text:
Why is the Red Fox colored bright orange?
They're not poisonous or anything, so it can't be aposematism.  As far as I know it doesn't come from diet like the flamingo.  They're not apex predators, so they can't get away with it (like tigers), and honestly it seems like a big risk factor given how many species prey upon them.  As well as something that would make hunting more difficult for them.  I understand they prefer dense brush, and I think hunting during low light hours, but orange against green is about as starkly contrasting as it gets.  So does that just leave sexual selection?  One of their sexes thinks it's pretty, basically?  Or is there some other reason for it, one that might have something to do with the rest of the odd coloring?

The orange colour isn't really all that bright. Photographs that make them look intensely orange (such as this one on Wikimedia Commons) have typically had the colour saturation cranked right up (notice that grass in that photograph is unrealistically intense green).

Most mammals don't have good color vision.  They're dichromats rather than trichromats like primates (including humans).  So you have to figure out what that red/orange color is going to look like to its dichromatic predators & prey.  Orange on green might be good camoflage to them - consider tigers :-)

Consider also that foxes are mostly crepuscular hunters... the low light levels around dusk and dawn mean that the orange/green clash is even less important. So maybe it really is just down to foxes like a nice orange mate.

Of possibly partial interest (given what I thought you might be asking from the title of your question -- "Why is the Red Fox coloured bright orange") is that at one time, English didn't use the word "orange" for the colour we now recognise as orange.  As this Wikipedia page notes, red deer, red hair and the robin red breast were all named "red" even though they were more orange than red.

The tiger doesn't just "get away with it" - it is very well camouflaged

Their fur colour is actually a pretty good camouflage

Ahahaha, I love how simple, and yet indisputable, this answer is :D

Good camouflage indeed

The difference between the name and reality is a linguistic rather than a biological issue. The word "orange" is a relatively modern English word. In the past "red" would have been a term applied to other creatures which are also the same colour, the "red" squirrel for instance, along with people with copper coloured hair who are said to are "redheads" and not "orangeheads".

From the question title, I also thought he was asking about the naming, until I read the body. :)


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What is the charge of (bacterial) ribosome?
Ribosomes are negatively charged and thus electrostaticaly repelled from DNA. However, I could not find a good reference that would allow me to estimate the magnitude of negative charge on a ribosome. Anyone could help with that?
This reference suggests it to be on the order of tens of e- or more.

@tyersome — Whoa! It's a fair question in itself if you look at the paper, even though it is not of interest to me, and the concern with DNA seems strange. The pH of the intracellular mileu can be assumed so that's not particularly important. In fact I am quite surprised that ribosomes are negatively charged, rather than neutral, as the negative charge of the RNA is balanced to a large extent by magnesium ions — you can't study ribosomes (as I used to do) without say 5mM magnesium. In all the  ribosome conferences I attended last century I never remember the topic coming up.

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(Genetics) Is a silencer the same as gene silencing (heterochromatin)?
Is silencer the same as gene silencing?
I know that gene silencing refers to those heterochromatin concentrated at the telomeres or centromere. It is also related to methylation. But what about a silencer. Are they the same? Or is silencer an opposite of enhancer (repressor)?

You are a bit confused with your terms here. Remember, when you are talking about natural regulation of a transcriptome, you can control it at the level of the genome, transcriptome and the epigenome.
The Repressor protein is a DNA- or RNA-binding protein that inhibits the expression of one or more genes by binding to the operator or associated silencers. Depending on where it binds, it regulates at the level of the genome or transcriptome.
The Gene Silencer Region, is a DNA sequence in the geneome that  that allows repressor proteins to bind to it. It is usually very near the promoter of the gene that it wants to control. This controls the expression of the gene at the level of the genome to repress the transcription of the gene. There exists a few types (Classc silencers, negative regulators and polycomb response) but lets not get into that).
An example is the regulatory element in the classical Lac operon.

Gene Silencing as you call it is epigenetic in nature. I'll point you towards the wiki as it is quite big and diverse to explain it here:
http://en.wikipedia.org/wiki/Gene_silencing
you can read more about it here:http://www.ncbi.nlm.nih.gov/books/NBK26872/

Never heard of NRE; what is it? Is PRE Polycomb Response Element? or is it negatively regulated and positively regulated. Please expand the abbreviations. Plus, lac operon is not an example of a "silencer". It is just a case of simple transcriptional repression. Silencers, like enhancers operate from a long distance and have more global effects but they function oppositely to enhancers i.e. they reduce the transcriptional activity.

@WYSIWYG Doesn't the Lac operon contain a regulatory element that keeps it off normally (LacI)? Also edited the post for the acronyms.

Yes it has a regulatory element at the promoter that is bound by LacI. These are usual cis elements and are frequently called operators; they only affect the proximal gene. Enhancers and Silencers control a bigger section of chromatin which may include many genes and they also sometimes interact with promoters via DNA looping.

@WYSIWYG Interesting. Never heard of it being called an operator before (was never taught that way) but thats a term. When you say tha Enhancers and Silencers control a larger section of the chromatin, I am assuming that you are saying that the enhancers are not gene specific right (in which case I undertsand)? Or are you saying that enhancers and silencers also control chromatin secondary structures (I have not really looked this up)?

Enhancers and silencers regulate several genes and can interact with their promoters, cause epigenetic changes or both. Both processes lead to a change in chromatin structure.

@WYSIWYG Thanks for the clarification. Do you have a reference for enhancers/silencers altering epigenetics mate ? I would very much like to read up on that. I know epigenetics can cover or uncover enhancers, but I have not heard of it being done other way around.

Many Polycomb/Trithorax responsive elements act as enhancers (that's how I got to know about them initially). Other examples include CTCF, CEBPs, etc. You can find many good reviews on these proteins.

CEBP does not mediate epigenetic modifications but the others that I mentioned, do.

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What will happen to transcription if histone acetyltransferases are removed from a eukaryotic cell?
If HATs are destroyed in a eukaryotic cell, how will gene expression level be affected? Will all gene expression be affected or just be slowed down and most gene will still be expressed?

There are many HATs, but I would expect many of them to be lethal knockouts, for example this.

Yes as March Ho said there are several HATs. Hat1 knockout is lethal [Ref]

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Would somebody born 'reversed' (e.g. heart on their right side, etc.) be completely healthy?
By reversed I mean their body is a complete mirror image of a normal human's.

Yes, such a conditions exists. It is called "situs inversus" (literally "inverted sites"). All major organs are placed on the opposite site, the condition is relatively rare with an incidence rate of 1:10.000. There are some even rarer forms occuring, when the organs are flipped, but the heart is still on the left side (levocardia) as opposed to the case when it is also on the other side (dextrocardia).
While some  of the patients are phenotypically normal (besides having their organs on the "wrong" side), congenital heart disease and ciliary disorders (also known as Kartagener syndrome) can occur. See the linked paper below for an overview.

For more information see here and here and the article:

Situs inversus and ciliary abnormalities: 20 years later, what is the
connection?

They're not always normal and healthy, situs inversus is related to primary ciliary dyskinesia: http://en.wikipedia.org/wiki/Primary_ciliary_dyskinesia

@CactusWoman I have updated the article, thanks for the critics.

And they tend to be sterile.  If the handedness of their MTOC is reversed then the spermatozoa tails cannot beat properly for swimming. Most XY's with situs inversus are identified via fertility clinics.


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In the Lineweaver-Burk Plot, why does the x-intercept = -1/Km?
Taking the reciprocal of both sides of the Michaelis-Menten equation yields the Lineweaver-Burk Equation:
$ \dfrac{1}{V} = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}+ \dfrac{1}{V_{max}} $
Plotting a $ \dfrac{1}{V}$ vs. $\dfrac{1}{[S]}$ graph, I am told that:
y-int $= \dfrac{1}{V_{max}}$ and
x-int $= -\dfrac{1}{K_m}$
How are these relationships derived from the lineweaver-burk plot?  I can see how the y-intercept can be equal to $\dfrac{1}{V_{max}}$ if $\dfrac{1}{[S]} = 0$, but I don't see how x-int $= -\dfrac{1}{K_m}$ by setting $\dfrac{1}{V} = 0$? Can someone demonstrate how these relationships were derived?

Equation of a line: y=mx+c or y=m(x-d) where c is y-intercept and d is x-intercept. The general equation of a line is y-y₁=m(x-x₁)

Set $ \dfrac{1}{V} = 0$ and solve for $\dfrac{1}{[S]}$:
$ 0 = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}+ \dfrac{1}{V_{max}} $
$ -\dfrac{1}{V_{max}} = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}$
$ -1 = {K_m}\dfrac{1}{[S]}$
$ -\dfrac{1}{K_m} = \dfrac{1}{[S]} = $ x-intercept


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What fruits will naturally ferment?
If left unpicked after the fruit ripens, what fruits may ferment instead of just rotting? My perception is that most fruits just rot.
I know figs will ferment. I'm guessing that this is because the wasp that pollinates the fig carries yeast inside what will become the fruit.
Eating ferment figs got me thinking about how humans first discovered ethanol. I'd guess that they ate ferment fruit and fiddled around until they could reproduce the process.

basically any fruit Yeast is everywhere. its more about conditions than type of fruit.

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Is intelligence (or mental ability) genetically transferred (inherited characteristic) from the parent to the offspring or is it an acquired trait?
The question is simple- whether our mental ability i.e. ability to acquire and store knowledge and comprehend and analyse the stored bits, an inherited trait (i.e. genetically transmitted from the parent to the offspring) or is it an acquired trait (depends on environmental, social factors)?
P.S. - Please attach the link of any reference/research (if any) with your answer.

This question is probably more appropriate on the Cognitive Sciences S.E..

Thanks for you suggestion @AMR, posted it on Cognitive Sciences S.E.

Standard IQ test are often considered the best proxy for intelligence. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref).
TO make sense of these numbers, you will need to understand the concept of heritability. You can find info on this important concept in the post Why is a heritability coefficient not an index of how “genetic” something is?. Other posts also offer an intro to this concept (see this, this, this or this post). You can also simply have a look at wiki. You might want for example to be able to understand the equation $H_N^2=\frac{V_A}{V_P}$ without further explanations.
The H2DB database may interest you as well and of course the wiki page on heritability of IQ

I think epigenetic factors and training will affects this more than heredity.

I think that this is a good technical starting point but it does not fully address the rather larger controversy. (And it's somewhat old)


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What is the attacking mechanism of RF on IgG?
Rheumatoid Factor (RF) attacks Fc portion of Immunoglobulin G (IgG), I want to know the underlying mechanism at molecular level. Also, what type of bond or attachment is made by RF and Fc portion of IgG?
// I'm a student of mathematical physics and have no detailed knowledge in biology, this question comes in my mind because my sister is suffering from Rheumatoid arthritis. All I want is to understand this disease from physical aspects//

RF factors comprise antibodies that your body makes that exhibit auto-immunity (recognition of self as an antigen). They often recognize and bind to IgG antibodies as illustrated in this picture:

So the answer to your first question is that the underlying mechanism is inappropriate recognition of self from your immune system.
For your second question, I am not an expert in the type of chemical bonds employed by antibody-antigen interactions, so I looked it up briefly. This article was quite informative for that: Antibody/Antigen Complexes.  The majority of binding seems to be hydrogen and ionic binding.
Hope that gets you going in your own searches.

Thanks sir, the link helped me a lot. I was searching something special in bonding of RF & IgG so that we can separate them via external forces. Here uniqueness and speciality is important in the RF-IgG bond because in breaking the bonds from external forces can destroy the bonding between another antigen and antibodies.

Great.  Mark my answer if it answered your question. That is how it works.

But I didn't get unique property of RF-IgG bond, the bonding between antigen and antibodies are generalized in that link.

Antibodies have variable regions that are just that.  Through VDJ recombination, this could be a multitude of ways. I don't know of a way to characterize a unique binding pocket for this process.  You might be able to do so if you could crystallize a monoclonal AB/IgG protein complex.  But my understanding in humans would be you would have many different auto antibodies coming from different B cells.  Anyone else that can chime in, please do.


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How does cancer of the larynx (laryngeal cancer) affect the respiratory system?
The larynx is part of the respiratory system and is responsible for producing sound (our voices). My question is how cancer in the larynx (voice box) affect the respiratory system overall? I appreciate any answer, but if it's not too inconvenient, please don't use too complex terminology (I'm in grade 10 Canada).
Thanks

Welcome to Bio@SE. What kind of googling have you done on topic? More precisely, what kind of information you want to get on that topic? Please, be advised that this site has policy on what questions are appropriate. Currently your question is too broad + you didn't provide any background or effort of your own.

According to this website:
http://www.spirometry.guru/fvc.html
it causes difficulty with inhalation but exhalation is normal...

"Typically the expiratory part of the F/V-loop is normal: the
  obstruction is pushed outwards by the force of the expiration."
  "During inspiration the obstruction is sucked into the trachea with
  partial obstruction and flattening of the inspiratory part of the
  flow-volume loop."

the exact symptoms of a laryngeal tumor depends on where it is located on the larynx... above the vocal cords, on the vocal cords, or below the vocal cords...
but more generally:
anatomy:
mouth/nose-->pharynx-->larynx-->trachea-->bronchi-->lungs
a tracheostomy may be necessary... basically the surgeon makes a connection between the skin outside the throat and the trachea... this bypasses the larynx (as well as pharynx and nose/mouth)...


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Wouldn't it be more efficient to let the kidneys flow into the intestines?
So I was thinking about how much fluids we lose when we pee. Then I realised that it would be much more efficient to remove the bladder and let it flow into the intestines so that the fluids can be reabsorbed.
What probles would arise from letting pee flow into the intestines? Also, where would be the optimal place to let the pee arrive? In the small intestine or closer to the anus?

You want continuous diarrhoea, and kidney infections?

Then I realised that it would be much more efficient to remove the bladder and let it flow into the intestines so that the fluids can be reabsorbed.

No. This would be very, very bad.
First, the kidney is very good at water conservation when necessary. If you're peeing up a storm, then you're drinking up a storm.
It is much more efficient to flush out waste products through the kidneys, and simply drink when thirsty. So you pee a lot. That's ok. It all ends up in the water cycle.
But emptying the ureters in any part of the digestive tract would mean terrible diarrhea, the kind that your bottom would burn like crazy every time you went (and you would hardly be able to control it, meaning large laundry bills) unless you used a protective ointment barrier between your skin and your diarrhea. To keep that skin from breaking down (yes, breaking down), you would need to bathe your bottom after every bowel movement. And it just would not be as good for fluid and electrolyte balance.
Also, the urinary tract is relatively sterile, protecting the kidneys from infection. The GI tract is anything but. The result would likely be so many ascending bacterial infections that your poor kidneys would be scarred and useless at a young age.
Nope, nope, nope.

Urine is acidic. It would irritate the bowels. It would also react with and spoil chemicals in the intestines that the body wants to recover like thyroxine. In general, the intestinal pathway is for fat-soluble materials and the urinary pathway is for water-soluble waste.
The body can absorb water from urine. For example, camels have very thick urine. Thicker urine is more acidic, so the camel's bladder has to be tougher.


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Why are antibacterial body soaps uncommon?
If body odor is caused by bacteria, and antibacterial soap kills bacteria, why aren't antibacterial body soaps hailed as the holy grail of getting rid of body odor? I can only find hand soap that is antibacterial.

Please don't use antibacterial soaps.. Unless you're a nurse or a doctor. This isn't a highly scientific link or anything, but I appreciate ASAP Science's work that they do in scientific literacy.

I recommend watching the video in the link I posted. And please, there is very little scenarios where you should be using antibacterials or hand sanitizer

Oh, but one occasion you should always use hand sanitizer - when entering a hospital/clinic/doctors office

@Bob: I had the impression hand sanitizer is pretty different from "antibacterial" soaps.

@Bob okay, I won't do it, but still my question stands. Shouldn't antibacterial soap be able to get rid of body odor altogether?

@sumelic It is! Usually hand sanitizer consists of 60-70% ethanol. Which isn't really harmful, and doesn't contribute to bacterial resistance. However, I do not see how killing your microbiota is beneficial. Hand sanitizer seems unnecessary, unless it's use is a job-requirement.

@vrwim I don't think so. I would even argue that it would make body odor worse since you'd be killing all of the microbes on your body - even the microbes that act to inhibit the growth of body-odor-causing bacteria

I think there are some misconceptions here. One, the bacteria on your skin are part of you normal flora and contribute to your body odor. If you kill everything, you leave yourself at risk for opportunistic infection and even worse body odor as the composition of your flora changes. Two, alcohol hand sanitizer will not kill all the bacteria on your hand in the 5 seconds you rub it to evaporation. Alcohol is a denaturing agent and requires 30-60s wetted contact time actually kill anything substantial. Three, triclosan isn't effective anymore: people have been using it improperly for decades.


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Plasmid: Empty Backbone?
When searching for a plasmid on Addgene what does it mean if it is said to be an "empty backbone"? Why would one want an empty backbone?

If you look on a very basic plasmid map, you usually see three different features: An origin of replication (often abbreviated ori or origin) which is necessary for the replication of the plasmid, a resistance gene (not necessary but useful to select for) and and multi cloning site (abbreviated MCS) which contains a number of unique restriction enzyme recognition sites, see the figure (from here):

In molecular biology plasmids are used to overexpress proteins in bacteria (or other cells) which are of any interest. To do this, you bring in the coding information for this gene into the plasmid using the MCS. Here you can cut the plasmid controlled (only open the ring on one site) and insert DNA of interest. An empty plasmid in this context means that it can readily used for cloning purposes as it does not contain any foreign DNA.

cause you want to put your own stuff in without worrying about other people's junk interfering with your stuff.
Something like why would you want an empty hard drive and not one which is almost full with stuff from somebody you don't know.


text:
How to read this diagram?
I have diagram of oxidative decarboxylation of pyruvate pathway. The pathway is between glycolisis and Krebs cycle.
How to read this diagram?
This excerpt from Harper's Illustrated Biochemistry, 30E, page 173.

The circles are like gears, where the points of contact are chemical reactions.

To me, it is unclear exactly what you are asking about, and the question also reads as unresearched homework.

Take a look on reaction catalyzed by dihydrolipoyl dehydrogenase. It acts upon $NAD^+$ according to following equation:
$NAD^+ + FADH_2\rightarrow NADH+H^++FAD$
Same way you can write other reactions, e.g. by pyruvate dehydrogenase:
$Pyruvate+TDP\rightarrow CO_2+TDP-Hydroxyethyl$

Texts usually have a verbal explanation of these kind of diagrams, so look in the text where it references Figure 17.5 and read the section before and section after.
That being said, if you start at the top with pyruvate, it enters the cycle where the curved circles touch on pyruvate dehydrogenase, which catalyzes its decarboxylation. That product then enters into the next cycle where the disulphide bond is broken and it is added to one of the sulfurs. Co-enzyme A then reacts with that and you get Acetyl CoA as a byproduct and dihydrolipoamide. The cycle continues and you get one hydride (I think) and one proton transfer to FAD and the reformation of the disulfide bond. You then have a hydride transfer to NAD+ and a deprotonation to regenerate FAD.
So each place a curved arrow touches another is what goes into the reaction and then following the split of the arrows is the product that comes out of the reaction. Where there are transfers to different circles means that there are different enzymes catalyzing the reactions.


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Do I not have any alleles from my mom's mom & my dad's dad?
So, I have an XX, & I got an X from my mom, & an X from my dad. My dad would have gotten his only X from his mother, & my mother could have gotten the X I got from her father or mother. That would mean I did not get either X gene from either my mom's mom or dad, or my dad's dad - does that mean that I have "less" of their genetics in me? Say I got my mom's dad's X, would that mean I have less of my mom's mom's genetic traits?

Speaking of your DNA in general, you have alleles from all four of your grandparents.  The 22 pairs of autosomes (non-sex chromosomes) can receive DNA from all four with random mixing.  On a few chromosome pairs you may be missing alleles from one of your grandparents due to the randomness, but on average you will have about a quarter of your autosomes from each of them.
The X (and Y, for males) chromosomes are special, though.  The X you inherit from your mother will have alleles from both your maternal grandparents.  The X that you, as a female, get from your father has no alleles from his father, so that grandfather's X alleles are always missing from your genome.
Because of the random mixing, you will have slightly varying amounts of DNA from each of your grandparents: it won't be exactly 25% for each of them.  Because of the special X inheritance, your paternal grandfather will on average contribute slightly less than the other three grandparents.  (Because of another quirk, mitochondrial inheritance, your maternal grandmother will contribute on average a very small amount more than the other three grandparents.)

Regarding your second paragraph, you should consider recombination between the pseudoautosomal regions of the X and Y chromosome.

Nice summary. Sex chromosome inheritance is interesting, for instance that paternal grandmothers are on average more closely related to their granddaughters than their grandsons: Fox et al. 2009. Grandma plays favourites: X-chromosome relatedness and sex-specific childhood mortality. Proc. Roy. Soc. B


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Is too much CO2 in the air toxic?
I know that if there is too much CO2 in the air we will have too much greenhouse effect.
I would like to know if there is too much CO2 in the room, something like 3% while there is also more that adequate oxygen for us to breath. will we live or die? why?

CO2 forms carbonic acid in water, which helps to dissolve rocks and mountains in envitonmental science. It would slightly acidify your body with what is called a weak acid.
5% can cause acidosis and loss of conciousness, without lack of oxygen.
3% would devastate most chalk based sealife, corals and shells.
Perhaps lifelong breathing of 3% co2 would have serious effect on alkaline processes in the body, osteoporosis, and would have to be counterbalanced by the body to maintain its blood ph above 7.35, with alkaline chemicals like sodium.
Also check out this fact sheet.

First, the toxicity of any  substance is a matter of dose. So the answer of your question is yes too much is toxic but the real question is how much is too much ?
This is still not clear in the litterature but effect are starting to appear over 3% see:
HAYWOOD C., BLOETE M.E. -
Respiratory responses of healthy young women to carbon dioxide inhalation. Journal of Applied Physiology, 1969, 27, pp. 32-35.
OR
ALEXANDER J.K.,WEST J.R.,WOOD J.A., RICHARD D.W. - Analysis of the res- piratory response to carbon dioxide inhalation in varying clinical states of hypercapnia, anoxia and acide-base derangement. Journal of Clinical Investigation, 1995, 34, pp. 511-532.
CO2 is the result of respiration as you know and a too high concentration in the blood result in a change a Ph of your blood and asphyxia. You can find more information on those effect here Permentier and al.
Hope this helps !

nice answer. You can add more information about physiological impact on hem, but it is still good :).

I know CO2 is toxic if it's too much in the blood. by question can somehow be reduced to how doe increasing the CO2 level of air increases the CO2 level of blood.


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Clarification for the anatomical terminology of the cerebellum
I've been trying to find descriptions for some of the fissures found on the inferior surface of the cerebellum, and so far the only source I've been able to find that provides an adequate description is Gray's anatomy (1918, 20th edition):

The prepyramidal fissure crosses the vermis between the uvula in front and the pyramid behind, then curves forward between the tonsil and the biventral lobe, to join the postnodular fissure.
The postpyramidal fissure passes across the vermis between the pyramid and the tuber vermis, and, in the hemispheres, courses behind the tonsil and biventral lobules, and then along the lateral border of the
biventral lobule to the postnodular sulcus; in the hemisphere it forms the anterior boundary of the inferior semilunar lobule.

So, that would make these fissures the following ones:

(the blue one being the postpyramidal fissure, and the red one being the prepyramidal fissure)
However, I checked a few atlases:

(here, 2 and 2' are the postpyramidal fissure and 4 is the prepyramidal fissure)
And on radiologykey, the descriptions it gives for these fissures is the following:

The postpyramidal (secondary) fissure separates the pyramis/biventral lobule above from the uvula/tonsils below
the prepyramidal fissure separates the tuber above from the pyramis below.

It seems like Gray's anatomy has the names swapped or something, is that the case? If so, that means I can still use these descriptions but just swap the names.
And is the secondary fissure the same as the retrotonsilar fissure/postpyramidal fissure?


text:
Why does dryness irritate mucosal surfaces, and what exactly is this "irritation"?
The mucosal surfaces of the body function to moisten the epithelial linings and keep them from becoming dry. Why is this important? As an example, the respiratory tract moistens and warms the air that we inhale before it gets to the lungs, to protect it from damage and "irritation". How would cold, dry air cause those things?

How do you think it would cause those things?

I genuinely have no idea, I sat down a few times and looked it up as much as I could, nothing really describes how dryness and coldness irritates a cellular lining.


text:
What do repopulation and expansion mean in stem cell biology?
I was studying a lecture on the effects of cytokines on hematopoiesis, and it uses these two terms often in the context of the effects of regulators on hematopoietic stem cells:

All repopulating bone marrow HSCs express a fibroblast growth factor (FGF) receptor that supports HSC expansion
TPO may has a role in promoting the survival of repopulating HSCs, however, it contributes to both generation and expansion of HSCs during definitive hematopoiesis.
Etc.

I looked online and honestly struggled to find any form of a definition on these two terms. They are used awfully alot though which makes it kinda weird too frankly.


text:
what is the role of granulation tissue in bone fracture repair
When a bone fractures, let's say with a large enough gap that repair has to occur through secondary healing, vessel rupture will result in a hemorrhage that then coagulates, there's inflammation that removes tissue debris, and granulation tissue forms as capillaries and fibroblasts infiltrate, using the hematoma as scaffolding. Next is the formation of the soft callus. What is the composition of this soft callus?
I understand that chondroblast precursors are activated, and cartilage forms to bridge the fracture ends, but what happens to the granulation tissue from earlier? The fibroblasts that infiltrated the site of the fracture, do they lay down fibrous connective tissue or do they differentiate into cartilage cells and lay down cartilage matrix as well? I've been reading from multiple sources, and none of them really specify it well enough for the ambiguity to not remain.


text:
What does it mean when a patient suffering from malignant tumor (cancer) has been declared cured?
Comment by Anongoodnurse, has made me curious as to what a doctor means when (s)he says "The cancer is cured" to a patient.
My idea up till this point (based on what I read and what I learned in my classes from my professors) was that the prognosis was declared based on the survival rates and that cancers could never be declared cured as no one could be sure that every single malignant cell has been eradicated.
However Anongoodnurse commented:

Curable cancers are not few and far between.

So I would like to know what it means when it is said "Cancer is cured"

Though the answer by Anongoodnurse has been accepted, I would like to have other answers too, please feel free to contribute

Being a programmer and not a medical practitioner, most of my knowledge on this subject can be summed up in this XKCD comic.

Lol, excellent one

TL;DR - ask someone who has survived 45 years after treatment of their testicular cancer. The patient (and most doctors) would consider that a cure.
I believe the kxcd cartoon explains prognosis quite well. There is something that @Crags has overlooked, though, and that is the caveat "Once most cancers spread out into your body, they're incurable".

I would consider that sentence to be quite correct. A good prognosis is very different from a cure. Most of the surgeons, radiation therapists and oncologists I have worked with make that distinction. (Even surgeons, whose mottoes include "A chance to cut is a chance to cure." and "Nothing heals like cold hard steel." are careful not to use the word cure, unless it is a cure.)
I am not an oncologist, but oncologists do write papers. From one of them:

METHODS: We analysed postmenopausal women with localised invasive breast cancer. The primary endpoint disease-free survival (DFS), and the secondary endpoints time to recurrence (TTR), incidence of new contralateral breast cancer (CLBC), time to distant recurrence (TTDR), overall survival (OS), and death after recurrence were assessed... FINDINGS: At a median follow-up of 100 months (range 0-126), DFS, TTR, TTDR, and CLBC were improved significantly in the ITT and hormone-receptor-positive populations.

Although this study only followed patients for 100 months (8.3 years), some studies are much longer, and a cure is what you or I would think of as a cure: disease-free survival, not of months, but for a lifetime, that is, non-recurrence of the cancer.
Your professors sound like they are using the standard approach to cure, which is to hedge one's bets:

In medicine, a disease is considered cured when it’s been successfully treated and does not return. The concept of “cure” is difficult to apply to cancer because undetected cancer cells can sometimes remain in the body after treatment, causing the cancer to return later (referred to as a recurrence or relapse). Many cancers are considered “cured” when there is no cancer detected five years after diagnosis. However, recurrence after five years is still possible.

In the past, cure was defined as 5-years cancer free. We now know that that is survival, not cure. The same can be said of 10 years (thought that one runs more true to cure). The fact is, most studies don't follow patients indefinitely. That doesn't mean no cancer is "cured". The patients (even many of those in the xkcd comic) without recurrence are cured. Therefore it is a fallacy to say cancer can never be cured. Semantics and statistics are at play.
As I said in my comments, there are curable cancers.
Curable cancers: non-invasive basal cell carcinoma:

Nearly every basal cell cancer can be cured, especially when the cancer is found early and treated.

(This is not a hedge. The authors are lumping aggressive BCCs in here with the less aggressive BCCs.)
Certain early prostatic cancers:

These results suggest that a patient has a high likelihood of biochemical cure after treatment for prostate carcinoma with conventional doses of external beam RT if he has not demonstrated biochemical failure within 5 years of treatment. Patients with lower pretreatment PSA levels and lower Gleason scores may require longer follow-up than those with less favorable characteristics to achieve the same certainty of cure. Patients who achieve a PSA nadir ≤ 0.4 ng/mL and require ≥ 2.0 years to reach this nadir have the highest probability of cure.

Cervical cancer:

Early cervical cancer can be cured by removing or destroying the precancerous or cancerous tissue.

Colorectal cancer:

Conclusion: Patients who survive 10 years appear to be cured of their disease, whereas approximately one third of actual 5-year survivors succumb to a cancer-related death. In well-selected patients, there is at least a one in six chance of cure after hepatectomy for CLM. The presence of poor prognostic factors does not preclude the possibility of long-term survival and cure.

Childhood acute lymphocytic leukemia:

Impressive improvements of survival rates in pediatric acute lymphoblastic leukemia (ALL) have been achieved during the last decades.1–21 Today, a long-term cure can be attained for approximately 75% of patients.

(Although good survival rates - defined by *event free survival - are defined at 6 years in this paper, there are papers which follow to 15 years with little change in the group. Like most studies, longer times mean more patients are "lost to follow-up".)
It goes on and on.
Finally, my comment was an admonition to you to be wise with your words, not an absolute.
Understanding Statistics Used to Guide Prognosis and Evaluate Treatment
The cure of cancer: A European perspective
Basal cell carcinoma: Diagnosis, treatment, and outcome
Cervical cancer
Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95

Thanks for the detailed explanation. I understand that the confusion is because of the interplay between statistics and semantics. But I gather that a cure seems mostly a retrograde statement rather than a prognosis given at then end of treatment

Or rather a prognosis based on statistics and confirmed only by the passage of years

You ignore the obvious. Some cancers, including BCC and cervical cancer, are curable. If you don't want to accept that, you don't have to. You can believe that a localized cancer which is completely removed will recur in the future. Who can prove you wrong? (Except for the millions who are still alive 40 - 50 years out, and who knows about them, really?)

While what you say is correct, what can you tell about those in whom it does recur, those millions who are in their graves? Then again dead men tell no tales!

Find me papers on the death rates of localized small BCCs. I found papers supporting my answer.

I am stating the obvious, that cure can be pronounced only on retrograde analysis on a case by case basis unless there are cancers with absolutely no chance of recurrence (0 % recurrence rate proven). I mean even if recurrence rate is say, only 0.1% that person could be you.

I am not disagreeing with you, as I said earlier. Just stating the obvious

If you know all the answers, why bother asking the question? You asked "what (does) a doctor mean when (s)he says 'The cancer is cured' to a patient.?" I'm a doctor. I explained it. That's all I'm going to say.

OK, I accepted your answer right? I guess it is subjective, based on doctors too. I agree that you represent a class of thought among doctors. And some cancers do have very low recurrence rates. But it is never zero.

As I mentioned, even among doctors different classes of opinions exist. That was the reason for my question


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Hot water bath and Infertility
From here:

Effect of temperature. Sperm cells will not mature at core body temperature in most mammals (spermatogenic DNA polymerase b and recombinase activities exhibit unique temperature optima); to adapt, the testes assume an external position. Testicular descent from the abdomen normally transpires during fetal or neonatal life.
If the testes fail to descend into the scrotum, a condition called cryptorchidism, the male will be sterile; gone uncorrected (by surgery or androgen treatment) spermatogonia will eventually degenerate.

How many minutes of exposure to hot water is tolerable?
Can regularly bathing in hot water lead to infertility?
Up to what temperature (of bath water - assuming the maximum tolerable temperature would not hurt skin) is tolerable?


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Genotoxic agent and their metabolic pathway
What are the mechanics (set of biochemical reactions) allowing a given genotoxic agent

to modify the mutation rate at a given spot?
to induce only a given type of mutation (from Gs to Cs for example)?
some other consequence of the kind that you think is worth talking about!

I am not necessarily seeking for a very detailed explanation of the biochemical pathway but rather some kind of understanding of how such things are possible (not evolutionary speaking but in terms of physiology and cytology).
This question comes in reaction to this post.

Here is a somehow related question I asked a month ago and which is still unanswered. It might interest you. http://biology.stackexchange.com/questions/10011/how-can-a-mutation-influence-the-recombination-rate-of-a-specific-sequence

In terms of DNA mutations, it's usually just pure chemistry.  The mutagens article gives a brief rundown of some of the usual suspects, but to pick a few of the ones I'm familiar with:

UV light can cause pyrimidine dimers, which clearly is a dimerization of Cytosines or Thymines, which can cause replication issues.
Deaminases, which remove amine groups, is probably the coolest example.  Deamination can occur naturally, turning Cytosine into Uracil, but is often done deliberately as part of bisulfite sequencing to determine methylation status.
Alkylation can occur, in particular of Guanine, which can lead to a preference in binding for Thymine; subsequent replication will result in an Guanine to Adenine conversion.

Similarly, there are many base analogs that will fill in for a given nitrogenous base.  These analogs often prefer to bind to an "incorrect" base as above (and in the figure below with 5-bromouracil) which will lead to specific errors.

On a more intentional basis, biotechnological tools such as zinc finger nucleases, TALENs, and the (oh-so-sexy) CRISPR system can be used to specifically alter genome sequences of choice.  ZFNs are in particular being used as a gene therapy tool for just that reason.
Otherwise, viruses (and transposons) that insert into the genome can cause specific mutations or errors if they do so non-randomly.  Figuring that out, though, can be tricky; most oncoviruses cause mutations through specific genes that allow uncontrolled growth and tumorigenesis, not in a site-directed manner.  There is, however, a growing hypothesis that certain retroviruses which tend not to cause cancer, in particular HIV, may be inserting into sites with certain characterizations, such as chromatin level.  That is far from known, though.
If you're looking for random causes, that's easy.  Anything that disrupts DNA repair mechanisms such as p53 or Rb will do that.  For chemicals, intercalators such as ethidium bromide and thalidomide insert in between DNA bases and prevent proper DNA repair.


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What is the biding site code recognized by the parts of the spliceosome
Another question about another Youtube video. At 0:50, the splicing process begins to remove the non-coding section of the DNA (intron), so the different parts of the spliceosome attach to the borders on the intron.
My question is, what is the code found in the borders of the intron which is recognized by the parts of the spliceosome, so they attach to it ?
For example, in the transcription of the DNA, the process begins after the transcription factor "TBP" recognizes the code "TATA" in the DNA string, then attaches to it. This triggers a whole process described by this video.

Did you try googling "splice site recognition sequences"?
In general, the first two letters of the intron must be GT, the next three are often ARG.
The last three letters of the acceptor site of the intron are virtually always YAG

Thanks !! Do some section inside the intron play a role in this process ?

Well the GT-AG motif is inside the intron (the actual consensus sequences for humans are 5'-(C/A)G|GU(A/G)AGU ... NCAG|G-3', | denotes the intron/exon boundary). Additionally, there is a branchpoint site near the 3' end of the intron which has consensus sequence YNYURAY followed by poly-Y. The A is highly conserved and its 2'-OH is used to join the 5' end of the intron, creating the lariat. Also, note that because splicing requires high precision (an indel of 1 nucleotide means a frame-shift mutation), the spliceosome has additional mechanisms to ensure the splice site is selected accurately.


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Different kind of M13 primer
I m looking for universal primers M13. I found different version. For instance :

M13 (-21) Forward TGTAAAACGACGGCCAGT
M13 (-40) GTTTTCCCAGTCACGAC

What's the meaning of (-21) and (-40 )

This dates back to the 1980's when these M13 primers were first cloned.
Heidecker G, Messing J, Gronenborn B. 1980. A versatile primer for DNA sequencing in the M13mp2 cloning system. Gene 10(1):69-73.
In this paper, they discuss the construction of a primer for sequencing of the M13mp2 phage vector. An EcoRI/AluI digest releases a 92 bp fragment from a portion of the lac operon. This fragment contains what are now called the M13 forward -21 and -40 primers. I do not know who first named these primers but, counting from the centre of the EcoRI palindrome, I think it's clear where these names came from:


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double PCR with tailed primer
I would like to make a double PCR with universal tailed primer. The first PCR would make a tailed amplicon. The second PCR would generate fragment labeled with fluorescent dye. Here is my protcole. Could you tell me if I am wrong ?

is my second PCR forward primer well designed to fit with the tail ?
What would be the ratio of primer to use if I want to merge the two PCR into one ?

Fist PCR ( works )
In bold, you have the tail M13(-20)
Forward : 5'-GTAAAACGACGGCCAGTTCTGCAGTTGTACTGAGTGAA-3'
Reverse : 5'-AAAGCGTGCAGCTGATATTT-3'
Mix for 1 sample

Water              = 15.8µL
MgCl2 (25mM)       = 18µL
Buffer (5x)        = 6µL
dNTP (4mM)         = 1.5µL
Forward(20pmol/µL) = 1µL
Reverse(20pmol/µL) = 1µL
GoTaq (5U/µL)      = 0.15 µL
DNA (50ng/µL)      = 1 µL

Second PCR ( not working = no fragment signal )
Forward : 5'-[FAM]-GTAAAACGACGGCCAGT-3'
Reverse : 5'-AAAGCGTGCAGCTGATATTT-3'
Mix for 1 sample

Water              = 15.8µL
MgCl2 (25mM)       = 18µL
Buffer (5x)        = 6µL
dNTP (4mM)         = 1.5µL
Forward(20pmol/µL) = 1µL
Reverse(20pmol/µL) = 1µL
GoTaq (5U/µL)      = 0.15 µL
DNA (50ng/µL)      = 1µL from my previous amplicon

Are you forced to use the reverse like this? I've been taught to avoid A/T ends and stretches of more than 3 consecutive C/Gs or A/Ts; your reverse has both. Besides that, did you try a gradient for the anneaing temperature?

No, I can change the primer ! Thanks for your advice.

I'm not sure to understand your query. I can say that in my lab we are also using fluorescent dye (for SSR detection). But we are doing it with a one step approach:
Our forward primers are like yours preceded by the fluo sequence (M13-forward primer). But instead of making a second PCR, we add directly the fluo primer (let's called it M13-FAM) in the first PCR. It is REALLY important to put your M13-forward primer in lower quantity than the reverse one (factor 10 for me). To achieve that I use 0.1mM primer solutions and I mix my primers before
For 96 wells (20µL/well)
Primer Mix

1.25 µL of M13-F primer
12.5 µL of R primer
240 µL of water

PCR Mix

200 µL of Primer Mix
20 µL of M13-FAM
Master Mix 1mL
Water 1mL

Thanks ! You answer to my question perfectly ! I was doing 2 PCRs to check my primers first . But my final goal is what you did .
Could you give me your primers ? To check if I am not wrong ? I m not sure if M13-tail primer and M13-FAM have to be in same orientation 5'-3'


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Example of impossibility in the nested hierarchy?
I have conversations with evolution deniers, and I've read that the best single piece of evidence for evolution is the congruence of the genetic and morphological nested hierarchies, and the fact that they are predicted on evolution, but not on intelligent design.
I think I have an example of what would falsify the nested hierarchy; please check me on this, I want to get this right.
Because evolution is a historical process, an organism can only share characteristics, or have varied characteristics, of one of its ancestors.  If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy.  An example of this would be a primate with two post-orbital fenestrae (see pic)..
And, we don't find such organisms.
This is not predicted on design because if you design from scratch, without the necessity of varying ancestors' characteristics, you are not limited by not designing a primate with two post-orbital fenestrae.
Do I have this right?

Your view of evolution is wrong

If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy

The expression "falsfying the hierarchy" does not mean much, so I won't comment on it.
Note two things
1) Convergent evolution
 - It is not so uncommon that different lineages evolve similar traits when facing similar selection pressures. This is called convergent evolution.
2) Horizontal transfer
 - It is not so uncommon that pieces of DNA find itself (via a number of different mechanism) in a different lineage. A gene can therefore jump from one lineage to another one. This causes the gene tree of a given gene to not match the species tree. Other processes can cause such mismatch though. This is called horizontal gene transfer.
So, in short, no your view of what you call "impossibility in the nested hierarchy" is wrong.
Intelligent design
Intelligent design is not a scientific hypothesis. It means that it does not make logical sense and it does not make clear predictions that can be tested. By contrast, the theory of evolution is a set of hypothesis all of which that have been formally tested have shown to be confirmed by evidence (that's why the theory of evolution is called a theory;
see here for the semantic).
It is therefore impossible to say whether intelligent design is correct or wrong because it does not say anything. One cannot compare the predictions of the theory of evolution with the ones of intelligent design as intelligent design does not make clear predictions. One can only argue why the theory of evolution
is a set of (confirmed) hypotheses while intelligent design is not a hypothesis (or set of hypotheses).

While evolution generally predicts a nested hierarchy for shared traits of organisms, it's not generally that simple - there are some cases that can lead to exceptions of strictly nested hierarchy.
The first (obvious) one is convergent evolution: if there is an easy biological 'solution' to a certain problem (caused by the environment), then evolution will often find that solution independent where it started from. A good example for this are back fins in fish and marine mammals, which are very similar but not actually related. Of course this is no argument against evolution, it's just a bit more complicated to explain, why different evolutionary starting points can lead to (seemingly) the same outcome.
A second possible exception is caused by the fact that organisms do not just gain new traits during evolution, they can also loose them (if they don't serve any purpose any more).
A very good example for this are teeth: sharks have them, some fish have them, mammals have them, as do many reptiles, but birds generally don't have teeth. Still this is no argument against evolution - first because birds don't need teeth so why should they keep them? Secondly, the genetic program to make teeth is not absent or missing in birds - its just disabled: when researchers tinkered around with this, they managed to make chicken with alligator (or dinosaur) like teeth

Nicolai, thanks very much.  Aside from those exceptions like the ones you mentioned, would you say that my example is a good illustration of the basic idea of why the nested hierarchy is predicted by evolution?

@Slothrop yeah your example is definitely right. Generally you expect a new trait formed at a junction in the taxonomic tree to be present in most species that are descendent from this point.

As an add-on, genetic evidence is often an excellent tool in cases of convergent evolution that are not as clear-cut. In most cases, convergent phenotypic solutions come with dissimilar genetic ones.


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Specialist evaluation for people aged under 40 years with stage 1 hypertension
Reading the NICE clinical guideline for Hypertension it says...

For people aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes, consider seeking specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage.

However it is not clear in the guidelines exactly what "specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage" would entail.
I understand that it is typical to carry out blood tests to look at kidney function, thyroid function, cholesterol and glucose levels; and that further tests such as a 12-lead ECG, echocardiography and renal ultrasound scan may be ordered if necessary to test for organ damage.
My question is what further tests would be performed by a specialist on a patient aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes? I have done several searches on Google but most of the papers I've read relate to patients who already have signs of organ damage or existing disease.

Alongside full guidance released by NICE they also produce treatment pathways which give further advice - here is the treatment pathway for hypertension.  You've listed most of the investigations that would be considered in your original question.
Investigations that may be considered as appropriate include:

Urine dipping for proteinuria or haematuria indicative of renal damage
Measuring of plasma urea and electrolytes and estimation of glomerular filtration rate, again as an indicator of renal damage
Measuring of plasma glucose, total cholesterol and LDL/HDL cholesterol to rule out additional risk factors as part of cardiovascular risk assessment - e.g. diabetes, hypercholestrolaemia
Fundoscopy to examine the retina for damage resulting from hypertension
12 lead ECG to show any changes compatible with left ventricular hypertrophy
Scanning for the presence of a phaeochromocytoma if clinically suspected

You may also find the professional reference page on hypertension from patient.co.uk useful.


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Plant Identification Help

Can someone help me identify this plant? Flowers bloom in summer, then red seeds form afterwards.  Leaf length is about 10 inches max.  I live in Southern California and it is grown in a container under my patio.
Thanks for your help.

This seems to be Scadoxus Puniceus, also known as the Paintbrush Lily (not to be confused with other species with the same common name). The dutch originally cultivated scadoxus puniceus, and your specimen could be one of several hybrids of the original.
Dave's Garden has plenty of pictures of the species. He didn't have any fruit at the same stage of ripeness as yours, but the likeness is still rather compelling.

For a slightly more reliable source (if a little older), the South African Medical Journal also identifies Scadoxus Puniceus in a study of accidental poisonings by herbal medicine. The flower might be a touch wider than yours, but you almost certainly still have a Scadoxus, and within-species variations can easily account for such a small difference.

Copyright Disclaimer: All included photos would typically fall under fair use due to their limited scope compared to the original work and due to their non-commercial use as a benefit to the public. If any of the copyright holders disagree, feel free to contact me so we can resolve the problem.

Welcome to the biology SE and congrats on your first answer, that I believe to be correct. However, on BiologySE it is required that you substantiate your claim with evidence, for example a picture or a description why it is this species.

@RHA Thank you. Is this more like what you had in mind?


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Technical Name for Bamboo Leaf Plant
Can someone provide a technical name for this plant.  Sometimes called "bamboo leaf plant" and is often used for plating of sushi or for cutting leaf for decorations for sushi plate.  Rhizomes for root system, does not bloom flowers, and prefers shade.  Found in Southern California.  Grows to about 36 inches tall.  See attached photo.

Does it have any distinct smell?

Right, I'm almost certain that this is an Aspidistra plant - the growth habit is  practically the same, and your description of it being used for plating sushi mirrors some of the traditional Chinese and Japanese uses for the plant. As for the flowers, it's probably had quite a few - Aspidistras bear rather strange-looking purple-maroon flowers just above or partially buried in the soil.

Interesting……..


text:
Gene silencing: relative or absolute number of methylated CpG sites?
CpG content varies a lot across the human genome. What does determine a promoter to be silenced through DNA methylation: the fraction of CpG sites that are methylated or the total number of methylated CpG sites? Any reference?

Total methylated sites in the genome or in the promoter?

In the promoter

Generally, robust silencing by DNA methylation requires that all or most CG sites be methylated and that there are a good number of CG sites to methylate.  (A 'good number' is relative to each species depending on CG content of the respective genome.)
A promoter with ~10% of its CG sites methylated would not likely be silenced.  However, the caveat with this is that one well-placed methylated CG can cause silencing or at least decreased promoter efficiency.  Also, many promoters are depleted for CG, which means they can be fully methylated, but still not have much absolute methylation.  These promoters can be active despite apparent 'hypermethylation' in the CG context.  Also, a caveat to this is that promoters with zero methylation can be silenced, even if they have CG sites.  Basically, if CG methylation is important in the regulation of a gene, it will have CG sites in functionally-important parts of the promoter.  The promoter will be well-methylated when the gene is silenced, but because placement of de novo CG methylation is not absolutely perfect, there is a high likelihood that there will be more methylation than is needed for silencing to be achieved.  A sort of overkill phenotype.
This paper from the Schubeler lab is a nice foray into the mammalian promoters, which they break into 3 different groups depending on CpG content, and then further analyze each group for CG methylation profiles.


text:
What is this tree in Sydney?
My family snapped this picture around Sydney, Australia. Could someone please advise what this tree is? Help! We are smittened with it :)


text:
is Xanthosine Xanthine plus ribose?
I'm so confused. I used to think Xanthosine is Xanthine with a ribose instead of H but it appears to me as if it isn't. If you look at the picture in top-right of its wikipedia page you will see that the Imidazole is reversed from the picture in here also the picture in the bottom of this page in additional images section is like the second one. I'm sorry if didn't use the right chemical terms! I'm no chemist. Also I while I was searching I saw different images for Adenine and Guanine where the Imidazole loop was reversed in some by reversed I mean like the position of NH and N was reversed with respect to the Benzene loop!
P.S. It would be great if you could also teach me the correct way to ask this question by means of the chemical terms I should use.
P.S.S I hope it is not a wikipedia problem!

All they’ve done is flip the picture…

Have you ever heard of PubChem? It's a great resource for chemical structures as well as other information.

@canadianer no it is not. pay attention to the relative position of NH in Imidazole to the Os in the Benzene Ring.

@anongoodnurse according to PubChem the image at https://en.wikipedia.org/wiki/Xanthine is wrong. but is PubChem completely reliable?

They are the same. The purine imidazole can exist in two tautomeric forms.

@canadianer I understand that they are tautomers but I don't understand how they are the same! I think they are not the same bc altho the imidazole  is symmetric, the other ring is not. and since there are two bonds between them they can't turn so it matters so much don't you agree that they will look differently under an electron microscope?

9H-xanthine (https://www.ebi.ac.uk/chebi/searchId.do?chebiId=17712) is a tautomer of 7H-xanthine (https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:48517)

I guess it depends on your definition of "same". Tautomers are often considered to be the same compound even though they are constitutional isomers.

On the question "Is PubChem/Wikipedia/etc completely reliable?" the answer is "not completely!". It is very hard to get all chemical data 100% correct, but there are efforts to cross-check and validate such data with experts...

@canadianer I was just imagining there were long carbon chains instead of hydrogen in imidazole and another chain in the other ring and then I thought the structure would vary so much because the angle between the carbon chains would be so different and thus different properties. But if you say tautomers are considered to be the same compounds then I suppose such things just don't happen often and the properties of tautomers are almost just the same. Thanks for your explanation.

The two structures are tautomers of one another:

Tautomers are often considered the same compound even though they are really constitutional isomers. Technically they are called 7H-xanthine and 9H-xanthine, respectively (thanks to gilleain for the links).


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why do we tighten out muscles against cold?
When I'm in shower and I want to open the cold water on myself suddenly I make my muscles so tight before I open the water and that helps so much in being able to handle the shock. Why does tightening of muscles help in handling the shock.

This question could be improved by rewording it to be more focused on the general human actions, this may be confused for a personal medical question.

@John I don't really know how to reword it in more than one small sentence to be more general. I don't know if other people do this in shower or before an impending cold shock so I can't say we humans instead of I there.. anyway, if you have any good way of making this general please edit. I will accept:)

Consider most animals instinctively recoil from unpleasant sensations. Resisting this often involves tightening the muscles. Think about the last time you had to get a shot or pull a splinter out of the skin, you often tighten the muscles in an attempt to resist your own instinctual reaction. Even non-physical reactions like resisting fear or disgust often have similar responses, the mind and body do affect each other. Physical actions can effect mental states. Tensing muscles has been shown to have a direct effect on our willpower.

Your question can be answered by focusing on both 1) physical, and 2) psychological changes that occur when you tighten up your muscle. Of the two, psychological changes

Muscle contraction generates some heat which may account for a very small sensation of heat; however this heat can't be so much to actually prevent cold sensation. Moreover, muscle contraction can insulate the visceral organs (imclitsong the blood vessels)  to lose heat due to conduction. Again, this is not very effective for your situation.
Mammals tend to curl up when the ambient temperature is low. This will prevent heat lose from the core. By contracting the muscles, you feel good and sense warmth as this behavior is associated with warming up. Therefore, you won't feel the cold as you get exposed to cold water.


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Are cloned spieces significantly more vulnereble to deseases than sexually reproducing species?
I would like to be able to compare the risk for species to go extinct implied by their reproduction mechanism in the very short term. Imagine we choose some species A that can reproduce both sexually and asexually and then we make three clones of earth and in one clone we spread 1 million specimen of A that are all reproduced sexually. In another one 1 million that are all asexually reproduced (not in one generation but in like a 100 generations) and in another one 1 million of cloned specimen of A. now I want to compare the probability of each of these three going extinct in 10 years assuming the next generations would also be reproduced like their parents of course.
At the end I would be happy to know if the reason I get for this question depends on how sophisticated the immune system of that specie is.
So if I can fill in the following table with normalized numbers from 1 to 100 I would be so happy.
╔═════════════════════════════╦═════════════════════════════╦═══════════════════════════════════════════════════════════════╦═════════════════════════════════════════════════════╗
║ disease toleration score    ║ clones of a single specimen ║ asexual reproduction of the same specimen through generations ║ sexual reproduction of a couple through generations ║
╠═════════════════════════════╬═════════════════════════════╬═══════════════════════════════════════════════════════════════╬═════════════════════════════════════════════════════╣
║ sophisticated immune system ║                             ║                                                               ║                                                     ║
╠═════════════════════════════╬═════════════════════════════╬═══════════════════════════════════════════════════════════════╬═════════════════════════════════════════════════════╣
║ casual immune system        ║                             ║                                                               ║                                                     ║
╠═════════════════════════════╬═════════════════════════════╬═══════════════════════════════════════════════════════════════╬═════════════════════════════════════════════════════╣
║ simple immune system        ║                             ║                                                               ║                                                     ║
╚═════════════════════════════╩═════════════════════════════╩═══════════════════════════════════════════════════════════════╩═════════════════════════════════════════════════════╝

Right now my intuition tells me it should be something like this:
80 85 100
40 50 70
1  15 30

But I know I can be so wrong.
Please note that I don't want the single "Correct" answer to this question. I would be happy enough with the best "wrong" answer from a biologist. I mean if you know some things and you have some ideas about it that are not so bad but you are not so sure and you think maybe in future science will prove you were wrong. Just tell me that incomplete answer. I just want to learn something more than what I know now. I don't want an ultimate answer.


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Could homoplasy occur within a clade?
Consider the below phylogeny. taxon1 and 2 are sister taxa but:
- share a brown color coat
- differ from their closest common ancestor (light color coat)
Is this a case of homoplasy (Analogous trait)?

The definition of a homoplasy is a common characteristic to 2 or more branches, not shared by their common ancestors, so I'd say yeah, this qualifies as a homoplasy.

@MoBo If you feel like one of the two answers answered your question, you can click on the check mark next to your favourite answer.

Could homoplasy occur within a clade?

Note that the all of life is a clade! A clade is any mono-phyletic tree. So any homoplasy observed on earth is necessarily within a clade!
Let's replace the term clade by species to further the discussion

Could homoplasy occur within a species?

Wether you consider two lineages as being part of the same species or not changes nothing to the question of whether their shared trait was already present in the common ancestor or not. You can have homoplasy within a species and even within a population. Of course, the lower level you go, the less likely it is to observe a clear case of homoplasy.
It is important not to view a clade (incl. species and subspecies) as something too atomic. As a whole and single clearly defined entity but rather a whole complex tree (or network) of lineages. Any lineage may have evolved a trait that has already evolved independently in another lineage whether the two lineages are very closely related (within the same subspecies) or very distantly related. In this regard, you might want to have a look at this post.
So, yes you can observe homoplasy when comparing lineages within a clade.


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Where are there analyzable signed directed network datasets?
I'm looking for biological datasets with specific properties that are available for me to analyze. Informally put, I have a hammer and I am looking for a nail. That is to say, I have an algorithm and I am looking for suitable data to test if it can tell us anything interesting about biology. Let me start by characterizing the properties that I'd like this data to have.
Math Properties
The data must be representable as signed directed graphs, which in less formal terms means that I am looking for a network where the connections between the nodes are arrows with a +/- sign associated with them.
The signed property of the edges must represent a property of the relation between discrete objects that only takes on one of two values. One way to get signed values from quantitative data would be to use the sign function, keeping only the relations whose sign of the quantitative variable were not equal to zero. Another way is to encode Boolean values, where False is - and True is +. I'd like to further clarify that the data should not only conform to this criteria, but should have instances of both positive and negative paths within the data.
The directed property of the edges mean that we care to distinguish 'A relates to B' from 'B relates to A'; order matters. Both, one, or neither of these relations can hold in these networks between any two nodes A and B.
Data Properties
The data must be analyzable in the sense that I can obtain the data in a form where I can either (1) immediately analyze the data or (2) transform/manipulate the data into a form that I can analyze. As a computer programmer, I'm likely to be able to find packages for (or code for myself) moderately arbitrary transformations as long as they are computable and interpretable. That is to say, in your answer I would like you to not worry too much about whether you have a ready-to-use software solution for analyzing or transforming the data. What I would like considered is whether there is (1) a direct download for a/the datafile(s) or (2) an application programming interface (API) for downloading the data in either pieces or as a whole.
Preference will be given to answers that do not cost money, and do not require creating accounts (although either are acceptable).
All else being equal, I'd prefer larger datasets (n > 1000) over smaller ones.
Preference will also be given to answers where the dataset has additional variables are available on the vertices. For example, if the vertices represent genes, then additional variables on the vertices would mean more data is available that describe those genes.
Academic Properties
The dataset(s) should be citable.
Examples
While I'm open to other biological subjects, there are two biological topics that I feel should be representable in the mathematical way I've described above.
The first is gene regulation data. The vertices would be genes, and for any two genes A and B we could have any of the following relations

Gene A downregulates Gene B
Gene A upregulates Gene B
Gene B downregulates Gene A
Gene B upregulates Gene A

The second example I've thought of is in biological signaling as the signals are sometimes directional (sender to receiver) and might have some sort of sign (turn on/off, increase/decrease).
Bonus points if the data is topical (COVID-19/coronavirus-related for example).
Data Sources
I've downloaded a few datasets from BioGrid, but I didn't see the kinds of mathematical properties I was looking for in those datasets. If there are datasets here that you think meet my criterion, please mention them.

While this does look like a very nice approach, I would actually argue that there are (almost) no biological datasets, that can be directly used for your algorithm - you can only do a sort of meta analysis using results/predictions based on other datasets.
The reason for this is that the nature of a signed graph requires you to look at effects that can have opposite directions, which in biology  pretty much restricts you to regulatory functions*. The problem with that is, that is nearly impossible to directly measure regulatory effects. In all cases I am aware of, one has to measure the magnitude of an effect under different conditions and then calculate regulatory interactions based on that data.
This means any set of regulatory interactions you can put out into your network is already based on a given analysis with inherent assumptions and (potentially) biases.
This doesn't make the approach impossible, but I do think, it is something you need to be aware of, especially if you want to use multiple datasets.
As for actual datasets that would fit well:

transcription factors have already been mentioned in another answer
other regulatory effects on transcriptions (promoters / enhancers) may also work, though in this case the 'class' of the objects effected (genes/mRNA) is different than the effector
Another type of biological network that might fit are metabolic / enzymatic pathways. For these you could either also look at regulatory interactions (which again may be tricky because both proteins and metabolites can have regulatory effects) or maybe also directly at metabolic flow: in this case nodes in the graph would represent metabolites and edges reactions that produce or consume them. The KEGG database has large numbers of metabolic pathways for many different species.

*I was trying to think of other things, but presence/absence of a signal probably doesn't fit and neither does classification into strong/weak signals (i.e. interactions)

Thank you for the suggestions. I appreciate your laying out of the difficulty of getting such datasets. I didn't mention in the original post, but it was a similar line of reasoning that led me to put this question to the SE community.

@Galen I think you need a collaborator in the field. It's super dangerous (or at least embarrassing) when people with an algorithm enter a domain they don't understand without help. SE is not a replacement for collaboration.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Here's some directed network graph data for regulatory networks of transcription factors (TFs), via http://www.regulatorynetworks.org/:
• Mouse TF: http://www.regulatorynetworks.org/results/networks/mm9/networks.v12032013.tgz
If you click on the site's About button, there is more information about this file. From the README, for instance:

Regulatory interactions were identified in each cell type by scanning the
  proximal DHSs (+/-5kb from the canonical transcriptional start site) of each
  transcription factor gene DNaseI footprints corresponding to the recognition
  sequences of known TFs.
The file genes-regulate-genes.txt contains two columns of gene names, at column
  4 and column 5 of the text file.
The gene in the first column is bound (i.e., contains a DNaseI footprint in
  proximal regulatory DNA) corresponding to the second column's TF gene product.
The final column (column 6) represents the number of times a motif for the
  regulating gene is found in the regulatory region (promoter) for the regulated
  gene.

The gene names are HGNC symbols and are easy to look up in resources available through UCSC, GeneCards, Ensembl, etc.
DS-numbers are internal identifiers for cell lines. However, the prefix uses that cell line's more general name and is usually easily searchable or parsable.
Disclaimer: I created the regulatorynetworks.org site and I was a contributing author on a couple papers which used the datasets rendered in it (1, 2).

Thanks for the suggestion. It looks like this data has directed edges. Can you elaborate on how the edges are also signed?

These are all positive values.

Ah, I see what you mean, you're quite right. I'll clarify in the question above that I'm looking for data that contain instances of both positive and negative paths. Sorry for the confusion.

To augment this with data that contain negative values, ChIP-seq peak overlaps may work. For TFs for which there are ChIP-seq peak datasets (on ENCODE, for instance: https://www.encodeproject.org/), you could use set operations (e.g., BEDOPS: https://bedops.readthedocs.io/en/latest/) to call overlaps of these proximal promoters with TF-specific ChIP-seq peaks as +1/-1, to specify overlap/non-overlap, true/false categories. ChIP-seq peak data would be useful, because it lends biological evidence to support that there is TF binding in the promoter (and associated regulation of the target gene).

That's just spitballing, though. The networks in my answer contain genomic intervals, and you could do set operations against any number of interval-based datasets, in order to get "signed" data. For instance: overlap/non-overlap with SNPs, overlaps with conservation values averaged over the TF binding site, etc. Conservation might be useful if you want to associate nodes with +/- values; I think either the phyloP or the phastcons conservation scores are ranged positive to negative, to specify the selection pressure over genomic regions: from highly conserved, to neutral, to highly evolving.

Enrichr has a huge (164 libraries) collection of term-to-gene relations in machine-readable format.
X2K can be more interesting for you, as it partially implements networks approach. It has a large collection of libraries as well. And two more - KEA3 (kinases to genes), and ChEA3 (transcription factors to genes).


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Do "non-human" animal like cat, dog, bird or fish think about future while sleeping?
I don't think "non-human" animal like cat, dog, bird or fish think about future while sleeping.
I think when sleeping, the "non-human" animal will feel rather think about anything. I think when sleeping, the "non-human" animal will feel  their breath just like when we are meditating. So, when we meditate we will feel our breath like "non-human" animal that are sleeping.
Do "non-human" animal like cat, dog, bird or fish think about future while sleeping?

I'm not sure we know enough about animal thought to even begin to answer this question.

Issue with your question
This question is full of terms that don't have a proper definition in Biology. I don't think there is any clear definition in the verbs "feel" and "think". Also, I don't fully understand what the differences between feeling or thinking (whatever that means) when sleeping matter for the question of whether some animals "think" (and its variants) about future while sleeping. I am not sure either what "thinking about future" really means. One doesn't know the future, he can imagine it and in some cases it is kinda complicated to really know whether a set of thoughts are encompassed within the concept of "thinking about the future". I vote to close for primarily-opinion based. Finally, your question might eventually be a better fit on CognitiveScience.SE.
Theory of Mind
You might be interested in the Theory of Mind (ToM). Having the ToM (I know it is weird formulation, ToM is not a theory per se) means having the ability to 1) be aware (might have various definitions for "aware") of its own existence and 2) be aware that others also think and have intentions and 3) more importantly be aware that others might be aware that you think and have intentions.
It is pretty hard to investigate whether an animal has the ToM. Here is a list of species (and lineages) where ToM has been found (or thought to exist at some level). The list is probably not exhaustive and the difficulty to accurately define ToM and awareness make those pretty arbitrary.

Chimpanzee
Orang-outan
elephants
dolphins
corvids
some parrots
bee-eater

Btw, your list of lineages is funny by the fact that you seem to weight equally two relatively closely related domestic species (cat and dogs) and two gigantic taxa that are fishes (fishes do not represent a monophyletic group) and birds


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Why do cats meow when they are adults?
Meowing for kittens is similar to a baby crying. As human adults grow, they stop crying, but as kittens grow up they continue to cry. Why is this?

I could not find a peer-reviewed paper, but there is a widespread popular belief that adult cats only meows to communicate with humans but never with other cats. Meowing allows a cat to obtain the attention of its human owner and eventually get what it wanted.
See this webpage from the american society for prevention of cruelty to animals for example or this quora post.


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Why is there symmetry in animals?
If cut a cut down the middle, both halves are symmetrical.
Why is it that most animals are symmetrical?
Is there an energetic reason for this? (as in, it is energetically favorable to create the same thing twice instead of making something new)

I believe this question has already been answered: https://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally

Intuitively, symmetry is useful for balance. A weight-nonsymmetric animal would have to expend additional energy to keep itself balanced (and this would also increase neural complexity for maintaining balance).
Mirror-image pieces only have to be coded once in the genome as a rule-of-thumb, allowing reuse of (mostly) the same genetic pieces with a few orientation and growth-origin markers thrown in. If you put vastly different parts on each side, you have to encode them (making the genome larger with more opportunity for mistakes and harmful mutation)


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Multi-protein drug treatments
Apologies if this an obvious question - I am very new to this. I am, as of now, under the impression that multiple SNP variations interact to create multiple mutated proteins, which ultimately results in a variant phenotype.
I am wondering if the standard method of treating is this is by creating a drug that has a combination of all of the non-mutated versions of the proteins, or if drug makers simply use the protein that they believe has the biggest impact?
Thanks for the help!

Proteins are long strings of amino acids.  Drugs are generally not proteins; they are small molecules.


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What animal has fat with the highest energy density?
Fat is more energy-dense than protein and carbohydrates, it is not only an energy deposit but also an organ with many functions such as cushioning and metabolism regulations. I want to know are animal fats similar across species (composition & function), specifically what animal has fat with the highest energy density?

In both humans and animals, the body fat stores appear as triglycerides, which can be composed of different fatty acids, but they all have about 9 kilocalories per gram (USDA).
There can be different amounts of fat in different fat cells, so there can be slightly different amounts of fat in 100 grams of different types of fat tissue.
Calories in 100 g of fat from different animals:

Lard = 902
Beef tallow = 902
Chicken fat = 900
Turkey fat = 900
Goose fat = 900

The fat mentioned above was white fat, which appears as a single fat droplet in a fat cell. Humans and some animals, especially rodents and bats, also have different amounts of brown fat in which the fat cells contain a lot of mitochondria and the fat is present in multiple droplets, so, logically, brown fat tissue has lower energy density.

I wonder what the measurement error is on those estimates.


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Why do some trees flower year round, others only once
Depending on latitude, rains, and pollinator behavior, etc. some trees flower only once a year such as oak trees, others twice (such as pipe organ cati as a response to pollinating bats) and yet others continously such as figs (I believe, not sure).
However I noticed that arbutus unedo (straberry tree) has both immature flowers, mature flowers young fruit and ripe fruit on the tree at the same time. To mky knowlesge, fig tress in amazonia behave differently: the whole tree is roughly in the same state at once, either "flowering" developing fruit, bearing ripe fruit.
My question is what ecological role does Arbutus U. fill that it has this feature?


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Reference for most up to date sport physiology
I currently have

Exercise Physiology Nutrition Energy And Human Performance, 7th Edition, 2012, McArdle et al.

as my reference book for Exercise physiology. However, based on a question I recently asked here on this very same board, I realise the book sometimes takes shortcuts and does not provide a complete explanation. Plus, the structure is sometimes a bit difficult or not to my liking.
I saw that the 8th edition (2014) has been issued. I don't know if it is significantly different from the edition I have.
Would someone have another solid reference for Exercise physiology? I am particularly interested in the energy pathways and their training.