What is the main challenge in creating a chemical male contraceptive? More than 50 years after hormonal contraception for women was invented, a contraceptive pill for males is still not available. With the obvious major biological differences in mind, why does it appear more difficult to create a chemical contraceptive for males? What are the main challenges that must be overcome to create a viable, reliable and marketable contraceptive pill for men?

I am going to summarize a few reasons for both why contraception is "easier" for women, and for why it is "harder" for men. They are both biological and sociological.

Easier for women

The female cycle is more complicated

The female cycle leading to ovulation is regulated by several hormones that interact. As such, it is easier to disturb.

  The system is so sensitive that even the slightest alteration in any of these factors can disrupt its fluidity and lead to anovulation

(Anovulation = a cycle where no ovulation occurs) Source: Anovulation: Background, Pathophysiology, Epidemiology

Even in young women, this occurs naturally.

  Estimates of chronic anovulation rates range from 6-15% of women during the reproductive years

Female bodies l already have a "built-in mechanism for contraception

As ovulation needs to be suppressed during pregnancy, there is already a mechanism in place by which this can happen.

Women are more affected by pregnancy

Since women are more affected by pregnancy and childbirth, the risk they feel they have when they don't use contraception or use it incorrectly is larger.

Contraceptives for women have more than one use

  More than half of pill users, 58%, rely on the method at least in part for purposes other than pregnancy prevention. Thirty-one percent use it for cramps or menstrual pain, 28% for menstrual regulation, 14% for acne, 4% for endometriosis, and 11% for other unspecified reasons.

Beyond Birth Control: The Overlooked Benefits of Oral Contraceptive Pills

Harder in men

It only takes one

While the saying "it only takes one sperm"  is probably an exaggeration, it carries a certain truth - you really need to shut down the production of sperm or the risk of a pregnancy is too high. Both the pill and the various IUD options have set a high bar for what's considered an acceptable risk.

Side effects and effectiveness

While hormonal contraception for women already has a multitude of side effects, often unrelated to the reproductive system, this is certainly not easier in men. The most prohibiting side effect encountered so far is impotence - not much use in taking birth control to have sex without risk of pregnancy when doing so leads to no sex at all.

  Progestins have been used in multiple small studies of men for suppression of spermatogenesis and testosterone production. Progestins used alone result in significant side effects such as loss of libido and erectile dysfunction.

Update on Male Hormonal Contraception: Is the Vasectomy in Jeopardy?

(Decreased libido is also a side effect in female hormonal contraception, though. The reasons why it's seen as more acceptable there are probably sociological)

That review is a good overview on what has been tried until 2010. Many solutions failed because of side effects or because they didn't work well enough.

On testosterone:

  Of note, this international study revealed that 91% of Asian and 60% of Caucasian patients became azoospermic, suggesting an ethnic difference in endocrine response

Testosterone proved to be rather good in other doses and combinations, but is not that easy to handle because it requires injections and can't be taken orally.

  Testosterone alone has side effects, including acne and oily skin, mood changes, increased hemoglobin and hematocrit, weight gain, decrease in testicular volume, sleep apnea, gynecomastia and possible effects on cholesterol. There are no long-term data with testosterone use and normal men regarding prostate symptoms, growth or cancer. In an era of fear of using medications on relatively healthy individuals, acceptability of routine use may be a major concern, given recent data on medical treatment of menopause with estrogen/progestin therapy. In addition, anabolic steroids are a controlled substance and regulation of this industry is very strict at this time. Abuse of these drugs could easily become prevalent with its widespread use and availability for contraception.

On cryproterone acetate:

  Doses ranging from 25 to 100 mg per day have suppressed spermatogenesis, but side effects have precluded subsequent studies.

And so on...

The market factor

A side effect of the contraceptive options for women being so well-accepted, women often feeling responsible for contraception and also using hormonal contraception anyway, for reasons unrelated to pregnancy, is that the market for male contraception is not that easy and pharmaceutical companies have been pulling away from it. Especially in light of the research difficulties.

  Although Bayer, Wyeth and Organon were once active in research and development of a male method, all three discontinued their programs between 2005 and 2008 although the industry continues to actively pursue programs for hormonal contraception and hormonal-replacement therapy for women. In withdrawing support, company representatives cited corporate changes in direction and the perception that safety standards demanded by regulatory bodies would require such extensive evidence as to make further research financially infeasible

Current challenges in male contraceptive research

This is not to say that there really is no market. As you mentioned in the comments, at least in questionnaires, many men say they would use male hormonal contraception and many women say they would like their partners to use it. See, for example, Market size for male contraception (plus the following pages of that paper)

But you asked about the challenges ;-)

I think it's also interesting to note that the search for hormonal contraception started for both men and women. It's just that the "solution" was found for women first and then got popular really fast.


Why Can't A Male Mule Have Offspring? I've read that female mules can sometimes have offspring, but that male mules are incapable of doing so. Why is that the case? Is their sperm not capable of entering the egg or is their a genetic reason?

It's essentially genetic. The mule is a hybrid of a male donkey and female horse. A donkey has 62 chromosomes, a horse has 64 chromosomes, and a mule has 63 (mix of 62 and 64). There is a mismatch between both number and structure of the chromosomes and as a result, most mules are infertile.


Can people with AIDS get a fever? It's my understanding that fevers are an immune system response to infection. Like the body's cells can take more heat than most viruses or bacteria.

So if that's the case then can you even get a fever if you have a non-functioning immune system due to AIDS?

With AIDS, the whole immune system is not non-functional. The condition results in a severe drop in CD4+ T-cells, which is what primarily predisposes AIDS patients to secondary infections.

Fever can be an immune response to infection, but it is not directly affected by the loss of CD4+ T-cells. Rather, fever occurs due to a complex cascade of events triggered by pyrogens, which causes a release of prostaglandin E2 (PGE2). In the hypothalamus, PGE2 signals a systemic response for the body to generate heat. More on the pathophysiology of fever can be read here.

AIDS patients still produce PGE2 in response to pyrogens (such as compounds produced by bacteria). Therefore, AIDS patients can certainly get fevers. In fact, AIDS patients may be more likely to get fevers because they may produce more PGE2.


How do organophosphates actually work? The common explanation as to what the primary mechanism of action for organophosphates (and carbamates) is is the inhibition of the enzyme acetylcholinesterase and resulting buildup of acetylcholine at neuromuscular junctions, which ultimately results in respiratory failure. However, there is evidence that this may not be the case.

Firstly, a study reported that the nerve agent VX has been found to attack at least 132 different proteins, some of which were associated with metabolism.
Source: https://www.ncbi.nlm.nih.gov/pubmed/28267914

Also, another study showed that, even when the enzyme was protected against the action of organophosphates, nerve agents still exhibited toxicity.
Source: (http://www.rand.org/publications/MR/MR1018.5/MR1018.5.chap5.html) (Found in the Chapter 5 PDF, under "Non-AchE Effects")

Also also, another study was conducted on the matter. The test subjects were mice genetically engineered to lack acetylcholinesterase. The study found that the mice that totally lacked the enzyme not only lived (For over 34 days, no less), but were also twice as susceptible to OP poisoning as mice with the enzyme and exhibited the same symptoms.
Source:https://www.ncbi.nlm.nih.gov/pubmed/11602663

So, how do organophoshates actually act to cause the symptoms associated with OP poisoning? What proteins do they affect? There seems to be a great abundance of evidence that the effects of poisoning are not due to AchE inhibition.

Hundreds of OP's have been made since the 1930's. Phosphoric acid is used in Coca-Cola and organophosphates are esters of H3PO4, you can study ester lipid/aqueous drug chemistry. They have many different targets: http://www.scielo.br/img/revistas/jbchs/v27n5//0103-5053-jbchs-27-05-0809-gf04.jpg

OP's are lipophilic. Lipophilic substances can dissolve into cell walls which are lipid bi-layers, straight into the DNA of cells and also into the nervous system.

They can travel through cellular membrane, alveolar and dermal membranes, through dermal glands, cell walls and from one organ to another. The degree of lipophilicity of drugs cause them to either stay inside the cell membrane or go through. Prozac also being lipophilic. The body is made of a mostly aqueous phase and also a lipid phase.

Many OP's contain Sulphur and they are bioactivated through desulfurative oxidation and turned into the corresponding oxon form by the liver so the organic chemistry inside the body is very complex: dealkylation, dearylation, phosphyrylation, carboxylation, hydrolysis and they are very reactive with metabolic compounds in different phases. They can be combined with absorption facilitators to pass the skin barrier and paired with radicals which are activated by the liver.

A recommended text on the toxicity: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-50532016000500809

OP and acetylcholine are both esters.

Here's a good chemistry animation of AChE enzyme inhibitor process: https://youtu.be/fIvF1rhp1nA

And this one, about non-competetive inhibition of AChE:
https://youtu.be/_jfGKbbZStw
general AChE info:
https://www.youtube.com/watch?v=-gIqZ8IxctE

AChE inhibitors that affect lots of organs such as peripheral and central nervous systems, muscles, liver, pancreas, and brain.

They lead to a characteristic toxidrome of hypersecretion, miosis, dyspnea, respiratory insufficiency, convulsions and without an antidote, death.

They can bind to fatty elements inside the body, like the central nervous system. They can exert damage through phosphorous-alkylation of cellular macromolecules (e.g., DNA, proteins) and intense activation of pro-inflammatory pathways.


Chromonema and Chromonemata A chromonemata is composed of two chromonema. Which are again composed of chromatin fibre. Thus my question is chromonemata is composed of how many chromatin fibre ?

To my understanding, a chromonema is the filament of DNA constituting a chromosome during interphase; its equivalent during DNA replication is chromatid. The plural of chromonema is chromonemata.

The chromatin is the form in which DNA is found within the nucleus of a eukaryotic cell, that is in complex with proteins such as histones.


why don't antibiotics reduce our weight? I know that a significant weight of the human body (in Kgs) is contributed by microbiota. I also know that antibiotics can often be broad spectrum and kill all the bacterias regardless of them being good or bad for us. So why doesn't antibiotic courses reduce our weight as the microbial population must've been demolished?

First, you present as fact that antibiotics therapy (say AT) does not reduce weight. To show this fact, a study must weigh persons before AT and after. Confounders to this measurement are 1. weight differences because of bladder content (up to around 1 liter urine = 1kg), 2. weight differences because of bowel content (100g-200g), 3. Food weight (up to 2kg and more). High salt foods can cause water retention that can easily reduce your urine output one day by 500-1000ml (=g), increasing it with the same amount the other day. So your confounders can add up to +/- 4kg easily. But what you want to measure is a change of 1kg.

This means that you need to account for all these. I don't know any study that did this. Please cite such a study before presenting as fact that there is no weight loss from AT.

Assuming there is no weight loss, there are several hypotheses that can be advanced: from the fact that no antibiotic (even broadband) can kill all bacteria, the remaining bacteria in the gut may simply feed off the highly nutritional content of those bacteria cells that were killed. Note that although we know which bacteria of those that we can cultivate in a lab are susceptible to AT, we don't know at all about those that we can't grow, and that is the majority of bacteria in the gut.


Protein purification: Linear elutions or stepwise elution, using imidazole or pH gradient? I now work in a lab with a protein and a pre-made purification protocol, were they purify a His-tagged protein using linear elution which then gives a steady increase in the imidazole concentration. However, I am curious to as if you plainly have to test which elution scheme you want to use, or if there are some "rule-of thumb" on what is a more standard way to elute protein, and what in general is more common?

Also, say for instance (just as an example) that I use a protocol which in the end loses about 80% of the protein before it's pure, is one of the first things you could do is to change the elution schemes to increase the yield? Are there other very basic things one can do to optimize a purification protocol which has not been so thoroughly optimized?

So basically:

Is linear "usually" better/more common than stepwise?
Is imidazole gradient "usually" better/more common than pH gradient?

Linear is better typically. The flow rate combined with fraction size and length of time gives you better resolution for which proteins are coming off the column at what point.

Once you've narrowed down the imidazole concentration at which your protein comes off the column, you can in future just stick to concentrations around that area, though it's still advisable to use gradients either side of that concentration as your preps are never likely to be completely consistent.

How do you know you're losing 80% of your protein before achieving purity? If your protein isn't separating from other contaminants during IMAC, you can try switching to an IMAC optimised strain (I use NEB BL21(DE3) NiCo21's).

Usually you'll have to do some downstream purification in any event. Gel filtration is common. You could also consider a different column chemistry such as anion exchange.

EDIT

Typically I wouldn't expect that you would need to mess with pH very much when performing IMAC. I certainly have never had to. You are likely to need physiological pH to ensure native folding of your protein.

You can however use other additives if your protein is recalcitrant. For example, I often add 1mM DTT and 2M urea to my samples and then heat them slightly as my protein binds things easily and is extremely stable. GE Provide a whole booklet of supported additives for their columns, you may have the same thing for yours too.


I did an agar gel electrophoresis but I could not see DNA, why? After performing a PCR, I ran the products (700 bp) in an agar gel electrophoresis along with a Genedirex ladder (100 bp), but the transilluminator did not reveal them.

One common reason you can't see your DNA is because you didn't put any EtBr / GelRed into your gel. Do you have enough PCR product to run it on another agarose gel?


What does +60mm mean in MRI scans? What do the -30 to +60mm markings mean in this MRI scan image?

Short Answer

They are marking distance from a reference plane.

Longer Answer

In the images you provided, you are looking at horizontal slices through a brain. The legends are indicating that each plane has that vertical distance from a reference point (if the subject were standing); the positive numbers are dorsal to that reference and the negative numbers are ventral.

A common reference point for MRI images (to define as [0,0,0]) is the midpoint of a line through the pre-auricular point, though ultimately it is an arbitrary distinction.

If the actual reference point is important to you, you will need to verify the reference coordinate system used in the study you are looking at. It's also possible you are looking at coordinates transformed to some reference brain rather than real-life coordinates for that particular subject, but again, whether that matters or not depends on why you care. If you are doing research across subjects, you probably want to know reference coordinates; if you are doing brain surgery on a particular patient you want real-life coordinates.


What would happen if two different viruses penetrated one cell? I want to know what would happen if two different kinds of viruses took over one cell.

Would nothing happen? Would the cell create both kinds of viruses? Would it make a fusion of the two viruses?

One infected cell may produce hundreds of new viruses. By the time the disease occurs, many thousands of cells may be infected and producing new viruses. These new viruses are released from the cell, often in bunches, and are almost identical. Sometimes the host cell makes mistakes in copying the virus nucleic acid, causing some genetic variation. However, the outsides of these new viruses tend to be pretty much all the same, and they will usually infect only some more of the same kind of cells that produce them ¯ either in the same host animal or, if they can get out, other animals. Viruses produced in the respiratory tract are usually shed in droplets from the mouth and nose; viruses produced in the digestive tract are usually shed in feces but sometimes also in vomitus.

One person or animal is usually infected with only one kind of virus at a time, so the bunches of virus they produce and shed are all the same. Then, if this virus infects another person, even if two of the same kind of virus bump into a single susceptible cell, the infection will still be all of one type. However (much less likely), if viruses from two different infections get mixed up in the air or in sewage and get into a single person, it is possible that two different viruses will attach to receptors on the same cell and infect that cell together. If the two viruses are closely related, their nucleic acids may "recombine" while they are being copied. When this happens, part of the genetic information from one virus is linked to the genetic information from another virus, and the new virus that is produced is a "hybrid."

If you read about influenza that is traveling about in populations you will see that the outside of the influenza virus has an H type and an N type. For example, you might read that this year's main influenza virus is type H3N2.A reason to get a new flu vaccination each year is that the vaccine has to be made to immunize us against this type. Somewhere out in the world, a double infection as described above may happen between two different types of influenza viruses and some of the new virus may be type H5N4. Once this new type is established, a new vaccine is needed, or people won't be protected. Development and production of vaccines are expensive, and distributing them and getting people to use them is difficult. So, here is at least one situation where your question about two viruses infecting one cell may have serious public health results. Of course, influenza viruses that develop in birds, and sometimes other animals, may also be transmitted to people. Not many other kinds of viruses can jump host species like this, but it is possible that Ebola was transmitted to people from apes, perhaps from eating "bush meat." Viruses and other infectious agents that are transmitted from animals to people are said to be "zoonotic"; once this happens, the virus can usually be transmitted from person to person after that. Obviously, this too is an important public health concern.

http://www.madsci.org/posts/archives/2007-12/1198562498.Vi.r.html


Primitive streak being only present in caudal half of embryo affecting gastrulation? It is my understanding that in gastrulation epiblast cells migrate to the primitive streak where they start to form the three germ layers; does this mean that gastrulation only occurs at the caudal half of the developing embryo

It would help a little in answering your question to know more about what organisms you are interested in, or the specific source that you are referencing, with e.g. the relevant quote.

For example, the primitive streak is specific to amniotes: avians, mammals, and reptiles. In other common model organisms such as flies or amphibians gastrulation happens differently.

Another thing to keep in mind is that gastrulation is a very large and structurally distending process, so it can't be really said to happen "only on one end" of the embryo. The whole embryo is going through gastrulation. We can however talk about the placement of certain gross morphological structures on the embryo. But really each cell is affected by gastrulation, whether it's immediately obvious under a microscope or not.

Looking at the Amniote section of the wiki page on gastrulation, it appears that the main morphological changes in gastrulation do occur on the caudal side - for amniotes.

However, in Drosophila, gastrulation involves the formation of an approximately homologous structure called the ventral furrow, which is obviously on the ventral side, extending most of the anterior-posterior axis. However the invagination event does actually happen on the dorsal/caudal side.

So, it's complicated, and it depends a lot on which organism you're talking about.

Update following response

Humans are amniotes, they follow more or less the normal amniote path in gastrulation according to the wiki link above.

An important note missing in my previous answer above is that gastrulation itself defines bilateral symmetry in embryos; prior to this establishment animal-vegetal is the only obvious axis. So we are kind of defining the rostral-caudal axis according to the formation of such structures as the primitive streak, which are formed during gastrulation.

So it's a little circular to say that gastrulation happens on caudal end only; as gastrulation includes the step that establishes the rostral-caudal axis. Without gastrulation that axis just doesn't exist.

Again, gastrulation is a process that happens to the entire embryo. It doesn't just happen in one area. Structures such as the primitive streak are just obvious clues that the process is happening. It might be proper to say that the primitive streak begins forming caudally (I don't know of exceptions, though I'm not an expert), but it would not be proper to say that gastrulation is a caudal process.


What are wave frequencies in the EEG? Here is a typical EEG reading:

(source: frontalcortex.com)
I understand that each row corresponds to the signal read between two sensors on a standard 10-20 (or 10-5) distribution setup (e.g. C3-P3).
What I'm missing here is: what waves are we actually seeing here - alpha, beta, etc.? Or do EEGs not really contain wave types, and instead just show voltage differentials between sensors?

EEGs are often analyzed in the frequency domain, where signals are subjected
to spectral analysis, typically by Fast Fourier Transformation, or FFT.

What an FFT basically does is decomposing a signal in the time domain into one in the frequency domain. It does this by decomposing the input signal (any signal, including EEG) into a series of sinusoids. These sinusoids are not present in the original signal; it is a mathematical trick. If you would add all the sinusoids back together, the approximate original signal is restored.

Typically not a single frequency is analyzed, but a band of frequencies, because the frequencies within these bands are associated with similar brain states. The frequency bands that are typically reported on are shown in Table 1, including the brain state they associate with as well as sample EEGs:

Table 1. Typical analyzed EEG frequency bands. Source: Conorrus Somanno

Reference
- Nelson Garcia et al. Device and method for cognitive enhancement of a user (2014). Patent EP 2681729 A1


Sensitivity vs. Limit of Detection of rapid antigen tests I'm comparing a bunch of SARS-CoV2 rapid antigen tests:

Source
Columns 4 and 6 list the values for sensitivity and limit of detection (LOD). How come that a test with a several times lower limit of detection can have a worse sensitivity?
As an example, consider tests #2 and #4:
#2 - Sensitivity: 97.7% - Limit of detection: 2.0*10^2.4 = 502 TCID50/ml
#4 - Sensitivity: 91.4% - Limit of detection: 2.5*10^1.8 = 158 TCID50/ml
Shouldn't these values correlate, i.e. the more sensitive a test is the smaller the amount it is still able to detect?

Not necessarily. Sensitivity and specificity are decision criterion-based measures. They are not actually separable from another, they are a consequence of choosing a threshold at which to say "the test reports positive" or "the test reports negative", a consequence of this binary result. As such they are weighed against each other. You can always make a test with 100% sensitivity as long as you always report "Yes". You can always make a test with 100% specificity as long as you always report "No".
Similarly, you can define what it means to have reached a limit of detection, but this need not be the same trade-off as the one you use for sensitivity and specificity. For example, you might declare this as the point where your readout is "significantly greater"  than baseline in a collection of known positives vs known negatives. But if you set your decision threshold right at that level of detection, you may still have, let's say, only 50% specificity at that level and accept too many false-positives, so you set a different decision criteria.
They are apples and oranges, there is no reason they need to correspond.


Where does the carbon in new spring leaves of a deciduous tree come from? When a leafless deciduous tree 'comes to life' in the spring and puts forth new leaves, where does the mass for these leaves come from? The tree has no leaves to make use of photosynthesis to get the carbon it needs to grow these leaves, so where does the carbon come from: has it been stored in the root system over winter just for this purpose? And if so, has enough been stored for the tree to produce most if not all of its new leaf growth for this season, or only enough to get a few leaves out that will 'take over' the task of providing carbon fixation (making sugars) via photosynthesis to grow the remaining new leaves?

It has been suggested in the comments that the new leaf buds were grown at the end of the previous season. It would seem to me that this strategy for new growth in the spring would be fraught with all sort of dangers from 'winter kill', so these buds would not remain viable come the next spring. So, are the sugars needed for new spring growth coming from the roots or last seasons leaf buds?

While I can't provide references to actual studies, simple observation suggests that it must be stored in the roots, at least in part.  That observation is the existence of maple syrup (and other tree syrups, such as birch: https://practicalselfreliance.com/trees-species-tap-syrup/ In the spring, before leaves start to grow, sugar-rich sap rises from the roots, and can be collected by tapping the tree.


What kind of microscope for ML/biological research? I am a computer science student, focusing on machine learning applications. I have been always interested in biology but I lack any training in it. Now, I had an idea that I could introduce myself to biology more by buying a microscope, and doing some small (still serious, if possible) experiments.

Now, the problem one I am facing is what kind of microscope should I get? Preferred answer would outline what kind of research is possible to do with such and such microscope, and what is the typical price range for the system.

If there are any safety (e.g. does any of the UV leak from fluorescence microscopes?) or ethical concerns I would like to hear about them too. Thanks!

I agree with @Jeremias Brand's answer.

Pretty much you will have to forget about fluorescence microscopy... you can probably find some dusty old one on eBay in your price range, but it probably won't be any good.

However, the good news is that seen that in your comment you mention

  a) plants, b) blood, c) liquids such as wine, d) food?

transmitted light (white light) would be perfect for a start.

eBay is surely a good place for finding used objectives at a cheap price. You may end up with a good collection of objectives for less than 100€.
That is surely tempting, and it may actually be OK as a start.
However, I personally think that it is better to own a good lower magnification objective than a cheap high-magnification one, so be always be a bit wary about offers that look too good to be true (especially for new piece of equipment).

I would strongly suggest getting a binocular microscope (so with two eyepieces), rather than a monocular one. Makes life much easier.
Also, be sure to have a camera attachment. While a camera may not be strictly necessary, especially at the beginning, it's better to have an attachment so that you can add one in the future, if you feel the need of taking pictures. Although many microscopes have specialized attachments for microscope cameras, you can get away with using your own normal camera, or even your cellphone, if you position it correctly (may need some DIY depending on the situation).
This page has very detailed explanations on how to connect a camera to a microscope.

As for your samples, plants are a very good and easy thing to start observing. Onions are probably one of the best samples to start with.

You may also want to stain your samples. Probably the easiest thing to get is methylene blue, which should be a few euros for 20-30 ml. However, fountain pen ink works as well.

Whenever you use chemicals, remember to look for their safety data sheet (MSDS). Methylene blue is pretty safe to work with, provided you don't swallow it (doh...) and use gloves (standard latex gloves are OK). Be careful because it stains and can be a bit messy, which is true for pen ink as well!

Crystals are also pretty cool to watch under a microscope: take a coverslip, put on a drop of sugary or salty water and wait for it to dry!


How do our eyes detect light at different frequencies? Here is my confusion: we can see colored light of different wavelengths: form red to violet. To my understanding, these stimuli cause a confirmational change in the photoreceptors in our eyes and results in a STP that eventually leads to an "all or nothing" action potential that sends another signal, again an all or nothing action potential through the optic chiasm to the occipital lobe and we perceive the colors as we see them.

My question is *how does this signaling work? *; How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?

Asked another way, how does variation in a confirmational change at a receptor that results in "all or nothing" signaling lead to specific signals being sent such as colored vision ?

PS: I dont know jack about sensory physiology

Short answer
Action potentials generated to different colors are indeed similar throughout the nervous system and do not encode color as such. Instead, the different color- sensitive cells in the retina are connected to different neurons and these color-specific signals are kept segregated up until the higher visual cortical areas.

Background
Action potentials are indeed pretty similar throughout the nervous system. However, the color-sensitive sensory cells in the retina, called the cones, come in three flavors: red, green and blue. These colors form the RGB system just like in your LED TV and can together make all the available millions of colors. These three cones synapse ultimately onto color-specific secondary sensory neurons (Fig. 1).

Hence, R, G and B cones indeed generate identical action potentials in downstream neurons, the trick is they do so in different retinal ganglion cells, and at different firing rates depending on the intensity of light that particular cone is sensitive to. These different classes of retinal ganglion cells project onto different classes of neurons in the brainstem (lateral geniculate nucleus, or LGN) and ultimately onto different neurons in the higher cortical visual areas in the brain.

Fig. 1. Different classes of cones synapse onto different classes of secondary sensory neurons in the retina. source: Discovery Eye Foundation

The reason why we can differentiate millions of colors can be explained by the Hering model of color vision (Fig. 2). Basically, the different cones converge pairwise onto opponent color-sensitive cells. The red-green opponent system, for example, operates by weighing the amount of red and green in the incoming signal. This weighting results in an analogue system that can code millions of colors along the red-green axis (Fig. 3).

Fig. 2. Hering model of color vision. source: Webvision

Fig. 3. Red-green color axis. source: SO


How would you model the evolution of two genotypes across generations? Say you have a genotype A that produces x offspring and another genotype B that produces y offspring, where x>y.  These x offspring are of genotype A but with modest differences in fitness due to mutation and these y offspring are of genotype B but with modest differences in fitness due to mutation.  How would you model how many offspring these x offspring can themselves produce and how many offspring these y offspring can themselves produce as a function of the quantity their original parents produced?

Obviously, you could say that each descendant of genotype A produces x and each descendant of genotype B produces y, but that would unrealistically benefit genotype A, since realistically, one of B’s offspring could have a chance to be fitter than A’s by developing a favorable mutation or one of A’s offspring could have a chance to be less fit than B’s by developing an unfavorable mutation.
You could say that each descendant of genotype A and B produce (x+y)/2, but this would not be fair to genotype A, since it is fitter, so its offspring would probably be fitter than B’s offspring.

You could use the breeder’s equation and say that each of A’s offspring produce xh+m(1-h), where h is the heritability of fitness and m is the population mean, and that each of B’s offspring produce yh+m(1-h).  But this is also unfair to genotype B because all of its offspring are less fit than all of A’s offspring, since x>y.  So, what’s a way of modeling how resultant mutations might occur, such that B has a chance of producing some offspring that are fitter than A’s offspring?

So, what’s a way of modeling how resultant mutations might occur, such that B has a chance of producing some offspring that are fitter than A’s offspring?

Here's one possible solution that fits your criteria. You could have something like this (with "d" being the distance between "x" and "y", i.e. d=x-y and "n" being the n-th offspring, so it varies between 1 and x for A and 1 and y for B) :

A: n -> x + r(n), where r(n) is a random number between x-d and x+d
B: n -> y + r(n), where r(n) is a random number between y-d and y+d

(I write r(n) not because r is a function n, but because a different number is drawn for each n. I also didn't specify r's distribution, that would also need to be decided when making an actual model)

This is your situation where some offspring of B have a chance of being fitter than offspring of A, and the least-fit offspring of B can even be fitter than the fittest offspring of A. I think it fits your criteria and thus answers your question. The sum of the grandoffspring is basically the basic x or y squared (that you would get if each offspring had the same fitness as their parent) + the sum of all the "r"s.


Is abiogenesis possible today? Life on earth started about 3.5 billion years ago. I would assume abiogenesis happened because the conditions were right.

Would the current earth conditions allow for new abiogenesis and completely independent (in terms of phylogeny, not ecology)?

I will argue that yes, it is POSSIBLE. It is possible on earth like on other planets. Given enough time, matter, and energy, "something" that resembles life will emerge. The problem I see, however, is that life has already conquered our planet, so any "new living thing" will have to compete with other long-time adapted living thing, in practice, no chance of survival. The right conditions you refer to are the ones that allowed "life as we know it" to emerge. Given other conditions (other chemicals, other energy forms, etc), something completely different will form.

Of course, without final proves, this is still speculation.

Some speculative links:

http://speculativeevolution.wikia.com/wiki/Alternative_biochemistry

http://www.dailygalaxy.com/my_weblog/2015/05/alien-life-habitats-nasa-brainstorms-alternatives-to-water.html

http://www.nature.com/news/2009/090513/full/news.2009.471.html


Why don't sodium Voltage Gated Channels open during Repolarization? During Depolarization the Sodium VGC open when they receive the Threshold Stimulus. But when Repolarization occurs there comes a point when the cell interior has exactly the the same potential that it had during Depolarization i.e.,60mV but the Sodium VGC remain closed. Am I getting something wrong? If no, please explain.

Voltage-gated sodium channels have three basic states that represent different conformations of the protein: closed, open, and inactivated.
When a voltage-gated sodium channel is open at depolarized voltage, there is space for part of the channel to shift into a position that blocks the pore. When this happens, it gets stuck blocking the flow of sodium, and it requires a negative membrane potential to remove the block. We call this the "inactivated" state, and this model is called the ball and chain model of sodium channel inactivation.
The inactivation gating process is also referred to as the "h-gate", because h is the variable representing the gating in the classic Hodgkin-Huxley model.
Wikipedia currently has a useful table on the sodium channel page showing the different states that a sodium channel goes through during different phases of an action potential.


Alder Tree Root Nodule Origins? I recently found out that alder trees have root nodules which contain nitrogen-fixing bacteria and that alders are primary colonizers in primary succession. That leads me to this question: since there are really no fungi in the soil and since the alder is a colonizing species, where does the fungi come from? Or is my assumption that there are no fungi in the soil incorrect?

Any soil microbiology textbook will tell you that there are a great number of fungi in most soils. I believe there are 12 or 13 species of non-legumes capable of fixing atmospheric nitrogen. Podocarpus is one of them. Look at the roots of podocarpus and you will see nodules all along the roots.


Evolution home experiment? If I were to take bakers yeast and put it in medium of minimal sugar(whatever quantity that would be) and rice(for a source of starch), could the yeast have a "evolutionary leap" and adapt to use the starch in its environment? I remember reading something similar in a report of E.coli bacteria and citrate adaption, under the heading:
 Catching evolution red-handed.

The passages in question are so:

  "Every night, the bacteria run out of the sugar glucose and go
  dormant. The following day around noon, a researcher plunges a pipette
  in and sucks up 1% of the culture to inoculate a fresh flask. Those
  faster at gobbling up glucose will send more of their descendants to
  the following day's pipette and, after a few weeks, descendants of the
  fastest one will be the only ones transferred as the mutation 'sweeps'
  to fixation."

Under the heading: The rise of Escherichia erlenmeyeri, (bold emphasis mine).

  "One morning, at the turn of generation 33,127 according to the lab's
  log book, a massive increase in turbidity was recorded on the vial
  labelled Ara-3. The sugar-starved bacteria had suddenly 'discovered' a
  vast new source of carbon by importing citrate, a pH buffer that had
  been in the growth media all along, and it sent the population size
  through the roof. "

So if I understand this correctly, there is evolution going on through the differential reproductive success of the bacteria, via their fitness which is affected by the glucose levels?

This "pressure" caused a type of "hopeful monster" in the form of Escherichia erlenmeyeri, the bacteria that could metabolize citrate, in which it didnt have the means to do so before.

So then could I replicate this concept with baker's yeast and starch metabolism and hope for similar results hypothetically? Or am I misunderstanding this?

Keep in mind that the citrate utilizing strain appeared after over a decade. Also, Escherichia coli could always metabolize citrate, but the citrate transporter that brings it into the cell is only expressed under anaerobic conditions [1]. The strain that evolved to import citrate under aerobic conditions had a duplication of the transporter gene which put it under the control of a different promoter that drives expression under aerobic conditions [2]. Baker's yeast doesn't have amylase or debranching enzyme genes [3], so a similar evolutionary mechanism cannot occur. Developing such enzymes de novo doesn't seem trivial, but perhaps the enzymes involved in glycogen metabolism can be repurposed. The only way to know is to try.

References:

Blount et al., 2008
Blount et al., 2012
Ostergaard et al., 2000


Does the anterior primary ramus of T6 innvervate the Rectus abdominis? Anatomy and Human Movement Structure and Function writes in the section about Rectus abdominis:

  Nerve supply
  By the anterior primary rami of the lower six or seven thoracic
  nerves (T6/7 to T12).

What does "or" mean? Does it means that in some humans this happens and in some it doesn't?

Because muscle (mesoderm) and peripheral nerves (ectoderm) develop from different embryonic germ layers, the pattern of innervation is somewhat variable. The muscles are condensing from mesenchymal tissues more or less in place, and nerves are growing out into the muscle masses to innervate them. Because of this, the specific spinal segments that innervate muscles can vary somewhat. This is particularly true in the brachial and lumbosacral plexuses. In the brachial plexus for example:

Grayed out text for C5 in the median nerve and C7 in the ulnar nerve suggest variable contributions from those segments.

In this case, rectus abdominis is "always" innervated by at least T7 to T12. But sometimes T6 as well in some, but not all, people.


Why does freshly cut grass smell like a watermelon? I found that, when I smell watermelon aroma outdoors, someone nearby has mowed  the grass. Is there an underlying basis?

cis-3-hexenal is probably the main reason.  It is one of the main chemicals in fresh-cut grass smell (lots of references besides wiki if you google it).  This fairly comprehensive paper on watermelon odorants also says that they find a lot of cis-3-hexenal in fresh cut watermelon.  See tables 3.1, 3.2 and 3.3.


Biological meaning of read length I have some FASTQ files in two datasets which are sequences from 16Srna region. The first dataset is amplicons form V4 region and the second is V3-V4 region.

However all the reads are 250 nucleotides long, whereas one region is strictly included in the other. So what is the biological meaning of the length?

I'm expecting reads to have the same length as the sequenced/amplified region. I don't know the size of the regions but one is obviously longer than the other.

Thank you
(I thought it was better to ask here rather than on bioinformatics.stackexchange.com)

The read length has absolutely nothing to do with what you are sequencing. It is a characteristic of the sequencing technology you use. NGS sequencing techniques typically produce this sort of short read you're seeing. The read length does not change because you are sequencing a longer molecule. You would still get ~250nt reads even if you were sequencing an entire genome. Your reads are something like this (image source):

So the vast majority of your 250nt are overlapping and cover slightly different parts of your target sequence. This is one of the reasons why NGS analysis is not trivial. The first step in any NGS analysis is to assemble your reads into a bam file that covers your target region. If you need help on doing that, come on over to http://bioinformatics.stackexchange.com.


How does a fungus protect itself from digestion by other fungi? If a fungus releases its digestive enzymes outside its body, how does it protect itself from digestion? How do fungi growing nearby protect themselves?

I have tried searching this on google but couldn't get an answer.

In general fungal cell walls are resistant to whatever enzymes or compounds they are excreting to break material down for consumption. Conceptually, it is a little like your stomach lining being resistant to stomach acid. For a more detailed answer you may have to head over to your local university and find a Mycologist.

There is ongoing research on how fungi actually "eat." You can look up fungal endocytosis if you wish to research it more. There may be other mechanisms as Shigeta mentions.


What are samples of "Outlaw Genes" I read this in a paper

  Keller and Ross describe their greenbeard gene as an ‘outlaw’.
  Admittedly, the comment is only made in passing, but are they correct?
  In this context an outlaw is usually defined as a gene whose action
  favours itself, but opposes the reproductive interests of the
  individual organism. Where there are outlaws, natural selection at
  different loci is pulling the organism in different directions.
  Theoretically speaking, green-beard genes...

Yes: http://www.sciencedirect.com/science/article/pii/S0140175083901562

Basically loving your children is outlaw because it makes you sacrifice resources for your children. However, if your interest is defined as maximizing the number of children, then it's just your stuff working properly. Outlaw genes will be something that makes you die for a cause or stuff like that I suppose.

The t locus, which is described in detail in this book by Robert Trivers, is the classic 'outlaw' or 'selfish' gene.

If a heterozygous (single) t allele is present in the paternal mouse, the t locus is evident in sperm 95% of the time.  Talk about "Breakin' the Law"!  As a locus whose main phenotype seems to be for mitotic cheating, t seems to convey little or no benefit to the other genes by way of helping the host survive.  t/t homozygotes are sterile.  Nice summary here.


Is there any research paper which identifies left and right brained behavior? There are many web puzzle to identify, but does it really have any scientific proof?

something like - http://braintest.sommer-sommer.com/en/

any logic behind it?

In general I'd say "left and right brained behaviour" is total nonsense. I guess the origin of this kind of claim is a bad press release or something.

Let's start with something simple. Say hearing. When you hear a sound to your left ear, it is projected strongly to the contra-lateral side (right hemisphere), and weakly to the ipsi-lateral (left hemisphere) of your brain. So the brain response to a sound presented to the left ear is lateralized. Typically, this means that the other hemisphere is "more" responsible for processing the input. Similar thing happens for the other senses too.

So what is interesting about lateralized brain responses? Well, it would be very interesting to know for example are memories lateralized. It would tell something about the system: is it a kind of distributed system, where parts of a memory are scattered here and there, according to some logic, or is a single memory stored on a small area (and maybe only on the other side of the brain), etc. The distributed hypothesis seems more plausible according to recent research.

Let's talk about handedness next. Are you right handed? Or left handed? Or ... something between? Actually, even something like handedness is not a binary thing. It is more like a value on a range from 0 ("very left handed") to 100 ("very right handed"). This is taken into account in decent research, where ~1 hr per participant is used to assess that value (if it is relevant to the study).

So we have now talked about lateralization. How about the "left and right brained behaviour" then? In the URL you have provided it is implied that certain behavioural attributes are somehow related to lateralization. Lateralization of what? All the attributes, e.g. "being rational" depend on so many things: seeing, hearing, thinking, retrieving memories, ... that saying such a thing is not plausible.

Anyway, many brain processes are lateralized. That is the word to look up for for more information. But a thing like "behaviour" is too complex to be put to one hemisphere.

Reference: Accumulated wisdom from being a research assistant in a neuroscience project. (so you should trust pubmed.org more than me).


How valid are GO (Gene Ontology) terms? I'm looking for papers quantifying the validity of ontologies such as GO.

I'm relatively new to using annotation terms, and I often hear things like "annotation is messy" and "GO is good but it's not perfect." So I'd like to find papers that give numbers for just how messy.

I'm looking for answers from any experts that have a sense of the "quality" of GO terms (however you want to quantify it). For example, what fraction of terms are just wrong? The more computational parts of me want to sum up GO (or other ontologies) with a few descriptive validation statistics. e.g. "GO terms have an 80% precision and an R^2 of 0.6."

I'd like to see a few more examples similar to this paper that shows that a good fraction of GO ontology can be rebuilt from the ground up from independent data. That seems like one way to validate GO quality. They include this line about lack of GO validation in general literature: "... problems [with consistency and bias] are difficult to assess due to the lack of any definitive gold standard for the rigorous validation of GO."

There are quite a lot of articles(1,2, etc.) which have investigated this, I think this article did a great job to give a visual representation of the specificity, reliability and coverage:

also this article noticed the following:

  Compared to electronic annotations, it is not surprising that curated
  annotations have a considerably lower average coverage (Fig. 8,
  vertical lines). Indeed, the main appeal of electronic annotations is
  precisely that they scale efficiently to large quantities of data. But
  in terms of reliability, and contrary to current beliefs, curated
  annotations that use evidence other than experiments from primary
  literature do not fare better than electronic annotations (Fig. 8,
  horizontal lines, Fig. S9 in Text S1). In fact, we observed a higher reliability for electronic annotations than for curated annotations (0.52 vs. 0.33). the figure blow is figure 8 from the article

I don't know if you are just curious in the reliabilty of GO or if you are searching for an other kind of hierarchical annotation method, but e.g. for enzymes there are also EC numbers.  I can continue citing the article but I would suggest to read the article from which I used the figures ( Quality of Computationally Inferred Gene Ontology Annotations). Secondly this article is more recent and  something similair was done here. Among other things they also compared the computional annotation from 2008 with manual annotation in 2010 for the same set of GO terms:

So I would also recommend to read The what, where, how and why of gene ontology—a primer for bioinformaticians. This article and the previous mentioned article will give you a good insight in GO terms.


What are the lifetimes of cellular components on organelle or molecular level? I was thinking that even though I know how generally the cell works, I don't really have a feeling of how volatile it is.
I want to know what is the lifetime/turnover rate of different constituents of the cell.

On the molecular level what are the lifetimes for various proteins, for ribosome, lipids, carbohydrates, DNA and RNA. What about aminoacids, nucleotides?

On the organelle level what are the lifetimes of the mitochondria, golgi apparatus. Does nucleus or ER ever change if not during meiosis.

I understand that the lifetime depends on the context. For example, for DNA, cells that replicate, half-life is about one replication as a whole new strand is generated. In neurons, that don't replicate for decades it's not the case. But the DNA can't just sit there. It is constantly unraveled, transcribed, damaged and repaired. So it has a different time constant.

I am still very interested to know any specific numbers.

Your question has several parts to it so I will attempt to address them one-by-one.

In terms of protein stability and turnover, this is a nice paper describing how human cell (HeLa) line, although this is a cancerous cell line, is used to measure the turnover of proteins (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316722/?report=classic). They have used labelled amino acid technique and mass spectrometry (SILAC) to make measurements of protein turnover. It is concluded that on average the turnover is 20 hours, which is correct in my experience when doing gene knockdowns in Drosophila (S2) cells using RNAis as we incubate the RNAi with cells for 72 hours to ensure most proteins that we targeting are degraded and we can see the desired effects in cells.

Now getting to your questions regarding organelle turnover, you have to consider that cellular organells are very precious to the cells as most of them consume a lot of energy to build hence they are maintained unless they suffer critical damage, and they would become detrimental to the cellular integrity. In that case organells such as mitochondria undergo a specific type of degradation called mitophagy, which is a subtype of autophagy. Now I'm sure there are specific average times for the so called turn-over of cellular organelle under "normal" conditions but thats a slightly misleading view since the turnover can be tipped through reactive oxygen species (ROS) or ageing leading to less efficient cellular maintenance and buildup of toxic aggregated proteins or ROS.

Now just to clarify the use of the word half-life in you last paragraph, half-life normally refers to the time it takes for half the molecules in a given system to degrade (or to be more correct Half-life is the amount of time required for a quantity to fall to half its value as measured at the beginning of the time period) so I do not agree with your use of the word half-life in the last paragraph of above question although human DNA does have a replication limit (Hayflick limit) of roughly 40-60 due to telomer shortening and afterwards the cells (due to the DNA) that no longer replicates will enter senescence and eventually die.

Now getting to non-replicating, highly differentiated cells such as neurons, it still remains a mystery as to how neuronal DNA remains so highly stable (although DNA is a highly stable molecule (compared to RNA) and its further stabilised through histones), while undergoing many dynamic processes such as transcription (since if anything goes wrong the cells cannot be replaced at least in CNS) and how axons of some neurone that can reach over a meter in length are maintained so well for decades. There is a lively argument amongst the scientific community about this, which you can find out about if you simply search for axonal maintenance in a search engine.

Hope this answers some of your questions.


How usable is the Human Metabolic Model to predict biomass? In order to use the Human Metabolic Model for Flux Balance Analysis of specific cancer cell lines, we would like to know what sort of flux values have been determined for the Human Metabolic Model.

Basically, how usable is it to predict biomass production in humans (to some extent)?  If it is not very good for this, what other options are there?

Thanks very much!

Firstly, it is important to remember that Flux Balance Analysis computes theoretical performance limits, i.e, the theoretically optimal behaviour of the system with respect to the objective and constraints. When growing bacterial cells growing in culture evolve under selection pressure for biomass production, the theoretical limit on biomass production may indeed be approached, see for example Ibarra et al: Nature. 2002 Nov 14;420(6912):186-9. (http://www.ncbi.nlm.nih.gov/pubmed/12432395) and Fong & Palsson: Nat Genet. 2004 Oct;36(10):1056-8 (http://www.ncbi.nlm.nih.gov/pubmed/15448692).

How closely other systems can be expected to approach optimality should be considered on a case-by-case basis, and the constraints should be realistic. In humans, you would for example expect that the physiology of the persons (blood glucose levels, etc.) would greatly affect the growth rate of any cancer cells, in addition to the structure of the tumour (especially blood supply). For cells growing freely in culture, one might expect FBA to be easier to apply.

For HeLa cells growing in culture, the results of at least one study suggests agreement between experimental and FBA-predicted growth rates: See Resendis-Antonio et al: Modeling core metabolism in cancer cells: surveying the topology underlying the Warburg effect. PLoS ONE, 5 (2010), pp. 1–11 (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012383)

Whether the precise biomass production rate is predicted or not may actually not be so important, and there has been considerable interest in applying FBA to studying various aspects of cancer metabolism. Here are some papers that may be of interest:

Ashwini Kumar Sharmaa, Rainer König. Metabolic network modeling approaches for investigating the “hungry cancer”. Seminars in Cancer Biology 23:4,2013, 227–234 (http://www.sciencedirect.com/science/article/pii/S1044579X13000436) (Review)

Shlomi et al.: Genome-Scale Metabolic Modeling Elucidates the Role of Proliferative Adaptation in Causing the Warburg Effect. PLoS Coputational Biology 2011 (http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1002018).

Lewis & Abdel-Haleem. The evolution of genome-scale models of cancer metabolism. Front. Physiol., September 2013 (http://www.frontiersin.org/Journal/10.3389/fphys.2013.00237/full). (Review)

And a relevant Master's thesis: Computational Metabolic Modeling of
Cellular Growth: From Bacteria to Cancer. http://www.cs.tau.ac.il/thesis/thesis/Benyamini.pdf


How do you see the stage of the second meiotic arrest in oogenesis in the given video? My old question raised this new question. After reading this page I can say now that metaphase is the stage in which the second meiotic arrest occurs within oogenesis:

  The oocyte is arrested again in the metaphase of the second meiotic
  division.

It is difficult to visualize the thing in my head. I could not find a video of specifically for oogenesis but probably the general model for meiosis holds true. The problem I am having is that I cannot see the arresting steps in this general meiosis video.

How do you see the second meiotic arrest of oogenesis in the above video?

I cannot even see clearly the first meiotic arrest. I only know that it is in prophase for the first and metaphase for the second.

I seem to understand the thing now.

The video is utterly simplified for animal cell meiosis I and II.
In oogenesis, you get after every anaphase one cell with very little cytoplasm, polar body, and another cell with much cytoplasm. In the video, the amount of cytoplasm is equal so the thing is idealized.

The video is better to explain male gametogenesis: spermatogenesis, since the amount of cytoplasm does not differ after each anaphase.

The video is too going too fast to teach you oogenesis, since in reality the things are arrested rather long time. The second meiotic arrest in oogenesis can lasts 12 - 50 years starting after puberty. The rupturing secondary oocytes lasts then again less in the second meiotic arrest of oogenesis, since they start to develop into ovum after the monthly release.


Is a double-yolk egg capable of producing two viable chicks? As per title: If fertilized, is a double-yolk egg capable of producing two viable chicks (that could survive to adulthood)?

Have there been any reported cases of such (presumably) fraternal twins?

According to the discussion here they normally fail to hatch because the chicks cannot get enough leverage to break the shell.

Here is a video of an assisted hatching. It is claimed that these two survived.


Blood urea nitrogen and usage of proteins? I have been reading some books and am getting slightly confused. Here is roughly what I have read.

  The greater the blood urea nitrogen the greater the usage of proteins (since blood urea nitrogen is created via the metabolism of proteins).

and

  A positive nitrogen balance (where nitrogen balance $=$ N intake $-$ N loss) indicates a greater usage of proteins.

To me these two seem to be contradictory, if you have greater blood urea nitrogen then surly you will have more nitrogen lost meaning the nitrogen balance would be more negative. So do these two statements contradict and either way please can you explain.

The quotes in the question provide incomplete information at best.

Let's focus on the nitrogen (N) that comes from protein, ignoring for now how metabolism differs among amino acids. We'll assume for simplicity that liver function is OK so that the urea N production rate is a reasonable measure of protein N degradation rate (say in units like moles of N per hour).

First, consider simple conservation of mass:

  Intake = Loss + Net Storage

If you think about this in terms of protein N from the perspective of the whole body, you start to see the limitations in those quotes.

First, loss from the whole body of metabolized protein N in the form of urea N mostly occurs via the urine. Impaired kidney function may lead to less urea being excreted than is being formed. You will then have "Net Storage" of urea N in the blood and body fluids, so BUN can rise even if metabolism of protein is unchanged. In fact, BUN tests can be used with other tests to provide information about kidney function. Thus BUN levels don't necessarily tell you much about the urea N production rate or protein degradation rate.

Second, you have to consider that one "use" of proteins can be "Net Storage" to build muscle mass. That type of "use" won't show up in increased urea N production. Alternatively, body protein in muscle can be broken down to be "used" for metabolism/catabolism during an overnight fast, possibly leading to increased urea N production rate depending on how the mix of protein, fat, and carbohydrate catabolism has changed. Furthermore, the effects on BUN levels will depend on kidney function.

Both storage and degradation/catabolism are important "uses" of protein N, but they have different implications for production of urea N, and BUN levels don't necessarily represent the urea production rate.


Reformulation of Hamilton's rule Who (and in which article) was the first to reformulate Hamilton's rule using the letters $B$ and $C$?. See below comments on this reformulation.

Hamilton, in his 1964's article gave a mathematical formulation to explain the direction of social traits. Below is its formulation. Note: Hamilton used quite a complicated formulation, I hope I am not misunderstanding its meaning. Please let me know if it is the case.

$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$ where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$. $w(x,y,z)$ is the fitness function of a focal individual expressing trait $x$ and interacting with an individual draw from a subpopulation expressing trait $y$ (expected value of the probability distribution of trait expression of individuals in the subpopulation) in a population expressing trait $z$ (expected value again).

Most often this formula is expressed in the following form:

$$RB>C$$

$B$ and $C$ are called cost and benefit of the social trait. I believe that $B$ and $C$ are often not understood as a consequence of a change of the social trait but rather as a cost and benefit of carrying the social trait (compare to not carrying it).

Tracing it backwards this was the earliest reference I found via google scholar, it's from 1988 and uses the $r B C$ notation in the format we are used to.

  Hamilton's rule states that for a social
  action to be favored under natural selection, rb - c > 0, where c is the cost to the
  actor in terms of the effect on (usually a reduction in) his expected number of
  future offspring, bis the benefit to the recipient in terms of the effect on (usually
  an increase in) his expected number of future offspring, and r is the relatedness of
  the actor to the recipient

However, I've traced back a bit further by going through the references and found this Michod paper from 1978 where they defined terms $b_i$ and $c_i$ as the

  "fitness effect of genotype $i$'s behaviour on others"

and,

  "fitness effect of genotype $i$'s behaviour on self"

respectively, which was the first such notation I could find which could be interpreted as $b$ = benefit via the increased fitness of others and $c$ as a cost to self.

As far as I can tell this leaves a 14 year gap between Hamilton's long version and the beginnings of the current notation by Michod in 1978, with the first "rB - c > 0" type of notation appearing in 1988. Obviously my search is not exhaustive - many papers from this period will be hard to find and text search (e.g. using "rB" as a search term) - but it's a good start. If I find an older reference any time I will update.


Cannot identify this insect Can anyone please help identify this insect. It seems to be some sort of caterpillar but I'm stumped.

Location is in Suffolk, United Kingdom
Length is around 1cm, width is perhaps 4 or 5mm.

Image opens a video clip on YouTube.

That appears to a "bag worm", which is as you surmised a caterpillar.

This suggest that it is from the family Psychidae, but I won't even try to guess at the species.  However, if you see any adults you may be able to identify them using this website.

An example image of an North American species:


Coalescent Theory - Probability for $k$ alleles that of one coalescence event occured $t+1$ generations ago From this textbook
Under the wright-Fisher model of genetic drift and under the assumption that all alleles are neutral, the probability that $k$ alleles had $k$ distinct parent alleles the previous generation is
$$Pr(k) = \prod_{i=1}^{k-1}1-\frac{i}{2N} ≈ 1-\frac{{k \choose 2}}{2N} $$
The chance of two alleles not coalescing for $t$ generations is $\left(1-\frac{1}{2N}\right)^t$ , and the chance that they coalesce in the next generation is $\frac{1}{2N}$. Therefore, the probability that 2 alleles had a common ancestor t+1 generations ago is
$$\frac{1}{2N}\left(  1-\frac{1}{2N} \right)^t ≈ \frac{1}{2N}e^{\frac{-t}{2N}}$$
I understand up to this point!
The probability that the $k$ alleles do not coalesce for $t$ generations, and then one pair coalesce to give $k-1$ alleles at $t+1$ generations ago is as follows:
$$Pr(k)^t \left[ 1-Pr(k) \right] ≈ \frac{{k \choose 2}}{2N}exp\left[ -\frac{{k \choose 2}}{2N}t \right] $$
Can you help me to understand this last part? (both the left and right part of the equation)

Is this the exact text from the book? The left side seems to represent the probability for

  "No coalescence in $k$ lines in $t$ generations (i.e. the $Pr(k)^t$ term), and at least one coalescence among those lines in generation $t+1$ (the $1-Pr(k)$ term)"

which is the same event as

  "First coalescence event in $k$ lines is exactly in generation $t+1$".

The right hand side is derived analogous to the second equation, with $1-\frac{1}{2N}$ ("no coalescence in two lines") replaced by $1-\frac{k\choose2}{2N}$ (approximation for "no coalescence in $k$ lines):

$$
\begin{align}
Pr(k)^t \left[ 1-Pr(k) \right] &≈ \left( 1-\frac{k\choose2}{2N} \right)^t \left [1 - 1 +  \frac{k\choose2}{2N} \right] \\
&\approx \exp\left( - \frac{k\choose2}{2N} t \right) \frac{k\choose2}{2N}
\end{align}
$$

were is first approximation is due to your first calculation. The second one seems to use a first order Tailor approximation of $\exp(x)$:

$$
\exp(-xt) = exp(-x)^t \approx (1-x)^t
$$


Why oxLDL accumulate to form foam cells? In atherosclerosis, why macrophage store all the cholesterol from oxLDL inside, and turns to foam cell, and not just degrade it and going back to blood? (there are some amount that leave the plaque, but much more stay (J Clin Invest. 2011 May;121(5):2025-36. doi: 10.1172/JCI43802. Epub 2011 Apr 18.))

Reading a lot about atherosclerosis, but no explanation about why macrophages stay there and form a plaque, instead leave or at least break the cholesterol.

In short, rate of expression of intracellular cholesterol removal proteins like ABCA1 in macrophages and cytokine waterfall molecules in T-lymphocytes beside other anti-inflammatory cytokines has an important role in AS and why oxLDLs accumulate in intima.

When there is high level of oxLDL, rate of removal mechanism must increase to take extra cholesterol out of macrophage and after that to the liver.
And it(increasing the rate of reverse mechanism) could be done by inhibitors or regulators(when natural way could not effort enough excretion). => drugs like TONSHINONE

There is huge amount of information about how regulation of adhesion molecules, costimulatory molecules, antigen presenting molecules and anti-inflammatory or inflammatory molecules could have effect on oxLDL accumulation in macrophages and T-lymphocytes which cause damage induced by hydrogen proxide.

So accumulation of oxLDL molecules in Macrophages has genetic reason and why human being evolved in this way is a question for geneticists but how this happens could be explained by tracing adhesion and signaling molecules.

This is one of the texts about oxLDL accumulation and AS.

Macrophages take in, a large number of oxidized low density lipoproteins (oxLDL) under the intima and then become foam cells, which is one of the early signs of atherosclerotic lesions.

ATP-binding cassette transporter A1 (ABCA1) is an integral membrane protein that transports lipid from the cells to the liver with subsequent lipid excretion by bile at last. This reversal transport inhibits the formation of lipid.

This text shows how regulating cytokine waterfall and pro-inflammatory cytokines could have impact on creation or removal of foam cells.

They experimented that Tanshinone IIA (a molecule extracted from root of Salvia miltiorrhiza) significantly increased expression of ABCA1 in macrophage-derived foam cells, raised the outflow of intracellular cholesterol, and inhibited the formation of oxLDL induced foam cells.

Furthermore, the liver X receptor (LXR) and peroxisome proliferator activated receptor (PPAR) which are members of nuclear receptor superfamily can increase expression of ABCA1 through coupling path. Tan IIA inhibited the formation of foam cells. The mechanism might be that Tan IIA increased expression of PPARa, LXRa, and ABCA1, facilitated reversal cholesterol transport, and ultimately promoted cholesterol efflux.

T-lymphocytes in plaques are mostly CD4+ T-lymphocytes which belong to Th1 subtype. Most of CD4+ T-lymphocytes are active and can induce “cytokine waterfall” as well as secrete proinflammatory cytokines interferon-gamma (IFN-y), IL-12, and other cytokines, eventually leading to inflammation. Experiments showed that Tanshinone significantly inhibited production of Th1-derived IL-12 and IFN-y in a dose-dependent manner. T-lymphocytes play a role in the formation of AS, mainly because of proinflammatory cytokines secreted by T helper type (Th) 1 or Th2. Therefore, Tanshinone can inhibit the formation of AS and stabilize plaques via reducing the secretion of Th1 or Th2. Moreover, T-lymphocytes are activated to express CD40L, and the expression of tissue factor and matrix metalloproteinases (MMPs) is then promoted by interaction between CD40L and CD40.
TanIIA could improve the activity of superoxide dismutase (SOD), decrease the level of malondialdehyde (MDA), and reduce both the expression of CD40 and the activity of MMP-2.

So normally macrophages could excrete cholesterols but problem occurs when your diet contains high level of cholesterol and oxLDL goes high in your blood.

Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 267976, 6 pages
http://dx.doi.org/10.1155/2014/267976


Mitosis and Colchicine I'm preparing for an Olympiad and while I was going through some of the old papers I found a question. I googled it but a lot of people have different answers to it. Please help.

A student treats some onion root tips with colchicine that is responsible for arresting cell division at the metaphase stage (by dissolving spindle fibres) and further prepared a slide of the root tip staining with acetoorcein (stains chromatin) and observed under high power of compound microscope. He is well aware of the cell cycle given alongside.

Question: Which of the following is not true about his observation?
a) Most cells are in Interphase
b) Most cells are in the metaphase
c) No cells are in anaphase or telophase
d) Chromosomes could be observed better than a slide prepared without colchicine
treatment.

According to me the answer should be (c) because if colchicine arrests cell division at metaphase, anaphase and telephase being the subsequent processes would not happen. But a lot of people are saying it should be (a) or (d). I'm stumped, any help would be appreciated.

The question is asking which is NOT true.  You are correct that C is true - very few cells should be found in anaphase or telophase.

D is also true.  When spindle fibres are dissolved, chromosomes/chromatin would not be tightly bundled or packed in the cell and it would be easier to see them with an acetoorcein stain.

A and B are trick answers.  In a regular tissue, most cells are in interphase at any given time.  Interphase is the regular functioning period for the cell.

However, the question is referring to onion root tips which are primarily comprised of actively dividing cells (meristem tissue). The colchicine would affect most cells and most cells would be found arrested in the metaphase.  http://w3.marietta.edu/~biol/introlab/Onion%20root%20mitosis.pdf

Therefore for onion root tips treated with colchicine, most cells are not found in interphase.  A is the correct answer.


How do you consider an organism to be a new species? How do you consider an organism to be a new species? Can a new parthenogenetic organism be considered as a new species?

There are various hypotheses and concepts proposed to define a species, but no definitive answer. Mostly a combination of these concepts are used because each hypothesis has exceptions. Classification is constantly being debated, reevaluated, and changed as we learn more. Some of the most notable definitions are:

The is the biological species concept in which Ernst Mayr defines a species as actually or potentially interbreeding populations that are reproductive isolated from other groups and produce viable, fertile offspring. But this doesn't by definition exclude hybridization between species, but often hybridization does not produce viable or fertile offspring. (This definition doesn't work with parthenogenesis. Also, hybridization is accepted as a mechanism that can lead to speciation, most notably seen in plants, where the hybrid offspring can interbreed with other hybrids, but are not able to reproduce with their parental species.)

There is also the morphological species concept which uses morphology and body features to classify organisms, which is more useful when there is little population information available, such as for fossils. But this can result in one sexually dimorphic species being classified as two. (The eclectus parrot was initially classified as two species because the males are green, while females are red.)

In the phylogenetic species concept Willi Hennig defines a species as the smallest group of individuals sharing one common ancestor and a set of fixed heritable differences to make up one phylogenetic branch. Genomics is often used to define this. There is debate that this method creates "taxonomic inflation" and creates more species than necessary because different populations may be able to interbreed, are not reproductively isolated, but are genetically differentiated enough due to local adaptation.

The ecological species concept defines species by their environmental niche--organisms that look, act, and share similar life history patterns. This definition includes parthenogenic species as a separate species from its non-parthenogenic relatives.

(It becomes much more complicated when trying to classify prokaryotes and viruses because mutation occurs at a much higher rate and many of the above definitions cannot be effective applied.)

Ultimately, yes, there are various accepted species that reproduce only by parthenogenesis (like the mentioned New Mexico whiptail lizard), and parthenogenesis can be a defining factor which separates them from a sexually reproducing counterpart species that is similar in morphology, niche, and evolutionary history.

Information comes from courses and textbooks from my Ecology & Evolutionary Biology major within the last year.


How do rodenticides with delayed effect work? Most modern rodenticides are claimed to cause death no earlier than several days after ingestion.

That's quite strange - once a chemical was ingested it will be absorbed in the digestive system and enter the blood stream and rapidly spread around the body (something like within ten hours - that's what most human medications claim in pharmacokinetics sections of their manuals). I'm pretty sure a rodent is very similar to a human in terms of digestive system functioning.

Then how do rodenticides not kill the rodent earlier than in several days after ingestion?

These poisons prevent recirculation of vitamin K and thus formation of prothrombin which is essential for coagulation of blood and are required for maintaining the integrity of capillaries. The depletion of vitamin K is slow and in a couple of days internal hemorrhage occurs extensively and the animal dies of shock. Early recognition of poisoning in humans and other animals can easily be treated with administration of vitamin K.
http://en.m.wikipedia.org/wiki/Rodenticide


Why is the  microbial ecosystem of the gut so susceptible to disruption by pathogens? From all accounts, it seems as if the Escherichia, Enterobacter, etc. that live and thrive in the human gut are pretty well entrenched.  I know that these microbial populations are often analyzed as an ecosystem.

What surprises me is that it seems like minor food poisoning can throw the whole ecosystem off.  I know superficially that Clostridium are contenders in the fight because they remain viable after traveling through the acid of the stomach, but why are these populations so sensitive to other invading bacteria?

There are two types of food poisoning:

Alimentary intoxication

This is the case when you consume food which is contaminated with some toxins, and those are responsible for development of the poisoning symptoms. The source organisms of these toxins might not be present anymore (killed by heating during cooking, for example). In this case there is no massive invasion of any foreign organisms into the gut.

Alimentary toxico-infection

This happens if you eat the food contaminated with microorganisms, and these start to massively proliferate in your alimentary system causing the symptoms of poisoning. The massive intake of the bacteria (even 2-3 spoons of contaminated food might contain millions of bacteria, like Staphilococcus in contaminated diary products). In this case the balance of gut microflora is dramatically changed due to introduction of a considerable amount of foreign microorganisms.

So, even the poisoning seems to be "minor" (e.g., its symptoms are not so dramatic), there could be different amounts of bacteria invading the guts.

The second important point here is the increased emptying of the gut due to diarrhea that leads to the washing out some of the "good" bacteria from the guts, especially in case of profuse diarrhea. The newly coming bacteria are not necessarily those that are present in normal microflora, and it takes days or even weeks until the microflora reaches homeostasis again.

One last point: even without poisoning, microflora varies, and the amount of different bacterial fractions can fluctuate over time. This is normal and depends upon your eating habits, your environment, immune status, and many other factors.


Why do animals only eat some parts of their food? For example monkeys/apes only eat part of a fruit and then throw the rest. Cats (big and small species) only eat some parts of their prey and then they abandon it.
Humans on the contrary leave as few leftover as possible.

What do we know about the parts that animals eat ? and how do we know it ?

It all depends on hunger. As in comment (@Remi.b), it has been mentioned, an animal won't throw if they are starving.

  For example monkeys/apes only eat part of a fruit and then throw the rest.

Monkeys and apes can differentiate between good and bad part of the fruits. So, they eat what they can and if the color looks different (or however they differentiate them) they will throw the rest of them.

  Cats (big and small species) only eat some parts of their prey and then they abandon it.

Cats in general are very picky eaters. They actually have a very short digestive tract, so, they need something easy to breakdown into energy rather than complex processes of digestion. Their main food consist of meat, they leave the inner organs as such.

Source:

http://en.wikibooks.org/wiki/Wikijunior:Big_Cats/Complete_Edition
http://bigcatrescue.org/feed-cats/

Image Source:

http://wordpress.as.edu.au/rspiers/2013/05/22/comparing-animals-digestive-systems/
http://cats56971.wordpress.com/2012/10/30/eating-habits-of-a-african-lion/


How do muscles help erect the spine? Muscles of the spine help to support it against gravity. For example, the multifidi interweave throughout the vertebrae and, as I understand, sort of reinforce the spine. So let's suppose muscles help to make the spine more stiff and rigid and this somehow helps it fight gravity.

What portion of support comes from the muscles? Would a spine by itself be able to support itself? In other words, to what extent is our ability to support our spine to remain upright due to muscles and how exactly do they help keep the spine erect in this capacity?

A biomechanical analysis can be done to determine how much support comes from the muscles vs other (skeletal) support structures. Assume the body is standing upright, in static equilibrium. Consider this (over simplified) free body diagram of the upper torso where the sum of the forces equals zero in static equilibrium.

Here the diagram over simplifies the analysis with one general equation: Fsupport = sum of all the weights. Since we are considering only how much weight muscle supports, we deduct Wbones from Fsupport.

A spine by itself would not be able to support itself because the sum of the forces do not equal zero in static equilibrium. (Wgravity + Wspine) > Fsupport.

In reality, each muscle, bone, and organ has many more forces with specific magnitudes in different directions that altogether equal the weight of the specific region of mass it supports. I imagine these forces as many vectors over an area/field. A more detailed analysis would require a program like MATLAB that uses triple integrals in calculus to visualize these forces in 3D. This kind of visualization can help us color code only the muscle vectors which answers your question, "to what extent is our ability to support our spine to remain upright due to muscles," as a percentage of the sum of all the forces input into the program. How the muscles keep the spine erect can be determined from such visualizations as descriptions of directional forces.

For an example of how this kind of analysis is done, see this paper on lumbar spinal support. http://www.uvm.edu/~istokes/pdfs/stab-model.pdf


Are there real world examples of one way isolation between two populations? I know that for two populations A and B, there are situations in which there is a two way exchange of individuals between the populations, and there are situations in which there is no exchange of individuals between the populations.  I have thought before of a situation involving one way isolation between two populations, in which it's easy for individuals from population A to immigrate to population B, but impossible for members of population B to immigrate to population A.
I tried searching to see if I could find any examples of one way isolation between populations, and couldn't find any examples, although I don't know if this is from not using the correct keywords to find it, not knowing where to look, or there being no known examples of it.
Are there any real world examples of the one way isolation I mentioned between populations?

You might want to look for asymmetric dispersal.
Asymmetric dispersal has been found in many freshwater fishes (such as bullhead; Junker 2012), freshwater mussel (Terui et al., 2014) and in marine kelp (bull kelp; Collins et al., 2010).
That being said asymmetric dispersal does not mean that dispersal goes exclusively one way. Maybe Blondel et al. (2020) reporting asymmetric isolation caused by waterfalls in guppies can be helpful to you.
I am also thinking of polyploid and invasive lines of sunflowers that often live along rivers and reproduce clonally through cutting, where cuts gets transported by the water stream. I co-authored a paper on the evolution of these invasive sunflower lines (Bock et al., 2018) so I should know the literature well but I don't and I am not able to cite a paper that really describes the dispersal and population structure of these sunflower lines. Such patterns might be found in Mimilus as well.
Planctons follow water streams and can therefore have very asymmetric dispersal too (Pringle and Franks, 2001).
I am also thinking of plants reproducing with seed flying in the air and living on a windy sea shore or in windy wide open plane (e.g. tumbleweed). But I cannot give you a reference.


Resilience to the neurotoxins of Indian King Cobra I read on Wikipedia about this:

King Cobra - Wikipedia

In Thailand, a concoction of alcohol and the ground root of turmeric is ingested, which has been clinically shown to create a strong resilience against the venom of the king cobra, and other snakes with neurotoxic venom.

Though, I have been in the village parts of India where King Cobra is frequently encountered, I have never heard of this knowledge.

Can somebody please explain the scientific basis of this statement and possible reasons for this?

[PS]: Can somebody also please create a tag for "Snakes"?

Well, turmerin, the compound in turmeric has been medically proven to help neutralize venom from King Cobras in snakes (reference1, reference2). It has also been used in ayurveda for snake bite treatment (reference) The alcohol I guess is just used to help ingest the turmeric and act as a pain reliever, though it strangely seems counter-productive since most snakebite help guides advice against the consumption of alcohol after getting bitten (reference1, reference2) due to its blood thinning properties.

Having said that, I guess personally, I would go for anti-venom rather than ingest turmeric. As a quick remedy until you get the anti-venom you should be able to depend on turmeric.


Why are 2 electrons transported from photosystem II at the same time? I only know that electrons are captured by the primary electron acceptor and then go through the electron transport chain, ultimately ending up at photosystem I. But why do 2 leave photosystem II in the first place? I thought the oxygen-evolving complex only replenishes the electron hole one-by-one?

So refer to the following diagram,

In the photosystem II complex, water is decomposed into oxygen and protons. That's two electrons liberated from each water molecule. Plastoquinone accepts two protons from the stroma by coupling it to the two electrons it receives from the photosystem complex. In this manner, the protons are transported to the lumen, and the electrons are sent into the electron transport chain. So PQ binds in a QB site in the D1 protein, and it's not released until it's double reduced/protonated. Another PQ binds in it's place when PQH2 leaves the binding site. Source

Short answer: Two electrons are liberated in splitting water, and that mechanism feeds into asymmetric lumen/stroma H+ concentrations and movement of electrons through the ETC.


On the premise of crop rotation, is there similarly a plant or organism able to provide nutrients into its environment that exists in water biomes? I know of the simple concept of crop rotation, and being able to use certain plants to replenish soil, and was wondering if there is a plant or organism that can or does function similarly but in water. I also know there are some plants that are more resilient (and even function or thrive) in soils high in certain compounds and metals (or, conversely lacking in certain nutrients or conditions), that are otherwise detrimental for other plants or organisms. I am therefore also wondering which plants or organisms function similarly, but again--in water, rather than on land.

I have a particular interest in saltwater environments, but also would like to know if there is something in freshwater environments that provides this function.

The question isn't worded very clearly. Scientifically you cannot talk about crop rotation for natural ecology. Ecology has mutualism, commencalism, companion plants that grow together, i.e. some lichen that have three organisms together, plant, mushroom and bacteria, in sponges growing on trees and on rocks.

Crop rotation is especially important on land because we do monocultures, and our sewage doesnt go back into the field, there is a net drain on the soil minerals. In forests and the sea, the situation is different, because plants adapted to the soil grow and build up nutrients over time by rotting with organisms, being fertilized by worms, snails, insects birds and so forth. In the sea, fish provide that function and there isn't the same net drain on a sea environment as there is in a crop.

If you study green life inside different pots of water, from river, tap, rain, and pond, from different sources and different geologies, you will learn some things about aquatic ecology and nutrients. It reacts  with different plants and at different speeds.

The sea is physically so different from land, that the matter falling from the top can be transported miles away, that little comparison is made between nitrogen fixing in soil and in seawater. Also, the zone with the most light also has the strongest currents, so less chance for exchange of nutrients in ecology micro-climates and biomes.

crop rotation is mostly for N P K fixation.

On land NPK availability is often due to the acidity of the geology, which is not quite the same in the sea, plants can live on basalt or chalk, but they have endless flowing water and a good detritus layer in either.

In the sea, NPK is mostly brought by algea and cyanobacteria, which fall and bring it to the phito-detritus layer.

There are not the same forest type ecosystems in the sea as on land, where forests create many meters of peat bogs and massive NPK reserves, as in jungles sometimes. Because forests are less complex in the sea, less green stuff exists on the sea bed, we can say that the situation for plants is less profitable than on land and that instead the biomass exists more in floating small algea, Coccolithophores and so forth, which account invisible for most of the algal biomass of the sea. I cant find if there is more phyto biomass in the land or in the sea. I figure it's on land.

In freshwater environmetns, lakes can have an over or under abundance of NPK, and can bloom more or less completely for a given Ph and environment, given specific adaptations that help them to cope with a particular Ph. it's a lot more variable that the sea with PH going from 4 to 10 and beyond, when the sea ph is about 7.5-8.4.


Immediate cause of death due to dehydration When we don't drink we get dehydrated and after some time we die. What is the cause of death on the lowest level?

I would assume the dielectric properties around/in the heart tissue get imbalanced and the heart stops beating.

Then lack of oxygen in the brain. Then...?

The simple answer is dehydration kills you by causing the blood flow to become completely ineffective.

Dehydration limits the amount of water in the bloodstream causing an increase in blood viscosity, and thereby an increase in blood pressure.  As this process gets more extreme the body has a difficult time getting the blood to the places it needs to be, and will limit blood flow to non-essential organs (kind of similar to what happens when it's cold outside and your fingers go numb).  At the same time waste is beginning to build up as the kidneys cannot filter the blood effectively, and the internal temperature rises because of the lack of sweating.  This process gets more extreme until one of your essential organs cannot take it anymore and shuts down, likely the liver first.

Most everything I got for this answer was from a PopSci Article. Although there is also a nice 1935 study with many measurements from real people.


Growing Mouth Bacteria in a bowl of sugar water I want to teach my nephew why brushing in necessary and how sugar in mouth reduced by bacteria to acid.

I plan to put sugar mixed water in bowl and take swab from his mouth and dip in bowl, and test ph using Litmus paper to show him that sugar is converted to acid.

Is it possible to grow mouth acid making bacteria in this solution and will it change pH enough to show in litmus paper?

I like the concept of this demonstration for teaching science!
As rotaredom's comment pointed out, bacteria does not grow in plain water with sugar. Bacteria require a nitrogen source, trace minerals and vitamins to grow in significant numbers.
I have a few recommendations that you can try, but I attached an extensive guide to kitchen microbiology below.

Growing the microbes in diluted milk (~ 1:10 dilution) + salt (a pinch for half glass) with and without added sugar (1 teaspoon for half a glass) might be a good starting point. Add yeast extract if you have some (not bakers yeast, but this is the killed version of that).

Make sure to boil and cool the milk, the container and other ingredients to keep conditions sterile.

Avoid a cotton swab if you can (as the cotton might not be sterile), I would take some milk solution, swirl it in my mouth and spit it back into the same container.

Also have a sterile culture in the experiment, without the oral microbes for comparison and a great teaching point.

Grow the microbes for 2-4 days with an air permeable cap (the air allows faster growing aerobic organisms, the cap ensures dust does not fall in)
Extensive source: Microbiology at Home: A short non-laboratory manual for enthusiasts and bioartists
PS: I'm studying PhD to be a microbiologist


Quantification of various amino acids from bacteria? I would like to characterise how much of various (uncommon) cytosolic amino acids  are produced in bacteria, and was wondering if there are good suggestions of how to go about doing this. I know that chromatography is a good end-point analysis once I have isolated a fraction of what I suspect contains the amino acids; however, I am unsure about the smartest way to do the 'rough' initial purification prior to chromatography.
I know that you in general lyse the cells, pellet cell debris and then start some form of purification. I have also heard of certain resins that can bind natural products (e.g. Diaion® HP20, synthetic adsorbent resin) had thus aid the first purification step of the amino acids. Do people have experience with this? Are there also good solvents for separation of amino acids from lysate, that could be used in the first step (phase separation)? Does someone have any experiences with this? Any alternative suggestions would be appreciated.

A good approach could be to use GC-MS to identify cytosolic metabolites. When focussing on cytosolic amino acids, it might be useful to precipitate the proteins in a purification step and continue with the soluble fraction. Subsequently, a derivatization is done. The mass spectrometry helps to better identify the amino acids. This article by Phelippe et al. can give a good start.


What is the name of this tiny creature? Place: South India,

Metropolitan, Year: 2017; Night Time.

Size: 1-2 cm (Very Tiny)

From the posture, it looks like it can belong to Geometridae (Larentiinae). But I haven't been able to find a species that has that particular color.


Conserved acetylation sites in a given protein I want to identify potential conserved Acetylation sites in protein X. As it is known, acetylation happens in Lysines (K), thereby I would like to identify conserved K residues for protein X during evolution. Eventually I would use different Acetylation site prediction tools to further filter the results, but initially I need the other data, does anyone know a user friendly but trust worthy bioinformatic tool to do so?

You can use the NCBI subpage HomoloGene

Halfway down page on left you can choose to show Multiple Alignment as seen in this screenshot.

I think you will then see what you are looking for as in this screenshot: