text:
Does orgasm cause a dopamine crash?
There's some theory around that orgasm will cause a dopamine surge and drop, and that this can lead to a period of low mood or depression. A come down.
Is this true, does orgasm have a negative psychological consequence ?

To answer your last question, I very much doubt it's true in general. It does have unplesant effects in some people though. Form a popsci account

He [a psychoanalyst] was puzzled about a 24-year-old man whom he viewed as psychiatrically healthy except for intense depression that lasted for several hours after sex. [...] Could it be that some patients have particularly strong rebound activity in the amygdala after orgasm that makes them feel bad?

And this post-coital dysphoria can happen to women too, for which there is some prevalence data:

Forty‐six percent of respondents reported experiencing PCD symptoms at least once in their lifetime with 5.1% experiencing PCD symptoms a few times within the past 4 weeks.

"No sex before game day" was a tenet in some sports psychology/physiology corners, but more recent research failed to find significant differences of sex acts on mental performance... at least in (healthy) athletes. A 2016 review notes

Despite the major differences found in the recovery phase, where higher values of HR [heart rate] were found 2 h after sexual intercourse, no significant differences were found in workload achieved and in mental concentration of the athletes.

And, yeah, I know sex doesn't necessarily mean orgasm, but it seems close enough to mention.


text:
Is the Opah a warm blooded fish?
In 2015 many sources, including USA TODAY, Discover Magazine, and National Geographic, ran stories about the Opah fish (Lampris guttatus) being warm blooded.

Image Source: http://discovermagazine.com/2016/janfeb/58-meet-the-first-warmblooded-fish
Headline from USA TODAY 5/14/2015:  First warm-blooded fish identified

In a discovery that defies conventional biology, a big fish that lives
  deep in the Pacific Ocean has been found to be warm blooded, like
  humans, other mammals and birds.

Article from National Geographic 5/14/2015: Meet the Comical Opah, the Only Truly Warm-Blooded Fish

The opah’s wonderful nets are in its gills, and that makes all the
  difference. The blood vessels carrying warm blood from heart to gills
  flows next to those carrying cold blood from the gills to the rest of
  the body, warming them up. So, while a tuna or shark might isolate its
  warm muscles from the rest of its cold body, the opah flips this
  arrangement. It isolates the cold bits—the gills—from everything else.
This allows its huge pectoral muscles, which generate most of its
  heat, to continuously warm the rest of its body. It also keeps that
  heat with the help of thick layers of fat, which insulate the heart
  from the gills, and the pectoral muscles (which produce most of the
  animal’s heat) from the surrounding water.

According to the Merriam-Webster Dictionary warm blooded is defined as:

having warm blood; specifically : having a relatively high and
  constant internally regulated body temperature relatively independent
  of the surroundings

This definition seems to agree with the stories about the Opah fish being warm-blooded.  However, it seems different from humans, mammals, and birds which generate and maintain body heat when muscles are at rest too.  Are there different definitions of warm-bloodedness that would fit the Opah fish that is different from humans, mammals, and birds?

Did you say warm-blooded?
Despite the definition you cite from Merriam-Webstre Dictionnary, the term warm-blood is very unclear. The correct terms are endo-, exo-, poikilo- and homeo- therm. In short…
Source of heat

endo = inside
exo = outside

Variation in inside temperature

Poikilo = varies
homeo = does not vary

Please note, that these terms refer to extreme cases. There are organism which temperature are extremely constant (homeotherm), organisms which temperature are extremely variable (poikilotherm) and anything in between.
Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. Also, some organisms manage to keep a quasi constant body temperature via behavioural actions (moving to the sun when cold, going into the water when it's hot). A fun example (although debated to what I've heard) are the large dinosaurs that are thought to be homeotherms because their metabolism produce some heat and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaur homeo-endo-therm individuals.
Opah fish
From what your second quote, it sounds like the Opah fish is endotherm. It is unclear from the quotes whether Opah fish are homeothermic.
Wegner et al. (2015) is a great read on the subject. Below is their abstract but I recommend reading the whole paper, it is easy to read and is very short (3 pages).

Endothermy (the metabolic production and retention of heat to warm body temperature above ambient) enhances physiological function, and whole-body endothermy generally sets mammals and birds apart from other animals. Here, we describe a whole-body form of endothermy in a fish, the opah (Lampris guttatus), that produces heat through the constant “flapping” of wing-like pectoral fins and minimizes heat loss through a series of counter-current heat exchangers within its gills. Unlike other fish, opah distribute warmed blood throughout the body, including to the heart, enhancing physiological performance and buffering internal organ function while foraging in the cold, nutrient-rich waters below the ocean thermocline.

In the whole, paper, I could not find a mention of how much variation in body temperature there is. They highlight however that the point of such adaptation is for foraging in cold waters suggesting that they would just make a boost of temperature in extreme cases but not necessarily actively maintained a constant temperature otherwise. I would tend to think that Opah fish are much more variable than birds or mammals. To reinforce my believes, in the wikipedia > Opah fish it is written (without reference unfortunately) "The opah is not homeothermic like birds and mammals".

FYI, this answer was written by partially recycling this other answer of mine.

IIRC, the opah is not unique.  Other large fish like tuna and swordfish also have various temperature-regulating mechanisms for keeping parts of their bodies (like eyes & brains) above ambient temperature: https://www.ncbi.nlm.nih.gov/pubmed/7079766

@jamesqf: That is correct.  However, from how I'm reading these articles, the opah is set apart because it heats it's entire body instead of just parts of its body.

source: Stack Exchange

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

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text:
What kind of grasshopper-like insect is this?
We found this thing in our basement. Not quite an average grasshopper. Any ideas?

Please include your location, or at least a country and state. That will make your question much easier to answer.

Looks like a cave cricket to me!

This is potentially a duplicate of the question asked here; if not a duplicate, the species involved appear closely related.

That is a "cave cricket", in the family Rhaphidophoridae. These are common in basements, and harmless.

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


text:
Proteins that cannot form biofilm?
I am trying to build a machine learning training set for bacterial protein sequences that form biofilm, and that cannot. I collected the positive sequences from the GO ontology website but for negative sequences I am not sure which sequences to incorporate into my training set.
Can anyone point me to resources for proteins sequences that are known to be not capable of forming biofilms?

Intracellular proteins cannot form biofilms. Additionally, many (but not all) extracellular proteins contain an N-terminal cleavable signal sequence.

Lory (1992) Determinants of extracellular protein secretion in Gram-negative bacteria. J Bacteriol 174: 3423-3428.
https://www.ncbi.nlm.nih.gov/pubmed/1592799
Schneewind & Missiakas (2012) Protein secretion and surface display in Gram-positive bacteria. Philos Trans R Soc Lond B Biol Sci 367:1123-1139.
https://www.ncbi.nlm.nih.gov/pubmed/22411983


text:
How is single nucleotide polymorphism denoted?
Currently I'm studying an article on TERT promoter mutations in human melanoma and find myself unfamiliar with included denotations,I would appreciate it if someone could explain to me what C228T in the sentence below means.

Two tumors with a C228T transition also contained an adjacent C>T transition (at position chr5,
  1,295,229), which is indicative of a dinucleotide CC>TT transition

C228T is a mutation from Citosin to Thymin at the 228th basepair.
Maybe this website helps? Nomenclature for the description of mutations and other sequence variations
I see they write the mutation different (following their format it would be 228C>T), but the general idea is the same.


text:
meaning of binding capacity and binding affinity
Actually, I am unfamiliar to biology, so when I read a thesis, the term "binding capacity" and "binding affinity" are really confusing.
Since my major is unrelated to biology, I don't know correct definition. Is there anyone who can explain differences between them clearly? Any references would be helpful, thanks!

Context would be useful, though there is nothing particularly special about the use of the words in this case. Binding affinity refers to how strongly two things bind (eg a protein-ligand interaction) and binding capacity refers to how much something can bind (eg in reference to a chromatography column).

references are really helpful, the key is "how much" and "how strong". right? you resolved my confusion

@victoria Yes, essentially.

Without any context... is hard to give a detailed answer.
I understand for bindind capacity the ability of a molecule to bind or attach to another molecule.
Binding affinity is the strength of the binding interaction between a single molecule and the other one.

oh l am sorry, since I am not familar to biology, I thought that the terms are often used in biology, so the only reason for confusing me is lack of my knowledge. So, I didn't add some context, but material I found is just about receptor's binding ability and affinity.


text:
Clarification on RefSeq Genes track on IGV
The following picture is a snapshot of the RefSeq Genes track (collapsed) on IGV. I know that the bold blue line indicates exons and the thin one indicates introns.
However, I cannot find what the medium line stands for. Is it part of the exon? Why is it different?
I have checked into the manual but I couldn't find any relevant info.

When you expand the track (bottom picture) even more diverse lines appear.

medium blue line without arrows
medium line with arrows
bold line with arrows

Can anyone explain to me what is the difference between all of them?

The thinnest blue line is intron, so not in your transcript.  The medium thickness segment is untranslated exon, the thickest blue segment is translated.

Thanks for the answer. It makes sense. Do you have any insight on the meaning of the arrows? Why some medium blue lines have it and some not?


text:
Please identify this tree in the Netherlands

Please identify this tree for me. It was found in a park in Eindhoven, Netherlands.

I suspect this is a hazel (Corylus avellana) based on:

the leaves
the male flowers (not mature in your photo)
the fact that it is a common tree in Europe)

This one has twisty branches, so it could well be of a particular variety called "contorta".
According to
https://en.wikipedia.org/wiki/Corylus_avellana#Cultivation_and_uses

A selection with twisted branches has been propagated horticulturally as Corylus avellana 'Contorta'.

Though providing links to supporting sources is ideal and often required when answering [tag:species-identification] questions, citing random non-reputable links is harmful to constructive learning and often inaccurate. This is especially true of google search results, which are very often inaccurate.  Please do the extra homework and find an image or description from a reputable source. (e.g., here or here). Thanks!

@theforestecologist Sorry for the link. I thought it would improve my answer because the male flowers in the wikipedia article or the link you suggest are mature ones. I removed it. Feel free to edit my post or propose another better documented answer.

Well, you don't have to remove the link necessarily, but use it as cautionary evidence instead of direct evidence. If that makes sense....In general, though, if your best line of evidence is a link such as one from google images, it probably just means you need to keep searching for better evidence. So, keep the link if you'd like (with some note signifying its lack of reputability), but take the time to keep searching for better support :). Thanks!


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How does kissing burst a person's ear drum?

A young Chinese woman was left partially deaf following a passionate kiss from her boyfriend.

..

The kiss reduced pressure in the mouth, pulled the eardrum out and caused the breakdown of the ear.

Source - BBC News
How exactly does this work though? With me not immediately being familiar with the inter-mechanisms of the mouth/jaw/ears, I'm not able to so easily discern the cause-effect of this; also, most all literature I come across is anatomically oriented, like this, as apposed to perhaps more "functionally" oriented.
Follow-up / Accenting question: is there any kind of anatomical disposition that would make the woman more susceptible to this happening? I mean, there are millions of people that partake in "passionate kissing" every day, however, this is the first I've ever heard of it bursting someone's ear drum.

The Daily Mail is not known for accuracy; it is known, though, for sensationalism.

@anongoodnurse I was also able to find this story on BBC News, and have updated my source link accordingly; I hope you find this [source] more credible.

Normally the pressure in the ear sinuses communicates directly with the nose, so the only way to change the pressure there is to pinch your nose, which is what divers do. Some people can have blocked sinuses and badly formed organs.

"The kiss reduced pressure in the mouth, pulled the eardrum out and caused the breakdown of the ear"

All you really need to understand the mechanism given this statement is anatomy: the nasal cavity and ears are connected through the https://en.wikipedia.org/wiki/Eustachian_tube so pressure changes in the mouth can be communicated to the ears. A typical individual would experience this when having the ears 'pop' in response to changes in outside pressure due to elevation or swimming underwater.

is there any kind of anatomical disposition that would make the woman more susceptible to this happening

Although I have not conducted a survey with a sufficient sample size, I don't believe most peoples' passionate kissing involves forming a mouth-to-mouth seal and then sucking/inhaling forcefully to create enough of a vacuum to damage someones' eardrum. It seems that the anatomical disposition most likely to make a woman or man more susceptible to this happening is having a kissing partner with this unorthodox approach. As commenter @kmm points out, you would also need to seal the nose, so having a partner who plugs your nose during kissing or having nasal congestion would also be necessary.
With 7 billion+ humans, though, there is a large enough sample that statistically rare events occur all the time, in part because there is also a near-infinite set of possible rare events.

You'd have to pinch off the nose as well to be able to generate the negative pressure.

@kmm That's a good point, so I suppose someone with a stuffy nose could be more susceptible.

This a splendidly amusing answer.


text:
Does GABA help or hinder anxiety?
This article
https://www.prnewswire.com/news-releases/smartphone-addiction-creates-imbalance-in-brain-300558945.html
Says both

The researchers performed MRS exams on the addicted youth prior to and following behavioral therapy and a single MRS study on the control patients to measure levels of gamma aminobutyric acid, or GABA, a neurotransmitter in the brain that inhibits or slows down brain signals

And

Having too much GABA can result in a number of side effects, including drowsiness and anxiety.

If GABA slows down brain signals, wouldn't that reduce anxiety? And if you have too much GABA, wouldn't that reduce anxiety also, not increase it?
DreamWater, a 5 Hour Energy counterpart, has GABA, 5-HTP, and melatonin, which promote sleep. It wouldn't make sense that GABA increases anxiety to promote sleep.

I wouldn't bother trying to interpret press-release science that doesn't even contain a citation or link to the original research. However, I will try to address some of the other content of your question.
It is indeed true that many anti-anxiety medications, particularly the benzodiazepines, act primarily to increase GABAergic activity by potentiating GABA receptors.
However, it is also true that GABAergic activity is not some monolithic attribute of the brain. Different brain regions have different functions, and some brain regions are associated with behavioral or neurochemical inhibition of other regions. An increase in GABA activity in a brain region that tends to inhibit others could theoretically be anxiety-inducing rather than anxiety-calming, even if the overall effect of increasing GABAergic effects is anxiety-calming. Looking at GABA levels is also only one part of the picture, and it fails to tell you a) how often GABAergic cells are releasing neurotransmitter, and b) how sensitive post-synaptic cells are to GABA. The overall effect of GABA is going to be roughly proportional to (GABA concentration) * (how often GABA is released) * (sensitivity to GABA).
An extreme example of why this is important are the delirium tremens that occur if a severe alcoholic suddenly stops drinking alcohol. Alcohol also potentiates GABA receptors, and with long term use the brain compensates by reducing GABA production. However, this adaptation is fairly slow, and alcoholics who quickly stop drinking can have motor symptoms and seizures as a result (some other neurotransmitter systems are involved as well, though, so this is a bit of a simplification). The opposite could be true as well: it's possible that increased GABA concentrations could be because not enough GABA is being released or because postsynaptic receptors have been downregulated. It is quite possible that you could have more GABA but less GABAergic inhibition. This study didn't test levels of inhibition, just levels of GABA.
Lastly, eating GABA to make you sleep is a bit silly and is far removed from brain levels of GABA or inhibition in the brain - I am not aware of any study that shows that eating GABA makes you sleepy; companies can freely put it in a drink and make abstract claims that suggest it aids sleep, but that doesn't mean it actually does, a beverage like that isn't regulated the same way that pharmaceutical drugs are.
In summary: be very wary of attributing a complex behavioral outcome to one particular element in the brain.

I know, I know, I' not supposed to do this, but this is such a good answer, I have to. Thanks! I'd upvote more if I could.

@anongoodnurse Agreed. Just in case you are not aware of this feature, if you still feel like that in 2 days, you can add a bounty.


text:
Details of Needleman–Wunsch algorithm
I try to understand details of the Needleman–Wunsch algorithm and use an example from the book [Nello Cristianini, Matthew W. Hahn. Introduction to Computational Genomics. A Case Studies Approach, www.computational-genomics.net].
To my opinion, the algorithm is described not very neatly, so the question arises.
Consider two sequences:
I: VIVALASVEGAS
II: VIVADAVIS
The first step is clear:

Also, the calculation of the score for diagonal neighbor is also clear,

because this is an alignment without a gap:
I: V
II: V
Unclear moment is the alignment for left (or above) neighbor. Say, the left  neighbor

corresponds to this
I: V
II: -
or this
I: -
II: V
alignment?

This is really off-topic here, but you need to read very carefully how this algorithm works, how the scoring matrix is constructed, how the traceback is done, and how that is finallly converted into an alignment. It takes me a 50 min lecture to explain it. I do not know the book you mention but have found the best explanation in Durbin et al. Biological Sequence Anlaysis.

This is a classic application of dynamic programming in bioinformatics, and is one of the first dynamic programs that I was exposed to in university! Let's begin..

Overview of algorithm
Step 1. Conceive of a scoring system.
Step 2. Create a table using the two character sequences.
Step 3. Iteratively fill in each cell, row by row, left to right. This is achieved by selecting the maximum (most positive) value coming from either:
(1) the cell that's located diagonally (top-left) to the current cell, plus the "cost" to align the two characters in consideration (cost value is obtained from scoring system).
(2) the cell to left of the current cell, plus the gap penalty (score issued for insertion/deletion mutation); looking at your example, the gap penalty is -1.
(3) the cell just above the current cell, plus the gap penalty.
Again, the greatest (most positive) of these three [sum] values will be placed in the current cell.
..
If you want the recurrence relation for this, then, if $T$ is the table being filling in, and $T(i, \ j) \equiv T(row, \ column)$, then
$$T(i, \ j) \ = maximum \begin{pmatrix}
T (i-1, \ j-1) + [alignment \ cost],\\
T (i, \ j-1) \ + [gap \ penalty],\\
T (i-1, \ j) + [gap \ penalty]
\end{pmatrix}$$

Scoring system
For simplicity sake, and to remain true to your example, I'll define and use the following:

Character match score: 0
Character mismatch score: -1
Gap penalty: -1

The character scores are potential alignment costs, and which to use is determined by if the two characters in consideration (row vs. column) are the same or not.

Now, to fill in table $T$..
Let sequence 1 run along the rows of $T$, and sequence 2 run along the columns, as you already have. If $T$ is initialized with a value of zero at location (0, 0), then, in order to fill in the first row [going from cell (0, 1) to (0, 9)], since there are no diagonal cells that exist yet, nor is there yet a row above the current row, for all cells in the first row we will use the second option that was mentioned above to obtain each cell value. So then, with the gap penalty being defined as -1, the first row will range from 0 to -9.

Make sure to keep track of which adjacent cell was used to obtain the value for each cell. This descriptive will later be used to trace $T$ once it's completely filled out, in order to obtain the optimal solution. If you're writing this on paper, people usually just draw arrows (from current to adjacent cell), however, if it's on a computer, an adjacency matrix is created & filled in.
In cases where more than one adjacent cell yields the greatest value, draw an arrow to each one. This is to say that there can be more than one optimal solution.

Next, we start with the first cell of the second row. Since a left & diagonal cell doesn't exist, that omits options 1 & 2, and leaves only option 3, which yields a value of -1 (only gap penalty). And, as you maybe have noticed by now, this behavior will always be true for the first row, and for the first column, and so, this is why you're able to so immediately fill out the table as you already have.
Continuing, to compute cell (1, 1), we now have to compare all three potential values and choose the maximum. For options 2 & 3, they both yield a value of $-1 + (-1) = -2$, however, option 1 yields $0 + [alignment \ cost]$, and, since both characters are the same (V and V), cell (1, 1) will have a value of $0 + (0) = 0$.
If we're to then fast forward a little and calculate cell (2, 1) ...

Considering option 1, we have $-1 + (-1) = -2$, since the characters being compared are I and V (and are a mismatch). Option 2 yields a value of $-2 + (-1) = -3$, and option 3 gives $0 + (-1) = -1$, hence, cell (2, 1) = -1.
Continue doing this for all cells until $T$ is filled.

Obtaining an optimal solution..
As mentioned, multiple optimal solutions may exist. In order to obtain an optimal solution, you must trace $T$, using the arrows you've been drawing (or the adjacency matrix), as a guide.
To obtain the path for best alignment, simply begin with the bottom-right most cell of $T$, i.e. the most recent/last computed cell, and trace your arrows to create a path back to the first cell (the top-left most).
To then construct the alignment, you will traverse this alignment path, beginning with the top-left most cell, and going to the bottom-right most cell, and, when considering the orientation of each arrow when going from cell to cell (diagonal, horizontal, vertical), you will do one of the following:
Diagonal arrow
For the first alignment sequence (top), simply add the character that's in the column of the cell you just moved to; for the second alignment sequence (bottom), use the character that's in that row. So then, when considering your example, and for both sequences, the first characters of an optimal solution when going from cell (0, 0) = 0 to cell (1, 1) would be:
V
V
Vertical arrow
When this happens, it means that there is a gap in the [initial] sequence that runs along the columns, since there are two rows for one column. Because of this, for the first alignment sequence, you will use a - to denote a gap. For alignment sequence two, use the character that's in the row.
Within the context of your sequences, for the optimal solution, a gap isn't encountered until the 7th character, at which point, the partial optimal solution will look like:
V I V A D A -
V I V A L A S
Horizontal arrow
This is the same concept as the vertical arrow rule, except it implies there is a gap in the row-oriented sequence, and so, a - will be placed in the second alignment sequence; the first alignment sequence will use the character in that column.

After all is said and done, your optimal solution is:
V I V A D A - V I - - S
V I V A L A S V E G A S

An interactive version of this algorithm can be found here.

Thank you very much for so detailed description. But I wished a very little detail of the algorithm. Now, due to the interactive version, all becomes clear.

@Konstantin I provided the entire algorithm because you mentioned the book not being clear to you in instruction, and, because the determination of alignment follows a specific set of rules, just as filling out the table does. I'm glad you were able to find your answer. :) Please mark this as the correct answer if this was helpful and accurate.


text:
CD4 Proteins & Antigen presenting cells
If Helper T-Cells express CD4+ proteins on their surface to bind to MHC Class ll proteins on antigen presenting cells, why do antigen presenting cells also have CD4+ Proteins?

This question has been asked previously. You can click on this link to get furthur information - https://biology.stackexchange.com/a/67948/11647


text:
Can domestic breeding be considered evolution?
Domestic breeding of animals (and plants) by humans seems to match some of the definitions of evolution I have been able to find:

"a process that results in heritable changes in a population spread over many generations." (the TalkOrigins website)
"cumulative inherited change in a population of organisms through time leading to the appearance of new forms" (Merriam-Webster)
"Changes in the heritable attributes of populations of organisms over time" (this SE's 'evolution' tag info)

But other definitions seem to be less of a fit:

"the way in which living things change and develop over millions of years" (Cambridge)
(domestic breeding does not take millions of years)
"The process by which different kinds of living organism are believed to have developed from earlier forms during the history of the earth" (Oxford)
(Does breeding lead to different 'kinds' or organisms?)
"The gradual development of more complex organisms from simpler ones" (Chambers)
(Breeding may not result in more complex organisms)

I've seen people argue that domestic breeding can not be considered evolution, because domestic breeding:

does not involve natural selection
doesn't direct towards 'fitness'
does not lead to new species
decreases, rather than increases, the size of the gene pool (is this actually true?)
does not (or may not) lead to more complex organisms

I was not able to find whether or not there is a general consensus among experts from relevant fields on whether domestic breeding can be considered evolution. Is there?
EDIT: I've made the list of arguments I've heard against calling it evolution a bit clearer, and also added an extra one.
EDIT 2: Added why the second set of definitions seem to exclude domestic breeding as evolution

Humans are a part of nature, therefore selection by humans is perfectly natural.  2) "Fitness" is something of a misnomer: whatever survives to pass on its genes is fit in the evolutionary sense, by definition, even commercial turkeys that have to be artificially inseminated by humans - and how are they different from say an orchid that's pollinated by one species of moth?

@jamesqf The second part of your comment is spot on, but the first bit is spurious. There is a reason evolutionary biologists define human-induced evolution as 'artificial selection' to distinguish it from natural selection, since they are categorically different phenomena. Natural selection is non-teleological, whereas artificial selection is.

@et is: I suppose the distinction between natural and artificial selection might be a good question for philosophy, but I didn't mean it like that.  What I meant is that genes don't care what is applying the selection pressure.

Yes, selective breeding results in evolution.
Definitions of evolution
I don't understand why you say that for 3 of the definitions you found, selective breeding would not be considered as evolution. To me, all of these definitions match with the idea that selective breeding results in evolution. If you think otherwise, can you please explain why?
There are a number of related definition out there, some of them being more clear and straight forward than others. The simplest definition is probably the classical population genetics definition which says

Evolution is a change in allele frequency over time.

See wikipedia > allele. You might want to have a look at How to define evolution? too.
Under this definition, any event of death or birth in a population is evolution as it affects allele frequency. In the human species for example, that means an evolution happens about 254 times per second (computed from these numbers from ecology.com)!
Specific statements
All these statements are stupid and none-sense! The easiest is probably for you to just have a look at an intro course to evolutionary biology (such as Understanding Evolution by UC Berkeley for example) and you will be able to refute those statements yourself.
Let's go through these statements...

There is no natural selection

First, evolution is much more than just natural selection. There is genetic drift, mutations, gene flow and plenty of interacting processes.
Second, it is silly to separate natural selection from artificial selection (aka. selective breeding). The only difference between these two is that in artificial selection someone is willingly affecting the environment of the individual to affect selection pressures. This is really it.
Note, btw, you never totally get rid of natural selection. Under selective breeding you may affect the environment but some things will remain the same. For example, a mutation causing the cell membranes to be extremely unstable will not be selected for whether under an artificial setting or a natural one.

It doesn't direct towards 'fitness'

The claim is unclear. What is "it" and assuming it refers to a population, then what does it mean a population is directing toward "fitness"?
Fitness is a function of survival and fecundity. Each genotype is associated to a particular fitness in a specific environment. Ignoring stochastic processes such as genetic drift, the mean fitness of a population is increasing from one generation to the other by the amount of the additive genetic variance. This is true for (artificial or natural) selection.
The only thing to consider is that the environments under which this happen is different. Under selective breeding, the population evolves to a higher fitness for the specific environmental conditions set by the farmer (or who ever who selectively breed). It is possible (and quite common in fact) that genotypes associated with a high fitness under one environment has a low fitness under another environment.

It does not lead to new species

In short, 1) it does lead to new species 2) the concept of species is often meaningless as poorly defined 3) evolution > speciation. In more details, below..

It does lead to new species. Different lineages of cabbage are considered different species. Cows and ox are different species. Pigs and boars are often considered different species. While wolves and dogs are considered same species, some lineages within this species (such as a Chihuahua and a Great Dane) are, I think, reproductively isolated. You might also want to have a look at the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
The question of whether selective breeding lead to speciation or not does not matter much on the question of whether it leads to evolution. Speciation is one outcome of evolution but is definitely not the same as evolution. Evolution does not need to lead to speciation. For example, evolution of the lactase gene in humans (see this post) did not lead to any speciation. It is still an evolutionary process.
The concept of species is mainly arbitrary. If you want to understand the concept of species, have a look at the post How could humans have interbred with Neanderthals if we're a different species?.

It decreases, rather than increases, the size of the gene pool (is this actually true?)

The term "size of the gene pool" is very undefined. I suppose, it just means genetic diversity, aka. expected heterozygosity.
All act of selection, whether artificial or natural, decreases genetic diversity. This is correct. Mutations is the fundamental process increasing this genetic diversity and selection selects the variants associate with the highest fitness.
Because, the selection pressures imposed under selective breeding are often extreme, the decrease of genetic diversity via selection is often faster in selective breeding than in nature.
Note however, that if we split a lineage in two and select the two populations under different optimas, then the total genetic diversity will increased (the within-population genetic diversity will still decrease). As such, via selective breeding we created a gigantic diversity of dogs and a fantastic diversity of cabbage but each cabbage lineage (e.g. brussel sprouts) and each dog lineage (cocker spaniel) have very low genetic diversity.
What the claim is suggesting is that because selection is often stronger (and therefore change in allele frequencies is faster) under selective breeding than in natural environments, we should not consider artificial selection as resulting in evolution? How silly is that!

The word 'it' in the second argument refers to domestic breeding. I will update my question to be more clear.

@Remi.b great answer as always, +1, but there is a mistake here: wolves and dogs are the same species, Canis lupus. Have a look at Mammal Species of the World: A Taxonomic and Geographic Reference, Volume 2, the comment at the bottom: https://books.google.com.au/books?id=JgAMbNSt8ikC&pg=PA576&redir_esc=y#v=onepage&q&f=false It says: "Canis lupus [...] includes domestic dogs as subspecies".

Whether or not it leads to separate species has nothing to do with evolution. I know you know this but you should probably emphasize it more; there's a widespread vague belief that speciation and evolution are the same thing, whereas in reality speciation is just one small and specialized aspect of evolution.

@iayork and Gerardo Thanks for your comments. I've edited my post accordingly.

@GerardoFurtado these is a lot of debate about whether wolves and dogs are the same species, and goes back to the problems with defining species. Technically all of Canis may be able to interbreed.

@John not anymore, this matter has been almost settled now.

@ Remi  I meant Canis as a genus, All the members of Canis are cross fertile, minus jackals, and may turn out to be polyphyletic . Also not everything from the same species can interbreed, that is one of the problems with defining species that way, ring species are a thing. I just wanted you to understand that referring to them as the same species or not is more opinion than anything else. https://www.ncbi.nlm.nih.gov/pubmed/16341006

sorry thats the link to the paoer about Canis being polyphyletic, this is the one about dogs not being domesticated gray wolves. http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004016

There is absolutely nothing in that paper saying that.

@Gerardo Furtado: If dogs and wolves are the same species, why not dogs and coyotes, or wolves and coyotes?  They interbreed quite successfully where their ranges overlap, and indeed, the eastern North American "coyote" seems to be a hybrid of coyote, wolf, and dog.

Nope. Coyote is Canis latrans, not related to what happened to dogs. Dogs came from a population of Canis lupus in east asia around 16kya. So, as a clade within C. lupus, they are C. lupus. Also, interbreeding - alone - doesn't define a species.

Anyway, I'm starting to become tired of this: dogs are whatever you say they are, just consider that I'm wrong and move on.

@Gerardo Furtado: But genetic studies show North American wolves and coyotes diverging around 6,000–117,000 years ago, with all modern populations being somewhat intermixed: https://en.wikipedia.org/wiki/Evolution_of_the_wolf#Divergence_with_the_coyote  That overlaps the ~16kya wolf-dog divergence.  Which just points up the fact that species are largely a matter of opinion.

The answer is "yes". Evolution is defined as a change in heritable characteristics of a population over generations, and to me, there is no reason not to define domestic animals as populations.
The statements you list can all be refuted:

Part of the selection human-driven, part "natural". You cannot control all genes.
The concept of fitness talks about offspring and contribution to the gene pool. Humans enhancing the fitness of desired individuals should also count as fitness. It is just the "human selection" that partly drives the evolution (i.e. human selection works as an environment).
Dog, chicken, cow are all species created by domestic breeding. They are all considered species by some biologists.
Strong selection pressure sometimes decreases the size of the gene pool, but again if you take dogs as an example: they are likely genetically more diverse than wolves. There are so many factors involved in domestic breeding that you cannot say that it decreases the size of the gene pool. It can go both ways.

But again, evolution is a human-created concept to understand our surroundings. If somebody wants to think that humans should not be a driving factor in evolution, that is fine for me.
Next logical question would be whether gene-manipulation is evolution. I will leave that for someone :)

There is not consensus among scientists, that human sciences of should be equaled to natural sciences.
Scientists don't agree if pets and farm stock are new species, and we all agree, domestic animals are in a different, recent, group to all other and selection processes. It's Yes and No andwer. It shares and conflicts with evolution and seems to deserves a human sciences category of it's own.
"Evolution of the chihuaha specif traits from the wolf", wouldn't qualify for a science journal.
Survival of the funny looking animal, for a dominant species, that has a large brain, that devises breeding methods. Contrary to survival of the fittest. It's a form of evolution that was seen only 50k years from 4 billion, that's 0.00125% of evolutionary history. You can compare it to evolution of captive algea used by coral, and ant-aphid relationships.
Darwin studied the topic for decades, and in the actual title of his book he wrote "Natural" selection, so he clearly made a mental difference between human and wild, natural processes.
The difference of the concepts is similar to human geography and physical geography. They are described by different books.
To make a language's semantics clear, it's best not to group different groups of processes with the same word, when new semantics be invented where a discussion is required to differentiate the two.
It's the only form of evolution that uses artificial foods, artificial walls and fences, artificial mating, to make funny looking animals for amusement, and social animals companionship and work.
The result is generally low fitness, stamina, immune system, fainting goats, deaf dogs, dogs that can't breathe well due to snout length, dogs which are tremendously unfit. and animals that are fit for human amusement.

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


text:
How does sexual reproduction generate more genetic variation?
I'm curious as to why sexual reproduction generates genetic variation. For me, the term genetic variation is a little ambiguous. The way I understand it, it's the number of alleles at a locus in a population or "group" of organisms.
But sexual reproduction only "reshuffles" alleles, and doesn't generate new ones (most of the time, at least). So why does it create genetic variation?
Thank you for reading.

Short answer it doesn't. Sexual reproduction generates new combinations of traits and increases the difference between individuals in the same populations.
New combinations means beneficial traits have a better chance of finding complimentary traits while the opposite are also true detrimental traits have a greater chance to find combinations that make them worse. It increases variance in the sense that individual genes can disperse easier in the population, and genes can form more unique combinations, but not in the sense of actually increasing the overall variability.
Likewise it also keeps individuals from being identical which makes a population more vulnerable to parasites and disease.

There are two questions here. 1) What is genetic variance? It is actually clearly defined. 2) How does sexual reproduction generate more genetic variation?

What is genetic variance?

Assuming bi-allelic loci, just assign a value of 0 to one allele and 1 to the other allele. Then compute the variance! Average this value over all loci. Done! Have a look at any intro book in quantitative genetic for more info (see here)

How does sexual reproduction generate more genetic variation?

You are right "sexual reproduction only "reshuffles" alleles, and doesn't generate new ones". It is a common misconception that sexual reproduction generate genetic variation. The details of whether it does or it does not depends upon the detailed distribution of dominance coefficient and distribution of epistatic effects.
There has been a lot of work on the subject and it is not an easy work to summarize it. Sally Otto does a great job to summarize this misconception in her speech On the Evolution of Sex and the Advantages of Recombination. You should definitely have a look at it.
Note however, in some species that preforms both asexual and sexual selection, it happens that sexual selection is coupled with higher mutation rate than asexual selection. In such cases, sexual selection does indeed increase genetic variance but only so because of tis correlated effect on mutation rate.

Having read over, I think in "common misconception that sexual reproduction generate genetic variation"  you seem to use two different terms "variation" and "genetic variation". So there is a definition of "allelic variation" that differs from "genetic variation"?

From your question: "... only "reshuffles" alleles, and doesn't generate new ones (...). So why does it create genetic variation?"
There are no trick questions, still my answer goes:
Because genetic variation is also created by independent assortment.
There are two ways of crossing-over in meiosis.
First, there is Chromosomal crossover, or crossing over, which "is the exchange of genetic material during sexual reproduction between two homologous chromosomes' non-sister chromatids that results in recombinant chromosomes." (Wikipedia)
Second, however, there is, much lesser known  Independent assortment of chromosomes:
"The physical basis of the independent assortment of chromosomes is the random orientation of each bivalent chromosome along the metaphase plate with respect to the other bivalent chromosomes. Along with crossing over, independent assortment increases genetic diversity by producing novel genetic combinations."
Without alleles being changed (if exchanged, as a result), chromosomes from on parent are exchanged with (homologous) chromosomes of the other parent. This, too, results in genetic variation, and - as such does not involve so called crossing over of allelic genes. Exchange of alleles as a result of independent assortment must be distinguished from creating new alleles by crossing over,i.e. exchanging genes or parts of genes.
Independent assortment can be differentiated from "allelic variation". Hermaphrodite reproduction as sexual reproduction shows that in one single individual there are a million combinations of alleles. By definition, however, not all alleles existent in a population. Interestingly, this rule is not valid in respect of the rather unknown mechanism of mingling of chromosomes (not alleles). Any indivual has got the potential to find any - among all - combination of chromosomes.
From this finding results that intercourse of different individuals in contrast to hermaphrodite interchanging of chromosomes and alleles can be distinguished by potenitally combining all alleles, whereas all chromosomes can - potentially - combined by one hermaphrodite individual.
Surprising about this answer is that, in the words of your question, "new genetic variation" that is not considered allelic variation as it does not involve the changing of genes is thus produced by sexual reproduction.


text:
Measure of relatedness between two animals
So I am aware there is such a thing as inbreeding coefficient which is a number allocated to an individual as a result of taking the average of it's parents' inbreeding coefficient.
(Note that I am working in terms of pedigree based relatedness, not genomic relatedness.)
Is there a number that quantifies the relationship level between 2 individuals?
If so how is this calculated? Can it be done in R using the pedigree package?
Where say a sire and ewe have a 0.5 value or something similar?

There are about an 25 thousands ways to measure relatedness between two individuals. The most obvious coming to mind  based on your description is the coefficient of relatedness. Relatedness is the probability that two individuals share an allele due to recent common ancestry. There are probably tens or hundreds of online tutorials. Consider this one for example.

I believe a good word for what I am after is "kinship," or a "kinship matrix."

Consider having a look at the kinship2 package.


text:
Are a child's traits truly random?
To me, there are two definitions of "random" in common usage: effectively random, where predicting the outcome is beyond most reasonable effort (e.g., drawing a card from a deck); and truly random, where predicting the outcome is beyond known science (e.g., radioactive decay/QM).
With this (possibly flawed) perspective, I'm very interested in sources of true randomness. I started thinking about how parents never know exactly what their child is going to look like. Is this because there are aspects of reproduction that are fundamentally unpredictable (true randomness) or because we lack the sophistication/motivation to predict it (effective randomness)?

Its unclear what process you are referring to, are you talking about recombination? If so then like all chemistry it is just effectively random and in a way not even be that since position on the chromosome has an effect.

You true randomness definition is partially wrong! Something does not need to be fundamentally random to be beyond known science.
Also, it is unclear what process you are referring to when talking about a child's trait. I would assume you are thinking about crossover but then, summarizing crossover positions by "child's trait" shows that you misunderstand a number of things!
To my knowledge, outside of quantum physics, in no field of knowledge has it been shown that true randomness has any measurable effect. So, no what chromosome an individual inherits is only random in the sense that it would be necessary to know exactly the position of every molecule in the cell to know where the crossover will happen.


text:
Is it possible for parsimony to estimate more state changes than stochastic character mapping
I'm mapping states (geographic regions) onto a phylogeny to estimate the number of transmissions between countries.
I'm using two methods, stochastic character mapping implemented in Phytools and parsimony implemented in Mesquite.
I was expecting parsimony to give lower results than stochastic character mapping, as it doesn't attempt any simulation along branches. This is generally true, and the number of transitions between states is generally lower estimated by parsimony. However, in a couple of cases, the number of transitions estimated by parsimony is higher than by stochastic character mapping.
I'm still developing an intuition in this type of analysis, so could someone tell me if this is feasible, or should I be looking for a technical problem somewhere?

If the number of taxa is large enough, an exhaustive search is not possible, and parsimony methods use heuristics to explore the tree space. It is therefore not guaranteed that the most parsimonious tree will be encountered.
This might explain your observation if your tree has a high number of taxa (> 20).
According to wikipedia:

However, although it is easy to score a phylogenetic tree (by counting the number of character-state changes), there is no algorithm to quickly generate the most-parsimonious tree. Instead, the most-parsimonious tree must be found in "tree space" (i.e., amongst all possible trees). For a small number of taxa (i.e., fewer than nine) it is possible to do an exhaustive search, in which every possible tree is scored, and the best one is selected. For nine to twenty taxa, it will generally be preferable to use branch-and-bound, which is also guaranteed to return the best tree. For greater numbers of taxa, a heuristic search must be performed.

How many taxa do you have?


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Health benefits & enzymes different between Thermophilic and Mesophilic Probiotic cultures?
Is there a difference between the Enzymes produced by Thermophilic vs Mesophilic Probiotic cultures ? are there any other differences in health benefits between the two types of cultures ?

Thermophilic and mesophilic enzymes differ in the optimal working temperature, due to a structural adaptation: thermophilic enzymes have more stiff surface-exposed loops than their mesophilic orthologs. Human is mesophile, which means that mesophilic enzymes, no matter whether human or bacterial, will work in human more efficiently.

Bjelic, Brandsdal, and Aqvist (2008) Cold adaptation of enzyme reaction rates. Biochemistry 47: 10049-10057; emphasis mine:

[P]sychrophilic, mesophilic, and hyperthermophilic citrate synthases
  ... have increasingly stronger electrostatic stabilization of the
  transition state, while the energetic penalty in terms of internal
  protein interactions follows the reverse order with the cold-adapted
  enzyme having the most favorable energy term. The lower activation
  enthalpy and more negative activation entropy observed for
  cold-adapted enzymes are found to be associated with a decreased
  protein stiffness. The origin of this effect is, however, not
  localized to the active site but to other regions of the protein
  structure.

https://www.ncbi.nlm.nih.gov/pubmed/18759500

Aqvist (2017) Cold adaptation of triosephosphate isomerase. Biochemistry 56: 4169-4176; emphasis mine:

The results show that the enzyme from the psychrophilic bacterium
  Vibrio marinus indeed displays the characteristic shift in
  enthalpy-entropy balance, compared to that of the yeast ortholog. The
  origin of this effect is found to be located in a few surface-exposed
  protein loops that show differential mobilities in the two enzymes.
  Key mutations render these loops more mobile in the cold-adapted
  triosephosphate isomerase, which explains both the reduced activation
  enthalpy contribution from the protein surface and the lower
  thermostability.

https://www.ncbi.nlm.nih.gov/pubmed/28731682


text:
Can action potential generating ion channels only be understood as assemblies of membrane proteins (and not as single proteins)?
I always believed to have roughly understood how voltage-gated ion channels and the creation of action potentials work: as and by single (or non-interacting groups of) membrane proteins, that behave somehow non-linearily by intrinsic means, each by its own. But suddenly I doubt.
Might it be the case that some of the non-linear dynamics of ion channels and the generation of action potentials cannot be understood when looking only at single ion channels as proteins? Or is it like Wikipedia says:

A voltage-gated ion channel is a cluster of proteins embedded in
  the membrane.

This means, that some of the non-linearities only occur when many membrane proteins (presumably in a fine-tuned mix of different types) interact?
Maybe only then some features of ion channels can be understood:

Action potentials are always of the same size, independent of the voltage (or current) that is applied/injected (which would be hard to understand for single membrane proteins).
Ion channels can exhibit many different firing patterns, which depend on intrinsic emergent mechanisms of assemblies of membrane proteins.

If this is so, one must be very careful when talking or reading about voltage-gated ion channels, because depending on context sometimes single membrane proteins are meant, and sometimes complex assemblies of non-linearily interacting proteins.

Wikipedia's statement

A voltage-gated ion channel is a cluster of proteins embedded in the membrane.

is most likely referring to the fact that most ion channels (maybe all? I hate to say "all" in biology) are made up of multiple protein subunits; usually these are all considered one protein's quaternary structure, though, so wikipedia's language is not ideal.
I think you are then running with a misunderstanding of this statement to make some conclusions that are not warranted. Of course multiple ion channels come in to play when you are talking about membrane potentials at the cellular level. Of course you need to consider multiple ion channels when considering the overal membrane potential, but it is sufficient to know only a) the gating properties of a given channel and b) the membrane potential to know the contribution of that channel.
Action potentials are only roughly the same 'size' in terms of voltage amplitude - they are certainly not identical, and this size is because of the gating properties of voltage gated channels and the reversal potential for sodium. The membrane potential can never exceed the reversal potential for sodium via sodium-based conductances, so that puts an upper limit on action potential size. In addition, hyperpolarizing potassium-permeable voltage gated channels will open at depolarized potentials, further limiting the maximum amplitude of an action potential.
Ion channels don't exhibit any firing patterns: neurons exhibit firing patterns that depend on all the channels present and the physical morphology of the cell.


text:
Potato with purple veins!
Today while cooking with potatoes when I cut open a potato(raw) which was looking perfect from the outside showed purple veins. I threw it in my kitchen garden but than I wondered what it could be

Questions

Why did my potato developed these purple patterns?
What could be that purple pigment?
Are such potatoes Edible?

PS: The potato was not old. It was quite fresh.

The potato developed this pattern because it's (probably) natural to cultivar you're growing or due to cross-pollination.
Purple pigment is anthocyanin. It's perfectly normal and considered as more healthy (as those varieties of potatoes contain more antioxidants and vitamin C) and even 'gourmet'.


text:
What really causes the toxicity of wrongly-thawed meat?
(Note: I've seen multiple related questions over at Cooking.SE, but I'm looking for a scientific explanation, not cooking advice!)
I've been researching this for a couple of hours but the more I read, the less I seem to understand the situation. Many sources claim that thawing meat in warm water is wrong and that I should instead opt for cold water to prevent bacteria from growing and producing toxins. I found a wide variety of toxin-producing bacteria that can live and reproduce in meat, such as Escherichia coli, Salmonella, Corynebacterium diphtheriae, Listeria monocytogenes and Clostridium botulinum.
There are two things I don't understand:

If I thaw the meat quickly, the bacteria have less time to reproduce before I cook the meat. This is especially true for Listeria monocytogenes which seems to be able to quickly reproduce in cooler temperatures. Why is it bad to thaw meat in warm water?
If the sources I've read are true, it leads me to believe that Listeria monocytogenes is not a bigger issue than the other species of bacteria growing in the meat. I suspect that bacteria compete for resources and that it is probably only one of them that is the main factor in making a piece of meat toxic for consumption even after cooking. What is the primary cause of meat toxicity?

Or is it possible that I've been overanalyzing the situation and the exponential relationship between bacterial growth and temperature is the main reason?

Not a full answer, but my impression was always that it was a temperature gradient problem. Thawing meat in warm water or at room temperature puts the outer layer of meat in the "danger zone" while the inside stays frozen. By the time the center is defrosted, the outermost meat isn't well-refrigerated anymore.

This is a really fascinating question and got me reading stuff all through the night. If my response seems tl;dr, then please skip to the fourth paragraph.
From what I've found in literature, it may be the case that prolonged exposition to certain temperature ranges may prove lethal to some pathogens. Shortening this time or shifting the temperature may cause suboptimal death rate of microbes. El-Kest et al. have found that Listeria monocytogenes would be most effectively killed by 5 to 6 freeze-thaw cycles with 35 degrees C as the thawing temperature and -18 degrees as the freezing temperature. Freezing at -198 degrees proved way less successful in killing the bacteria. This suggests that not only the thawing temperature and rate have the influence on microbial diversity in meat but also the actual temperature of storage!
Here is the link to the publication by El-Kest et al.: http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-55.8.639?code=fopr-site
Freezing rate also has a significant influence. If freezing occurs slowly, ice crystals will mostly appear mainly outside cells with rapid freezing having the exact opposite effect. It is quite logical why it happens: spots within the food that are freezing will slowly make the unfrozen surroundings rich in ions and osmotically active substances, the water will gradually seep out from bacterial cells to the surroundings and subsequently freeze up. (https://books.google.pl/books?id=o6kJCAAAQBAJ&pg=PA25&lpg=PA25&dq=Inactivation+by+cold.+In+Inhibition+and+Inactivation+o+f+Vegetative+Microbes.&source=bl&ots=zlH-dMFiqo&sig=AfglM7piuvMnjI3q3JV0ovHy-FE&hl=pl&sa=X&ved=0ahUKEwjS-6fAypTYAhWiJJoKHe-gDJAQ6AEIQTAE#v=onepage&q=Inactivation%20by%20cold.%20In%20Inhibition%20and%20Inactivation%20o%20f%20Vegetative%20Microbes.&f=false)
From that perspective slow freezing is more likely to get microorganisms killed, as there is no cold-shock response and the cells do not become desiccated prior to freezing.
Now, let's look at the big question: why can't we use warm water to thaw meat. As one of the commenters pointed out, there is something called "danger zone" in frozen food safety, in fact USDA keeps talking about it all the time. This might be counterintuitive but by rapidly increasing the temperature in outer layers of meat, you will quickly provide microbes with ideal conditions for cellular division. As time progresses each next layer will be infested by bacteria from the outer layer as well as those that will just start undergoing cellular division, and so on, and so on, until you reach the very center. You end up with a pretty nice bunch of bacteria throughout your meal, though you shouldn't probably worry to much about it, unless you like your meat half-raw.

What happens during cold-water thaw or refrigerator thaw is different because you essentially increase the temperature of each consecutive layer but without providing enough thermal energy to give microbes a near-optimal temperature for intensive cellular division. Sure, they will start dividing anyway but to a much lesser degree. The temperature increase is not rapid therefore there is no abrupt resumption of life-cycles of microbes. Think of it as waking up on a cold winter day vs. warm, pleasant summer morning.

Still, you can use hot-water thaw safely if you're dealing with thin cuts of meat, if fact USDA approves it: http://onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2010.02037.x/full
Further reading:
https://www.fsis.usda.gov/shared/PDF/Big_Thaw.pdf
https://link.springer.com/content/pdf/10.1007/978-1-4615-5975-7_10.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662152/

Now, regarding your second question, I'll mostly answer from my own experience. We used to test meat in our microbiology lab during studies and we tested different kinds of meat. Teachers who teach the subject for 10+ years, when asked, admitted that there is generally a pattern of how many bacteria and what types of bacteria populate different kinds of meat, so there is no safe way to say that there is a single major pathogen that is responsible for food poisoning from meat in general. I'd say what's most dangerous are exotoxins produced by those bacteria, e.g. botulinum toxin is the most potent toxin known to mankind and Clostridium botulinum loves to populate meat stored at room temperature. Listeria is a popular example because of its great survivability in cold temperatures. But it really depends on the kind of meat and even on the specific batch of meat. You simply never know what you'll get with it.
Either way, you were not just overanalyzing the topic. There are really many factors to the quality of food preparation safety, especially when it comes to meat. To summarize:

Hot-water thaw can be used for thin slices of meat (I still use it for bigger slices as well, but only if I'm certain I'll fry the meat very thoroughly)
Cold-water thaw is better due to lower probability of serious bacterial infestation, especially recommended for thicker slices of meat
Freezing as well as thawing rate both influence meat quality
Freezing temperature cannot be too low, nor too high to ensure optimal death count of certain species of bacteria
Meat toxicity is generally caused by pathogenic bacteria that multiplied within or were previously present (e.g. due to improper meat handling by the producer), in most cases due to the toxins produced by the bacteria

Hope I helped a bit :)
[EDIT]
There was a request in the comments to include some more info about the toxins produced by food-borne pathogens. There's a good review here:
https://www.ncbi.nlm.nih.gov/pubmed/8750662 (not sure if paywalled though, I'm using library internet right now). You could group those toxins into 4 arbitrarily defined groups:

heat-liable enterotoxins – these generally can be destroyed in the process of cooking or frying; produced by Salmonella spp., E. coli, Campylobacter spp., Vibrio cholerae (yes, this one causes cholera)
heat-stable enterotoxins – these cannot be efficiently removed by heat preparation of food; produced by Yersinia enterolytica and some strains of E. coli
Shiga-Like toxins – they resemble verotoxin of Shiga spp.; produced by E. coli O157:H7 (this strain is very pesky, as it induces hemorrhagic diarrhea and kidney failure)
Unique toxins – some bacteria produce unique toxins, e.g. Bacillus cereus, Clostridium botulinum, Clostridium perfringens

Generally E. coli strains have many subtypes of heat-stable as well as heat-liable enterotoxins and some strains have other types of toxins like the O157:H7. The name "enterotoxins" refers to toxins that are secreted by microorganisms targeting intestines and generally they are cytotoxic, which essentially means they cause cell lysis of the host. Mechanisms of action are varying, e.g. cholera toxin triggers a cascade of reactions that overdrive CFTR channels (chloride ion transporters) and alters osmotic balance, which macroscopically manifests itself by a production of characteristic watery stool.
Worth noticing: some of those pathogens require other factors to cause disease, e.g. Vibrio cholerae requires a toxin-coregulated pilus to be pathogenic and some even do not produce any toxins directly (for instance Listeria monocytogenes overdrives lysosomes and doesn't let them take the bacterium apart, then it spreads from cell to cell by the means of actin filaments).
In the context of detox diets, there is a large dispute going on about their effectiveness whatsoever. I'd recommend confronting these two articles, which, to me are well written:
https://link.springer.com/chapter/10.1007/978-3-319-49929-1_33
http://onlinelibrary.wiley.com/doi/10.1111/jhn.12286/full
Some animal models have indeed shown some anti-toxic effects of certain foods, other researchers argue that most of the toxins eventually get to the liver and get broken down. The liver does its job pretty well, so running for two weeks on a "kale juice" would be a bad idea. People seem to forget that usually the dose is the poison: if you ingest highly diluted cyanide, it won't harm you, while drinking 7-8 liters of water at once could kill. Switching to an unbalanced, monotonous diet could be actually detrimental to health a lot more than those minuscule amounts of food-borne toxins ingested. The best way to live a healthy life is still: move, eat well and diverse, follow food safety guidelines, take care of your physical and mental health.

Thanks, that's a great answer. Did you learn something about the toxins which you didn't include? If so, could you add it? The reason I'm asking is because I think the internet is full of posts mentioning unspecified toxins (especially on non-scientific forums), but no one ever bothers to do the research or there are no toxins in the first place (detox diets etc.). Your answer is different, which is awesome, but if you can add more, that would be great.

I've updated the answer with what I found on the topic, hope you find it helpful ;)

Thank you, here's your bounty, you very much deserve it. And I learned some pretty cool stuff too!

Thanks for the bounty and for the question. I love questions that make me learn too, so this one was splendid ;)


text:
Can we estimate longevity from menopause age?
This is from an answer in other question, about the age at which menopause occurs:

Aristotle's assessment was similar to those of Hippocrates and also
  Roman authors, so it seems that 2000 years ago most women entered the
  menopause in their early 40s. Mediaeval authors, however, gave the 50s
  as the age when menses ceased-much closer to the timing for twentieth
  century women.

Considering that, throughout history, menopause starts at about 40-50 years, shouldn't this point to a stable and long life expectancy? (Considering also that menopause is an adaptation.) When we read that humankind used to live much less than today, isn't it just the effect of newborn mortality, and thus adults lived just about as long as we do today?

these author may not be the best sources for anatomical/biological information. Especially for trying to gauge the average anything about women, Aristotle thought women grew fewer teeth for crying out loud. medieval "doctors" were even worse.


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How does radiolabeling work?
Protein turnover can be measured by calculating the "decay" or loss of radio-labeled proteins in the blood, for example, but I am confused at how this calculation works. Wouldn't the radioactive isotope that you're using be decaying due to being unstable and not just due to protein turnover? Would you have to account for that in your calculations?

Which calculation are you using?

A=Ao*e^-kt, where A = tagged protein at any time, Ao = tagged protein at zero time, t = time in days, and k = turnover rate as fraction of the protein pool turned over per day. By rearranging the equation you can get turnover rate (k).

Technically yes, but practically it depends on what the half-life of your isotope is relative to the half-life of your protein. For example, tritium has a half-life of a little over 12 years, but most protein labeling experiments take place over only a few days at most (it depends on your protein). So while technically the tritium is decaying during your experiment, the amount of decay will be below your detection limit, and therefore is negligible over the course of the experiment.
So basically it works best to choose an isotope that will not appreciably decay over the time course of your experiment so you don't have to worry about it. If this is not possible, then yes, you would need to correct for this.

I've read some papers that use Iodine 131 to label proteins, which has a half life of 8 days. So I have another question: how do people detect these isotope labels? Do people rely on their decay to measure it (for example the release of beta-minus and gamma emissions? In that case, wouldn't you want to use something as radioactive as I-131?

Detection depends on the isotope used. Tritium is a low energy beta emitter, so it would need to be removed from the place you are measuring and put into scintillation fluid or something analogous.For something that is higher energy, like P-32, you could use film or a geiger counter. For imaging in live organisms, I think you do need something fairly strong like I-131, unless you are harvesting samples from the organism. For I-131 you can do a PET scan, since it is a gamma emitter. Typically, this does rely on the decay of the particle. 8 days is still plenty of time for most imaging though.


text:
At what point does muscle mass overcome muscle strength to affect speed?
I'm trying to think in terms of "how fast" someone can do something, like swing a bat or push a crate. Someone might have a lot of muscle mass, but that also increases how much mass an arm has to move which also increases the torque. Is there anything referable in biology that has found at least some estimate of where these two factors trade off?


text:
What is this fleshy-stemmed plant?
This plant came (seemingly by accident) with another pot plant a few years ago in a plant sale.  Unfortunately, we do not remember what the original plant was that it came with.

It was initially one of the small 'fleshy stems' you can see in the photos, about 2cm in length.
If you do not water it, the leaves fall off and leave the fleshy stems
If it is watered, a new section of stem is grown with leaves.
Its existing stems do not seem to regrow their leaves if they drop off.
It was acquired in the South-West of England.
It does not appear to be affected by the time of year.

Photos (click to enlarge):

Does it ever grow flowers? If so, can you provide pictures or a description of them?

I've never seen it flower.  Also, whilst I appreciate the "click to enlarge" change to my post, please don't correct the grammar in my post from British English to American English, thanks.  I'm also a little unsure why you removed the disclaimer from the top of the original question.  You describe it as unnecessary in your Edit, but surely it was important to put in case this was the wrong StackExchange site?

sorry didn't realize some of the phrasing was British! Of course feel free to roll back edits if you don't like them. I removed the disclaimer paragraph to indicate that, yes, this post is ok here and therefore the paragraph was not needed. Thanks for including it initially, but it would only serve as clutter moving forward.

Also, FYI: gardening.stackExchange also accepts plant ID questions -- it's really up to you where to post, but they are probably a bit more horticulturally inclined. I don't spend much time there, so I can't comment on their accuracy, though :p.

Reminds me of Senecio articulatus (Candle Plant; hot dog cactus), a succulent plant in the broad (aka polyphyletic) Senecio genus (Asteraceae).

 Source: U. Wisconsin-Eau Calire
Based on my limited knowledge of the plant and the variable leaf shape, I am not sure if this is your species or not. However, I'm sure some additional searching using this species as a guide will get you to the correct species/cultivar.
World of Succulents provides some additional information on Senecio articulatus.
You can see a video of a Senecio succulent identified as S. articulatus for better comparison to your plant:

This does certainly look like it!  The leaves certainly seem similar, and the colour seems right, not to mention fleshy stems!  The picture in the World of Succulents link does look like it has grown very differently though, but I don't know if that would be because the growth has been carefully managed?

Again, I'm not too knowledgeable on this plant. It's very likely that yours is a different species or cultiva in the genus. I welcome you to dig around a bit yourself and let me know if I can update this answer in any way to make it more accurate/useful.

It is likely that I'll accept this answer at some point once I'm done digging, and I'll post another comment if I feel that it could be improved with another comment.  Rest assured that I've not forgotten about this answer!

@Interminable no worries. I encourage you to dig around as I'm not 100% sure this is a correct answer. No rush. Feel free to add/update/comment about anything you find! (or feel free to add your own updated answer if appropriate!)

@Interminable please feel free to accept the answer if you are satisfied and found no further information. Thanks :).


text:
For humans, why is red the color of distinction rather than green?
The human eye is most sensitive to the color green. However, for some reason red is often selected as the color of distinction or alert. For example, in Renaissance times, painters would outline their figures in a thin red line. In manuscripts, a "red letter" (or "rubric") was used to emphasize an initial capital. Today, we routinely use red for emergency lights or whenever we want to call attention to something. Considering that red is the color our eyes are least sensitive to -- and green the most --  it seems counter-intuitive that we would use red when we want to draw attention to something. Why is this?

I think strictly you're mixing two concepts of color.  We can talk about a frequency of pure light (or a single photon) in terms of a color under the purview of optics.  But optic colors are poor metrics of what we see; instead, we incorporate a theory covering multiple frequencies of light with various intensities (spectra), combined with how they affect our cone sensitivities across an average of humans, under the purview of colorimetry. That in mind, our eyes are most sensitive to optic green, but red lights/paint is colorimetric red.

you make a number of unsupported claims throughout your question. Please indicate some prior research to support these claims and to indicate your own effort to answer this question.

Related question: https://biology.stackexchange.com/questions/24481

Perhaps because (at least in Western Europe and eastern North America, where these conventions originated) most of the world is green for most of the year, while only occasional ripe fruits and flowers are red.  Thus red stands out against the green background, while green blends in.

The reason is more historical than biological.
Our own eyes are more sensitive to green light, and ambient light is mostly green (we are a diurnal being). If you start doing real botany, you will notice that you can distinguish a lot of species just from the shade of green (and for trees, this also from far away).
Red is a difficult colour to produce, and often not very stable over time, and in nature is not so frequent. But it was used because it was also not very common in constructed environments. For example, for the Romans it was a symbol of power (and richness) because it was very expensive to produce red dyes. So red is visible because of the contrast with other colours.
The most visible colour is yellow: the "red" cones are really centred on yellow, and the "green" cones are still very sensitive to yellow. A good yellow appears brighter than any other colours because it stimulates both  the medium-wavelength cones and the long-wavelength cones in the human eye. Now emergency services tend to use yellow.
Note: red is not so special (but having a third type of eye cone is very special). Blood is red, but one rarely sees it as red: it quickly turns dark. Fruit? I think blue, green, yellow, orangeish, and dark brown were more common than red (and I recognize a tree by its leaves, from far away, so I'll know what fruit there are).
Traffic light: lights were already very yellowish, and blue, purple, and violets are not that visible, so green, orange, yellow, red, and also white are the most logical colours. I think yellow and white were too similar (especially in cities), because they were the colour of illumination and headlights. Note: in maritime traffic, red, green, yellow, and white are used (not orange).

This answer needs citations. Please see our guide to writing good answers in the help section. Thanks!

@theforestecologist: Adding citations is complex: I like the area of colours, but it is not my field, so I know it mainly from secondary sources (and technical point of view, so just as a "user"). If you tell me what one or two important points which requires a reference, I can add, but I give hints to "students", I would really not do their homework. Also considering the most controversial parts of my answer (IMO) are outside biology.


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Clatherin Mediated endocytosis is pinocytosis or phagocytosis?
This was a question in a test. Clatherin mediated endocytosis is which of the two: pinocytosis or phagocytosis?
Precisely what is the difference between the two and CME?

My answer would be pinocytosis
Eukaryotic cells are also able to take up macromolecules and particles from the surrounding medium by a distinct process called endocytosis. In endocytosis, the material to be internalized is surrounded by an area of the plasma membrane, which then buds off inside the cell to form a vesicle containing the ingested material. The term “endocytosis” was coined by Christian de Duve in 1963 to include both the ingestion of large particles (such as bacteria) and the uptake of fluids or macromolecules in small vesicles. The former of these activities is known as phagocytosis (cell eating) and the latter as pinocytosis (cell drinking).
During phagocytosis, cells engulf large particles such as bacteria, cell debris, or even intact cells.In contrast to phagocytosis, which plays only specialized roles, pinocytosis is common among eukaryotic cells. The best-characterized form of this process is receptor-mediated endocytosis, which provides a mechanism for the selective uptake of specific macromolecules.The macromolecules to be internalized the first bind to specific cell surface receptors. These receptors are concentrated in specialized regions of the plasma membrane, called clathrin-coated pits. These pits bud from the membrane to form small clathrin-coated vesicles containing the receptors and their bound macromolecules (ligands). The clathrin-coated vesicles then fuse with early endosomes, in which their contents are sorted for transport to lysosomes or recycling to the plasma membrane.
For more information please see this link https://www.ncbi.nlm.nih.gov/books/NBK9831/
Hope this helps!


text:
Can platypuses communicate via electroreception?
I know at least some electroreceptive fish are capable of basic communication with other members of their species via varying their own bioelectric signals.  However, I can't find any information as to whether platypuses (or, for that matter, any of the handful of other electroreceptive mammals) are capable of communicating in a similar manner.  Does anyone know if they're able to do this?

Electrocommunication is used by weakly electric fish only and it is limited to aquatic environments where the electrical conductivity of the medium allows to transmit electric signals. The best studied fish species that use this communication method are The African Mormyriformes (which comprise the Mormyridae or elephantfish and the Gymnarchidae with Gymnarchus niloticus as the only species) and the South American Gymnotiformes (or Neotropical knifefish).[1]
The mammals that are capable of electroreception use it for passive electrolocation which means locating the prey by detecting the weak electric fields of the prey with electroreceptors. These mammals are the three living species of monotreme; the Australian duck-billed platypus (Ornithorhynchus anatinus), the Australian short-beaked echidna (Tachyglossus aculeatus) and the Western long-beaked echidna (Zaglossus bruijnii) of New Guinea; and more recently discovered, the Guiana dolphin (Sotalia guianensis) from the cetacean order.[2][3]
Note: Electroreception was reported in star-nosed mole, Condylura cristata, based on limited behavioral data (Gould et al., 1993) but the theory remains unexplained physiologically.[4]
The electrosensory system of platypus (and probably other mammals) is evolved independently and the electroreceptors belong to the trigeminal system. The physiology of the electosensory system of mammals reveal why they can't use their electroreception for conspecific communication.

In African mormyriform and South American gymnotiform fishes this sense has evolved to an additional active system using an electric organ as a source for a.c. impedance measurement of the environment and for communication. All electroreceptors found in fishes and amphibians that do not have electric organs are of the ampullary receptor type and probably form part of the acoustico-lateralis system. In contrast, the electroreceptors in platypus belong to the trigeminal system. Their sensitivity to d.c. as well as to high-frequency pulses [2] contrasts with the mostly d.c. or lowfrequency responsiveness of ampullary receptors, which are less well-adapted to detect rapid muscle action potentials.
Langner, Gerald & Scheich, Henning. (2009). Electric Senses in Monotremes: Electroreception and Electrolocation in the Platypus and the Echidna. 1056-1060. 10.1007/978-3-540-29678-2_2919.
https://www.researchgate.net/publication/299656487_Electric_Senses_in_Monotremes_Electroreception_and_Electrolocation_in_the_Platypus_and_the_Echidna

References:
1. Map of Life - "Electrolocation and electrocommunication in weakly electric fish"
http://www.mapoflife.org/topics/topic_578_electrolocation-and-electrocommunication-in-weakly-electric-fish/
January 24, 2018
2. Passive electroreception in aquatic mammals.
Czech-Damal NU, Dehnhardt G, Manger P, Hanke W.
https://www.ncbi.nlm.nih.gov/pubmed/23187861
3. Electroreception in the Guiana dolphin (Sotalia guianensis)
Nicole U. Czech-Damal, Alexander Liebschner, Lars Miersch, Gertrud Klauer, Frederike D. Hanke, Christopher Marshall, Guido Dehnhardt, and Wolf Hanke
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248726/
4. Edwin Gould, William McShea, Theodore Grand; Function of the Star in the Star-Nosed Mole, Condylura cristata, Journal of Mammalogy, Volume 74, Issue 1, 19 February 1993, Pages 108–116, https://doi.org/10.2307/1381909

Further reading:

1. Electroreception (edited by Theodore Holmes Bullock, Carl D. Hopkins, Richard R. Fay)

2. Neurobiology of Monotremes: Brain Evolution in Our Distant Mammalian Cousins
(edited by Ken Ashwell)

3. Sensory receptors in monotremes ( Proske U, Gregory JE, Iggo A.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692308/

4. Electroreception in monotremes (John D. Pettigrew)
https://jeb.biologists.org:2083/content/jexbio/202/10/1447.full.pdf

5. Perceiving in Depth, Volume 3: Other Mechanisms of Depth Perception (By Ian P. Howard)

6. Electroreception and Electrogenesis (James S. Albert and William G.R. Crampton) http://www.ucs.louisiana.edu/~jxa4003/Albert%20PDF%27s/Albert-Crampton-Electroreception-proofs.pdf


text:
Mutate from non-GM to GM?
Would non-GM crops such as Grains, Fruits, & Vegitables retain their non-GM make up if they were to be re-planted in soils that have been made entirely of composted GM plants and GM plant matter?
Or would the GM plant matter still retain those properties enough mutate the transplanted or planted crop?

Can you please rephrase Or would composted GM plant and non organic plant matters still retain those properties enough mutate the transplanted or planted crop?. It is unclear to me

I am not sure I understand the question, but it appears to me as the question is about labelling and therefore is a question of policy and not biology. I am therefore voting to close.

You've rephrased the sentence I asked you too but I still don't get it. Maybe you misunderstand the concept of mutation. Note by the way, the in a single reproductive event, several mutations will typically happen. See for example estimates in humans from this question

I have reworded your question to relate solely to genetic manipulation (GM) as your question relates to mutation. Organic is a subjective concept, and this site is not about labels on food, which in any case vary between countries.

@Remi.b I modified the question so it is no longer about food labelling. I assume the poster knows nothing about genetic transformation, but you could interpret this as a question whether DNA from dead plants in the soil could transform growing plants, perhaps with the aid of soil bacteria. I'd still be happy to close under the portmanteau homework/lack of research heading.

@Remi.b  Tough crowd. Yes i'm very new and i'm keen on learning new things. obviously i'm behind the curve. i do appreciate assistance with the edit.  this is a Q&A site and i believe the question to be a valid one.
[eartheasy.com guide to compost][1]
[wisegeeks.org definition of flash freezing][2]
[wikipedia.org/wiki/Food_fortification][3]

@JeffreyBoettger Don't worry. It is not easy to ask a clear question, esp. as a new user. Do you think your question could be rephrased as Can plants absorb DNA from the soil and integrate it into their genome?. If you think it is not a goo reformulation, can you explain why?

@jamesqf no need to be rude. How is this related to religion? And, anyway, there isn't a "Religion SE", there are at least 4 I can think of for various different religions. Yes, the OP is showing ignorance, but there's nothing wrong with that! Not everyone is a biologist and, sadly, given the misinformation spread about what GM actually is, this sort of confusion is reasonable from a lay person.

@terdon: I don't see any rudeness.  WRT to religion, that is what most of the objections to GMO are based on.  Not reason or logic, but just the faith-based belief that GMOs are somehow "unclean".

@jamesqf the rudeness lies in ascribing motives with no evidence. Yes, some people object to GM based on religion. Many object for socioeconomic reasons. Others because the idea of fiddling with things we don't understand perfectly scares them.  What bothered me was your off-hand dismissal of "go ask on 'religion SE'" (a site which doesn't even exist). You are unlikely to find anyone who objects to religion as vehemently as I do, which might be part of why I found it insulting, but I don't think it's polite or fair to make such assumptions with not evidence.

The process of genetically modifying crops is performed in a lab. Genes would not leak into planted organic crops from compost any more than they would move from decomposing soil nematodes, earthworms, or manure. So no, organic plants would not be genetically modified. However, the labeling of a crop as "organic" is not always standardized, so it could be a cause of concern for some people who do not understand the process.

This is called horizontal gene transfer. In general, it's quite difficult to get a plant or animal to pick up foreign DNA and integrate it into its own genome, requiring special reagents and laboratory conditions. That's why we didn't have GMO fifty years ago. Note that you will spend your entire life consuming plants and animals for food, but you won't integrate cow, apple, or potato DNA into your own genome.
However, some viruses and bacteria can and do swap DNA with each other, and with their host organisms. In particular viruses can carry DNA into eukaryotic cells, and can even integrate the DNA into the host genome. Specially engineered bacteria and viruses are typically used as the vectors to create GMO in the first place. There has been concern about horizontal gene transfer from GMO organisms, but it's widely thought that it would be rare enough to not be a significant hazard. As far as I know there in nothing about GMO that would make them more susceptible to horizontal gene transfer in your compost pile than non-GMO.

It has been brought to my attention through further research on this subject matter that it is possible to obtain " DNA into your own genome"    http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.503.7552&rep=rep1&type=pdf.                                                    As specified from minute 23:00 to 23:38 https://www.youtube.com/watch?v=gjNtyFtJdho " the aleuts are so dependant & so integrated with the marine ecosystem that in fact their  tissues the same carbon 14 molecule reservoir as the sea lion."

Neither of those references say anything about integrating non-human DNA from food into human DNA. The thesis by Rubicz is just tracing the influences of surrounding human populations on Aleut genetics, that is, determining to what degree they are intermarrying with Russian and other neighboring native populations. The YouTube video doesn't say anything about integrating DNA either. Integrating carbon molecules from your food into your body tissue is very different from integrating their DNA into your genome. Carbon in itself doesn't carry any genetic information.

Should I remove comment and question all together? And ask the question of “How do carbon molecules enter human body tissue from a food source.”

That's up to you. That's certainly a very different question from the one you originally asked here.


text:
Are centrioles really absent in human neurons?
A booklet (issued by my school) claims,

Centrioles, formerly believed to be absent in neurons, have been described in neurons and may be associated with the production and maintenance of neuro(micro)tubules in them.

I was under the impression that mature human neurons are totally devoid of centrioles.
Being something circulated at a school, it lacks niceties such as citations/references. I've done a spot of Googling, but that didn't yield anything confirming the claim in the booklet.

Q- As per latest studies/info. do (mature) human neurons really possess centrioles?

You asked for "latest studies/info"... Funnily enough, mature neurons with centrioles were described by Cajal (who needs no introduction) in 1911.
If you want a more modern source, you can see Jacobson (1978):

Microtubules associated with the cilia and centriole are present in all young neurons and many mature neurons and glia. Neuronal cilia and centrioles can be seen very easily by light microscopy in sections impregnated with silver by the Nauta method (H. A. Dahl, 1963). Centrioles can also be shown by light microscopy in neurons stained by other histological methods. (emphasis mine)

Sources:

CAJAL, S. RAMON Y. (1911). Histologie du système nerveux de l'Homme et des Vertébrés (trans. L. Azoulay, 1952), vol. i. Madrid: Consejo Superior de Investigaciones Cientificas.
Jacobson, M. (1978). Developmental Neurobiology. Boston, MA: Springer US.

Aha! So they do have centrioles! :D Follow-up question please: Does that mean the answer to this question is incorrect? Cornelius says neurons lack centrioles (he cites stuff for that) :(

There are several sources that will state (incorrectly) that mature neurons never have centrioles. Besides that, the link in that question is not a peer-reviewed paper or a reputable book. Also, it's not " they do have centrioles", as you said... some mature neurons have centrioles.