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Antibacterial hand soaps (and related products); what are they good for?
From Wikipedia:

Household use of antibacterials in soaps and other products, although not clearly contributing to resistance, is also discouraged (as not being effective at infection control).

Following the links led me to this paper:  Larson EL, Lin SX, Gomez-Pichardo C, Della-Latta P.,  Effect of antibacterial home cleaning and handwashing products on infectious disease symptoms: a randomized, double-blind trial.  Ann Intern Med. 2004 Mar 2;140(5):321-9.
They conclude:

The tested antibacterial products did not reduce the risk for symptoms of viral infectious diseases in households that included essentially healthy persons. This does not preclude the potential contribution of these products to reducing symptoms of bacterial diseases in the home.

Upon reading this, my thoughts were:  Why would one test whether antibacterial products have an effect on viral infections diseases?  Since the authors used a control group (those whose soaps didn't have an antibacterial agent), they are only testing for the effect of the antibiotic.
This leads me to the main question:

Question:  Which common diseases would likely be more affected by antibacterial hand soaps (and other antibacterial products) than their non-antibacterial counterpart?

psychosomatic illnesses?  Soap is a pretty potent anti viral and anti bacterial all by itself.  Hospitals and doctors use Purelle or other alcohol based gels to keep their hands clean.  The weak antibiotics in antibiotic soaps like triclosan are probably encouraging the formation of antibiotic resistance.

This may be related to this question on Skeptics SE:  Does regular handwashing with antibacterial soap prevent disease?  Since it is closely related, I will copy my answer from there to here:
See this related answer.
To answer your specific questions:

Has something changed?

Well, we have access to these products now, whereas we didn't before.

Does this sanitizing really make people healthier?

That is a subject of debate.  While it can prevent rapid spread of some things, keep in mind that anti-bacterial soaps should only have specific uses.
The CDC has concerns about the prevalent use of these products.

Scientists are concerned that the antibacterial agents will select bacteria resistant to them and cross-resistant to antibiotics. Moreover, if they alter a person's microflora, they may negatively affect the normal maturation of the T helper cell response of the immune system to commensal flora antigens; this change could lead to a greater chance of allergies in children. As with antibiotics, prudent use of these products is urged. Their designated purpose is to protect vulnerable patients.

Also, there is some concern as outlined by the hygiene hypothesis (WP).  However, that is mostly associated with childhood immunities and allergies as opposed to the effects on adults.

“The natural immune system does not have as much to do as it did 50 years ago because we’ve increased our efforts to protect our children from dirt and germs,” says McMorris.
“Allergies are on the rise because our society has changed the way we live. As a result, people with allergies are having children with others who have allergies, which in turn creates a natural increase in the prevalence of allergies in our society.

The bottom line on this hypothesis is that more research is required.

He (Richard G. Barbers, M.D., USC professor of medicine at the Keck School) also gives credence to the hygiene hypothesis in that "we may be over-protecting kids, and their immune systems, consequently, do not become well-developed."
Barbers notes that only time and a lot more research will tell whether the hygiene hypothesis is valid, and whether, once again, parents should let their kids play in the dirt.

It is generally understood that interaction with beneficial germs is good for you.  However, normal cleaning will not destroy these germs since they reside within you (unless his germaphobia induces him to take antibiotics).  The human immune response doesn't particularly work that way.

The investigators show that "good" bacteria in the gut keep the immune system primed to more effectively fight infection from invading pathogenic bacteria. Altering the intricate dynamic between resident and foreign bacteria - via antibiotics, for example -- compromises an animal's immune response, specifically, the function of white blood cells called neutrophils.

Using too many anti-bacterial soaps has raised quite a few concerns even still.

Soaps and lotions that include antibacterial agents have no benefit over ordinary soap and water, but more research is needed to allay or substantiate concern that these substances may be leading to increased rates of antibiotic resistance. This is the conclusion of the Food and Drug Administration's Nonprescription Drugs Advisory Committee, which met last month to consider the use of these products outside of the health care setting.
"In the absence of proven benefit, there's no real reason to encourage the use of these products," said Alastair J.J. Wood, MD, committee chair and associate dean at Tennessee's Vanderbilt Medical School.

That is not to say that their use should be discontinued entirely.  Two MDs weigh in and conclude:

Opt for regular soap and water, unless you’re at a hospital or doctor’s office, where it’s best to use antibacterial soap. But if you’re out and about and antibacterial soap is the only kind around, it’s fine to wash with it—and it’s worth keeping in the kitchen to use after handling raw meat.

Hope that helps.

I thought I would attempt to answer my own question.  The only other answer currently (by Larian LeQuella), while a helpful comment, I feel it doesn't answer my original question.
To begin, we need to put the results into context.
Fact: Hand-washing using tap water alone will reduce the amount of bacteria and viruses on hands (they might not be actually killed, but no longer on your hands).
Some examples:

Ansari et al. (1989) performed an experiment where a fecal solution was placed on participants' hands and subsequently washed off using one of a range of soaps.  They found a reduction in around 83% of the human rotavirus and 90% of the E. coli.
Shojaeia et al. (2006) randomly selected 150 food handlers in Iran, and instructed them to wash and scrub their hands with sterile water.  Before the intervention, around 73% were contaminated with bacteria (primarily with Staphylococcus aureus or E. coli), and afterwards 32%.

Fact: More bacteria and viruses are removed from hands by hand washing by using some type of soap (not necessarily antibacterial).
Some examples:

Ansari et al. (1989) (op. cit.) found that certain agents (e.g. 70% isopropanol) can increase the reduction in E. coli and human rotavirus to around 98%.  However, this was not true of all possible hand-washing agents.
Mbithi et al. (1993) also conducted a experiment consisting of placing a fecal solution on participants' hands that was subsequently washed off using one of a range of soaps.  In this case, the hepatitis A virus (HAV) and poliovirus type 1 (PV) was considered.  They found that tap water gave a reduction of HAV of around 80% and PV of around 85%.  The reduction increased to around 88-92% for HAV and 90-98% for PV for most soaps tested.

[There will be zillions of additional examples to the above.]
A large survey was conducted by Aiello et al. (2007) which considered the efficacy of triclosan (one of the common active ingredients used in antibacterial hand soap) found that, overall, previous research has indicated no significant additional benefit vs. ordinary hand soap.  They write:

Soaps containing triclosan within the range of concentrations commonly
  used in the community setting (0.1%–0.45% wt/vol) were no more
  effective than plain soap at preventing infectious illness symptoms
  and reducing bacterial levels on the hands.

This is probably not the last word on the matter, e.g. Fischler et al. (2007) claimed a significant difference in the transmission and acquisition of E. coli and Shigella flexneri after using an antibacterial soap.  It is also plausible that antibacterial agents other than triclosan (where the focus has been) provide a health benefit (for example, methylchloroisothiazolinone/methylisothiazolinone).  In fact, the Aiello et al. (op. cit.) paper itself indicates a non-negligible effect from >1% triclosan.  Kimberly-Clark give a 99.9% or more bacterial killing efficacy for a range of bacteria in a 2003 in vitro experiment of their product; obtainable via Googling "kimberly-clark killing efficacy".
(Side note:  There is also a suspicion that the use of triclosan will give rise to triclosan resistance or cross-resistance to antibiotics (e.g. by Levy (2001), Aielloa and Larson (2003), Yazdankhah et al. (2006)).  Although, Cole et al. (2003) and Weber and Rutala (2006) claim otherwise in the case of antibiotic resistance.)
This leads to the original question:  Which common diseases would likely be more affected by antibacterial hand soaps (and other antibacterial products) than their non-antibacterial counterpart?  I.e. if we wanted to test the claim that a certain antibacterial hand soap has some positive effect (vs. a non-antibacterial version), what would be some common diseases that we could test for, and expect to find a non-negligible result?
I offer the following candidate for a bacterial disease whose effect should be noticeably reduced by the use of antibacterial hand soaps:

Staphylococcus aureus is a bacterial species that causes a range of noticeable illnesses and can be transferred by skin-to-skin contact and contact with contaminated objects.  We can thus reasonably expect it to be affected by an effective antibacterial hand soap.  In fact, washing hands is recommended for reducing the prevalence of S. aureus, along with zillions of other diseases (by e.g. Better health channel).  This is one of the bacteria that Kimberly-Clark give a 99.99% kill efficacy of their product in vitro.

Although, not directly related to hand-washing, Brady et al. (1990) used a 1% triclosan preparation and Zafar et al. (1995) used 0.3% triclosan to control methicillin-resistant Staphylococcus aureus.

The single additional measure of changing handwashing and bathing soap to a preparation containing 0.3% triclosan (Bacti-Stat) was associated with the immediate termination of the acute phase of the MRSA outbreak.  -- Zafar et al.

Similarly, a 1.5% triclocarban bath has been used to treat atopic detmatitis Breneman et al. (2000):

The antimicrobial soap regimen caused significantly greater
  improvement in the severity and extent of skin lesions than the
  placebo soap regimen, which correlated with reductions both in S
  aureus in patients with positive cultures at baseline and in total
  aerobic organisms.

The above results suggest that antibacterial soaps could have a beneficial effect against S. aureus (more than a non-antibacterial counterpart).  However, it is unclear as to how much of this effect implies a comparable effect for hand washing alone (and in an ordinary household setting).  Moreover, there are many different antibacterial hand soaps and other products, whose active ingredients might be at different dosage, all of which would further affect the outcomes.


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Why do most breast cancers occur in women?
According to Korde et al. (2010):

Male breast cancer accounts for less than 1% of all cancers in men and less than 1% of breast cancers.

This raises the question: Why do most breast cancers occur in women?
Two plausible explanations I can think of:

A male is less likely to get breast cancer for anatomical reasons (such as a smaller quantity of breast tissue, or breast tissue that is less susceptible to cancer),
Women have higher significantly levels of estrogen, which is linked to mutations that cause breast cancer (see Cavalieria et al. (2006)).

Although, I have no evidence to suggest that either of these is predominant factor.

There is another problem with breast cancer in men: Its usually not detected and searched for. Its probably happening more often than doctors think.

Interestingly, a greater proportion of male breast cancer is estrogen receptor positive (90%) than female breast cancer (80%)

Yes, this is mostly about estrogen. Most breast cancers rely on endogenous estrogen to sustain proliferation.
Some general reading: Cancer Medicine, Chapter 18
More in-depth reading: Endogenous Hormones as a Major Factor in Human Cancer
Requested summary of mentioned readings:
First of all, there is an established link between breast cancer cell proliferation and concentration of estrogens and progesterone, which is logical, because normal breast cells divide in response to those hormones (e.g. puberty, pregnancy, even luteal phase of the menstrual cycle). Secondly, the incidence of breast cancer in women correlates with major changes in their hormonal profile - girls and elderly women (i.e. women with lower levels of sex hormones) don't get breast cancer.
Many factors, that influence the risk of developing breast cancer are in fact tightly connected to the hormones' levels. For example - early age of menarche (or, more importantly, first ovulation, because physical activity at young age disturbs ovulation AND is protective against breast cancer) and Hormone Replacement Therapy raise the risk, early age of first full-term pregnancy or any form of artificial menopause (such as preventive oophorectomy for women with mutations in BRCA1 or 2) reduce the risk.
The first table from the book chapter lists known risk and preventive factors. The review article explains the same ideas, but connects them to other types of cancer (e.g. ovarian cancer) and suggests mechanisms, which might be the cause of those risk changes.

Can you summarize some important points of those links?

estrogen and prolactin are hormones that stimulate mammary development and growth of the breast tissue.  They greatly enhance the chance of cancer since that tissues is proliferating at a great rate.  Males do not typically experience these developmental phases.

This is a bad and poorly referenced answer. The age vs. cancer incidence for breast cancer follows essentially the same curve as every other adult cancer. There's no drop at menopause, and the highest incidence is in women over 70. There's a decrease in diagnosis in very elderly women, but this is seen in all adult cancers. Autopsy studies show us this isn't due to a magical protective age threshold, but different clinical choices due to age.

For two reasons: Women are

exposed to estrogen,¹ and
the lobules in a woman's breast go through 4 stages:

Type 1: prepubescent & Type 2: pubescent

Type 3: reproductive & Type 4: lactation lobules²

The sooner a woman progresses to Type 3 and Type 4 lobules, the lower her risk of cancer. An interruption of the progression from Type 1 to Type 4 lobules (such as with a late-term miscarriage or induced abortion) increases the risk of cancer, as cancer generally arises in Type 1 and Type 2 lobules.³
References

Miller, Katherine. Estrogen and DNA damage: The silent source of breast cancer? J Natl Cancer Inst 2003: 95:100-102.
Schwartz, Shires, Spencer, Principles of Surgery (McGraw Hill) Russo J, Tay LK, Russo IH. Differentiation of the mammary gland and susceptibility to carcinogenesis. Breast Cancer Res & Treatment 1982;2:5-73.
Daling JR, Malone DE, Voigt LF, White E, Weiss NS. Risk of breast cancer among young women: relationship to induced abortion. J Natl Cancer Inst 1994;86:1584-92.

"or induced abortion" Isn't a(n adult) woman already at phase 3 (or what does it mean)? According to the source 3 non-adult women are in the category of increased risk. Women above 30 have increased risk of breast cancer probably due to the same reasons as people have other types of cancer, though.

@rus9384 All adult women, regardless if they have ever been pregnant, have reached at least phase 3?

That was a question. I guess your responce is "no". But after the woman stops breastfeeding what phase does she turn to?

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Random Mutagenesis vs Directed Evolution as Strategies to boost expression
Do people use random mutagenesis (say using UV) to generate host variants that have high expression of a metabolite / enzyme? I've seen it mentioned as a strategy but it confuses me as to why.
How does that compare to using Directed Evolution for the same purpose? Intuitively, random mutagenesis seems highly inefficient (since you have no control over which genes you mutate) given the combinatorial explosion even in something like E Coli's genome size. Am I making a mistake in this reasoning?
What are situations where one may prefer random mutagenesis over directed evolution? Are there any pros and cons to consider?

Well, you already mentioned it. Random mutagenesis (with UV or chemical mutagens) targets the entire genome and you select the organism for certain traits.
In a directed evolution experiment, you are just targeting a gene or a group of genes. With the progress of synthetic biology, it might be possible to synthesize small genomes (already shown by Craig Venter and group) and apply directed evolution methodology genome wide. This would still not be considered directed, as the mutations are actually random over the genome.
The pros and cons depend on what exactly you aim to do.

Thanks! The aim is something like this: I'm interested in getting yeast to express  a secondary metabolite by inserting a hetrologous gene. The goal is to develop & select a yeast strain that produces high levels of the precursor substrate.

@curious_cat That is the ultimate goal. In that case you can go for random mutagenesis. However, if you are improving the catalysis rate of a specific enzyme, lets say, then apply directed evolution to that specific gene.

Thanks! So it isn't entirely impractical to attempt random mutagenesis? i.e. With 12 Million base pairs & random mutation is it a viable strategy? Have other attempts using similar approaches succeeded?

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Can oral bacteria be targeted by white blood cells?
Today I was told from a dentist that a leukocyte is much larger than a bad bacterium. So a leukocyte cannot remove bad bacteria when they hide in very places like the space between the gums and teeth for example, because leukocytes cannot exit the body.
So am I right that a colony of bad bacteria cannot be removed from the oral cavity by leukocytes, because they are too big to exit the gum?

A colony in the gums or teeth are protected by building a strong film around them. There are leukocytes in the mouth, but they can't really breach this strong barrier. It has nothing to do with size.


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What is effect of sperm in blood?
Staphylococcus aureus, Streptococcus pyogenes, and Clostridium perfringens all produce hyaluronidase.
Each of these bacteria are pathogens (use hyaluronidase as a virulence factor to destroy the polysaccharide that holds animal cells together, making it easier for the pathogen to spread through the tissues of the host organism)

The role of hyaluronidases in cancer is controversial, however there is substantial evidence of increased hyaluronidase activity in malignancies.

We know, human sperm also produces hyaluronidase (for penetration of ovum),
So what would happen if sperm enters blood (Like:via cuts or wounds on genitals)?

Ciliary Dysentery(Balantidiasis) is caused by Balantidium coli(ciliated protozoan) which causes ulcers in colon and invades mucous membrane by secreting "Hyaluronidase"

Not much really, blood would be a really hostile environment for sperm. And they would get targeted by the immune system rather quickly. Fertilization of oocyte by sperm is a very specific process, sperm would not be able to "drill" through any type of cells.

Would there be any effect in body after hyaluronidase is secreted by sperm? You can guess it by examples given by me.@Maljam

could you link the evidence to your claim The role of hyaluronidases in cancer is controversial, however there is substantial evidence of increased hyaluronidase activity in malignancies.?

link   is the required link.@gone

The problem with bacteria in tissues is that they can multiply, causing more damage. A sperm can't multiply. It's effect would be negligible.


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Is there a special reason why ferns are so early in evolution?
Reading about plants in history it seems that ferns where already in the Devonian period (400 million years ago) growing. Probably the climate in that time was very different from now, but what made them so good surviving in that time?

Could be due to them "having" Neochrome, a protein which enables them to respond simultaneously to red and blue light in both the way that they grow and the way the photosynthetic elements in their cells, the chloroplasts, organise themselves. I'd recommend reading into http://www.economist.com/news/science-and-technology/21600856-survival-ferns-present-depended-ancient-accident-time-and (mostly about why fern survived for so long) and http://www.britannica.com/plant/fern (general information about fern) and https://u.osu.edu/eeob3320/category/ferns/ (properties of fern)


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Can cirrhosis be caused by physical compression of the body?
On a random forum, a member speculated that their cirrhosis was caused by wearing tight-fitting clothing such as a girdle or corset.  This leads me to the following question:

Question: Can cirrhosis be caused by physical compression of the body?

The list of causes on Wikipedia does not include this.  However, this may just be because the list is incomplete.  Alternatively, it may be because physical compression is unlikely to contribute to cirrhosis.
A plausible mechanism that springs to my mind is that physical compression leads to the constriction of hepatic veins, arteries and/or their tributaries.  But I suspect the rib cage would provide significant protection against this (see below).

There is the term “corset liver”. It describes changes (“grooves”) on the liver’s surface following external compression and subsequent local atrophy, e.g. from wearing a corset for a long time. (see Dancygier: Clinical Hepatology)
A paper from the 1980s describes some abnormality in the histological findings of liver tissue of dogs after chronic abdominal compression but without providing any details in the abstract (I don’t have access to the full version). They measured an increased pressure in the Vena cava and the portal vein. (Ueyoshi, Shima: Studies on spinal braces. With special reference to the effects of increased abdominal pressure. PMID 4093227.)
A (chronic) Budd–Chiari syndrome can also cause liver necrosis and consequently cirrhosis and can be the result of venous compression from e.g. tumors.
I doubt that a comparable chronic compression is possible from wearing clothing. Corsets are still used in orthopedic conditions. I have never heard about long-term side effects on liver tissue. The explanation for cirrhosis seems unlikely to me.

Thanks for that.  I think you're right... my suspicion is it's likely that any link with cirrhosis would have been discovered along with "corset liver" etc., and would be reasonably easy to find in the literature.


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Does cooking ginger reduce its anti-nausea effect?
There seems to be strong evidence to support the hypothesis that eating ginger helps reduce nausea e.g. during pregnancy (e.g. Vutyavanich et al.).  It seems that gingerol is the active ingredient in preventing nausea (cf. Qian et al.).  Wikipedia writes: "Cooking ginger transforms gingerol into zingerone...".  Presumably, zingerone does not affect nausea.
Question: Does cooking ginger reduce its anti-nausea effect?
A Google search will reveal numerous suggestions for giving ginger tea to pregnant women to help with morning sickness.  But boiling the ginger could conceivably defeat the purpose of taking the ginger in the first place (and any effects are primarily due to the placebo).
There's an article (Basirat et al.) which describes an experiment in which biscuits with ginger were given to patients (instead of ginger tablets), although their results alone have not convinced me one way or the other.  The authors conclude that their results indicate an anti-nausea effect, but some of their tests do not match that conclusion (i.e. a placebo was comparably effective).  Also, the group given the ginger biscuits started off with worse conditions on average.

Good news! Some Australians have published on the stability of aqueous gingerol at elevated temperatures: http://onlinelibrary.wiley.com/doi/10.1002/jps.1116/full
Gingerol turns out to be stable enough to make a cup of tea with at neutral pH. They also note that gingerol and its primary decomposition product form a 50-50 mixture that doesn't degrade further over shortish time periods, and that the decomposition product is probably restored to gingerol in the stomach's acidic pH -- so you're good to make your tea, and probably to hold on to it for at least a few days.

Excellent!  That certainly answers my question.

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How does a tiger have stripes?
A vague question, but let me try to explain. My friend explained to me that in females, some cells use one X chromosome, while all others use the other X chromosome. This can result in some differences of appearance of certain individuals. The Wikipedia page on X-inactivation shows an example. There is a picture there that shows a cat with fur of two colors, each showing in seemingly random groups. My friend had explained that when one cell "deactivates" its X chromosome, all of its descendants have the same deactivated X chromosome, so it makes sense that the similar colors appear in groups on the cat's coat.
But it seems tigers' coats are much more complicated than that. The pattern on a tiger's coat is not completely random. They make very discernible shapes. There are clear borders inside which only black fur grows, and outside of which only orange fur grows. How is this possible?
I'm not suggesting that the patters on tigers' fur is in any way related to X-inactivation, since I know that only applies to female mammals. But X-inactivation seems like a "natural" phenomenon, while the stripes on a tiger (or other animals with complex patters) seem a bit more bizarre. How do the cells on a tiger's body know which color to show and still follow the pattern?

Although not exactly what you ask, but you may want to have a look at this: http://biology.stackexchange.com/questions/3299/how-did-butterflies-evolve-to-have-eyes-on-their-wings/3357

It turns out that this was a question that was answered by Alan Turing in the 1950s.
Turing hypothesized there would be two morphogens, an inhibitor/ activator pair, each of which would produce a one of two phenotypes by activation or suppression of a trait.  He hypothesized that this would produce a pattern like stripes or other patterns (e.g. black and orange stripes).
This year just such inhibiting/activating pairs produce patterns like ridges in the top of the mouth of mice.
In a broad way, this seems like X-inactivation, where there is an X-inactivation center (XIC) that is inhibited or activated when the cell is created in mitosis.  XIC is still hypothetical and undiscovered, but it can create patterns and is non-random.
So I would say that this tiger stripes and X-inactivation may share Turing's mechanism, but the stripes, found in male and female tigers alike is not linked causally to X-inactivation.


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What drives male fish to spray their milt?
In mammals the sexdrive of the males is because the intercourse provides a satisfaction where after, the sperm is ejaculated into the female. However, the male sperm doesn't enter the female fish but reproduces by spraying this fluid which contains the sperm, onto roe (fish eggs).
But what kind of (physical) drift is urging them to spray, while they probably don't have an orgasm, or do they?

From a human perspective, it's easy to understand how feelings of sexual attraction and an urge to have sex result in people reproducing. For men, this may be most apparent in the extreme pleasure found at the moment of orgasm, which coincides with insemination. However, there are many behaviors that people have a tendency to perform that don't involve any sort of immediate pleasure comparable to an orgasm.  For example, if someone cuts their finger, often their initial instinct is to stick their finger in their mouth. This is a type of wound licking, which is observed in a number of different species of mammals and is believed to promote wound healing due to clotting factors, growth factors, and/or antimicrobial factors present in saliva. However, a young child who cuts his finger sticks it in his mouth without any knowledge of these biological processes. It's a behavior that we are genetically programmed to perform because it promotes healing and reduces the risk of infection, thus promoting survival, thus promoting eventual reproduction. It has therefore been favored by natural selection.
There are many behaviors in animals that are clearly genetically programmed, and which animals perform consistently given the right stimuli (i.e., the right "triggers," whether they be visual or via other senses). Here are a few examples off the top of my head:
In birds, the process of mating and raising young is long, complex, and laborious. The process begins well before and continues well beyond the actual act of copulation (when insemination occurs). This suggests that there is some sort of more general internal mechanism that motivates the birds to go through these costly, time-consuming, stereotypic behaviors, generation after generation, in order to reproduce.
As a quick overview of some of these reproductive behaviors:
Many birds go through the effort of migrating long distances to very specific locations that they use as their breeding grounds and/or nesting grounds. The travel alone is energy-intensive and can be dangerous or even fatal. Mating is often preceded by complex courtship behaviors, sometimes involving elaborate song-and-dance performances by the males (video), in an attempt to impress the typically picky females. In some species, such as manakins, juvenile males may practice their courtship performance (video) for several years before using it to actually find a mate, as the execution needs to be flawless in order to sufficiently impress a potential mate. The young males use their male peers as stand-ins for the female during these practice sessions or rehearsals.
If the female is satisfied with a male suitor, then they may pair up and create a nest. The parent birds build their nests in very exacting and particular ways, even though they themselves don't even live in a nest the rest of the time. It's constructed purely for the purpose of raising chicks, and is abandoned after the chicks leave the nest. Yet the parents have some desire or "push" to build it, and to do so in very precise and structurally sound ways (in terms of climate, location, distance from the ground, materials used, size, shape, etc.). Eggs are laid, and when they hatch, a great deal of effort goes toward feeding the hungry chicks with their gaping mouths and helpless cries for more food, day in and day out, often for several weeks or months. I doubt that the motivation of either the mother or father bird is comparable to the human experience of sexual pleasure, so there is something else that prompts them to go through this ordeal, year after year.
Would we say the parent birds experience intense pleasure that motivates them to do all of this, in the right order, at the right time, and with such precision? It's impossible to know what a bird is "thinking," but remember that there is a danger in trying to project human emotions onto animals, whose brains may function in ways rather different from our own.
Interestingly, the sight of a young bird's open mouth is apparently a strong trigger for the parent bird to "want" to put food in that mouth. Evidence of this includes the fact that some bird species don't build their own nests or raise their own young at all, but rather lay their eggs in other birds' nests (quickly and sneakily, while the parents are away). The parent birds residing at the nest (i.e., the hosts) often don't notice the difference between their real offspring and the intruder that's a different species (i.e., the parasite), even though the difference is often obvious to any human observer. As a result, the the unwitting host parents feed and raise the parasite bird as if it were their own, often to the detriment of their actual chicks. The parasite chick species is often larger and grows faster than the host species, so the parasite outcompetes its host siblings for food (and sometimes pecks them to death or pushes them out of the nest). The parasite often grows much larger than its parents, yet the parents continue to expend lots of energy feeding it, as if they are unable to override whatever program that normally guides their behavior, because the sight of the parasite chick's open mouth is such a strong trigger.

Even stranger, perhaps, is the fact that multiple different species of birds have been observed feeding fish (often koi/goldfish in ornamental ponds or parks) as if the fish were their own offspring. The fish swim to the water's surface and open their mouths, and the sight of this drives certain birds to go find food and bring it back to feed to the fish. According to one source (in the following video), the feedings occurred up to six times per day.  Here's that video: A cardinal feeding several hungry goldfish.
Enough about birds, though; let's talk about bees.  Actually, not bees, but their close relatives, wasps. Among wasps, parasitoid wasps are a large group estimated to contain over 600,000 different species worldwide. An example that you may have heard of is the tarantula hawk wasp, which attacks, stings, and paralyzes (but does not kill) a tarantula "victim," then drags the tarantula to a prepared burrow/nest location, lays an egg on the tarantula's body, seals off the nest with the paralyzed (but still living) tarantula and wasp egg inside, and then flies off, never to see the offspring again. When the wasp egg hatches, the wasp larva bores a hole into the spider's abdomen, eating the living spider's insides while carefully avoiding the vital organs for as long as possible. This keeps the spider alive as it gets eaten from the inside out, and thus prevents the larva's food from rotting. Interestingly, as adults, these wasps subsist on nectar and plant material. The males don't hunt prey at all, and the females go through the process of attacking tarantulas (which are much larger than themselves) just so that they can drag the spider to the prepared burrow for their offspring to eat later. They don't even witness the fruits of their labor — but they are motivated to go through this process nonetheless.
While the process would seem to require some skill and intelligence on the part of the mother wasp, in some ways it seems overly pre-programmed and inflexible.  For example, consider the following description of the behavior of the parasitoid wasp genus Sphex, relayed by D. E. Wooldridge in The machinery of the brain in 1963:

When the time comes for egg laying, the wasp Sphex builds a burrow
for the purpose and seeks a cricket which she stings in such a way as
to paralyze but not kill it. She drags the cricket into the burrow,
lays her eggs alongside, closes the burrow, then flies away, never to
return. In due course, the eggs hatch and the wasp grubs feed off the
paralyzed cricket, which has not decayed, having been kept in the wasp
equivalent of a deepfreeze. To the human mind, such an elaborately
organized and seemingly purposeful routine conveys a convincing flavor
of logic and thoughtfulness — until more details are examined. For
example, the wasp’s routine is to bring the paralyzed cricket to the
burrow, leave it on the threshold, go inside to see that all is well,
emerge, and then drag the cricket in. If, while the wasp is inside
making her preliminary inspection, the cricket is moved a few inches
away, the wasp, on emerging from the burrow, will bring the cricket
back to the threshold, but not inside, and will then repeat the
preparatory procedure of entering the burrow to see that everything is
all right. If again the cricket is removed a few inches while the wasp
is inside, once again the wasp will move the cricket up to the
threshold and re-enter the burrow for a final check. The wasp never
thinks of pulling the cricket straight in. On one occasion this
procedure was repeated forty times, always with the same result.

On a similar note: Normally, the female wasp grabs the paralyzed cricket by its antenna to drag it into the burrow. However, if both antennae are cut off while the wasp is briefly away, then she is unable to pull the cricket inside and complete her task. She doesn't even attempt an alternative, such as pulling it by one of its legs, even though that would seem like an obvious backup plan to the human mind.
So, what motivates the female wasp to go through all this trouble in this way?  Is this even an example of true "motivation," or is it simply a form of genetic determinism in which she is an automaton, unable to modify her actions? It's food for thought.

Although this comment was very well written regarding animal motivations in general and how we should be careful with ascribing human emotions to animals, I think you forgot to relate it back to the original question, which was specifically about fish.

@ETam If someone asked what causes an apple to fall downward from a tree, the most meaningful response would not consist primarily of a lesson in botany or horticulture. In order to understand why an apple falls downward from a tree, one ultimately needs to have some understanding of gravitation as a general physical phenomenon. Whether the mass being acted upon by gravity is an apple, a boulder, or a planet, the underlying explanation is the same, and it has little to do with apples, boulders, or planets, specifically. Likewise, this question, ultimately, is not about fish.

came here to say the same thing; this is an awfully long answer that bizarrely evades the actual question

Assessing the motivation of gamete release in fishes is difficult, but most if not all organisms have a drive to reproduce, which likely instills some feeling of satisfaction if the species is capable of such feelings. From numerous observations of fish spawning, I am not sure that I would use the word spray for the release of milt. Such fishes are only capability of external fertilization, where females either deposit eggs or release them into the water column. Males will release milt either over deposited eggs or pelagically at the same time of egg release. The observed spraying is caused by the release of milt into a fluid that disperses and mixes it in the water column with eggs for fertilization. Water movement coupled with the movement of the male fish results in the perceived "spraying." The functionality of this type of dispersal is to mix the sperm with eggs, both of which are subjected to fluid dispersal. Numerous videos show this behavior in Rowell et al. 2018 supporting info videos https://onlinelibrary.wiley.com/doi/10.1111/jfb.13888 There are numerous other videos out there as well.


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Can animals also get Down syndrome?
I heard that animals cannot get Down syndrome or trisomy. Is that true and why can't they get it? They also have chromosomes.

Note that Down's syndrome and trisomy are two different things, where the former is a special case of the latter.

Animals can be generated with genetic defects similar to Down Syndrome, but not that exact condition, except in the case of great apes.
Down Syndrome is a kind of defect called a chromosomal abnormality, meaning that either there is an extra chromosome or an excessive repetition of the same genes on a particular chromosome. In the case of Down Syndrome, that repetition in on a region of the 21st chromosome. Similar abnormalities in other chromosomes are possible, such as the abnormality which causes Klinefelter Syndrome.
Although animals do have chromosomes, they have different chromosomes than human beings do. For example, a horse has 32 chromosomes whereas a human has 23. Apes are most similar to humans, having 24 chromosomes. Therefore, if trisomy is to be found, apes would be most likely to have it. Researchers have attempted to answer this exact question and there is a paper on the subject entitled "Conservation of the Down syndrome critical region in humans and great apes".
The result of this study was that the area on chromosome 21 in humans that is responsible for trisomy is found analogously on chromosome 22 in apes and that apes can, indeed, get Down Syndrome, if they have duplication of this region. There do appear to be apes that suffer from this condition. The band diagram for both chromosomes is shown below:

where "H" indicates human and "C" indicates chimpanzee.

It depends on the animal, some can get it, others cannot.
Down syndrome is the result of an extra copy of the twenty first human chromosome. So, it is a rather humanly genetic problem.
However, the closer an animal is to humans, the greater the chance of it being at risk of suffering from down syndrome.

There have been several chimpanzees found with Down Syndrome. As the syndrome is caused by an extra copy of a specific chromosome (chromosome 21 in humans) only animals closely related to humans have a similar syndrome. Extra copies of other chromosomes cause even more serious syndrome and most are not compatible with life. To study Down syndrome, scientists have created mice that have extra copies of the same genes found on human chromosome 21. These mice have some of the features of Down Syndrome.$^1$

There had been some uproar a couple of years ago around a tiger (they have 19 chromosomes) who supposedly had down-syndrome. The tiger "Kenny" was called the tiger with down syndrome, however that is not true. His appearance and mental retardation was due to aggressive inbreeding.

A great benefit of having two copies of each of our genes is that damaging recessive mutations are seldom expressed. However, where parents are closely related there is a high chance of them both carrying the same rare version of a gene, with a one in four chance their offspring will inherit it from both sides. With enough damaging alleles in common this becomes like a repetitive game of Russian Roulette.

References:
1. https://www.genome.gov/dnaday/q.cfm?aid=788&year=2008


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Black bumps on the cut surface of an avocado
I cut an underripe avocado in half and put half of it, without the pit but with the peel, in the refrigerator. A day later, I see very small black bumps along the cut surface. What are they? What causes them?

If this is off-topic here (which I doubt), please consider migration to [cooking.se] in lieu of outright closure.

That avocado does not look underripe to me...

This is on-topic, the answer is about plant anantomy

@nico, the parts closer to the pit were too hard to be palatable (to me), so either it was underripe or I like avocados overripe.

It looks to me (although I'd want to use a microscope to check) like the black dots are xylem. When you cut the fruit, you've severed the xylem and also exposed the flat surface. Three main things have then happened:

The increased surface area has led to the 'fleshy' part of the fruit contracting as the cells dehydrate.
The stiffer, lignified xylem tubes have retained their structure and have not contracted with the rest of the fruit, so they've become exposed.
The exposed xylem have blackened due to oxidation - this eventually happens to all the flesh but, again speculating here, the oil in the fleshy tissue might protect it from oxidation longer than the exposed xylem which don't have the oil coating.


text:
Whence fecal E. coli (et al.) if swallowing it is dangerous?
I don't know much about medicine, and I know even less about microbiology, but I understand that there are organisms in the lower gastrointestinal tract (and in feces) of a human, like Escherichia coli, that can cause dangerous disease if swallowed (or injected intravenously) by a human. So how did they get to the lower gastrointestinal tract in the first place? I assume either (or some combination of)

its prevalence in feces is less than I'm led to believe, so my question as to how it got there doesn't arise;
the percentage among cases of swallowed E. coli of those that lead to disease is low; or
E. coli-caused disease is more common than I'm lead to believe.

Does anyone know which of these is true? Or is it something else? (Perhaps they enter the gastrointestinal tract from below and not via swallowing?)

normal ecoli wont cause any disease.. certain pathogenic enterobacteria use the fecoral route for transmission.
blood infection (septicaemia) is a different thing altogether.

E. coli is mostly harmless; only a few strains are harmful.
I don't believe the route by which gut biota is established has been entirely established for any species but, for example, koala feed their faeces to their offspring to help them establish biota capable of digesting eucalyptus. It seems that a small proportion of ingested bacteria somehow survive passage through the stomach to the gut and then begin multiplying and colonising the intestines.
It's also important to realise that just because an organism is sometimes harmful doesn't mean it always is. There are many microorganisms that are pretty much ubiquitously found on or in your body which are capable of causing disease but only do so very rarely; usually when the body's defences have already been compromised (e.g. Pseudomonas aeruginosa, Candida albicans aka thrush, and so on).

There are many varieties of E. coli, with differences in their chromosomal DNA, different plasmids (independent loops of DNA that replicate autonomously inside the host cell and can be transferred between bacteria), or both.  Some are harmless, some beneficial, and some deadly.  E. coli of various kinds are found in the feces of cows, dogs, people, and more; but are also found in the environment.  Of course, even normally harmless bacteria can be harmful if they are in the wrong place in the body (e.g., in the blood) or if the body's microbial balance is out of whack.
Your second thought is correct:

the percentage among cases of swallowed E. coli of those that lead to
  disease is low

E. coli is found practically everywhere in homes, in concentrations ranging from very sparse to very dense. A good eye-opener is [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709336/], which makes it very clear that children (and adults) are exposed to E. coli constantly. We hardly notice until a strain comes along that happens to make us seriously ill.


text:
Diabetes-diabetes comorbidity
Is it possible to have both type-1 (insulin-dependent) and type-2 (non-insulin-dependent) diabetes mellitus? That is, to have both insulin resistance and zero (or negligible) insulin production? If not, why not? And if so, then how common is this (among humans with each type of diabetes)? Any information on why the comorbidity may be high or low is also most welcome.

I've been thinking about the "how common" part of your question, and it's tricky to awnser world wide as we see significant cultural variation.  Perhaps you would settle for prevalence in a group of countries you are interested in?

@AtlLED, any answer that answers that part of the question about any region would be most welcome.

Yes you could think of an individual as having both(1).  A good place to start looking at "newer" diabetes other than the classic 1 and 2 is latent autoimmune diabetes (LADA).  Though, I don't know if one would say you had no insulin production.  It would seem as though patients exhibit some characteristics of both types(2), and indeed there maybe a continuum possible(3) between ether "pure" type on each extreme.
(1) The type 2 diabetes-associated variant in TCF7L2 is associated with latent autoimmune diabetes in adult Europeans and the gene effect is modified by obesity: a meta-analysis and an individual study. Diabetologia. 2012 Mar;55(3):689-93. doi: 10.1007/s00125-011-2378-z. Epub 2011 Nov 23.
(2) Latent autoimmune diabetes (LADA) is perched between type 1 and type 2: evidence from adults in one region of Spain. Diabetes/Metabolism Research and Reviews 2013; 1520-7560.
(3) Latent autoimmune diabetes in adults: evidences for diabetes spectrum?.Chin Med J 2013;126:783-788

Latent autoimmune diabetes is interesting and even answers my question, but I was thinking more of, and looking for, cases of independently contracted types 1 and 2 diabetes.


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Where does meiosis II of oogenesis end exactly in tuba uterina - uterus?
I know that metaphase II ends at ampulla tuba uterina, but I am not completely sure where the telophase II ends. Is it in the triangular section of cervix uterii?
I just have an intuition that the thing is not ending at the ampulla, since there is some time to get to the uterus. The thing must happen before implantation to the uterus, since the egg is blastocyst at the stage.
2. When does meiosis II of oogenesis end exactly?

The location is exactly tuba uterina infundibulum, source, since the processes results in the following things before LH peak:

The correct placement of the uterine tube infundibulum upon the
  ovarian surface
The rupture of the follicle wall and the flow of the
  follicle fluid with the oocyte into the infundibulum
The inhibition of
  the maturation of further follicles


text:
Does prokaryotic transcription have activators / enhancer regions involved?
I am designing a biosensor, and I need to know whether prokaryotic transcription involves or can involve (if a gene needs to be regulated) enhancer regions. Also, where are enhancer regions located (how far away from the promotor), and when isolating a promotor region, how do you make sure you are also isolating these enhancer regions?

This question is too broad. Prokaryotic also have enhancers and repressors, of different kinds, their distance from the promoter may vary a lot. If you can list a particular gene you are interested in then I can have a look. In general, however, the right choice of promoter is often enough for a biosensor.

I am deriving the promotor from a silver resistance mechanism found on plasmid pMG101. The SilE is transcriptionally controlled by enhancers known as silS and silR (they are sensor / enhancer responder units). What I need is this promotor with neighbouring enhancer regions. I am not sure how to do this....

Good, you should edit your question then.

You can find the sequence of the plasmid, with all the detailed coding regions, here: http://www.ncbi.nlm.nih.gov/nuccore/AF067954 . Once you have the sequence you should design a pair of PCR primers to take out what you need.

Dang it, primer design. Thanks for your help!


text:
Energy input during ATP Dephosphorylation?
What is the energy input needed to break the phosphor bond during ATP Dephosphorylation? How and when this will occur?
Many thanks for your answers.
Edit 1: I know how much free energy (∆G) is released with the hydrolysis of ATP, but I dont know how much energy is needed to start the hydrolysis of ATP.
Updated Question/s:
To break the phosphorus bond of ATP, must there be some input energy? What is the amount of this energy? Else how can break any bond of ATP without the supplement any energy?

read into https://en.wikipedia.org/wiki/Dephosphorylation and https://www.boundless.com/biology/textbooks/boundless-biology-textbook/metabolism-6/atp-adenosine-triphosphate-71/atp-adenosine-triphosphate-349-12938/

I know how much free energy (∆G) is released with the hydrolysis of ATP, but I dont know how much energy is needed to start the hydrolysis of ATP. To break the phosphorus bond of ATP I think there must be suplied some input energy? What is the amount of this energy? Else how can break any bond of ATP without suplying any energy?

It sounds like you are asking about the activation energy of the ATP hydrolysis reaction. This paper estimates the activation at 35--39 kcal / mol, depending on details of the reaction mechanism. So yes, energy is needed to break the phosphate bond; this ensures that ATP does break down spontaneously (which would make it a rather useless molecule for cells).
Note that this concerns ATP hydrolysis without enzymatic catalysis. Enzymes that break the phosphate bond of ATP to drive reactions lower this reaction energy substantially.


text:
What is this creature?
I found this small creature in my water bucket which i filled from my water tank. I would like to know what kind of creature I have found here.
Features which ought to help for identification:

Size = 1 cm
2.Transparent or semi Transparent
4 thread like legs
6 tentacles
2 black dots possibly eyes
It can swim
Triangular tail (Fish Like)
Found in Karachi City, Pakistan.

I think I see 6 legs in the picture. Could that be?

I looks a bit like a shrimp (Caridea)

The triangular "tail" is actually the tail fan made of five parts. The central part of it is the final segment of the body and either side is composed of the two parts of a modified leg. Were you to investigate it more closely you'd thus discover it is not at all "fish like"

It looks very similar to the grey shrimps that can be catched on sandy beaches of Normandy (on the English Channel).

It looks very similar to freshwater shrimp from this site:


text:
What is the difference between these worms: Caenorhabditis elegans and Eisenia fetida?
I love worm composting (I use red wiggler worms), but wondering how similar or different the Caenorhabditis elegans and Eisenia fetida are?

It's possible that the gardening stack exchange might provide better answers if you're interested in their differences in regards to composting.

@Mys-721tx's answer (excellent, by the way!) is the type of response you'll get here.

Caenorhabditis elegans is a nematode. Eisenia fetida is an annelid. They both are lophotrochozoans (more specifically, trochozoans).
Time of Divergence
According to Michael Lynch, there are about 41 amino-acid substitutions per site between Annelida and Nematoda. According to Lynch's data, I estimated that this difference is roughly equal 100 million years.
Therefore, assuming the rate of molecular evolution was constant, their common ancestors lived about 100 million years ago.
Difference on Anatomy
Nematodes have pseudocoelom while annelids have eucoelom. Therefore nematodes do not have a vascular blood system. However, annelids do have one. Nematodes also lack a layer of circular muscle, which annelids have. This layer of muscle allows annelids to move by shorten and elongate their bodies.
C. elegans in particular does not have a female gender. There are only male worms and hermaphrodite worms. Only the male can fertilize other worms.
E. fetida is hermaphroditic and two of them can fertilize each other.

The time of divergence within the nematodes is already estimated to be >500 million years http://www.timetree.org/pdf/Blaxter2009Chap28.pdf -- so the divergence of annelids and annelids must be even earlier

What does "there are about 41 amino-acid substitutions per site" mean?

@MichaelKuhn It's probably true. Also notice that the Lynch paper was published in 1997, the sequence data he used might simply be not good enough.

@JackAidley Lynch compared 10 proteins encoded by mitochondrial genes between organisms in 12 phyla. The "substations per site" are the differences in protein sequences coded by homologous genes in two compared organisms.

@Mys_721tx: I don't see how you can have 41 amino-acid substitutions at a single site between two homologous genes. Surely you can have at most one substitution per site on each gene?

@JackAidley I think by site Lynch meant the entire gene.


text:
Will neurons live after the death of a human? If so, how long?
I don't know if this is correct or not, but I have heard this from a friend and I want to get a clear explanation about this.I hope there is some one who can help me.

This is called "necrobiosis".

isn't brain death the definition of death in many medical cases?

Yes, brain death is what medical professionals [generally] use to define death, as modern medicine is often able to keep a human body physiologically functioning for an extended period of time through technology and medication - and it is often possible to do this well past where the body would have originally died on its alone.  This is done when there remains hope that the body will recover and consciousness will return.  However, if additionally cerebral function is also convincingly lost (discussion of how we test for that is another topic), the concept of medical futility comes into play.

I think that depends somewhat on how the human dies - in particular on the conditions. If they die in a very cold environment (say at the top of some icy mountain range), they'll freeze and metabolic processes will slow down considerably, and so will cell death. But such hypothermia-based slowing down is a special case. Normally, if your heart stops or you are not getting oxygen to your brain (perhaps due to a stroke), your neurons will start dying pretty quickly. Within many minutes there will certainly be considerable permanent cell loss - certainly within hours. If oxygen is significantly depleted, ATP production will also significantly drop. If this happens, the various ATP-dependent processes will slow to a crawl (including the Na/K ATPase and other ion pumps and channels that are needed for maintaining and changing the voltage difference between the inside and outside of the cell). This in itself is bad enough as a lot of the enzymes and mechanisms that are dependent on the voltage difference will fail (and probably enough of a reason for many cells to start dying), but one of the effects of this is apparently an increase in the extracellular glutamate, which ultimately leads to (via NMDA receptors for example) an influx of calcium ions into the neurons. Too much of the calcium ions is once again toxic for a variety of the processes inside the cell and is an additional and big reason for neuronal cell death.
In short, as far as I know, neurons don't have a good time living without sufficient oxygen and therefore after a typical human death.


text:
Why does Glutamine have the symbol Q?
Spent a half hour googling this and the best I could find was this:

Now for some rhymes: Arginine = R. R we having fun yet?
  Asparagine = N The kNights of Ne say "Ne".
  Glutamine is a cute amine = Q
  I say "glutamate"/a former vice president says "glutEmate" = E
  ditto with AsparDic acid = D
  Fenylalanine makes tasty italien sausage = F
  Theres are two rings in tryptophan, and there are two v's in W = W
  Tyrosine = Y, Y? Because we love biochemistry. Source: One letter codes, rhyme and reason

Because glycine took G?

Did you want a mnemonic or did you want to know why it was assigned that particular code? The cute-amine was the mnemonic I learned.  It may be related to the rationale behind the code, but that could be something else entirely.

@dd3 I want to know why it was assigned that particular code

@Kevin That reasoning makes sense for Lysine (since its the letter before L) but Q is several letters away from G. Though I suppose Q could have been the next available. That may be the simplest answer, thanks.

The Biology Project from the University of Arizona provides the best explanation of Dr. Margaret Oakley Dayhoff's logic for the non-obvious single letter AA abbreviations:
Glutamine ~ Q-tamine therefore, Q

Initial letters of the names of the amino acids were chosen where
  there was no ambiguity. There are six such cases: cysteine, histidine.
  isoleucine, methionine, serine and valine. All the other amino acids
  share the initial letters A, G, L, P or T, so arbitrary assignments
  were made. These letters were assigned to the most frequently
  occurring and structurally most simple of the amino acids with these
  initials, alanine (A), glycine (G), leucine (L), proline (P) and
  threonine (T).
Other assignments were made on the basis of associations that might be
  helpful in remembering the code, e.g. the phonetic associations of F
  for phenylalanine and R for arginine. For tryptophan the double ring
  of the molecule is associated with the bulky letter W. The letters N
  and Q were assigned to asparagine and glutamine respectively; D and E
  to aspartic and glutamic acids respectively. K and Y were chosen for
  the two remaining amino acids, lysine and tyrosine, because, of the
  few remaining letters, they were close alphabetically to the initial
  letters of the names. U and O were avoided because U is easily
  confused with V in handwritten material, and O with G, Q, C and D in
  imperfect computer print-outs, and also with zero. J was avoided
  because it is absent from several languages.
Two other symbols are often necessary in partly determined sequences,
  so B was assigned to aspartic acid or asparagine when these have not
  been distinguished; Z was similarly assigned to glutamic acid or
  glutamine. X means that the identity of an amino acid is undetermined,
  or that the amino acid is atypical. "Nomenclature and Symbolism for Amino Acids and Peptides"

U is the code for selenocysteine.

IUPAC-IUBM add it in 1999.http://onlinelibrary.wiley.com/doi/10.1046/j.1432-1327.1999.news99.x/pdf

I know, it's just that I did my PhD on selenoproteins and everyone forgets selenocysteine and that makes me sad :(.


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What species of spider is this?
I'm trying to find out what kind of spider is this little fellow:

It really seems to like our garage and is the bane of my girlfriend (as evidenced by all the screaming when on two occasions one got into our home somehow). I was never able to spot this kind outdoors, which is rather odd (there are plenty of Araneus diadematus spiders in the area which are fairly easy to spot).
It's hard to tell on the photo, but these spiders seem rather big (at least as far as spiders in Poland I was able to spot go)... somewhere around 5cm at least (legs included)? They really do make for rather large, black spots against an otherwise white garage wall.
I'd really like to find what kind of species this is so that I can, hopefully, convince my GF that it's harmless to humans. Unless it isn't, in which case I'll start getting scared of walking into our garage. ;)
PS. We live in Poland, Poznań.

This is a giant house spider, Eratigena atrica complex group. It could be one of the species of E.atrica, E.duellica, E.saevus. It is too dark for E.agrestis.
Eratigena is a genus spun-off from Tegenaria. But the other suggested answers of T.domestica is a spider that remains in the Tegenaria genus. This spider in the question does not exhibit the leg-bending (annulations) that are present in T.domestica.
The abdominal pattern is the classic 'herringbone' pattern that places this in Eratigena, while Tegenaria abdominal patterns are a different sort of a spotty pattern.
The habitat of giant house spiders overlaps fairly consistently with T.domestica - human-made structures, indoors, garages, etc.
Giant house spiders are typically larger than E.agrestis and T.domestica, particularly in their leg spans.

I think this is just
Tegenaria domestica. I am from Czech republic and this is really big and kinde everywhere. Specialy in garages.

Just a minor note - it would be helpful if the link wasn't for the mobile version of Wikipedia and was for an English article...

I am sorry for that but I thought when you are from Poland u would prefer something a bit closer to your language.

Well, no offence, but those are still different languages. ;) Plus, this is StackExchange, which is English-based, AFAIK.

This is a giant house spider, not Tegenaria

I'm not a European spider pro, so although I think it looks rather like a Tegenaria, I can't be positive it isn't something else that I'm unfamiliar with.
However, I can state confidently that it is not any of the problem biters known on Earth.  In Europe, you're going to be careful around any of the Black Widow group (Latrodectus spp.) and perhaps be cautious if you should come across a Mediterranean Recluse (Loxosceles rufescens) - but this isn't either of those possibilities.  Widows are small, globular cobweb spiders with relatively short, arched legs, and Recluses are very plain spiders with a dark central 'fiddle' mark on the 'head'.
By elimination, if it isn't any of the known problem biters, it's harmless.
However, what you can do to get a better identification, is to submit your photo to Ed Nieuwenhuys at his website which deals with European spiders.


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Is this Heracleum sosnowskyi?
There's a relatively big scare in local news about the Heracleum sosnowskyi plant, considering how dangerous it can be.
I was strolling through the park when I noticed these plants - the ones I photographed were rather small, but there have been a lot bigger examples in the park as well. For reference, I live in Poznań, Poland.
I have a feeling this isn't Heracleum sosnowskyi, but the only reason I'm thinking this is because it was in a local park where there are a lot of people / kids, and if there were any dangerous plants there there would be an uproar... but I'd rather be sure, thus I'm posting this question.

Is this Heracleum sosnowskyi?

Just out of curiosity, are the leaves belong to this plant? Although it looks like  "Stalin's revenge" to me. read https://en.wikipedia.org/wiki/Heracleum_sphondylium Similar species.

Given what I know about Heracleum sosnowskyi I didn't want to touch the thing, and I took the photos with my phone (questionable quality, I know). As such, I cannot really tell which leaves belong to the plant in question and which belong to other, nearby plants @DevashishDas...

Added a source for the danger posed by the plant (and related members of the genus).

Where were the pictures taken? Species ID questions are very hard to answer without that info.

@fileunderwater I'll add that information to the question.

No, I don't think it looks like Heracleum sosnowskyi. To me, the plant in your pictures looks similar to Angelica sylvestris (which is common in Poland), but there are many species in Apiaceae with a similar apparence and I'm not familiar with all of them. Species in the Heracleum genus has leafs that are "lobed" and all leaflets aren't as separated as the plant in your pictures (overall, the leafs of Heracleum look quite different), and the stem is usually "swollen" where the leafs connect (i.e. the leaf stems are swollen). Plants of Heracleum sosnowskyi (and H. mantegazzianum) are also much larger, and they often have a fussy apparence because of the bristle hairs.
Angelica sylvestris (picture from from wikimedia commons)

I'd say it's an imposter, but depending on the stage of it's life cycle, characteristics may differ. The following webpage lists identifying factors for giant hogweed, as well as some plants that may be mistaken for it (but of course, they aren't). The lack of purple splotches and white hairs around the stalk bases, and leaves are signaling to me that this is not giant hogweed. It looks like it may just be wild parsnip. Take a look at that webpage, giant hogweed is quite... giant.

The reason I was worried is that before something gets big... it starts out small. ;) Unless only fully grown plants are harmful... PS. I'm getting a time-out on that page...


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Clarification on the "orientation" of chromosomal rearrangements
I need some clarifications on the concept of "orientation" in case of chromosomal rearrangements.
Given a deletion event on a chromosome for example, is the resulting DNA at the breakpoint always in TH (Tail to Head) orientation? Do all duplications lead to HT orientation? And in case of translocations, inversions, etc..?
Can someone give a clear definition of "orientation", and make some examples?
Here some specific examples found in the Cosmic database:
CRC-3  large_intestine  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  28066  0  2  53774826  53774826  +  2  53775947  53775947  +    21892161

CRC-3  large_intestine  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  28072  0  2  60783417  60783417  -  2  60786447  60786447  -    21892161

0006_CRUK_PC_0006_T1_DNA  prostate  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  113193  0  18  60375963  60375963  +  18  77010169  77010169  -      538

0006_CRUK_PC_0006_T1_DNA  prostate  NS  carcinoma  adenocarcinoma  intrachromosomal inversion  113314  0  7  153608258  153608258  -  7  153610727  153610727  +      538

As you can see, they have inversions having all of the possible strand orientations, '++','--','+-','-+'.
How is this even possible?! How to convert to H/T orientation in this case?
P.S. This is the description of the header of the data:
               HEADER[IDX] : IDX : DATA[IDX]
               Sample name :   0 : 0006_CRUK_PC_0006_T1_DNA
              Primary site :   1 : prostate
              Site subtype :   2 : NS
         Primary histology :   3 : carcinoma
         Histology subtype :   4 : adenocarcinoma
             Mutation Type :   5 : Interchromosomal unknown type
               Mutation ID :   6 : 113196
          Breakpoint Order :   7 : 0
         GRCh37 Chrom From :   8 : 6
  GRCh37 Location From min :   9 : 129148581
  GRCh37 Location From max :  10 : 129148581
        GRCh37 Strand From :  11 : -
           GRCh37 Chrom To :  12 : 7
    GRCh37 Location To min :  13 : 153610712
    GRCh37 Location To max :  14 : 153610712
          GRCh37 Strand To :  15 : -
     Non-templated ins seq :  16 :
                 Pubmed ID :  17 :
                  ID_STUDY :  18 : 538

Adding a NCBI bookshelf link.

I think the picture will help you. In fact, to determine which kind of rearrangement for the chromosomal, we need to define an "orientation". However, this orientation is not fixed. It is a definition compared with the two chromosomes before and after the rearrangement. As the picture shows, the duplicated sequence after rearrangement should be in the same orientation, if one of them not, it should be described as "inversion after duplication". For deletion, there is no difference in the orientation if the remain parts still in their previous pattern. The key point to understand,  is to check the sequence before and after the rearrangement and find difference(s) between them, then compare to this picture(which is the definition of rearrangement) to find if the chromosome has one or multiple rearrangements.
Hope this could help you.

Translocations are often between two different chromosomes (that situation is not depicted here).


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

Welcome to Biology, this question is about treatment of disease, a purely medical subject which is off-topic here (see this meta post on our discussion on that. Questions about the biological basis of diseases are welcome, but questions about treatment are off-topic here.

lots of biologists and biochemists study this topic.  why be so over defined?  This question should be answerable here. in my opinion.  The first line treatment for such things is to use rare and expensive antibiotics that still can work like Vancomycin.  antibiotic resistant strains keep popping up because (among other reasons) people don't take all their antibiotics and this creates an environment for more antibiotic resistance to develop through selection.  SEe http://www.ted.com/talks/paul_ewald_asks_can_we_domesticate_germs.html

A second vote for reopening. The question is not "What drugs should I use to treat X", the question is how they are treated. That question is very much in the domain of microbiology and epidemiology, neither one of which are medical fields.

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

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

Combinations of antibiotics are now becoming essential due to quite widespread resistance to single antibiotics in bacteria such as MRSA, E coli, K pneumoniae and P aeruginosa. Physicians often give two or three antibiotics. However, few of the combinations used have actually been rigorously tested for safety and efficacy (hence widespread side-effects, as the former icu nurse reported above). The odd thing is that there is only one approved combination of two antibiotics available for Gram-negative bacteria, the combination of trimethoprim and sulfamethoxazole. This seems to be a very obvious gap that needs filling. Which other dual combinations would be very useful?

References for your claims are missing.

As a former icu nurse and also a molecular biologist who specialized in genes for antibiotic biosynthesis I can tell you theory is world's apart from practicality. New antibiotics are least tested agents and very expensive, often the patient suffers more from the antibiotics side effects than they do from the infection. Monotherapy is basically old hat now, use of a single agent to treat massive drug resistant infection only increasea the odds of  increasing drug resistance. The general rule now is combitherapy using two or more cheaper and better known antibiotics and save newer agents as a drug of last resort for future cases. We are rapidly evolving into a post antibiotic Era according  to Dr Stuart Levy https://www.amazon.com/Antibiotic-Paradox-Antibiotics-Destroys-Curative/dp/0738204404

see my common on your other answer... please include some references to back up your claims - thanks!


text:
How do you break up cell clumps when passaging?
I am working with HepG2 cells, and they really like to form clumps.  Pipetting up and down in TrypLE does not seem to be very effective in breaking them up.

Rob: can this question be answered by Google?  If it can, please come back and post an answer to your question.
Here's a hint: http://hepg2.com/index.html

I find that I only get clumps (with HeLa and similar cell types) if I leave them in Tryple too long. Generally I leave them in room-temp (not hot) Tryple for ~8 minutes, then I angle the dish, lid off, so that I can see the "sheen" of cells on the dish (this happens in the hood, of course). Then I blast the sheen with Tryple using a 1000ul pipetter, which de-adheres the cells. These are generally much less clumped than if I let the Tryple de-adhere the cells.

Cell clumps that not dissociate with rigorous pipetting might very well be caused from free DNA in your cell suspension (i.e. if you trypsinized for too long). Free DNA attracts cells which bind altogether forming clumps.
Two possible ways to get rid of these clumps:

Centrifuge your cell suspension at 5000 rpm for 2 minutes with acceleration on (at 4) and brake (at 3) allowing the way heavier molecules to precipitate. Then aspirate ~0.5ml from the top of the suspension and transfer to a new flask. Repeat if needed.
Use DNAse at concentrations from 20-100µg/ml (concentration resulted from personal use) as long as you will not intend to carry out DNA related experiments.

You can always go back and buy a fresh ampule of the cell line you want clumps free :)

In some protocols for setting up primary cultures (for example from mouse bone marrow or rat endometrium), there is a step that requires pushing cell suspension through a large needle to get rid of clumps. Of course, this carries a high risk of damaging the cells, so sometimes collagenase is used instead.
It might also be helpful to wash your cells with PBS without ions before passaging and use tripsin with EDTA. That should get rid of at least some calcium from the plate, so that action of adhesion proteins would be inhibited.


text:
Which extinct creatures were most genetically distant from everything alive today?
The more distant the common ancestor of two creatures the more genetically distinct the creatures will be. For example I am more genetically distinct from a mushroom than an ant. I am more genetically distinct from an ant than a fox. Etc.
Extinction in the deep past has cut off some evolutionary branches. Which extinct creatures (including all living organisms) were most genetically distinct (alien) from living creatures today?

I vote for the Edicaran fauna.

from http://ediacaran.blogspot.com/2008/11/introduction-to-ediacaran-fauna.html
from en.wikipedia.org/wiki/Ediacaran_biota

Most macroscopic fossils are morphologically distinct from later
  life-forms: they resemble discs, tubes, mud-filled bags or quilted
  mattresses. Due to the difficulty of deducing evolutionary
  relationships among these organisms, some palaeontologists have
  suggested that these represent completely extinct lineages that do not
  resemble any living organism. One palaeontologist proposed a separate
  kingdom level category Vendozoa (now renamed Vendobionta)[8] in the
  Linnaean hierarchy for the Ediacaran biota. If these enigmatic
  organisms left no descendants, their strange forms might be seen as a
  "failed experiment" in multicellular life, with later multicellular
  life evolving independently from unrelated single-celled organisms.[9]

No-one can say what the DNA of the Edicaran organisms were, or whether they were related to what came after.  Apparently these fossils do not resemble the fossils of the subsequent Cambrian or much of anything else.  The triskelion fossil I put in here looked the coolest to me.  If they were a "failed experiment" or some sort of false start on multicellular life, they might have been totally alien.

I think this works for Eukaryotes. But I wonder if there are bacteria that are further still. Though, It could be hard to tell.

Stromatolites are fossils of bacteria colonies.  Some people think the edicaran fauna is the same sort of thing.

The very first ones to go extinct would be the most genetically distant; at that distance, the issue becomes more "how do you define life?" or "how do you define a species?" to get the actual most distant. Overall, it sounds like an interesting question, but it really isn't: extinction isn't special, it's the norm. There are most certainly extinct organisms or pre-organisms of some level of development that never contributed to the existing life on earth and have no descendants or relatives.

The first to go extinct could have been a part of a family or genus that still exists today. So, this isn't just about who went extinct first?

@futurebird No, it's certainly not. The first life to go extinct would have been relatives of the very earliest life to exist; these would also be the most genetically distinct, because everything since then is more genetically related than anything extant now is to the first life to exist.

that make sense do we know anything about these organisms?


text:
What is the difference between muscle tension and muscle tightness?
Is there any difference between muscle tension and muscle tightness?
I want to study the relation between forearm muscles tightness/tension and tendinopathy (specifically, medial and lateral epicondylopathy) in humans. In that context, I wanted to understand whether muscle tension and muscle tightness are synonymous, and if not what the difference is.

In what context do you mean? It's not clear what you are asking.

@kmm Thanks for the comment. I want to study the relation between forarm muscles tightness/tension and tendinopathy (specifically, medial and lateral epicondylopathy) in humans. In that context, I wanted to understand whether muscle tension and muscle tightness are synonymous, and if not what the difference is.


text:
How does an excessive amount of beta carotene affect skin colour?
How much is the daily need of beta carotene and how many carrots have to be eaten in order for one's skin to turn "orange".
I found 2-4 mg/ day as basic need, 30 mg daily over three weeks turns white skin orange. Is this correct? And what is the reason behind this?

How much beta carotene does it take to change someones skin colour?
To turn the skin yellow, rather than orangish, a person would have to eat about 10 carrots a day for a period of at least two weeks, consuming at least 51 grams of beta-carotene each day. The average carrot contains about 5 to 6 milligrams of beta-carotene

What is the reason behind this?
A very high diet of food which contain carotenemia (such as carrots, squash, sweet potatoes and others) can cause skin discoloration. The skin, and especially the palms of the hands, turn yellow, rather than orange. This change in skin colour fades and eventually disappears when the individual's diet changes back to normal.

Carotenoderma is deliberately caused by beta-carotenoid treatment of certain photosensitive dermatitis diseases such as erythropoietic protoporphyria, where beta carotene is prescribed in quantities which discolor the skin.

What does an excess of carotenoids do?

An excess of carotenoids, being eliminated via sweat, may cause a marked orange discoloration of the outermost skin layer. This benign and reversible condition – which is most easily observed in light-skinned people and may be mistaken for jaundice – is known as carotenosis or carotenoderma.

sources:

https://en.wikipedia.org/wiki/Carotenosis
http://www.webmd.com/vitamins-supplements/ingredientmono-999-beta-carotene.aspx?activeingredientid=999&
http://umm.edu/health/medical/altmed/supplement/betacarotene
http://emedicine.medscape.com/article/1104368-overview


text:
What are golgi blobs?
From a general google search I have come to know that golgi 'blobs'(also referred to as "golgi haze") are tubular vesicles formed during the interphase of mitosis.
I would like to be reassured and also learn more about this topic. If possible please include a diagram in your answer.

What are golgi?

Stacked array in the cisternae which are ought to connect vesicles and tubules
Made of >1000 different proteins
Has the ability to transform/alter in response to a cellular stimulation such as mitosis

Fragmentation of golgi during mitosis

During interphase, the Golgi receives secretory cargo from the ER via the COP II vesicle formation pathway. Depending on their nature, secretory cargo then travel through the Golgi apparatus by a combination of vesicular transport involving COP I vesicles and cisternal maturation. A retrograde COP I vesicle pathway connects Golgi cisternae and the ER to allow recycling of Golgi enzymes and integral membrane proteins of the transport machinery such as the SNAREs. Two models have been proposed to explain the fate of the Golgi in mitosis. The first is the direct fragmentation model, where Golgi cisternae are consumed by continued COP I vesicle budding in the absence of membrane fusion, which is blocked in mitosis. This generates a pool of tubules and vesicles (Golgi haze) containing Golgi enzymes and structural proteins. The second is the ER recycling model, where forward transport into the Golgi by COP II vesicles is blocked, but COP I recycling back to the ER continues until Golgi proteins are redistributed to this compartment. Some Golgi proteins may then exit the ER via the COP II pathway, but these vesicles are unable to fuse with a Golgi compartment during mitosis, and remain in equilibrium with the ER.

A more detailed outline of the process of fragmentation of golgi apparatus can be found here and here

As I know "golgi blobs" are also referred to as "golgi haze".
Sources:

http://www.clfs.umd.edu/classroom/mocb639/Hamza_Golgi_Apr5_2005.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175146/
http://www.cbi.pku.edu.cn/chinese/documents/cell/xibaoshengwuxuecankaowenxian/cocb/15/15-4/15-462.pdf

@SanjuktaGhosh You're welcome. Let me know if you have any follow-up questions.

Golgi blobs are larger fragments and are resolvable by light microscope.  The golgi haze is not resolvable and just causes scattering of light in the microscope as if it were a fog.


text:
Do they have scales?
Do Channa striatus and Channa punctatus have scales?
They are both snake headed species of the genus Channa. I'm trying to figure out the distinguishing characters.

Did you try to google the species names and the word "scale" and either look at pictures or one of the first links. Here is the search result I got with "scale Channa-striata" (the answer is in the second link).

I'm sorry. I shouldn't have created this post in the first place.

Channa striata
Environment/climate/range

Freshwater; brackish; benthopelagic; pH range: 7.0 - 8.0; dH range: ? - 20; potamodromous (Ref. 51243); depth range 1 - 10 m (Ref. 2686), usually 1 - 2 m (Ref. 4515).   Tropical; 23°C - 27°C (Ref. 1672), preferred ?; 35°N - 18°S

Length at first maturity / Size / Weight / Age

Maturity: Lm 18.0, range 23 - ? cm
  Max length : 100.0 cm SL male/unsexed; (Ref. 2686); common length : 61.0 cm TL male/unsexed; (Ref. 44091); max. published weight: 3.0 kg (Ref. 40637)

Short description

Dorsal spines (total): 0; Dorsal soft rays (total): 38-43; Anal spines: 0; Anal soft rays: 23 - 27. Body sub-cylindrical; head depressed; caudal fin rounded (Ref. 2847). The dorsal surface and sides is dark and mottled with a combination of black and ochre, and white on the belly; a large head reminiscent of a snake's head; deeply-gaping, fully toothed mouth; very large scales (Ref. 44091).

More information here

Channa punctata
Environment / Climate / Range

Freshwater; brackish; benthopelagic; potamodromous (Ref. 51243).   Tropical; 22°C - 28°C (Ref. 2059), preferred ?

Size / Weight / Age

Max length : 31.0 cm TL male/unsexed; (Ref. 4833); common length : 15.0 cm TL male/unsexed; (Ref. 6028)

Description

In Sri Lanka, the young have a chocolate-coloured body with three yellow stripes which are lighter ventrally. There is also a golden lateral stripe from the snout, through the eye to the middle of the caudal fin. At 13 mm, black body scales appear along with three dark bands on the caudal fin. Adult colouration arrives at a size of 70 mm upwards ( Deraniyagala 1929 ).

More information here and here


text:
How does reversibility of lactic acid fermentation work?
For the production of lactic acid we need pyruvate from glycolysis.
This process is known as lactic acid fermentation. One of the features of this process is reversibility. How does this reversibility work?

The enzyme catalysing this reaction in mammals is lactate dehydrogenase of which there are two major isoforms: LDHA and LDHB. The general reaction scheme can be shown as:

In muscles LDHA reduces pyruvate to lactate consuming one NADH. This gets rid of the electrons which would normally go through the respiratory chain. The lactic acid is then transported to the liver where it is turned back into pyruvate by LDHA producing one NADH. This is know as the Cori cycle.
Both enzymes however are very similar and can catalyse the reaction into either direction, they are just slightly different in structure which make them have a greater affinity for pyruvate or lactate.

You need to add the H+ to the left hand side of your equation.

Thanks for the comments, I adjusted the text and figures


text:
What is so difficult about mushroom cultivation?
I am just wondering why it is so cheap and easy to cultivate this type of mushroom: Agaricus bisporus, however a typical forest mushroom such as Boletus edulis  has to be harvested. What makes one mushroom species much more difficult to cultivate compared to another?

Like many other strictly mycorrhizal fungi, B. edulis has to date eluded cultivation attempts.[107][117] The results of some studies suggest that unknown components of the soil microflora might be required for B. edulis to successfully establish a mycorrhizal relationship with the host plant.[118][119][120]

What makes some mushrooms easy to cultivate is that they grow profusely, they aren't tree symbionts, where as sponge gilled culinary musrhooms are symbionts. Cheap mushrooms can easily be controlled with temperature and or light to fruit year round with minimal labour, they have cheap and easily obtainable substrate, and that are very appreciated for cooking and transportable. Also Argaricus doesn't even need light as a signal to trigger fruiting bodies and can be grown in complete darkness, and the harvest can be with robots not even manual, https://youtu.be/iBENPHl4mBA?list=PLw1YvKXHZymsoJbFGRI_OFSWZ5Wwg_fVD, which makes them particularly cheap.
Mycorrhizal mushrooms like boletes and many forest associated mushrooms differ from Argaricus and
commonly commercially produced saprotrophic
types (such as shiitake and button mushrooms).
Saprotrophic mushrooms live and feed on dead
organic matter, whereas mycorrhizal mushrooms
grow in a close, symbiotic (mutually beneficial)
relationship with the living roots of a tree.
Field and dead wood mushrooms generally have simpler substrate that can be transported in boxes in the dark, and almost all cultivated mushrooms are of saprotrophic.
Saprotrophic nutrition /sæprəˈtrɒfɪk, -proʊ-/ or lysotrophic nutrition is a process of chemoheterotrophic extracellular digestion involved in the processing of dead or decayed organic matter. It occurs in saprotrophs or heterotrophs, and is most often associated with fungi (for example Mucor) and soil bacteria.
That's slightly different to Saprophytes are more generally plants which live on dead or decomposing matter and which can also be more accurately be called myco-heterotrophs because they actually parasitize fungi, rather than dead organic matter directly.
They say that Argaricus was first discovered in 1650 on melons! but as any theory, there were probably precedents. Any farmer that discovered sizeable populatons of fungi near horse and cow middens could have easily have experimented with placing some compost in a basement.
Morelles and truffles are such expensive mushrooms that the man who learns how to grow big truffles will be payign himself up to a 1000 dollars a kilo for his efforts, it illustrates the difficulty of micorrhizal cultivation.
If you are interested in fungi there is a fascinating ted talk about them from Paul Stamets.
and
https://en.wikipedia.org/wiki/Mycorrhiza


text:
Why do Hot/Cold drinks taste sweeter once returning to room temperature?
Now, I know this is a very bizarre question, and I tried to find a correct exchange for this, but it might relate to biology/science as it being our taste buds and everything.
I am so sorry if there is a better exchange for this, but (I hate using this excuse) I'm new to StackExchange, so please be gentle and point me in the right direction.
Now, to meat and bones (Unintended pun; meat...bones...biology hehe), over the last few days I have noticed that after my drink returning to room temperature, it is so much sweeter than it originally tasted.
Drinks

Hot Tea - I normally only add 1-2 teaspoons of sugar into my tea and it tastes just right, though after taking a sip when it had returned to room temperature, it tastes about 3 or 4 times sweeter than when it was hot/warm. (Milk)
Iced Tea (Bubble Tea) - Just today I had a bubble tea with the smallest amount of sugar possible, it was still too sweet but I stuck with it, and again when it reached room temperature, it was almost unbearably sweet. (No milk)
Slurpee - Again, after returning to room temperature, it is extremely sweet, with it being much lighter with respect to sweetness.
Hot Coffee - Come to think of it, I have also had the same experience with sugared coffee.
Coke - Also, when coke (or any other soft drink) is flat and room temperature, it also produces the same super sweet taste.

So, I tried to think of possible reasons why this happens but, I cannot think of any possible explaination other than magic.
If anyone knows why this might happen, it would be greatly appreciated since I am tripping out trying to figure out why this happens!

This doesn't address all your issues, but with 1,2, and 4 - I would bet that the sugar is simply sinking (e.g. coming out of solution) to the bottom of the cup. If you drink your beverage as it comes to room temperature, a substantial portion of the sweetener has descended to the bottom of the cup where you are now drinking from. Regarding 3 - ice is less dense than water, so as your drink turns to liquid, there is more sugar per cubic centimeter than before. In neither case is the temperature making the beverage taste sweeter, it is just a coincidence with the sugar concentrations.

Generally, cold suppresses sweetness. As an example, consider soft drinks that are usually served cold: they taste sweeter when warm (like you said with your examples of drinks).
Our taste receptors send a stronger signal to the brain when activated by warmer substances and so the perception of sweetness, in this case, is lessened when we consume cold food or drinks.
There are taste receptors on the surface of our tongue which refer to the proteins TAS1R2 and TAS1R3 which, which bind to the “sweet-tasting” molecules.
When the molecules bind to the receptors, they trigger a series of actions which increase the number of positively charged potassium ions (K+) in the cell to which the receptor is attached. In order for the signal to continue along to the brain, the cumulative positive charge of the potassium ions must be high enough to activate a TRPM5 channel into the cell, so that calcium ions (Ca2+) can pass through. The Ca2+ ions are required for the release of neurotransmitters which send the signal. This channel requires a much lower positive charge for activation when it is warm than when it is cold.
Now if you were to put, e.g., a cold coke into your mouth, it decreases the temperature of the entire tongue and consequently the TAS1R2 and TAS1R3 proteins, and the TRPM5 channel. This will result in it requiring a greater positive charge in order for the signals to travel to the brain. This means overall also less signals are even received by the brain, thus resulting in us perceiving less sweetness.
Sources:

http://www.ncbi.nlm.nih.gov/pubmed/25963040
http://www.ncbi.nlm.nih.gov/books/NBK236241/
http://www.foodnavigator.com/Science/Food-temperature-affects-taste-reveal-scientists
http://www.ncbi.nlm.nih.gov/pubmed/17180301

What about hot drinks?

@moonman239 Upvoted your comment, because the answer really does not answer that. Yet, my guess only could be that is due to the damage caused by hot. Even if you drink something sweet and not hot (only room temperature) right after drinking hot drink, it still will not be as sweet as usual.

Don't both hot and cold reduce nerve activity and conduction rate? Isn't that why we apply hot water compress or ice to reduce pain ?  Maybe pressure reduces it as well since we grasp tightly the area of pain

I found an article (1) which may help you understand what happened on your tongue:
Light cooling from 37 to 21°C of beverages increases your sweet taste adaption, but not actual sweetness of your drink!
Another article (2) states, that a certain receptor for sweet taste perception is heat-activated.
So I guess there is no universal rule for any drink, you must look into further detail what the sweeteners are and which receptors would detect the taste.
(1) http://www.ncbi.nlm.nih.gov/pubmed/25963040
(2) http://www.ncbi.nlm.nih.gov/pubmed/17180301