Does the entire surface of the earth contain organisms?

That will depend on many things. How do you define surface? Is one meter underground still "surface"? How about a kilometer?

Also, how large an area are we talking about? You could probably find a square millimeter in, for example, Antarctica that has no organisms. I don't think you would find a square kilometer with no organisms though.

There are organisms (called extremophiles) that thrive in the most hostile environments we know, they can survive extreme heat, cold, acidity, salinity etc. I found this very nice list:

  Cold – The McMurdo Dry Valleys in Antarctica are some of the coldest, driest deserts on Earth, with average annual temperatures of
  -20oC (-4oF) and less than 10 centimeters (4 inches) of precipitation a year. Scientists have found bacteria in liquid water pockets
  embedded about twelve feet deep in “solid” lake ice. Some of these
  bacteria use chemical nutrients from particles of dirt in the ice and
  use energy from sunlight for photosynthesis.
  Hot – Large concentrations of microbes thrive in Yellowstone National Park’s Grand Prismatic Springs, a hot spring with water
  temperatures up to 90oC (188oF). Other hot springs in Yellowstone are
  extremely acidic, yet are home to many different kinds of bacteria and
  microbes. Many of these microbes use chemical nutrients in the waters
  and energy from sunlight for photosynthesis. Deep underground –
  Scientists have discovered bacteria living in ground- water 5
  kilometers below the surface in deep gold mines of the Witwatersrand
  Basin in South Africa. These microbes thrive in cavities and cracks in
  rocks. Scientists are also are investigating life within and below
  permafrost in north- ern Canada.
  Bottom of the sea – Scientists have found abundant life clustered around hydro- thermal vents on the ocean floor, including bacteria,
  mussels, clams, shrimp, and giant tubeworms that can reach ten feet in
  length. Water pouring out of the vents in the complete darkness
  thousands of feet under the surface of the sea can reach temperatures
  of 113-120oC (235-248oF). The high pressures keep the water from
  boiling. Bacteria use chemicals in the vent’s water, primarily
  hydrogen sulfide, as their energy source instead of sunlight. Other
  creatures survive by eating the bacte- ria or each other.
  High Acidity – The water in the Rio Tinto in southwestern Spain is very acidic, a result of chemical reactions between the water, and
  iron and sulfur minerals in the ground. The river has a deep red
  color, like wine, because of iron dissolved in the water. Microbes
  living in the water use chemical reac- tions with iron and sulfur
  minerals to generate the energy they need. Products from these
  metabolic reactions contribute to the low pH in the environment. Many
  algae and fungi also live in the acidic waters.

As far as I know, there is no evidence of life in molten lava. Apart from that though, just about every habitat you can find on the earth has been colonized by life. Ask your teacher what parts of the earth she is talking about, and report back here.

UPDATE:

MCM's very interesting answer prompted me to do some more research. It seems that life has now been found even in the Atacama (taken from Azua-Bustos
et al):

  For a long time it was thought that regions of the Atacama could not
  uphold any type of life forms. However, recent culture-independent
  methods (metagenomics, transcriptomics, in situ hybridization, etc.)
  have improved the sensitivity for life detection. Thus, microorganisms
  have been found even in the driest areas of this desert, which makes
  scientists wonder about the true limit of water availability needed to
  sustain life as we know it. In this review, we summarize the efforts
  devoted to the characterization of microbial life in the Atacama
  Desert.

So, it seems that life can exist even in the Atacama. That leaves only molten lava...

Reference

Azua-Bustos et al, Life at the dry edge: microorganisms of the Atacama Desert, FEBS Lett. 2012 Aug 31;586(18):2939-45


How do you know which organisms are keystone species?

According to the wikipedia page, a keystone species is:

  A keystone species is a species that has a disproportionately large effect on its environment relative to its abundance.

Thus, you could work out the keystone species in an ecosystem by sampling population size and and what size 'effect' the removal of the species from the ecosystem would have. If you standardised the units of 'effect' for all species in the ecosytem, the keystone species would be those with the highest effect/population fraction. I don't know if there's a critical size of this fraction for a species to be determined 'keystone', but if there is it would allow you to explicitly define a keystone species. This would rule out the problem of interdependency as you mention.


If they are made in different animals you should be fine.  You could do a western with those antibodies though, to double-check.  Looks like Cenp-C is about 106kD and Rod1 is about 60kD.  So on a western, if you see bands at both those sizes with one of the antibodies, you have cross-reactivity between those proteins.  And if you just see the specific band you're looking for, you're good.


Can life subsist on anything else but water?

This may not completely answer your question, but provide some information.

Looking at this Wikipedia outline Non water solvents, other possible candidates are ammonia, hydrocarbons even hydrogen fluoride.

Digging a little deeper, this abstract of the article: "Many chemistries could be used to build living systems." (Abstract only) describes the possibilities of ammonia and liquid nitrogen as being potential suitable solvents.  Page 678 onwards of the article: "Is there a common chemical model for life in the universe?" also describes other solvents such as ammonia (I should say that there quite a lot of Star Trek references in that paper).

I hope this goes part of the way to help.


Do primates other than humans have a consistent sleep schedule?

This is only a partial answer, but a reasonable starting point.

In a blog-article "The Evolution of Primate Sleep", the author identified 3 main patterns - the third pattern seems most relevant to your question.

What he found was that there are 2 divisions of sleep patterns - several primates, such as some species of lemurs are nocturnally active, whereas apes, gorillas etc tend not to be active at night.  Seemingly adapting to the diurnal cycle.  In the article "Mammalian Sleep Dynamics: How Diverse Features Arise from a Common Physiological Framework " (Phillips et al.), primates uniquely undergo monophasic sleep.


Not an experimentalist, so take this with a grain of salt.  But for motility you often need some external factor, e.g. a chemokine or chemoattractant (FMLP is a common one for white blood cells).  Also some cell types may not crawl on bare glass, and might need a protein or gelatin coating.

White blood cells on slides can look like this: https://www.youtube.com/watch?v=JnlULOjUhSQ

Unfortunately, I don't know the conditions used there.  My recommendation is to look through Google Scholar for white blood cell motility or neutrophil motility, and see what turns up.  For instance, the first paper I found was: C S Spada, A L Nieves, A H Krauss and D F Woodward, J. Leuk. Biol. 1994 (PDF) which gives some details about how they got their assays to work, including a gelatin coating for the slides.  However, the details probably depend on the origin of your cells and the type of white blood cell you're looking at.


What non invasive methods of estimating Body Time are there?

For circadian rhythm, the gold standard is melatonin secretion (blood or saliva). Also, core body temperature.

see: Circadian temperature and melatonin rhythms, sleep, and neurobehavioral function in humans living on a 20-h day

James K. Wyatt , Angela Ritz-De Cecco , Charles A. Czeisler , Derk-Jan Dijk
American Journal of Physiology - Regulatory, Integrative and Comparative PhysiologyPublished 1 October 1999Vol. 277no. R1152-R1163


What's the advantage of autocrine signalling?

Why doesn't it just exert an affect while it's already inside the helper T cell?

Because it interacts with membrane-bound receptors. Those are outside so there is no way IL-2 (or any autocrine factor) could signal while inside the cell. It has to exit.

Now, the next question is why the receptor is membrane-bound and outside. As far as I understand there are two parts to this answer:

Receptors are evolutionarily related so they follow similar synthesis pathways.
Membrane-bound receptors are (all?) transcribed while being secreted into the endoplasmic reticulum. This causes their agent-binding portion to reside inside the ER. From there, vesicles bud off, are transported towards the cell membrane, merge with it, and hence the formerly inside portion of the protein ends up on the outside.


Is it possible for a human to get rabies from a rabies vaccine meant for dogs?

It would depend on which vaccine you're talking about, as there are several. Some use attenuated strains of the Rabies virus, others use killed, and some are recombinant glycoprotein vaccines. Here is a list from the CDC of all the rabies vaccines available in the US in 2011 (I wasn't able to find anything newer). Generally speaking, through, one would expect the FDA in the US and the relevant authorities in other companies to require vaccine manufacturers show that their product is safe in other species, in case of accidental exposure, such as you are talking about here. This is especially true of something being given to an animal that is quite often a family pet.

If you think you've been exposed to any type of medication which has not been prescribed for you, including dog rabies vaccine, you should seek medical attention immediately, if not sooner, but based on my experience in the pharmaceutical industry and dealing with regulatory agencies, you should be pretty safe, as the regulations surrounding vaccines are quite stringent.


During the process of correcting mutations via gene therapy, is the defective gene removed?

To be specific: I am talking about adult, somatic gene therapy here, and germline gene therapy experiments is still a landmine when considering ethical reasons.

The defective gene codes for a defective protein, that usually plays a part in pathways. Since the protein is also defective, that pathway is also rendered defective because of this protein, and usually when pathways go defective, bad things happen.

There are three target approaches to gene therapy:

Gene silencing by Antisense Oligonucleotide Therapy
Genome Surgery by ZFN, Crispr/Cas9 etc..
Gene Replacement by viral vectors

The only method that corrects the defective gene here is the genome surgery method. By using Zinc Finger Nucleases, or Crispr/Cas9s, TALENS or other methods like that, the defective protein is corrected at the genome level, which automatically corrects the mRNA and protein, and everything works as it should.

Other methods like Antisense, just prevent the incorrect protein from forming. This is really useful if the defective protein is itself toxic to the body, and a replacement protein can be achieved by masking the defective region to produce a truncated but functional protein.

Gene replacement usually puts in a healthy copy of the gene in, that functions along with the defective copy, and this solves majority of the problems as the affected pathway is no longer rendered inactive, as the healthy protein takes over the defective pathway. The defective protein is still produced, but doesnt do anything (or rather, is rendered moot as the healthy protein takes over) and gets removed during regular maintenance of the cell.

Now depending on the type of disease the individual has, gene replacement may also take place along with gene knockout (depending on if the defective gene is toxic), but obviously many considerations have to be thought about before the combinatorial therapy can be used (toxicity of treatment itself being the primary concern, followed closely by efficacy).

Now obvious question with gene replacement, antisense or any other form of gene therapy is how we get the therapeutic agent to all cells, and yes that is a major challenge, and that's why gene therapy is expensive. And no, the therapy doesn't correct all the cells in your affected tissue, but it aims to correct majority of the cells, and that should restore function (atleast in myopathies like the muscular dystrophies)

As you can see here, in DMD, dystrophin gets muated due to a mutation We can either mask the mutation by Antisense therapy at the level of the RNA (which leads to a functional protein forming), put in an alternative form of dystrophin (mini or micro dystrophin) that takes over the function of dystrophin in majority (if we are so lucky) of the cells, and the overall phenotype of the individual improves. Recent advances in genome surgery are also being investigated for ameliorating disease symptoms. The reason I concentrated on DMD is that, gene therapy for DMD is my PhD. So apologies for the bias.


What would happen if some neurons are unmyelinated?

From a physiological perspective, what could be the consequences if cold receptors were unmyelinated?

Per the resistor-capacitor model of a neuron, one would expect signals conducted through myelinated axons to be faster, more sharply localized in time (spikes don't broaden out as they propagate down the axon), and less costly of energy, vs in unmyelinated axons.

I wouldn't read too much into significance as there's all kinds of ways to accomplish the same effect at any level, e.g. faster conduction is also accomplished through larger axon diameter, and better temporal localization is also accomplished through signal coding, and energy consumption is also modulated by tweaking membrane composition of ion channels etc.

  Would that pose some detrimental effect?

Generally, if it's normal for axons to be unmyelinated then one would expect things to be running normally. Demyelination of normally myelinated axons pretty much always leads to loss of function in sensation or motor control.

The question to ask here is rather "Would myelination of normally unmyelinated afferents pose some detrimental effect?" I'm actually not aware of any disorders in which there is "extra myelination" -- Even the dysmyelination disorders are all loss of function in the proteins, not extra insulating myelin or myelination in the wrong place. That doesn't mean there aren't overmyelination disorders, but does suggest that our nervous systems are less sensitive to overmyelination if it is a thing that happens.

One would expect conduction velocity and energy consumption to decrease, okay. Probably not an issue unless temporal synchronization in that signal is important; even then "plasticity" usually irons out these problems.

If the normally unmyelinated afferent axon normally has synapses homogeneously distributed along its shaft, then abnormal myelination could cause abnormal development of these synapses. As contact area would only be available between myelin "nodes," synapses would be crowded into smaller area. Also depending on how development works in the systems you're considering, overmyelination might affect the spatial pattern of secreted growth factor concentration which could affect synaptic development along the axon shaft. But this is all completely hypothetical.


Does all cells in individual has same mitochondrial DNA?

In a homoplasmic individual, all mitochondria is the same. Therefor will be the same amongst cells and between siblings/mother. Unless some mutation occurs. A homoplastic individual either has all mutated mitochondria or all functional mitochondria of the same type.

A Heteroplasmic individial (more than one type of mitochondria) mitochondria occur when a mitochondria has accumulated sufficient mutations. When a hetroplasmic mother has children, the siblings have varying ratios to each other and the mother.

When you produce oocytes, a selected number of mitochondria are transferred into each. During maturation, there is a rapid replication of mt-DNA, which can lead to a random shift in mutated DNA between the offspring and the mother. This is the mitochondrial bottle neck. Bottlenecks enforce mechanisms that omit cells or individuals, in this context mitochondria, ideally such that only the healthiest mitochondria are transmitted.

In a heteroplastic individual, different cells or populations can have varying amounts of of the mutant mitochondria (including complete homoplasmy).


Surprisingly, it is indeed possible! But, the fact is that the actual process is a bit more complex and might actually require more compounds along with cysteine to give such effects in living beings. First of all, see this image1:

As is clear from the diagram, GSH (glutathione) is also a factor for pheomelanin production, along with cysteine. Another factor on which one might not pay heed is Tyrosinase protein expression. High amount of L-cysteine is thought to decrease the expression of tyrosinase in cells2 (but since I found just one article, I'd suggest to not pay much attention on this point).

Apart from gene expression, cysteine affects tyrosinase itself too. High concentrations of cysteine and glutathione have been shown to inactivate tyrosinase in cells, and the cause has been suggested to be the thiol-group of GSH and cysteine, which somehow generates oxygen radicals and inactivates tyrosinase3. A concentration of 10mM cysteine is sufficient to inhibit tyrosinase activity in cells4. It is because of these kinds of effects that GSH and cysteine are now being used in cosmetics as skin whitening agents as they, in higher concentrations, inhibit tyrosinase activity and hence, melanin production in skin cells5.

Just to add, when it comes to gene regulation, then it seems that cysteine has some more effects too. As pointed out by @Chris, eumelanin production in skin is stimulated by a cascade which involves a receptor known as melanocortin-1 receptor (or MC1R). When activated by one of the variants of MSH, typically $\alpha$-MSH, MC1R initiates a complex signaling cascade that leads to the production of the brown or black pigment eumelanin6. Now, a research has concluded that 0.07 mg/ml concentration of L-cysteine greatly reduces expression of MC1R gene, thus literally leaving no way (not really) for eumelanin production7!

Thus, in short, it is not as simple as "Hey, you want a red skin tone? Here is some cysteine for you!" Cysteine, and other related compounds like GSH, have more complex effect on melanin production than just promoting production of pheomelanin over eumelanin. You can also have a look at this answer (by @Chris) for some more information.

EDIT: To tell where you're going wrong, I'll make two reaction flowcharts. First, this is (IMO) what you're expecting as an answer:

But this is what is actually happening:

The red line is what we're interested in. But as you can see, the diagram is already quite complicated (and expected to get more complicated as more factors are discovered). So, giving a simpler explanation than this would be, very much, impractical or impossible.

References:

Malathi M, Thappa DM. Systemic skin whitening/lightening agents: What is the evidence?. Indian J Dermatol Venereol Leprol 2013;79:842-6
The Inhibition Effect of L-cysteine on Melanogenesis in B16F10 Mouse Melanoma Cells; In-Sook An, Ji-Hye Kim, Hoe-sook Yoo, Rui Zhang, Sang-Mo Kang, Tae-Boo Choe, Tae-Jong Kwon, Sung-kwan An, Gi-Yeon Kim
The effect of catalase on the inactivation of tyrosinase by ascorbic acid and by cysteine or glutathione; Lindbladh C, Rorsman H, Rosengren E.
Inactivation of human tyrosinase by cysteine. Protection by dopa and tyrosine.
Jergil B, Lindbladh C, Rorsman H, Rosengren E.
Mechanisms Regulating Skin Pigmentation: The Rise and Fall of Complexion Coloration; Jody P. Ebanks, R. Randall Wickett, and Raymond E. Boissy
Melanocortin 1 receptor - Wikipedia
Substantial Effect of Melanin Influencing Factors on in vitro Melanogenesis in Muzzle Melanocytes of Differently Colored Hanwoo; Touseef Amna, Kyoung Mi Park, In-Kyung Cho, Tae Jeong Choi, Seung Soo Lee, Kang-Seok Seo, and Inho Hwang


The mushroom suggestive for one of the inki ones of Coprinus family, especially Coprinus comatus. The black color can be very intensive in some stage of their development, since it is a part of the spread mechanism.

"Members of the genus Coprinus have been collectively known as the "inky caps" because of the curious character of autodeliquescence of their gills-- in other words self-digestion to release their basidiospores. Most of these species have gills that are very thin and very close to one another, which does not allow for easy release of the spores. Moreover the elongated shape of mushroom does not allow for the spores to be shot off the basidia and get caught in air currents as in most other mushrooms. Coprinus species "compensate" for this by a sequential maturation of the spores from the bottom of the gill towards the top. After the spores have matured and been released, the gill tissue digests itself and begins to curl up, allowing easy release of the basidiospores above. In other words, the digestion opens up the fruiting body so that spores from further up the gills become exposed to the air and a clear path of spore release. The self-digestion continues until the entire fruiting body has turned to black ink. In the olden days this ink was actually used for writing. The self-digestion is also a way of releasing the spores over a longer period of time, and allowing the release of spores from very closely spaced narrow gills borne inside a longitudinally tall pileus. If any Coprinus species are collected for eating or for scientific study, they must be cooked or dried right away, since the self-digesting enzymes seem to kick into high gear after the mushroom is removed from its substrate. They're pretty easy to find too-- the genus name Coprinus gives you a pretty good idea where to look for these mushrooms-- in dung or very rich organic soil."

examples:
1.

2.

3.


This is not a direct answer to your question, but I want to point out that your basic premise is partially incorrect. Other felines also form social groups. For instance, male cheetahs form coalitions (also see Cheetah outreach at http://www.cheetah.co.za/c_info.html), often for life, which generally makes them more successful in defending territories. Female feral cats also form social groups in some environments (see e.g. Natoli et al, 2007), where females sometimes co-rear kittens. There is even evidence that tigers share kills with related or unrelated individuals (see Wikipedia: Tiger for examples), and tiger home ranges can overlap in complex ways. On the other hand, lions (both males and females) are sometimes solitary, and this partially interacts with their living environment.

My point is mainly that sociality (in general or in felines in particular) is not either/or for a particular species, and other felines also show social behaviours and sometimes form groups (so sociality should be viewed as a sliding scale). Granted, lions are definitely the feline with the strongest social behaviors, and they form the largest social groups. It is therefore interesting to think about why that is the case, and what group dynamics and tradeoffs that determine the social behaviours of lions.


Neuroscience of temperature regulation and perception

I've found a good resource for this--an open-access review by Nakamura, "Central Circuitries for Body Temperature Regulation and Fever." In it, the author provides a nice summary figure of the circuitry involved in temperature regulation (see below). As I suspected, the hypothalmus is pretty central to temperature regulation. I had forgotten about the involvement of the peripheral nervous system in responding to environmental temperatures, which, now that I think about it, makes some amount of sense, but is still pretty interesting. It appears that there's a difference in the specific circuitry and neurotransmitters used in responding to warm and cold temperature (especially GABA v. 5-HT), so I think a reasonable hypothesis regarding the basis of individual differences in the perceived temperature of an external environment might be differences in peripheral 5-HT systems (in addition to differences in body composition). Perhaps someone with a background in the peripheral nervous system could speak to this better than I can, but single nucleotide polymorphisms (SNPs) leading to differences in central 5-HT systems has been an active area of research in the neuroscience community of late (e.g., Nordquist & Oreland, 2010, Gonda et al., 2010), which I think lends some face validity to this idea.


Is it possible to detect whether an organism has been gene edited (by humans)?

If you had access to the DNA of the organism's parent(s) then you could make an inference about whether the child's genome is consistent with being edited, assuming that the edit was done early enough in the embryo's existence for the edit to be present in all/most of its cells. If the organism is a chimera/mosaic, then it may be possible to detect the edit by comparing different tissues within the organism, and identifying differences which do not look like 'natural' somatic mutations.  However, I don't think we have a good handle yet on what the natural range of somatic mutations looks like, so it might be difficult to assess whether any difference found were of an engineered origin.


How does sucrose protect bacterial cells in lysozyme solutions?

This is an interesting question and as often, it has been noted by someone before. In this case it has been a researcher named Claes Weibull, who did his research in the 1950s. He noted (as you did) that sucrose has a protective function on the generation of protoplasts from Bacillus megaterium) with lysozyme. He published the following figure (from the first paper below):

He did not really explain the phenomenon, but speculated about protective function of the sugar in solution when the bacterial cell wall is removed. This also works with PEG in solution (see the third paper below).
He published a number of papers on this (if you look him up in Pubmed, you will find more articles, but these seem most relevant):

The isolation of protoplasts from Bacillus Megaterium by controlled treatment with lysozyme
Characterization of the protoplasmic constituents of bacillus
megaterium.
Osmotic properties of protoplasts of Bacillus megaterium.

It seems also possible to cultivate these protoplasts on agar plates and let them form "normal shaped" bacteria again:

Morphological study of the reversion to bacillary form, of Bacillus
megaterium protoplasts.


Electrocardiogram: Difference between Atrial Fibrillation and Atrial Flutter

A-Flutter will have discernible waves that can be counted, usually. The R-R interval will be regular or maybe slightly irregular if there's a variable conduction block in the AV Node. A-Fib will ALWAYS be completely irregular without discernible pattern.

You can also modify the position of your limb leads. There is an EKG placement called the S5-Lead that basically makes it where the QRS disappears because it's electrical impulse is perpendicular to the monitoring leads. The Atria however, become super-visible on the EKG.

To do S5:
Place the RA electrode on the patient's manubrium.
Place the LA electrode on the 5th intercostal space, right sternal border.
Place the LL electrode on the right lower costal margin.

Then set the EKG to view Lead I


What is the reason behind studying seroprevalence of a disease?

Seroprevalence tests people for the presence of a disease based on serologic methods. Often you do ELISA (or related methods) to test for pathogen specific antibodies.

This gives you information on how common a disease is, especially when it might infect people without them showing symptoms. It also can help detecting cross-protection when the seroprevalence is lower than expected. This is something shown in micronesia, where the seroprevalence was much lower than expected (from: Zika Virus Seroprevalence, French Polynesia, 2014–2015)

  Our findings show that <50% of the population of French Polynesia had
  detectable Zika virus IgG. This seroprevalence rate is much lower than
  the 86% attack rate estimated by Kucharski et al. (14) using a model
  that assumed the French Polynesia population was 100% susceptible to
  Zika virus infection. However, in a setting where DENVs are highly
  prevalent (8), the possibility of cross-protecting immunity preventing
  infection from Zika virus (12,13) cannot be excluded. The attack rate
  and the asymptomatic:symptomatic ratio in French Polynesia were also
  lower than those described for the 2007 outbreak on Yap Island (73%
  and 4:1, respectively) (4); this finding supports the perception that
  the drivers of Zika virus transmission vary depending on geographic
  context. For other flaviviruses, such as DENV, previous model-based
  studies showed that the herd immunity threshold required to block
  viral transmission is ≈50%–85% (15). Thus, if Zika virus has the same
  epidemiologic characteristics as DENV, the seroprevalence rate of 49%
  would not be sufficient to prevent another outbreak.

It can also help to make predictions about the spreading of a disease. With a high seroprevalence epidemic spreading is unlikely, while this is pretty much different with a low prevalence. This is something which was observed in Brazil when Zika occured there first.


SNP

Let's start with the definition that has nothing to do with the rest of the question :). A Single-Nucleotide-Polymorphism (SNP) is a kind of genetic variation that you find in population. This genetic variation is defined as a variation caused by only one single nucleotide (as its name indicates it). For example if you have in the populations the two following variants at the same locus: AGCCGT and AGCTGT, then you have a SNP at the position of the C and T. This type of variation is very common. We estimate that there are about 10 millions SNPs in the human genome. We often use these SNPs as genetic markers.

Ancestral vs derived alleles

An ancestral allele or an ancestral trait (depending on whether you look at the phenotype or a t the genotype) is the trait/allele that was carried by the common ancestor of the taxon you consider. For example: as you may know the taxon Reptilia includes lizards, snakes, turtles, birds, mammals and some other lineages. In the taxon Reptilia, the scales is the ancestral state (still exist in lizards for example) and the hairs and feathers are derived states. Usually, the ancestral state is the one that carried by the most basal lineages.

Identity by state (IBS) and Identity by descent (IBD)

If two sequences are exactly identical, then we say that they are identical by state (IBS). Such identity can occur either through convergent evolution or through common ancestry.

To understand the concept of "identical by descent" (IBD) it is important to understand the concept of coalescence. A coalescent event is, when looking backward in time, an event where two sequences were actually the same sequence. Often IBD is defined relatively to a given threshold in time. If the coalescent event occurs after this event then the two sequences are not IBD. If the two sequences coalesce before this time threshold and that the two sequences are still IBS, then the two sequences are IBD

Bridging everything together

So, if you look at sequences in a given group of lineages and see that they are all exactly the same then they are identical by state. If you know that all these sequences come from a common ancestor and even they all coalesce to a single individual in the common ancestor, then all sequences are identical by descent. But some mutations may have occurred since the last common ancestor resulting in some SNPs, then all the sequences are not IBS anymore and therefore not IBD either. You can use such sequence variance in order to create a phylogeny for example.

Hope that helps.


Have I identified this species correctly? Weird ocean blob

A coworker of mine was able to identify the specimen as a Lightbulb Tunicate, Clavelina huntsmani. The distinctive "lightbulb filaments" that give the species its name can be clearly seen in the pictures I posted:

So it was indeed an ascidian.


Please identify this bone found on the beach

It's an atlas vertebra from a large herbivore, a goat, a young horse, a deer. Also know as the C1 vertebra it's probably a sheep from a mechoui party.


It doesn't matter where the $H^+$ comes from in the context of this information. The textbook is just saying that the aquaporin is permeable to $H_2O$ but not to $H_3O^+$ (nor, presumably, to $OH^-$).

In any aqueous solution, especially in the presence of acids, some of the molecules will be $H_3O^+$. The pH tells you how many. It doesn't really make sense to think about what a solution of $H_3O^+$ would look like.


Is it really detrimental to humans as a species to reproduce with one's own first cousin?

Inbreeding depression, "the reduced survival and fertility of offspring of related individuals" (quoting the linked article), is a well-known and well-understood biological effect. It does, indeed, affect humans.

The problem is that recessive mutations become more likely to affect the survival of the offspring of relatives. Imagine that you have a mutation affecting, say, some gene that's critical to your metabolism, which is entirely possible. But, since you have two copies of the gene and only one of them is faulty, you are not affected by this. Nevertheless, you, by chance, pass the non-functional one on to a couple of your kids, who are also not affected due to only having one copy as well. They, in turn, pass it on to one or more of their kids. Now, two of them, cousins, have a kid. The kid gets both copies and can no longer properly metabolize something due to having two faulty copies of the gene. This can prove to be fatal or at least severely debilitating.

Now, lest you think this is improbable, there are on average 70-something mutations per generation. Some of those will be neutral in effect, others will be detrimental. Once an offspring gets two copies of those detrimental alleles, then there could be serious health effects. The likelihood of an offspring getting two copies decreases as the relatedness of its parents decreases. So, sibling or parent/child pairings would be the most likely to produce offspring with the problems. Pairing between 3rd generation (First-cousins) or any pairings between them and their siblings, parents, aunts/uncles or grand-parents would be the next most likely.

So yes, first-cousins marrying and having kids is a bad idea for very basic scientific reasons.

I missed the "as a species" part of your question. Inbreeding will only likely have an effect within small, closed populations, though it will continue to have a lasting effect even as those populations grow and open up. Two textbook examples are French Canadians and Ashkenazi Jews. Even now, there is continued elevated risk of certain rare genetic diseases in these populations. As for the species as a whole, it is likely to be really detrimental only if the effective population size of the species becomes really low: a general rule of thumb used by conservation biologists is that the effective population size should be at least 50 to avoid the effects of inbreeding (and 500 to avoid the effects of genetic drift) (50/500 rule).

Sorry about the confusion.


Which animals live in trees and make noises like rubber ducks at night?

It is most likely a Tawny Owl (Strix aluco), or Waldkauz in German, one of the most common owl species in Central Europe. These owls have many different calls, and you can hear them often here in Karlsruhe at night. Particularly their "kewick" call sounds similar to squeezing a rubber duck. It is usally emitted by female individuals during the mating season, but also males can produce it. Juveniles have a similar call as well. But most of the time - as far as I have noticed - you only hear their more common "hoo-hoo" calls (listen here or here).

Photo of a Tawny Owl:

Image Source:

https://commons.wikimedia.org/wiki/File:Waldkauz-Strix_aluco.jpg


A currently active cell database is SHOGoiN, which says it is a significant extension of the world-first human cell database, CELLPEDIA.  It focuses on human cells but also has information on mouse, sea urchin, and C. elegans.

The site says:

  The database consists of several modules that store cell lineage maps, transcriptome, methylome, cell conversions, cell type markers, and cell images with morphology data curated from public as well as contracted resources, based on sophisticated cell taxonomy.


Birds have a few adaptations and behaviors to keep their legs warm in cold weather:

Blood vessels (veins and arteries) run very close together or are intertwined:

The arteries and veins intertwine in the legs, so heat can be transferred from arteries
back to veins before reaching the feet. Such a mechanism is called countercurrent exchange. Gulls can open a shunt between these vessels, turning back the bloodstream above the foot, and constrict the vessels in the foot. This reduces heat loss by more than 90 percent. (Wikipedia)

Birds have specialized scales on their feet and legs which act as an insulator.

Birds often alternately tuck their legs into their body feathers to minimize heat loss. (Audubon)

Other survival mechanisms such as shivering and torpor come into play with extreme cold.

Other sources: Mother Nature Network. I don't have my texts handy, but can highly recommend Manual of Ornithology: Avian Structure and Function by Noble S. Proctor and Patrick J. Lynch.


In many hormonrs, the hypothalamus produces a hormone which acts on the pituitary gland which subsequently acts on an end organ. Taking your example of the thyroid gland let's take a look at it.

The hypothalamus produces TRH which acts on the anterior pituitary causing it to release TSH which in turn stimulates the thyroid gland to make thyroid hormones T3 and T4.

Abnormal levels of thyroid hormone may be caused by problems in any one of the three stages. Problems on the end organ are termed primary, in the pituitary gland are termed secondary and in the hypothalamus tertiary.

For simplicity let's look at abnormally high levels of thyroid hormones called hyperthyroidism. In a patient with a primary or thyroid gland problem we expect high levels of thyroid hormones but low levels of TSH. The pituitary gland is trying its best to tell the thyroid gland, "No more!" but it won't listen. In secondary or pituitary disease, the pituitary gland is the bully pushing the thyroid gland to make lots of thyroid hormone by over production of TSH. Usually there are other hormone disturbances too in this case as the pituitary gland has a range of hormones it secretes. Also the swollen pituitary gland puts pressure on the nerves carrying vision leading to visual loss (specifically in the temporal fields). In this case the hypothalamus will be secreting low levels of TRH (which isn't routinely measured) trying to get the pituitary gland to stop acting out. The rarest situation is when the hypothalamus has the problem where every hormone is increased. However again this will be causes by something or the other detectable usually on imaging.

So the short answer is yes, but there will be other features. Primary or end organ dysfunction is most common and will cause characteristic findings in blood tests and examination (e.g. swollen thyroid gland) but secondary and tertiary disease can be figured out when other features are found in association.


Storage of energy in muscles vs fat depos

The  regulation of metabolites and signals in general (glucose (Glc) or FFA in this case) and their selective uptake by cells, depends on the number (from few hundreds to many thousands) of receptors expressed and displayed to the surrounding environment, the type of receptors (what they can bind, and do as a result) and their properties.

The regulation of glucose storage and use in muscle cells is determined largely by the dynamic energy state of the cell, which is can be described (to first approx at least) as the cellular equilibrium between ATP<-->ADP<-->AMP. The key here is to be aware that nothing is happening in isolation and the whole metabolism of the cell is one giant equilibrium. You make a change at one place that will result in proportional changes elsewhere to compensate.

If you start exercising, that is using ATP rapidsly, suddenly AMP spikes, the increase in [AMP] results in the upregulation of key enzymes in Glycolytic and TCA pathways, which causes and increase in ATP producting. How much is made? Whenever possible always just enough enough to meet the demand (assuming cell has resources to supply it and manufacture it).
Absolutely, in the same way, the energy state of the cell, and the availability of Glc in and outside the cell (which it knows, because increase in blood Glc causes insulin to be release, muscle cell can bind to insulin, which results in activation of more GLUT4 to be expressed and expressed) directs how Glc is used, stored as glycogen, converted to FFA etc. When cell energy state is low, or exercising, signaling from muscle cells to liver (via lactate in blood/ Cori cycle) tell liver to release stored Glc into the blood.  l
If Glc in high in blood, insulin released from the pancreas, which tells the liver, to start sucking up Glc from the blood, and the way it does that is a lot better than muscle. Why? because of the binding properties of the different isozyme receptors expressed (same function but slightly different physical properties).
FFA metabolism is a same general concept, but different key enzyme players. The increase in metabolite availability causes or is a signal, which results in the appropriate response to balance level out the steady state dynamic equilibrium.

The strategy is basically, if available in excess and can be stored it's stored until the limit of cell is reached, which is determined by the thermodynamic equilibrium of metabolite inside and outside the cell.

Nelson, D.L.,Cox, M.M.(2013) Lehninger Principles of Biochemistry, 6th Ed.

In response to your comment questions,
In general, like I mentioned, the strategy for coordinated fat uptake holds.

Majority of insulin-stimulated glucose uptake occurs in skeletal muscle, with about 10% of insulin-stimulated glucose uptake occurring in adipose tissue. However When it comes to FFA, these are largely delivered, absorbed and stored (as triglycerides) from bloodstream into adipose tissues. This process is definitely actively controlled and regulated, as you do not want fat globules floating around in your bloodstream. When energy state of the organism as whole is low, adipose tissue can sense and release FFA that can be take up by other cells (muscle, liver) and energy in molecules extracted during FFA catabolism pathways. How exactly adipocytes translate changes in glucose uptake or storage into signals that affect global energy balance is not completely understood it seems.

For a good place for much more detail, check out

Leto D., Saltiel A.R (2012) Muscle and adipose tissue in energy homeostasis, Nature reviews of Molecules Cell Biology, 13, 383-396
http://www.nature.com/nrm/journal/v13/n6/box/nrm3351_BX1.html


What do you see if you look at your own retina with the same eye? (optical feedback)

You would see your retina and that's all. There would have no "mise-en-abyme".

In order to experience this feedback loop you describe, you need to see something which includes the total picture of what you see. For example: You might see a woman holding a frame of the totality of what you see.

When you look at your retina, you can't see something which includes the total picture of what you see, you just see your retina! It would probably work if the retina was a mirror (or any output device)

This question might not really a good fit for Biology.SE. You might have a chance to make a good fit by asking a question on the mechanistic nature of the process called mise-en-abyme on Phylosophy.SE. And ask wether one can live this same process with any of their sense (perception). You can ask whether the Larsen effect (audio feedback) is a similar process to the one we experience when looking at this picture and in what terms they are similar and in what terms they differ. If you ask such question, I welcome you to add the link on this post (except if the post get closed)!


When our brain works out where a part of our body is in relation to another part of our body, or in relation to anything for that matter, we combine:

visual information
information about how much our muscles are contracted
how much our joints are contracted
different forces being applied on our arms/legs or other body parts
where it remembers we used to be
how much force we applied to move where we wanted to move
where we would therefore expect to be
and many other things

That's quite a few things that our body relies on! The one that's most fine tuned is our vision. Let's face it, whatever we are actively doing with our hands requires the most skill and knowledge of where our hands etc. are. It is also the system that we rely on the most. But other systems are helpful to make sure we don't fall, grabbing on to things and making sure we reflexively contract the opposite muscles to prevent falling, stop us dropping things and lot's more. It doesn't matter if they're not accurate, they just need to be fast and in doing so they can't be extremely exact.

When we don't use vision, we rely on these other things. They're made to quickly adapt (e.g. hold a shopping bag for a while and when you let go your arm feels light or when you get out of a swimming pool your body feels heavy) and it is important that they do this to allow their functions as listed in the last paragraph.


This appears to be a jackfruit. Jackfruit are a large, tropical fruit, commonly reported as smelling similar to banana.


How does menstruation proceed during one period?

The answer is both. Different women experience menstruation differently depending on the levels of different hormones in their body, personal medical conditions, medications, on their age, and the activities they do in their lives. Bleeding is due to the sloughing off of the highly vascularized endometrial lining of uterus which is no longer receiving the appropriate levels of progesterone for its maintenance from the corpus luteum, in the absence of an implanted embryo in the uterus. You can imagine how different this common event would be if a woman was taking warfarin, had a bleeding or coagulation disorder, had polycystic ovarian syndrome, was a runner, or was a 13-year-old vs a 41-year-old. It varies!

Source:

Welt et al. Physiology of the Normal Menstrual Cycle. Last updated Feb 28, 2014. http://www.uptodate.com/contents/physiology-of-the-normal-menstrual-cycle.
http://www.womenshealth.gov/publications/our-publications/fact-sheet/menstruation.html


At what minimum distance the direction at which eyes point becomes parallel?

Mathematically, the eyes are parallel when they fixate at, and only at, infinity. Now, because of noise, there is a distance after which it's not really going to make a difference (otherwise you would be able to tell the distance between stars at night). There are 2 parts for your question. First, at what distance it doesn't matter because the eyes won't stay still enough to accurately maintain this vergence angle. Second, at what distance it perceptually makes no difference because you can't tell if the object is closer or not. Concretely it means looking at the distance where each of these metrics is smaller than detection threshold (the value below which your performance on a detection task is lower than a specified value). Conveniently, Chopin et al. (2016) measured both values (these numbers can of course be found in older papers too).

For the first question, they measured vergence noise of 225 arcsec (or 225*pi/(60*60*180)=0.0011radians). The distance for which vergence becomes smaller than that is approximately 55 meters (vergence~=IPD/FD, with IPD interpupilary distance of approx 6cm). So farther than that you wouldn't be able top tell whether they fixate at infinity or not.

For the second question they measured relative disparity thresholds. Relative disparity is the difference in vergence angles between 2 points. So for relative disparity angles lower than threshold you cannot tell whether point A is closer or farther than point B. They unfortunately don't report the exact value but from the graph it looks like 300arcsec, corresponding to a distance of about 40 meters. In other words, after this distance you can't tell whether an object is farther than where you look at.

Finally, you could also ask: at what distance can't I tell whether an object is at infinity or not? The distance of a point in isolation is called absolute disparity, and is known to be much worse than relative disparity (i.e. it is much easier to compare the distance of 2 points than to report the distance of a single point in isolation). This distance turn out to be quite shorter. From the same paper the absolute disparity threshold is about 3000arsec (again, they unfortunately don't report the exact value). This gives a fixation distance after which you cannot tell whether you fixate at infinity or not of about 4 meters.

This is all very approximate and making lots of assumptions but I hope this more or less answer your question.

Chopin, A., Levi, D., Knill, D., & Bavelier, D. (2016). The absolute disparity anomaly and the mechanism of relative disparities. Journal of vision, 16(8), 2-2.


How efficiently does the human body convert the energy stored in fat into kinetic energy?

this depends on largely how you define it, what we normally measure is efficiency including how much energy is used on metabolic upkeep and heating the body in addition to muscle output. we use oxygen consumption to know exactly how many calories we have "burned" when doing this.  In this study we get between 18-26% efficiency, thats calories ingested to work done. Most of the loss is in converting to ATP (~60% loss) and how much ATP we "waste" heating the body. Note efficiency drops quite a lot when you switch to anaerobic exercise.

keep in mind however the body will not start out burning fat, it has glycogen reserves it will start using first.


Is a nucleus more dense than the rest of the cell?

When you hang up your shirt does it fall to the bottom of your closet?

The nucleus is a dense fibrillar network of DNA, RNA, and proteins, yes, but the subject you should take a look at is the cytoskeleton of the cell. It will will answer all your unanswered questions on the intracellular network that stabilizes, supports, and aligns the organelles within the cell.


Do women tend to have longer legs and shorter torsos than men?

We seem to have a preference for proportionally longer legs (see comment here for a good summary around that study).  So when you are observing "pedestrians" they have probably tended to dress and comport themselves to skew your perception of their leg lengths.  Perhaps in your cultural environment females have a greater capacity and/or motivation to alter that perception than do men.

The reality is that adult female legs are on average proportionally shorter than those of men.  See, for example, this detailed 1977 U.S. Army study comparing body proportions in adults by gender.

For readability I would highly recommend this much broader survey of the subject, which contains not only clear illustrations of how proportions are measured but also an extensive survey of cross-cultural and historical variations: Leg Length, Body Proportion, and Health: A Review with a Note on Beauty.


Factor causing Methicilin-resistance in MRSA?

I think you can normally think about similar pressures leading to extended-spectrum beta-lactamase (ESBLs) and  methicillin/oxacillin-resistant Staphylococcus aureus (MRSA).

Going to the core of your question:

"Currently, the reported mechanism of methicillin resistance in S. aureus is the production of a distinctive penicillin binding protein 2a (PBP2a), which exhibits low affinity toward β-lactams"

But to really read on it you need to back to Liu et al.

Again Todar's is a great source for a good broad reading on staph including MRSA.

Response to Edit [inclusion of full question]:

TSDR: The answer is C.

Let's break down the three options given in the question and learn about MRSA along the way.

  a. its MIC is increased to methicillin, but not to penicillin

First, for people who may not know, MIC is short for minimum inhibitory concentration.  Simply, the MIC is a basic measurement of how much of any given agent is need to stop the growth of a bacterial colony.  Often we think of current medical antibiotics when thinking of MIC, but even simpler things like table salt and sugar have a MIC for a given species.  Thus this sentence is making the assertion that the bacteria found in the patent have an increased resistance to methicillin but not to penicillin.  This leads us to ask the obvious question:

Can Staphylococcus aureus (staph going forward) be methicillin resistant but not penicillin resistant?

This is a bit of a trick question, but let's break it down to the needed components: What is Methicillin, what is/are penicillin(s), and how are staph resistant to them.

First that it should be noted that penicillins can actually refer to a whole class of antibiotics which all use β-Lactam and the specific set of antibiotics:

  benzylpenicillin (penicillin G), procaine benzylpenicillin (procaine
  penicillin), benzathine benzylpenicillin (benzathine penicillin), and
  phenoxymethylpenicillin (penicillin V). (from wiki)

It should be noted that more correct way to address the whole class of antibiotics would be β-Lactam antibiotics, not penicillins, and that if you wanted to talk about more specifically penicillin derived compounds you would be discussing penams.  For even further clarification, penicillin as drug most likely refers to benzylpenicillin, and for the rest of this answer I will use penicillin to refer to benzylpenicillin.

Thus we should think of penicillin as an early antibodic that work by preventing the dividing/genesis of cell walls and certain organelles via binding to penicillin binding proteins (PBPs).

Methicillin is also a β-Lactam antibiotic, and it's MOA is similar to penicillin.  It was developed/discovered after penicillin and was seen a answer to Gram-positive bacteria that were breaking down penicillin via β-lactamase.  Methicillian still works by binding to PBPs, but it escapes the bacteria's counter to penicillin.

This leads us to address how penicillin resistance and methicillin resistance commonly occur in staph.  First, many staph strains and other bacteria use β-lactamases to breakdown antibiotics so they no longer can bind to PBP's (1).  But methicillin is particularly suited by its side chains to not be degraded by β-lactamases.  In their ground breaking work on the subject, Hartman and Tomasz identified that methicillin resistance was not in the acquisition of a β-lactamase, but in a mutation in PBP's that prevented methicillin binding (2).  There they tested 4 strains of staph, two were methicillin resistant (MR), and two were methicillian susceptible (MS).  You will note that all but 1 didn't have β-lactamase activity, and where more susceptible to penicillin than methicillin (ibid).

BUT this does not mean that MR strains are not also penicillin resistant, instead it shows that the resistance can be independent of each other.  Therefore "A" is wrong because it tries to draw a correlation that is not there.  In reality many MR strains are also β-lactamase positive.

This also address the problem with "B."  While it is possible that a β-lactamase could bind to methicilin and lead to degradation of the antibiotic, the main mechanism of methicillin resistance is the mutation of PBPs (ibid, 3), in particular BPB2a (4, 5).

We are then left with the task of figuring out why "C" is the correct choice.  Indeed "C" is the given reason for the failure of "A" and "B," but we can still go deeper into how and perhaps why BPB2a mutated.

For that I think it is best that we turn back to Chambers' review of the subject.  Forgive my over quoting, but it's done so well there and the text is now open.

  Methicillin resistance is associated with production of a novel PBP
  that is not present in susceptible staphylococci. Resistant strains of
  S. aureus produce an additional 78- kilodalton PBP (Fig. 1), termed
  PBP2a or PBP2' (assumed to be identical for the purposes of this
  review), that has a low binding affinity for beta-lactam antibiotics.

...

  PBP2a is highly conserved. Limited proteolysis of PBP2a from unrelated
  strains of S. aureus (123) and coagulasenegative staphylococci (31),
  whether homogeneous or heterogeneous, generates remarkably similar
  peptide fragments.

...

  Presumably PBP2a can substitute for essential PBPs when these have
  been saturated by drug and can perform the functions necessary for
  cell wall assembly (22, 122).

...

  In some strains, PBP2a is inducible by beta-lactam antibiotics and its
  production differs according to growth conditions (34, 122, 125, 159).

Unfortunately, they didn't quite have the staphylococcal cassette chromosome mec (SCCmec) figured out at that point.  The genetics is quite complex.

How does MRSA genetically accomplish resistance?

As we already established, the resistance comes from the production of an alternate PBP, PBP2a.  SCCmec is interesting for several reasons.  First of all, it's much larger than a plasmid, and contains information for several genes.  That's why it's called cassette chromosome.  Further it normally incorporates into the same part of the genome in staph, in an area know as OrfX (6).  This means that even during horizontal transfer, that the cassette has to direct it's integration into the genome, which is exceedingly uncommon, or at least there are not many other know examples (7, 8).  This cassette can be spread horizontally between staph, and even with other species (ibid, 9).  Even if the integration site (integration site sequence, ISS) is slightly different, this specificity is carried out by cassette chromosome recombinases (ccr), wich are also on SCCmec (8).  This is carried out by ccr-medated recombination of the target chromosome, and further details on the process are considered outside the scope of this question.

The actual gene that encodes PBP2a is called mecA.  But as we mentioned above, PBO2a production can be induced and regulated.  It is likely less favorable to produce it in the absence of antibodies, and after serial passage of bacteria in antibiotic free broth, you find that PBP2a expression can drop drastically.  Therefore regulatory and other useful proteins encoded by SCCmec.  When placed in a β-Lactamase environment, MecR1 causes a single transduction cascade to start transcription of mecA (10).  Conversely, MecI provides a negative feedback loop to MecR1, and in the absence of β-Lactamase, will lead to the down regulation of mecA (ibid, 11).  The actual action of MecR1 is to cleave MecI, thereby remove the suppression of mecA by MecI.  I actually learned something new when reading the wiki on MRSA, but didn't do further research on the subject:

  mecA is further controlled by two co-repressors, BlaI and BlaR1. blaI
  and blaR1 are homologous to mecI and mecR1, respectively, and normally
  function as regulators of blaZ, which is responsible for penicillin
  resistance. The DNA sequences bound by MecI and BlaI are
  identical; therefore, BlaI can also bind the mecA operator to
  repress transcription of mecA.

This represents the general pattern of resistance of MRSA, but there is a rich diversity in the particulars of how each strain manages expression.  Two of the main identifiers are how the mecA gene complex and ccr gene complex are configured (carriage).  The other two identifiers are the ISS and whether or not the ISS is repeated in the target chromosome (and how many times it's repeated) (8).  If we just consider the mecA and ccr carriage, then we get a great summary from IWG-SCC (ref 8):

  The mec gene complex is composed of mecA, its regulatory genes, and
  associated insertion sequences. The class A mec gene complex (class A
  mec) is the prototype complex, which contains mecA, the complete mecR1
  and mecI regulatory genes upstream of mecA, and the hypervariable
  region (HVR) and insertion sequence IS431 downstream of mecA. The
  class B mec gene complex is composed of mecA, a truncated mecR1
  resulting from the insertion of IS1272 upstream of mecA, and HVR and
  IS431 downstream of mecA. The class C mec gene complex contains mecA
  and truncated mecR1 by the insertion of IS431 upstream of mecA and HVR
  and IS431 downstream of mecA. There are two distinct class C mec gene
  complexes; in the class C1 mec gene complex, the IS431 upstream of
  mecA has the same orientation as the IS431 downstream of mecA (next to
  HVR), while in the class C2 mec gene complex, the orientation of IS431
  upstream of mecA is reversed. C1 and C2 are regarded as different mec
  gene complexes since they have likely evolved independently. The class
  D mec gene complex is composed of mecA and ΔmecR1 but does not carry
  an insertion sequence downstream of ΔmecR1 (as determined by PCR
  analysis).

And

  ccr gene complex.The ccr gene complex is composed of the ccr gene(s)
  and surrounding open reading frames (ORFs), several of which have
  unknown functions. Currently, three phylogenetically distinct ccr
  genes, ccrA, ccrB, and ccrC, have been identified in S. aureus with
  DNA sequence similarities below 50% (Fig. 2 and 3). The ccrA and ccrB
  genes that have been identified to date have been classified into four
  allotypes. In general, ccr genes with nucleotide identities more than
  85% are assigned to the same allotype, whereas ccr genes that belong
  to different allotypes show nucleotide identities between 60% and 82%.
  All ccrC variants identified to date have shown ≥87% similarity; thus,
  there is only one ccrC allotype. We suggest describing their
  differences as alleles by using previously used numbers, e.g., ccrC1
  allele 2 or ccrC1 allele 8.

All of this is nicely summarized in their table:

\begin{array} {|r|r|r|}
\hline
SCCmec ~type  &ccr ~gene ~complex  &mec ~gene  ~complex \\
\hline
I &1 ~(A1B1) &B \\
\hline
II &2 ~(A2B2)&A \\
\hline
III &2 ~(A3B3)&A \\
\hline
IV &2 ~(A2B2)&B \\
\hline
V &5 ~(C)&C2 \\
\hline
VI &4 ~(A4B4)&B \\
\hline
VII &5 ~(C)&C1 \\
\hline
VIII &4 ~(A4B4)&A \\
\hline
\end{array}

To sum up, methicillin-resistance is caused by the encoding of a novel PBP, PBP2a, along with other factors, which is both genetically stable and transferable via the use of SCCmec.

References:

(1) Pathak A et al. High prevalence of extended-spectrum β-lactamase-producing pathogens: results of a surveillance study in two hospitals in Ujjain, India. Infect Drug Resist. 2012;5:65-73. doi: 10.2147/IDR.S30043. Epub 2012 Apr 5. [Note that many of the great sentinel studies on drug resistant bacteria occur in the massive hospitals in India].

(2) B Hartman and A Tomasz. Altered penicillin-binding proteins in methicillin-resistant strains of Staphylococcus aureus. Antimicrob Agents Chemother. 1981 May; 19(5): 726–735.

(3) Liu, H. et al. Detection of borderline oxacillin-resistant Staphylococcus aureus and differentiation from methicillin-resistant strains. Eur J Clin Microbiol Infect Dis. 1990 Oct;9(10):717-24.

(4) Tawil N. et al. The differential detection of methicillin-resistant, methicillin-susceptible and borderline oxacillin-resistant Staphylococcus aureus by surface plasmon resonance.  Biosens Bioelectron. 2013 Nov 15;49:334-40. doi: 10.1016/j.bios.2013.05.031. Epub 2013 Jun 4.

(5) Chambers HF. Methicillin-resistant staphylococci. Clin Microbiol Rev. 1988 Apr;1(2):173-86.

(6) Huletsky A et al.  New real-time PCR assay for rapid detection of methicillin-resistant Staphylococcus aureus directly from specimens containing a mixture of staphylococci. J Clin Microbiol. 2004;42(5):1875-84. DOI: 10.1128/JCM.42.5.1875-1884.2004

(7) Schoenfelder SM et al. Success through diversity - how Staphylococcus epidermidis establishes as a nosocomial pathogen. Int J Med Microbiol. 2010 Aug;300(6):380-6. doi: 10.1016/j.ijmm.2010.04.011. Epub 2010 May 6.

(8) IWG-SCC. Classification of staphylococcal cassette chromosome mec (SCCmec): guidelines for reporting novel SCCmec elements.  Antimicrob Agents Chemother. 2009 Dec;53(12):4961-7. doi: 10.1128/AAC.00579-09. Epub 2009 Aug 31.

(9) Stürenburg E. Rapid detection of methicillin-resistant Staphylococcus aureus directly from clinical samples: methods, effectiveness and cost considerations.  Ger Med Sci. 2009 Jul 6;7:Doc06. doi: 10.3205/000065.

(10) Jensen SO and Lyon BR. "Genetics of antimicrobial resistance in Staphylococcus aureus". Future Microbiol 4 (5): 565–82. doi:10.2217/fmb.09.30. PMID 19492967

(11) Oliveira DC, de Lencastre H.  Methicillin-resistance in Staphylococcus aureus is not affected by the overexpression in trans of the mecA gene repressor: a surprising observation. PLoS One. 2011;6(8):e23287. doi: 10.1371/journal.pone.0023287. Epub 2011 Aug 2.


What is the difference between a dermatome and a sensory neurone?

This is just a confusion of English.
"Supplied" is a bit of a weird term to use, I agree, due to the direction of information flow, but feel free to substitute in just "connected to". It seems pretty common to use this word, for example Wikipedia says:

A dermatome is an area of skin that is mainly supplied by afferent nerve fibres from the dorsal root of any given spinal nerve

and I see similar phrases elsewhere (not sure which is your original source). Afferent nerve fibers, as you describe, are those carrying information into the central nervous system from the periphery, so yes, the information is coming in from the skin.
If you interpret it instead as the spinal nerve providing the connection rather than information flow, then it makes a bit more sense to say "supplied". I suspect the phrasing is borrowed from blood supply since nerves and major vessels tend to develop and travel together. I also suspect the phrasing comes from anatomy, which is sometimes not particularly interested in function which can lead to some confusing results. You'll also see similar phrasing in standard English in other contexts, like roads, even when movements of goods or people are two-way. Merriam-Webster also provides a definition addressing exactly this circumstance:

to furnish (organs, tissues, or cells) with a vital element (such as blood or nerve fibers)

So yes, a given spinal nerve is "supplying a single dermatome with nerve fibers", even if the information ultimately moves the other direction.


Relation between goose bumps and temperature

Goose Bumps (a.k.a. - Goose Pimples) are caused by the Arrector Pili muscles in your skin:

Their purpose is to increase the distance from epidermis to the top of the follicle, and increase the area between follicles. This has the effect of increasing the amount of air trapped between the hair and surface of the skin. In other mammals the end-result is an increase in the insulatory properties of their fur, meaning they will stay warmer or cooler depending on their current needs.

Another function in our mammalian cousins is to simply appear larger, and thus more of a threat to any predators or dangerous animals. Much like the shoulder and lower back hair on this dog:

Thermoregulation in humans has evolved since our furrier ancestors; we sweat to cool off, and shiver to keep warm. We also use tools and weapons, can create fire, and have other ways to communicate our lethal capabilities.

Goose Bumps are the human body utilizing old instinctual reflexes in the proper situations, but we lack the thick mattes of hair our ancestors had for the reflex to have any significant effect. They're a fun Easter-egg, a leftover that doesn't do us any harm and are an easy way to tell if someone is cold or scared - which might be useful under the proper circumstances.


Is it possible to accurately measure micronutrient levels with the blood volume from a Dermal / Capillary puncture?

Detection methods are constantly getting better, requiring lesser amounts of blood to make a determination. In newborns, a heel blood sample (of capillary blood) is used to detect up to 40 (sometimes more) disorders from maple-sugar urine disease and hypothyroidism to hemoglobinopathies and organic acid conditions. If such large molecules can be detected in capillary blood, smaller molecules should as well.

There are differences in central venous sampling and capillary blood sampling, but it could be argued that since the capillaries are the site of exchange of nutrients, this is the most accurate site to determine availability of micronutrients in blood.

One reason labs take more blood than required for the test is to run a second analysis if the first is abnormal. Although it's not done for every abnormal, clinicians often want to confirm significant abnormals before treating a possible lab error.

Newborn screening tests
Newborn Screening
Conditions Screened By State
A Layperson's Guide to Tandem Mass Spectrometry


I have not used the assay myself, but Bhuiya and Liu "A cost-effective colorimetric assay for phenolic O-methyltransferases and characterization of caffeate 3-O-methyltransferases from Populus trichocarpa." Anal Biochem. 2009 384(1):151-8 [link] seems to have a relatively straightforward protocol.

Roughly, you make a 0.4% (w/v) solution of Gibbs reagent in ethanol, and then add one fifth volume of that to your enzymatic reaction mix. You then observe the solution spectrophotometrically.

The biggest issue I see is that it looks like each phenolic compound has its own absorption maximum, and widely varying extinction coefficients. In their protocol it seems they look at full range scans, rather than single wavelength measurements. You'll definitely need a standard curve for your particular phenolics in order to get quantitative results. (Also, any background phenolics or medium absorption in the 400-600 nm range may throw off measurements - use appropriate blanks.)


Is this a large bee? (species identification)

Note: My mistake. I did not notice the OP info that he is in china. There are giant honey bees in China, such as Apis dorsata Fabricius, however their size is only 17-20mm.

========

I suggest  Bombus dahlbomii. It can grow up to 40 mm long, 1.6 inch

Picture

Wiki


Primary cilia: what cell types have non-motile cilia that migrate?

It's hypothesized that planar cell polarity is many cases functionally associated with asymmetry of (primary) cilia (Axelrod (2008)). So, the phenomenon of primary cilium migration could be not that infrequent. One example is the development of ependymal cells in brain ventricules: They are multiciliated and the cilia are motile, but ciliogenesis starts from a single cilium, which is not motile and which migrates from the apex to the rostral end of the cell:

Mirzadeh et al (2010)
Bayly & Axelrod (2011)

Seemingly less clear (for me, at least) cases are non-motile single cilia on the lens fiber cells and may be, embryal node cilia (which are motile in the mature state):

Wallingford (2010)
Sugiyama et al (2010)


How to calculate or know by experiment the entropy of enzymes or protein?

In practice, like Energy calculations, Entropy is a relative numbers and difficult to get.  Computational chem and bio have been working on this problem with mixed success.  The summary of what I'm going to say here is that when you try to calculate the differences in entropy (or energy for that matter), the Gibbs Free Energy differences in most biological processes such as enzyme/substrate binding, protein/protein or protein/DNA interactions or protein folding etc is so small compared to the errors in these calculations that the computations are hard to believe.

Entropy is ultimately a term one would use in calculating the Gibb's free energy which will tell whether a given chemical or molecular process will occur.  So it's a valuable number to have.  Gibbs Free Energy (G) equals Enthalpy (heat) minus the temperature (T) times the change in entropy.

G = H - T$\Delta$S

The Entropic term, $\Delta$S is described in chemical systems often as a change in the combinatorial change of the system and the change in the heat capacity of the system. The first of these could broadly described as a 'mixing' term.  When more than one solvents or a solvent and a solute diffuse into each other mix completely, the number of possible states is maximized.

The heat capacity of the system is a more often the focus of entropy calculations for proteins and biological molecules.  This is because the conformations of the biological molecules, especially how free they are to move around are thought to contribute to the entropic part of G.

So attempts have been made to estimate from NMR and crystallography as well as molecular dynamics how much domains and side chains are free to move.  Unfortunately this is only an insufficient proxy for biological entropy.  A substantial if not dominant contribution to the T$\Delta$S term comes from solvent.

How is this so?  Water molecules form structures around proteins which are not static, but do involve many water molecules residing there on the average to see them in crystal structures and NMR experiments.  While the individual waters are exchanging rapidly, they are not in the same entropic state in water solution as they are when they form a hydration shell around an aromatic or charged side chain.

Attempts have been made to parametrize the solvent entropy by looking at the buried nonpolar surface in a folded protein, looking at the mobility of sidechains before and after folding/binding, but these metrics appear to be configuration dependent to the point that they can't calculate the protein entropy via these efforts, at least heretofore.

Conventionally, molecular dynamics tries to calculate this by surrounding the proteins or other molecules with water molecules and some approximation of the overall entropy is calculated on the entire system.  It turns out that small differences between the water molecular models and the simplifications in ball and stick/Hooke potential water models we make are also problematic approximations when there are hundreds or thousands of water molecules in the simulation.


B-cell and T-cell activation by parasites

I've found a great article that says:

  Mitogens   and   superantigens   have   been   described   to
  explain the strategy used by microorganisms to avoid the
  host specifc immune responses and to ensure persistence.
  These  moieties  are  responsible  for  the  initiation  of  non-
  specifc  (polyclonal)  immune  responses.

Mitogens are chemicals (usually proteins) that promote mitosis. Superantigens (sAg) form a subclass of antigens and are capable of inducing massive polyclonal T-cell activation and cytokine release (Cytokines crucial role in immune system mediation). Their ability to inflict massive T-cell activation comes from the fact that they bind directly to MHC-II without any pre-processing, and stimulate T-cell activation.
Source: https://escholarship.org/uc/item/47g8w51m
Also there are B-cell sAgs that stimulate B-cells, and their activation.

These altogether (mitogens cytokines, sAgs) result in rapid expansion of B-cells and T-cells.

Also this paper might help to understand why parasites trigger polyclonal T and B-cell activation. Namely to avoid host specific immune system, dilute the pathogen specific anti-bodies. It is important to note that chronic infections could lead to several auto-immune diseases.


I found two references that talk about the circle of Willis in different kind of mammals so i think it's right to say that this particular anastomotic system of arteries is not exclusive to humans.

Here are the two references:

http://www.neuroanatomy.org/2008/054_065.pdf

http://www.ncbi.nlm.nih.gov/pubmed/14651482


Simply because it has neurotropic receptors. Why did acquiring these receptors seem evolutionarily advantageous? Well the immune system doesn't target nerve cells for destruction as well. There are few if any white blood cells in the CSF within which the neurones are bathed. The immune system is about protecting against damage, it doesn't care as much if a virus doesn't cause damage as it isn't geared to respond as well if that's the case.


There are several ways you could go about identifying species through DNA. If you want to do everything yourself, the simplest option in terms of equipment needed consists of evaluating fragment lengths observed during gel electrophoresis after amplifying specific DNA sequences using PCR.

If you are content with some outsourcing, you can also send DNA samples to a commercial company for sequence analysis.

A compromise between these options in terms of information obtained, is to do study Restriction Fragment Length Polymorphism (RFLP) by amplifying DNA fragments and using restriction enzymes to cut the fragments, before analyzing the fragmentation pattern using gel electrophoresis. To perform RFLP analysis, you would need to obtain restriction enzymes in addition to the chemicals mentioned below, and they can be a bit pricey.

The minimum equipment would consist of a PCR machine, one or more pipettes with matching pipette tips, a gel electrophoresis tray with power supply and a transilluminator (preferably blue-light/non-UV). A centrifuge is not strictly necessary, but can be useful for processing/filtering your DNA source.

Some chemicals will also be needed: Polymerase and dNTPs for the PCR reaction (or a pre-made "master mix" containing both), electrophoresis-grade agarose and running buffer for the electrophoresis, along with a DNA dye specific to the type of transilluminator (Usually UV or blue light). For a blue-light transilluminator, GelGreen is a suitable DNA dye. You will also want to use a "loading dye" to mix in your DNA sample before applying it to the electrophoresis gel. This can either be purchased or prepared yourself by mixing sugar and food coloring in water.

You need some form of heating to dissolve the agarose - a microwave oven is convenient for this, but take care to avoid over-heating, glass explosions or flash boiling. It is convenient but not strictly necessary to have some lab glassware. Preferably use a screw-top bottle to mix your agarose solution. Always leave the top off when heating bottles.

Photographic equipment can be also useful for documenting results of gel electrophoresis.

Finally, you will need single-stranded DNA oligomers (primers) specific to the DNA regions you want to amplify. DNA primers can be bought from a number of companies, but it varies how easy it is for non-affiliated individuals to order and make payments. Macrogen has been my choice: They both deliver DNA primers and perform DNA sequencing.

You may be interested in the following thread on the DIY Bio e-mail group: https://groups.google.com/forum/#!topic/diybio/cPzfEuiZH58

I have collected some of the primer sequences mentioned in the thread on a page on OpenWetware: http://openwetware.org/wiki/User:Jarle_Pahr/Meat


Why is alcohol purged from the body more slowly when we sleep?

You are right, Culprit is Ethanol in Alcohol. It contains 2 carbon atoms, 6 Hydrogen atoms and 1 Oxygen atom.

Ethanol is readily soluble in water, so it easily dissolves in the
bloodstream and gets carried to various parts of the body. The most
affected areas of the body include the liver and the brain. In the
brain, ethanol adversely affects Glutamate receptors, which causes
slurred speech, memory loss, slow reaction to stimuli, and other
common side effects of being a bit too tipsy.
Not only this, ethanol molecules bind with GABA (gamma-aminobutyric acid) receptors, which is able to slow down the
activity of brain. Unlike glutamate receptors, ethanol actually makes
GABA receptors more receptive, causing the brain to slow down even
further. However, alcohol doesn’t just act to slow everything down in
the body. It also stimulates the production of dopamine and
endorphins, chemicals that produce feelings of pleasure. This is the
reason why people choose to get that alcohol “high”, despite knowing
the negative consequences that it may lead to.

So basically when you are physically working body needs more oxygen while Ethanol only has one oxygen atom, and Since Liver starts to work on regular pace, Which plays a central role in all metabolic processes in the body.
Everyone's oxygen levels in the blood are lower during sleep , in fact while sleeping or in meditation body needs very less oxygen to survive.

Why would I need to wear oxygen while sleeping?
Everyone's oxygen levels in the blood are lower during sleep, due to a
mildly reduced level of breathing. Also, some alveoli drop out of use
during sleep.
If your waking oxygen saturation is greater than about 94 percent on
room air, it is unlikely that your saturation during sleep will fall
below 88 percent. However, your doctor can order an overnight oximetry
test if there is a question about your oxygen saturation levels while
you are sleeping.

In general, metabolic rate is higher when you are awake, because then you tend to be moving about doing stuff.


As @dd3 stated, it's a spiny (or prickly) sow thistle. It's an annual common in most of the US.

The leaf itself does not have a stem, and if you break the central stalk, it should be hollow and there should be a milky exudate. The plant spreads by fluffy seeds produced from a small dandelion-like flower.

If you pick it while young, it won't hurt (as much); if you prevent it from flowering, it should not spread, although unsprouted seeds can sprout still for a few years (it can come in on the wind as well.)

Prickly Sowthistle


Why do we only initially feel the bending of a hair?

Short answer
Touch receptors become unresponsive after continuous stimulation, a process called neural adaptation.

Background
There are various touch receptors in the skin (Fig. 1). One of them is the hair follicle receptor. These receptors form sensory nerve fibers that wrap around each hair bulb. Bending the hair stimulates the nerve endings.

All the afferent fibers of the skin receptors in the skin show neural adaptation. A rough classification of the various skin receptors is grouping them in rapidly and slowly adapting fibers.

Rapidly adapting fibers respond mainly to pressure changes. Typical examples are the Pacinian and Meissner's corpuscles, but also the hair follicle receptor.

Fig. 1. shows a static stimulation of the various receptors. Upon initial stimulation, the hair follicle receptor (Fig. 1a) vigorously fires action potentials. Because the hair follicle receptor rapidly adapts, however, it soon stops responding when the hair is continuously, statically bent in that same direction. Once the stimulus is removed it fires another volley of action potentials because the hair moves again.

In other words, the hair follicle receptor responds to strokes, stretch and skin vibrations, as it is a novelty detector; it detects change, just like Pacinian and Meissner's corpuscles do (Fig. 1b,c). This opposed to Merkel cells and Ruffini endings (Fig.1d,e) - these receptors are designed to continuously fire action potentials upon a static pressure stimulus (Fig. 1), although even these receptors eventually give up and become unresponsive.

Fig. 1. The skin receptors and neural adaptation. source: Delmas et al., (2011)

Reference
- Delmas et al., Nature Rev Neurosci (2011); 12: 139-15


Why are the shells of birds' eggs fragile but not those of other creatures?

Your question is, I think, based upon a false presumption: that avian eggs are more fragile than those of other oviparous animals.
The paper Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds1 suggests that increased calcification of the avian eggshell is an evolutionary response to protect against predation and microorganisms, particularly in soil. The trade off was less permeability and water absorption. To offset that "cost," birds' eggs evolved the albumen or "egg white" which adds liquid content.
This is discussed more (and referenced) in Frank B. Gill's Ornithology2, which goes on to further explain that the shells additionally protect eggs from the weight of incubating parents.
Other functions, such as that of oxygen exchange, are permitted by the calcium shell due to microscopic pores. Also, crystalline calcite (the main ingredient of the shell) can be used by the embryo to form calcium in development of its bones.
1 Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds by Gary C Packard and Mary J Packard; American Zoologist, Volume 20, Issue 2, May 1980, Pages 351–362
2 Gill, Frank B.. Ornithology. United Kingdom: W. H. Freeman, 2007.


How does food intake affect medicine? Why pill instructions recommends taking them before (after) meal?

From the Merck website :

Drug absorption is the movement of a drug into the bloodstream after administration.
Absorption affects bioavailability—how quickly and how much of a drug reaches its >intended target (site) of action. Factors that affect absorption (and therefore >bioavailability) include
1.The way a drug product is designed and manufactured
2.Its physical and chemical properties
3.Other ingredients it contains
4.The physiologic characteristics of the person taking the drug
5.How the drug is stored
If a tablet releases the drug too quickly, the blood level of the drug may become too high, causing an excessive response. If the tablet does not release the drug quickly enough, much of the drug may be eliminated in the feces without being absorbed, and blood levels may be too low. Drug manufacturers formulate the tablet to release the drug at the desired speed.

Essentially, most drug's absorption rates are slowed down by food in the digestive tract, which is beneficial for various reasons depending on the drug.
Some pills are irritants to the stomach, in which case they usually have a coating that may need an acidic environment to break down. Food would assist in this, as well as serving as a sort of diluting agent and even a physical barrier for the stomach.
Conversely, some nutrients (and certain pharmaceuticals) are absorbed by the stomach lining and small intestine much more efficiently when the body is actively digesting food, which is why vitamins and other supplements have the food recommendation.
I think that 'before or after' food should be read as 'shortly before or after', i.e., so food and pill are digested simultaneously. Otherwise, I believe they just don't mention it. Of course, this is a simplistic rendering of pharmacological absorption vis a vis food (there are some very specific interactions; grapefruit and various blood pressure medications come to mind), but this is the general answer to your general question, I believe.


Among primates, is it true that homosexual behavior is extremely unnatural and uncommon?

First Antonio Pardo is not a biologist, he is a professor of bioethics and his degrees are in medicine and philosophy.

Second, Clearly he does not know anything about primates, since there is one famous great ape that has sex even more often than humans do, the Bonobo. Bonobo have sex for everything, hello, goodby, conflict resolution, social bonding, ect. Bonobo engage in homosexuality and a hundred other sexual practices, including some things humans can't do, like penis fencing. Bonobos along with chimps are also our closest living relative.

As for other animals there are hundreds of examples of homosexuality in nature. I hate using all these wiki links but this is such general biological knowledge I would need either dozens of links or a link to a textbook.

As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name.

Now for her argument, it is true that in nature sex is most often directed towards reproduction (that is why it evolved in the first place* and just consider how many sexual animals have very simple behavior), but as I have pointed out there are notable exceptions one of them our closest relative. And not just homosexuality, masturbation is observed in nature as well. Also consider monogamy is also extremely rare in nature with the exception of birds, arguing humans should behave based on how other animals act will not help their argument. It is also a common fallacy, what is natural and what is ethical are not related, Sanitation, science, religion, medicine and reading are also not natural.

If you want to read more about humans and our relatives I suggest the book (the Third chimpanzee" by Jared Diamond as a t least a good starting book.
"Wild Connection" by Jennifer L. Verdolin is even better, both have actual degrees in biology.

*Of course your legs originally evolved as fins,  so what something starts as is not necessarily what it is used for now.


The word "Afrothere" comes from Latin Afer (referring to Africa) and Ancient Greek θηρίον (thēríon, meaning “beast”). In other words, "Afrothere" etymologically refers to animals with origins in Africa.
So really, Afrotheria and it's members are referred to based on their origins and not their physical characteristics. In other words, they needn't share morphological characteristics, but rather they all evolved from the same common ancestor from Africa.
From the Afrotheria Wikipedia page:

Afrotheria is a clade of mammals, the living members of which belong to groups that are either currently living in Africa or [are] of African origin...
They share few anatomical features but many are partly or entirely African in their distribution

These animals are all chordates of the class Mammalia, and therefore do share the common "basal" characteristics shared among all members of these higher taxanomic levels -- for example, a notochord (and backbone), hair, three middle ear bones, mammary glands, etc.


Chaos theory and population cycles of odd periodicity

The chaotic behaviour you are referring to (at least the one described in your link in the comments) is a property of the discrete version of the logistic equation, where you get chaotic dynamics at growth rates above ~3.55 (see the logistic map). The behaviour of this equation has been described in a classic paper by Robert May (1976). As you increase growth rate (a in your link) from one you go from a stable attractor (approached directly or by dampened occilations) to cycling behaviour (between 2 to 4 to 8 states as growth rate increase) to chaotic dynamics, which is shown in this bifurcation diagram.

And to be clear, nothing of this has anything to do with period/cycle length per se (in the sense of species interactions or lagging feedback loops), but is a property of the model and the population growth rate. The statement about period 3 implying chaos probably refers to a brief window around r ~3.83 ($1+\sqrt{8})$ where you get cycling between three values, and at higher values then this you only find chaotic behaviour (which you get at lower values as well though).

Addition:
I now realize that the statement "Period three implies chaos" comes from the theoretical paper with the same name (Li & Yorke, 1975). This paper proves that all one-dimensional models (not only the equation above) that has a period 3 cycle will also show chaotic behaviour. This proof is a special case of the Sharkovsky's theorem, which is older but was unknown to Li & Yorke at the time.

There is also a question at MathSE that deals with the same problem, and some of the answers there link to useful resourses:
https://math.stackexchange.com/questions/2901/period-of-3-implies-chaos


How scientists can be confident that human embryo tail is really a tail?

We can be sure it's a tail because it is an extension of the vertebrae, and we define "tail" as an extension of the vertebrae, among other things.

  tail

  tāl/

  noun: tail; plural noun: tails

  the hindmost part of an animal, especially when prolonged beyond the rest of the body, such as the flexible extension of the backbone in a vertebrate, the feathers at the hind end of a bird, or a terminal appendage in an insect.

Emphasis mine. Source: www.oxforddictionaries.com


There is only one main "coloring" agent, or pigment, in the eyes.  That pigment is melanin.  To a much lesser extent, at least in health individuals, you can have lipofuscin produced which gives a golden-amber color to the eyes.  It should be noted that lipofuscin is most likely produced because of oxidation damage/stress in your eye, and not something to be hoping for (Beatty et al has a good review of the subject (1)).
Indeed, lipofuscin in the eyes can be seen as a symptom to physicians, so for the rest of the answer I will only consider melanin, eumelanin and pheomelanin in particular, as the normative pigment in the iris.
To make additional colors, we would need to develop an additional pigment, and or modify eumelanin so that it produces different scattering properties.  So why do we have melanocytes in the eye producing melanin in the first place?
As much as we might consider it as a factor now, sexual selection was probably not the main pressure for having pigment in the eyes.  Instead UV protection almost assuredly is (2, 3).  Thus for another pigment to be selected for, it would probably need to do a better job protecting us vs. UV (also, further selection in humans is hampered by all kinds of things like behavior, medicine, and life span).
Eumelanin does a good job protecting us from UV (2, 3) and in fact does a better job than phenomelanin (4).  It seems incredibly unlikely that we would develop the necessary evolutionary pressure to have our pigment epithelium to produce a totally foreign pigment.
And that is what prevents us from naturally having a whole rainbow of colors in our iris.  One could conceivably engineer a better pigment, and have the genetic information needed to produce it delivered in gene therapy (I hate to think of people purposefully infecting their pigment epithelia).  I, for one, wouldn’t sign up for that.
(1) Beatty S. et al. The role of oxidative stress in the pathogenesis of age-related macular degeneration. Surv Ophthalmol. 2000 Sep-Oct;45(2):115-34.
(2) Hu DN. et al. Role of ocular melanin in ophthalmic physiology and pathology. Photochem Photobiol. 2008 May-Jun;84(3):639-44. doi: 10.1111/j.1751-1097.2008.00316.x. Epub 2008 Mar 8.
(3) Simon JD, Peles DN. The red and the black.  Acc Chem Res. 2010 Nov 16;43(11):1452-60. doi: 10.1021/ar100079y. Epub 2010 Aug 24.
(4) Hu DN et al. Uveal melanocytes, ocular pigment epithelium, and Müller cells in culture: in vitro toxicology. Int J Toxicol. 2002 Nov-Dec;21(6):465-72.


Are ectopic beats considered sinus rhythm for pNN50 purposes?

No, the beats originating outside of the sinoatrial node are not considered for pNN50. Moreover, this metric cannot be applied to the rhythm featuring any type of ectopic or non-sinoatrial activity.

NN50 has its name from an acronym "normal-to-normal", this acronym is used instead of RR ("from R to R") to emphasize that only the normal, e.g. sinoatrial beats are considered for evaluation.


Do the primers used for Covid-19 test work with all new strains?

I TRY to answer. First of all, no we cannot be 100% sure that the primers are effective against all strains.
However, the strains that are under media attention right now are due to variants in the spike protein, while RT-PCR primers are designed on different genes.
One WHO document (I do not know if it's the official guideline) targets RdRp (RNA-dependent RNA polymerase) and a gene called E gene.
While the document itself nor the paper on which it is based explicitly addressed conservation of the target genes, I found evidence for relatively high conservation of at least RDRP in this paper.
Personal opinion here: in looking for RT-PCR primers, you always need a balance between targeting genes that do not vary in the species, and targeting genes that may aspecifically amplify in different species (e.g. SARS-CoV).
Final answers:

how can we be sure that there are not new strains with sequences not complementary to the primers?

We cannot. However, as far as the variants media are talking about, we know that RT-PCR has some ability to detect them, since they have been sequenced as a consequence of some patient testing positive to RT-PCR.
We cannot exclude the existence of unknown strain. They could be identified by e.g. sequencing patients with COVID-2 symptoms testing negative to RT-PCR (and possibly testing positive to the antigenic test). I don't know if such cases have been observed.

Does the current covid19 test target highly conserved RNA regions?

Yes, the current RT-PCR based tests target conserved genes (although I wouldn't call the highly conserved, because of the caveat I expressed above as a personal opinion)

If that is correct, how do we know that those regions are highly conserved?

Mostly by sequence similarity. Regions that have the same sequence in all the individuals of a species and in related (or distant) species are conserved.


It doesn't become volatile nor is it degraded. Neither is really possible because the dye (lawsone) forms very strong bonds with protein molecules and also penetrates the skin quite well [source: here].

Henna fades with time via exfoliation. In other words, it fades progressively as additional layers of skin die and fall (or "slough") off.


How is the probability of a sequence occuring with BLAST calculated?

According to BLAST documentation statistics of local sequence alignment, when doing database searches, is done

  by treating the database as a single long sequence of length N.

N is therefore a sum of all sequences with varying sizes from a given database.

Underlying assumption is that

  query is a priori more likely to be related to a long than to a short sequence, because long sequences are often composed of multiple distinct domains.

To calculate the probability, we need to choose a scoring scheme (for ungapped example: choose a mismatch penalties), which for a query sequence gives us a statistically significance score $S$. Expected number of alignments with score of at least $S$ follows Gumbel extreme value distribution:

$$
E = Kmn\cdot e^{-\lambda S}
$$

where m is query length, $n=N$ and $K$ and $\lambda$ are distribution params.

Again, according to docs and its references, probability of finding at least one such seq would be $P=1-e^{-E_{(N)}}$, where $E_{(N)}$ is E-number for concatenated N-sequence and query sequence.