I've been doing some reading, and have come up with the following interesting information.

Telomeres

During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess nucleotides – at the ends called telomeres (Silvestre, 2012).

Mammalian cells do not replenish their telomeres after cell division, giving them a replicative lifespan;  a maximum number of cell divisions before the telomeres run out. The cells then either enter a state of senescence and no longer divide, or initiate programmed cell death. However each cell has the genetic information for telomerase – the enzyme that can replenish the telomeres – but cannot use it. Only embryos and stem cells are able to express telomerase in mammalian cells - this protects against the build up of damage to DNA causing uncontrolled cell cycle progression. Activated telomerase is a core feature of many cancers (Campbell, 2012).

Plant Telomeres

You mention telomeres in your question, and it is an interesting question I had never considered. Plants have no germline preserved, so their progeny must bear all the defects of their particular parent cell, and that plant cells must therefore all have the capacity to regenerate their telomeres. I found a paper by Fajkus and colleagues that finds telomerase activity in plant cuttings grown in culture (Fajkus, 1998). Their hypothetical Plant Telomere-Length Regulating (PTLR) protein must arise in the early stages of the culture and last only a few cycles. Interestingly it seems that the efficiency of this process varies between different plant species. The authors note that their plant of choice – tobacco – is particularly proliferative and that other plants such as barley were harder to grow from cuttings, which may be down to a different way of regulating the telomerase (for instance it could only be activated occasionally at low amounts).

Do Plants Get Cancer?

It seems to me the next obvious question. One of the first papers I came across (published in 1916 by the Journal of Cancer Research!) talks of Crown Gall in plants and its relation to human cancer (Smith, 1916). Many websites cite galls as being the equivalent to cancer in plants, but it appears that the outgrowths (galls) that appear very tumour-like are in fact caused by bacteria encouraging their surrounding cells to proliferate. (See this question for more detail on galls).

I later found an abstract (I cannot access the full paper) from a paper published in Nature in 2010 called “Walls around tumours — why plants do not develop cancer” (Doonan, 2010). It appears that Plants can and do develop tumours, but they are less frequent and less lethal due to fundamental differences in development between plant and animal cells. Singh and colleagues found that in 2 plant species (Arabidopsis and rice) there were DNA damage repair pathways well conserved but with variation; there were several gene duplications in different DNA repair pathways (Singh, 2010).

Plants Do Not “Age” As We Do

Although I could find no conclusive evidence, it seems to me likely that plants may also have enhanced maintenance against other cellular stresses than DNA damage, such as build-ups of aberrant proteins. It therefore appears that in a protected environment some plants could live indefinitely. I say some, because others deliberately end their lives after reproduction. Traits such as longevity are inherently hard to be selected for, as the advantages come long after reproductive maturity and are therefore under much less selective pressure.

We see plants wither and die, but this is because they are constantly subject to environmental insult. Animals and insects may eat them, there may not be enough food or water, or sunlight, or the plant may become infected. All of which are at the macroscopic level. Due to completely different evolutionary constraints and pressures plants are highly resilient to cellar stresses, possibly due to differences in metabolic rate, and apparently have indefinite replicative potential.

Edit:
Although the more I think about it, the more it seems that most plant must have an ultimate lifespan, in that as they forever grow and expand their tissues would gradually harden and become less functional (I am mostly imagining bark plants here). Although as the layers of bark are pushed out the layers below take the place. In this way a tree could possibly live indefinitely by continuously remodelling it's layers.


A single picture of aged and polished horns is not going to be that easy to give a confidently correct answer, but I can at least say that they appear to me to be horns of a yak or cattle steer.

See for example, the horns of a female domesticated yak (Bos grunniens):

  the horns sweep out from the sides of the head, and then curve forward; they typically range from 48 to 99 cm (19 to 39 in) in length. The horns of females are smaller, only 27 to 64 cm (11 to 25 in) in length, and have a more upright shape.

Wild Yak (Bos mutus) have similar, though smaller and sometimes curvier horns:

  The Wild Yak’s horns are grey to black and curve outwards, forwards, back, and slightly inward. The horns of males are larger than those of females. The horns of male Wild yaks average 42.6 centimetres (16.8 inches) in length, from tip-to-tip, and 35.2 centimetres (13.9 inches) in circumference. The horns of females average 32.2 centimetres (12.7 inches) from tip-to-tip and 19.5 centimetres (7.68 inches) in circumference. [Source].

 Yak (Bos mutus) in the Lüneburg Heath wildlife park, Germany. [Source].

Both Yak species are present in Asia:

  Though there are over 12 million domestic yaks in the Central Asian highlands, fewer than 10,000 Wild yaks survive.

However, as I said, these could just as likely be the horns of any of a number of variety of steer cattle. (There are over 800 varieties!).

See for example, this Corriente cow in California:

If you Google "steer horns" you get dozens of shapes and varieties of mounted horns. You could comb through looking for similar specimens...

If I had to guess, since your grandparents are from Russia where yak are present, it seems to me it would be more interesting/impressive to mount yak horns vs just steer cattle horns. But that's just a personal guess.

Here's a picture showing a variety of species and their horns:


Why doesn't local anesthesia affect muscles?

@Nicolai's answer is not entirely correct.

Background

The most common local anesthetics are all the "-caine" drugs - like novocaine, lidocaine, - and even cocaine has some of the same pharmacology, as well as other effects (in movies this is why cops might rub some white powder on their lips - if it's cocaine, it will make their lips tingle; this is not standard training for non-movie police; also not advised for drug sellers or purchasers, because for exactly this reason cocaine is often cut with other -caines or other compounds that give a tingly feeling).

What all of these drugs do is to block voltage-gated sodium channels. These are the channels that propagate action potentials through axons and excitable dendrites. Other local anesthetics that aren't used in the clinic, like tetrodotoxin from pufferfish, block the same types of channels. At sufficient concentrations, local anesthetics block all nervous activity: unlike @Nicolai's answer, they do shut down nerves (as a brief note for terminology: nerves are bundles of axons containing many many individual fibers).

So back to your original question: how come the muscle isn't impaired during dental surgery?

Geometry of innervation of the face

Take a look at this picture of the nerves innervating the facial muscles and the muscles themselves: https://bmc.med.utoronto.ca/cranialnerves/wp-content/images/c_07/Facial-vii12_labelled768.jpg (note: I wasn't able to find a good image that has a license allowing me to reproduce it here; if someone finds one and wants to edit it in, please do - thanks!)

They mostly come in from the sides of the face, and so they are further away from the site of local anesthetic injection. The muscles themselves also extend further away. It may be that the muscle is partly anesthetized, but you don't realize it.

Limited diffusion and location of injections

Diffusion of local anesthetics is limited because they actually act inside cells, and only the unionized form can diffuse across cell membranes. Once inside the cell, the tend to be ionized and therefore get "stuck". Therefore, they don't typically diffuse nearly as far as other compounds of similar size, especially lipophilic compounds.

The nerve endings that sense pain, on the other hand, have to be at the surface of the skin/mucous membranes. That is, they are exactly where the local anesthetic is being injected. The objective of local anesthesia is often to inject enough to affect only those surface tissues, trying to spare the deeper tissues.

Effects on nerves

However, it isn't too uncommon to overdo it and to paralyze the underlying muscles or nerves. Even nerves far away can be affected, for example see this paper discussing cases where the local anesthetic travels near the eyes and impairs eye movement. There are also other non-dental procedures where block of a particular nerve is the intended result: this can be seen as an alternative to general anesthesia. One example is the use of an epidural (essentially into the space around the spinal cord) injection during childbirth or surgery. The extent of paralysis depends on the dose, however, and usually the intent is to avoid major paralysis and use other drugs like opiates to assist in preventing pain.


Does the cell internal temperature changes in response to a change in external temperature?

Homeothermic multicellular organisms have special tissues that burn resources to warm up (usually this involves breaking the electron-transporting chain at the final stages of respiration to transform all chemical energy into thermal energy). And they have special tissues (fat) and enough body mass (this is more about the volume/area ratio) to keep this energy from dissipating. If you recall physics, any unicellular organism has insufficient body mass to accumulate thermal energy for any perceptible amount of time, hence it's useless to burn resources that it can spend to adapt to lower temperatures, i.e. synthesise cold-shock proteins, modify membranes, restructure metabolism. This is basically the same reason why small mammals and birds have to eat all the time to stay alive.

As you can see, the smaller you get the more energy you need to burn (hence increase ${O}_{2}$ consumption) to maintain body temperature. That's why we don't see truly homeothermic insects (some of them can warm up for short periods of time) or other small animals.


Why are monarch butterflies attracted to particular flowers but not others?

It's the Monarch caterpillars that only feed on milkweed. Adult Monarchs, like many butterflies, feed on the nectar from flowers. https://www.fs.fed.us/wildflowers/pollinators/Monarch_Butterfly/habitat/index.shtml


Fastest observed biologically evolution rate?

Theoretically, it really depends how crazy you want your model to be! Also it depends what you mean by "evolution rate".

Let's consider a very simple and quite crazy model. Let's assume that by evolution rate you mean the difference between mean phenotype between one generation and the next. Let consider a trait (which heritability is $h_N = 1$) which takes only two values $x_1$ and $x_2$. In a given generation, half the individual carry the trait value $x_1$ and half the trait value $x_2$. If the relative fitness of $x_1$ and $x_2$ are 1 and 0 respectively, then the evolution rate is simply $| \frac{x_2 + x_1}{2} - x_1 |$. Allow $x_2$ and $x_1$ to be very big values and the rate of evolution will be very fast. In the most extreme case, $x_1 = \infty$, then the evolution rate is simply infinite.


Recommendation for a molecular biology book that explains how we know what we know

This is not my favourite book on molecular biology (Alberts is my favourite, and Lodish is the runner up), but I'd recommend The Cell, A Molecular Approach, by Geoffrey Cooper

This book has, for every chapter, one or more boxes called "Key Experiments", in which the author describes famous experiments that allowed us to know what we know now about that subject.

For instance, at chapter 10, titled "Protein Sorting and Transport", the Key Experiment box shows the discovery of the peptide signal by Gunter Blobel:

And the best news, the book is completely free at NCBI bookshelf:

https://www.ncbi.nlm.nih.gov/books/NBK9839/

It's searchable, but unfortunately not browsable. However, the workaround is very simple: just type the chapter title in the search box!

Of course, some concepts are so old (for instance, you asked "how do we know that there is such a thing as "protein" in the first place") that you probably are not going to find them in molecular biology textbooks, but on a book about history of science instead.

PS: By the way, both Alberts and Lodish are also free to read (and browsable) at NCBI bookshelf!


As described in the abstract of Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al., protein cyclization improves:

resistance to proteolytic degradation and conformational stability. The latter property leads to an increase in binding potency and increased bioavailability due to increased permeation through biological membranes.

In simpler terms, a protein that is cyclized is less likely to:

Fold into an unhelpful shape.
Be broken up by an enzyme.

Thus, they are more likely to:

Act as better binders for a given target
Make it across a cell membrane


Is PrEP used for anything other than HIV?

Prophylaxis is typically prior to exposure. Condoms, for example, were historically referred to as prophylactics, in that they prevent pregnancy and many STIs. The reason the pre-exposure bit is given special attention in this context is that it refers to use of drugs with substantial risk of harm. Because of their associated risk, these drugs were previously only used for post exposure prophylaxis. Similar to rabies vaccination after an animal bite, this strategy involves preventative treatment given after exposure but before a critical point in the progress of an infection.

To more directly answer your questions

  Are any diseases other than HIV prevented using pre-exposure prophylaxis?

Many, many, many diseases. Vaccines are a good example of prophylactic treatment, typically given prior to exposure. Malaria prophylaxis is another example, where a medication (with non insignificant risk of harm) is given to healthy people traveling to an endemic area.

  Do they use a different term?

In most cases, as you can see by searching for the words used in the linked references, the term is simply prophylaxis, rather than pre-exposure prophylaxis.


This is not a moss, but a fungus of the family Clavariaceae. Most likely this is Clavaria zollingeri, commonly known as violet coral, but there are a few resembling species. Microscopy might be needed to be entirely sure.

The species is saprotrophic, so it grows on the woody debris in your picture.


Looks like Lumbar Vertebrae or Sacral Vertebrae of a Cow like @Brian Hanson Said above.

Studying closely in laboratory can elaborate more secrets about the bones.


How much cost would artificial pollination add to common products (fruits etc.)?

The cost would increase; either because pollination services are not provided and the supply is decreased; or because the cost to producers goes up as they must pay for artificial pollination. See the extremely detailed analysis in Winfree et al.

edit

I imagine what you're actually asking for is a $ figure "per apple". This depends on the location, crop, market, etc., but just for a ballpark, if I'm reading the supplementary tables in Allsop et al correctly, the replacement value of insect pollination to apples in the Western Cape of South Africa would represent a 6%-25% increase in production cost (and, if the producers pass that along to the consumers, an equal increase in the cost to consumer).

 Allsopp MH, de Lange WJ, Veldtman R. 2008. Valuing insect pollination services with cost of replacement. PLoS ONE 3: e3128–e3128.
 Winfree, Gross, Kremen. 2011. Valuing pollination services to agriculture. Ecol Econ 71: 9–9. [behind paywall, but posted free here]


How are mitochondrial diseases like MERRF inherited?

Mitochondria are primarily thought to be inherited from the mother but there is evidence now that the father can also contribute mitochondria (Schwartz and Vissing, 2002; Luo et al., 2018).

Even if the mitochondria were purely maternally inherited, a cell (including oocyte) typically contains many mitochondria and not all of the mitochondria may have the (deleterious) mutation. This phenomenon is called heteroplasmy.

MERRF is associated with a loss of function mutation in mitochondrial tRNAs (See NIH, Genetics Home Reference). The extent to which a cell will be affected would depend on number of mutated mitochondria it contains. Therefore different cells would be affected differently.

The trait inheritance would therefore not be in the typical Mendelian fashion.


Why do you get prion diseases from eating animal brains but not other parts of the animal?

The notion that you get prion diseases like BSE only by consumption of brain is not correct. Any part of the infected animal that contains nervous system tissue or lymphatic tissue can be infectious, although I guess this is dose-related.

Quote from OIE, "BSE. General disease information sheet" ([1]):

  The risk linked with consumption is addressed by the requirement for
  routine removal of all visible nervous and lymphatic tissue (Specified
  Risk Materials (SRMs)) from carcasses during the processing of
  cattle as well as the removal of any suspect animals from the human
  food chain.

  Appropriate handling of nervous and lymphatic tissue tissues from
  BSE-suspect animals in abattoirs and laboratories is indicated to
  avoid accidental exposure (ocular or oronasal). Milk and milk products
  are considered safe.

[1] http://www.oie.int/fileadmin/Home/eng/Media_Center/docs/pdf/Disease_cards/BSE-EN.pdf

The OIE is the animal equivalent of the WHO.


There are many reasons for why people eat meat. Some of them are to be discussed here and some of them have nothing to do with biology.

Reasons that have nothing to do with biology

There are many reasons that are not to be discussed on Biology.SE. These include cultural reasons, the reasons related to taste and appreciation, farming and availability, price and economy and of course for reason related to political ecology (incl. water and energy consumption of meat production).

Reasons that has to do with biology / medicine

We can talk about nutritional value though. According to a number of websites (sorry nothing peer reviewed; monitor.co.uk; rd.com; sparkpeople.com), people not eating meat may suffer from lack of

protein
iron
zinc
calcium
vitamin D
vitamin B12
omega–3 fatty acids

It is not impossible to get all of these nutrients without meats. However, when becoming vegetarian, some people need to be careful and rethink their diet to ensure not to suffer from the lack of these nutrients.


Yes, they’re edible and even eaten in some places.
https://culinarylore.com/food-science:are-earthworms-edible/


Are there seeds intended to feed eaters?

There's a very interesting case of mutualism between the species Homo sapiens and Oryza Sativa (also Triticum aestivum...). The humans have bred the plants to produce highly nutritious seeds, much greater then non-adapted species, and in return the humans save a small fraction of the seeds and will cultivate the plant for many generations.

It goes further then that in that humans also will protect their mutualistic plant partners from other invasive species and cultivate them, ensuring their mutual survival.


Accurate surveys of urban pigeon and bird populations

You can find population data for lots of species at The Global Population Dynamics Database, which can be used to test and fit population models. When searching for Columbidae (the dove family) I find 16 datasets of different lengths, but none for Columba livia though.

To search and download data you first need to register for a user account.


How would ecology be affected if 100km² of an ocean surface was covered by a floating object?

The vast majority of light only penetrates the top 200 metres of the ocean, the euphotic zone, so your answer is roughly "what ever lives in the euphotic zone which requires light." In all likelihood I would expect this to cause:

anything  which is not highly mobile but, is dependent on sunlight (phytoplankton etc.), would die.

the more mobile ("free swimming") which rely on either sunlight or the (now dead) slower resources would move out of the area.

reduced flow of nutrients in to the lower parts of the ocean - biomass from the upper regions dies and sinks to the lower levels, if it no longer grows in the upper 200m then there will be less down flow after time.

Overall, the impact would be low because the area of the pacific is >165,000,000 km2 so the density of biota would only increase marginally in the top 200 metres of the pacific (the sunlit water volume decreases from 33,040,000,000,000 cubic metres to 33,039,080,000,000 cub. metres). Also, if we assume that the platform is free floating that means it would drift thus only causing short term loss of sunlight for the less mobile organisms.
EDIT:
Upon reading @Kotatsu's answer I feel they have made a very good point and I should add the following:
By providing a solid surface it could also benefit oceanic life by increasing area available to live for sessile organisms (just like shipwrecks, oil rigs etc.). Further if the panels were broken up (I assume this would be the likely design because sitting a huge sheet across the ocean will leave it prone to twisting by wave motion) light would be able to pass between the gaps. I agree with @Kotatsu, and this "floating panel" could even be beneficial to the ocean ecosystem.

note: I am not an expert on this so it is purely an application of logic and my best guess


That's an Echinoid, or Sea Urchin (Phylum Echinodermata). We can clearly see the five rows of ambulacral groves and the base of the spines.

Here is an image of a fossil Echinoid, from the Melbourne Museum, for comparison:

Fossil echinoid (sea urchin), Lovenia bagheerae; late Miocene (c. 8 my old), Portland, Victoria
Photographer: Frank Holmes / Source: Museum Victoria

According to the museum:

  Victoria contain fossils of many different kinds of echinoderms, including sea stars, brittle stars, crinoids, cystoids, blastoids, edrioasteroids and carpoids. They occur in the Heathcote, Kilmore, Kinglake, Melbourne and Lilydale districts. In much younger rocks of the Cainozoic Era (less than 65 my old), the most abundant echinoderms found in Victoria are the echinoids or sea urchins. They occur mainly in limestones exposed in coastal areas including the Portland, Port Campbell, Torquay, Geelong and Lakes Entrance districts. (emphasis mine)

Your second image, from below, really seems like this image of Lovenia bagheerae:

Source: Museums Victoria


This is a part answer (as this is outside of my field), but the article Self Regulation of the Heart: Natural Frequency and Damping of the
Heart Contractions  (Bahramali et al. 2009) imply that 'normal' frequencies may not be possible to precisely define, due to:

  ECG frequency analysis is complicated by the fact that ECG signals are non-stationary, that is, their activity
  patterns change slowly or intermittently as a result of variations in a number of physiological and physical influences.

The article extensively reviews the general frequency analysis, divided into P, Q, R, S and T components.  However, they define 'optimal conditions' (i.e. 'normal and healthy) as:

  optimal conditions of the heart contraction as those under
  which the dynamics of contraction shows the best
  agreement with underdamped harmonic oscillation

An example of this is visualised in the diagram below:

this example is provided on the University of Pennsylvania tutorial site ECG Tutorial

In the article Comparison of Power Spectral Density (PSD) of Normal
and Abnormal ECGs (Das and Chakraborty, 2011), note comprisons for the QRS component, as

  QRS complexes are chosen because
  it shows distinct differences for different heart diseases

In other words, distinguishing healthy from not-so-healthy.


Is it safe to feed an adult fire salamander with slime maggots?

Although I am afraid I don't know much about fire salamanders specifically, it is certainly possible for ingested fly larvae (or larvae hatching from ingested eggs) to survive ingestion and subsequently cause intestinal damage. Parasitic infestation by fly larvae that grow inside the host while feeding on its tissue is called myiasis. Enteric myiasis (also called gastric, rectal, or intestinal myiasis to indicate the affected part of the digestive system) occurs occasionally in humans following the ingestion of cheese infested with cheese fly maggots. Casu marzu, a traditionally produced Sardinian cheese, is supposed to have live cheese fly maggots in it, and cases of bloody diarrhoea following its consumption are known. If they're dead the cheese is considered unsafe to eat (although personally I'd correct that to 'more unsafe').


Percentage of mutations caused by radiation?

You might use the frequency of thymine-thymine dimers to extrapolate the rate of UV induced damage. This has been studied but I couldn't find a paper in human cell lines. It appears different cell lines have different susceptibilities to thymine-thymine dimers. The majority of DNA mutation in healthy people comes from endogenous sources, not radiation. Recombination during fertilization may also contribute significantly to changes in DNA sequence. Wikipedia nicely breaks down some of the different sources of mutation.

Manifestations of mutations from endogenous sources is measurable as our bodies become genetically more chimeric with time. Regions of our bodies become deferentially susceptible to disease due in largest part to errors in DNA repair and replication, unrelated to electromagnetic insult.

Damage due to UV radiation, like the creation of a thymine-thymine dimer, can be repaired readily by base excision and replacement. While DNA is dividing, it is cut many times to allow the molecule to unwind. Single strand breaks resulting from DNA damage have robust mechanisms for repair. For example, when a thymine-thymine dimer is excised or single strand break is otherwise introduced, enzymatic recognition makes identification of a template for repair possible. It is also very unlikely in a single strand break that another break will occur in the same location, decreasing the mutation effect of UV.

Double strand breaks and errors in DNA replication are intrinsically more permanent as a substituted base is chemically indistinguishable from any other of the same type. Much of the new genetic information introduced into any mammalian genome comes from endogenous sources, not the environment.

Error rate of human DNA polymerase
Deamination is a major contributor to mutation rate


Natural selection is environment-dependent. A mutation that makes an individual more fit in one context, might make it less fit in a different context.

The mutations that make bacteria more fit in an environment where they're exposed to antibiotics generally make them less fit in a "natural" environment where they don't have to deal with antibiotics. That means that MDR bacteria are often out-competed by their less-resistant competitors, unless they're in the "right" environment for them, such as a hospital or an infected, antibiotic-treated patient.

Some references:

Barnett M, Busby SR, Mitchison DA. Tubercle bacilli resistant to isoniazid: virulence and response to treatment with isoniazid in guinea-pigs and mice. Br J Exp Pathol 1953; 34:568–81.
urgos M, Deriemer K, Small PM, Hopewell PC, Daley CL. Effect of drug resistance on the generation of secondary cases of tuberculosis. J Infect Dis 2003; 118:1878–84.
Davies AP, Billington OJ, Bannister BA, Weir WR, McHugh TD, Gillespie SH. Comparison of fitness of two isolates of Mycobacterium tuberculosis, one of which had developed multi-drug resistance during the course of treatment. J Infect 2000; 41:184–7.
Gagneux S, Long CD, Small PM, Van T, Schoolnik GK, Bohannan BJM. The competitive cost of antibiotic resistance in Mycobacterium tuberculosis. Science 2006; 312:1944–6.
Li Z, Kelley C, Collins F, Rouse D, Morris S. Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs. J Infect Dis 1998; 177:1030–5.
Middlebrook G, Cohn M. Some observations on the pathogenicity of isoniazid-resistant variants of tubercle bacilli author. Science 1953; 118:297–9.
van Soolingen D, Borgdorff MW, de Haas PE et al. Molecular epidemiology of tuberculosis in the Netherlands: a nationwide study from 1993 through 1997. J Infect Dis 1999; 180:726–36.


What is the role of the tissue surrounding neurons in decision making and taking control of impulses?

Short answer
This question is pretty broad as it basically translates to "what purpose serves neuroglia in neuronal communication"? In short: next to everything.

Background
In the adult brain there are three types of glia: oligodendrocytes, astrocytes, and microglial cells (Purves, 2001). A few notable examples of their functions:

Oligodendrocytes (peripherally called Schwann cells) generate myelin sheaths around neurons, which increases conduction speeds (saltatory nerve conduction) and increases the metabolic efficiency of neural communication.
Astrocytes are a highly heterogeneic group of supportive cells. To put the impact of glia in perspective: this class of cells is considered to contain as many cell types as there are types of neurons in the brain. They are thought to mediate transfer of nutrients from blood capillaries to neurons, and they also assist in removal of neurotransmitters from the synaptic cleft and thereby speed up the recovery from synaptic activity and hence they increase the speed of information transfer (Tsacopoulos & Magistretti, 1996).
Microglia are the brain's immune cells, and are similar to peripheral macrophages. They act as the major inflammatory cell type in the brain, and respond to pathogens and injury.

References
- Purves  et al (eds). Neuroscience, 2nd edition. Sunderland (MA): Sinauer Associates (2001)
- Tsacopoulos & Magistretti, J Neurosci (1996); 76(3): 877-85


The answer might be a little late, but it was published after you asked the question. See the following publication for estimated global BMI averages from 1975 to 2014: http://thelancet.com/journals/lancet/article/PIIS0140-6736(16)30054-X/abstract


Genetic variation can affect the levels of protein; consider a variant that reduces the amount of mRNA transcribed, this could have a profound effect on the amount of mRNA available to translate into a protein.

Consider another variant that does not affect the abundance of the mRNA transcribed, but alters one of the many important sequences that are required for translation (co-factor binding sites, ribosomal binding sites, start site, etc.).

These are just a couple of examples that first came to mind, but there are many more. For instance, a variant may increase expression of a particular microRNA that in turn inhibits the translation of another mRNA molecule. I have not included any references as this is more a logical exercise - doubtless there are many more ways a genetic variant can affect protein abundance.


Can there be an equilibrium between humanity's increase of carbon dioxide output with plants since plants harness CO2?

Yes, with 2 caveats.

More CO2 encourages plant growth up to the local plants' limit. After that limit, the plants are saturated and extra CO2 backlogs into the air. If you intend to prevent atmospheric CO2 buildup, you're better off gradually supplying CO2 rather than deploying it in large surges.

The other caveat is dead trees and other plants that should be harvested or logged to make way for new growth (while providing lumber, fuel, and employment).


What does the species name 'fistula' mean?

The botanic and medical term fistula is directly derived from the latin word fistula meaning tube or pipe.

Both the medical fistula and the fruits of the Cassia fistula tree show phenotypes similar to a tube.

I will spare everyone the medical example picture, but here are the fruit of Cassia fistula, which are sold as "manna":


How was Crisper Cas9 function discovered?

The two "classic" papers cited in terms of Crispr/Cas9 discovery include the Doudna/Charpentier initial discovery, and the Feng Zhang application to gene editing.  There is an ongoing, famous patent dispute as to whom really discovered the Crispr/Cas9 gene editing technology.

As a quick timeline that better answers your question, a good publication is Cell Paper and there is actually a great podcast, but I will summarize:

Yoshizumi Ishino et al. in 1987 Discovers Crispr mechanism - the authors simply noticed the odd regular repeats of DNA in bacteria and noted: “no sequence homologous to these has been found elsewhere in procaryotes, and the biological significance of these sequences is not known.”
Francisco Mojica in 1993-2005 - Furthers research into CRISPR, at this time the terms has been coined by Jansen, however it is Mojica who really notices the Crispr pattern in several bacterium and suggests that it is involved with an immune response.
Alexander Bolotin in 2005 - Looking into the bacteria Streptococcus thermophilus, Bolotin discovers that the genetic material in between the spacers is viral DNA, providing definitive evidence of the Crispr hypothesis.
Marakova in 2006 - First proposal that the protein Cas9 can be used in a bacterial adaptive immune response, although Bolotin is also credited around this time from noticing the use of Cas9.
Koonin in 2006 - The first one to piece the Crispr storage of viral DNA and the Cas9 reports of an immune response together as a related system that might be able to use the Crispr DNA with Cas9 in an immune system.
Marraffini in 2007 - Studying the Crispr-Cas9 system further, he provides the first definitive microbiological evidence that Cas9 is a programmable restriction enzyme, and that it targets DNA not RNA. At the same time Philippe Horvath, Danisco France also provided the best evidence yet of the adaptive immunity system.
Doudna and Carpentier in 2010 - Through sequencing, definitively put the Crispr and Cas9 system together as complete unit that is able to cut DNA, they also described tracRNA as the RNA piece that join with Cas9 to program DNA cutting.
Feng Zhang in 2013 - While Doudna previously suggested that the Cas9 system could be used to target mammalian DNA, Zhang was the first one to actually that it was possible and therefore open to the door as the Crispr/Casa9 system as a tool that easily edit genomes.

While I definitley missed several key steps, and did not fully explain the actual mechanism of Crispr/Cas9, I think this provides a decent timeline.  For more information about the actual mechanism see: Harvard, Wired, Science News.


Mitosis versus Meiosis I: What's the difference?

At the start, all the cells are 2n, diploid cells. By far the largest difference between meiosis I and mitosis is that mitosis results in genetically identical, diploid somatic cells. Meiosis, in it's entirety, results in gametes of haploid genetic information, but the genetic information is not identical due to crossing-over events that happened during meiosis I.

What you should also note from the figure: Each chromatid represents 1 DNA molecule. In mitosis, the cell will begin with 4 chromosomes and 8 chromatids. After cytokinesis, the somatic cell will have 4 chromatids and 4 chromosomes. This propagates during the next round of mitosis. In meiosis: The cell starts with 8 chromatids and 4 chromosomes. After meiosis I each cell has 4 chromatids and 2 chromosomes. After meiosis II, each cell has 2 chromatids and 2 chromosomes. You're halving the amount of genetic material each round of meiosis, and this can't be propagated indefinitely.

Source: Tortora, GJ (2008). Principles of Anatomy and Physiology. 12th ED.


What hair color will result in someone inheriting both blond and ginger genes?

Hair color is not so simple as that.  Most traits, especially those as complex as color, are controlled by many alleles at many loci.  That's why there are different kinds of brown, blond, and red hair in the population.  There is no "hair color gene."  A fascinating paper came out a few years ago, identifying dozens of SNPs playing a role in hair and eye color.  It's a deep, deep rabbit hole that we have only begun to plunge into.

EDIT: To summarize, it's very complex.  This paper performed genome-wide association scans looking at two comparisons each for eyes (Blue and green, blue and brown), hair (red or not, blond or brown), and skin (freckles, sun-sensitivity).  The researchers looked in a group of Icelandic and Dutch individuals, which means they only looked at a small portion of human variability (i.e., very few African or Asian genomes, for example).  Still, just from those simple comparisons, their scans:

  revealed 104 associations that reached genome-wide significance, accounted for by 60 distinct SNPs, of which 32 showed genome-wide association with only one pigmentation trait, 12 with two traits and 16 with three traits.

That is to say, they found 60 DNA bases that explained their data.  Roughly half of those only affected one thing (eye, or hair, or skin, but only one), a fifth of those single base changes contributed to two different traits, and a full 25% of those SNPs were related with three traits.

That's still pretty hefty.  Basically, they found 60 things that can affect hair, eye, or skin color, and some of those can affect some or all of those at the same time.  And they only looked at people from two countries.  Here's a figure where they summarize the seven strongest SNPs; you can see how tricky it can be to explain colors.


Can we estimate effective population size from DNA sequence data (CR or cytB sequence)?

It sure is possible.

Very simple model

It is often hard to decompose the effective population size $Ne$ from the mutation rate $\mu$ though. But it is quite common to estimate $N\mu$. For example, it is a classical result from coalescent theory assuming a single panmictic population of constant size and no selection (and a few other assumptions) that

$$N\mu = \frac{S}{\sum_{i=0}^{k-1} \frac{1}{i}}$$

, where $S$ is the number of segregating sites and $k$ is the number of sampled individuals.

More advanced models

You will probably want a slightly more advance model though.

There exist a number of estimators including Colony2, CoNe, Estim, MLNe, ONeSAMP, TMVP and LDNe. I recommend having a look at Gilbert and Whitlock (2015) who compares these estimators under different demographic scenario.


Understanding the configuration of channels in the 10-20 EEG montage

EEG 10-20 system. source: Wikipedia

  How many actual channels are there?

21 in the figure, i.e., the number of active electrodes.

  What's the difference between reference and active channels?

The active electrode is the electrode under investigation. Basically this is arbitrary. Consider electrode F2 and F3. When you measure the potential difference between them and F2 is the active electrode and F3 the reference, the signal will be exactly identical as in the reverse situation, only the polarity (the sign of the voltage) is reversed. That's all there is to it. The active electrode is typically the electrode linked to the location you wish to record. The reference is elsewhere.

  What is the difference between a bipolar and a normal
  (unipolar/monopolar) setup?

In a regular unipolar setup, each of the electrodes is either measured against a distant reference (e.g. the earlobe) or against the aggregate of all the electrodes. Either way, the reference is distant. This means that the signal will be high, but artifacts will be large too, because artifacts from both the electrodes will be merged into the signal. Consider a reference in the neck; neck musculature activity will add artifacts (EMG) to the signal. Likewise, a reference in the chest area will add ECG to your signal.

In a bipolar setup adjacent electrodes are recorded. This means that large artifacts occurring through eye blinks or whatsoever are recorded by both electrodes and as their polarity is opposite, the large artifact responses will be cancelled and the signal is much cleaner. However, the downside of the coin is that commonalities in the signal, which will be larger when the electrodes are closer will also be subtracted and hence your signal will decrease accordingly.

I have used bipolar setups when measuring eERGs and eCAPs, i.e., electrically evoked activity. The electrical stimuli generated large artifacts and actually so large that their amplitudes were approximately similar between active and reference electrodes. The reduction in artifact by far outweighed the loss in signal. It depends on the situation you are at.

An authoritative work in this field is listed below.

Reference
- Pivik et al., Psychophysiol (1993); 30: 547-58


This is Crane fly, of the Tipulidae family. They don't bite humans, adults feed on nectar. Larvae prefer moist environments such as wet soil or decomposing vegetable matter and can consume roots and vegetation, damaging plants. Among others, bats and some Coleoptera are its predators.
Further informations can be found in the Wikipedia article linked above.


Are there comprehensive species descriptions on most species?

To suggest a new species, someone must necessarily makes a rather thorough effort of description. A good solution to get some info could be to go to the original paper however, these papers can be very old and hard to find. Also, the standards at that time might be very different from today's. After all, K. Linnaeus managed to describe 13,000 species also maybe because the description were more simple than they are today (see this related post). Andrena hattorfiana was described by Fabricius in 1775 but I could not find the original paper.

Note that the english wikpedia article for A. hattorfiana is relatively decent.

The IUCN red list is also a good source (see here)

The page for the Encyclopedia Of Life is unfortunately a little empty.

Here are some amazing pictures on flickr

You can also just search papers that refer to a given species. Here are a number of papers on A. hattorfiana.


Females are defined as the sex that produces that bigger gamete (ovule) while the males are those from the gender that produce the smaller gametes (spermatozoid). Because producing big gametes is costly, the number of females fix the reproductive limit in the population and in other words the variance in reproductive success in males is higher than in females. In the same logic, because females fix the reproductive limit in the population, males have to compete to access the females while the females are choosy. You may want to have a look at the wikipedia articles for Bateman's principle and Parental Investment.

The conclusions of Bateman's principle holds in general but not systematically. In some species males produce huge amount of parental care and therefore, the females become choosy for example.

  [..] men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females.

Yes, in many cases but not everytime. Human are an example of the cases where this statement is wrong.

  [..] for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival.

It sounds a bit weird! The reason is that the sentence almost implies that individual's strategy evolved in order to increase the probability of survival of the species which is totally wrong. By the mechanisms of natural selection a population evolve in the direction so that each individual favors its number of offsprings which can be in some cases very detrimental to the species as a whole.

Reading some bits of what I found no the webpage you linked i your question, it doesn't seem to me that the author is a good evolutionary biologist…but I haven't read much.


Why is DNA replication so much faster in prokaryotes than eukaryotes?

The difference in DNA replication rate between prokaryotes and eukaryotes is still under current research, but the basics are understood. It is very much a matter of complexity, as eukaryotes are more complex in many different ways. I found a very useful reference for this and other kinds of related questions. Briefly, some possible reasons:

[...] in eukaryotes, the DNA template is compacted by the way it winds
around proteins called histones. [...]

The DNA-sequence is not as easily accessible in eukaryotes, the unwrapping and re-wrapping of the DNA takes some time.

[...] The coordination of the protein complexes required for the steps of
replication and the speed at which replication must occur in order for
cells to divide are impressive, especially considering that enzymes
are also proofreading, which leaves very few errors behind. [...]

This underlines another rather important factor. The speed of the polymerases replicating DNA is very much related to their accuracy.

[...] This proofreading capability comes with some trade-offs: using an
error-correcting/more accurate polymerase requires time (the trade-off
is speed of replication) [...]

And just for completeness, here is a compete overview of DNA replication in the three big systems.


How to distinguish those flowers in outskirts: hawkweeds (Hieracium), hawksbeard (Crepis) and hawkbits (Leontodon)?

It's quite hard to answer this question and the best would be to follow a flora, which I'll not just copy informations from to past here.
So following are general observations subject to numerous exceptions.

Hieracium generally have lanceolate to oval leaves, not or little toothed, most hairy.

Crepis and Leontodon have generally Taraxacum-like leaves, that means, dentate to lobed.

Some Crepis have leafy stems (but some don't), while Leontodon always have their leaves concentrated to the base, forming a rosette.

[edit on 2014, october 2]

Be aware that there is another genus of the Asteraceae family which may be mistaken with the Crepis/Leontodon/Hieracium group, although it's easier to distinguish. It's the Hypochaeris genus.

Hypochaeris have few but not so homogenous species as there are within the other genera.
Hypochaeris radicata (which may be the most common species in France and wester Europe) have all its leaves basal, forming a rosette and sticking to the ground (never erected). These leaves are always lobed (neither entire, nor toothed), with erected hard hairs covering there upper faces.
Hypochaeris maculata may be mistaken with some Hieracium : it have hairy smooth entire leaves wich are (all or mostly?) basal forming a rosette.

[Addition on August, the 5, 2014]

Also Leontodon and Hypochaeris have hollow stem just below the capitulum(1). When you press the stem just below the capitulum, you fell it flattens under your finger, and if you use the nail to make an incision in the stem, you will see it is hollow like a pipe.

  NB : Taraxacum also have hollow stems but they are fully hollow (from the base up to the capitulum), while Leontodon just have the upper part of the stem which is hollow.

Leontodon are almost always monocephal, that means, the stems are not branched : they have only one capitulum per stem, while Crepis and Hieracium and Hypochaeris mostly (if not always) have branched stems carrying several capitula.

(1) the capitulum is the type of inflorescence in the Asteraceae family. It's also called "head" (and actually, "capitulum" is the latin word for head).

You may like to have a look at this page [in french] presenting some common yellow and ligulate weeds from the Asteraceae family to get some illustrations of what I explained here.


Possible complications due to gene-therapy?

Your question is too broad. It is better to take some specific example.
Not all cell's in the body divide. If you take cell out of the body and want to return it back, it must divide. So we probably could talk about stem cells for example. The stem cells don not really sit in one place. And it almost impossible now to get such cells from the place that they sit in it, and then return in back. It is possible with bone marrow for example.

If we take some example, like ALS - some percent of the disease is thought to be genetic. But the mutation is in all the body cells. Mostly it's affects astrocytes, microglia and motor neurons. You cant take them out of the body, fix and return back. The only chance to fix is to work inside the body. For example by using some sort of virus (AAV for ex.) And CRISPR.

However, if we follow your story and we insert cells with genomB, they will live together with cells with genomA, if there is not some bigger mortality of the original cells.


Will the climate change help the trees to grow?

I don't think anyone knows for sure. It will certainly depend on which spatial location, and which tree species, you're thinking of: while "global average effect on growth (e.g. measured by change in net ecosystem exchange of forested ecosystems) of all tree species" is at least well-defined, it will be an average across an enormously variable set of communities, and species within communities. Some of the relevant factors:

if you count the direct effects of increased CO$_2$, this will generally increase growth rates, although it will be highly variable across ontogeny (life stage, i.e. seedling vs sapling vs adult) and species. In general changes in growth rate will be higher for seedlings and for early-successional/fast-growing species, which may in turn change community structure: see Bolker et al. 1995 for one synthetic study of this.
increased temperature would be expected on average to increase growth rates
decreased moisture availability (potential evapotranspiration) would be expected on average to decrease growth rates
increased microbial activity (e.g., due to increased temperature and/or moisture availability) would be expected to lead on average to increased nutrient availability, increasing growth rates
if you're just measuring "net biomass accrual to trees", then changes in large-scale disturbance (wildfire, windstorms, pest and pathogen outbreaks ...) will tend to decrease standing biomass (although it may also lead to temporary pulses of increased carbon accrual as forests re-grow after disturbance)
note that almost all of these driving factors (temperature, precipitation, water availability, frequency of disturbance) will themselves vary a lot in space.

For a summary, you could start by looking at Purves and Pacala 2008 for some of the ways in which people are trying to put these pieces together.


How to know the gestation time of pregnant mice?

This is generally done by checking for the vaginal plug in the female after you have set up the breeding. If the plug is visible then it means that copulation has happened. However, this is not a foolproof test because the vaginal plug just indicates copulation and not pregnancy. This, nonetheless works in most cases and helps you in timing the pregnancy (Reference: JAX notes).

  For most strains, the rate of pregnancy is highest among
  estrus-suppressed females with vaginal plugs found the third day after
  being placed with a male. As examples, whereas the rate of pregnancy
  is ~100% and 44% respectively for C3H/HeJ and BALB/cJ females with
  plugs found on the third day, it is only 62% and 31% respectively for
  those with plugs found on the fifth day. In contrast, whereas the rate
  of pregnancy for C57BL/6J females is only 39% for those with plugs
  found on the third day, it is 69% for those with plugs found on the
  fourth day.

  If the plugged female is pregnant, the first day of gestation is
  considered to be the day after the plug is found.

You can also monitor for an increase in weight of the mouse. This is not a foolproof technique but serves as a secondary evaluation method.

If you have not timed your breeding and checked for these markers, then you may have to rely on ultrasound.


Why has our nose evolved with the nostrils facing down?

I have not been able to find any studies that look specifically at the genetic mechanism for nose development. I certainly do not know but I'll offer up two hypotheses.

My first hypothesis is that the elongated nose is a remnant of the elongated lower face of our ancestral species, as you note in your answer. Take a look at this brief YouTube video (1:17 long, the part relevant to this answer begins at 33 seconds) of a time-lapse composite showing the develop of the human face. Our face develops as two separate halves that meet together in the middle. That's what creates the philtrum under our nose.

Watch the especially carefully from the 54 second mark to 1 minute mark. Note that our nostrils are pointing directly forward and the overall region looks somewhat like a pig snout. The mouth is vertical aligned with the front of the nose. The overall face is much more rectangular and the eyes are on the sides of the face.

Then, the face begins to become rounder and flatten. The eyes move to the front of the face and the recesses our our eye sockets recede. The lower face below the nose recedes, becoming flatter. The only part that does not recede is the nose area. The flattening of the lower face may actually cause the nostrils to turn downward.  Our nose does not develop outward from a flat face but instead is left behind as the rest of the face flattens.  This would be my initial thought as the primary reason for the shape of the nose and direction of the nostrils.

My second hypothesis (and honestly independent of the comment by @Remib) is related to our sense of smell and taste. Although our ability to detect flavors is a complex process, the primary sense involved is smell (Shepherd 2006). Therefore, downward-pointing nostrils are located directly above the mouth so we get a good smell of the food just before it enters the mouth, perhaps enhancing our flavor-sensing ability.

  Shephered, G.M. 2006. Smell images and the flavour system in the human brain. Nature 444: 316-321.

Note that these two hypotheses are not mutually exclusive. The downward pointing nostrils may be a remnant of our facial development but provides an (adaptive?) advantage for flavour perception.


What is indirect vs direction selection of genes?

Direct selection is when the fitness is directly associated with a certain gene. The beneficial alleles of this gene get selected.

When an allele gets selected not because of its direct effect on fitness but because of other reasons for e.g. strong linkage with other genes which in turn are being selected, then it is said to be undergoing indirect selection.

From Kirkpatrick and Barton (1997)

  Female preferences have caused the evolution of extreme male mating
  displays throughout the animal kingdom (1–3). One mechanism that might
  establish these preferences is indirect selection, which occurs when
  preference genes are associated (that is, in linkage disequilibrium)
  with other genes that are spreading under selection. Indirect
  selection is invoked by two types of theories (2). The first are “good
  genes” theories, which interpret male mating displays as indicators of
  high viability. In this view, the expression of the male display is
  correlated with the presence of alleles that increase viability.
  Because associations naturally develop between preference genes and
  male trait genes, as the high viability alleles spread by natural
  selection, preference alleles for extreme displays also spread. The
  second class of theories that postulates indirect selection involves a
  “runaway process.” Here alleles that exaggerate a male mating display
  decrease survival but nevertheless spread because they enhance male
  mating success. Genes for extreme preferences can then be established
  as the result of their associations with these spreading male trait
  genes.


What hold and inject pressure to be used in microinjection?

It depends on volume that you want to inject and the width of your needle! Try to optimize the pressure by measuring the volume that you inject in mineral oil (I use grid in the objective to measure the drop size). You will decrease the volume by decreasing the injection pressure, of course. I work with zebrafish embryos so I am not sure if it is the same since it's in the water, but for DNA injection (1-2 nL) I normally use Hold Pressure 2 kPa and Injection Pressure 20-30 kPa.


In plants why are potassium and nitrate ions absorbed faster than any others?

Since plants absorb minerals, like potassium, calcium, sulfur, etc. in their ionic form, like K+, NO3-, SO42-, Ca2+, they need to absorb them actively. Since these ions are charged, they have difficulty while passing through the plasma membrane. Hence, plants need to expend energy in order to transport them. For this, they use ATP and membrane transporter proteins. These transporters transport ions across cell membrane with an accompanying ion (H+) so as to maintain electrochemical gradient. As a result (partly), these transporters are highly selective for the ions they carry. For example, a K+ transporter will not transport SO42- or another ion. See this answer to see how transporters achieve this selectivity.

The above part explains how ions are transported in plants. Now, lets come to the main question i.e. why some ions are transported faster than others. Well, there is no definitive answer to this (at least none that I know of). But I can think of two possible reasons for this (using only the examples of K+, Ca2+, NO3- and SO42-):

Magnitude of Charge: one fact here is that both K+ and NO3- have a charge of $\pm$1, whereas Ca2+ and SO42- have a charge of $\pm$2. So what? This makes their transport a bit more difficult. For example, to transport K+ across the membrane, the transporter would antiport 1 H+ for 1 K+, whereas a similar antiporter would transport 2 H+ out to bring 1 Ca2+ in. Obviously, this does not explain the difference between ions with same charge, which the following point seems to do.
Requirement: one of the most important points to keep in mind here is the difference in requirements of different ions by the plant. This is why plant macronutrients (i.e. required in large quantities) have been divided into primary macronutrients (N, P, K) and secondary macronutrients (all others, including Ca, S, Na). As you see, nitrogen and potassium are mostly the limiting factors of crop production. This is why plants require them in large quantities, and hence try to absorb them as fast as possible. This, partly again, explains why K+ and NO3- (the only artificial nitrogen source other than NH4+) are absorbed faster by plants while Ca2+ and SO42- are absorbed slowly.

References:

Mineral Absorption - Wikipedia
Secondary Plant Nutrients: Calcium, Magnesium, and Sulfur - Mississippi State University


How can we know or measure pain in animals?

Pain is subjective

Pain is a subjective experience; you cannot even tell with certainty how much pain your fellow human is experiencing, which is why we ask people; they then can tell us. Pain relief (both physical and emotional) is a significant part of medicine, yet we still have "pain scales" for self-reported pain, one of the more common ones being the Wong-Baker Faces Pain Rating Scale:

Now, note well that even this scale must be interpreted for the patients. For instance, a patient might look like a 6, but be reporting a 10, in which case, a nurse must try to ascertain their actual level of pain.

My point is evaluating pain is contentious even in humans who can express themselves.

Definition of pain

The International Association for the Study of Pain (IASP; www.iasp-pain.org) defines pain in humans as

  an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Pain usually involves a noxious stimulus that activates nociceptors in the body that carry signals to the CNS where these signals are processed (and generate responses) including the “unpleasant sensory and emotional experience.”

The following are examples of common types of noxious stimuli for different tissues:

  Skin: thermal (hot or cold), mechanical (cutting, pinching, crushing), and chemical (inflammatory and other mediators released from or synthesized by damaged skin, and exogenous chemical stimuli such as formalin, carrageenan, bee venom, capsaicin)
  Joints: mechanical (rotation/torque beyond the joint’s normal range of motion) and chemical (inflammatory and other mediators released into or injected into the joint capsule)
  Muscle: mechanical (blunt force, stretching, crushing, overuse) and chemical (inflammatory and other mediators released from or injected into muscle)
  Viscera: mechanical (distension, traction on the mesentery) and chemical (inflammatory and other mediators released from inflamed or ischemic organs, inhaled irritants).

Animals need us to interpret their pain into language. For political and emotional reasons, humans are ill-disposed to do so (how could we then justify eating, exploiting, experimenting on animals, etc.). Even into the late '80's, veterinarians were taught that animals didn't perceive pain per se.

How we know animals understand pain

To determine whether animals can experience actual pain (not simply nociception), it is necessary to show that they

  can discriminate painful from nonpainful states; make decisions based on this discrimination in a way that cannot arise from evolved nonconscious nociceptive responses; demonstrate motivations to avoid pain; and display affective states of fear or anxiety if threatened with noxious stimuli. In addition, animals experiencing pain might be expected to exhibit spontaneous behavioral changes including sustained signals of distress and impairments in normal behaviors such as sleep.

Animals show all these behaviors. Additionally, there is ample evidence that emotional pain in animals is real. The mere threat of foot shock (electric) induces signs of stress in rats and mice that can be alleviated with anxiolytics (drugs that reduce anxiety).

Even fish show responses to a painful event: guarding behaviors, unresponsiveness to external stimuli and increased respiration, all of which improve with morphine. This is called analogous evidence: evidence that they are, mechanistically at least, directly analogous to pain responses in more complex animals.

Humans are animals

The nervous system of mammals is fairly identical to our own (we are animals). A chimpanzee who is afraid of a pin after being stuck with one 20 times in a row clearly feels physical pain and fear. That a chimp can mourn the death of a parent by not eating and not moving for days clearly indicates that they can experience emotional pain.

In summary:

Pain is subjective. I cannot really tell exactly what you feel if your arm is ripped off (your bird-wing example) or (don't read if queasy type)

   if you are given an electric shock, your throat is slit and, while still bleeding, you are dipped in boiling water to remove your body hair in a whole body hair plucker (which is how most poultry - usually males, not hens, btw - meet their makers).

By definition, only you can tell us.

But common sense and experience tells us it would be painful. And, yes, animals feel pain pretty much exactly like we do. Because we are exceedingly "more alike" than we are "slightly different".

Can animals feel pain?
Pain in Research Animals: General Principles and Considerations
Which Responses Indicate Pain and Which Nonhuman Vertebrates Display Them?<- read this if you really want to know
Evolution of pain


Is there such thing as "half-life" of dopamine?

Dopamine (DA) secreted by neurons is selectively reuptaken by the dopamine transporter (DAT), present on nerve terminals.

(source: inist.fr)

Image source: Plasma membrane monoamine transporters: structure, regulation and function - Torres et al. - Nat Rev Neurosci., 2003

DAT acts as a symporter, using the Na+ and Cl- gradients to generate the energy required to transport DA back in the cytosol.

The mechanism of reuptake has been investigated in vitro allowing the description of a model for DA reuptake by DAT.

In particular, from the abstract of this paper:
A multisubstrate mechanism of striatal dopamine uptake and its inhibition by cocaine. - McElvain and Schenk, Biochem Pharmacol., 1992

  Dopamine uptake was found to be first order in dopamine with a Vmax of 582 pmol/sec/g wet weight and a Km of 1.2 μM. The results of experiments in which choline and isethionate were substituted for Na+ and Cl−, respectively, suggested that the uptake process is second order in Na+ and first order in Cl−. Multisubstrate analyses of the initial velocities of uptake over the concentration range of 0.025 to 1.5 μM dopamine suggested that the mechanism of binding of dopamine to the uptake carrier is a partially random, sequential mechanism where dopamine or Na+ binds first with the uptake carrier and Cl− binds last.

A transport scheme is reported in:
Dopamine Neuronal Transport Kinetics and Effects of Amphetamine

  Scheme 1 is a kinetic scheme for a simple carrier adapted from that of Stein (1986) for the DAT. The subscripts o and i represent the outside and inside, respectively, of a DA neuron. Scheme 2 describes a possible mechanism for
  the cotransport of another species. All symbols are as in scheme 1 except that A corresponds to amphetamine.

From the text

  This scheme describes transport as a series of steps: the competition between binding and dissociation of the substrate to the transporter on the  extracellular side, a similar process on the cytoplasmic side, and an equilibrium between the unoccupied transporter facing toward the extracellular or cytoplasmic side. The driving force for inward transport arises from the cotransport of Na1 and Cl2 as well as the membrane potential difference
  (Stein, 1986; Sonders et al., 1997). Biochemical (Krueger, 1990) and electrophysiological (Sonders et al.,1997) studies have established that DA transport is accompanied by transport of at least two Na1 ions and one Cl2 ion and that DA transport can be bidirectional in isolated preparations.


Can the concentration of a kinase be used to identify its substrate?

The concentration of a kinase is completely independent of the concentration of the substrate, and vice versa. In a typical kinase cascade (such as the Ras→Raf→MEK→Erk pathway), signal transduction is generally amplified with each successive step. A relative small population of one kinase (like Raf) phosphorylates orders of magnitude more of its substrates (like MEK1/2), which in turn phosphorylate orders of magnitude more p44/42 MAPK (Erk1/2) molecules. These then phosphorylate transcription factors like c-Myc which translocate to the nucleus and affect the expression of target genes. Over time, protein levels inside the cell are changed, including the levels of the various components of the pathway or their inhibitors (such as phosphatases, components of the protein degradation machinery like ubiquitin ligases, etc.), allowing for regulation of the signal.

Therefore, for any given kinase at any given time post-stimulation, such as with a growth factor, the concentration and phosphorylation state of its substrate(s) can vary tremendously. For example, in the classical NK-κB pathway, activated by TNFα, one of the main substrates of the IKKα/IKKβ kinase complex is the inhibitor IκBα, which upon phosphorylation is rapidly ubiquitinated and degraded by the proteasome. However, one of the first target genes of the activated NF-κB p65/p50 transcription factor dimer is Ikba itself, which negatively regulates activation of the pathway.

I don't know exactly what information your data set contains, so I can't comment too much on your results. However, just graphing substrate concentrations that correspond to kinase concentrations at various time points will only give you one piece of information - that some substrates have grossly similar concentrations to the kinase - which means nothing. All that is is confirmation bias - you've decided on your result, then picked the data that confirm it. I bet if you were to graph the concentrations of direct substrates along with your kinase, you would find no relationship whatsoever, because as I've described above, there is none biologically.


How does an octopus eye react in free fall?

Statocysts are composed of a spherical structure with smaller granule statoliths inside; the orientation of these granules is recepted by cilia receptor cells. So in a situation like the ISS, statoliths would be randomly floating around, being recepted by cila receptor cells. At some times, the distribution of statoliths may be concentrated on one side, triggering random changes in the direction of the eye. So in this situation, the direction of the eye may be constantly changing.


Understanding food composition data from USDA for Vitamin A

The corrected answer: It seems that the both rows from your table show the same thing: the sum amount of all vitamin A-related substances, but in different units; the 1st row in RAE and the 2nd row in IU.

As I said before, according to ods.nih.gov, 1 IU retinol = 0.3 mcg RAE, but this conversation is true only for retinol (the true, "pre-formed" vitamin A), which is found only in animal foods.

The main vitamin A-like substance in plant foods, such as carrots, is beta-carotene and the conversion rate is: 1 IU beta-carotene = 0.05 mcg RAE, so the 20-fold difference between 835 mcg RAE and 16,706 IU now makes sense.

Why to complicate this?

Large amounts of vitamin A (retinol) can be toxic. The upper tolerable level (the amount that should cause no side effects and is not nearly toxic) for retinol for adults is 3,000 mcg RAE. For example, 100 g of chicken liver contains 4,296 RAE of retinol. (You can also see that for the liver, 4296 RAE/14378 IU = 0.3, so this explains again that the two rows are the same thing.)

You can see that the same IU of vitamin A in animal foods is translated into much more RAE than in plant foods. This is also why high IU of vitamin A in animal foods can be (potentially) much more toxic that the same IU of plant foods.


How to run agar gel electrophoresis at home

There are a few reasons why this is usually not suggested.

DNA itself is not visible (at least not in the quantities you'd run on your gel). You need a compound (dye) that binds to the DNA to make it visible, and because they bind to DNA most of these compounds are carcinogenic. Even if you use such a dye, many of them only show up under UV light, an additional difficulty. You could also buy a safe dye that works and is visible, but that makes staining also more laborious. Food coloring will be visible all the time, already when running the gel.
The nice CSI gels you see on TV are showing (supposed) PCR products of short tandem repeats, giving you nice bands at different heights on the gel. These bands also have a convenient size for gel electrophoresis. Restriction analysis of plasmids is also something you'd see more often, and also here the pieces are between 100 and 10,000 bp. DNA extracted from plants consists of genomic DNA, huge strands (millions of base pairs) that will not really run on an agarose gel. Getting a selection of discrete-sized DNA fragments is really not so easy in your kitchen, that's why they go for food dyes.


More extreme phenotypes when parents are from diverged populations

Yes, it would be reasonable to expect greater variation in the offspring of the Canadian woman.
Human genetic variation is the genetic differences among populations. Populations have access a pool of genes and over-time polymorphisms may arise to create greater variation.
Human populations within a species are defined by, divergence times and rates of gene flow - From mitochondrial, X and Y chromosome re-sequencing data.
Genetic Distance is the genetic divergence between species or between populations within a species (as in your example above). Populations with many similar alleles have small genetic distances. This indicates that they are closely related and have a recent common ancestor.
E.g. Height as you use for your example is a polygene. The inheritance of many genes alter phenotypic height of offspring.
Thus, it would be reasonable to expect a difference in allelic variations pertaining to height from the Canadian woman. The offspring may have a different height profile of alleles, and thus a different phenotypical height.
I should mention that:

"individuals from different populations can be genetically more similar than individuals from the same population"

But the above example - should not be expected.


ANF (Atrial Natriuretic Factor more commonly known as ANP - atrial natriuretic peptide) squeezes (vasoconstricts) the efferent arteriole. This means the pressure in the glomerulus is higher (like if you squeeze the end of a hose) and so more fluid is squeezed out i.e. the glomerular filtration rate (GFR) is higher. It also dilates the afferent which means more fluid is going in, further increasing GFR (Marin-Grez et al.)


Advanced books about molecular biology and genetics

Molecular Biology of the Cell is a great text book, and an older edition is available for free on NCBI bookshelf. However, the book covers a broader range of topics than perhaps you're interested in and may not go into the same depth as others (though I haven't actually done a side-by-side comparison).

Watson, who along with Crick developed the central dogma of molecular biology, literally wrote the book on this subject: Molecular Biology of the Gene. It sounds exactly like the text book you’re looking for, and was one of my favourites as an undergrad. You can check out the contents of the book yourself to make sure it's what you want.


For the neurobiology I'd recommend to read: Mapping the Mind and The Quest for Conscioussness , but these are kind of long books.

For shorter articles as (merely) an introduction, I'd recommend:

Manoli, D. S., Meissner, G. W., & Baker, B. S. (2006). Blueprints for behavior: genetic specification of neural circuitry for innate behaviors. Trends in Neurosciences, 29(8), 444–451. https://doi.org/10.1016/j.tins.2006.06.006

Good philosphical and historical viewpoint can also be found here:

Marler, P. (2004). Innateness and the instinct to learn. Anais Da Academia Brasileira de Ciencias, 76(2), 189–200. https://doi.org/10.1590/S0001-37652004000200002

For something more practical: The Little Black Book of Neuropsychology.

Looking forward to suggestions by others :)


What is the distinction between the terms detrivores, decomposers, saprotrophs and saprozoic organisms?

Detritivores consume (eat) detritus.

Saprotrophs feed on dead organic matter by the means of extracellular digestion.

Saprozoic organisms are protozoans that are saprotrophs. This actually comes from an obsolete classification of plants and animals where bacteria and fungi were grouped with plants and were therefore called saprophytes if they are saprotrophic. Protozoans were considered animals; so saprozoic.

Decomposer is a broad class including both detritivores and saprotrophs.

Scavengers also consume dead organisms. They are distinct from detritivores because the former consumes a relatively larger amount of dead matter. Often, scavengers are the first to consume dead organisms; the leftovers are processed by decomposers.

I could not find any authoritative source for these definitions. A peer-reviewed article by Getz (2010) attempts to classify organisms based on their eating habits.


Why calf thymus DNA is widely used instead any other body part?

I have crawled through google and many, many journal articles. What I can make of it, is:

"It is generally agreed that from mammalian cells (as, for example, calf thymus..." are capable of yielding high molecular weight DNA from cells, with very little protein present to decrease purity. [From Welsh and Vyska]

Additionally:
"Calf thymus gland is a fairly good source of replicatiue deoxynucleotidyl
transferase (deoxyribonucleic acid polymerase)" [From Yoneda and Bollum]

So we have a good DNA coming from the calf thymus. Calf thymus is also something we have in great abundance (worldwide slaughter of cattle) and I don't know of any other demand for it (don't know of anyone eating it?). So it should be effective and not too expensive, relatively.

Perhaps there is a difference between the thymuses (thymi?) of calves and adults, given the immune role of the thymus, it's possible. But I can only speculate on that.

And yes. It does seem a bit weird. But it works and everybody does it, so we seem stuck with it.

My two sources:

Richard S. WELSH / Karel VYSKA, Relationship between the Purity and Molecular Weight of Calf Thymus DNA, Hoppe-Seyler's Z. Physiol. Chem.
Bd. 362, S. 969-981, Juli 1981

M. YONEDA AND F. J. BOLLUM, Deoxynucleotide-polymerizing Enzymes of Calf Thymus Gland, THE JOURNAL OF BIOLOGICAL CHEMISTRY, Vol. 240, No. 8, August 1965


What is the minimum population size that Hardy-Weinberg calculations can be applied to?

You can use power analysis to work out answers depending on the specifics of your data. The things you need to consider are:

The power of the test. This is the probability that the test will
fail to reject the null hypothesis even if in truth it is false
(Type II error). If the population is not in equilibrium, what is
the probability that the test will fail to detect this? This will largely depend on the costs of a Type II error. If the experiment is expensive in terms of time/money/animals used etc. you would want to make sure it will give a sold answer at the end.
The significance level. 0.05 is commonly used. The probability that
the null hypothesis is rejected even though it is true (Type I
error). If the population is in equilibrium, what is the probability
that the test will erroneously say it is in disequilibrium.
The degrees of freedom. The number of alleles.
The effect size. This is how far away from equilibrium you expect
your samples to be. The largest effect size would be extinction of
one allele. However, if two alleles are in a ratio of 100:101 across
the full population, this is a small effect size.

For the Pearson's Chi-squared test we can use (in R)

library(pwr)
pwr.chisq.test(w = 0.3, N = 40, df = 4, sig.level = 0.05 )

A rough guide for effect size (w) is 0.1, 0.3, and 0.5 for small, medium, and large effect sizes. There is more detail here. N is the total number of data points, df is the number of alleles. This function will give us a value for 1 minus the power of our test. A value of 0.9 means there is a 10% chance of failing to detect an effect that truly exists.

If we want to work out a suitable number of data points to collect we must decide what power we want. Say we decide that a 0.01 chance of doing the test, but failing to detect disequilibrium if it exists is acceptable.

pwr.chisq.test(w = 0.3, df = 4, sig.level = 0.05, power=0.99 )

tells us that 280 data points are needed.

Without estimates of effect size or a number of genotypes it is hard to give a straight answer to your question, but 5 per genotype seems very small.

If you have only two genotypes, you might choose to use the Fisher Exact Test in which case you can use power.fisher.test() in the statmod package. The definitions of effect size and degrees of freedom are slightly different but the idea is the same.


What is the difference between an antibiotic and an antibacterial?

An antibacterial is any compound that will kill or at least slow down the growth of strictly bacteria, a domain of prokaryotes.

An antibiotic is often used synonymously, but denotes a compound that kills or slows down the growth of any cellular pathogen, prokaryotic or eukaryotic. So, certain antibiotics can kill bacteria, fungi and parasites but antibiotics have no effect on viruses and prions.


Can stem cells from male convert to cells of female-only organs, and vice versa?

I am assuming you are talking about embryological stem cells and embryological development of genitalia.

The answer is no.

Male stem cells have XY chromosomes. Y chromosome is the sex determining chromosome with SRY gene that determines testes development. Absence of the Y chromosome leads to female development by default. That is why XX forms women and there are people with only one X chromosome which are women. (Turner's syndrome)

It might be possible that SRY gene undergoes a mutation and the gene isn't expressed. There are Y chromosome linked diseases.

You should read up about Y chromosome and development of genitalia.

https://en.wikipedia.org/wiki/Y_chromosome
https://en.wikipedia.org/wiki/Development_of_the_reproductive_system


What is the extent of the effect of Tris on E. coli?

The cited article describes effects of Tris on the outer membrane of E. coli. Like all Gram negatives E. coli has an inner (or cytoplasmic) membrane which is a typical phospholipid bilayer membrane containing many membrane proteins including transporters and, of course, an electron transport chain. Surrounding this there is a layer of peptidoglycan, and then the outer layer of the cell envelope is the outer membrane, which is a special (highly atypical) bilayer structure containing phospholipid and lipopolysaccharide as well as a number of proteins including the porins. The space between the two membranes is the periplasm, or periplasmic space which contains a number of small secreted proteins.

The outer membrane is susceptible to disruption by a number of treatments including EDTA treatment. For example, many cell lysis procedures for E. coli use EDTA to disrupt the outer membrane sufficiently to allow lysozyme to gain access to the peptidoglycan.

Cells with destabilised outer membranes could display increased fragility, but in general I would imagine that this would not normally cause any specific problems: obviously this would depend upon exactly what your experiments are.

Finally it is worth noting that the concentration of Tris that you will be adding with your kanamycin must be pretty low. Even if you have used 0.1 M Tris you are presumably using a 1000x stock, so the final concentration of Tris will only be 0.1 mM. The work in the cited paper looked at cells resuspended directly in 0.1 M Tris. I don't think that you need to worry about this at all.


I'm in year 5 too; and (with a bit of help of my dad) I have some bits of answers (my challenge of the day).

A paper tissue is principally made of cellulose. And cellulose is a polar molecule. And so is water. So, the paper will easily absorb water.
See these short clips [1] for water polarity and here for cellulose [2].

In plants, xylem vessels are also made of cellulose and that helps the small molecules of water to stick to the vessels walls.
Think of it as a lot of tiny drinking straws made of wood.

There are at least two reasons why water manages to 'climb up' from the roots to the leaves through the xylem.

During the day, when the sunlight is available, water will be consumed by the leaves during photosynthesis [3]. For each molecule of glucose, 6 molecules of water are needed.
So the water already present from the xylem in the leaves needs to be replenished by water (sap) from the twigs, which is replenished by the water from the xylem in the branches,... And so on, till the water is pulled from the roots.[4]
Remember little molecules of water cling to each other because they are polar.  This is why they tend to pull each other up, as they are consumed in the leaves [1'].

And this is why it is important that both the water molecule and the cellulose molecule are polar.  If H2O would be like CO2, there would be no vascular plants as we know them.

But there is no sun, so no photosynthesis, during the night.
Then the stomata, which are holes used by vascular plants to "breath" (
transpiration), are usually closed.
There is also another reason why water moves up the xylem. Here it is.
Roots not only 'pump' water, their role is also to capture nutrients.
These nutrients are like salts, not table salt, more like ions (potassium, phosphorus, zinc, mangnese, etc) which are needed by the plant cells.
So the water is a bit more 'salty' inside the roots.  Water outside the roots tends to try to diffuse into the roots in order to compensate the relative saltiness [5].
This in turn pushes the water from the root below the ground towards the branches.[4]

What is remarkable is that the whole cycle of water is passive, the plant does not spend energy to move the water 'upwards' to the leaves.

Here are a few sources which I can recommend and from which I learned most of these things. Crash course biology.
They talk fast but it's quite funny.

[1] water polarity: 'Water - Liquid Awesome: Crash Course Biology #2'
https://youtu.be/HVT3Y3_gHGg?list=PL3EED4C1D684D3ADF&t=171
[1'] To picture molecules of water pulling one another up the xylem... well:
https://youtu.be/IlmgFYmbAUg?t=154 (Monkey chain in Madagascar 3)

[2] cellulose: ' Plant Cells: Crash Course Biology #6'
https://youtu.be/9UvlqAVCoqY?list=PL3EED4C1D684D3ADF&t=255

[3] Photosynthesis ' Photosynthesis: Crash Course Biology #8'
https://youtu.be/sQK3Yr4Sc_k?list=PL3EED4C1D684D3ADF&t=75

[4] For a simple presentation of xylem, I use Simple English in
https://simple.wikipedia.org/wiki/Xylem_vessel
and 'Vascular Plants = Winning! - Crash Course Biology #37'
https://youtu.be/h9oDTMXM7M8?t=373

[5] Osmosis (water compensating solutes) "In Da Club - Membranes & Transport: Crash Course Biology #5"
https://youtu.be/dPKvHrD1eS4?list=PL3EED4C1D684D3ADF&t=148

Ian (and dad <= all errors and approximations are his :) ).


Does a piezoelectric organic substance exist?

I think your question is a bit specific, but piezoelectric organic substances do exist. There was a paper in nature that researchers at Berkeley published.

Please see the following journal article:
http://www.nature.com/nnano/journal/v7/n6/full/nnano.2012.69.html#affil-auth

Also see the following public article:
http://www.extremetech.com/extreme/129389-berkeley-scientists-turn-harmless-virus-into-piezoelectric-generator


can the face of a person be accurately predicted from DNA information?

Not accurately. Assuming the DNA information is the DNA sequence, you can't tell which genes are being expressed and which are being silenced. These are through chemical groups on the DNA which aren't generally picked up.

Also there's the environment that grossly affects what you look like, how much you weigh, your skin colour and cosmetic surgery.


I'm surprised this term shows up much anymore. Though it's a part of history now, the following paper by Woese demonstrated the three domain system long ago.

This, however, is the net result of the sequenced genomes of eukaryotes, archaea and bacteria:

Source: Toward automatic reconstruction of a highly resolved tree of life.

The phylogenetic differences between these organisms shed light that bacteria and archaebacteria were not as closely related as was initially though, hence the abolishment of Monera.


Chlorophyll is a dye that makes leaves green, it plays a key role in photosynthesis. It is present also in unripe fruits, young peas etc. Maybe I should say chlorophylls, because it is a group of similar chemicals. They get degraded by heat.

(No assistence of microbes needed).

Bonus: Chlorophyll contains magnesium at the molecule core, which facilitates the green color. There were some creative people, who were upset, that the canned cucumbers are not green enough, so they added some copper-containing molecule during canning. It replaced magnesium and was more stable, so beautiful bright green cucumbers were on the market for a while. However, they turned out to be slightly poisonous and are not sold anymore.

Bonus 2: Most varieties of peas change color also naturally as they rippen. The seeds become yellow. The chlorophyll gets degraded in plant metabolism. The chloroplasts, i.e. the cell organelles responsible for photosynthesis change function to become storage organelles called leucoplasts.

(Edit: Ooops, I first wrote that chlorophyll supposedly contains iron. That was wrong, it is magnesium. Iron is present in a similar die called heme, which makes blood red. Probably I am getting too old :-) )


Are progenies factually half-clones of the parents?

A progeny is not a half clone of its parents.

Each cell expresses both maternal and paternal genes. There are no parts of the body or even a cell for that matter that is identical to one of the parents.
When haploid gametes form, chromosomes are randomly segregated. So the gamete receives either paternal and maternal chromosomes (grandparents of the progeny) randomly. This technically means that the gamete is not an exact half of the parent's genome.
During gameteogenesis (production of sperm/ovum), genetic recombination happens between nonsister chromatids of homologous chromosomes (meiotic crossover). This mechanism creates a small shuffle in the haploid genome that the gamete is carrying.


What's the difference between physical (direct) and functional (indirect) protein interaction?

As I understand it, "physical" and "functional" are just two different ways of analyzing an interaction between proteins.
Proteins can and do interact physically, meaning they can bind in specific ways and sites, and this binding can produce changes in those same proteins (like conformational changes), which alter their properties. This is the purely physical analysis of the protein interaction. The functional analysis begins when we ask the questions "What is the role that this interaction performs in the cell/organism/living system?"; "What effects do these changes in the protein are going to create in the cell/organism/living system?". Often a conformational change in a protein induced by an interaction with another activates or inactivates it. In other words, an interaction can create a conformational change that enables (activation) or disables (inactivation) the protein to catalyze a given reaction, and so the referred interaction plays an important function in regulating the protein's activity. For instance, phagocytes (cells capable of phagocytosis) have in their membranes proteins capable of physically interacting with proteins present in pathogens membranes. They physically bind to them, changing their conformation in the process. This is the physical part of the interaction, it is what happens purely physically (and can be studied more deeply). This conformational change will enable the protein to catalyze a series of reactions inside the phagocytic cell that will ultimately lead to the phagocytosis and destruction of the pathogen. This is the functional analysis of the interaction, it is understanding what is functionally achieved by the interaction, in this case enabling phagocytosis (and can be studied more deeply).


You can use this equation to very generally describe the one-compartment pharmacokinetics of a drug:

Cplasma = (Dose*F/Vd)e^(-kt)

Where F is the fraction that is bioavailable and Vd is the volume of distribution of the drug.  These values can be obtained from the Lexi-comp monograph.  If a drug is administered i.v., F = 1.  k in this equation is your elimination rate constant.

Your description of steady state is not correct.  Steady state is reached with multiple administrations of the drug after 3-5 half lives.  We usually assume steady state is reached in 5 half lives.  Here you are only dealing with one administration of the drug and a steady state is never reached.  The drug will be continuously cleared from plasma until Cplasma = 0.  The time that this takes is usually 5 half lives (50% of initial plasma concentration excreted after 1 half life, 75% after 2 half lives, 87.5% after 3 half lives, 93.75% after 4 half lives and 96.875% after 5 half lives).

Without any plasma concentration data, a route of administration, volume of distribution and bioavailability, a proper elimination rate constant cannot be calculated.  Consider the case where an oral drug is only 75% bioavailable.  This means that 75% of the administered dose reaches the plasma and systemic circulation while 25% is cleared initially by stomach acid, digestion, poor absorption from the GI tract, etc.  The elimination rate constant for this drug will be different than for one that is 100% orally bioavailable.


How do I get the current "camera position" in PyMol so I can reuse it in scripts?


If a dead snake reflexively attacks itself, why does it not always attack itself?

It seems that National Geographic were just as curious, in their interview in this article with James Murphy, he states the answer to your final question - that even though the snake is dead, it can still reflexively 'attack' the nearest object - in this case, the remains of its own body - as it is not attached, it is a 'foreign object' and the reflexes result in an 'attack'.


Is There An Initiative To Sequence The Genomes Of Critically Endangered Species?

The seedbank terdon mentions is the Norwegian Svalbard Global Seed Vault located at Spitsbergen island:

http://en.wikipedia.org/wiki/Svalbard_Global_Seed_Vault

However, the closest thing to a concerted initiative for sequencing animals I know of is the Genome 10K project:

http://genome10k.soe.ucsc.edu/

Their list of first 101 vertebrata proposed for sequencing contains 29 species with status RED from the red list. Most of them are only proposed, but the sequencing of the following are already in progress:

crested ibis (Nipponia nippon)
Amur tiger (Panthera tigris altaica)
cheetah (Acynonyx jubatus)
lion (Panthera leo)
domestic yak (Bos grunniens)
bactrian camel (Camelus bactrianus)

and that of the Chinese softshell turtle (Trionyx sinensis) has funding secured. Already complete are the giant panda, the chiru, and the polar bear.

And some surprising fact: where the funding is secured it is/was funded by the Beijing Genome Institute. A shame if this would remain the only one.


Anesthetics, specifically inhaled anesthetics

The following is one of the many elegant statements in General Anesthetic Actions on GABAA Receptors:

  It is the fervent view of the authors that general anesthesia is no different from any other pharmacological process: exogenously administered drugs interact with key sites on cellular proteins in the body which results directly in the alteration in the function of these proteins, in the present case, neuronal proteins that control how information is conveyed through the nervous system.

Isoflurane, Sevoflurane, and Desflurane, the current inhalation general anesthetics, along with Halothane and the intravenous anesthetics Propofol, Etomidate, Methohexital and Thiopental, enhance the function of GABAA receptors (GABAARs), the most abundant fast inhibitory neurotransmitter receptor in the CNS (ligand-gated chloride ion channels) by increasing the affinity of the receptor for GABA. Since these receptors are abundant in parts of the CNS that process higher-order brain functions, it stands to reason that GABAAR function is central to memory, awareness and consciousness. GABAARs are involved in mediating hypnosis, depression of spinal reflexes, and amnesia, three of the classical components of general anesthesia. Isoflurane, Sevoflurane, and Desflurane enhance the amplitude of responses to low concentrations of GABA and prolong the duration of GABA mediated synaptic inhibition.

A very good starting point for your investigations can be found by clicking on the linked article above.

Agent-selective effects of volatile anesthetics on GABAA receptor-mediated synaptic inhibition in hippocampal interneurons
The sedative component of anesthesia is mediated by GABA(A) receptors in an endogenous sleep pathway


What is the name of this beautiful white trees?

If you do a Google Image search with the picture in the question, you'll see the screenshot is from the 2000 movie The Patriot starring Mel Gibson. The movie's filming locations were mainly scattered around South Carolina, on the southern East Coast of the United States. I've spent a lot of time in the region, and the gray-ish fluffy stuff hanging off the branches is almost certainly Spanish moss (Tillandsia usneoides), which is very common in the area.

While it is more difficult to identify the tree, as the bark and leaves are not clearly visible up close, a good educated guess based on the size and shape of the tree would be live oak (Quercus virginiana), which also happens to be one of the primary hosts of Spanish moss.