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Book recommended for neurobiology
I am looking for a good explanatory book concerning Neurobiology. I am interested on how the brain works but prior to this I believe that I have to start learning things about the biology of neurons. So I searched on the net and found a book called "From Neuron to Brain" from John G. Nicholls et. al.
Actually there are so many books out there and because I have never worked on that subject, all these results are confusing me.
So i would like someone's opinion who has dealt with this subject to help me choose a book for beginners.
Thank you.

I can highly recommend Kandel's "Principles of neural science". I have not had any biology courses since highschool, but I was able to understand it well. It is really a book meant to teach. The style is beginner friendly, and not tedious/boring at all.
It is an expensive buy and a very long read (I think the paper version is close to 2000 pages), but given the complexity of the subject matter, I find it reasonable.
If you decide to go for it (or for any other neurobiology work, actually) get the newest edition. Getting an older one is a false economy here - our understanding of how this stuff works gets better by the year, and there is lots of missing (or sometimes even not-valid-any-longer) information in the older editions.
A few examples of what might make the book hard to understand for beginners
"Principals of neural science" does not require much preexisting biology knowledge. It is sufficient to roughly know that a cell has a nucleus, plasma with organelles swimming inside, and a membrane. But you have to be comfortable with a bit of biochemistry. This is an example passage concerning the behavior of ions in solution. I found this perfectly understandable with my prior knowledge, I don't know if you need brushing up on chemistry or not.

The cell membrane is selectively permeable to K+ because the otherwise impermeable membrane contains proteins that form pores called ion channels. The channels that are active when the cell is at rest are highly permeable to K+ but considerably less permeable to Na+. The K+ ions tend to leak out of these open channels, down the ion's concentration gradient. As K+ ions exit the cell, they leave behind a cloud of unneutralized negative charge on the inner surface of the membrane, so that the net charge inside the membrane is more negative than that outside.

And then there are examples like this one:

Isoprenylation is another post-translational modification important for anchoring proteins to the cytosolic side of membranes. It occurs shortly after the synthesis of the protein is completed and involves a series of enzymatic steps that result in thioacylation by one of the two long-chain hydrophobic polyisoprenyl moieties (farnesyl, with 15 carbons, or geranyl-geranyl, with 20) of the dulfhydril group of a cysteine at the C-terminus of proteins.

Here, my own chemistry is bad enough that I could only understand that a protein is modified by attaching some molecular structure to it, and this makes it possible to attach the protein to the cell membrane. The lack of understanding of the details (what is a geranyl-geranyl?) did not stop me from understanding the rest of the section, so I don't mind, but I know that there are readers who'd have a problem with that. Sadly, I don't know of a source which does not require such knowledge, and if you feel the need to know every single word, you might need to use a reference while reading, or start with a course in biochemistry first before switching to the neurobiology.
Finally, if you don't have a life science background, there might be words outside of the chemistry you might have to look up, or understand from context, but they will be unfamiliar at first. For example, I was surprised to see the word "process" used in the meaning of a physical protrusion from the cell body. But this is not such a high hurdle, you have to either read ahead and puzzle such words out, or use a dictionary. They are not so frequent to prevent comfortable reading.

This was the book used in my undergraduate Neurology course and I thought it was wonderful.  It's one of the few textbooks I've held onto.  Granted, I try not to hold it for too long, as the thing weighs a ton.

I totally agree with Rumtscho. Kandel's Principles of Neural Science is excellent. Eric Kandel is a Nobel Laureate and one of the gurus in the field. As to the biology of neurons I can refer you to:
Part II: Cell and Molecular Biology of the Neuron, and Part III: Elementary interactions Between Neurons: Synaptic Transmission.
These sections cover the basics petfectly. The following sections bring the reader to higher level of processing in the brain, namely Part IV-IX that cover Cognition-Perception-Movement-Arousal-Development-and Language/Thought, respectively.
So it is a nice build-up to exactly the things you are looking for.
But as Rumtscho says: it's quite a buy, but worth every penny. I have been using the book for about a decade during my studies as well as beyond.

Can you please expand you answer? Actually it is more a comment.

I concur with Old Chris — some details such as what all it covers etc would be nice. New Chris, I suggest that you can slightly modify your profile name so that the name confusion can be avoided.

I added details and changed my profile name. thanks for all your patience and help guys

@ChrisStronks Thanks. I now feels less like I am talking to myself. :-)

No worries old Chris!

I have no worries about this :-) BTW: Welcome the biology.stackexchange.


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What effects does being cryogenically frozen have on a person's body?
I'm wondering what effects are known to happen to a person's cells when a person is cryogenically frozen, especially those that need to be overcome in order to "bring them back to life."
From a cellular and maybe even molecular level, is the person exactly the same as before?

It's not possible to freeze a person and bring it back to life later.

Possible or not, I'm still curious what effects have been observed - the study of Cryonics still seems to active.

@Chris wrong! Well, maybe. Check out this frog

You need to add details or stick to one domain- molecular/physiological. In any case since this has not been done on humans the answer can be based only on speculations.

@tel: More to point, we know that it is possible to freeze human sperm for later re-use. That leads me to wonder if we can someday freeze human BEINGS for re-use. After all,who would have ever guessed that we could clone sheep.

@Chris Can you prove that statement?

@JBentley Which one?

@chris I can only see one - "It's not possible to freeze a person and bring it back to life later."

Short Answer
Death!
Longer Explanation
In terms of the cellular and molecular level, many of the relatively weak interactions holding a person together are disrupted by cold temperatures. As a cell freezes, most of its  proteins and lipid membrane content will denature and "fall apart", the same as if you boiled it.
As with many things in biology, the problem is water. At room temperature, the lipid bilayers and proteins of a cell are held together largely by way of a complex network of interactions with the surrounding water. If the cell gets too hot or too cold this network of interactions between biomolecules and water falls apart. This leads to a disruption of the cell's overall organization*, which in turn can cause problems up to and including complete cell rupture and death.
So in order to preserve a living creature under cryonic conditions you need to replace the water in and around its cells with a different molecule that will maintain most of the normal intermolecular interactions even under conditions of extreme cold. There are protocols for freezing cell cultures that use various different substances as replacements for water, such as glycerol or DMSO, and there's a frog that loads its own blood with carbohydrates at low temperatures in order to turn it into a better cryonic medium.
footnote
*The disruption of a cell's organization at extreme cold is likely to persist even if the cell is brought back to room temperature. See Gulevsky, et al for a complete review of the thermodynamics of cold denaturation.

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Do Blanding's Turtles die of old age?
I have recently found articles and various claims that turtles (Blanding's turtles as an exact example) could possibly live indefinitely. http://discovermagazine.com/2002/jun/featturtle
This is said to be due to the fact that they

don't senesce— deteriorate physically— as they grow old

I am highly skeptical of that claim, and on the other side are links such as this http://www.nature.org/ourinitiatives/regions/northamerica/unitedstates/indiana/journeywithnature/blandings-turtles.xml which say they can live up to 70 years (though in the actual article it says 70+)
I realize in the wild that predation, disease, and other causes other than old age could kill turtles, but my question is:
Can blandings turtles die of old age? If so, around what age would this be?

It looks like as in fishes, the lack of an intrinsic cause of death in turtles in general is seen:

Like in fishes, the reptiles appear to show three types of senescence. The African skink, Mabuya buettneri, shows rapid senescence similar to death at mating observed in Salmon and marsupial mouse. Most of the lizards and snakes undergo gradual senescence comparable to the pattern exhibited by a majority of vertebrates. On the other hand, turtles, tortoises and crocodiles continue to grow throughout life and are thus credited with slow or negligible senescence.
  Patnaik 1994 Gerontology 40(2–4):200–20.

The main article by Congdon, the researcher who the Discover article profiles, also seems to be fairly definitive about this lack of senescence (or negative senescence?) in Blanding's Turtles specifically:

Survivorship, reproductive frequency and size-adjusted mean clutch size were all higher in the Oldest age group compared to the younger age groups.
  Congdon et al 2001 Experimental Gerontology 36(4–6): 813–827

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How do single-celled predators chase other cells?
From my understanding, single celled organisms have been seen avoiding, and chasing, potential food or other organisms.
How do they accomplish this? They do not have eyes or ears or a nervous system. My understanding is that chemical reactions are involved somehow.
How do single-celled predators chase other cells? What happens on a chemical level?
Edit:To help keep a more constrained question, the single-celled organism I am considering is Paramecium

This is actually a very broad question. Chemotaxis (the response to changes in a chemical in the environment) is only one of the "taxis". If you could refine this, say by singling out one single celled predator, I think it would be a less broad question.

@anongoodnurse I am trying to find a common predatory Ciliate that does the behavior that I have described - is Paramecium a good example?

Yes, paramecium is a good example.

it is always useful to show work you've done yourself to answer the question.

@aaaaaa my work so far is essentially google searches leading to links which fail to answer the question. All I can find is definitions of "single-celled organisms", "paramecium", or broad explanations of the digestive system.

It could be I just don't know the correct terms to search for, if this is readily available information

Detection of and movement according to a gradient of a chemical species is a strategy that single cells use to track a target across space. There are very many strategies of movement depending on the cell and its environment, but a common problem that while cells can sense the concentration of chemicals, they cannot sense its gradient (the direction in which it increases) because they are of too small a size to rely on the difference of concentration on one side and the other. Howard Berg and his co-workers have discovered a mechanism that allows single cells to move toward increasing concentration zones by a combination of concentration sampling and movement. See his webpage, http://www.rowland.harvard.edu/labs/bacteria/projects/track.php


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How to tell if a beverage will hydrate or dehydrate?
Beverages of any type generally contain some measure of water. However, in the case of some liquids, the non-water components take more water from the human body to filter out than the water contained in the beverage.
The most-known example of this is salt-water from the ocean - there is too much salt so the body tries to use water from the body to "water down" the salt water.

Given a beverage with unknown additives, how would one determine if the beverage would actually hydrate or dehydrate a person?
If you knew the ingredients (and the amounts), could you tell that way?
Edit:comments seem to indicate that it depends on the solutes and tonicity of the solution: are there any other factors to be aware of?
What (common) solutes will have the largest affect on whether the human body will be hydrated and why?
if you need "common" to be defined, consider it defined as: contained in many[more than 3] store-bought beverages

It will depend on the tonicity of the fluid, I guess. Sea water is hypertonic while distilled water is hypotonic. Hypotonic fluids would move into the body faster due to osmosis. By the same reasoning hypertonic fluids would pull water from the body into digestive tract till sufficient electrolytes have been absorbed.

@CRags Thanks for the info! I guess what I'm looking for is how to measure the tonicity of a fluid. A quick google search didn't come up with much, but I didn't have much time to look. I'll have to check it out later.

It depends on the solutes. Glucose can be metabolized. Some things inhibit vasopressin (anti-diuretic hormone) excretion, others stimulate it, influencing the outcome. This question might be too broad.

Yes it depends on the solutes; it is not just tonicity. Note that marine fishes do drink seawater; the salt is actively filtered out. @anongoodnurse You can expand on your comment and post it as an answer. So the question "Is it possible to know if some beverage is hydrating or not" can be at least answered by "no".

I think at the least a list of things that will determine if a drink will cause hydration or dehydration can be provided for this question. It is an interesting one after all!

I'd say the diuretic effect of the drink is more important than the plasma osmolality it might alter. Alcohol is far more "common" than sea salt as solutes in beverages, and it has strong diuretic effect. Also, thirst-triggering is not necessarily equal to dehydration, but water in the bladder is probably not available for the rest of your body.

Osmolarity does not depend on type of solute (as long as the solute is not a huge molecule that actually forms a colloid). Osmolarity depends on the van't Hoff factor of the solute molecule.


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Active & passive transport question
If an element, ion or molecule is found in a cell is it possible to tell which method of transport was used? for example if a hydrogen or sodium ion was found in the cell could you tell if it got there by diffusion, or facilitated diffusion, or endocytosis, pinocytosis etc? If not could you at least narrow down the number of transport methods it could have used?
I'm very interested in which substances are let throught the cell membrane and by which method.

How should you be able to distinguish how a certain atom or molecule entered the cell? They are not getting a sticker on them saying "got through the Na-K-ATPase".

Welcome to BioSE! As @Chris mentioned, transported atoms and molecules don't typically retain a record of their past history, so just by looking at a molecule in the cell you can't in general tell how it arrived in the cell (an exception might be proteins that have some chemical modification on them that allows them to be imported via a specific mechanism, such as the mannose-6-phosphate enzyme re-uptake system). In order to infer if a molecule typically enters a cell by a particular method, you will have to do several different types of experiments. I'll list a few off of the top of my head. Note to other SE contributors: since this is not my area of expertise, I'm not sure how feasible some of these experiments are, or how they are typically done, so please edit my answer to be more accurate!

Diffusion If you want to know if something can diffuse across a membrane, then the easiest way would be to try it in vitro. One way I can imagine doing this is to use a phospholipid bilayer to separate two compartments: one with your molecule of interest, one without. By measuring the concentration of your molecule that transfers from one compartment to the other, you can see if your molecule can diffuse across a lipid bilayer. Note that this will only tell you if diffusion is possible for your molecule. It may be that cells have ways to actively prevent your molecule from diffusing across your membranes, which you wouldn't be able to know from this assay.
Endocytosis or pinocytosis One way to assess if your molecule is taken up by endocytosis or pinocytosis would be to knock out (genetically or with an inhibitory drug) these processes in your cell and see if your molecule of interest still ends up in the cell. Depending on the context of the molecule you're interested in, you might be able to simply place cells in solution with your molecule of interest and measure the concentration of the molecule outside the cells over time. You could compare how much of your molecule is lost from solution when cells can't endocytose and compare to when they can; if your molecule stays around when cells endocytose, you have some indication that process is necessary. Note that there would have to be a lot of other controls for this experiment as well: e.g. ensuring the effect you observe is specifically caused by endocytosis being inhibited. Since endocytosis and pinocytosis form vesicle intermediates containing your particle of interest, one check to see if endocytosis might be reasonable is to see if you can see vesicles containing your molecule of interest in the cell. Of course, this requires a method for being able to visualize your molecule of interest (maybe it's fluorescent, or can be modified with a fluorescent marker? Or maybe there is a fluorescent protein that binds your molecule and can change color on binding? These things all exist, they just depend on your particular molecule and context).
Transport channels: In a similar vein, how does the uptake of your molecule change when you inhibit or remove from the cell a particular type of channel? You could measure this in a similar way as the bullet point above.
Active vs passive transport: If you wanted to see if uptake of your molecule requires active transport, you could try inhibiting ATP synthesis with a drug and see if transport of your molecule decreases over time. Note that this is in general not good for the cell (really!), so you might also have to have some more controls for this, maybe showing that transport of a molecule known to travel by passive transport is not affected on the timescale you're looking at, for example.

This list is by no means exhaustive, but I hope it gives you a sense of the type of experiments and ways of thinking you might be able to use to figure this out. Some general thoughts:
This tends to be case-by-case. While the type of experiments you might do to determine the mode of transport for different molecules are similar, the controls you will have to do to shore up your conclusions will really depend on the system involved, what type of effect a molecule has on your cells, whether your cell imports and exports this molecule, under what circumstances you might expect the cell to take up this molecule (so you have a way to trigger the cells to take up this molecule for your experiment). I don't know of a completely generic method for resolving this type of question.
Being able to measure abundance of your molecule is important. All of the experiments above rely on being able to measure the concentration of your molecule, either outside of the cell, or inside of the cell. This is often easiest if you can modify your molecule to be visualizable in a microscope or spectrophotometer, but however you do it, you need a good, reliable, robust assay in order to make strong conclusions with this assay.
Controls are really important. Thinking up all the different alternative possibilities and trying to come up with ways to rule them out is the heart of experimental science. Fortunately, it also happens to often be rewarding and thought-provoking! I certainly had fun thinking about this.
Best of luck!


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Is "Cisternal Twins" an actual classification of twin types and if so, describe it
I always assumed my brother and I were identical twins. Now my mother, in her eighties, says we are cisternal twins, but I cannot find any references on the matter. Is there such a thing? If so, what traits make them so?
appended: also, we've been called mirror twins. In a study by a student, we learned that our fingerprints are nearly exact opposites.

Most likely she means fraternal, or dizygotic twins. http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Twins_identical_and_fraternal

that's not it; ty for the guess but I'd like something more definitive. I explicitly mean "Cisternal". I know what fraternal means.

Cisternal doesn't make sense in this context, so either your mother is using an obscure term (quite possible, these things change a lot) or just has the wrong word.
However, mirror twins are a known thing (and quite cool): http://www.twinsuk.co.uk/twinstips/4/140/twin-pregnancy--multiple-births/types-of-twins--identical-fraternal--unusual-twinning/.
She may have meant something like "chiral twins" or "cis-trans twins", which would be borrowing from a similar concept in chemistry to describe your mirror-image nature (but is, again, not a phrase I've heard in the twin literature.)


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Mitochondrial inner membrane
I know that the cristae of the inner membrane can be tubular or vesicular but I would like to know what are the functions of each .

Can you add more details in your question? Anything that you searched for.

@WYSIWYG The answer to this question is unknown yet, however probably in 20 years we can come back to this question and answer something reliable. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219563/

There is a reasonable speculation. That is to get more areas where ATP synthases are localized in order to produce ATP. But this doesn't tell why the structure has to be the exactly that shape.
As the review Ilan show, the shape seems to be determined by ATP synthase dimerizetion. The shap may be just a consequence of ATP synthase dimerizetion, although it successfully enlarges the area where ATP synthase is localized.

The general morphology of cristae is dictated by ATP-synthase Complex dimers, which form rows along the edge of cristae, sort of pinching the inner mitochondrial membrane together (see http://www.pnas.org/content/108/34/14121.short). The angle at which the dimers form, which is different in various species, causes different cristae morphologies. In organisms that don't have ATP-synthase or in yeast strains that are devoid of key subunits required for dimer formation, the cristae of their mitochondria are much more irregular and have a less defined shape, often described as 'onion-like' in the literature (see http://www.jbc.org/content/279/39/40392.short).
Therefore, I guess you could argue that actually it's the form that is a product of the function, rather than the other way round i.e. different cristae morphologies having different functions. The purpose, or selective advantage, of mitochondria having cristae is most likely that they create a greater surface area that can facilitate a larger number of complexes of the electron transport chain, which would enable greater ATP production per organelle. This explains why in eukaryotes that don't produce ATP via the electron transport chain there is no selection to maintain cristae in their mitochondria, or homologous organelles such as hydrogenosomes and mitosomes, and so usually the cristae are lost altogether in such species.
Other protein complexes are also involved in cristae formation and general architecture. Search for MICOS and MIB complexes to find out more.


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How can some enzymes work faster than the diffusion rates of the molecules it catalyzes allow?
Quoting Wikipedia: "Some enzymes operate with kinetics which are faster than diffusion rates, which would seem to be impossible." Which are those enzymes and how can they be so fast?
One example is catalase which Lionel Milgrom discusses in Water Journal no. 7.

Is this a homework question?

No. I ask since some surfing didn't give any answer.

Diffusion rates of what? Please provide some explanation in your question. As it is now, the question is unclear.

What is the source of your assertion?

@WYSIWYG I presume he's referring to diffusion-controlled reactions and diffusion limited enzymes. It's a rather standard concept in enzyme kinetics.

@David Here is one such claim: "One of these enzymes, superoxide dismutase, actually catalyzes reactions FASTER than the diffusion-controlled rate. That's because the active site is surrounded by charged residues that attract oppositely charged substrate molecules!"

OK. Now we know what you are talking about. I can't imagine there are many more — there's obviously something about the chemistry that allows the enzyme to develop such an extreme kcat.  I imagine you need to surf kcat to find others. Not many of us have a "Guinness Book of Records"  mindset.

Here is one article trying to explain why catalase is faster than diffusion rates allow. https://www.researchgate.net/publication/316504611_Why_is_catalase_do_fast . Please open this question.

Is this more of a chemistry question? I asked the same question in Stack Exchange Chemistry without reactions: https://chemistry.stackexchange.com/questions/118608/how-can-some-enzymes-work-faster-than-the-diffusion-rates-of-the-reactants-allow

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When is it reasonable to assume selection for an observed change?
In speciation events, a lot of changes seems to appear simultaneously. How can a specific partial changes, occuring together with a lot of other changes, be said to be advantageous or disadvantageous?
For example, can we conclude that the loss of photolyase in placental mammals was disadvantageous? Was selection at work for that specific loss?
Another example is the change from GULO to GULOP. In an answer on Stack Exchange Biology a lot of people vote that this change was advantageous because it hadn't been selected against in natural selection, according to the book they cite.

Thanks for your efforts to improve the question, it looks like you've cleaned out a lot of the issues raised in the comments. I've reopened your question, though people might still suggest some improvements. It might be helpful for you to cite specific cases (including links/DOIs/etc) where scientists argue a given past change was due to selection; you mention a couple but there is no direct path from your description to where you found the information.

Some genetic changes occur too fast for selection to take place.

Can you please define "genetic change"? Selection can only change the frequency of alleles in a population. It cannot make a new mutation. If by, "genetic change", you mean "mutation", then selection just can't do it. If by "genetic change", you mean change in allele frequency, then the change resulting selection is not necessarily much fast than if genetic drift alone is at play.

Often scientists presume that selection has taken place for an observed genetic change. Is this assumption still valid, based on the current knowledge of genetic changes?

No, really not! Whatever you mean by "genetic change", there is no false assumption made here.

For example genetic changes caused by viruses and transposons seems to have the capacity to establish fast in populations.

Again, do you mean "mutation" or "change in allele frequency" by "genetic change"? Assuming you meant "change in allele frequency", can you please cite a peer-reviewed paper as an example but the claim is really not that obvious to me.

Can a genetic change established in a population be disadvantageous?

Yes! Most mutations are deleterious and genetic drift can lead to some drift load. No one has ever assumed that genetic drift could not happen. Even Darwin knew about it!

Can it be advantageous to make a pseudo gene functional again?

Sure! I have no idea how that relate to the rest of the question that being said.

I don't know what you mean by "changing order". You are maybe confounding "mutation" with "substitution". A mutation any any sudden change to a DNA sequence. It can be a substitution, an indel, a whole chromosome duplication, whatever. You should have a look at What is the definition of a mutation?

Your post and comment are completely full of wrong definitions. You should probably have a look at an intro course to genetics or to evolutionary biology otherwise it is near impossible to understand what you mean. You should at least make sure you have a good understanding of the definitions of the terms: allele, gene, locus, substitution, indel, mutation, selection, and genetic drift.

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Enzyme inhibitors against common cold viruses
Would some inhibitors of viral enzymes work against common cold viruses? Are there any studies? What could a treatment look like?
A lot of common cold viruses are rhino viruses which are picorna viruses. All picorna viruses contain two cysteine proteases, designated 3C and 2A according to Handbook of Proteolytic Enzymes
Volume 2, 2013, Pages 2402-2406
David S.Wishart Would it suffice to inhibit either of them?

Common cold seems like the most damaging disease of all. With on average two weeks sickness per year and person that equals to an annual loss of GDP by 300 billion EUR in EU.

A human enzyme involved in the production of rhinovirus capsids has been successfully inhibited.

Fragment-derived inhibitors of human N-myristoyltransferase block capsid assembly and replication of the common cold virus https://www.nature.com/articles/s41557-018-0039-2

The article also says that targeting a human enzyme could be more efficient since the risk of mutation is lower compared to a virus enzyme.

Pfizer has the orally administered Paxlovid which is the protease inhibitor nirmatrelvir in combination with its preserver ritonavir.

Can you please combine both answers into one by using the edit function?

Then there would be no way to vote separately, and the two solutions are basically different.  One inhibits a virus enzyme and the other a human enzyme.

These are two possibilies for the same problem. Please put them together, otherwise I will do it.


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Can New Caledonian crows survive on their own in Europe?
Is it possible to insert New Caledonian crow in Europe and have them survive on their own, mate, lay egg, hatch and so on?
The motive for the question is to find cheap labor, highly capable animals similar to working dogs, since the New Caledonian crow is among the ablest land animals known.

This question could be improved by adding in your own research on what introduced bird species are present in Europe.

This question is potentially about invasive species introduction. The motives for the question would be welcome. That species has lived in temperatures always warmer than 15 degrees for many generations and would have some disadvantages, compared to european crows. Yes they can breed a bit, but there is no scientific information to say if they would proliferate.

What kind of work would a New Caledonian crow do?  They're pretty small, couldn't herd sheep or carry anything big.  I suppose they could act as rather unusual service animals - they wouldn't take up much space!  Also, there seems to be a fair bit of research that shows that some of the native crow species in Europe are capable of doing some very clever things - the gap might not be all that big, it might just be that the New Caledonian crows were studied earlier.


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Can bottlenecked potato immunity defence be increased with knockouts?
I read in a Swedish newspaper advertisement some years ago that genetic intervention had been used to knock out part of the plant immunity defence. This advertisement was paid for by starch producer Lyckeby. The potato's own gene repair introduced variation in the resulting repaired genes, giving the plants a broader defense against various possible threats. What is the background to this story?
The reason given for why common agricultural potato varieties have low variation in their defence genes was genetic bottlenecking post-domestication (other potato strains in the endemic range retain substantial diversity).

Please provide a reference for this claim.

The rewrite of Maximilian Press goes beyond my intent in regard to how bottlenecking occurred. I see no need to mention it, especially since it likely occurred after domestication when the plant went to Europe. Is there any problem in removing it?

@DavidJonsson just fyi, you have to @ tag anyone so that they get notified that you respond. I don't now recall my chain of logic in introducing that edit, I think that I added it to provide more context. I will further edit to try to clarify what you mention in your comment.

This sounds to me like a CRISPR approach used to create S (blight susceptibility) gene knockouts that are then screened for blight resistance, though it's a little hard to know for sure due to the lack of a reference. CRISPR approaches do indeed exploit endogenous repair machinery to introduce mutations at targeted locations.
Here is one paper that follows that rough outline. The take home message is that, yes, you can use this kind of workflow to optimize resistance to particular blights. What it does not seem to address is the part of your question regarding the generation of variation at R genes via this approach, unless you refer to the specific variants introduced by such mutation. While such variants are not "unnatural", you cannot really replace population diversity removed by bottlenecks with CRISPR, they operate at different scales.
A more general review of CRISPR applications in potato is here, which may include more information if I have misunderstood something.
Another application that may be relevant is using CRISPR to modify the genes governing self-incompatibility in potato, which makes it easier to breed potatoes.


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Why do mountain gorilla eat just 1.7% fruit, while lowland gorillas eat 25%?

Eastern lowland gorillas have more diverse diets, which vary
seasonally. Leaves and pith are commonly eaten, but fruits can make up
as much as 25% of their diets. https://en.wikipedia.org/wiki/Gorilla#Food_and_foraging

The mountain gorilla is primarily a herbivore; the majority of its
diet is composed of the leaves, shoots and stems (85.8%) of 142 plant
species. It also feeds on bark (6.9%), roots (3.3%), flowers (2.3%),
and fruit (1.7%) https://en.wikipedia.org/wiki/Mountain_gorilla#Habitat_and_ecology

Have you checked what is the availability of fruits in the two environments? My first guess is that in the mountain environment you find fewer fruits due to altitude and climate.

Mountain plants have to be hardy, especially if they grow above the frost line. They are more likely to be tough vegetation (leaves, shoots, and stems) as mentioned in the mountain gorilla diet.
The lowlands have much more plant diversity (and generally better food). Sweet fruits have better calories for the effort required to forage and digest them, so you would expect the lowland gorillas to prefer fruit.


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Why are successful human rock climbers so dissimilar to Hominidae primates who spend extended time periods climbing?
In rock climbing, the sport considers the Ape Index when evaluating the factors critical for success.
However, the majority of successful climbers are lithe and slim with less than 8% body fat.  As one professional described it

“I feel very pressured to be thinner for climbing. I’m very strong, but I will likely never be thin, and I think that it holds me back…I don’t have that classic thin, long-limbed climber body…”

However, this seems completely at odds with the primates that we see on documentaries and in zoos which appear to be heavy, muscular, powerful and with considerable upper body strength.
Professional human climbers, while strong, rarely have significant quantities of muscle (Bodybuilder-esque) on their skeleton. They seek a power to weight ratio through weight-loss.
What accounts for this difference in development?  How do primates move such heavy masses through the upper canopy and why have they not evolved slimmer, smaller or more lithe frames?

I don't understand. Monkeys that are particularly agile at climbing tend to be very thin as well. A famously agile monkey species is the spider monkey.

Orangutan, Gorilla,  Chimpanzee...

Gorillas typically are pretty bad at climbing. I think you make the mistake to put all primates into a single pack and assume they are all alike and are all good climbers and then you make comparison with humans. A human is probably a better climber than a gorilla.

Remi...please dont make uninformed comments.  If you have an academic answer backed up with references then please make it otherwise assumptions benefit no one. http://www.berggorilla.org/en/gorillas/general/everyday-life/do-gorillas-often-climb-trees/ Gorillas can spend 20% of their day climbing

Venture, humans don't have exoskeletons (and you call others uninformed?) Please don't come here and be rude. We like questions, and we like answering good ones, but Remi.b is right that you've grouped a large number of species then compared them to one. You have your answer in your question. Finally, how closely related is climbing rocks to climbing trees? If trees disappear and primates have to resort to living on cliff faces, you'll have your definitive answer in a few million years maybe.

Do gorillas spend their time rock climbing?

@Seeds: Do ANY primates (other than a small subset of H. sapiens) spend much time rock climbing?  Some, but by no means all, of them spend a lot of time climbing trees & other jungle vegetation, but that's rather different from rock climbing.

@jamesqf Aye, that was the point of my question. H Saps do it infrequently, for recreation, all the other apes climb/swing in trees, which is a totally different activity. (closer to some of the things gymnasts do, like the ring thing)

I have specifically said Hominadae @anongoodnurse.  I did call others uninformed to state that gorillas are poor climbers.  I stand by that.  It was uninformed. I made a mistake in using the word exoskeleton but that doesn't make Remi's assumptions and your own any less rude. If you cannot answer, simply don't comment on the question.  I have grouped a large number of species, you are right, they are called the Hominidae family and all display similar traits and characteristics in climbing abilities.

@Venture2099 I don't want to fuel the discussion any more... but I am pretty bad at some things I sometimes spent a lot of time on. The fact that gorillas spend a lot of time climbing does not make them good at it. In fact, maybe if they were better they would have to spend less time doing it and more resting. You were asking for competitive climbers. Just because someone has a better Ape index it does not make them automatically a more avid climber.

And no source has been posted to prove that Gorillas are bad at climbing.  It was merely an assumption by a commenter, like much of this discussion thread.

Of course it varies from one species to the other. The silverback typically don't climb. Few branches would be able to hold their weight anyway. Other gorillas don't climb much in general (although see Western lowland gorillas do climb quite a bit) except for playing and foraging on fruits. They are in any way very bad in comparison with spider monkeys or other monkeys that are thinner and have longer limbs.

No one is comparing them with Monkeys.  Just you.

@Venture2099 Your OP says "primates" in every place except where you mention an "Ape Index". If you want comparisons only to apes, then say apes, don't say primates. You changed your title after the comment thread started talking about monkeys and then wonder why people are still on monkeys.

Actually I said Hominidae

There is an edit history here. You did not say Hominidae in the body of your question, and you added it to the title only after @Remi.b made a comment about monkeys.

After his first comment.  And I clarified in the comments as well but he kept referencing monkeys. shrug

As a rock-climber myself I’ll attempt to answer:  The selection criteria for competitive rock-climbing is exclusively based on sustain non-resting, extremely challenging moves up a rock-face.  The two most challenging aspects are 1) ability to ‘crimp’ (climbing term) on micro-holds without slipping and 2) being able to keep that up without resting throughout the climb.  I personally have a real problem with the later, because of my weight.
Primates selection criteria is not isolated to non-resting climbs.  They don’t get penalized for sitting on the branch.

I have to say, as someone who did a bit of climbing now & then, that the idea of competitive rock climbing just boggles my mind.  It seems to run contrary to everything I enjoyed about climbing...

@Venture2099 If you think this answer answered your question then upvote and accept it instead of posting unnecessary comments.

I will post the comments that I see fit and I will mark the question as answered when I think it is appropriate.


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Does Methanol cause similar intoxication as Ethanol?
Take two average healthy adult males weighing 80 kg. Neither has, ahem, developed their alcohol tolerance to any significant degree.
One imbibes 1 shot, 40 ml of 40% Methanol, and another 40 ml of 40% Ethanol (vodka) to empty stomach.
Now the vodka drinker should feel the drink going to their head, and he'd become just slightly drunk, and that's about it. No hangover expected from 1 shot of vodka, either.
What would be the effects on the Methanol drinker? Info on other effects would be nice too, but most importantly, would he become drunk, and how much compared to the vodka drinker?
If 16 ml of absolute methanol seems so much, that other toxic effects will dominate over "feeling drunk", then you can consider a smaller amount. The crux of the question is, does Methanol cause one to "become drunk" same way as Ethanol.

WARNING, just in case, to offset the casual tone of above question: Never drink anything which even just might contain Methanol! It's an easy way to die, or just go blind if you're "lucky"! It is not a useful way to get drunk or high, ever.

According to Wikipedia the density of methanol is 0,79 g/ml. Your 40ml of 40% Methanol contain about 16ml pure methanol which translate into 12,6gr. According to this paper the toxic dose starts around drinking 8g, so you would have some other, severe problems.

@Chris Yes, I'd expect so. I tried to choose an amount, which should feel like going to ones head (1 shot of vodka to empty stomach), yet shouldn't be lethal amount of Methanol.

A starting point could be this review which states  :   "With respect to GABAA receptors, a number of alcohols [...], including methanol, [...] potentiate GABA-gated current. The potencies of these alcohols tend to increase with chain length.". Not a definitive answer, though, because this is mole-for-mole at the receptor site, only for GABAaR, and does not take into account kinetics of absorption/passage of the BBB.


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Were Telomeres the Master Key to Abiogenesis
Knowing as we do now that all manner of complex organic molecules and viscelles/micelles form spontaneously in various environments, from hot vents perfect for basic hydrophobic H-C fatty acids and stable charged H-C-O-P hydrophobics - to volcanic glass micro-chambers, clay-layer geometry and water ice fractal symetry,  that all combine to create ideal nanoscale everywhere rapid self assembly scenarios for various amino acids etc that in turn can form RNA like segments and combinations... I can't help but wonder what scenario is best situation pre-biotic that can form Telomeric sequences.
It seems to me, an instinctive feeling after viewing so many bioscience and life origin videos, that in all the random prebiotic assembly and disassembly of molecules, the perfection of replication lies in repetition that first needed a master start and stop sequence control, as master of other sub gene start stop codons.
Of course a myriad of biophysics factors come into play in origin theory and I am far from expert but I wonder if anyone can provide solid
references about abiogenisis and telomeres?
Tough question to word here, and too vast a topic when I try and narrow the web searches.  However, the amino squences for telomeres are finite I believe and so before life kept repeating itself what molecules in what environment crates the combination best?

When you refer to amino acids (twice) I assume that you mean nucleotides?

I believe that is correct Alan. Being uncertain I used the word amino sequence, although that might be ambigous.

This lecture discussing the crebs cycle, along  with a beautiful animation illustrating the natural harmony of sequential assembly and disassembly  of H C and O building blocks, maybe be more the answer to my phrase "Master Key"  https://youtu.be/0cwvj0XBKlE?t=41m16s

No, they weren't. Interesting hypothesis though!
However, that hypothesis is missing a very important piece of information: prokaryotes don't typically have telomeres.
Because their DNA is typically circular, rather than linear, telomeres aren't necessary, and there is no shortening problem.
See the Wikipedia page on telomeres for more information. There are various theories on the origins of telomerases and telomere evolution, check out Google Scholar.


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Why does the kidney of a cow have lobules, why the kidney of a human hasn't any?
The kidney of a cow has lobules, while the kidney of a human hasn't any.
I can't think of any reason why it would be good for a kidney to have lobules. It would be good if the kidney needed to have a large surface area, but I don't see a reason why it would have to, since there is no diffusion or another proces that needs larger area.

Is there any reason why it would be beneficial for a kidney to have
lobules?
Is there a known reason why the kidney of a cow has lobules,
while the kidney of a human hasn't any?

Please edit your questions to provide links that reference the facts you are questioning. This will help future readers of your question that may not be aware of these facts to learn more, should they be interested. Thank you.

@AMR Thank you for your answer. But I am not sure what you meant by your comment. Do you want me to add a link to a picture of a human kidney and a cow's kidney?

I basically meant that you should add the sources of your research. How did you learn that bovine kidneys are lobular? If it was an article or a book you could say something like "The kidney of a cow has lobules, -X..." where X is the title of the article or a link to the source where you read it. I suggest it because it may not be common knowledge and someone may want to read more than your question and my answer on the subject. Also, general guidelines for asking questions on the site can be found here.

It appears that the invagination of the renal kidney is vestigial from development and unlike human and other mammals, the bovine kidney does not form a smooth outer cortex.

The kidneys of the bovine do not lose their foetal lobulation.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net
However this is not related to its function.

Despite what it’s externally lobulated appearance may suggest, the cortex of the bovine kidney is continuous and the kidney is of multipyramidal type.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net
If you want further information on the subject, The bovine kidney as an experimental model in urology: external gross anatomy; Carvalho, et. al. Cells Tissues Organs. 2009;190(1):53-8. doi: 10.1159/000159370 made measurements of the bovine kidneys and compared then to human measurements. This article is unfortunately behind a pay wall, so you will need academic access to Medline to access.
One observation that they do make is that

There are few publications about bovine kidney anatomy. The available information is general, contains little detail and is limited to the classical texts [Bossi et al., 1909; Nickel et al., 1979; Sisson, 1981; Dyce et al., 2004].

The question seems based on a partially incorrect premise (i.e., that human kidneys don't have lobules), but I could not discover any known reason for the variation in external appearance.
To start, all mammal kidneys contain renal lobules that form during fetal development and are necessary for the organ's function; so they are certainly beneficial.
In some mammals the kidney develops a smooth covering cortex that leads to the well-known "kidney bean" shape (as far as I can tell this is the case across all adult primates). Dogs, cats, sheep have the bean shape, and also have thicker kidneys than pigs, who have a more flattened shape. In some animals the left and right kidneys appear nearly "mirror image" in size and shape; in others (such as horses) the left and right are very different in shape. In the context of all this variation, cows are not that unusual among mammals, they do have a larger rumen that can force both kidneys to be on the right side, and the cortex that covers the lobules just doesn't develop to be as smooth as it does in humans. Since the lobules are universal across all the kidney shapes, and are often visible in a fetus with the cortex forming later, it is likely that is the original structure to evolve, whereas the smooth cortex was only selected later in evolution, and only in certain species where it was useful.
source: I have seen a lot of kidneys.


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Are there testosterone receptors in female mammary tissue?
Does female mammary tissue have receptors for testosterone hormones?
Do male hormones influence female mammary glands, as female hormones influenced the male mammary tissue, such as in gynecomastia?

The female mammary gland tissue contains androgen receptors (testosterone is an androgen). So this tissue is sensitive to androgens, and they inhibit the estrogen-induced proliferation. The inactivation of the androgen receptor on the other hand leads to an accelerated growth of the pubertal mammary gland and to the upregulation of estrogen receptor α expression in female mice. See references 1-3.
And the androgen receptor also seem very important in the formation of the nipples, as testosterone here directs apoptosis in the forming breast tissue. Mice without a functioning androgen receptor were born without nipples. See reference 4 and 5 for details.
To answer your question shortly: Yes, androgen hormones (among them testosterone) have a profound influence on the female mammary gland.
References:

Testosterone inhibits estrogen-induced mammary epithelial
proliferation and suppresses estrogen receptor expression.
Minireview: The Androgen Receptor in Breast Tissues: Growth
Inhibitor, Tumor Suppressor, Oncogene
Androgen receptor inactivation resulted in acceleration in pubertal
mammary gland growth, upregulation of ERα expression, and
Wnt/β-catenin signaling in female mice.
Hormone Action in the Mammary Gland
Specificity of tissue interaction and origin of mesenchymal cells in
the androgen response of the embryonic mammary gland.

@esi72
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The effects of auto-brewery syndrome
Why are some people affected so differently by auto-brewery syndrome differently if the syndrome seems to be caused by the single organism saccharomyces cerevisiae? It is known that the syndrome has been used to waive DUI charges — like most recently for this New Yorker whose blood alcohol level was 0.4 but she had none of the usual symptoms of intoxication, even though she had ingested alcohol earlier that day. She also carried out most of her daily activities normally, even with high levels of alcohol in her system.
On the other hand, there was another case where the carrier experience the effects of auto-brewery syndrome differently:

Cases involving the yeast Candida albicans and Candida krusei have
  popped up in Japan, and in 2013 Panola College Dean of Nursing Barbara
  Cordell documented the case of a 61-year-old man who had frequent
  bouts of unexplained drunkenness for years before being diagnosed with
  an overabundance of Saccharomyces cerevisiae, or brewer's yeast, the
  same yeast used to make beer.

The quote can also be found at the link of the CNN article.
Could the difference in symptoms and effects due to variations in how the carrier bodies could deal with the overabundance (maybe depending on age, gender, or ethnicity) or are they attributed to variations in the nature of the yeast?

Did any of the people in those cases have diabetes? They likely have high levels of blood glucose. Women with diabetes are prone to recurrent complicated fungal vaginosis as they have higher than average amounts of blood glucose creating an environment where yeasts have abundant nutrients. The metabolic byproduct of yeast is ethanol.

People could also have a disruption in their bacterial microbiome, as is the case when we take antibiotics that allow the fungi more room to grow. The more space they take up, the more access to resources they have, the larger their numbers get and the more metabolic waste they produce. Yeast produce ethanol. So more yeast equals more ethanol. Also if the person has a defective alcohol dehydrogenase gene, then they are not going to be able to process the alcohol that the yeast are excreting.

The gut microbiome is extremely complicated, and almost anything related to it is only partially known, therefore prone to oversimplification. Trying to explain the phenomenon of gut fermentation syndrome in such a limited fashion (age, gender, ethnicity, quantity of one particular yeast, etc.) will not help us understand it.

Common yeasts (C. albicans, C. tropicalis and Torulopsis glabrata) and Saccharomyces cerevisiae are able to ferment sugars through the homolactic, heterolactic or mixed acid fermentation pathways, with ethanol as the major end product.

Candida is a very common yeast found in the environment and in and on our bodies wherever it's warm and moist (therefore the GI tract.) Candida species are the most common cause of invasive fungal infections in humans (followed by Cryptococcus and Aspergillus) and can involve any organ. Yet it's omnipresence does not result in clinically recognized cases of ethanol intoxication in even a minute fraction of people who carry it in their gut.
Case reports started appearing in the literature starting in 1972, yet it is still a rare event to see one. In 2001, the case of a 13 year old girl was published. She had short gut syndrome and became intoxicated after ingesting carbohydrates. She had been placed in a rehabilitation facility with no access to alcohol, but still had positive blood alcohols. Aspirates from her small intestines grew Candida glabrata and Saccharomyces cerevisiae. Short-gut syndrome is complicated.
We have no idea how common fermentation into alcohol is in the gut, or what the results are, but it is probably far more common than recognized, can probably result in effects other than intoxication (for example fatty liver disease in non-drinkers), and probably has a role in other illnesses.
It's complicated:

Carbohydrate metabolism by gut microorganisms is a central process allowing supply of nutrients and energy to the host. This fermentative process is complex and involves several functional groups of bacteria with complementary metabolic activities that interact to ensure the biotransformation of polymers (resistant starch, nonstarch polysaccharides, proteins, mucins…) into end-products (mainly short chain fatty acids and gases). Hydrolytic communities transform complex substrates into smaller fragments that can also be used by other bacterial groups unable to hydrolyse polymers. Other microbial cross-feeding interactions are related to the utilisation of fermentative products such as succinate, lactate or hydrogen and involve specific groups of microorganisms.

All we know is that it happens in some people, and that it can respond to antifungal treatment and some probiotic supplementation. "Why" is still a mystery, and speculation only.
Gut fermentation syndrome
Invasive Fungal Pathogens: Current Epidemiological Trends
IwataK., “A Review of the Literature on Drunken Syndromes Due to Yeasts in the Gastrointestinal Tract,” University of Tokyo Press, Tokyo, 1972, 260-268. Not available online
Functional dysbiosis within the gut microbiota of patients with constipated-irritable bowel syndrome
Obesity and female gender increase breath ethanol concentration: potential implications for the pathogenesis of nonalcoholic steatohepatitis

Interesting. Also how often do we routinely test for blood alcohol levels? Plus as one of the science writers in those articles put it, if we think about alcoholism and how the body grows accustomed to increased blood alcohol levels, then that could mean that it is very prevalent, it is just that we never look and we don't feel the effects because we are acclimated to it. Though I also wonder how much diabetes and elevated blood sugar levels might play in the syndrome.

@AMR - It is. In one study after a 50 g glucose challenge of people suspected of gut fermentation into ethanol, 61% (311/510) had positive blood alcohol levels, whereas "almost none" of the controls did. What a summary! It makes one wonder.


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How do microbes develop resistance to anitmicrobial peptides?
I would like to better understand how bacteria use the "strategy" of alternations to lipid A and membrane proteins in order to resist antimicrobial peptides of the immune system?
It is my understanding that the by altering its lipid A, the bacterium makes its membrane less hydrophobic, increasing hydrophilicity, resulting in an increased amount of fluidity for the outer membrane.
This should then inhibit the hydrophobic portion of antimicrobial peptide embedding into the lipid membrane of bacteria.
Is this accurate? Is there anything I am missing about these alterations than confer resistance?


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What determines whether the maternal or paternal allele is expressed?
I am taking cell biology and have this question:
During the process of gene expression, it is possible to express either the maternal allele or the paternal allele.
When and how is the determination made to express one allele over the other?

Are you talking about X chromosomes in females only?

Except in the case of X inactivation in females, and genes on the Y chromosome in males, generally speaking both alleles are expressed in cells.
A good example is the ABO blood type marker system. If the mother is type AA, she will pass on an A allele, which codes for the A antigen. If the father is type BB, he will pass on a B allele, coding for the B antigen. Therefore, any children will be type AB, as the maternal chromosome 9 will express the A form, and the paternal chromosome 9 will express B.

I see.. thank you. But, when does this happens? I assume that two different mRNA's for each pair of homological chromosomes are leaving the nucleolus? So, when does the merging happen?

@user135172 Yes, two different mRNA sequences will leave the nucleus after transcription. They don't "merge", each one is translated separately. In the case of my ABO example above, one set of mRNAs is translated to the A antigen, and the other set to the B antigen, and both are expressed on the cell surface (I'm simplifying the exact process tremendously, please read the wikipedia link if you'd like to know more).

Answer is yes. The term you are look for is parental imprinting
http://mcb.berkeley.edu/courses/mcb142/lecture%20topics/Amacher/LECTURE_13_Imprinting_F08.pdf
Take the  insulin-like growth factor 2 (Igf2) on chr7 (autosome). This gene is imprinted such that only the parental copy is active. So if a mouse inherits a defective copy from its father, it will be stunted. However if it inherited a defective copy from its mother, it will be normal.
Last I looked (about 2 years ago) there were over 1000 genes in humans that are paternally imprinted. It also should be noted that the imprinting may only be present at certain stages in development. It is even possible that one parent's allele to be active in one development stage (father in fetus) but the other at a different stage (mother, rest of life).
This is a very exciting field. How the more complicated switching between imprinted allele occurs is still understudy. However for simply imprinting... it is caused by DNA methylation and DNA silencing by heterochromatin.
Female mammals have an additional system for differential allele expression...ChrX inactivation. In a tissue, one ChrX is randomly inactivated by heterochromatisation. So most of the gene on one ChrX are off. So some cells in a tissue will express the maternal allele, while others the parental allele....


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Blood draw from the elderly or those with tiny veins
A lot of people have very small veins making it next to impossible to draw blood.
Would a nitroglycerin tablet (or some other vasodilator) before drawing blood help to enlarge veins?

When we need to collect blood from patients we typically draw blood from peripheral veins that are superficial. These are the veins that you can see in some individuals hands and forearms. There are superficial leg veins that are visible. Drugs like nitroglycerin or other vasodilators do not have significant effects on the superficial veins that you'd be trying to withdrawal blood from in the extremities (i.e. arms and legs).
If you wanted to really engorge someone's veins, you'd likely have to load them up with intravenous fluids. However, this would not be safe in patients needing routine blood draws; especially elderly people who might become fluid-overloaded to the point at which the develop congestive heart failure. Younger patients might temporarily have minimal increases in their circulating blood volume, but their kidneys would very quickly eliminate the excess fluid as urine.

I think the use of drugs for simple things like a blood draw should be a last resort. Having a cup of tea or two can work wonders at raising your blood volume and making the blood draw easier.
A nitroglycerin tablet would risk systemic side effects in many patients, so a topical ointment could be used to minimize these effects. Nitroglycerin has been applied topically over the venipuncture site to cause a transient vasodilation, and potentially make the blood draw easier. There are varying reports on its efficacy - Hecker et al. (1983) found nitroglycerin ointment helped venipuncture, Griffith et al. (1994) found it made no difference in vein size.

the Hecker et al. study is a small, poorly conducted study - you can't even tell if they used the proper statistical analysis. I wouldn't get very excited over it - I would bet someone could not reproduce this experiment. The size of the veins doesn't even appear to be changed with the nitroglycerin in almost all of the patients, and it appears that 2 or 3 patients were particularly difficult sticks (and just happened to be in the placebo group). We don't routinely use this clinically in the ED or anywhere else in the hospital/clinics - I doubt nitroglycerin ointment actually helps.


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Why are kidney discard rates so high?
A recent report from UNOS states:

The kidney discard rate has returned to pre-KAS levels, dropping from 20.2 percent in the first six months to 18.4 percent in months 7-10.

To me, this seems quite high considering the number of people waiting for a kidney. Why is this rate not lower?

If you click through the link on the page you linked to is a presentation, https://www.transplantpro.org/wp-content/uploads/sites/3/KAS_analysis_6month.pdf Towards the end is a slide that shows reasons for discarding. The majority were biopsy findings (probably some infection or precancerous lesion) no donor found in time (Not all organs are a match of the people on the transplant lists)

Not a transplant surgeon, but... we're not going to rush to put a mediocre kidney in someone when that kidney may not do well in the long term. There's always a chance of developing renal failure again - and, if you've already exposed the patient to those foreign antigens on the donor kidney, then they are even more highly sensitized to any future transplant kidneys.


text:
Why are fifth order Markov Models, the ones most often used for gene prediction?
As far as we know that smallest polypeptide chain length is 60 amino acids - so if we found an Open Reading Frame (ORF) of about 60 codons without the interruption of stop codon we can consider it to be a possible coding region or gene.
The fifth order Markov Model uses hexameric frequency to predict coding regions, however this doesn't seem very specific.
Why wouldn't we use higher order Markov Models with higher frequencies and more specificity? Wouldn't increasing the order of Markov models prevent false positive results?

We do not, in fact, know that "the smallest polypeptide chain length is 60 amino acids".  That is a purely artificial cutoff, not a biologically meaningful one.  There are undoubtedly many, many functional polypeptides that are much smaller but that have not been correctly annotated.

You also have to remember that higher order Eukaryotic genes are interrupted. If the exons in the gene you are looking for are all less than 180 nucleotides, then you are going to miss it. you also have to factor in splice acceptor and splice donor sites, alternate splice forms, codons for methionine that do not indicate the start of the reading frame, etc. Think of it this way; by increasing the stringency, you are throwing out more information. Most of that information is bad, but not all of it, which means that you are creating the situation where you miss things you want.

Why are you so sure that people stick to 5-order Marcov Chains? 2. This boils down to training the state transition matrix, i.e. increasing order leads to increasing the number of possible k-mers exponentially, hence at some point your sample becomes insufficient to estimate transition rates with enough confidence, let alone the computational complexity.

The problem with increasingly complex HMMs is that their parameter space tends to explode with the nth-order of the HMMs. Higher number of parameters is often not great because it reduces the possible number of observations that go into training each parameter and can increase overfitting of the model.
From the information that you are providing it is possible that the 5th order model reaches the sweet spot of having great performance with a reasonably contained parameter space.
It is not clear how your model also works.
Is each state a single nucleotide or a single KMER?
Is it a generalized HMM with separate states for exons and introns with the KMERs being observations?
Work by the Bier lab has shown that 5-mers are very good at telling apart enhancers from background using a SVM model for classification. In your context it seems pretty reasonable to use 6-mers to find genes given this finding.
For more details please check "Biological Sequence Analysis" by Sean Eddy and the work of Dr. Michael Brent @ Washington University in Saint Louis (his lab has done a lot of research on HMMs for gene finding).
It'd be useful to have one or few paper references behind your question.


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How long can a human neuron live outside the body in a controlled environment?
Have there been any experiments that have kept neurons alive (stationary), without preserving methods such as freezing? If yes, then how long were the cells kept alive for?

Do you mean primary cultured neurons?

You can look into culture protocols. For example this one suggests 7-10 days for culture maturation, then 2 weeks harvest time (scroll down to the last step). While a protocol won't tell you the longest time, it will give you a lower limit for the longest time. This is about nonhuman neurons of course, but there are also human cultures started from stem cells.

According to this paper from 2001, they've got the survival time up to about a year on average. The trick is sealing the neuron inside a permeable membrane so you don't actually risk contamination when feeding. This paper lays out experiments that take many weeks to perform, so as far as I can tell the science of keeping neurons alive has advanced to 'as long as I keep feeding them and nothing bad happens'.


text:
What is the effect of garlic on intestinal flora?
Now that we can compare whole microbiomes, has there been investigations on the effect of garlic (or diallyl disulfide, its main ingredient) on intestinal flora? From the proven antimicrobial activity, it should work like antibiotics. But does it leave "good bacteria" counts untouched?

From studies,

lactic acid bacteria were found to be more resistant to GP (garlic
  powder) compared to the clostridial members of the gut microbiota.
  While for most bacteria the antimicrobial effect was transient, the
  lactobacilli showed a degree of resistance to garlic, indicating that
  its consumption may favour the growth of these beneficial bacterial
  species in the gut. Once the strains of other bacteria (eg:
  Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium
  nexile A2-232) became resistant, they retained their resistant
  phenotype upon sub-culturing. Garlic intake has the potential to
  temporarily modulate the gut microbiota (reference).

Overall garlic can prove to be beneficial, because it seems to have more of an effect on detrimental bacteria like Helicobacter pylori (H. pylori), even when its strains were resistant to antibiotics. Overall garlic was found to be more detrimental to pathological bacteria when compared to normal gut flora (reference). Garlic’s diallyl disulfide has also been found to effectively cause cell death in Candida albicans which is a fungus in our gut which if not kept in check can cause health problems (reference).
Inulin and fructooligosaccharides present in garlic can also serve as nutrients for the probiotics colonizing your body (reference).


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Transmission of HIV from Mother-to-Child Through Breastfeeding
If a mother is HIV+ and was on medications which would help her deliver a HIV negative baby, can the baby contract the HIV through her breast milk?

Hi there and welcome to biology.S.E. Currently the question is a bit unclear. To try to move this away from being to hypothetical, what medication is the mother taking? Also note that this site shouldn't be used to seek personal medical advice.

I am not seeking personal medical advice ,i was just curious to know.Thanks for the answer

In short, yes. Breast milk can contain virions which can be transferred from Mother-to-Child.
These are the guidelines from the National Institute of Health in the United States regarding the Prevention for Mother-to-Child Transmission of HIV and how the prevent Mother-to-Child Transmission of HIV After Birth
While the guidelines in the US are geared towards the fact that we have alternatives to breast milk, the World Health Organization has compiled evidence that suggests that Antiretroviral therapies along with exclusive breastfeeding may provide the most benefit for the health of the infant. This likely has to do with the access to suitable nutritional alternatives, clean water, and vaccines in developing countries, and in fact, it appears that mothers in wealthy countries that have HIV are advised not to breastfeed at all. This site outlines the different guidelines in place. The choice between breastfeeding and not in lesser developed countries has to do with the fact that the risk from waterborne illnesses and their impact on infant mortality rates is likely far greater than the risk of HIV transmission from mother to child through breastfeeding while both are on Antiretroviral therapy. The reason that exclusive breastfeeding is recommended is that it keeps the viral concentration in breast milk lower than if the baby was suckling only part of the time.
Italics in previous paragraph indicate an edit to the answer in order to clarify the reason why breastfeeding is recommended in lesser developed countries, even though it poses a risk for HIV transmission
Please note that these guidelines are in flux and as more evidence is obtained and as the virus mutates, things may change. It is always best to consult with a physician on the most current recommendations in the care of your infant if you are HIV+.

Wow, I would never have expected a 'yes (maybe)' on this question... +1

@AliceD I think that we in the developed world forget that what works for us may be untenable for the rest of the world. The WHO guidelines are likely a lesser of two evils approach....

@AliceD Breastmilk is a really easy way to spread the virus, but part of the problem is that in many sub-Sarahan communities access to clean water is not reliable.  Thus, the option frequently becomes a choice between breastfeeding and giving your child HIV, or mixing formula with water and giving your child life-threatening illnesses.  Not good.

@Amory, my goodness, that is terrible. I never realized HIV to be transmitted orally via breastmilk.

@AliceD It's fairly efficacious too; transmission rate is somewhere around 20%, if not higher.  Only birth (25%?) and blood transfusions (90%) are higher.


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What kinds of cells does human saliva contain?
I have heard that our saliva contains cells. What cell types can be found in human saliva?

I clarified the question and vote for reopening.

It contains white blood cells (leukocytes) and cells from the inner lining of the mouth (buccal epithelial cells). The DNA obtained from these cells is the basis of DNA profiling based on saliva samples.
Source: Salimetrics


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Does photosynthesis occur on cloudy days or does it require direct sunlight?
In my basic science classes in high school, I have learned that during photosynthesis, plants absorb sunlight and produce food by converting carbon dioxide and water into sugar and starch.
To me, this seems similar to the analogy of solar cells that convert sunlight into electricity. When sunlight falls directly on the solar cell, it produces electricity, but even when it is cloudy with no direct sunlight available, electricity is produced, but with less efficiency.
So can photosynthesis occur in plants only when they are in direct sunlight or does photosynthesis also occur during cloudy weather when the light is diffuse or indirect?

I recently took a trip to a nearby abandoned ore mine. Deep in there, I was surprised to see plenty of mosses around the installed neon tubes. So, photosynthesis does not even need actual sunlight to occur. I also agree with WYSIWYG's answer regarding the performance of leaves under diffuse light conditions.


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What "emotions" can a snake feel?
Short:
Thinking in particular of a Royal Python (US: Ball Python) such as some people keep as exotic companion animals, what sorts of "emotions" or "feelings" are they capable of?

Long: http://simonsnakesite.tripod.com/snakebasics.html says that

scientific studies show that snakes just don't have the cerebral capacity for [emotions like joy, anger, and affection] but do have "primitive" feelings like aggression, fear, and pleasure

Based on the parts of the human brain where we develop emotions, and on the more primitive brain in a snake, this makes sense, but beyond being able to tell whether it's feeling the primitives such as "fear" or "safety", what "emotions" or "feelings" can we realistically ascribe to a snake?

Interesting thought. I'd recommend diving into google scholar.

You seem to be confusing emotions and feelings. They are not necessarily the same thing. Definitions vary, can you make your question more precise? What do you mean by emotion?

I think the emotionial capacity of an animal is directly related to it's inteligence.By this mean the more intelligent species can be more emotional.

We can only very indirectly and tentatively ascribe emotions/feelings to animals if we understand their brains functionally, and use functional imaging. This is difficult in practice. There is also a crucial difference in science between the subjective world (happy) and objective world (smiling).
In ethology, you can only observe behavior and its consequences. Stimuli can be appetitive and aversive, positive or negative. Insects, reptiles and mammals can similarly differentiate between sweet water (which they seek out) and bitter water (which they normally avoid). Those are easier behaviors to identify. Of course, in reality, an emotional state is made up of a complex multi-dimensional spectrum of multiple measures (satiety vs. hunger, anxiety vs. relaxation, happiness vs. unhappiness, fear vs. safety, sadness vs. unsadness, etc.) simultaneously. There is also a difference between the measurement and the internal reality. Additionally, there's the choice of measurement and the internal reality, too. One could measure happiness by width of your smile at a given time, but that would not be a very valid and reliable measurement. This is the general difficulty with measuring and detecting emotion - behavior is a more objective quantification.
If you were studying a new species of human, which could not talk or report to you using a language about how it 'felt', and had a brain significantly different from ours, we would also be unwise to ascribe specific emotions so callously. Not because the specimen would be incapable of feeling emotions, but because we wouldn't have the tools to check and verify internal emotional states, or probe whether the snake was conscious of an emotion regardless of its behavior.
However, we do believe that emotions require a big central nervous system to exist. Snakes certainly have large enough brains to experience fear and pleasure. It seems that most large vertebrates can, certainly mammals can such as mice. Whether reptiles or even insects have the 'cerebral capacity' for non-primitive (read: non-humanlike) is an open question.

Pleasure and Displeasure certainly if you have a brain you have these.
Pain, Fear, and Anger is also highly likely just based on their general behavior. these are fairly basic and likely exist in all vertebrates.
Since they can be taught food avoidance likely Disgust as well.
Some snakes show familial ties so Affection/Love may be possible, although this is very tentative.
As SPr points out determining exact emotion ins ethology is extremely difficult, we can't even agree on what emotion humans have.This is partially due to not being able to define basic emotions.


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Do human anal glands have any function?
Anal glands in all kinds of animals play a range of diverse functions - providing fat for preening feathers or waterproofing fur, generating distinct scent, even repelling predators.
None of the resources I found about human anal glands ever mention their function. There's info or infections, location, treatment of problems related to them, but never a word about a role they might serve - if any. Are they vestigial organs without any role or do they have some evolutionary purpose?

never heard of a human anal gland

@WYSIWYG: Here.

my anal glands produce a distinct scent...

@MattDMo: uh... comparing to whose? No, wait, scratch that question.

This question may have more to do with a depreciation in the ability to detect anal secretions than with the function of the glands themselves.

They are vital if not incredibly useful in many other mammals but not humans. People have tried to look for a role and seen that they activate in times of stress or anxiety. However this probably only serves to heighten both stress and anxiety as you now also don't smell that great either. There is no identifiable role in humans apart from causing a variety of disorders such as an abcess.
When physically examining a patient with a very painful condition, doing something that greatly provokes symptoms will often cause the anal glands to secrete. As a doctor, I interpret it as a clear warning that the patient is in distress, and that I need to exercise greater caution. I don't know of any science supporting this, but the function seems self-evident.


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Is a stab wound to the back lethal?
How deadly is a stab in the back?
Video games, movies, and other fiction would have us believe that a backstab against a foe with a modestly-sized blade leads to immediate and certain death, having a 100% success rate and causing death virtually instantaneously.  How close is this to reality?  How does the lethality of a puncture wound to the back compare to such wounds delivered to other areas of the body?  What is the primary target in such an attack in terms of internal organs, and what variables effect its projected success?

It depends on a lot of factors like the size of the blade, where you stab etc.. I would think that a stab through the heart would mean instantaneous death..

Check out the sources of Wikipedia article: the mortality rate is up to 4%.
The main causes of "immediate" death in penetrating trauma are shock (low blood pressure due to external/internal hemorrhage, especially arterial hemorrhage), pneumothorax, penetrating heart injury (with resultant hemopericardium) and other less frequent causes.
The same causes account for "later" lethal case plus some specific causes like infections, emboly etc.
The overall mortality rate of stab wounds is far from 100%, and according to different studies is between 1% to 4%, but rarely more. The morbidity depends on depth of wound, place of injury, overall health status etc, thus multifactorial analysis is required to get an overall image of the penetrating wounds of the body.
Some sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627025/ -
 (4.3% mortality in stab wounds to the anterior abdomen, back, and flank).
http://www.ncbi.nlm.nih.gov/pubmed/3798182 - the mortality in back/flank stab wounds was 1.3%.

I think there is a possibility for significant selection bias in those studies as they only include patients who made it to hospital alive

@RoryM You are right about the "selection". However, it is very rare occasion  to see an isolated back stab wound on autopsy as a cause of prehospital death, thus even if this bias were extremely significant, the mortality rate could not exceed 15%....


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Microbiome Data
How is it possible to access microbiome data like that found here? I'd like to perform analyses on similar type of data, but cannot find OTU data like that at the Human Biome Project. Thanks for any leads.

Purely computational questions are better suited for http://biostars.org

This .csv files (comma-separated value) can be imported into Galaxy (usegalaxy.org)
I recommend that you take a look at that web app, it has many build in applications for analysis.
Also this site has a lot of quick video tutorials.

Thanks for the link. I'll check it out. My goal was to get OTU prevalence data (like at the exploredata.net site) and not just the Human Biome Data (regardless of format [e.g., csv, FASTA,etc.]) on what constitutes a particular OTU.

The data that you are pointing to are files in .csv (comma-separated value) format. They can be opened, after downloading, by any standard spreadsheet programme, including Excel, as well as programmatically (e.g. in Python using the csv module)
Apologies if you understood this and were asking for something more.


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Why do vaccines cause your arm to hurt?
When you get a shot for a vaccine (for example, the annual flu vaccine), the nurse frequently indicates that your arm will ache for a day or two, maybe more. This ache is typically not just a pain from having your skin punctured, but is actually an ache of the entire arm.
What mechanism causes the entire arm to ache from a vaccine? Why doesn't that ache extend to other parts of the body, like the hands or the shoulders? Why do non-vaccine arm punctures (such as drawing blood, injecting drugs) not cause the ache?

My guess would be local inflammation, but it's just a guess

I would also say local inflammation. Since vaccines are designed to trigger an immune response, and inflammation is one of the initial mechanisms of the Innate response, it would make sense.

Vaccines contain adjuvants. They are designed to enhance the immune response, which means creating something like an inflammatory response.

i think it may partially be "just in our heads"

@tryingToGetProgrammingStraight No, it's an aching arm, not a headache. ;-)

The goal of the vaccine is to provoke an immune response, therefore some degree of inflammation is expected in order for the vaccine to work. As swbarnes2 says, vaccines contain adjuvants, pro-inflammatory molecules that produces local inflammation and recruits immune cells to the site of the inoculation.
Since you get the shot intramuscularily, intradermally or subcutaneously, it is local, and the inflammation does not spread. The reason why your whole arm seems to hurt (rather than the place where the vaccine was deposited) is, I think, that where you got your shot, you have not many pain receptors, and your brain is not able to determine the pain source very exactly.


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Are the intestinal microbiota substantially different within a diverticulum of the colon?
From the Wikipedia page for the vermiform appendix:

This proposal is based on a new understanding of how the immune system supports the growth of beneficial intestinal bacteria, in combination with many well-known features of the appendix, including its architecture, its location just below the normal one-way flow of food and germs in the large intestine, and its association with copious amounts of immune tissue. Research...showed that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile.

This quote seems to be implying that the appendix can act as a breeding ground for certain gut flora that are slightly less common (like C. difficile) and not as ubiquitous as E. coli or Enterobacter sp. The appendix could be seen as an ideal spot for this growth of microbial populations in the gut.
Given that, to a first approximation, anatomically, the appendix and a common diverticulum of the colon are both outcroppings of the large intestine: to what extent would a diverticulum also be able to support less common or more diverse flora, and how likely is this to be due to a difference in extracellular environment (pH, ion concentration) and how likely is it simply due to shape?

This is a very interesting question given the rising importance of the gut microbiome, as well as the American Gut and British Gut microbiome sequencing projects

The appendix is a type of true diverticulum of the colon, although it is one that is present in everyone (unless a surgeon has removed it). There are bacteria in the gut from the mouth all the way down to the anus, and the numbers and types of bacteria change along the length of the intestinal tract. A recent review from J. Ridlon published in the Journal of Lipid Research (2006) is available online and has documented these observations from a number of investigators. In that paper the bacterial species are described as changing as well as the relative abundances of bacteria which increases along the length of the intestinal tract. Figure 1 from that paper which is open access available from the link above is below.

I think its interesting that the wiki page you're citing states that individuals without an appendix were more likely to develop a recurrent C. diff infection. One could interpret that as they did on that site that somehow the appendix is repopulating the colon and making that individual more resistant to a repeat or "Recurrent" infection. However, I don't know of any studies that have directly tested that hypothesis.
In terms of whether or not the gut flora - aka "gut microbiota" - are significantly different in the appendix is possible, but I don't think anyone has identified that just yet. One of the problems with this would be that we don't routinely remove appendices unless they are infected/inflamed which intrinsically would alter the microbiome locally.
So, is it possible that the microbiome could be significantly different in the appendix itself compared to the cecum just a few centimeters away? The answer would be - potentially, but no one has been able to address that question to date.

These may help: http://www.ncbi.nlm.nih.gov/pubmed/25588621 ,  http://www.ncbi.nlm.nih.gov/pubmed/24883147 , http://www.ncbi.nlm.nih.gov/pubmed/24039352 , Though it appears that you may have to decide whom to believe.

I thought the 5% colectomy with appendix versus 10% without was pretty telling, but there are just too many uncontrolled variables with humans or knowledge on the microbiome yet to say definitively what the exact cause of anything actually is. Maybe they all went swimming in Griswold Springs....

@AMR nice links, but all retrospective (and biased)... an interesting hypothesis though... I agree with you, numbers look convincing - but only 388 patients for a multivariate logistic model... definitely not enough power in that paper to be reproducible - that reeks of irreproducibility to me.


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What is an organism?
The definition of an organism Wikipedia gives is

An organism is any contiguous living system.

I understand that these are not organisms according to this definition:

A bird and a tree it's perching on are living and contiguous, but they don't form a system.
All humans are living and form a system, but they are not contiguous.

But some things are unclear to me. My veins and my skin are contiguous and living. Do they form a system? I think so, at least according to what I read about systems in Wikipedia. They are definitely interconnected; they have behavior; and I believe they have structure, though I'm not really sure what structure is. Perhaps if we carefully define what we want "structure" to mean, we can save the definition from allowing (skin + veins) to be an organism?
Is (mother + her unborn child) an organism? I think it definitely is according to the definition. Is the unborn child an organism?
Is an apple that's just fallen off a tree an organism? Was it an organism before it fell?
Is (human + their microbiome) an organism? Is a human without the microbiome an organism?
I think the part of the definition that the least clear to me is the word "system", and in the definition of the word "system", it's the word "structure".

Cf. this question http://biology.stackexchange.com/questions/8745/polymorphism-in-cnidarians/9148#9148, and especially part B in my answer about "Organism Concepts"

I think the definition in Wikipedia is simply bad because it depends on another debatable definition.
I prefer something which follows from an observation made by Ricard Dawkins in The Extended Phenotype (the following is my definition, but I think Dawkins had something similar in mind):
An organism is any system of components which depend on each other for survival and cooperate in proliferating potentially unboundedly.
A single-celled organism is by this definition an organism since it proliferates by coordination of its components.
A single-celled organism with organelles deriving from endosymbiosis (think mitochondria) is an organism: even though mitochondria do proliferate on their own inside the cell, they don’t do so outside of the cell, hence have a bounded proliferation only; and they depend on the cell as a host. On the other hand, they cooperate with the cell division.
Endosymbionts, on the other hand, are organisms because even though they depend on a host (and the host on them), they may theoretically switch host or even survive a limited time without a host.
Similarly, the cells in a multi-cellular organism can sometimes divide independently (in organs) but they cannot survive without the rest of the organism, and the unbounded reproduction of any organ in fact requires going via the germ line of said organism.
A virus which depends on a host to proliferate does not form an organism with the host since it doesn’t use the host’s germ line; if, on the other hand, it does use the host’s germ line (consider virally derived pseudo-genes on our DNA) then, yes, it forms a common organism with its host.

Is (mother + her unborn child) an organism?

I wouldn’t say so, since the child is only temporally part of the host.

Is an apple that's just fallen off a tree an organism?

Interesting; I’d say yes, as long as it retains the potential ability to proliferate (it’s a separate organism from the tree though).

Is (human + their microbiome) an organism?

No. Humans can survive (albeit only shortly) without a microbiome; in the same vein, the bacteria of the microbiome can change their host.
Unfortunately, this definition also has a drawback: there are organisms which cannot reproduce because they are sterile, yet they are clearly still organisms.
Note that other definitions (e.g. “an organism is a collection of components sharing common genetic material”) also don’t work universally since they also break down – the example of genetic commonality would preclude mosaicism and organelles derived from endosymbiosis.

Thank you. I'm not sure I understand the part on mitochondria. Do you consider a mitochondrion an organism or not? You say "endosymbionts are organisms", but also "mitochondria . . . have a bounded proliferation only". Aren't mitochondria endosymbionts?

@ymar No. They form an organism with their host cell. Endosymbionts are organisms but mitochondria are derived from endosymbionts. They are no longer endosymbionts (according to the common definition of the term).

OK, I see. Could you explain what you mean by potential unbounded proliferation?

@ymar Literally, proliferation without (theoretical) limit. Mitochondria can try as hard as they want, they cannot proliferate beyond their host cells. On the other hand, humans can theoretically proliferate to the bounds of the biosphere, which, itself, has no fixed bounds (except the edge of the Universe if you’re so inclined).

I don't understand. Let's forget about humans for a moment because technology makes things complicated. But a cod cannot live on the desert unless there is a caring human that supplies water and food for it. There surely are limits to where cods can live and proliferate by themselves, right?

@ymar Sure. But a desert is not an organism which can proliferate by itself: mitochondria are restricted in their proliferation by the surrounding cell, but together with the cell they can proliferate beyond that single cell. The cod can proliferate more or less limitless within its biotope but the biotope itself isn’t an organism with which the cod can cooperate to reproduce further.

OK, this seems to be related to something I decided to leave out of my question. Can organisms be nested? Of course, an organism can live within another organism. But can an organism be a part of another organism? It seems to me that your answer is no.

I believe you are using the incorrect definition of "Contigous." The most common usage is basically "sharing a border," but it can also be:
-touching or connected throughout in an unbroken sequence contiguous row of houses
http://www.merriam-webster.com/dictionary/contiguous
You also need to include the part about what defines "living":
"... can react to stimuli, reproduce, grow, and maintain homeostasis."
Your organs form a system, which results in you. A mother and her unborn child could also be considered an organism under this definition. The apple would not, nor would the tree and bird combination.

I think that's the definition of "contiguous" I'm using. Why do you think it's not? I know all of my organs together form a system. What I'm not sure about is whether my skin together with my veins forms a system. Is being made of living cells enough for being living? I think it should be if a colony of bacteria is considered an organism.