Which plant's part is this? I found this plant in Rajasthan, India.
This sample is 4-5 cm long.
This is an ornamental plant. It was a potted plant.
I put my fingertip in the photo to give an idea of size of the specimen.
I can't figure out which plant this part belongs to.
Please give the species name if you can.
I would be very thankful to anyone out there who will help me.

This is a bit hard to say exactly, since there is a number of possibilities. We can be pretty sure that these sample is from a Cypress, belonging to the family of Cupressaceae, but which subfamily or species this is exactly, can't be identified here. Therefore a wider image would be necessary, but since this is a potted plant, even this might not be enough, as a lot of these plants are used in gardening.


Thickness / size / volume of a macrophage What is the thickness of a macrophage? From some available literature it looks like a macrophage has a 'circular' shape of radius ~10 microns. But I need the thickness to calculate its volume.

BioNumbers is a good database for different values (numbers) in biological systems. From BioNumbers*:

Volume of an alveolar macrophage ( Homo sapiens ) = 4990 (±174) µm3

Diameter of an alveolar macrophage ( Homo sapiens ) = 21.2 (±0.3)  µm

So, your thickness should be (assuming a circular shape of the cell):

Volume/(pi×(0.5×diameter)2) = 14.15 (±1.52) µm

Apparently, the size of the alveolar macrophages varies a lot between different species.

  The AM from humans were significantly larger (p < 0.05) than those
  from all other species studied, corresponding to a 4-fold larger cell
  volume of human AM (4990 +/- 174 microns 3) compared to hamster (1328
  +/- 123 microns 3) and rat (1166 +/- 42 microns 3) AM

*
The paper that BioNumber refers to is this:
Krombach, Fritz, et al. "Cell size of alveolar macrophages: an interspecies comparison." Environmental health perspectives 105.Suppl 5 (1997): 1261.


Dilute DNA plasmids with distilled water I just extracted the DNA plasmid from E.Coli and dilute them in EB buffer. However, I've just figured out that the next step, which is electroporation, required that the DNA plasmid be diluted in Distilled H2O. Can anybody help me to know how to transfer the DNA plasmid from EB buffer to Distilled H2O?
To be clear, the EB buffer I used is from Qiagen. It contains 10mM Tris-Cl, pH 8.5.
https://www.qiagen.com/sg/resources/faq?id=d8ef773f-6a37-4993-908b-8bbc7bc5c8d6&lang=en

Buffer EB is simply 10mM Tris buffer, ph 8.5. I think you are worried about the ions present in your electroporation. There are two things to consider:

What is the concentration of your DNA and how much do you need for the electroporation?
In which final volume is the electroporation taking place?

In my experience, usually you add a very small amount of DNA (a few microliters) to 100, 250 or 400µl (depending on the cuvettes used) final volume. Here a tiny amount of Tris does not interfere or cause a short circuit.


I am interested in Sociobiology. Which academic field should I study? I like to study Sociobiology and evolutionary psychology. Which academic fields concentrate on these sciences in bachelor and master degrees?

What fields are sociobiology and evolutionary psychology?

Sociobiology (aka. social evolution) is a subfield of evolutionary biology.

Evolutionary psychology is a subfield of both evolutionary biology and psychology. Evolutionary psychology is, for the moment, very theoretical without much (if any) empirical testing. For this reason, not only natural scientists
 and social scientists work on the subject but some philosophers have also contributed (such as Daniel Dennett for example).

How to become a researcher in one of these fields?

Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give reliable career advice anyway. Also, I am not trained in any way to give you carrer advice.

That being said, a priori, start with a Bachelor in Biology and follow up with a master in Evolutionary Biology. Because evolutionary psychology is very inter disciplinary, I would personally advice to go with whatever broad field of study attracts you most. If you are more into psychology than biology, please go with psychology. If you are more into philosophy than biology, then go into philosophy.

Short intro to evolutionary biology

For a very short intro course to evolutionary biology, you can have a look at evo101 by UC Berkeley.


Anabolic reactions and reaction energy My textbook says,

  In general, the formation of a [chemical] bond releases energy

and continues to state,

  Anabolic reactions (collectively called anabolism) link simple molecules to form more complex molecules. Anabolic reactions require an input of energy because strong bonds within the smaller molecules must be broken to form the more complex molecules.

Do these two statements contradict each other? The first statement says that when two chemicals combine to form a bond, energy is released; the second statement says that when simple molecules are linked, presumably through a bond, an input of energy is required.

Any help is appreciated.

Both statements are correct, but an understanding of why they are not contradictory requires a bit of explanation.

For "spontaneous" reactions, those which occur naturally, entropy must always increase.  As a general rule, one of the easiest ways to increase entropy is to release energy, so we generally find that spontaneous reactions release energy.*  It's a pretty decent rule of thumb to use.

In the case of an anabolic reaction, we're putting together complex molecules from simple ones, and for these particular reactions we see they don't release energy.  They in fact "consume" energy in their formation.  This is reasonable, so what we find is that such reactions are not "spontaneous."  We don't see them just occurring on their own.

To make an anabolic reaction occur, we need to change the environment such that the reaction becomes spontaneous. We need to change the environment such that the reaction releases energy.  To do that, we start off with inputs which have even more energy than the final product should (such as extra kinetic energy from heat, or a strong oxidizer to reduce one of the reagents, or any one of a number of chemical and mechanical approaches).  Now the formation of the complex molecule can release energy, so it can occur spontaneously.  When we do this, we release some energy, but not all of it.  The rest of the energy is consumed in building the bonds of this molecule that would not otherwise have spontaneously come into being.  The released energy is typically seen as waste, and the energy pent up in the molecule is your desired product.

So in the end, the reason why there's no conflict is the "In general..." bit in the first quote.  You can cause a reaction to occur that consumes energy, but you typically have to do some clever things to put the energy into it.  Reactions which release energy occur spontaneously.  In general, we find "spontaneous" reactions occur far more often, hence the rule of thumb.

* I'm pretty loose with energy and entropy here to try to paint a simple picture without all of the confusion that entropy always brings to a discussion.  As you learn more, do expect to need to be more precise than I am here.


Why is there no herd immunity against common cold coronaviruses? In discussions of herd immunity against SARS-CoV-2 the underlying assumption usually appears to be that the virus basically stops spreading once a sufficient percentage of the population has overcome an infection.
My understanding is that this approach does not work for the seasonal flu, for instance, because the flu virus mutates too quickly. Since coronaviruses do not mutate so quickly, herd immunity "can work" for them.
Question: Given how long common cold coronaviruses have been spreading in the human population, why does there not appear to be herd immunity against the common cold coronaviruses? To what extend can we expect herd immunity to SARS-CoV-2 if there is no herd immunity against common cold coronaviruses?

The following review has extensive answers to the complex of this question. They also include MERS and SARS-Cov-1 in their discussion, as there is good data on them.
Huang et al., A systematic review of antibody mediated immunity to coronaviruses: antibody kinetics, correlates of protection, and association of antibody responses with severity of disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217088/
The best data comes from challenge experiments which, with common-cold CoV, are not ethically problematic. They write:

Several studies exposed volunteers to two challenges of virus, some months apart. Reed re-challenged 6 volunteers who had been experimentally infected 8–12 months previously(ref.9). On the first challenge, all 6 developed symptoms and detectable viruses and 5 of 6 experienced significant rise in titer. In the second, 0/6 experienced illness, detectable virus or significant rise in titer. Callow et al re-challenged volunteers with the same dose of coronavirus, one year apart(ref.8). Of 9 volunteers who were infected in the first exposure, 6 (67%) were infected in the second exposure. However, none of these individuals developed respiratory illness symptoms and they experienced a mean duration of detectable virus of 2 days compared to a mean of 5.6 in the initial challenge.

So, reinfection can occur even after 1 year with HCoV 229E, and this does not support the idea of herd immunity against that virus.
Note however that it is not known to date if, when reinfected after some years, you will also shed active 229E virus. If not, this would be just as good as neutralizing immunity and would support herd immunity.


Why are the fertility rates of large predators kept low? Predators at the top of a food chain, like lions, seem to have a relatively low fertility rate, which fits well to the ecosystem and avoids overpredation. But what is the mechanism that keeps the fertility rate at this level? A mutation that increases fertility among the predators should quickly spread in such a population, eventually leading to an increase of the predator fertility rate followed by overpredation. But it seems that this is usually not the case. What does keep the fertility rate of predators at the level they are?

P.S: Many explanations on population dynamics cite Lotka Volterra, including the existing question on Bio.SE "What prevents predator overpopulation?". Population dynamics predict orbits for the population sizes of predator and prey. Still this does not explain why the fertility rate of predators shouldn't go up.

This question can be tackled in several ways, and also seems to contain a couple of misconceptions about ecological processes (e.g. problematic group-selection ideas and how species 'fit' into the ecosystem).
However, I think it is most usefully answered from the perspective of life history theory and the evolution of life histories (see e.g. Roff, 2002 and Fabian & Flatt, 2012 for background), and at its core this question is dealing with tradeoffs between e.g. fecundity and mortality.

All organisms act under a limited energy budget, and when they spend energy on some activities that will limit what they can spend on other activities.
This lies at the core of life history tradeoffs.
If organisms use resources to produce or raise offspring, this can therefore have consequences on growth, maintenance (e.g. disease resistance), predator avoidance and many other traits and behaviours, which all affect fitness.

With regard to your question, there is a well-known tradeoff between survival and fecundity (an intraindividual effect), which has been shown both between individuals within species and across species.
As with almost all species traits, there is also variability between individuals within populations, so that some have higher fecundity than others, but may then also suffer lower adult survival rates (maybe under certain environmental conditions).
Therefore, there are certainly already "mutation(s) that increases fertility among the predators" within populations.
The reason that fertility is not continuously increasing over time, is that this would have negative fitness consequences overall.
So the reason that the (average) life history traits within a particular species are what they are, is that they are the result of the evolutionary pressures that the species have been experiencing over evolutionary timeframes, acting on the entire life history.

To be sure, hypothetical mutations/changes in life history traits that would increase fecundity with no negative tradeoffs whatsoever for either parents or offspring (i.e. no negative fitness consequences) would definitely increase in frequency.
From the perspective of life history theory, everything else equal, selection will maximize the survival function, $l(x)$ (survival to age x) and the reproductive function, $m(x)$ (number of offspring at age x), while minimizing maturation age.
However, tradeoffs between these functions (directly or indirectly) and between generations will prevent these from being optimized one by one.

Population growth in long-lived predator species is usually also very sensitive to changes in adult survival rate (Caswell, 2001).
This result comes from analysing stage or age structured population models, and is the result of a life history strategy with high adult survival rates, fairly high age of maturation and relatively low fecundity.
To increase fecundity in this situation with negative effects on adult survival will risk adult death and therefore loss of many future years of reproduction.
These kinds of results and models are often used to identify which life history traits and stages to target in conservation actions, but can also be used to understand evolutionary processes, since population growth rate can be used as an overall measure of fitness.

It should also be added that many other ecological processes must be considered.
For instance, large predators often care for their young for quite a long time, since their hunting/foraging behaviours are complex, and it takes a long time for young to learn how to hunt successfully by themselves.
This means that adults need to bear not only the direct cost of producing offspring, but also to support them until they are self-sufficient.
For an extreme case, look at the Orangutan (not a predator, but still) where the young stay with their mother and nurse for up to 5-6 years (sometimes more).
To increase fecundity in such a situation will put a large strain on adult mothers.
You also need to consider trade-offs between offspring number and offspring "quality", which have been demonstrated in many species (an intergenerational effect).
This means that an increase in fertility can result in lower offspring survival over longer timeframes, with overall negative effects on fitness.

Finally, life history evolution is a large and complex field, and these are just a couple of examples and suggestions for why the situation isn't as simple as your question makes it out to be.
Environmental variability and the predictability of the environment are other factors that I haven't considered at all, but are both important processes when you try to understand life history evolution.
This question can also be approached from a more theoretical perspective, but without a background in life-history evolution I think it is more useful to start reading about different processes and tradeoffs, and then later if you are interested to go into the theory for a deeper understanding.


Are Measles patients infectious until death? I'm examining a dataset of a measles outbreak, and for each patient I have the date of first appearance of symptoms $t_1$, date of appearance of rash $t_2$, and if applicable, date of death $t_d$. According to the literature, patients are infectious for one day before appearance of symptoms, and up to about 4 days from appearance of rash, so the interval of infectiousness is approximately $\left[t_1 -1, t_2 + 4\right]$. After this, most of the time their symptoms gradually abate and they get better.

However, if a patient dies, presumably they remained sick until they died. If $t_d$ is like, 10 or 15 days after $t_2$, are they infectious during all of this period? Or is it reasonable to conclude that they're infectious for the same length of time as everyone else, and the symptoms that kill them are non-infectious complications?

The characteristic rash of measles is itself an immune response, and is a good marker for progression of the immune response. Patients with immunodeficiency can  have a much more limited or even absent rash. In most patients, if it's been 4 days since the appearance of the rash, and they have improvement in fever, runny nose, and conjunctivitis, without a productive cough, they probably aren't infectious. If you have that data (fever and mucous membrane inflammation), I'd pay attention to that as well as the time since the appearance of the rash. A sick patient with measles should be kept in respiratory isolation regardless, but if you're looking at modeling disease transmission, you can follow the symptom progression.

As far as death is concerned, there are several pathways. Measles can cause a poorly understood immunosuppression and immune dysregulation, which certainly contributes. The most common cause of death is pneumonia (often secondary pneumonia), but early diarrhea can be a major cause in malnourished children. Otherwise immunosuppressed individuals (e.g., HIV, and primary immunodeficiencies) can develop a fatal measles encephalitis (a brain infection). Some deaths result from a fatal post-infectious autoimmune syndrome.

Some of these individuals are probably still shedding virus (diarrhea, primary measles pnuemonitis or encephalitis), many of them aren't (secondary pneumonia and autoimmune cases).

Many texts focus on vaccination and the current epidemiology of measles in developed countries, but Cecil Medicine has a very good chapter (375) on the clinical manifestations of measles. There is an interesting article in Lancet Infectious Diseases about the US army outbreak in 1917-18 that is a good example of the interaction of measles with other respiratory pathogens.


Lysosomal Storage Disease In my biochemistry class today we did a problem detailing two lysosomal storage diseases.

In the first scenario, a cell line for I-cell disease can synthesize lysosomal hydrolases that are perfectly functional which are then secreted outside of the cell instead of being sort to the lysosome. However there is a mutation that inhibits the the kinase domain that normally phosphorylates Mannose-6-Phosphate (M6P), so there is no M6P-labeling in these cells.

In the second scenario, a cell line for Hurler's disease has a mutation that eliminates one lysosomal glycosidase so that it cannot degradte certain classes of oligosaccharides. This results in the cells of this mutant cell line to have engorged / bloated lysosomes.

Now when these two cell lines are co-cultured in the same flask, it is observed the I-cell culture correctys the defect in the Hurler cell culture, while the Hurler cell culture was not able to correct the defect in the I-cell culture.

My question is how can this phenomenon be explain? And why are the Hurler cells still growing?

I-cells produce the normal functional lysosomal hydrolases, however they are secreted outside of the lysosome.

The Hurler cells lack a functional lysosomal hydrolase to degrade the certain oligosaccharides.

When the two cell lines are mixed together in the same media, through non-specific endocytosis, the Hurler cells will simply arbitrarily want to endocytose things such as nutrients from the media into the cell, and some of the times, the Hurler cells may endocytose the functional enzymes secreted outside of the extracellular matrix / membrane from the I-cell.

Thus, the Hurler cell's lysosomal contents can then be degraded to some extend and restore the defect exhibited in normal Hurler Cells.


Function of an VEGF inhibitor in the treatment of macular degeneration I'm working on a short presentation of treatments of macular degeneration for a biomedical
optics seminar on macular degeneration.

Since I don't have any relevant medical or biological background (B.Eng. Electrical Engineering, now M.Sc. Biomedical Engineering w. a major in Biophysics) I need some help with
understanding the function of VEGF inhibitors, and how they work.

It doesn't need to go into all details as it is one of three treatments that I'm supposed to present, but enough to explain how it works, in about roughly 5 minutes.

Could anyone help me please?

The Wikipedia page for vascular endothelial growth factor (VEGF) looks pretty useful - it explains that VEGF stimulates the growth of blood vessels. If this gets out of balance, for example in diabetic retinopathy and wet form age-related macular degeneration, one treatment is to attempt to reduce levels of VEGF in the circulation, using monoclonal antibodies directed against VEGF, or to antagonise the action of VEGF using drugs that target the VEGF receptors.
Two milestones in anti-VEGF therapy are described in these papers:

Ng et al. (2006) Pegaptanib, a targeted anti-VEGF aptamer for ocular vascular disease. Nature Reviews Drug Discovery 5: 123-132 (This paper describes the first approved aptamer drug: an RNA directed against VEGF.)
Ferrara et al. (2006) Development of ranibizumab, an anti-vascular endothelial growth factor antigen binding fragment, as therapy for neovascular age-related macular degeneration. Retina 26:859-870 (This paper describes a therapy based upon an antibody fragment directed at all isoforms of VEGF-A.)

A very recent review of anti-VEGF therapies is:

Freund et al. (2013) An update on the pharmacotherapy of neovascular age-related macular degeneration. Expert Opinion on Pharmacotherapy 14:1017-1028


What is the so called "hepatic glucose production" I came across this term in my readings but I do not understand how this works. Can someone direct me to some reference as to what this "hepatic" glucose production is all about?

"Hepatic glucose production" is the gluconeogenesis process (the opposite of the gycolysis process), that is the formation of glucose primarily from lactate and amino acids. This process takes place in the liver's cells and it is regulated by hormones (insulin and glucagon).
Look here and here for a better explanation!


After getting fully vaccinated for HBV why does the antiHBs titer last for so long? When a newborn child is fully vaccinated with HBV and let's assume he's responsive, his antiHBs titers will be high. But since the antigenic stimulus is withdrawn, shouldn't the titre fall to nill in some time? Rather, the titers stay significant for around 40 more years. (>10 IU/L is significant)

So, how are there circulating antibodies for so long if there is no more antigenic stimulus?

I understand that memory cells have large half lives but what is producing the antibodies is the plasma cells which have very short half lives.

So how do the antibodies persist for so long?

There is such a thing as memory plasma cells, discovered only relatively recently. Here is a review from 2010 discussing them, here is another review from 2012, and here is a pre-publication manuscript of an upcoming review in Leukemia (I apologize if any are behind paywalls, let me know if you can't access any of them).


How does the brain alter/inhibit muscle reflexes? I can find lots of information on how stretch-reflexes/reciprocal-inhibition/autogenic-inhibition work but from them all it's unclear how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

Can it alter the weighting of inhibition in antagonistic muscles?  As well as 'set the length' for a stretch reflex to target?  Or does it somehow control both 'with one value'.  Where and how exactly does it interject into the feedback loops?

I am trying to understand it more from a programmers pseudocode or equation point of view rather then get lost in meandering biological terms I have seen everywhere that gloss over this point.

how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

A: At multiple places within a hierarchical system:

In a  simplified way, the Motor cortex is the executor of movement via projections to the brain stem and spinal cord, this is accomplished via excitatory signals to a muscle, the agonist, and inhibitory signals to the antagonist, so in one sense, spinal interneurons would be the answer, since they interface with the motor cortex and alpha motor neurons at the muscle site.

There are also feedback loops all over the motor hierarchy, premotor and supplementary motor cortex regions for instance help plan the movement direction, we don't seem to code a target in the strict sense, but rather a movement direction and then correct via sensory feedback.

The cerebellum projects to premotor, motor cortex and the brainstem, and receives projections from premotor areas, it is involved in stopping and timing movement,the brakes for action if you will.

The circuitry of the Basal Ganglia  which loops with premotor and projects to the motor provides the go, no go and graded modulation via inhibition to the motor cortex, which in turn affect less spinal interneurons, so in another sense this circuitry would be responsible.

  Can it alter the weighting of inhibition in antagonistic muscles?

Yes, via spinal interneurons (Henshaw cells, Ia inhibitory interneurons and Ib inhibitory interneurons)

  As well as 'set the length' for a stretch reflex to target?

Yes, via a the motor,basal ganglia,cerebellum motor hierarchy, although as mentioned, there is no target but rather a direction vector and feedback that tells you when to stop the movement, i.e. you reached your target. ( Higher cognitive areas do seem to have a representation of the target though).

  Or does it somehow control both 'with one value'.

Depends on the interneuron, but basically they serve as information relays ( they also convey sensory information )

  Where and how exactly does it interject into the feedback loops?

As mentioned there are multiple feedback loops, the brain is not a unit, but a system and as such I would rephrase the question as which subsystems, brain regions, neuronal tracts and neurons create feedback loops in the motor system.

  I am trying to understand it more from a programmers pseudocode

I am a software developer myself, so let me try switching hats, this is one scheme:

If all you want is to control agonist/antagonists, tie up 2 or more variables together such that when one goes up, the other goes down, and presumably change 2 effectors ( virtual or real ) and their position relative to each other,

If you want specific control, you would then need to send 2 channels of information and modulate both variables, if you just send one to either one, the other will respond based on the above configuration.


Species identification: what kind of fungus is this? Found in a cave
Location: Israel

The white tentacles appear to be sticky. When they touch something, they stick to it and detach from the main body

I think these are parasitized insects.

Fungi of various types can infect insects.  The end stage produces these fruiting bodies.  Here is an example I found on the excellent site WhatsThatBug.

Here is another example.

http://www.anura.it/the-parasites-parasite-everyone-has-a-bad-day/clasp04/

The second site notes

  Entomopathogenic fungus (Clavicipitaceae sp.) killed a troglophile
  moth, Veins cave (Grotta delle Vene), Italy

I would guess something similar for what you found.

I must say your images are incredible.  The long fungal tendrils on the second image are the most amazing example of this I have ever seen.


what the best E-value cutoff in the miRNA homology search I'm trying to use miRBase database to annotate some microRNA sequences in length 22-24bp. I highly appreciate if someone let me know whether I should do this BLAST against mature miRNA or stem-loop sequence database? and the other main question is that which number of E-value is reasonably accepted as a lowest E-Value in the miRNA BLAST results? Also, what tool you suggest to perform miRNA enrichment analysis? for example we can use DAVID for gene (coding sequence) enrichment analysis. Using such analysis we are able to assign probable functions and biological roles to a group of miRNA (not only one miRNA). Any comments and idea is welcomed.

If you are using BLAST for short nucleotide searches then you should reduce your word size to <=7. It is better to align with mature sequences.

E-value depends on the database size. If your target database is huge then you should increase the e-value cutoff. If miRBase (for a few organisms) is your database then there is no need to run BLAST, also. You can simply run SSEARCH (Smith-Waterman Local alignment algorithm).

If you are running BLAST against miRbase you can set the e-value cutoff at 10. This is fine because there are many similar looking miRNAs with different function. If you reduce the e-value cutoff then you may lose these.

There are some other criteria for miRNA conservation- e.g there should be very high (almost exact) similarity at the seed region. After the BLAST, make sure that seed region is conserved.

  Can we can use DAVID for miRNA functional analysis.

I don't think DAVID can be directly used (miRNAs have to be annotated in their database). What you can do is that you can predict the targets of your miRNA and then pass them to DAVID. DAVID won't do the predictions but there are other programs (see this post). You can also try BioMart (provided by ENSEMBL) for getting GO details. Even BioMart does not provide functional annotation for miRNAs (I just tried, to verify). So best thing is to check for the targets.


multiple HIV infection in same T cell I was wondering can multiple HIV virus infecting same T cell ?
Coz in flu virus they have SA to cleave of those sialic acid residue preventing re-infection of the same cell by other viruses to maximize the amount of cell get infected.
I was wondering is there any mechanism found in HIV virus like what found in flu virus to prevent re-infection of an already HIV-infected T cell.

(little bit more about HIV virus that is irrelevant to the question, coz i was told that there is some HIV possible to hide in our body, but then i don't understand what it is the meaning of this hiding? Q1:Is the "hiding" refer to the genome of HIV that integrated into T cell. some of these infected T cells circulating in the blood Q2: will some of them reside in lymph node? Q3: and what make these infected B cell proliferate so to keep these B cell with the hiv genome long existing? will the virus transform these T cells into self proliferating? but will that be like cancer cell uncontrollably proliferating or well controlled?)

Thank you everybody

Yes, HIV does attempt to prevent multiple infection of the same cell. Once a T cell or other cells are infected, HIV downregulates the CD4 receptor which it uses to gain entry. Because of this, there are less receptors so another HIV is less likely to infect that cell. Meanwhile, the infection itself upregulates CD4 receptors on other cells which means the downregulation is even more effective. There are other mechanisms but this is a major one.

Hiding means it is somewhere where we don't know where it is and it isn't that active. When HIV is active it is destructive but also the cell is aware it is there. The cell can then try to alert other cells that it is infected. If HIV isn't active but instead hiding, it can stay where it is without really being detected. Even the drugs we use usually only affect HIV whilst it is replicating. So again if it's in a cell that's long lasting and the HIV is not replicating then it is essentially hiding. Such a cell includes macrophages and memory cells when we are just talking about the immune system.

Will HIV reside in the lymph node? Well yes, this is an exciting place for it. There's loads of exposed CD4 receptors and lot's of it's favourite T cells about. An infected cell will transmit HIV to other cells when they are signalling to each other. Even worse is when a dendritic cell is infected. Instead of instructing the immune system how to detect HIV infected cells, it is infecting them.

HIV is an infection. As soon as the body detects it, it goes into overdrive trying to eradicate it. This means there are more cells for HIV to infect. More foreign material means the immune system is even further stimulated to make even more cells. However it doesn't want CD8 cells to proliferate too much nor too many HIV specific cells so driving too much proliferation is a bad idea. What HIV does do is make lots and lots of useless copies of itself. HIV particles that are so badly made they aren't functional. The body tries to fight these and makes more cells to combat these but there's no point because they aren't the problem. But this immune diversion and a larger target number of cells is exactly what HIV wants. Proliferation of HIV specific cells, particular CD8, is associated with delayed disease progression or control.

Usually the cancers caused by HIV are because of other viruses running unchecked. Kaposi's sarcoma or lymphomas for example.


How is it that ionic diffusion is independent of other ions? This question arises from the explanation of what the resting potential of a cell membrane is. In the Goldman formula, there is no interaction between different ion types.

If diffusion is caused by random movement of ions and collisions, then how is it that the K+ ions do not seem affected by the very high concentration of Na+ ions outside of the membrane? Shouldn't there be an effect due to the fact that outside, the ion concentration overall is higher than inside? How come they are all independent?

Most importantly, the whole Goldman-Hodgkin-Katz model is, well, a model. It is a way we would like to find and explain phenomena, given pen and paper.

Often, scientists build models in order to explain data in hand, but even then, they will have to add something from their imagination. For example, early astronomers saw planets moving differently from stars, and came up with the idea that, you know, planets do not circle the earth, but maybe around some points in space, which in turn circle the earth. That didn't work well, so they created the heliocentric model, where planets and the Earth circled the sun. That was still perfectible, and Newton suggested the planets do not move on circles, but on ellipses. Each generation of astronomers had almost the same data in hand, but chose to make some assumptions in their models.

The same goes with the lack of interaction between potassium and sodium ions: it is a theoretical assumption. As models go, the GHK model is quite good, because it fits experimental findings better than any other model. Its assumptions have a great chance of being true, of reflecting the physical world. I guess you really asked what are the physical facts that underlie the assumption of ion independence. The fact is, you are looking for explanations for a fact that may be or may not be - so any response you will receive is, to a degree, speculation.

My thought is that the number of water molecules (55 molar) that may collide with an ion is far greater than the number of cations (up to a few hundred nanomolar, about 100 million rarer). Perhaps the number of ion-ion collisions is negligible. There is one bottleneck, in the actual channels, but there different species do not meet, because each has its own channels.

Another, more factual, is that the model is imperfect, and independence is more of a wish than a complete truth. Quoting from http://books.google.com/books?id=SmJoSwnwSh0C&lpg=PA353&ots=3fvI19Sk5Q&dq=ghk%20ion%20independence%20fails&pg=PA353#v=onepage&q&f=false : "The rich literature on how ion channels fail to obey the independence principle is reviewed in Chapter 14 of Hille (1991), and some specific models will be studied in the following chapter."


Catenation and decatenation by DNA Gyrase Decatenation is done for the replication of DNA and why is Catenation done and is it related to Crossing over

Both DNA Catenation & Decatenation are crucial to the equal distribution of DNA to the daughter cells during the mitotic crossing over. While catenation plays structural role in chromosomal architecture , decatenation facilitates the separation of sister chromatids.


Open protocol for Ligase Independent Cloning Ligase Independent Cloning is a protocol that allow an insert to be integrated into a vector without ligation.  It uses T4 DNA polymerase with only ATP to first chew back from blunt ends to create long sticky ends and then a polymerase treatment with full dNTP compliments to fill in the vector.

While there are several nice articles and resources that describe the procedure, I really would like a protocol with concentrations, temperatures and timing, which I'm having problems finding.  OpenWetWare for instance has only stub pages with no details.  Can anyone point to a full step by step recipe to make this work, once you have designed the primers?

You can look up Gibson Assembly or Circular Polymerase Extension cloning (CPEC).  For both of these the website for J5 has some good protocols.  Here is the one for CPEC:  http://j5.jbei.org/j5manual/pages/80.html

For CPEC you can look at the 2011 Quan paper: http://www.ncbi.nlm.nih.gov/pubmed/21293463

Hopefully that helps.


Why is only the donor's antigen seen during a blood transfusion? I am a high school student and I am a little confused that why only donor's antigen matters during blood transfusion? for e.g if the donor's blood is O- so it means that it will antibodies against all antigens so if he donated blood to say some A+ blood group then those antibodies will attack on that antigen and agglutination will occur, isn't it? At first I thought may be the antibodies do not work outside our body then later I heard of passive immunity so this thought is not correct then what's the correct reason?

Blood transfusions are done with erythrocyte concentrate and not whole blood. The antibodies are dissolved in the blood plasma. Grafting parts of the donor's immune system by transfusing white blood cells (the leukocytes) would cause even more problems than just agglutination in most cases. That's why care is taken to separate the red blood cells.


Are there any predators without camouflage? Are there any predators that don't use camouflage?

Poison dart frogs have aposematic colouration, making them the exact opposite of camoflaged.

They are also predators, since they feed on ants, termites and beetles.


Does increasing the value of k in k-fold coverage requires more memory? Study:
Here is what is k-fold coverage which is know as sequence coverage.
According to this, 2-fold coverage means the whole DNA is sequenced more twice in average.
Question:
If I have a genome sequence of length x with 30-fold coverage, then which of the following is correct?

I have to occupy 30x memory for the genome sequence, it means I would be given the genome sequence of length 30x.
It means I would be given the genome sequence of length x, but the sequence is more purified according to the calculation.

In Next Generation Sequencing (or better called 2nd generation sequencing) you are sequencing many many small genome fragments cut from many DNA molecules. Multiplying molecules, cutting them into fragments and amplifying them is known as library preparation (library of fragments to be read). During that process (of which PCR is important procedure) different errors or biases could be introduced.
What you get from a sequencer is many many short reads in form of FASTQ files that you need to assemble into genome sequence (by de novo assembly or more commonly by alignment to reference genome). It is important to know how sure are we for each nucleotide in assembled genome, which depends on how many times (and with what quality score) sequencer read each nucleotide (see image below).

(source: davidson.edu)
Coverage could mean average coverage across whole genome or coverage of some smaller portion of it (different coverage across genome is usually because of mentioned biases introduced in library prep).
To answer question: In final representation you get one whole genome assembled, if all you need is final representation (so answer 2). If you also store reads, then more coverage means more memory, but final genome is of same length.
NOTE: Coverage is even more ambiguous term that I just described, so you should look at this thread for possible different meanings (for example: which portion of whole genome is covered by sequencing).


What is the general term for tree-dwelling animals? Many different types of animals live primarily in trees, from birds to monkeys and beyond.

Is there a general term that I can use to refer to all of them?

The closest I've been able to come is "arboreal", and I'm not sure that that particular term is appropriate for the broad range of animals encompassed by the casual usage of "tree-dwelling."

You answered your own question - arboreal.

Another term that is somewhat related is scansorial, describing animals that climb trees. For example, black bears and raccoons are scansorial, though they aren't really arboreal. Conversely, there are probably some arboreal birds that aren't really great climbers; they simply fly or glide between branches.


What does the Gini index mean in a biochemical context? What is the meaning of the Gini index, as specificed in this link, which describes the Gini index of beta-glucopyranose bound to hexokinase?

Is this true that if Gini index has a very low value that means it doesn't interact much? If Gini index is high for a compound, it will interact?

The paper by Graczyk (2007) is probably relevant for you. It says that the Gini index is a measure of reactive selectivity of kinases, with values close to zero indicating no selectivity and values close to one indicating high selectivity, and it is created in direct parallel to the Gini index in economics, which is used to describe economic inequality. In its basic form, the Gini coefficient is a measure of statistical disperson. Also see Anastassiadis et al. (2011) for a more recent example where the index is used.

  Abstract
  A novel application of the Gini coefficient for expressing selectivity of kinase inhibitors against a panel of kinases is proposed. This has been illustrated using single-point inhibition data for 40 commercially available kinase inhibitors screened against 85 kinases. Nonselective inhibitors are characterized by Gini values close to zero (Staurosporine, Gini 0.150). Highly selective compounds exhibit Gini values close to 1 (PD184352 Gini 0.905). The relative selectivity of inhibitors does not depend on the ATP concentration.

References:

Graczyk. 2007. Gini coefficient: a new way to express selectivity of kinase inhibitors against a family of kinases. J Med Chem. 50(23)

Anastassiadis et al. 2011. Comprehensive assay of kinase catalytic activity reveals features of kinase inhibitor selectivity. Nature Biotechnology 29: 1039–1045


Where does the 'C' in exhaled CO₂ mostly come from? When a human being exhales CO₂, what is, by the numbers, the main source of carbon atoms exiting the body in this way? I mean what class of cells, or which tissues are the biggest on a pie chart of where carbon atoms breathed out in the form of CO₂ molecules came from?

CO2 is a product of Cellular Respiration, which generally takes Glucose and molecular Oxygen to produce Carbon Dioxide, water, heat, and allows ADP to be regenerated into ATP (or other various oxidation reactions). The Carbon comes from wherever the acetyl-CoA used in the Citric Acid Cycle came from - either carboyhydrates or fatty-acids (saturated carbon chains).

Simplified reaction:   C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat

So, you are correct. CO2 transferring out of the lungs is mostly the result of burning sugars (or fats) for energy (the regeneration of ADP/GDP with respect to human biology).

To that end, the tissues that produce the most CO2 will be the cell-types which constantly require energy. Nominally, muscle tissues.

Per your comment, broken down fat, or rather, the process of Fatty-Acid Catabolism, results in the production of acetyl-CoA, which is a primary player in the Citric-Acid Cycle. The Citric Acid Cycle, which you should recognize as the Cycle that Pyruvate - the end result of Glycolysis (the breakdown of Glucose into 2x 3-Carbon Pyruvates) - also goes into after being converted into acetyl-CoA by Pyruvate Dehydrogenase.

The sum of all reactions in the citric acid cycle is:
Acetyl-CoA + 3 NAD+ + Q + GDP + Pi + 2 H2O → CoA-SH + 3 NADH + 3 H+ + QH2 + GTP + 2 CO2

So, for a basic breakdown with respect to CO2:

Carbohydrates (Sugars, Starches) → Glucose → Pyruvate + ATP + NADH
Pyruvate → Acetyl-CoA
Lipids (fats) → Lipolysis → Acetyl-CoA
Acetyl-CoA + ... + H20 → ... + CO2


Influence of eating at late night on sleep I have often heard the saying that one shouldn't eat a mountain of food because blood will go to the stomach and it'll be difficult to sleep well because the stomach can't rest at night.

I see that the blood goes to the stomach when you eat something to digest the food. Have any studies been done on whether it does actually affect the quality of sleeping?

According to Crispim et al 2011, caloric intake late at night is correlated negatively with sleep quality:

  We conclude that food intake during the nocturnal period is correlated with negative effects on the sleep quality of healthy individuals. Indeed, food intake near the sleeping period (dinner and late night snack) was negatively associated with sleep quality variables.

The paper is an interesting read. Here's their figure 1 which shows the correlation between sleep latency (how long it takes to fall asleep) and nocturnal caloric intake:

Thick line: men
Thin line: women

Basically, it shows that people who eat more at night take longer to fall asleep, and other results show that it's also correlated negatively with other sleep quality indicators.


What jellyfish is this? I saw this jellyfish at Brighton Beach, Victoria, Australia. I have searched jellyfish images but there is nothing similar. It is round with a diameter of approximately 80cm and the blue part looks like hundreds of thin tassels.

Looks like Pseudorhiza haeckeli. Based on cross motif, and long tail. Grows over a metre across. There is a photo at https://www.abc.net.au/science/photos/2012/01/11/3406019.htm?xml=3406019.mediarss.xml#bigpicturepos
but dont copy it here - copyright.


Why PPD test in patients without M.tuberculosis often slightly positive? I got this question which I interpret as

  Why PPD test in patients without M. tuberculosis often have slightly positive PPD reaction i.e., a lifelong slightly positive skin test reaction?

because slightly positive -phrase does not make so much sense to me.
I first thought it is about false positiveness, but it does not make sense.

I am reading Murray Microbiology book.
It says there

  [An alternative to the PPD skin test,] is in vitro IFN-gamma release
  assays. The tests use immunoassays to measure IFN-gamma produced by
  sensitised T cells stimulated by M.tuberculosis antigens. If an
  individual was previously infected with M.tuberculosis, exposure of
  sensitised T cells present in whole blood to M.tuberculosis-specific
  antigens results in IFN-gamma production.

The question asks PPD test in patients without M.tuberculosis.
It does not say if the patient has previously had infection with M.tuberculosis.
I think this question implies that the patient has never had before infection with M.tuberculosis.
I am not sure how it can be in reality possible for adults, since M.tuberculosis spreads in air.

The reason for false positiveness can be that assays that use PPD use unspecific antigens, in contrast to IFN-gamma and second-generation assays.

The other reason is that once you get infected you always have some degree positive skin test reaction.
So to say patient without M.tuberculosis is faulty in a way because I think most people get exposured to this bacteria at least little in life.


What are the essential criteria for sleep in living organisms? I was reading this fascinating article about how sleep evolved before brains, and it got me thinking "can plants sleep" and "what is sleep anyway".
A line in the article states:

Studies by a team in South Korea and Japan showed that the hydra
periodically drops into a rest state that meets the essential criteria
for sleep.

But after looking around I am unable to find the "essential criteria for sleep" - Before I am able to answer questions like "can plants sleep" I think I first need to understand what these essential criteria for sleep actually are.
Can anyone here help me out?  Many thanks in advance.

I take it you did not even read the article. The article quite nicely expounds on this question. The whole idea is that sleep used to be considered as a human or psychological phenomenon that could only be studied by EEG, and clearly sleep was a phenomenon that goes deeper and wider in biology than just EEG waves. From the same article, just a little below:

She distilled a set of behavioral criteria to identify sleep without the EEG. A sleeping animal does not move around. It is harder to rouse than one that’s simply resting. It may take on a different pose than when awake, or it may seek out a specific location for sleep. Once awakened it behaves normally rather than sluggishly. And Tobler added a criterion of her own, drawn from her work with rats: A sleeping animal that has been disturbed will later sleep longer or more deeply than usual, a phenomenon called sleep homeostasis.

The keyword is behavioral criteria.
This is cited, I recommend a read-through.
I also recommend reading the rest of the article, it guides you through the status quo in sleep science which may further answer more of your questions. At the end, there is an exposition on animals without brains that seem to be sleeping. The hydra is one of them.


How do mutations come to be shared by all cells? It's my understanding that various hazards can damage the DNA in our cells, causing mutations.

But whenever I picture this, I see the damage being done to one of our tissues (for example, our lungs due to smoking, or our skin due to UV rays).

When I think about this, I see that... many cells in a smoker's lungs, or many cells on the back of a beach-goer's neck, may have mutations in their DNA. But only the cells in that tissue have these mutations... the other cells in our body would not have the same mutations.

In particular, sperm and egg cells would not have the same mutations, so the mutations due to smoking and UV rays shouldn't pass on to children.

Are there instances where mutations that occur over the course of our life are spread to every cell, including sperm and egg cells, so that every cell reflects the mutation, and the mutation is passed onto our offspring?

Goods question! Only mutations that occurred when we were in the early stages of development will affect all cells. That's why pregnant mothers shouldn't smoke. The reason for this is that one cell goes on to divide and become all our cells so any mutations in that cell are passed on to cells formed when it divides. That same principle explains your smoker example. In the lung we have two types of cells which are called Type 1 and Type 2. Type 1 cells are constantly dying as they get old and they get replaced by type 2 cells whose job it is to divide continuously to replace Type 1 cells. So we have lots of type 1 and few type 2. When type 2 divide they make one type 1 cell and one type 2 cell, so type 2 cells never run out. If smoke causes a mutation in type 1 cells generally they're okay because they'll die before enough mutations occur. Of course something that causes lots of mutations could make it cancerous before it dies but that's rare. Now if it occurs in Type 2 cells every subsequent type 1 or type 2 cell that cell makes is mutated.

The last thing you mentioned are mutations that occur to eggs and sperm. When making sperm you have the same as above. One cell makes sperm and a sperm maker cell. The sperm is like type 1 cells and the sperm maker cell is like type 2. So mutations affect them as they do above, where a mutation in a sperm maker cell is way worse. As for eggs women are born with all the eggs they'll ever have and there's no egg maker cells. So mutations just occur, and the older women are the more mutations. That's why the older a mother is the much higher risk of genetic diseases like downs. But an older man only has a slight increase in risk.

Mutations that affect eggs and sperm tend to be really harmful, as they affect every cell, so these cells or "babies" die before the mother even realises she's pregnant or as a miscarriage. I've not given the scientific names for things but if you request them, I'll give you the real names, but hope you enjoy the principles.


Development of vitreous humor I have tried reading about development of vitreous humor but it is all very confusing. When does it first developed ? Does it renew itself ? Please provide reliable sources..

Look at this scheme -

As I stated before, vitreous is 99% water and is not an organ itself, thus the "replacement of vitreous" is actually = 99% water re-production and the only organ inside the eye which can perform this - ciliary body.

Consequently, if the vitreous was removed and replaced by gas or saline it will be replaced by aqueous which produced by ciliary body - this process takes 8 weeks to completely replace foreign substance as a gas by aqueous.


Understanding common identifier codes (IDs) in biology databases I know this is very basic but I would like to understand it and it's difficult to know where to begin with a new database.

I have the output:

sp|Q9NZT1|CALL5_HUMAN

However I'm not sure exactly what this is referring to.

Is Q9NZT1 q unique identifier?
Is CALL5_HUMAN unique too?
Should one use both together to get information?
How many types of ID are there?

Common biology ID codes.

PDB: 2BIB for example. 4 letter code for a specific structure.

Uniprot: Q9NZT1 for example. A six letter combination of numbers and letters for either a TrEMBL or Swissprot record. This record contains information on domains, and Uniprot links out to lots of useful things like interaction databases, redundancy datasets etc.

Pfam: X1WG39_DANRE A uniprot ID followed by an identifier. Tightly linked with Uniprot, but with an emphasis on domains.

NCBI: NP_000108.1 For example. These IDs link to either a gene, transcript or protein in refseq. In an NCBI record there are two main distinctions in prefix of the ID code: hypothetical/automatic assertions (XM_, XR_, and XP_) and manually curated assertions (NM_, NR_, and NP_). This is followed by a 6 digit number, and sometimes followed by a "." and a number, indicating an splice isoform.

Uniprot IDs
I'm not sure where you got this output so this seems a strange concatenation of Uniprot information.
Q9NZT1 is indeed the unique Uniprot ID. This is specific to uniprot.
CALL5_HUMAN is the "gene name" or "Identifier" and often spans across different databases for that gene. It's a little more back end, but is essentially not unique due to splice isoforms.
There are many IDs in uniprot, and many types. Already below you'll notice some are swiss prot, others are Trembl. These are the main types. Swissprot are manually reviewed, whereas Trembl is an automatically compiled collection.

There are many many different accession code types with each database using it's own nomenclature that you'll come across. Unfortunately, there are too many to list here comprehensively.


Help identifying a mushroom found in Raymond, WA, USA Hello dear mycology wizards!

Could you help me figure out what's the name of this species.
I found the mushrooms in a forest near to Raymond, WA. The area was quite wet and mossy, but not a swamp. There was a creek ~50-75 feet away. The forest is mostly coniferous trees with a few birches.

Here are the photos of the mushroom of interest:

To me that looks like Chrysomphalina chrysophylla, which is one of several fungi superficially similar to the chanterelles.
(The chanterelle in contrast has gradual increase in the diameter of the stalk rather than a sharp demarkation between the stalk and cap.)
Chrysomphalina chrysophylla is a species that has been reported in Washington:
 Source: Burke Herbarium Image Collection (for Washington state)


Nervous System : Organ or Gland Failure If an organ was to start failing, not total failure, such as the thyroid gland, is it possible that the fault may not lie in the failure of the organ but in the nerve signals coming from the brain?

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

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

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

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

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


How does this small brown crescent-headed land planarian(?) "look around" and sense its envirnoment? This 2-3 cm long, thin brown worm with a wide "anchor" or hammer or crescent shaped head was seen in northern Taiwan slowly moving along a damp tile outdoor surface. It moved by contraction/extension and regularly lifted its head appearing to explore its environment, as if to say "where should I go next"?
Comments suggest that this is a land planarian.
Question: Is it possible to confirm that this is a land planarian and to understand what sensory organs it has on its head in order to "look around" and decide where to go next?

Given that "hammerhead worms" are Bipaliinae, I expect you can find your species from this bibliography1.  Bipalium or Diversibipalium ruteofulvum and cosmopolitan Bipalium kewense are mentioned, but I did not find images of these species online just now.
A paper about the sense organs of B. kewense (Abdel-Haleem, 2014) mentions many small pigment cup eyespots, as well as papillae and pits that may be chemosensory in nature.

1Kawakatsu et al. 2004 An Annotated Bibliography of Taiwan Land Planarians, with Lists of Linked Papers on This Animal Group


How do veins's valve pocket sinus tend to become hypoxic? For context, this question relates to the formation of deep vein thrombosis as I read that hypoxemia in vein can trigger coagulation cascade and cause a thrombus to form in vein.

I read that vein's valve pocket sinus tend to become hypoxic due to vortical flow. The diagram I attached below has oxygen tension color coded with a gradient from red to blue; the darker the blue is, the greater the hypoxia.

However, how exactly does vortical flow have to do with hypoxemia in those regions? From my understanding, the lack of blood circulation in vein's valve pocket shouldn't affect the amount of O2 bound to the haemoglobin stucked in the vein's pocket? As veins are not permeable to O2 thus O2 can't escape into surrounding cells.

References:

Bovill EG, van der Vliet A. Venous valvular stasis-associated hypoxia and thrombosis: what is the link? Annu Rev Physiol. 2011;73:527–545. doi: 10.1146/annurev-physiol-012110-142305.

Mackman N. (2012). New insights into the mechanisms of venous thrombosis. The Journal of clinical investigation, 122(7), 2331–2336. doi:10.1172/JCI60229

https://www.jci.org/articles/view/60229

As veins are not permeable to O2 thus O2 can't escape into surrounding cells.

Veins are not like impermeable rubber tubes, they are 'living' structures requiring, like all cells, Oxygen and glucose to survive. Smaller veins get the O2 from diffusion, while the larger veins need help from vasa vasorum, small blood bessels that bring blood to the walls of the veins.

The innermost cells lining veins are epithelial cells. They also line valves.

In the picture you posted, blood is not circulating well behind valves. The cause of hypoxia is that epithelial cells are continually removing O2 from the blood.

When enough O2 is removed to cause hypoxia, the endothelial cells may become damaged by the lack of O2, causing inflammation and (possibly) potentiating clot formation.

  Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis.

Mackman N. (2012). New insights into the mechanisms of venous thrombosis. The Journal of clinical investigation, 122(7), 2331–2336. doi:10.1172/JCI60229


If there is such known "Mitochondrial Eve", does it means that all the mitochondrial dna in everyone's body is same? P.S. I know not that much, just some basics, but this question really interested me :)

The mitochondrial genome has a nonzero mutation rate, though estimates differ according to method. Estimates are approximately 10^-8 per bp per year on average, and the mt genome is ~20,000 bp. So we can do some math and expect that many (or most) people experience heteroplasmy, which is to say that they carry various different mitochondria (in the same person).
Note also that you inherit multiple mitochondria from your mother, not just one.
So- no, not everyone has exactly the same mitochondria, even if we can trace them all back to a single hypothetical human.


How does a cell regulate what leaves its vacuole? Suppose a plant cell wants to take something out of its central vacuole. Some specific substance. Well if the vacuole is a bit of a soup of water and other dissolved substances, how does the cell get some specific substance out? Without letting any of the water/solution into the vesicle that's budding off? Or do they just let the solution right in?

Clarification: Since a vacuole is full of water and other dissolved substances, wouldn't that solution get into a budding vesicle? How is this prevented? Is it prevented?

When the cell is creating a vesicle, it starts pinching off part of the membrane, correct? My question is how the solution in the vacuole stays out of the vesicle, if it does at all.

Your question is not entirely clear, even after the edit. However, I believe it's worth mentioning that the vacuole, just like any other membranar organelle1, is surrounded by a biomembrane.

Such biomembranes have transport proteins, which can be channels, carriers or pumps, and those transport proteins can determine which substances will get in/out of the vacuole, either down the electrochemical gradient (channels and carriers) or independent2 of it (pumps).

Here is a diagram showing the membrane of the vacuole with some transport proteins:

Therefore, since the cell can open or close a give gate or activate/deactivate a given pump (just like the transport proteins in the plasma membrane), that helps to explain how the cell decides what gets in or goes out the vacuolar lumen.

1: Unfortunately, there is not a consensus around the definition of organelle. The definition I use states that all organelles have a surrounding membrane (therefore, a ribosome is not an organelle), which renders the expression membranar organelle pleonastic.

2: It's very common reading that pumps will transport the substance against the electrochemical gradient. That's not correct. They will transport the substance independent of the gradient, that is, they can pump a substance against the gradient or down the gradient.


Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion? Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion? How severe would the effects be if a patient came to the hospital after the recommended 1 hour time frame?

Gastric lavage only washes out ("lavages") the stomach ("gastrium"). Gastric emptying time is generally ~60-120 min, probably on the lower end of that for ingested liquids. After that amount of time, most of the toxic substance will be beyond the level of the pyloric sphincter (i.e. in the duodenum) and not accessible to lavage.

The second question is not possible to answer without some information about what specific toxic ingestion you are interested in knowing about.


Mechanical cause of loss of consciousness Consciousness is an electrical and chemical interaction in the brain, caused by neurons firing and chemical interactions. How does a mechanical "force" cause this to stop working?

i.e. How does a mechanical action (such as a punch to the head) cause this electrical/chemical system to stop working (leading to unconsciousness)?

Mechanical force can compress neurons and cause action potentials as you probably experienced in the form of hitting the funny bone. Strong enough acceleration of the brain tissue may be causing massive excitation of neurons as indicated by animal EEG study. It suggests that the loss of consciousness is due to generalized epileptic seizure. However, it is not fully agreed upon: quoting wikipedia entry on Concussion:

  It is not known whether the brain in concussion is structurally
  damaged or whether there is mainly a loss of function with only
  physiological changes.[14][needs update] Cellular damage has
  reportedly been found in concussed brains, but it may have been due to
  artifacts from the studies.[15] It is now thought that structural and
  neuropsychiatric factors may both be responsible for the effects of
  concussion.[16]

And following quote is from this

  The brief loss of consciousness that characterizes concussion appears
  to be the result of rotational forces exerted at the junction of the
  upper midbrain and thalamus that cause transient disruption of the
  functioning of the reticular neurons that maintain alertness.
  (Allan H. Ropper, M.D., and Kenneth C. Gorson, M.D.; N Engl J Med 2007; 356:166-172 January 11, 2007)


Why do raw prawns turn red after sitting in vinegar? Yesterday morning I put some raw prawns (shell removed) into vinegar (more specific this one), and put them in fridge. When I came back at night all of them turned red, which looks cooked, except those not covered by vinegar.

Why do the raw prawns change colour?

The prawn has proteins (meat, muscles).

Beef is red because the muscle proteins in it have a molecule that binds oxygen called myoglobin (whereas our red blood cells have hemoglobin that allows them to carry oxygen better).

In fish you know the meat is white because there is no myoglobin present (in the muscle proteins), but another molecule that still binds oxygen but doesn't look red.

When you add heat or acids (vinegar) to the meat, the proteins get denatured, change their shape and their colour too. You get red shrimps by heating the proteins in them.

Hope this helps


Two heterozygote mice for skin color are reproduced. Find the probability that in 3 children 2 will be dark and one white Two heterozygote mice for skin color are reproduced. Black is dominant to white color. Find the probability that in 3 children 2 will be dark and one white. How did you do the ordering. Well I found it that in F1: 1/4 are AA, 1/2 Aa, 1/4 aa or 3/4 black and 1/4 white.Now nI think I should multiply the chances: 3/4*1/4*3/4, but it would be according to an order. What should I do? Is my answer correct?

You are on the right track, but you have to keep in mind there are multiple ways to have two dark and one child in a group of three. You have to add the probabilities of each unique outcome that results in two dark and one light child. So, the probability is (1/4) x (3/4) x (3/4) PLUS (3/4) x (1/4) x (3/4) PLUS (3/4) x (3/4) x (1/4)


Does sweat contain DNA information? I was reading this article : Perspiration
The first question which came to my mind after reading the composition of sweat was whether it contains any information about the DNA or not?

I haven't had much interaction with biology since 12th grade (2010), so kindly answer in layman's terms and detail as well.

The Wikipedia page you linked says that sweat is composed of a liquid similar to blood plasma. As all DNA in humans is stored in the nucleus of a cell, it seems unlikely that the sweat itself would contain any DNA.

However, when someone sweats significantly, I can't imagine that no skin cells end up in the sweat. In any case in which this occurs, then the DNA in the cell is in the sweat. Additionally, with small amounts of sweat, I can't imagine how it would be collected without getting any skin cells in it.

This source confirms that sweat contains DNA in some form. Additionally, I think the following quote from here shows that it is stored in cells:

  In every case, what is being tested is the DNA contained in cells of human tissue


Mitochondria variability per tissue in humans? I would like to know the distribution of mitochondrial content per tissue type in humans. I understand the simple metric that energetically active or energy requiring tissues will have more mitochondrial content, however is there any study/link for a more quantitative estimate ?

BioNumbers is a great site to answer this kind of question.

This search produced a link to this paper , which has measurements for mitochondria per cell for multiple species and cell type.


Why some tissues like small intestine epithelium are able to be replaced so often, yet they are not one of the most common cancers? My small intestine epithelium cells are replaced thousands times more than my prostate. Yet I'm much more likely of getting a prostate cancer than cancer on my intestine epithelium. Is there a known cause for this?

Does our body have better DNA-repairing mechanisms or something like that for those tissues ?

The human prostate has two main epithelial cell types, basal and luminal, as well as a minor population of neuroendocrine cells. Primary prostate cancer nearly always has a luminal phenotype characterized by atypical glands, strong androgen receptor (AR) signaling, and an absence of basal cells .                  Intestinal epithelium. The intestinal epithelium is the single cell layer that form the luminal surface (lining) of both the small and large intestine (colon) of the gastrointestinal tract.


Potential to destroy viruses using prions? Could a prion be used to sufficiently deform a viral protein in order to make the virus it is a part of incapable of reproducing? For example, take the common cold's VP1 protein and turn it into a prion, then inject that prion into someone with a cold. Would this prion ever come into contact with the virus? Would it actually deform the virus? Can we make prions?

Prions are misfolded "versions" of proteins already present in the genome. These tend to bind to their properly folded counterparts and catalyze their misfolding into prions. Although unlikely, it is not impossible to imagine that they might interact with other macromolecules. That being said, injecting a human with prionic particles for any reason (especially in a clinical trial for the common cold) is EXTREMELY unlikely. Even if you prove that it works in animal models, injecting a person would be considered too risky. Additionally, the "benefit" of that would be marginal - curing the common cold, from which > 99% of people recover even without any medication. Given that there is great risk and very little benefit, we will most likely never know for sure how feasible this is (at least for the common cold). As a concept, it could work, but would be extremely difficult to get right.


Are stem cell lines cryogenically preserved or commercially available like HeLa cells are? There are HeLa cells, which were taken from sick cancer patient and now is growing worldwide in different laboratories for experiments. HeLa cells can be kept because they are immortal and so they are an instance of immortal cell line.

What about stem cells? They are also immortal. Such cells can be taken from normal healthy person and also kept forever. Do scientists do this? Why don't we hear about it then? For example, they are distinguished in Wikipedia article, referred above.

Are there some special properties of stem cell lines, making them different? For example, being low differentiated they may be useless for experiments.

This is too long for a comment, so I have to write it in here:

Mostly this is because other cell lines are more practical in the lab.

Stem cells are much more tricky to maintain - especially if you want to keep their stem cell properties. They only grow very slow, tend to differentiate when they get too much stress, cellular signals and so on and need special media (these need to be defined, so that they are not containing factors which promote differentiation for example).

For everyday experiments (like expression profiles, experiments on the effects of certain substances on the growth, gene expression or whatever of cells) "normal" cell lines are much more suited as these are much easier to keep in the lab using standard media. Additionally,experiments can be more easily repeated and reproduced, since these cells should behave always the same.


Is it possible for a human to get rabies from a rabies vaccine meant for dogs? What would happen if a human was injected with a rabies vaccine meant for dogs? I know vaccines can contain weak or dead strains of the virus, but is it possible that the human could become infected with rabies from a vaccine meant for dogs? My thinking is that maybe a dogs' immune system is more suited to deal with a weak strain of rabies that would otherwise infect a human.

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

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


Reattaching body parts Is there any living organism that has the ability to remove and reattach body parts at will?

I'm not talking about regeneration (like in starfish). Say I'm chasing prey, and I decide that my tail will be a hindrance. So I leave it behind, and reattach it after the hunt.

I dont think this would be possible from the simple idea that all cells need energy, and if there's no nutrient flow, then how would the cells inside the detached body part stay "alive".  Doctors can currently reattach body parts right now if it's within a certain amount of time, but no animal yet can just reattach at will.


Ebola: cleaning of protective suit As far as I know, in developed countries protection suits used by people who treat patients with Ebola are disposed of after a shift.

From a rather ambitious costume last year, I still have a hazmat suit like this one and this full-face gas mask.

More out of curiosity than out of real concern, I was wondering whether it would be possible to use this equipment in a potential outbreak of the virus. My greatest concern would be reusing the suit, as it might not be safe after the first use.

Is there a way to disinfect the suit and mask with publicly available chemicals? For example, I could imagine a friend spraying me with a solution of chlorine. Would that be feasible and make wearing the suit reduce the risk of an infection?

Notice: the only select agent I've worked with is VSV which was a USDA select pathogen (not as big of a concern for humans).

TLDR:  It would provide some protection, but I would be most worried about a false sense of security.  It would unlikely be up to rated standards, but it would likely be better than a t-shirt.

First let's start with ebolaviruses.

Ebola, like HIV and many other viruses, doesn't do well outside a host.  This might be because the protein structures beneficial in the host are not the same as needed for stability in exposed air and room temperature.  A counter example of a very stable virus would be something like human rhino virus (HRV).  If HRV was compared to be like a rock, ebola would be over cooked spaghetti.

Certainly the virus has to maintain some stability in the environment, otherwise it wouldn't succeed evolutionary.  As I'm sure you've heard on the news, ebola is spread by contact with contaminated fluids.  I would like to point out a wonderful info-graphic that was made for public consumption, especially the image on viral life cycle:

Assuming that you're not going splunking in bat inhabited caves in West Africa, it's safe to assume that what we are worried about is human to human transmission through infectious fluids.  Ebola actual isn't that stable in water, so just soaking a surface in water and a little oil might help you out (if you don't have bleach handy).  I want to be clear that I'm not recommending this, in reality you should just avoid contaminated objects.  I think that we have clearly established that what we're really concerned about is infectious bodily fluid.

This leads me to the wonderful note by Jose Martin-Moreno titled "Is respiratory protection appropriate in the Ebola response?"  I don't think I can express the problem better than he can, so hopefully I will be allowed a substantial quote:

  This transmission [of ebola] occurs via close family contact or in
  health-care settings, particularly when placing orotracheal intubation
  or when caring for a patient who is vomiting or bleeding. Ebola is
  rarely transmitted via an airborne route. Although these routes of
  transmission are well known, most agencies, including governmental
  agencies responsible for repatriating western patients, apply
  infection-control measures appropriate for airborne diseases.
  Excessive precautions could offer reassurance to those responding to
  Ebola, yet complete respiratory protection is expensive,
  uncomfortable, and unaffordable for countries that are the most
  affected. Worse, such an approach suggests that the only defence is
  individual protective equipment, which is inaccessible to the general
  population. Moreover, the image of workers with spectacular protective
  clothing might contribute to the panic in some communities. If this
  leads people to flee affected areas it could increase the spread of
  infection.

With that said, all your full face gas mask is going to help with is prevention of fluids from hitting your head.  You could probably take the actual filters out to breath more easily (I find breathing in them a giant pain).  And as @Chris pointed out, they are easily clogged which could necessitate the need to take off the whole mask (which might be doing some good) to prevent suffocation.

Moving to hazmat suit.

It's actually good news that you don't need the air containment of the suit, as that's the hardest element to maintain.  To state the obvious, the main purpose of the suit is to prevent your body from coming in contact with infectious fluids (in this case).  To do that you don't need to be in positive pressure personnel suit (PPPE), or follow BSL4 considerations.  The respiratory concerns from in an BSL4 environment come from other select agents, and the personal working in such a facility are going to be doing very different activities from what you should be doing as person trying to avoid an outbreak (they could be purposefully growing up purified high-titer virus stocks and running around with pointy things as an example).

Here I'm going to run into citation problems because no one (that I could find) has tested the kind of scenario I'm about to discuss, so it should be seen as informed conjecture.  Assuming yous suit is actually an analog of a Tychem QC suit, it's probably not a rated OSHA unit (A-D), but that doesn't necessarily matter.

On it's first use it would likely be sufficient to protect against incidental exposure.  Let's assume for the sake of argument that you didn't run into any Ebola when you used it as a costume, and don't the next time you put it on.  At this point decontamination (decon) isn't the concern, failure of the material is.  In other words, are you sure you don't have any holes, tears or cracks in the material?  I think this is going to be the real limiting factor in the life of the suit.  Using good old fashioned duct tape will be give you a few more uses, but the suits are just not designed to last through prolonged use.

Now let's assume the worst and that you get substantial blood splatter on you (while wearing your suit) from an ebola patient.  And not a little that could easily be wiped of with a spray bottle of 10% bleach and a paper towel (how most decon could be done).  Instead let's assume you're standing next to someone who suffers a traumatic injury on top of having ebola virus disease (EVD).  I'm imagining something like a point-blank shotgun wound or, given the probability of this scenario, a falling grand piano. In this case, you're going to want to decontaminate the suit before you take it off, which is the same thing professionals are going to do.

If you're friends with your local fire department, and you live in an area with a large enough population to have a HAZMAT team, you can probably get them to at least give you a run through of how it's done in ideal conditions.  YouTube videos are also not hard to find, just search JESTC and decontamination.

Presumably you would have a hard time going through several rinse and wash steps, but you would want emulate this as much as possible.  With ebola, you would be fine to decontaminate with a 10% bleach solution (or if you use bargain/cheap bleach 15%).  The trick is that you would want to do it a few times, and with a friend (also hopefully in a suit).  Thus if you got two generic soap sprayers, filled one with 10% bleach, and the other with water, and then alternated spraying your partner with bleach and water, wiping down as you went, you should be able to decon the suit pretty well.  If possible you're going to want to collect all the run off an rinsate.  Again professionals tend to use actual kiddie pools for this.

But just the act of using so much bleach on the suit is going to weaken the fabric, again leading to the principle problem of failure of the fabric. Thus I would be worried that such a suit would provide a false sense of security, leading one to go into dangerous infectious environments when one shouldn't.  Just avoiding and going away from contaminated individuals is going to be the best solution, regardless of a suit.

I considered going into why I think it's highly unlikely that any of the ebolaviruses would evolve to be airborne, but I consider that outside the scope of the question.


What triggers the release of gonadotrophin-releasing hormone with the onset of puberty? I am interested to know the process of development of puberty. During puberty, when boys/girls reache 12-14 (puberty) years of their age, their hypothalamus releases gonadotropin releasing hormone (GnRH) and then this hormone in turn affects the pituitary gland which releases FSH and LH. FSH/LH hormones promote male/female features. For e.g. girls start their first menstruation cycle and males start to produce sperm; their voices become smooth and intense respectively. So all these phenomena are dependent on GnRH.My question is that if those hormones are produced due to the effect of GnRH then how is GnRH production itself regulated. In other words how does our body "know" that we are in the age of puberty and it should secrete GnRH?

GnRH-secreting neurons are not fully independent. To date, their most studied regulators are kisspeptin-secreting neurons. During childhood, kisspeptin-secreting neurons are off, due to GABAergic higher level structures and to lack of free leptin. So both brain and body fat have a word on it.

Caveat: most of the evidence is circumstantial (for example, higher circulating kisspeptin in naturally occurring precocious puberty) and I am oversimplifying, so the picture is more complex and will become even more so.


When muscles contract is the process similar to how non-newtonian fluids react? I'm trying to understand how muscles contraction/tension works but getting loss in on the cellular level. From my understanding, when muscle tissue need to contract, the cells are flooded with calcium? Does that mean they get filled up with calcium? If so, are the cells hollow or does the calcium replace the fluid that was originally there? Or does the calcium cause the reaction in the cell for it to firm up?

I'm asking because there's an alien character who's quite thin but is also very strong and I was wondering about the science of that. I know them being alien means that their biology wouldn't necessarily follow earth rules but they could also share similar traits.

Calcium ($\ce{Ca^{2+}}$) is a signalling molecule and it acts like a chemical switch that tells other chemicals in the cell to enact the contraction. It's not accurate to think of the cell "filling up" with $\ce{Ca^{2+}}$ since $\ce{Ca^{2+}}$ wouldn't significantly change the volume of the cell alone *. Also, during contraction, the muscle cells contract in on themselves - they don't swell out.

It's also not accurate to think of the cells as hollow. Other chemicals inside the cell (such as actin and myosin) act like machinery that enact the contraction. Instead of thinking of the cell filling up like a balloon, I think it would be better to think of it containing a chemical winch (as in the figure below) whose pulling force causes the contraction. Similarly, instead of thinking of $\ce{Ca^{2+}}$ as a fluid, think of it as a bunch of particles that cause a chemical reaction to turn on this winch when they're allowed into the cell.

Reference: https://www.ncbi.nlm.nih.gov/books/NBK21670/

* During a $\ce{Ca^{2+}}$ spike, intracellular $\ce{Ca^{2+}}$ rises around 10-100x from 100 nM. Assuming $\ce{Ca^{2+}}$ has a 100 pm ionic radius, the volume of the cell ($x$) is only increased by around $10^{-9}x$ to $10^{-8}x$, which is negligible.


Why does mint oil feel cold on the skin? When putting (japanese) mintoil on the skin it produces a cool feeling.

You can experience this, when adding it to your bath or using a spray with mint oil on your skin. The cool feeling occures even if the actual temperature of the spray or bath is quite warm.

Where does this sensoric impression come from?

Anything related to mint usually contains menthol. What does it do? It triggers the TRPM8 ion channels, causing your skin's cold receptor to become sensitive, and causing it to overfire.

This causes the brain (receiving cold signals from skin) to feel cold, and that's why you feel cold.

I have summarised it in a few sentences, but as with any scientific discovery, it took quite a few years to fully understand what was going on. NCBI have summarised this quite nicely over here (http://www.ncbi.nlm.nih.gov/books/NBK5238/)


How does the size of insert affects the rate of Homologous Recombination in yeast? When performing genetic knockouts in yeast using homologous recombination to replace a target gene sequence via a vector DNA, does the region between the flanking regions in the vector have to be the same length as the site of recombination in the host cell's gene?

As pointed out by aandreev, the greater the size of the insert relative to the flanks lower will be the recombination rate. This is because the donor DNA essentially becomes non-homologous. See the figures below:

  Figure1: Effect of insert size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

  Figure2: Effect of flank size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

However, you mentioned that you want to make gene knockouts. In this case you just need to make a small mutation (for example introducing a premature stop codon).

Use of genome editing tools such as Crispr-Cas, ZFN and TALEN increase the rate of transgenesis by introducing DNA double strand break.

These can also be used for making knockouts when NHEJ dominates over HR as the DNA repair mechanism. NHEJ is error-prone and can cause indels that can disrupt gene function.


Might new bones evolve from soft tissue? I wonder how bones evolve where there are none. (This is the question, read the sub-questions as examples :) )

Lets take an elephant as an example. If it was adaptive for the elephant, could bones somehow evolve in their soft-tissue trunks? If so, what tissue would they develop from?

Perhaps the sheet of cartilage in their ears are more likely to somehow calcify and become a new bone?

And would then several connected bones and joints evolve from the new bone tissue?

Is it very rare for new bones to evolve from scratch? Or, do today's bones entirely trace back to the set that evolved in early tetrapods?

New bones do form occasionally so it is not impossible, Ornithischian dinosaurs are defined by a evolution of a new bone (predentary). There are many pieces of cartilage in the body that become ossified in some animals and not others, the kneecap is a great example since a bony kneecap has evolved and been lost many times independently, it is just a matter of ossifying existing tissue. The trunk however is more difficult since it does not have any suitable cartilage.

Cartilage however is not necessary to form bone, but it is the most common way to get it. Endochondral ossification forms bone from cartilage and is responsible for the majority of the bones in the body. Intramembranous ossification forms bones in other connective tissue, the bones of the skull and dermal bones are examples of this process. Dermal bone has evolved separately many times but tends to form in the skin.

Given enough time  and the right selective pressures it is certainly possible for bones to evolve in the trunk but it is not going to happen quickly.


Are there any parasites that alter human behavior in a self destructive way? There seems to be quite a few examples of parasites taking over the behavior of insects in a way that leads to the death of the host.  A couple of examples include:

Spinochordodes tellinii:  A nematomorph hairworm that causes crickets and grasshoppers to jump into water, and likely drown, as
part of their life cycle.
Ophiocordyceps unilateralis: A fungus that causes ants to leave their desired habitat for the habitat required for the fungus
to reproduce while consuming the ants internal organs.

In mammals, a common example is:

Toxoplasma gondii: A single celled parasite that appears to make rats attracted to cat pee in an attempt to continue its life
cycle within the cat.  Additionally, humans can be infected with
Toxoplasma gondii via contaminated meat, vegetables, and cat feces.  In fact, there is a study of Danish medical records from 45,788
women in which the rate of self harm increased 50% for women
suffering from chronic toxoplasmosis and the rate of attempted
suicide was 80% higher.  However, direct correlation between the
increases could not be linked to the these higher rates due to the
possibility of other factors such as depression.

So it seems that there is some widespread evidence of parasites causing a host to act in a potentially lethal way, but the evidence that I could find for humans seems to be minimal and yet to be proven.  Are there any examples of parasites causing humans to act in a risky, potentially deadly, manner?

There is a link established between Candida and Aspergillus fungal infections and mental illness of schizophrenia and depresssion. Over prescriptions of antibiotics and use of antibiotics in cattle ranching, subject people to excessive antibiotics. This causes a die off of natural gut flora and consequent fungal overgrowth.
Fungal metabolites (aflatoxins) have been linked to anorexia,depression and schizophrenia. Pubchem lists lists behavioral acute anorexia for aflatoxin G1.
Research published in Journal of Antimicrobial Therapy, suggest that some SSRI antidepressants have an antifungal effect.
Ethyl alcohol (alcoholic beverage) is a fungal metabollite of brewers yeast that is well known to impair human behaviour in a negative way.
I have been unable to find any research into using antifungal agents to treat mental illness.

A fungus that thrives in soil, contaminates grain, is distilled into a beverage that causes drunk driving and death, and returns the host to the soil has also completed its life cycle. Similar to the ant example in your question.


How would one calculate the availability of nucleotides to an enzyme? How would one calculate the availability of nucleotides to an enzyme like a polymerase ?

I imagine an answer in units like nucleotides per second per enzyme, but I'm also imagining an answer that is not a simple rate of reaction. k_on calculations and k_off do not offer mechanistic explanation.

I'd like to know, specifically, if there is a theoretical approach to this question:  how does a polymerase reject an incorrect nucleotide?

I could read this question more than one way.  Are you talking about an enzyme in a cell or in a reaction in vitro?  Kinetics and mechanical explanations can overlap, but are not entirely the same and are usually dealt with separately - kinetics with watching the rate of reactions in a tube and mechanism in a crystal structure or possibly Nuclear Magnetic Resonance.

Protein structures are usually static- you only get a time lapse snapshot of the reaction in most cases. kinetics allows you to see how fast these things go and can help you understand the order of binding when more than one component is needed for the reaction, etc.

The polymerase has a binding pocket where the template strand and the growing strand are used to build a double helix together.  if the base being introduced does not form Watson Crick base pair bonds, the geometry of the reaction will not allow the base to be added to the growing strand.

Hope this helps? If I can make this clearer, can you drop me a comment and I'll revise...


Infection of urinary tract if the pH of urine is made alkaline It is very well known that drugs like phenobarbiton,morphine are unionized, lipid soluble.So,in case if there is toxicity due to these drugs,the only way to save the patient is make the pH of urine alkaline and thus facilitating its excretion.But,the normal pH of the urine is acidic which protects the person from various urinary tract infections,if the pH is made alkaline is there a increased for the patient to have urinary tract infections?

There is a huge misconception here.  Morphine overdose is treated with Narcan (naloxone).  Phenobarbiton overdose is treated with artificial respiration (in extreme cases), blood pressure medication, and management of low heart rate.  The concept of lowering the pH of the urine to increase a drug excretion is (to my knowledge) never used in emergency settings.  Dialysis, which filters the blood, would be used to 'clean' the blood of toxins.  Think about it.  Time is life, and changing the composition of your fluids would take a lifetime compared to the implemented measures in emergency rooms.  You body has an extremely sensitive acid-base balance.  You do not want to try to increase or decrease the pH of your bodily fluids.