Can a human acquire a memory of an animal?

No, it can't be done for a lot of reasons. Here are just a few.

1) Memories are stored in electrical pathways, not the the cells themselves. You don't have 1000 memories in a chunk of brain that contains 1000 neurons. If you don't get the entire pathway, you won't get the memory.

2) Once a nerve is cut, it won't fuse with another cut nerve. All you'll have is a chunk of dying animal brain in your head. Even if a skilled neurosurgeon united the blood vessels of your brain to those of the chunk to keep it alive, the nerves themselves wouldn't become a working part of your brain. All you'd have (at best) is a useless chunk of another animal's brain sitting where your now-missing chunk was.

3) Animals are different from us. Your body would recognize the different-animal brain matter as foreign, and would make antibodies to it and reduce it to mush (if one didn't die of infection before then).


Loss of taste and smell during a SARS-CoV-2 infection

This is not completely clear to say the least, but there are some hints. Please keep in mind that there was not much time for extensive research, since this disease is still quite new. What seems clear (at least at the moment) is that most like the nerve cells (in the olfactory bulb as well as in the taste bud) are not directly affected, since they do not express the ACE2 receptor on their surface which is needed by the virus to enter a cell.
In the nose, there are two studies, which link the loss of smelling to massive damage of the epithelial cells surrounding the nerve cells. These cells have a lot of ACE2 receptors and are thus susceptible for an infection with SARS-CoV-2. An infection leads to the death of these cells, which disturbs the balance of ions for the nerve cells leading to loss of smell. Specifically this seems to affect sustentacular cells. Since the epithelial cells recover over time, smelling comes back. This also fits the description of affected people, who describe the loss of smell as a sudden event, while the recovery happens gradually.
For the tasting it is less clear, but it also seems that supporting cells (which carry ACE2 receptors) are affected. For sensing of sharp (for example Chili), which is not chemical sensing but via pain sensing, it seems that at least a part of the cells are also susceptible to the virus as they express ACE2.
Taken together this seems to indicate that important cells in the vicinity of the nerve cells are hit by the virus, causing anosmia and ageusia. It is also important to note that not all people who lose their sense of smell also lose the sense of taste.
For furter reading have a look at the references, the first one is a nice article in the scientific american, the second goes deep into the topic with a lot of nice images.
I will have a deeper look into the topic later and probably update the answer.
References:

Mysteries of COVID Smell Loss Finally Yield Some Answers
COVID-19 and the Chemical Senses: Supporting Players Take Center
Stage
Massive transient damage of the olfactory epithelium associated with
infection of sustentacular cells by SARS-CoV-2 in golden Syrian
hamsters
SARS-CoV-2 Receptor ACE2 Is Enriched in a Subpopulation of Mouse
Tongue Epithelial Cells in Nongustatory Papillae but Not in Taste
Buds or Embryonic Oral Epithelium
Real-time tracking of self-reported symptoms to predict potential
COVID-19


All neuromodulators (dopamine, serotonin, acetylcholine, histamine, and norepinephrine) act only on metabotropic receptors?

Not all neuromodulators act only on metabotropic receptors. However, you are correct to observe that this is a general rule of thumb.

Of the substances you have listed:

Acetylcholine is not primarily a neuromodulator, but rather a "normal" neurotransmitter. As such it acts on both ionotropic and metabotropic receptors.
Serotonin - the one exception among the neuromodulators you have listed - acts on numerous classes of metabotropic receptors, but also on the 5-HT3 receptor, which is ionotropic.
All other neuromodulators you have listed act on metabotropic receptors only.

This tendency of neuromodulation to be metabotropically mediated is possibly a consequence of the nature of the neuronal function itself. Neuromodulatory systems do not per se relay information, but change how other information relays work. As such there is no need for the most rapid, temporal, coding (best achieved via the more rapid ionotropic signal transduction), and a slower coding may even be more efficient.


can self-fertilization in flowers be called asexual reproduction?

According to this article from Berkeley, asexual reproduction is:

  Any reproductive process that does not involve meiosis or syngamy

Using this definition of asexual reproduction and knowing self-fertilization involves meiosis and syngamy, it is not asexual.


Do large animals experience a meaningful delay when moving their most distant appendages?

Yes, larger animals do experience larger delays in movement.

There have been studies of size difference vs sensorimotor delays in terrestrial mammals, https://www.ncbi.nlm.nih.gov/pubmed/30158304

That graph is for innate reflexes of a needle to the hind versus a kick-time. Perhaps no one dared to prick a blue whale.

Elephant vs shrew, heartbeat of 30 vs 1500 BPM, elephant 50 times slower than the shrew. Larger animals compensate with a better ability to predict physics and kinematics using their larger brain.

There are other kinds of movements which have more complex neural pathways that the graphs of pin-prick reflexes, that are even slower compared to size, you can study the physiology of eye to hand response in humans which varies from 120ms to 270ms for different humans.

It does have an effect on survival for example with a mongoose versus a snake, the mongoose has more versatile and faster reactions.

There are also weasel attack videos on the web.
some graphs here


Do male mammals other than humans have nipples?

Most mammalian males have nipples. The duck-billed platypus does not have nipples but you begin to see development of nipples in marsupials (Park and Lindberg 2004) like the opossum and kangaroo.  Development of a complete nipple begins in the eutherian (placental) mammals.

The mammary glands develop early in the embryo along a pair of ridges called the mammary ridge, mammary lines, or milk line (shown in an adult human in the figure below, taken from Wikipedia). The nipples form along this line. In humans, this happens during the fifth week of development. Within a few days, nipples begin to form. The number of nipples pairs that form is characteristic of the species (e.g., 1 pair in humans to 9 pairs in pigs). The development of nipples occurs before sexual differentiation begins which, in humans, is during the sixth week of development. That's why both males and females have nipples. This same order of develop occurs in other mammals, revealing our common ancestry.

However, because the process is under genetic control, mistakes can happen. Occasionally, humans (and other mammals) can develop extra nipples, the so-called supernumerary nipple(s). The most common places that humans develop one or more supernumerary nipples are identified by the circles in the figure above. The actor Mark Wahlberg is not shy about showing his.

For a general overview of mammary gland development, Dr. Jacqueline Veltmaat has a nice web page that highlights her research in this area. For those interested in the more technical genetic aspects of mammary gland development, a paper by Watson and Khaled (2007) reviews the genetic processes that regulate development of the mammary gland in mammals, based on the mouse model system. The article covers all stages of mammary gland development, from the embryo through puberty to pregnancy. Their Figure 1 shows one row of embryonic mammary buds (labeled MB1 - MB5) in the embryonic mouse. In the case of the mouse, all of the mammary buds will develop into fully functioning mammary glands.  Another paper by Robinson (2007) discusses the signalling pathways during development of the mammary glands.

Literature Cited

Park, C.S. and G.L. Lindberg. 2004. The mammary gland and lactation. pp. 720-741 in Dukes' Physiology of Domestic Animals, W.O. Reece, ed.  (Publisher not identified.)

Robinson, G.W. 2007. Cooperation of signalling pathways in embryonic mammary gland development.  Nature Reviews Genetics 8: 963-972.

Watson, C.J. and W.T. Khaled. 2008. Mammary development in the embryo and adult: a journey of morphogenesis and commitment. Development 135: 995-1003.


Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.

Since it's connected to the head trauma by definition, there is in principium no other cause of it.

The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:

the acceleration of brain causes increase of pressure
the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)

These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:

  Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.

The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and

  Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.

Microinjury is also linked to triggering of cell death pathways in brain cells.

The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.

Sources:

Overview study
Robbins and Cotran pathologic basis of disease


Reference Request: Human visual system takes in $10^7$ bits/sec at the periphery and compresses it down to 50 bits/sec deep inside

How about this:
https://www.springerprofessional.de/data-compression-and-data-selection-in-human-vision/3218014

The original link in the Abstract referenced (https://link.springer.com/content/pdf/10.1007%2F978-3-642-04954-5_7.pdf) above isn't available anymore, but I found a repository:

https://webdav.tuebingen.mpg.de/u/zli/prints/ZhaopingNReview2006.pdf

I don't think the review is peer reviewed, but maybe you find a reference in there (it's not my field, so I guess you know more on where to look ;-)

She's now in Germany:
https://www.researchgate.net/profile/Li_Zhaoping

If you don't find anything, maybe you can ask her on researchgate directly.


Is there redundancy in the auditory system like there is in the visual system?

There is certainly redundancy in the auditory system, well demonstrated by Gal Chechik et all

It is also clear that there is pronounced intersensory redundacy, involving auditory systems here

Another article discusses clear auditory redundancy in adults when participating in a task to discriminate between two sounds as quickly as possible

...the auditory system maintains and tolerates functionally independently represented redundant and contradictory predictions.

In terms of redundancy in development, it seems there have  been shown links in mice discussed by Dr Thomas Braun

Hope this helps!


There aren't any animals like hornets that hunt large prey (like a rabbit, or even up to a deer), right? Why not?

They're not fast enough

A hornet has a top speed of around 40 kph, while a rabbit is only a touch faster, a deer can hit 75 kph (all figures from Wikipedia). In order to act as hunting insects they need to match the speed of these large animals in large enough numbers to surround and overpower them but these animals could easily match their speed or outpace them. Let's suppose they can overcome that limitation somehow and bring the prey down. They've now bagged a big lump of protein but it's a long way from the hive because they've had to chase it down first. That means that a long round trip is required every time they visit the kill and thus reduces the energy yield as well as increasing the chance of losing it to scavengers.

Against this you have the simpler option of eating smaller, easier to catch, prey as they do now.


Brown fat is so-called because it contains a large number of mitochondria, certainly greater than its white fat counterpart. The reason for the excess in mitochondria is to participate in thermogenesis (incidentally, brown fat is also called thermogenic adipose tissue). Nearly all mammals have brown fat (excluding pigs), especially those that hibernate. Brown fat require larger numbers of mitochondria in order for the fat to be used in beta oxidation (which is carried out directly by mitochondria), and subsequently produces heat via the electron transport chain. This also requires greater access to oxygen from the blood, and as a result, greater capillary density also darkens the appearance of the gross tissue. Mitochondria themselves are dark because of the iron content; vitamins B2, B6 and B12; as well as the pigmented flavins (FADx).


Richard Prum (the author of Evolution of feathers) says that ornithology is mostly a science about dinosaurs. He insists that dinosaurs were very close to birds, part of them had feathers and these feathered dinosaurs "shed (molt) them as birds of our days do".

Thus, we can conclude that dinosaurs probably possessed at least one molting-like mechanism, while others are the subjects for consecutive investigations.

sources
Moulting tail feathers in a juvenile oviraptorisaur. Nature, 2010.


No. MHC works differently from any other antigen. MHC is involved in the maturation of T lymphocytes in the thymus. Forming lymphocytes need to recognise the MHC with a certain affinity (lymphocytes with too much affinity for the MHC are destroyed). In all this process there is no intervention of foreign antigens, so the system you propose won't work because the lymphocytes would search the MHC of the graft and they would attach them with abnormal affinity. This would trigger autoimmune response.

What you propose is the main functioning of allergy vaccines. You expose the immune system to low dose of antigen during long time, and that would make the body to not react aggressively to the substance. However, this phenomenon is based in B lymphocytes, which recognaise soluble antigens and little cells (humoral immune system) instead of whole cells (cellular immunity).

In the domains of science fiction, however, it would be technically possible to transfect thymal cells in order to express the MHC of the donor, since it would express both. Actually, this should be theoretically easy (The thymal cells seems to express almost any protein in the body, in order to prevent autoimmunity), but it face the problem of thymal degeneration.


How long does it take for a person to lose all offsprings due to inheritance?

I think your question conveys some misunderstanding.

A child is related to each parent by a factor of ½. Humans have a diploid genome, meaning they have two copies of each chromosome (see: autosome). When two humans reproduce, they each contribute one copy of each chromosome to the offspring, in other words, they contribute a haploid genome to make a diploid child. Genetic information is not "lost" - the genome is not shrinking by a factor of ½ every generation.

However, relatedness does decrease from generation to generation. You are related to each of your parents by a factor of ½, each of your grandparents by a factor of ½ $\times$ ½, your great-grandparents by a factor of ½ $\times$ ½ $\times$ ½... You are also related to your children by a factor of ½, you are related to your grandchildren by a factor of ½ $\times$ ½... You get the picture, right?

For example, imagine the genome carries just one gene. Your father carries alleles $AA$ at that locus, and your mother $aa$. You would then be $Aa$ and, because half of your alleles came from your father and the other half from your mother, be related to each by a factor of ½, but all three of you have the same number of genes (1) and that gene is the same length (in nucleotides, barring mutations) in all three.


Can other animals see black differently?

Yes, animals can see 'black' differently, in terms of different shades, similar to what you stated about humans perceiving different hues of 'blue'. It is all relative to the cones in the eye of the referenced animal. Animals that see in black-and-white see several different hues of both, black and white. Animals that depend on color to judge the ripeness of a food also see in several different hues of black. For example, a parrot differentiating between seeds that humans may perceive as both being 'black'. Here is a color chart showing the colors that bees can perceive in juxtaposition to humans; it indicates high differentiation between hues of black, as opposed to humans' low differentiation.


As @Ilan wrote, this is a Cantharidae but most probably Cantharis fusca, which is very common species in northern Europe. Cantharis rustica is similar but has reddish femurs and the black spot is more centered on the pronotum. It is not C. lecontei, which is a North American species.

If you go looking at flowers of Anthriscus sylvestris for an hour or two, you will most likely see at least Cantharis fusca, Cantharis rustica and Cantharis obscura - they are all very common in Scandinavia during early spring/summer. The larvae of all these species live on the ground/in plant litter as predators.

Cantharis fusca

Cantharis rustica         .................... Cantharis obscura


When was it determined that Type 1 Diabetes is an autoimmune disease?

This question has two answers: The difference was first described in 1936 by Harold Percival Himsworth, which described it in this article.
At this time it was established that there are two forms of Diabetes, one sensitive to insuline while the other is not.
The terms Diabetes type 1 and 2 where established somewhere between 1974 and 1976, for details see the review "The discovery of type 1 Diabetes".


Should heart-to-body energy consumption ratio equal oxygen consumption ratio?

At first glance there are a few major issues with your calculation and assumptions.

You're comparing the energy output in work (pumping action) with the energy consumption of the rest of the body in input (oxygen consumption). I don't know how efficient the heart is, but I'd guess only somewhere from 20-40% of input energy is actually converted to pumping action.
Oxygen consumption is correlated with energy consumption, and would be a good way to measure energy consumption if you know exactly what the subject is burning. However, if you have a big difference between the preferred fuels between the heart and the rest of the body, this doesn't really apply  anymore. A quick google leads me here: https://www.ncbi.nlm.nih.gov/pubmed/17081788, showing that the heart prefers to burn fat over glucose, and this creates a significant difference:

  Carbohydrate oxidation typically generates approximately 120 kcal per mole of respired oxygen, whereas fatty acid
  oxidation typically generates only approximately 100 kcal per mole of oxygen.

This means that the heart needs more oxygen than the rest of the body to generate the same amount of energy.

I think combined this could explain the 5-fold difference.


I recommend to filter using transcript_type value from description column. You need only proteine_coding genes. Now you have extra ~10K unprocessed pseudogenes, ~5K antisense genes, ~4K miRNA, ~7K lincRNA and more than thirty other categories of unprocessed pseudogenic stuff.

As far as I know current release for GRCh37 is 19th version, not 18.


Biodiversity is restricted by genome combinatorics?

Yes, we can say the number of species is limited as you conjecture.  However, quick estimation shows that the limitation has no apparent usefulness:

A reasonable estimate of the largest known genome is 150 GB (150,000,000,000 or 1.5e11 nucleobases).  The limit would be 4 raised to that power.  That limit is so high that it is too large for most calculators to calculate.  For instance. Wolframalpha.com fails to calculate 4 raised to 1e11, its maximum being about 4 raised to 1e9.  The result of 4 to the 1.0e9 power is about 1.0e602059991 or 10 raised to the 602059991'th power.

That rough result, 1.0e602059991, is so enormous that it is exponentially greater than the number of atoms in the universe (which is less than 1.0e100).  Hence, assuming the definition of species requires an organism to use at least one atom for its body, there is no consequence to saying the number of species must be less than this number.

The number of possible combinations of nucleotides is so outrageously large that it does not constrain the number of unique individual organisms or species.


Where can I find hemagglutination inhibition (HI) assay data?

I don't think there's any universal database containing ongoing, widely representative HI assay output. The Antigenic Cartography group has made available some historical datasets that were used in published articles, such as

Influenza A/H3N2 data published in Smith et al. 2004. Science 305:371-376
Data from H1N1pdm09 assays in 2009/2010 (click on the links for html/Excel/OpenDocument tables)
Data published in Koel et al. 2013. Science 342:976-979

Trevor Bedford et al. make their large set of historical HI data described in Integrating influenza antigenic dynamics with molecular evolution available in DataDryad.


Can a Turner syndrome patient develop male characteristics artificially?

After a lot of research, I've finally found an answer.

In the case of humans, it is practically impossible. See this article from wikipedia:

  During gestation, the cells of the primordial gonad that lie along the urogenital ridge are in a bipotential state, meaning they possess the ability to become either male cells (Sertoli and Leydig cells) or female cells (follicle cells and Theca cells)...Once proper SOX9 levels are reached, the bipotential cells of the gonad begin to differentiate into Sertoli cells.

This part is just to clarify why it is not possible. In embryonic stage in turner syndrome patients (and females), since SOX9 is not expressed (due to absence of SRY), the bipotential gonad cells in the urogenital ridge (Müllerian/paramesonephric ducts) of embryo develop into female reproductive system i.e. become mature into that state. After this has happened, any amount of SRY cannot develop male reproductive system as all bipotential cells have differentiated into female reproductive system.

It is practically impossible, but virtually it can happen if you can insert Y chromosome or TDF in the bipotential cells of embryo. Practically, doing such experiments on embryo might not be possible (at least for now).

Source

Source

However, it only means that they can't develop primary sexual characters. Secondary sexual characters can, obviously, be developed by efforts as small as hormone injections. In fact, hirsutism is a condition in which females devlop hairs on chest, face, etc. and even beards! Its causes are as common as obesity. See this article:

  Some medications can cause hirsutism. These include danazol, which is used to treat women with endometriosis; systemic corticosteroids and fluoxetine (Prozac) for depression...Being obese causes increased androgen production, which can worsen hirsutism.

So, if a Turner syndrome patient wants a moustache or beard (just in case), it can be achieved by androgen injections too.


I've always wondered about mesosomes. They were controversial 35 years ago when I was working in a related field. I decided to check the current status of the term.
I checked for research activity in this area using a Web of Science search "mesosome" in Title: this gave just 54 hits. I list the most recent here (unless otherwise indicated, these are single hits per year).
2010; 2008; 2004 (human cell mesosome??); 1994; 1988 (geology); 1983; 1982 (2); 1980
So it doesn't seem to be a very active area of research. The 2008 and 2010 papers are from the same group. The earlier paper is:

Li, X et al. (2008) Mesosome formation is accompanied by hydrogen peroxide accumulation in bacteria during the rifampicin effect. MOLECULAR AND CELLULAR BIOCHEMISTRY 311: 241-247   DOI: 10.1007/s11010-007-9690-4
Abstract: Ultrastructural alteration and hydrogen peroxide localization were examined in Xanthomonas campestris pv. phaseoli during rifampicin effect using transmission electron microscopy. Bacterial cells were treated with rifampicin and then were examined by electron microscopy to observe the changes of ultrastructure or hydrogen peroxide accumulation in living cells that took place before lysis. Intriguingly, rifampicin treatment led to presence of an additional location of hydrogen peroxide accumulation within the cells. There was an association between the frequency and size of the additional location of hydrogen peroxide accumulation and the concentration of rifampicin. Furthermore, an additional ultrastructure, mesosomes, was also present in cells during rifampicin effect. The frequency and size of mesosome increased with the increasing concentration of rifampicin. Result of multiple linear regression showed that the size of mesosome plays as a key factor in the quantity of excess hydrogen peroxide accumulation in cells during rifampicin effect. Linear correlation was confirmed between quantity of excess hydrogen peroxide accumulation and the size of mesosome in cells during rifampicin effect. This finding intensely indicated that mesosomes are just the additional location of hydrogen peroxide accumulation in cells under cellular injury caused by rifampicin treatment. The mesosome formation is always accompanied by excess hydrogen peroxide accumulation in X. campestris pv. phaseoli during rifampicin effect.

This paper has been cited 7 times. One of those citations is from:

Saier, MH. & Bogdanov, V. (2013)  Membranous Organelles in Bacteria. JOURNAL OF MOLECULAR MICROBIOLOGY AND BIOTECHNOLOGY 23: 5-12   DOI: 10.1159/000346496

Free full text here.
The language used in this review seems to support the existence of mesosomes as some sort of intermediate in the formation of intracellular membranes in prokaryotes. This review is a polemic in favour of the idea that prokaryotes do indeed contain intracellular membrane-bounded compartments. It has no abstract, but the first paragraph gives a flavour of its stance:

The traditional view of life on Earth divides the living world into two major groups, prokaryotes and eukaryotes. These two groups were originally suggested to differ in very basic respects. While eukaryotes had complex cell structures including a cytoskeleton and intracellular membrane-bounded organelles, prokaryotes were believed to lack them. In fact, numerous textbooks and current sources still note this distinction and hold it to be true. For example, in Campbell’s Biology [Campbell, 1993, p. 515] it is stated without equivocation: ‘Prokaryotic cells lack membrane-enclosed organelles.’ In ‘Functional Anatomy of Prokaryotic and Eukaryotic Cells’ [Tortora et al., 2009, chapt. 4] it is similarly claimed that ‘Prokaryotes lack membrane-enclosed organelles, specialized structures that carry on various activities’. In the current Wikipedia, under ‘Prokaryote’ the following statement can be found: ‘The prokaryotes are a group of organisms whose cells lack a cell nucleus (karyon) or any other membrane-bounded organelles’. In the same online compendium under ‘Organelle’, one can read: ‘whilst prokaryotes do not possess organelles per se, some do contain protein-based microcompartments’. Proteinceous microcompartments will be the subject of a forthcoming Journal of Molecular Microbiology and Biotechnology written symposium, but this one will show that these generalizations, suggesting a lack of subcellular compartmentalization in prokaryotes, are blatantly in error [Murat et al., 2010a].


What are the differences between Signaler and Primer pheromones?

A good example of a primer and a signaler pheromone could be in the recently discovered pheromone system in pennate diatoms (unicellular algae). When diatoms reach a certain size as a result of successive divisions (they get smaller with each vegetative division) both mating types start to produce a first pheromone that provokes cellular responses in their mates: 1) to stop dividing vegetatively and 2) to produce either another pheromone (a cell attractant, by one of the mating types) or to induce a sensing system to locate their mates. So, the 'Primer' pheromone would be the first, and the 'Signaler' the second pheromone, i.e. the attractant. A similar system exists in fungi. The evolutionary explanation is likely that organisms don't need to invest in pheromones and their associated repertoire of sex genes when mates are not present.

References:

Metabolomics Enables the Structure Elucidation of a Diatom Sex
Pheromone
Pheromone signaling during sexual reproduction in algae


Is the prostate problem unique to humans?

Dogs get benign prostatic hypertrophy, so, yes, other animals (in fact most old male dogs, so that would mean a whole lot of other animals) do get BPH.

  The most common conditions affecting the canine prostate include benign prostatic hyperplasia, prostatitis, prostatic cysts, and prostatic neoplasia.

However, you're almost correct.

  [T]here is no risk for prostate cancer in any other aging mammal except the dog.

Though this article addresses cancer, the same appears to be true for BPH.

The prostate and breast appeared at the same time with the origin of mammals (possibly as long as 195 million years ago). While all male mammals have a prostate, seminal vesicles only appear in  primarily herbivorous species with the exception of man. The human male has seminal vesicles and consumes meat. Thus, it has been postulated to be a dietary cause. Bonobos, on the other hand, exist primarily on a high fruit and vegetable diet. They don't get BPH.

It isn't known what dogs ate before domestication (were there 'dogs' before domestication?) But it's postulated that ~10-15,000 years ago, humans (and their newly domesticated partners, dogs) dramatically altered their diets, breeding animals for food.

Why haven't we evolved a solution? Well, on the one hand, if BPH is only 15K years old, that's only a fraction of a blink in the human evolutionary scale of things, so not enough time to "evolve" a way around it (maybe reroute the urethra?)

On the other hand, we have. We've evolved medications and surgery for treatment of prostatic hypertrophy.

Similarities of prostate and breast cancer: Evolution, diet, and estrogens
New concepts in tissue specificity for prostate cancer and benign prostatic hyperplasia


Are there any alternatives to DNA as the hereditary material on Earth?

First of, depending on your definition of life (which is a matter of philosophy, not science) you may even accept as living something that has not heritable information passed onto 'offspring'. But let's consider only those hypothetical life forms who would have heritable information.

Of course, it is possible for different life forms to use some other mean of transferring heritable information. In fact, there are life forms based on RNA instead of DNA on earth (see RNA virus) and it is even thought by many that life first evolved using RNA and not DNA (see RNA world hypothesis).

To go further in this discussion you should have a look at wikipedia > Hypothetical types of biochemistry (I got the link from @RoniSaiba 's answer).


Not "all of them". But yes, plants suck up water from the soil, with everything dissolved in this water - nutrients, heavy metals, poisons. And also they breathe air, and absorb stuff via this route.

There probably are some toxins which will not enter the plant, because their molecules are too large and/or fragile. For example, should a plant root come in contact with snake venom, I cannot imagine that any venom will end up stored in the plant leaves.

Plants also have their own metabolism, so they will change/deactivate some toxins. I've seen claims that some plants "purify" formaldehyde, although I don't trust the sources enough to be sure of that.

But the smaller the poison molecule, and the less similar to stuff which is usually digested in nature, the more likely that it will enter the plant and stick around instead of being broken down. The heavy metals you mentioned are prime candidates. If they are present in the groundwater - or also lead from air pollution, before we banned leaded gasoline - they end up in plants, including food plants. And mushrooms are even more at risk.

Growing food near waste dumps is a known problem in farming, and sometimes makes the news, for example here:
http://bigstory.ap.org/article/mafia-toxic-waste-dumping-poisons-italy-farmlands


Why is it said that bacteria have no membrane-bound organelles, when they often have one or more flagella?

Prokaryotic flagellum is very different from eukaryotic flagellum: it's not surrounded by a biomembrane (as in eukaryotes) and its composition is distinct. Actually, they only have in common the name and the function:

  The term flagella is ambiguous. It refers to bacterial structures composed of flagellin protein and to eukaryotic structures composed of microtubule proteins.

Source: https://www.ncbi.nlm.nih.gov/pubmed/7378551

It's clear that prokaryotic flagellum is just a protein-made structure that crosses the membrane and grows outside it, as represented in this image (notice the TEM at the bottom right):


From Henderson's Dictionary of Biology 14 ed. An operon is: a type of gene organization in bacteria, in which the genes coding for the enzymes of a metabolic pathway are clustered together in the DNA and transcribed together into a single mRNA. This mRNA is then translated to give the individual proteins. The expression of all the genes in an operon is controlled by a single promoter.

I'm not sure what an overlapping gene is, but according to this definition, yes genes on opposite directions of a promoter or different loci cannot be a part of an operon because they wouldn't be on the same mRNA.


Antibiotic resistance of Staphylococcus epidermidis and S. warneri

Here some studies concerning the antibiotic resistance of Staphylococcus epidermidis and Staphylococcus warneri:

Antibiotic resistance patterns of coagulase-negative staphylococcus strains isolated from blood cultures of septicemic patients in Turkey - Koksal, Yasar & Samasti [2009]

The abstract of the study above reads as follows:

  The aim of this study is to determine antibiotic resistance patterns
  and slime production characteristics of coagulase-negative
  Staphylococci (CoNS) caused nosocomial bacteremia. A total of 200 CoNS
  strains were isolated from blood samples of patients with true
  bacteremia who were hospitalized in intensive care units and in other
  departments of Istanbul University Cerrahpasa Medical Hospital between
  1999 and 2006. Among 200 CoNS isolates, Staphylococcus epidermidis was
  the most prevalent species (87) followed by Staphylococcus
  haemolyticus (23), Staphylococcus hominis (19), Staphylococcus
  lugdunensis (18), Staphylococcus capitis (15), Staphylococcus xylosus
  (10), Staphylococcus warneri (8), Staphylococcus saprophyticus (5),
  Staphylococcus lentus (5), Staphylococcus simulans (4), Staphylococcus
  chromogenes (3), Staphylococcus cohnii (1), Staphylococcus schleiferi
  (1), and Staphylococcus auricularis (1). Resistance to methicillin was
  detected in 67.5% of CoNS isolates. Methicillin-resistant CoNS strains
  were determined to be more resistant to antibiotics than
  methicillin-susceptible CoNS strains. Resistance rates of
  methicillin-resistant and methicillin-susceptible CoNS strains to the
  antibacterial agents, respectively, were as follows: gentamicin 90%
  and 17%, erythromycin 80% and 37%, clindamycin 72% and 18%,
  trimethoprim-sulfamethoxazole 68% and 38%, ciprofloxacin 67% and 23%,
  tetracycline 60% and 45%, chloramphenicol 56% and 13% and fusidic acid
  25% and 15%. None of the strains were resistant to vancomycin and
  teicoplanin. Slime production was detected in 86 of 200 CoNS strains.
  Resistance to methicillin was found in 81% of slime-positive and in
  57% of slime-negative strains. Our results indicated that there is a
  high level of resistance to widely used agents in causative
  methicillin-resistant CoNS strains. However fusidic acid has the
  smallest resistance ratio, with the exception of glycopeptides.
  Additionally, most S. epidermidis strains were slime-positive, with
  statistically significant (p<0.001) association between methicillin
  resistance and slime production.

The other two studies contain information on the aforementioned strains with regards to penicillin susceptibility.

Antibiotic-resistant Staphylococcus epidermidis in patients undergoing cardiac surgery - Archer & Tenenbaum [1980]

Clinical significance of Staphylococcus warneri bacteremia - Kamath, Singer & Isenberg [1992]

In addition, I would recommend to acquaint yourself with Google Scholar for these kind of questions. It normally makes for a good starting point.


Does the process of making a sourdough starter involve Darwinian selection?

Yes, continually diluting the mix like this encourages the organisms (bacteria, yeasts, fungi) to have more constant conditions (maximum nutrients, fewer waste products) and be in log phase growth. The mix selects for particular faster-growing organisms. if you did not dilute, the nutrient levels would change (lower) and waste products accumulate much faster. Then the conditions would be more different day-to-day.

Practically, the dilution adds more nutrients while still allowing the pH to fall. Without the dilution, particular bacteria tend to take over and lactic-acid producers dont get a chance.

refs
https://en.wikipedia.org/wiki/Bacterial_growth
https://en.wikipedia.org/wiki/Sourdough


Real-world examples of Darwinian extinction

Although you don't mention it in your question, I guess you'd like examples of extinction in (more or less) constant environment? Then I guess you'd like cases of extinction due to the introduction of an overseas species out-competing the original one.

Red squirrel is not extinct yet, but its sharp population decrease is mostly linked with competition with newly introduced grey squirrel, although habitat loss and concurrent introduction of a virus are also part of the causes. Read at https://en.wikipedia.org/wiki/Red_squirrel


Differences in the action of Scopolamine and Atropine

It seems that the reason for the different effect of Atropine and Scopolamine on the brain is related to the structural difference between them.
From the chemical structures below it is evident that the two molecules are almost identical, save for an epoxide group that is found in Scopolamine but not in Atropine.

According to Brody's Human Pharmacology: Molecular to Clinical, 5th edition, 2010, pp. 113-115, this epoxide reduces Scopolamine's base strength and enables it to penetrate into the brain more readily than Atropine.
Faster penetration into the brain = earlier appearance of psychotropic effects.


Do men have a higher genetic variance than women?

This question is very interesting and I would love to have a reference to an article that provides such evidence.

Decomposing your question:

Is it true that there is more genetic variance among males than among females (in humans I guess)
If the answer to (1) is yes then: Why is it so?

I am trying to address these two points below

1. Is it true that there is more genetic variance among males than among females ?

There are different ways of understanding your question 1. Do you want to talk about…

Allele richness
Heterozygosity
Polymorphism
Part of the genetic variance in phenotypic variance (heritability). I don't think it is what you meant though!

Therefore, the question is slightly unclear and I don't know of any paper who address any of these questions anyway. So... I don't know!

2. Assuming (1) is true, then Why is it so?

There are many possible explanations for such observation (assuming this pattern has been observed). Below I give some hypothesis I can think of.

There might have a higher selection (survival differential) among females than males. In a consequence, genetic variance among young females is higher than among older females. In total, genetic variance among females would be lower to that of males.
There might have a very high variance on the Y-chromosom but not on the X-chromosom. This might for example be a consequence of the arrest of recombination that occur on the Y-chromosom. As a consequence of this arrest of recombination, selection hardly purge deleterious mutations (see Muller's Ratchet). See Shigeta's answer for a more detailed overview of this point. See shigeta's answer for more information.
Males might migrate more. If one look at the sex-specific genetic variance in a population (and not on the world-wide metapopulation), this variance might be greater for the sex that migrate more because different genetic background might be brought from other neighbor populations.
Higher selection within mitochondria in females very early in life (in the egg for example) resulting in a decreased mitochondrial genetic variance in females. This is maybe a bit far-fetched.
There might have other hypotheses for species for which sex of an individual is not determined by sex-chromosomes. (see Sex Determination System)
Depending on what you mean in your question, I guess we might find many other hypotheses when thinking of migration, different fitness landscape (different optimum), different selection intensity.
We might as well think of genetic variance of gender-specific gametes (especially for haplon-diplontic species for example)
This evidence (assuming it has been observed) was a False Positive!

Note:
@terdon provided a very good explanation (which was deleted) of why males might cause most of the genetic diversity but as @terdon and I discussed (in the comments that were also deleted) this is not an explanation for greater diversity among males. The reason is that the variation is created via mutation in the testis and the ovary. The fact that most mutations happen in males does not influence the sex-specific diversity because males sire as many male offsprings than female offsprings (so do females!).


Do animal muscles atrophy slower than humans?

Animal muscle does atrophy and gain depending on use.
First, animal muscle does atrophy if the animal is too sessile. However in nature it is hard to be sessile. Consider how physically fit hunter-gatherer humans are in terms of their cardiovascular systems. If you are constantly active you don't need to "exercise" to build muscle - you are getting loads of physical activity. Walking 10km a day or more is normal for most humans without advanced technology. We used to see atrophy in animals a lot more, but with animal welfare laws we usually don't keep animals in tiny cages that prevent them from moving anymore.
Some animals are less lazy than humans: many animals will also instinctively stay active even when provided with the conditions to be sessile, but when forced to not be active we do indeed see muscle atrophy. This is especially true of less intelligent species, because the conditions to be sessile are too rare to waste "instinct space" on, but humans who have a much more broader range of behaviors with far more learning behaviors, so we can become very sessile. The downside of intelligence is that you can use it in self-destructive ways.
Just like humans, animals can also build extra muscle by doing the same thing over and over again: a draft horse will build different muscles than a race horse just because it is using them differently.
Many animals also have physiology that makes atrophy harder. Hibernating bears are known to have special adaptations to prevent atrophy because hibernation is defined as long periods of inactivity. But we only only see this in animals that have something like hibernation or have drastically different muscular systems.
So why is a gorilla so much stronger?
Well to start, wild male gorillas mass between 130 to 260 kg. Note that gorillas in captivity often become overweight weighing even more. They have short legs so we don't realize how much bigger than us they are. For scale, Andre the giant (a human far outside the normal range) masses about as much as a large but normal range male gorilla. But there are several other factors.
Humans’ muscles are weaker than other primates’ in significant ways. We have traded strength for much better endurance and fine control of muscles - we do indeed have a significant difference in muscle composition and possibly muscle fiber recruitment, although it is hard to test the latter - you can't tell a gorilla to contract one muscle as hard as they can. As a gain however humans have amazing endurance for any animal and far finer motor control than any other primate. An active human can have better endurance than almost any other terrestrial organism, humans can walk a horse to death, that is a human walking side by side with a horse can keep going long past the point the horse has died from exhaustion.
Gorillas are only stronger in some aspects, a gorilla upper body is certainly stronger, gorilla have large arms and a deep chest drastically increasing the muscle mass of the arms compared to a humans. But the best human could probably beat the best gorilla at kicking power, gorilla legs are comparatively small. To use Andre the giant again, Andre has a lot more muscle mass in his legs than a gorilla and the gorilla has a lot more in the arms, humans have long well-muscled legs. Like all things, genetics can set you up with better musculature, and you will keep it as long as it gets some use.


I think the definitions of inhibitory and excitatory neurons are currently defined as a matter of convenience based on observations made by synaptic staining, electrical feature and its morphology.
In other words, neurons with more inhibitory synapses are inhibitory neurons, and neurons with more excitatory synapses are excitatory neurons, and so on.
By detecting inhibitory and excitatory synaptic-specific staining in different colors on the same section, we may be able to determine whether all synapses in a single neuron are inhibitory or excitatory.
Also, I think there are events happening in the process of neural differentiation that distinguish excitability/inhibition, but we don't seem to know how they are happening.
It may be determined by signals from neighboring neurons, Ca++ concentration, etc.
If, at the neuronal precursor stage, the differentiation mechanism that determines excitability/inhibition could be confirmed at the level of gene expression, it might explain why inhibitory neurons only make inhibitory synapses.
22th June 2020 added;
I find a good example of Excitatory synaptogenesis on dendrites of hippocampal-mediated (inhibitory) neurons, here;
https://www.nature.com/articles/ncomms1736
In short, this article shows what will occur after generating spine on inhibitory neuron.
(A)The synapses move along the microtubule from the tip of the process to the shaft. (B) Morphological changes in parallel fibers of cerebellar granule cells during synapse formation. When the parallel fibers come into contact with Purkinje cells, the neurexin-Cbln1-δ2 glutamate receptors A complex of synaptic vesicles is formed and synaptic vesicle accumulation occurs. Synapse matures after microprojections extend from the parallel fibers and encircle the spine to form an annular structure. (C) In early postnatal hippocampal pyramidal cells, DCLK1 accumulates at the tip of the process to promote process elongation and Inhibition of synaptic maturation.


Do you know of ways that help a plant to produce more flowers?

Each species of flowering plant produces a set number of floral parts, more or less. Having three styles and three stigmas per flower is a trait that is determined genetically. Mutations can cause floral parts to be duplicated. Heirloom tomatoes have mutations in the fascicated and locule-number genes, resulting in more locules being produced per fruit. Mutations in the fascicated gene also cause increases in other floral parts, such as petals, sepals, and stamens. If you compare a regular tomato to an heirloom, you'll notice that heirlooms tend to have around 10 petals and sepals compared to a regular tomato's 5.

Now the question is, do such mutations exist for Crocus sativus? A quick Google search didn't turn up anything other than the normal three-stigma flowers, so it doesn't look like such a mutation is common, if it exists at all. My answer to your question is: there is no easy way to get a saffron flower to produce more stigmas, for if such a method existed, everyone would be using it. I don't doubt that a dedicated botanist could come up with something (crossing with a related species, perhaps), but it's not something you can likely accomplish in your home garden.

Edit:
User Sleepses found an article where a high-yielding mutant with 5 stigmas was obtained through gamma radiation mutagenesis. I'm not sure whether or not this mutant is for sale commercially, though.


What is the number of cells in a line of a fingerprint?

I am not sure that this can be accurately estimated because the outer layer of skin is ill-defined in terms of cells and cell boundaries. The outer layer or epidermis is composed of dead cells and dead cell parts that is tough and interconnected by design. Individual cells are not readily discernible.


The answer to the first part of your question is: diffusion. After transcription and some processing, the eukaryotic mRNA is exported to the cytoplasm. Here it floats around until it meets a ribosome. Binding of ribosome to mRNA is facilitated by proteins called initiation factors (IFs) and the 5' cap of mRNA$^1$.
The second part of your question basically asks about cell-free protein synthesis using an RNA template. This has already been shown to work: one is reminded of the famous Nirenberg–Matthaei experiment$^2$, which ultimately led to the cracking of the genetic code. Nirenberg and Matthaei worked with bacterial cell extracts, but systems based on eukaryotic cell extracts have also been developed$^3$.

References and further reading:

Nelson DL, Cox MM. Lehninger principles of biochemistry. 7th ed (international edition). Basingstoke, England: Macmillan Higher Education; c2017. Chapter 27, Protein metabolism; p. 1077–1126.
Nirenberg MW, Matthaei JH. The dependence of cell-free protein synthesis in E. coli upon naturally occurring or synthetic polyribonucleotides. PNAS. 1961 Oct 1;47(10):1588–1602. https://doi.org/10.1073/pnas.47.10.1588
Chong S. Overview of cell‐free protein synthesis: historic landmarks, commercial systems, and expanding applications. Curr Protoc Mol Bio. 2014 Oct 1;108(1):16.30.1–11. https://doi.org/10.1002/0471142727.mb1630s108


Comparing angles between population vectors of neural activity

They are not writing about "after conditioning" as you write, but, importantly, after extinction.
What they observe is that, during learning, the response to the conditioned stimulus (CS+) becomes more similar to the response to the US. In the n-dimensional space in which a population response lives, you can describe this as the population vector evoked by CS+ pointing closer to same direction as the population vector from the US.
We expect that during extinction, the CS+ vector will become different from the US compared to at the peak of conditioning. There are two general possibilities for how that could happen. The first possibility (perhaps the simplest one to expect) is that with extinction the CS+ vector returns to where it was initially, before the conditioned stimulus was paired with the US. You could describe this as merely forgetting what has been learned: responses to the US and CS go back to how they were before conditioning and it's as if nothing was ever learned.
However, that's not what these authors observe:

During within-session extinction, the CS+ representation did not revert and gained no more similarity to its initial representation before learning

Although they do observe that with extinction the CS+ vector moves away from the US, it doesn't move back towards the old response, it points in a new direction that is further both from the US response and from the original CS response. That can be described as an "out of plane" rotation, not towards either of the other vectors.
In case it's hard to think about these things in N-dimensional space, we can think of a more familiar situation in our own 3-dimensional world.
Let's say the US causes a response corresponding to "12 o'clock". The conditioned stimulus causes a response corresponding to "3 o'clock" before any training. As you do some conditioning training, pairing the US and CS, the CS response moves towards "1 o'clock", beginning to resemble the US response. During extinction, we might expect the CS response to move back towards "3 o'clock", maybe we'll find it at "2 o'clock". This would represent rotation in the "plane of the CS and US" made by the clock. Instead, the hand points out away from the wall, so it is further from both the original US at 12 and original CS at 3. That's the "new learning".


Intracellular proteins cannot form biofilms. Additionally, many (but not all) extracellular proteins contain an N-terminal cleavable signal sequence.

Lory (1992) Determinants of extracellular protein secretion in Gram-negative bacteria. J Bacteriol 174: 3423-3428.
https://www.ncbi.nlm.nih.gov/pubmed/1592799

Schneewind & Missiakas (2012) Protein secretion and surface display in Gram-positive bacteria. Philos Trans R Soc Lond B Biol Sci 367:1123-1139.
https://www.ncbi.nlm.nih.gov/pubmed/22411983


What animal / insect carcass is this? (Victoria, Australia)

This is a tadpole shrimp. The most common species here down under is Triops australiensis.

Here is an image of it:

Source: https://www.flickr.com/photos/euprepiosaur/23782620153

Here is some info from Western Australia Museum (I found nothing on Victoria Museum): http://museum.wa.gov.au/creature-feature-tadpole-shrimp

PS: This is not a duplicate of this question because the species here is clearly different.


How do we know how long hermit crabs live in the wild?

Hermit crabs increase in size over time and this is used to provide a minimum estimate for their age1.

You may also find this article interesting.

Reference:
SantAnna, Bruno Sampaio, Christofoletti, Ronaldo Adriano, Zangrande, Cilene Mariane, & Reigada, Alvaro Luis Diogo. (2008). Growth of the hermit crab Clibanarius vittatus (Bosc, 1802) (Crustacea, Anomura, Diogenidae) at São Vicente, São Paulo, Brazil. Brazilian Archives of Biology and Technology, 51(3), 547-550. https://dx.doi.org/10.1590/S1516-89132008000300014


What is this insect with scary antennae?

Actually, the antennae of that insect are not scary at all!

In your image, the antennae are pointing down; those forceps-like structures pointing up are part of abdomen, and are called cerci.

That insect (probably a male) is an earwig, from the Order Dermaptera. In the image below, the antennae are at the left, while the abdomen and the cerci are at the right:

Narrowing down the the Genus of your specimen is more complicated, but here is a list of earwigs from Sri Lanka: https://en.wikipedia.org/wiki/List_of_Dermapterans_of_Sri_Lanka

Regarding the danger: earwigs are not dangerous. The cerci may be scary, but they normally are not capable of hurting a human. Also (and I hope you don't believe urban legends), they do not lay eggs in human ears: http://www.snopes.com/horrors/insects/bugear.asp


Atelectasis due to decreased surfactant in lungs

Long-term exposure to excessive oxygen will lead to damage in pulmonary tissue. This damage resembles the same damage which is seen in patients with Acute Respiratory Distress Syndrome (ARDS). In these patients surfactant specific proteins are damaged by proteolysis. This proteolysis is caused by the neutrophil elastase enzyme, after a massive influx of activated neutrophils.

The damage done by exposure to excessive oxygen is thought to be done by Reactive Oxygen Species (ROS).

  Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen...

These ROS can cause oxidative damage to DNA, RNA and proteins. They can form covalent bonds between molecules in the surfactant, thus inactivating them. Damaging of molecules can lead to cellular damage, causing ROS-mediated necrosis or apoptosis. Therefore there will be less surfactant production possible.

Also interestingly:

  An important feature of pulmonary oxygen toxicity is that it is almost impossible to distinguish from damage caused by other lung injury processes. Consequently, it is unclear whether deterioration of lung function during high concentration oxygen therapy is due to worsening of the primary disease process or to oxygen-free radical-induced damage; the administration of high concentration oxygen may be perpetuating lung injury in some patients.

So in patients who undergo long-term 100% oxygen exposure, for example due to lung problems, the problems could be perpetuated or even worsened due to oxygen therapy and the oxidative stress caused by it.


How many Watt-hours can an electric eel produce in a day?

This research states that an eel whose size is 90 cm can provide 6.05 mW, which is 145 mWh every day. They say you'd need 165 eels to be able to read for 24 hours using a 1W lightbulb like the one on a phone.
An electric eel should be able to flash a 0.6W L.E.D. light for 10 milliseconds at full power every second, which would be very visible in daylight, and would light up the room.


You might want to pick something that has little or no homology with anything that exists in any organism in the databases, just in case.

Gut feeling says to go for balanced oligos in the middle between AT-rich and GC-rich, and not have repeats or homopolymers.  If you go for AT-rich, then your complementary will be GC-rich, and vice versa. I'm pretty sure there would then be a differential in the mechanical properties of the two oligos - maybe this would be something useful to have for other reasons though?

It seems like most of the design principles might be constraints (do nots) rather then goals (dos), so you could do worse than have a generator churn out random sequences, and score each one against the various constraints.  Random seems OK, if you are then checking each randomly chosen pair against some strong rules.  Then pick ten or so pairs that all score well, get them synthesised and see whether any work...


Why are the posterior and anterior inferior temporal cortex called area TEO and area TE respectively?

These are very old names for primate cortical areas, originally from the anatomist Constantin von Economo and also used by von Bonin and Bailey (1947) (where the TEO region name seems to originate).

Like Brodmann areas these regions were defined by cytoarchitecture well before most functions were determined.

I discovered another work that I can access from 1935, Rose (1935) that is quite helpful for the TE terminology. From Rose it is clear that von Economo labeled areas in the temporal lobe TA, TB, TC, etc. up to TH. So they seem to be simply "temporal"+letters of the alphabet. Rose refers to "Area temporalis propria" as area TE, comprised of Brodmann areas 21 and 20; Rose calls Brodmann 21 "TE1" and Brodmann 20 "TE2" which are separated based on the size of layer 3 pyramidal cells.

As far as the TEO terminology, Boussaoud et al (1991) write:

  In their study of  the cytoarchitecture of  macaque cortex, von Bonin and Bailey ('47) labeled this region with a question mark on their section drawings but showed a photomicrograph through the region that they labeled  “TEO.”

This is the best evidence I can find that the TEO name a) originated with von Bonin and Bailey, and b) that the further origin or meaning of the name is unclear; it's just a label on a photomicrograph that wasn't even used in the drawings by those authors who instead used a ?. I suspect further authors preferred the TEO terminology rather than confusingly referring to "area ?" and yet they felt like giving credit to von Bonin and Bailey for their work on the macaque cortex.

It's unclear to me whether TEO is meant to be an acronym; "temporal" is part of the name, but whether O stands for a word (perhaps occipital, as it is toward the occipital lobe?) or if it is actually the number 0, or a non-English word (possibly German or Latin?). However, when more modern neuroscientists refer to area TE and area TEO, they are simply intending to refer to "area TE and area TEO in the von Economo/von Bonin & Bailey terminology."

Other terminology, such as referring to posterior or anterior inferior temporal cortex, may seem more descriptive but there isn't anything inherently wrong with referring to the older names as long as people know what area you refer to. TE and TEO are clear, short names that have been used for decades, whereas inventing a new acronym like PIT or AIT would be unfamiliar at this point.

References

Boussaoud, D., Desimone, R., & Ungerleider, L. G. (1991). Visual topography of area TEO in the macaque. Journal of Comparative Neurology, 306(4), 554-575.

Rose, M. (1935). Cytoarchitektonik und Myeloarchitektonik der Großhirnrinde. Handbuch der Neurologie, 1, 588-778.

von Bonin, G., & Bailey, P. (1947). The neocortex of Macaca mulatta.(Illinois Monogr. med. Sci., 5, No. 4.).

von Economo, C. F., & Koskinas, G. N. (1925). Die cytoarchitektonik der hirnrinde des erwachsenen menschen. J. Springer.


Albizia julibrissin (Persian silk tree) is doubly compound (AKA bipinnate) and has a conspicuous pink/white fluffy flower. This tree is an Asian native, but it's a commonly cultivated (and equally commonly escaped) plant in the U. S. You should be able to find it in numerous locations. Look in yards and along roads.

http://www.missouriplants.com/Pinkalt/Albizia_julibrissin_plant.jpg

For native species: Gleditsia triacanthos (honeylocust) is a fairly widespread (though uncommon) example of bipinnate leaves. Here is an image from Will Cook's wonderful website:


Could not fit in a comment...

To my understanding, paralogs and orthologs refers, as you said, to the relative isolation of gene copy to the isolation of populations (and eventually species).

Gene conservation on the other hand refers to the variability of a given gene along many species. If a gene does not show any variance along many species, than we say that it is a conserved gene.

Eventually, gene duplication may allow for neo-functionalisation, sub-functionalisation or loss yielding to variance among this gene copy. Aside the philosophical problem of what is the identity of the gene, there is no relationships between the concepts of orthologs versus paralogs and gene duplication.


Evolutionary rationale behind migration proteins

This would be a very long answer but just to give you some hints, the migrational mechanisms are already there and the cancerous cells makes use of them to metastasise. So in short its deregulation. What is under selection pressure tho are cancerous cells themselves to constantly change and evade cellular fail safes which kill (apoptosis) uncontrollably replicating cells. You can find out about this here (http://www.nature.com/onc/journal/v22/n42/abs/1206757a.html)


How does reversibility of lactic acid fermentation work?

The enzyme catalysing this reaction in mammals is lactate dehydrogenase of which there are two major isoforms: LDHA and LDHB. The general reaction scheme can be shown as:

In muscles LDHA reduces pyruvate to lactate consuming one NADH. This gets rid of the electrons which would normally go through the respiratory chain. The lactic acid is then transported to the liver where it is turned back into pyruvate by LDHA producing one NADH. This is know as the Cori cycle.

Both enzymes however are very similar and can catalyse the reaction into either direction, they are just slightly different in structure which make them have a greater affinity for pyruvate or lactate.


How can paleontologists identify morphologically different fossils as members of the same species?

Radically different body shapes and sizes represent overall phenotype. Overall phenotype was used briefly in the 1960s and 1970s for species identification under a statistical distance method called "phenetics". However, phenetics has been rejected as a valid method of species identification. Similarly, although ecologists widely use the Biological Species Concept (Mayr) based on reproduction, taxonomists generally prefer some form of the Phylogenetic Species Concept. In addition, paleontologists find species concepts that require assumptions about reproduction in fossils to be difficult. The phylogenetic species concept uses the presence of fixed morphological characters to identify individuals as members of a species. Fixed characters need not be major, obvious differences. They need only be present in all members of a hypothesized species, and absent outside the species. That they are fixed in all members of a species implies a lack of gene flow, but the definition does not require that. So in the example you gave, juvenile T-rex must have some unique characteristic morphological feature that define them as members of the species (a synapomorphy). In addition, when there are a series of intermediate juvenile fossils, it becomes possible to link them together.


How to model missing residues on a protein from multiple PDB files?

I suggest you to use modeller - advance modelling (https://salilab.org/modeller/tutorial/advanced.html), Where you can use multiple template PDB to get final model structure.

All the best..:)


Mammalian advantage at filling large-animal niches after the KT extinction?

Birds have to feed and guard there eggs for 30-40 days, against the elements and against predators, whereas mammals can bear larger offspring in exposed environments. That's especially an advantage for swimming mammal megafauna, because the birds can't lay eggs in water, and also for predator-intensive environments and for forests.
Birds lack hands and teeth and four sets of claws for manipulating leaves and prey and defense. Birds can only have a hooked bill to peel up prey, and less sophisticated molars for herbivory. The sheer range of mammal teeth shapes appears to be an advantage compared to beaks.
Quadrupeds have some advantage for running and turning without falling over, whereas birds mostly have long necks which are a bit of an easy target for horns and claws and teeth.
It's interesting to think about a pack of wolves attacking an ostritch, and a pack of predator ostritches attacking a springbok... The wolves and the springbok have a wider range of attacks and defenses to use for survival.


BLAST 16s rDNA: Everything alligns to Bacillus sp

As you guessed in the last sentence, it's hard to answer your question without some more information.

For example, how much of the 16S rRNA gene did you sequence? Most people just sequence the v3-v4 regions which are the most variable, but they only comprise a few hundred bases. Sequencing the entire 1500 bp gene gives more specificity when doing searches, but is also more expensive.

With regards to selection of colonies, do you know from the literature how selective your two different types of media are? We did similar studies with environmental E. coli including several rounds of screening and selection, and you would be surprised how much "junk" we got. If you're isolating from soil, Pseudomonas and Bacillus spp. are going to both be highly prevalent.

With that in mind, it is not enough to grow on selective media, do one transfer, and call it good. Really, you should have a screening method in addition to your selective media. Maybe some compound that yields fluorescence or a visible change to the surrounding media that you can use to differentiate your target bacteria from contaminants. Once you have your candidates, you need to isolation streak them onto fresh selective media. Then screen again and isolation streak again. Repeat this process 2-3 times, or until you have monomorphic, pure cultures. Only then should you start doing genetic/genomic testing on your isolates.

Hope this helps.


Lindeman's "law" is not a true "law" like the laws of thermodynamics, it's more of a catchphrase for a concept.

The true, valid concept from Lindeman is that "lots of energy is typically lost as you go to the next trophic level, especially at early stages...but there might be exceptions." This is characteristic of most of the "laws" of biology: there is always a lot of flexibility and leeway in biology.

The data in the chart you provide support this generalized version of the law: namely, most of the energy is lost at each trophic level, and a rough average or rule-of-thumb is that it's about 10%.

The usefulness of the 10% number is that it presents a nice benchmark: when you look at these data, you should notice and remark on the relatively high 22.3% level for secondary consumers on the Cedar Bog Lake: you should wonder "what features of this ecosystem or these consumers mark the relatively high energy transfer here?" Without the "10% law" you wouldn't know which numbers should stand out and which are unremarkable.


By what mechanism is NADP+ converted to NADPH in Photosystem I?

OVERVIEW (verbatim from the article)

  Plastidic ferredoxin−NADP+ reductases (FNRs) accept electrons
  by two sequential one-electron transfer steps from two
  molecules of the one-electron donor ferredoxin to generate
  their fully reduced hydroquinone state, FNRrd, through the
  formation of an intermediate neutral semiquinone form, FNRsq.
  FNRrd then transfers both electrons as a hydride to the
  nicotinamide adenine dinucleotide phosphate (NADP+
  )
  coenzyme in a single step (Figure 1A).1,2

Theoretical Study of the Mechanism of the Hydride Transfer between Ferredoxin–NADP+ Reductase and NADP+: The Role of Tyr303 (Institutional access will be required!)

Basically, FNR is a flavoprotein with a stabilized FAD prosthetic group that can alternate 3 oxidation states with 0, 1 or 2 electrons. NADP+ binds in the FNR active site, and recognition of the AMP group causes a conformational change that brings the nicotinamide portion in proximity with the isoalloxazine group of the FAD. Ferredoxin is a single-electron carrier where two molecules of ferredoxin sequentially donate electrons to the FAD group that produces a hydroquinone FADH2. The actual architecture of the charge transfer complex formed in the active site mediates the formal hydride transfer that produces NADPH*. As far as I can tell, the hydride transfer occurs while the ferredoxin is still bound due to the effect electron transfer to FAD has on the pKa and protonation of a Glu312 that stabilizes NADP+ too much in the absence of ferredoxin (source).

NADPH ends up getting released after the catalytic cycle.

*I'm still trying to find some more detailed information on the catalytic mechanism.


Is the human ovum visible to the naked eye?

The line that you quote from the Wikipedia page is talking about ova in general, whereas your question relates specifically to human ova. The "Human and mammal ova" section of the same article states that

  The ovum is one of the largest cells in the human body, typically
  visible to the naked eye without the aid of a microscope or other
  magnification device.

With the stated average size of 0.12 mm in diameter (same Wikipedia article), an ovum is very, very small, but presumably a person can still see it unaided.


How does a tree trunk sprout and grow after being cut?

This is basically the same that happens after pruning and involves a basic hormonal regulation mechanism in the plants.

What happens is that the cut piece of the wood forms a new meristem which allows the growth of new organs. What’s important is that there is no other growth happening nearby, since that would hormonally inhibit any further growth. This is why such growths happen once you’ve cut the wood, not before (on the healthy stem). This inhibitory effect is known as apical dominance, which has now been disabled.

As to where the energy and water comes from, to some extent it is stored within the branches themselves. That’s why you need to dry them before being able to use them in a fire. However, this growth is pretty limited. Further water is probably collected by condensation of water vapour in the air.


Are tendons and ligaments classified under the muscular or bone system?

Tendons are intrinsically part of muscles. Ligaments are not. So for your question, we need to create a classification system which is a bit artificial, based on the tissue structure of the various components of the musculoskeletal system.

  The musculoskeletal system is made up of hard and soft tissues. The hard tissue includes bones and cartilages (articular cartilages), while the soft tissues are the muscles, tendons, synovial membranes, joints capsule and ligaments. (emphasis mine)

Here is an illustration of the biceps brachii muscle (arm) from Kenhub:

It looks a little different in real life, but this clearly illustrates how tendons (the white things at the ends of the muscle) are part of the muscle. So, to answer your question, tendons are part of the muscular system (a term that I have never used as a physician. I would just say "muscles".)

Ligaments are supporting structures of fibrous tissue of nearly the same composition as tendons, but do not arise from muscle per se. (For a reason I cannot comprehend, little research is devoted to the embryonic development of ligaments.)

These are the ligaments of the elbow (and more fibrous connective tissue):

Clearly they are not bone, and they are not muscle.

If you need to artificially divide muscle vs. skeletal systems, then:

Muscle: muscle and tendons
Skeletal: bone and cartilage
"Other": ligaments, bursae, synovial fluid and membranes, etc.

The easiest thing to define is what is bone and what is not bone. Then bone may well stand alone, even without cartilage. But no one would say cartilage is part of the "muscular system".

So I hope you see that this way of separately classifying tissues which are meant to work together is artificial and perhaps misleading.


As a simplified response:
Propensity score is used to predict protein secondary structure. It is derived from looking at the aa residue of the accessible surface of the protein and also the interface which enables interactions between other proteins.

The equation is as follows:

Propensity= [probability of the residue in the interface / probability of the residue on the surface]

where,

prob of the residue in the interface = [number of amino acids in the interface / total number of amino acids of any type of interface]

and,

prob of the residue on the surface =  [number of surface amino acids / total number of surface amino acids]

Check out this PLOS paper for an example. PLoS One. 2014; 9(5): e97158.


Are there other mechanisms for mutation besides imperfect DNA replication?

Absolutely. Ionizing (X-rays, neutrons, electrons, heavy ions) and non-ionizing radiation (UV), chemicals, etc. are able to induce DNA Damage, which is then imperfectly repaired. So it's not an issue of imperfect replication, but also of imperfect damage repair.


Why do people and animals stretch out their bodies and what is causing this behaviour?

Humans and other animals have lots of innate behaviors that are not learned from observation, i.e. behaviors that are hard-wired into our nervous system, and this is one of them. Suckling reflexes in mammals and the Moro reflex is human babies (which we grow out of) are other simple examples.

The stretching behaviours you are referring to are usually labelled pandiculation in humans (defined as involuntary stretching of the soft tissues), and yawning is often considered a special case of this. These kinds of behaviours are also normally related to transition periods between high-low activity in animals (Walusinskie, 2006). In practice, stretching functions as a way to reverse the muscular atonia during REM sleep, and is in this sense a way to restore homeostatic functions (Fraser, 1989; Walusinskie, 2006).

A paper by Rial et al (2010) deals with the evolution of sleep and wakefulness in mammals from our reptile predecessors, and indicates that stretching behaviours might have originated/evolved from post-basking activities, more specifically risk-assessment behaviours, such as:

  ...risk assessment behaviour (RAB) and consists of the suspension of current behaviour, to be replaced by head dipping movements, eye scanning, rearing and
  adopting stretch attending postures...

There is most likely much more to be said about this, and the paper cited above contains many references that can provide further clarification and evidence. A short comparative discussion of pandiculation is found in Frasier (1989).


Does homeopathic or herbal treatment of cancer have any scientific recognition?

The methodology behind homeopathy is scientific nonsense.  If you dilute anything a billion times, it will have no chemical effect, not even if you shake it all the while.  So no, homeopathy does nothing for cancer, or any medical condition at all.

Of course plants can have active compounds in them, once scientists have identified those compounds, they can be tweaked to make them act better in the human body, and then manufactured under strict guidelines to ensure purity, and tested to determine the optimum dosage; then it's just medicine.  Taxol comes from yew trees, it doesn't mean that native herbalists were successfully treating cancer with it for hundreds of years.  Native herbalists were using willow bark, which contains salicylic acid, which has anti-inflammatory properties, but chemists improved on it, reducing some of its negative side effects, by modifying it to acetylsalicylic acid.

Millions of people get cancer.  Doctors get cancer.  Herbalists get cancer.  If curing cancer was as easy as mixing some leaves in a poultice, people would do that.


What advantages could there be for using the unseen variant chosen by He Jiankui instead of the naturally occurring CCR5-∆ 32 mutation?

Possibly He Jiankui was using Cas9 without a template DNA.  If so, this generates double-stranded breaks that are repaired through processes such as non-homologous end joining (NHEJ) that often produce small indels (deletions and insertions) 1.

This is consistent with the apparently random small deletions and insertions around the cut site seen in both girls.

An additional, unflattering possibility is that this way he could prove that these were his edits and didn't happen spontaneously.

Useful starting points for understanding how Cas9 works can be found at the Addgene website and on Wikipedia.

Reference:
1: Brinkman, Eva K et al. “Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks.” Molecular cell vol. 70,5 (2018): 801-813.e6. doi:10.1016/j.molcel.2018.04.016


Can multiple overt/covert intentions produce identical EEG readings?

To curtly answer your question: given the sheer amount of different thoughts possible (billions I guess) and the limited spatial resolution of the standard EEG as well as the restricted number of characteristic parameters to describe EEGs (frequency, amplitude, latency) it is safe to say EEG is not suitable to characterize all of the brains processes. In fact, no state-of-the-art technique can do so, as far as I can see.


Why aren't plants and animals capable of assimilating $\ce{N2}$ directly from the atmosphere?

As @Wolfgang Bangerth commented, inertness just means that nitrogen gas doesn't undergo reactions because the NN triple-bond has a very high bond energy and the activation energy for reactions that break the bond (even though thermodynamically favourable) is therefore high. So I suppose that you could say that a major chemical factor in the reactivity of gases is their bond energies.

The key reaction of biological interest for nitrogen is reduction to ammonia, as referenced by the comment of @aretxabaleta. Stryer makes a couple of points that seem chemically relevant (http://www.ncbi.nlm.nih.gov/books/NBK22522/). He says that the reaction pathway for the reduction of nitrogen involves unstable intermediates, and he also mentions that the nitrogenase enzyme in Rhizomium is extremely sensitive to inhibition by oxygen. I am no expert, but I presume that the instability of the intermediates is related to their ease of oxidation. Leguminous plants maintain a very low concentration of free oxygen in their root nodules by synthesising the protein, leghaemoglobin, which mops oxygen up.

So the answer to the question in the title — why animals (at least) don't fix nitrogen — could well be because as aerobic organisms they would find it very difficult to provide an oxygen-free environment to do this. And the fact that animals can get their metabolizable nitrogen second- or third-hand means that there is no evolutionary pressure to develop such a mechanism. (Most bacteria and plants manage without too.)


Understanding conclusions that functional regions are under negative selection?

Lets assume for simplicity that DNA is globally subjected to the same mutation rate (which is probably not a fully correct assumption).

Now let take a DNA region which is functional (what you meant by giving a fitness benefit), mutations in this region will occur as anywhere else in the genome. Some mutations will be deleterious and reduce the fitness of (or kill) the cell therefore, on the long run, cells that do not carry those deleterious mutations will propagate. This means that now if you look at the genome in the cell that propagated, certain genomic regions will contain less mutations than other because of the negative selection. They were "protected" against deleterious mutation.

Similarly, In multicellular organisms any mutations that reduces the fitness of the germline cells will be negatively selected (again functional regions will be more conserved).

The author was likely referring to regulatory regions. These are regions that do not encode proteins but are very important for gene regulations. Regulatory regions include enhancers, silencers, insulators and locus control regions (Maston GA, 2006). These regions will also be more conserved as deleterious mutations in regulatory elements could reduce the fitness of the cell/germline.


Sansevieria species specification needed

You could use this key to the genus. The differences between both species should become obvious when tracing back the decision tree. It seems that they can be distinguished mainly by the leaf size/shape of adult plants.


On which chromosomes were the traits studied by Mendel?

The yellow/green color of seeds is on chromosome 1, but the color for for the pods is on chromosome 5. The smooth/wrinkly seed shape is on chromosome 7; however for the pods a similar contrast is governed by chromosome 4. The pea has 14 chromosomes (diploid).

What you mentioned however are not all of the pea genes Mendel studies. He actually studied 7 genes (see table above) but only 4 chromosomes host all of the genes he studied. Mendel was lucky that two combinations don't usually show linkage because of the large distance between them (on the chromosome 1 and 4 respectively). There was one linkage which he should have detected though between plant height and the shape of the pods (both close enough on chromosome 4); apparently Mendel never published anything on that combination though. I don't know whether it was because it befuddled him or he just didn't study it.
Referernce: Blixt, S. Why didn't Gregor Mendel find linkage? Nature 256, 206 (1975). doi:doi:10.1038/256206a0


Inexpensive way to determine mass of tiny seeds?

A pharmacy is a public business, and they should have a scale sensitive enough to weigh seeds.  They will have to let you in back to use it of course.  If you show up with her and she has the seeds and she asks the manager nicely, they might let you back and help you use it.  I would show up rather than call; if you show up you will see the manager / pharmacist but if you call you will not talk to the manager.

If this works she needs to be sure to credit the pharmacy in her project!

I recommend she weigh several seeds of each type - they might vary.

Your 100 seed idea is a better one, I think.  I understand your sentiment.

You did not ask about volume but this could be done with a graduated cylinder.  Put some water in it up to, say, 5 ml.  Then drop in a seed.  How much farther does the water level rise?  That is the volume of the seed.


Engineered CD8 T-cell therapy for HIV infection

People in the comments suggest that this would "Drive the patient into AIDS sooner", or that this will be ineffective because of dormant virus.  Neither is correct.

The question is asking about engineering CD8 with engineered T cell receptors specific for HIV.  This is a logical approach, and multiple groups have tried it:

In Vivo Suppression of HIV by Antigen Specific T Cells Derived from Engineered Hematopoietic Stem Cells
Reconstitution of anti-HIV effector functions of primary human CD8 T lymphocytes by transfer of HIV-specific alphabeta TCR genes
Development of CD8+ T cells expressing two distinct receptors specific for MTB and HIV-1 peptides
T-cell engineering by a chimeric T-cell receptor with antibody-type specificity for the HIV-1 gp120

A brief search on Pubmed will turn up many other articles. Some of these approaches have entered clinical trials; for example:

Redirected High Affinity Gag‐Specific Autologous T Cells for HIV Gene Therapy

The problem with this approach is not that it will "drive the patient into AIDS sooner".  A strong CD8 T cell response controls HIV well, and although it might be one contributor to CD4 T cell loss it's no longer believed that it's a major cause, especially in the early stages of HIV infection.

The general problem with CD8 control of HIV is that the virus is capable of mutation to avoid control by CD8s. Essentially, every case of HIV is effectively controlled by the CD8 T cell response in the early stage of infection, but the virus then mutates and escapes control, then the CD8 response adapts and controls the virus once again, and the virus mutates and escapes ... This can and has been tracked in many patients, showing repeated rebounds of the virus in the blood correlated with CD8 changes.

Better CD8 control of HIV is linked to a broader CD8 response -- that is, attacking many viral proteins, so that viral escape requires multiple simultaneous mutations (exponentially more difficult for the virus).  (Alternatively, the CD8 response can attack a small number of proteins that are very constrained, so that the virus can't successfully mutate them.  However, for reasons related to MHC restriction, that seems to only work in a small minority of people.)

An engineered CD8 T cell response will inevitably be to one or a small number of viral proteins.  That's conceptually similar to the natural situation following HIV infection, meaning that the outcome could be the same -- viral mutation and immune escape.

Because engineering the TcR means you can pick your targets rationally, you might be able to do better than the natural situation, but it's not obvious.  Overall, the fact that groups have been working on this approach for decades, without a breakthrough cure yet, suggests that it might be useful but isn't going to be a slam-dunk.


Restriction Mapping of Plasmid Assignment

A) Here is the correct map:

You made a mistake on your map at the PvuII site (it is not on 6.5kB from the start of the plasmid, but on 6kB).

  Can the Kpn I not go on the 8.5 site, it still creates the 2 and 8.5, so isn't there more than 1 correct option for plasmid map?

Yes. What you need to do in order to make the correct map is try all possible positions of the restriction sites:

You start with HindIII and place it at position 0 of your vector.
The KpnII site can be either at 2kb (left of HindIII) or at 8.5kb (right of HindIII). Draw both versions of the plasmid.
You place the NotI site that can either be at 2.5kb or at 8kb. Now you have four different possibilities for the plasmid:

HindIII[0], KpnII2, NotI[2.5]
HindIII[0], KpnII[8.5], NotI[2.5]
HindIII[0], KpnII2, NotI[8]
HindII[0], KpnII[8.5], NotI[8]

Then you do the same for the rest of the restriction sites. When you get to the last two digests, there is only one option for the correct plasmid left in the following order, depicted on the plasmid map below.

I have to point out though that StuI and SstI can both be at 3kb (they can be next to each other). Then the 2 fragments from the digest will be ~3kB and ~7.5kB. So technically, there are two possible versions:
correct

a) HindIII[0], KpnII2, NotI[2.5], StuI[3], PvuII[6], SstI[7.5]

b) HindIII[0], KpnII2, NotI[2.5], StuI[3], SstI[3] PvuII[6]

  If u can, can u please elaborate on question b as to why there is one correct option for the plasmid map? Also, what do they mean by double digest to confirm ur analysis?

A double digest means that you cut your plasmid with two different restriction enzymes at the same time. As you already have a putative map of the plasmid, you can predict which would be the expected bands. If you observe the expected sizes, then your design is correct and your analysis are confirmed.

To check which one is correct I would do a double digest with:
1) SstI and PvuII, generating a 1.5kb and a 9kb bands if design a) is correct or                              3kb and a 7.5kb bands if design b) is correct
2) StuI and SstI, generating a 4.5kb and a 6kb bands if design a) is correct or                             a 10.5kB band if design b) is correct

  To confirm the "ampicillin gene" starts at kpn I 2.0 and end at the 3.0 stu I site right?? So the amp gene is 1 kB long?? So the relative position of the amp gene starts at 2.0 and ends at 3.0.
  Why is it that in the question it says cloning into the kpn I and sst I sites abolishes ampicillin resistance whereas cloning on other sites does not?
  What do they mean by this? Is the ampicillin resistance gene diff from the ampicillin gene??

The ampicillin resistance gene and the ampicillin gene are the same. It refers to an enzyme (beta lactamase) which degrades ampicillin, and thus the cells that harbour the ampicillin-containing plasmid can survive when plated on ampicillin.

Are you sure that the resistance is disrupted if cloning into SstI site and not StuI? If this is really the case, then the StuI site and SstI sites are next to each other, as first you have the SstI site, followed by StuI. The amp gene
The gene is a little above 1kb, so it starts upstream of KpnII and ends right after SstI, but it doesn't disrupt StuI. If something is cloned into KpnII or SstI sites, then the open reading frame of amp is disrupted, and the protein cannot be functional.


Because mother invest the most material and time into producing the offspring, so there is a stronger pressure on them to not waste it. Males can go impregnate other females so there is a stronger possible disadvantage for child rearing, few mates thus fewer offspring. Whereas a female can't have more offspring by finding other males while currently carrying offspring so they are forced to sink a lot of time and energy into the offspring. So evolution strongly disfavors females who waste those resources by abandoning the offspring.

Strong K strategists like human tend to override much of this becasue of how much investment the offspring need. So there is a strong pressure for the female to only accept mates that can provide a great deal of resources, including time. And males can seriously hurt the chances of their offspring surviving by abandoning them. But there is still more built in investment on the part of the female.

There is one other factor, A female knows who her offspring are, males do not, so the offspring they invest in might not be theirs, so there is a pressure to not put all their eggs in one basket so to speak, this is also why males tend to be more worried about physical infidelity (cuckolding) while females worry more about risk of abandonment (loss of support).

Now remember this is males an females in general, individual species can have different pressures. And remember that humans have very complex behavior so much of this just amounts to tendencies on average, not hard and fast rules.

More on the ethology of mating here. http://www.tandfonline.com/doi/pdf/10.1080/11250008409439461


Species Identification: Liberian "kiss-meat" snail

It's Tympanotonos fuscatus from West Africa. They harbor near the roots of mangrove at low tide. Due to their tendency to bioaccumulate heavy metals, they have been used in studies of environmental presence of heavy metals, and the samples taken from markets have been found to be excessively high in cobalt and manganese.


What differences in effect does fast repetitive exercise have compared to slower muscle-building exercise?

Your body creates muscle after an exercise through a process where it fuses muscle fibers together to form new muscle protein strands called myofibrils. these myofibrils increase in size as workout intensity increases, leading to muscle growth. Muscle growth occurs when muscle protein synthesis happens faster than muscle tissue breakdown 1.

Since you are never really increasing the amount of strain on your muscles(i.e. by adding more weight to a workout) there is no incentive for your body to create more myofibrils, rather it will just replace the ones that were torn during your drumming.


What is a "noninvasive" biomarker for a disease?

A biomarker, or biological marker, generally refers to a measurable indicator of some biological state or condition. - Wikipedia

The presence of certain 'things' (sorry for being vague) in a tissue obtained invasively - via biopsy, for example - are considered biomarkers for, say, a cancer. It could be histopathological - a particular abnormality seen on staining the tissue - or it could be the presence or absence of a membrane receptor, etc.

A non-invasive biomarker is simply one that can be obtained easily and without "harm" to the (patient?), for example, to identify the potential presence of a cancer without the need for a biopsy. (Obviously, this doesn't eliminate the need for invasive methods. It just adds to the arsenal of detection methods.)

That is the usual meaning of non-invasive biomarker in the many, many papers using the term (at least medically), such as the one cited.

Serum microRNAs as non-invasive biomarkers for cancer


Can you tell the sex of a white willow when it's not flowering?

I remember overhearing a botanist some 10 years ago, that he cannot tell male poplar from female when they are not flowering or producing seeds. Poplars and willows are related, so it is a weak indication for you, you will likely not find any visible features in willow neither. But it is an old information, too.    (Are you interested in DNA sequencing evidence or not ? I can look it up for you, but it seems your statement in comment question was ironical.)
EDIT: have just found an article which says: "In Salix viminalis, the sex of plants cannot be confirmed until the first time they flower." At that time, 1997, there were no DNA markers for plant sex determination, but it is apparent, they did not know how to differentiate the sex of this willow just from morphology. This example is even closer to Salix alba than poplar. I find it even more likely now, that you will not find the morphological features.
I took the suggestion of Oreotrephes. This is what to look for under the tree - fruit and seeds:
.
Source.
( C. Alström-Rapaport, M. Lascoux, U. Gullberg. Sex determination and sex ratio in the dioecious shrub Salix viminalis L. Theoretical and Applied Genetics 1997, Volume 94, Issue 3-4, pp 493-497).