How does one calculate the resolution of a crystal structure?

Hi sorry i missed this one - not too hard for "biology"

If you look at a protein crystal (or any crystal really) in an x-ray beam, it scatters lots of spots (diffraction reflections).  If you look at a picture of crystalline diffraction, at larger angles from the center of the x-ray beam, the reflections get weaker and weaker and basically just stop, if the wavelength is short enough (in all crystallography labs its plenty short - from 1.5 to 0.9 Angstroms).

The resolution is marked by the angle of scattering to the last measurable spot (aesthetics can vary here, but there is little variance from personal judgement here).  Once you have the angle of scattering, you can calculate the resolution from the Bragg scattering equation:

lambda = 2d sin(theta)

which is rearranged to solve for 'd'

d = lambda / 2 * sin (theta)

where lambda is the wavelength of the incident radiation and theta is the scattering angle.
d = the apparent width of the 'slit' which caused this highest resolution reflection is called the 'resolution' of the X-ray scattering experiment.

There is one part that's a bit tricky as in the typical diagram, depicting Bragg reflection/scattering, you would take the incident x-ray beam as first beam and the scattered angle as the beam of the high resolution scattering, which is more easily measured as 180 - 2* theta.


Function of the alpha subunit in mitochondrial ATP-synthase?

From: Uniprot

  Mitochondrial membrane ATP synthase (F1F0 ATP synthase or Complex V) produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain. F-type ATPases consist of two structural domains, F1 - containing the extramembranous catalytic core, and F0 - containing the membrane proton channel, linked together by a central stalk and a peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F1 is coupled via a rotary mechanism of the central stalk subunits to proton translocation. Subunits alpha and beta form the catalytic core in F1. Rotation of the central stalk against the surrounding alpha3beta3 subunits leads to hydrolysis of ATP in three separate catalytic sites on the beta subunits. Subunit alpha does not bear the catalytic high-affinity ATP-binding sites.

From: InterPro

  There is a substrate-binding site on each of the alpha and beta subunits, those on the beta subunits being catalytic, while those on the alpha subunits are regulatory. The alpha-subunit contains a highly conserved adenine-specific non-catalytic nucleotide-binding domain, with a conserved amino acid sequence of Gly-X-X-X-X-Gly-Lys. The alpha and beta subunits form a cylinder that is attached to the central stalk. The alpha/beta subunits undergo a sequence of conformational changes leading to the formation of ATP from ADP, which are induced by the rotation of the gamma subunit, itself is driven by the movement of protons through the F0 complex C subunit [PMID: 12745923].

Sources:

http://www.ebi.ac.uk/interpro/entry/IPR005294
http://www.uniprot.org/uniprot/P25705
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278611/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1679692/


I made the large-scale in a falcon tube and then moved the mixture to PCR tubes each containing 50 μL, so the PCR conditions should be the same as the single PCR amplification

If all reagent concentrations and cycling conditions are the same, I suspect that you did not sufficiently mix your large-volume reaction prior to dispensing as 50 μL aliquots.

It should be mentioned that the single PCR was performed in the summer, and the large-scale was performed now

If you were using the same polymerase and primer stocks for the small- and large-volume reactions, were the stocks properly stored in the interim? Recombinant DNA polymerases in glycerol buffers have shelf lives of months to years depending on the supplier specifications and storage conditions, though you should expect some decreased activity after several months.


Why do men have a higher hematocrit (red blood cell count) than women?

I found a nice article that has insights to this matter. As posted before me it is true that only adults, but not juvenile individuals show this difference. Direct and indirect effects of sex hormones on bone marrow erythropoiesis and renal erythropoietin production has been proven, but it works in both sexes the same way. Females are capable to elevate their haemoglobin / red blood cell levels to external stimuli, yet at same conditions (same altitude etc) the difference remains. Also:

  Men, premenopausal women and postmenopausal women have similar plasma erythropoietin levels, indicating that women do not attempt to compensate for their lower haemoglobin levels by increasing erythropoietic drive. These observations show that the prevailing lower haemoglobin level in females cannot be ascribed to a lack of bone marrow or renal erythropoietic capability: they indicate that adult females maintain their venous haemoglobin levels at a lower level than adult males as a physiological steady state — they do not try under physiological conditions to maintain the same levels as adult males.

This could be achieved by modulation of the juxtaglomerular apparatus signal (JGA) of the kidney. The JGA has important role in the regulation of the haemoglobin level - it is the main input for erythropoietic red blood cell production by regulating renal filtration and thus regulating the amount of oxygen that gets to the EPO producing peritubular cells.

It is noteworthy to say that similar difference exist in mammals and even there are examples among birds and reptiles.

It is described in the linked paper that both men and women achieve the same or very similar microcirculatory haematocrit level inspite the different mean venous haemoglobin levels.

This implies the very interesting theory / reasoning in the article:

  (...) that both sexes set their mean optimum level separately and to some degree independently.(...) the red cell mass is an enormous resource in animals — one third of the body's cells by number in adult humans, and demands enormous effort to establish and maintain.(...)This price must be paid for by increased fitness.(...)The excess red cells over the critical minimum that circulate in the large vessels (and slowly through in the spleen in some species) and that constitute half or more of the venous haemoglobin level probably provide a storage function for the reserve red cell mass for use when the need arises for increased work — fight, flight, food and reproduction. They may also act as reserves for heat exchange and iron storage. It is likely that the return in fitness from this reserve differs between the sexes, and therefore that the optimal size for maximal cost benefit also differs.


There are no roses (that is, flowers of genus Rosa species) that naturally express a "true" blue color. Through cross-breeding, there are lilac-mauve rose horticultural varieties ("Blue Nile","Blue Moon","Lady X", etc.), and through genetic engineering (actually inserting delphinidin-producing genes) there are mauve-lavender varieties ("Applause"). The insertion of delphinidin-producing genes did not yield blue colour roses as hoped is due to the acidity of the rose petals, which itself changed the delphinidin blue to mauve-lavender instead. The next breakthrough will be to switch off the acidity of the rose petals to create a true blue rose.

More info

Wikipedia article Blue Rose gives good coverage.

Here's a nice scientific bibliography of rose pigments with some good information on blues.


Short answer
Moss plants form spores; minute, invisible, typically one-celled, reproductive units that are carried off by the wind and into your pots.

Background
Mosses belong to the Bryophytes. Bryophytes are embryophytes; i.e., non-vascular land plants. They are spore-producing, rather than seed-producing and they do not bear flowers.

The leafy moss plant you are describing is the sexual phase of the moss life cycle. When mature, most mosses develop sex organs. Under wet conditions, sperm cells are released from male sex organs (antheridia) and swim to the female organs (archegonia), attracted by a chemical released by the female organ. After fertilization, the egg cells that are embedded in the female organ form a spore-producing plant. This consists of a stalk with a spore capsule and stays attached to the parent moss plant. As the spore capsule matures, it releases its spores into the air, and then dies. If moss spores fall in a damp place, they germinate and grow into leafy moss plants, and the cycle is completed (Fig. 1).

Hence, to answer your question - moss appears in your pots when spores land into it and enough water is available for their outgrowth.

Fig. 1. Reproductive cycle of moss. source: Encyclopedia of New Zealand


Relationship Between Evolution and the Increase of Entropy of Earth

However, I do not understand. Biological evolution does cause the system (living organisms)'s entropy to decrease. So, by the second law of thermodynamics, the entropy of the universe (in this case Earth), must have overall increased.

The universe and the earth are not equatable. Earth is not an isolated system. Life causes entropy of the earth to decrease. This is offset by increased entropy of the sun, which is the primary source of energy for the earth. Overall, the entropy of the universe increases.


Colorblindness in females and random X chromosome inactivation

In heterozygote females with colour defect genes on the X-chromosome, even if approximately half of their photoreceptors are dysfunctional they usually have enough functional cone photoreceptors to have normal colour vision.

From Molecular genetics of colour vision deficiencies:

  Due to X-chromosome inactivation during early development,
  heterozygotes are mosaics for two populations of cones, one expressing
  visual pigment genes encoded by an X-chromosome that would cause
  colour vision defects in males, and the other expressing genes that
  would confer normal colour vision on a male. In support of this,
  patches of defective colour perception were detected by shining a very
  narrow beam of red or green light into the retinas of female
  heterozygotes for X-linked colour vision defects. The majority of
  heterozygote women (carriers of colour vision defects) have normal
  colour vision.

This means that  – in most cases – for a female to be colourblind, her father must be colourblind and her mother must be either a heterozygote (carrier) or homozygote colourblind. In a male, only the mother's X-chromosome determines whether he inherits the defective genes, so he is more likely to have the colourblind trait.


How animals maintain their body shape after development to maturity?

Normally, cells do not proliferate without a "command". The "zones of genetic activity" you mentioned are defined by gradients of morphogenic molecules (and cell interactions). In the adult organism the original "map" of concentrations of these molecules is already realized and the pattern they defined before is no longer present.

Another closely linked idea is that most cells in mature tissues are not able to proliferate, because they have already undergone the process of differentiation. In contrast, stem cells maintain their ability to reproduce. [There are still some ways to de-differentiate some types of cells, i.e. to obtain induced stem cells in vitro.] Thus, embrya are composed of embryonic stem cells, while adult organisms have several restricted pools of stem cells (for example, in haematopoetic organs, where new blood cells are produced.)


Is there anything that tells me how Lichens Grow?

Just from conducting a Google search using the phrase, "lichen modeling pdf", I was able to find several studies/publications that address your need(s). Though its dated 2004, this article seems extremely relevant to your application.

Simulating and Modeling Lichen Growth

  In this paper, we present a system for modeling lichens
  and simulating their propagation and growth in a virtual
  scene.

In the article, they mention:

Aging and Weathering
Ecosystem Simulation
Lichen Seeding and Propagation
Environmental Charateristics
Theoretical Aggregation
Complex Modeling

And here are (a few) examples of what they produce:


Can female Drosophila melanogaster lay eggs without males?

Yes, I regularly have to collect female virgins (12500 of them in the last week). They will lay eggs especially when there is extra yeast available. It is actually a good way to check virginity (in case a fly hatched early and was already mature, or a male made it through sorting etc.) - put some extra yeast grains in the vial when you collect them, leave them for a few days and then check for larvae, if they are not virgins there will be eggs and larvae, if they are virgins there will only be eggs!


What's a good and reliable database on the pharmacodynamic and pharmacokinetic data of drugs both approved and unapproved?

For approved drugs, the Drugs @FDA database at CDER (Center for Drug Evaluation and Research) aggregates labeling information (which includes at least a cursory PD explanation and a listing of or reference to common PK data for the substance) for most modern drugs.

Unapproved drugs may be a bit trickier to find out about, but the FDA maintains a list of contract research organizations (CROs) who are running trials here, and the actual trials can be found on http://www.clinicaltrials.gov/, which will have citations for the papers that have been published.

Drugs in their earliest stages of development, i.e., internal to a pharma company, are likely to be kept pretty tightly under wraps.

I don't know enough about the governing bodies in other countries to know where any international data would be, but I assume you can find published papers for substances in those countries as well.


Determining net charge of amino acid at given pH

You are right in your reasoning: at any pH for any titratable group, there is a distribution between the protonated and deprotonated species. We can calculate this distribution and therefore the average charge of the species with the Henderson-Hasselbalch equation:

$$\mathrm{pH = pKa + log\left(\frac{[B]}{[A]}\right)}$$

Or, rearranged:

$$\mathrm{\frac{[B]}{[A]} = 10^{pH - pKa}}$$

Where A is the conjugate acid and B is the conjugate base. For carboxyls and primary amines, this can also be written as $\ce{\frac{[COO-]}{[COOH]}}$ and $\ce{\frac{[NH2]}{[NH3+]}}$, respectively. As a simple example, if the pH was 2.28, the ratio between the protonated and deprotonated form of the carboxyl group (pKa = 2.28) would be $\ce{\frac{COO-}{COOH} = 10^0 = 1}$. This means $\ce{[COO-] = [COOH]}$ and the average charge of the carboxyl is thus -0.5.

Now, for cases where $\mathrm{pH \neq pKa}$, we need to determine the mole fraction, $\chi$, for each charged species. Given that $\mathrm{\frac{[B]}{[A]} = \frac{\chi_B}{\chi_A}}$ and $\ce{\chi_A + \chi_B = 1}$, we can derive these equations:

$$\mathrm{\chi_{COO^-} = \frac{1}{1 + 10^{pKa - pH}}}$$
$$\mathrm{\chi_{NH_3^+} = \frac{1}{1 + 10^{pH - pKa}}}$$

Plugging in the numbers, we get:

$$\mathrm{\chi_{COO^-} \approx 0.999981}$$

$$\mathrm{\chi_{NH_3^+} \approx 0.993872}$$

To state it another way, ~99.9981% of the carboxyl groups are in the deprotonated (negative) state and ~99.3872% of the amino groups are in the protonated (positive) state. The average charge of methionine at pH 7 is simply the sum of these mole fractions, accounting for the charge of each species, and is approximately equal to -0.006109. I assume your textbook is rounding.

You can plot these functions to see how charge varies with pH:


Why are 2 electrons transported from photosystem II at the same time?

So refer to the following diagram,

In the photosystem II complex, water is decomposed into oxygen and protons. That's two electrons liberated from each water molecule. Plastoquinone accepts two protons from the stroma by coupling it to the two electrons it receives from the photosystem complex. In this manner, the protons are transported to the lumen, and the electrons are sent into the electron transport chain. So PQ binds in a QB site in the D1 protein, and it's not released until it's double reduced/protonated. Another PQ binds in it's place when PQH2 leaves the binding site. Source

Short answer: Two electrons are liberated in splitting water, and that mechanism feeds into asymmetric lumen/stroma H+ concentrations and movement of electrons through the ETC.


Colchicine inhibits the formation of the microtubules by binding to tubilin and rendering it unavailable for the polymerization. Thats why the cells get arrested in the metaphase and can not go on further in the cell cycle and divide. For chromosome studies this is very useful since this is the phase where the chromatin is most condensed and can be viewed best. It inhibits the positive side producing the microtubules to prevent it from moving to the negative side, in cell division.


Can estimating the likelihood of protein sequences adopting functional enzyme folds show life is too complex for evolutionary timescales?

I think your acquaintance is trying to fit real science to some of his personal beliefs (that are obviously wrong).

If you read the article you'll see that it's not about evolution at all, but about protein folding and what proportion of possible sequences gives a working protein. It turns out random sequences are not that likely to fold, which leads to some conclusions about the probable mutational pathways to folded proteins.

The argument of your friend is sort of analogous to the infinite random monkey theorem. If you put a monkey behind a typewriter and wait long enough, eventually he'll write the complete works of Shakespeare. This doesn't mean we waited billions of years for this monkey to type it up, because the world doesn't work like that. There was just a guy with a brain.

In case of the proteins, evolution doesn't work by generating newly (random) 300 residue proteins that work 1 time in a billion. Probably in one generation a copy of the protein is made with the same function, and during many generations the function of this protein drifts towards a new function, while all the intermediate proteins stay folded because they're not that different.


Are there any organisms, extant or extinct, that have only one neuron?

In evolution things don't just pop into existence. So, it's unlikely that a single neuron originated by itself. The question is, what would that neuron do? It would communicate to at least one other cell, right? Otherwise the transmitted signal would be lost and useless. And where is the signal coming from? Neurons generate signals either by receiving signals from other neurons or, for specialized sensory receptors, through some changes in the environment. The receiving cell could be a muscle cell, so your minimal network would consist of a sensory neuron and a muscle cell. Upon a detected change in the environment, the neuron would signal the muscle to contract.

In evolutionary basic organisms we can find action potential like excitability and synapse-like cell-cell contacts in non-neuronal cell types. This hints towards a step-wise development of these functions before actual neurons arose (wiki, paper). Even one-cell-organisms have neuron-like features (sensory input dependent polarization, intracellular signal propagation, coordinated movement). If cell-cell communication or excitability are not limited to neurons, what makes a neuron a neuron? This is also a matter of definition, as discussed in the paper mentioned above.

What makes neurons unique is their property to propagate signals in a network. That's why the neuronal nets of jellyfish are usually seen as the first appearance of neurons in the evolutionary tree. While organisms without a nervous system are able to respond to their environment by signal transmission between non-neuronal cells, I am not aware of any organism that possess only a single cell which we would now call a neuron. At the stage where neurons arose, animals were already a more complex arrangement of specialized cells for different functions. You would therefore assume, that also the neuronal predecessors were a group of cells within the organism.


What happens if you intake pure magnesium?

Because like a lot of material we need the ion not the pure form. Pure sodium is explosive metal and pure chlorine is horribly toxic gas but change them into their ionic form and they are essential nutrients, sodium chloride, table salt.

In the case of magnesium however the problems one of reactivity and absorption. If you swallowed a solid lump of magnesium, not much will happen, the molarity of stomach acid is fairly low, it reacts too slowly to get significant amount of magnesium (or hydrogen) out of it before it passes. Your body just is not equipped to break down solid magnesium since it does not occur naturally often. We can only absorb it in it's ionized state.

More importantly we take in some ion combinations better than others, this is called bio-availability and is influenced by a number of factors. Magnesium oxide for instance has very low absorption rates and basically just passes through without doing much, while magnesium glycinate has a fantastic absorption rate, some combinations can actually be mildly toxic like magnesium sulfate. This is a reoccurring issue with dietary supplements many do not contain bioavailable forms of the mineral they list, which is how people can end up with deficiencies even while taking supplements for that mineral.


The main mechanism behind the scar changing its color is the dilation of blood vessels within the scar tissue. The dilated vessels lead to the congestion of blood flow. The red blood cells moving more slowly leave more oxygen due to its diffusion to the tissue and the hemoglobin -- the oxygen holding protein -- changes its color from scarlet (bound to oxygen) to cyan (released/bound to CO2). Since scars are not covered by skin, the blood vessels are clearly visible here and you see this characteristic color.

The triggering mechanism here is cold that increases the energy barrier for many biochemical reactions, first of all those required for smooth muscle contraction.

Cold-induced vessel dilation (that can be seen, for example, on cheeks and extremities) with mild circulatory disturbances ultimately undergoes into so-called cold vessel paralysis when smooth muscles of blood vessel walls completely loose their ability to contract and are maximally dilated. The cyan color of the scar is usually seen at the very last stage, that can occur unexpectedly quickly because scars do not have any warmth insulation layer compared to the regions covered by skin.


Soap kills nearly all the bacteria it comes into contact with by dissolving the bacterial membrane.  Some viruses with protein coats can resist soap, but many viruses have similar membranous coats (like HIV) and are usually disrupted by soap.  I'm sure it washes some away too, but to say they don't kill bacteria is misleading. In the end, though, they are gone.

Antibacterial soap with triclosan does not kill bacteria on contact and are no more effective than if they had no triclosan at all.  That's actually a good thing since really using an antibiotic would probably accelerate antibiotic resistant bacteria which is a serious - probably catastrophic public health failure. A recent study showed that killing bacteria by soaking with triclosan took 9 hours to start showing an effect.

To achieve full sterility, surgeons bathe their gloves in iodine (see details in the comments below) and their instruments will be sterilized by heating them beyond the boiling point in an autoclave under pressure.   That's useful when you are breaching the skin in surgery, but the skin needs some bacteria to be healthy long term and works well to fend off bacterial infections.

Your confusion seems to come from finding a page full of errors. Alice didn't really do her homework.


Reporting observation of a bird outside its seasonal presence

It is NOT a Great Grey Shrike (Lanius excubitor).

It is a young Lanius minor Lesser Grey Shrike (which breeds in Bulgaria).
I say young (born the same year) because of the white tips of the feathers (they are new) and not so extended black mask (which probably induced you into the ID mistake).

I attach a picture of young Lesser Grey Shrike for comparison.

Generally you can report your observation on ebird.
There is a team checking the unusual observations (although for Europe at least many mistakes are not picked up).


Why do neurons die so quickly (relative to other cells) when deprived of oxygen?

There is a good review in the Journal of Experimental Biology (Bickler and Donohoe 2002, JEB 205, 3579–3585) I will just summarize for those that do not have access to the review.

Neurons use lot of energy to maintain their polarized state, this is not required to other cells. When O2 or blood flow is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.


With over 400 chromosomes, does mitosis in a species of butterfly happen in the same way as in humans?

Mitosis was displayed in a lot of organism, also in organism with a very high number of chromosomes. Here's an example of the analysis made in a fish with an average count of 280 chromosomes. Look at the metaphasis of a cell with higher number of chromosomes (Acipenser transmontanus):

This doesn't mean that every chromosome is equal to others: there're microchromosomes, acrocentric chromosomes, meta, sub-meta.. So, the size required into the nucleus (because where're obviously talking about eukaryotic cells) isn't strictly connected with the chromosomes number.

The answer to your question isn't a clear "yes" : the high number of chromosome in a butterfly is connected with a karyotype instability, where some cells received a wrong number of chromosomes into an alterated mitosis. Actually isn't fully clear why and how these errors come out. Here's something else about butterfly karyotype and phylogeny.


Can you vaccinate against bacterial diseases? Are there existing vaccines for such diseases?

Of course we can - and do - vaccinate against bacterial diseases, as these are some of the dangerous infectious diseases.
Among these are:

Tetanus (although here the vaccination is targeted against the toxin, not the bacterium itself)
Tuberculosis
Diphtheria
Pertussis
Haemophilus influenzae type B
Cholera
Typhoid
Streptococcus pneumoniae
Meningococcus: against the strains ACWY, B

A list of the vaccines against bacterial diseases can be found here.


How fast do different organs turn over cells?

1) cell growth

You should look into chemotherapy and cancer medicine in general.  Because chemo is mostly effective because it kills fast dividing cells, this has been worked out reasonably well.  the 7-10 year number is not really correct, some cells are replaced a lot more slowly.

This is why hair often falls out in cancer treatment, because the follicle cells are growing quickly.  Neurons divide very slowly - if at all - and often are never replaced.  Fat cells are in between - probably replaced in the 7-10 year range.  Heart cells are replaced albeit quite slowly - less than 1% per year, which implies that many cells are with you your entire lifetime.

2) atoms/molecules change

The cell itself is in a continuous state of flux, but different parts of the cell, like cells in the body, change at different rates. Some proteins which make up the cell matrix or the DNA in the nucleus are replaced very rarely (through repair or rearrangement of the chromosome for instance) and most of the chromosome DNA is with the cell for the entire life of the cell.

Most proteins are labelled for degradation and are recycled after a few hours of function.  Metabolic compounds such as sugars or salt might drift in and out of the cell continuously, maybe turning over in an hour or so. Fats can be incorporated into the cell and last for years I think.


Could a person become physically transgender through artificial means?

A "high level of testosterone" must be made within the context of a particular sex. Men tend to have much higher levels of testosterone than women, but the testosterone production and levels within women vary widely - just as many hormones. Genetics, environment, diet, drugs, and workout regimes can all affect testosterone levels. A qualified physician will be able to tell where a person is after a test.
As for the rest... Every case of gender reassignment I've heard of and read about has occurred after birth. Read through this Johns Hopkins Magazine article from Sept. 2000 to get a fairly good understanding of when gender reassignment occurs and how it's handled. Here's a quick rundown (summaries, NOT quotes from the article):

Inadequate exposure to Testosterone in utero can result in ambiguous genitalia or other conditions such as 'micropenis' for an XY fetus. Up until the 1990's, regardless of chromosomal gender, children with the conditions would be reassigned as 'female' and had reconstructive surgery very early on.
Androgen Insensitivity is when an XY fetus is genetically incapable of utilizing male hormones and can involve several levels of insensitivity from "Complete" to "Partial". Complete insensitivity usually leads to fully feminine genitalia, while "Mild" or "Partial" can lead to partially or fully masculinized genitalia. Genitoplasty is an option for the latter cases.
CAH - congenital adrenal hyperplasia. This genetic disease causes the adrenal glands to produce excess androgens--the steroids that cause masculinization--a process that begins in the womb and can result in ambiguous genitals. However, CAH girls are generally more aggressive and display behavioral tendencies that more closely coincide with boys of the same age. Important to note: CAH children are genetically female (XX) and identify as female.

An extensive review of gender reassignments in 1997 had this to say about the consequences of surgically altering an infant's sex:

Considering this case follow-up, and as far as an extensive literature review can attest, there is no known case where a 46 chromosome, XY male, unequivocally so at birth, has ever easily and fully accepted an imposed life as an androphilic female regardless of the physical and medical intervention.

HOWEVER - as with all things scientific - there is dissent from the Johns Hopkins article above:

Preliminary analysis of the data, says Migeon, indicates that almost all of the patients are content with the gender in which they were raised. All but two showed a gender identity and gender role in accordance with their gender of rearing.

There is significant divergence that has not been reconciled in any trustworthy article I could find. The modern practice is to raise the child as their genetic sex unless significantly afflicted.
In adult transgender individuals, things like Hormone Replacement Therapy are part of a regime - along with surgery, acclimatization courses, and psychological evaluations - that can successfully result in a person presenting themselves and physically resembling another sex.
With adequate surgery, hormone therapy, and proper treatment all-around, it is practically impossible to tell whether a person is transgender without getting invasive or performing genetic tests.
As with all things that veer into a hazy area between medical knowledge (medical advice is not allowed on this website) and human biology: DO NOT use the above information to diagnose yourself or anybody you know. ONLY a qualified medical professional can perform the necessary tests required and give a qualified interpretation of the results.


How do cells determine what size to grow to before dividing?

All eukaryotic cells have 'checkpoints' during their cell cycle (1)1. They will only commit to cell division or the next phase of mitosis until all requirements have been fulfilled. The cell needs to have enough energy and the right external stimuli before it starts the irreversible commitment to cell division. The proteins effecting these changes are the cyclins and the associated CDK's. These proteins integrate a wide array of signalling inputs (e.g. DNA duplication complete or no major DNA damage) and steer the proteins actually duplicating the DNA and the other machinery needed to split a cell. You can learn more about these proteins and their signals by googling 'restriction point'

If you interfere with cyclin D modifying proteins you can get very large or very small cells. One of the best understood proteins involved is WEE1 from fission yeast. If you knock this one out, you get very small cells (2).

In mammalian cells the size of the spindle during anaphase also seems to be crucial in splitting cells equally (although some divisions are asymetrical)(3).


That is the male of the Indian peafowl species (Pavo cristatus), also called the blue peafowl or common peafowl.  The male is called a peacock and the female a peahen, collectively peafowl, although often "peacocks" is used instead of peafowl.  The hen does not have the impressive tail of the peacock (although she does have a similar crest on the head).

They are not native to Kentucky, or anywhere else in the Americas, but have been widely introduced (because of their appearance).  There are only 3 species of peafowl, the green peafowl being similar and native to southeast Asia, and the Congo peafowl being much more subdued and native to Africa.


What is the name of this about 5cm high, grey, Beanie shaped fungus?

I think this is Coprinellus disseminatus, also known as "Fairy Inkcap". Size (they are pretty small) and also the color fits pretty well. See the image from the Wikipedia:

Some more information can be found here.


How can I isolate live Wolbachia endosymbionts from Drosophila

You can see this protocol for Wolbachia isolation:

See this protocol for infecting cell lines with Wolbachia.

In this study the authors have established a cell line from a Wolbachia infected tissue of Aedes albopictus. You can have a look at that too.


Can environmental pressures affect genes in one generation?

Yes. Environmental pressures that cause a change in allele frequency will always produce changes in a single generation. If the environmental pressure is present for more than one generation, it will affect changes in allele frequency over a longer time span.

I'd encourage you to look at this set of case studies from UC Berkeley's Understanding Evolution

To clarify what "pressure" means in the context of evolution. Selective pressure, or evolutionary pressure, as wikipedia describes it, is anything that changes the reproductive success of an organism. It is, by definition, something that has an effect in one generation. Selective pressure causes organisms with certain heritable characteristics (and certain alleles) to reproduce at a different rate from organisms with other heritable characteristics (other alleles). The pressure selects for certain alleles.

Considering the comments, it sounds like you're describing a disorder (psychological ailment, e.g., PTSD, GAD), which may have a heritable diathesis, and an environment (trauma) that causes the expression of that disorder. To consider that environment to be selective pressure, it would need to be present at a population level and cause individuals with that heritable diathesis to reproduce at a different rate than individuals without it. If it did, you would see changes in allele frequency over one generation. Indeed there is no way for selective pressure to cause a change in allele frequency without it occurring in a single generation.  I'm not aware of any study that has demonstrated this to be the case for any anxiety disorder.


Why are melodies/harmonies perceived as pleasurable by humans?

There are strong connections between the auditory cortex and the limbic system, which includes such structures as the hippocampus and the amygdala.

A recent paper [1] builds on earlier notions of emotional "significance" of music without any lyrics.  It adds in lyrics, so giving a perspective of which portions of the brain are reacting to which component of the music.

  Additionally, contrasts between sad music with versus without lyrics recruited the parahippocampal gyrus, the amygdala, the claustrum, the putamen, the precentral gyrus, the medial and inferior frontal gyri (including Broca’s area), and the auditory cortex, while the reverse contrast produced no activations. Happy music without lyrics activated structures of the limbic system and the right pars opercularis of the inferior frontal gyrus, whereas auditory regions alone responded to happy music with lyrics.

One of the limitations of this particular study is that the subjects self-selected their own pieces, which may limit the reliability of the results.  Of course, defining "happy" or "sad" for every individual is slightly subjective and difficult.  They cited an earlier "pioneering" study which standardized the musical selection between subjects.  Without consideration of the lyrics:

  The first pioneer study using functional magnetic resonance imaging (fMRI) by Khalfa et al. (2005) chose a controlled manipulation of two musical features (tempo and mode) to vary the happy or sad emotional connotations of 34 instrumental pieces of classical music, lasting 10s each. Sad pieces in minor-mode contrasted with happy pieces in major mode produced activations in the left medial frontal gyrus (BA 10) and the adjacent superior frontal gyrus (BA 9). These regions have been associated with emotional experiences, introspection, and self-referential evaluation (Jacobsen et al., 2006; Kornysheva et al., 2010).

As an aside to answer your final thought, in cases like this I think trying to jam everything under an umbrella of one "neurotransmitter system" or another can make things overly simplistic to the point where you lose focus of the diversity of receptors expressed.  You can say a system is driven by Dopamine, but D1 and D2 receptors have exactly the opposite effects on the neuron.

  [1] Brattico, E., Alluri, V., et al (2011) A functional MRI study of happy and sad emotions in music with and without lyrics.  Frontiers in Psychology, 2: 308.  doi: 10.3389/fpsyg.2011.00308 (free pdf)

(see also, http://www.sciencedirect.com/science/article/pii/S0028393206003083 and related)


How significant is the genetic component of homosexual behaviour?

This is not an area I know well, but I'm familiar with a couple of studies that have tried to estimate the heritable (genetic) component of homosexuality in humans. A review paper by Rice  et al (2012) points out that:

  Pedigree and twin studies indicate that homosexuality has substantial heritability in both sexes, yet concordance between identical twins is low and molecular studies have failed to find associated DNA makers.

Here is a selection of papers that should be of interest to you:

Pillard & Bailey. 1998. Human sexual orientation has a heritable component. Hum. Biol.
Bailey et al. 2000. Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. J Pers Soc Psychol.
Kirk et al. 2000. Measurement models for sexual orientation in a community twin sample. Behav Genet
Rice et al. 2012. Homosexuality as a consequence of epigenetically canalized sexual development. Q Rev Biol.

Kirk et al (2000) find a rather strong heritable component (30-60%), which also differs between males and females (stronger in females).

  Abstract
  Multivariate structural equation modeling techniques have been applied to examine the causes of individual differences in responses to several items concerning sexual orientation. To minimize potential ascertainment and response biases, the study sample involved a large (N = 4901) community-based cohort of Australian twins aged 18-52 who answered an anonymous questionnaire on sexual behavior and attitudes. The statistical power of the analysis was increased by the availability of multiple measures of sexual orientation (behaviors, attitudes and feelings), providing stronger evidence for the existence of additive genetic influences on this phenotype than in a previous analysis (Bailey et al., 2000). Estimates of the heritability of homosexuality in this sample ranged between 50 and 60% in females but were significantly lower (heritability of approximately 30%) in males.

Note however that is it often difficult to separate genetic and environmental components in these types of epidemiological data, especially when twins have grown up in the same environment. I'm also not in a position to judge or comment on the quality or methods of these studies.


Can the absorption of vitamins be enhanced?

There are two types of vitamins:

Fat soluble vitamins - Vitamins A, D, E, K
Water soluble vitamins - B complex Vitamins and Vitamin C

Fat soluble vitamins get better abosorbed when fat content of food is good. The bile secretion is also very important. These vitamins form miscelles with the fat molecules and get absorbed as such. The absorption of these vitamins can be enhanced by taking fatty diet.

The water soluble vitamins are absorbed freely and they are also excreted freely - Excess are expelled through urine.

There are inter-vitamin competition and some food biomolecules can inhibit vitamin absorption. For example avidin in the egg would bind to biotin and prevent its absorption. The articles below deal a little with such inhibitions.

For more see:

http://healthyeating.sfgate.com/improve-bodys-absorption-vitamins-2898.html
http://www.ncbi.nlm.nih.gov/pubmed/17023940
http://health.howstuffworks.com/wellness/food-nutrition/vitamin-supplements/body-absorb-vitamins.htm


Multi-nucleated cells: advantages and examples?

Muscle cells are the only cells I know of that are polynuclear. With respect to monocytes, a concise review of their nomenclature can be found in this paper by L Ziegler-Heitbrock, P Ancuta, S Crowe, et al. (Blood, 2010). Apparently it has had quite a complex and confused biochemical characterization, but the article states the name indeed derived from its single lobed, mononuclear morphology. This is in distinction to other phagocytes which have multi-lobular nuclei (polymorphonuclear cells).

With respect to advantages, a multinucleated cell makes sense when the speed of intracellular signalling is important (e.g., calcium diffusion). It may also be useful in the case of cells when the cell needs to coordinate the synthesis of large amounts of protein.


What is happening in each iteration of PSI-BLAST?

PSI-BLAST is Position-Specific Iterated BLAST.

I'm probably out of my depth here, but my understanding is that the results of the first, essentially standard, BLAST search are used to create a multiple sequence alignment. This alignment is then converted to a Position Specific Scoring Matrix (PSSM). (The linked Wikipedia entry shows this for DNA sequences, but the principle is exactly the same for protein sequences.) This matrix can then be used as the probe for the next round of BLAST, and the results of that alignment can be used judiciously to improve the matrix, and so on until the results converge.

Here is a link to some slides by Stephen Altschul which go into lots of detail.


Question regarding an Escherichia coli reaction

As far as I can tell, enterochelin esterase (Fes) utilizes an Alpha/Beta hydrolase fold to catalyze it's reactions, which means there's a triad of catalytic amino acid side chains. Where Fes differs from other proteins in the pathway is an amino terminal lid domain which confers specificity to the substrates of Fes ((1) dictates this forms a deep pocket in the protein). I'm having trouble finding the exact catalytic amino acids, but homology modeling between IroE and Fes from the same source shows this may be a triad of Glu, His and Ser. If we kind of visualize what a catalytic triad's mechanism looks like, and the following image is a generic lipase/esterase catalytic site,

A sort of transition state is formed between the target molecule and the serine, where the water reacts with help from the asp/glu and histidine to catalyze the hydrolysis. You'd just call it protein-ligand interactions.


Range of feasible coefficients in an unlimited growth model

A solid limit: k must be greater than zero. Unless you're talking about some cannibalistic species or something that isn't suited to the model at all.

As long as the species is productive in the new environment: k is greater than 1. The population is probably growing or again you probably won't be using an exponential growth model.

As mentioned before you would need to know the species for more information. But if you look at generation times and litter sizes:

Some bacterial generation times (from here) range from 10 to
2000 minutes (33 hours). So that is $k=2$ per generation time. Per
day you're looking at a lower bound of 2 per day and an upper bound
of $k=2^{14}=10^{43}$ per day.
Mice are something like 12 week generation time and a litter of 10
giving something like $k=10^{10}$ per year.
Elephants are one young every 25 years. So $k=16$ per century or so.

Of course this is all based on gross assumptions. But you're looking for guidelines for a unrealistic model so hopefully they'll do.


How to find the location of a gene, starting with the gene name and the DNA sequence of nucleotides?

To find the genomic location of a gene when you start with a gene name;

Use the UCSC Genome browser. This has a number of advantages. There are a number of species to choose from. It provides a representative image of the gene and regulatory elements that surround it. It can display a lot of extra information if you want to see it. The disadvantage ot the UCSC Genome browser is that the information density may overload non-professional users.

To find the genomic location of a gene when you start with a DNA sequence;

Use the search tool that links to the UCSC browser.

The alternative option is to search for your gene ID or sequence in NCBI Gene.

To search for a DNA nucleotide sequence using the link above, select Reference genomic sequences (refseq_genomic) from the pull-down tab in the Database field. Limiting the search to a species using the Organism field is also wise.

Both of these sites provide the information you are after. Taking time to read the help instructions will be useful.


Are specific primers or detectors, or both, used in COVID-19 tests?

When you run a PCR reaction, you are making copies of a DNA sequence of interest (cDNA in case of retrotranscription, since retrovirus have RNA as the genetic material). The sequence of interest is presumed to be in a sample, that you take from the patient, or some organism (I say 'presumed' because the PCR is precisely to confirm this). These copies are made by a group of 'generalist' enzymes, called polymerases, and by generalists I mean that they do not discriminate on which DNA sequence they are copying. But, they cannot copy DNA de novo (from scratch). The copying process needs to be 'primed' by a short sequence of nucleotides that is complementary to the DNA of interest. These are called primers, and they effectively serve as probes to target the copying of the specific sequence you need to amplify. And this is where scientists put a lot of care on: primer design. Bad primers will not be very specific, or will not be very efficient during the amplification process. As for the 'machine' that actually detects the copies, there are many variants. The most typically used in research and diagnostic laboratories, involves staining the amplified DNA with some molecule that binds nucleic acids (which there are many), and visualize it via DNA electrophoresis. What you visualize is a population of DNA copies (via the staining you make), so you need to know beforehand what to expect. For instance, do you expect a small fragment (a couple hundred basepairs) or a big one (a few thousands?). You have a 'ladder' (also called marker) that gives you a reference to compare, like in this image:

People know what to expect because they already know the DNA (or RNA) sequence they are amplifying (otherwise they could not have designed the target primers). They know the sequence because they've done some form of nucleic acid sequencing (labs, health institutes, and so, do this all the time and deposit the sequences in some platform, for instance GeneBank).

A 'positive' amplification will give you a band in the expected size range, and no other bands (because your primers are targeted for a particular DNA sequence). But as you mentioned, there exists also a multiplex PCR reaction. In it, you design multiple primers to target different sequences (using the same DNA sample -e.g. from a patient or organism-), but the verification process is basically the same. Here people are extra careful to avoid cross-interactions among the primers added to the reaction.

PCR is a family of techniques, not a single one. There are variations in the actual process, and also in the 'detection' (for instance, qPCR uses real time detection of copy numbers). But the general principle is the same: primers are specific, while the 'detection device' is not really.


Gamma thiophosphate-analogues of nucleotides were first synthesized in the 70s (Goody and Eckstein, J. Am. Chem. Soc., 1971) and have been used to decipher many intracellular pathways.

To understand why GTP-γ-S is not (or very slowly) hydrolysed by GTPases, we can look at the structure of a GTPase-GTP complex.

GTP binds to various sites on GTPases. This is the binding of GTP to Rap2A, as described in (Cherfils et al., EMBO J. 1997).

As you can see four different sites bind to the γ phosphate.

From the paper:

  The interaction of Tyr32 with GTP suggests that its general conservation in small G proteins may have structural or functional advantages. Tyr32 is located three amino acids upstream of a threonine (Thr35 in Ras) which is extremely conserved in most G domains. The alpha subunits of heterotrimeric G proteins have a conserved arginine equivalent in sequence to Tyr32, which was shown from crystal structures to interact with the γ-phosphate of GTPγS

In particular, the position of Tyr32 is different, when Rap2A is crystallised with GTP-γ-S. This figure shows the position of the Tyr32 with GDP (A), GTP (B) and GTP-γ-S (C)

  Crystals of Rap2A–GTPγS, whose structure we also report at 3Å resolution, are isomorphous to the Rap2A–GTP crystals. Both structures are essentially similar, except that Tyr32 no longer forms a hydrogen bond with the corresponding atom of the γ-thiophosphate, which is probably the sulfur atom. The Tyr32–γ-thiophosphate distance is 7.2 Å. The conformation of switch I and II and their interaction with the nucleotide are otherwise identical. Thus, the Tyr32–γ-phosphate hydrogen bond forms only in the presence of the true ligand, but is probably not essential for the triphosphate conformation of Rap2A nor for proper binding of the nucleotide. In particular, the position of Thr61 compares well between the GTP and GTPγS complexes.

The author conclude that:

  Our study shows that the complex with the natural ligand GTP is similar to the complex with GTPγS, and thus justifies most conclusions obtained from previous structures of G proteins with GTP analogues. However, the structure of Rap2A with GTP reveals a novel interaction of Tyr32 with an oxygen of the γ-phosphate of GTP and with the amide group of Gly13. In the GTPγS complex, Tyr32 is shifted away from the corresponding atom. The Rap2A–GTP and Rap2A–GTPγS complexes are otherwise identical, and form isomorphous crystals. Thus, the interaction of Tyr32 with GTPγS is prevented solely by the presence of the gamma-sulfur, but the conformation of switch I and II is similar whether GTP or a GTP analogue is bound. GTPγS probably introduces a different charge distribution on the gamma-(thio)-phosphate and/or modifies the polarizability of the β–γ P–O bonds as compared with GTP


Artificial Propagation and it's relation to asexual reproduction

Artificial propagation is (generally) human-directed, while asexual/vegetative reproduction is a natural process. Take a look at the wikipedia article on vegetative reproduction for more information on how and why artificial propagation is sometimes preferred to vegetative reproduction.


What are these shrimp-like insects in my cat's water bowl that appear overnight

They are probably some species of amphipod.

According to that link, two species common to Florida are Talitroides topitotum and Talitroides allaudi, though there are dozens of species in the US alone. In some areas, amphipods may be known commonly as "scuds."

These guys like to live in fairly wet places, depending on species - on the beach, in decomposing mulch/leaf litter/grass. They seem to be finicky with moisture: they tend to seek drier areas when it rains, often bringing them onto sidewalks or indoors, then they get dry and look for moisture. I'm guessing this is how they end up in your cat bowl: you certainly are not the first one to observe this.

https://www.whatsthatbug.com/2004/11/10/lawn-shrimp-3/

I'm not sure at all about the precise species...the species most commonly encountered by people on the sidewalks and such don't seem like they would survive long truly immersed in water since they avoid rain, but I wasn't able to find anything definitive on that - maybe their behavior is to avoid very wet but they can still survive immersed for awhile.


Is there any record of an Albino (Not leucistic) peacock

There is a breed of White Peacock. I could not find any record of 'Albino' Peafowls (the gender neutral term for peacock is peafowl (females are peahens). This white variety of peafowl is similar to how there are white chicken which have been bred over many years.
Albino animals do not produce the pigment 'melanin'. Albinism can be a dangerous trait in some organisms such as birds. The lack of melanin makes albino animals very sensitive to the sun's UV rays which can cause their vision to become impaired. Therefore most birds that are adult and white are usually either a variety of bird that is naturally white or is suffering leucism which is similar to albinism but does not remove melanin from organs such as the eyes.
But not all white birds are albino and not all albino birds are white. Just because the melanin pigment is non-existent in albino birds, doesn't mean other pigments couldn't still exist. Some animals don't even need pigments to achieve a certain color and do so instead by reflecting light in interesting ways.
It must also be noted that sometimes, white varieties of birds (or birds with leucism) are interpreted as albino and mistakenly presented that way online. This goes for other animals as well.


Do humans have skin cells that trigger oxytocin release in the brain?

Short answer
Oxytocin release has been associated with the cutaneous low-threshold (CT) afferent fibers in hairy skin.

Background
Oxytocin is released from the paraventricular nucleus in the brain in response to low intensity stimulation of the skin, such as touch, stroking and warm temperatures.

In a recent review Uvnäs-Moberg et al. (2015) report that the specific sensory nerve type mediating oxytocin release in the brain is unknown. Although myelinated somatosensory fibers mediating the discriminative sense of touch may be involved, a more likely candidate mediating affective touch are the unmyelinated low-threshold mechanosensory nerves, called C low-threshold mechanoreceptors (CLTMs) in animals or C-tactile afferents (CTs) in humans. Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown. The fibers have been characterized mainly through  electrophysiological and electron microscopy research (McGlone at al., 2014).

The association of CT fibers with affective touch stems mainly from the finding that their activation patterns with various stroking velocities correlates with subjective pleasantness ratings. Specifically, the relationship between brush-stroking velocity and firing rate was distinctly different between CT and myelinated afferents. CTs showed an inverted U-shaped relationship,
whereas mean firing rates increased monotonically with brushing velocity in all myelinated afferents (McGlone at al., 2014).

However, CT fibers have only been identified in hairy skin in mammals, and the fibers mediating affective touch through glabrous skin (including the fingertips, palms and lips) are unknown (McGlone at al., 2014).

References
- McGlone et al., Neuron (2014); 82: 737-55
- Uvnäs-Moberg et al., Front Neurosci (2015); 5(1529): 1-16


Over what range do Thyroid Stimulating Hormone (TSH) levels tend to fluctuate over the course of a day?

I wrote an answer about the circadian rhythm of TSH for a question over on Health.SE: How does one's TSH tend to vary over the course of a day. That answer also has some information on how this is different in people with hyperthyroidism and hypothyroidism.

The paper Physiological variations in thyroid hormones: physiological and pathophysiological considerations has a section on circadian and seasonal rhythm and a table with some values. Quoting from the paper:

  There is a clear circadian variation in circulating TSH concentrations in animals and in humans. TSH concentrations are low during the daytime, increase in the evening, and peak shortly before sleep.  Amounts decline slowly during sleep. Table 3 summarizes studies of mean, nadir, and peak serum

This is table 3:

A chart is available in figure 2 of the paper Modulation of Endocrine Function by Sleep-Wake Homeostasis and Circadian Rhythmicity

As for test error, it's important to note that TSH itself is not used for or at least should not be used for diagnosis of Hypothyroidism and hyperthyroidism. T3 and especially T4 need to be measured.


there are actually more than one process, but in the case of high detail wood fossils the process is the slow filling in of all the spaces in the wood (filled with water in life) with dissolved minerals from the groundwater. this is called permineralization. Of course this only works is the wood is buried so it cannot rot while this is happening. Since permineralization happens on the molecular level is can preserve great detail as the minerals form around the remaining hard tissue.

This video is a decent representation,


How does loss of the electrochemical gradient result in heat production?

ALiceD's comment is perfectly true. (Though in real cases, the short circuiting is seldom absolute as there is usually some finite resistance in the short circuiting wire.)

You can understand this in two ways.

Intuitively, the uncoupling provides a channel for the hydrogen ions to move across the membrane in the direction of their electrochemical gradient without having to do any work. Therefore, the energy it gains by traversing a potential difference, can be thought of as being converted to kinetic energy, i.e. the hydrogen ions are accelerated by the potential difference which causes them to gain speed and hence move at a higher speed than the average in the final compartment. This will cause increased collisions (and more energetic) with the surrounding molecules, slightly increasing their kinetic energy too, which will ultimately increase the average kinetic energy, the measure of which is called temperature. If it was coupled, the hydrogen ions would not have gained the kinetic energy, as the energy they gain by traversing the potential difference would have been used to do work in the ATP synthase machinery.

Rigorously, you can show this using some chemical thermodynamics which includes using $\Delta G$ functions, $\mu$ functions and some related thermodynamic variables. Let me know if you want that explanation.(though I stand the risk of having lost the touch to the mathematical aspect of thermodynamics)

PS:- While the thermodynamic explanation also accounts for the increase in temperature due to obliterated concentration gradient, it is difficult to explain with the former model. You can think of this, as the neutralising of the concentration gradient changes the number of collisions per unit volume (and time), and hence also contributes to the observed temperature change.


What is the human energy consumption by organ?

Percent of basal metabolic rate by organ (BC Campus Open Education):

Liver and spleen : 27%
Brain: 19%
Skeletal muscle: 18%
Kidneys: 10%
Heart: 7%
Other tissues (lungs, intestine, skin, bone, fat tissue, glands...): 19%

Basal metabolic rate by 1 kg of specific organ tissue (kcal/kg of organ/day) (Table 5 from American Journal of Clinical Nutrition, 2010):

Heart: 440 kcal/kg
Kidneys: 440 kcal/kg
Brain: 240 kcal/kg
Liver: 200 kcal/kg
Skeletal muscle: 13 kcal/kg
Adipose tissue: 4.5 kcal/kg
Residual tissues (lungs, intestine, skin, bone...): 12 kcal/kg


Are All Taxonomic Groups Uniquely Named?

There are quite a few biological homonyms (especially at the genus level, which apparently you aren't asking about).  At the family taxonomic level, the Interim Register of Marine and Nonmarine Genera (IRMNG) currently lists 100 family names which are used for two or more distinct taxa.


Can radiation exposure cause cancer later in life even if no traces of radioactive material are present in the body anymore?

Yes it can, because exposure alone can cause mutations in your genes which is usually the main cause of cancer.

For example, when we get exposed to UV light for longer periods of time, we can get skin cancer/melanoma. Here , of course no traces of these rays are present in our body, its just all due to prolonged exposure.

Now to the fact that why does it even happen , according to wikipedia is

  Cancer is a stochastic effect of radiation, meaning that the probability of occurrence increases with effective radiation dose, but the severity of the cancer is independent of dose. The speed at which cancer advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the person is exposed.

So since once induced, it just keeps on increasing even though you are not exposed to that particular rays anymore, you most probably are going to have it. This is the reason why cancer is so dangerous, because once it is there you can't stop and even can't make any precise stats about it until a certain stage.

For more details , visit https://en.wikipedia.org/wiki/Radiation-induced_cancer#Mechanism

I hope this answer helps you :)


Why can't we feel pain when the eye lid touches the eye ball?

TL;DR: It's psychological.

Pain is a tricky thing, and it's certainly possible to feel pain when pressing your eyelids against your eyeballs if you press hard enough ("hard enough" in this context is generally quite a lot less hard than is required to cause damage, by the way).

However: Since your eyeballs don't have skin, they also don't have nociception; i.e. they don't have pain receptors in the same way your skin at large does. Eye pains, like headaches, are largely caused by a combination of psychological responses to perceived stimuli and pain responses in associated structures.

Basically, the pain you experience when fingering your eye isn't pain in the same sense as the pain you feel from touching a hot stove or pricking yourself with a needle, it's generated by the brain in response to novel stimulus. Your brain knows what eyelids feel like, and it's okay with them, but once you start introducing fingers into the mix, all sorts of disturbances in salinity and moisture crop up, and your brain freaks out (and rightly so).

The same phenomenon can be seen with regards to swimming in the ocean: If you try to open your eyes under water, you'll find it a painful and disconcerting experience, but if you keep at it and practice holding your eyes open under water, you'll get used to it, and the pain will go away. Similarly, contact lens wearers will soon learn to deal with these stimuli, and be able to handle eye touching.

While I wouldn't advise you to go pawing at your eyeballs, if you for whatever reason have a need to do so, acclimating yourself to the feel of it will make the associated pain go away in short order.


How can I align more than 2 sequences locally?

You have to do it pairwise (there is no other option).

You can do that with BLAST or even SSEARCH (Smith-Watermann). If you have a fasta file of your sequences then do this:

make index of your sequences using makeblastdb -dbtype nucl -in <yourfastafile> -out <yourdbindex>
Run BLAST with your <yourfastafile> as input and <yourdbindex> as database with desired parameters. This will do a pairwise alignment between all sequences

Similar strategy can be used for SSEARCH.


Help understanding cell replication animations

When these animations are made by experts, they are actually not abstractions. Animations like this one [https://www.youtube.com/watch?v=X_tYrnv_o6A] actually don't show you an "idea" of how this looks but the actual shape of the individual molecules involved.

The reason we can now for many proteins draw pictures of how the molecule looks on the tiny scale that it is, is the field of structural biology. The scientists working in this field use techniques like X-ray crystallography, nuclear magnetic reconance spectroscopy and cryogenic electron microscopy to determine the structure of a protein at resolutions down to 2.7 Å (Angstrom, 1Å = 0.1nm). Once they manage to get a reliable picture of how a protein molecule looks, they publish their work and submit it to the world-wide protein data bank, which you can access freely using one of three websites: PDBe, PDBj and RCSB.

I tried searching for the proteins in your animation (CD4 and the HIV envelope protein gp120). Some structures do exist for them (e.g. http://www.ebi.ac.uk/pdbe/entry/pdb/2ny1) but they seem to contain only part of what's shown in the animation. Often certain parts of proteins can't be identified by structural biology for technical reasons, but we know they must be there based on the genetic information we have, and we can make some educated guesses about what those bits of the protein might look like. It seems in this animation, there was quite a bit of educated guessing involved.

A lot of biological science nowadays goes by the paradigm "seeing is believing". Many modern animations are reproduced from actual recordings where the process shown in the animation can be seen happening in reality. Cell divison for example is an intensively researched process that has been filmed using many different microscopic techniques and focussing on many different parts of the cell, figuring out what each protein or other molecule does during the process. Putting together knowledge from many different teams, you can generate a full picture of what everything is doing at the same time.

As far as reading recommendations go, any basic molecular biology textbook like Molecular Biology of the Cell by Alberts et al. (pick it up from a library), or lectures freely available online should allow you to gradually wrap your head around it.


The source you link does not report that certain neurons only use glucose, and I am unaware of any reputable source that makes this claim.

Neurons do tend to use glucose as an energy source when it is available, and the brain does not tolerate sudden drops in glucose. However, as your source notes, other energy sources can be utilized given enough time to adjust, such as during starvation/fasting as well as suckling.

Cahill, G. F., Herrera, M. G., Morgan, A., Soeldner, J. S., Steinke, J., Levy, P. L., ... & Kipnis, D. M. (1966). Hormone-fuel interrelationships during fasting. The Journal of clinical investigation, 45(11), 1751-1769.

Hawkins, R. A., Williamson, D. H., & Krebs, H. A. (1971). Ketone-body utilization by adult and suckling rat brain in vivo. Biochemical Journal, 122(1), 13-18.

Nehlig, A., & de Vasconcelos, A. P. (1993). Glucose and ketone body utilization by the brain of neonatal rats. Progress in neurobiology, 40(2), 163-220.

Owen, O. E., Morgan, A. P., Kemp, H. G., Sullivan, J. M., Herrera, M. G., & Cahill, G. J. (1967). Brain metabolism during fasting. The Journal of clinical investigation, 46(10), 1589-1595.

Pollay, M., & Alan Stevens, F. (1980). Starvation‐induced changes in transport of ketone bodies across the blood‐brain barrier. Journal of neuroscience research, 5(2), 163-172.


Protocol for measuring stamina of arthritic mice

I believe the standard is an graded-speed treadmill test.  An example pub:

Genetic variability in forced and voluntary endurance exercise performance in seven inbred mouse strains

If there is a particular ethical concern, you should always have your institutional review panel review it.  If you call up your department of animal resources (or what ever it is called in your institution) they will almost always give lists of preferred LOPs.

Another option would be to score time sleeping if you have them under behavioral surveillance.  The problem with this is the large amount of man hours needed, even watching tapes at high speed.  Instead I recommend you check this paper out:

Evaluation of two automated metrics for analyzing partner preference tests

Then to get accurate scoring, I would put a strongly colored bedding pad in a corner so the computer could pick it up.  Be sure to put the bedding in at least a week before so the mice get used to it and actually sleep on it.


Is it possible to identify the wasp species/family by the nest?

Ok, my bad. Should've googled better.
It seems that it might be a common wasp aka Vespula vulgaris. It's said that the colour of the nest is caused by material being collected from the rotten tree trunks.

See the identified sample:

It's said that they don't make nests in houses too often that's why I'm not accustomed to the look of the nest.


It looks like a Rhizostomae, or crown jellyfish, but it's hard to tell. The  article here does mention that it's edible though and it's found in Thailand so I'm pretty happy with that guess.

More specifically, it looks similar to the jellyfish asked about here, which was eventually classified as a Lobonemoides, perhaps Lobonemoides robusta


Where can I find an image of the gut/anatomy of the mealworm?

The best I could find which showed the inside of a mealworm not just the outside was this:

Taken from here. Hope this helps with your dissection.


Short answer

Optogenetics can be used to make cells responsive to light. One striking use of this technology is to restore vision in the blind by making the surviving neurons in the retina light-sensitive. This can be done by transfecting the retina with genetically engineered viruses that induce the expression of bacterial channelrhodopsin proteins in retinal neurons.

Background

I will explain optogenetics by focusing on one of the most striking applications: to make the blind see. In humans light is sensed by photoreceptors in the retina (see further reading #2). Rods infer grey-scale vision (i.e., night vision), while cones provide color vision when there is enough light available. Rods and cones contain light-sensitive proteins: the photopigments. The pigment in rod photoreceptors is called rhodopsin, in cones they are referred to as cone pigments, which are used for color vision. When light hits the rods and cones, the photopigments catch the light and activate a cascade of second messenger reactions, eventually causing hyperpolarization of the membrane. This hyperpolarization in turn activates secondary neurons in the retina, which eventually carry the receptor signal to the brain, where it is processed and used to generate a visual percept.

Light sensing across single-celled and multicellelar animals is mediated by two large families of proteins: the opsins. Opsin genes are divided into two distinct superfamilies: microbial opsins (type I) and animal opsins (type II). The rohodpsin and cone pigments found in humans belong to type II. Among other differences, type I opsins are bound to ion channels, while type II is not. Type II opsins therefore need a battery of intracellular second messenger molecules to operate. In contrast, the type I opsins, being channel proteins, directly cause intracellular changes by changing the membrane potential upon activation due to ion flow. Type I opsins, being channel proteins are referred to as channelrhodopsins.

In retinal degenerative diseases such as retinitis pigmentosa (RP) the photoreceptors degenerate and patients eventually loose their vision. The secondary neurons in the retina, however, partly survive. As explained above, these secondary neurons are responsible for processing the photoreceptor signal and sending it to the optic nerve. Hence, although RP patients miss the photoreceptors, the rest of the visual pathway is ready to rock! Hence, somehow these neurons should be activated. There are a battery of approaches to do just this. Retinal implants activate the neurons directly by electrical activation (see further reading #3).

Optogenetics (Fenno et al., 2013) is another approach where the secondary surviving neurons are made photosensitive, thereby bypassing the photoreceptors by turning the secondary neurons into photoreceptors. The neurons are made photosensitive by making them express channelrhodospins. This is done by injecting a viral vector into the eye such that the virus infects the retinal cells. Instead of a viable virus, however, it is tinkered aound with and the only thing the virus does is incorporate the channelrhodopsin into the genome of the neurons, which start to express it.

Channelrhodopsins are cation channels, and therefore, upon light activation, they allow positively charged ions (notably Na+, but also Ca+) into the cell. This depolarizes the neuron and can induce action potential firing (see further reading #1). Action potentials is the neuron way of transmitting signals to the brain. Hence, by activating the secondary neurons through channelrhodopsin transformation, they start sending light-induced neural activity to the brain. The brain will handle this input as if evoked by photoreceptors and hence will interpret it as light-evoked visual stimuli.

With regard to cancer: It has been shown that expression of channelrhodopsin and illumination of whole-mice resulted in diminished subcutaneous cancer cell counts (yang et al., 2013).

With regard to your first added question: dependent on the exact peptide regulatory sequences added to the protein, or by using viral vectors specifically targeting axons, expression of channelrhodopsins can occur wherever one likes.

Your second added question: Cation channels activate neurons, anion channels inhibit them. This means you can play around with different variants to control neurons at will.

References
Fenno et al. Annu Rev Neurosci 2011;34:389–412
Yang et al. Cell death and disease 2013;4:e893

Further reading
 1. Action potentials and neurons: how-do-the-brain-and-nerves-create-electrical-pulses
 2. Photoreceptors: parallels-between-pixelized-image-and-the-human-retina
 3. Retina and retinal implants: does-the-retina-encode-visual-information-like-a-bitmap-or-an-svg


Is there a difference between macroevolution and group selection?

Is there a difference?

Yes, they are quite different things.

What is group selection?

Group selection is an view of evolution where selection acts at the level of the group, rather than the individual. It suggests that selection is mediated by fitness of the population, and leads to conclusions of things occurring for "the good of the species". It is generally excepted that group selection arguments can rarely be invoked (but see haplodiploid social insects and kin selection). There is a long and controversial history to group selection and it's well worth reading about in further detail if you are interested in the history of science!

What is macroevolution?

Macroevolution is the evolution which occurs at larger scales, things like speciation, extinction, and the history of life. It often involves comparing species or lineages for example.

  "Macroevolution generally refers to evolution above the species level."

Microevolution on the other hand is, generally considered, evolution which occurs within lineages, or (more often) within populations. Researchers of microevolution would consider problems of adaptation for example.

  "Microevolution is evolution on a small scale — within a single population."

Macro- or microevolutionary trait?

I've never heard anyone refer to something in this way, traits can be studied in both micro- and macroevolutionary contexts.


WARNING: This answer is very tangential to the question. Confused Morus sp. with Rubus frutticosa (don't use "common name in questions"! luckily I wrote the answer using scientific names). So, as addendum: some trees tend to lose some leaves later (in my region, such trees can recover easily with broken branches).

"Always" is "always" a strong word in biology.

You describe your mulberry (Rubus sp.) as deciduous: the leaves are changed every year.

Many plants (especially trees) lose leaves in autumn/winter and they get new one in late winter/spring, few plants are marcescent, e.g. various oaks (Quercus sp.), so the leaves dry in winter and the plant lose it just when the new leaves appeaers. Some plants lose the leaves in summer.

Mulberries, like various "small plants", tend to keep the leaves until they form the new one (eventually, replacing all the shot). In my zone mulberries tend to keep old leaves until the new one are already developing.

Why this habit? Mulberries lives at borders of forests, so they try to have more energy/sun when the tallest tree lose leaves. On the other hand, being shrub and tending to radicate easily, it keeps safer in case of frosts, and it is also not a long living organism (as "plant", not as clone).

Note some decidouos young trees have also the same habits: they keep their few leaves in winter, to try to catch up. Being young also means few investment for the original plant, so it could be still a gaining habit. Look this winter on undergrowth.

Not so different to strawberries and many grasses, which replace the leaves in springs. But they are not "decidouos", just because they doesn't have a trunk or just they replace the entire shot the shots.


This is a multi-part series of books, with each volume numbered with roman numerals I, II, III, IV, etc meaning 1, 2, 3, 4, etc, followed by a subtitle, in this case the subtitle is "Modern Genera."

There is no meaning to "Genus VI", the title of the book series is "How to Identify Mushrooms to Genus" which indicates it will help you identify mushroom genus but will probably not bother with differentiating species of the same genus (even that is quite a lofty goal).

The authors could have instead called this book "How to Identify Mushrooms to Genus; Volume 6: Modern Genera" to convey the same meaning.


Hormones explain the sexual dimorphism.
Expose females to androgens and they develop masculine facial hair.  See hirsutism.  Also research:

... women’s intermediate facial follicles respond to men’s higher androgen levels by synthesizing more hair over several days ....


Is it appropriate to say "selection of" or "selection for" an allele that evolves by genetic hitchhiking?

The expressions "selection for" and "selection of", their definitions and their usage have been subject to a number of semantic issues throughout the literature. Good and Griffith (1995) is a good read on the subject.

I would argue that neither "selection for" or "selection of" is appropriate to use in the context of genetic hitchhiking because, in this context, by definition, the increase in frequency of an allele is only due to a different locus nearby that is under selection. So an allele that evolves due to hitchhiking is not directly under selection and only changes frequency indirectly due to nearby selection on a linked site.


Can we produce sugar using chlorophyll dissolved in ethanol?

The mechanism of photosynthesis proceeds via light-dependent reactions and light-independent reactions within the chloroplasts (organelles in cells which house the photosynthetic machinery, and indeed chlorophyll itself).
To produce glucose via photosynthesis, you certainly need the pigment chlorophyll - it is necessary but not sufficient by itself. For that, you need the Calvin cycle, which is part of the light-independent reaction within photosynthesis.
The light-dependent reaction requires chlorophyll and uses H2O and sunlight to produce ATP and NADPH, with oxygen as a byproduct. ATP and NADPH are necessary for the Calvin cycle to proceed, which takes atmospheric CO2 and produces glucose and other sugars. This is simplified into basic photosynthetic equation which you are familiar with.
     6 CO2     + 6 H2O  -->  C6H12O6 +  6 O2
carbon dioxide + water  -->  glucose + oxygen

Here is an illustration:

The red arrows point to the light-dependent ("light"), and light-independent ("dark") reactions.
Take a look at this slideshow, which answers all your questions with illustrations.

We CAN extract chlorophyll by dissolving the boiled leaf in ethanol! So can't we just bubble CO2 in and let the sun shine on it and add some water? Shouldn't that make sugar in the solution?

Unfortunately you destroy the chloroplast structures during the extraction you describe. These structures, and especially the membranes, are necessary for photosynthesis in its entirety to proceed.


Difference between strand-specific and not strand-specific RNA-seq data

It may be worth checking out the paper "Comprehensive comparative analysis of strand-specific RNA sequencing methods".

The most common techniques sequentially ligate different RNA adapters to the 5' and 3' ends of each RNA molecule prior to cDNA synthesis.  You will end up with an RNA molecule that looks like this (where A and B are the two adapters):

  5'-AAAAAA---------------BBBBBB-3'

These adapters are then used for cDNA synthesis and library preparation.  Finally, since each adapter is ligated to a specific end of the RNA the library can be generated in a stand-specific fashion; ie. the reads derived from the antisense strand should align to the antisense strand of the genome.

** Note that there are other variations of this technique but Illumina's protocol is one of the most popular.


I have a black tiny bug crawling all over the house

Insect 1 is a:

Booklice
Introduction
Booklice, also called psocids, are not true lice. While they resemble lice in size and shape, booklice feed only on fungi or mold. If you find them in grain or other stored food products, it is an indication of high humidity which encourages mold growth. In addition to food products, psocids may be found under wallpaper, in furniture, along the sides of windows or on window sills around potted plants. Booklice do not bite, transmit disease, or damage food or fabric, but they can be very annoying when present in large numbers.
Biology

Booklice found inside homes are wingless and very tiny: less than 1/16 of an inch long. While their back legs are thicker than the other four, and resemble the legs found in jumping insects, booklice do not jump, but run about rather quickly.
Adult booklice range in color from translucent white to gray or brown. Females can produce about 60 eggs during the warm summer months and their life cycle (from egg to adult) can be completed in less than one month. When cool temperatures prevail, female booklice produce fewer eggs and the time required to complete their life cycle is over three months. Females deposit their eggs singly and often conceal them by covering with debris. Booklice undergo simple metamorphosis, that is their nymphs look just like adults except that they are much smaller and sexually immature. The common house-infesting booklice normally have four nymphal stages.
Injury
Booklice feed on molds and will overrun cereals and similar materials that support mold growth. Their presence, therefore, is a nuisance and can render some foods unfit. The starchy paste of wallpaper and books also can support mold growth or may be attacked directly by booklice. Outside of annoyance, their damage is insignificant.
Management
The best way to control booklice is to eliminate moist environmental conditions. Reducing the humidity in your home will eliminate the mold on which the booklice feed. Lowering the relative humidity to less than 50% will prevent their development. An air space under potted plants on windowsills will help keep the humidity down and reduce mold growth. Throw away any infested food material and make sure other foods are kept dry. Pesticides are not normally necessary to control booklice in homes.
Warning
Pesticides are poisonous. Read and follow directions and safety precautions on labels. Handle carefully and store in original labeled containers out of the reach of children, pets, and livestock. Dispose of empty containers right away, in a safe manner and place. Do not contaminate forage, streams, or ponds.

Source: Penn State, Entomology: Booklice


Are centrioles really absent in human neurons?

You asked for "latest studies/info"... Funnily enough, mature neurons with centrioles were described by Cajal (who needs no introduction) in 1911.

If you want a more modern source, you can see Jacobson (1978):

  Microtubules associated with the cilia and centriole are present in all young neurons and many mature neurons and glia. Neuronal cilia and centrioles can be seen very easily by light microscopy in sections impregnated with silver by the Nauta method (H. A. Dahl, 1963). Centrioles can also be shown by light microscopy in neurons stained by other histological methods. (emphasis mine)

Sources:

CAJAL, S. RAMON Y. (1911). Histologie du système nerveux de l'Homme et des Vertébrés (trans. L. Azoulay, 1952), vol. i. Madrid: Consejo Superior de Investigaciones Cientificas.
Jacobson, M. (1978). Developmental Neurobiology. Boston, MA: Springer US.


Why does smoking change the human voice?

Smoke is hotter than air and passes through your vocal cords (before getting to your lungs), irritating them.
Irritation produces inflammation and inflammation produces mucus and general edema that could affect the biomechanics of your vocal cords, especially if you're a seasoned smoker.
The edema of the vocal cords is called Reinke's edema, which is classified as a benign polyp and will definetely make your voice more low-pitched.
I just saw that you added vaping in your question.
Since vape contains irritating chemicals too, I think its effects wouldn't be much better than smoke..obviously it depends on how often you smoke/vape.
Also, check this article:

Significant research has been conducted about the effect of cigarette smoking on the larynx and vocal cords. Several studies also suggest that exposure to electronic nicotine delivery systems can cause cellular hyperplasia (growth of cells) and metaplasia (change in cells) in mucosal lining in rats. It is theorized and likely that the same would occur in human tissue. Another experiment assessed the toxicity of vegetable glycerin, which is known to be harmless in liquid form. Its effects change in aerosol form. The experiment concluded that the substance led to squamous metaplasia of the epiglottis epithelium. Other research shows that nicotine in cigarettes is likely to lead to cancer, including in the mouth and larynx.
If the delicate lining of the vocal cords are exposed to hot, vaporized chemicals, the tissues are likely to undergo change and lose their ability to behave normally. This may produce hoarseness, loss of vocal range, voice fatigue, or vocal injury.

and finally:

These diseases and their effects on the voice can deeply affect singers and other people who use their voice for  a living. The only option to avoid these is to abstain from vaping completely.


Let's do a quick mind experiment. Imagine a ray of UV light hitting a white molecule in the skin. White generally reflects light, so that UV light would bounce off, and potentially could hit something much more critical. Black, on the other hand, absorbs light, so the energy in the UV light would be absorbed by melanin rather than other, more sensitive molecules. According to this article:

  eumelanins are capable of dissipating >99.9% of absorbed UV and
  visible radiation through nonradiative means.

Eumelanins are the most commmon type of melanin. Incidentally, not all melanin is black.

Another quick note, somewhat relevant: Try not to think of evolution as having a goal or purpose. Melanin being black is a result of random changes that happened to result in a beneficial phenotype. It didn't conclude that something was needed to counteract UV light and try to reach that goal.


Human Embyronic Stem Cells (hESC) can be programmed to differentiate into a number of different types of tissue depending on the signals you give or withhold.

Source: BioTime

The company Viacyte is actually developing a technology based on hESC that can be used to rescue loss of function in type-1 diabetes, just as an example. Their process takes hESC to pancreatic endoderm after about a month. The pancreatic endoderm has the capacity to differentiate into beta cells, ductal cells and so forth. He could have also been talking about human induced pluripotent stem cells (hiPSC). Like embryonic stem cells, these can differentiate into "anything," but are derived differently.


There are indeed periods of fast evolution and period of evolutionary stasis. The term "burst of evolution" is never used in the literature but below are three common terms when discussing these concepts.

First we have to realize that the term 'speed of evolution' does not mean much. We can be talking about change in phenotype through time (See Punctuated Equilibrium and Evolution and Ecology time scales) or speciation rate (See Adaptive Radiation and Mass Extinction). Also, we have to realize that we can talk about such speed of evolution on a given taxon or for the entire life on earth.

Punctuated Equilibrium

We often refer to the fact that there are periods of evolutionary stasis and periods of rapid evolution as punctuated equilibrium

  Punctuated equilibrium (also called punctuated equilibria) is a theory in evolutionary biology which proposes that once species appear in the fossil record they will become stable, showing little evolutionary change for most of their geological history. This state is called stasis.

Here is a representation (from the above wikipedia link) of phenotypic divergence following an extremely gradual view of evolution and an extremely "punctuated" view of evolution

Evolution and Ecology time scales

Since the 2000s, there has been increased recognition that evolutionary processes even matter on a ecological/demographics scale. That is ecological/demographics processes and evolutionary dynamics influence each other dynamically and the old view that evolutionary processes are much slower than ecological/demographics processes is sometimes wrong.

See the post History: Do evolutionary and ecological processes occur at the same timescales?

Adaptive Radiation / rapid diversification

The speciation rate also varies through time. There are "burst in speciation rate" if you like the term. A sudden burst in speciation rate is called an adaptive radiation

  In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches. Starting with a recent single ancestor, this process results in the speciation and phenotypic adaptation of an array of species exhibiting different morphological and physiological traits. An example of adaptive radiation would be the avian species of the Hawaiian honeycreepers. Via natural selection, these birds adapted rapidly and converged based on the different environments of the Hawaiian islands

You can find a list of classical examples of adaptive radiation on the above wikipedia link or at the post Is there a taxa that radiates faster?. If you don't want to be too extreme, you can as well just use the expression rapid diversification.

Mass Extinction

There are essentially two differences between an adaptive radiation and a mass extinction. 1) one is about an increase in speciation rate while the other is an increase in extinction rate. One is about a single taxon, the other one concern most of life on earth.

Because, a mass extinction sounds quite apocalyptic and because we seem to be at the start of a new mass extinction, most people are familiar with this term.

  An extinction event (also known as a mass extinction or biotic crisis) is a widespread and rapid decrease in the biodiversity on Earth. Such an event is identified by a sharp change in the diversity and abundance of multicellular organisms. It occurs when the rate of extinction increases with respect to the rate of speciation. Because most diversity and biomass on Earth is microbial, and thus difficult to measure, recorded extinction events affect the easily observed, biologically complex component of the biosphere rather than the total diversity and abundance of life.

I want to highlight that when thinking of a mass extinction, many people think of a single event clearing up the surface of the earth in a day but the reality is very different. In fact, a mass extinction can well last thousands of years.


How we can localize sound vertically (up-down) and front-to-back?

The Wikipedia article is quite good.

In brief, as you state, the wave phase can be used only to localise sounds in the plane of the ears. To have an approximation of the position in the median plane (above-below/front-back), we use asymmetries that distort the sound differently at different frequencies.

In humans, it seems that these asymmetries and their processing are not genetically programmed but evolved by each listener.

This is different in owls, although different species have each a specific asymmetry. https://en.wikipedia.org/wiki/Sound_localization_in_owls


These are floral formulas, a way to succinctly describe how many petals/sepals/pistils/... the flower contains, and their relations (free, fused, ...). The wikipedia page describe the meaning of each symbol.

For example, for the first one :

Up arrow : symmetry along the vertical axis
K(6) : 6 sepals (K), which are joined (parenthesis)
C(2.3) : Two large petals, three smaller, joined. (not sure on the exact signification of 2.3)
A2 : Two stamen, not joined
[C(2.3) A2] : the petals and stamen are fused
G(2) : two fused carpels

Continuing with that example, it seems to me the first formula is not correct given the schematics below : there are 4 carpels. Though I'm no botanist.


Background:
Most fungi can reproduce sexually and asexually, and some even parasexually. Fungal reproduction is complicated!
Idiomorphs  are at the exact same locus (like alleles) but produce a completely different protein rather than a variant of the protein.
Heterothalic - also called outbreeding: male and female reproductive structures are in different individuals. Partners have opposite mating-types with compatible MAT idiomorphs
Homothalic - also called inbreeding: male and female reproductive structures in the same individual. Partners have the same mating type but both MAT idiomorphs are present in the same genome and used in mating-type switching.
Heterothallic species are said to be homogenic incompatible, heterogenic incompatibility occurs when the offspring of a heterothallic cross between different strainss shows negative heterosis. There are forms of heterogenic incompatibility that appear to act only in the sexual phase.
Note that mating type and sex are not the same as sex is determined by mating structure and mating type may have no effect on sexual structure only on the nucleic content.
Answers:
1. I am not certain, but my understanding is that a haploid spore will generate a haploid mycelium of the same mating type. Note that things can get more complicated because you can have bifactorial incompatible mating types (e.g. two unlinked mating loci)
2.  Homothallism and heterothallism are properties of the of the species
3.  I am not entirely sure I understand the question here. In Basidiomycota (Club Fungi) Mycelia of + or - mating type will fuse to form a dikaryotic (two nuclei) mycelium for the majority of the life cycle. Only under unfavorable conditions will karyogamy (the fusing of the haploid nuclei) occur to form diploid hyphae and fruiting bodies where meiosis will take place to create haploid spores with mating types which will generate the new mycelia. Part of what makes the lifecycle here difficult is remembering that diploid somatic cells will have both mating types. (Life Cycle)


What is the scientific name of this leaf?

Looks very similar to Naringi crenulata which is found in India.  More information can be found on this Encyclopedia of Life page.

Image source: https://commons.wikimedia.org/wiki/File:Naringi_crenulata_leaves_and_flowers.jpg


Do antigens protrude through the capsule/slime layer in prokaryotic organisms where these features are present?

They don't have to -- there are times in life of a bacteria (cell division, hunger, mutations, attacks of lysozyme and other enzymes, cell lysis) when any possible antigen gets less or more exposed.

About escaping phagocitosis, there are numerous strategies to achieve it -- from forming a large slime-covered colony, through killing or disabling phagocytes up to stopping digestion, escaping the phagocyte back to the environment or even living inside it (Listeria monocytogenes is a prime example -- it can even directly move from one cell to another).
EDIT: Here is a nice overview.


Here are a few hints that might help:

Talking about Maria's pedigree:
Firstly, it seems as if you have mixed up with $X^a$ and $X^A$, see that the disorder is X-linked DOMINANT. Anyone with either heterozygous or homozygous dominant expression would have the disease expressed. So the first generation male should have a genotype: $X^aY$, because if it were $X^AY$ then Amelogenesis imperfecta would be expressed as his phenotype and the first generation female should have a homozygous recessive genotype. Also no child in the second generation would suffer from the same.
(NOTE: The one suffering from Amelogenesis in the second generation would have genotype $X^AY$)

As for Gunther disease, both the parent in the first generation should have a heterozygous dominant expression and the offspring suffering must have a homozygous recessive expression. And you can apply the same basics in Peter's pedigree.

I think this much should be enough to complete the task, but if you still have some doubt you can put it forward in the comments.