What is basis of multifunctionality of "master glands" in the endocrine system? I have just started reading about the endocrine system and I am having some difficulty understanding the basis of distribution of glands and associated hormones.

I am using multifuntionality to describe the amount of relatively independent input and output that are shared through a same organ or proximal space. Many of these organs have a heterogenous mixture of endocrine cells sharing the same glandular space.

There appear to be some glands that are considered "master glands" such that they take a variety of relatively independent input, apply some control logic via a diverse set of endocrine cells and tissue and secrete a diverse hormonal output. The pituitary and hypothalamus are the best examples, however the adrenal cortex and the pancreas also fit this definition to a certain extent. Many times the diversity of hormones and cells within an organ have no obvious connection (eg thyroid). Some glands appear more specialized with a relatively straightforward endocrine axis of input and output (eg testes).

Some of this multifunctionality seems unnecessary, in that insulin secretion could occur anywhere and be effective in the manner of an insulin pump, or contain risks due to excessive centralization as in a pituitary tumor or renal artery stenosis, so there must be some advantages I do not understand.

My textbook (Headley, Levine, 6th) seems to minimally cover multiplexing, signal cross-talk and competition between diverse endocrine cells sharing an organ. Its focus on discrete pathways and axes suggests these are evolutionarily unfavorable.

Are there synergistic advantages in shared endocrine infrastructure such as vascularity or metabolic pathways?

Is there some overlying logic that can be used to explain this distribution of glands and hormones regarding multifuntionality-specialization, or is it necessary to view the distribution of vertebrate endocrine system as the outcome of evolutionary contingencies?

Thanks

It would seem to me that in the examples that you have listed that proximity to necessary input is the overriding logic behind gland geography. Take the hypothalamus as the first example. This gland receives input from diverse regions of the brain from the amygdala and hippocampus to the retina and brainstem. The brain can tweak levels of various releasing hormones entering the  hypothalamic-hypophyseal portal veins in order to produce a response that is appropriate to the situation perceived by the brain. It makes sense to have all of these co-located because they are all receiving input from the brain. Similarly, it makes sense to have all of cells that are uptaking the releasing hormones close-by to protect these vital peptides from degradation in the systemic circulation. Their collectively unique circumstance makes sharing a specialized vasculature a logical choice.

The pancreas is a good example of the importance of cross-talk within some endocrine tissue. Within the islet, alpha, beta, and delta cells are feeding back on each other to get the balance of insulin and glucagon just right. To whit, glucagon secretion provides a paracrine signal for insulin secretion. This makes sense because the body knows that once glucagon is released the blood sugar will soon rise. Ergo, it makes sense to trigger some insulin secretion as well in preparation. Their co-location makes that possible.

In short, I would say the overriding logic to the placement of each of these glands is their proximity to the necessary inputs and outputs that each of these glands interacts with.


The "truce of the watering hole" -- is it completely discredited? In short, the idea comes from Kipling that animals observe a sort of truce around watering holes and prey animals do not have to be on guard (as much?) from predators in the vicinity.

I have read that this is false, that predators might even wait around watering holes for prey. However: Cleaning stations in the ocean seem to have rules and a truce (and a fish violating these rules, primarily not to attack other fish waiting to be cleaned is attacked by other fish of various species). So the idea of a truce at waterholes, perhaps only partially observed, is not that far fetched.

I wonder too if lions, for example, at some level understand that in order to survive they need prey to be able to eat/drink and breed. While this also sounds too sophisticated, is it any more sophisticated than the behavior of killing cubs so that females come into heat?

Cleaning stations offer a pretty strong individual incentive not to attack, those that attack do not get cleaned and thus get riddled with parasites. Watering holes are just the opposite there is no advantage to not attacking and in fact a decent advantage for attacking, (a meal) many predators hang around watering holes just because the draw prey.

To put it another way the genes from lion A say hunt things at the watering hole, the genes from lion B say don't, Lion A is going to have more meals and thus more offspring than lion B therefore the genes to hunt at the waterhole will spread. Lion B gains no benefit from not hunting at watering holes that can offset the very large and immediate advantage lion A gets. This is a good general test to why group selection generally doesn't work, even if all lions were type B as soon as lion A occurs from a mutation it has a huge advantage and drives out lion B's genes.

There is quite a lot of evidence that predators often concentrate around watering holes, heck this is how crocodiles make a living. The idea that lions do not is an out dated and stems from early observations done only during the day (when lions are mostly inactive yet close to watering holes to hunt at night), spread by fiction writers and reinforced by advertising and poorly researched articles.

https://www.nrcresearchpress.com/doi/abs/10.1139/z77-235#.XkxeG2hKhPZ

https://academic.oup.com/beheco/article/23/5/970/232520

The Serengeti Lion: A Study of Predator-Prey Relations
By George B. Schaller

Seasonal Diet and Prey Preference of the African Lion in a Waterhole-Driven Semi-Arid Savanna


If one endures the same form pain over a long period of time, would the pain begin to lose intensity? Metaphorically thinking, if one endured the pain of constant burning for decades, would the pain slowly lose its strength?

Under the assumption that the temperature experienced is not high enough to simply burn the nerves responsible for the pain (which would lead to insensible regions), yes and it would due to what is called receptor desensitization. In the case of burning pain the receptor involved is called the transient-receptor potential channel V1 (TRPV1). It is the same receptor involve in the oral burning sensation of spiciness.

Now two scenarios are possible given your question, namely a constant stimulus over a long period and "oscillating" stimuli (i.e. a repetition of stimuli followed by non-stimulated periods).

Constant stimulus

I provided a similar answer to this question: What features cause mechano sensory adaptation?. This is the scenario where you keep the painful stimulus constant over a period of time. Here desensitization, i.e. reduction in pain feeling, is due to a direct receptor desensitization. This happens because the receptor is internalized (also called receptor-mediated endocytosis) into the cell after being activated and it takes some times for the receptor to reach the cell membrane again meaning if the stimulus remains constant, pretty much no receptors will be left on the cell membrane.  After decades long term desensitization will occur and is slightly different in it's mechanism compared to standard desensitization as described hereafter.

"Oscillating" stimuli

In the case you are talking about a chronic pain interrupted by periods of non stimulation then long term desensitization will occur. In this scenario, the concentration of receptors will be reduced semi-permanently (i.e. reduced expression of the receptor) in the receptor cells reducing the pain signal. This is what happens with spiciness sensation. People eating regularly very spicy will physiologically be less sensitive to spices as they have less receptors sensing the spices provoking a reduced burning sensation.

Just as a footnote, very long chronic pain will also change the brain wiring of the pain signal but as I don't know enough about neurobiology I will leave that appart.


Without plant breeding and domestication, would most of the foods consumed by humans evolve to become inedible? Would this happen? Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

Plant defense against herbivory

Plenty of plant species evolved defense mechanisms. There is a large variety of defense mechanism. Have a look at the wikipedia article Plant defense against herbivory for more information. Such defense mechanism often comes at a cost and therefore the mechanism can be maintained only if herbivory is sufficiently common and costly. Note that herbivory might be beneficial to some animal species typically as it can help to disperse the seeds.

plant-herbivores Co-evolution

Herbivores co-evolve with plants and develop mechanism to deal with plant defense mechanism. Such coevolution often yield herbivores to specialize in feeding in a handful of plant species only.

Human consumption

Most of what human consume is artificially selection. We specifically allow the breeding of individuals that present trait that are pleasant to us. In such condition, a defense mechanism would be a highly deleterious trait.

  Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

I don't understand this sentence. Do you mean "[..] especially plant species being consumed by animal species that don't help spreading the seeds"?

If this is what you meant, then yes. If herbivory comes at non benefit for the plant, the overall cost of herbivory will be more important for the plant. All else being equal, a mutant that present a defense mechanism would have a higher fitness if the herbivores do not offer any benefit to the plant being eaten.


Fabric melting spider juice I live in the southern rocky mountains of Canada. I was in bed the other night when I saw a small scurrying shadow out of the corner of my eye. The source of the shadow was a small spider (95% sure it was a barn funnel weaver), approx 2cm in diameter. I killed the spider.

Interestingly, what intrigues me is that the place on my bed where I killed the spider the jus of the spider had melted to the sheet (!). How could that happen?

Some spiders are known to eat their own silk when breaking down a web and reconstructing it (https://en.wikipedia.org/wiki/Spider_web#:~:text=It%20is%20common%20for%20spiders) or even stealing the web of other spiders and eating it (https://frank.itlab.us/photo_essays/papers/Argyrodes_kleptoparasite_spider.pdf). It may very well be that some types are able to digest various silks or other fibres. I'm not aware of any studies that test whether a spider could digest - say - wool or other natural fibres.
If your sheets were silk or other natural fibres, it's feasible that their digestive juices were strong enough to break down your fibres. Who knows, maybe their digestive juices are even strong enough to break down synthetic fibres (unlikely, but I don't know any study that has looked at that).


Does copper exacerbate wounds? There is a three edged stiletto (weapon, not shoe) with a triangular cross-section that is often touted as being "extra dangerous" because of the triangular puncture it makes, and its copper construction. The claim is that the copper inclusion causes something colloquially referred to as "blood poisoning."

Is there any basis to the idea that a copper blade would cause some kind of secondary toxic effect?

Excess copper in the body can be toxic but I'm not sure a copper blade would be especially toxic unless it was coated with something else or it remained in the wound. Copper can be acutely toxic when ingested, or chronically over a long period of exposure (like lead), but is more often associated with a failure in copper excretion. Since the body has ways of dealing with excess copper, I just don't see much merit in the super-toxic copper blade, unless it is designed to break off in the target.


Why do sparrows jump instead of walk when they are not flying? I want to talk about sparrows, one of the most common birds around the world. I noticed that when one slowly walks into them (so that they are not frightened enough to fly away), these tiny birds would jump away, rather than walk away, as if they are not able to walk.

Why?

As pointed out by @jamesqf in the comment below, there exist many birds like quail and pheasants that run and walk rather than hop. Also, there are several flightless birds like  ostriches, emus, rheas that do the same. But it is also true that sparrows don't walk or run but hop. The question now is- why?

There is an interesting fact- both Quail and Pheasant are ground nesting birds.

Now, the reason why we do not see sparrows running like pheasants is because sparrows rely more on their ability to fly for survival and getting around. So, a sparrow will rather fly the distance than run. The reason for this might be its smaller size which makes it more efficient and safe during flight.

But the question is- why don't sparrows walk? Why do they hop? Quails (video) and Pheasants(video) certainly walk even for short distance.

Just before a flight, all birds jump to power their flight. So, if a sparrow hops around rather than walking around, it can convert any of these jumps into a full flight in the case of an unexpected need. This again comes down to sparrow's heavy reliance on flight to escape danger. Because of their light weight, hopping rather than walking is less costly for a sparrows.

Whereas in a normal situation, Quails and Pheasants would rather run to build the necessary  momentum to initiate a flight. But they walk even for shorter distance because they are heavier than a sparrow, and walking for them is more efficient than hopping. But in worst case scenario, even birds like Quails can simply jump into a flight, as can be seen in this video if you watch it in slow motion.

Edit: another factor that might influence whether a certain bird hops or walks is the irregularity of the terrain with respect to the size of the bird. The terrain is relatively more irregular for smaller birds (there are obstacles like twigs, stones, grass etc), hence making hopping a better option than walking.

There are many kinds of birds that each choose whether to walk or hop. Here i present a small categorization with video evidence to bring out some pattern if any. You might need to watch some of the videos in slow motion.

Birds that hop:

sparrows
American robin
blue jays

Birds that walk

Crow
magpie
Quail
Pheasant
an unknown small bird that the video title says is American robin but which walks


Are Purkinje Action Potentials Neuronal and Cardiac? I first thought that action potentials of His-bundle i.e. Purkinje fibers are Cardiac.
However, I started to think that this is not enough.
I think now that they are neuronal and cardiac.
My conjecture. They have first short-acting neuronal part and then long-acting cardiac part.

Are Purkinje Action Potentials Neuronal and Cardiac?

The His-Purkinje fiber system is a network of one type of specialized conducting cardiac cells that carry an action potential in the heart. There are other cells which perform this function in different parts of the heart. The initiation time, shape, and duration of the action potential are distinctive for different parts of the heart, reflecting their different functions. These distinctions arise because the myocytes in each region of the heart have a characteristic set of channels and anatomy. You can completely dissociate the nervous system from the heart, and the heart will still pace itself. Think of what happens with heart transplants. This completely eliminates neuronal influence. See the following brief excerpt which explains one type of cells conduction method. Please note there is no reference to neurons.

  The positive charge that enters cell A not only depolarizes cell A but also produces a flow of positive charge to cell B—intracellular current. This flow of positive charge discharges the membrane capacitance of cell B, thereby depolarizing cell B and releasing extracellular positive charges that had been associated with the membrane. The movement of this extracellular positive charge from around cell B toward the extracellular region around cell A constitutes the extracellular current. The flow of intracellular current from cell A to cell B and the flow of extracellular current from around cell B to around cell A are equal and opposite. It is the flow of this extracellular current in the heart that gives rise to an instantaneous electrical vector, which changes with time. Each point on an electrocardiogram (ECG) is the sum of the many such electrical vectors, generated by the many cells of the heart.

This has been extensively studied, so much so that cardiac electrophysiologists can pinpoint the location of a small group of cells that are misfiring by the nature of the impulse they are giving off. The annual median salary for an electrophysiologist in the US is $480,000. :-( There is a lot of grant money in this area. It's a big deal.

For in-depth study of electrophysiology of cardiac cells, please see Electrophysiology of Cardiac Cells or any other of a number of reliable sources.


How do roots absorb water instead of presence of waxy - material suberin in the form of casparian strips on the wall of endodermis? I found that in the endodermis, the tangential and radial walls have deposition of the waxy, and hence water-impermeable, material suberin in the form of casparian strips. The endodermis comes before the vascular bundle so how is water absorbed in roots?

The plants do  have waxy walls and stuff, the plants use "Suction Method" to suck the water from the ground. Due to transpiration plants loose water from the top or aerial region of the plant and since water is absent in that region there is vacuum present so it sucks water from the ground. This is how plants absorb water.

[Reference--- https://en.wikipedia.org/wiki/Xylem ]

[Ref. Wiki Images and text part and cross check for better understanding]


Does the octopus have an anus? What does it look like? Octopuses are cephalopods, which have separate anal and oral openings. Indeed, descriptions of the cephalopod GI tract clearly depict an anal opening.

However, I am very confused about how this applies to the octopus. I don't think I've ever seen the anus depicted - where is it? What does it look like? Does anything much come out?

My first instinct would be to simply do a google image search for this. Unfortunately, those results are flooded with unrelated hits (apparently the octopus is a popular motif for tattoos... in a certain part of the body).

The anus of Octopus is channeled into its siphon.

Image taken from Carina M. Gsottbauer

Note:

  Siphon is a tube that leads from the mantle to the outside. Octopuses use their siphon to force water out in jets for propulsion and to flush waste products from the anus.

From Encyclopedia of the Aquatic World, Volume 6
By Marshall Cavendish Corporation


What is the difference between orthologs, paralogs and homologs? These three terms are often misused in the literature. Many researchers seem to treat them as synonyms. So, what is the definition of each of these terms and how do they differ from one another?

First, a note on spelling. Both "ortholog" and "orthologue" are correct, one is the American and the other the British spelling. The same is true for homolog and paralog.

On to the biology. Homology is the blanket term, both ortho- and paralogs are homologs. So, when in doubt use "homologs". However:

Orthologs are homologous genes that are the result of a speciation event.
Paralogs are homologous genes that are the result of a duplication event.

The following image, adapted (slightly) from [1], illustrates the differences:

Part (a) of the diagram above shows a hypothetical evolutionary history of a gene. The ancestral genome had two copies of this gene (A and B) which were paralogs. At some point, the ancestral species split into two daughter species, each of whose genome contains two copies of the ancestral duplicated gene (A1,A2 and B1,B2).

These genes are all homologous to one another but are they paralogs or orthologs? Since the duplication event that created genes A and B occurred before the speciation event that created species 1 and 2, A genes will be paralogs of B genes and 1 genes will be orthologs of 2 genes:

A1 and B1 are paralogs
A1 and B2 are paralogs.
A2 and B1 are paralogs.
A2 and B2 are paralogs.
A1 and A2 are orthologs.
B1 and B2 are orthologs

This however, is a very simple case. What happens when a duplication occurs after a speciation event? In part (b) of the above diagram, the ancestral gene was duplicated only in species 2's lineage. Therefore, in (b):

A2 and B2 are orthologs of A1.
A2 and B2 are paralogs of each other.

A common misconception is that paralogous genes are those homologous genes that are in the same genome while orthologous genes are those that are in different genomes. As you can see in the example above, this is absolutely not true. While it can happen that way, ortho- vs paralogy depends exclusively on the evolutionary history of the genes involved. If you do not know whether a particular homology relationship is the result of a gene duplication or a speciation event, then you cannot know if it is a case of paralogy or orthology.

References

R.A. Jensen, Orthologs and paralogs - we need to get it right, Genome Biology, 2(8), 2001

Suggested reading:

I highly recommend the Jensen article referenced above. I read it when I was first starting to work on comparative  genomics and evolution and it is a wonderfully clear and succinct explanation of the terms. Some of the articles referenced therein are also worth a read:

Koonin EV: An apology for orthologs - or brave new memes. Genome Biol, 2001, 2:comment1005.1-1005.2.
Petsko GA: Homologuephobia. Genome Biol 2001, 2:comment1002.1-1002.2.
Fitch WM: Distinguishing homologous from analogous proteins. Syst Zool 1970, 19:99-113. (of historical interest, the terms were first used here)
Fitch WM: Homology a personal view on some of the problems. Trends Genet
2000, 16:227-31.


When in Ampicillin degraded (gone) in liquid TB-media? Concerns about selectivity Question: Specifically regarding Ampicillin; When growing cells in TB (terrific broth) for protein expression - when should I expect the ampicillin to be gone due to degradation by b-lactamases? (and how much Ampicillin do people add in addition to standard 100 ug/ml)

Background: I have heard rumours that all Ampicillin (100 ug/mL) is degraded within few hours (2-3) due to the enormous amount of b-lactamases secreted by the bacteria.I have also heard that some are not concerned about this, because 2-3 hours is anyway enough for the culture to outcompete anything else that will grow after the ampicillin is gone. On the other hand, some people are also writing that they add more ampicillin every 2-3 hours to maintain selectivity; however, I dont really see the point in maintaining selectivity as long as I have plenty of protein I will anyway lyse the cells and not use them for anything else.

My growth conditions: Grow at 37 degrees till OD600=1 (takes around 3h), then induce with IPTG and grow at 25 degrees for 18h, 200 rpm the entire time.

End comment: I know you can generally change to the more expensive carbenicillin which is degraded slower, but i'm more interested in knowing "how bad" Ampicillin really is for my general knowledge (and I will anyway keep on using it). Also: Any general thoughts or references to literature on this topic, specifically for Ampicillin is appreciated.

rather interesting question. Selection pressure is very important for any type of work. And it is true, amplicilin will degrade in media due to the secretion of beta-lactumase. This is a limitation that we must face, though there are ways of getting around this.

For example, when cloning, on a plate sometime you will notice "smaller" colonies growing around a central large one. This is due to beta-lactumases. They are not a problem if you are going to take the central colony and place it into fresh media with new amplicilin. They will simply die out. No harm done.

In liquid culture it is good to not "oversaturate the culture". Usually, do not let it get over OD600 = 1. In addition, do not use old stocks, as this causes problems with selection and use higher concentrations of ampicillin if you are still having troubles selecting!

Generally speaking, 100ug/ml is standard for most selection with cloning, and should be sufficient for what you are doing. It seems that your protocol should work fine for protein isolation.

Last remarks -- it is a problem that most microbiologist do not think of. Ampicillin has its limits!

https://www.addgene.org/mol-bio-reference/antibiotics/

https://bitesizebio.com/10188/whats-the-problem-with-ampicillin-selection/


Can cells show negative growth? I know that growth is an irreversible increase in mass or overall size of a cell, organ or whole organism. I also found that growth occurs due to the net result of anabolism and catabolism.
My teacher said;
           When anabolism > catabolism - growth occurs
                 Anabolism = catabolism - no growth
                Catabolism > anabolism - negative growth
But on searching about this negative growth, I couldn't find any information. What is this negative growth? Where do you see it?

When you look at a certain mass of cells (in a petri dish, a tumor, whatever) which are in principle viable, growth can go in both directions. It can be poitive which means that the number of cells is growing over time.

It can also be negative, which results in a declining number of cells over time. We see this effect in cell growth assays, when we analyze the effect of certain treatments to our cells. Since we want to "kill" our cells with the treatment, a positive growth would indicate an unsuccessful treatment, a negative cell growth a positive treatment effect.


Immunological factors for the cause of headaches following SAR-CoV-2/COVID vaccination It is generally-accepted that headaches are a common side effect from receiving the COVID vaccine.

Vaccine recipients with pre-existing immunity experience systemic side effects with a significantly higher frequency than antibody naïve vaccines (e.g., fatigue, headache, chills, fever, muscle or join pains, in order of decreasing frequency, P < 0.001 for all listed symptoms, Fisher’s exact test, two-sided).

— Florian Krammer et al.: "Robust spike antibody responses and increased reactogenicity in seropositive individuals after a single dose of SARS-CoV-2 mRNA vaccine" doi: https://doi.org/10.1101/2021.01.29.21250653
I am trying to understand why. What theories or known biological, immunological or otherwise physiological mechanisms would cause recipients of the vaccine to report headaches as a common side effect?

Headache is one of the various side-effects of vaccination. Typically, a person will have pain in the site of injection, muscles throughout your body and head.
The immunological reason is the network of our immune system. Whenever a foreign antigen (vaccine) is detected by our immune system, antigen-presenting-cells (macrophages, dendritic cells) takes the antigen to nearest lymph nodes where it is presented to the adaptive immune system. Due to this invasion, strong immune response starts which leads to the pain.

Image Source: wikipedia.org/wiki/Lymphatic_system


How do cis-regulatory elements and trans-regulatory elements behave differently? Suppose you are working with an operon in a diploid organism.

I'm looking for either a biochemical or genetic explanation.

What I'm having trouble with mainly is understanding how something would only be able to regulate a gene on one chromosome but not the other. I was thinking cis would be favored because the gene is close by, but everything is just floating around randomly in the cell so it should favor cis either way and level out if you waited long enough.

I was thinking cis would be favored because the gene is close by

Your intuition is correct.  Cis-regulatory elements like enhancers are more efficient at enhancing transcription of genes in cis than genes in trans, but trans interactions of cis-regulatory elements do occur.  Take a look at figure 2B of this paper and the accompanying text:

  ... quantitative RT-PCR showed that relative levels of GFP transcripts from constructs inserted at 37B were similar to those from transgenes at 53F, with 1.7% [95% C.I., 1.6–1.8%] of total GFP transcript in eye discs where GMR acts in trans relative to those where activation is in cis ...

The interaction of alleles between homologous chromosomes is called transvection, and this can be realized as binding of the enhancer associated with one allele to the promoter of the other allele.  Figure 9 of this paper is a good explanatory graphic.


Difference between mice and rats What is the actual biological difference between mice and rats? Are they actually the same thing with two different names depending on appearance (are they all mice for instance and we call the larger ones rats or vice versa) or is there some fundamental difference in their genetics?

Mice (Mus) and rats (Rattus) are definitely separate species, by whichever definition of species you choose to use. They are genetically distinct, and both genera are members of the clade Muridae, along with Acomys ("spiny mice") and Gerbillus ("gerbils").

Moreover, what we call colloquially "mice" and "rats" encompass a great deal of variation within rodents. The genus Mus is one of several subgenera with ~15 species.

A recent phylogenetic study of rodents by Blanga-Kanfi et al. (2009), revealed that Mus and Rattus are sister groups, meaning that each is the other's closest relative. The image below from the paper above shows the complete tree. Muridae is about 2/3 of the way down in blue.


What does "out-titration" mean? I am reading an article on developmental biology and cannot understand (even after searching the internet) what is meant by "out-titration".
For example, in this phrase:

  We have previously shown that Drf1, together with Cut5, Treslin and Recq4, are out-titrated on chromatin by increasing N/C ratios in vitro.

From this article: Chk1 Inhibition of the Replication Factor Drf1 Guarantees Cell-Cycle Elongation at the Xenopus laevis Mid-blastula Transition

Thank you!!

It does seem oddly phrased, but is still understandable. The paper explains how the combination of low zygotic transcription and increasing amount of DNA due to rapid cell division can function as a switch to trigger the mid-blastula transition. Before this event, most factors in the cell are of maternal origin (ie they are not being expressed in the zygote) and are thus in limited supply. As cell division progresses, the stoichiometric ratio between these factors and DNA decreases until, eventually, there is more DNA than these replication factors. At this point, you could say that the DNA has titrated the replication factors in that there is no unbound form left. This is analogous to the equivalence point of acid-base titrations commonly encountered in first-year chemistry courses.


Have there ever been as many mammals as there are now? I apologize for the weird question, but based on a Google search it looks like this topic hasn't been discussed before. I'm hoping that enough information about population biology is stored in the fossil record to answer this question.

Humans have wiped out a lot of animals in a very short time, but I realized that mammals might be doing very well.

First off, humans are mammals, and there are 7.6 billion of us. That's quite a lot. I don't believe any other animal species of our body size has such a large population.

Second, humans have pets. A lot of them. And they're almost all mammals. Everywhere we go we take our cats and dogs with us. Many of them become feral and multiply prolifically.

Third, our livestock. With the growth of human civilization came the growth of meat consumption, which, naturally, meant a lot more cattle. I think I read somewhere that cattle are contributing more to global warming than cars, through burping.

Lastly, and probably most importantly: rodents. Cats chased us everywhere because rats chased us everywhere. They thrived on the grain we grew and their population exploded to the point that they became a global pest, and possibly humanity's greatest enemy.

So, my hypothesis is that there are more mammals now than ever before in the history of life. Not in terms of species diversity, but in terms of headcount. If this is true, it would be remarkable, since the rest of the Animal Kingdom is currently suffering through a mass extinction.

There can be perhaps 10 trillion rodents and bats on the planet, so the humans and livestock probably are small compared to a rainforest rodents and bats. The biggest bat colony is 40 million, they decline without unmanaged forests, can reach 4-10 bats per hectare, and the world population might normally be in 10s of billions, save for the use of pesticides and deforestation.

Here's a bit of maths to say that we have erased 1 trillion rodent habitats through monocultures and ploughing. Every cow and sheep field would have previously supported 10-20-50 times more rodents, and they aren't adapted for pesticides and ploughs.

37% of the world's land is farmed
Extent of total cultivated land in 2006: 1.5 billion hectares.

If there were 14 mammals per km2 of farmland, then we have displaced 20 billion mammals.

If the pristine habitats previously supported 1 rodent/mammal every 5m2, we would have destroyed the homes of 2000 mice,voles,shrews,squirrels and other mammals by hectare, that's 3000 Billion mammals (worst case scenario) due to monocultures and farming, and 1000 Billion in a best case scenario. Bangladesh rice farms and UK fields both are hostile to mammals.

A 20g mouse for 5m2 comes to the same as one human for 15 square kilometers. A mouse only needs a 3g of seeds/roots/beetles/snails per day to survive, that's about a kilo per year. "blue oak, interior live oak, and black oak respectively produce 2955, 1074, and 616 kg/ha of tree canopy" invertebrates provide 100-300kg/ha.

Perhaps we have erased 1 trillion mammals in the amazon alone.

https://www.worldatlas.com/articles/list-of-primates-by-population.html

Also we have depleted the fish stocks. It is reported that in medieval times, the seas heaved with incredible amounts of dolphins, whales and fish stocks, pristine seal and dolphin numbers could have been about 1 billion. Perhaps today it's about 1/4 of that.

If i had to bet all I own on your theory, I'd say it happened at another time in the previous 60mn years, probably not today.


Additive genetic variance components from LMER in R I've set up some dummy data in R which makes 40 genetically related lines, they are all siblings within a line so are genetically related by a factor of ½ thus additive genetic variance should be twice the variance explained by line. For the lines there are 200 individuals being measured, for three characters/traits. The first trait has low phenotypic variance, the second has high environmental variance, and the third has high genetic variance.

rm(list=ls())
re = 200 # replicate individuals per line
li = 40  # lines

# setup
set.seed(5)
data = data.frame(rep(1:li, each = re))
colnames(data)="Line"
library(nlme)
library(lme4)
par(mfrow=c(1,3))

# trait 1: little variance (Va or Ve)
data$Trait = rnorm(li*re,10,1)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("Low V"[A]*"& Low V"[E]))
var1 = var(data$Trait); mean1 = mean(data$Trait); m1 = lmer(data$Trait ~ (1|data$Line))

# trait 2: high enivronmental variance, little Va
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait + rnorm(re*li,0,3)
boxplot(data$Trait~data$Line, ylim=c(0,20),main = expression("Low V"[A]*"& High V"[E]))
var2 = var(data$Trait); mean2 = mean(data$Trait); m2 = lmer(data$Trait ~ (1|data$Line))

# trait 3: high additive genetic variance, little Ve
data$Trait = rnorm(li*re,10,1); data$Trait = data$Trait+rep(rnorm(li,0,3),each=re)
boxplot(data$Trait~data$Line, ylim=c(0,20), main = expression("High V"[A]*"& Low V"[E]))
var3 = var(data$Trait); mean3 = mean(data$Trait); m3 = lmer(data$Trait ~ (1|data$Line))

Plots of the three traits,

Then to estimate additive variance ($V_A$) I extract the line variance ($V_L$) from the lmer model and double it,

# line variances (variance in additive effect of each haploid genome)
m1_line = unlist(VarCorr(m1))[[1]];
m2_line = unlist(VarCorr(m2))[[1]];
m3_line = unlist(VarCorr(m3))[[1]]

# additive variance (double the line variance because it is a hemiclone)
m1_add = 2*m1_line;
m2_add = 2*m2_line;
m3_add = 2*m3_line

Residual variances should be (assuming perfect experimental design, no measurement error etc.) the estimate of environmental variance ($V_E$) and phenotypic variance ($V_P$) should be the sum of $V_L$ and $V_E$,

# residual variance
m1_res = attr(VarCorr(m1), "sc")^2
m2_res = attr(VarCorr(m2), "sc")^2
m3_res = attr(VarCorr(m3), "sc")^2

# phenotypic variance
m1_phe = m1_line + m1_res
m2_phe = m2_line + m2_res
m3_phe = m3_line + m3_res

Heritability is additive variance divided by the phenotypic variance

$h^2 = V_A / V_P$

But I think it is correct in this case to use line variance rather than additive variance (if someone could explain in an answer that would be useful), so I've done,

# heritability (line/ (line+ residual))
m1_h2 = m1_line/ m1_phe
m2_h2 = m2_line/ m2_phe
m3_h2 = m3_line/ m3_phe
m1_h2; m2_h2; m3_h2

My question(s):

Is it appropriate to use the lmer function in R to extract variance components in this manner?

Have I calculated $V_A$, $V_E$, $V_P$, $h^2$ correctly? I think $V_A$ and $V_E$ are correct, $V_P$ could perhaps be the sum of $V_A$ and $V_E$ rather than $V_L$, and subsequently $h^2$ may be $V_A/V_P$.

From what I understood of your code and what you are asking I am guessing that you do the following:

Generating a virtual set of 40 individuals (lines) of which you have 200 measurements (repetitions). You say that they are full siblings, so they share both parents. Then you use the lmer function (which I am not familiar with) to give you the total variance, within-group variance and between-group variance, ($V_{T}, V_W, V_B$ respectively). What you call $V_L$ would be the $V_W$.

We know that $V_P=V_A+V_D+V_E$

In full siblings we also know that $V(A,A')=\frac{1}2V_A+\frac{1}4V_D$ where $A$ is the additive value and $D$ is the dominance value because they share a quarter of their gene combinations.

If you are treating with full siblings the $V_W$ should be then the $V_E$ and the $V_B$ would be the $\frac{1}2V_A+\frac{1}4V_D$ as you are seeing the variance between siblings.

So no, you are not calculating correctly the $V_A$ because you are missing your $V_D$ on your counting. The code itself looks fine for what I understood, but maybe you should take that to corssvalidated with the R tag


The onset of hair loss in men I've seen men starting to lose hair in almost all ages. Why is the onset of hair loss in men different? Is there a normal distribution?

Mostly it is because of the scalp and a decrease in the hair follicles ability to maintain production of sturdy hair (keratin along with melanin for hair color). In some cases, it is also genetic such as in Male Pattern Boldness.

Hair thickness changes with age. Hair is made of many protein strands and a single hair lasts between 2-7 years on your head. The hair then falls out and is replaced with a new one. How much hair you have on your body and head is also determined by your genes. With age, the rate of hair growth also slows down. Source

I would say however that the major impact-factor ought to be testosterone production especially in the case of MPB. More specifically DHT (Dihydrotestosterone) which is a derivative of testosterone. The amount of DHT is higher in balding scalp than non-balding ones.

In addition, it has been shown that the number of DHT receptors on the hair follicles also increases in balding scalps. Also, blocking the conversion of testosterone to DHT delays progression of hair loss and onset of MPB. That is why DHT is usually held responsible for miniaturization of hair follicles leading to hair loss, and this can happen at any age based on the DHT amount, but usually happens as we get older. Source

Testosterone is mainly found in man, but women certainly do produce it, even though it is present in minuscule amounts. Under normal conditions, women have a very small fraction of the level of testosterone that men have. However, even a low level of it can be converted to DHT and trigger hair loss in women. Source


Are drugs made bitter artificially to prevent being mistaken for candy? All drugs I remember tasting (with the notable exception of Aspirin) have bitter taste. Is the taste due to the active substance, or is a bittering agent added to them, perhaps to prevent overdose?
Take Paracetamol for instance: adult pills taste bitter, while the syrup for babies is sweet without any noticeable bitterness. Or is the dosage simply so low that I couldn't distinguish the drug taste behind all that sugar they put in?

Short answer
A bittering agent may be applied to therapeuticals to prevent pediatric poisonings, but many drugs inherently taste bitter by themselves.
Background
Bitter taste is thought to have evolved as a way to decrease the risk of ingesting toxic substances, which may explain why many drugs taste bitter. In other words, classes of compounds that may harm the body often taste bitter (Menella et al., 2014). These include the often dangerous compounds like alkaloids and glycosides (source: University of Delhi). These include the familiar psychotropic compounds found in hallucinogenic plants, and the potentially deadly heart glycosides found in Digitalis species, respectively, among other classes of substances.
Paracetamol can be regarded as an alkaloid (Fig. 1), but not aspirin, as it lacks a nitrogen atom (Fig. 2). An alkaloid is defined as

any of a class of naturally occurring organic nitrogen-containing bases. Alkaloids have diverse and important physiological effects on humans and other animals. Well-known alkaloids include morphine, strychnine, quinine, ephedrine, and nicotine...

All of which are quite toxic. As cleverly noted in the comments, aspirin is not an alkaloid in its strictest sense, as it is not naturally occurring. However, it is chemically obtained by acetylation of salicylic acid (Mund et al., 2016), as shown in Fig. 2. Both of the reactants in themselves are naturally occurring; salicylic acid can  be sourced from willow bark, and acetylation is a widely occurring biochemical reaction (Gibbs, 2017).
I myself have never had the chance to taste aspirin, unfortunately (although I performed the acetylation shown in Fig. 2 for my Organic Chemistry class :-). Originally, aspirin was developed from salicylic acid (Fig. 3) just because the taste of salicylic acid was so bitter. Acetylation diminished the bitterness, yet the anti-inflammatory action remained (Wu, 2000)). Besides reducing bitterness by chemical modification, masking the bitterness of drugs with, e.g.., sweeteners, can help to overcome the aversion to the bitter taste. This can aid in helping patients, especially pediatric ones, to take their medicine and adhere to their treatment regime (Chauhan, 2017).
Reversely, coming back to your question, adding bitter-tasting additives to drugs indeed seem to be an effective way to reduce pediatric poisonings (Menella et al., 2014)
References
- Chauhan, J stem cell Bio transplant (2014); 1(2): 12
- Gibbs, Trends Plant Sci (2015); 20(10): 599–601
- Menella et al., Clin Ther. 2013 Aug; 35(8): 1225–1246
- Mund et al., J Occup Med Toxicol (2016); 11: 32
- Wu, Circulation (2000); 102: 2022–3

Fig. 1. Paracetamol, or acetaminophen. source: Wikimedia Commons

Fig. 2. Synthesis of Aspirin, or acetylsalycilic acid, from salicylic acid. source: Imperial College, UK


What is the molecular basis of hangovers? Well, most of us have experienced the wonderful feeling of the dreaded hangover. How does it work exactly? I imagine it has something to do with dehydration but what are the underlying mechanisms?

Extra points for explaining why mixing drinks makes it worse and why (or if) a hair of the dog (another drink) the next day can help. Someone once told me that hangovers are the first symptoms of withdrawal and if you drink (anecdotal evidence suggests that it should be the same drink as the night before, but I doubt this is true) a small amount of alcohol, the symptoms are alleviated. I don't really see how that can be true.

First, the hormonal and hemodynamic changes seen in hangover are distinct from those seen in alcohol withdrawal, so the advice to drink more is not good, even if some symptoms are in fact improved. See tables 2/3 in the cited review.

It appears the molecular mechanism of veisalgia (HA, a new word) is not well known.

1. acetaldehyde Part of it may be attributed to acetaldehyde but there is clearly more to it. The liver enzyme alcohol dehydrogenase 1 (ADH1) produces acetaldehyde from ethanol, and aldehyde dehydrogenase 2 (ALDH2) makes acetate from that, so the aldehyde does not exist for a long time, and is rather responsible for short-term illnesses.

2. ADH and diuresis

  Hangover severity is proportional to antidiuretic hormone
  concentration (46). Alcohol inhibits the effect of antidiuretic
  hormone on the kidneys, thereby inducing  diuresis that is out of
  proportion to the volume of fluid ingested. As blood alcohol
  concentration decreases and dehydration persists, the serum level of
  antidiuretic hormone increases, maintaining water retention in
  dehydrated patients with hangover. In our clinical experience,
  hydration attenuates but does not completely relieve hangover
  symptoms.

3. cytokines

  The constellation of hangover symptoms (nausea, headache, diarrhea)
  resembles that seen in conditions related to dysregulated cytokine
  pathways (for example, in viral infections and after administration of
  interferon-alpha). Alcohol alters cytokine production through a
  thromboxane pathway. Levels of thromboxane B2 are elevated during
  experimentally induced alcohol hangover (42), and the administration
  of tolfenamic acid, a prostaglandin inhibitor, at the time of alcohol
  consumption has a small prophylactic effect in reducing hangover
  severity (9).

4. further substances

  Congeners, the byproducts of individual alcohol preparations (which
  are found primarily in brandy, wine, tequila, whiskey, and other dark
  liquors), increase the frequency and severity of hangover (24, 39,
  40). Clear liquors, such as rum, vodka, and gin, tend to cause
  hangover less frequently.

So there are factors that aren't even identified exactly, and these could fit the mixing of drinks observation.

There are several reviews out there, just search for hangover at Google Scholar.

Wiese, Jeffrey G., Michael G. Shlipak, and Warren S. Browner. "The alcohol hangover." Ann Intern Med 132.11 (2000): 897-902. Online at http://dionysus.psych.wisc.edu/lit/topics/Hangover/WieseJ2000a.pdf


How does a Na+/H+ antiporter drive osmosis in this "osmotic motor"? This recent paper in Cell describes a cancer cell using osmotic pressure to move in confined spaces. The cell preferentially inserts Na+/H+ antiporters in the leading membrane. I want someone to double-check my osmosis before I make students reason it out:

The normal Na+/K+ pumps cause an increase in Na+ ions outside the cell, but little change in osmotic pressure across the membrane.
Increased Na+/H+ antiporters will allow Na+ in while pushing H+ out at the "front" end of the traveling cell.
While this causes little net solute change, it increases water flow into the cell via aquaporins (?? this part I find mysterious)
Na+ continues to be pumped out of the cell by the Na+/K+ pump at the "back" end of the cell
Water follows the Na+ through aquaporins out the "back" of the cell, moving the cell forward

I don't feel convinced that moving ions around like this is causing osmotic gradients. Can anyone convince me?

Since posting, I did some more research using background refs from the intro (who knew?). The trick seems to be that when protons are pumped out, the cell regenerates them from water in order to maintain pH. So the solute concentration DOES increase inside the cell with more Na/H transport.


Performing PCR on samples whose DNA concentration is nul Is it vain to perform a PCR on samples whose DNA concentration was measured as nul by a NanoDrop?

Nope, you could get amplification from samples that are orders of magnitude below the nanodrop detection limit (~2 ng/uL). To compare: most manuals for polymerases recommend 1 ng of plasmid template, and will probably work with much less, especially if you use a few more cycles.

But if you expected to see something on the nanodrop, and you get nothing, something else might be completely wrong.


Could a human become infected with rabies in such a way that even prior vaccination wouldn't stop the infection? Given the highly persistent nature of rabies after entering the brain, I was wondering whether certain ways of exposure to this virus could be risky even for a previously vaccinated individual. I understand that no vaccine is 100% effective, but would the risk of infection be particularly increased in case of exposure at some particular site on the body? Which mechanisms of the rabies infection would play role in this situation?

Reframing your question as:

  Are rabies exposures at specific sites on the body riskier than other sites, even for a vaccinated individual?

Possibly for post exposure prophylaxis, but probably not for pre exposure vaccination.

Rabies transmitted by a bite or scratch (almost all cases) involves a period of slow replication in muscle tissue at the site of the bite or scratch (see Murray Medical Microbiology Ch. 60 for a general discussion). This is called the incubation phase, and it is highly variable. The incubation phase is followed by a prodrome phase (virus binds receptors of sensory neurons at the site of exposure, and travels to the CNS) and neurological phase (infection of the brain).

An effective immune response is believed to be the result of both an antibody response and cell mediated immunity during the prodrome phase. Post exposure vaccination is effective because the incubation period provides enough time for a naive immune system to mount a protective response (same reference). Regardless, rabies post exposure prophylaxis (PEP) includes both active and passive immunization, i.e., vaccine and human rabies immune globulin.

Both post and pre-exposure prophylaxis failures have been reported. As discussed here cases with pre-exposure vaccination failure involve immunocompromised individuals. Cases with post-exposure prophylaxis tend to involve failure to fully follow guidelines (some are summarized here), but there is a recent case where guidelines were followed. These cases tend to involve bites or scratches to the head and face, which tend to involve a more rapid progression from incubation through prodrome to the neurological phase.

So, since reports of post exposure prophylaxis failure tend to involve specific locations of exposure (head and face), it's reasonable to assume that an exposure there has a higher risk. There is no data supporting this risk for cases with pre-exposure vaccination.


A biological system to measure time First of all I am a physicist, so I apologise for my non-existent understanding of basic biology. However, I have what I think is an interesting question and this seems like a good place to ask it...

I’ve recently been thinking whether there is a way to measure time using biological processes. In other words some system, a characteristic of which can be correlated to elapsed time. One example I can come up with is counting the number of divisions of a cell. I guess this can be done, but will most likely be highly inaccurate…

So this is my question: Do you know of any papers even tangentially related to the idea of a biological system that can be used as a clock?

Any ideas will be greatly appreciated!

There are lots of biological clocks, or clocks made of biological components. The circadian clock is an important, though complicated, example. There are excellent engineered clocks that form some of the neatest examples of systems / synthetic biology. See for example Elowitz & Leibler's "repressilator" (link, link). The basic idea in all of these is to have gene regulatory circuits with feedback that lead to oscillation of the gene expression dynamics. Books on systems biology, or Philip Nelson's Physical Models of Living Systems (aimed at physicists), are good places to read more.


Species Identification: Bulbous root on plant, Southern California, USA In Southern California, I was pulling out some roots and grasses and weeds in our backyard, and I noticed something weird. It appeared like there was a grape-sized bulb of something connected to one of the roots below the top layer of dirt. I didn't puncture it or anything, but do you have any idea what this could be?

It reminded me of two things: an air sack on kelp and a potato.

Edit: I took some more photos, and I tried to break it apart. I was able to break it in half with one hand, easier than a potato but harder than a grape. It was a little juicy inside. I took more photos too.

Edit number two: We have dandelions. Does this seem like it could be a potato dandelion?

Edit #3: So we have a lot of Dandelions and I thought these roots appeared to be connected to dandelion plants, so at first I thought they were potato dandelions. However, we I pulled out a different plant nearby, and it had very similar looking tubers connected to the roots. It was a small plant, but here's the picture, and a picture of a larger plant that I think is the same species as this one, but mixed with a bush. Can anyone positively identify it?

Edit #4: Here's more pictures of the plant I'm seeking to identify, which appears to be a more developed individual on a neighbor's property, and it even has berries:

This is an Asparagus species, and the root bulbs are storage organs. Unfortunately, I can't identify the species. There are 219 accepted species currently in TPL. I presume this is an ornamental plant. As far as I can see, the species is not recorded as naturalized in California.


What kind of snake is this? Seen on Koh Lanta, Thailand We had this snake in our bungalow on Koh Lanta, Thailand. From the reaction of the employees at the resort I can tell that it is venomous, but that's all I know. I am curious, does anybody know what species it is?

Thanks and cheers, Philip!

If the resort is near a water body then it is highly likely that it is a keelback snake.
For determining whether it is poisonous or not it is extremely important to look at the scale pattern on its ventral side(belly). Unfortunately that is not visible here.


When running a gel, what could cause a standard to run "faster" than usual? We are running a gel on the products of a restriction digest to determine the size of an insert. We know the vector backbone size should be ~2.9kb; however, the standard appears to be running too quickly (or our samples too slowly), causing the backbone size to be about 4kb (which distorts our results for the insert size).

What could possibly cause this? Thank you.

If the salt content or pH is different than "normal," run time can be affected. After all, you're applying an electric current to the sample(s) and ion concentrations and pH are sensitive to that current. Of these two, salt/ion levels are more likely to have an effect as your samples/markers are likely to be adequately buffered.


What does the total membrane current vs time plot of an action potential look like? What does the total membrane current vs time plot of an action potential look like? I see that there are voltage vs time plots, but I can't seem to find the current plots.
Thanks

Check out panel b for total current, panel c for K+ and panel d Na+ currents separated...

This is from this website: imageWebsite


What's the name of this bug from Toronto, Canada? It's about 3 millimetres in length. Found on September 10, 2015.

It's a moth fly. They're cute fuzzy little things. Most people consider them pests.

  An annoying and troublesome pest that concerns numerous homeowners is the moth fly, also commonly known as the drain fly, filter fly, or sewage fly. Moth flies are frequently found indoors on windows, sinks and walls.

They're often found around sink drains because the eggs and larvae survive on the biofilm in your, well, drains.


What is the actual size of a nucleotide? I found in this website that the dimension of a nucleotide is 0.34 nm. Is there any experimental paper confirming this statement?

If you want experimental papers, we should be precise about what we're measuring. "The dimension of a nucleotide" is rather imprecise, as a nucleotide is a rather oblong, knobbly thing.

0.34 nm is a relevant measurement related to nucleotides, but it's specifically the distance between consecutive bases in a standard B-form DNA helix - that is, what's the spacing between the "rungs" on a DNA ladder.

This measurement can be confirmed by several experiments, primarily those involving X-ray or neutron crystallography or scattering. For example, both the Wilkins and Franklin papers that were published back-to-back with the famous Watson & Crick DNA structure paper referrence the strong 0.34 nm reflections from X-ray fiber diffraction which Watson & Crick reference as the spacing of the bases in their model of DNA structure. Other papers have confirmed the measurement. This 1983 Biomed Biochim Acta paper uses wide-angle X-ray scattering to find it. Additionally, there are a large number of structures in the Protein Databank which contain DNA structures - these have been determined by a number of different approaches (X-ray crystallography, neutron diffraction, NMR, electron microscopy, etc.) and all of which are consistent with the 0.34 nm average spacing of base pairs. (Modulo minor structure-to-structure variations.)


Why are Chloride Anions necessary for gastric acid functioning? Why do parietal cells of the gastric mucosa release Chloride anions along the H+-ions, which are pumped into the lumen by the proton-pump. Wouldn't the presence of protons alone be enough to denature proteins?

Mebrane divide basicly enviroment to two disimular sections. This sections differ in lots of chemical/ phycical properties. One of those is electrochemical potential which it can be in the very simple way describe as whole charge of disimular section divided by biomembrane.

So if cell  pariental cells pumped into stomach that section will have too much positive value of electrochemical potencial which can repulse pumping more hydrogen ions back to the pariental cell. This lead to freeze hydrogen pumping to  the stomach area. Than chloride aniont came to the scene basicly to reduse positive charge and enable to pump tremendous amount of hydrogen to the stomach.


Ratio of bleach to water required to disinfect COVID-19? I am confused about the needed ratio of bleach to water required to disinfect COVID-19 from surfaces.

The guide on CDC states that: https://www.cdc.gov/coronavirus/2019-ncov/community/home/cleaning-disinfection.html

  Diluted household bleach solutions can be used if appropriate for the surface. Follow manufacturer’s instructions for application and proper ventilation. Check to ensure the product is not past its expiration date. Never mix household bleach with ammonia or any other cleanser. Unexpired household bleach will be effective against coronaviruses when properly diluted.

  Prepare a bleach solution by mixing:

  5 tablespoons (1/3rd cup) bleach per gallon of water or

  4 teaspoons bleach per quart of water

This is a 2% ratio. My problem is that it is not clear what "bleach" means. Chemically I guess it's Sodium hypochlorite. What's not clear is that what is the strength of the solution I can buy in shops.

Wikipedia states that bleach in stores can be anything between 3-25%.

Does CDC recommend the final strength of Sodium hypochlorite : water to be 2% or "bleach in stores" : water to be 2% (which can be anything between 0.06% - 0.5%

Disregarding this confusing CDC direction: What is the scientific recommendation for the required sodium hypochlorite : water ratio needed for disinfecting COVID-19 from surfaces?

I have also been frustrated by use of percentages in protocols when making dilutions of stock bleach.  It's helpful to look at the product labels, as they often have dilution factors for different uses as well as concentrations in parts per million.

I have a bottle of Clorox brand concentrated bleach sitting next to me, and the label says this solution is 8.25% sodium hypochlorite.  The label also says that 8.25% sodium hypochlorite yields 7.85% available chlorine, and that 4 oz. of this product in 1 gallon of water yields 2,400 ppm chlorine, implying that the stock concentration is 76,800 ppm if 1 gallon (128 oz.) is the total volume or 79,200 ppm if the 1 gallon is added to 4 oz. (that is, 132 oz. total).  For simplicity, let's say that the stock solution is 78,500 ppm so that 1% available chlorine is exactly 10,000 ppm chlorine.

The CDC website cites a study that states 200 ppm chlorine is sufficient to inactivate 25 different viruses.  Sadly, I cannot find the text of that study.  Here's the citation:

Klein M, DeForest A. The inactivation of viruses by germicides. Chem. Specialists Manuf. Assoc. Proc. 1963;49:116-8.

So, using the low end of your given values, a 3% stock solution of bleach will have ~2.85% available chlorine, following the yield ratio above.  Diluting 5 tbsp. (2.5 oz.) of this stock in 1 gallon of water (total volume 130.5 oz.), as recommended, will yield ~0.05% available chlorine, or 500 ppm, which is sufficient for viral inactivation.

Edit - a bulletin from Clorox (PDF, cached HTML) states that 2400 ppm available chlorine is recommended for disinfecting hard, nonporous surfaces.  The bulletin also lists enveloped and non-enveloped viruses against which this product is effective (at the "99.9%" level), including Human Coronavirus (Strain 229E, ATCC VR-740)


Placebo Effect Reactions Why do some people actually experience measureable effects when given a placebo(fake drugs) versus the actual drug?  Is is the power of suggestion, belief, or something else?

Few examples in which placebo looks effective even if it isn't (Wikipedia):

The condition, for example, common cold heals on its own in participants who received a real drug and in those who receieved a placebo.
In psychological and other conditions in which the participants are asked only how they feel after the treatment, some of them may just think that they feel better.
Sometimes neither the real drug nor the placebo work, but the condition has a naturally fluctuating course, so it looks that they both work.


Could a prolonged amount of Antibiotics severely affect the digestion Gut Microbiota? Could taking antibiotics for a prolonged amount of time severely harm or even worse kill off a large proportion of Gut Microbiota responsible entirely for  digestion, Resulting in lifelong digestion problems similar to Crohn's Disease?

Yes, even if you will not kill ALL the bacteria in your gut, you can mess up your flora pretty badly by using antibiotics for prolonged time.

For how long? It depends from person to person, from antibiotic to antibiotic.

Similar to Crohn's disease? Some symptoms like abdominal pain, diarrhoea and weight loss can occur in case of messed-up flora like in Crohn's disease (and many other diseases!).


Material recommendation: molecular biology for mathematicians and computer scientists I am wondering if there are some introductory learning resources on molecular biology designed specifically for scientists with heavily math-oriented curricula (math/physics/computer science).

They should be capable of conveying the main ideas in a concise way; if they could represent some concepts in a mathematical language, that would be a big plus.

Additional details

As it was pointed out in the comment, molecular biology is a very broad field so I should be more specific - although it is difficult for me. Personally, I would like to acquire some basic knowledge to interpret NGS data and go in the direction of system biology.

I have also come from purely non-Bio background (I am a Software/Electrical engineer who didn't study Bio even in his high-school).
As others have pointed out in comments above that Molecular Biology is a vast field. But if you want resources covering all the basics of Genetics/Molecular Genetics, then I can easily recommend the following to anyone (which are both easy to understand and very authentic ones):

Nature Scitable
Genetics by PS Verma, Agarwal, S Chand.

There are other books like this one but they all are on bioinformatics/advanced and expect some knowledge of Molecular Biology. My recommendation (proved one) are above two. Best of luck!!


What's the percentage similarity between human individuals (and other primates) when comparing only exons? In popular science books and articles, I often see it stated that humans are >99 % similar to each other (wikipedia has it a 99.5 %, referencing Craig Venter and this PLOS Biology article) and ~96-99 % similar to chimpanzees or bonobos (Smithsonian Institute, National geographic). I have previously thought that this referred to the entire genome, but the wording on the Smithsonian Institute page I linked, makes it appear that it might refer to genes only, which also seems to be the case according to the answers to this post Do apes and humans share 99% of DNA or 99% of genes? What is the difference?.

How big are these percentages when comparing only the coding regions (exons) instead of entire genes, both within our species and compared to other species, such as primates? And, not as importantly, what are these numbers when including the entire genome with all non-coding DNA?

One of the references to the chimpanzee genome paper linked by Maximillian is Inferring Nonneutral Evolution from Human-Chimp-Mouse Orthologous Gene Trios, where the authors seems to have focused on exons only:

  Here we apply evolutionary tests to identify genes and pathways from a new collection of more than 200,000 chimpanzee exonic sequences that show patterns of divergence consistent with natural selection along the human and chimpanzee lineages.

They conclude that:

  Perhaps the best way to understand the relation between DNA sequence divergence and the differences between human and chimpanzee physiology and morphology is to compare these differences to the variability among humans. Human-chimp DNA sequence divergence is roughly 10 times the divergence between random pairs of humans.

Unfortunately, they didn't compare this to the fold-difference of non-exonic DNA, so the comparative quantification between coding vs non-coding regions remains to be determined.

However, this does directly answer the question of how big the genomic differences are between individuals of the same species vs those of other species, when comparing only coding regions. I also found it useful to quantify the differences in these relative terms in addition to the previously stated percentages.


Evolutionary reasons why you cannot tickle yourself but masturbate There are obviously good reasons that explain why you cannot tickle yourself (see e.g. here). This got me thinking why it is possible to masturbate...

Wouldn't it make more sense to not being able to do that so that you are more inclined to have real sex. Individuals who were not able to relieve themselves in this manner should have been more actively producing offspring. And the tickling example shows that self-produced sensations can be inhabited.

Does this make sense? I know that it is always hard to reconstruct evolutionary processes but are there reasons that explain this?

I think there is a bit of a logical leap here (or at least in the title).

The simple answer is that there are many biological phenomena for which there is no logically satisfactory explanation. For instance: why do people have wisdom teeth? We come up with some hand-wavy explanations about ancestral diets, but at the end of the day we just have wisdom teeth (or at least most of us do) and there isn't a great immediate causal pathway that tells us why this rather inconvenient thing exists in modern humans and hasn't been lost.

Getting back to the question at hand, there are a number of assumptions that seem to come along with this question:

Most importantly, why is it assumed that there must be an evolutionary "reason" for a biological phenomenon? In many/most cases there is no such reason. Most (molecular) evolution is neutral and random.
Why is it assumed that there is an equivalence between tickling and sexual stimulation? (then again, a cursory google search suggests there is a relationship...)

Both tickling and masturbation are phenomena that seem to occur in primates. However, this does not require that there be a link between them even if they appear to be similar superficially. Furthermore, it is not logically required that either of them satisfy any particular purpose, even if we can imagine a possible purpose (as some of the commenters have).

Of course, there are lots of reasons why these things exist if you're willing to drop the evolutionary mumbo-jumbo. For instance: both of these things can be fun and God loves us and wants us to be happy. This is the same as the platitude from Ben Franklin on why booze exists. Substitute your favorite demiurge.

These arguments are not much different from arguing that constant ejaculation leads to better sperm on evolutionary time scales. There is equally good (better?) evidence that having to produce more sperm leads to a higher prevalence of birth defects and other disorders. So maybe masturbation is bad from one reasonable point of view, and is in fact a deleterious vestigium like wisdom teeth. The "scientific" answer depends a bit on which literature you pay attention to.

Evolutionary answers of this type tend to be this kind of just-so stories. They give an air of precision and authority with uncertain logical backing, and they don't even have the folksy philosophy as a consolation.

This may not be an answer in the fashion the OP intended, but hopefully it does at least give a perspective on thinking about these kinds of questions.


Carcinogens, how do they work? The easiest carcinogenic thing for me to grasp is radiation, as it directly messes with DNA. Then it seems there are other compounds that simply mimic hormones, but these shouldn't necessarily cause cancer, right? Then there are things that can accelerate mitosis or mess with other processes, which can inadvertently mess with DNA. So my question is, in general, how many different flavors of carcinogens are there? I know there are a lot, but can someone list a good few? Maybe some examples? I'm most interested in how plastics and things like smoke cause cancer. I think a few examples would be best in aiding my understanding. Thank you!

Edit: I also just realized this is not the Chemistry Stack Exchange, I think I am more interested in the chemistry side of this question, but it might need to be migrated.

"So my question is, in general, how many different flavors of carcinogens are there?"
As mentioned in the comments, almost all carcinogens act by damaging DNA.  In general there are three ways to do this:

Alkylation, a good example is pyridine.  These compounds covalently modify the DNA and either cause a mutation by misincorporation during DNA replication (where the wrong base is incorporated across from the alkylated base), or by generation of double strand breaks during DNA replication that result in a mutations during the repair process (the details of which are not in-scope here).

Intercalation, my favourite example being ethidium bromide.  These compounds literally insert themselves between the bases of the double helix, where they cause "fork collapse" during DNA replication, and the ensuing repair process mutates the DNA.

Ionization through radicals.  Yes, carcinogens can generate radicals that will generate DNA damage.  A good example is doxorubicin, which is a highly effective chemotherapeutic, but also a carcinogen in its own right.  Some heavy metals can also generate radicals under the right circumstances.  These compounds typically oxidize the bases of DNA, and result in broad misincorporation during DNA replication.  Radicals can also result in breakage of the phosphodiester backbone, which cause mutations during repair. This mechanism is taken advantage of in some methods for studying the primary and secondary structure of RNA molecules, and in "foot printing" methods.  Incidentally, it is this mechanism of carcinogenesis that causes antioxidants to be associated with the prevention of cancer.  Compounds like vitamin C soak up the radicals generated by the carcinogen (or radiation), thereby preventing the damage from occurring.

An interesting point: pyrimidine dimers, which are generated whenever you get a sunburn, are a carcinogenic form of DNA damage somewhere between the ionization and alkylation mechanisms.  UV light induces a redox reaction that results in covalent linkage of two neighboring pyrimidines.  A dedicated repair process can cause a mutation at the site of the dimer.

However, the take home point is that the DNA damage itself is not usually the mechanism of mutation!  Mutation occurs when the damage is repaired, either as part of a dedicated repair process, or by (non)homologous recombination after a stall in DNA replication.

I hope this answers your question.  It is a complicated subject, and I doubt I covered everything here.


How is honey not toxic to our epithelial cells? Being a supersaturated solution of sugar, honey pulls the water out of cells it comes in contact with via osmosis - killing the cells. It also contains the inactive enzyme glucose oxidase, which when diluted with water activates and then converts glucose into gluconic acid and hydrogen peroxide - both of which are bad news for cells.

Honey also likely contains an antibiotic protein Bee Defensin-1, which is also bad news for bacteria. I didn't yet look into how it works so I don't know if it affects our epithelial cells.

Then some honey types (manuka) contain Methylglyoxal. Damage by methylglyoxal to low-density lipoprotein through glycation causes a fourfold increase of atherogenesis in diabetics. [1] Methylglyoxal binds directly to the nerve endings and by that increases the chronic extremity soreness in diabetic neuropathy.[2][3]

How is it safe to eat?

I'll change my initial comment into a real answer.

The human digestive tract has evolved to allow us to be broadly omnivorous, safely consuming a wide range of vegetable, animal, and mineral-based foods. While honey can be damaging to exposed cells, the epithelial cells lining the digestive tract are not exposed like the endothelial cells that line the circulatory system. Eating honey is not the same as injecting it into your veins.

A layer of mucous covers the cells of the digestive tract from mouth to colon and provides both lubrication as well as protection to the cells underneath it. It is protective to varying degrees against such challenges as acid, osmotic stress, mechanical damage, and foreign microorganisms. Additionally, the cells themselves are layered and are continually being sloughed off and regenerated, so even if the mucosal lining isn't 100% effective, damaged cells will be replaced fairly quickly.

Food quickly travels from the mouth through the esophagus to the stomach, not allowing enough time for osmotic stress or enzymes to damage anything to any significant degree. (Obviously, if you swallow something extremely harsh like bleach, lye, or concentrated acid, that's a different story.)

Once in the stomach, a food like honey is diluted by the digestive juices and any other food or drink already present -- it's not like the stomach is totally empty and globs of honey can just sit in direct contact with cells for an extended period of time, allowing for osmotic or enzymatic damage. Digestive enzymes and the acidic environment quickly attack proteins and other substrates, so even if the glucose oxidase can become activated, it will be cleaved by proteases into inactive fragments long before damaging levels of H2O2 can build up.

Low-density lipoprotein (LDL) is found in the bloodstream, not in the digestive tract, so any methylglyoxal present in food would need to be actively transported into the blood to do any damage. The work in the paper you cited was done completely in vitro, with no evidence that MG-mediated glycation as a result of eating honey actually occurs in people.

Many foods we commonly eat would appear to be dangerous to our bodies in one way or another, yet we have evolved strong mechanisms to minimize harm. However, it's pretty clear that some foods are damaging in various ways over time, so we still need to moderate what we eat. I don't know if honey (or certain kinds of it) is one of those foods, so more research is needed.


What exactly does adaptive mean? This is a quote from Dey et al 2014:

  Hatching asynchrony is thought to be adaptive because...

What exactly does adaptive mean here? Does it mean hatching asynchrony has fitness benefits? Or does it mean hatching asynchrony is likely to be selected for?

The question is probably more complicated than it seems because, if I am not wrong, the word adaptation here is understood at the group level.

Definitions of adaptation

Unfortunately, there is not such thing as a single, standard definition of adaptation. But for most cases the accurate definition the author is using is not of much importance as all of the usual definitions totally fit in the sentence without changing the meaning of the concept they want to express. In you case however, the concept of adaptation seems to be a bit more complicated (and interesting) because it refers to a group-level adaptation.

Note that most people does not really care about the exact definition they're using and this might yield to some confusion. It will probably be a bit hard to know exactly what the authors  (Dey et al.) of your article had in mind.

Definition of Group-level adaptation

I am here going to talk about how the term adaptation can be understood for a (social) group. This is important as I suspect the authors to use the term adaptation on a group phenotypic trait (emergent trait if you want).

Pareto optimality

To my experience, the concept of group-level adaptation is defined in relation to the concept of Pareto optimality which is a concept used in evolutionary game theory. Shortly speaking, in a system that is at Pareto optimality no individual can by any change of the trait under consideration increase its fitness without decreasing the fitness of another individual. In other words, a population that is at Pareto optimality has the greatest achievable population mean fitness. Therefore, it makes sense to consider a group to be (perfectly) adapted when it is at Pareto optimality.

Nash equilibrium

Depending on the underlying evolutionary game, the Pareto optimality may or may not be a Nash equilibrium. Shortly speaking, a population is at Nash equilibrium if no individual can increase its fitness by changing the trait under consideration. Therefore, group-level adaptation can only be stable if the Nash equilibrium is Pareto optimal. An example of game where the Nash equilibrium is the free-market game.

In your case

At first sight, because asynchrony is a group level trait, it seems to me that the sentence "Hatching asynchrony is thought to be adaptive [..]" means that hatching asynchrony is thought to be at Pareto optimality. In other words, it means that hatching asynchrony is thought to be the state of the system where the mean fitness of the group is maximized, that is no individual can increase its fitness without decreasing the fitness of another individual by being synchronous.


Glycolysis step 5: isomerization by triose phosphate isomerase On the 5th step in glycolysis, triose-phosphate isomerase converts dihydroxy-acetone-phosphate to glyceraldehyde-3-phosphate.
Now my question is: Why?

Most books and sites I've read only say that glyceraldehyde-3-phosphate has a direct pathway compared to dihydroxy-acetone-phosphate. Anyone with additional info on this would help much if they shared.

"Why" questions in biology tend not to make sense-
https://en.wikipedia.org/wiki/Teleology_in_biology

But perhaps if I narrate the reaction it will connect with your intuition.
Let's look at the reactions in question:

https://en.wikipedia.org/wiki/Glycolysis#Summary_of_reactions

Step 4 in glycolysis cleaves fructose 1,6-bisphosphate into two molecules that are isomers. One isomer (glyceraldehyde 3-phosphate, GADP) is a reactant in step 6, and fuels the “payout phase” where glycolysis reactions begin to yeild ATP and NADH. So what happens to dihydroxyacetone phosphate (DHAP), the other product from step 4? How can we extract energy from this?

Reaction 5 is the interconversion of GADP and DHAP. So as GADP is consumed by reaction 6, reaction 5 will, by Le Chatlier’s principle, lead to net conversion of DHAP to GADP. The GADP produced by this isomerization then also feeds reaction 6. In this way, both of the products of reaction 4, GADP and DHAP, are channeled down the chain to fuel NADH and ATP production.


Plant identification What plant species is this?

Its stalk looks like a grapevine, but the leaves & flowers not. It bloomed this week (Mid-June). I have found it in Turkey, Amasya.

If you want, I can add more shots of plant.

That is a kind of honeysuckle. The picture below is for Japanese honeysuckle (Lonicera japonica), but your specimen is different in the way the flowers are arranged and that the distal-most paired leaves are clasping the stem.

It might be Lionicera periclymenum, or Lonicera etrusca (there are about 150 species of honeysuckle); L. etrusca is pictured below (the color is irrelevant) which is native to Europe.


Is chlorophyll living or non living? Is chlorophyll living or non living, and after boiling the water out of a chlorophyll extract would it still live, as in would it still maintain its properties after re-adding liquid to the dried chlorophyll?

Thank you for any help.

Chlorophyll is organic, not living, which is a fancy way of saying that it contains carbon. As for your question about boiling, it depends on whether or not the heat from boiling will disrupt the chemical bonds and destroy the molecule. According to Wikipedia, chlorophyll a will melt at around 117°C (I'll assume that chlorophyll b is similar), which is higher than the boiling point of water, so if the temperature is strictly maintained, the chemical should stay intact.


Why do humans hear better between 2kHz and 5kHz? I've recently seen the following image:

Source: https://commons.wikimedia.org/wiki/File:Hoerflaeche.svg

Translation (from German):

The upper boundary (Schmerzgrenze) is where it starts to hurt
"Musikwahrnehmbarkeit" is where you can hear music
"Sprachwahrnehmbarkeit" is where you can recognize speech
"Hörschwelle" is absolute threshold of hearing (ATH)

While the ATH seems to be relatively smooth, there is a noticeable "gap" between 2kHz and 5kHz. Does anybody know why this is the case?

Some possible explanations I've heard are:

Evolution: Hearing a baby cry
Evolution: Hearing leafs rustling
Coincidence: There is no good reason for that.

The image is from wikipedia commons and has no references. It might be wrong. Do you know similar graphs? Do you eventually have this kind of information for other animals?

Acoustically, we hear better in the 2-5 kHz range because our auditory canal resonates in that range (specifically, around 3 kHz). Our ear looks something like this (U Miami):

The auditory canal is part of the outer ear, which amplifies sound so that it can be converted into electrochemical signals by the middle and inner ear. We hear better in the 2-5 kHz range because the resonant frequency of the auditory canal is in that range.

The mechanical question of "how does this work" is usually easier to answer than the "why did this evolve?" question. Since reproductive fitness is the driving force of evolution, hearing babies crying (between 1-5 kHz) is the best guess I can come up with.


Can a cell survive temporarily without oxygen? Can temporary denial of oxygen to a cell damage the cell? Will the cell continue to live in partially damaged condition if the supply of oxygen and nutrients are restored?

This is really interesting because the answer largely depends on the severity of the damage, the length of the damaging condition, the type of damage incurred, and the type of cell incurring the damage.

For a real life example, irreparable DNA damage as by irradiation or drugs tends to be lethal to a cell. The severity of the damage may affect how long a cell has to live, however. For example, PBMC we irradiated with X gy tend to stay alive for 10-15 days (they actually don't divide though, due to the damage). Why did we pick that number? Too low a dose the cells persist, and too high you obliterate them. For reference, my experiements require my PBMC to be alive for a few days but disappear from the culture over time, so X gy is just an optimized value. Gy (gray) is an SI value for dose of ionizing radiation.

What you call a temporary denial of oxygen is actually referred to as intermittent hypoxia, or in a prolonged case just hypoxia. Human cells regularly survive in hypoxia by altering their metabolic pathways when OxPhos can't be utilized anymore. These changes are assisted by oxygen-sensing molecules that change the transcriptional profile of the cell. HIF1a comes to mind, a hypoxia inducible factor, which is regularly induced by PI3K and MAPK (typical cellular signals). It's typically kept in check by other oxygen sensitive proteins like VHL, but in hypoxia the effects of HIF1a action are entirely beneficial. So when the cell returns to "normoxia" it can typically reprogram into OxPhos (caveats exist, tumors for example).

So to answer your question yes, the cells will survive (in nutrient deprivation, too, but with a different mechanism), but they have to make a lot of changes first.


Are there animals / mammals which only have one eye? Do all animals (of a certain size and not thinking about worms) have the possibility to perceive depth?

Do all mammals have at least two eyes? Are there mammals with more than two eyes?

All mammals have exactly two eyes, though the eyes are vestigial in some species, some of which are even blind.

Small fossorial (burrowing) mammals generally have very tiny externally visible eyes or eyes that are covered with skin (e.g. golden moles). Some river dolphins (e.g. "blind dolphins") also have very small, vestigial eyes.

Some reptiles (and amphibians?) have a "third eye" called a parietal eye. However, it isn't a true eye. (See How Humans Lost Our Chance at a Third Eye).

I'm not aware of any vertebrates that have just one eye. As far as I know, all vertebrates have two eyes. The anableps is a fish that is nicknamed "the four-eyed fish," or something like that, though it actually has just two eyes.

However, there are one-eyed invertebrates, including copepods. (One copepod genus bears the scientific name Cyclops.) Answering your first question, copepods reportedly lack depth perception. There may be other one-eyed invertebrates, but I'm not an expert on inverts (there are too many species to count let alone study!).


More informative phylogenetic trees In the presentation of phylogenetic trees, the geometric shape of the trees often seems somehow arbitrary and is more driven by aesthetics than by informative reasons.

But wouldn't it make sense to give the geometry (distances and angles) specific meanings? Or is this already done (when it's done right)?

Some basic principles:

The vertical axis represents time (on a linear, logarithmic, or "anti-logarithmic" scale).
The horizontal axis represents the amount of genetic change (measured in appropriate units).
The line of one species (= population with virtually identical DNA) goes vertically from bottom to top.
The line ends when the species becomes extinct.
A new species branches off of an existing species by a horizontal line perpendicular to the line of the latter.
The length of the new (horizontal) line reflects the amount of genetic change.
At its end the line continues vertically.
There are no other branchings along the horizontal line.

By these principles and with perfect knowledge (and a good measure of genetic change) we would have a perfect rectangular tree like this:

But our knowledge isn't perfect: we know little to nothing about lots of intermediate species which didn't leave traces. Hypotheses about these unknown species can be reflected by inclined lines whose slopes can tell for example:

a) Their have been many pronounced genetic changes in a short period of time after the new species branched off. (grey: hypothesized intermediate species)

b) Their have been few small genetic changes in a long period of time after branching off.

  I'm looking for discussions/considerations of this kind of drawing
  phylogenetic trees (papers, web pages, or simply good search terms).

An interesting - and new to me - point of view is given in Joseph Ahrens' answer to this Quora question:

How do you interpret ancestry in phylogenetic trees?

What slowly becomes clear to me: It's about the interpretation of straight line segments, maximal straight lines, of horizontal vs. vertical lines, and nodes (= branching points) in phylogenetic trees, especially: which of them is to interpreted as a species?

Here's the issues with your well considered project:

1/ Temporal datasets to proportion trees: That's probably the most absent thing in species measurement. You'd need data sets of time for beetle species, for mammals, plants in millenia and million years. 90+% of that information is absent.

2/ Genetic proximity to arrange trees. Scientists publish their genome studies into the ToL project. There is lots of distance data to compare all animals.... Genetic distance doesn't graph easily because on the same tree, some distances can be 500 times longer than others. On a tree of 20 extant species, you will have branches 5mm long and 5 meters long, half the the species are on your screen and the other half are higher than the ceiling. It's best to represent them with another symbol, else interactive 3D trees where you can switch compact/large views and the tree zooms out crazily, it's illustrative and cool, else use a weighted proximity length which is 1+ similarity/50, that doesn't really work either. either way, I couldnt find a way of clearly displaying that info on the tree.

Phylogeny trees don't lend themselves well to being informatively measured. You start by thinking "Oh I could find a pretty way of doing that" then when you apply the datasets, your trees become uncontrollable and jumbled up because of exponential branch lengths.

I programmed phylogenetic trees based on the 81MB ToL tree of life project to represent many millions of species, to do 3D physics trees and HTTP lookups to provide wiki texts and images for all species. There is www.biostars.org a very kind and helpful bioinformatics forum for postgrads that do trees all day.

There are many (dozens) of informative tree graphics programs coded by academics, to visualizw and analyzw species data, arranged into different trees and sorting through them.


Semi permeable membrane "The knowledge about semi-permeable membranes is applied for various purposes. We know that semi-permeable membrane is capable of separating substances when a driving force is applied across it. Artificially synthesized semi-permeable membranes are used for separation of bacteria from viruses, because bacteria cannot cross a semi-permeable membrane."
My Question is Why Bacteria cannot cross a semi-permeable membrane? Reason?

In my opinion, it should work by size exclusion. Bacteria are on the size of few microns, whereas the pores in semi-permeable membranes are on the size of nanometers. Therefore, bacteria will not pass through the membrane.

Viruses are usually smaller than bacteria, and so maybe more likely to pass through such a membrane. However, you have not included the pore size of the semipermeable membrane in question, and so I am unable to give a more specific answer at this point. If the pores of the membrane are very small, even viruses will not be able to pass through it.


Would constant light or fading light be registered as more wakefulness promoting by the Supra Chiasmatic Nucleus? During the fall and winter season, a number of people are experiencing Seasonal Affective Disorder. One of the way it has traditionally been treated is with a dedicated lightbox - a very high intensity light (5k-15k lux) that is positioned somewhere the user can see it.

One of the possible ways such light affect the brain is through being picked up by Melanopsin receptors in the eye and this info being transmitted to the Suprachiasmatic Nucleus (SCN). The SCN makes sleep/wake decisions by suppressing melatonin release.

It has been tested that melanopsin receptors in the human eye respond most strongly to the light at around 470nm wavelength.

My question is about the mechanism by which this light influences the brain - which would have a stronger influence on the brain:

A constant, high intensity source of light that is ignored by the conscious mind (fades into background)?

OR An alternating, moving or fading, less intense source of light that the eye is drawn to, such as dancing light, a moving lamp or some other form of light that the conscious mind might be drawn to watch?

To clarify my question, I know that brain has a number of self-attenuating circuits (for example dopaminergic system), where extended release of some hormone numbs the sensitivity to the hormone. I'm interested - are SCN, melanopsin receptors or melatonin suppressing process are also self attenuating, where prolonged exposure to constant light would attenuate these processes?

There is no light adaptation (such as Arrestin-mediated light adaptation http://www.sciencedirect.com/science/article/pii/S0896627303003908) or other negative feedback loop that attenuates melanopsin that I have ever heard of. Rodents in constant light lose behavioural circadian rhythmicity (http://www.ncbi.nlm.nih.gov/pubmed/23714074), which could technically be due to some sort of long-term depression of melanopsin-mediated signaling, but I have always hypothesized that the rhythm disruption comes from aberrant Period gene expression in the SCN due to constant light signals stimulating its transcription via retinohypothalamic tract->SCN->cAMP->PKA activation->CREB phosphorylation->PER transcription. This paper shows the rescue of rhythms in  in VIP knockout animals using constant light (http://www.nature.com/articles/srep14044), suggesting melanopsin signaling remains intact. They also claim that light may be providing tonic input to the SCN, so they are thinking melanopsin is still intact.

In terms of light influencing the brain? That sounds very vague, as light influences the brain in many ways. How would you want to delineate light input via the visual pathway from circadian light input via the RHT? Light can produce an image on your eye, and the higher thought representation of that image could evoke an emotion or an arousal state. This would be wholly different than a circadian effect.


What is an explanation of the dual role of calcium hydroxide in teeth? Calcium hydroxide induces dentine formation in permanent teeth, while it causes resorption of tooth in deciduous teeth. How is this dual role explained?

For more than 70 years calcium hydroxide has played a major role in endodontic therapy, although many of its functions are now being taken over by the recently introduced material MTA. Calcium hydroxide may be used to preserve the vital pulp if infection and bleeding are controlled; to repair root fractures, perforations, open apices and root resorptions [1].
Calcium ions released from calcium hydroxide stimulates fibronectin synthesis in dental pulp cells. Fibronectin might induce the differentiation of dental pulp cells to mineralized tissue forming cells that are the main cells to form dentine bridges, via contact with cells [2].
Calcium hydroxide ($Ca(OH)_2$) is known to cause internal resorption in the deciduous dentition. Though this has been attributed to chronic inflammation and odontoclasts, the exact mechanism has not been elucidated. $Ca(OH)_2$-induced odontoclastogenesis could be multifactorial. Odontoclasts may result from fusion of cells of monocyte/macrophage series either due to inflammatory mediators or through stimulation by stromal odontoblasts / fibroblasts. Pre-existing progenitor cells of primary tooth pulp because of their inherent propensity may transform into odontoclasts [3].

References:

Carrotte P. Endodontics: Part 9. Calcium hydroxide, root resorption, endo-perio lesions. Br Dent J. 2004 Dec 25;197(12):735-43. doi: 10.1038/sj.bdj.4811897. PubMed PMID: 15608732.

Mizuno M, Banzai Y. Calcium ion release from calcium hydroxide stimulated fibronectin gene expression in dental pulp cells and the differentiation of dental pulp cells to mineralized tissue forming cells by fibronectin. Int Endod J. 2008 Nov;41(11):933-8. doi: 10.1111/j.1365-2591.2008.01420.x. PubMed PMID: 19133082.

Ravi G R, Subramanyam R V. Calcium hydroxide-induced resorption of deciduous teeth: A possible explanation. Dent Hypotheses [serial online] 2012 [cited 2014 Jun 7];3:90-4.