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Question about using Mendelian inheritance to reverse-guess the parent genotype
I would like some help with a question about Mendelian inheritance, based on the following information (I assume this is autosomal and not sex linked):
-- Start of information --
"As flatfish (Pleuronectiformes) develop, they lose their bilateral symmetry. One of their eyes migrates across the top of the head, so that both eyes end up adjacent on the same side of the head. As a result, the adult fish is able to lie flat on its side on the sea floor with both eyes facing up. In some species of flatfish the right eye migrates to the left side of the head (they are left-eyed); in other species the left eye migrates to the right side of the head (they
are right-eyed).
In one species of flatfish, the starry flounder (Platichthys stellatus), different populations have different proportions of left-eyed and right-eyed individuals. Off the west coast of the USA the population is evenly divided between left-eyed and right-eyed individuals. However, in the north Pacific, midway between the USA and Japan, 70% of the population is left-eyed and in Japanese waters all the starry flounder are left-eyed.
Consider the following hypotheses (I – III) about the starry flounder. The hypotheses assume that a single gene locus determines the final location of the eyes on the head.
I. The Japanese fish are homozygous for a dominant left-eyed allele (LL), whereas west coast fish are homozygous for a neutral allele (ll) and have an equal chance of developing into either left- or right-eyed individuals.
II. The Japanese fish are homozygous for the left-eyed allele (LL), whereas in the west coast fish both left-eyed (L) and right-eyed (R) alleles occur in equal proportions. Heterozygous individuals (LR) have an equal chance of developing into either the left- or right-eyed form.
III. There are three alleles of the controlling gene: the left-eyed allele (L) is dominant to both the right-eyed allele (l) and the neutral allele (l’). Further, the right-eyed allele is dominant to the neutral allele. Fish that are homozygous neutral (l’l’) have an equal chance of developing into right- or left-eyed individuals."
-- End of information --
Question:
The question says: When a left-eyed mid-Pacific female and a right-eyed west coast male were crossed and the offspring were all kept in standard laboratory conditions on the west coast of the USA, 50% of the thousands of offspring were right-eyed and 50% were left-eyed.
Of the following this result completely rules out:
A hypothesis I.
B hypothesis II.
C hypothesis III.
D none of the hypotheses
The 3 hypotheses only talk about Japanese fish and west coast fish, there is no mention of mid Pacific fish, and, if it is talking about the North Pacific fish, the info state that "However, in the north Pacific, midway between the USA and Japan, 70% of the population is left-eyed and in Japanese waters all the starry flounder are left eyed."
From this we infer that:

the 70% part refer to the non-Japanese fish due to the word 'and'
the non-Japanese fish must be the north Pacific fish since there are no other fish mentioned.

So:

What are mid Pacific fish? And what are their genotypes/alleles?
Some fish have equal chances of being left or right eyed, so that specific genotype represents 12.5% and 12.5% where each square of a Punnett square is 25%. So you add 25% + 25% and + or - 12.5% or 25%. Therefore the closest thing to 70% is 50+12.5 = 62.5% or 50+25% = 75%, either under or over, when trying to determine how to get the mid Pacific fish.

So I can't get the 70% and still don't know what mid Pacific fish are.
I know how to do Punnett squares. But my issue is the wording of this question. It says "left-eyed mid-Pacific". None of the genotypes mentioned in any of the hypotheses mention Mid-Pacific.
Unless it means midway between Japan and USA, which the question info state is NORTH Pacific.
So my question is, do we need to and if so how, to reverse-guess the female North Pacific fish' genotype. Or if we don't, how to do this question.
My reasoning is, the only way Hyp 1 can create a right eyed fish, as opposed to Hyp 2 (which say R is right eyed) is if I take each hyp 1 as it is (ie, the available alleles are LL for homozygous dominant left and ll for homozygous neutral where there is a 50:50 chance of being either left or right), without trying to figure out what a Mid Pacific fish is (I believe if a Mid Pacific fish is a cross between a West Coast fish and a North Pacific fish, then we need to look at all the possible combinations of this, in which the result is 70 left eyed. There are 2 problems with this, one this is a practise exam question where you have 1.5 minutes per question, and 2, there is no way to get 70 from adding or subtracting 12.5, 25, and 50.) then, Hyp 1 says LL and ll. A cross between that is 100% Ll, which is 100% Left, ruling it out instantly since we want 50% left and 50% right.
However, the answer was D, no hypothesis is ruled out.
This is a Punnett square I did for each combination listed in the 3 hypotheses, based on a West Cost male and a Japanese fish.

(So, in total we have 4 fish types, the West Cost male and a Japanese fish mentioned in the hypotheses, the North Pacific fish mentioned in the information and the Mid Pacific asked for in the question.)
Can someone help explain this?
Thank you.

Homework questions are usually closed here, but you certainly have given it the appropriate amount of thought, so +1 from me. :)

@anongoodnurse Please clear me of confusion, is the biology stackexchange closed to homework questions? This question is actually not homework nor homework related but it is the closest tag I could find, and, I have asked other questions here that are 'homework'.

If you had enough rep to close vote, you'd see that the second reason (of 5 possibilities) is that it's a homework question. But as I said, I think you've been very diligent in your thinking and explanation of same. I wouldn't worry about it, but do take the "Homework help" out of the title.

This is found on Course Hero (can't see it because I haven't signed in). I'm not saying that this is a HW question - but I was looking for it because I wondered where it came from; since it seems that a lot of the problem has to do with interpretation of the question, the best thing to do would be to go back to the person who asked it ... can you give any more context about why you're trying to solve this particular Q?

Also: https://www.coursehero.com/file/pc9ee9i/offspring-F1-of-many-crosses-between-Japanese-starry-flounder-and-randomly/

@BenBolker This is a GAMSAT practise question so a lot of people would ask it, and, there is no way to ask the person who asked it.

First of all, let's distinguish between the three populations. The Japanese fishes are all left-eyed, midway between the US and Japan the population is 70% left-eyed, and in US (or the west coast) the population is 50% left-eyed.
Let's take a look at the US population. I want to emphasize on the point that this trait is genetically determined. That is, it does not have environment factors influencing the phenotype. Next, let's look at this logically. In order for the entire population to be 50% left-eyed, the trait needs to be 50%. That is, every fish needs to have (roughly) equal chances of producing an offspring with left eyes as well as an offspring with right eyes. This does not strike me as following the dominant-recessive pattern, since that will ensure 75%-25% phenotypes. On the contrary, I'm thinking off a heterozygous genotype which will result in a random phenotype. However, we don't have proof for this yet. All we know is that the population is 50% left-eyed.
Moving on, the Japanese population needs to all be left-eyed, so any newborn fish will be left-eyed (or so we can assume, for simplicity's sake). The genotype of this population ensures left-eyed fish.
The population midway between the US and Japan is trickier. Since they are 70% left-eyed, the eye position is not controlled by chance. However, if they were like the US population, then they would all be left-eyed. Hence, we can safely assume that this population is a mix between the US population and the Japanese population. This assumption is not only based on the location (midway between both the populations), but also based on the information that they give us. Since a single gene determines the location, you cannot have a population with 70% having one phenotype. You rightly mention this when you say:

So I can't get the 70% and still don't know what mid Pacific fish are.

This is because only genetic factors determine the phenotype (given or assumed from the question). Hence, I'm thinking of an approximately 50-50 mix between the Japanese population.
50 Japanese fish + 50 US fish = 100 fish
Since 50% of the US fish are left-eyed - 25% of the total fish are left-eyed (50% of 50%)
Since all the Japanese fish are left-eyed - 50% of the total fish are left-eyed (100% of 50%)
Adding this gives us 25 + 50 = 75% of the 100 fishes are left-eyed.
This is very close to the 70% that we have been given.
Now let's look at each hypothesis in turn.
Hypothesis I
If the Japanese fish are homozygous dominant LL, that means that they will all be left-eyed. On the other hand, if the US population is neutral ll, then they have an equal chance of being left-eyed or right-eyed. Since this is what we have observed, this hypothesis could be true.
Hypothesis II
This hypothesis states that LL individuals are left-eyed, RR individuals are right-eyed, and LR individuals have an equal chance of being left or right eyed. The Japanese fish are LL, so all of them are left-eyed. The west coast fish are LR, and hence the population is 50% left-eyed. Again, this agrees with our observations, so this hypothesis can be true.
Hypothesis III
Since the L gene is dominant to both l and l', fishes with at least one copy of the L gene must be left-eyed. Hence the Japanese fish must be LL, Ll or Ll'. However, since all newborn fishes are left-eyed, the population most likely carries the LL gene. Moving on, the US population must have the l'l' genotype since they are 50% left-eyed. If they were Ll' or Ll, they will be almost 75% left-eyed (or even more because the l' gene gives a random phenotype). On the other hand, if they were ll' then they will be 75% or more right-eyed. However, the l'l' genotype works without a problem. So this hypothesis is plausible too.
Notice that I said that these hypotheses could be true. We don't know for sure that they are true, since as you noted, the hypotheses do not talk about the midway population. There are also multiple possibilities, and we don't know for sure which one is correct. However, none of these are incorrect based on the information given. Since the question asks for the false hypothesis, the answer is None of the above. Hope I made this clear!

Thank you very much!

Re: 1: "mid Pacific" is just a short way of referring to "in the north Pacific, midway between the USA and Japan".
Re: "what are their genotypes/alleles" Yes, that is what they want you to consider. For each of the 3 stated hypotheses, you should be able to come up with possible genotypes and rough genotype frequencies for the mid Pacific fish of different eye phenotypes.
Re: 2: Consider the genotype frequencies of the mid Pacific parental fish under each of the 3 hypotheses.  A Punnett square only represents 2 specific parental genotypes. If multiple parental genotypes are present in a population, you will have to make a Punnett square for each different combination of 2 parental genotypes, and adjust overall resulting offspring genotype frequencies according to the proportion of that combination.
From comment: "Ultimately my question is how do you determine the genotype of that "70% left eyed J-WC mid-Pacific hybrid"?"
Since the 70%... is a population, there may be more than one genotype among them.

If mid-Pacific refers to midway between USA and Japan, then, the hypotheses only mention pure Japanese and pure West Coast. This means I have to cross a pure Japanese that according to Hyp 1 and 2 have only LL, and a pure WC which is neutral L and R. As I mentioned in my question, the hybrid J+WC mid-Pacific fish are known to have 70% left eyed. That means you need to somehow combine the possibilities of the alleles with 12.5%, 25% and 50% to get 70%, how do you do this? (Eg 50% LL left and 12.5% LR since LR has equal probabilities of producing either left or right)

"If multiple parental genotypes are present in a population, you will have to make a Punnett square for each different combination of 2 parental genotypes, and adjust overall resulting offspring genotype frequencies according to the proportion of that combination." I know this, that is not my question. Ultimately my question is how do you determine the genotype of that "70% left eyed J-WC mid-Pacific hybrid"? So that I can then use this to cross with a pure right eyed WC to get 50:50 left and right?

It seems like you are assuming there is only one genotype represented in the "70% left eyed J-WC mid-Pacific hybrid" population. If so, why?

My reading of the hypotheses is that they do not all specify each of the Japanese and West Coast populations as having only a single genotype.

I interpret the hypotheses as, the J and WC fish have only 1 genotype - and the hypotheses are there to try and figure out which genotypes they have. That's why it is a hypothesis and not the fact.
To answer your question about why I assume there is only 1 genotype for the 70% left eyed hybrid fish: Since 1), and since there is nothing to suggest the 70% left eyed fish are made of anything else, and, since they specifically mention that some genotypes gives a 50:50 chance of either, I believe this is there to tell you that one genotype can have more than one phenotype, so, one genotype.

I'd re-evaluate your assumption of always one genotype and try seeing if more than one genotype in a population makes things work better.  Remember, "absence of evidence is not evidence of absence" - just because they don't say the 70% population has multiple genotypes doesn't mean that isn't the case. Just for fun, what would you expect to see in terms of phenotypes if the mid-Pacific population were 1/2 Japan genotypes and 1/2 West Coast genotypes?

So what is the answer and what is the correct interpretation? No one has answered my question.


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Quantifying DNA in a band on gel electrophoresis
I am a first year science undergraduate and I am just asking this as a more theoretical question rather than for carrying out a protocol, so I would appreciate if answers do not involve lots of complicated chemical names.
I was wondering how one would go about quantifying the amount of DNA in a given band on a gel electrophoresis. Some ideas I have had so far are:

Cut out the DNA band and extract the DNA. Quantify using some known method such as measuring the absorbance at 260nm of the DNA in solution to find the concentration.
When the DNA is stained with ethidium bromide, clearly there will generally be more stain uptaken in a band region if it has more DNA so it will fluoresce with greater intensity when illuminated with UV light. However I would have reservations to using this method because I would think that the amount of stain uptaken would depend also on the state of the DNA (i.e. if it is supercoiled or not), but then again I do not know how much of an impact this could have on how much stain is uptaken. Of course, if you know that all of your DNA is in the same state then there shouldn't be a problem with this method I think. Although here you would have to be aware that the concentration of ethidium bromide in a certain band depends on the concentration of nucleotides there, which depends both on the number of the DNA fragments and their size (which is known from the position of the band). Compare this with the final method...
Finally, if one is making the DNA for example using dideoxy chain termination/Sanger sequencing in PCR, then you can use a radioactively labelled primer. The intensity of the image on the radioautograph would then directly tell you the number of molceules of that DNA fragment present in the band.

I was wondering which of these are viable options to use in the lab, and why/why not.

All three methods could be used to measure the amount of DNA. However in practice, method 2 (estimation by dye brightness) typically works best in a normal workflow. It really depends on what you plan to do as your downstream application.
Problems with method 1:

Yield from gel purification methods is sometimes finicky and prone to loss.
Absorbance of remaining agarose can influence the results. DNA cleanup is a must.

Problems with method 2:

Quantification is difficult as you must estimate the band brightness against a known standard (add a known quantity of your ladder and use that for estimation).
Supercoiling of plasmids causes multiple bands to appear, so the estimation must be performed multiple times and then added (now it's less of an estimation and more a guess)

Problems with method 3:

Working with radioactivity adds a significant amount of safety protocols into a simple procedure
All products from radiolabeling must also be handled as radioactive material
Using an image has the same issue as method 2 where you're estimating instead of actually quantifying.
You could get more quantitative results from a scintillation counter, but then the products become more difficult to use because of purification from the scintillation fluid (maybe this is possible but I never tried it).
You're limited to procedures which would incorporate the radiolabeled nucleotides
If you do something like dA-tailing, then you're not quantifying the amount of DNA, but the amount of copies of a transcript.

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Exact definition of 'convergent' and 'divergence' in cell signalling?
From what I understand, we refer to 'signal convergence' as being when two different ligands/stimuli lead to the same (at least in part) responses inside a single cell. This may or may not be due to activation of the same pathway, so for example we can refer to the response of a muscle cell to adrenaline and to stimulation by the nervous system via acetylcholine as convergent because they both lead to the release of calcium. We can also refer to the activation of the phosphoinositide pathway by both activation of beta phospholipase C via a heterotrimeric Gq protein, and activation of gamma phospholipase c via the tyrosine kinase pathway, as signal convergence.
So it seems to me that 'convergence' is defined on the level of the cell with it being, in a nutshell, different stimuli resulting in the same effect regardless of at which point in some internal signalling pathway the two responses 'converge' (at least in part).
Now with divergence I am getting slightly more stuck, and I have not seen a single, clearly stated, definition. Firstly, does divergence refer only to the level of the cell, or also for the whole organism? In particular, I am thinking of cases where a single ligand has different responses in different cells, such as adrenaline leading to increased contraction in muscle cells and glycogen breakdown in the liver (I know this isn't the best example because adrenaline technically leads to glycogen breakdown in both cell types).
Perhaps instead divergence is only referred to on the level of the cell, as with convergence? So for example generally tyrosine kinase stimulation activates several different proteins, which trigger different responses: ras, gamma phospholipase C etc. Even the phospholipase C pathway produces DAG and IP3, which have different responses. But then it seems to me like practically all pathways are divergent if this is the case, because generally pathways lead to several responses inside the cell. So with the case of phospholipase C which cleases PIP2 to DAG and IP3, the DAG can regulate metabolism and transcription etc via protein kinase C and the IP3 leads to calcium ion release that causes muscle contraction. Would this be referred to as divergence?
I would greatly appreciate if someone could just state what exactly convergence and (especially) divergence refer to. I am relatively new to cellular and molecular biology.

In my experience those terms are primarily used intracellularly, but I wouldn't argue that it is wrong to use them more broadly, it's just that essentially everything released extracellularly is going to have some level of divergence, so it makes more sense to use a separate classification scheme (i.e., endocrine/paracrine). Between cells, the terms are also used in other contexts such as the nervous system to refer to inputs from multiple neurons synapsing on one neuron (convergence), and outputs from one neuron synapsing on many targets (divergence).
Convergence just means multiple signalling pathways converging on the same target: like multiple pathways that can activate phospholipase C.
Divergence just means that one effector, which could be a protein such as a kinase or a second messenger like IP3, has multiple targets.
You are quite likely to get both convergence and divergence within any given signalling pathway. In my opinion, this is one of the ways that biology is not taught well in schools: textbooks might make it seem like convergence and divergence are these concrete, specific classifications, but they are really just descriptive terms. Phospholipase C pathways are a great example that displays both. If you are talking from the perspective of activation of phospholipase C, you are probably talking about convergence because there are so many ways to activate phospholipase C, but at the same time, if you talk from the perspective of the G protein subunit that is activating phospholipase C, that G protein probably has other targets as well, so that's divergence. And downstream of phospholipse C you have divergent effects of DAG and IP3.

Ah, I see. I like how you stated that convergence and divergence are 'really just descriptive terms'- it makes a lot of sense; in any pathway you can probably find a point at which several different inputs can activate a certain protein or have one given effect, or a single protein will have several different effects- divergence. A whole pathway itself won't just be an example of convergence or divergence.

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What is the mechanism behind ventilatory acclimatization?
In my respiratory physiology lectures, my professor explained that hypoxia-induced hyperventilation occurs in 2 stages when people try to acclimate at high altitudes. My question is about the long-term 2nd stage, listed as #2 below:

there's an immediate increase in alveolar ventilation triggered by peripheral chemoreceptors, but this only leads to a small increase, and also decreases levels of $p_{CO_2}$.
over 8 hrs, there's a slow rise and 2 mechanisms are involved:
a) bicarbonate ion ($\ce{HCO_3^-}$) in cerebrospinal fluid is shuttled out and chemoreceptors increase their sensitivity to $p_{O_2}$
b) kidneys excrete more $\ce{HCO_3^-}$ to normalize blood pH

I get that the $\ce{HCO_3^-}$ and $\ce{H^+}$ comes from $\ce{H_2CO_3}$ being broken down through carbonic anhydrase. But she never mentioned where the $\ce{HCO_3^-}$ is shuttled to or which chemoreceptors are increasing their sensitivity to $p_{O_2}$ (I assume peripheral since it's mentioning sensitivity to $\ce{O_2}$). She then says that because of this $\ce{H^+}$ and $\ce{CO_2}$ levels increase, stimulating central chemoreceptors to increase ventilation to help decrease the acidity/$\ce{CO_2}$ levels. I don't understand how $\ce{H^+}$ and $\ce{CO_2}$ levels are even rising because I don't know where the $\ce{HCO_3^-}$ is even going and what it's role is. This professor is terrible at explaining things, and I'm just so confused at this point! Any sort of direction would be so helpful! Thanks!

not a complete answer, just a comment: $CO_2 + H_2O$ <--> $H_2CO_3$. This is going on all the time (e.g. in a soda bottle) without the need for an enzyme.

Some links might help you: http://fblt.cz/en/skripta/vii-vylucovaci-soustava-a-acidobazicka-rovnovaha/7-acidobazicka-rovnovaha/ http://www.ccmtutorials.com/renal/Acid%20Base%20Balance%20in%20Critical%20Care%20Medicine-NELIGAN.pdf http://mcat-review.org/excretory-system.php

@Michael Kunh Carbonic anhydrase is used in the human body to tip the balance of the reaction  $H_2CO_3\rightleftharpoons H^++HCO_3^-$ to the right side, and is an important player in acidobasic homeostasis.
To answer the question:
$HCO_3^-$ is excreted through the kidneys. This represents the metabolic compensation to respiratory alkalosis that appears in altitude.
To summarize:

ascension leaves us in with a lower partial pressure of oxygen. This will stimulate the peripheral chemoreceptors of the carotid bodies and aortic arch to increase ventilation (hypoxic ventilatory response). In consequence, an acute respiratory alkalosis develops.
renal adaptation begins after more or less 8 hours, and reestablishes homeostasis after 24-48h. To do that, the kidney will excrete $HCO_3^-$, which will tend to acidify blood (metabolic acidosis to counterbalance respiratory alcalosis). To accelerate this phase, one could take some acetazolamide, a diuretic drug that causes $HCO_3^-$ excretion.

Please note that enzymes do not tip the balance of any reaction in a direction. They specifically speed up reactions that are already thermodynamically favourable.

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Why does Haidinger's brush tilt depending on rotation direction?
Based on the Wikipedia explanation of Haidinger's brush I would expect it to remain oriented to the light polarization, no matter which way I rotate my head.
However that is not what I observe. When I rotate my head, the pattern tilts by about 20 degrees to the opposite direction. This is compared to the LCD monitor vertical direction, so total shift is around 40 degrees. I can also hold the pattern vertical by slight counter-rotation, but then it quickly disappears.
The tilt angle doesn't exceed about 20 degrees, no matter how far or fast I rotate. The tilt seems to reverse immediately when I reverse the direction of rotation, even if I haven't yet passed the original orientation. Thus it seems to be related to the rotational motion, rather than the angle itself.
I haven't found explanation for this effect, though I did find a description by    Stephen James O'Meara where he observes the same tilting. I think it may be related to Troxler's fading because the pattern quickly disappears if I keep my head still.

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Is metastatic cancer always lethal if uncured?
Can matastases spread in different parts of the body of an animal suffering from cancer grow in a limited way, such as not to cause much more harm that a benignant tumor in those parts of the body would, or are metastases guaranteed to eventually cause death, if left uncured?

What you're asking is essentially to prove a negative ("Are there no ways an unchecked cancer can be non-lethal?"), which is unfortunately more of an exercise in imagination than anything else. The best way I can answer is by highlighting what about cancer actually kills, from which you can personally evaluate if a particular type of cancer fits and would be lethal.
You need to remember that it is not the metastization per se that kills something, it is the growth interfering with critical systems that causes death. Many systems in a body will prove lethal if sufficiently compromised. The brain is an obviously vulnerable point (a sample of one of its mechanisms can be found here), but even something like the lymphatic system, which is notably able to maintain its duties with some components compromised or removed, are ultimately necessary (a compromised lymphatic system will, among other things, leave one vulnerable to otherwise harmless infections). The primary checks to take away from this are "Can a body survive with this system compromised, or to what degree?".
Even in the case of a hypothetical cancer that is not particularly metastatic, but simply growing in a particular area (we'll even be generous and say the particular area is not vital to survival), tumors take resources to maintain, both chemically and mechanically (pulmonary issues are known to occur with this sort of unguided growth). Many of these effects can be highlighted in overgrowth diseases such as in Proteus syndrome (Note - My apologies, this is behind an academic paywall). Considerations for this part are "How many resources can a body afford to lose?" and "Can the heart support this extra mass?".
As an additional factor, tumors that don't allow infiltration by cells from the immune system can be prone to infections, both internally and externally. This is circumstantial, though, and not a core component of a cancer's lethality (mostly).
The mere presence of a tumor is not guarenteed to be lethal, but I would say, ultimately, any continuously-growing tumor will lead to death, simply by subverting the proper mechanisms of the body to a sufficient level.
References:

Papadopoulous et al., Neuroscience (2004);129,1009–1018
Cohen, AJMG (2005);137C,38–52

Thanks! There's a few other documents I'm looking to put in. Is the academic paywall that I'm citing through an issue?

Please add more, great! Paywalled stuff is more than fine. To me, it testifies of someone with an academic background :)

Honorable mention for paraneoplastic syndromes which add insult to injury.

@HarrisWeinstein You can also possibly include the case of benign tumours of endocrine glands (such as thyroid/adrenal etc ) that cause problems due to hormone oversecretion.


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Are there animals that can deliberately manipulate their metabolism, apart from hibernation?
Are there animals that can slow down their metabolism deliberately? I know that hibernation would be one mechanism, and maybe being cold-blooded, but I was wondering if there was maybe an animal that could crank up or slow down metabolism based on food resources?
Are there chemical compounds that could have this effect?

By deliberately do you mean voluntarily? Pythons are known to modulate their metabolism. Are you looking for examples like this?

Yes, sorry, voluntarily would be a better word!

Humans.


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does life make or break?
Ok, this question seems like it may be impossible to answer, but would be interesting to see if anyone has an idea.
Throughout the course of a human life, do we make more molecular bonds than we break, or vice versa?

Metabolism ≈ Anabolism + catabolism
Metabolism is the set of all chemical reactions happening inside a living body. These reactions can either breaks down big molecules and build up big molecules. The set of reactions the breaks down big molecules is called catabolism. The set of reactions that build up big molecules is called anabolism.
Energy
Generally speaking, anabolism cost energy and catabolism yield energy. The molecule that is directly used to transfer this energy is Adenosine triphosphate (ATP).
Any energy transfer is coupled with some loss of energy from the system (see Energy conversion efficiency).
Entropy
For any chemical reactions, there is always an overall increase of entropy. As a consequence, a living organism increases the entropy in its surrounding. In other words, it breaks more than it builds.
Your question

does life make or break?

Life does both! But on average, it mainly breaks things up (just like any other chemical reaction).
Want to learn more?
The concepts of energy and entropy are studied in physics and chemistry but not so much in biology. I cannot really give you a good source of information.
Khan Academy offers a very good introductory course on metabolism (here), you should have a look!

that's a great answer, thankyou. But if the breaking of molecular bonds is endothermic, and life 'mainly breaks things up', does that mean life is negative entropy? http://www.masterorganicchemistry.com/2010/10/28/the-marriage-may-be-bad-but-the-divorce-still-costs-money/

My guess would be that, as complex organisms, we make more complex molecules than we break ---> net exothermic ---> entropy


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Data on Gene Position in Human Genome
I am trying to get some data on gene position in the human genome and I need some help
What I tried
I downloaded ftp://ftp.sanger.ac.uk/pub/gencode/Gencode_human/release_18/gencode.v18.annotation.gtf.gz
I am only interested in gene position, so I kept only the first columns.
awk -F "." '{print $1}' /Users/remi/Downloads/gencode.v18.annotation.gtf  >> HumanGenomePositions.txt

This operation will take a few minutes. The file contains information on exon position and transcript. I subsetted the table to get only the lines that concern genes
sed -i.bak '/gene/!d' HumanGenomePositions.txt

I am left with 57445 entries. 9872 are annotated by ENSEMBL and 47573 are annotated by HAVANA. Note that there is partial overlap between the two. According to Church et al. 2009, there are 19042 annotated genes in the human genome (reported from bionumbers). There is obviously something I am getting wrong!
Question
Can you help me to get data on gene positions in humans in a handy format (see below)?
start   end
15648   65487
129841  124984
...

I used the <homework> tag even though this is not a homework. The reason is that I think the question is introductory enough to be asked in an introductory course to bioinformatics.

Why did you pick GTF vs. GFF3? I only ask because I have way more experience using GFF3; also, in GFF3 column 2 tells you the type of sequence feature that is being annotated in a given row, so by using cut -f 2 | sort | uniq -c you can get a list of all the "known" features in that file, as well as a count of the number of them.  A potentially trivial explanation for the discrepancy you found is that Church at al., are only counting the protein coding genes, while your regex search will match tRNA genes, rRNA genes, miRNA genes, snoRNA genes, and pseudogenes, wouldn't it?

One extremely useful tool (in my hands) is the intermine family of data warehouses. I have primarily used modMine and FlyMine, but there is also a HumanMine. If you had a list of identifiers for those human protein coding genes you could upload that list into HumanMine and then use their query tool to generate a table of the genomic coordinates for those human genes.

I used GTF completely randomly. I don't know any of these format and I never heard of "interMine family of data warehouse" before either. Oh do you think we might have about 30,000 non-protein-coding genes? It seems huge to me but that would be a good explanation.

I recommend to filter using transcript_type value from description column. You need only proteine_coding genes. Now you have extra ~10K unprocessed pseudogenes, ~5K antisense genes, ~4K miRNA, ~7K lincRNA and more than thirty other categories of unprocessed pseudogenic stuff.
As far as I know current release for GRCh37 is 19th version, not 18.

Oh I missed this column. So is there really so many genes that do not code for proteins? I would have never guessed right. I'll just subset what I need based on this column. Thank you.

I took the 18th version completely randomly. I felt a little lost and just picked some random data to start doing things with it.

Side Question: Looking at ftp://ftp.sanger.ac.uk/pub/gencode/Gencode_human/ I can see 24 releases. Is the 19th really the newest one as you claim?

@Remi.b I suggested using the 19th release because I supposed that you use the 18th release and it is the GRCh37 assembly. As you do not have any specific needs, I think it is fine to use the latest stable release.

Gencode is 24th version afaik.


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How many genes of an individual are homozygous?
We have 20000 to 25000 protein-coding genes. Considering an individual, how many of his\her protein-coding genes are homozygous? I am looking for an estimation of gene homozygosity ratio in human individuals and\or other organisms and appreciate any help (preferably with the support of an academic paper).

Do you mean the number of homozygous genotypes? A single gene contains many different genotypes, some which are homozygous and some heterzogygous.

@user438383 I mean how many of genes of a person are homozygous and how many are heterozygous? I think you meant that a person has many genes, some are homozygous and some are heterozygous.

No, I meant what I said. Unless you are using a different definition of 'gene', then to my knowledge, a single gene contains many different genotypes, which may be either heterogyous or homozgous.

I do think this could be caused by 'gene' having multiple, related definition. How are you defining it?

A single gene across a population may contain many genotypes, but an individual can't have more than 2 genotypes for a single gene (barring trisomies or other gene duplications)

I think it's going to vary quite a lot...someone with one parent who is pure Chinese, and the other parent is pure Swedish is probably going to have more heterozygosity than someone who can trace their ancestry on both sides to, say, Limerick.

Recall that a gene generally consists of DNA sequences, which may yield numerous alleles, each of which is a variant at a discrete positions within the DNA sequence of the gene. For example, there are numerous known variants of the beta-globin gene, some of which cause inherited anemias such as sickle-cell anemia. A variant at coding position 40 causes beta-thalassemia, and a variant at coding position 6 causes sickle-cell disease.
It is possible (though unlikely) for a person to be heterozygous for each of these variants independently (when the variants are so closely linked, i.e. the same gene, this might be called "compound heterozygosity").
The terminology is admittedly confusing, and there is a tendency to be sloppy with language particularly in medical genetics and population genetics talking about "genes" being heterozygous, or "gene frequencies" meaning allele frequencies. This is very old terminology from before when we knew what genes were made out of (DNA).
But when we talk about heterozygosity in the sense that you mean ("how many [x] are heterozygous?"), we can only answer this where [x] = positions, not when [x] = genes.
In terms of positions of the human genome, estimates differ among populations but I believe that something like 0.5%-1% of variable positions are heterozygous (see e.g. Figure 1 of this paper, note scaling of axis). Of course, the number of variable positions in the genome is relatively small (0.6%). So you might expect that on the order of 0.001% to 0.01% of positions in the human genome are heterozygous in any given person, depending on their population of origin.
I was unfortunately not able to immediately find a study that directly estimated this number, though I'm sure it exists somewhere.


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Why do ants live so long?
I was surprised to learn that worker ants in some species live many years. I would have expected a lifespan of a few weeks or months (which is apparently the case for many species).
What factors might account for the length (and/or variation) in ants' lifespans?   (ie, is there some evolutionary preference? Some fundamental limit on the reproductive capacity of the queen?) Is there any relationship between these lifespans and different structures of ant communities?

Can you name the species in which the ants live long?

There will always be a tradeoff in terms of resource allocation between reproduction and self maintenance. Since worker ants forego reproduction to perform other roles (gathering resources, caring for young etc.) within the colony, it makes sense that this would favour a longer lifespan. This idea works for most animals (i.e. higher reproduction = lower lifespan across species in general) and is well documented (Partridge et al. 1987, Gems & Riddle 1996 (PDF link), Westendorp & Kirkwood 1998 - to name a few). However the relationship is reversed in eusocial animals: the queens of ants, some bees and naked mole rats (which are all eusocial) tend to be longer lived than their sterile workers (Hartmann & Heinze 2003). Aging patterns within ants and other eusocial organisms are a very popular research topic at the moment, but the mechanisms causing differences between social castes are not fully understood.
Eusociality is strongly associated with increased lifespan, indeed many studies on the evolution of aging have focussed on eusocial animals which have appeared to overcome aging effects to an extent (Keller & Genoud, 1999, Buffenstein 2005). The naked mole rat is one of very few species of eusocial mammals and the relationship between its lifespan and body mass is very dissimilar to that of other rodents (ignore the bat points):

Image from Buffenstein & Pinto (2009).
If a queen has a longer reproductive lifespan then over the course of its life it will create a higher number of offspring. This will cause their increased longevity genes to be more prevalent in the gene pool over time - as long as they are able to reach the limit of their reproductive lifespan and are not killed by externalities (accident or attack) in the meantime. Therefore this trait (longer reproductive lifespan) will be selected for as long as the queen is protected.
Within eusocial colonies, there is often a protective environment (Buffenstein & Jarvis 2002): there is usually a physical structure (nest or burrow); symbiotic bacteria and/or fungi creating a more hygienic microflora; and queens are also protected by other castes. This gives queens a lower incidence of death due to accident or attack which (from the reasoning in the previous paragraph) supports the selection of a longer reproductive life. This is likely to lead to longer lived workers since they share the same genes.
However queens do tend to live much longer than their workers (O'Donnell & Jeanne 1995). This is probably due to their reproductive role. All the ants in the colony are investing in reproduction (whether by physically giving birth to young or by providing it with food and protection) therefore the normal relationship (reproduction and lifespan tradeoff) mentioned at the start is not relevant, but since the queen is the only individual reproducing, it will be the only one for whom lengthened lifespan is beneficial evolutionarily.
A mean lifespan of 20 years has been observed in Formica exsecta, and a maximum lifespan of 28.5 years observed in Lasius niger. Pogonomyrmex owyheei has an observed maximum of 30 years, and mean of 17 years. These (and many more) figures were obtained from a review by Keller (1998).
Other references on this subject include (Svensson & Sheldon 1998), (Keller & Genoud 1997) (PDF link), (Calabi & Porter 1989), and (Amdam & Omholt 2002).
References

Amdam, G.V. & Omholt, S.W. (2002) The Regulatory Anatomy of Honeybee Lifespan. Journal of Theoretical Biology, 216, 209–228.

Buffenstein, R. (2005) The naked mole-rat: a new long-living model for human aging research. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 60, 1369–1377.

Buffenstein, R. & Jarvis, J.U.M. (2002) The Naked Mole Rat--A New Record for the Oldest Living Rodent. Sci. Aging Knowl. Environ., 2002, pe7.

Buffenstein, R. & Pinto, M. (2009) Endocrine function in naturally long-living small mammals. Molecular and cellular endocrinology, 299, 101–111.

Calabi, P. & Porter, S.D. (1989) Worker longevity in the fire ant Solenopsis invicta: Ergonomic considerations of correlations between temperature, size and metabolic rates. Journal of Insect Physiology, 35, 643–649.

Hartmann, A. & Heinze, J. (2003) Lay eggs, live longer: division of labor and life span in a clonal ant species. Evolution, 57, 2424–2429.

Keller, L. (1998) Queen lifespan and colony characteristics in ants and termites. Insectes Sociaux, 45, 235–246.

Keller, L. & Genoud, M. (1997) Extraordinary lifespans in ants: a test of evolutionary theories of ageing. Nature, 389, 958–960.

Keller, L. & Genoud, M. (1999) Evolutionary Theories of Aging. Gerontology, 45, 336–338.

O’Donnell, S. & Jeanne, R.L. (1995) Implications of senescence patterns for the evolution of age polyethism in eusocial insects. Behavioral Ecology, 6, 269–273.

Svensson, E. & Sheldon, B.C. (1998) The social context of life evolution history. Oikos, 83, 466–477.

I know I'm late to this, but longer worker lifespan could be beneficial because colony size is a function of birth rate and death rate. Longer lifespans means a slower death rate and colony size can increase without forcing the queen to produce more workers than normal. If workers died quickly, the queen would have to lay a lot more eggs to increase colony size.


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Why is there an extended delay before G.M. liver cells are attacked by the immune system?
In this BBC article a trial is described where patients with B-Haemophillia are infected with modified Adeno-associated Virus 8 which contained the genes for Factor IX clotting protein.  Trials seemed to be successful, however the article later mentions

There was an immune response against the infected liver cells around seven to nine weeks after the virus was injected.

I am interested to know why there was a delay period of such length?  Would this be true of all cells and is it due to a long duration of clonal selection in the humoral immune response or is something else at play?  Also, I'm presuming that the Adeno Virus would be attacked long before the cells it has infected?

The delay in immune attack is common for many viral infectious deceases where auto-immune response plays substantial to significant role in pathogenesis of the decease. The classical example here are the viral hepatitis B, C and D where it is auto-immune attack that causes the massive death of liver cells (hepatocytes).
The delay in immune attack is explained by the following mechanisms:
The immune attack is developed against the surface antigen, in case of hepatitis it is the HbS Antigen. "Surface" means that this antigen has to appear on the cell surface in order to elicit immune response: the virus itself as well as the parts of destroyed cells are not immunogenic enough for this.
The second point explaining why the attack takes so long to develop is that it is primarily cell-mediated attack, the humoral factors play the secondary role here.
So, the usual "workflow" in this case is the following:

Contamination with hepatitis virus.
Virus propagation to hepatic cells and their infection.
Processing of the viral DNA (either as DNA or first reversed-transcripted from RNA) so that it is integrated into cell normal processing pathways.
Expression of viral proteins (=antigenes) and their anchoring in the cell membrane.
Surface antigenes are detected by macrophagues, processed and expressed on their membrane for T-helpers
... (continuation of the usual cell-mediated immune response via T4 and T8 lymphocytes).

Every stage takes some time, the total duration can sum up to 4 to 12 weeks depending upon the viral activity and the immune system status.

I've encountered cell mediated and humoral pathways as part of my studies so far, so I understand most of your answer.  However why is it that the response to this pathogen is more cell-mediated than humoral?

There is no clear answer here, possible causes are high mutability of the RNA hepatitis viruses (similar to that of AIDS) and the positioning of many viral antigens deeply within the liver cells, so that they cannot be accessed by antibodies. Humoral response is also here, but during the successful course of therapy it is supposed to go down, not up.


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How many gigabases of DNA are there on earth?
The human genome is about 770 MB, the C. elegans genome is about 100 MB, the yeast S. cerevisiae is about 12 MB. Different other genomes have been sequenced: how many GB of genomic DNA we have now?
Let say we would like to make a Noah hard-disk ark: how much space would it take to represent the genomes of all known species on earth? There is a way to provide an estimate?
I'm also interested in the total biodiversity: for instance, if two species each have 1 GB genomes and have half of their DNA in common this would count as 1.5 GB.

I think this is an unanswerable question - there are a handful of species whose genomes have been sequenced, and many millions on the earth that remain completely uncharacterised!

The human genome has highly repetitive (“low complexity”) regions though, which means that it can be compressed much further. This is the real measure of biodiversity “size” since it measures the actual information content. And adding genome sizes is much more complex than you make it out, your 1.5 GB approximation isn’t very precise.

@KonradRudolph You have to choose between the most reductive representation of the genome and the fullest one.  I'm sure we'll have records of hundreds of millions of variants in the human genome alone by the end of the next decade.  There are proposals to move away from a single reference build for the human genome.  Not only storing the sequence itself, but annotation describing how the variants are used already blows the doors off of 770 MB.

@shigeta I don’t think this is relevant here. What Craig wants to measure is the combined information content of all genomes, and the information content is by definition the entropy which, again by definition, corresponds to the size of the data in its tightest (theoretically) possible representation.

It really depends on what you are trying to understand.  Total information measures are convenient for bookkeeping, but considering the recent work that shows how frequently horizontal gene transfer occurs in bacteria, http://phys.org/news205389256.html, its probably true that you will never run out of bacterial genomes to add to the sequence database as @MarkSchltheiss is pointing out.  I'm definitely more of a pessimist w.r.t. the tractability a complete genomic sequence catalog.

Why is it more interesting to talk about megabytes, rather than megabases?

@nico Because people are used to thinking in bytes; they have a relative impression of how much "1GB of information space" can hold.

@Armatus: OK... although to me it makes much more sense to talk about megabases. Personally I don't have an impression of how much of a DNA sequence can be stored in 1Gb... also because it really depends on how you store it.

@nico: I suppose we like to convert things into units that we can relate to known quantities. E.g. I'm used to metres so I'd always rather convert inches and miles. I can't imagine how far "5 miles" is exactly. But I know that it's roughly 1:1.5 so about 7.5km which is about 3/4 the way to work which I cycle in about 25 minutes and so on. :)

If you want to represent all genetic information on Earth, you need to get all individuals, not all species. There is significant variation between two humans or two birch trees, so you can't just take a single sample per species and say 'got it!'.

What's with compression algorithms?

If you simply take one order of insects, Coleoptera, there are just under 400,000 described species with estimates from 850,000 to 4,000,000 species total in just this order.  The number of primates is under 1,000.  If your assumption of say 10MB for all other primates would be accurate, just adding in the low end estimate of 850,000 at 10MB per 1000 we are quickly at 8,500GB which seems to be a factorial out of the GB range.
So, we have a broad estimate of non-bacterial of plants, animals etc. at say 8,700,000.
Jason Gans found in a 1 gram of soil survey approximatly 1,000,000 bacterial species.
SO the total accounting for species number is totally impossible to estimate for anything at this time, let alone the genome.
Even for something as "common" as a giraffe, there are up to 9 sub-species with genome differences within each subspecies.
So, once we get them all decribed, we can then work on the genome sequence for each and get you some answers!

Recent genetic work on the Giraffe now indicates multiple species of what were once thought to be sub-species, some of which are now viewed as endangered of extinction due to the low population numbers in some.

According to this paper there is ~ $5.3 \times 10^{34}$ base pairs of DNA on earth. One base pair contains approximately 2 bits worth of information (4 possibilities). So that would be ~ $8.48 \times 10^{35}$ bytes of information.
or more than the total information in all digital and analog technological storage media on earth combined.

I was mostly wondering about thy total information content in all dna on earth. This number is probably much higher than the total information content as many of those strands will be duplicates, but I upvoted your answer as this still provides a good upper bound and possibly some good places to start with other calculations. Thanks!

duplicate information is still information, most of the information in books or on digital media is duplicate as well. Any estimate you compare it to will contain a lot of  duplicate information. Alos the original paper lists the number in megabases, I converted for convenience.


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What is this fruit found in a market in Uyuni, Bolivia at the end of December 2019? (orange skin, 4cm, white flesh)
What is this fruit found in a market in Uyuni, Bolivia at the end of December 2019?

Fruit diameter: ~4 cm. Seed: large, spherical, black. Flesh: white. Taste: sweet but not as sweet as a lychee.

I found the name: it appears to be Garcinia humilis, known commonly as achachairú or achach:

Garcinia humilis, known commonly as achachairú or achacha, is a small, prolifically-fruiting tree related to the mangosteen. It grows in the southern part of the Amazon basin in the central area of Bolivia, but has recently been planted on a commercial scale in Burdekin, Australia.

That matches the area, appearance and season.


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Why do parasites sometimes kill their hosts?
It's bothered me for a while now. I understand why a parasitoid would do this, as it only temporarily requires the host, and that not all parasites kill their hosts.
There seems to be no evolutionary advantage in killing a host, because the parasite relies on the host for resources. Yet some organisms, usually microscopic pathogens, seem to fatally damage the host with no immediate benefit to themselves. Why is this? Won't it be better to have a commensalism relationship with the host so both exist healthily?
I know this is asking for a broad soft answer, but I don't want the question to get bogged down by a specific species, although it would be good to have examples.

Great question. I wonder if metapopulation dynamics could have something to bring to this conversation. That is, it can be appropriate to exhaust your resources in one "patch" (eg., glade, island, host organism) if it's relatively easy for you or your offspring to move to another "patch"

I can think of several (non-exclusive and probably non-exhaustive) hypotheses:

Maladaptive. It is maladaptive. Maybe because it is a virus coming from another species (e.g. SIV and HIV) or because it is not adapted to our modern lifespan.
Benefit of the host immune system to the parasite. Some parasites might benefit from host immune defence (e.g. sneezing helps bacteria to spread) and death is a consequence of the selection for increasing disease symptoms to the host.
Pathogen's and host's fate. The pathogen's fate is not linked to the host's fate. This is especially true if the pathogens spread well (easily jump from one host to another) I guess or for parasitoïd because the pathogen leaves its parasitic life after the death of its single host.
intra- and inter-host selection. Among hosts, there might have a selection for reducing resource consumptions and therefore for decreasing the probability for the host to die. But within a host (among individuals of a parasite population or even among parasite species), it is a prisoner's dilemma (tragedy of the commons). The more you invest in foraging, the more competitive you are. This might not be adaptative at the population level but it is at the individual level. We might think of this prisoner's dilemma happening among individuals of a single parasite species or among several parasite species. You may want to have a look at the work of Martin Nowak on the subject incl. Consider for example his book; Evolutionary Dynamics.
Consequence of harming on trade-offs. Harming an individual will cause him not to spend energy into reproduction in order that more energy is available for the pathogen use. Moreover, by causing symptoms, the infected individual will be sexually less attractive and will again have less opportunity to spend energy into reproduction.
The pathogen does not mean much harm. When fighting pathogens, many of the symptoms we experience (such as fever typically) are actually caused by the immune system and not the pathogen itself. A maladaptive overreaction of the immune system can cause our death.

The book Why we get sick by Randolph Nesse and George Williams, will probably interest you.

#3 is a common answer, and linked to #2,4,5.  Lots of viruses for instance simply reproduce and spread to other hosts.  If a host dies it doesn't hurt the pathogen if it's timing is good.

I like #3, but what exactly do you mean by well spread? Are you talking about method of infecting new hosts, or general population?

@GoodGravy I meant "if pathogens have good dispersal abilities (good abilities to jump from one host to another), then it is likely that the survival of the parasite is not linked to the survival of the host". Does it make sense? I don't really understand your question above. But I said "spread well" not "well spread".  Maybe here comes the doubt.

I think you should make the 4th paragraph more clear.

@Mockingbird I'm not sure how to edit it to clarify this point. I made some modification but I am not sure it helps. If you have specific ideas, feel free to suggest them.

Some parasites aren't natural hosts of humans, instead we are an accidental host in which they cannot replicate. Zoonoses such as this can be quite fatal as the parasite is not adapted to us. Although viruses are often separated, they are parasites and you can see just in influenza that the animal derived flus are more fatal than those that are well adapted to humans.
Otherwise because there is no need for the host they can be fatal. If they have finished their round of replication or require death of the host to be able to spread. Still this is less common than simply a badly adapted parasite.
HPV causes cervical cancers. It is adapted to increase replication of its host cell which is obviously beneficial, but this also kills the host in the long term. Thus some viruses are not yet adapted to the new longer lives we live, but may never do so due to less of a survival pressure hence vaccines.
Please feel free to ask questions.

+1 - a number of the parasites that cause human disease aren't supposed to be in us. We're an odd side-note in their lifecycle.

This is related to Remi.b's answer, but a common reason is that sometimes parasites/pathogens actually need to kill the host to spread.  A lot of viruses, in particular phages, are only released from their host by bursting out of the cell.  If the parasite can't leave the host, there's no point in any of it, and death may be a good way to achieve that.  A number of diarrheal diseases in humans cause death because massive diarrhea (aka water loss) is how they spread.

A virus usually destroys its host cell to get released (this cell has been reprogrammed by the virus to produce only viral products anyway) but this does not necessarily mean the death of the host.


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Tissue grafting in marine invertebrates
I'm trying to source a procedure for a transplanting tissue in regenerating polyps. Would anyone happen to know where I can find a method of adhering to donor to host tissue?
Thanks

I think what @bonCodigo is trying to ask is what kind of polyps you are talking about (their habitat etc).

Colonial anthozoans located in the intertidal region. Truthfully, I can't find a procedure for grafting tissue in any aquatic invertebrate. I'm just looking for a good starting point.


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Why are bovines different genera if they can interbreed?
Why are bovinae a "subfamily", above Genus, when members can interbreed?  Some like the beefalo are fertile, which is the normal defining characteristic of a species. And Genus are groups more distantly related, so by definition they should not be closely related species.

Different genus doesn't mean that they are very far away genetically, it means that they can be classified at a clear level above species.
Genus are not strict and codified, they give order in the animal world for groups of the nearest affiliation after species... based on: common ancestry, reasonably compact groupings, distinctness (of ecology morphology etc).
There are 143 bovidae in 50 genera, sheep to gazelle to wildebeest. cows are in the subfamily bovinae, made of 9 or 12 genera and three tribes.
They have decided that cows are of three types, buffalo's, bison's and bos/ox, in the tribe bovini, and that there oryx, kudu and bongo antelope are cousins of cows from a different bovinae tribe.
Scientists have agreed that bison can be grouped in a different group, genus, that zebu and cattle. It's logical.

vs

vs

They have agreed that indian cows, zebu, from indian aurochs, is in nearly the same as a cow derived from eastern aurochs, compared to the 5 species of buffalo.
For example with pigeons, they have decided to group all the species related to the wood pigeon into one group, and the columbidae family actually has 42 genera of pigeons, mostly exotic and tropical ones, and even stuff like dodo's.
https://simple.wikipedia.org/wiki/Bovinae
They make mistakes regarding genus as often as for species, and may have to swap around a species from one genus to another based on genetic evidence, even if two genus have members with parallel ecologies and appearances.
Taxonomists will say "Tragelaphus and Taurotragus genera are sometimes included with bovinae", the groups can be blurred and flexible.
It's a messy job for taxonomists.
http://bioweb.uwlax.edu/bio203/s2007/hayes_katy/images/ruminants.bmp
https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcSWBirAqviIKqUNdGHbxfhZJ9JcK57jU8mYD5iydpV5wFIARCQJ
https://www.researchgate.net/publication/225666813_DNA_barcoding_of_18_species_of_Bovidae
https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/9b140afd9d0d3eaf61ac9bde4560f8c9c207e380/9-Figure4-1.png

Species are not defined by whether they can interbreed, not even close.
In fact, there is no objective, scientific standard for what defines species, or genera, at all. What is a species is determined by little more than the "feels" of the individual naming it, or the committee approving it.
And the same is true of the entire rest of taxonomic structure. It's not really science, it's just a way of organizing ideas that got popular, and in fact is under constant assault now by somewhat more scientific things like genetic testing. The hierarchy of the taxonomic system changes pretty much daily, and has no official structure or definition at all. Even the number of kingdoms is entirely up in the air.
Getting back to the specifics here, since there is no objective, scientific standard for what is a species or genus, it's no surprise that separate ones can interbreed.
And it's not like bovines are the only ones. There are many other intergeneric hybrids possible, like sheep and goats, wheat and rye, camels and llama, house cats and servals, marine and land iguanas, et cetera.
Perhaps someday there will be objective definitions to establish a truly scientific taxonomy. But for the moment, it's just whatever people in positions of power feel makes sense, at any given moment.
List of Intergeneric hybrids

Although binning organisms into "species" is an artificial construct to allow conceptualization and organization of life's diversity, your post is misleading and seemingly misinformed. There are dozens of ways to "define " a species, which we term species concepts -- many of which do not rely on the ability for interbreeding as part of the "definition". These concepts are not defined by "people in positions of power", but rather used to varying degrees in the scientific literature as support for certain taxonomies.

...In other words, it's the peer review process that ultimately decides the value for binning species according to the concepts defined in various papers; not "people of power". Perhaps becomign more common are concepts based on genetics/phylogenetics as they seem to be somewhat more objective than more historically utilized concepts (e.g., morphology).

You say that as if peer review were in any way a valid part of the actual scientific method, instead of being an impediment to it that cultivates conventional wisdom and censors ideas that sometimes turn out to be correct.


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where can I find microarray images?
I have investigated some of the links to known microarray databases, such as arrayTrack, omnibus (NCBI), TCGA. I find that when trying to get microarray images I either get an exotic file format (such as .sdf or .cel) or text base information. Does anybody know of publicly available microarray images (preferable with metadata too) in .svg, .png, .jpg or another well known image file format?

Welcome to Biology.SE I am not quite what exactly you want to be displayed on those images. If you just type microarray on GoogleImages, you'll get many pictures of these dots of colours on a black background. Is it what you're looking for?

yes, it is. But I would like them to be available through a database system so I may get a lot of them with description of which genes are on the array.

Oh ok. That makes sense. I would tend to guess that researchers rarely upload the pictures directly (as it is a very costly way of storing data) but only the results in a .txt (or other) file (I have never worked with this kind of data). Out of curiosity, why do you want a lot of those pictures?

I would like to analyse them on a GPU as I think they are the perfect for data based parallelism.

Microarray images (at least for Illumina arrays) will come in .tiff format and are huge compared to the summarized formats (.sdf/.cel). Most places will not archive the raw images (so you won't find them online) and even when you run the microarray, you will often times need to make a special request to output raw images. iirc .jpg images are useless due to compression artifacts.
You can use the proper bioconductor libraries to extract data from the 'exotic' file formats. There are many bioconductor workshops archived online that will go through the steps of microarray analysis.
http://www.bioconductor.org/packages/release/bioc/html/affy.html
http://www.bioconductor.org/packages/release/bioc/html/beadarray.html
http://master.bioconductor.org/help/course-materials/2007/BioC2007/labs/oligo/BioC2007-oligo.pdf

sad that its not possible to get raw pictures ..

@hotGopher You might to directly contact the authors but that's a pain and it takes time.


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Why is untreated trypanosomiasis invariably fatal in humans?
If left untreated, African trypanosomiasis will invariably kill the patient. The human immune system is unable to clear the infection.
I am aware of a few other infectious diseases with this property and I have a rudimentary understanding of the reason why. For example, I'm told that rabies has evolved to be uniquely good at attacking the brain because that's the only way it can spread to other hosts, and the neuroimmune system, being quite different from the peripheral immune system, is not capable of dealing with a virus that has this property.
I do not understand why the human immune system is ineffective against trypanosomiasis. One explanation I was offered is that the human immune system is just not very good at fighting parasitic infections (compared to viral and bacterial infections). However, this can't be the full answer, because there are other parasitic infections that may go away on their own without treatment.

Welcome to SE Biology. As a veteran contributor to StackOverflow you will know how important it is to follow the guidelines of a SE community. Our guidelines, like most, specify the audience (biology researchers, academics, and students) which is important in that answers will assume a certain level of knowledge, just as on SO) and that posters are expected to show that they have researched a question before asking it. If you search for "trypanosome immune evasion" you will find many articles on a very broad field.

African trypanosomiasis, or sleeping sickness, is caused by the protozoan Trypanosoma brucei, a single-celled eukaryote.  Being eukaryotic, it has a cell nucleus and a larger genome than most bacteria; it also has a flagellum with which it can propel itself.  Infection with T. brucei occurs via the bite of a blood-sucking fly, one of several species of tsetse fly.
The mammalian immune system has a difficult time with T. brucei because of an effective set of adaptations.  The protozoan's surface maintains a dense coat of a particular glycoprotein on its surface which generally hide other necessary surface features such as chemical receptors and ion channels. Since it is this glycoprotein that the adaptive immune system will encounter, that molecule is the one which it will develop antibodies to recognize.
Within a few days the protozoans would be recognized and soon eliminated by the immune system except that T. brucei at random times changes the glycoprotein used as its surface coat.  The mechanism that does this is called a variant surface glycoprotein (VSG) expression system.  The organism has a repertoire of about 1500 different proteins to  select from to use for a new glycoprotein coat.  The overall effect is that by the time the immune system is able to flood the body with the antibody type it has developed, most of the T. brucei population is not recognizable by those antibodies. T. brucei devotes a significant portion of its genome and its protein production to this immune evasion system.

good answer!, also, the trypanosome gets through the blood-brain barrier where immune system options are fewer, and fewer chemicals can get there.

This makes sense. I wonder if you have an opinion as to why a VSG-like mechanism hasn't evolved in other kinds of infectious parasites, though? It seems that it the trade-off involved would be similar for them (i.e. the benefit of being more effective at infection versus the cost of the additional genome size and protein production)

@Brian That's probably wide enough topic for a separate question, but I think the fly-mammal-fly lifecycle might have something to do with it. Malaria has a somewhat similar, but apparently separately evolved, mechanism of varying its surface characteristics. More here: https://en.wikipedia.org/wiki/Antigenic_variation

I hope you're not trying to give a new idea to our newest coronavirus, @brian!

Viruses are dumb, eukaryotes are smart.

@Brian Evolution isn't forward-looking. It doesn't seek out adaptations which would be useful; it merely preserves any adaptations which it happens to come across which turn out to be useful. (Of course, there isn't really any "force of evolution" which causes these things to occur. Evolution is merely the name we give to the self-evident fact that adaptations which propagate themselves propagate themselves.)


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Cat herpes and behavior
We have 2 cats, aptly named "Fatty" and "Tiny".
"Fatty" is a 6 year old house cat that hasn't seen the outside world in years.
"Tiny" is a cat we rescued about 45 days ago and she's roughly 2.5 months old.
Tiny came in with what looked like an eye infection, a million fleas and intestinal worms.
We kept the cats isolated until Tiny could be seen by a veterinary doctor. She had treatment to kill fleas and worms and we just washed her eye and it cleared quickly.
Soon after Fatty started to develop a cough; the doctor at the clinic said it was some cat flu, probably brought over by Tiny and she got some antibiotics.
If the flu is a virus, I question the antibiotics.. but we went through anyways.
Now we're a month and a half later and Fatty has completely lost her voice and she articulates sounds that are like 'krr'; she is unable to make any normal cat sounds anymore.
The doctor said it may be cat herpes that was introduced by Tiny; if this is the case, she'll never 'speak' again. In the meantime, Tiny is doing very well.
The most striking change is in her behavior; at first she didn't accept Tiny, now they are friends, but she has become slow, uninterested in any form of play, doesn't really purr anymore, doesn't come close to us and walks away when we pet her.
So, my question is: if she had the herpes virus, which is very common in stray cats where we live, can it have any effect on her brain that would explain a huge change in behavior? (her blood test is normal)

I'm so sorry to hear this. I hope it's just a temporary adjustment. You might have more luck with this on Pets.SE.

yes; I was a bit on the fence since it's about a specific virus.. but it's about cats :) I followed your advice and posted in Pets as well.

https://pets.stackexchange.com/q/17764/11132


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heart rate vs pulse strength when exercising
I have noticed, depending on the exercise I am doing, two different patterns (and probably every combination in between):

if I do an exercise like biking, I can feel I have a faster heart rate but the pulse (touching my neck) doesn't feel very strong.
in opposite, I have noticed that if I do an exercise like push-ups, the heart rate is not as high, but the pulse feels stronger.

why the difference?

Get a portable BP  tester, they are inexpensive and accurate ( those I have used).

I used to have one, but I don't see the link as to why some exercises seem to favor a high heart rate and others seems to elicit a stronger pulse.

Position matters. You are sitting upright when cycling, but are horizontal with pushups, affecting the way the blood volume moves. Also, when cycling, no Valsalva maneuvers are done, whereas with pushups, weightlifting, etc., people tend to do Valsalvas, which makes the blood volume 'stuck in your neck', so to speak, larger, so the pulse "pressure" will seem greater. Other factors also apply, and it depends when you check your pulse for "pressure".


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PCR efficiency or DNA yield with single primer
How to calculate number of DNA molecules synthesized after 'n' no. cycles with single primer (either only forward primer or reverse primer)? Is there any formula to calculate the DNA yield after such PCR?
Supposing, I am setting a PCR reaction for 100 template DNA molecules for 30 cycles, with only one primer - forward primer for target gene. How many DNA molecules will be generated at the end of 30 cycles. All other conditions remain the same.
Thanks.

Technically, if you use only 1 primer, it will not be PCR anymore.
But that's what gonna happen if you have 100 template DNA molecules (made of strand A and complimentary strand B) and abundance of primer (say, 10x, or 1000 molecules):

At first cycle primers will bind to template DNA, but only to one strand (for example, A)
DNA polymerase will extend those primers, creating complimentary strands B'. Some strands B' will be shorter than template because DNA pol is not perfect
DNA-primer complex will melt at the beginning of cycle 2
At the beginning of cycle 2 primer molecules will again bind to template, again to strands A, and process continues

Since there is no step where strand A is being copied, this process will be linear, not a "chain reaction". At each cycle you will get the same amount of strands B'.
It is hard to say how much B' molecules you will get at each cycle, but at the end of 30 cycles, it will be at best 30x of the first cycle. Remember, though, that DNA polymerase degrades, and cycle 30 will be less efficient than cycle 1.
Assuming perfect polymerase, and that extension time is long enough, you will get 100 strands B' on cycle 1, 100 strands B' on cycle 2 and so on. At the end of 30 cycles you will have 30x100 strands B', and 100 strands A and 100 strands B.


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Difference between curated publications and additional publications in nextProt database?
With reference to reference papers listed in nextProt database, what is the difference between curated publications and additional publications? Anyone using nextProt, kindly explain the terms. For example, when I search for SLC22A23 in nextProt simple search engine, I get as mentioned below on the left side toolbar.
References
Curated publications (21)
Additional publications (2)
Patents (0)
Submissions (0)
Web resources (0)
Link: https://search.nextprot.org/entry/NX_A1A5C7/
Thanks


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What is this small insect called?
It is about 1-2 mm long. It also can fly and it stays on the wall.
Location: Lebanon.

Your country/state will help in getting an answer; a more-in-focus photo (if available) would also assist ... the best anyone can do at the moment is "it's a beetle."

It is in Lebanon. That's the maximum zoom my cell have. Sorry. I want to identify them so I can get rid of them.

If you are taking pictures with your cellphone it's usually better not to use the zoom. Cell phones, at least the ones I am aware of, don't usually have a real optical zoom, just a digital zoom. Essentially its the same thing as cropping the center out of a picture and then stretching it bigger. You don't actually get any more information.

It looks to me like a cigarette beetle- they can infest many different types of products so I would definitely check everything carefully. Here's the link I used as a source, you can find more info here: https://www.orkin.com/other/beetles/cigarette-beetles/

Welcome to Biology.SE! Although this answer might prove to be helpful, you still need to add more details and some images for comparison.


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Biological basis for the illusion of being pulled uphill on a *magnetic hill* when, in fact, one is coasting downhill?
A "gravity hill" is one where a downhill slope appears to be uphill, such that an object such as a car will appear to roll uphill when in fact it is moving downhill.
This is described in a wikipedia article as a feature of the lie of the surrounding land.
What relevant feature of the land would cause this misperception/illusion in human beings? I assume it’s related to some aspect of vision, but would have thought our proprioceptors would feed us opposing information, inducing discomfort of some kind.
What is the biological basis of this illusion?
Edited to add my research: the phenomenon is explained here as a gentle decline between two steeper declines. The illusion is explained as comparable to the Zöllner illusion in which  lines intersected by oblique line segments appear to tilt (Kitaoka, 2007; Oyama, 1960; Robinson, 1972/1988; Zöllner, 1860).

The American Psychological Association’s definition of the Zollinger illusion is

a visual illusion in which parallel lines appear to diverge when one of the lines is intersected by short diagonal lines slanting in one direction, and the other by lines slanting in the other direction.

The illusion in 2 dimensions is clear. But how does that translate into the 3D illusion? Are the “parallel lines” the edges of the road? Or is the road the line (visually implied) transacted by oblique angles of the landscape?
If That question is confusing, it’s because I am confused. Sorry.
This is not original to me but the original poster chose to leave in a huff. Now I really want to know, because when I was a girl, my mom told me great stories about the strange things she herself had experienced. One of the stories involved being pulled uphill in a car placed in neutral at the bottom of a hill. TIL… it was true, for her at least!

I don't have any sources, but usually these sorts of things in the outdoors are related to the layout of the landscape, perhaps with a horizon that appears horizontal, but isn't actually, or maybe with a horizon that is steeper than your brain interprets. I've been on one in a "puzzle world" with a chair that rolls "up" the slope, but it's actually that the wall decor and floor are sloped.

I recall doing instrument flying (IFR) in pilot school and how difficult it is to maintain spatial orientation without a visual horizon. Under these conditions, it is actually impossible to maintain level flight without reference to the instruments, especially the attitude indicator/artificial horizon. I have heard of plane crashes caused by instrument failures during IFR flight: the pilots thought the plane was straight and level when in fact it was in a banking dive. I don’t know if this is related, but it seems like it could be.

@bob1 - I didn’t consider the horizon. I just assumed (a dumb thing I often do) it would be hilly. Good point.

I've found some footage of the one I went to here (youtube; timestamped, but it's only 2min anyway) with a couple of similar illusions. Not easy to see what's going on though, other than a sloped floor and ceiling.

@bob1 - write this as an answer! It may not say exactly what is going on. But your comments do help (as did canadianer’s) and the bounty should go to one of you!

I don't have any proof, but these illusions are typically by visual effects, much like was postulated in the question.
Basically it is a matter of subverting the expectations of the viewer. In most cases this seems to be through a horizon that the viewer interprets as horizontal, but isn't.
An couple of examples of this can be found at Puzzling World in Wanaka in New Zealand, where there are illusions of balls rolling up a pool-table, and a rail (with chair) that the chair rolls "up". Footage of these can be found at this timestamp on Youtube. In both these cases, the floor and/or ceiling are sloped, but the eye interprets them as horizontal (I think through expectations/familiarity).
As commented by @canadianer on the question, pilots doing instrument flying find it difficult to maintain spatial orientation and level flight if their instruments fail and tend to bank the plane, and in some cases dive/rise, when flying without artificial horizons.

The YouTube video is impressive! The brain is a funny thing, and I think you’re right when you say familiarity is behind it. Much more simple example of familiarity is interpreting a broken circle as a circle still. No reason to think illusions can’t be very complex.


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How did the moray eel evolve a pharyngeal jaw?
I am referring to the retractable second set of jaws in the moray eel.
How can one imagine such an evolutionary step to have occurred? Just by chance an eel grew a second internal jaw and it was luckily attached to some muscles which made it useful for swallowing prey?

What have you found so far? I got a number of hits when I search for moray eel jaw evolution on google or google scholar.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

well considering jaws originally evolved from the first set of gill arches and eels still have gill arches, so it's not that much of a stretch. Most fish gill arches already have muscle attachments that aid in swallowing and breathing. Many bony fish already have  pharyngeal teeth to aid in swallowing (they teeth prevent the prey from being pushed back out of the mouth by water pressure. Moray eels have a much more direct mechanism becasue they live in burrows and can't fold the gill arches out to generate suction and pull food down the mouth as other fish do. So instead the muscles pull the arches backwards and the shape pulls them together pulling food down the gullet.
it has actually happened independently in cichlids and something similar happened in Snakes and Mosasaurs


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Presence of MHC on red blood cells
Do red blood cells have no MHC? (I have often heard that they do not.)
If so why are they not destroyed by immune cells?

Actually, effete red blood cells are eventually removed from circulation by immune system phagocytes. While this would not involve an MHC-mediated mechanism, the means the immune system recognizes dying RBC's is an interesting field of current research.

They do not, at least not normally or noticeably.  MHC I occurs on all nucleated cells, and red blood cells do not have nuclei.  If they did indeed have MHC on them, blood transfusions would be as successful and as tricky as organ donation.  There are reports of MHC detection on red blood cells, but the amount is orders of magnitude smaller than elsewhere, only present for certain MHC alleles, and often transient.

So why are they not rejected by immunity cells ?

@biogirl I'm not sure what you're asking.

@Biogirl - They can be if they have the wrong blood-type or Rh factor.

@Amory I think immune system kills those cells who do not have MHC molecules on them. So why shouldn't RBC be killed?

@biogirl Ah, I see.  It's not particularly well known, but the two main theories are that either RBCs lack additional markers needed for natural killer cells to engage, or that RBCs express additional proteins that inhibit destruction, such as CD47 in the case of macrophages.  I'm actually doing research on a very related topic so I'll just say that I think it's closer to the latter.

@Amory Ok, I get it now. Thanks !Hope you find something really exciting with your research !

There are other histocompatibility antigens on the surface of blood cells, e.g. A, B, Rh, etc... (There are probably a lot more which change less by person to person, so they have lower effect on the outcome of blood transfusion.) These antigens can be recognized by immune cells as self, that's why they don't destroy them. Before complete differentiation RBCs have nuclei, so they can have MHC1 remnants on their surface from that period of their development. RBCs are relatively well tolerated by the immune system especially with coverage.

wikipedia - Blood type
2012 - Transfusion in the absence of inflammation induces antigen-specific tolerance to murine RBCs
2014 - Simultaneous Camouflage of Major and Minor Antigens on Red Blood Cell
Surface With Activated mPEGs

you are right.red blood cells do not have noticeable MHC 1 molecules.But rather the have high levels of CD47 markers which are recognized by the immune system as self.On the other hand red blood cells during development are nucleated they may contain small traces of MHC 1 molecules.I hope this answers your question.

Welcome to Bio. Can you add sources to your answer?


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Please identify this moth from Bangladesh
Sorry for bad resolution of the picture. This picture is taken from JU campus, Savar.

I think I have found the identification. It is a planthopper from ricaniidae family. Most likely Ricanula stigmatica.

Image source: https://en.m.wikipedia.org/wiki/Ricanula_stigmatica


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Why is the probability of fixation of an allele equal to its frequency?
Introduction
In a panmictic population, the probability of fixation of an allele at a neutral locus is equal to its frequency at that time. I will refer to this probability of fixation as calculated at time $t$ as $P_{fix,t}$.
If $p_t$ is the frequency of the allele $A_1$ at time $t$, then the probability of the allele $A_1$ to reach fixation (rather than disappearing) is $P_{fix,t}=p_t$. Typically, the generation when the mutation occurred, the probability of the new allele to get fixed is $P_{fix,0}=p_0=\frac{1}{2N}$, where $N$ is the population size.
Question
This simple and classic result makes very good intuitive sense to me. However, I would fail to provide a mathematical proof.
Can you please demonstrate that $P_{fix,t}=p_t$?

Several proofs are given here (p. 9). My favorite comes from the genealogical argument:
Consider the situation where there are $2N$ alleles: $A_1$, $A_2$, $A_3$ ... $A_{2N}$.
By the genealogical argument, we may state that at $t = \infty$, all alleles at this locus will be direct descendants of one particular allele present at $t = 0$.
Allelic variants at this locus are selectively neutral, so $Pr(A_{1fix})$ $=$ $Pr(A_{2fix})$ $=$ $Pr(A_{3fix})$ $= ... =$ $Pr(A_{2Nfix})$. For any given allele present at $t = 0$, the probability of fixation is therefore $\frac{1}{2N}$.
Now define allelic variants $A$ and a as complementary, non-overlapping groups of the initial alleles, such that $n_A$ + $n_a$ $=$ $2N$. From the above, the probability of fixation of an allele within group $A$ is $n_A * \frac{1}{2N} = \frac{n_A}{2N} = p_0$.

Sorry for digging this topic after 2 years. I am studying evolution these days and was reading basics from the book by Hartl and Clarke. There, this proof is given using the Markov chain approach. However, the way it is proved doesn't make sense to me (also shown in the slides that you have linked). In the Markov chain approach the probability is a vector with each element denoting the probability of having i number of alleles in the population. Can you, if possible, please show how to prove this result using the Markov chain approach?


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Is it possible to have a mechanism to use carbon dioxide as a source of oxygen in human body?
Is it possible to seperate O2 from CO2 and use it for energy In Human? Why Plants and not Humans can do it?

It's possible, though complicated, and I believe is done on the ISS.  I'm not really up on the exact method, but searching NASA web sites should provide info.  The problem is that it takes energy to do the separation, as explained in the answer below.

Most energy in humans is generated by reducing O2 to water and CO2, using something like sugar or fat. Converting CO2 into oxygen would require energy, not generate it.
Plants do have mechanisms to convert CO2 into oxygen, but they use light as an extra energy input to push this energy-costing process.


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Retina Transplant Difficulties
Why is retina transplant not as easy as the normal eye donation and transplant (I think the latter involves the cornea ) ?
This says that a new method has come up but why isnt the process similar and simple as the normal transplant ?
What are the difficulties in retina transplant ?

This is a diagram of a cross-section of the cornea:

It is an amazing but relatively simple structure, the shape of which is responsible for about 60% of our focusing power, and the clarity of which allows light to enter. It is avascular (no blood vessels), and the non-mylenated nerve endings are very tiny and present in the epithelium.
Transplanting this relatively simple tissue is easy (well, not do-it-at-home easy, but easy.) The only problem with cutting all those nerve endings is that the new cornea will feel nothing if there's dust in the eye, etc. This is a problem, but nothing compared to blindness.
This is a diagram of a cross section of the retina:

As you can see, it is not nearly as simple as the cornea. The nerves (to the left: yellow, light blue, medium blue and darker blue), which collect information from the rods and cones (pink and purple) are very numerous, and absolutely vital to the ability of the brain to interpreting information from these photoreceptors. Therefore, a cut piece of retina immediately loses the ability to send any information to the brain. To transplant it into an eye with a damaged retina would do nothing to improve vision. Also, it is not easy surgery. It's very difficult.
What has been called "retinal transplants" in the recent past have been tiny pieces of embryonic retina, about...

4 millimetre square of retinal tissue, complete with retinal progenitor cells and the retinal pigment epithelium that nourishes them. The tissues were placed in the sub-retinal space beneath the fovea, the area of the retina responsible for sharp central vision.

Note, they didn't try to connect nerves or blood vessels. And, it came from an embyro (so the supply is a problem.) The improvement in vision - which was significant in 7 out of 8 recipients (one patient going from 20/800 to 20/160) - is not long lasting, and believed to have been not from the transplanted retina connecting to the existing retina, but from the release of growth factors from the embryonic tissue improving the health of the degenerating retina.
The newest in "retinal transplants" (which might be better called stem-cell-supplied growth factors implanted in the retina) actually derives from the patient's own stem cells:

A Japanese woman in her 70s is the first person to receive tissue derived from induced pluripotent stem cells, a technology that has created great expectations since it could offer the same regenerative potential as embryo-derived cells but without some of the ethical and safety concerns. [No news yet on whether it worked.]
In a two-hour procedure... a team of three eye specialists lead by Yasuo Kurimoto of the Kobe City Medical Center General Hospital implanted a 1.3 by 3.0 millimetre sheet of retinal pigment epithelium cells into an eye of the Hyogo prefecture resident, who suffers from age-related macular degeneration, a common eye condition that can lead to blindness.

TL;DR: It's not as easy as taking cadaver retina and replacing a patients retina (that would result in immediate and permanent blindness). Whereas corneal transplantation is very easy.
Corneal Innervation and Cellular Changes after Corneal Transplantation: An In Vivo Confocal Microscopy Study
Retinal transplants see fleeting success
Japanese woman is first recipient of next-generation stem cells

Great answer +1 - but - was the transplanted material effective? Just curious :) Interesting stuff!

@AliceD - D'oh! Sorry, I've edited my answer.

That was great . +1


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MTHFR recessive alleles and B-vitamins
I know that being heterozygous or homozygous recessive for the MTHFR gene prevents that person from being able to process and use folate and B-12. It causes an unhealthy level of homocysteine to accumulate in the bloodstream which can cause more serious problems. Taking methylated B-vitamins, specifically Methylfolate and Methylcobalamine will prevent homocysteine from building up, but I am not sure why.
Can someone explain how this process works? I am wondering how the body uses folate and B-12 (cobalamine) normally and how the recessive MTHFR genes interfere with this process.

Folate, or rather its active form tetrahydrofolate (THF), is a coenzyme that carries a 1-carbon group. The carbon group can occur in various redox states: CH3-THF (methyl-THF), CH2-THF (methylene-THF), CH-THF (methenyl-THF) or CHO-THF (formyl-THF). These can be interconverted by a variety of enzymes, and are used by cells to synthesize a number of products, including nucleotides and methionine.
MTHFR (methylene-THF reductase) converts CH2-THF into CH3-THF. The CH3-THF form is the most abundant folate in blood, and is therefore considered the "transport" form of folate. CH3-THF is also the form used to synthesize methionine, in the reaction
CH3-THF + Homocysteine $\rightarrow$ THF + Methionine
catalyzed by methione synthase (gene symbol: MTR). This enzyme requires cobalamin (B12) as a cofactor. Actually, the reaction occurs in two steps,

CH3-THF + Cobalamin --> THF + CH3-Cobalamin
CH3-Cobalamin + Homocysteine --> Cobalamin + Methionine

Loss of MTHFR leads to deficiency of CH3-THF, causing methionine synthase to run out of substrate, and homocysteine to accumulate. Lack of the B12 cofactor also blocks methionine synthase, and it should be clear from the reactions above why supplementing with either CH3-THF or CH3-cobalamin can alleviate the problem (at least in theory). I would guess the phenotypes seen in this condition is mainly due to lack of methionine though, rather than excess homocystine, since methionine is required for a variety of methylation reactions in cells.
This is a simplified view. There are many other interactions between B12 and folate; for example, the methinine synthase reaction is needed for cells to take up and store folates, and therefore B12 deficiency can create a folate deficiency as well. See for example http://www.ncbi.nlm.nih.gov/pubmed/6115113 and http://www.ncbi.nlm.nih.gov/pubmed/10466189 for further reading.