What coronaviruses have been identified in racoon dogs? Christian Dorsten says in an (Apr 26) interview in the Guardian that racoon dogs as [intermediate] source of coronavirues have been overlooked (in China):

Q: What do we know about that intermediate host – is it the “poor pangolin”, as it’s come to be known?
A: I don’t see any reason to assume that the virus passed through pangolins on its way to humans. There is an interesting piece of information from the old Sars literature. That virus was found in civet cats, but also in raccoon dogs – something the media overlooked. Raccoon dogs are a massive industry in China, where they are bred on farms and caught in the wild for their fur. If somebody gave me a few hundred thousand bucks and free access to China to find the source of the virus, I would look in places where raccoon dogs are bred.

So what studies are there on coronavirues in racoon dogs up to now? (A quick search found a 1992 US paper that some coronavirus [unsurprisingly] infects racoons too. But I can't find much else. Is there more up-to-date survey? Also, duh, racoon dogs aren't even the same family [Canidae vs Procyonidae].)

Here's an abstract for a paper from 2006: https://www.ncbi.nlm.nih.gov/pubmed/16450706

  An RT-nPCR assay was used for testing fecal samples of dogs, foxes, raccoon dogs and minks for the presence of canine coronavirus (CCV). The animals were raised in homes, dog schools or farms... Among 24 raccoon dogs samples, 22 were CCV type II-positive, and from those 16 were additionally type I positive.

Here's another paper from 2003: https://www.ncbi.nlm.nih.gov/pubmed/12958366

  A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS)... Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market.

So at least a couple types of canine coronavirus and other strains closely related (but not identical) to the coronavirus that causes SARS.


Are cells electrically neutral or charged to setup the membrane potential across them? While studying about membrane potential I usually come across the Na K pump . But I can't understand does it cause any generation of net charge in the cell If yes then how do charged cells stay together with other similarly charged ones ,  if not why and how not .

It isn't neurons that are charged, it is their membranes. From the distance of other cells, they "see" both the charges inside and outside the membrane, so there isn't any substantial repulsion on that scale.

The charge across a membrane comes mostly not from the Na+/K+ pump directly, but due to differential permeability of the membrane to different ions. Ions normally tend to flow down their concentration gradients, but that flow can be influenced by an electrical potential. From the perspective of just Na+ and K+, there is more K+ inside the cell and more Na+ outside, and more permeability of the membrane to K+ than Na+. Therefore, the inside of the cell will be negatively charged at equilibrium where the net flow of ion charges is equal. At a negative resting potential, the negativity of the inside of the cell equalizes the net flow of potassium out with the net flow of sodium in. However, the actual concentration changes involved are miniscule. From the perspective of ion counts, there are basically as many positive ions inside as there are negative ions inside a cell; it's the very minute imbalance (fractions of a %) that gives a potential of ~-70mV.


Why is the mosquito a definitive host in malaria? I thought that the definition of a definitive host was that the parasite had to sexually reproduce in that particular host.

I've been told that mosquitoes are the definitive host for the plasmodium parasite, but I thought that the fertilization (and thus the sexual reproduction) takes place in the human?

Plasmodium falciparum (the main causative agent of malaria) and other Plasmodium species have a very complex life cycle, with stages in the female host Anopheles mosquito, in the human liver, and in the human circulatory system, where it primarily resides in the erythrocytes (red blood cells, or RBCs):

During a blood meal, a malaria-infected mosquito injects sporozoites in its saliva into the human host (1). Sporozoites travel through the circulatory system and first infect hepatocytes (liver cells) (2, stage A) and mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony (A), which can last a minimum of 5.5 days), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony (stage B)). Merozoites leave the liver and enter the circulatory system where they infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing more merozoites, which continue the cycle of infection of RBCs (6). Some immature trophozoites, in the so-called "ring stage," differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.

It is important to note here (in answer to your question) that while the male and female gametocytes are formed at this stage in the human (the equivalent of meiosis), sexual reproduction does not occur until the micro and macrogametocytes are taken up by a mosquito.

The male (microgametocytes) and female (macrogametocytes) gametocytes are ingested by a female Anopheles mosquito during a blood meal (8) - only female mosquitoes (of pretty much any species) drink blood. The parasites' multiplication in the mosquito is known as the sporogonic cycle (stage C). While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle (1).

Sources

The Centers for Disease Control and Prevention: Malaria
Wikipedia: Plasmodium falciparum biology


Is this long black insect with semi-long antennae and a large segmented abdomen caught in the kitchen a larva or an imago? And what is it? This is in Northrhine Westfalia in Germany/Europe: we have those large longish and comparatively flat bugs (taking my hand below the plastic as reference, it should be about 4cm or 1 5/8in in length) or larvae in our kitchen occasionally.  For a larva, it seems to be lacking any soft parts.  It can raise its behind "threateningly" in the style of a scorpion but I doubt it's anything but mimicry.  Its large head reminds me of ant soldiers, though it is obviously out of scale.  I think it's mostly in the evening or night that we find one (and it's often because a cat stares at it in an obvious manner) and while it's usually the kitchen, that may just be because we are most frequently there.

That is an adult rove beetle (Coleptera, Staphilinidae). https://en.wikipedia.org/wiki/Rove_beetle
Rove beetles have very short elytra (forewings), so they don't look like other beetles. This one looks a lot like Ocypus olens, which is common in Europe https://en.wikipedia.org/wiki/Devil%27s_coach_horse_beetle


Difference between sexual and asexual spore This Wikipedia article on Spores mentions this:

  In biology, a spore is a unit of sexual or asexual reproduction that may be adapted for ....

What is the difference between the sexual spore and asexual spore?
Are they any different on basis of formation, diploid or haploid, role in life cycle?

By Sexual Spores, I mean the spores that arise in the sexual reproduction process and similarly for Asexual Spores, i.e. spores which arise in asexual reproduction process.

To add to the context, this image shows the Sexual and Asexual spores in a certain fungi (Mycelium) life cycle.

In the same wikipedia page of spores you cited, you can find that they have said:

  Fungi commonly produce spores, as a result of sexual, or asexual, reproduction. Spores are usually haploid..

Again,

  Vascular plant spores are always haploid.

So, sexual and asexual spores have no difference in ploidy- both are haploid. (There are exceptions- zygospores in fungi are diploid)
Now, coming to mode of formation, they are different. For example, in Ascomycetes, sexual ascospores are produced endogenously whereas asexual conidiospores are produced exogenously.

Spores that are formed by the process of meiosis are sexual spores and when formed from mitosis are asexual. The term 'sexual' means meiosis is involved.


How is Cas9-gRNA-tracrRNA complex lysed in mammalian cells? I am interested in degradation of Cas9-gRNA-tracrRNA complex. I would like to understand how do the cas9 enzyme, gRNA and tracrRNA degrade in mammalian cells (with references, if possible).

There has not been much research on this part of CRISPR-Cas system, as everybody is interested in geting gene editing done, but very few think about what actually happens to the things we leave inside. So, the mechanism of its degradation is not well understood. But there has been some research on this, which leads to the conclusion that the Cas9-gRNA, being a ribonucleoprotein (RNP), degrades by the normal protein degradation pathways, and is indeed very quick process. See this article:

  By contrast, Cas9 RNPs are delivered as intact complexes, are detectable at high levels shortly after transfection, and are quickly cleared from the cell via protein degradation pathways...Second, rapid clearance of Cas9 RNPs from the cell may increase CRISPR specificity by reducing the amount of time that Cas9 is available for off-target cleavage...Cas9 RNPs are active immediately following transfection and are quickly degraded within the cell. These fast degradation kinetics enable Cas9 RNPs to modify target genes with reduced off-target effects.

For more information about RNP degradation, you can have a look at this article. An example of RNP degradation pathway is this too:


Trick fruit trees into flowering later in the spring There is a common problem with fruit trees in temperate climates where the trees flower before the last frost. Generally speaking, if the tree has flowered, and the temperature drops below freezing, the flowers die and do not produce fruit.

This is certainly not a new problem. It's my understanding that the problem affects almost the entire fruit farming industry in temperate climates.

I've heard that fruit farmers have large-scale commercial techniques that they use to mitigate the issue, such as:

Covering
Fog or smoke
Wind Machines
Sprinkling
Heating

While these methods might be practical for commercial farmers, not all of them are practical for small-scale urban farmers like me.

Instead of actively protecting the open flowers, would it be possible to trick fruit trees into not flowering as early?

I'm dealing specifically with plants in the prunus genus:

Examples:

Prunus tomentosa
Prunus besseyi x prunus salicina hybrids
Prunus avium x prunus salicina hybrids

Note: I have a related question here: What triggers plants in the prunus genus to flower?

You are on the right track, but snow is the wrong way.  When the snow is around it insulates the ground.  Soil surface temps stabilize at close to freezing.

Instead, do the reverse.  Remove, or firmly pack the snow.  Do so about 1.5 times the dripline radius.  (If the dripline is 10 feet from the trunk, pack out to 15.)

This allows the ground to freeze deeper.  However see other answers.  I'm not nearly as confident about this now.

Now once melt starts in earnest, cover the ground with a couple of layers of the insulated tarps used by contractors to pour concrete in freezing conditions.  This will keep the ground cold, both by reflection (most tarps of white) and by insulation, and by wind reduction.  This should slowdown bud break by at least a week, and more likely two weeks.

For a single tree, you may be able to do protection with an oscillating sprinkler (for a big tree) or a impact rotary.  Key thing with these is to start them before the temperature gets down to freezing.  The initial few minutes while it's working with dry air you can get supercooled droplets that kill your buds instantly.   Start the sprinkler when the temps are about +6

A third way that may help is to graft onto a different root stock.  The russians work with pear on cotoneaster.  This dwarfs the pear strongly, but also forces it into dormancy earlier.  I haven't read what it does to bud break, but given that pears also tend to be early bloomers, it must help.  These interspecies grafts are working in Siberia in zone 2.

Look at using prunus that tend to go into dormancy early in the fall.

Another way to experiment with would be to keep them a bit thirsty in the fall.  If the roots are slightly dehydrated, then the first moisture they get in spring will be used to rehydrate.  This may delay bud break by a day or two.

Some trees do their budding on reserves in the bud and twig itself.  I see this some years when a winter has killed roots.  The leaves break bud, inflate about to about 1/4 size, then wither.  For these guys it's a matter of enough degree days or the day length on the bud itself.

If it's degree days, you may be able to stretch things out by making the tree lighter coloured.  Many people spray dormant oil in late winter anyway.  By adding some cheap latex paint to the dormant oil mix, you lighten the colour of the twig, and so reduce sun warming.


Detection of bacteria to measure quality of water I have been working on a science project were I have built a water filter.

To prove that it works I would need to test if there are bacteria in a sample which has been treated vs a sample that hasn't been treated.

I really just need to know if there are bacteria not how many. I looking to do this at home.

IF you are looking at a much faster technique but don't mind spending a bit and have some research equipment access, there are ways by which bacterial contamination can be detected by measuring ATP (Adenosine tri-phosphate). See this research publication. There are commercial kits available which you can use: Here is one of them by Thermofisher.

Again, this is only if you have access to the research equipments and funds.


How do you keep track of past/new lab protocols? Does there exist a list grouped my subject (e.g. 'microscopy') for keeping track of what protocols have been designed and used?

Closest I could find is http://www.protocol-online.org/ but it's fairly sparse and out of date.

Any recommendations/tips and tricks? Thanks!

The best match to what you're looking for is probably https://www.protocols.io/, which hosts protocols for free and generates a digital object identifier (DOI). It is not indexed by PubMed or other similar engines, however.

Some journals permit methods papers, but not a high proportion (and it sounds like you're looking for a place to find them, not to send them).


Does the Human Eye White Balance? OK, this may be a stupid question…but here goes.

Does the human eye “white balance” itself?

I assume that each human perceives colour slightly differently according to the peculiarities of their own eye, but within parameters (notwithstanding colour-blindness).

But does our eye (or brain) white balance? Or do we simply all see our own personal colour balance?

If the eye can white balance in real life, can it also colour balance a photograph that has been taken at the wrong colour temperature.

So, say I shoot and print an image shot at 2000K. The image printed will have its luminance information intact, but colour-wise, it will be very, very orange.

If I could somehow exclude all other vision from my eye and fill my entire viewing capacity with that single image, would my eye balance the colour back to a true white?

If it does not, why not? What goes on in our brain to say “this is an image at a fixed colour temperature, so you will see it as an orange hue”

Please excuse me if this is an eye-roller of a question. I’m not a Biologist, so I am well aware I may be demonstrating my own ignorance in asking the question!

The human brain white balances, the eyes do not, but the process is not instantaneous.

the easiest way to see this is to make a person wear colored lenses they will soon see colors normally again, but will need to readjust, taking a similar length of time,  once the glasses are removed.

Your eyes will balance an image back to white , but it takes time, and may happen faster in a landscape image.
https://www.sciencedaily.com/releases/2005/10/051026082313.htm

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820566/

there is a great ted talk showing a major aspect of this visually.

https://www.ted.com/talks/beau_lotto_optical_illusions_show_how_we_see?language=en

you can also see it with common photo negative color illusions.

Stare at the center dot on this for a minute then look at the second image.

you will see that the as the brain adjusts color balance you can use the lag as the eye readjusts to see false color in black and white images.


B -Cell activation by helper T cell When Dendritic cell travels to nearby lymph node with antigen presented on MHC II molecule, the helper T-cell residing there gets activated. But what happens to B- cell residing there? Does it get activated too when helper T-cell is activated and start producing antibodies for that specific antigen?

Naive T cells hang out in the lymph node waiting for antigen presenting cells (APCs) like DCs to present processed antigens on their MHC molecules. Naive B cells similarly hang out in the B cell zone and are capable of interacting with other T cells and follicular dendritic cells (FDCs). Antigen that ends up in the lymph ends up traveling to the lymph node, where B cells internalize, process and display them on MHC molecules. This is because B cells are also APCs.

Activated (and differentiated) T cells that were previously activated by DCs can identify some of these B cells clones through the TCR-MHC interaction. The B cells process the antigens like DCs, so the resulting heterogeneity of the processed peptides means a fair chance a T cell will recognize it. The result is that B cells receive an activating signal through the BCR and costimulatory receptors.

Differentiated T cells also secrete different profiles of cytokines. For example, Th1 cells secrete IL-12 and IFN-y whereas Th2 cells secrete IL-4, IL-5 and IL-13. Not exclusively, just predominantly or in greater amounts.

The receptor signaling in conjunction with certain cytokines can induce class switching to the resulting antibody production. This swaps the constant or Fc region of the antibody to a different isoform. So Naive B cells are IgM/IgD, and if the cells is receiving Th2 cytokine stimulation, class swtiching results in IgE antibodies, for example.

For elementary immunology I like to reference Cellular and Molecular Immunology, 8th ED. by Abbas et al., but 9th ED is out so keep that in mind. The field somewhat rapidly evolves.


Why aren't introns found on the ends of pre-RNA? We recently learned in genetics class that exons always cap the ends of nascent RNA. I have been trying to figure out the reason why introns can't instead be found on the ends instead of exons. The end introns would still have their 5' and 3' splice sites, and assuming the splicing machinery functions correctly, these introns would be removed. The only thing I could imagine occurring is inappropriate nucleophilic attack of the end 3' hydroxy group at the end 5' phosphate leading to a single circular RNA. However, in a normal situation where exons are at the ends, if introns in an RNA are  all removed simultaneously than it is possible that the free 3' hydroxy group of say intron 2 could attack the 5' end of another intron leading to inappropriate cleavage of the intervening exon so having exons at the ends does not solve that problem. I don't think my explanation is correct, any ideas?

RNA splicing refers to a certain kind of RNA processing mechanism which leads to the excision and exclusion of some regions of the primary transcript. You should note that this is not the only method by which such a thing can happen; Endo-ribonucleases can clip the ends of the transcript and this happens in the case of tRNA-processing. But as "splicing" happens it is essential that the excised region be in the interior of the transcript. See the figure.


Why are the Galápagos islands so special? Why did Darwin formulate his theory of evolution just after his visit to the Galápagos islands? Why were they so special from an evolutionary point of view?

Charles Darwin formulated his theory after travelling the world aboard the Beagle, here's the route. He found the Galapagos Islands particularly inspiring,

  'The natural history of this archipelago is very remarkable: it seems
  to be a little world within itself.'

This is a more detailed account of his relationship with the Galapagos islands, and there is also a book called "Voyage of The Beagle" (I think it is available as a free kindle download) which is basically his diary.

A big part of the reason it is so famous is because of "Darwin's Finches," which are 12 species of finch on the island that have all evolved to specific niches. This is one of the classic examples of evolution. Darwin noted the differences between the birds, thinking they were of different families, but it was later discovered they were all finches and the differences had evolved because of factors like the food they eat (seed eaters had fatter beaks.. etc).

The Galapagos islands offer opportunities to study evolution and adaptation because the islands are distant from the mainland, have differences between the islands, and migration between the islands is difficult. Studies like this one (which I happened to be reading at the time of the question being asked whilst writing a manuscript) are an example of how cool a place it is!


What attacked my peach tree? Help me please! I have to get rid of these!

These are definitely some sort of aphid (small sap-sucking true bugs in the superfamily Aphidoidea).

Based on the coloration and shape of the pest and the host plant, my best guess is that you're looking at Hyalopterus pruni (or the Mealy Plum Aphid).

Note: the scientific name of this species has changed at least 21 times!

 Photo by Jack Kelly Clark

Looks like this person also found this species of aphids on a black cherry tree if you want to see more picture.

Description:

  Wingless adult aphids are pale green with three dark green longitudinal stripes on their backs. Their bodies are covered with a white, mealy wax. [source].

Host Plants:

Typically trees in the Prunus genus: cherries, plums, almonds, apricots, nectarines, and -- you guessed it --  peaches. [source].

Damage:

Plant can become stunted from high numbers of aphids, but the primary concern is the development of mold that grows on the aphid's honeydew. [source].

Management:

See this University of California Agriculture and Natural Resources site for management suggestions.

Suggestions:

Biological: lady beetles, lacewings, or soldier flies
Organic: biological control + sprays of neem oil
Pesticides (typically not needed): Phosmet, Diazinon, and others in the fall; neem oil, flonicamid and others in the spring.

Final Notes:

Just because an aphid shares a name with an individual plant (e.g., the green peach aphid mentioned in the comments) doesn't mean that the species is limited to just that plant or that any aphid found on said host is that species. Many aphids feed on a wide range of host plants, so limiting your host to an individual species doesn't necessarily rule out a wide range of pests. However, it is not uncommon for an aphid species to stick to a single genus, narrow set of genera, or narrow set of families of host plants.


Why do fruits have to ripen? It seems like most fruits that we consume undergo some sort of ripening process either before or after they are picked from the vine, tree, etc. I understand that sugars are released during the ripening process and this is why ripe fruits are sweeter and more palatable than non-ripe fruits.

Why, though, do fruits have to undergo this process of ripening?

Wouldn't it be simpler to just grow and already be "ripe"? Does the ripening process confer some sort of advantage to the plant?

Mature, viable seeds have to form in most fruits, which involves the maturation of embryonic tissue. That can take a little time, from just a few days in some weed species to months and perhaps longer in some fruits like pineapple.


Is human vision sensitive to frequency or wavelength? In a vacuum, there is a one-to-one correspondence between light frequency ($\nu$) and wavelength ($\lambda$), ie. $\lambda=c/\nu$. But in a refractive medium, $\lambda=v/\nu$, so while the frequency may remain constant, the wavelength may not.

I've seen that in biology, wavelength is mostly used. But, I recall reading that human vision is sensitive to frequency. So, is human vision sensitive to wavelength or frequency?

It is not the wavelength or frequency that determines light absorption- it is the energy of the photon that matters. The energy of incident light should match the excitation energy of the chromophore. The medium itself can also affect light absorption by electronically interacting with the chromophore. Frequency is proportional to the energy (given by the relationship $E=h\nu$); while wavelength and velocity change in different media, frequency and energy remain constant.

The chromophore in the opsins (retinal) absorb energy to become active and you can say that they detect the frequency. However, sufficient number of opsins have to become active for the retinal cells to transmit the signal. So the overall light flux is also important. An interesting thing to note is that activation of the opsins hyperpolarizes the photoreceptor cell and reduces its tendency to fire.

Wavelength plays a role in diffraction and therefore diffraction is less in a medium with higher refractive index. Wavelength also determines scattering. So, while the opsins actually detect frequency, the wavelength can slightly affect the overall "vision" because of scattering/diffraction effects.


What's the frequency resolution of the human ear? I was thinking about audio compression (namely mp3), that "filters" out sound that we would not likely hear.

  The MP3 lossy audio data compression algorithm takes advantage of a perceptual limitation of human hearing called auditory masking.
  from: http://en.wikipedia.org/wiki/MP3

I've also checked the wiki entry for auditory masking, and found this:

  If two sounds of two different frequencies are played at the same time, two separate sounds can often be heard rather than a combination tone. The ability to hear frequencies separately is known as frequency resolution or frequency selectivity. When signals are perceived as a combination tone, they are said to reside in the same critical bandwidth.

My question is how much is this critical bandwidth or what's the smallest frequency difference we can perceive as two different tones, if you wish. Let's assume that both tones are equally loud, are coming from the same direction and distance and we are in a quiet room - so basically we eliminate as much noise and affecting phenomenons as possible.

As @ sanchises pointed out (thank you again!) in the comment section the frequency resolution is 3.6Hz between 1 and 2kHz. But since perception threshold is a function of the pitch of the sound I'd assume that the ability to resolve two tones would change with pitch too. Does anybody have any data on that? For example resolution X pitch graph.

The frequency limen, or frequency resolution can be determined in various ways using psychophysical measures. You refer to a simultaneous method, in which two (or more) frequencies are presented at the same time. This has consequences for the test as different frequencies are perceived with different perceived loudness under constant sound pressure levels, meaning that additional cues are present besides pitch cues.

One carefully controlled study Zwicker et al (1957) in this regard defined the critical band basically as "those frequencies where no intensity summation occurs", meaning that adding those frequencies (below or above the center frequency) do not result in differences in loudness perception (as expressed in acoustic threshold of the center frequency). This method nicely prevents loudness summation cues by deploying them in the criterion. This article shows the following picture (after Zwicker et al. (1957)):

The critical band (upper graph) is dependent on frequency, and ranges from 0.1 kHz to >2 kHz.

The markedly lower difference limen of 3.6 Hz as touched upon in the comments may have been obtained using an alternative psychophysical test where the test frequency is modulated by another frequency (bottom graph). This procedure is based on adding a frequency to a certain sinusoidal stimulus, basically resulting in a single stimulus instead of two (or more). This procedure is technically not defined as a critical band and indeed results in a difference limen of ~3.5 hz and up. The other graph plotted in the figure is a masking procedure (middle plot), which basically determines the physiological overlap between frequencies in the cochlea in the intensity domain by determining the amount of masking from one frequency by another.

NB: The authors worked with headphones so no effects of direction.

Reference
Zwicker et al. JASA 1957; 29: 548-57


What is the point of toxins without remarkable coloring? As far as I know, some toxic species (eg: some mushrooms) have no remarkable coloring. Therefore, what is the purpose of their toxins?

Toxic species often have colorful appearances to warn predators. Therefore, if a species has toxins but no vibrant coloring, this seems to me to not be beneficial for either this species or potential predators. But still, some toxic mushrooms (for example) have plain coloring.
What is the point of being toxic without vibrant coloring?

This is a really great question. To take a specific example, let's consider Amanita phalloides, the death cap mushroom. It doesn't advertise its poison; in fact, it resembles several edible species of mushrooms, including Caesar's mushroom and the straw mushroom. It contains alpha-amanitin, an extremely potent poison that inhibits RNA polymerase, shutting down protein synthesis. The estimated minimum lethal dose is 0.1 mg/kg or 7 mg of toxin in adult humans. The poison has a delayed effect, taking between 10-24 hours for significant effects to appear, so it's not like a poisoned animal can learn to avoid the mushroom in the future. None of the amatoxins appear to have any purpose except as a mammalian poison. They aren't specific to humans, and are capable of poisoning dogs. So what's the evolutionary advantage of this poison?
According to an essay written on the California Native Plant Society blog by John Chesnut, a horticulturist, the answer might lie in where the mushroom grows -- on tree roots as ectomycorrhiza (emphasis mine):

Death cap is an ectomycorrhizal symbiont. This means it forms connections on the root-tips of forest trees; in California, its typical (but not exclusive) partner is coast live oak. [...] Ectomycorrhizal (EC) fungi collect major nutrients, nitrogen and phosphorous, and exchange these with the host tree for sugars. Delicate hyphal strands extend outward from the root tip mass into the surrounding soil and mulch. EC also allows efficient active transfer of macronutrients, micronutrients, and soil water to the tree. The chronic phosphorous limitation in serpentine soils makes the EC symbiosis especially important for local forest types on this soil. Studies in Norway discovered up to 50% of a birch tree’s sugar is exchanged at the root tips with EC symbionts.

So the poison might not be intended as a way of preventing itself from being eaten, but as way of defending the tree it lives with from nematode pests (emphasis mine):

So why are Amanita so poisonous? It is an unlikely deterrence to vertebrate predation of the fruiting caps, as the effect is slow-acting (36-72 hours before the toxic crisis in humans) and the toxin is not concentrated in the cap. Evidence supports the hypothesis that the fitness obtained from synthesizing the toxin is secured within the hyphal network. Perhaps toxic Amanita obtain nitrogen from poisoned nematodes, or protect themselves (and their symbiont hosts) from plant parasitic nematode predation.
Perhaps the toxin suppresses the growth of competing fungal webs. It seems clear the toxic effect of death cap is intrinsic to its invasive success worldwide.

Interestingly, he points to some research suggesting that some mushroom flies might have co-opted this mechanism to keep themselves parasite-free (link and emphasis mine):

An evolutionary entomologist working in New York State, John Jaenike, has discovered four species of mushroom flies in the genus Drosophila that lay eggs in the gills of fruiting Amanita phalloides. The fruit fly taxa are related to ones that inhabit rotting skunk cabbage, but in New England have recently transferred to the recently introduced Amanita fruitings.
Jaenike discovered that Amanita phalloides is toxic to the damaging parasitic nematodes Howardula that reproduce in the stomach of fruit flies. The toxicity of the death cap to the parasitic nematodes results in much greater egglaying (fecundity) by the fruit flies. The fruit flies are affected by the toxic amanitin, especially the males, but the poison is more than offset by the increase in reproduction.
Janike also discovered that most other insects using mushrooms as egg laying sites (craneflies and forest gnats) shun use of the Amanita (due to its toxicity).


Pseudoautosomal regions of the X chromosome showing heterozgyosity I've always had questions for myself about sex differentiation, mostly on account of an unusual history & puberty. I won't go into details, but needless to say it was unique.

My question is... I got results back from 23andme showing hetereozygosity at the beginning & ending of the X

I've been diagnosed as XY androgen insensitive & pseudohermaphrodite with mullerian structures intact.  Born with questionable stuff internally, only definitive thing is nothing male (no prostate, no seminal etc..)

They also did show a Y, but it was apparently missing half of it (though I've read thats not unusual for half of it to be --)

Can you have a hetereozygosity at the ends of the x and not have another x?

rs6644972   X   178624  AG
rs28475515  X   182276  CT
rs28463388  X   191998  TT
rs28669107  X   195014  CC
i6033542    X   200928  CC
rs6655397   X   201935  GG
rs7890186   X   202458  GG
i6033543    X   209741  CC
i6033544    X   215805  CC
rs28736870  X   220770  GG
i6033545    X   228250  GG
rs6603204   X   298440  GG
i6033547    X   301596  CC
rs2738344   X   310897  AA

A normal male can show heterozygosity in the "X" results of a 23andMe SNP test despite having only one X chromosome.  This is because there are very short regions at the ends of the Y chromosome, called pseudoautosomal regions, that match up with equivalent (homologous) regions at the ends of the X chromosome.

Because the pseudoautosomal regions of the Y are homologous to the matching regions of the X, the SNP results for those areas cannot be distinguished in the SNP tests, so the results appear along with the X results in "X" chromosome file.  The results in those two areas of the file can be either homozygous or heterozygous at each location.  Most of the locations in the "X" file are for  locations outside of those regions, so most of the file entries cannot report heterozygous results.


How diverse are species in remote, isolated areas on Earth? If we consider land areas that have been largely isolated from each other from a human point of view, but with a similar climate – for example, a part of Europe and a part of Americas with a similar climate before the time of Columbus – generally how different can one expect the flora and fauna to be between the places?

I realize there can be quite different approaches to measuring the biological differences. Not being a biologist, I probably miss some quite important metrics. Some ideas that come to my mind:

How distinct are the species in each environment? For example, can we expect to see the same ant species? Same grass species? Same bacteria?
DNA difference based approaches: How much of the DNA material in each environment does not exist in the other one? How large a proportion of organisms in one environment does not have a close relative on the other, given some threshold closeness value?
Historical approach (probably overlaps the DNA approach quite a bit): How long ago (alternatively: how many generations ago) did the common ancestor of similar organisms in each environment live? Do the organisms share this number, i.e. is the common ancestor of, say, humans in Europe and America as ancient as that of ants and grasses?

The concept that you hint at, has been studied at the example of the island of Australia, where marsupials often look quite similar as their counterparts in the same ecological niche, which live outside Australia and have a placenta, and are less related on the DNA level (e.g.: squirrel-like animals, wolf-like, and the now everywhere extinct saber-toothed tiger-like...).

If you are interested to learn more, I would highly recommend to read Jerry Coyne's "Why evolution is True" ( http://jerrycoyne.uchicago.edu/index.html )

The specific example of Europe and Americas (which does not fully capture the complexity of your question), also is quite interesting - although it is very short on an evolutionary time-scale. E.g.: American squirrels, which lack predators in Europe, and only arrived in Europe because of human journeys following the rediscovery of Americas, are partially outcompeting the beloved red squirrels ( https://en.wikipedia.org/wiki/Eastern_grey_squirrels_in_Europe )


How do plants maintain air spaces in leaves? As we know, there are air spaces in the mesophyll layer which allows carbon dioxide to diffuse in and oxygen to diffuse out, but cell membranes are partially permeable and allow water to diffuse to regions with lower concentration. Yet these air spaces still manage to not get flooded by liquid water.
How does this happen?

There has not been not much research on this topic, which has caused lack of definite answer. Sibbernsen et al, 2017 performed a study on response of stomatal opening on filling these air spaces with water. They suggest the existence of a vapor-phase signal (from water) that originates in the mesophyll and causes stomata to open in the light. In another research, Wiebe et al, 1976 were able to remove the air spaces with the use of paraffin oil which infiltrated the spaces. They show that leaf air spaces contain invaginations which are extensions of air space system and increase conductivity of CO2 to the chloroplasts which line these invaginations.

Stomatal transpiration gives a clue to this. When the stomata open, they expose the internal environment to the atmosphere. Due to this, the air spaces get filled with water vapors which, due to concentration gradient, flow outwards from the leaf. To maintain the inner water vapors, more water is evaporated from the nearby cells, which leads to more transpiration. This hints that some water is present all the time in these air spaces in the form of water vapors. However, when the concentration of vapors becomes high, the nearby cells might take in some water or the stomata might open to maintain the concentration. See this article for some details on this.

At last, there is Woolley et al, 1983 which concludes that the mechanism behind the maintenance of these air spaces is still largely unknown.


Why do DNA and RNA have the functions they have? I know that there are two most important directions of genetic information transfer in living organisms: DNA->DNA and DNA->RNA. The first is replication, and the second is transcription. I wonder if there is a reason for this choice of directions. According to this article, all other directions are possible. Why do we use DNA for example? RNA is capable of self-replication since it happens in viruses. And why do we use RNA, not DNA, as messenger molecules? Is it just an accident or is it possible to explain why this is the right way of doing it?

DNA is more chemically stable than RNA, which makes it ideal for long-term storage. RNA viruses like HIV have a short lifespan and must replicate to survive, which is why they can get by with a less chemically stable genome.

RNA is a useful format to transcribe since it has multiple forms and functions (e.g. rRNA, mRNA, tRNA, siRNA, snRNA, miRNA, etc.). RNA can sometimes function like a protein in which it carries out cellular actions without needing to be translated. It has been hypothesized that RNA were the first molecules as precursors to life since they can function for both storage and action. The theory is that RNA was the first molecule but was then able to be translated into proteins (which were more variable/useful) and able to be stored as DNA (which was more stable as a storage medium).


What is the distance between the 3' 18s rRNA (the Kozak consensus sequence) and the A-site of eukaryotic ribosomes during protein translation? Reposted from Quora

The Kozak sequence is shown to be important in translation initiation, and the A-site is the anti-codon recognition site. If the distance is not known, how could I find out what it is? Is the crystal structure of the whole mRNA-rRNA-tRNA complex determined? If so, what modeling program would be best for establishing intermolecular distances?

Kozak consensus sequence (KCS) is present near or overlapping with the start codon. I am not sure what you mean by distance between that and A-site. Start codon is localaized at P-site at the time of translation initiation. Distance between start codon/KCS and A-site at initiation is same as distance between P- and A- sites (I guess ~20Å). A-site keeps moving during translation and hence the distance keeps increasing. Crystal study is available; See here.

See this figure from the abovementioned study for the relative positions of start-codon, P-site (exit) and A-site (entry).


What does "tumour budding" mean? tumour budding, lymphocytic infiltration and resection margins are established factors that influence the outcome of colorectal cancer (1)

In this context what does "tumour budding" mean?

Reference

(1) A. Bolocan, D. Ion, D.N. Ciocan, D.N Paduraru. Chirurgia (2012) 107:555-563. Introduction/0

Tumor ‘budding’ is loosely defined as the presence of individual cells and small clusters of tumor cells at the invasive front of carcinomas. A study of the measure of budding can give an insight into how fast the disease might propogate.

Reference


Does every human eye see the same visible spectrum? It is said that human eye can see light with wavelength approximately between 400nm and 700nm.

Are these upper and lower bounds same for every human? If not, what are the means and standard deviations of these upper and lower wavelength values for human eyes?

Human eyes all use the same optical pigment photopsin, so they all have the same basic frequency response.

There are differences. For example cataracts will change the sensitivity of the eye to colour, and people with colour blindness have various defect to cone cells that affect colour response. However these are secondary effects.


What is the actual speed of nerve impulses in humans? For an undergrad assignment I read a biology paper that mentioned the speed of nerve imuplses to be 440 km/h in myelinated fibers. However, our biology teacher told us that this reported conduction speed is not true. So my question is:

What is the actual speed of myelinated fibers?

Short answer
A conduction velocity of 440 km/h is possible in thick, myelinated fibers. However, this number is probably more representative of the upper range of conduction velocities, rather than a conservative average.

Background
First off, there are a heap of variables that affect neural conduction velocities (in myelinated fibers) in complex ways (Waxman, 1980), including but not limited to:

axon diameter;
myelin thickness;
internode distance;
temperature;
axonal milieu;
age of the subject.

Having said that, in humans myelinated, thin A-delta fibers the average conduction speed was established at 19 m/s (Gyberls et al, 1983), or 68 km/h. A range of pain-conducting fibers exist, with different diameters. As a result, they range in their conduction velocities from 0.5 m/s (2 km/h for thin C-type fibers) to 120 m/s (432 km/h for thick A-alpha type fibers).

Hence, the 440 km/h is certainly possible in thick myelinated fibers. Note I just highlighted pain-conducting fibers here as an example, and other classes of neurons may feature even faster conduction in their axons.

References
- Gybels et al., J Neurophysiol (1983); 49(1): 111-22
- Waxman, Muscle & Nerve (1980); 3(2): 141–50


Is 'disorientation event' a common term among biologists? On the South Carolina Department of Natural Resources web page about the marine turtle conservation program it says, "When a hatchling sea turtle is attracted away from the ocean towards a direct or indirect source of light, biologists describe this as a disorientation event."

Does something like the disorientation event describing the sea turtle behavior also occur in other species?

As sort of a "teach to fish" answer, let's approach how to answer a question like this:

Google Scholar is a pretty good index of scientific literature: good enough for this purpose. If you search:

"disorientation event" -turtle

you will return all results that use the specific phrase "disorientation event" except those that mention turtles.

You can also do the search:

"disorientation event" turtle

to find the turtle papers. As of today, "disorientation event" returns 57 results; 14 also include the word "turtle", 43 do not.

Among the 43, it looks like the majority of papers are discussing human disorientation, particularly in the context of human pilots but also in the context of cognitively impaired individuals or simply lost pedestrians. There is one paper that uses the term referring to rats in a maze-like task.

Overall, these results lead me to conclude that "disorientation event" is not a common general term used by biologists to refer to non-turtle species losing their way, although I would also say that I would expect a biologist to understand the meaning of the term given sufficient context.


What is two photon calcium imaging? I have encountered the term "two photon calcium imaging" in a few papers.
I have tried to look in the internet but can't understand what this technique actually is.
I will be very happy for recommendations for a good internet source.
For example:

what does the "two photon" means?
how does the implement look like?
Is it sensitive to absolute voltage or voltage changes?
Does all relevant (genetically engineered) neurons light in the same color?
Is it the color that is measured or the intensity of the color?
Is the purpose of this technique single neurons or brain pathes?

Thanks!

what does the "two photon" means?

Ordinary confocal microscopy uses single photon of laser light to excite the molecule of fluorescent dye.

In two photon microscopy you use two photons, with lower energy, which cannot excite the molecule of dye on their own, but their interference in a specific place leads to summation of their energies and to excitation.

This has benefits such as decreased phototoxicity and increased precision (resolution) especially in z-plane.

  how does the implement look like?
  Does all relevant (genetically engineered) neurons light in the same color?

There are two types of fluorescent dyes for 2-photon Ca2+ imagining. Since you want to measure local concentration of Ca2+, you can either use a chemical which chelates the calcium ions and changes its conformation and fluorescent properties based on that e.g. fura-2.

Alternatively, you can prepare fused protein from calmodulin ( CALcium MODULated proteIN) and some fluorescent protein e.g. GFP and transfect the cells with this product.

This means you can transfect different cells with different GFPs and get different colors. Depends on the actual experiment design.

Source

  Is it the color that is measured or the intensity of the color?
  Is it sensitive to absolute voltage or voltage changes?

You can analyse fluorescence intensity changes. The derived fluorescence intensities and ratios are plotted against calibrated values for known Ca2+ levels to learn actual Ca2+ concentration. Source

  Is the purpose of this technique single neurons or brain paths?

Actually, with a good interpretation of the data it can be used for analysis of both.

For more information about calcium imaging, see for example: http://www.cell.com/neuron/fulltext/S0896-6273(12)00172-9
or http://www.pnas.org/content/100/12/7319.full

or corresponding wiki articles:
https://en.wikipedia.org/wiki/Two-photon_excitation_microscopy
https://en.wikipedia.org/wiki/Calcium_imaging


Why does music give you emotions? Why do we feel emotions when we hear music?

Click to see video

How can a set of tones arranged in a specific order and timing make you feel sad or happy?

I read that music can somehow trigger the part of the brain which is responsible for language processing. Whatever be the mechanism of emotions, why do we feel that certain emotions are connected with certain tunes?

What may be the evolutionary origin of this?

The evolutionary origin is alleged to be recent: Other animals do not have a preference for dissonance and consonance.  (McDermott & Hauser, 2004).

Humans have new auditory regions in the brain for predicting and processing speech, and processing the emotions conveyed in the voice. The human voice mostly has harmonics in the 3rd and 4th note due to the properties of the vocal tract. There have been some basic studies of the 12 notes of the piano as represented in the human voice, which concluded that the "consonant" sounds from chords and melodies correspond to the the sound of the human voice.

This article suggests that dissonant/amusical frequencies are uncommon in natural ecology, because of the way physical objects resonate. Bird melodies are atonal and not particularly dissonant or consonant.

Some people may suggest that animal alarm calls are more dissonant than mating calls, especially those that are made to scare you like a cat hiss, a gecko scream, baby marmots which are separated from their mother, a rabbit being eaten.

Actually, many studies have identified brain regions used for emotional processing, the same that react when they see a beautiful or unnerving image, by MRI tomography and also from people who have had strokes which make them non-reactive to music, and people with amusia known as amusics.

  They also
  found an increase in frontal-midline (Fm) theta power
  for consonant music, indicating greater coherence of
  neural firing in certain population of neurons. This is
  interpreted as reflecting activation in the anterior cingulate cortex (ACC), which has been implicated elsewhere in processing pleasant music (Blood & Zatorre
  2001). The ACC’s role in emotion is also supported by
  its inputs from other key emotion-related areas, such as
  the amygdala, hippocampus, and parahippocampal gyrus (Devinsky, Morrell, & Vogt, 1995).

There are a lot of studies on the topic, this is a well written summary of recent research.

Musical sensory stimulation is a fascinating topic with complex ecology and brain quirks, it's best to research the topic individually to find which aspects of music do what to the brain:

Music rhythms vs cardio/breathing/cerebral rhythms, individual sound consonance/dissonance, and complex auditive patterning of sounds found in rhythmic chords and melodies. The conflict-resolution of harmonies are what you are referring to regarding the sequence of notes, there are studies on musical expectation, it's a sub-field of consonance/dissonance neuroscience.


Why are there both stop and start codons? Based on my understanding from wikipedia, there is the (RNA) start codon AUG and the stop codons UAA, UGA, UAG.  AUG can also encode Methionine, I'm assuming if it appears in the middle of a mRNA sequence.

But is there a chemical reason there are both start and stop codons?  Eg, if I only had a stop codon, would that also imply the next codon was start? Are there cases where there is a stop codon and the next codon isn't start?

Start and stop codons are instructions for the ribosome to start and stop protein synthesis, respectively.

The region between the start and stop codon (inclusive of them) is called ORF (open reading frame) or sometimes CDS (Coding sequence).

Why does ribosome need explicit instructions for start and stop?

Ribosome recognizes an RNA as a mRNA if it has certain features. In bacteria and other prokaryotes there is a region on the mRNA called the Ribosome Binding Site (RBS) that helps in initial recruitment of the ribosome. In eukaryotes there are Kozak consensus sequences that help in identification of a start site. When the ribosome encounters an AUG codon then the initiation reactions take place (there are some proteins called initiation factors that help in this process). The ribosome just keeps moving along the mRNA and producing a polypeptide unless it encounters a stop codon. When it does other proteins called release factors come into play and they dislodge the ribosome from the mRNA.

What about a second AUG codon?

If the ribosome encounters another AUG codon after the start then it would consider it as a codon for methionine. However there are situations when the second AUG can act as an alternative start site. You can see this paper for details.

Why is stop codon essential?

You can imagine a situation where ribosome just goes till the end of mRNA — why stop it? The reason for this is that the mRNA 3' terminus usually has regulatory regions and most importantly poly-A tails (in eukaryotes) that should not be translated. Moreover stop codon also signals the ribosome to dislodge from the mRNA. If such processes didn't exist then ribosome will remain attached to the RNA.

If I only had a stop codon, would that also imply the next codon was start?

No. Because stop codon works only when translation has already started. However it is not essential that the stop codon should be followed by the 3'UTR. Usually in bacteria a single mRNA codes for multiple proteins. There are many ORFs that are lined one after the other; such mRNAs are called polycistronic mRNAs. In these cases there is another start codon a few distance ahead of a previous stop codon.


Horizontal Gene Transfer I understand the different ways bacteria can undergo horizontal gene transfer (transformation, transduction (phages), conjugation (plasmids)).

Is there an experimental method to tell how a specific gene got into the host (during evolution)? For example if a gene A got into host X from species Y, is it possible to know how gene A was transmitted?

If you're looking at evolutionary timescales, then the only available source of information is the target organism's genome sequence. At least some of the methods of horizontal gene transfer you mention leave a distinctive signature in the genome. For example, retrovirus particles that have become incorporated into the human genome are easily identified by their local DNA sequence.

So in terms of an experiment, you would sequence your specific gene of interest as well as the surrounding local sequence (say, 10,000 base pairs downstream and upstream of your gene). In at least some cases you would be able to say for sure "this gene arose from retroviral incorporation", whereas in others it would be more ambiguous.

References:
Belshaw, R. et al. Long-term reinfection of the human genome by endogenous retroviruses. PNAS (2004)


Propensity Score for amino acid What is the meaning of propensity score of amino acid? How is it calculated? (I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

As a simplified response:
Propensity score is used to predict protein secondary structure. It is derived from looking at the aa residue of the accessible surface of the protein and also the interface which enables interactions between other proteins.

The equation is as follows:

Propensity= [probability of the residue in the interface / probability of the residue on the surface]

where,

prob of the residue in the interface = [number of amino acids in the interface / total number of amino acids of any type of interface]

and,

prob of the residue on the surface =  [number of surface amino acids / total number of surface amino acids]

Check out this PLOS paper for an example. PLoS One. 2014; 9(5): e97158.


PCR primer in highly repetitive region Is there any way to design a PCR primer if region of interest is highly repetitive (tens of kilobases only SINE's & LINE's)?

This paper describes some PCR strategies with LINE and SINE PCR identification (Shedlock and Okada. SINE Insertions: powerful tools for molecular systematics. BioEssays (2000) 22:148-160.).

I have no experience with PCR amplification of SINEs or LINEs, however I can think of two strategies right now.

1) You may be able to find a unique 18-20 nt region flanking those regions. If you can, great. If not, perhaps there is a unique site somewhere in the middle of these regions, then you can amplify from the middle outward to both upstream and downstream regions.

2) If there are no unique sites that you can exploit, that would imply a highly regular (ie, repetitive) pattern, but you can take advantage of this too. You can pick primers such that they are on the extremes of the repetitive subunit within these structures. For example, if your sequence looks like this:

A------>BA------>BA------>BA------>BA------>B

Then you can pick primers A and B for PCR use. You will have non-specific primers, and therefore when you amplify the DNA, you will get all possible permutations of DNA that these primers will produce. Specifically, you will get:

A------>B

A------>BA------>B

A------>BA------>BA------>B

A------>BA------>BA------>BA------>B

A------>BA------>BA------>BA------>BA------>B

         A------>BA------>BA------>BA------>B

                  A------>BA------>BA------>B

         A------>BA------>BA------>B

and so forth.

This last approach is obviously inefficient, because your possible products scale exponentially, and will be produced with equal likelihood, minimizing the DNA yield of any particular segment.


What is the function of clot retraction? I am thinking how clot retraction and fibrinolysis work together.
I think that clot retraction is a process that gets clot towards fibrinolysis process.
Fibrinolysis process then lyses the clot.
However, I am not sure if it is so simple.

Some seems to be discussing about how to differentiate start of fibrinolysis from clot retraction morphologically.
So they probably seem to be at this stage similar processes visually, but not functionally.

What is the function of clot retraction?

The platelets in the clot contain contractile proteins. They bring the edges of the wound together, which also reduces the chance of further bleeding. The contraction process also supports the wound healing process as it brings the ends of the wound together.

For more information see this article: "Mechanics and contraction dynamics of single platelets and implications for clot stiffening"


About the formation of protein There is a question in my textbook which asks: "What does the glucose produced from photosynthesis form?" However one of the answers said that glucose forms protein.  But I'm quite sure that amino acids form protein, don't they?  I would be grateful if anyone out there could help me out.

Photosynthesis results into formation of a carbon skeleton (a 3C or 6C skeleton). These newly formed carbon skeleton can be used to form a large number of bio-molecules which are required by a cell. For example the glucose can enter into aerobic respiration and the intermediates thus formed are used for synthesis of several molecules.

As you can specifically see from the above figure, alpha ketoglutarate is converted into glutamate which is then used for synthesis of proteins.

Alpha ketoglutarate is a keto acid can easily be aminated to give rise to amino acid.


Axial skeletal system I was curious about a fact given in my biology textbook as to why the Japanese have  3 pairs o floating ribs unlike the rest who have just two?

Because your textbook is probably worded poorly.

It appears that the Japanese (and several other ethnic groups) apparently have a higher proclivity for the 10th rib to be a true floating rib, but every ethnic group has the chance of having a floating 10th rib.

With that said, the one McGraw-Hill book cited in the Wiki article is the only source I've seen for this higher morphology rate. I, personally, wouldn't trust just one source, and (if true) the rate may not be much higher.


Can a human increase cold resistance through some practice? Can cold showers, moderate underdressing in cold weather increase your cold resistance?
What is responsible for cold tolerance? It's physiology/psychology or it's genetic thing?

By increasing cold resistance I mean feeling more comfortable/survive in low temperature environment comparing to state before practice(cold showers, underdressing, etc).

The advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga allows control of aspects of body temperature.

Physiological measurements on practitioners are described in the paper Benson et al. (1982) Body temperature changes during the practice of g Tum-mo yoga. Nature 295: 234-236

  Since meditative practices are associated with changes that are consistent with decreased activity of the sympathetic nervous system it is conceivable that measurable body temperature changes accompany advanced meditative states. With the help of H.H. the Dalai Lama, we have investigated such a possibility on three practitioners of the advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga living in Upper Dharamsala, India. We report here that in a study performed there in February 1981, we found that these subjects exhibited the capacity to increase the temperature of their fingers and toes by as much as 8.3 °C.

In this paper the authors report measurements made on three subjects. The Figure shown below is the data for the third of these. The authors describe these results as follows:

  His finger temperature rose 3.15 °C while toe temperature  increased 8.3 °C (Fig. lc). There were no other large changes in skin temperature. Rectal temperature was unchanged…The most likely mechanism to account for the increase in finger and toe temperature is vasodilation.

If you wish to try this for yourself, here is a description of the practice as quoted in the paper:

  g Tum-mo yoga is a form of meditation which allegedly allows its practitioners to alter body temperature. Previously, only subjective descriptions of this phenomenon existed: "The neophytes sit on the ground, cross-legged and naked. Sheets are dipped in icy water, each man wraps himself in one of them and must dry it on his body. As soon as the sheet has become dry, it is again dipped in the water and placed on the novice's body to be dried as before. The operation goes on in that way until daybreak. Then he who has dried the largest number of sheets is declared the winner of the competition".


How does a metronome help in controlling breathing rate? I'm new to the Bio/Medical field so kindly bear with me. I am doing studies on volunteers to formulate algorithms for evaluating Respiration rate from ECG and accelerometer data. I learned about this device when I read this paper. I'd like to know how exactly the metronome device helps in controlling the breathing rate, how is it to be used and precautions to be taken?

The paper in question used metronome to aid test subjects control their breathing rate. This seems like a good approach, much better, than asking "please, breath with 0.1Hz frequency".

  The subjects were asked to remain at rest in a supine position for 10 min, and then to control their respiratory rate with the help of a metronome at different breathing rates: 6 (near 0.10 Hz), 10 (near 0.16 Hz) and 16 (near 0.27 Hz) breaths/min.

Metronome is a device that produces any perceivable ticks (sound clicks or, maybe, light flashes can be used) with given and constant frequency. So patients were asked to synchronize their breathing with metronome clicks.

Only precaution in mentioned experiment is that high frequency of breathing can cause voluntary hyperventilation. Or if preset frequency is low and patient is trying to follow it, hypoventilation might occur. Fainting seems among the worst of consequences in both conditions (if person is relatively healthy).


Predictable microchimerism I read in New Scientist recently that microchimerism occurs between previously born siblings and grandparents, not just the mother.

Do we know which parts of the genome are likely to be transferred? Is it possible, given a genetic sample of relatives, to predict which genetic traits might be transferred by microchimerism?

Microchimerism, as defined by wiki, is the presence of a small number of cells in an organism that are genetically distinct, and originated from a separate organism. The example they give is an unborn child and the mother can 'swap' immune cells, and retain these for many years.

Your question about which parts of the genome are transferred is therefore not really valid, because the cells are transferred, rather than bits of genetic information. Therefore 'traits' are not transferred either, but distinct immune cell lineages can be transferred and persist - this can confer an immune advantage, so this 'trait' could be said to have transferred, but no genetic information has been swapped by the cells.

Although it does not say it on wiki, this presumably only applies to cells of the same species, but a different organism, otherwise infections would also count.

Update 20th July 2012

The New Scientist article you have linked to in the comments can be found online here.

It says that we may be more microchimeric than we imagined, because a recent study in Blood found that half of the mothers studied were positive for male T-cells (Dierselhuis, 2012). The authors note that it is remarkable that the immune cells from neither the parent or the offspring attack the other, and that this may explain the observation that siblings make better donors.

Another finding that mothers are found positive for cells from their own mothers, and even their own grandmothers, and that the cell numbers increase during pregnancy (due to clonal expansion of the inherited immune cells) reinforces the opinion that microchimerism is commonplace (Gammill, 2011).

So to reiterate, immune cells can be inherited from your mother, and she may also end up with leukocytes from her offspring, which can in turn be passed on. This is a very fascinating way in which the immune system seems even more complex and helpful.


How much does 10g of glucose raise the blood glucose level? If you would calculate it:
~5 liters of blood = 50 deciliters
10g glucose = 10000 milligram

so the glucose level raises by 10000mg/50dl = 200mg/dl

However, it is known that ingesting 10g glucose only raises the blood glucose level by ~40mg/dl

Why?

If you get an intravenous injection containing 10 g of glucose, all glucose will enter the blood within few seconds and your blood glucose level will temporary rise by ~200 mg/dL.

If you take 10 g of glucose by mouth, the glucose will be dissolved and distributed within the stomach and small intestine and will be gradually absorbed into the blood, let's say within 30 minutes. In this time, some glucose will already move from the blood into the cells, so you will never have 10 g of additional glucose in the blood at a given time.

The actual blood glucose rise after ingestion of 10 g of glucose is not a fixed number, but a range that depends on several factors:

  The gastrointestinal tract plays a major role in the regulation of
  postprandial glucose profiles. Gastric emptying is a highly regulated
  process, which normally ensures a limited and fairly constant delivery
  of nutrients and glucose to the proximal gut. The subsequent digestion
  and absorption of nutrients are associated with the release of a set
  of hormones that feeds back to regulate subsequent gastric emptying
  and regulates the release of insulin, resulting in downregulation of
  hepatic glucose production and deposition of glucose in
  insulin-sensitive tissues. These remarkable mechanisms normally keep
  postprandial glucose excursions low, regardless of the load of glucose
  ingested.** (Role of Gut in Glucose Homeostasis, Diabete Care, 2016)


Can tardigrades survive being eaten? Compared to a tardigrade, the cockroach seems fragile.

But can tardigrades survive the acidic environment of being eaten by most animals?

In there natural state no, tartigrade have absolutely no way to survive the acidic content of stomachs and are fragile.

In their cryptobiosed form (extremely resilient form) there has been no research to determine if they could survive extremely acid environnements. The things that we know they can survive is:

Temperature
Pressure
Dehydration
Radiation
The outer space environnement
Toxins

However, very few organisms possess mechanisms to tolerate highly acid environnement since acid affect cell membranes by "attacking" mainly the proteins and lipids. These organisms have evolved these traits because they live in acidic environnements, tartigrades on the other side don't.

Another point to add is, entering cryptobiosed form takes time, if the tartigrade would be eaten in it's natural form, it wouldn't have the time to cryptobiose and thus it would die.

Tartigrades

I hope this gives you some useful information


What is the expected effect of pH on the activity of a fungal pectinase? I am working on an enzyme assay for a fungal pectinase.I assayed the enzyme in different buffers from pH 1-12.5 However,the enzyme has good activities starting from pH1-10.5.

Is it possible to have enzyme activity over such a broad range of pH?

I actually doubt that the pectinase has such a broad pH range in which it works optimally. Searching the web I found two figures which support my doubts:

The first is from an article ("Immobilization of pectinase by adsorption on an alginate-coated chitin support") which compares the activity of native and immobilized pectinase under different conditions. The second is from the datasheet of a company which sells the enzyme. Both show an activity over 50% roughly between pH 3.5 and 5.5 but not at higher or lower pH values.


I added ethanol to my TRizol RNA extraction I added ethanol instead of chloroform to the cell suspension in Trizol. Can I still obtain my aqueous phase?

My answer is based on my experience in the lab and something like a best guess - it may or may not work. But given the fact that added 100µl of ethanol to 500µl of total volume and since water and ethanol mix completely, I would give it a shot.

I don't think that the ethanol would change the polarity of the solution so much that phase separation is inhibited. The only thing that I can image is the contamination of the aqueous phase with traces of phenol, so I would probably clean up more carefully and do an additional NaOAC/ethanol precipitation at the end of the procedure. If you expect a small pellet with little nucleic acids, add some glycogen to get a better outcome there. I would appreciate it, if you could comment on your experience (and the outcome) when you try to save you sample.


Can coronavirus contaminate public water systems? It's been reported recently that people are panic-buying stuff as the coronavirus epidemic worsens. I've even noticed that the local grocery store is low on hand sanitizer, paper towels, and bottled water.

I did some reading and traced links back to the DHS's ready.gov website, and it recommended preparing a 2-week supply of food, water, medicine, and hygiene products for ISOLATION, though I expect if you're sick you're supposed to plan a trip to the hospital. Most of that makes sense to me. The exception is the supply of water. We have public water systems that send drinkable water to us, so why do we need to prepare a stash?

I tried finding an answer online, but I couldn't. The only guess I have is that coronavirus can contaminate the public water system, and it's not guaranteed water treatment will work. Who here has the know-how on waterborne viruses and water treatment to address this speculation?

Viruses can survive a few days in water, i.e. SARS can survive 22 days in lab grade reagent water and 7 days in pasteurized sewage. That is the time the virus takes to be at 99% of it's original concentration. (from "survival of surrogate coronavirus in water").

Viruses can also spread via swimming pools, i.e. hepatitus A and norovirus have been associated with swimming pools. (from "a review of waterborne viral deseases associated with swimming pools").

Boiling water will kill viruses. Children have very little reaction to the virus when they carry it, so it's likely that they act as a transmitter more than water does. I'm not worried about it at all by the way, just do what the doctors advise.


How likely will 2 normal bacteria "attack" each other if they infect the same parts of your body? I read this interesting article online about how deadly bacteria are known to attack other deadly strains of bacteria.
https://www.google.com.sg/amp/s/phys.org/news/2013-02-deadly-bacteria-remarkable-precision.amp
I am wondering how normal bacteria that infect us like those that cause strep  throat and so on also have the capabilities to attack other bacteria and how feasible it is to use this as a treatment for bacteria infections by introducing harmless strains od bacteria to fight pathogenic versions (maybe like probiotics?)

Mixed bacterial populations, where not engaged in some kind of mutual or commensalistic relationship, are constantly at each others throats over resources. Even then, sometimes it's just rate of growth isn't terribly bad for each commensal. Not just nutrients, for example, but also precious space to colonize or attach to. There's a good review here, and among some of the tactics direct killing by antimicrobial production is an option. You also have other factors, however, such as secretion of molecules that impair attachment or quorum sensing. Also, virulence factors that give a competitive edge such as evading immunosurveillance (encapsulated B. anthracis strains vs unencapsulated, for example).

So here's the hard part: you want to engineer an attenuated bacterium that goes in and attacks a pathogenic strain. While I'm sure possible, you would certainly need to ensure that what you take away to attenuate your strain doesn't gimp it in vivo. You also need to realize that your target pathogen is very capable of simply "changing" itself to avoid dying to the engineered strain. Once your mechanism of action has been defeated, your product has been defeated. I think that it's fundamentally different from commercial virus-based products like T-VEC, as well, due to the level of variability.

One of my thoughts is your strain needs to be able to compete with the pathogen in the first place to stand a chance, which may be difficult if you cut out too many virulence factors trying to make it "safe."


Ethics in Paleontology Ethics in Paleontology

Fossils help researchers understand the evolution of many lineages of plants and animals. But, who actually owns fossils? What if an important fossil (say a transitional fossil like Tiktaalik or Basilosaurus) were found by an amateur fossil hunter and sold to a private collector? Should there be regulation of fossil hunting to prevent loss of scientific information? Should all "important" fossils be turned over to museums?

It depends entirely on where the fossils were dug up. In the US fossils on private land belong to whomever owns the mineral rights to the land, that landowner can do with the fossils as they will. On public land the fossils belong to the government and to get a permit to dig them a paleontologist must have a place to store them, this is part of the permitting process (digging on public land without a permit is a felony). Most of the time this place is something called a repository, a public institution that has facilities to store and care for fossils, usually a museum or university and has contingencies so that the fossils will not be lost if the facility were to fail or close. Now this is for vertebrate fossils becasue of the nature of invertebrate fossils (chalk for instance is made entirely of fossils) the laws can be a bit more lax.

Private collectors can only collect on private land, which usually involves making an agreement with the landowner. Keeping collection records is always a good idea if for no other reason than to show where a fossil was found.

I have worked with both types of collectors private and public, good private fossil hunters will differentiate rare fossils and common ones and will donate rare ones to museums while selling common ones. Bad one will sell everything, which often does lead to fossils disappearing or in some cases being outright destroyed by those who disapprove of evolution and the fossil evidence for it. For this reason most journals will not accept publication made using private collections, becasue it makes repeatability impossible.

Now this is all in the US, other countries have different laws some more strict some less so.


Is tolerance unavoidable? Do all psychoactive substances induce tolerance eventually?

For that matter, do all receptor-binding substances induce tolerance eventually?

It seems certain that different substances take different amounts of time to produce tolerance. Is there a pattern here? Do all receptor antagonists take similar amounts of time, or does it vary by receptor type?

(How do we know medications are not a zero-sum game?)

In general receptor-binding substances cause an "overflow" of your own already produced neurotransmitter. Your brain reacts by reducing the receptors. Also your own neurotransmitter production may be down-regulated by negative feedback. When you take away the "medication" afterwards, there are less receptors together with less neurotransmitter, causing withdrawal symptoms.

When you put in more substance in a control loop, there will always be some sort of "adaption" in order to reinstate a new balance (1). If you take in just enough drugs to balance the neurotransmitter-receptor system in a way, that the signal transduction in terms of nerve pulses remain the same, you have reached a tolerance stage, but not an effect stage. Still, medication is not "useless", since not all receptors will be dissipated. It is a matter of dose rate to increase the nerve pulses; once there is relatively more neurotransmitter (2) available than before medication, one should obtain a constant effect or an effectively altered control loop balance.

(1) https://books.google.at/books?id=z9TUch7m144C&pg=PA34&lpg=PA34&dq=receptor+regulation+up+down+neurotransmitter+drugs&source=bl&ots=2-4GRChqBi&sig=6e0YM-UrfgnMlw6e-rXR2Or7Qxc&hl=de&sa=X&ved=0ahUKEwixr_D25ZDMAhWB7RQKHcF9DqYQ6AEIHzAA#v=onepage&q=receptor%20regulation%20up%20down%20neurotransmitter%20drugs&f=false

(2) http://www.merckmanuals.com/professional/clinical-pharmacology/pharmacodynamics/drug-receptor-interactions


Do you know of ways that help a plant to produce more flowers? In Crocus sativus, or saffron crocus, the most commercially important part is the stigma of flowers. Each plant produces one flower (so there is more than one plant in this picture) and each flower has three stigmas (stigmas are red in this picture). What are the possible mechanisms to produce more stigma in a plant for commercial cultivation?

Each species of flowering plant produces a set number of floral parts, more or less. Having three styles and three stigmas per flower is a trait that is determined genetically. Mutations can cause floral parts to be duplicated. Heirloom tomatoes have mutations in the fascicated and locule-number genes, resulting in more locules being produced per fruit. Mutations in the fascicated gene also cause increases in other floral parts, such as petals, sepals, and stamens. If you compare a regular tomato to an heirloom, you'll notice that heirlooms tend to have around 10 petals and sepals compared to a regular tomato's 5.

Now the question is, do such mutations exist for Crocus sativus? A quick Google search didn't turn up anything other than the normal three-stigma flowers, so it doesn't look like such a mutation is common, if it exists at all. My answer to your question is: there is no easy way to get a saffron flower to produce more stigmas, for if such a method existed, everyone would be using it. I don't doubt that a dedicated botanist could come up with something (crossing with a related species, perhaps), but it's not something you can likely accomplish in your home garden.

Edit:
User Sleepses found an article where a high-yielding mutant with 5 stigmas was obtained through gamma radiation mutagenesis. I'm not sure whether or not this mutant is for sale commercially, though.


Are centrioles really absent in human neurons? A booklet (issued by my school) claims,

  Centrioles, formerly believed to be absent in neurons, have been described in neurons and may be associated with the production and maintenance of neuro(micro)tubules in them.

I was under the impression that mature human neurons are totally devoid of centrioles.

Being something circulated at a school, it lacks niceties such as citations/references. I've done a spot of Googling, but that didn't yield anything confirming the claim in the booklet.

Q- As per latest studies/info. do (mature) human neurons really possess centrioles?

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

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

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

Sources:

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


Is there a favoured mathematical model of bacterial growth? One of the most regularly measured phenotypes in bacterial synthetic biology is growth. Anyone who does wet lab microbiology or synthetic biology will have performed a growth curve measurement. However, it is quite rare in synthetic biology papers for growth to be characterised using a mathematical model - even though growth curves are regularly shown in supplementary materials.
There are a plethora of growth models around - from basic logistic growth to the more biologically grounded Monod growth. I recently discovered the Richard's model which seems to be a more general form encompassing logistic, Gompertz etc. Is there a favoured model for the microbiology and/or synthetic biology community? Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

Some clarifications:
Commonly used models for bacterial isothermal growth curves (which represent the growth curve directly) are for example:

Exponential

Logistic

Generalized logistic

The Monod equation expresses how the growth rate changes with the availability of substrate see a related question here.
The Monod equation can be incorporated into an exponential growth model (differential equation) like this:
$$
\frac{dX}{dt}=\mu X
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X$ is the biomass concentration and $[S]$ is the substrate concentration. Or into a logistic growth model:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X_{max}$ is the carrying capacity.
Other growth-substrate relations like Haldane which takes into account growth inhibition by the substrate can be used instead of Monod one.
Regarding this:

Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

It depends on what branch of synthetic biology you are looking into. Model-based design engineering biology interpretation of synthetic biology goes around the DBTL cycle. In the DBTL cycle, there are always (at least) models of both growth and gene expression.


Are all genetic instructions in DNA? Wiki says

  DNA is a molecule that carries most of the genetic instructions used
  in the growth, development, functioning and reproduction of all known
  living organisms and many viruses.

What bugs me is the "most" there, it implies some of the genetic instructions are elsewhere, but where?

Genetic information is the heritable information used by organisms to guide their self-assembly. It's why traits can persist across generations. DNA is, by far, the primary material used (by life) to encode genetic information, but it's not the only one. RNA is a pretty common alternative to DNA.

If we're looking to Wikipedia, this is actually referred to (in passing) on many pages about genetics. They usually link to the page on the best known edge case, RNA viruses:

  An RNA virus is a virus that has RNA (ribonucleic acid) as its genetic material. This nucleic acid is usually single-stranded RNA (ssRNA) but may be double-stranded RNA (dsRNA). Notable human diseases caused by RNA viruses include Ebola hemorrhoragic fever, SARS, influenza, hepatitis C, West Nile fever, polio, and measles.

While viruses fall into a weird middle ground between life and inanimacy, they still all need genes, and many of them use RNA for that. Side note: retroviruses get their name from the fact that they use reverse transcription to synthesize DNA from an RNA template.


I found this on the beach at Breamlea in Vic Australia and wondered if you could tell me what it is please It is about 6.5 x 5 centimetres and semi transparent.
It has quite a tough skin and is hollow inside. Like a tight clear tooth shaped balloon. I have put a coin next to it for you to see the size.

It's a swim bladder, probably a porcupinefish swim bladder. They can be found washed ashore still inflated. They've been described as "molar shaped". (Picture from Australian Museum.)


Why do bacteria adapt quickly to antibiotics but not to much more common threats? People cook food all the time, why don't common bacteria adapt to extreme heat? It's winter in either hemisphere every year, why don't common bacteria adapt to extreme cold? People use soap or spray cleaners, why don't bacteria adapt to those chemicals?

Why is it specifically only antibiotics that bacteria adapt to so quickly?

Antibiotics usually target a single protein (most commonly components of the ribosome machinery). If you have a large population of bacteria, there are bound to be cells with mutations in the gene encoding for the target of the antibiotic that render the antibiotic ineffective. Microbes also have drug efflux systems that can help with resistance to antibiotics. Temperature on the other hand has broad lethal effects from disrupting the cell membrane to damaging DNA and affecting the reaction rates of vital enzymes so that it's impossible to adapt in such a short time by gaining a few mutations.


databases for plant growth temperature and altitude Does anyone know databases which have info for plant growth temperature.It could be specific numbers or categorization as 'cold, warm,tropical and etc' ?

You might find these maps useful. I am not sure where you live, but most plants will list what region they will grow in on their seed packet or online.

You might also find luck by searching ESRI or ArcGIS maps to find more information.

http://www.ahs.org/gardening-resources/gardening-maps


What is the difference between silent and synonymous mutations? Several sources all caution that silent mutations and synonymous substitutions are not the same thing and should not be confused. But they seem to draw different actual distinctions between the terms:

This Wikipedia page and this biology dictionary entry define a silent mutation as a point substitution that replaces a single codon by another codon that codes for the same amino acid, and therefore does not directly change the amino acid sequence that is coded for. It defines a synonymous substitution as a silent mutation that occurs in an exon. Under these definitions, a synonymous substitution is a special case of a silent mutation.
This Wikipedia page and this blog post define a silent mutation as any mutation that does not have any phenotypic effects, and defines a synonymous substitution as a point substitution to a degenerate codon (anywhere in the genome, as far as I can tell). It points out that such synonymous substitutions can still have indirect phenotypic ("nonsilent") effects by affecting translation and transcription. Under these definitions, a silent mutation is a special case of a synonymous substitution (namely, one that doesn't have any indirect phenotypic effects).
This Wikipedia page uses similar definitions to the one in #2, except it explicitly requires that a synonymous substitution occurs in an exon.

Clearly these definitions are not all compatible. (#2 and #3 are very similar and could perhaps be excused as minor variants on the same definition, but they clearly conflict strongly with #1 - they disagree on which of "silent mutation" and "synonymous substitution" is a special case of the other!) Is there a standardized distinction in the biology community between these terms, or is it just the case that everyone uses conflicting definitions and we should ask people to clarify the senses in which they're using these terms?

I would say that silent mutations, as they have been defined, are a subset (or perhaps even same as) of synonymous mutations. However, the term, "silent mutation", is not used so much these days. Almost every research paper that I have read pertaining to this topic has always used the term "synonymous mutation" irrespective of whether or not it has a phenotypic effect. It seems that the term, "silent mutation", is confined only to textbooks.

If you consider silent mutations are mutations that are not reflected in the phenotype then there some points that you should consider.

As canadianer mentioned, these mutations can be present in non-coding region. However, mutations in non-coding regions can also affect the phenotype. Moroever, as they mention, synonymous mutations can cause changes in translation rates because of the codon bias which in turn can lead to phenotypic differences (Kimchi-Sarfaty et al, 2007; Waldman et al, 2011; Buhr et al, 2016). These phenotypic differences can arise due to altered protein concentration or altered folding states. So a synonymous mutation is not essentially "silent"
A non-synonymous mutation may not affect the phenotype (neutral mutation).

I would say that this definition should not be used unless the majority of the scientific community agrees on redefining the term. Till then, you can possibly use the term, "neutral mutations", to mean mutations that do not affect the phenotype. Remember that neutrality of "neutral mutations" is defined with respect to fitness. However, if your measure of fitness pertains to the molecular function of the gene then this definition works.


How do CD 8+ Tc cells reach the site of tumors? In normal humoral immunity, dendritic cells present antigens to the Th cells by arriving at the Lymph node. This is fine. But consider a tumor cell. How does the Tc cell sitting in the lymph node know that there is problem out there? Consider there is a single cell which has undergone mutations and is expressing altered proteins. This wouldn't cause much inflammation to attract the Tc cell there.

So, is there continuous surveillance by the Tc cells? Where exactly do the Tc cells reside? Do they roam around like Th cells? How about the NK cells? do they too roam around in the tissues?

Cases of viral and intracellular pathogens, there may be some inflammation which draws the Tc cells there. Maybe. This can not be in tumors. So how do the Tc cells reach there?

I do not remember enough details to share a mechanistic insight.

However, chemotaxis is a likely answer, which basically means moving along concentration gradient of certain ligand of interest.

Also relevant to your question: a hypothesis called 'immune surveillance' gaining support over the past few years.

http://www.biolegend.com/cancerimmunoediting


Whole genome sequence analysis software Please help to choose Bioconductor R packages and other software for the whole genome sequence data analysis and, in particlular, the goals of false discovery mutation rate, mutations exclusion, mutation contribution and data dimensionality reduction. I could find Expander, MeV, Genesis software for the microarray experiments, however, could not find similar tools for the whole genome sequence analysis of mycobacteria. Sorry, that my question has no code.

There are couple of them. First if you want to sequence analysis basic packages are :

http://www.bioconductor.org/help/workflows/high-throughput-sequencing/

Also, Maqweb seems promising.

http://maqweb.sourceforge.net


How many traits can a multivariate breeders equation handle? The multivariate breeders equation (MBE) by Lande predicts the change in a trait $\Delta \bar z$ (response) as

$\Delta \bar z = G \beta$

where $G$ is a genetic variance-covariance matrix and $\beta$ is a vector of the selection coefficients. What are the limitations on the number of traits the MBE can tolerate? Is there a theoretical limit on the number of traits $G$ and $\beta$ could contain? Or does the calculation lose power with increasing complexity?

Theoretically as an example, could I take the expression of 10000 genes, compare them to fitness to to make a 10000 row $\beta$ vector, and generate a 10000 * 10000 G-matrix from estimates of male and female gene expression in some lines, and then put them through the MBE?

Noting that the right hand side can also be written $\mathbf{G}\mathbf{P}^{-1}\mathbf{s}$, we see that the only theoretical limitation of the multivariate breeders equation is the invertibility of the matrix $\mathbf{P}$. This happens when the measures of two traits are the same for all individuals, making two columns of the matrix the same I.e. It becomes singular.

This theoretical concern can become a practical concern quite quickly when multiple traits are measured. The solution is to effectively consider two traits as one.

The 'power' of the equation, by which I assume you mean something like 'accuracy of prediction', actually improves with the number of traits measured. Indeed, a big concern with measuring only a few traits is that the response to selection on those traits is actually 'caused' by selection on some other correlated but unmeasured trait.


Could an exposure to a small amount of viruses result in an easier course of the disease? According to Gunther Hartmann (Professor of Clinical Chemistry and Pharmacology at the University of Bonn) cited in this article (Süddeutsche Zeitung, in German)

  Die Zahl der Erreger hat bei Erstinfektionen Einfluss auf den Schweregrad der Erkrankung.

My translation:

  The number of pathogens during the initial infection affects the severity of the disease.

Leaving ethics aside I was wondering about the following:

Might it be an option to get infected by only a tiny amount, suffer only light symptoms and reach immunity (similar to a vaccination but probably more risky)?
Does the transmission path also affect the severity of the disease(inhaled vs. infected vs...)?

Edit: As Chris pointed out in his comment there is not enough research for Covid-19 yet so I would be also interested in findings from other viral infections.

I think the answer to your question is actually found in the paragraph surrounding the quoted statement:

  Auch Gunther Hartmann, Professor für Klinische Chemie und Pharmakologie an der Universität Bonn, berichtete, nach ersten vorsichtigen Einschätzungen sei davon auszugehen, dass der Schweregrad der Erkrankung über Hygienemaßnahmen reduziert werden könnte. "Die Zahl der Erreger hat bei Erstinfektionen Einfluss auf den Schweregrad der Erkrankung."

Approximate translation:

  Gunther Hartmann, Professor of Clinical Chemistry and Pharmacology at the University of Bonn, also reported that, after initial careful assessments, it could be assumed that the severity of the disease could be reduced via hygiene measures. "The number of pathogens influences the severity of the disease in initial infections."

Notice that the language is not absolute but rather asumptive: "initial careful assessments," "It could be assumed," "could be reduced."  It's tentative language and suggests that research is ongoing.  Furthermore, if you search for that quote, you'll find that this is not published in peer-reviewed journals; it's simply a preliminary observation to encourage the public to limit intake of pathogens.

We already know that in some other cases the viral load affects the severity of symptoms. But we don't actually know that that's the case with COVID-19.  In fact, initial reports from Italy suggest that there is no statistical difference between viral loads between symptomatic and assymptomatic cases of COVID-19. So Chris's short answer is absolutely right; we don't know.  For all practical purposes, it's just as well to assume that it's the case, as it will lead to more hygeinic practices, but further research will be required to demonstrate that it is actually the case.