Can one see flickering of a light bulb at 50 Hz?

Short answer
Yes, the flickering of a light bulb may be noticeable, and yes, that's directly related to the mains frequency. However, since the flickering of a bulb is about two times higher than the temporal limits of our visual system, it is unlikely to be perceivable.

Background
The temporal resolution of the visual system can be quantified in a number of ways. As you are referring to a relatively simple flickering stimulus, the critical flicker fusion frequency is probably the most relevant. At a certain critical frequency, a flickering stimulus will appear as a continuous stimulus. This critical flicker fusion frequency limit is around 50 Hz, but variable between 5 - 50 Hz, dependent on the lighting conditions (Kalloniatis & Luu), see Fig. 1 below.

For example, the turn signal of a car is obviously flickering (flickering in the 1 Hz region). But an object displayed on a standard flat-screen computer seems steady. A monitor's refresh rate is typically 60 Hz, which is indeed above the critical flicker fusion frequency (Holcomb, 2009).

However, the good old CRT screens can sometimes seem to be flickering. The mains, as you indicate, is indeed 50 Hz (Europe, Australia) or 60 Hz (US), and indeed the flickering is at this frequency. Similarly, well functioning fluorescent tubes seem to flicker on occasion (when they are reaching their end they start to flicker too, but that's because of a failure of the device rather than the mains frequency peaking through). Due to a similar effect, light bulbs may seem to flicker too. However, because of the sine wave characteristic of the mains alternative current, featuring two peaks per wavelength (a negative and positive peak, the flickering of a light bulb is actually two times the mains frequency, or 100 - 120 Hz. This is quite far above the critical flicker fusion limit and hence will likely not be noticeable.

It's interesting to see that you mention that it was around sunset. Scotopic vision (night vision) is mediated mainly by the rod photoreceptors. The rod visual system mediates gray scale vision at low-lighting. While spatial resolution is poor, it's very well adapted to process fast-moving stimuli. Hence, the flicker fusion frequency under scotopic viewing conditions may indeed be higher; i.e., flickering of light bulbs may not be perceived during the day (Federov & Mkrticheva, 1938). Nice add-on there.

To add to this as alluded to in the comments, whether the flicker of mains-grid powered appliances are actually visible depends on a lot of factors other than flicker frequency. CRT screens, for instance, may have improved phosphors that have delayed response times, 'smearing' out the flickering into invisibility. In other words, it's not a simple matter of 'ON' and 'OFF'. Likewise, light bulbs heat up and hence the temperature difference might not be noticeable to us, as the temporal flickering depends on heating and cooling of the wire.

Fig. 1. Flicker fusion as a function of stimulus intensity. Note that the shape of this graph means that photopic vision is less sensitive to temporal changes; the intensity scale relates to the stimulus intensity, as alluded to in the other answer. Scotopic vision to promote the temporal resolution of vision in the sense mentioned in this answer alludes to the ambient lighting conditions conditions. source: Kalloniatis & Luu (2007)

References
- Federov & Mkrticheva, Nature; 142: 750–1
- Holcomb, Trends Cog Sci 2009; 13(5): 216-21
- Kalloniatis & Luu, WebVision, chapter "Temporal Resolution" 2007


Why can blood group O be given to all blood groups?

Good question! Let's start with an overview and explanation of the ABO blood grouping system (Dean, 2005):

Blood groups, antigens and antibodies: Subjects with blood group A carry the A antigen on their red blood cells (RBCs) and have antibodies to antigen B; subjects with blood group B have the B antigen and anti-A antibodies, blood group AB carries both the A and B antigens and have no antibodies, and finally folks with group O have no antigens but both antibodies.

Blood groups and transfusion: Circulating antibodies in a person's blood will attack transfused RBCs from unmatching blood groups. These antibodies fix complement and cause rapid intravascular hemolysis, triggering an acute hemolytic transfusion reaction that can cause disseminated intravascular coagulation, shock, acute renal failure, and death (Dean, 2005). As people with blood group AB have no antibodies, they can receive all blood groups without issues. People with blood group O can only receive RBCs of blood group O, because they carry both antibodies. Blood group A can receive A and O, and blood group B can recive B and O. Hence, blood group O can be received by all other groups, and is therefore the universal donor.

Typically, literature on transfusion deals with the haplotyping the antigens of the donor RBCs. The question whether the antibodies in the donor's blood with blood group O would start attacking cells in recipient with blood group A, B and AB is, therefore, a very good question. And the answer is: yes, they will. Why then is O still the universal donor as they have both anti-A and anti-B antibodies?

First, whole blood is not used for "routine" blood transfusions (Torrens University Website). Instead, blood component therapy has largely replaced the use of whole blood (Patient.co.uk website). For routine transfusions, only the fraction containing packed red blood cells is transfused (Mayo Clinic website). Hence, in these cases, the blood plasma containing the antibodies is (virtually) removed after centrifugation. Since O-type red blood cells contain no antigens (Dean, 2005), and the plasma with the antibodies are not transfused, it can be donated to everyone, barred that the rhesus factor matches.

Secondly, even if plasma is transfused, antibodies in the donor's plasma are a minor problem, because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation (Dean, 2005).

Reference
- Dean (2005) Blood Groups and Red Cell Antigens. Chapter 5.The ABO Blood Group


BLAST(Basic Local Alignment Search Tool) is heuristic?

You might be confused about what "heuristic" means. "Heuristic" doesn't mean random or arbitrary, instead, an algorithm is termed "heuristic" if it employs a shortcut which means that it does not necessarily yield the theoretically best result.

For BLAST, this shortcut is the assumption of first matching the fixed-length words prior to extending the match. Hypothetically, there could be a query sequence and a database where the best scoring match for the query sequence doesn't contain any k-length sequences in common with the database sequence. In this case, BLAST would be unable to find that match. - So the heuristic portion of the algorithm isn't in the dynamic programming portion, it's in that first step of finding pairs which are to be aligned.

The failure of BLAST to find a match is likely to be rare, though, especially with short word lengths. If you find a decent match, it's highly likely that there is a 3-mer (5-mer, etc.) of identical sequence in the pair. But because it's not a guarantee, the use of k-mer word in the process means that BLAST is a heuristic algorithm.

The ability for BLAST to provide quality and statistical metrics is not limited by its heuristic nature. To build an e-value, you don't need to know that BLAST is able to find the absolute best match. Instead, you just need to be able to build a model of the sort of matches BLAST would find by spurious random chance, when applied to a similar database with no "true" matches. Similarly for bit-score. You don't need to know what the absolute best match would be, you just need to know how BLAST would behave on a hypothetical true-match-free database of similar properties.


Do organisms have a mechanism to control how fast mutations occur?

The ability of a population to respond to environmental change through evolution occurs over generations, and so the generation time of an organism has to be less than the time scale of the environmental change for such an increase in mutation rate to be beneficial.

For bacteria at least, the answer to your question is yes. Bacterial stress responses involve upregulation of error prone polymerases and thus lead to an increased mutation rate. Check out this paper (links and emphasis added):

Foster PL. 2005. Stress responses and genetic variation in bacteria. Mutat Res 569(1-2):3-11.

  Under stressful conditions mechanisms that increase genetic variation can bestow a selective advantage. Bacteria have several stress responses that provide ways in which mutation rates can be increased. These include the SOS response, the general stress response, the heat-shock response, and the stringent response, all of which impact the regulation of error-prone polymerases. Adaptive mutation appears to be [a] process by which cells can respond to selective pressure specifically by producing mutations. In Escherichia coli strain FC40 adaptive mutation involves the following inducible components: (i) a recombination pathway that generates mutations; (ii) a DNA polymerase that synthesizes error-containing DNA; and (iii) stress responses that regulate cellular processes. In addition, a subpopulation of cells enters into a state of hypermutation, giving rise to about 10% of the single mutants and virtually all of the mutants with multiple mutations. These bacterial responses have implications for the development of cancer and other genetic disorders in higher organisms.

This mechanism may be involved in the evolution of antibiotic resistance, for example (emphasis added):

Cirz RT, Chin JK, Andes DR, de Crecy-Lagard V, Craig WA, Romesberg FE. 2005. Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance. PLoS Biol 3(6):e176.

  The emergence of drug-resistant bacteria poses a serious threat to human health. In the case of several antibiotics, including those of the quinolone and rifamycin classes, bacteria rapidly acquire resistance through mutation of chromosomal genes during therapy. In this work, we show that preventing induction of the SOS response by interfering with the activity of the protease LexA renders pathogenic Escherichia coli unable to evolve resistance in vivo to ciprofloxacin or rifampicin, important quinolone and rifamycin antibiotics. We show in vitro that LexA cleavage is induced during RecBC-mediated repair of ciprofloxacin-mediated DNA damage and that this results in the derepression of the SOS-regulated polymerases Pol II, Pol IV and Pol V, which collaborate to induce resistance-conferring mutations. Our findings indicate that the inhibition of mutation could serve as a novel therapeutic strategy to combat the evolution of antibiotic resistance.


Common name: Stonefly completely harmless!
(the terrestrial adult does not have mouthparts) and is an indication that the stream nearby is somewhat healthy.
Below is great info from online site. I just now joined Biology Stack so not sure if we can post links but I’ll try it at the end.

Neither a stone nor a fly, the stonefly is in an order of insects called "Plecoptera," which means "braided-wing", due to the prominent network of veins in its wings. The common name “stonefly” refers to the fact that the larvae live among stones in rivers and streams, and the adults fly.
Like most insects, the larvae and adults live radically different lives.
By far the majority of the stonefly’s life, two to four years, is spent as a larvae or naiad (the term for larvae that live in water). The naiads are entirely aquatic, living secretive lives in cool streams where they feed on plants, algae and decaying matter.
Giant stoneflies are the largest stonefly species, with adults reaching nearly two inches long. They emerge from the water in late May to early July and live only a few days — just long enough to mate and lay eggs. To attract a mate, the males drum their abdomen on the substrate or surface on which they're resting. The female feels these vibrations and moves towards it, sometimes drumming a response call. Adults have no mouthparts so they do not eat or bite. As large and imposing-looking as giant stoneflies are, they're completely harmless.
While most people would find the giant stonefly to be an interesting-looking insect, fisherpeople get particularly excited about them because they indicate good water quality — and possibly trout. Like trout, stoneflies need fairly cool, stable water temperatures and a high amount of dissolved oxygen. Stoneflies are also a favorite food of trout, so they can be used as lures. Finding these critters in the Mississippi River is another indicator of how water pollution has greatly improved from historical conditions in the early and mid-1900’s.

https://www.fmr.org/news/2017/12/27/nature-notes-its-sign-giant-stonefly-found-downtown-st-paul


Does exercising increase the rate at which UV rays are absorbed and cause affects?

The only pathways in which I would see more sensitivity to UV light would be

If you were drenched in sweat and somehow the sweat focused the light/UV.   This is highly unlikely as I don't believe any studies have been done to show that a water based solution causes a more intense sunburn.

(Here is a further explanation by another poster on wetness and sunburn https://physics.stackexchange.com/questions/71263/why-does-wet-skin-sunburn-faster )

The increased dilation of blood vessels results in a more red thus darker and more absorbent skin tone leading to more of a sunburn

Both of these are highly unlikely of increasing the sunburn, so in my opinion exercising shouldn't increase UV absorption or make a sunburn worse. Hope that helps.


Is the amount of the soil reduced when plants grow?

The vast majority of the mass of a plant is carbon-based which is obtained directly from the air via photosynthesis. So trees are, in a loose sense, solidified air!

And most of the mass that comes from the ground is water which, of course, is constantly being replaced when it rains (or by Charlie with her watering can).


What does "melanistic phase" mean in regards to black jaguars?

In this context, "phase" means the same thing as "color phase". Here's the definition from Merriam-Webster:

  1: a seasonally variant pelage color
  2: (a) a genetic variant manifested by the occurrence of a skin or pelage color unlike the wild type of the animal group in which it appears (b) an individual marked by such a variant

So it sounds as if "phase" originated in the case of animals that spent a season with a particular pelage (meaning "fur, hair or wool"), such as the snowshoe hare, which is brown in summer and turns white in winter, and the term then began to be used for animals that might be a different color from other individuals of that species. If the alternate color was caused by a recessive allele, most offspring of that individual would have the wildtype color unless bred with another double-recessive individual, and alternate offspring might spontaneously be born to wildtype heterozygous individuals, so pre-Mendel biologists might have seen it as a "phase" between wildtype generations.

As you can see from the illustrations on the snowshoe hare Wikipedia article, "morph" is much more commonly used today for this kind of visible variation within a species. Wikipedia has a fuller description of the nomenclature of this and related terms.


Displaying nucleotide at a single position from RNA-seq reads in a BAM file

Your best option is to create a tab delimited position list file:

chr3    1000

You can then use the samtools mpileup -l pos.txt option

-l FILE      list of positions (chr pos) or regions (BED)

This file can also be in bed format if you are interested in specific regions


To start off with your last question, strandedness is something the reverse transcriptase does not care about. If you use random hexamers it will simply translate your -ssRNA into a + single stranded cDNA. Perhaps this diagram from Wikipedia makes things more clear, it is for an mRNA but the principle is the same:

This cDNA will then serve as a template for your primers in the qPCR which will turn it into a double stranded DNA molecule. In other words, after one round of amplication in a PCR reaction the DNA products of the + and the - RNA strand would be indistinguishable!

It therefore does not matter which strand you synthesise as DNA to make your standard curve. It will be double stranded so you just need to compensate for the other strand being a template in the PCR as well.


Could habitat selection pattern be deformed in environment with low variability?

If I understand your question correctly, I've seen this idea in many papers, sometimes stated clearly and sometimes in more implicit terms. After a quick look I found a paper which should be relevant as a starting point for you: Mayor et al. 2007. Spectrum of selection: new approaches to detecting the scale-dependent response to habitat. Ecology 88(7).

In my mind, there are two questions here. First, to what extent will low population size in sub-optimal environments (leading to a smaller sample to work with) lead to more uncertain inferences of preferred habitat/substrate; basically saying that noise might swamp signal in sub-optimal environments. Second, to detect selection for a particular habitat/substrate, you must sample a wide enough range of environments so that you capture both preferred and unpreferred habitats and transitions between them. In the paper I linked to this issue is touched upon in the discussion:

  Second, evidence of habitat selection depends on the scale of analysis. To understand scale dependence, investigations must encompass a spatial scope sufficiently wide to uncover scale domains of selection and the thresholds or transitions between them. In both cases, spatial scale is the empowering principle, and scaling continua are the means of application.

I've seen similar ideas as this show up in papers on habitat choice in birds living in agricultural landscapes as well, where some species are often found in rather poor environments (because these environments are common). Looking at habitat preferences only in these environments might then give a misleading view, since individual choices are constrained. Also relevant, even if not mentioned in your question, is the concept of maladaptive habitat selection (sometimes called ecological traps), where you can have situations where species use environmental cues that used to indicate high fitness habitats, but might now result in maladaptive choices, see e.g. Pärt el al. (2007). However, in this case you will still have a clear preference/selection (as in your high variability environment), the problem being that the organism is selecting suboptimal habitats from a fitness perspective.


How did shellfish and coral survive acidic oceans in earlier eras?

They didn't survive when carbon dioxide levels in the atmosphere passed certain thresholds in the history and increased ocean acidity significantly; leaving less carbonate for marine life to use for shells or skeletons. For example, up to 96% of marine life (including organisms with CaCO3 skeletons) went extinct in the Earth's most severe known extinction event, Permian–Triassic extinction. Another event called Paleocene–Eocene Thermal Maximum caused a mass extinction of benthic foraminifera.

  Five times in the Phanerozoic [the past 542 million years (My)], more than three-fourths of marine animal species have vanished in mass extinctions. Each of these events is associated with a significant change in Earth’s carbon cycle. However, there are a great many disturbances of the carbon cycle  whose imprint in the geologic record is almost exclusively environmental. These other events are relatively benign, with extinction rates barely, if at all rising, above background levels.

  Two well-studied examples illustrate these distinctions. The end-Permian extinction [~252 million years ago (Ma)], the most severe mass extinction in the Phanerozoic, plays out over a period of 104 to 105 years; the extinction interval immediately follows a perturbation of the carbon cycle of similar duration. The Paleocene-Eocene Thermal Maximum (~55.5 Ma) is a carbon cycle event of roughly similar time scale, with unambiguous signs of global warming and ocean acidification. It is associated with a significant extinction of benthic foraminifera, but there is no evidence of other major extinctions. What makes these two events so different? The unambiguous co-occurrence of the end-Permian extinction with massive volcanism provides one indication, as does the greater magnitude of the end-Permian carbon isotopic excursion compared to that of the Paleocene-Eocene Thermal Maximum. However, no general distinction, applicable throughout the Phanerozoic, exists.

  Thresholds of catastrophe in the Earth system
  By Daniel H. Rothman
  Science Advances | 20 Sep 2017 : E1700906
  http://advances.sciencemag.org/content/3/9/e1700906.full

  (emphasis mine, removed citation numbers)

Here is an excerpt from a relevant study of Knoll et al. about the affects of end-Permian mass extinction on biomineralization  which includes the extinction percentages of animals that
form skeletons of calcium carbonate and vulnerable to elevated CO2
levels:

  Within the marine realm, animals with active circulation and elaborated gills (or lungs) for gas exchange compensate for elevated PCO2 better than organisms that lack these features. Also, animals that normally experience high internal PCO2 , including infauna and metazoans capable of exercise metabolism at high rates, tolerate experimental increases in carbon dioxide differentially well. And among animals that form skeletons of calcium carbonate, species that can exert physiological control over the pH balance of the fluids from which minerals are precipitated fare better than those with
  limited buffering capacity. Based on these features, Knoll et al. (1996) divided the Late Permian marine fauna into two groups, with high and low expected survival, respectively.

  As predicted, 81% of genera in the “vulnerable” group disappeared at the boundary, while only 38% of nominated “tolerant” genera became extinct (Figure 6A). The selectivity is even more pronounced when skeletal physiology is considered alone (Figure 6B; Bambach and Knoll, in preparation). Fully 88% of genera disappeared in groups that formed massive carbonate skeletons but had limited capacity to buffer fluids (sponges, cnidarians, bryozoans, calciate brachiopods). In contrast, groups that built skeletons of materials other than calcium carbonate lost only about 10% of their genera. Intermediate taxa—groups like mollusks that have a substantial commitment to carbonate skeletons but some physiological capacity to regulate the chemistry of internal fluids—lost 53% of
  their genera. Of these, those genera considered vulnerable on the basis of the other criteria noted above went extinct at twice the rate of those otherwise considered tolerant.

  Biomineralization and Evolutionary History
  By Andrew H. Knoll
  Department of Organismic and Evolutionary Biology
  Harvard University
  Cambridge, Massachusetts, 02138 U.S.A.
  https://web.archive.org/web/20100620222809/http://www.geochem.geos.vt.edu/bgep/pubs/Chapter_11_Knoll.pdf

  (emphasis mine)


What is the lowest pressure at which plants can survive?

I like your question!

Low surface pressure on Mars (averaging 600 Pa or about 1/170 of Earth's at sea level) is only one difficulty that an organism would have to contend with. In addition, mean surface temperatures are ~210 K (- 63 °C), the surface ultraviolet flux is extremely high (no ozone layer) and an aridity comparable to the Atacama desert. On the plus side, a 95% CO2 atmosphere might promote photosynthesis.

So, higher plants are extremely unlikely to prosper on Mars. Purely in terms of pressure, experiments suggest that at 1/10 Earth atmospheric pressure vascular plant transpiration increases significantly. So much so that they enter into a drought response which often leads to plant death.

However, lichens may be another matter. These are often adapted to low precipitation/pressure environments such as high mountains. Indeed, this article addresses exactly your question (sadly it is not open access). The authors suggest that the lichen Xanthoria elegans experiences no loss in vitality after 22 days exposure to laboratory Mars-like conditions (low pressure, low temperature etc.)!

Having skimmed this article I am frankly amazed (and slightly dubious) at the result. However, it should be noted that they only ran the experiment for 22 days, applied no ionising radiation (to simulate the high UV flux) and make little mention of the precise metabolic state of the lichen. If it has entered into cryptobiosis (cessation of metabolic processes) then it can't exactly be regarded as prospering.

de Vera et al., 2010, Astrobiology, 10, 2, Survival Potential and Photosynthetic Activity of Lichens Under Mars-Like Conditions : A Laboratory Study


How to safely conserve my current DNA methylation marks?

To record the current methylation state of your DNA, you can use bisulfite sequencing. Basically, you take half of your DNA sample and treat with bisulfite, which deaminates cytosines (C->U) , so they read as T instead of C. Methylated cytosines are protected, so they still read as C. You run two sequencing reactions, one with bisulfite-treated and the other with untreated DNA, so you can tell where the true Cs are in the genome. See the below diagram:

Wikimedia commons

Note that if you're thinking of doing this from a longevity point of view, that there are hugely different methylation patterns in different cell types; I'm not sure which cell type you'd want to pick. Also, methylation is not the only covalent modification of DNA that exists, there's also hydroxymethylation, and I'd bet there are more that we haven't discovered yet. There certainly are in bacteria and phage (glucosyl-hydroxymethylcytosine, for one). The hard thing about saving things for the future is that we really don't understand the full picture of what's happening now epigenetically, and as such, we don't have assays to detect things we don't know about.


Do species ever move into new territory and then die out because of the local diseases?

So how come the story is always that the invading species kills off
  the locals, when you would expect the invading species to have
  hundreds of totally new threats and strange foods to handle, would be
  unable to cope, and would die out?

There is a problem of observation bias for these two scenarios.  In the first scenario a few members of an invasive species enter a new range, transmit a novel disease to the pre-existing species, which suffers a massive (easily observable) die off. In the second scenario, a few members of an invasive species enter a new range, catch a local disease, and die in short order (unobserved and unnoticed).

In other words, a few individual deaths from any cause will generally go unnoticed. Thousands or millions of deaths of deaths from a novel disease are more likely to attract attention.


Why do neurons have long axons but short dendrites?

Axons are used to transfer electrical signals from Point A to Point B.
Dendrites are for receiving electrical signals from different neuron cells via their respective Axons.

There are mainly two different types of Axons, insulated and non-insulated.

Insulated Axons allows extremely high velocity of electrical signals to propagate from Point A to Point B. Please note that insulated axons are not entirely insulated, the axons are only insulated at every given interval for a certain length (in measurement of distance). This forces the electrical signal to jump from one gap to another gap between insulation and result in extreme speed of electrical signal propagation down the axon.

Non-insulated axons still allow high velocity of electrical signal propagation but it is very much slower as compared to insulated axons. This is why when you have a stomach ache, its a slow and dull pain due to non-insulated axons which gives you prolonged pain signal. However, if you accidentally knock into a sharp object, you receive an instant sharp pain for a split second for you to react at that instant (Its a biological life saving function) due to insulated axons that gives you extreme speed of pain signal propagation.

On the other hand, dendrites are not built for signal transmitting but for signal receiving. Dendrites comes in different configurations, one such examples are your color sensory cells in your retina.

This is why dendrites are short while axons are long. They are configured for different purpose. Just a bit more information, electrical signal in biofluid are actually ionic current. Ionic current are different from electron current, the charge carrier are different. Lastly, electrical signal are generated due to electrochemical gradient on cellular level. When a certain membrane potential threshold is reached, action potential will be triggered and they resulted in the firing of electrical signal down the axons.

I hope you find these useful.

Best Regards

Price


Do low light levels during development affect the distribution of rods and cones in the retina?

I found a few studies in fish that showed constant light exposure changing rod density. First one in goldfish:

Raymond PA, Bassi CJ, Powers MK.
Lighting conditions and retinal development in goldfish: photoreceptor number and structure.
Invest Ophthalmol Vis Sci. 1988 Jan;29(1):27-36.
http://www.ncbi.nlm.nih.gov/pubmed/3335431

  The retinas of 63 goldfish were examined after varying durations of exposure to one of three environmental lighting conditions beginning before hatching: constant light (340 lux), cyclic light (12 hr 320 lux, 12 hr dark) and constant dark. Up to 8 months, no effects of constant light or dark on photoreceptor numbers or structure were apparent. Densities of rod and cone nuclei were normal and all retinal layers appeared normal by light microscopy. Exposure to constant light for 12 months or longer resulted in a reduction in rod density by 37%. Cone numbers were unaffected by constant light, even with exposures of 3 yr, and rod and cone outer segments were normal in length at 11-20 months under all environmental conditions. Due to poor survival, only one animal was available for quantitative examination from the group reared in constant dark 12 months or longer. Photoreceptor size and number in this retina were similar to those in the constant light condition. The results suggest that the formation and maturation of rods and cones in goldfish retina is unaffected by rearing in constant light. However, long-term exposure (greater than or equal to 12 months) may disrupt maintenance of differentiated rods.

See also http://www.vision-in-cichlids.com/fenotypic_plasticity.htm where they say rod density changes in early retina development of Tilapia leucosticta.


The pET vectors family is what you are looking for.


You are not far off the mark I would say. Strictly speaking it's not correct to say that mitochondria oxidize fat. By "fat" we usually mean triacylglycerides, and these must first be hydrolyzed into free fatty acids (by enzymes known as lipases) that can be oxidized in the mitochondria. But many researchers and textbook authors are not always careful with this distinction.

Most fatty acids are indeed oxidized ("digested" sounds strange to me) in the mitochondria into acetyl-CoA units, in a process known as beta-oxidation. The acetyl-CoA units produced are then further oxidized into CO$_2$ by the TCA cycle. These processes generate NADH and FADH$_2$ which is converted into ATP by the respiratory chain.

There are exceptions though. Very long-chain or branched fatty acids are instead oxidized in peroxisomes, which contain enzymes specialized for this purpose.

There is no such thing as "anaerobic respiration": in animals, respiration always uses oxygen as the terminal electron acceptor. Mitochondrial beta-oxidation is coupled to the respiratory chain, and therefore requires oxygen. Peroxisomal oxidation is not directly coupled to respiration, but the process still requires oxygen, which in this case is reduced directly by the fatty acid oxidases. So there is no truly anaerobic form of fatty acid oxidation.


The idea that memories could be stored as RNA or proteins is an old one.  It got a lot of attention decades ago when James McConnell did a number of experiments where he conditioned planarian flatworms to respond to certain stimuli, ground them up, fed them to worms that hadn't gone through the conditioning.  He claimed to have observed that the worms fed conditioned worms learned to respond to the stimuli faster.  This supported the idea that memories were just RNA or proteins, and thus survived the grinding up process.  His results were not readily reproducible, and so the idea fell out of favor.

There have been a number of studies at this point that have been able to look at the firing of individual neurons and shown that there are unique patterns that respond to different stimuli, for example: http://www.ncbi.nlm.nih.gov/pubmed/10966627  So I think it is pretty well established that there are certain connections between neurons that are critical, sometimes even individual neurons.

That doesn't necessarily rule out that there are unique RNA or proteins in those specific neurons, and they are whats actually storing the memory.  I'm not a neuroscientist, but I think the biggest argument against such a storage system is simply the speed with which you can recognize something.  When you see a face you know you nearly instantly recognize the person, and have a flood of memories about that person.  If the memories were somehow stored in RNA or protein structures, I think it would take much longer to somehow "read-out" that data from the molecular structure.  The only thing that really works that fast are the action potentials in neurons.

An interesting comparison might be made to the system in our bodies that DOES have molecular-based memory, the immune system.  When you get sick with a cold you've never been sick with, your immune system doesn't immediately recognize the antigens that come from that virus.  Through the process of somatic hypermutation, your body produces B- and T-cells that have protein receptors that recognize the viruses and the cells infected by the viruses and go and kill them.  A small subset of the T and B cells that have the molecular recognition of that cold become 'memory' cells.  These memory cells that go into a quiescent phase, waiting around until the next time that cold infects you.  But that time they 'remember' it immediately, and you dont get nearly as sick, if at all, because the genes for those recognition proteins are stored in the memory cells.  The activation of immunological memory cells takes a long time as compared to remembering a face, or some other normal memory function, so such a molecular system couldn't be responsible.


Is this plant with very asymmetric leafes Aegopodium podagraria (aka ground elder)?

A man, collecting herbs, confirmed my suggestion about Aegopodium podagraria. Together with what I read about this plant, I can set my question as being answered with Yes.


Detecting cancer in the hyperplasia phase using image processing and SEM

Not exactly spectroscopy, but microscopy is common for detecting pre-cancerous tissue as part of the standard Pap Test given to women at regular intervals throughout their life:

https://en.wikipedia.org/wiki/Pap_test

This is typically done by a team of cytologists (with pathologists confirming results, particularly in abnormal cases), but is beginning to have automated screening (with human oversight).

One of the problems with any form of screening is that the potentially problematic tissue needs to be observed, which is typically quite an invasive procedure. A potential melanoma is usually cut out prior to analysis, and I expect that any procedure involving a scanning electron microscope will also require tissue removal prior to analysis.

A more interesting development in the area of cancer screening is in looking for cell-free genomic DNA in blood; blood tests are much better tolerated for screening purposes in comparison to other tissue removal. With high-throughput short-read sequencing, it's possible for some cancers to see DNA changes before their effects are detectable through histological methods.

Here's a review paper on cfDNA screening, which is is generally negative about the whole thing:

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002205

And one that is generally positive:

http://cancerres.aacrjournals.org/content/76/14_Supplement/LB-136.short


Image Dataset for Cardiac cells for Mus musculus?

Sure help yourself with the broad institute image sets collection

Broad Bioimage Benchmark Collection - Annotated biological image sets for testing and validation:
https://data.broadinstitute.org/bbbc/image_sets.html

And the EMBL-EBI:
https://www.ebi.ac.uk/bioimage-archive/

No mouse cardica cells, but I am confident you can easily do transfer learning after training on those.


is there a way to do batch download for all gene pathways?

Try using KEGG REST.

http://rest.kegg.jp/link/pathway/hsa ## list of all genes and pathways in Humans


Are the sister chromatids exactly the same?

A new chromatid is synthesized by copying the other chromatid. As such two sister chromatids are (quasi) perfectly identical.

Why did I say quasi? Because there are sometimes "errors" when replicating DNA. These "errors" are called mutations. As far as I know, most mutations occur during meiosis though and only very few occur during mitosis. So, to a pretty good approximation, yes sister chromatids are identical.


When we talk about 'can something happen', then I don't think the answer would need a reference.

Of course, humans can attain the ability of magnetoreception, but the main question is What good will it do to us? Instead it'd prove to be disadvantageous as:

We already have smartphones, compass for identifying magnetic field, so why will the body prefer to waste energy on something which can be done without wasting energy?
We all know that the earth has its own magnetic field. So whenever you wake up or go for a walk (just do any movement), you'll feel an irritating magnetic sensation. Why would that be useful?

Even if we don't talk about disadvantage, then also magnetoreception wouldn't prove to be much useful in whole human population. Randomly, some guys might get a few genetic mutations which would allow them to feel magnetic field, but that wouldn't be of any use to them.

BUT, to your interest, humans do have magnetoreceptors, in retinas. See this article:

  But cryptochrome isn’t unique to birds – it’s an ancient protein with versions in all branches of life. In most cases, these proteins control daily rhythms. Humans, for example, have two cryptochromes – CRY1 and CRY2 – which help to control our body clocks. But Lauren Foley from the University of Massachusetts Medical School has found that CRY2 can double as a magnetic sensor.

or this Wikipedia article:

  Humans are not thought to have a magnetic sense, but there is a chemical (a cryptochrome) in the eye which could serve this function.(2)

Source                                                           Source

So, acquiring magnetoreception might be easier than you'd expect, but it doesn't happen even in this condition. Why?, who knows? Maybe because our body rejected magnetoreception as useless. Maybe at some point of time, humans had the ability to feel/see magnetic field, but this feature now seems vestigial.

EDIT: Regarding "magnetic bones", every article that I could read only points to this Nature article you referred to in your question. So it doesn't seem like there has been much research on it, or maybe this article itself is enough to conclude the topic.

References:

1.http://blogs.discovermagazine.com/notrocketscience/2011/06/21/humans-have-a-magnetic-sensor-in-our-eyes-but-can-we-see-magnetic-fields/

2.https://en.wikipedia.org/wiki/Magnetoreception

3.http://www.ks.uiuc.edu/Research/cryptochrome/

4.http://www.microsystem-components.com/html/magnetoreception.html

5.http://www.nature.com/nature/journal/v301/n5895/abs/301078a0.html


Like you said the sexual X chromosome inactivation is random in each different cell, this means women have some cells with the maternal x chromosome active and others with the paternal x chromosome active. Now if a woman carries the daltonism gene mutation (heterozygous for color blindness) she can actually manifest signs of the disease if the retinal cells randomly silenced the healthy x chromosome instead of the mutated one in more cells compared to the opposite pattern of silencing (meaning she can present daltonism out of pure bad luck).

It is worth mentioning that the magnitude of this disease will never be as strong as it presents itself in males since women (even the unlucky ones who present signs of daltonism) will always have the protection of a certain percentage of retinal cells with the healthy x chromosome active. The only way a woman could have classic daltonism to the same extent as a male is if she presents the color-blindness gene mutation in combination with Turner syndrome.

In conclusion recessive X-linked diseases aren't "everything or nothing" since woman could present signs in function to the number of cells that randomly inactivated the healthy X chromosome. They will fully express themselves in males all the time though.

References:

Scitable by nature education - Q&A

X chromosome inactivation - Nature education


Insect Egg Case, and if so, What Insect?

A local graduate student relayed the answer to me.  It is an ootheca of a praying mantis.  There is some additional background on the egg life history here.  Wikipedia reports there are three mantid species.  The upper-left picture of the ootheca here is essentially what I observed, so we may be looking at the genus Stagmomantis.  There are some other great pics at that last site.


Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\cdot 2 + 1\cdot 3)/10 = 2.1$.

The Price equation or theorem is:
$$(1)\hspace{10mm}w\cdot \Delta z =  \text{cov}(z_i,w_i) + E(w_i\Delta z_i)  $$

While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do:

  "The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection..." p. 376.

We work with reference to the following data and will define variables below.

$$\begin{array}{c | c | c | }  n_i & 3 & 2  \\ \hline
z_i &1  & 2  \\ \hline
w_i &1& 5   \\ \hline
n_i' & 3 & 10  \\ \hline
z_i' & 1 & 2.1  \\ \hline \end{array}$$

All cites WK are to the Wiki page on the Price equation:

(1) We can write $\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\hspace{10mm}$ WK eq. (7).

Explicitly:

$$ \text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$

$$ = \frac{1\cdot1\cdot3 + 5\cdot2\cdot2}{3+2} - (2.6)(1.4) =\frac{23}{5} - (2.6)(1.4)= 0.96$$

(2) We can write $E(w_i\Delta z_i) = E(w_i z_i') - E(w_i z_i).\hspace{10mm}$ WK eq. (8).

Now $E(w_i z_i') = \frac{1}{n}\sum w_iz_i'n_i\hspace{40mm} $ WK eq. (9a).

$ = \frac{1}{2 + 3}(1\cdot 1\cdot 3 + 5\cdot(2.1)\cdot 2) = 24/5.$

$E(w_iz_i) = 23/5$ from (1) above.

So  $ E(w_i z_i') - E(w_i z_i) = \frac{24}{5} - \frac{23}{5} = 1/5$

(3) Finally we have $\Delta z =  z' - z = \frac{2.1(10) + 3(1)}{13}-\frac{3\cdot 1+2\cdot 2}{5} = \frac{29}{65} $

and $w = \frac{3\cdot 1+ 2\cdot 5}{3+2} = \frac{13}{5} = 2.6$

So $$w \Delta z = (2.6) \frac{29}{65} = 1.16 $$

$$= \text{cov}(z_i,w_i) + E(w_i \Delta z_i) = 0.96 + .2 = 1.16 $$

  $n_i$ is the number of elements in group $i.$

  $n_i'$ is the same for the filial generation.

  $z_i$ is the value of a character for group $i.$

  $z_i'$ is the same for offspring of $z_i.$

  $w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have.

  $w$ is the average fitness for the parental generation.

  $z$ is the average value of z for parental generation;

  $z'$ is the average of z for the filial generation.

  $z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial
  generation minus the average of $z_2$ in the parent's generation.

$^1$ This site condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended.


How long do the periods of systole and diastole last?

The following image from wikipedia answer what you need. You can check corresponding page for details.

The top part shows the details of the different processes during a heart beat. Corresponding to these events the ECG reads are marked. As you can see the distance between the T wave ( the small bump after the QRS complex) and the next P wave corresponds to the diastole. As you can see the pressure changes correlate well with the electric reads from the heart. This wiki page has great descriptions of the features of the ECG and the corresponding events.

For example P to QRS corresponds to the conduction of stimulus from the sine node to AV node, or QRS depicts the rapid depolarization and repoliarization of the ventricles. This latter leads to strong muscle contraction and this causes intaventicular pressure rise, that is followed by aortic pressure change.

Edit: Sorry, for missing the key point, I totally misunderstood what you needed. I'll try to correct my mistake (I'll leave the previous info as it may be useful for others) The authors of this paper did a really nice work on modeling and measuring left ventricle contraction time and other things.

The reference: (Beyar and Sidman 1984)
Long story short: the contraction of the ventricle depends on the initial amount of blood (preload), aortic blood pressure at the end (afterload), and intial contractility. The results are summarized in three tables:

As you can see in the last columns, the ejection time varies with the parameters. The ejection time that is required for the ventricle to push the blood out to the aorta. Under normal circumstances a complete heart cycle is about 0.8s (or 800ms) this pie char shows the time ratio of main events. (Image taken from: tutorvista.com)

Note that complete cardiac diastole is when all the heart muscles are relaxed (this can be shortened if higher heart rate is required).

According to wikipedia

  Isovolumic relaxation time (IVRT) is an interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve. A normal IVRT is about 70 ± 12 ms, and approximately 10 ms longer in people over forty years. In abnormal relaxation, IVRT is usually in excess of 110 ms.

Isovolumic relaxation is when the muscle relaxes, yet the volume of the ventricle remains the same, thus only the internal pressure changes (it is analogue to isovolumic contraction - when the volume is unchanged, but pressure is built up, this happens at early ventricle contraction).


Why doesn't glucagon promote glycogenolysis in muscle?

Glucagon needs glucagon receptors to have an effect on the tissue or organ in question, and your answer can be found there.  Glucagon receptors are found in the liver, like you say, but they're also found in other tissues like intestinal smooth muscle, and brain tissue (http://www.glucagon.com/glucagonreceptor.html) - but, crucially, not in skeletal muscle.  So glucagon-stimulated glycogenolysis isn't actually restricted to the liver, it's also found elsewhere.  Liver-based glycogenolysis has a significant role in blood-sugar control though, so it's often only the liver that gets mentioned.


It would depend on the type of tissue. But if you are interested in any tissue, then have a look at this BioNumbers entry. It says that there are 100000 insulin receptors per cell in rat adipose tissue. Divide it by the surface area of the cell and you'll get the density. Cell dimensions can also be found in BioNumbers


This phenomenon is called polyspermy and results in an embryo which is not viable. This is because it has more than the usual two sets of chromosomes (one from each parent), but one from the mother and multiple (depending on how much spermcells enter the egg) from the father.

To avoid this, most species (including mammals) have protective mechanisms against it. The so called cortical reaction which starts upon fertilization (the first sperm penetrating the zona pellicula) and releases cortical granules to prevent further sperm cells from entering.


Why antipyretics do not bring the body-temperature below normal?

Antipyretics doesn't work by reducing the body temperature but blocking pathways that make it higher.

For paracetamol/acetaminophen the mechanisms implied are not currently completely clear (as reported on Wikipedia or on Katzung's "Basic & Clinical Pharmacology").

For the most common NSAIDs (aspirin, ibuprofen, naproxen, ...) the mechanisms instead are more clear as they block some enzymes that are involved in production on inflammatory molecules (enzymes COX1 and COX2 that are implied in the arachidonic acid pathway as said on this article).

When these inflammatory molecules rise concentration in blood they can get to the hypothalamus so it will set the body temperature at an higher level; when these signals stop coming (inflammation stops or no more molecules are produced because of drug's block) the hypothalamus sets the temperature to the normal range.

More infos about hypothalamic temperature set point.


Why Didn't Evolution Cause the Human Body to become Streamlined?

If streamlining makes movement/locomotion quicker and easier, why didn't the apes evolve into life-forms that had streamlined bodies (much like fish)?

As with everything in Evolutionary Biology, you must ask yourself: Gain vs. Cost?

In your specific case, the Gain is very little.  Air isn't nearly as dense as water, so a streamlined form won't show a major benefit unless the organism is traveling very, very quickly. This is why you see it in birds; raptors can travel over 100mph while diving, and at those speeds small changes in drag can mean the difference between dinner and starving. Smaller birds often make very quick turnabouts and changes in direction mid-flight where, again, small changes in efficiency can mean the difference between life and death. The cost was is worth it.

For apes and monkeys, moving very quickly isn't a case of living or dying. That's what we evolved opposable thumbs and prehensile feet(/tails) for. You don't need to run fast when you can climb a tree and simply get away from any predators on the ground. After we came down from the trees permanently, our larger brains allowed us to use tools to fend off predators - which, again, is much simpler than evolving an aerodynamic form that won't make a difference until you're running at the speed of a car.

So, in lieu of becoming a land-shark, we have hands that can use keyboards and minds that can invent the keyboard. Unfortunately, while the gains are many, the costs do include both a very long period of time where humans are helpless without parents, and an absolutely terrible form of locomotion with our upright stance on forward-pointing knees. Though you won't catch Cheetahs digging sewers anytime soon.


What's the smallest size a human eye can see?

Very nice question!

First of all, the 'smallest size' that a human eye can perceive is called visual acuity, and can be expressed in various ways. It cannot simply be expressed by means of size measures, as objects with a fixed size are perceived as smaller when viewed from a distance (perspective). A familiar example is the train track:

Hence, visual acuity has to be measured as a function of viewing distance, i.e,  in degrees of visual view. Measured in degrees, the visual acuity of the average normally sighted person is 1/60 degree, or 1 minute of arc (1 MAR) (Webvision, chapter "Visual Acuity", by Kalloniatis & Luu).

Using the basic structure of the eye and some trigonometry one can deduce the smallest visible size :

The trigonometric formula becomes: $2d \times tan(\frac{\alpha}{2})$ with d being the viewing distance and alpha ($\alpha$) the visual acuity expressed in radians ($\pi \times \frac{degrees}{180}$) (NDT resource center).

Assuming the closest distance an adult can focus (~100 mm) and an average maximal acuity of 1 MAR, the smallest visible size boils down to 29 microns.

A young child can focus at distances down to ~50 mm, and can have a visual acuity of 0.4 MAR, which yields 6 microns.

Note that 1 MAR encompasses 288 microns on the retina, and some 180 photoreceptors. The optical limitations of the eye (such as diffraction by the lens and light scatter by the neural cells in the retina) limits the resolution of the human eye below the theoretical 'pixel limit' of the eye.

So to sum up, depending on one's age, one should be able to see targets in the order of 6 - 29 microns. The lower bounds of this range are indeed in the range of the waterweed cells and cloth fibers you describe.

PS - the values described are representative under ideal conditions, i.e., under situations of abundant lighting and high contrast.


What is this plant with some seeds around its leaf?

It is Andrographis paniculata also know as Kalmegh or Kalamegha

It has close resemblance to Mexican Tea Plant also.


Why does HIV belong to a group of retroviruses called lentiviruses?

In Latin, lente means slow, so lentiviruses are retroviruses that are characterized by long periods of latency.

lentivirus A group of retroviruses that include human immunodeficiency virus, HIV-1. They cause disease after a long incubation period.
latency A state in which a virus infects a cell but does not replicate.

-Janeway's Immunobiolgy, 8th Edition, Kenneth M. Murphy
HIV-1 is characterized by long incubation periods. It can often take months before the virus is detectable on HIV tests.
It is also known that HIV reservoirs will exist in a patient, such that even if they have undetectable viral loads when on Antiretroviral Therapy, once they come off of the treatment, they will begin to produce virons again. The likely reason for that is that the immune cells that they infect can be very long lived, and as the viral genome has been incorporated into the host cells genomic DNA, it is incredibly stable. It will stay dormant for years until it is able to replicate again.


Is this some kind of parasite crawling about in my yard?

It looks like a terrestrial ribbon worm.

https://upload.wikimedia.org/wikipedia/commons/a/ad/Terrestrial_Ribbon_Worm_%28Nemertini%29_%2822799575773%29.jpg

Nemertean worms are not leeches, but a different group of worms.  Most are marine but there are a few terrestrial ones.  This depicted worm is from Borneo and other terrestrial nemertean worms are from South Asia also.  But I have read that these can stow away in plants and are turning up in other parts of the world.  I found some small ones in San Diego that I thought were terrestrial leeches but were nemertean worms.

I would be very curious where you are in the world that big ribbon worms are partying in your yard.


Substitution rate at neutral sequences

The rate of substitutions at neutral sequences is given by the mutation rate. It si a very simple and classic result. It is because the probability of each new neutral mutation to fix is $\frac{1}{2N}$ (which you can calulate from a Moran branching process as well as from a simple Wright-Fisher model of genetic drift) and there are $2N\mu$, new mutations at each generation (where $N$ is the population size and $\mu$ the haploid mutation rate), resulting in a substitution rate of $2N\mu\frac{1}{2N} = \mu$.

Substitution rate at non-neutral sequences

A beneficial mutation has a probability higher than $\frac{1}{2N}$ to fix, while a deleterious mutation has a probability lower than $\frac{1}{2N}$ to fix. Therefore, the more beneficial mutations there are, the higher is the substitution rate. There are a number of approximations to the fixation probability of a non-neutral mutation. For example, using diffusion equations, one can approximate the probability of fixation of a deleterious mutation with selection coefficient $s$ by $\frac{1-e^{-\frac{4s}{N}} }{1-e^{-4Ns}}$ from some Kimura paper.

This rate of substitution therefore depends upon the selection scenario. It is lower than $\mu$ in conserved sequences and it is high than $\mu$ in sequences that undergo positive selection. So, the reason for such fast evolving sequences is just that they are under positive selection.

How about HAR1?

Without looking for more accurate statement form the scientific literature, the same wikipedia article you cite says

  HAR1A is active in the developing human brain between the 7th and 18th gestational weeks. It is found in the dorsal telencephalon in fetuses. In adult humans, it is found throughout the cerebellum and forebrain; it is also found in the testes.[1] There is evidence that HAR1 is repressed by REST in individuals with Huntington's disease, perhaps contributing to the neurodegeneration associated with the disease

It already gives you a vague idea of potential selection pressures on those sequences in the human genome.


What part of the body holds the most pain receptors?

There is anecdotal evidence that the cornea is indeed the most sensitive tissue. Just think of it: our eyes well up with tears when slicing an onion. A tiny insect who flew into our eye feels enormous, and a corneal injury, say a scratch, can leave us severely compromised for a number of  days. Luckily, the cornea has rapid healing powers.

The cornea is so sensitive that part of determining the amount of brain injury one has sustained is by measuring the corneal reflex. The way this is done is to take a cotton swab and pull off some cotton fibers and twist them into a tiny tail (so to speak), and tough the cotton fibers to the cornea. If there is no reaction, that's a bad sign.

The Sensitivity of the Cornea in Normal Eyes
Evidence-based guideline update: Determining brain death in adults
Report of the Quality Standards Subcommittee of the American Academy of Neurology


What is the top speed of muscle contraction?

Your question is a good one. The velocity of muscle contraction depends on the:

Initial length of the muscle
The Load on the muscle

Source: Medical Physiology : a cellular and molecular approach by Walter F. Boron, Emile L. Boulpaep - 2nd ed. Page 248

From the above picture we can see that:

The velocity of muscle contraction is not constant. Initially it is zero and then it accelerates to reach a peak
The maximum velocity of muscle contraction is constant at any different initial muscle length
The lower the load the steeper the rise of velocity

So the velocity of muscle contraction should be calculated on a case by case basis.

What can be calculated

What can be calculated is the displacement and frequency of actin myosin cross-bridging.

Under microscopically isotonic conditions, the quantal displacement of a single cross-bridge is ~11 nm.

The frequency of actin-myosin cross-bridging depends on atleast:

ATP concentration
Temperature

At an ATP concentration of 1 µM the frequency is 3.8 ± 0.4 M-1s-1

At 170C the mean time for single displacement was 15±20 ms. While at 250C the mean was 6.4±3.6 ms.

Source: Characterization of Single Actin-Myosin Interactions by Jeffrey T. Finer, Amit D. Mehta and James A. Spudich.
Biophysical Journal, Volume 68, April 1995, p.291s-297s

Concerning your actual question regarding the quadriceps velocity and the velocity of the swing, you should keep the following in mind while calculating:

Quadriceps acts over a second order lever: The Knee is the fulcrum, the effort is put over the tibial tuberosity where the quadriceps is inserted and the load is the foot and whatever it hits/lifts...
The contraction of the quadriceps is calculated as linear velocity while the kicking action is circular - so what you actually observe is the angular velocity. So appropriate angular velocity to linear velocity conversion should be made.

All the best!


Can the spike protein created by the Covid mRNA vaccines be created independently of the human body, and is there a higher cost to that?

It is quite costly and difficult to manufacture and store proteins. It's very likely more efficient to have the human cells create as much protein as they can, from a relatively small amount of mRNA. Remember than one mRNA molecule can be translated into protein many many many times, so the manufacturers need to only make one mRNA molecule to get many protein molecules, whereas it would be more expensive to manufacture many protein molecules.
It's kind of a "give a man a fish, he eats for a day, teach a man to fish, he eats forever" situation. Better to give the body the instructions (mRNA) than the product, for cost effectiveness.


Growth mediums required for human cell cultures

So this paper probably has what you need.
Isolation and cultivation of human keratinocytes from skin or plucked hair for the generation of induced pluripotent stem cells

The first part of that paper covers just the cultivation of keratinocytes.
It's actually moderately difficult to culture keratinocytes, so if you just want to try out cell culture I wouldn't recommend this as your first step.

A good first step to learning the techniques of cell culture would either be bacterial, fungal, or yeast cultures because they are cheap, hardy, and don't require expensive equipment. Yeast culturing would be closest in technique to mammalian cell culture among the three  Yeast culture info here


Based on what I learned from my comp vert anatomy class, the clavicle does not articulate with other skeletal elements, thus allowing the scapulae to retract further along with the forelimbs


Not very common, and not found so far in nature, but they exist and are called deoxyribozymes.

Additional information:

Deoxyribozymes are the equivalent of ribozymes in the DNA world and can function as catalysts for different biochemical reactions, such as DNA cleavage. While DNAzymes (short name) were synthesized in a laboratory context (In-vitro) and proved to be active, no observations were made of DNA molecules having an enzymatic activity In-vivo which is of course not a definitive proof they don't exist in nature.

The latter point is a major difference compared to ribozymes which were proved to be active and functional in living cells.


How would cloning affect conservation of rare species?

Cloning become an important method for conservation genetics. However, it is not a magical solution and doesn't solve all of the the problems. There are two key considerations with conservation: short term issues which are causing the immediate threat such as poaching, habitat destruction etc. and long term issues of genetic variation. Genetic variation is critical to the long term survival of a species because low genetic variation results in inbreeding depression (reduced ability to survive and reproduce resulting from higher expression frequencies of deleterious mutations) and reduced potential for adaptation. The rate of adaptation is determined by the strength of selection and the volume of genetic variation; without genetic variation there can be no adaptive evolution. Therefore, genetic variation is key to the long term success of a species.

Where cloning can come in is it can be used to increase the gene pool, sometimes quite substantially. Consider the meta-population of a species, this could be allowed to include all of the wild sub-populations and all captive or managed (semi-captive) populations. For example, there are ~3900 wild tigers in the world, and ~5000 in captivity. Among all of those, only a subset contribute offspring to the next generation of wild animals, reducing the effective population size, and increase rates of inbreeding and genetic drift. For example, often very few males fertilise the females of a population with strong effects on the effective population size. What cloning could be used for (to various levels, depending on the specifics of the method) is to allow other individuals to contribute. For example, by cloning the members of a wild population that were unable to secure mates during a reproductive season (there is often high variance in mating success which reduces effective population), conservation managers can artificially re-inflate the effective population size to more closely resemble the census population size. In other cases, conservation managers may chose to clone particularly viable/fertile individuals that are approaching old age or nearing death, and are therefore at risk of being lost from the population. Conservation programs could use cloning of (semi-)captive individuals and introducing clones from (semi-)captive populations in to wild populations allowing genetic variation to be drawn from the gene pool of (semi-)captives in to the wild populations. Increasing the variance in the gene pool will increase the adaptive potential of the wild population. Another option is to clone wild animals in threatened areas (e.g. where populations are in decline as a result of poaching) and to put the clones in to safer areas such as national parks, or even zoos, to preserve genetic variation while conservation managers try to bring the other issues under control. Effectively this would act a bit like a seed bank.

However, there are some issues to consider, and this is a non-exhaustive overview. What if there was a good reason for some individuals not mating? The action of selection, which causes adaptation, is to induce variance in reproductive success as a result of the genes an individual carries: in principle selection reduces genetic variation and allows the "better" variants to prosper. So if we clone a wild individual that produced no offspring in the reproductive season we may just be maintaining genes in the population that selection would otherwise be removing. In other words, cloning efforts could be counter-productive to the long-term success of the species and make conservation more difficult. What if we reintroduce bad genetic variance to the wild population? Captive populations have adapted to some degree to the environment that they are in, this may have selected genes out of those populations that are more beneficial in the wild. For an extreme example, dogs are descended from wolves and have adapted to an enormously different environment, so it would probably be very counter-productive to start cloning chihuahuas and introducing them to wild wolf populations as a conservation strategy to get genetic variation from captive "wolf" populations (but maybe the chihuahuas would be a good food source at least). Can clones be effectively, and efficiently, reared and introduced to wild populations? It will be extremely hard to actually get to the point where clones can be successfully introduced to wild populations. Resources (including money), are extremely limited in conservation, so there may be better ways to use those resources. Are populations under remaining threat from short term issues such as poaching and habitat loss? If there is continued extrinsic threat to the wild population then there is not much use in cloning, because clones will also be threatened by the same issues. Many places are still under serious threat from poaching. Adding some clones would be like trying to stop a ship from sinking and using a tiny bucket to bail out the water; you need to plug the hole first or use a really big bucket (can cloning be a big enough bucket?).

Bonus: You could read here about the issues faced in the Isle Royale system of wolves and moose, where wolves are on the verge of extinction, and the impacts it will have on the ecolsystem.


Solution based measurement of Solvent-Accessible Surface Area of macromolecules

I only know of one method, but here it is.  You create a sphere the diameter of the VdW radius of water, and then 'roll' it along the surface.  I know this as a Richards-Lee surface, wikipedia has another name for it.

This looks complicated, but its not.  you move the probe sphere along the surface of the molecule in the XY plane until it just touches the vdW radius of the protein, keeping the center of the sphere as the surface, all the way around the molecule.  If you like, you can color the surface by the charge of the position too, which is useful for discussing solvent interactions.

Then you translate along the z axis and do another contour until you run out of protein.  Apparently jmol and other packages will do this for you.

Wikipedia references a more mathematical method LCPO, which I am not so familiar with.

Is this accurate?  As usual with such calculations its more of a guess than an answer.  You can do the calculation on any structure or any ensemble of structures (like NMR gives).  It doesn't understand how the molecule might be flexible or dynamic.  If you read up on your physical chemistry you see that proteins breathe and can allow diffusion into the core rather readily.  If I recall right, you can get rather large molecules quenching heme flouresence in hemoglobin at room temperature.

If you are looking to dock 2 proteins, SAS might be more useful.  Its an important piece of information, but not an ultimate answer.  I'm afraid with proteins that doesn't happen so easily.

@bobthejoe asked about SAS for which no structure exists.
This is an extremely difficult thing to even guess at.  The non helpful answer is that the surface of the protein goes as the cube root of the molecular weight of the protein.

By getting a solution of the protein and shooting it in a syhcrotron, you can get a mean radius of gyration pretty easily which will give you an ellipsoidal volume (and surface area) for a protein.  Again most of the particulars would be lost and this could easily be off by 25% for an irregularly shaped protein.  For a regular globular protein it might give an answer similar to the power law above.

I have seen physical chemistry experiments that look for changes in osmotic pressure when the salt concentration in a solution of the protein changes substantially (Adrian Parsegian's work at NIH in the late 80s).

I doubt you will find any of these answers useful as their mean error is going to be very large (20-200%) and also assumes the protein is soluable and amenable to the experimental conditions.

Solvent probes can help too.  For instance exposing the protein to D20 then doing mass spectroscopy on the protein. This is still only going to give you a general idea of how much of the peptide is surface exposed.  Protein structure is still pretty necessary to getting any accurate measurement of SAS I think.


According to Furtado and Pessoa (2014):

Homology: A similarity due to common ancestry.

Homoplasy: A similarity not due to common ancestry.

And, according to Futuyma (2006):

Homology: Possession by two or more species of a character state derived, with or without modification, from their common ancestor.

Homoplasy: Possession by two or more species of similar or identical character state that has not been derived by both species from their common ancestor

Therefore, the answer is quite clear: the trait here is an homoplasy, since it's not present in the common ancestor of A and B.

PS: Homoplasy and analogy are not, technically speaking, synonyms. Analogy is a special case of homoplasy.

PPS: A clade is just a monophyletic group. For instance, the hominids form a clade, Mammalia is also a clade, Vertebrata is a clade, even Animalia is a clade. Therefore, a clade can be very exclusive or very inclusive. Because of that, I'm skipping the title of the question ("Could homoplasy occur within a clade?"), whose answer is obviously yes1, and focusing only on your second question: "Is this [image] a case of homoplasy?"

PPPS: Furtado is me, and that quote was translated from the original.

Sources:

Furtado, G. and Pessoa, F. (2014). Liçoes sobre sete conceitos fundamentais da biologia evolutiva. Brasília: Editora UnB. (translation: On seven fundamental concepts of evolutionary biology)
Futuyma, D. (2006). Evolutionary biology. New York: W.H. Freeman.

1For instance, my metamery and the metamery of an earthworm is an example of homoplasy. Both myself and the earthworm belong to a clade called Animalia. Therefore, there is homoplasy within a clade


What factors govern the variable age of onset in Huntington's Disease?

There is quite a bit of data available from Venezuelan HD families, but they haven't identified the factors themselves. From the abstract of the paper, emphasis mine:

  Analysis of the 83 kindreds that comprise the Venezuelan HD kindreds
  demonstrates that residual variability in age of onset has both
  genetic and environmental components. We created a residual age of
  onset phenotype from a regression analysis of the log of age of onset
  on repeat length. Familial correlations (correlation +/- SE) were
  estimated for sibling (0.40 +/- 0.09), parent-offspring (0.10 +/-
  0.11), avuncular (0.07 +/- 0.11), and cousin (0.15 +/- 0.10) pairs, suggesting a familial origin for the residual variance in onset*. By
  using a variance-components approach with all available familial
  relationships, the additive genetic heritability of this residual age
  of onset trait is 38%. A model, including shared sibling environmental
  effects, estimated the components of additive genetic (0.37), shared
  environment (0.22), and nonshared environment (0.41) variances,
  confirming that approximately 40% of the variance remaining in onset
  age is attributable to genes other than the HD gene and 60% is
  environmental.

*This paper also suggests the same, with a smaller (but different) samples.

A recent study of an Italian sample suggests that a polymorphism in Atg7 (autophagy-related gene) is a modifier of age-of-onset, but this result does not generalize to a European cohort.

What is apparently not linked to age of onset in HD? β-defensin copy number variation.

Also, CTCF doesn't appear to be linked to the CAG repeat instability (mutations in CTCF have previously implicated in triplet repeat instability).

Mutations in PGC-1α, mitochondrial regulator, were previously associated with age of onset, but a more recent study suggests that this might have been due to stratification of the sample.

Similarly, a polymorphism in HAP-1 was previously associated with age of onset, but a subsequent study found no evidence of association.

Altogether, these results suggest that population stratification needs to be taken into account when evaluating associations between age of onset and genetic polymorphisms.  It is also possible that there are population-specific genetic factors that affect age of onset.


$g_0$ is the standard gravity.

You can look up the rpm-equivalent using a nomogram or calculate it yourself.

On some centrifuges you can switch between both. Some vendors provide conversion tables in their centrifuge's manual.


Do any RNAs directly inhibit transcription

Yes there are reports of RNA directly inhibiting transcription.

RNA induced transcriptional silencing (RITS) is a well known pathway in Schizosaccharomyces pombe (fission yeast). Initial heterochromatinization is dependent on the RNA (as a DNA identfication module) that guides other functional proteins to the target (Also see Djupedal et al., 2009).

piRNA in higher eukaryotes are known to cause methylation of target DNA regions and thereby the repression of genes at these loci (Aravin and Bourc'his, 2008).

Some classes of small RNAs in C.elegans (such as 22G RNA) are also known to cause transcriptional silencing.

Many lncRNAs are known to inhibit transcription of their target genes. The most famous example would be that of XIST which causes epigenetic silencing of one of the X-chromosomes in the female.

On a purely biochemical note, RNAs can also form triplex with target DNA regions and impede transcription and replication (Bacolla et al., 2015).


Is blood pressure in the aorta and brachial artery the same or different?

Blood pressure is mostly dependent on the height from the heart. Therefore, if it is below the heart it will have higher blood pressure and if it is above the heart it will have lower blood pressure.

Here you are asking from two parts of body that have same height as the heart,

so they will have approximately the same blood pressure.

For more see:
Netter's Anatomy Page 136 and Campbell Biology


Probably not! There are certainly some physical reasons to doubt it. Looks like the mass difference between X and Y sperm is on the order of 0.1 picograms: X chromosome "weight"?

First, mass differences are not likely to affect swimming and motility of sperm, because sperm are at low Reynolds number -- the forces of fluid drag vastly overwhelm inertial forces. See, e.g. Purcell's lecture "Life at Low Reynolds Number" (http://aapt.scitation.org/doi/abs/10.1119/1.10903 but also available online). For this reason, even much larger differences in mass are not likely to matter to swimming.

If motility is not the issue, you could imagine that, during the fertilization or insemination process, sperm might be under the force of gravity, leading to different sedimentation rates. A sperm's sedimentation speed is equal to the force on it divided by its friction coefficient $\gamma$,
$$v_{sperm} = \frac{(m_{sperm}-m_{displaced}) g}{\gamma} $$
where $g$ is the gravitational acceleration and $m_{displaced}$ is the amount of mass displaced by the sperm. You can estimate $\gamma$ with Stokes' law (https://en.wikipedia.org/wiki/Stokes%27_law) as about $6\pi R \mu$ with $R$ being the sperm size and $\mu$ the fluid viscosity. We're interested in the maximum possible difference in speed, so we'll choose $R$ to be at the small scale of sperm size, $5$ microns and $\mu$ to be that of water $\mu \approx 0.01 \frac{g}{cm s}$. This gives us $\gamma \sim 10^{-4} g/s$. The difference between $v_X$ and $v_Y$ is then
$$v_X - v_Y = \frac{(m_X - m_Y) g}{\gamma} \approx 0.01 \,\textrm{micron}/s$$

This means, for there to be a significant difference between X and Y sperm you'd have to keep them sedimenting under force for quite a while. This can be used (especially in a centrifuge, where you can increase the gravitational force) to select between genders - but it seems unlikely to happen in vivo.

To see why this is a small speed in practice, you have to ask whether the sperm would also have diffused a larger distance or managed to swim while it was sedimenting. Sperm velocities are on the order of tens of microns per second, so anything that changes the sperm swimming speed by even 0.1% is more important than the mass difference in sedimentation.

Putting this together, it suggests that mass differences are not a likely origin for sex ratios slightly deviating from one - if they are tuned, it would make more sense to change sperm length or swimming stroke. In fact, I believe there are some small geometric changes between X and Y sperm - but could those geometric changes happen simply because there is less chromosomal material in the Y? That, I'm not sure.


You are asking explanations about a creationist argument. One could provide explanations about some hypothesis that you may found in a science paper but not explanations for a creationist argument just because, by definition, a creationist argument is not supported by any evidence and logical thoughts. However, you may want to link to a creationist website making a specific claim of interest and we may eventually talk about whether the claim is wrong/misleading. It would be very handy to have the claim in quotes rather than an explanation of what the claim is.

You say

  [..] after the evolution and speciation [..]

This piece of sentence sounds weird. You could say after the evolution of something (meaning the appearance of this something through evolutionary processes that are mutations, natural selection, drift and eventually others) but just "after the evolution" sounds as if evolution may not exist during some periods of time.

Talking about speciation in fruit flies, you will likely be interested in reading this post.

UPDATE

In general, when talking about fruit flies we talk about the Tephriditae. Tephriditae is a family of flies which contain about 5000 described species (including the model organism Drosophila melanogaster).

So, there is definitely different species of fruit flies. Of course, within any population (to the exception of populations of exact clones by definition), you have variation. This variation is a key concept in evolutionary biology. If this is unclear to you you may want to learn a bit more about evolutionary biology, including the concept of heritability ($h_N=\frac{V_A}{V_P}$).

Speciation took place in Tephriditae (otherwise we wouldn't have the species we have today) and is still taking place. The post I linked above gives an example of speciation between lineages of Drosophila melanogaster that has been directly observed in the labs.

Your issue seems to likely be a semantic one. As there is variation within a lineage and this variation is associated with groups that are in reproductive isolation, then the two lineages you consider do not belong to the same species anymore. Therefore, there was a speciation event.


Depending on the neuron, small/large could mean one of two things:

1: Axon diameter, larger axons have lower resistance, so transmit action potentials faster see tables here. Important for neurons that cover long distances to convey information quickly.

2: What I think you mean though is the size of the cell body, where some neurons, e.g. Purkinje cells are much larger than nearby golgi cells. In which case the size is related to the function, large cells tend to have large dendritic fields and integrate many inputs into a single output, often relayed to a different area of the brain. Small cells are typically interneurons that only have an effect over a very small area.


Is there an advantage to antibacterial soap?

Short answer: There is no benefit for their use in households.

Long answer: These soaps (see here for the complete list) contain the so called quaternary ammonium compounds Benzalkonium chloride and Cetrimonium chloride which indeed have antimicrobial properties.

While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.

There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.

This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.

References:

Use of germicides in the home and the healthcare setting: is there a
relationship between germicide use and antibiotic resistance?
Plain soap as effective as antibacterial but without the risk
Consumer antibacterial soaps: effective or just risky?
Effect of antibacterial home cleaning and handwashing products on
infectious disease symptoms: a randomized, double-blind trial.
The Burning Question: Is It Safe to Use Antibacterial Soap?


How to compare SNP from genotyping results for multiple people with a known phenotype?

Each rsid identifies a unique SNP in the genome. Thus there should not be any entry in the files that have the same rsid but different chromosomes and/or positions. If you do find this, it is likely that you have data from different versions of the assembled genomes.

To find genetic variants associated, i.e. correlated, with your trait, you need to focus on the genotype at each of the SNPs. For example, SNP rs3094315 is an A/G polymorphism, i.e. an individual can either have the genotype AA, AG, or GG. To find if it is associated with tongue rolling, you would count the number of AA, AG, and GG individuals (alternatively you could sum the number of A and G alleles) in the group that can roll their tongue and compare those numbers to the group that cannot. You would then repeat this for each SNP that you want to test. For most SNPs, there will be no difference in proportion.

That being said, this is not a modest undertaking as this a cornerstone of human and statistical genetics. There are many issues that could strongly bias your results (e.g. population stratification, genotyping error, linkage disequilibrium, multiple testing). To learn more, you can read about the Cochrane-Armitage Trend Test and the PLINK software. If you are really serious I recommend Applied Statistical Genetics with R by Andrea S. Foulkes.


Most species of birds have 2 foveas, the temporal fovea and the central fovea.

  temporal fovea, which is like ours in the sense that it looks straight
  ahead and offers binocular vision (i.e. the temporal foveas of both
  eyes point in the same direction). But birds also have a central
  fovea, which points sideways and is, obviously, monocular (i.e., the
  central foveas of both eyes look in opposite directions).

So the bird has a choice of which fovea it wants to look through.

  It can look straight ahead with its temporal foveas, to the left with
  the central fovea of its left eye, or to the right with the central
  fovea of its right eye. And this is not a hypothetical possibility:
  Birds actually do switch between foveas all the time! This is why they
  tend to swing their heads erratically in turns of about 90° (reference).


Are there any proteins not found in the brain that are affected by prions?

Yes, malformed prion proteins can affect tissues outside of the brain.

Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/overview-of-prion-diseases

  Another familial prion disease has been recently discovered. It differs from other prion diseases because it causes diarrhea and affects nerves throughout the body years before symptoms of brain malfunction develop. It is described as prion disease associated with diarrhea and autonomic neuropathy.

Via: https://www.merckmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/prion-diseases/prion-disease-associated-with-diarrhea-and-autonomic-neuropathy

  Symptoms begin when people are in their 30s. People have persistent watery diarrhea and bloating. They may lose weight. Because the nerves that control body processes are affected, people may not be able to pass urine (called urinary retention) or may lose control of their bladder (urinary incontinence). Their blood pressure may drop when they stand up, causing them to feel dizzy or light-headed (called orthostatic hypotension). People may lose sensation in their feet. Later, when people are in their 40s or 50s, mental function deteriorates, and seizures may occur.


Why are semi log graphs used in drug Dose response curves?

The reason is to make it easier to determine a suitable dose from the graph.
Normally, using a arithmetic scale, the response curve is a hyperbolic, with most of the information squished together in a small section of the graph. By using the log the function usually becomes somewhat sigmoid, with a relatively linear section in the transition from low-high response. This means that this dynamics in this section can be studied more carefully.

See e.g. this example (with data from https://www.idbs.com/media/396649/dose-response-comparison-example-hr.jpg), where I have reversed the x and y-axes, and used a secondary y-scale to show the log dose (so the graph is flipped compared to a normal dose-response curve). Here, the orange line shows a semi-log dose-response curve, and the blue line shows the same data using a normal arithmetic scale. Note that the orange line (log dose) should be read against the right scale and the "normal" dose against the left scale):

Here it is obvious that the normal scale doesn't give any possibility to interpret the region where the dose is effective, while this is obvious in the log graph.

The statistical modelling of these data is to some extent a separate issue though, where probit model or logit models along with data transformations are often used to analyse the data. Note also that the "usefulness" of the semilog-plot only lies in the visual presentation, and whether it will add anything depends on the dose series used in an experiment. If the doses used are not exponential (as in this example), the semilog-plot will not add much. In the statistical test of an effect the log dose is also usually not important, and I suspect (as someone not working in pharmacology) that the semilog plot is to some extent a historical artifact from the time before computer analysis of results, when the appropriate dose was determined in  a more manual way (e.g. linear analysis of the middle portion of the semilog graph).

Example data:

dose (conc.)    response
0.00001         0.993
0.0001          1.02
0.001           3.12
0.01            6.36
0.1             31.97
1               51.2
10              75.96
100             89
1000            97.932
10000           98.8


Does our immune system react on all bacteria?

The immune system is capable of recognizing pathogenic ("bad") bacteria, either by components of the innate (non-specific) or adaptive (specific) immune system. Pathogenic bacteria will have antigen on their surface that mark them as 'foreign', leading to an immune response targeted to the bacteria. In contrast, the immune system tolerates the normal flora of the body. The precise role that the human immune system takes in tolerating and regulating the populations of the normal flora is not known, it is currently a hot area of research.

Current research suggests that microbiota induces host immune tolerance to commensal bacteria directly via a microbe-associated molecular pattern (MAMP) and polysaccharide (PSA) signalling. The immune system continuously monitors the resident microbiota, and certain antimicrobial mechanisms are constitutively engaged to prevent overgrowth of the colonizing microbes: this maintains what is loosely called immune homeostasis. The mechanisms that control (intestinal) tolerance include those that:

1) minimize exposure to and 2) immune recognition of intestinal microbiota, and 3) those that down-regulate immune responses through intra-cellular and inter-cellular mechanisms.

Research has shown that he tolerance of the normal microbiota of the gut seems to require an extensive network of regulatory immune cells including Tregs and (tolerogenic) dendritic cells.
Thymus-derived Tregs were discovered by Dr. Leszek Ignatowicz to be a crucial  player involved in "educating" the immune system about the diverse bacterial colonies in the intestinal flora of mice. In response to the diversity of gut bacteria found in the gut, the Tregs express a 'repertoire T cell receptors' (TCR) that recognize the antigens characteristic of individual bacterial colonies in the gut. Upon engagement of these receptors, Tregs suppresses the adaptive immune response, specifically through the release of immune-modulatory cytokines such as interleukin-2. Moreover, it was found that gut bacteria can also be recognized and protected by a distinct innate lymphoid cell population (ILC) in the intestinal lining of mice. These cells behave like antigen presenting cells, and can recognize and present antigens from gut bacteria through the major histocompatibility complex class II (MHCII). But rather than activating CD4+ T lymphocytes through MHCII engagement, these ILC works by suppressing CD4+ T lymphocytes through MHCII engagement. CD4+ T lymphocytes are involved in clearing pathogen/bacteria, and thus the suppression of CD4+ T lymphocytes is involved in the immune-tolerance of normal flora.

http://www.sciencedirect.com/science/article/pii/S2352345X14000083

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007055/


Is "reaction center" the same as "photosystem"?

Reaction centers are specific sites within the photosystems where the adsorbed photon energy is transferred to electrons.


Crick’s Central Dogma was actually:

  The Central Dogma
  This states that once ‘information’ has passed into protein it cannot get out again. In more detail, the transfer of information from nucleic acid to nucleic acid, or from nucleic acid to protein may be possible, but transfer from protein to protein, or from protein to nucleic acid is impossible. Information means here the precise determination of sequence, either of basesin the nucleic acid or of amino acid residues in the protein.

So, although in my comment I stated that the discovery of reverse transcriptase was the first violation of this — as was generally regarded — this turns out not to be the case.

I remember that the case of reverse transcriptase was felt to be different from the existence of RNA viruses because it involved the flow of information from RNA to genomic DNA, which were generally represented by a unidirectional arrow in the opposite direction in diagrams of the dogma. The following is a typical illustration of that, taken from some University lecture notes that I found on-line and which are described as:

  These diagrams ..., created originally by Crick, summarize the basic processes of information transfer within cells.

But the NCBI collection of facimilies of Crick’s documents include a 1956 diagram that is quite different and much more sophisticated:

And, so the central dogma has not been violated (certainly not by lncRNAs), unless you consider that it has by prions, where information of sorts is transfered from protein to protein.

Morals

It’s amazing what you can find on the internet.
Never believe what you find on the internet.

Footnote

I’ve seen the DNA → Protein arrow repeated as if it were fact in diagrams, although Crick only said ‘may’. I know of no example of this.


Does tea have its effect if you have a sleep after drinking it?

Caffeine is the stimulant in tea. It has different effects on different people, but if you can sleep right after drinking it, it probably isn't strong enough to have long term 'refreshing effects', And yes, the duration of your sleep does matter. If you sleep for 12 hours, much more caffeine will filter out of your blood stream than after a 1 hour nap.

Some info on how caffeine works, from here:

  Caffeine, a component of tea, coffee and cola, induces wakefulness. It binds to adenosine A1 and A2A receptors as an antagonist, but the receptor subtype mediating caffeine-induced wakefulness remains unclear. Here we report that caffeine at 5, 10 and 15 mg kg-1 increased wakefulness in both wild-type mice and A1 receptor knockout mice, but not in A2A receptor knockout mice. Thus, caffeine-induced wakefulness depends on adenosine A2A receptors.


Do people of the same height walk at the same speed?

People of the same height can easily have different leg lengths. Think western women models - currently they are typically women with relatively long legs while ordinary people can easily have shorter legs for the same total height. There's even leg-to-body ration section in Body proportions Wikipedia article.

This is why pedometers always require calibration - the procedure in which you have to walk a known distance and count steps and then know how much steps you need per mile. There're no tables that would assist by assuming certain steps-per-mile ration for known height.


Would a hole in a heart make it unsuitable for transplantation?

I am assuming you are referring to a patent foramen ovale.

A Google Scholar search for donor heart "patent foramen ovale" returns many results about transplanted hearts with PFO, which suggests to me that this is not a contraindication for donation, though that may be up to the transplant team or hospital. In most cases, PFO is not symptomatic; it could also be potentially repaired at the time of transplant if it was deemed significant.


How can octopus walk if muscles can only contract?

Kier and Smith wrote a paper on how tongues tentacles and trunks worked. It explains in detail exactly how their legs (and our tongues) elongate, shorten and move about without any bones for support. It's called muscular-hydrostat.

Movement of the limb actually depends on which muscle is being contracted. If it's contracting the muscles longitudinally it will make the limb short and wide, while if it contracts laterally it will cause the limb to extend and be short and thin.

If you watch the video carefully you can actually see the changes in thickness of the limbs as the lateral muscles release and the longitudinal muscles contract so the octopus can move its leg forward.

If you want to see it work in person, go into the bathroom and move your tongue around and watch in the mirror. It uses the same mechanics to move your food around your mouth, lick your teeth, help you get that bit of food that is stuck up against your gum, and who can forget rolling the tongue into a cylinder or making tongue clovers.