surface (which brings us to nr.3), but it's a lot less efficient than, for instance, lungs that can exhale air filled with carbon dioxide and replace it with fresh air. While the intake of oxygen of the skin remains more or less the same even with different metabolic demand, lungs can quickly adjust the breathing rate depending on the metabolic demand of the moment.

So, the answer to the question

  why does the intake through the skin vary slightly while through the lungs dramatically?

is that skin cannot regulate its gas exchange rate, while lungs can. This brings us to your first question:

  Why does a frogs oxygen intake through the skin and lungs vary throughout the year?

The answer lies in the biological cycle of the frog throughout the year: during cold months, frogs hibernate. In winter, frogs slow dramatically their metabolism and they don't need so much oxygen; thus, in this season they are able to rely only on cutaneous respiration. In other seasons they are active, and they have to breathe actively through their lungs to supply their blood with the necessary quantity of oxygen.


Starting out with RNA data is great, since you already have fully spliced entities, despite  being in a different dynamic regime.

As the chromatin landscape itself is dynamic and High throughput data exploration has only begun in the last decade, consider the following tools and results with care...

You may find the following tools helpful:

Archalign , Publication (didn't work well during my day of trials)
Ensembl chromatin-state map data (See the database layout, Regulatory Build, and the lincRNA
genes in the web-interface of the Ensembl databases)
HaploReg, Publication (the most recent)


Does taking a shower have the same effect on muscles as warming up?

Hot shower will definitely affect your muscles health. Hot water shower results in Vasodilation,which will decrease the vascular resistance and allows blood to flow easily through the blood vessels. As the vasodilation (increase in diameter of blood vessels) allows blood to move without resistance and which in turn nourish the tissues with sufficient oxygen and nutrients. Also it affects in the removal of metabolic wastes from cells. There is another process called  Vasoconstriction (decrease in blood vessel diameter) which makes the blood vessels to contract and may lead to increased blood pressure.

There is a technique called as Heat therapy which will be effective in muscle and body health.

  Heat therapy, also called thermotherapy, is the use of heat in
  therapy, such as for pain relief and health. It can take the form of a
  hot cloth, hot water, ultrasound, heating pad, hydrocollator packs,
  whirlpool baths, cordless FIR heat therapy wraps, and others. It can
  be beneficial to those with arthritis and stiff muscles and injuries
  to the deep tissue of the skin. Heat may be an effective self-care
  treatment for conditions like rheumatoid arthritis.

  Heat therapy is most commonly used for rehabilitation purposes. The
  therapeutic effects of heat include increasing the extensibility of
  collagen tissues; decreasing joint stiffness; reducing pain; relieving
  muscle spasms; reducing inflammation, edema, and aids in the post
  acute phase of healing; and increasing blood flow. The increased blood
  flow to the affected area provides proteins, nutrients, and oxygen for
  better healing.Reference

While taking a hot water bath we are just making our muscles and tissues nourished, which means the muscles will be in a healthy state for expansion and contraction. So it is recommendable to take a hot bath before exercising.


Separation of smaller DNA fragments and larger fragments without using gel electrophoresis?

One option is to use SPRI beads, like those sold by Ampure (Ampure XP beads) to separate DNA fragments by size. By adjusting the ratio of beads to sample, you can selectively bind fragments of certain lengths by excluding those of other lengths, as seen in the following image:

From this image, you might try using a beads-to-sample ratio of 0.7 to exclude fragments below 200bp, or a ratio between 0.7 and 0.6 to exclude only those fragments below somewhere between 200 and 250bp. The advantage to beads over a gel is the time it takes. Size selection by beads takes only around 10 minutes, versus maybe 30 minutes or more for a gel (including the extraction).

As with any molecular biology procedure, it's important to test it and make sure that it works for you. For instance, it might be a good idea to take aliquots of your samples and compare the lengths and yields that you get from a range of bead concentrations and/or to compare the yields that you get from using gel vs (in this case) beads.


Are antibodies removed before blood transfusion

I quote from the below.
Groups and Red Cell Antigens
by
Laura Dean (page 7). Available at:
http://www.ncbi.nlm.nih.gov/books/NBK2265/
"Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation."
I dont think the antibodies are removed, but in countries with a good medical system I believe the matching blood type is always used.
http://en.wikipedia.org/wiki/Acute_hemolytic_transfusion_reaction


How is silica transported to the leaves of genus Dendrocnide trees to form stinging needles for toxin delivery?

Biosilicification is a good search term to use.
The silicic acid present around the roots can be actively transported into roots, and later into specific cells or cell compartments. It is deposited preferentially onto lignin or polysaccharide surfaces.
For free articles giving an overview there is:
Nawaz, Muhammad Amjad et al. “Phytolith Formation in Plants: From Soil to Cell.” Plants (Basel, Switzerland) vol. 8,8 249. 26 Jul. 2019, doi:10.3390/plants8080249
found at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724085/
and:
"From biosilicification to tailored materials: Optimizing hydrophobic domains and resistance to protonation of polyamines"
David J. Belton, Siddharth V. Patwardhan, Vadim V. Annenkov, Elena N. Danilovtseva, and Carole C. Perry
PNAS April 22, 2008 105 (16) 5963-5968; first published April 17, 2008 https://doi.org/10.1073/pnas.0710809105
found at:
https://www.pnas.org/content/pnas/105/16/5963.full.pdf
Keywords silaffins, frustulins, pleuralins (used by diatoms) silicatein (used by sponges)


Why was the evolution of large, slowly reproducing organisms preferred?

The simple answer is that the evolution of large, slowly reproducing organisms is not preferred: it is simply not selected against.

The key mistake in your thinking is this statement:

  One of the main goals of living organisms is to reproduce

Most living organisms have no such goal, they simply take actions that have, historically, led to the continuation of their lineage.

In a complex world, there are many different strategies that can lead to survival and propagation of an organism, and cooperation between cells is one of them.  Even simple bacteria often form large multicellular aggregates, which can provide physical advantages for their members over dissociated individuals, such as resistance to physical damage and formation of protected microclimates. The inside of your body is another such protected microclimate. So multicellularity can be quite advantageous.

As for limiting reproduction: remember that the closest competitors every new organism has are its own relatives, who occupy the same space and compete for the same resources.  Even bacteria will often limit their reproduction when resources are limited. Reproduction also takes significant resources. A faster reproduction then, is also not necessarily advantageous for long-term survival.

Bottom line: neither large nor small, fast nor slow is preferred.  Instead, the study of evolution predicts that we will see what we do see: a multiplicity of forms and strategies adapted for different niches in the ecosystem formed by their interactions with other species and the external environment.


The explanation I got when learning how to do qPCR was that you need run both replicate experiments and parallel experiments to get publishable data.

Replicates (or biological replicates) would be qPCR runs on independently collected samples. That does not count your control vs your experimental groups. So for my work I had to collect 3 sets of control tissue and 3 sets of experimental tissue from independent sets of animals (in my case 3 generations but for mammalian work I think three different animals would be ok).

Parallel does imply that you ran the the samples together in the qPCR machine. I think the standard is that for each sample in a particular replicate you need to run three qPCR reactions in parallel. So in total you need to run 9 wells of qPCR reactions for each test group.


Are there any non-pathogenic gram-positive bacteria in human gut?

A recent Nature article, entitled A new genomic blueprint of the human gut microbiota, contains the following Figure:

[Fig. 3 Phylogeny of reference and uncultured human gut bacterial genomes]

I don’t know much about bacteria, but, according to their entries in Wikipedia, Actinobacteria, and most Firmicutes are gram-positive and, as these appear to be present in abundance in the human gut of healthy individuals, one assumes that they are not pathogenic to humans.


How is ATP involved in muscle contraction?

ATP prepares myosin for binding with actin by moving it to a
  higher-energy state and a "cocked" position.

  Once the myosin forms a cross-bridge with actin, the Pi disassociates
  and the myosin undergoes the power stroke, reaching a lower energy
  state when the sarcomere shortens.

  ATP must bind to myosin to break the cross-bridge and enable the
  myosin to rebind to actin at the next muscle contraction.

  The muscle contraction cycle is triggered by calcium ions binding to
  the protein complex troponin, exposing the active-binding sites on the
  actin. As soon as the actin-binding sites are uncovered, the
  high-energy myosin head bridges the gap, forming a cross-bridge. Once
  myosin binds to the actin, the Pi is released, and the myosin
  undergoes a conformational change to a lower energy state. As myosin
  expends the energy, it moves through the "power stroke," pulling the
  actin filament toward the M-line. When the actin is pulled
  approximately 10 nm toward the M-line, the sarcomere shortens and the
  muscle contracts. At the end of the power stroke, the myosin is in a
  low-energy position.

  After the power stroke, ADP is released, but the cross-bridge formed
  is still in place. ATP then binds to myosin, moving the myosin to its
  high-energy state, releasing the myosin head from the actin active
  site. ATP can then attach to myosin, which allows the cross-bridge
  cycle to start again; further muscle contraction can occur. Therefore,
  without ATP, muscles would remain in their contracted state, rather
  than their relaxed state.

Summary from: https://www.boundless.com/biology/textbooks/boundless-biology-textbook/the-musculoskeletal-system-38/muscle-contraction-and-locomotion-218/atp-and-muscle-contraction-826-12069/

Also this:

Essentially look up the cross bridge cycle (http://muscle.ucsd.edu/musintro/bridge.shtml)

I would also suggest reading it from the master himself here:
Huxley, A. F. "Muscular contraction." The Journal of physiology 243.1 (1974): 1-43.


What does "chlorophyll photosynthesis peak" mean in relation to photon wavelength?

First thing to note is that the absorption spectrum of chlorophyll A and chlorophyll B is similar but not the same. The reason for the appearance of absorption spectra is because the light is composed of photons of light.  Different photon has different  oscillation frequency and energy. The essence of Chlorophyll absorption is absorbing photons. After chlorophyll absorption of a photon, the electron transition from the ground state to the excited state, and get water electronic from the water cause decomposition. Only phonton that has resonant vibration frequency with electrons, and can meet the energy requirements of electronic transitions in order to be absorbed by chlorophyll. The Photon energy of different wavelengths of light is different. This is also the reason of different wavelengths of light affect chlorophyll light absorption.

Simply explain the absorption spectrum:

280 ~ 315nm  has small effect of plant morphology and physiological processes
315 ~ 400nnm absorption rate is small, impact the photoperiod, prevent stem elongation
400 ~ 520nm (blue) Absorption ratio of of chlorophyll and carotenoid in this light is maximum, it has the greatest impact on photosynthesis
520 ~ 610nm absorption rate is not high
610 ~ 720nm (red) low absorption rate.  It has a significant effect on photosynthesis and light cycle effect of  chlorophyll.
720 ~ 1000nm Low absorption rate, stimulate cell elongation, impact of flowering and seed germination
1000nm converted into heat

p.s. white light is a mixture of light


Source of hydrogen in reduction of oxygen in electron transport?

The equation you've shown is similar to other cellular respiration equations that I've seen, in that, it is trying to simplify a pretty complex process.

My guess is that you're doing first year cell biology like I am, so you probably know that there is a difference between the pH of the mitochondrial matrix (7.8 - making it alkaline) and the inter membrane space (roughly that of the cytosol - usually about 7). The lower the pH of a solution, the greater the concentration of H+. My point is that the solutions on either side of the inner mitochondrial membrane both have a concentration of H+.

So even though, when NADH is oxidised, it loses a H+ to solution, thereby contributing to the pH of the mitochondrial matrix, what is the likelihood that that particular H+ will be the H+ that is part of the molecule that takes the electrons at the end of the electron transport chain? I think low.

Indirectly, NADH does contribute H+ to the overall pH of the mitochondrial matrix but it doesn't directly give the H+ to "half an oxygen gas molecule".

Check the video below which is from the publisher of the textbook my course uses.

http://www.garlandscience.com/garlandscience_resources/resource_detail.jsf?landing=student&resource_id=9780815344544_CH14_QTM02


The Mystery of The Cretaceous' Songbirds

The short answer is that we will never know.
Luck can sometimes be a factor of who lives and who dies. But such an answer doesn't feel satisfactory given such a diverse group such as dinosaurs and other groups like Enantiornithes.

Together with hatchling specimens of the Mongolian Gobipteryx[35] and
Gobipipus,[36] these finds demonstrate that enantiornithean hatchlings
had the skeletal ossification, well-developed wing feathers, and large
brain which correlate with precocial or superprecocial patterns of
development in birds of today. In other words, enantiornitheans
probably hatched from the egg already well developed and ready to run,
forage, and possibly even fly at just a few days old.[34]
A 2006 study of Concornis bones showed a growth pattern different from
modern birds; although growth was rapid for a few weeks after
hatching, probably until fledging, this small species did not reach
adult size for a long time, probably several years.[37] Other studies
have all supported the view that growth to adult size was slow, as it
is in living precocial birds (as opposed to altricial birds, which are
known to reach adult size quickly).[26] Studies of the rate of bone
growth in a variety of enantiornitheans has shown that smaller species
tended to grow faster than larger ones, the opposite of the pattern
seen in more primitive species like Jeholornis and in non-avialan
dinosaurs.[38] Some analyses have interpreted the bone histology to
indicate that enantiornitheans may not have had fully avian
endothermy, instead having an intermediate metabolic rate.[39]
https://en.wikipedia.org/wiki/Enantiornithes

So we have this. Enantiornithes weren't completely bird like. They may have invested less energy in parental care. Perhaps taken longer to reach adulthood, longer to reach reproductive age. May not be as warm blooded as birds but not as cold blooded as a crocodile.  Maybe that is why they went extinct.
The Enantiornithes did not care much for their young, since they were born pretty much hardwired to be independent. This hard wiring probably worked find in a stable environment, allowing adult to spend more time and energy making more independent chicks. But in a hostile, changing world of post-impact, that was simply too much for a hard wired, semi-warm blooded chick. Especially one that took longer to reach reproductive age than most birds did. And birds by and large do invest in parental care of their offspring.
The answer is perhaps obvious if we could go back in time and observe the entire genera of Enantiornithes. But in the absence of a time machine and only fossils and estimated growth rates... we can only speculate.


Difference between Condensin and Cohesin proteins?

Condensin

Condensin I: present in cytoplasm during interphase, has access to chromosomes after prophase. Contributes to condensed chromosome assembly during prometaphase and metaphase [1].

Condensin II: present in nucleus during interphase, involved in chromosome condensation. Contributes to condensed chromosome assembly during prometaphase and metaphase [1].

Cohesin

It keeps sister chromatids connected with each other during metaphase and ensures that each sister chromatid segregates to opposite poles. "It facilitates spindle attachment onto chromosomes. It facilitates DNA repair by recombination." [2]

References:

Wikipedia contributors, "Condensin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Condensin&oldid=606814199 (accessed July 29, 2014).
Wikipedia contributors, "Cohesin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Cohesin&oldid=617481362 (accessed July 29, 2014).


Short answer
In a way, yes.

Background
One prime example where the sense of touch is diminished is when peripheral sensory neurons degenerate, which is called sensory neuropathy. Diabetes is currently a common cause of this disorder, resulting from the high blood glucose levels that damages the small blood vessels which supply the nerves. This prevents nutrients reaching the nerves, eventually damaging nerve fibres, which may end up in a disappearance of the nerve altogether (source: diabetes.org).

Sensory neuroptahy can lead to a multitude of complaints, including weakness, numbness and pain, usually in the hands and feet (source: Mayo clinic).It can also lead to the loss of ability to feel pain, changes in temperature and coordination when you lose proprioception is affected. The loss of the sense of pain is dangerous. An often heard complaint is that wounds to the feet are not noticed. If ignored, even minor injuries can develop into infections or ulcers (source: diabetes.org). I fact, my grandmother-in-law recently underwent an amputation of the lower leg, because of a diabetes-related, neglected injury to her toe. It lead to an ulcerating wound and eventually necrosis. At a certain point it caused terrible pain, but the initial wound had gone unnoticed.

A related condition is Carpal Tunnel Syndrome, also called median nerve compression. It is a condition that causes numbness, tingling, or weakness in your hand. It is caused by pressure on the median nerve that traverses a passage in the wrist called the carpal tunnel.

This may not be exactly the answer you are after, as sensory neuropathy mainy causes numbness of the extremities, rather than a complete loss of sense of touch. Remember, however, that blindness rarely results in a complete blackness. Beside the fact that the great majority of blind people are 'only' functionally blind, as they still have rudimentary visual function left, perceptions of phosphenes are in fact really common, and some people even start seeing complete visual scenes with people and objects included (Charles Bonnet syndrome). This is not unlike deafness, where many people still have residual hearing, yet too little to be of any functional use. For instance, people that are eligible for a cochlear implant often still have substantial residual hearing left. Like phosphenes in the blind, tinnitus in the 'deaf' emerges akin to 'phantom' sounds. These 'hallucinatory' sounds are actually generated more centrally by the brain after prolonged deafness. In short, blindness and deafness are relative, the great majority of folks don't lose their senses, they have reduced functionality of them.


Consider doing triplicates of just 4 combinations of cycle/dilution: low+low, low+high, high+ low, high+high.  Simpler.
Most important: prove you can extract DNA from a clean room.  If you extract from a real clean room and get no result from the PCR, maybe it is because you failed to collect anything or maybe nothing was there.   Idea - spray a known quantity of DNA into a room that will serve as your sham clean room.  Then do your extraction protocol.  You can test the cycle / dilution parameters with the sham clean room extraction and have those variables optimized for when you collect from a real "wild" clean room you did not dope with DNA.


Yes, HIV does attempt to prevent multiple infection of the same cell. Once a T cell or other cells are infected, HIV downregulates the CD4 receptor which it uses to gain entry. Because of this, there are less receptors so another HIV is less likely to infect that cell. Meanwhile, the infection itself upregulates CD4 receptors on other cells which means the downregulation is even more effective. There are other mechanisms but this is a major one.

Hiding means it is somewhere where we don't know where it is and it isn't that active. When HIV is active it is destructive but also the cell is aware it is there. The cell can then try to alert other cells that it is infected. If HIV isn't active but instead hiding, it can stay where it is without really being detected. Even the drugs we use usually only affect HIV whilst it is replicating. So again if it's in a cell that's long lasting and the HIV is not replicating then it is essentially hiding. Such a cell includes macrophages and memory cells when we are just talking about the immune system.

Will HIV reside in the lymph node? Well yes, this is an exciting place for it. There's loads of exposed CD4 receptors and lot's of it's favourite T cells about. An infected cell will transmit HIV to other cells when they are signalling to each other. Even worse is when a dendritic cell is infected. Instead of instructing the immune system how to detect HIV infected cells, it is infecting them.

HIV is an infection. As soon as the body detects it, it goes into overdrive trying to eradicate it. This means there are more cells for HIV to infect. More foreign material means the immune system is even further stimulated to make even more cells. However it doesn't want CD8 cells to proliferate too much nor too many HIV specific cells so driving too much proliferation is a bad idea. What HIV does do is make lots and lots of useless copies of itself. HIV particles that are so badly made they aren't functional. The body tries to fight these and makes more cells to combat these but there's no point because they aren't the problem. But this immune diversion and a larger target number of cells is exactly what HIV wants. Proliferation of HIV specific cells, particular CD8, is associated with delayed disease progression or control.

Usually the cancers caused by HIV are because of other viruses running unchecked. Kaposi's sarcoma or lymphomas for example.


Is there a way to chemically detect the presence of Fungus in a sample?

You could test for the presence of chitin, which is a fundamental component of fungal cell walls.  There is precedent for this: https://apps.dtic.mil/dtic/tr/fulltext/u2/a036986.pdf

Chitin is not only present in fungi though, it is also fundamental to insect and crustacean exoskeletons, and the occasional plant species (e.g. Aegagropila).


Short Answer: Fever cannot cure Ebola simply because the virus is not temperature-sensitive.

Background: Fever is a defense mechanism of the body which is specific to temperature-sensitive virus and bacteria. It is so because high temperature induces stronger immune response and makes the body hostile for the pathogen1. Ebola virus, on the other hand, is not affected by this mechanism because it can survive over a much broader range of temperature. Ebola virus is moderately temperature-sensitive, and can survive in temperatures as low as 4°C2 and as high as 60°C3 (at least for half an hour). So, in practical sense, it is not possible to cure ebola disease by heating or cooling the body, either naturally or artificially. But, if we ignore practicality, then Yes, you can cure ebola disease if you take an ice bath or a steam bath for hours so that your core body temperature drops to 4°C (in former case) or 60°C (in latter case). However, it wouldn't be a very nice idea as your body would become hostile for yourself before becoming hostile for the virus.

Having cleared the point about making body hostile for the virus, we are now left with another option: inducing stronger immune response. However, this will not work either because of a peculiar, but dangerous, property of such viruses: they use our defense system against us. Ebola virus, coming under the category of Filoviridae4, attacks host's immune cells, specifically monocytes and macrophages, to replicate inside them. This serves dual purpose; first, the virus has its work done, and second, it kills the host's immune cells. Although how ebola enters into immune cells is not understood, but it has been shown that the virus is helped by the host's antibodies in entering into immune cells5 (quite ironic). Ebola virus can also accomplish this through a process known as macropinocytosis6 (a form of endocytosis). You can refer to this page for its life cycle as well as the diagram of the ebola virion which I've used above, or just have a look at the diagram below from here:

References:

What is the benefit of fever during infections? - Biology Stack Exchange
Okware SI, Omaswa FG, Zaramba S, Opio A, Lutwama JJ, Kamugisha J, et al. An outbreak of Ebola in Uganda. Trop Med Int Health. 2002;7:1068–75. doi: 10.1046/j.1365-3156.2002.00944.x
Mitchell SW, McCormick JB. Physicochemical inactivation of Lassa, Ebola, and Marburg viruses and effect on clinical laboratory analyses. J Clin Microbiol. 1984;20:486–9
Wikipedia contributors. "Filoviridae." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 24 Sep. 2016. Web. 5 Apr. 2017.
Takada, A. & Kawaoka, Y. Antibody-dependent enhancement of viral infection: molecular mechanisms and in vivo implications. Rev. Med. Virol. 13, 387–398 (2003).
Hunt, C. L., Kolokoltsov, A. A., Davey, R. A. & Maury, W. The Tyro3 receptor kinase Axl enhances macropinocytosis of Zaire ebolavirus. J. Virol. 85, 334–347 (2011).


The bacteria wouldn't see any benefit from the warm water in the ~30-60 seconds you're washing your hands, neither would hot water "sterilize" your hands at temperatures you could tolerate. The reason you wash your hands with hot water is because the hot water+detergent soap mix is better for removing oil and dirt than cold water+detergent, which is supposedly where bacteria reside.

Interestingly, there was a study published saying that washing with hot water doesn't have much of an effect on bacterial load. Hot water for handwashing--where is the proof? (Laestadius and Dimberg, 2005). I'd be interested to look more into their methods but the paper is behind a paywall and I don't have access at home.

Also, this paper, Water temperature as a factor in handwashing efficacy by Michaels et al. is open and shows no evidence that hot water is any better than cold water for removal of microbes.

  [W]ater temperature exhibits no effect on transient or resident bacterial reduction during normal handwashing with bland soap.


Did vertebrates diverge from other deuterostomes via neoteny?

echinoderms are sort of bilaterally symmetrical, imagine if you took a velvet worm and then twisted it around in a big loop with the legs sticking out until the head was stuck to the tail end but still pointed away from each other. That is basically how echinoderms went from bilateral to radial. of course in practice this is done by rearranging hox genes but it is a good way to visualize it.  https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-5-22

as for chordates look at hemichordates (which also have endoskeletons) and you can see why the general belief is that tunicates evolved that life stage after branching off(kinda like barnacles) instead of vertebrates losing that life stage.


Does testosterone increase female sexual behavior?

I'll point you to this article by A. Tuiten et al.

To quickly answer your question, yes,  testosterone does have an enhancing effect on the sexual behaviour of human healthy adult females.

The (admittedly small) study indicated that after an dose of testosterone was given to the women there was found:

a statistically significantly [sic] increase in genital responsiveness (P = .04)
a statistically significant association between the increase in genital arousal and subjective reports of "genital sensations" (P = .02) and "sexual lust" (P = .01)

A time lag was reported from the administering of the dose to effects being seen of approximately 4.5 hours.

References

 Tuiten A. 2000. Time Course of Effects of Testosterone Administration on Sexual Arousal in Women. Archives of General Psychiatry 57: 149–153.


Hundreds of Red Spiders in Individual Webs

It is a black-tailed red sheetweaver, Florinda coccinea.

Identified by its red body colour , location (USA) and black caudal
tubercle.

More images to be found on bugguide.net

  It is a species of web-building spider belonging to the family Linyphiidae. It is the only species in the genus Florinda. It is sometimes known as the red grass spider. This species is common in the southeastern United States, inhabiting grasslands, lawns, and agricultural fields.

Reference: Wikipedia


What is the translation termination efficiency in mammalian cells?

There is a paper for transfection of mammalian cells here which has a bit of comparison of stop codon and protein yield.

Otherwise this article suggests having a 'rare' codon after the stop to prevent readthrough. But yes, I'm not sure why one wouldn't simply put two stops after each other.


Can flow-FISH be used on metaphase cells?

Don't know if this will help but Maurizio Carbonari in cytometry A in 2016 published on methods which allow for cell cycle analysis.

The abstract

  Formamide has long been one of the most widely used reagents in the study of nucleic acids. However, the use of formamide for treating cells to be analyzed by flow cytometry is a recent development and is restricted to measuring telomere lengths by flow‐FISH. In this field, we have published several papers in order to observe the effects of formamide treatment on cells at room temperature. We therefore discovered that, with suitable modifications, a short and simple incubation in this ionizing solvent facilitates cell cycle analysis by flow cytometry, equivalent or superior to that obtained with treatments in alcohol, acetone or detergent in hypotonic solution. Even using a bulky and problematic stain (low quantum efficiency and G‐C base preference), such as 7‐aminoactinomycin D (7‐AAD) which, on the other hand, has the advantage of being excited at 488 nm and does not bind to the RNA, it is possible to obtain excellent coefficients of variation and (G2–M) mode/(G0–G1) mode ratios. These parameters, especially if stained cells are washed before acquisition, arrive at optimal values. It is noteworthy that the ability to wash the cells stained for DNA content analysis without affecting the stoichiometry of the staining has not been described elsewhere in the literature. With formamide treatment the doublets are practically absent, sample recovery is efficient, as well as the preservation of physical parameters, and the stained cells can be stored for at least 10 days at room temperature before acquisition.

As for Flow-FISH, it is a method used to measure telemore lengths.

Vyacheslav I Borisov et al. in Current Protocols in Cytometry. 2014
Published on applying flow-fish to look at M phases.


Can exercise strengthen tendons and ligaments?

yes..It takes approximately 10 weeks of regular resistance exercise to strengthen your tendons, and it takes longer for them to thicken. You can expect up to 20 percent increase in strength and thickness of your ligaments and tendons with regular training.


Is "exhaustion" of the Hodgkin-Huxley membrane at constant stimulation a real phenomenon?

This phenomenon is called depolarization block and it occurs in real membranes in current-clamp experiments.

The key mechanism is that the membrane has not been allowed to repolarize sufficiently to relieve the inactivation of sodium channels. The Hodgkin-Huxley model reflects this in the "inverted" voltage-dependence of the h gate (sodium inactivation gate)--inactivation is greater at higher voltages. This means that sodium channels cannot open again, or trigger another action potential, until the membrane is repolarized. Canonically, the need to relieve inactivation of sodium channels is the reason for the afterhyperpolarization phase of an action potential where the AP downstroke becomes transiently more negative than the resting potential.

The relevance of depolarization block in in vivo physiological conditions is not well studied. It is not likely that depolarization block occurs in well-behaved neurons under physiological conditions. However, it's possible that it does occur during pathological states.


A congenital disorder or disease is a disorder that is present at birth.  This term can be applied to many conditions, including some that are infections.  More typically, the term is used for developmental birth defects such as spina bifida and cleft palate.

Although HIV/AIDS can be congenital (since a mother has about a 25% chance of passing it to her newborn), most cases of HIV/AIDS are not transmitted by pregnancy and birth, but rather by sexual contact between adults.  Hence it is inappropriate to call AIDS congenital since most cases do not occur in newborns.  This can be contrasted with, for instance, spina bifida and cleft palate, which essentially only occur in newborns and so can reasonably be called congenital disorders or diseases.

A specific case of HIV/AIDS, one which has occurred in a newborn, can be called congenital HIV/AIDS, but HIV/AIDS cannot, in general, be called congenital.


Difference between Medical and Airport scanner radiation

The type of radiation is quite different in a medical X-ray vs. an airport scanner.

Medical X-rays are high frequency (beyond ultraviolet) radiation, typically on a wavelength of a few angstroms.  While I would emphasize that @Ram is right to point out that there is not very much radiation in a medical X-ray since electronic detectors have been in place over film, the radiation itself is capable of penetrating the entire body and causes ionization.  The body can tolerate a certain amount of this, but that's why we use X-rays - they go through just about anything but bone/minerals and metals.

Airport security scanners emit terahertz radiation, which has a wavelength between microwave and infrared.  This is a very low level of energy per photon.  Terahertz radiation will not penetrate more than a centimeter of light material, which is more suitable to find hidden metal objects (which reflect terawaves).  Relative to X-rays it causes practically no radiation damage.  The intensity of the radiation is also pretty low since these scans are also detected by digital cameras, which are quite sensitive.

Compare the machinery.  X-ray technicians, who might have to take dozens of X-ray exposures a day, usually go behind a protective screen to take a medical x-ray.  The airport body scanners are open to the air and the terahertz radiation spills out into the crowd and the workers stand by it every day.  It has practically no expectation of being hazardous.  This device is pretty good as frequent fliers can have as many scans per year as are needed and health concerns are not significant.

Its always possible we might find some issues with Terahertz radiation in the future, but its hard to imagine it - its safer than standing 2 feet away from a working, closed oven.


How to Extract RNA and perform RT-qPCR from very few cells ( ~5,000)?

You can consider use of single-cell RT-qPCR kits such as this one if you have the budget for them. (Note: I have not personally used this kit, just putting out an idea)

  The Ambion® Single Cell-to-CT™ Kit contains a complete validated
  workflow for gene expression analysis for samples containing 1–10
  cells. Each kit contains reagents for sample preparation, reverse
  transcription, pre-amplification, and qPCR that have been optimized
  together in a simple workflow that can be completed in only 5 steps
  (see figure).


Finding different Proteins with same function

There will be a lot!  Chromosomal dihydrofolate reductase and type II (plasmid) dihydrofolate reductase have not been derived from common  ancestor but catalyze completely the same reaction including stereochemistry by the authority of Brito.

Bacterial phenylalanine hydroxylase too is completely different in sequence of amino acids from phenylalanine hydroxylase from mammals (where plants have no such protin). The literature shows this paper Cloning and nucleotide sequencing of phenylalanine dehydrogenase gene of Bacillus sphaericus.


Fairy flies can be so small because they mooch off other insects' eggs, this is one of the reasons why they need to be small, then after that, they don't need to eat as they will die in only a few days. Information can be found on the "how do they manage to be so small" section of this PDF: https://www.cell.com/current-biology/pdf/S0960-9822(18)31343-5.pdf


What would cause crows to be attracted to a human body?

I think the key is "his fragrant corpse." When an animal dies and begins to rot, a number of quite smelly chemicals are given off, including putrescine and cadaverine. Crows and other carrion birds like vultures are probably very sensitive to these compounds, rather like sharks are to the smell of blood.


I would argue that the orbiculares do have antagonists. To some extent, levator palpebrae superiorus antagonizes orbicularis oculi, and zygomaticus major/minor as well as risorius antagonize orbicularis oris.

I can think of three muscle that don't have obvious antagonists:

Stapedius
Tensor tympani
Articularis genu

1 and 2 essentially perform the same action, to dampen sounds reaching the cochlea. 3 elevates the suprapatellar bursa.


How does the brain know what to remember and what not?

The body of work on this topic huge, so I'll just try to mention a few things.

On the cognitive level, one possible answer is salience (also see here for an article specific to the visual system). You can think of this (in a somewhat circular answer) as the thing that makes certain stimuli stand out from others. Salient stimuli capture bottom-up attention. Another possible answer is top-down attention. This is where you actively/deliberately pay attention to something.

In terms of mechanism, we have to think about different types of memory. For example, there are separate long-term and short-term memory systems (among many other distinctions). In general, there are hypothesized gating mechanisms that determine the information that can enter memory. The gating systems are controlled by some signal that says 'store this information' or 'ignore this information'. Different memory networks can have different gating systems.

There's a lot of work looking at neuromodulators as gating signals. Dopamine and acetylcholine are some prominent examples. For example, people have found that dopamine can modulate synaptic plasticity (the strengthening and weakening of connections between neurons, which is thought to be a primary mechanism of long term memory storage). It can also cause cortical remodeling. For just a couple examples, see:

  Zhang et al. (2009) Gain in sensitivity and loss in temporal contrast
  of STDP by dopaminergic modulation at hippocampal synapses.

  Bao et al. (2001) Cortical remodelling induced by activity of ventral
  tegmental dopamine neurons.

  Froemke et al. (2007). A synaptic memory trace for cortical receptive field plasticity.

On the behavioral level, stimulating the dopamine system can induce particular forms of learning (which you can think of as a form of memory). For example, if you stimulate the dopamine system, an animal may tend to repeat the behavior that led to the stimulation. A pathological version of this is thought to be what happens during addiction with certain classes of drugs that stimulate the dopamine system (e.g. cocaine, but not lsd).

Interestingly, many of the same mechanisms appear to work across species, from sea slugs to humans). Although,sea slugs can't remember going to a shop after work.


Is it possible for an organism that is polypoloid with an odd number of sets of chromosomes (e.g. 5 sets) to be fertile?

Yes, it is possible. There seems however to always come up with a cost in fertility eventually of the order of 2/3!

You should have a look at Ramsey and Schemske 1998. I don't remember it well enough to make a good summary (maybe someone else could do that?!) but it is a classical article. Here is a sentence from their abstract

  In contrast to the common claim that triploids are sterile, our results indicate that the triploid bridge pathway can contribute significantly to autopolyploid formation regardless of the mating system, and to allopolyploid formation in outcrossing taxa.


Picture is not very good, but I think this might be an Eastern Buckmoth Hemileuca maia caterpillar.

 Photo credit: Gary L. Spicer ; Source: butterfliesandmoths.org
Description: From the University of Kentucky:

The two-inch long Buck Moth caterpillar is brown to purplish-black with numerous yellow spots. The body is protected with branched reddish spines that may have red or black tips....
Common...from spring to mid-summer.

Reaction: Your wound/reaction would not be an unexpected reaction from touching this caterpillar species. From UFL IAFS:

The spines in the buck moth occur on raised, sclerotized (hardened) portions of the larva's cuticle that are known as tubercles and scoli. The spines found on these structures are associated with venom glands that occur within the caterpillar's body... The sting produces pain immediately, which then spreads to nearby lymphatic nodes. The caterpillar's sting then causes swelling and redness to occur. These symptoms can last for as little as a day to over a week. Wagner (2005) reported that the stings he received from a buck moth caterpillar were still present after ten days and the venom of the caterpillar caused a small hemorrhage where each spine had stung him. According to Diaz (2005), severe reactions to the venom of the buck moth (such as anaphylaxis) are rare.

Treatment: The video here suggests running your hand under cold water, air dry, use tape to get out remaining spines, and then apply some ice. UFL IAFS corroborates this approach as well.

Range: According to the incidence map on butterfliesandmoths.org, H. maia is found in Texas:

Wikipedia corroborates the range of this species to include Texas.


Vaccination and population dynamics of an epidemic

I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate.

The number of people who have this disease will be fewer each week.  I think this makes sense because at 16 / km^2, you can expect that practically nobody will ever see each other.

This is a flawed model though because it assumes that the mean density is uniform.  In a city like Helsinki (2,800 / km^2) you would expect the disease to get caught by nearly everyone in just a week.

Helsinki: n = 94.5%

In Lapland (which has a population density of less than 2/km^2) , the transmission rate (beta) of 0.0015 translates to 0.003 incidents per week.  This is not a terribly catchy disease, you probably have to kiss someone, wear their clothes, or eat off their plate to get it. With only 2 people per km^2 the chances of this happening appear to be poor, though even here families tend to get the disease and the model breaks down.

So to sum up, the model is consistent within itself, BUT it is a baby model and makes some broad assumptions that do not help it describe the dynamics of the disease in a national scope or in a highly detailed scope.  It probably describes the chances balls will collide in a box as well as disease spreading.


Can someone identify this plant I saw in NYC (might not be native idk)

That looks like it is probably a single leaf coming up from a tuber.

That fact combined with the mottled pattern on the petiole (leaf stalk) and the shape and branching pattern of the leaflets makes me guess it was something in the genus Amorphophallus.

Example image:

Other images for the "voodoo lily".


What is this? Found in southern Illinois

Nice find! It looks to me like a Bush Cicada or scientificly Neotibicen dorsatus. It also looks like its injured, because we can see the white liquid around its wings and abdomen. Bush Cicadas tend to have a yellow or brown color but as shown here there is a wide variaty to the colourations that it might have:

Size (Adult, Length): 35mm to 57mm (1.38in to 2.24in)

Identifying Colors: yellow, brown, white, gold, black

North American Reach (Though Not Limited To*): Arizona; Arkansas; Colorado; Illinois; Indiana; Iowa; Kansas; Kentucky; Louisiana; Minnesota; Mississippi; Missouri; Nebraska; New Mexico; North Dakota; Oklahoma; South Dakota; Texas; Wyoming; Mexico.

Here are and some photos:

Adults:


Why are animal births not taken as seriously as human births?

Our heads are bigger.

There's some debate on the issue, but in essence, human brains, and therefore heads, are very large relative to our body size.  This is handy for all the intelligent things we like to do, but can be rather painful during birth.  Because we walk upright, the size of a newborn's head is actually a non-trivial fact during the birthing process.  There are two major implications.

The first is that human birth hurts.  You can watch the birth of other animals and they seem to brush it off, but for humans, forcing that huge head through a relatively small birth canal is difficult.  Evolution has (supposedly) limited the size of the hips because, while that would allow an easier birthing process, it would negatively impact our ability to walk.  As such, it has to hurt.

Secondly, in order to make the process easier, humans rotate during birth.  The end result is that, unlike even other closely related primates, humans come out backward in a way that is very difficult for a birthing female to attend to.  This almost requires having another person or two on hand to help out.  This would, of course, be a huge reinforcement for social connections.

A few books I know of touch on this.  Up From Dragons deals with the brain size/hip size issue and The Invisible Sex talks about rotation during the birthing process and the social implications.


The complexity of the immune response requires foreign proteins to be bound first by presenting cells which happen to be like macrophages - cells that are like garbage disposals. Why some proteins are simply gobbled up and yet others are preserved and presented to the resident T cell helper population is related to the size and sequence of the protein. In other cases, even small molecules (allergens) can bind to native normal proteins and make them look abnormal.
The use of immunoglobulin (semi purified blood) was used in treating certain diseases in the past. These sera were usually developed from animals purposely infected with the disease. Though these proteins also elicited their own immune response (side effects) the kinetics of that event was days to weeks whereas the binding of the immunoglobulin to its target(the virus protein) is a first order event occurring in minutes. Clearance of that antibody antigen complex over hours to days Avoids the catastrophic exponential growth of the virus by keeping the numbers low. Eventually tho side effects WILL happen if you keep giving the serum


How can a pathogenic bacterium be avirulent?

Streptococcus pneumoniae is a pathogenic species. Streptococcus pneumoniae R6 is an avirulent strain of this species. Presumably this means that specific virulence genes that are present in virulent strains of Streptococcus pneumoniae are missing or mutated in the R6 strain. In fact the most likely difference would be that virulence factors are encoded by a plasmid that has been lost in the avirulent strain.

The use of avirulent strains is a common strategy for studying pathogenic bacteria, although obviously it precludes studying mechanisms of pathogenicity directly.


Which life is supported in sterilized 100% pure water?

Of course many life forms can survive for some time in 100% water. A human for example can survive about 4 minutes in 100% water but I doubt this is what you are interested in! Although there is no commonly accepted definition of life, I think we can say that we all agree that any life form needs to reproduce or somehow grow. So I take your question as

  What life forms can reproduce or at least grow "potentially indefinitely" in 100% water?

Any life forms, to grow or reproduce needs matter to make its own constituents. As such, pure water won't provide with such nutrients and no life form can survive in the long run in 100% water.


I think you need to consider that oxygen is toxic to large groups of microorganisms, because it poisons their electron transport chains.

Strict anaerobes does not tolerate the presence of oxygen at all and as such I would argue that life can survive and thrive without O2.

Also life on earth evolved under conditions were O2 levels were extremely low, in fact when some organisms started to release oxygen into the atmosphere it caused an extinction event (Great Oxygenation Event).

So I think you need to change your question to why did life adapt to the presence of oxygen?


Any forms of pneumonia that can be caught?

Pneumonia means inflammation of lungs- especially alveoli.
There can be many causes of it including infectious agents, autoimmune condition and  chemical irritants. Pneumonitis is a more accurate word for lung inflammation, the causes of which includes the abovementioned agents; Pneumonia in common usage refers to the condition due to infectious agents such as bacteria, viruses and fungi.

In almost all the cases the infectious agents are airborne in the form of aerosols (spread by cough) and infect the respiratory tract directly. Some cases of fungal pneumonia (Pneumocystis, Penicillium) are observed more commonly in immunocompromised individuals, such as AIDS patients, and dissemination happens via spores.

As you can intuitively figure out the infectivity is different for different pathogens.


Do omnivore mammals vary food preferences based on dietary needs?

For what concerns amino acids, mice rapidly reject meals that are not balanced in essential amino acids and continue to look for other kind of foods. This behavior is called aversion response and it is an adaptive phenomena that can be observed already 20 minutes after exposure to the unbalanced food. The mechanism involves brain sensing of uncharged tRNAs. The significance of the aversion response is to minimize depletion of essential amino acids that can not be directly synthethized but are required for protein synthesis. You can find good reviews in PubMed, for instance Gietzen et al. 2007, Annual Review of Nutrition, and Gietzen and Aya 2012, Molecular Neurobiology.


What is the average volume of the hippocampus?

The average values of right hippocampus were recorded as follows weight 4.11572 gm, length 6.996 cm, width 1.998,volume 13.978 and surface area11.839 cubic centimetre while left hippocampus mean values were weight 3.96458gms,length 6.995, width 1.998,volume 13.976 and surface area 11.713cc. B. Narasinga Rao, K.R.S. Prasad Rao, R. Ramana Rao. 2012. Morphometric study of hippocampus in adult human brains. Int J Basic Appl Med Sci 2: 139-143.

Men and women had identical volumes of amygdala and hippocampus, as well as dorsal prefrontal cortex Ruben C. Gur, Faith Gunning-Dixon, Warren B. Bilker, Raquel E. Gur. 2002. Sex Differences in Temporo-limbic and Frontal Brain Volumes of Healthy Adults. Cerebral Cortex 12: 998-1003

Hippocampal volume change with age: Hippocampal volume diminished by 20% from 3,584 ± 136 mm3 at age 36 to 2,870 ± 220 mm3 at age of 85, corresponding to a volume loss of about 14.6 mm3/year (Schuff N., et al. 1999. Age-related metabolite changes and volume loss in the hippocampus by magnetic resonance spectroscopy and imaging. Neurobiol Aging 20: 279–285).


Can the regeneration mechanism of lizards be used in humans?

Actually there are some studies to find out your answer. Some of the studies claim that they have found a special enzyme and some say micro RNAs give salamanders the capacity of regeneration. But until now, humans couldn't use salamander's regenerative ability. Maybe you would like to know there is a mammal (african spiny mouse) with special regenerative capacities which include regeneration of its skin and cartilage without scarring.

References:

'Skin shedding and tissue regeneration in African spiny mice (Acomys)' Ashley W. Seifert,   Stephen G. Kiama,   Megan G. Seifert, Jacob R. Goheen, Todd M. Palmer & Malcolm Maden
Microarray analysis of microRNA expression during axolotl limb regeneration.
For further studies I recommend searching "salamander and regeneration", "african spiny mouse and regeneration" in pubmed ;)


As far as it can be deducted from the picture you ask about Appendix or just Coecum. This is a normal finding and not abnormal one. (You can see a terminal Ileum as well).
If other pictures were provided it could be possible to give more exact answer.


Is there any problem with using a single stop codon with a single CDS in prokaryotes?

If there is only one CDS, presumably there will be a transcriptional termination directly after the CDS (after the stop codon actually), which makes any read-through coming from using a single stop codon almost negligible.


Is it possible to produce a tangible mass of DNA/RNA using a PCR reaction?

PCR amplifies only DNA not RNA.

A PCR reaction is typically within the  micro liter volume, and can go down to the nano liter volume for qPCR. The maximum volume of a PCR tube is 200 microliters. The maximum volume a 96 well thermocycler can handle per well is usually 100 microliters. So the maximum amount of reagent volume one thermocycler can handle at a time us 9.6ml

I have never seen anybody scale a PCR to mili liter volume, as that would be rather expensive and excessive.

However if some some reason, somebody did do as you say, yes it is possible to obtain visible quantities of DNA. (Removal of impurities would be required first... ie unreacted dNTP, primers) And given that we can obtain visible quantities of DNA by extracting DNA from bacteria or salmon sperm.. I am sure a chemist somewhere would be able predict the physical properties of that DNA mass.


What is the length of the centromeric repeat sequence in a human?

No specific length for centromeres. Actually in a real chromosome in a cell, centromeres are usually very condensed sequences of DNA, they are winded and folded (if you know about the DNA structure). Thus you cannot measure the length of the centromere unless you decondense the chromosome first.


The main difference between tracheal gas exchange, and other forms of gas exchange (except simple diffusion) is that it is generally a passive process. Organisms with lungs, gills, or other modified respiratory organs can actively pump the oxygen-containing medium (usually air or water) across their respiratory surface, and some also pump their blood across in the opposite direction to cause a countercurrent exchange to enable maximum efficiency of oxygen/CO₂ transfer.

The tracheal system is a more efficient mode of gas exchange than diffusion since it does not only involve the oxygen passing over the organism's body surface (a semi-permeable membrane) which limits the rate of movement. Instead the epidermis is invaginated to form tracheae (tubes) through which air can travel passively. The tracheal system is highly branched and terminates at tracheoles (fluid-filled sacs) which closely line respiring tissues to provide oxygen and allow release of CO₂.

Tracheal respiration limits the size of insects since their oxygen demands will not be able to be met if the air has to diffuse very far. Some insects require more oxygen than others: many larger insects and more active insects have evolved to supplement the tracheal system with pumps, gas gills (permanent or temporary bubbles of air which aquatic insects carry), or mechanically ventilated air sacs (honeybees have these, see Gullan & Cranston, 2005; and Snodgrass, 1956).

Furthermore, tracheal systems can be 'open', 'closed', or the insect can engage in discontinuous gas exchange. Insects with open tracheal systems have spiracles (holes in their cuticle). Closed tracheal systems are more common in aquatic insects, they come in two major designs: highly branched systems over the internal surface, allowing cutaneous gas exchange; and filamentous or lamellate  arrangements, which are analogous to a primitive gill (see Wigglesworth, 1964 or Gullan & Cranston, 2005 chapter 10 for more on aquatic insect adaptations). Discontinuous gas exchange involves co-ordinated opening and closing of different spiracles which results in a uni-directional current allowing more effective ventilation.

References

Gullan, P.J. & Cranston, P.S. (2010) The Insects: An Outline of Entomology. John Wiley & Sons.
Snodgrass, R. (1956) Anatomy of the honey bee, Comstock Publ. Assoc. Ithaca, New York,.
Wigglesworth, S.V.B. (1968) The Life of Insects. New American Library.


During weight loss, do we inhale more oxygen?

First one needs to make it clear that oxidation of foodstuffs, either those in the diet or from deposited reserves, occurs in order to generate energy (ATP) for life’s processes — the most evident to the non-biochemist being to perform muscular work. So, as the poster correctly implies, this will occur in both fasting and non-fasting individuals, and the fairest comparison would be between the same individual performing the same amount of energy-requiring processes.

Let us consider this comparison in the simplest situation where the person “losing weight” is fasting, i.e. has no food intake (rather than being on some fancy diet). After his glycogen has been depleted, the fasting individual will be producing all the energy for his various needs by oxidizing triglycerides that had been deposited previously in his fat cells. The amount of oxygen he inhales (assuming this is strictly related to requirement — I’m not a physiologist, so I don't know) will be that required to oxidize the triglycerides to produce this required energy.

Now compare this to the same individual, not fasting. His energy needs have been assumed to be the same as in the fasting state, but he is generating this energy from his food intake. Making the unlikely assumption for comparison that this were all triglyceride, the amount of oxygen needed to oxidize this would be exactly the same as the fasting individual.

I think that deals with the fallacy in the question, perhaps caused by not reflecting on what the oxygen inhaled by the non-fasting individual is used for. Technically one should admit that if the simplistic assumptions do not hold, the strict equivalence would not either. Different foodstuffs (carbohydrates, fats, proteins) are in different oxidation states, so the amount of oxygen required to oxidize them in the fed individual would depend on diet. If the food intake of the fed individual were greater than his needs and he was depositing glycogen or fat, extra ATP would be required to do this, which would likely be generated by oxidative phosphorylation. No doubt one can think of other possibilities, but these were not the focus of the question.


First and foremost, it looks like the original article is slightly less dramatic:

  Parasitoid ovipositor tips have a higher content of the transition metal zinc compared with the cuticle elsewhere on the ovipositor

So a 'higher concentration' isn't quite the same as 'tipped with'. It looks like they are describing a higher numbers of metal ions, rather than pure metal:

  The presence of transition metals in insect cuticle and mandible is hypothesized to increase material hardness to permit cutting through hard substrates with minimal wear

There are many examples of organisms using inorganic chemistry to make materials. The overall topic is called biomineralization and you even mention teeth - which is hydroxyapatite (not really organic chemistry!).

However, a pure metal like zinc is unusual, I think. There are examples such as the snail that has an iron pyrite 'armor' or even the iron nanocrystals in ferritin.

More spectacular examples include the bacteria that produce gold particles

  As a result, Au
  detoxification is mediated by a combination of efflux, reduction, and
  possibly methylation of Au-complexes, leading to the formation of
  Au(I)-C-compounds and nanoparticulate Au0.

Where Au0 is pure gold. I don't know of any other examples of pure zinc in organisms, but there is a nice review here of zinc biochemistry.

When you say 'synthesise' I assume that you mean 'deposit'.