Where are action potentials initially created?

Action potentials are initiated where there is a high density of voltage-gated $Na^+$ channels and that may vary from cell to cell, as you guessed. For an illustrative example see the figure below, reproduced with permission from Kole et al. (2008).

Density of voltage-gated $Na^+$ channels and $Na^+$ influx along the axon of a cortical pyramidal neuron.
Reproduced with permission © Nature Publishing Group

As you can see, in this cell type voltage-gated $Na^+$ channels, labelled in green in the left-most image, are predominantly expressed away from the axon hillock. We can also observe that the expression of voltage-gated $Na^+$ channels correlates with the degree of $Na^+$ influx in a monotonic relationship (right-most panel).

In smaller cells action potential initiation can happen closer to the axon hillock and in cells of some invertebrates even in multiple locations (Kole and Stuart 2012). What may be the advantage of using the axon initial segment (AIS) as the sole site of initiation of action potentials (APs)? Here is a direct quote from Kole and Stuart (2012):

  [The AIS] has a small local
  capacitance ($C$) and therefore requires less inward current ($I$),
  that is, a smaller number of $Na^+$ channels per unit area, to
  generate APs compared to larger structures, such as the soma
  or proximal dendrites. Hence, the AIS is also an energetically
  favorable site for AP initiation. Furthermore, the small capacitance
  of the AIS favors rapid changes in membrane potential,
  as occurs during the upstroke of the AP ($dV/dt = I/C$). Finally, it
  is worth noting that having a single site of AP generation provides
  neurons a single locus where inhibition can gate AP initiation. [...] Initiation of APs
  further from the soma, taking advantage of the electrical isolation
  of this region, is a strategy used in some neurons to increase their
  capacity to discriminate the arrival time of different synaptic
  inputs.

References
M. H. P. Kole et al., Action potential generation requires a high sodium channel density in the axon initial segment. Nat. Neurosci. 11, 178–186 (2008). doi: 10.1038/nn2040
M. H. P. Kole, G. J. Stuart, Signal Processing in the Axon Initial Segment. Neuron. 73, 235–247 (2012). doi: 10.1016/j.neuron.2012.01.007


DNA supercoiling can be described numerically by changes in the linking number $L_k$, it's the most descriptive property of supercoiled DNA.

The linking number $L_k$ is equivalent to the sum of $Tw$, which is the number of twists or turns of the double helix, and $Wr$ which is the number of coils or writhes.

$$L_k = Tw + Wr$$

  [...]  If there is a closed DNA molecule, the sum of $Tw$ and $Wr$, or the linking number, does not change. [...] Since the linking number L of supercoiled DNA is the number of times the two strands are intertwined (and both strands remain covalently intact), L cannot change.

I don't know how to explain it more but I think the main idea is represented in the image below.

Edit:

From DNA Topology: Fundamentals :

There are two important features of the $L_k$:

$L_k$ is always an integer.
$L_k$ cannot be changed by any deformation of the DNA strands, i.e. it is topologically invariant. The only way to change it is to introduce a break in one or both DNA strands, rotate the two DNA strands relative to each other and seal the break. This is precisely the role of DNA
topoisomerases.

Related question: Reason behind formation of positive supercoils during DNA replication/transcription.

Sources : DNA supercoil and DNA Topology.


I am unsure that how much does it answer your question, but have a look at the homepage of DeltaSVM - In his work, Lee et al. have used similar datasets (only for GRCH37 I reckon) and I am sure they will address some of your queries.

As you yourself can better determine which dataset(s) are ones you need.


Centriole genes Knock-out Experiment in Common experimental animals?

One of the chief components of centrosome is γ-Tubulin.

In this study the authors have reported the effect of γ-Tubulin knockout in mice.

Quoting the abstract:

  Gamma-tubulin regulates the nucleation of microtubules, but knowledge
  of its functions in vivo is still fragmentary. Here, we report the
  identification of two closely related gamma-tubulin isoforms, TUBG1
  and TUBG2, in mice, and the generation of TUBG1- and TUBG2-deficient
  mice. TUBG1 was expressed ubiquitously, whereas TUBG2 was primarily
  detected in the brain. The development of TUBG1-deficient (Tubg1-/-)
  embryos stopped at the morula/blastocyst stages due to a
  characteristic mitotic arrest: the mitotic spindle was highly
  disorganized, and disorganized spindles showed one or two pole-like
  foci of bundled MTs that were surrounded by condensed chromosomes.
  TUBG2 was expressed in blastocysts, but could not rescue the TUBG1
  deficiency. By contrast, TUBG2-deficient (Tubg2-/-) mice were born,
  grew, and intercrossed normally. In the brain of wild-type mice, TUBG2
  was expressed in approximately the same amount as TUBG1, but no
  histological abnormalities were found in the Tubg2-/- brain. These
  findings indicated that TUBG1 and TUBG2 are not functionally
  equivalent in vivo, that TUBG1 corresponds to conventional
  gamma-tubulin, and that TUBG2 may have some unidentified function in
  the brain.

Another important gene is pericentrin. Fibroblasts from pericentrin knockout mice show abnormal spindles during mitosis have been studied.

  In agreement with a model in which pericentrin is required for correct
  spindle orientation, fibroblasts isolated from PCNT knockout mice show
  a significant increase in cells with disrupted astral microtubules and
  misoriented spindles (Fig. 2; unpublished data; Zheng, G., personal
  communication). Spindle misorientation is shown by an increase in the
  angle formed by the pole-to-pole spindle vector and the cell–substrate
  adhesion plane in pericentrin knockout compared with wild-type
  fibroblasts.

Apparently both TUBG and PCNT deletions (individually) are not lethal.


New infectious diseases appear mainly as a result of chance mutations in pathogen genomes?

Mutations happen all the time when DNA is replicated. These random mutations are the building blocks for evolution under natural selection. So when a single nucleotide is changed, (or deleted or added), there are three possible outcomes. 1. the mutation is neutral, so nothing happens. 2. The mutation is lethal or mal-adaptive for the organism, in which case natural selection will remove the individuals carrying the mutation from the population, or 3. the mutation results in some change in function that helps the organism compete under natural selection. This 3rd kind is the rarest, but with pathogenic viruses and bacteria, with huge populations, the evolutionary test pool is much larger because there are so many new mutations being put to the test with every generation. So, for example, a mutation in a pathogen adapted to spread through chickens, could change the pathogen to be better adapted for spreading through humans.


Are there chromosomes that we inherit that are not recombinated?

As you say people, I will assume you are talking about humans only.

Except for the small pseudo-autosomal regions (PAR1, PAR2), the Y-chromosome and the X-chromosome do not recombine together. This means that if you are a girl, then you have inherited a X chromosome from your father who did not recombine in your father (but might have recombined in your father's mother if that's where this chromosome come from). If you are a boy, then you have inherited a Y chromosome from your father who never recombines.

There is also mitochondrial DNA (mtDNA) that does not recombine but mtDNA is not organized into chromosome.


Short answer
The structural anatomy of the cerebral cortex is closely related to its functionality. The cortex is a thin sheet of only a few cell layers deep. Expansion of processing power requires enlargement of the surface area of this sheet, and simply increasing its volume doesn't help. As a consequence, gyri and sulci developed during evolution to accommodate this restriction.
Background
The human brain is characterized by a prominent and enlarged cortex, much larger than that of other primates. This is mainly due to the great expansion of the cerebral cortex during evolution. The underlying structures have, however, remained stable (Toro et al., 2008). The cerebral cortex houses the higher cognitive functions that separates us from other animals, allowing us to reason, talk, write books, develop culture and so on. As a result, to allow the development of these higher cognitive functions in man, it was the cortex that needed expansion, and not the deeper more ancient brain structures that govern more basic needs of life (breathing, heart beat etc.).
Because the cortex forms only a thin sheet a few cells thick that overlies the rest of the brain, a solution had to be found when the cortex was expanding in our early hominid ancestors, because the whole brain did not need inflation, just the cortex. Folding of the cortex increases the surface-to-volume ratio such that an expanding cortical surface fits onto a relatively stable base.
To take this a step further - why not increase volume in order to fit those extra neurons in? Since the volume of a ball increases by a third power with radius, why on earth would nature keep holding onto increasing the surface area, and not simply inflate the cortex by enhancing its thickness?
This has to do with the fact that the vertical architecture of the cortex has remained remarkably stable during evolution. In other words, evolution of a bigger cortical area to enhance higher cognitive processes has occurred in the most parsimonious way so typical for evolution: take an existing structure and enlarge it when there is need for more.
The cortex typically consists of a thin sheet covering the brain, and is not more than 3 mm thick. The neocortex represents the great majority of the cerebral cortex. It has six layers and contains between 10 and 14 billion neurons. The six layers of this part of the cortex are numbered with Roman numerals from superficial to deep (Fig. 1). Layer I is the molecular layer, which contains very few neurons; layer II the external granular layer; layer III the external pyramidal layer; layer IV the internal granular layer; layer V the internal pyramidal layer; and layer VI the multiform, or fusiform layer (Review of Clinical and Functional neuroscience, chapter 11).

Fig. 1. Cortical layers. source: Mental Construction.
Basically, layer IV receives most input from the periphery via the thalamus (visual, auditory, tactile inputs etc.), layer II/III takes care of horizontal projections for further processing, while layer V takes care of the output (motor output etc.). This basic architecture cannot be changed easily without changing the entire core workings of the cortex. As an analogy - to speed up computers in a parsimonious way, one can expand the number of processors quite easily. Coming up with a speedier processor is difficult these days, as evolution of single processor capabilities is pretty much at a dead end.
Thus, to increase the number of cortical neurons, the cortical surface must be enlarged. As the basis (subcortical structures) remain pretty much the same, creating folds (gyri and sulci) is the best way, and perhaps the only way to increase cortical surface area.
Reference
- Toro et al., Cerebral Cortex (2008); 18(10): 2352–7


How does a ribosome gather tRNAs at a fast enough rate for Translation?

The answer is simply due to the random walk of the amino acids. Over small volumes, this process is incredibly quick and is also responsible for nucleotide delivery to polymerases as well proteins searching for their substrates, in fact, only a few enzymes/proteins are limited by the rates of random walk motion. I'm sure there are lots of papers which discuss the rates of trna movement in the cell, but this is the first one that I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2727733/
(You are completely right about competing tRNAs and the orientation of the tRNA entering the ribosome, all of these factors are taken into account in calculations. Ribosome animations are also a massive oversimplification, they illustrate certain points well but they are by no means accurate, they are useful for reaching purposes!)


There is no reason for why a certain codon came to represent a certain amino acid. But some reason is attributed to similarity of degenerate codons. Usually the degenerate codons only differ in their last (third) nucleotide. The corresponding first anticodon in tRNA usually bears a modified nucleotide such as inosine which can (promiscuously) pair with A, C and U.

You can see the wikipedia page on wobble base-pairing.


Finding the number of chromosomes of an organism

Answer

An comprehensive online database of the chromosome numbers of all living species most likely doesn't exist. This Wikipedia article is the best and most complete reference comprising animals that I can personally find on the internet.

This source in Spanish, which I've translated with Google Translate reads:

  Canedo Delgado (1999) performed the karyotype description of the three species of the genus Pygoscelis , noting that there is a high homology both numerically and morphologically: Pygoscelis antarctica presented 2n = 92, Pygoscelis papua 2n = 94 and Pygoscelis adeliae 2n = 95 in females and 2n = 96 in males.

Also, note that chromosome number cannot be "guessed" or "assumed" for closely-related species. As shown above, the three Pygoscelis species have a high homology, but have very different chromosome numbers.

The other chromosome number you found for the species (38) is actually that of the Emperor penguin, as a simple Google search shows.

References

Ledesma, Mario A., T. R. O. Freitas, J. Da Silva, Fernanda Da Silva, and R. J. Gunski. “Descripción Cariotípica De Spheniscus Magellanicus (Spheniscidae).” El Hornero 18, no. 1 (August 2003): 61–64.


Presence of reaction module in bacteria but not in Eukaryotas (human)

That module represents Entner-Duodoroff pathway, which is an alternative pathway to the Embden-Mayerhof-Parnas pathway of glycolysis.

Entner-Duordoff pathway exists only in prokaryotes.


I can't pinpoint on the species name but a quick common fruit fly should give you a image which look very similar to the one in your photos.

these Bois are around 1/8 in inches long
-striated abdomen

Hope this is the one


Can anyone help me identify this insect?

This a long-horned caddisfly (gallery), which belongs to the superfamily Leptoceridae, though, due to a combination of the quality of your image, as well as limited available resources online, I'm currently not able to confidently suggest a genus or species. At any rate, here are a few pictures of various caddisfly that resemble the characteristics of your posted insect.

Unkown genus & species

Ceraclea dissimilis

Ceraclea sp.

Ceraclea slossonae

From where the majority of what I believe to be the closest matches mostly all belong to the genus Ceraclea, I am currently leaning towards that, however, I will continue to search for further validation.


Why is there no herd immunity against common cold coronaviruses?

The following review has extensive answers to the complex of this question. They also include MERS and SARS-Cov-1 in their discussion, as there is good data on them.
Huang et al., A systematic review of antibody mediated immunity to coronaviruses: antibody kinetics, correlates of protection, and association of antibody responses with severity of disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217088/
The best data comes from challenge experiments which, with common-cold CoV, are not ethically problematic. They write:

Several studies exposed volunteers to two challenges of virus, some months apart. Reed re-challenged 6 volunteers who had been experimentally infected 8–12 months previously(ref.9). On the first challenge, all 6 developed symptoms and detectable viruses and 5 of 6 experienced significant rise in titer. In the second, 0/6 experienced illness, detectable virus or significant rise in titer. Callow et al re-challenged volunteers with the same dose of coronavirus, one year apart(ref.8). Of 9 volunteers who were infected in the first exposure, 6 (67%) were infected in the second exposure. However, none of these individuals developed respiratory illness symptoms and they experienced a mean duration of detectable virus of 2 days compared to a mean of 5.6 in the initial challenge.

So, reinfection can occur even after 1 year with HCoV 229E, and this does not support the idea of herd immunity against that virus.
Note however that it is not known to date if, when reinfected after some years, you will also shed active 229E virus. If not, this would be just as good as neutralizing immunity and would support herd immunity.


Help identify the insects I keep finding at my house (Auburn, WA)

It is a Halyomorpha halys, commonly known as a stink bug.  Your photo shows a brown marmorated stink bug.  More information can be found on this Wikipedia page.

As far as your two questions:

Stink bugs do not normally bite people and are not poisonous.
A good way of controlling them in your home is by sealing any
openings that they are entering through.

Source: http://stinkbugsguide.net/facts.htm


Cardiac pacemaker: how can different nodes have different frequencies?

The AV node and any other nodes are suppressed by the SA node because it is the fastest.  If the SA node is sick or slow or there is a conduction problem one of these other nodes can take over calling the beat.

http://www.cvphysiology.com/Arrhythmias/A018. bold emphasis mine.

  The higher frequency of SA nodal firing suppresses other pacemaker
  sites by a mechanism called overdrive suppression. If a latent
  pacemaker is being depolarized at a higher frequency than its
  intrinsic rate of automaticity by an adjacent cell that is driven by
  the primary pacemaker, then the increased frequency of depolarizations
  leads to an increase in intracellular sodium ions because more sodium
  ions enter the cell per unit time. This increased sodium stimulates the Na+-K+-ATPase (increases its activity) to expel more sodium from the cell in exchange for potassium (see figure). Because this pump is electrogenic, increased pump activity increases the amount of hyperpolarizing currents generated by the pump. This drives the membrane potential more negative, thereby offsetting the depolarizing pacemaker currents (If) being carried into the cell. This effectively prevents the pacemaker currents from depolarizing the cell to its threshold potential, and thereby prevents the spontaneous generation of action potentials. If the cell ceases to be driven by the SA node (e.g., because of AV block), then the additional hyperpolarizing currents will be lost and spontaneous depolarization and action potential generation can occur.


Red Blood Cell Size Vs White Blood Cell Size

there are several types of white blood cells (at least 4) and they vary greatly in size from type to type.
white blood cells are not rigid, they can squeeze through very small openings. it always buts me in mind of watching a octopus squeeze into a bottle.


How much do urban pigeons move around cities?

I'm only aware of two studies that have looked at Rock Pigeon home range size. Note that this isolated research and may not be representative of Rock Pigeons everywhere nor of other pigeon species.

Rose and Nagel (2006) tracked 80 feral pigeons using GPS receivers and found 32% remained within 0.3 km of their roost location. Only 7.5% traveled over 2km from their roost location. Individuals of this species typically have 1-2 primary feeding locations within their home range which ranged from 3 - 151 ha in size (Rose et al. 2006).

Rose, E., D. Haag-Wackernagel, and P. Nagel. 2006. Practical use of GPS-localization of Feral Pigeons Columba livia in the urban environment. Ibis 148(2):231-239.

Rose, E. and P. Nagel. 2006. Spatio-temporal use of the urban habitat by Feral Pigeons (Columba livia) Behavioral Ecology and Sociobiology 60(2):242-254.


Why does the open tree of life have 2600 species of rose?

There are at least three possible explanations (and quite likely more):

1) You may be correct in suggesting that the OTT isn't "very coherent."* In other words, they may have a little work to do. I don't know enough about the site to offer a solid opinion.

2) The OTT may be unintentionally repeating someone else's error(s).

3) The OTT has to work with the information that's available, and, in the realm of taxonomy, that information can be very confusing. Different authorities recognized different classification schemes. Scientific names also change over time; for example, the polar bear (Ursus maritimus) used to be Thalarctos maritimus.

I don't know enough about OTT to really understand exactly how it works. However, I typed in Ursus (a subspecies in the bear family), and it listed 22 "Descendant tips." Curiously, it didn't display a list of species and subspecies, however. When I type in Panthera (the "big cats"), it does display a list of species and subspecies. I don't know if that reflects a problem with OTT or not.

You're focusing on the genus Rosa, which, as you say, is complex. In fact, I just thought of a fourth possibility...

4) Domestication - Many species in the genus Rosa have been domesticated and/or hybridized. It's possible that OTT is including the names of cultivated species. (It shouldn't be too hard to determine if this is the case if you're familiar with the Latin names of some cultivated species.)

Ultimately, the people best qualified to answer your question are probably the people behind OTT. I'm very interested in finding a definitive answer myself, because taxonomy is a major personal interest. I also find it endlessly confusing. ;)

P.S. I once wrote an article about a particular phylum of marine invertebrates. I stated that there were X number of species in the phylum, using a similar website as a reference. However, a specialist later told me I was way off base. I can't remember the details, but I believe there was either an error with the "master database" or there were conflicts between two or more databases. Like I said, taxonomy is confusing.

*Regarding coherence, we might also consider the target audience. This definitely is not what I would call a user-friendly site. I'm a lifelong naturalist with a degree in ecology/biology, and I find it very confusing. But rather than call it "incoherent," we might just say it isn't user-friendly.


Its a black Cricket .

Crickets, (family Gryllidae) are related to the Grasshoppers Family.

It should have grasshopper like hind legs .
Crickets usually emit  noise from its body.


Why don't carrier proteins require energy to change shape?

The carrier proteins that participate in passive transport do not require energy in the form of ATP molecules, which is the primary form of metabolic energy of the cell, but this does not mean that the transport process is energetically 'neutral'. Many proteins bind their ligands via hydrogen bonds, partial or full ionic bonds, van der Waals interactions, etc. These interactions build up a type of energy known as 'binding energy', which can be enough to induce a conformational change in the transporter. In addition, consider that a chemical gradient in itself is a form of energy, which effectively drives the movement of many solutes across the membrane. In fact, the gradient of a molecule can be used to transport another type of molecule, without using ATP. For instance, consider the Lactose permease. Its mechanism is, I quote:

  Hydronium ions from the outside of the cell bind to a carboxyl group
  on the enzyme that allows it to undergo a conformational change. This
  form of lactose permease can bind lactose from outside the cell. The
  enzyme then everts and lactose is transported inward.

Below a diagram of this protein, with its ligands in the center:

That being said, some proteins that are involved in passive transport do not require conformational changes like these I described, because they are simply 'open' (like a tunnel), and the solutes can freely diffuse across the channel. This is the case, for instance, of aquaporines. The advantage of the carriers that need to change conformation is that the binding to their transported molecule implies a recognition mechanism, which gives high specificity, whereas the proteins that are simply 'open' are less selective and thus transport many different solutes. See, for instance, the central pore of an aquaporine:

Regarding your last question, the hydrolysis of ATP can release enough energy that (similarly to the binding energy described above) can induce a conformation change in the transporter protein (active transport). This is often used when going 'against' the gradient because, as I mentioned, the gradient in itself contains energy that if not used passively (as in passive transport) then it is not favorable to transport something against the gradient. Thus, an external source of energy is needed (ATP!).


Possible? When a pregnant woman suffers an organ damage, fetus would send stem cells to the damage organ to help repair it?

Fetal RNA - mRNA and microRNA - has been detected in maternal blood as shown in this report. Here's a second report showing how fetus gives back to repair the maternal myocardium - fetal cells traffic to an injured maternal myocardium and undergo cardiac differentiation.


Can we influence evolution by teaching primates to control fire? Should we?

Is it conceivable to influence the course of their evolution so that it becomes more likely they gain the intelligence to support a civilization in the distant future?

No, I don't think so, based on what is known about evolution.

Your idea is in keeping with the opening of Kubrick's 2001: A Space Odessey, where the monolith inspires one of the primates to see a femur as a weapon. He picks it up, hits an opponent with it, and the idea catches on within his group; the implication is that this inspired male's (female's?) group goes on to domination and are the progenitors of the human race.

In real life, that's not how intelligence is passed on. You can teach a gifted bonobo how to build a fire, but if he's not into roasted meat, or really cold, or trying to scare away predators (or if he doesn't realize that's what fire is good for), all you have is one bonobo who can start fires. It doesn't influence his genes.

To actually influence evolution of bonobos, I imagine it would look like this: You capture 4/5ths of all the bonobos in the world (leave the 1/5 for genetic pool variation). You test them for basics of quick-wittedness. Kill all the bonobos that fall below a certain threshold, and release. Repeat several generations later. Keep doing so for 50 cycles. What you will have are a race of quick-witted bonobos - maybe. Because if the quick-wittedness you selected for doesn't provide them with a survival advantage, it (and they) will die out. What if the smarter bonobos all want to be alphas, and all that fun cuddling and sex-as-peacekeeping were to disappear? They might not survive the bonobo-chimpanzee wars, because they won't live in large, peaceful, cooperative groups any more. Maybe you can teach the bonobos to plant crops, assuring a food source. Will they irrigate, too? What would this decrease in roaming mean for pygmies who hunt bonobos for food?

My point is, we can't control evolution very much unless we also control the total environment they live in. That's one way we have been able to have such an impact on a rather extraordinary species: dogs. But in the end, a dog, whether it's a sheep-herding or rat-catching or boar-hunting or bull-baiting or duck-fetching breed, is still only a dog. Invaluable helpers, but after all that selective breeding, they're just dogs. The smartest dog in the world still likes to play fetch more than anything in the world. Even eating, if she's anything like my two Border Collies.


At what total rate is water used in metabolic processes over the entire biosphere?

The lifetime of a water molecule is less than 1 millisecond, in the sense that two particular protons will not remain bonded to same oxygen ion for longer than that order of time.  Also, the protons of water are constantly exchanging with protons of other molecules and ions, such as alcohols, amines, carboxylic acids, bicarbonate, and countless acids.   So it would only make sense to discuss the rate at which the oxygen atoms of water become atoms of another substance (beyond just hydroxide or hydronium) such as dioxygen or sugar.

For photosynthesis, one molecule of water is consumed for each molecule of carbon dioxide.  The link says that about 110 billion tons of carbon undergoes photosynthesis per year and since a water molecule is 1.5 times the mass of a carbon atom, this means 160 billion tons of water consumed in photosynthesis.

So at a minimum, biological processes destroy and create 160 billion tons of water per year (on the basis of whether an oxygen atom is or isn't part of a water molecule).


How many cells need to be damaged before a human can feel it as pain?

Although any number estimation would be inaccurate, I can think on two factors that can influence the count.

Cells location: Pain is trigger when specialize cells (Nociceptors) fires action potentials. The density of those nociceptors is greater in the tip of your finger than in your back. So the number of cell damage that trigger the pain would be different in those areas too.
Cell death rate: The delay that you mention is a key factor. Slow death like the normal on skin is done by a regulated mechanism (Apoptosis), in this process the cellular components are recycled. In fast cell death, the cellular components are released causing inflammation, which increases the nociceptors sensitivity.


What is this insect seen in Northern Italy?

This looks like some kind of bagworm moth. Their larvae would use silk and plant debris to construct a protective case around themselves. It’s hard to tell the exact species unless you open up the case or wait for it to emerge as an adult moth.

There are species on pretty much every continent and definitely some in Northern Italy. You can check out a list of observations and photos here: https://www.inaturalist.org/taxa/61415-Psychidae


The measurement that decreases during vasodilation is flow velocity, $v$, or a change in distance over change in time $\frac{\Delta x}{\Delta t}$. Prior to a reflex response, the same rate of flow, $Q$, or $\frac{\Delta V}{\Delta t}$ enters the capillary bed (here we use a capital V to represent volume, where $\Delta V$ is a change in volume, and $\frac{\Delta V}{\Delta t}$ is the change in volume over change in time. Because volume is area times a third distance dimension (e.g., if we say area is height times width, then volume is area times depth or thickness), we can describe flow as flow velocity times cross sectional area ($Q = A \cdot v$, or  $Q = A \cdot \frac{\Delta x}{\Delta t}$). If you increase the cross sectional area, $A$, and maintain the same flow, $Q$, then flow velocity, $v$, has to decrease.

A more intuitive explanation would involve turning on a garden hose and covering part of the end with your thumb. The smaller the opening you allow, the greater the flow velocity through the end of the garden hose. The same volume of water leaves the hose per unit time. It's just moving at a faster flow velocity if you decrease the cross sectional area (and at a slower flow velocity if you increase the cross sectional area).

This is discussed in Chapter 4 of Costanzo Physiology, in the section on hemodynamics.

The actual physical measurements end up being more difficult to predict in a situation with parallel capillary beds and reflex responses. $Q$ does not stay constant, for both the specific capillary bed, and for the entire circulatory system. However, you can say that, as a general rule flow velocity, or $v$, will decrease when cross sectional area, $A$, increases. As @BryanKrause points out in particular, provided the series resistance for a capillary bed doesn't change, the initial $Q$ for the capillary bed won't change, which means this caveat isn't relevant.


If you measure the O.D. of cells at one wavelength, is it possible to find its equivalent O.D. at another wavelength?

O.D. can mean 30 different things, many of them being related to science and to optics (see here)! I'll assume you mean absorbance (for Optical Density I'd guess) or light scattering as @canadianer said

Each substance has its own absorption spectrum and reflectance spectrum. Knowing only the absorption is a given wavelength does not tell much about the absorption at another wavelength (at least not without some other a priori knowledge about the substance studied).

So, the answer is 'no'.


swallowing of food or water from mouth to stomach is done with the help of peristalsis action of esophagus

Then rhythmic, unidirectional waves of contractions will work to rapidly force the food into the stomach. This process works in one direction only and its sole purpose is to move food from the mouth into the stomach.

In earth it also happens but it is assisted with gravity but in space Peristalsis action is the only process by which food or water is taken to stomach .


Why are my faeces black in color after eating Oreos

This is a perfectly reasonable question based on a self-adminstered (human) trial. Morever, the proposer bases their observations not on one subject but several reports. The impromptu survey of friends etc. is also acceptable. By the way, self-reported intakes/output records are an accepted method in nutrition research.

My 2-year-old child exhibited the symptoms described above, after consuming two Oreo biscuits in the afternoon. That evenings soiled nappy (diaper) revealed a dark but otherwise well-textured stool. When my concerned partner brought this to my attention, it immediately reminded me of the use of carmine red and related food dyes for the measurement of gastrointestinal transit times. The principle here is that the dyes are not absorbed in the gut, so the time from consumption to excretion gives a measure of bowel function. Short transit time means no constipation and is considered a sign of great bowel function.

Based on the observations reported for Oreos, my educated guess would be that Oreo products contain miniscule amounts of non-absorbed colorants - something that is generally regarded as safe. Self-reported symptoms are generally considered valid by health professionals. I am still intrigued by the Oreo colouring puzzle, as this colourant must be natural.


Do drugs always degrade after they have passed their expiration date?

Drugs do not have to degrade after their expiration date and passing the expiration date has more than one possible meaning.

First of all chemical compounds vary in their susceptibility to breakdown over time.  If they are kept away from oxygen, high temperatures (or kept in very low temperatures), and they are of a robust chemical nature, they might be stored for much longer than their expiration date and remain just as strong.

Over time, pharma compounds will chemically break down and lose their potency.  In many cases, you will find that they simply don't do anything when you take them.  This link cites a study that many drugs can retain their potency 15 years after they are made.

There are important exceptions.  Two examples are tetracycline and acetaminophen (tylenol) whose breakdown products can increase the tendency for these drugs to induce liver damage.


Are there organisms with fewer than 1000 neurons?

Short answer
As far as I know, a complete neural map (a connectome) is only available for the roundworm C. elegens, a nematode with only 302 neurons (fig. 1).

Fig. 1. C. elegans (left, size: ~1 mm) and connectome of C. elegans (right). sources: Utrecht University & Farber (2012)

Background
Looking at the least complex of animals will be your best bet and nematodes (roundworms) like Caenorhabditis elegans are definitely a good option. C. elegans has some 300 neurons. Below is a schematic of phyla in Fig.2.

You mention insects; these critters are much more complex than roundworms. The total number of neurons varies with each insect, but for comparison: one of the lesser complex insects like the fruit fly Drosophila already has around 100k neurons, while a regular honey bee has about one million (source: Bio Teaching).

Complexity of the organism is indeed an indicator of the number of neurons to be expected. Sponges, for instance (Fig. 1) have no neurons at all, so the least complex of animals won't help you. the next in line are the Cnidaria (Fig. 2). The Cnidaria include the jelly fish, and for example Hydra vulgaris has 5.6k neurons.

So why do jelly fish feature more neurons? Because size also matters. Hydra vulgaris can grow up 15 mm, while C. elegans grows only up to 1 mm. See the wikipedia page for an informative list of #neurons in a host of species.

A decent neuronal connectivity map (a connectome) only exists for C. elegans (Fig. 1) as far as I know, although other maps (Drosophila (Meinertzhagen, 2016) and human) are underway.

References
- Farber, Sci Am February 2012
- Meinertzhagen, J Neurogenet (2016); 30(2): 62-8

Fig. 2. Phyla within the kingdom of animalia. source: Southwest Tennessee University College


The plant is Convolvulus tricolor, the dwarf morning-glory. It belongs to the family Convolvulaceae.Blue, white, red and pink flowering cultivars of this plant are available$^1$. It is a annual/perennial growing to 0.3 m (1ft) by 0.2 m (0ft 8in) at a medium rate$^2$.

Image source
References:

Plantasm

PFAF database


Which spider species is this, and is it dangerous?

It is a female, the males of this genus are quite distinct. The genus is Argiope, and the specific epithet most probable is bruennichi. It is not a clinically important spider.


Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions?

My initial reaction upon reading this question was to think that the answer was: no, denitrification is a process in which nitrate is used in the absence of oxygen as an alternative electron acceptor. However I decided to check the literature, and I have discovered that there is, in fact, a lot of new evidence that many bacterial species may be able to use both of these electron acceptors simultaneously. This article is a good place to start if you want to find out more:

  Chen & Strous (2013) Denitrification and aerobic respiration, hybrid electron transport chains and co-evolution. BBA Bioenergetics 1827: 136-144

This is a review which summarises the area from the point of view of bioenergetics, but most importantly for this question, includes a Table summarising the experimental evidence for the phenomenon.  Referring to this Table, they state:

  It appears that in most cases, the evidence presented is not sufficient to support the conclusion that denitrification really proceeded in the presence of excess oxygen. It should be noted that the aerobic denitrification rates were much lower than the anaerobic denitrification rates measured for the same strain while aerobic respiration rates remain high. This implies that the major electron flow in the respiratory chain is towards complex IV rather than the NOx reductases, and that aerobic respiration is still the preferred pathway for growth. Apparently aerobic denitrification can be an auxiliary pathway next to aerobic respiration.

The last sentence answers the OP question.


I had a quick look in my books (for the British Isles and Europe) but although I found a couple of candidates I don't feel confident in either identification.

I suggest that you have a look at Roger Phillips' online identification guide  - this will suggest a few identification criteria that you haven't considered in your question.


Are Measles patients infectious until death?

The characteristic rash of measles is itself an immune response, and is a good marker for progression of the immune response. Patients with immunodeficiency can  have a much more limited or even absent rash. In most patients, if it's been 4 days since the appearance of the rash, and they have improvement in fever, runny nose, and conjunctivitis, without a productive cough, they probably aren't infectious. If you have that data (fever and mucous membrane inflammation), I'd pay attention to that as well as the time since the appearance of the rash. A sick patient with measles should be kept in respiratory isolation regardless, but if you're looking at modeling disease transmission, you can follow the symptom progression.

As far as death is concerned, there are several pathways. Measles can cause a poorly understood immunosuppression and immune dysregulation, which certainly contributes. The most common cause of death is pneumonia (often secondary pneumonia), but early diarrhea can be a major cause in malnourished children. Otherwise immunosuppressed individuals (e.g., HIV, and primary immunodeficiencies) can develop a fatal measles encephalitis (a brain infection). Some deaths result from a fatal post-infectious autoimmune syndrome.

Some of these individuals are probably still shedding virus (diarrhea, primary measles pnuemonitis or encephalitis), many of them aren't (secondary pneumonia and autoimmune cases).

Many texts focus on vaccination and the current epidemiology of measles in developed countries, but Cecil Medicine has a very good chapter (375) on the clinical manifestations of measles. There is an interesting article in Lancet Infectious Diseases about the US army outbreak in 1917-18 that is a good example of the interaction of measles with other respiratory pathogens.


Do females living on mountains have more RBCs than a normal male

Currently impossible to give a definite answer... It depends what altitude you look at.

Going from @Alan_boyd's answer the normal range is 40-50% for males and 36-44% for females. If the altitude at which a person is acclimatized to correlates well with red blood cell count (RBCC), and this effect is not gender specific (i.e. both sexes are affected similarly), then an average woman from high altitude should have a higher RBCC than an average from low altitude. But whether or not the high altitude female RBCC exceeds that of the male depends on the altitude of the two measured.

This rough graph, assuming RBCC and altitude correlate and that male RBCC is higher than female RBCC, shows the problem. Female (red dashed line) A is from a higher altitude than the selected male (blue dashed line) and has lower RBCC. Female (red dashed line) B is from a higher altitude than the selected male (blue dashed line) and has higher RBCC.

Define altitudes and the question may be answerable.


How much total RNA can be extracted from Drosophila brain

In my opinion you should try low input library prep protocols because in my experience even with a decent quantity of RNA, standardizing the sequencing is not an easy job. The manual says that this kit works with 10-20ng of RNA; always assume the higher limit to be true. There is a higher chance of loss (relative) during extraction also. Try doing precipitation with 5M LiCl and a little glycogen along with alcohol; but assuming your yield is 80ng you can still run replicates for statistical comparisons.


How long does a signal from the brain take to reach the limbs?

Speed of transmission is going to vary depending on the neuron fiber subtype.

Specifically, the biggest gains will be seen with cross-sectional area (feel free to ask why on physics.stackexchange.com) and neurons with myelin sheathes (fat wrappings which affect saltatory conduction rates).

You're specifically asking about Efferent neuron transmission rates, but here's a general idea:

Keep in mind that the entire circuit (from pre-motor cortex to muscle spindles) will involve several different types. In-general, your central nervous system (brain, brain-stem, spinal chord) are A-alpha, and if I recall correctly - the somatic nervous system (the voluntarily-activated neurons throughout the rest of your body in the PNS [peripheral nervous system]) are A-delta. If I'm wrong, somebody please correct me.

On average non-voluntary reflexes (which is actually information going to the CNS, being processed, and then going out to the motor neurons) take about 0.3 seconds. However, the average human can blink in about 0.1 seconds, which is probably a better measure.


Thanks to MCM's advice I know for almost-certain that this is Lepista personata.


Difference between Sphyraena obtusata and Sphyraena novaehollandiae

I think you may have looked at these species too quickly.

They are in fact different species.

Sphyraena obtusata is referred to as the obtuse barracuda, the striped barracuda, or various other names that your linked website (fishesofausralia.net) provides:

  Dingo Fish, Obtuse Barracuda, Pike, Sennit, Short-finned Seapike, Short-finned Sea-pike, Short-jawed Sea-pike, Striped Sea Pike, Yellowstripe Barracuda, Yellowtail, Yellowtail Barracuda, Yellowtail Sennit

Sphyraena novaehollandiae, on the other hand, is referred to as the Australian barracuda, arrow barracuda, Australian sea pike, sea pike, snook, or shortfin barracuda.

Even your linked post doesn't provide "striped barracuda" as a common name for this species.

Differentiating the two species:

Your fishesofausralia.net links demonstrate these fish are found on different sides of Australia (S novaehollandiae in the south and S. obtusata in the North of Australia.

The Wikipedia articles for these fish (linked previously ion my answer) indicate that S. obtusata only reaches maximum lengths of 55cm, while S novaehollandiae can reach sizes exceeding 1 meter.

Both sources also list a number of additional color and morphological variations you can use to differentiate the two species.


Which amino acids can be phosphorylated?

There's a Wikinome page called Phosphorylation of unusual amino acids describing phosphorylation of histidine, aspartate, cysteine, lysine, and arginine. Lysine and arginine are apparently phosphorylated on the nitrogens. I was a little surprised to see histidine and aspartate on the list, as histidine kinases seem to come up often in my area of research.
I'm also aware of at least one non-proteinogenic amino acid, creatine, which is phosphorylated by a dedicated creatine kinase. It functions as a sort of phosphate shuttle for rapid regeneration of cellular ATP from ADP in situations of high metabolic demand.
References:
Phosphorylation on unusual amino acids. (http://kinase.com/wiki/index.php/Phosphorylation_on_unusual_amino_acids)
PubMed Abstracts: https://pubmed.ncbi.nlm.nih.gov/?term=18558627%2C10772951%2C10698688%2C1654322%2C9553104%2C8577821%2C19498169%5Buid%5D
Guimarães-Ferreira L. Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles. Einstein (Sao Paulo). 2014;12(1):126-131. doi:10.1590/s1679-45082014rb2741


Do human beings have pheromone receptors?

From what I have gathered, I would think that humans do have receptors that are able to detect pheromones.

For example, some studies that have indicated human responses to pheromones.  Of these pheromone responses, some have been traced to the olfactory mucosa and olfactory epithelium.

The trace amine-associated receptors (TAAR) for which humans have 7 genes (TAAR1, TAAR2, TAAR3, TAAR5, TAAR6, TAAR8, TAAR9) and 2 pseudogenes (TAAR4P, TAAR7P) are found in the olfactory epithelium whereas androstadienone receptors are found in the olfactory mucosa.  As suggested by the anatomical location, these receptors interact with the human sense of smell and the olfactory system

More information: http://en.wikipedia.org/wiki/Pheromone#Humans


Fibrinous inflammation, exudate and scarring in monotonous movements and ageing

I would now say that the hardening is just local acute venous congestion if in the short term.
Without stretching after practice, it just takes more days to recover.
So lymphatic drainage is the one which helps the muscle get its needs and nutrients.

If this happens during years, it is difficult to say what is the causal factor.
It depends on many factors.
One key factor is how well the lymphatic circulation can recover the body back.
So genomics of the patient comes in the picture.
Many other factors too like anatomical structure of chest.
Then, depending on these factors and other pathological processes may happen many processes like

accumulation of fibrinoid
accumulation of calcium deposits
shorter diffuse distances
smaller total area of cells

which are some adaptation processes to the ageing (also of prolonged monotonous weight lifting).
They can lead to

acute lymphangitis (reddening of the skin)
Chronic lymphangitis
Chronic Granulomatous Lymphadenitis (fibrosis happening between muscles and connection points - not in all cases granulomatous - rare only)
lymphadenopathy (very, very late - after many years)

during ageing (adaptation).

Better question would probably be: what are processes happening during ageing?
And then cover pathologies of ageing separately and also the physiological processes on the weight lifting separately.


Is the serum concentration of calcitriol different at different times in the day?

Calcitriol, or 1,25-dihydroxyvitamin D, is produced in the kidney by 25-hydroxyvitamin D-1α-hydroxylase from it's precursor, 25-hydroxyvitamin D.

Calcitriol has a plasma half life of about 6 hours. It is tightly regulated. This regulation involves a negative feedback loop on its own synthesis and via an inhibitory effect on PTH synthesis, and control by downstream effects (plasma phosphorus, calcium, FGF-23 and others).

25-OH-D, the precursor, has a plasma half life of about 2-3 weeks, and except in chronic deficiency or other pathologic states, is in plenty of supply for the appropriate production of calcitriol. Because of this, it is unlikely that, for example, daily changes in sun exposure or nutritional intake would propagate down to production of the active metabolite.

The image and a good review of Vitamin D can be found in this NEJM article

References ranges at my lab and in Lange's guide to diagnostic tests do not include any interpretation suggestions for plasma or serum 1, 25-dihydroxy vitamin D (calcitriol) at different times of day. Notably, though, this test is not often done clinically. It's primarily for the case where a patient has high calcium, low PTH, and no malignancy has been found.

Despite this (reference ranges do not distinguish between times of day), there may be a circadian rhythm within that range. Regulators and downstream effects of calcitriol do show a circadian rhythm, as is demonstrated in this classic 1972 study:


I think you may have been misled by graphic representations of the process: The actual replication fork is very small as, like Rex Kerr mentions, it costs a lot of energy to keep DNA single stranded.

Have a watch of https://www.youtube.com/watch?v=yqESR7E4b_8 at minute 1:45, it contains a relatively realistic representation of the replication fork. Of course you have to imagine all of the space around the molecules in this video to be filled with other DNA, RNA, proteins and small molecules zipping about.

On top of this, we like to think of DNA as a lone double strand where occasionally a protein might attach and do something. Realistically however, most of the DNA is constantly being manipulated by all sorts of proteins (mostly histones for compression, but also transcription factors, methylating and demethylating enzymes, DNA repair enzymes,...). DNA replication has to minimise the interruption it causes to all the mechanisms going on around it, and the most effective way to do this is by replicating the lagging strands in fragments which can be zipped up quickly and left to whatever other proteins might do to it.


How can I compare rates of evolution for two sets of proteins?

If protein alignments are sufficient for you, I suggest that you look at the eggNOG database. There you can download mappings from proteins to protein families, and for the families you can also download pre-computed multiple (protein) sequence alignments.

I guess depending on the type of analysis you want to do you would have to trim the alignments to get only homologous regions (for example, see this recent paper[1]).

Wu M, Chatterji S, Eisen JA. 2012. Accounting For Alignment Uncertainty in Phylogenomics. PLoS ONE 7(1): e30288, doi:10.1371/journal.pone.0030288.


I don't understand your calculations and I don't understand why you're trying to use Bayes formula. I don't know the $\frac{1-p}{2-p}$ formula and I don't understand what it is supposed to calculate. It seems to me that you're overthinking a simple problem.

We don't have all the information and need to make a bunch of assumptions but if I understand the question correctly then..

Probability that the father carries the mutant allele

I neglect the probability that a new mutation occurred and that the son is the first carrier of the mutant in the lineage. I assume that we have a probability of 0 of being sick if we don't carry the disease. Because MEN is a pretty bad disease, the autosomal dominant alelle causing the disease is probably kept at pretty low frequency. From wiki, I read that MEN 2A has a frequency of 1/40000. This means that the probability of being homozygous mutant is $\left(\frac{1}{40000}\right)^2 ≈ 10^{-9}$. I think we can safely assume that the sick kid is heterozygous. Given that the kid is heterozygous, the mutant allele comes either from the mother or from the father with equal probability. So the probability it comes from the father is $0.5$ and the odds are $\frac{p}{1-p}=\frac{0.5}{1-0.5}=\frac{0.5}{0.5}=1$

Knowing that the father is heterozygous, what is the probability that a given kids receives this mutant

By the law of segregation, the probability is 0.5 and the odds are 1.


Is it PSI-BLAST or BLASTP if I use PSI-BLAST for only one iteration

You simply used BLASTP against a consensus sequence. The first iteration of PSI-BLAST is identical to BLASTP.


Do fish increase or decrease pH of aquarium water?

Like a glass of beer going flat, any excess CO2 that your fish produce will quickly and irreversibly escape into the atmosphere. Thus, at least in terms of the pH battle between NH3 and CO2 that you describe, NH3 would win.

boilerplate "science is complicated" disclaimer

That said, it's likely that the total environmental effect that fish have on a tiny non-circulating volume of water will be much more complicated than the interaction between two basic chemicals. For example, say one of your fish sheds some scales and they start to rot. All sorts of things would be happening at that point which could affect the pH.


Why does hair thicken and become more rough after a razor shave but not after one using a trimmer?

Hair does not grow back thicker when it is cut. This is somewhat of an optical illusion because when you shave with a razor it leaves the top of the hair flat rather than pointed so it appears thicker. For instance see this picture:

As you can see the hair is tapered at the top and when cut loses this taper to leave a large cross-sectional area. I would say that for your question with with the trimmer that it is probably cutting the hair further up the taper where the hair is 'thinner' to begin with. A razor cuts closer to the base and thus gives a thicker appearance.
Evidence: http://www.scientificamerican.com/article/fact-or-fiction-if-you-shave-or-wax-your-hair-will-come-back-thicker/
http://www.sciencedirect.com/science/article/pii/S0190962299701817


I'm just going to give a broad idea of what a biological circuit is.  There's definitely more than one way to define them, but hopefully this will give you some idea.

Broadly, biological circuits are reminiscent of electrical circuits in that energy or information flows through the cell.  In biological pathways (a more typical terminology), genes in the cell (usually proteins) will use a signal (usually in the form of a chemical compound or a modification of a protein, but sometimes a simple ion or even electrical current (rarely)).  The signal then can be transmuted into a different chemical compound or it can even alter a protein so that it functions differently.

Here are a couple of classic examples.  The first is the Citric acid cycle (also called the Krebs cycle), discovered in the 1930s.  Here you can see that Citrate is chemically transformed into acetate and carbon dioxide and chemical energy in the form of NADH (reduced nicotinic acid dinucleotide).  Each step of the cycle has a different compound which is handled by a different protein enzyme.  While all the proteins and compounds may coexist in the same part of the cell, there is nonetheless an orderly circuit of chemical energy mediated by the genes of the cell and controlled by the cell as it adjusts the amount of enzymes available for each step of the cycle.

Another example of an entirely different sort of gene pathway works differently but has the same set of concepts.  Mitogen Activated Kinases (MAPKs) are proteins which have generally two states an activated state and an inactivated one.  As you can see below, an outside signal like high salt osmolarity or a signalling molecule is sensed by a receptor on the cell surface.  By some method a MAP Kinase is activated, perhaps by the addition of a phosphate to the surface of the protein or by dimerizing the MAPK.  Once activated, the MAPK will then phoshphorylate another kinase, which may activate yet another.  Finally a protein in the nucleus will be activated and cause transcription of some target genes.

In the latter case, a very small change to the protein costs little energy and information is being transmitted, but by biochemical signals where proteins are modified and affect other proteins.  That's a more subtle circuit than in the former case where relatively many individual molecules might be processed by enzymes together.

This hopefully gives you some idea of what a biological circuit looks like.  There are many other examples and subtle variations but that's a quick tour.

Experiments involving these pathways are too numerous to mention - individual proteins may be modified, their concentration within the cell can be altered by say mutations in the chromosome, pathway intermediate compounds like Succinate might be added to see how the citric acid cycle responds, isotopic labeled compounds can be added to see where they go in the cell.  There's nearly 100 years of experiments here.  that's a lot.

Hopefully this will just give you some idea of where to start.  Nearly any biochemistry textbook covers these topics in better detail, but then they are often over 1000 pages long!


Resource for finding what proteins bind?

Go to the NAR database site and look for protein domain databases. You have multiple options. Here is the link.


Why do fruit flies go so close to large reservoirs of liquid when they are likely to fall in due to surface tension?

Although this is from  a popsci article, a biologist says that fruit flies can normally land on liquids and take off from them thereafter:

However, simply leaving a shot glass full of fruit-vinegar will only serve to feed the flies. The surface tension of the liquid [Ed. note: You remember surface tension, right?] allows fruit flies to land on liquids but not drown.
To break the surface tension you’ll need a tiny bit of dish soap. Dish soaps contain surfactants, which are molecules with a head that likes water, and a tail that doesn’t. Because of this property, the surfactants tend to situate at the interface of air and water, forming molecular “cliques” that disrupt the surface tension of water.
By putting a tiny bit of dish soap on your finger, and touching it to the surface of the vinegar in the shot glass, you will add enough surfactant to break the surface tension. (Add too much and the molecules in the dish soap will alert the fruit flies to danger).
Now fruit flies will unknowingly attempt to land on the vinegar for a little sip, then, before they can react, will break through the surface tension and begin to drown.

So if this is true/confirmed, then they do have enough of an evolutionary adaptation to the [surface tension of the] usual liquids of their diet. Just not to [trace] dish-soap contaminated liquids.
And I can confirm from a peer-reviewed paper that dish soap is indeed used even in science trapping experiments:

The cup trap (figured by Beers et al. 2010) is a 946-ml clear plastic
drinking cup with a clear plastic lid (Solo, Urbana,
IL), with four 1-cm-diameter holes in the sides of the
cup near the top. A drowning solution or drowning
solution plus bait was placed within the cup. Forty
grams of boric acid and 0.5-ml liquid dishwashing
soap (Palmolive Pure and Clean Spring Fresh Dishwashing Soap; Colgate-Palmolive Company, New York, NY, USA) were added to a batch of 3.8 l of
water or aqueous bait to make a drowning solution
used in all traps. Boric acid served to inhibit microbial
activity of baits and captured insects, and soap
reduced surface tension to promote capture and submersion of trapped insects. For both types of traps
and all treatments in all experiments, each trap contained either 300 ml of drowning solution or 300 ml
of bait in drowning solution

0.5ml of soap to 3.8l of water is very little, but that's all it takes to drown the little flies. It seems entirely plausible to me to have this level of trace contamination on glasses that have been dishwashed.
And as a complementary survival mechanism, fruit flies can apparently survive 12 hours of drowning at room temperature (or more in lower temperature):

Flies submerged at 23°C did not survive after a submersion time of 12 h whereas flies submerged at 3°C survived up to 72 h of submersion.

@Frieke may be on to something, namely that ethanol lowers the surface tension of the solution (with water) by itself, significantly. At 20-25 degrees C, pure water has a tension of about 72 mN/m. Adding 10-15% ethanol lowers that to about 47-42 mN/m. Also, the trapping science paper does mention that

Very few flies were captured in traps baited with 10% ethanol in water.  Traps baited with a combination of acetic acid and ethanol in water captured more SWD flies than traps baited with acetic acid or ethanol solutions alone.  These results indicate a synergy of the two materials, and of the two chemicals, as lures for SWD.

Interestingly wine has substantially higher attractive effect than an equivalent ethanol solution though:

Wine is about half as effective a vinegar and about a quarter as effective as a combination of wine and vinegar. On the other hand, a 10% ethanol solution was 20-50 times less effective than alcohol 10% plus acetic acid 2%. So there's more to wine than ethanol that attracts the flies.
So the flies probably do avoid the higher alcohol concentrations... unless there's also vinegar.
Another paper finds that wine's surface tension is mostly determined by its alcohol content.

So it does look like:

Fruit flies are fairly strongly attracted to wine (on the same order of magnitude as to vinegar).
The surface tension of wine is substantially lower than that of water.

I'm still not sure what the surface tension of (2%) vinegar might be, in comparison. Pure acetic acid has substantially lower surface tension compared to water, about 27 mN/m at room temperature. And if Wikipedia is correct, 10% acetic acid solution has about 55mN/m around temperature. So acetic acid lower the surface tension less than ethanol, but not by much less. On the other hand, fruit flies are much more attracted to acetic acid than to ethanol (alone). So perhaps that's enough to explain why they drown easier in wine.
Actually it look like Wikipedia is wrong here. From an authoritative source, acetic acid has nearly the same effect as wine on surface tension; at 11.4% it has 43.5 mN/m; just 3.2% is enough to lower the tension to 55.6mN/m; at 1.6% it's 61.7mN/m.

So probably just the fact that acetic acid is much more attractive to flies than ethanol is the only factor (other surfactants excluded). Perhaps they "confuse" a higher concentration of ethanol to a lower concentration of acetic acid, which they would be able to handle as far as surface tension goes.
Yet another source (actually quoted in the previous one, on the next page) gives even lower values for ethanol surface tension.

Apparently determining surface tension is a hard problem, both experimentally and theoretically. So I'm not sure we can properly compare figures reported in different sources. Alas no single experimenter has done both ethanol and acetic acid in the same paper/setup. But what was observed about their relative attractiveness to flies is probably sufficient...
And for ballpark comparisons, a similarly or lower surface tension as that of 10% ethanol (or acetic acid) i.e around 30-40mN/m can be obtained by a adding a few ppm (parts per million) of a surfactant, such as LAS or AE.


Does every protein starts with Methionine amino acid

No, not every protein starts with a methionine. When the methionine is removed, it is called N-terminal methionine excision. Abstract excerpt below:

  N-terminal methionine excision (NME) is the major proteolytic pathway
  responsible for the diversity of N-terminal  amino  acids  in
  proteins.  Dedicated  NME components have been identified in all
  organisms, in all compartments  in  which  protein  synthesis  occurs:
  cytoplasm, plastids and mitochondria. Recent studies have revealed
  that NME is regulated at various levels and plays an important role in
  controlling protein turnover. NME is essential  in  Eubacteria  and
  lower  eukaryotes  and  is  the target of many natural and synthetic
  inhibitors. Such inhibitors  have  considerable  potential  for  use
  in the  treatment of various human diseases, from cancer to bacterial
  and parasitic infections.

And from a recent review focusing on the methionine aminopeptidase enzyme that cleaves the first methionine:

  Protein synthesis is initiated by methionine in eukaryotes and by
  formylmethionine in prokaryotes. N‐terminal methionine can be
  co‐translationally cleaved by the enzyme methionine aminopeptidase
  (MAP). When recombinant proteins are expressed in bacterial and
  mammalian expression systems, there is a simple universal rule that
  predicts whether the initiating methionine will be processed by MAP
  based on the size of the residue adjacent (penultimate) to the
  N‐methionine.

Mitochondria and other organelles also have different start codons. Their alternate start codons are well-characterized (AUA and AUU in humans and mainly - but not exclusively - GUG and UUG in prokaryotes).


Why social animals attack odd members of their own group?

Persecution is not a term often used in zoology, compared for example to the notion of social exclusion and hierarchy disputes/social animal hierarchy. That is because humans incarcerate animals which would otherwise flee to safe distance from the group if they are attacked. Wild Mammals, birds, fish, other animals with free movement can normally get safe distance from an aggressive group in order to be safe from persecution.
Fish and insects/island animals sometimes have restricted ranges, and "social exclusion of a mutant" - studies are difficult to find and perhaps won't give masses of information to know why it happens, for categorization and prevalence of different reasons.
I found only one research on social aggression based on appearance:Aggressive biases towards similarly coloured males in Lake Malawi.
Useful related terms for further research for your question are i.e.:

"social exclusion mutants traits aggression"
"social exclusion zoology"
"social exclusion injury zoology"
"social exclusion zoology mutation"
"hyerarchy disputes appearance zoology"

It's an interesting notion for research that you have found, for which a lot can be written, because it gives a complex range of potential reasons for the given behaviour: warding off a contagious individual, warding off a tribe from far away that could displace the current group, inability for the brain to average the mutant's appearance to associate with it, habituation of species to a type of social companion since their birth (i.e. birds sometimes think they are humans)
And so a research requires a broad understanding of juvenile establishment of appearance recognition of other individuals of the group, i.e. where humans search for an average appearance compared to the social group, and chimps recognize close relatives and mate with the most distant, chickens can adopt humans... and animal behaviour towards an ill individual, it's difficult and takes a while to gather actual sci documents for.
When you have found all the closest related research, the given write up would be very fascinating!!! i hope you can search the given topics and give a summary of some previous examples of vaguely related research.


Will humans ever evolve to cope with the rising temperature of our planet?

A change in temperature of 1 degree, or even 4 degrees, is less than the variation in temperature that is seen between different areas that are inhabited by humans and less than the variation which is seen annually in those areas. Accordingly it seems that humans are already adapted to these differences in temperature and that our response to the temperature changes are more likely to involve habituation and cultural changes in behaviour and technology use than evolutionary change.


Has synthetic biology created new plants or animals as of 2013?

Answering your question

Well, considering there is a plethora of facilities that deal with the cloning of plants and animals, as well as altering specific DNA in order to create a better plant or animal. Tests have been done with rats to try and create stronger and smarter rats, and tests have been done on countless other animals to try to develop immunity to dementia and Alzheimers. In the agricultural industries of the world, new types of corn, tomatoes, rice, and other types of crops are engineered on a daily basis, and new versions of these plants are made very commonly. The problem, however, is that a vast quantity of these plants are rejected from being planted. Some plants that are engineered either taste too bad, or they are less efficient than the plant at which they were modifying. As far as inventing a new species, you have to be more specific as to what you are asking. If science creates a new animal from another animal, it is likely of the same family and genus, like breeding a dog from another dog. Creating another type of mammal or reptile or bacteria that isn't part of a specific genus would be a breakthrough, as I am sure that all types of cloning and scientific pairing have been done to the same general Genus and Species... I am assuming, however, that it will be possible to engineer lifeforms at the molecular level by the next 50 to 100 years, as science and technology is getting more and more advanced. So, by the next few centuries, it would only seem logical to assume that new species would be created. However, the practice of creating new species, or even operating a laboratory/facility that deals with the concept, is illegal in a large number of countries, and has several guidelines in others.

I am only 13, so if any of this information is to be used anywhere else, I would advise not to cite me as a credible source. All this information is from my knowledge, and my knowledge is from school studies and personal readings. This is all my information, though. If any wording sounds similar to another source, keep in mind that one human brain functions similarly to another on several accounts and coincidences are often found.  I can assure you that if the documented information above is verified by plagiarism experts as my own wording, as I have taken the liberty to scan my own work. I hope I answered your question, and I am sorry for the long disclaimer ranting of this paragraph.


Both pasteurisation and irradiation work by killing micro- (and macro-) organisms in food. The two processes are broadly similar and in both cases the objective is to reduce the number of bacteria or other microorganisms in the food rather than completely sterilise it. Due to this and other similarities food irradiation is sometimes called cold pasteurisation (for example in this paper).

Food sterilisation has some advantages over pasteurisation: for instance, it can be used on (most) solid foodstuffs, including fruits, vegetables, grain foods, spices and meats (such as chicken), while pasteurisation can only be used on liquids. However, irradiation cannot be used on dairy products or eggs as it results in changes in flavour and texture (source).

There are other reasons why irradiation is not used as widely as it might be. One is that some markets were already saturated with pasteurisation, which is an older technology. Another is that public acceptance of irradiation is lower, with (for example) concerns about safety of the products, although these are not rational concerns and Crawford and Ruff note that similar concerns affected acceptance of pasteurisation when it was introduced. This may also partially explain why irradiation is sometimes called cold pasteurisation, although by international agreement irradiated unprocessed food sold in stores (not in restaurants, or processed foods) is labelled with the Radura symbol anyway.

I also have a suspicion that the startup costs associated with food irradiation plants are relatively high, but couldn't find a reference for this yet.

Some further reading

Lester M.Crawford, Eric H.Ruff (1996) "A review of the safety of cold pasteurization through irradiation" Food Control Volume 7, Issue 2, April 1996, Pages 87-97

"Advantages and disadvantages of the use of irradiation for food preservation" Journal of Agricultural and Environmental Ethics March 1991, Volume 4, Issue 1, pp 14–30

"Food irradiation", Better Health programme, Victoria State Government website (accessed 2017-10-24)


What is the concentration of ATP in an average cell?

Answer

This article covers the energy charge and ATP concentrations of an array of muscle cells from many different organisms. Since many factors come into play (amount of glucose available, rate and regulation of glycolysis and cellular respiration, use of energy in metabolism, etc.) it is expected for the ATP concentration within the cell to vary significantly. The ATP concentrations reported span from approximately 1 to 10 mM.

References

 - Beis, I, and E A Newsholme. “The Contents of Adenine Nucleotides, Phosphagens and Some Glycolytic Intermediates in Resting Muscles from Vertebrates and Invertebrates.” Biochemical Journal 152, no. 1 (October 1975): 23–32.


Short answer: many species can drop a regrown tail again and again again, however a few can only drop it once, while some lizards cannot drop their tails at all. It all depends on the species.

Background information:

According to this site the tail will only be able to be shed above the site it originally broke off. Although according to UCSB there are a few species of lizard that only have their tail grow back once.

Every site I've visited has said that the tail is nearly a completely different structure than the one it originally had. The original tail has "score marks" (fracture planes) which were studied by Sanggaard et al. (there are a few figures that you can see in their paper).

However, according to W. N. F. Woodland, D.Sc. (Lond.), there is no apparent limit to the amount of times a Gecko can drop its tail, "save the longevity of the animal". His paper goes into great detail, and has a lot of information about autotomy (limb dropping) of the gecko. I highly recommend going through it if you're interested.

So tail re-dropping looks like it primarily depends on the lizard that you're studying.


I'm no biologist but here are two answers to your multidimensional question. "How is it decided what type of food we want to eat?"
There is new research into neuroscience and microbiological science about a phenomena where bacteria in our gut that produce vitamins and digest things that we cannot digest, contribute to the choices we make for our diet. Don't ask me how, but from my understanding they must somehow communicate with the brain to release dopamine while stimulating neurons responsible for choosing a certain food to crave. "Is there something that measures for example what is level of glucose or amino-acids or some fats in blood...?" Well yes actually, let's take the pancreas for example. It knows when blood sugar is high from digested materials and will begin to produce insulin. I won't go much further because already there is a response based on the detection of sugars. Your entire digestive tract is based on these detective processes in order to appropriately digest and react to digested material. Are there processes that tell your brain what to eat next? Well besides the bacteria, there are plenty of hormones produced by your gastrointestinal tract such as Ghrelin which is the most common "hunger hormone" and is responsible for homeostasis aka energy regulation/distribution throughout your body.

It's better not to ask how but to ask why when researching topics similar to this, the how is almost always provided. I'm not entirely sure how those hormones communicate with the brain, my knowledge of the brain is less biochemical and more neurological (e.g. neuron formation).


How does Iota-Carrageenan achieve an antiviral effect?

Through two different pathways, one relying on a non-specific (innate) response, and another through a reactive oxygen species, the level of NF-kB(**) is amplified, as such a response would have happened as a result of the presence of the virus anyway.

  In thousands of experiments, carrageenans have been used to
  induce inﬂammation, since inﬂammation is a predictable effect of
  exposure to carrageenan in animal and cell-based models. For the
  most part, these experiments were designed to test the effectiveness of anti-inﬂammatory agents or to study the mediators of inflammation

  The innate immune pathway is mediated by toll-like
  receptor (TLR)-4 and B-cell leukemia lymphoma (BCL)10, leading
  to increased Interleukin (IL)-8 secretion by both canonical and noncanonical pathways of NF-kB activation. The ROS-mediated
  pathway of inﬂammation does not involve TLR4-BCL10, but
  requires Hsp27 and IkB-kinase (IKK)b, leading to increased phosphorylation of IkBa, and thereby enabling the nuclear translocation
  of NF-kB.

From the intro to:

  Yang B, Bhattacharyya S, Linhardt R, Tobacman J. (2012) Exposure to common food additive carrageenan leads to reduced sulfatase activity and increase in sulfated glycosaminoglycans in human epithelial cells.  Biochemie, Mar 5,epub ahead of print, doi

(As an aside, the direct conclusions of this study are that these changes in GAGs may further influence transcription and play a role in determining cell fate, and perhaps may influence cell/cell interactions)

  (**)NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens  wiki


Unfortunately, the answer to your question isn't as well researched as other areas, I believe...let's add some complexity into this.

You're correct, teeth does "grow" in the gums. And it does start off surrounded by cells (look up: tooth bud, cap, bell stage)!

The tooth originates from an interaction between the ectomesenchyme (likely originating from the neural crest cells) and the epithelium of the mouth when it is forming while you're still an embryo in your momma's tummy.

Unlike sharks, which are homodonts (meaning, their tooth are all of one morphology), we are heterodonts (e.g. we have different shaped teeth - e.g. molars, canines, incisors, premolars). There are a couple of theories to why this occurs (look up: clone model, field model, odontogenic homeobox code - a combination of all these theories). Basically, a bunch of genes transcribe for proteins and signalling factors that create the complexity of your tooth shape and position in the mouth.

Basically, this means, our teeth are going to take longer and require more energy and effort to carve into (yes carve! lot's of the tooth shape is create by apoptosis of the regions around the "cusp" area when it is developing).

When your primary/baby teeth pop out, they serve functions such as developing speech, allowing you to eat, strengthening your jaw muscles (which in turn helps to develop your mandible and shape of the face), all this so you can have a great bite when you get older!

Luckily, sharks don't speak much underwater, so they probably don't give a poop about having properly lined up teeth. Their teeth grows everywhere. Proper bite for eating various nuts, fruits, meats and vegetables? NAH. WE JUST CHEW OFF LEGS. WE CAN ONLY SHRED STUFF. Sharks need strong ankylosed teeth (ankylosed = like an anchor? teeth are anchored into the mandible of the shark).

In contrast, humans have teeth in gomphosis (sockets), which gives our teeth some cushioning and sense of proprioception (the sense knowing how hard you're biting) when we bite on something extremely hard, to prevent us breaking our teeth - thus helping us preserve our teeth. Sharks don't have that, they just break their teeth.

Humans do finally replace their teeth, after our jaw grows enough for us to accommodate them at a genetically planned stage. This happens by tooth germs (cells) being bud off (like a flower yes :D) from the baby teeth. Note though, your 1st adult/permanent molars are already beginning to form when you're still in your momma's tummy.

I believe that the continuous creation of teeth requires more energy, but takes less time (sharks). For humans, one time creation of teeth requires less energy, but takes wayyyyy more time (and also has to be timed correctly with all our other growing bits).

TL;DR Evolutionary reasons and different functional uses of teeth between sharks and humans probably determine why we only have two sets of teeth (diphyodonts). That being said, it would be cool if we were like rats (have molars/incisors) though, which replace their teeth anytime its lost. Maybe one day we can evolve into it? Yay!

Some interesting points: You mentioned teeth "healing".

Your teeth is made up of enamel on the outside, which is NEVER replaced. It "heals" by remineralisation which is not exactly the same as growing new crystals on top of it. Kinda complex, won't go into it.

However, your teeth is always forming new dentine, which is below the enamel. In a way, your tooth really is growing back all the time. Because a new layer of dentine is deposited everyday (like...4 micrometers). This is because the dentine producing cells, called odontoblasts, are still around. In contrast, the enamel producing cells, called ameloblasts, are removed when your tooth has developed. I THINK, the reason is to make space in your enamel so it can be fully mineralised and completely filled up by hydroxyapatite. (Too much fluoride when young can block this removal of ameloblasts and its proteins like amelogenin and enamelin = forming holes, which cavitate resulting in fluorosis).

Hopefully all that answered your question. But, it was fun for me to rant anyway. Cheers.


Are peanut proteins similar to chicken meat proteins?

I posted an answer to a similar question here: https://health.stackexchange.com/questions/9124/is-all-protein-the-same/9130#9130

  You're not using protein as it is to maintain your body. It's first
  broken down to the individual amino acids, which your body can then
  use to build new stuff.

  If you're lacking one of the essential amino acids, you can only build
  as much new protein until that runs out, and all the other amino acids
  are just excess. A protein that contains all the necessary amino acids
  is called a complete protein, and you could calculate the differences
  in the so-called quality of the protein.

  A perfect protein (i.e. from egg/milk/soy) will contain amino acids in
  exactly the ratio you need, some protein contains so little of a
  certain amino acid that you'd need to eat twice as much of that
  protein (for example rice or peanuts).

  In your case, if beef is making you recover fastest, you'd need to eat
  30*0.92/0.70 = 39g of peas for the same effect.

  You could get around this by combining different sources of protein.
  For example grains are limited in lysine, while beans are limited in
  cysteine/methionine.


What is the definition of an opioid, beyond that it's something that stimulates opioid receptors?

First there was opium. Then the active components of opium (morphine etc.) were defined and called opiates. Then the receptors for opiates were discovered, along with their endogenous ligands (enkephalins etc.), and since those endogenous ligands were not derived from opium and indeed (being peptides) were not chemically related to opiates, a new term was needed. This term was opioid, and yes, the definition of an opioid is that it is something which binds to an opioid receptor.

The perceived circularity lies in the shift of emphasis from the drug to the receptor as the central player - when the first binding studies were being done in the early 1970s the search was for opiate receptors, not opioid receptors.


Why might long telomeres be selected for in laboratory mice?

Their arguments for increased telomere length in lab mice are:

Rate of tumour formation is dependent on the number of cells within an organism. Additionally, tumours take time to form. Therefore, small animals that only need to reproduce early in life, like lab mice, are less prone to tumours and there is then less selective pressure favouring telomere shortening.
Senescence has a negative effect on reproductive success, even early in life, and there is therefore selective pressure favouring increased telomere length that reduces senescence.
While the lack of selection on senescence due to the short window for reproduction could have the opposite effect of reducing telomere length, point 2 is the dominant factor.

To be frank, this all sounds extremely speculative to me and the supporting evidence they did provide was not entirely convincing (though I am far from an expert in the field). Keep in mind that it’s a hypothesis only.

In case you don’t have access to their article, I quoted the relevant section below:

  The unusual telomere system of lab mice may be an unintended consequence of captive breeding. Retirement of breeders after 8 months eliminates selection on late-life effects. Tumor-forming mutations take time to occur, tumors take time to become lethal, and the likelihood of tumor initiation is presumably a function of the number of cells in the body, so in small bodied animals like mice, tumors may be rare and inflict minimal cost in the first eight months of life, even absent a telomeric fail-safe. Further, selection for sustained high reproductive output (beginning early and maintained for 8 months) should strongly favor a reduction in senescent effects occurring in that window. Selection acting to eliminate senescent effects and increase early reproductive output may tend to elongate telomeres. Because of the inextricable connection between tumor suppression and somatic maintenance, telomere elongation should dramatically increase the risk of eventual tumor formation, but any effects manifesting after the breeding cut-off will be selectively irrelevant. By our model, selection for early high rates of reproduction in the absence of selection for longevity or tumor suppression should produce long telomeres and a strong propensity for eventual tumor incidence. Despite diminished senescence, we expect these mice to have reduced maximum longevity compared to wild conspecifics. At all ages, lab mice (with elongated telomeres) should be more likely to die of tumors than wild mice. These mice should also be unusually resilient to somatic damage and show few signs of aging other than tumor formation.

  ...

  The hypothesis that an 8 month breeding cut-off should select for non-senescent, tumor prone mice seems paradoxical. One might expect the elimination of selection on late life effects to accelerate senescence, not retard it. But in lab mice, selection for high, sustained rates of breeding appears to be the dominant factor. The tumor fail-safe has effectively been turned off, condemning these animals to form tumors, but leaving an early-life window of reproduction within which there is minimal senescent decline.


Technically agar has first been used (and still is) in the kitchen and then adopted to the lab.
In the 19th century, gelatin was used in the microbial laboratory. The problem is that gelatin is much less thermostable than agar and at higher cultivation temperatures plates will melt and get liquid again.
In 1882 the german microbiologistt Walther Hesse (at that time an assistant in Robert Kochs laboratory) followed the suggestion of his wife Fannie Hesse to use Agar instead of gelatin. See the two references for some interesting details.

I personally would never use anything which comes from the lab in my kitchen since you never know if there are any contaminants in there. This is also probably the reason, why your lab manager doesn't want you to have it.

References:

Walther   and   Angelina  Hesse-Early Contributors  to  Bacteriology
History of the agar plate


How much variation in mutation rate in there in the human genome?

Cool question. Unfortunately, I don't have a complete answer; the best I can do is summarize some literature. I'd be happy to look more if you want to discuss though. Also, sorry the answer is a little scattered and I apologize if you were already aware of all this!

One thing I will suggest though is that this is hard to do for the human genome in isolation; hence why much of the literature draws on other animals as well.

In any case, the literature on this topic is quite expansive, so I am afraid this is merely the tip of the iceberg. Hopefully it's helpful though.

Firstly, I know of two genomic mutation rate maps that might interest you (as you suggest in your question). One in Genome-wide patterns and properties of de novo mutations in humans by Francioli et al, looking at de novo mutations in humans (obviously more concerned with germline mutations), and another in Mutational heterogeneity in cancer and the search for new cancer genes by Lawrence et al, which (unsurprisingly) is concerned with somatic mutation rates and the resulting oncogenics.

A great review, although not entirely human-specific, is Variation in the mutation rate across mammalian genomes by Hodgkinson and Eyre-Walker. They note that:

Small-scale effects: G & C mutate more than A & T, CG dinucleotides are highly correlated to higher mutation in non-coding DNA, and there appear to be hyper-mutable sites (conserved across species) that are susceptible to SNPs. These effects vary across the genome as well. Indeed, certain regions of mitochondrial DNA also have highly variable mutation rates. Oddly, GC-rich islands may be less mutable (for certain mutation types), and may affect nearby nucleotides, particularly methylated ones.
Transciption sites: somatic tissue has lower mutation rates of transcribed areas than non-transcribed ones. In germ tissue, there is an interesting effect for certain types of mutations increasing as one moves away from the transcription start site, but not others.
Other mutations: indel mutations tend to co-occur with point mutations
Mutation rates are spatially correlated at multiple scales.
Chromosomes: for humans, it seems the Y chromosome is the most mutable, followed by the X, and then the autosomes. There is also a difference in the mutation rate between autosomes, but it appears this is overshadowed by the intra-autosomal mutation rates.

Not explicitly noted by the paper, but intutive and sometimes implied, is the lower mutation rate in coding and regulatory regions (e.g. enhancers, promoters,...).

Another paper is Evolution of Local Mutation Rate and Its Determinants by Terekhanova et al. They note local mutation rates in primates (obviously including humans) are highly correlated across the genome. This correlation weakens as evolutionary distance grows (e.g. humans to mice). They also look at the influence of several genomic features on local mutation rates.

Not in humans, but Evidence of non-random mutation rates suggests an evolutionary risk management strategy by Martincorena et al look at mutation rates across E. Coli genomes, finding enormous variability, particularly lower rates in highly expressed genes.

Since we have not yet seen chromatin structure pop up much, I'd like to point out the cool paper The effects of chromatin organization on variation in mutation rates in the genome by Makova and Hardison. Therein, they find that mutations of different types are affected differently by open vs closed chromatin states; roughly, closed chromatin encourages base substitutions, whereas indels occur more often in areas with open chromatin.

Finally, some of the difficulties in assessing mutation variability are explained by Eyre-Walker and Eyre-Walker, in How Much of the Variation in the Mutation Rate Along the Human Genome Can Be Explained?

Some related work

For mutation rates in germ-line cells specifically, see:

Properties and rates of germline mutations in humans by Campbell and Eichler
Determinants of Mutation Rate Variation in the Human Germline by Segurel et al
Variation in genome-wide mutation rates within and between
human families by Conrad et al

which describe some patterns in mutation variability across the genome, but are often more concerned with inter-individual factors.

Also here are two early papers using comparative genomics to look at mutation rates:

Mutation rates in mammalian genomes by Kumar and Subramanian
Deterministic Mutation Rate Variation in the
Human Genome by Smith et al

which focus on inter-species comparison, but also discuss compositional differences (e.g. GC richness).


Difference between Bioscience and Lifescience

I agree with the comments and largely see them as the same thing, and many dictionaries would probably agree with this. However, in practical use (from my experience) Life science is used somewhat more broadly (everything from ecology and agricultural science to genomics and biochemisty), while Bioscience is more often applied to "whiter" lab-based biology and more technical applications (biotechnology, genetics, etc.). Personally, I would feel comfortable to label my research as life science but a bit more uneasy with bioscience. However, the terms are so vague that I wouldn't pass judgement on the content of research just based on these labels.


What happens to a human body once a sugary snack is consumed?

The human/animal digestive tract breaks down food chemically (with low pH/acid), enzymatically (like proteases and glycolytic enaymes which break down protein and sugars respectively), as well as symbiotically (bacteria participates in the breakdown of some compounds in the gut).  The results are released into the blood stream for the most of the body to assimilate.

With foods with complex carbohydrates (scenario 1), the results can be only a modest change in the glucose level in the serum.  This depends upon the specific food which you can understand better by researching the 'glycemic index'.  Highly glycemic foods result in rather short term release of simple carbohydrates glucose/sucrose into the blood.  Lower glycimic food contain complex carbohydrates (which are elaborate chains of sugars) which need to be broken up into simple carbohydrates before they are metabolized the the cells.

Foods which contain a lot of simple carbohydrates change the sugar levels in the blood nearly immediately and it can go quite high.  simple carbohydrates are monomers or dimers of sugars.  BTW complex carbohydrates have few pictures on the web, but you can imagine them as chains and networks of many many simple carbohydrates linked together.

Not all simple carbohydrates are used by human beings for energy.  For instance the glycosamine in 'joint juice' is the sort that makes cartilidge, which just to show you how different some complex carbohydrates can be. BTW i don't recommend joint juice, just trying to give a familiar example.  Its unlikely that the glucosamine you drink will be directly used for your joints!

So glucose is the energy currency in the blood.  when the glucose level goes up insulin is secreted by the pancreas which tells the cells to take up the glucose for glycogen (internal cell energy storage in a complex carbohydrate) or to be metabolized directly.  Diabetes results when insulin is not produced (type I) or when the cells stop responding to insulin (type II).

Human tolerance to glucose in the blood is estimated to be up to about 100 mg/dl long term. higher than this on the average is not healthy and can go up to several hundreds and cause lots of degeneration in the kidney, liver, and eyes, and more.  Exercise and fasting increase insulin sensitivity and athletes have blood glucose that is quite low even if they have a sugary beverage.

hope this helps - many keywords embedded within...

One last note.  Fructose, which is about 45-60% of high fructose corn syrup (the rest is sucrose) is almost entirely metabolized in the liver.  This is why fructose can be harmful to people who drink too much sweetened beverages.  With the liver taking in the vast majority of fructose, it tends to make fat out of it, sort of overdosing it to make it fatter than the rest of you relatively quickly.  Fatty liver is a marginally disfunctional liver and can cause health problems down the way.  Abdominal body fat (not on your love handles, but amongst your chest cavity and internal organs) is particularly harmful as it interferes with all sorts of organ function.  Probably something everyone should be aware of.


What is the name of this yellow / orange fungus?

Most fungi need to be studied under a microscope to determine a species. I think this belongs to the genus of Pholiota. I couldn't find an English name, if I translate the Dutch name, it would be 'Bundle mushroom'. This name refers to the fact that they always grow in groups, usually on (dead) trees or trunks.

At first look thought this was a Honey fungus, but these are parasitic so usually don't grow on dead wood.