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Is hydrochloric acid suitable for pickling food?
I was wondering whether it is possible to pickle food using hydrochloric acid (HCl), rather than acetic acid. I am not very familiar with the biology of the fermentation process involved in pickling and I do not know if HCl would give rise to a suitable environment. Is HCl-based pickling possible? What percentage of HCl should be used?

Short answer
Weak organic acids are more effective for food preservation then strong mineral acids, mainly because undissociated weak acids can cross the cell membrane and disrupt cell physiology from within.
Background
Natural fermented, or pickled materials are traditionally cured in a brine solution (salt, water, sometimes spices and sugar). Desirable anaerobic bacteria convert carbohydrates to acetic acid that “pickle” and preserve the food. The brine protects the vegetables from aerobic organisms. However, most contemporary pickles are not fermented at all; instead they rely upon the direct addition of acetic acid (vinegar, a product of fermentation), and usually heating for additional preservation. This way the acetic acid production through the fermentation process is simply bypassed.
So the basis of the traditional and contemporary pickling is the addition of organic acids like lactic and acetic acids. These small organic acids are known to be more effective against bacteria than inorganic mineral acids like HCl (Rode et al., 2010)
Acetic acid is a weak acid. In undissociated form, it is lipid soluble and able to rapidly diffuse through the plasma membrane (source: World Nutrition Science blog). It is thought that diffusion of acetic acid and other organic acids into the bacterial cell is the main mechanism of action behind its preservative effects. Preservation by acidification is especially effective in certain species of pH-sensitive bacteria such as E. coli and Salmonella. In contrast, strong mineral acids are nearly completely ionized in solution and ions do not pass the cell membrane's hydrophobic lipid bilayer.
The mechanism of action of small organic acids in food preservation are thought to be at least threefold:

Once diffused in the cell, organic acids will dissociate because the internal pH is near or above neutrality and thereby lower the bacteria's internal pH and disrupt cell physiology;
The anionic part of the organic acids, which cannot escape the bacteria in its dissociated form, will accumulate within the bacteria and disrupt many metabolic functions. This is one advantage of using organic weak acids like acetic acid, because they are normal constituents of the cells. Acetic acid and lactic acid for example are both intermediates in glucose metabolism. Accumulation of these metabolites will disrupt the glucose metabolism essential to the cell's survival.
Eventually, upon progressing accumulation, osmotic pressure increases become mechanically incompatible with bacterial life.

Another advantage of acetic acid is that it is a natural metabolite in human metabolism, and because it has been used in food preservation for thousands of years it is not classified as a food preservative, at least in the EU, and can be freely added to foods. Last but not least, acetic acid has a certain taste to it that may be preferable over inorganic acids.
Reference
- Rode et al., Can J Microbiol (2010); 56(9): 777-92

But wouldn't metabolic acidosis become a concern with such inorganic / mineral acids? We can certainly metabolize many of those organic acids (acetic, lactic, citric, etc......) just fine (down to water and exhale $\ce{CO2}$), but I'd imagine those "inorganic" ones ($\ce{HCl}$, $\ce{H2SO4}$, etc.....) could well become more problematic -- especially if one eats too many of those pickles!

Granted -- the body does have ways of dealing with occasional metabolic alkalosis just fine from ingested "inorganic bases" like baking soda & common antacids ($\ce{CaCO3}$), so perhaps the dangers of inorganic-acid metabolic acidosis may be somewhat exaggerated as well...


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Nucleoside triphosphates vs nucleotide diphosphates
A nucleoside can be defined as a nucleotide without its phosphate group. Thus, a nucleoside triphosphate (NTP) is a nucleoside bound to 3 phosphates.
This in turn must be equivalent to a nucleotide (whose name implies the inclusion of one phosphate already) plus an additional 2 phosphates. Thus, would it be appropriate to refer to an NTP as a nucleotide diphosphate?

I don't think this is technically incorrect, but why on earth would you want to give it a deliberate confusing name?

Did you check on Wikipedia or in Biochemistry at NCBI bookshelf before posting? Posters to this list are expected to make a reasonable attempt to find an answer from a standard source.  Or are you trying to make some sort of clever point? If so, it is not "appropriate" here.

Nucleoside is nucleotide without a phosphate group. That is something we say to understand and correlate nucleotide and nucleoside. But if followed Terminology by IUPAC a nucleotide should contain only one phosphate group, not more than that. Though NTP is a type of nucleotide, however, for the sake of technical terminology, nucleotides are given classifications as nucleosides with a suffix describing the number of phosphates present in a specific unit. For example, if a nucleotide has one phosphate, it is a nucleoside monophosphate (NMP). If the nucleotide has two phosphates, then it is called a nucleoside diphosphate (NDP), and for three, it is a nucleoside triphosphate (NTP). So you can say NTP as  nucleotide diphosphate, but considering the fact that nomenclature also indicate the chemical property of the compound, it would not be right.
Wikipedia

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Part of a fish outside the intestinal sac on the back?
I saw an expert Japanese chef fillet a mackerel (Scomber scombrus). He cut off the head and the whole intestinal sac came out with it as a single unit. Then he took the knife and scraped something from inside on the back. The object(s) were dark and bloody. Would those have been the kidneys?
You can see the video here: https://www.youtube.com/watch?v=udTHiRg34KI. The moment is at 2:20.

Yes, those are the kidneys. They're quite different from mammalian kidneys.
This is a picture highlighting the kidneys in a salmon dissection from the Pacific Streamkeepers Federation (http://www.pskf.ca/sd/). A very different fish, but similar enough to show the kidneys.

You can also see a dissection of the fish urogenital system here: http://necropsymanual.net/en/teleosts-anatomy/excretory-and-osmo-regulatory-system/, though I can't tell what fish species they're dissecting.

Are you going to upvote my question considering that you took the time to answer it?

I just did. Sorry, I'm new here-- is that generally expected?

@Kara welcome to bio.SE! Like any community-driven Q&A site, we hope that you vote frequently so as to acknowledge the efforts of others (or help to downvote bad/wrong answers once you have enough rep). However,  you should only vote when and how you want to -- no  one should pressure  you to do so.  It's perfectly acceptable to answer a question that you don't think qualifies for an upvote (or even one that you downvote). See here for more info.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Does the body have specific mechanisms for healing burns, or is it general purpose stuff?
I burned my thumb lighting sparklers (fireworks) a few nights ago. I've been pleased with how it's healing, and have been especially impressed because it's not a scenario that really could have come up in our evolutionary history. Then I started thinking that fires are not that common in nature. This prompts the question: do our bodies heal from burns using burn-specific techniques, or do they just follow general “procedures” for repairing damaged skin?

general applies to many specifics.


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Can vitamin B17 cure cancer?
I have heard that a 'vitamin B17' can cure cancer, but that the medical industry never talks about it, since making it legal would cause them loss of billions. But I have never found a reliable report on whether B17 really works or not. There is a question on 'vitamin B17' deficiency as a cause of cancer (see this post), however, not on 'vitamin B17' as a possible medication for cancer. What are the proposed mechanisms? And is there evidence that 'vitamin B17' really works in curing cancer?

The short answer is "no", but if you find a notable referenced claim saying that, you could try your luck on [skeptics.se] for confirmation.

@Mesentery: Even though related and heading towards the same direction I would not see it as a duplicate. Supplementing a deficiency or using a substance as a treatment for a disease are fundamentally different, justifying both questions independently. I will edit my answer to address that more directly.

@AlexDeLarge - duplicates are marked as such because of question similarity, not answer differences. If you could edit the question and stress the difference between this and linked question?

I'm voting to close this question as off-topic because it is better suited to SE Skeptics http://skeptics.stackexchange.com.

@AliceD: In the proposed edit, the question is rephrased and I added a query for possible mechanisms by which 'vitamin B17' could potentially cure cancer - which also makes it suitable for Biology.SE.

@David Just because a question is a "better" fit for another SE network site doesn't mean that it's off topic on this one. While SE Skeptics would be a good place to find sources which refute a particular claim, Biology SE is a perfectly fine spot to ask about the underlying biology of the topic.

@R.M.— No. But it is an excuse that can be employed to off-load stuff that is obviously undesirable but not covered by the criteria presented to one when one votes to close a question.

No such thing as B17: https://en.wikipedia.org/wiki/B_vitamins

@David I see no reason to close these sorts of questions if they can be answered with biology. This is my interpretation of the current meta as well. If you disagree, I would suggest raising the issue in meta.

@BryanKrause — I certainly did not and do not solicit a discussion here. I voted to close and had to explain why, which automatically generated a comment. This provoked other comments to which I replied. I suppose it could be raised on meta, but for various reasons I'd prefer to leave it a while.

I agree that, although this question would be well fit for posting on Skeptics.SE, this question is on-topic here.

Look here for an explanation why the "medical industry" wouldn't want any cancer cure to be kept secret, and wouldn't "loose billions" if such a cure existed and was made public: http://skeptics.stackexchange.com/questions/22770/has-the-cure-to-cancer-been-hidden-by-pharmaceutical-companies

Obligatory XKCD: https://xkcd.com/1217/

Of course a mere vitamin can cure cancer. That's why millions of scientists world wide are spending their lives looking for a cure. /s

There is no such thing as "vitamin B17". You can take TNT, call it "vitamin B52" and try to sell it to people but it doesn't make it a vitamin.

See also Is laetrile an efficient drug against cancer? on [skeptics.se].

@Agent_L I see what you did there.

Laetrile/Amygdalin has been claimed to be a suitable treatment for 'cancer' (which is a summary term for an extremely heterogeneous class of diseases). Even though laetrile/amygdalin in these claims is often called a vitamin, it in fact is not a vitamin as the molecule is not essential for the metabolism (Greenberg (1980)).
The claimed effects of laetrile/amygdalin are not only based on supplementing the molecule to balance a putative deficiency (with the false assumption that it is in fact necessary), though. Both other putative mechanisms are based on reactions that form HCN/cyanide: the enzyme $\beta$-Glucosidase breaks down laetrile/amygdalin and this reaction releases HCN. The argument now is that tumour cells have higher levels of $\beta$-Glucosidase which leads to accumulation of cyanide in tumour cells - with the effect of killing the tumour cells selectively. This would be great... if healthy and tumour cells actually had different levels of the enzyme. Unfortunately, they seem to have similarly low levels of $\beta$-Glucosidase (Greenberg (1980)). Even more problematic, Greenberg (1980) also reports elevated levels of $\beta$-Glucosidase in the liver and small intestine ... and you would not really want to release cyanide there.
There is a second mechanism, though: The enzyme $\beta$-Glucuronidase is claimed to be at higher levels in cancer tissue than in healthy tissues (leading to the same desirable effect described above). But again, there does not seem to be a difference in enzyme levels between healthy and cancer tissues (Dorr and Paxinos (1977)), and even more: $\beta$-Glucuronidase does not even break down the molecule as laetrile/amygdalin has a glucoside bond - so there is not even any cyanide release in that case (Holzbecher et al. (1984)).
Additionally, there is no clinical evidence that laetrile/amygdalin is an appropriate treatment for any form of cancer. This topic has been reviewed substantially (see Milazzo et al. (2006) for a review and this fairly recent Cochrane review by Milazzo and Horneber (2015)) and none of the studies included and analysed indicate any positive effect of laetrile/amygdalin. On the contrary, the in vivo cyanide formation after laetrile/amygdalin uptake makes the treatment very dangerous as it can lead to cyanide poisoning (and death, eventually) - especially after oral uptake due to higher $\beta$-Glucosidase concentrations in the digestive system. The authors of the Cochrane review therefore conclude that

The claims that laetrile or amygdalin have beneficial effects for cancer patients are not currently supported by sound clinical data. There is a considerable risk of serious adverse effects from cyanide poisoning after laetrile or amygdalin, especially after oral ingestion. The risk–benefit balance of laetrile or amygdalin as a treatment for cancer is therefore unambiguously negative.

"deficiency as a cause of cancer" and "the molecule is not essential for the metabolism" seem contradictory. Maybe I'm being overly simplistic in my understanding. Nevertheless, how could one have a deficiency in something that is not necessary to begin with? It either is necessary therefore causes a problem when deficient, or not essential, therefore its deficiency would not be a cause of any problem, namely cancer.

@jlaverde: Yes, you are right. The 'deficiency as a cause of cancer' builds on the false assumption that the molecule is in fact essential for the metabolism - which it is not. I clarified.

@jlaverde The whole point is that it is quackery: it is not a vitamin. There can not be a deficiency because it isn't needed at all.


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Why honey bees built hive in perfect hexagonal shape instead of irregular shape?
Why honey bees built hive in perfect hexagonal shape ?
Due to Hexagonal shape, I can go near without any anxious or fear.( Apart from Honey bee's stings)
From this Question, Most creatures look like or tries to look like irregular to fear the other creatures to attack.

What @iayork said. In plain English, they are making circular tube cells, but when placed so closely together, they form hexagons. Look at bubbles. Alone, they are round (perfect spheres), but the more bubbles are packed together, the forms will take on angled geometrical shapes, including perfect hexagons. It has nothing to do with fear, as hives are usually hidden.

With reference to the honey bee cells how could a slight modification in structure provide a survival benefit. If two individuals were starving would the person who was given a few milligrams of extra food have a survival advantage?

Why honey bees built hive in perfect hexagonal shape ?

Honeycomb cells (not the hive or the honeycomb itself) are hexagonal, in some species of bees but not all.  The regularity of this shape has puzzled people for a long time, and Darwin (and others before him) addressed the reasons for it.  Darwin did a series of experiments with bees, and summarized his results in Origin of Species.  You can search for "hexagon" in the linked text for his long explanation, or read the (still long) summary 'Evolution of Honeycomb on the Darwin Correspondence Project, but the short explanation is that it's the most efficient way to pack cells without wasting wax, and Darwin identified a bunch of intermediate (less efficient) cell structures in various bee species that supported his hypothetized mode of evolution.

Thus, as I believe, the most wonderful of all known instincts, that of the hive-bee, can be explained by natural selection having taken advantage of numerous, successive, slight modifications of simpler instincts; natural selection having, by slow degrees, more and more perfectly led the bees to sweep equal spheres at a given distance from each other in a double layer, and to build up and excavate the wax along the planes of intersection. The bees, of course, no more knowing that they swept their spheres at one particular distance from each other, than they know what are the several angles of the hexagonal prisms and of the basal rhombic plates; the motive power of the process of natural selection having been the construction of cells of due strength and of the proper size and shape for the larvae, this being effected with the greatest possible economy of labour and wax; that individual swarm which thus made the best cells with least labour, and least waste of honey in the secretion of wax, having succeeded best, and having transmitted their newly-acquired economical instincts to new swarms, which in their turn will have had the best chance of succeeding in the struggle for existence.

The bees don't make hexagonal cells. This paper shows how bees construct multiple cylindrical tubes which are then molded based on temperature and contact with other cells.

As you can see, the cells start off cylindrical (day 0) and transform into the common hexagonal shape by day 2. The paper also goes into details of the physics involved (it is in a physics journal). I strongly suggest reading the paper if you wish to go more in depth.

in "the origin of species" pages 178 and 179, Darwin has stated that if a bee could build a cell slightly more hexagonal than the other bees then this bee would have a survival benefit since a perfect hexagon is the most economical structure in storing the greatest amount of honey with the least amount of wax, but unfortunately there is nothing in his analysis that proves the point. He concludes on page 179 that the saving of wax by largely saving honey would be an important element in the success in any family of bees.
The problem with that analysis is that a slight modification of structure in this case a slightly more regular hexagon cannot provide a survival benefit as the two structures are almost identical.(the old cell and the slightly modified cell)

The problem with that analysis is that a slight modification of structure in this case a slightly more regular hexagon cannot provide a survival benefit ...  This is not a site where your unsupported opinion is considered a useful answer. Please supply references for this (that don't come from the deliberate liars associated with "intelligent design" and other religious dogmatists).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Do brain cells regenerate in the adult brain?
I know that most cells in the body regenerate, dying and being replaced with new cells. For example, in bone special enzymes move radially outward from the marrow in a narrow tunnel, destroying the old bone as they go and replacing it with new bone cells. In this way, our bones are slowly regrowing and being replaced constantly.
Is a similar process at work in the adult brain? Do neurons in the adult brain die and become replaced with new neurons? If so, how are the connections re-established? Each neuron is connected to other neurons by a complex network. If cells are regenerated, how do they re-connect to existing cells?

Short answer
Neural regeneration in the adult brain is confined to two localized hot spots, namely the hippocampus and the anterior lateral ventricular wall. Establishing connectivity between new cells and existing neurons is mediated, at least in part, by the growth cones present on axonal tips of newly formed cells. The growth cone responds to various stimuli and guides the axon towards it new target.
Background
As to your first question: Also adults can regenerate brain cells, albeit in a few restricted, specific regions of the brain. A continuous level of neural regeneration occurs throughout adult life in at least two locations. The first is the subgranular zone of the dentate gyrus of the hippocampus, the region of the brain involved in learning and memory. The other is located in and near the anterior lateral ventricular wall of the cerebral cortex. While neurogenesis in the adult hippocampus is relatively limited, the subventricular zone is thought to continuously replace interneurons in the olfactory bulb (Clarke, 2003).
Studies have shown that neurogenesis folloing neuronal cell loss due to injuries occurs only within the germinal structures mentined above, and not in cortical or striatal structures. Even when neurogenesis in the striatum (but not cortex) has been reported following ischemic injury, the resulting neurons survive only a short time. Hence, under normal circumstances structural or functional recovery in non-neurogenic brain regions is limited (Hallbergson, 2003).
Re-establishing connectivity between new cells and the existing tangle of neurons in the neurogenic regions of the brain is complicated. An important structure in this regard is the growth cone (Fig. 1); it is present in developing axons that are not yet synaptically connected. They are motile structures present on the tip of the growing axon and guide axons to their synaptic targets. They control the cytoskeleton and determine the course and rate of axonal outgrowth. Neurons and growth cones can detect a variety of external signals to establish neuronal migration and neurite outgrowth. A key in this process is chemotaxis. Several classes of molecules, e.g., secreted factors, adhesion molecules and cues from the surrounding extracellular matrix and adjacent cells are involved in the process of neuronal pathfinding and growth. To advance over larger distances however, gradients are insufficient and neurons use mechanical cues (durotaxis). For instance, neurite outgrowth has been shown to be affected by the mechanical stiffness of the substrate. Glial cells have been shown to be softer than their environemnt and neurons preferentially seem seek out glia to grow to (Lu et al (2006); Park (2002); Pawlizak (2009)).

Fig. 1. Fluorescently labeled growth cone on the tip of an axon. source: wikipedia
References
- Clarke, Bone Marrow Transplantation (2003); 32: S13–S17
- Halbergson, J Clin Invest. 2003 Oct 15; 112(8): 1128–1133
- Lu et  al., PNAS (2006); 103(47): 17759-64
- Park, et al., Bioessays (2002); 24(9): 821-7
- Pawlizak, Thesis, University of Leipzig (2009)

So when you write that neural regeneration is confined to particular places, are you implying that most of the cells in the brain do not regenerate? They form once and never die, the neuron lives for decades and is not replaced?

@ImprisonedRhesus - correct. Some small-scale migration may take place, out of the zones where neurogenesis takes place, but that is negligible.

Ok, so that means that many of the neurons in a person's brain are 30, 40, 50 years old, or however old the person is? I thought that cells had fixed lifespans that were short, not lasting years. From what you are saying there are cells that can live for decades?

I'd be a little careful with the word "regeneration" - it might be appropriate to the subventricular zone replacement of olfactory neurons, but I think "neurogenesis" is a better term for the other types of adult processes that form new neurons. Regeneration implies that they are directly replacing neurons that have degenerated, and I don't think there is good evidence for that.

@ImprisonedRhesus Cell lifespans vary greatly among tissue types. In the adult mammalian nervous system, almost all of the cells come from fairly early in development. Even the growth that AliceD is talking about is in some very small areas and contributes even a small fraction of the cells to those areas. Indeed, most brain cells are around for decades. There is definitely no broad-scale replacement of neurons like you have for blood, skin, etc.

@BryanKrause That is very interesting that some cells like blood cells should only last for a few months, but brain cells last for a lifetime.


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How long does immunity to influenza last when contracting the disease vs vaccination
The long term efficacy of flu vaccines are well documented, however I cannot seem to find a good source showing how long immunity lasts when contracting the disease.
I suspect it can't be much longer than vaccines since the virus mutates so quickly.

I you feel I can improve my question, please let me know. I don't quite understand why the downvote.

The effect on adaptive immunity are often stronger when contracting the flu than for getting the flu vaccination. The backside of this is that the flu is a quite dangerous disease which could end fatally, so getting the vaccine is always preferrable.
Getting infected by a specific flu strain (or receive a vaccination against it) generates specific immunity against this strain. If it mutates to strong or you get infected with another strain, you will have no immunity (and will have to develop a new immune response.
It seems that immunity against the flu can be livelong (against this strain) after you went through an infection and survived it. There are two studies showing long term response against antigens from the 1918 flu pandemic. The first (summarized in reference 1, the original article is reference 2) shows specific antibodies against the reconstructed haemagglutinin protein (H1) from the 1918 virus strain.
Serum from people born 1915 or before showed specific activity against this virus antigen, even more than 90 years after the infection.
The second study analyzes cross-reactivity of antibodies against the 2009 A/H1N1 pandemic flu strain. Here the cross reactivity of people born before 1930 was the highest - the 1918 strain (with which these people most likely had contact) was also a H1N1 virus. Although these viruses mutated between 1918 und 2009, there is still enough similarity that they are recognized by H1N1 specific antibodies (see reference 2).
A study which compared antibodies responses of people who contracted the 2009 flu against people who where vaccinated against it, showed that the antibody response was more longlasting in the people who got the infection (see reference 3).
So I think it is safe to say that the immune response is stronger after the infection compared to the vaccination, but the vaccination is much safer.
References:

How Long Does Flu Immunity Last?
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors
Antibody Dynamics of 2009 Influenza A (H1N1) Virus in Infected
Patients and Vaccinated People in China

Thanks for the well thought out reply. I came across the exact same references you did in my preliminary searching. Just to be clear, immunity from influenza is less than a year due to how much it mutates between flu seasons? I know this is true for vaccines, so it stands to reason that it will be similar when contracting the disease.

@niobe Nope, immunity for a certain strain seems to last for a long time, possibly life long. But the strains change from season to season, thats why they need to be adapted. Surface antigens (haemagglutinin and neuraminidase) don't change too much between two seasons, but different strains might get into circulation. Over time they change, this is why we have different strains.

@niobe You may want to have a look at "The Pathology of Influenza Virus Infections".

Perhaps I misspoke, I am aware of antigen drift, which is why I was curious whether immunity to contracting the disease(taking antigen drift into account) is significantly different between the two groups of people as mentioned in the above post. Due to antigen drift, I suspect immunity is seasonal for both groups.


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Small vs Large neurons
What is the criteria for classifying neurons as small and large?
Is this classification based on gross size or the length of axon?
Do they have any physiological difference?
For instance it is said that Substantia gelatinosa of Rolando contains small neurons .
What is so special about calling those neurons as such?
Aren't they doing the same function of conduction of impulses?

I have googled it but couldn't find any explanation for such naming.

Spinal cord isn't my forte, but when there are references to "small cells" these are always in my experience related to histological appearance, and though there is no specific criterion for what makes a cell small, it usually means "relative to other tissues" - I would expect these cells to be small relative to others in the spinal cord. I looked for a couple examples, and in the situations I found so far "small cell" always seemed like a description, rather than a designation.

My guess, though based on knowledge of other areas, is that the Substantia gelatinosa of Rolando is (or was originally) defined by the presence of smaller cell bodies that distinguished it from the surrounding areas before any function was elucidated.

(note that this terminology goes back to the early 1800s)

Depending on the neuron, small/large could mean one of two things:
1: Axon diameter, larger axons have lower resistance, so transmit action potentials faster see tables here. Important for neurons that cover long distances to convey information quickly.
2: What I think you mean though is the size of the cell body, where some neurons, e.g. Purkinje cells are much larger than nearby golgi cells. In which case the size is related to the function, large cells tend to have large dendritic fields and integrate many inputs into a single output, often relayed to a different area of the brain. Small cells are typically interneurons that only have an effect over a very small area.

So, what kind of small neutrons are present in substantial gelatinosa of Rolando? Do they have large cell bodies or axons?

I pretty much have no idea, I've never heard of it, but a quick look at wikipedia suggests that small slow-conducting sensory neurons synapse with neurons here, so I guess it forms a relay, where information from the sensory neurons is sorted out before being sent up to the brain. For some reason this kind of sensory information is transmitted slowly, so small diameter fibres. I'd guess the cell bodies are pretty small as well, but I can't be sure.

In my experience, calling a neuron "small/large" is always in reference to the size of the cell body. In some areas there may be a correlation with axon or dendrite length but it is usually based on Nissl stains of tissue so people are just referring to the soma.


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Are there people who can change one of their eyes' depth of focus, while not changing the other eye's?
Are there people who can change one of their eyes' depth of focus, while not changing the other eye's depth of focus, without any surgical or other external mechanical intervention?
Edit: let's assume both eyes are functional and not obstructed.

Have to tried to find an answer to your question, please share as queries with low or no effort are off-topic in Biology SE?

I'm voting to close this question as off-topic because the asker doesn't show any attempt at an answer.

What is the fun people have in closing questions? You can also just let it rot away in silence. What is the important difference?

Don't quote me on this, Stack Exchange started as Stack Overflow with the aim to build an open access online library of good (quality) questions and answers on computer programming. So to maintain the quality of the site these measures; downvoting,editing, flagging and closing others' posts have been implemented. About why not leave questions with low effort open? [...]

[...] Well, just to maintain the quality. Leaving them open would mean questions the site wants to discourage (low effort/ unclear/ opinion-based / too broad) are being entertained. Mostly questions are answered by biologists here (and concerned experts in other  communities) who donate their time to help others find an answer, this just ensures that they are not spoon feeding the asker which disinterest them and anybody who wishes to take up the challenge of answering good questions. Our help page can be found here.


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Aquatic forest insect identification
I found it in the forest but I've never seen anything like it so I took it home to see what it is. Does anyone know?

There are few things a species identification query must fulfill; locale, dimensions of the species and clear picture(s) (ideally from as many angles possible - so that all parts of the specimen are conspicuous to the one trying to ID your specimen).

This is a caddisfly larvae (Trichoptera). They live in streams and other water that are rich in oxygen.
They protect themselves by building there own 'house', with whatever is available, e.g. plant or wood fragments, gravel or even snail shells (see picture below)

Picture from Dutch wiki
https://en.wikipedia.org/wiki/Caddisfly

Id to species level probably requires microscopic work.


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Examples of heterologous expression in human cell beside viral expression
Usually, people are interested in expressing human proteins in fast-growing organisms like bacteria to yield a maximum of protein within a short time lapse. Codon usage harmonization/optimization have been used to increase the protein production. The role of codon usage have been studied in the context of viral protein expression, but outside this viral context, is there any example of using human cell lines for heterologous expression?

Are you asking for examples of human cell lines being used for preparaive protein production?

That should say "preparative".

Besides research (as mentioned by mxwsn), there are a lot of actual protein based medicines and vaccines produced in human cell lines. One of the first mass cultures of a human cell line was in the monkey free production of a polio vaccine
   (source). Almost every researcher working in a molecular lab has grown HeLa cells at one point during their career!

Expressing GFP in human cell lines for research purposes is an extremely common example of heterologous protein expression.
For research purposes, it's usually unnecessary to optimize codons for increased expression, especially since using more efficient enhancers and promoters produces a far greater improvement in expression levels than codon optimization which is non-trivial and species-specific.


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Why did plants evolve to use opioids?
I'm reading about medicine and specifically opioids. There seems to be a wide variety of forms of these chemicals, I'm curious as to what purpose these serve in these respective plants, and why they function the way they do in mammals.

Please tell us what you found in your reading. :)

Welcome to Bio and thank you for this interesting questions. I must say this question is too broad imo. A way to narrow it down, for a starters, is split this question up in two separate questions. One on plants, one on brains. Does that make any sense?


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Why are mammals not very often (never?) toxic?
Often reptiles or insects have poison to defend themselves or to offend their prey. But I don't know any mammals which are toxic. So are there any mammals using poison and why aren't there so less/any?

The platypus has a venom, there's that.

A list of venomous mammals is available at https://en.wikipedia.org/wiki/List_of_venomous_animals#Mammals. It could be worth noting that, although there are nine venomous mammal species listed amongst the ~5500 species of mammals, there are no venomous birds amongst the ~10000 species of birds, which makes avians an even more extreme group in this regard.

Note that "toxic" and "venomous" are not the same.  E.g. a rattlesnake is venomous but not toxic (you can eat it), while a puffer fish is toxic (you die if you eat it) but AFAIK not venomous.

Answering the first part of your question: The cuban solenodon has venomous saliva. It's a mammal -- rather shrewlike in appearance. But yes, venomous mammals are rare!


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What is the impact of the invasiveness of the European Starling in North America?
Currently there is a campaign to eradicate the European Starling from North America because of its threat to other species. Are there actual data regarding the extent of the ecological risk to native species, and are there data on the effects of the current eradication programs (are they working)?
Background
In North America, there an estimated 140 million European Starlings, or about 45% of the global total. The species was introduced to the continent over 100 years ago when only 120 or so were released in the New York area. Those few have quickly spread across the whole continent, competing easily with other native birds of similar type, especially for nesting holes, because they are naturally far more aggressive. It is currently listed in the IUCN List of the world's 100 worst invasive species. Annually, the US kills over 1 million of them with the sole purpose being extermination. There is even a specific poison commercially available. However I am having difficulty finding data to show how invasive the Starling really is in North America and the extent of the ecological risk to native species because of their presence. I would also be interested in data showing the impact of current control methods (do they actually reduce the impact on native species?).

Australia has also taken great measures to eradicate the species from their country.

For the record, I shoot Starlings all the time. Just got one today. First of the season, which prompted the question (should I actually be doing this?). I'm fairly confident the US killing of 1 million of them doesn't bother me.

@fredsbend: Perhaps surprisingly, starlings are edible, and supposedly quite tasty.

@james And about three bites each.

These control measures usually are extremely ineffective and unnecessarily brutal towards the introduced species. Ecosystems change for various reasons, humans introducing species is just one of them. It is an idiotic idea to kill European Starlings in order to putatively benefit local species to give them an artificial fitness advantage.

@Alex Are you saying there's no inherent value in preservation? Exotic species have caused the extinction of native species in the past.

Yes, that's exactly what I'm saying. Either you don't introduce new species or you have to live with it. There is no inherent reason for artificially selecting a 'native' species over a 'migrated' species, especially if this involves mass killings of innocent lives.

@Alex I think you might be letting an emotional response (mass killings of innocent lives?) affect your conclusions. That's a little to close to philosophy rather than biology. Science is amoral. The question is about the Starlings impact and whether control methods mitigate that. Whether we should attempt mitigation at all is not a biology question. I must confess, your opinion on this is the first I've heard like it. I take it as a given of preservation practices that invasive species that negatively impact native species must be controlled.

@fredsbend: Well, people eat shrimp, which are usually less than one bite each :-)

@AlexDeLarge: What of the "innocent lives" destroyed by the starlings?

@jamesqf: It is not an emotional response. It is rational ethical reasoning. Starlings are not able to reason morally. Additionally, I am not aware of any 'successful' population control measure.

@Alex "I am not aware of any 'successful' population control measure." Great. That's the start of part of an answer. The rest of your comment is a value judgement, and distinctly outside of the domain of biology.

That's why I commented and did not write an answer (even though as a biologist I do believe that ethics of biology are within the domain but we should leave it at that). :)

@AlexDeLarge NP. I found an interesting claim: "About 42% of the species on the Threatened or Endangered species lists are at risk primarily because of alien-invasive species." Is this not concerning to you, that nearly half of endangered species are because we've introduced foreign species?

Related question with a good answer: Do invasive species cause long-term damage to ecosystems they invade?

@AlexDeLarge: Where did I say anything about an emotional judgement?  It's simple fact: starlings are not herbivores: they eat other creatures, thus destroying "innocent lives".  In addition, they displace other species from similar ecological niches, destroying the lives of those creatures.

First, for the record, I do not know the North American Starling situation well. However, I know of one study (Koenig, 2003) that failed to find strong effects of Starlings on other cavity nesters (i.e. looking at effects from cavity competition). When trying to control for other effects, only one species was potentially negatively effected by Starlings.
Starlings cause quite large economic effects though (Linz et al, 2007), and it wouldn't surprise me if this is the main reason for the control measures. The paper refers to a previous study which estimates that Starlings cause crop damage costs of \$800 million/year as well as \$800 million/year in health costs, due to disease transmission to livestock and humans (both figures from Pimentel et al., 2000).
So my feeling, based on a couple papers and some quick searches, is that the ecological impacts are uncertain (or to a large extent unknown) but that the economic impacts are quite large. Given the North American population sizes of European Starlings it would however surprise me a lot if there weren't any ecological effects on other species (negative and positive). These issues are hard to study though, especially without long-term data of high quality.

Very good point. I did not think of the economical impact being the motivation for control measures. I'm surprised that I didn't, considering most control measures are economically motivated, or at least, environmentally motivated control measures remain underfunded and under implemented.

Yes, that might explain the control measures. Since they are on the IUCN top-100 list I would have expected them to also cause well-known ecological problems though. Maybe there are other papers or reports that show this. In the ones I've seen (after brief searching) it is mostly the study by Koenig that is cited though.

Giving the selection now, but welcome future answers to attempt a steal. Thank you for the answer.


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Where can I find comprehensive data on animal distribution?
I'm looking for vertical distribution or tidal height of several intertidal species, specifically from the Pacific Northwest.
I considered looking for published research for each species however, my search likely would not be comprehensive and perhaps be biased in site-specific differences.
Is there some kind of open database where I can find this information?
I've found that EOL draws some data from the Ocean Biogeographic Information System, but when I go to the site directly, I can't find the tidal height data. I've also looked through suggestions in response to this question but none are applicable.
Any help with these databases or suggestions on other relevant databases would answer my question.

This sounds both difficult and fascinating. I hope you can find these data!

I like your question a lot! I think what you're trying to achieve is the best way of solving your problem. Unfortunately, although I do have a few links for you that might get you a little bit further, a perfect solution is, I fear, not available. Tides are extremely complicated and depend on many factors. Some of these are large scale effects such as the relative positions of earth, sun and moon, but others are more local, such as ocean currents or the shape of the coast. Especially the latter can make a surprisingly large difference on a relative small spatial scale. Luckily, it is possible to come a long way and have very decent approximations.
The best option, as far as I'm aware, is to use XTide, a software program that can calculate tides at thousands of locations worldwide, making use of actual measurements as well as mathematical models. This will give you by far the largest amount of information, and the most detailed information. better still, it's open source software and completely free. The drawback is that it is complicated to use. Also, if you are a windows user, it is even more tricky as this is an X-windows program, developed for UNIX and UNIX-like operating systems (it should run fine on linux and macos). It is definitely possible to run it on windows, but I wouldn't recommend it for the faint of heart.
My second option would normally be to use rtide, an add-on package for the statistical program R, though in your specific case it's probably not good enough. The rtide package is fairly easy to use if you're familiar with R, and runs equally easily on all operating systems supported by R. The drawback is that it doesn't give as much detail as XTide, and it is based on data from a mere 637 stations, all of which are in the USA, so it's only of limited use for the Pacific Northwest. In addition, it takes more work to calculate certain variables such as the tidal range than to do the same calculations in XTide
A third option would be to use a website like https://www.tide-forecast.com/ where you can click your way to the relevant data. The number of stations they cover is even smaller than those offered by rtide, but they do cover the entire world. If you do not want to go the XTide way, then combining rtide with https://www.tide-forecast.com/ would probably be the best way to go: the former gives you a large number of stations in the Pacific US, while the latter will add some stations in the rest of the Pacific Northwest.
I hope this helps!

Hi Yuri, I appreciate your thorough answer however I'm looking for the vertical distribution (aka tidal height) of species. Effectively their vertical range along the shore. I'm not so concerned with the height of tides in a region but rather where animals live with respect to chart datum.

Oh, sorry. From your question I had understood that you had found the animal data in EOL and only needed the tidal height data that were missing there.


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How to send many samples to a lab for testing mosquito-transmitted diseases?
I am doing a project for the science fair in my school on mosquito-borne diseases in Panama. We want to collect mosquitoes from three different areas in the country to document what diseases they had, which place had more diseases, which species was more common, etc.
We will take a dead mosquito, document which species it is and, with a special tool, extract the blood that the mosquito had extracted from their host and put it in a small container to test for disease. We want to extract 300 samples per area of the city (900 samples in total) to have the best results. The problem with this is that we can not send 900 samples to a laboratory for testing and I do not think we can collect fewer samples because the results will not be as good. One idea we had was to put the 300 samples in the same container so we only have to send 3 containers to a laboratory.
Will mixing 300 different blood samples from mosquitos in the same container affect the results, especially if there are any diseases? If this wouldn't work, what other procedure could we do to avoid having to send 900 samples to the lab?

Welcome to Biology.SE. This is an interesting topic, but I think it needs some clarification. When you are talking about extracting the blood from the mosquito, do mean the insect blood (hemolymph) or the blood that it sucked out of a host?

I would strongly suggest sending the samples in either eppendorf/pcr tubes (with unique barcodes/labels) or alternatively in sealed 96well pcr plates. Put the samples in sealed styrofoam boxes together with plenty of dry ice and it should be fine


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What are the factors that contribute to genetically identical individuals behaving differently?
If you run the same task on a pair of identical computers, you will end up getting the same results, even with the same response time.
But let's say you line two different person, and ask them the exact same question. Each will answer totally different, even if they are twins, raised in the same family, went to the same school and shared the same roof, and probably had the same experience in life. One of them may love carrots, one may not.
The question is, what is generating such different behaviour and way of thinking? Aren't they sharing the same genes?
If yes, the question is still standing.
If no, then we'll have another question:
If we create 2 identical clones of a person, raise them in the same situation, will they think identical too? If not, why? And what's the reason of this?

This is a classic and in my opinion interesting debate; nature versus nurture. It has filled textbooks, journal articles, and popular books. This question isn't a good fit for the site because it's too broad, unclear (what constitutes "thinking identically", how do you want to measure that), and a matter of opinion. If you're interested in the topic, consider narrowing down your question to "what evidence suggests they would think similarly" and ask over at cogsci.SE. This still, however, may be too broad.

Thanks for your comment. I'm not expert in biology, my first question here. Please suggest / direct edit the question if you think it can be improved. I think you know what i'm after. As a computer programmer this question is bothering me for a long time, that why humans don't produce same results as computers.

Your example is flawed.  If you have two identical computers (that is, identical hardware), and install Windows on one and Linux on the other, they will behave quite differently.  Even two different versions of Windows or Linux will have differences, or two copies of the same version of Linux with different choices made during install.

@jamesqf Even the same program with identical command-line parameters may produce different results or execute faster/slower if you use a random number generator or multithreaded code, or just have other programs running at the same time (the OS itself included).

@jamesqf i mentioned to run the same task.

@Jack Johansson: Yes, I understand that, but I'm considering 'task' to be at a high level, similar to your example of two people being asked a question.  So if the task is for instance "display a web page", the Linux browser will do it somewhat differently than Windows/IE.

Your question has actually more to do with developmental biology and the origin of phenotypic variance in populations than with neuroscience.
Here is a list of factors which variance explain observed phenotypic variance in a population:

Genetics (incl. additive, dominance and epistatic variances)
Environment (incl. macro and micro environments)
Developmental noise (incl. cellular noise)
Epigenetic
All the covariances among above factors

Of course, when you consider a pair of monozygotic twin as your population, there is little to no genetic variance. They will also likely experience little epigenetic variance. Assuming they live together, practice the same sport, eat the same type of food, etc... then they will also experience little macro-environmental variance. Micro-envrionmental variance and developmental noise are probably the main factors causing these two hypothetical twins to differ.
You might want to read the post Why is a heritability coefficient not an index of how “genetic” something is? to better understand the current post.

Can you please expand on what remains unanswered?

If you create 2 clones from an individual person (assuming it's technically possible) and put them under same circumstances, will their brain function identically?

Yes as you will still observe micro-environmental variance, variance due to developmental noise and epigenetic variance (and their covariances). If it is unclear you might want to read the post that I linked at the end of my answer.


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What is Oncogene, and how do you get it?
I was looking at my family tree and it said that one of my family members died by Oncogene. What is it and how do you get it?

An oncogene is a gene that has the potential to cause cancer. If an oncogene is activated, it will contribute towards cancer, though there are typically many other factors necessary before cancer becomes noticeable and potentially lethal.
In short, your family member presumably died of cancer, though writing the cause of death as "oncogene" is highly abnormal.
Many normal and healthy genes can cause cancer when they are overly active. For example, PDGF produces a growth factor required for normal health, but if too much growth factor is produced it can cancer like breast cancer.

Oh. Thank you. Well now I know why she died. Have a good life, live it to the fullest (but not by smoking or drugs) and have fun. I hope I get to talk to you again.


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Where does moss come from?
I've been growing plants in pots for several years, and in some of my pots a patch of green moss appears and steadily grows to fill the whole surface area of the soil. But that doesn't happen in other pots. I've used different bags of soil for different types of plants, but moss doesn't seem to appear only in one type of soil from the same bag.
How does moss appear in the first place? Or is it present in all soil and only grows to a visible size under certain conditions?

Moss produces spores that can travel great distances. If these spores land in favourable conditions, then it will grow there.

Almost seems like a question for the Gardening SE, but I've always wondered about it myself. Always just assumed that humidity + soil = moss. Um... 'cuz reasons.

Short answer
Moss plants form spores; minute, invisible, typically one-celled, reproductive units that are carried off by the wind and into your pots.
Background
Mosses belong to the Bryophytes. Bryophytes are embryophytes; i.e., non-vascular land plants. They are spore-producing, rather than seed-producing and they do not bear flowers.
The leafy moss plant you are describing is the sexual phase of the moss life cycle. When mature, most mosses develop sex organs. Under wet conditions, sperm cells are released from male sex organs (antheridia) and swim to the female organs (archegonia), attracted by a chemical released by the female organ. After fertilization, the egg cells that are embedded in the female organ form a spore-producing plant. This consists of a stalk with a spore capsule and stays attached to the parent moss plant. As the spore capsule matures, it releases its spores into the air, and then dies. If moss spores fall in a damp place, they germinate and grow into leafy moss plants, and the cycle is completed (Fig. 1).
Hence, to answer your question - moss appears in your pots when spores land into it and enough water is available for their outgrowth.

Fig. 1. Reproductive cycle of moss. source: Encyclopedia of New Zealand

I fail to see how the leafy plants are  neccessarily the sexual phase, the sex organs of the mosses are the spore capsules shown in your picture. Some moss plants do not even produce these. Otherwise good answer.


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How does cartilage become bone?
It's a famous fact that bones begin as cartilage and later become bone, but I never was clear how exactly
 this changeover occurs. Could someone please explain this to me?

What research have you done? What exactly you are unable to understand? Show your efforts.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

FYI: Why is cartilage replaced by bones in an vertebrae adult?

The process is called endochondral ossification.
It is important to point out that not all bone is derived from cartilage. For example, when a bone is fractured and is healing, the new bone does not always come from cartilage, rather intramembranous ossification occurs. There are therefore multiple mechanisms at a microscopic level by which bone may form. Additionally, bone formation in the long bones is different to that in, for example, the flat bones of the skull.


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LacZ' selection: blue colonies despite ligation of insert
It has been suggested that bacteria transformed with pBlueScript vector, containing an insert in the middle of the lacZ' gene, can still give blue colour on X-gal, if the insert is small and ligated in-frame with the lacZ' gene (source: my course, ResearchGate).
I don't understand how it is possible that translation doesn't end at the stop codon encoded by the insert. Is this something to do with leaky termination? Moreover, even if leaky termination was possible, this would mean that there is ALWAYS a 1 in 3 chance of the insert being in-frame.

Transcription doesn't stop at the stop codon.

@canadianer Thanks! But why does it not? And also, if it doesn't stop at the stop codon, doesn't this mean that in 1 out of 3 cases, an insert would be ligated in-frame and the assay wouldn't work?

Transcription has nothing to do with codons. Perhaps you meant translation?

@canadianer Oops, this is awkward! Yes, this is what I meant!

Most inserts will disrupt beta-gal expression (by shifting the reading
  frame and introducing stop codons) and therefore remove the enzymatic
  activity required to cleave X-gal and produce the blue color.

Your source is agreeing with you - inserting a stop codon will stop translation (not transcription) and keep the white color.

Thanks! But the source also says that "In rare cases, when the insert is very small and does not disrupt the reading frame, beta-galactosidase activity will occur even in the recombinant clones, so blue-white screening becomes irrelevant." Am I interpreting this incorrectly?

I'm understanding the implication that, to still have beta-galactosidase activity, the insert needs to not have a stop codon. I think this is reasonable because the stop codon case is explicitly addressed in the previous paragraph.

But doesn't this mean that without a stop codon blue color will be produced in 1 in 3 cases (probability of in-frame ligation) and the assay is kind of pointless, so why would anyone use it like that?

The insert needs to not disrupt protein folding on top of being small, not having a stop codon, and being in frame.

@mxwsn You should add this to your answer.


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Database of known human proteins
Is there an up-to-date database of known human proteins that is easily accessible using Python libraries?

GenBank includes human proteins and provides APIs for constructing HTTP requests to make searches. Examples are given in Perl, but if you prefer another programming or scripting language you are expected to write your own:

Equivalent HTTP requests can be constructed in many modern programming languages; all that is required is the ability to create and post an HTTP request.

This approach has always served me well.
Uniprot seems similar in this respect.
SwissProt provides a package for BioPython which may be of interest. I don’t know if this is the library you are referring to — you don’t say, and I don’t use Python.

The human proteome can be retrieved from the UniProt Knowledgebase (http://www.uniprot.org/help/human_proteome).
All data on the UniProt website is accessible programmatically via a REST API. The documentation http://www.uniprot.org/help/programmatic_access also includes a few python code examples (among other programmaing languages).
Please don't hesitate to contact the UniProt helpdesk if you have any additional questions.


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Understanding a Chromosomal formula in a karytope analysis
I am reading a medical reporting results of a karyotype analysis. On it it is written:

Chromosomal formula
46,XX,del(7)(q11q36)[12]/46,XX[13]

I understand that 46 is the number of chromosomes, XX refers to the pair of sexual chromosomes, del(7)(q11q36) means a deletion on the long arm of chromosome 7 spanning the bands 11 to 36.
What do [12] and [13] mean?

Cytogenetic nomenclature is standardized in the International System for Human Cytogenetic Nomenclature. Unfortunately it is not free and my institution does not have access. However, looking at a preview of the 2013 version in Google Books, it would seem that the number in square brackets is the number of cells scored with that karyotype.


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How can I list genes present on a given series of bands?
My question is related to this one. My interest relate to this deletion:

del(7)(q11q36)[12]

as defined by ISCN.
I would like to access a list of the genes found on the bands 11 to 36 of the 7th chromosome in humans. How can I do that?

There's a brief tutorial here on how to search by band. Here is a more extensive help document, and here is a human-specific help page, Basically:

Select the species and annotation release. We're Homo sapiens, by the way...
Select the chromosome you are interested in.
On the left side of the page, it says Region Shown: followed by two input boxes. You can search by band using standard cytogenetic nomenclature: 7q11 and 7q36. Enter these into the input fields and click Go. Here is 7q11:7q36.
There are various links to download data. Perhaps most relevant to you, there is a link on the left of the page which says Data As Table View. Here is said page, a list of genes at various levels of characterization.

Here is a table of different search queries you can use. There are a couple of ways to analyze the data:
Interactive Genome Browser:

Click on Genome Browser.
In the search field, enter the cytogenetic coordinates: 7q11;7q36. Press Go. Here is the resulting page.

Table Browser (for downloading data):

Click on Tools > Table Browser.
There are a lot of options. A tutorial can be found here. Most important for your search is region. Select the position radio button and enter your cytogenetic coordinates. I'll leave the rest of the options to you.

Nice answer! I like you offered directly the small tutorial and not only links to explainations. I also like you used the slogan for each data collection. Thanks

@Remi.b You're welcome, hope you find what you're after.


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Do humans learn to distinguish different senses?
Does a human being learn to differentiate between its senses at some stage in their development? Is there a time when it, for example, cannot tell if an input is a taste or a visual image?
The question came to me because food may taste different when the sense of smell is impaired, although these are two separate senses with their own receptor organs. Is it possible for other senses to be mixed up in a similar way?

Taste is really not a separate sense.  Taste receptors on the tongue only react to a few things - sweet, sour, salty, bitter and umami, IIRC.  (And possibly chili peppers, though IMHO that probably involves pain receptors :-))  Everything else is really smell.

there may be another taste that responds to starches. https://www.researchgate.net/publication/306550362_Humans_Can_Taste_Glucose_Oligomers_Independent_of_the_hT1R2hT1R3_Sweet_Taste_Receptor

Short Answer: Though the concept of development of perception in children is known (Vernon et al, 1961), the process of differentiation between different senses is largely innate, though some disorders related to sensory processing may be acquired during infancy.
Background: The processes involved here are sensory processing and sensory integration. Sensory processing is a process that organizes sensation from one’s own body and the environment, thus making it possible to use the body effectively within the environment (Stein et al, 2009). It deals with how the brain processes multiple sensory modality inputs, like proprioception, vestibular system, auditory system, vision, etc. into usable functional outputs.
The second process is known as sensory integration. Sensory integration is the process through which the brain organizes different sensory informations. In short, it is the organization of different sensations for use by the brain (Ayres et al, 2005). The theory of sensory integration was put forward by Anna Jean Ayres.
As it seems obvious now, sensory integration is an innate process (Cronin et al, 2015). However, sensory integration disorders can be acquired by a child in the early stages of life. This can cause results similar to what you say. For example, according to a 2009 study, every 1 in 6 children has sensory issues which make it difficult for them to process different sensory stimuli. In fact, some symptoms which are common for children with sensory processing disorders are4:

They can’t sit still through a half-hour lesson and disrupt the class.
They often seem distracted and don’t pay attention to what teacher is saying.
They bump into kids in the lunch line, making them angry.
They can’t hold a pencil correctly, so they struggle with handwriting.
They get upset when asked to switch from one activity to another.
They melt down during assemblies and have to leave the gym.

Such activities are often seen as indications of problems with sensory processing and sensory integration i.e. they cannot differentiate between different senses or have problem organizing these sensory inputs to get meaningful output. However, I didn't find a case study where a person is unable to tell whether the input stimulus is touch or taste. This might be because (mostly) different senses are processed in different areas of the brain (Pirotte et al, 2008).
References:

M. D. Vernon, The development of perception in children, Educational Research 3 (1961),
no. 1, 2–11.
Stein BE, Stanford TR, Rowland BA (December 2009). "The neural basis of multisensory integration in the midbrain: its organization and maturation". Hear. Res. 258 (1-2): 4–15. doi:10.1016/j.heares.2009.03.012
Ayres, A. Jean (2005). Sensory integration and the child : understanding hidden sensory challenges (25th anniversary ed., rev. and updated / by Pediatric Therapy Network ; photographs by Shay McAtee. ed.). Los Angeles, CA: WPS. ISBN 978-087424-437-3.
A. Cronin and M.B. Mandich, Human development and performance throughout the lifespan,
Cengage Learning, 2015.
How Sensory Processing Issues Affect Kids in School - Child Mind Institute
Pirotte B, Voordecker P, Neugroschl C, et al. (June 2008). "Combination of functional magnetic resonance imaging-guided neuronavigation and intraoperative cortical brain mapping improves targeting of motor cortex stimulation in neuropathic pain". Neurosurgery. 62 (6 Suppl 3): 941–56. doi:10.1227/01.neu.0000333762.38500.ac

Mixing up input from different senses is actually a known neurological phenomenon called synesthesia. Synesthetes (ie. adults experiencing synesthesia) might see numbers in colors for example. Some may even "taste" colors as you say.
Now do all infants have synesthesia before some stage in development is another question. It is actually a rather old hypothesis called "neonatal synesthesia". One piece of evidence comes from this study which tested shape/color association in infants. I do not see any other study concerning this hypothesis though. I guess the main reason might be the difficulty to develop an objective experimental design on small infants who hardly communicate...

Nice answer, +1! According to Wikipedia, synesthesia is a neurological phenomenon in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second sensory or cognitive pathway. which is IMO different from mixing up of two different sensory stimuli.

Thanks. That's true. I was meaning that signals "mix up" in the brain and stimulate two senses when it should only stimulate one. But that's not clear you're right.

Indeed the signals do not "mix up". As per one theory, when a stimulus activates a specific brain area, another area gets cross-activated by the first receiving area of brain. According to ideasthesia theory, synesthesia is fundamentally a semantic phenomenon. Don't misinterpret this, I just wanted to clarify it (all points from wikipedia).

To me, this would suggest that senses are not "learned", but are automatic and controlled by the brain. You can't, for example, choose not to feel something, there has to be a problem with the wiring in your body. This would suggest to me that a human can't mix up its sensory inputs through lack of learning on a basic level.

@another'Homosapien' I was saying that based on your answer I feel my response to OPs question would be that human's don't "learn" to distinguish their senses, the brain does it for them. Humans may have to learn what the feelings mean, but the feels themselves aren't confused naturally.

@sgr in a way, you might say so, though I won't say that thus view is completely correct or should be the primary view on the topic


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Plasmid transformation yields only empty vectors
I have to electroporate pMAD cloned with an insert of 7.4 kb in my S. aureus isolate. When I electroporated in RN4220 I had no problems but when I put it in my isolate I just recover few colonies and they have the empty plasmid. Has anyone had this problem?

How do you know they're empty? Are you doing blue-white screening or actually isolating the plasmid?

I ask because if your isolate contains an endogenous beta-galactosidase gene, blue-white screening will not work.

I have the primers to amplifie the region of the multiple cloning sites and it gives me the fragment of an empty plasmid. Also I cut the plasmid with the same enzymes of the cloning and it gives me no fragment of the insert size, only the empty plasmid. When I do the same thing with the plasmids from RN4220, I have the good fragments...

A qualified guess is that either your insert is somehow toxic to the cells or you have a contamination issue with the empty plasmids far outweighing your plasmid with the insert concentration wise.


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Significance of lip end curve
What is significance of curve at point where lips meet, how it is determined and what effects it has on attraction and other factors? For some people it is a downward curve, for others it's an upward curve, while for some it is straight.
Is it genetic?

I don't think it can be called as a trait, since that region is highly mobile and changes according to emotions. But its well known that it gives an impression of downward curve in oldage.

@JM97 it is my observation that when lips are closed some people do have upper curves while most has downward, i thing upward and straight one is more attractive, so may be it is a trait. I checked on my self too, you can check on urself too.

this may help you:http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003375


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Why X-chromosome linked diseases happen due to recessive gene?
All the X -chromosome linked genetic disease I have studied (Color-blindness, Haemophilia, Muscular dystrophy) happen due to a recessive gene.
At first, I thought it was because there could be a 'good' copy of that gene on the other X chromosome (in case of females). So that's why these genes are recessive. But this is a bogus reasoning, I soon realised.
So, why X-linked genetic diseases happen due to a recessive gene? Maybe not all. But why some are recessive?

You might be interested in this

First of all, most observed mutations are recessive (see the answer to this question; in brief: homozygous carriers are strongly selected against, heterozygous carriers are not affected only if the allele is recessive). So you wouldn't be surprised to find the same pattern on the sex chromosomes.
A good way to think about the specialty of recessive alleles on the X chromosome, is to think about why these diseases are most often visible in males (and you are on the right track there) ... Most alleles causing heavy disease - be it a mutation on the autosomes or the sex chromosomes - are rare (it is for the same reason they are recessive which is described in more detail in the answer linked above; it is due homozygous carriers being affected by purifying selection again) and therefore female carriers are most likely heterozygous and therefore healthy. In males, however, a carrier is always affected by the disease because the carrier is hemizygous.


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How do similar environments on islands in close proximity result in allopatric speciation?
I would like to ask a question on the very classic example of allopatric speciation seen in the Galapagos finches. Adaptive radiation occurred because the finches flew from island to island, so there is gene flow, and the different environments on the different islands provide different selective pressures that causes relative fitness of the same species of birds to change. Over time, more drastic changes occur and speciation event occurred.
What I am doubtful of is the extent of different selection pressures on speciation. Given that the islands are so close to each other, wouldn't it be safe to assume that these islands generally have similar types of plants, similar types of insects, similar climate, similar predators. If gene flow between populations of finches can occur across islands, why can't it happen for the other biotic factors "contributing" to the islands' characteristics? So how can such similar conditions/environments provide selection pressure that is different enough to result in speciation?
Your clarifications are very much appreciated!

The question is a bit confusing because it seems to be built on at least 5 misunderstandings.
Allopatry and gene flow

[..] allopatric speciation seen in the Galapagos finches. Adaptive radiation occurred because the finches flew from island to island, so there is gene flow [..]

By definition, an allopatric speciation is a case of speciation where there is no gene flow. If there is gene flow, then you may still end up with a reduction of gene flow and a speciation event but that would not be called allopatric speciation.
The first event leading to isolation (that is to an allopatric scenario) might be caused by birds flying over to another island but this does not mean that the divergence between populations occurred with gene flow.
Relative fitness

[..] the different environments on the different islands provide different selective pressures that causes relative fitness of the same species of birds to change.

It makes little sense to talk about relative fitness of a species. The relative fitness of an individual is the absolute fitness of this individual divided by the absolute fitness of a reference individual (generally a theoretically super fit individual) in the population.
Did you want to talk about competition between species? I don't think so as I don't know how this concept would fit in the rest of the question.
Assumption of similar ecology

[..] wouldn't it be safe to assume that these islands generally have similar types of plants, similar types of insects, similar climate, similar predators.

No, it really is not a good assumption. In some extreme cases, climate can actually radically differ between two locations at less than 20 meters apart! The same is true for other variable making up the ecological conditions.
Species dependent migration abilities

If gene flow between populations of finches can occur across islands, why can't it happen for the other biotic factors "contributing" to the islands' characteristics?

Because birds have wings! It is easier for a bird to fly to the next island than it is for a mouse.
Implicit assumption that selection is needed for speciation

So how can such similar conditions/environments provide selection pressure that is different enough to result in speciation?

Speciation can happen in absence of divergence selection (esp. in allopatry). Genetic drift alone yield to population divergence too and can lead to reproductive isolation.
To my knowledge, the relative role of selection vs drift in causing speciation is not well understood though.


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A Designer Virus
An article at Wikipedia describes color changes that viruses have produced in tulips (without any human intention). And another article (elsewhere on the web) describes viruses that were designed to fight diseases in people. This makes me wonder:
Would it be possible to design a virus to produce certain coloration in tulips -- for example, if I want tulips to have white petals with blue streaks? Would this create a new strain of tulips that propagate that coloration without further human interference?

Welcome to Biology.SE! What research have you done before asking it here?

@another 'Homo sapien' In response to your comment I enhanced the question yesterday.


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Why do cyanide and arsenic smell like almonds and garlic, respectively?
Why do humans smell arsenic as garlic or cyanide as almonds? Do both smells activate the same receptor? Is there any reason why our brain interprets these smells the same?

Almonds indeed contain cyanide but I can't assure almond's smell is due to cyanide.

However we can assume you have took the information from textbook only.  cyanide and arsenic-compounds are very poisonous, so not recommended to smell anyway.

Why do you think almonds have a smell?

@jamesqf volatile organic compound

@murmansk: Do you really think the human nose is capable of detecting all volatile organic compounds?  Different people can smell different things.  For instance, my ex thought alyssum (the flower) had a wonderful fragrance, but I can barely detect a sort of grass-like smell.  Same with almonds: to me, they have no smell at all.  I've never tried cyanide, though.

Related: Why do sulfur compounds smell?

This question already has been asked on https://chemistry.stackexchange.com/questions/80564/do-almonds-smell-like-they-do-because-of-cyanide

According to CDC.gov and Toxnet, bitter almonds contain cyanide, which, gives them the characteristic odor, but this can be also due to benzaldehyde (PubChem), which is, by the way, used as almond flavor for cooking (Wikipedia).
Garlic has its odor due to allyl methyl sulfide (Wikipedia) and not due to arsenic, which is not present in garlic in significant amounts. Arsenic as such does not have garlic odor and foods high in arsenic, such as rice, chicken, fish, beer and wine (Prevention) do not smell like garlic.
However, poisoning by toxins, such as arsenic, thallium, organophosphate pesticides, selenium and tellurium (FPNotebook, PubMed) is followed by addition of the methyl group (CH3) to them by normal intestinal bacteria, which gives them the garlic-like odor.
So, the connection between the garlic odor of garlic and arsenic (or other) poisoning is in the presence of methylated substances: allyl methyl sulfide in garlic, trimethylarsine in arsenic poisoning, dimethylselenide in selenium poisoning, etc (PubMed).


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Why does Stereology use Systematic Random Sampling?
I am a student of Neuroscience and in all my textbooks and lecture notes it is written that in Stereology, Systematic random sampling (SRS) is used to obtain sections.
Why it's that and not any other type of sampling? For example, why do we not use completely random sampling? What are the advantages of SRS over any other type of sampling when applied to stereology?

I really like questions like this, thank you! I am glad you are curious about why approaches like this are used - I strongly recommend that all students try to think critically about techniques, you can learn a lot from this approach!

Systematic sampling refers to a method where all samples have an equal probability of being chosen but the spacing between samples is constant. That is, although each individual section is equally likely to be chosen, the combination of samples is not. The Wikipedia article on systematic sampling provides a good overview.
Stereology refers to the analysis of a three-dimensional structure using two-dimensional slices. Such an approach is common with histological techniques. A block of tissue is sliced into thin sections that allow for examination of the tissue with light microscopy, usually with the aid of stains.
If you sampled purely randomly, by chance, you are likely to obtain "gaps" in your analysis by random chance. For example, imagine you section a 3mm block into 40um sections. This process gives you 75 sections. It is too time-consuming to analyze all 75 sections, so you want to choose just 15 of them.
Let's try generating 15 random numbers from 1 to 75 and look at the maximum gap. I do this by taking the first 15 numbers of a random permutation of 1 to 75. In MATLAB, one can do: x=randperm(75,15), max(diff(x));
Here are some results:
23    26    33    34    35    37    44    54    55    58    60    69    72    73    74

Max diff: 10
12    14    15    16    17    20    22    27    28    34    44    47    58    59    73

Max diff: 14
 8    14    15    18    19    20    29    32    40    41    47    67    70    71    72

Max diff: 20
 3     7    16    19    30    32    33    34    38    39    50    57    61    65    75

Max diff: 11
 3     7    17    18    21    26    29    37    42    46    49    52    60    61    69

Max diff: 10
If we were to instead use systematic sampling, the difference between sampled sections would be fixed at 5: you skip 4 sections to get 15 evenly spaced sections out of 75 total. But with purely random sampling, the largest gaps are bigger, sometimes much bigger! 20 skipped sections means there is a 800um gap with no data! Even worse, I noticed later that in the first draw, the lowest number was 23! So the first 22 sections are completely omitted from analysis! There can be major morphological changes and entire brain nuclei missed within a gap that size, whereas 100um gaps are no problem.
I didn't print out the minimum gaps, but you can look at my examples to see the other side of this problem: in the first set, numbers 33, 34, 35 and 72, 73, 74 are right in sequence! There is likely little or no morphological difference on those short intervals and yet with random sampling one can waste time analyzing those adjacent slices. Because these draws are completely random, you can notice similar adjacent stretches in all of these random draws, even though I made no effort to select particular examples: these are just the first 5 results I got from MATLAB.
References

Gundersen, H. J. G., & Jensen, E. B. (1987). The efficiency of systematic sampling in stereology and its prediction. Journal of microscopy, 147(3), 229-263.
Gundersen, H. J. G., Jensen, E. B. V., Kieu, K., & Nielsen, J. (1999). The efficiency of systematic sampling in stereology—reconsidered. Journal of microscopy, 193(3), 199-211.


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Does human brain store duplicate data?
There are several answers and articles about how the brain stores data, but none specifically cover whether a human's brain stores duplicate data.
I was reading in this article that a human brain can have a capacity of 1 terabyte to 2.5 petabytes. But for example, if you read a book a dozen of times, will it be stored as data several times?
Let me put it this way. When we read a book a couple of times, we remember it better. Is that because it's stored in several synapses and then retrieved better while trying to remember, or is it because reading it over and over makes the missing parts be stored?
We do recognize a familiar phrase when reading a book, which means the brain can differentiate the unknown from known. What matters is that does it decide to store it again or not? Just like a computer who refuses to save a file if the file already exists.

You might think about what gets stored when reading a book.  First there's the actual text, which (if you read it a number of times and make an effort) you might memorize and be able to recite, and which can be stored in a Mbyte or so of ASCII.  Then there's the story the book tells, which you could remember even if you can't remember the actual words.  Then there are the various experiences of reading a book that you might have read multiple times over the years.  How much space does it take to store the memory of those experiences?

@jamesqf Yes, i mentioned this in my comment to the answer indeed. Some phrase in other language that you don't even know, but you remember how to repeat it.

The way neuroscientists currently think about storage in the brain, it doesn't make any sense to think about "duplicate" data but rather about the "robustness" of a given memory to interference or confusion, which increases with consolidation and reconsolidation of memories or can degrade over time.
Repeated exposure can contribute to the robustness of a memory, but so can other factors such as the emotional content of a memory (which, depending on the emotional state, can increase or decrease memory robustness, and this can also vary with the "jist" versus "detail" of a memory).
Note that there are also very different types of memory, so that repetition is very important for motor plans and "muscle memory" whereas episodic memory can get lost in the repetition of daily recurrent events, such as parking your car or eating lunch: you might remember where you parked or ate today, but if you have a routine this can blur into all one memory, where you have a notion of eating at a particular restaurant many times, but you would struggle to remember specifically eating there on December 14th, 2011, unless there was some other special event on that day.
In your example of reading a book, there would likely be two types of memory: 1) memory for the episodic event of reading the book, which would be a separate memory because it is a separate event, though it could be confused with other similar episodic events. 2) Semantic memory for the content of the book: this would be a single memory, reinforced with subsequent readings of the book, and supplemented with all your other semantic experience with the content of a book: discussing the characters of a fiction book with your friends, learning about molecular genetics from a textbook and from a lecture course, etc.
Note also that talking about the "data capacity" of a human brain compared to a computer is a bit silly, because data isn't stored in the nervous system in bits, and a "fair" accounting of human memory needs to consider the vastly multidimensional interactions that are easily coded in a nervous system but not at all easily in a binary system. Note that other papers have come up with estimates that diverge greatly from the numbers you cite, for example Wang et al 2003 which gives a value of 108432 bits based on the number of synaptic connections. That number is truly inconceivable to our conscious experience even if it is within the capability of our brain. Clearly there are other limiting factors not involved in a simple binary system, for example confusion with similar memories, and there are types of memory that computers excel at (such as the pixel values of an image) whereas human memory deals in abstractions and hierarchical representations.
References

LaBar, K. S., & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Reviews Neuroscience, 7(1), 54-64.
Walker, M. P., Brakefield, T., Hobson, J. A., & Stickgold, R. (2003). Dissociable stages of human memory consolidation and reconsolidation. Nature, 425(6958), 616-620.
Wang, Y., Liu, D., & Wang, Y. (2003). Discovering the capacity of human memory. Brain and Mind, 4(2), 189-198.

Thank you. Here i have to mention: 1- What do you mean by Robustness? For example, a signal's robustness can be divided into signal strength, signal quality, etc. 2- By reading book, i meant simply remembering words and their orders, such as you remember a phrase from a language you don't even understand.

I meant resistance to factors that interfere with signal. In memory, two of these are interference and confusion. Interference I would say is roughly equivalent to signal-to-noise, the inability to recall a particular memory. Confusion has a particular meaning in theoretical descriptions of memory as well, slightly different from the colloquial usage, but it basically means the ability to distinguish two different patterns. Also called "pattern separation" from the other direction. 2) This meaning would be the "semantic" type of memory that I mentioned.

For 1) in robustness I would also include, to some extent, the level of detail of the memory, though it could be possible for a memory to be very clear but not detailed, all of those qualities are not necessarily dependent on each other.

Nature preserves redundancy by duplicating certain parts of living things - two lungs, two kidneys, two testes, two ovaries. I believe that as an instinct of self-preservation the brain does duplicate memory in some form.  Otherwise a caveman who was clubbed on the head or fell and hit his head badly would (if he recovered) be bound to forget how to do some basic task - like remember where his cave is, or how to hunt, or how to eat.
This would explain why most Alzheimer's patients can remember the distant past, at least initially.  It also explains why they have 'good' days (where they seem like their old selves - at least until the ravages of the disease take their toll) and 'bad' days, rather than 'bad' then immediately, 'much worse'.
Another example – you hear an old song from your childhood that's not played on the radio very often. You knew you used to know the title, song, and artist very well – but now you can't remember who the artist is anymore.  You try to resist temptation to look it up immediately on the Internet because you know this can't be good for your memory recall, but curiosity eventually gets the better of you.  When you do finally look it up you say, 'No way - it can't be HIM!".  Reluctantly you accept this new memory but you realise that somewhere in the recesses of your mind this information is already stored (later you remember that you mixed this artist up with another artist at the time and performed some research and found it was this artist after all).
So what have you done?  You have a piece of information already stored in your brain and you've now stored an exact duplicate - and, because of the emotional situation attached to each piece of information, these remain as backups of one another.


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Is setting high mismatch and gap penalties sufficient to distinguish perfectly mapping reads?
I have a fat pile of 125bp whole genome shotgun reads that have undergone quality control, and I would like to pull out just those reads that do not map perfectly to the genome. When I set extremely high penalties for mismatches and gap opens/extensions (with bwa mem -B 1000 -O [1000,1000] -E [1000,1000]), it looks like the alignments for perfectly mapping reads are shown, and the rest of the reads are reported as unmapped. If this is true, I could then pull out the unmapped reads with samtools -f 4.
Are there any holes in my reasoning here, or will it work to discard all of the reads that map perfectly to the genome?

The short answer: No, setting extremely high penalties (100 or 1000) does not seem to work. I'm not sure why.
The medium answer: Since I posted the question, I did a bit of exploring, and it looks like the reads that perfectly match are the reads that are not soft clipped and that have an edit distance of zero, as indicated by the CIGAR string and NM tag, respectively.
The long answer: See https://standage.github.io/how-to-distinguish-perfectly-mapped-reads-from-a-sambam-file.html.

The preferred way is to map normally and then filter out imperfect matches downstream:
bwa mem ref.fa reads.fq | perl -ane 'print if /^@/ || ($F[5]=~/^\d+M$/ && /\tNM:i:0/)'

Changing the scoring scheme hurts mapping accuracy.

"Changing the scoring scheme hurts mapping accuracy." This is a concern if you want to keep all of the alignments around for other purposes, but is a non-issue if I only want to distinguish perfectly mapped reads vs imperfectly mapped.

I used to consider myself quite the Perl-slinger (I code mostly in Python these days), but I never knew about the -a flag. That's a game changer! +1


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question about fast/slow muscle twitch fibers
Here are my questions (I have several)
1) Are the fast twitch muscle fibers dominant or recessive as opposed to the slow?
2) Are people of mixed race/greatest genetic diversity in their background, tend to be the best athletes and the healthiest in general?
Allow me to clarify the first point:  Obviously no one in the world is either 100% fast twitch or 100% slow twitch.  Let's put this another way:  (and I'm just using random numbers here that are probably unrealistic, bear with me).  Let's say someone who is 80% fast twitch and 20% slow twitch has a baby with someone who is precisely the other way.  Would the child develop more of the fast twitch or more of the slow twitch?


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Does vaccination make the immune system "lazy"?
I was having this discussion with a friend over vaccination against the flu. Although he agrees that vaccination against almost all diseases is necessary, he said that flu shots are not. He argued that the immune system is like the muscular system. It constantly goes through training. Flu shots deprive the body from "natural exercise" since, he believes, we need to train our immune system by getting "the right amount" of the real viruses from the environment. In other words, if we do too much vaccination (and flu shots are "too much") we make our immune system lazy.
Is this true? I know that there is a difference between natural immunization and vaccination, is it correct though to say that the latter makes your immune system lazy? I was under the impression that vaccination's function resembles more the way we learn and memory and less the musclar system which can get lazy.

Vaccines are intended to provoke the exact same immune response as the actual pathogens they're derived from. There is not a fundamental difference between natural immunization and vaccination. I'm not sure what "lazy" would even mean in this context.

@ Harris Weinstein: He argued that flu shots will lead the body to a state of complacency . I believe this is false but I am no expert therefore I could not convince him.

In your friend's language: vaccination means infection by dead viruses. Thats it for the difference.

@ David: I had this discussion and could not convince my friend because of my lack of expertise. I thought I might ask the experts. Sorry.

OP's friend's opinion feels to me potentially pseudoscientific or that-type. Rather opposite should be true. over-vaccination = overtraining at gym.

I feel the same way. From the very little I know vaccination helps a lot in the recognition of an agent. It does not prevent "a fight" (or "training", in my friend's terminology  ) of the immune system when the virus comes into the body. This fight will happen anyways every time. Therefore there is no harm in any vaccination.

Please ready about the hygiene hypothesis; there is a lot of evidence that not being exposed to pathogens weakens our immune systems. Vaccines are boosters of the immune system, not suppressors. We rarely get tetanus any more (quite common once) because our bodies, thanks to vaccines, have been given an immunological boost to fight it. Ask your friend if his mind is stronger if he uses it or if he doesn't.  The answer is obvious. It's similar for the immune system (up to a point.)

Hi Welcome to Bio.SE. I'm +1-ing this question simply because this might be a misconception shared by others, and we should try to properly address it in the answers. Your friend's theory, however, is way off. As @anongoodnurse mentions: vaccines are boosters of the immune system, not suppressors.

No, that is ridiculous. Chris has it right. What you are doing is exposing the immune system to a target (piece of, or inactive viral particle) that it can then prepare antibodies for in advance of encountering the actual flu virus. This way your body can quickly recognize/attack/neutralize the virus before making you ill.

Contrary to many beliefs our immune system needs no "training". It is permanently active and confronted with dozens to hundreds of antigens in our food, from dust we inhale and so on. This all happens to protect our body from the environment and the immune system is pretty efficient with that and certainly it is not getting lazy.
By vaccinating against a certain disease, you generate immunogenic memory against this disease. When you then get exposed to the disease, this memory helps to speed up the immunogenic reaction against the disease - ideally you are not getting sick, in some cases the progression of the disease is much milder.
Further reading:

Wikipedia on adaptive immunity
The front line of host defense from Janeway at the NCBI Bookshelf

although there is evidence that lack of exposure may contribute to atopic immune reactions (allergies). The fact these reactions involve the adaptive immune system supports this. Immunization would have nothing to do with this one way or the other though. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)06252-3/abstract


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Are all non-breeding naked mole rats the same sex?
In many eusocial species, all the non-breeding members are the same sex.  Honeybees are a good example, with only female workers.
Are naked mole rats that do not breed also all either male or female, or are they mixed?

Naked mole rat colonies contain individuals of both sexes, with one breeding female and one to three breeding males, and the rest non-breeding individuals of both sexes.
The other individuals in the colony have an additional caste system that seems to depend on size but not sex (i.e., there does not seem to be a hierarchical relationship between non-breeding males and females).
Non-breeding females, but not males, have suppressed reproductive tracts. In the absence of a queen, some non-breeding females' reproductive systems will begin to activate, until one becomes dominant and the others return to being non-breeders.
References

Clarke, F. M., & Faulkes, C. G. (1997). Dominance and queen succession in captive colonies of the eusocial naked mole–rat, Heterocephalus glaber. Proceedings of the Royal Society of London B: Biological Sciences, 264(1384), 993-1000.
Jarvis, J. U. (1981). Eusociality in a mammal: cooperative breeding in naked mole-rat colonies. Science, 212(4494), 571-573.