Studying effects of alcohol on cells I am wondering about the logistics of a simple experiment with say 3 types of alcohols, and various concentrations of each, with a control(s)

I would like to research the effects of alcohol on mitosis. Do I need any expensive equipment or is it do-able with standard equipment? I am looking specifically at what I expect to be a negative impact on cell growth. Potential cell death and slowing of mitosis.

"We expect mitosis to slow and stop entirely or become corrupted as the amount of alcohol used increases. Of the three alcohols we will be testing, we expect some to be more damaging than others. The 3 chosen alcohols, listed in order of their hypothesised toxicity are Methanol, Ethanol and 2-methyl-2-butanol."

I am basically trying to see if tertiary alcohols are safer due to ethanols main metabolites acetaldehyde & acetic acid being more harmful/toxic? Since Tertiary alcohols for example, aren't metabolised into aldehydes. Which makes them less toxic than ethanol in theory.

Now I am unsure as to which cells to use to test upon, I'm also unsure as to the legitimacy of my hypothesis. Budget, time and a lack of knowledge is against me. I am researching as much as possible as quick as possible. Thankfully I have help available soon or I would be totally out my depth. This is me out of practice in the field trying to get a head start and help a friend out as best I can. I'll be his assistant and feel thats more than appropriate.

I realise I can't test for too many things. I need one clear goal. If we choose to test certain cells over others do you have any suggestions? and why?

The liver processes ethanol into acetaldehyde & acetic acid. So I would need these chemicals potentially in order to properly test ethanols effects on cells?

I am so out of my depth I feel right now I'm hoping for a prod in the right direction.

The 3 chosen alcohols, listed in order of their hypothesized toxicity are Methanol, Ethanol and 2-methyl-2-butanol. - concentrations of each yet to be considered.

I suffer from dyslexia and my wording is bad at the best of times. But please realize this is a very first draft / ideas on the table. Any help at all is appreciated, apologies for my lack of knowledge in the field. I'm trying to refresh my studies from 10 years ago in 2 days.

Great idea! It seems that this research has been done before and your hypothesis is correct, but testing a wide variety of alcohols and testing your hypothesis for each one of them would be a great project.

Now, to do this, I would expect you would need to check the growth of the cells after certain periods of time. How would you do this? Well, the best device would be a hemocytometer. It looks like the price varies from 10.00 - 400.00 which is pretty cheap. Of course, there would be mitosis if there is growth during periods of time, which means there would be more cells after certain periods of time.

What cells to choose? I would choose something easy to work with, such as E.coli. It is safe and easy to work with. It needs minimal resources. Here's a link to a simple culture you can probably make at home:

http://makezine.com/projects/how-to-make-bacterial-brothagar/

Later, however, when you get good data, you can use mammalian and human cells to show that the research is relevant to human beings. However, mammalian cells are harder to grow because mammalian cells grow slower than bacteria and fungi and moreover contamination can cause problems. You would also need biosafety cabinets or laminar flow hoods and learn of aseptic and sterile technique.


Is there an RGB equivalent for smells? Millions of colors in the visible spectrum can be generated by mixing red, green and blue - the RGB color system. Is there a basic set of smells that, when mixed, can yield all, or nearly all detectable smells ?

There are about 100 (Purves, 2001) to 400 (Zozulya et al., 2001) functional olfactory receptors in man. While the total tally of olfactory receptor genes exceeds 1000, more than half of them are inactive pseudogenes. The combined activity of the expressed functional receptors accounts for the number of distinct odors that can be discriminated by the human olfactory system, which is estimated to be about 10,000 (Purves, 2001).

Different receptors are sensitive to subsets of chemicals that define a “tuning curve.” Depending on the particular olfactory receptor molecules they contain, some olfactory receptor neurons exhibit marked selectivity to particular chemical stimuli, whereas others are activated by a number of different odorant molecules. In addition, olfactory receptor neurons can exhibit different thresholds for a particular odorant. How these olfactory responses encode a specific odorant is a complex issue that is unlikely to be explained at the level of the primary neurons (Purves, 2001).

So in a way, the answer to your question is yes, as there are approximately 100 to 400 olfactory receptors. Just like the photoreceptors in the visual system, each sensory neuron in the olfactory epithelium in the nose expresses only a single receptor gene (Kimball). In the visual system for color vision there are just three (red, green and blue cones - RGB) types of sensory neurons, so it's a bit more complicated in olfaction.

References
- Purves et al, Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Zozulya et al., Genome Biol (2001); 2(6): research0018.1–0018.12

Sources
- Kimball's Biology Pages


Are some facial features more important than others in human facial recognition? I'm often surprised by the human ability to correctly identify other individuals despite significant modifications due to ageing, hairstyle, injury, etc. But, sometimes the addition of a beard and a hat can radically increase the identification error.

I wonder whether all facial regions are equally important when we try to recognise human faces? Do we focus more on some regions than others? I doubt that this is the case, but I'm not certain.

Update:

So far I've read through the following:

1) http://en.wikipedia.org/wiki/Face_perception

2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998394/

So far I haven't found an answer so I decided to try Biology.StackExchange.

The most important features are the eyes, followed by the nose and mouth, respectively.

An elaborate answer can be found on the duplicate question on Cognitive Sciences SE:

Are some facial features more important than others in human facial recognition?


Why would lactate be high in diabetics? Why are lactate level high in diabetes? For example, type II diabetes are resistant to insulin. If those patients are insulin resistant their gluconeogenesis should be working at a high rate and, because of that, lactate uptake by the liver should be removing lactate from the blood.

Alternatively, type I diabetics don't produce insulin, so the ratio insulin/glucagon would always be very low and gluconeogenesis should be stimulated... So I don't understand why lactate levels are high in diabetes... Can someone help me?

PS. This question came up after doing an experiment in school, with diabetic rats and normal rats. Diabetic rats had higher levels of lactate and my professor said that it was because the diabetic rats don't perform gluconeogenesis and so, lactate accumulates in the plasma. But it doesn't make sense for me.

This condition is also known as "lactic acidosis" and can be pretty dangerous, since it influences the pH of the blood.
When we metabolize glucose to produce ATP and NADH it is metabolized finally to pyruvate in a process called glyolysis (I am not going into detail here since this is nicely explained in the Wikipedia). Pyruvate can then be used further in the body in the Gluconeogenesis, the Citric acid cycle and other pathways.
If a lot of energy is needed Pyruvate is converted by the pyruvate dehydrogenase into acetyl-CoA.

The problem with diabetes is that the pyruvate dehydrogenase can be inhibited in diabetes. If the body then needs a lot of energy pyruvate will be converted into lactate which is released by the cells into the bloodstream.
Gluconeogenesis cannot be activated since this needs either Pyruvate, Acetyl-CoA or Oxaloacetate as starting material. The other problem with this process is that this happens in the liver and when the glucose is released into the bloodstream, it cannot be taken up by the cells due to the lack of insulin.

The conversion from Pyruvate to Lactate is katalysed by the Lactate dehydrogenase and needs NADH + H+ as a co-factor. The image below is from the Wikipedia article on Lactate dehydrogenase.

This reaction is highly exergonic which means its preferred direction is to the right side. To change this and make Pyruvate from Lactate you need an excess of NAD+ which usually only happens in the liver.

There is also an epidimiologic study available showing a strong correlation between elevated blood lactate levels and diabetes type II: "Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study."


Does the human body metabolize what it smells, even in trace amounts? I conjectured to a friend that some small amount of anything we smell is likely metabolized by the body. He disagreed. My thinking is that, if you are smelling something, some portion of molecules are being sensed by the olfactory tissue and some portion is taken into the lungs. Of the portion taken into the lungs, some portion is exhaled and some portion remains. I didn't propose a mechanism for the part that "remains" at the time, but it seems reasonable that some of it gets caught in mucus, some of which is then swallowed.

Obviously, a very, very small portion of whatever we're smelling would go through this process if my conjecture is even correct. For context, we were discussing people who have elected to restrict their diets for ethical or similar reasons. I was comparing what I proposed to when food products are labeled with "may contain trace amounts" due to "shared equipment".

So I guess my questions are these: was I right in my guess, and if so, was the mechanism correct or not?

Olfaction is the result of the neuronal impulse of ligand / receptor binding. To smell something requires 1) Specificity between the receptor and the ligand, 2) Concentration of the ligand molecule, and 3)The receptors that are on the surface of neurons in the olfactory bulb.

As for metabolize, then you need to be much more specific in defining what you are considering metabolism. Is the molecule broken down further; does it pass into the cells directly; does it need to be the unaltered molecule to qualify as metabolizing the molecule that you sensed as a smell.

The majority of our mucus in our airways is moved to the digestive tract as the result of ciliated epithelial cells "sweeping" the mucus and everything trapped in it to our esophagus, where it goes into the stomach and is digested. It is hard to say whether or not the molecules that you detect as smell are reactive, and if they are, whether or not they would chemically react with something else before it got to your stomach.

Also the volatile chemicals which you sense as an odor, aren't necessarily what would constitute the substance that they emanated from. So I would probably argue against your conjecture that someone who decides to be vegetarian or who has a peanut allergy is metabolizing something just because they inhaled it. It is likely the proteins in a peanut that cause an allergy, and that is not what you are inhaling, and as for the vegetarian, I think the justification is that it would be the protein that constitutes the consumption of a meat and not the molecules that come from the cooked or uncooked tissue.

If you want to broaden what you are calling metabolize, then you would only need to look at inhaled medicines such as corticosteroids or compounds to bronchodilate, to make a case for the fact that you are metabolizing what you inhale.


Why do Type II Restriction Endonucleases cleave at palindromic sequences? Type II Restriction enzymes usually cut only at palindromic sequences. Is there any specific reason for that? Is there any advantage for bacteria if they cleave phage DNA at this type of sequence?

Short Answer

  The palindromic symmetry of the restriction site allows a dimeric
  enzyme to bind the DNA in a manner that bends the double helix in a
  way that facilitates the endonuclease reaction.

More Detailed Answer

The ‘palindromic’ nature of the recognition/cleavage site of restriction endonucleases, such as EcoRV (illustrated here) results in a form of symmetry (A) that allows a dimeric enzyme — that forms a tunnel — to bind symmetrically at that site in the DNA (B).

This binding causes the DNA to bend (C) bringing a catalytic magnesium ion into a position in which it can interact with phosphate of the phosphodiester bond that is being cleaved (D). (The dimeric nature of enzyme allows force to be exerted at two points, to produce the bend. Compare bending a thin pipe over one’s knee, applying equal force with both hands.)

Methylation of the adenine nucleotide in the recognition sequence prevents hydrogen bonding of the enzyme to the DNA. DNA lacking the recognition site is not cleaved by the restriction enzyme because it does not bind specifically to the protein so that the magnesium ion remains too far away.

Reference

This answer is based on chapter sections 9.3.2 and 9.3.3 of Berg et al., which is available online at NCBI Bookshelf and is well worth reading in full. There is also a PDB Molecule of the Month item on this, although unfortunately the bending of the DNA is not apparent in the images there.

Comment on Last Two Sentences of Question

There is no particular “advantage for bacteria”  other than “it works”.  So I think the last sentence is looking at things from the wrong perspective.


Possibility of orthogonal view for a creature? Just a pure curiosity: Does there exist a creature with an orthogonal view to the world instead of perspective? What would be an optical explanation for possibility/impossibility?

Many creatures have eyes on the sides of their head where they cannot have both eyes simultaneously look at the same target. For example whales. Chameleons are well known for having independently moving eyes (though they can align them for binocular vision)

Since all the significant processing of vision occurs in the brain's occipital lobes there is no problem with optics.


Technical term for a mutation that only occurs after a preceding one Consider a hypothetical population of 1000 organisms.

(a) 300 of these 1000 have a T to G substitution at a specific position 1.

(b) 200 of these 1000 have an A to T substitution at a second position 2.

(c) All of the 200 with the substitution at position 2 (b) also have the substitution at position 1 (a).

As a non-geneticist, I would call the second mutation a refinement of the first mutation. Would that seem reasonable, or is there a specific technical term for this phenomenon?

The description of the second mutation depends on the nature of its relationship to the first mutation.

If the first mutation reduces fitness of the organism, and the second mutation tempers the fitness reduction, then the second mutation would be compensatory.

Compensatory mutations are common in bacteria that acquire antibiotic resistance.  Consider a strain of E. coli that acquires resistance to streptomycin by mutating the rpsL gene, which encodes a 30S ribosomal protein targeted by streptomycin.  In the presence of streptomycin, the rpsL mutant is obviously more fit than wild type E. coli.  In the absence of streptomycin, however, ribosomal mutations lead to inefficient translation.  Compensatory mutations may then arise elsewhere in rpsL or within another gene involved in the ribosomal complex, partially alleviating the fitness defect caused by the initial mutation to rpsL.

If, instead, the mutations are synonymous and otherwise unrelated in their functional potential, I would simply call those mutations coincident in the genome, though this isn't really a "technical" term. If you wish to describe the relevance of these synonymous mutations in context of the three distinct genotypes given in the question, you could say that the first T to G transversion differentiates strain X from ancestral Wild Type, and the second A to T transversion differentiates strain Y from ancestral strain X.  This assumes that both of these mutations occurred once in the genetic history of this population.


Female preference for males who are already in a relationship A common saying is that women are generally more attracted towards men who are already in a relationship, and this phenomena does seem to have its own place in popular culture that is not matched by a corresponding male preference for women who are already in a relationship.

From an intuitive viewpoint I think it would make sense from the woman's viewpoint in an system of information economics where the fact that a male is engaged in a successful relationship with another female, or several other females, might provide extra and positive information about the evolutionary value of the male.

But how about the possibility for a male to use the same trick?

Is there any empirical evidence for this behaviour at all either in humans or in other species, or is this just a cultural artefact in some human societies? If there is empirical support, is there a consensus on the plausible evolutionary pathways involved here?

This is a widely researched topic in the overlap between social sciences and evolutionary biology.  Evolution has become very influential in understanding human interaction and preferences.

This chapter from "The Adapted Mind : Evolutionary Psychology and the Generation of Culture" will give you an idea of how all this plays out in the big picture - its a fairly comprehensive review of many factors considered in human mate choice.  The study may be psychological, but the logic is derived from biology these days.  (stackexchange won't let me link to google books - you can search for the title and look at chapter 6).

Evolutionary tendencies will favor more successful offspring.  But for people it includes not only the genetic qualities of the mate (appearance, height, disease resistance, health) but also social qualities (how reliable or willing a mate is to support offspring).

First off you can see that there are many many factors which women take into consideration in their preferences.  Its commonly said they are more complex than men, but that's another question.  You have to take a range of factors holistically including the social environment.

I can't find this particular issue addressed in the literature, but I think that it might be attractive to women in some social settings.  If there is a lot competition for 'quality' mates or resources for instance - if you have very few secure males or pessimistic females might create pressure which would cause females to prefer males which were successful.

Its pretty easy to feel good about hypotheses like this.  I couldn't find a specific study, but perhaps someone else will.  There's a lot of such papers out there.

I should say that men are as easily led to do things by 'mate choice' psychology that aren't totally healthy or socially acceptable.  That's biology.


Can ingesting substances that are produced by the body cause a permanent withering of the organs that produce the substance? This question is about substances such as insulin and some vitamins that the human body is able to produce on its own.

Some substances that are produced by the body are also present in various body building supplements.

What I wanted to ask is, is there evidence that ingesting these types of substances for prolonged period leads to (permanent?) withering of the organs that produce the substance?

Yes it is possible but in most cases it will not occur as the body simply halts production. The most infamous manifestation of this is in adrenal insufficiency. That's where when we take glucocorticoids (e.g. prednisolone used in management of lots of inflammatory diseases like asthma and autoimmune diseases) for a prolonged period at high dose. This causes the adrenal glands to atrophy (physically shrink) and following this sudden withdrawal can be dangerous for a patient. That's why we always slowly withdraw steroids when a patient has been on them for a long period of time.


Synthesis of immunoglobulin Fab fragments: Where can I learn about Fab? I wanted to know the chemical reaction involved in Fab synthesis. I looked everywhere for it. No luck. I know I will find it here.

All I know for now is:

Fab is a monovalent fragment that is produced from IgG and IgM, consisting of the VH, CH1 and VL, CL regions, linked by an intramolecular disulfide bond.

Molecular basis of Fab will make more sense.

For the generation of Fab-fragments antibodies, (possibly genetically modified) which can be made in large quantities by cells or animals, are used. Antibodies as a whole are not synthesized.

The Fab fragment is obtained from antibodies using the enzyme papain, which cleaves the antibody over the disulfide bonds in the hinge region. This results in two Fab fragments (which contain the antigen binding sites) and one Fc fragment (which contains the constant region of the antibody). See the image (from here):

If you want to go further into the topic, read one of the references below.

Preparation and separation of Fab and Fc fragments from human
immunoglobulin G with papain digestion
Fragmentation of IgG Using Papain


How is instinctual information encoded? If instincts are passed on through genetics, how is that information encoded in DNA?

For example, spiders instinctively know how to spin webs. Does that imply that the algorithm for web spinning is directly encoded in spider DNA?

Web spinning in spiders is a complex behavior and probably involves a number of different factors, genetic and environmental. Genetically there are surely many different genomic regions underlying the development and expression of the behavior.

Is the algorithm for web spinning directly encoded in the DNA? Not directly. There is not a single region of contiguous DNA sequence that codes for all the steps involved in building a web. Instead, there is a sequential and parallel developmental process beginning at fertilization (earlier if you include parental epigenetic modifications) - encoded and regulated by the genome and its products - that, without too many errors, generates a viable and fertile web-spinning organism. But the DNA sequence involved in that algorithm is spread all over the genome and includes coding genes, non-coding (ncRNA) genes, and regulatory regions. And the genome alone will not carry out an effective algorithm without proper environmental inputs like nutrition and parental provisions.

The act of constructing a web, when and where, and the design of the web is likely carried out via brain architecture and neuronal patterning, but of course these structures are built based on the DNA-based, developmental algorithm. In that sense, there are many nested levels of algorithms.

One of the best models used for studying behavioral genetics is the fruit fly Drosophila. Many different behaviors have been studied at the genetic and molecular level in Drosophila including courtship, foraging, sleeping, and memory-related tasks. A popular science book on behavioral genetics worth checking out is Time, Love, and Memory by Jonathan Weiner. It details the work of Seymour Benzer and provides a lot of background and easily understood explanations of how genes and their products can work together to exhibit complex phenotypes like sleeping patterns. It includes a detailed (though not up-to-date) description of circadian gene circuitry and how it develops.

At the moment, the best that I can think of for an algorithm directly encoded for by DNA is the sequential activation of HOX genes for animal body plans. But even in this case DNA code does not progress through correct development without other factors.


Blackgram leaves. SDS page. Phosphate buffer method I am doing protein analysis in blackgram leaves by using phosphate buffer method. But I cannot get proper bands on my SDS-PAGE. What should I do to get proper bands?

You should de-stain your gel longer. I can see at least one thick band at the top, but without de-staining longer you are probably missing other fainter bands.

Also, please explain what you mean by "proper bands". The top one looks fine to me. There might be others but we cannot see them.


Immune System - B-cell receptors How do the B-cells, which are a part of our body, develop antibodies against antigens of the outside world (outside of our body), which they don't even know about? Is it just a random match?

This is an excellent question. You are on the right track with the random match idea. B-cells (as a group) develop receptors that bind every possible antigen and then get rid of the receptors that match antigens in our body. Some textbooks are a little more careful in their language, though, and say almost every possible antigen.

See Alberts

  The preimmune repertoire is apparently large enough to ensure that there will be an antigen-binding site to fit almost any potential antigenic determinant

I'd note, though, that we've yet to identify an antigen that can't be bound by an antibody.

The process by which an individual's set of B-cells is able to generate all these different B-cell receptors was discovered by Susumu Tonegawa. He was given a Nobel prize in physiology or medicine for the discovery in 1987. You can read about it at nobelprize.org.

In broad strokes, each B cell has multiple copies of different types of gene segments that make up the B cell receptor. When the B-cell develops, it selects one of each kind of segment at random and pastes them together. At the level of the human organism, this generates an awful lot of diversity, but not quite enough to produce receptors that bind every possible antigen. The additional diversity is produced by adding or deleting additional DNA bases at random.

This produces a new problem, though, because with B-cells that have receptors that would bind every possible antigen, we would end up attacking ourself. The details here are the answer to a new question, but the basic answer is that B-cells that would recognize self are selected against, leaving us with a complement of B-cells that have receptors that bind literally every possible antigen that is not self.

Lauren Sompayrac has an excellent introductory book on the immune system that makes these very difficult concepts much more approachable. It's called How the Immune System Works, and I highly recommend it.

Here's a diagram from that book, showing the random selection and pasting together involved in one of the parts of an antibody (the heavy chain):


Where do the 2 electrons and H⁺ go when NADPH is turned into NADP⁺ during the Calvin Cycle? I was wondering where the 2 electrons and H+ go when NADPH is turned into NADP+ during the Calvin Cycle? I know that during the light dependent reaction, 2 electrons (from water) and H+ combine with NADP+ (from the Calvin Cycle) to form NADPH, but after NADPH is used and is turned into NADP+, where do those electrons and H+ go?

A reasonable source of information about the Calvin Cycle is Berg et al., but for this reaction the full structures are not shown. I therefore show them below in a diagram of my own:

I have coloured the hydrogen atoms to show where they go in reducing the phosphoglycerate (acid) to an aldehyde. You can think of the two electrons being used to form the additional covalent bond.

(The hydrogen phosphate is actually in equilibrium with other phosphate species, but this is not relevant to your question and so is not shown.)


Addax in the Land of Israel The Addax (Addax nasomaculatus) is critically endangered species of a desert anetelope with impressive long horns. Today there are small populations in the Sahara desert and the Arabian desert (Saudi Arabia). The addax is mentioned in the bible ("Dishon"), though the identification is not uninomous. Today in Israel there are breeding centers for the addax, one in Hai-Bar Yotvata (near Eilat, the rift valley, bay of the Red Sea) and the other in the Zoological Center at Ramat Gan ("The Safari"), but as far as I know, there are no plans to release addax in the wild in Israel (although I think it can survive and flourish there).

The question is: was the addax native to the Land of Israel (before it was eradicated from it by overhunting)? Do the conservation organizations support reintroduce it to the wild in Israel (in addition to the Sahara and the Arabian desert) addax herds from the breeding centers? The reintroduction of Oryx to the wild in Israel was pretty successful.

According to Yossef Braslevi, "HaYadata Et HaHaretz - Yam HaMelach Saviv Saviv" ("And you shall know the land - The Dead Sea and its Surroundings", 1956, Vol. C, page 199 -- the answer is positive. There were native addaxes in the Land of Israel.


Oldest Triceratops fossil In most books, Triceratops is listed to live between 68-66 MYA (million years ago), however some books list Triceratops as living between 70-66 MYA. The Campanian age ended about 72 MYA and then came the Maastrichtian. Many articles state that Triceratops is "late Maastrichtian" dinosaur. All these citations do not give a clear answer: when did Triceratops live? All sources agree that Triceratops lived up to the K-Pg extinction 66 MYA, but when did the earliest Triceratops live?
This may be vague question so put it more empirically: what is the oldest age that a Triceratops fossil is dated to? Not when the first fossil of Triceratops was found but what is the earliest age (in MYA) at which Triceratops are known to have existed? Are there Triceratops fossils from 68 MYA? And from 70 MYA?

late Maastrichtian is probably it.

Part of the problem you are running into is the Triceratops genus is in flux, there is debate about whether certain species belong in the genus. Such as whether triceratops and torosaurus are the same species.

The other problem you are running in to is the accuracy of dating methods, many fossils are dated indirectly, by bracketing (distance in section) with ash beds but this means they have a decent margin of error, 69MYA +/- 2mya is completely possible. Many were collected before such dating was even done or suche detailed measurements were taken leading to an even wider error bar. Especially given the best dates for the Hell Creek Formation itself has an date range error of about +/- 0.7MY and begins with a unconformity. Many studies are just going not going to calculate a date that has a high degree of uncertainty. The date for the end is more solid because it is an ash bed, thus directly datatable.

The most recent analysis of triceratops I know of is here many of the specimens were collected in the 1800's so late Maastrichtian is about the best you are going to get for an uncontroversial date.


Do goldfish really have a 5 second memory span? I heard that when people place goldfish in another tank, they just forget where they where previously? True or False ?

My answer might sound unscientific, since I haven't had tanks filled with goldfish. However, I have had fish and other pets over the years, including cats, turtles and a very sick lizard. I have a scientific background, and on this strength, I will report based on personal observation, albeit with a small sample size.

My fish always "knew" me. When I approached the tank, they knew it was their "feeding person", and even when they were not getting fed, left what they were doing aside and came to the surface to "greet" me, or more likely, impending food. I even experimented by asking others to walk up to the tank and saw that most of them did not respond in a similar fashion, although sometimes they did. With me, I enticed the same reaction every time, even  after a new tank was populated or new additions were made.

This makes me conclude fish, and goldfish, which I did keep, have "better than expected" memory.

When they are put in a new tank - well, I suggest you move to a well crowded city that is new to you, and see how long it takes for you to get your orientation right.

Hope it helps.


autosomal recessive population numbers This question is background research for a science fiction / fantasy novel, my knowledge of genetic is very basic.

It seems obvious to me that for genetic disorders that are autosomal recessive, if those disorders prevent affected individuals from reproducing, the carrier and affected rates in a population will naturally be smaller. I'm not sure if this is the entire reason why say, blue eyes are more common that cystic fibrosis, but it definitely seems to be a contributing factor.

My question is this: say you have a (fictional) autosomal recessive trait that does not prevent reproduction. Let's call the initial carrier rate in the population for this trait C and the initial affected rate A.

In case it matters, the fictional trait I'm considering might reduce the chance of reproduction (as the people may be shunned, or considered less desirable as a mate) but there is nothing preventing reproduction. Something like "bright purple hair" where there is a stigma against affected individuals -- "your hair marks you as tainted" or something. I'm thinking A is around 0.1% (1 in 1000 births). (And if I understand the math right, C would then be around 6%, or 1 in 16 -- so that C * C / 4 gives A.)

Now let's say an oppressive government decides to prevent all affected individuals from reproducing (but carriers are left alone). Let's assume a 100% success rate for the government at rendering affected people infertile thus preventing their reproduction. What will happen to C and A over time? Is there some simple way to estimate how they will trend over several generations?
I don't need exact numbers but I'm having trouble with even coming up with a guess.

In population genetics, with a simple one-locus two-allele model, we consider the frequency of the two alleles to be $p$ and $q$ where $p + q = 1$ (and thus $1-p=q$ and $1-q=p$). When an allele is recessive it is only expressed at the phenotypic level when the individual carries two copies of the allele.

Following from your example, gene $A$ might be responsible for hair colour, with alleles $A_1$ and $A_2$ where $A_2$ is a recessive allele responsible for purple hair. I will denote the frequency of $A_1$ with $p$ and frequency $A_2$ with $q$. This means that the frequency of individuals with purple  hair ($f_{A_2A_2}$) is $q^2$ and the frequency of people with not-purple hair is $p^2 + 2pq$ (assuming an idealised population). As such, a population of 500 diploid individuals* where there is 100 copies of the $A_2$ allele would have the following genotypic (& phenotypic) frequencies:

$$f_{A_1 A_1} = p^2 = 0.9^2 = 0.81$$
$$f_{A_1 A_2} = 2pq = 2 \times 0.9 \times 0.1 = 0.18$$
$$f_{A_2 A_2} = q^2 = 0.1^2 = 0.01$$

So the allele for purple hair would be present in 19% of the population, but the trait would only manifest in 1% (only ~5.3%, $\frac{1}{19}$, of the people that carry the purple hair allele exhibit the trait). Therefore selection would be quite inefficient at removing this allele from the population, even if you could prevent all purple-haired individuals from reproducing. To find the frequency of $q$ required to give a genotypic/phenotypic frequency where 1 in $x$ individuals have purple hair just take the square root of $1/x$. E.g. to get 1 in 1000 individuals expressing purple hair

$$q = \sqrt{q^2} = \sqrt{(1/1000)}$$

What does this mean for evolution? Alleles that are recessive deleterious are very hard to remove from the population because, at low frequencies, they rarely produce the detrimental effect. Assuming complete dominance ($A_1 A_2$ = exactly like $A_1 A_1$), denoted by $h = 0$, selection only acts on $A_2 A_2$ homozygotes. The frequency of the $A_1$ allele increases at the rate $1/(1-sq)$ where $s$ is the relative fitness advantage. Mutation can also introduce more copies of the $A_2$ allele to the population such that there will be an equilibrium, balanced by the rate of loss due to selection, and rate of gain by mutation. Furthermore, to further build on your analogy, a neighbouring population, where purple-hair is not selected against, may bring copies of the allele in by migration.

Suggested further reading on evolution here and reading on eugenics would likely be of interest to you.

* 500 diploid individuals = 1000 gene copies. Thus $q = 100/(500 \times 2) = 0.1$


Meaning of Phred score - probability of base calling error I learned that Phred quality scores are logarithmically linked to error probabilities. For example, if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10.
How is it possible to have 10 possiblities when you can only have 4 bases (ACGT) ?
When assigning a base, there are only three ways to be wrong to me.

Phred score is a measure of the probability that a base call is wrong/right.

Your understanding of this probability as "if Phred assigns a quality score of 10 to a base, the chances that this base is called incorrectly are 1 in 10", is not entirely accurate.

Quality scores calculation and base calling are specific to the machine. The way an Illumina HiSeq calls a base is different from how PacBio does it.

For example, Illumina uses high precision cameras to record the colors generated during sequencing (each color represents a base). Moreover, it does not sequence a single molecule of DNA but a cluster. Now, the machine's base calling software will calculate the reliability of the light signal being interpreted as a base (let's say A). Several parameters are considered in this calculation.

  For each base call, a number of quality predictor values are computed.
  Quality predictor values are observable properties of clusters from
  which base calls are extracted. These include properties, such as
  intensity profiles and signal-to-noise ratios, measure various aspects
  of base call reliability. They have been empirically determined to
  correlate with the quality of the base call.

   Illumina Technical notes: Understanding Illumina Quality Scores

Likewise, different machines have different techniques for reading a base signal and computational models to calculate the accuracy of the signal.

  How is it possible to have 10 possiblities when you can only have 4
  bases (ACGT) ?

Why not? You are just calculating what is the probability that a base is not adenine. The minimum probability should be more than 1/4, at or below which the base call wouldn't probably even assign the base as adenine.

Imagine it like this: if adenine is represented by blue light and you see that in the spot there is not a pure blue signal but some interference of other colors (noise) which represent 10% of the signal. There can be other parameters too that make the calculated blue signal to deviate from the "ideal signal". The percentage of non-overlap with the perfect signal would be the error.


Why can nervous inflammation radiate symmetrically in the limbs? I have had carpal tunnel syndrome in my hands this week, when the nerve in the pith of your palm, through thumb and index, is pinched, and swells, inside the wrist ligament tunnel.

In a few days, the inflammation declared itself in the other wrist. It's usually the case with CTS, it's rare that a person will have problems in only one had.

As soon as one hand is injured, the other tends to seize up and stop functioning as badly as the first one, within a week or so.

Why and how does a nervous injury such as CTS radiate symmetrically through the nervous system, differently from a sprain or a contusion?

What other factors in neuroscience demonstrate nervous symmetry, related to the CTS symmetry problem?

Padua et al. (1998) did find that 87% of followed patients developed bilateral CTS (i.e., carpal tunnel syndrome in both hands).

Most patients that develop unilateral symptoms, eventually have the symptoms spread to the contralateral (opposite) arm.

Bagatur & Zorer (2011) found that 59% of patients they followed reported bilateral symptoms initially, while 73% of remaining patients had symptoms eventually develop in the contralateral arm (even after receiving surgery on the first!)

So why? From what I could gather, we don't really know. From Bagatur & Zorer (2011):

  we assume that bilaterality may be time-dependent... [but] a definite conclusion could not be drawn.

However, research regarding "double crush syndrome" suggests that perhaps issues closer to the cervical spinal cord may play some role:

Pierre-Jerome & Bekkelund (2003) found that cervical intervertebral foramina were narrower in observed patients and affected nerve roots.

Although their research provided evidence for ipsilateral double crush symptoms, their study provides credence to the fact that more cervically-oriented issues (often which should show up bilaterally) could lead to CTS symptoms.

Not the greatest of answers, but a thorough search really didin;t turn up anything more recent or helpful. I'll update if I find additional info.

Citations

Bagatur, A. E., & Zorer, G. (2001). The carpal tunnel syndrome is a bilateral disorder. Bone & Joint Journal, 83(5), 655-658.
Padua, L., Padua, R., Nazzaro, M., & Tonali, P. (1998). Incidence of bilateral symptoms in carpal tunnel syndrome. The Journal of Hand Surgery: British & European Volume, 23(5), 603-606.
Pierre-Jerome, C., Bekkelund, S. I., Pierre-Jerome, C., & Bekkelund, S. I. (2003). Magnetic resonance assessment of the double-crush phenomenon in patients with carpal tunnel syndrome: a bilateral quantitative study. Scandinavian journal of plastic and reconstructive surgery and hand surgery, 37(1), 46-53.


Why spermatogenesis is an independent process while formation of ovum is dependent on fertilization by sperm? At the time of ovulation,secondary oocyte is arrested at Metaphase II and goes into the fallopian tube.If fertilization occurs, sperm binds with secondary oocyte and releases Anaphase promoting factor which leads to completion of meiosis II,ovum is formed and it subsequently gets converted into zygote.
My question is that why formation of ovum is dependent on fertilization by sperm and why formation of sperms is independent process? Has it some benefits for nature?

This can only be answered logically. Imagine bellow paragraph.
If secondary oocyte does not require fertilization for completing 2nd meiotic division then it will become an ootid (female gamete). Once formed lots of hormonal changes occur in female example individual's diet increase, mammary glands differentiate and all necessary changes for pregnancy which will be unnecessary at end of every month.
I hope u understood and comment if u want to ask about above imaginary paragraph.


How does sodium ion increase blood pressure? So I have been reading about the RAAS system and I was wondering how  natrium (sodium ) ions increase blood pressure.I have been looking up on the internet and have yet to find an answer.Help

Sodium acts on the juxtaglomerular cells of the kidney, which are then activated to produce and secrete renin. Renin hydrolyses angiotensinogen into angiotensin I. Next angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II.

Angiotensin II is the product that causes the increase in blood pressure, because it is a potent vasoconstrictor. With peripheral vasocontriction the heart has more resistance to pump blood against, thus higher blood pressure. Additionally, angiotensin II stimulates secretion of aldosterone from the adrenal glands, which acts on the distal tubules and collecting ducts in the kidney to retain sodium and water, thereby increasing blood volume and thus blood pressure.

Image: RVC 2008

This pathway is one reason why ACE-inhibitors, such as benazepril, enalapril, lisinopril, or perindopril, are used to treat hypertension (high blood pressure). With less activity of ACE, there is less angiotensin II, and blood pressure goes down. Hypertensive patients are told to consume a lower sodium diet because that will lead to less activation of the JG cells in the kidney, which will eventually result in less angiotensin II, and thus lower blood pressure.


Banana peel bruises after a hit When a banana fall on the floor or get a certain impact, the impact location gets darker (it bruises) after a certain amount of time. The darkening affects the peel as well as the fruit itself. Why does this happen?

Fruit is discolored in the first place because, when certain compounds are altered (oxidized), they turn brown.

In a banana (and most fruit) those compounds are phenolic compounds, and polyphenoloxidase is the thing that oxidizes them.

In an undamaged banana, the phenolic compounds and the polyphenoloxidase (that can turn them brown) are physically separated.

When the banana is crushed/dropped/etc, the structure of the banana is damaged so that the phenolic compounds and the polyphenoloxidase come into contact.  The polyphenoloxidase oxidizes the phenolic compounds, and you get that brownish color.

A nice summary (which links to a more detailed reference) can be found here: https://www.scientificamerican.com/article/why-does-bruised-fruit-tu/


When is really necessary to visit field to observe sample collection process? I know this could be a bit generic question, but for the sake of providing context this applies to a Transcriptomics Thesis.

Yesterday I've seen two researchers discussing about if it was really necessary for a post-doc geneticist to visit the place where the blood, weight, height, hair (and other) samples are taken.

From your experience, it is really necessary for a post-doc to travel and visit the field? Does that add real value to a Thesis? Shouldn't the sample collectors report everything like their name, how they measured a sample, etc?

After being a lab tech, just because they should report everything, doesn't mean that they are doing exactly what you think/wish. I would say it is important so you can see if the process of sample collection and processing is exactly what you need for your thesis. I had to follow a written report on how to feed a certain insect, after a few nights the post doc came in and realized there was something missing from the report and we were feeding the insects one the wrong side of the leaf. May not happen to you, but I think its always good to verify.


Use of salt as preservative I know that salt is used as preservative as it dehydrates microbes. Is there any other advantage like - altering pH or inactivating microbial enzymes ?

High salt environments are strongly hypertonic and disrupt the osmotic gradients of cells.  Excess salt gets forced in (disrupting function) and cell water gets drawn out.

In simpler terms, it dehydrates them.

This link has more info regarding what is required to live in high salt environments (and by corollary, why organisms without such features die):

http://en.wikipedia.org/wiki/Halophile


While in motion, why do closer objects appear to move faster? When I look outside the window while travelling by a car, why do closer things seem to be moving faster and appear unclear but the farther ones seem to be moving slower and appear clear?

Why do closer things seem to be moving faster?

This is due to parallax. A very simple phenomenon exhaustively explained on wikipedia.

  Why do faster moving things appear unclear?

This is primarily due to retinal persistence also well detailed on wikipedia.

It takes time for the retina to detect a change in light at a given position on the retina. Things that move quickly across your visual field (i.e. retina), or that reflect very low amounts of light tend to blur or simply be invisible. Car headlights moving close to you will blur because it takes time for photoreceptors to 'switch off' and the headlights would appear as a streak or trail of light for you. And similarly, if a car were to move at an incredibly large speed, the car wouldn't reflect enough light to trigger a response in the retina, so it would be unseen by you. Remember that what matters here is how much range of your visual field an object crosses, not the speed of the object itself. For example, a fast car in the distance does not blur since it's crossing a tiny fraction of your visual field, but a slow car right in front of your nose will be crossing your entire visual space very quickly.

These are properties of the retina. It is also possible the encoding of visual information in the brain also plays a role in how your perceive something. However, the illusion you describe is entirely explained by these retinal phenomena due to sensory neuron biology.


Probability of carrier for recessive trait given parents are carriers and sister affected I'm trying to understand more about inheritance of an autosomal recessive trait that runs in my girlfriend's family. How could I start looking at this?

My girlfriend's sister, C, is affected with a recessive trait. Her parents, A and B, are confirmed unaffected carriers. Am I correct to assume my girlfriend, D, is a carrier with probability 50%? Or must I take into consideration that we know the state of C given she is affected.

Furthermore, if I (E) have a child with my girlfriend, what is the probability that our children are either carriers or affected? My carrier status is unknown.

Assuming the trait is caused by a single gene, she would indeed have a roughly 50% chance of being a carrier. If both parents are carriers but unaffected they will both be Aa (with a being the recessive mutation). For your girlfriend to be a carrier she will have to be Aa, of the 4 possible combinations her parents could have passed on (AA,Aa,aA,aa) two lead to this outcome, thus 1/2. If you are sure that she is unaffected the aa option is eliminated and she thus has a 2/3 chance of being a carrier.

If you are not a carrier but your girlfriend is it will be impossible for your child to express the trait (but would still have a 50% chance to be a carrier!). If you are both carriers you loop back to the original situation of her parents, your child would have a 25% chance of being affected and have a 50% chance of becoming a carrier. I must emphasize that real life genetic inheritance is more complex than these textbook calculations, chromosomal crossing over and whatnot can seriously alter these percentages.

I am not a health professional, consult your physician and/or get your girlfriend tested (if possible).


Is each generation getting older? So we know that our sperm and egg cells get set aside relatively early so that they aren't going through unnecessary cell divisions and causing DNA damage or telomere shortening, but since each new generation starts from one cell each generation has germ cells that have divided more than the previous generation's germ cells.

So, does this have an effect on age?

Is a second generation baby technically older than a first generation baby due to these extra cell divisions, or is telomerase and DNA repair able to keep each generation at the same relative life span?

In germ cells telomerase enzyme is active and elongates telomeres, so youngsters are not born older than their parents due to telomeres.

Still, they do receive mutations, accumulated by their parents' germ-line cells, i.e. eggs and sperm. Most of the mutations occur upon division of the cell. Egg cells don't undergo many divisions - they are created in the course of embryonic development of a woman and then are spent one-by-one. At the same time, precursors of sperm cells divide constantly, thus accumulating mutations at a constant rate.

Got no time to look for a hyperlink, but I read that no matter what is the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations for each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1/70 leads to a change in aminoacid sequence of some protein, usually harmful.

So, although babies don't get older, but alas, they get uglier as generations pass :( Natural selection is what saves us from deterioration, so that the weakest are sentenced to childlessness.

EDIT:

Added a couple of hyperlinks as requested: decay of cognitive indicators of children with parent's age:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040

Another link: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation:
http://www.ncbi.nlm.nih.gov/pubmed/9371795


Dwell time equations for ATP-sythase? I have read that every 120 degree rotation of the F1 complex of ATP-synthase can be split into a 30 degree rotation and a 90 degree rotation. In between these two are dwell times, the one before the 90 degree rotation been called the ATP-binding dwell time and the one after been called the interim dwell time and that both of these fall of exponentially. I cannot, however, find a derivation of the probability density function of these dwell times, or there exact form. If anyone knows such a derivation or where to find one this would be much appreciated.

ATP Binding dwell time

Here is a very dodgy derivation of the binding dwell time (note I am the OP). For this we have $$E+S\rightarrow ES$$
Where $E$ is the enzyme and $S$ is the substrate (keeping this general). We can write our rate equation as:
$$rate=k[E][S]$$
But we can also write the rate as:
$$rate=-\frac{d[E]}{dt}$$
so that:
$$\frac{d[E]}{dt}=-k[E][S]$$
Now here is the bit that I think is a bit dodgy, we are going to assume that $[S]$ is approximately constant. So that:
$$[E]=Ae^{-k[S]t}$$
We can take $n=[E]V$ to represent the number of enzymes left, where $V$ is the volume, then letting $n_0=VA=constant$:
$$n=n_0e^{-k[S]t}$$
The probability of been within the time $t$ is then given by:
$$F(t)=1-e^{-k[S]t}$$
Which is our commutative distribution function. Differentiating this gives our probability density function:
$$f(t)=k[S]e^{-k[s]t}$$

Interim dwell time

The interim dwell time (also called the catalytic dwell time) involves two steps[7]:
1. The cleavage of the enzyme bound ATP.
2. The release of the hydrolysed products.

Each of which is going to follow the distribution (analogous to the above) of:

$$p_i(t)=k_i e^{-k_i t_i}$$
For $i=1,2$ respectively. The joint probability distribution is found by the convolution of these two [8]:
$$p_T(t)=\int^{\tau}_0 p_1(t) p_2(\tau-t)dt$$
Which gives:
$$p_T(t)=\frac{k_1 k_2}{k_1-k_2} (e^{-k_2 \tau}-e^{-k_1\tau})$$

Edit

Although starting from deterministic equations (which actually doesn't really matter), this method does hold and is simple. The type of reaction is called a pseudo-1st-order reaction (or 2nd order class 2) which explains my approximation for $[S]$ been constant. See [9] and [10]

Sources for additional info

https://youtu.be/X_YXTWU2maY?list=PLbKSbFnKYVY3j6ubaW1zgTXj5C4443v8s
http://www.nature.com/articles/srep08773
http://www.ks.uiuc.edu/Research/atp_hydrolysis/
http://www.pnas.org/content/85/17/6314.full.pdf
https://books.google.co.uk/books?id=uIxwICNmLKEC&pg=PA199&lpg=PA199&dq=catalytic+dwell+time+distribution+%5Batp%5D&source=bl&ots=u8oBcVNCDc&sig=PKvdVAwT0WxdqTuVwMxhU3RfSwM&hl=en&sa=X&ved=0CCAQ6AEwADgKahUKEwiGhKDalufHAhXkadsKHc54ADs#v=onepage&q=catalytic%20dwell%20time%20distribution%20%5Batp%5D&f=false
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://www.ncbi.nlm.nih.gov/pubmed/16258036
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://glutxi.umassmed.edu/grad/GradKinetics.pdf
http://chemwiki.ucdavis.edu/Physical_Chemistry/Kinetics/Reaction_Rates/Second-Order_Reactions/Pseudo-1st-order_reactions


What is this insect found in Malaysia? Found in Malaysia, South East Asia. Small insect with wingspan of around 1 centimetre. Its back legs and abdomen are pointed away from the wall.

Front View:

Diagonal View:

That is a moth, (Lepidoptera), in the family Pterophoridae. It looks very much like Stenodacma wahlbergi.  https://en.wikipedia.org/wiki/Stenodacma_wahlbergi


Why do veins undergo vasoconstriction during physical activity? How would this help increase blood circulation?

I believe that the answer is in the same cited source (BioSBCC).

Veins are considered a blood reservoir and undergo constriction to mobilize blood.

  [...] the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest. [...] When the body needs to mobilize more blood for physical activity, the sympathetic nervous system induces vasoconstriction of veins.

The result is an increase in circulating blood volume. This changes cardiac output and arterial blood pressure (CV Physiology: Blood Volume).

I also recommend reading on Biology.SE: Where does extra blood come from to fill your muscles during exercise?


Can oil be used instead of water in preparing wet mounts for microscopy? Is there a reason that oil (e.g., vegetable or clear mineral) is not used to make wet mounts in microscopy? I am not referring to oil immersion technique but substituting oil for water in wet mounts in bright field microscopy.

The question is mostly about moss or mold, things that appear plantlike on a slide. The optical properties may be good and the viscosity, as with glycerine, gives a little depth to the slide. Maybe it causes some sort of distortion? I don't see this listed as a suggestion on microscopy sites.

Thanks.

Typically wet mounts are used to observe the mobility and behavior of microorganisms. A classical use for a wet mount would be to study something like pond water were you could see all the different organisms swimming around like they would in their natural environment. Oils are more viscus and would impede mobility and might impact behavior or even be toxic to the microorganisms.

If you were an olive oil manufacturer, and you thought you had some odd microbial contamination of your olive oil you might look at a drop of your olive oil between a slide and cover slip thus using an oil based wet mount like you are describing. You might also do this if you were studying the microbiology of an oil spill in water.

There is nothing saying you could not suspend a sample in oil. There may even be a unknown benefit of using this method in certain circumstances, that is waiting to be discovered.


Suggestion about head transplant The success of the head transplant surgery depends on the acceptance of the immune cells of the body on which the head is going to be inserted. Can stem cells from thymus gland and bone marrow of the head donor be transplanted into the body on which the head is going to joined, then those stem cells will produce lymphocytes which will accept the transplanted head. Can this be a way to increase the probability of success of the head transplant operation?

I think that immune rejection is not the only major problem in head transplantation.

We are quite skilled at suturing vasculature, but it's not fully solved yet how can you make new and proper connections in the spine?

Concerning your questions, if you just took these naive lymphocytes, they would probably get destroyed by the acceptor's immune system pretty soon. If this wasn't the case, the approach would already probably be in use for other transplantations too.

What you possibly could do is a bone marrow transplantation, where you would replace the bone marrow of the acceptor with that one of a donor. However this would cause the opposite problem, the donor cells attacking the acceptors body.

For now, lifetime immunosuppresion is the only working way to go.

To get a better idea about how exactly the mechanism of rejection works and the prospective future therapies, see for example: http://emedicine.medscape.com/article/432209-overview#a8


Are the alleles that code for the same phenotype all the same exact sequence? The idea that you can be homozygous for a gene means that there are limited options or alleles , correct ?

My question is, if the mom has the allele b which codes for a blue eye, and the dad has an allele which codes for a blue eye too, are these alleles the exact same ? Do they have the same nucleotide sequence ?

This is probably a basic question but no matter how I phrase it, I can't seem to get an answer off of google.

No the same phenotypes do not mean the same sequence. For example some phenotypes are associated with alleles that are caused by non-functional gene products (like proteins). But there many ways to alter a gene to produce a non-functional protein.


Do body lotions enter into bloodstream of people? And how do they do it? I found this

very disturbing: bombastic tabloid-style writing in capital and the content is doubtful. If it was correct or close "does it really take something like 26 seconds for a body lotion to enter into bloodstream?", you select a lotion with very high level of fat -- now your heart will pump  blood with a very high-level of fat, possible source for heart failure. If you have a dry skin and you put 40%-fat lotion to your skin, it makes it more flexible. I am very-very skeptical whether any fat gets into your bloodstream. I am new to things such as blood lipids (blood fats) and mechanisms how the body lotions really penetrate into the skin. How? And which factors determine the time and does any get actually into bloodstream and after which kind of processes by the body? Is this just a hoax?

Lotions, like any other drug, can effectively enter the blood system. However, the fraction of the applied lotion that actually enters is really small, and it only achieves a significant concentration in the zone near the application. The skin, if healthy, offers a very high resistance to the passage of substances. Moreover, the bloodstream actually dilutes even more the little fraction it achieves to enter, further reducing its effects. If the skin is damaged the penetration is greater, though you'll never be able to get drunk by dropping booze in an injury.


In plant cells, is water stored only in the vacuole? In the turgor of plant cells, is water stored only in the vacuole or can it be stored in the cytoplasm and the other cellular organs too?

One of the properties of "storoge" is that in can be filled or empied when needed. Contents of cytoplasm and all organelles are aqueous solutions so all of them contain quite some water. However, thease solutions need to maintain precise concentration of many solutes in order to facilitate proper enviroment for various biological processes. Therefore, radical changes in amount of water in cytoplasm would be detrimental to life of the cell. Vacuole is not as sensitive and it can expand or shrink and act as a sort of water availibility buffer for the rest of the cell.


Predatory insect - what kind? I've seen several of these insects near my house in southeast Michigan this summer, including the one seen here feeding on a green bottle fly. What are they?

That looks like a type of "robber fly" — compare with this image:

BugGuide is a great resource for identification of insects, spiders and their ilk.


Why DNA needs histones to be packaged and ordered? I know that histones are proteins that package and order the DNA into structural units called nucleosomes, my question is Why DNA needs histones to be packaged and ordered ? Why DNA cannot do that by itself ?

Sort of like having one of these:

instead of this:

Surely you could simply wrap DNA up in a coil, but to do it in a neat fashion that allows you to package and repackage sections as needed, it's a lot better to have some dedicated machinery.

It is also difficult to organize DNA without a supporting structure because the negative charge of the DNA polymer repels other parts of the molecule, whereas histones are rich in positive charges.

As Galen mentioned in comments, histones both pack DNA into a smaller space (human DNA from one cell would be about the height of an adult if it was all in a straight line) and contribute to gene regulation. Modifications of histones control whether the DNA around that histone can be accessed by transcription machinery and therefore whether those genes will be expressed.


Database of medically validated SNPs I'm looking for all possible sources of clinically tested human SNPs. There is a handful of databases that store SNPs (like dbSNP), but I only need those that have validated presence/absence of phenotypic effects with some additional metadata. Thank you in advance.

You can search by traits (mostly diseases) for genome wide association, in these databases:

Gwasdb2
Human genome variation Database: it also links to a Copy number Variation (CNV) database.


What is the cause of the packaging capacity limit of recombinant adeno-associated viral (AAV) vectors? I am working with recombinant AAV and I am puzzled by the limit of their  packaging capacity (around 5Kb ssDNA), that is really a huge drawback for gene delivery.
I have tried to look more in deep into this problem but I couldn't find any paper that could clarify what is the reason of this limitation. Is it the size of the capsid or something else? I suppose that it is the size of the capsid but there are smaller capsids able to accommodate more DNA so it could be due to other factors. Either way, I could not find the proper literature to solve my doubts.
Do you know the answer? Or, can you point me to good papers on this topic?

It's not the size that counts, it's how you pack it (sorry couldn't help myself).

Wild-type bidensoviruses do a lot of interesting things to pack genome like splitting its genome into two virions(1), inverted terminal repeats (ITRs) that form panhandles that can stack instead of hairpins (2), and overlapping positive and negative ssDNA strand ends (2 and 3) that clip closely together.  So on the whole, I don't know that it's a fair comparison.

Also remember that you can go too small with AAV genome size, not just too large (if you go too small you will even get 2 genomes per virion).

If you want to orderly pack ssDNA (or DNA in general), you have to use some nucleoproteins to help.  Free ssDNA has the added problem of being unstable.  Going back to basic biology, you can think of nucleosomes allowing the packing of eukaryotic DNA at a much higher density than would otherwise be energetically favorable.

Viruses use a wide variety of methods to pack genetic material, one of which is through binding directly with the capsid as with AAVs.  One should remember that the capsid proteins also are tasked with entry into the cell, trafficking, and entry into the nucleus.  All while protecting and packaging the genetic payload.

AAVs, being small (wt is ~4.7kb w/7 proteins), only have the capsid proteins VP1-3 to work with.  The ITRs are known to be the cis active sequences of the genome (4, 5), and these ITRs form normal hairpins.

A portion of the AAV ITR binds (hooks onto) an interior facing portion of the VP3 gene (6, 7).  But the virus has to push in this ssDNA, and it uses the Rep proteins to do it (8).  The Rep proteins (Rep52 and Rep78 specifically), are larger than the capsid proteins, and bind the ITRs at multiple sites.

While the exact insertion pore hasn't been identified at the structural level, the way I like to picture it is a series of hairpins have to bind on spokes of the Rep proteins to be pushed into the virion, where in turn the hairpins have to hook onto the inside of the capsid.  If you put too much ssDNA between your ITRs, then you lose the ability to be passed along (or bind) to both proteins in packaging.  You start to lose the tight packing onto VP3 found in wt virus, and instead get more sporadic VP3 binding (every 3rd as opposed to every other).

It would be incredibly hard to just "increase" the size of the capsid without messing up the assembly and the other functions of the capsid.  The VPs only oligomerize in the cytoplasm (9) suggesting that host proteins are required for proper assembly.  I think the process of successfully increasing the optimal genome size would be quite a task and achievement if done.  One would likely have to optimize additional ITRs, the internal binding bind sites on VP3, and the structure of Rep52 before such a thing would be possible.  Alternatively bringing in a novel or chimeric packing mechanism, but again this would be exceedingly difficult (probably prize worthy).


What are these two insects (or at least one of them)? I need to catch and identify insects for my biology project, but I cant identify those two bugs.

Can I get the genus and the species (or it can be just general name of what this type of bug is called?)

They were found in Chicago suburban area.

I the first insect is a cricket, female Fall Field Cricket,Gryllus pennsylvanicus.

It is widespread across much of North America.They are  often found around areas of human habitation.
The the coloration ranges from dark black to dark brown, although some specimens show a slight reddish tint. The black antennae tend to be longer than the body span of the species.

It is a female because it has a long blackish brown ovipositor.

References:

Wikipedia

pbase.com

bugguide


Effect of arteriole dilation on vein If  an arteriole leading to a capillary bed is dilated will the pressure in the vein coming out from the bed decrease ? Will the velocity of blood in the vein change ?

All else being constant, velocity of the Venous blood will be reduced.

The Flow-Rate Equation: Q=AV

Q = Flow Rate
A = Area (of the "pipe")
V = Velocity of the Fluid

If we assume that the body will try to maintain a constant Q, then an increase in the A of the Arteriole means a reduced V to compensate and a corresponding drop in Venous fluid velocity.

If we start to assume that things are not constant, then the story becomes more complicated. Since Venous pressure is largely maintained by musculature and other actions, not heart contractions (though the system is essentially closed-loop), an increase in Arteriole flow-rate doesn't always correspond to an increase in Venous flow-rate. When there is an imbalance - either due to mechanical interference or something else - conditions like subcutaneous edemas can occur where the interstitial (between-tissues) fluid builds up enough to cause discomfort or damage.

*Normal Disclaimer: I am not a medical professional. The above us based upon an Undergraduate level of knowledge.


What is the name of the property of viruses that can go dormant in the host for 30 years? The Varicella zoster virus causes chickenpox in children and shingles in adults.

It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.

My question is: What is the name of the property of viruses that can go dormant in the host for 30 years?

As far as I know dormancy in viruses like the above stated chicken pox virus is known as virus latency which wikipedia defines as:

  The ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle.


How does dsDNA become ssDNA when binding to a nitrocellulose membrane? I would like to know how double stranded DNA becomes single stranded when binding to nitrocellulose membrane in southern blots. Does it require a special reagent? Is denaturing a special property of the membrane itself?

The DNA is denatured in-gel prior to transfer using alkali conditions, most commonly a solution containing 0.5 M NaOH (buffered with 1.5 M NaCl). Following that the pH of the gel is neutralised in 0.5 M Tris-HCl, pH 7.5; 1.5 M NaCl.

I have found the Roche DIG application manual to be a well-written and reliable resource for performing Southern and Northern blots. The section on Southern blots starts at page 94 and you can modify the protocol to suit other detection systems.


Do adipose cells divide in adults? I have a dim recollection of having heard that when humans gain weight, adipose cells just get larger, rather than dividing.  True?

My foray into the literature suggests that mature adipocytes do not divide. See, for example:

  Lefterova, MI et al. (2009) New developments in adipogenesis. Trends in Endocrinology and Metabolism 20:107-114

In the context of looking at the possibility of stimulating the conversion of white adipose tissue to brown adipose tissue, the authors outline the way in which the expansion of adipose tissue occurs by a process in which fibroblast-like pre-adipocytes differentiate into cells capable of storing lipid droplets and responding to insulin.

It appears therefore that expansion of adipose tissue occurs by the generation of new adipocytes. Thinking of the morphology of a fully-loaded adipocyte (a lipid droplet surrounded by a narrow band of cytoplasm) it seems rather unlikely that these cells would be capable of division. The Wikipedia citation linked to by QuietThud in the comments to the OP is to a popular book on nutrition, not an authoritative source.


Calculating Protein Concentration from Kilo Units (KU) I am looking to purchase Pyruvate Kinase from the Sigma Website, they state the volume in Kilo Units (KU) i.e. 1, 5 or 25 KU. It also states there are 350-600 units / mg protein.

Does this mean one unit is one protein? so 1KU is 1000 units of protein?
What is the relationship between the KU and mg? and how can I use this relationship to calculate my concentration in um or mg.

EDIT

In this paper (look at the methods section) they calculated the concentration of 25,000 units of calmodulin in 0.5 ml to be approximately 75um which is 40,000 units/mg. How did they calculate this?

From the page linked from your link:

  Unit Definition

  One unit will convert 1.0 μmole of phospho(enol)pyruvate to pyruvate
  per min at pH 7.6 at 37 °C.

So, the unit is defined by activity, and there is no way to know how many molecules or milligrams of protein are included


How does extracellular potassium ion concentration and calcium ion concentration affect the excitability of a cell? When extracellular $K^+$ concentration increase by a certain amount, excitability of cells is higher because the resting potential shifts toward a higher equilibrium potential of $K^+$, therefore causing depolarization. However, when there concentration of extracellular $Ca^{2+}$ increases, excitability of cells decreases. If $Ca^{2+}$ and $K^+$ are both positively charged ions, what is the cause behind their opposite physiological effects?

I'm not a biology student, so detailed answers would be kindly appreciated. Thank you!

If extracellular $Ca^{2+}$ concentration increased, it makes the extracellular membrane more positive then it used to be, then it would take the membrane potential to lower level then the excitability of the cells will be decreased

if extracellular $K^+$ increased more than the concentration inside the cell than it will make the $K^+$ on extracellular space move inside the call down the concentration gradient, it would take the potential membrane to higher state make it easier to reach the threshold (easier to be excitable)


How does the cornea breathe during sleep? The cornea is not supplied with blood vessels and so exchanges gases directly with the atmosphere. So how does it breathe during sleep when our eyes are closed?

As you noted, the cornea needs oxygen, yet it's not vascular. It needs to get it's oxygen supply from diffusion. In the daytime, diffusion occurs from air through the tear film covering the cornea.

The cornea spends about a third of it's lifetime under closed lids. At night, the tear film remains intact and is continuously replenished. The inner aspect of your eyelids, called the palpebral conjunctiva, are highly vascularized, with capillaries just below the surface (and accessory tear ducts and tiny mucosal glands to keep it moist).

When you sleep, oxygen (and nutrients) diffuses from the palpebral conjunctival capillaries through the tear film to your cornea.

The blood vessels in the palpebral conjunctiva are more permeable than most other capillaries and contribute fluid and nutrients to tears by leaking plasma. The surface epithelial cells are also a source of tear fluid because of a special arrangement of the cells such that there is more intercellular space allowing fluid, antibodies, and other plasma constituents to the surface of the conjunctiva.

This very issue was of great concern to ophthalmologists when people started wearing extended-wear contact lenses.

The Conjunctiva and Lacrimal System (www.eyecalcs.com/DWAN/pages)
Organization of Capillaries in the Primate Conjunctiva
The Conjunctiva—Structure and Function (oftalmologia/enciclopedias)
The oxygen tension and temperature of the superior palpebral conjunctiva
Facts About the Cornea and Corneal Disease (cool article)


Heart Rate being normal when under treatment for the bends When you surface from diving too quickly; you get "bends" - these are caused by gas bubbles forming in your lungs (especially nitrogen). This causes breathing problems if not treated since the bubbles are essentially blocking oxygen transport.

For treatment, you have to be in a hyperbaric chamber for several hours.

Why is it you don't get nitrogen and carbon dioxide bubbles in your bloodstream while being treated? I would think that in the machine the nitrogen, carbon dioxide and water concentrations would rise causing you to start having signs of low oxygen like loss of brain function.

As I stated previously, nitrogen bubbles block oxygen transport and thus carbon dioxide transport. Since there is nowhere else to go, it goes into the bloodstream where oxygenated blood is supposed to be. This is detected by the chemoreceptors in your arteries; this then tells the heart to beat faster in attempts to rid the body of CO2. Once again; however, this doesn't happen because now there are more nitrogen bubbles from breathing in more nitrogen and water. This leads to a progressively higher heart rate (Ventricular Tachycardia - V-tach) which is dangerous as it can lead to MI (Myocardial Infarction) symptoms - like chest pain. Ventricular tachycardia that lasts a maximum of a few minutes can then lead to V-fib (Ventricular Fibrillation) which, if not treated with epinephrine or defibrillation on time, will lead to asystole and death.

Summary:

When someone has the bends and is being treated in a hyperbaric chamber; how do they not end up having an acute MI (due to accumulation of nitrogen gas in the bloodstream)?

You are wrong on several accounts:

Bends occur due to bubbles that form in muscles and joints and not lungs - They fall under Mild or Type 1 Decompression Sickness (Type 1 DCS).
Formation of bubbles in blood stream do occur in the Decompression process - Hyperbaric chamber is used to treat this condition.

What happens when diving:
During deep sea diving the pressure surrounding a person increases at the rate of 1 atm (atmospheric pressure) for every 10 m in sea water and 10.3 m in fresh water. This relation is linear.
The pressure inside the body equalises with the pressure outside to prevent any deformation. The solid and liquid components of the body can withstand pressures upto 151 atm (depth of 1.5 km underwater) without undergoing any noticeable compression. But air, being extremely compressible undergoes compression.
So at 2 atmospheric pressure the space occupied by the air in our body is halved. This would shrink the lungs to half the total volume. To circumvent this the divers breathe air compressed at the same pressure as the water pressure around them, so that the pressure gradient across the chest wall is normal.
Pressure Concentration relationship:

Dalton's Law:
This law states that the Barometric Pressure is the sum of the partial pressures of the individual gases in the air mixture.
Barometric Pressure - The total pressure measured

In air at 1 atmospheric pressure (760 mm Hg) the partial pressures of various gases are:

Nitrogen ~ 593 mm Hg
Oxygen   ~ 159 mm Hg
Co2 ~ 0.2 mm Hg
Others   ~ 7 mm Hg

According to this Law, as the pressure inside the Lungs increase, the partial pressures of each gas increases. At 2 atm, the partial pressures of every gas doubles.
The gas exchange in the lungs is based on partial pressure of the gases. Thus due to increased partial pressure, the amount of gases dissolved in blood increases (This increase is proportionate to the pressure levels).

During a extended dive (one lasting several hours) the body tissues gradually equilibriate with the high-pressure gases. At sea level our body contains 1 L of dissolved nitrogen, equally distributed between body's water and fat. As partial pressure of Nitrogen rises, the nitrogen equilibriates with the body's lipid stores because adipose tissue is relatively underperfused.

Once equilibrium is achieved the volume of nitrogen dissolved in tissues is proportional to the alveolar partial pressure of nitrogen. Thus at 4 atm the body will contain 4 L of nitrogen.
The same principle applies to oxygen as well, though the solubility of oxygen and the speed at which equilibrium is attained are different.
Decompression
During ascent from the depths, the Barometric Pressure (surrounding pressure Pb) falls. As the Pb falls the pressure inside the alveoli fall as well. This causes a fall in the partial pressures of all gases in the lungs creating a gradient of gases from the tissues to the alveoli.
So the diver has to ascend slowly to give enough time for the gases to move into blood from the tissues and then get washed out. If the ascent is too rapid, gases dissolved in the tissues - due to high pressure - attains the gaseous form (due to pressure drop) and become bubbles. This is similar to opening a pressurised coke can where one can observe gas bubbles forming.
The bubbles are the reason for the bends. Bubbles can also cause serious problems like arterial gas embolisation, CNS disorders (due to formation of bubbles in the myelin sheath of axons which compromise nerve conduction), pulmonary symptoms (due to pulmonary emboli), sometimes even Disseminated Intravascular Coagulation.
Solution
The decompression is done in stages - in which the divers spend various amount of time at various under water levels to allow complete diffusion of dissolved gases into blood and into the alveoli which is consequently breathed out.

Hyperbaric Chamber
The hyperbaric chamber is used when the above solution is not applied i.e. the diver has surfaced rapidly without spending sufficient time at various levels to allow proper decompression.
In a hyperbaric chamber the diver is recompressed to the pressures equal to the pressure experienced at the level to which the diver dived. Due to the increase in pressure, the bubbles get dissolved again. This instantly relieves many symptoms - like the nerve conduction delay, bends, niggles etc... Now the decompression is carried out by under controlled environment, simulating the various intervals the diver has to stay at various pressure levels under water.
Hope this explains your doubt.
So coming to myocardial infarction, the hyperbaric chamber redissolves the gas bubbles thus preventing myocardial infarction.

For more info read chapter 61 of Medical Physiology, 2nd edition, by Walter F. Boron and Emile L. Boulpaep.


Why are there few tetrapod dinosaur carnivores? Today, most big carnivores are quadrupeds. Bears, Tigers, wolves.

During the Jurassic and the Cretaceous, carnivores were mostly bipedal, dinosaurs mostly from the Therapod family.

Why was bipedalism previously a very efficient predator mode for dinosaurs, when evolution could have made some quadruped familes, at least for the 10-400 kilo carnivores? For the Paleogene, there were briefly terror birds, and since then all the major carnivore families have been quadrupeds, and mammals have not evolved dinosaur convergeant evolution towards Therapod body formats. Why not?

Most of the dinosaur predators were derived from a common ancestor. The body plan was efficient, and the theropod predators speciated widely (including birds). But statistically, the number of therapod predators are not independent observations, but linked to each other through ancestry. Similarly, most mammalian predators (Carnivora) are linked to a common ancestor. Both forms worked, but there is not evolutionary pressure to evolve toward a particular form; only pressure to favor successful accidents. So it is an interesting question, but it could be that the predator niche was filled by bipeds in dinosaurs and quadrapeds in mammals.


How reversible is decerebrate posturing caused by brain stem damage? This is a follow-up question to How likely would Abraham Lincoln be to survive his wounds today?

You don't have to see a CT scan or autopsy to know if the brainstem is
injured (directly or indirectly), if it doesn't work right.
The description of the first doc at the scene mentioned that Lincoln
was not breathing, and one pupil was dilated (the latter a clear and
unequivocal sign of dysfunction of the third cranial nerve or the
upper brainstem, from where it comes). Unfortunately, the second doc
described the enlarged pupil being the right one (it's extremely
unlikely to have been one and then the other - one of the doc's was
probably mistaken as to the side).
By 3 hours after injury, both pupils were fixed and dilated, and
Lincoln showed extensor (decerebrate) posturing - again, all signs of
profound brainstem dysfunction (but not yet brain death, though pretty
close to it).

Now, what is decerebrate posturing? See http://en.wikipedia.org/wiki/Abnormal_posturing#Decerebrate

Decerebrate posturing is also called decerebrate response, decerebrate
rigidity, or extensor posturing. It describes the involuntary
extension of the upper extremities in response to external stimuli. In
decerebrate posturing, the head is arched back, the arms are extended
by the sides, and the legs are extended.[6] A hallmark of decerebrate
posturing is extended elbows.[12] The arms and legs are extended and
rotated internally.[13] The patient is rigid, with the teeth
clenched.[13] The signs can be on just one or the other side of the
body or on both sides, and it may be just in the arms and may be
intermittent.[13]
A person displaying decerebrate posturing in
response to pain gets a score of two in the motor section of the
Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale
(for infants). Decerebrate posturing indicates brain stem damage,
specifically damage below the level of the red nucleus (e.g.
mid-collicular lesion). It is exhibited by people with lesions or
compression in the midbrain and lesions in the cerebellum

The decerebrate posturing is a sign of major brainstem dysfunction.

The reversibility of this state (which is considered to be very critical and hardly reversible) depends upon the origin of the brainstem dysfunction.

The primary brainstem dysfunction means that the brainstem was directly damaged (by a bullet) and there is no way that this can be quickly reversed. This is exactly the case here and there are no chances that the brainstem might recooperate with time.

The secondary brainstem dysfunction may be caused by cerebral edema and thereby dislocation of the brainstem towards foramen magnum, where the brainstem is coned. The coning of the brainstem can be reversible if the brain edema is treated quickly and effectively (by administration of diuretics in the intravenal catheter.

With brainstem regaining its normal functions the decerebral posture will eventuall resolve and depending upon the residual brain injury the recooperation of the brain function (and compensation) may be almost entire.


Does DHA increase the effects of clarithromycin? I've read on this publication that every drug that induces CYP3A can reduce the effectiveness of clarithromycin. Clarithromycin inhibits CYP3A.

But it does not say anything about the opposite situation: does a low concentration of CYP3A increase the effect of clarithromycin?

This research shows how DHA can inhibit CYP3A.

Now the final question is: does a high concentration of DHA increase the effect of clarithromycin?

You've misread the paper. Clarithromycin is metabolized in part by CYP3A, but to an active metabolite. A significant proportion of clarithromycin and its active metabolites are excreted unchanged in the kidney. Clarithromycin, and other macrolide antibiotics do inhibit CYP3A enzymes, as you noted in your answer. You can read about this in chapter 55 of Goodman & Gilman's the Pharmacological Basis of Therapeutics.

We certainly worry about clarithromycin and other macrolides increasing the half-life of drugs that are primarily metabolized by CYP3A4 (again, see Goodman and Gilman). Midazolam is an example, and is what the paper you cite was about. If you give clarithromycin together with midazolam, expect the effects of midazolam to last longer. The important relationship between CYP3A induction and clarithromycin discussed in the paper is not that it reduces the effectiveness of clarithromycin, but that CYP3A induction does not overcome clarithromycin mediated CYP3A inhibition.


How are antibiotic resistant bacterial infections treated? For example, how are infections of antibiotic resistant strains of MRSA, Streptococcus, or Gonorrhea treated?

There are a number of ways to address antibiotic resistance in infectious bacteria. What one gets used depends on exactly what organism we're talking about. But below is a short list of some ways:

Changing the antibiotic being used. Not all antibiotics have the same molecular target within a bacterial cell. Some interfere with the formation of the cell wall, others interfere with protein synthesis, some mess with DNA replication, etc. Similarly, resistance mechanisms don't work equally well on all antibiotics. So often the solution is simply to switch antibiotics. Or, quite often, treating all infections with a combination of drugs that should get around most resistance. This is why you see people getting skittish about things like multi-drug resistant organisms - because it removes this solution.
This isn't as much a treatment as a preventative measure, but increasing antimicrobial stewardship and the appropriate use of antibiotics to prevent widespread resistance from arising in the first place.
The use of non-antibiotic antimicrobials. The most "common" of these is phage therapy - using preparations of bacteriophages that naturally prey on the infecting pathogen to help combat the infection. This was a major "contender" for how we treated antibiotic infections, but has fallen away due to a bad reputation early in its history (due to difficulties purifying phage treatments) and the discovery of antibiotics which were vastly easier to use. But there's still ongoing research, and it may pose a potential to help treat highly resistant infections in the future.


Missing 4 $\ce{H_2O}$ (per glucose) in Cellular Respiration... Where can they be? I having trouble understanding the equation of the cellular respiration. The thing that bothers me is the number of $\ce{H_2O}$ molecules. Generally, cellular respiration is written thus :

$\ce{C_6H_{12}O_6 + 6O_2 + 6H_2O -> 6CO_2 + 12H_2O}$

Yet studying the reaction on a molecular level, I realized that the water molecules just don't add up to be six! (on the left side) What I obtained from my textbook and Wikipedia is that (per 1 glucose molecule)

(Glycolysis) (in the reaction that 2-Phosphoglycerate(2PG) forms Phosphoenolpyruvate(PEP)) 2 molecules of $\ce{H_2O}$ are out of the reaction
(TCA cycle) (in the reaction that combines Oxaloacetate and Acetyl-CoA to form Citrate) 2 molecules of $\ce{H_2O}$ are into the reaction
(TCA cycle) (in the reaction that Citrate form Cis-Aconitate) 2 molecules of $\ce{H_2O}$ are out of the reaction
(TCA cycle) (in the reaction that Cis-Aconitate form D-Isocitrate) 2 molecules of $\ce{H_2O}$ are into the reaction
(TCA cycle) (in the reaction from Fumarate to Malate) 2 molecules of $\ce{H_2O}$ are into the reaction

These sums up to a net of (only) 2 molecules of $\ce{H_2O}$ into the process of glycolysis and TCA cycle... additional 6 molecules of $\ce{H_2O}$ comes from oxidative phosphorylation. Then, where can the remaining 4 molecules of $\ce{H_2O}$ possibly be?

First thing to make clear is that net $6 \, \ce{H_2O}$ go out of the reaction.($12 \,\ce{H_2O}-6\,\ce{H_2O}$)

Let me tell you my calculation, you should then be able to figure out what went wrong.

For the Left hand Side, $6\,\ce{H_2O}$ are accounted here :

$2\,\ce{H_2O}$ go in conversion of 2-Phosphoglycertae to phosphoenolpyruvate.
$2\,\ce{H_2O}$ in TCA from conversion of Oxoloacetate to Citrat by combining with Acetyl CoA.(One for each Acetyl CoA molecule)
The aconitase -cis-aconitase-isocitrate water molecules cancel out. Equal no go in and out.
$2\,\ce{H_2O}$ in TCA from conversion of fumarate to Malate.

For the right hnd side, if we calculate the no. of NADH formed = 10 and assume that each participates in respiratory chain, we have $10\,\ce{H_2O}$ from there. The other $2$ will be from the $2$ FADH produced.

So we have 6 on the LHS and 12 on the RHS. Hope this makes sense !