text:
Formation of splint bones in ungulates
I do know that the splint bones are vestigial (reduced non functional toes in this case) , in odd and even toed ungulates. Is there any evolutionary reason of why is it so?
What were the conditions that lead to it?

what are you asking why they are reduced, or why they have not been lost completely?

@John -Why did they get reduce in the first place?

One easy way to make an animal faster (especially if it is larger than a housecat), is to make the ends of the limbs lighter, the more mass there is near the end of a limb the more energy it takes to move it and the slower you can swing it, that translates into moving slower because you cannot get the limb back into position for the next step fast enough.
Because of this reduction in the mass and number of toes in lower limb is an adaptation we see over and over again in animals focusing on running speed. We see it in dinosaurs, we see it in ungulates and artiodactyls. We see five toes reduced to three then eventually one toe, or sometimes we see a reduction from four toes to two paired toes instead.
Source

Wow! That's a really pretty simple(and awesome) logic if i think about it now! thanks =)


text:
Immune response to shock
I am studying nursing and have a question regarding the physiological response to shock (decreased perfusion).  In lecture notes supplied by the lecturer, he indicates that there is a neural, hormonal and immune response to shock that is compensatory.
The neural component is the activation of the sympathetic nervous system, and hormonal response is through RAAS, etc.  This makes sense, as these mechanisms attempt to increase blood pressure and blood volume
I don't understand the immune response, though, which is described as the release of pro-inflammatory mediators, which lead to endothelial cell damage, making the vessels leaky, leading to oedema.  So how is the compensatory, it seems disruptive?  And why exactly would pro-inflammatory mediators be released in response to shock in the first place?

While I'll try to flesh out an answer when I can, try to access this article. There are some fair points, but importantly that tissues release inflammatory mediators in response to damage and stress.

Also this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846925/

Great articles, thanks.  I think this basically fills the gap in my knowledge.  So ischaemia from any form of shock causes endothelial damage, which leads to inflammation, etc...

First: what is inflammation.  From wikipedia
https://en.wikipedia.org/wiki/Inflammation

Acute inflammation is the initial response of the body to harmful
  stimuli and is achieved by the increased movement of plasma and
  leukocytes (especially granulocytes) from the blood into the injured
  tissues. A series of biochemical events propagates and matures the
  inflammatory response, involving the local vascular system, the immune
  system, and various cells within the injured tissue.

Second re shock: why does it happen?  If I go into shock from blood loss after a terrible knife juggling accident I will probably not have the inflammatory piece: I am dying from lack of blood and consequent low blood pressure.
What if I am in septic shock?  That means shock caused by organisms, usually bacteria, in the blood stream.  Bacteria are the ancient enemy and we have layers upon layer of defense accumulated over evolutionary time.  The reason we have them is that somehow, our ancestors that had them had some fitness advantage - probably because they survived having bacteria in the blood.
Some of the stuff that comes with that package does not seem very adaptive - like the leaky vessels and lungs filling up with fluid.  Maybe we see the wild extreme of this reaction but to a lesser degree (lesser infections?) those inflammatory responses are good?  Maybe releasing a storm of neutrophils has unavoidable side effects for the surroundings - like the Avengers fighting an alien army in NYC?  It was tough on NYC.  Maybe those extreme shock reactions save the organism 1 time in 10, which is better than the odds otherwise with an overwhelming bacterial infection.
Bottom line though is that bacteria in the blood in great numbers is an existential threat to the organism.  Desperate times call for desperate measures.

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What are these creeping cacti tendrils?
During a trek through a small forest-type area on the main island of Hawaii, I came across the following plant:

It did not cover very much area from what I could tell (there was a continuation of the bed just behind me from where I took the picture). I believe it was near Punalu'u Beach but I can't say with certainty.
It's creepy, looks like a tractor load of snakes got loose, and something I find fascinating. Could someone tell me what this cactus-y, bed of vines-like plant is?

I don't know what plant this is (a closer picture would help) but I was surprised on a recent trip to Maui by the large number of large cactus invasions. Mostly central american jungle species, but some prickly pears too. Really unfortunate. Don't get me wrong, I like cactus, they just don't belong in Hawaii, in my opinion.

It's creepy ... something I find fascinating.

Creepy & fascinating indeed!

Could someone tell me what this cactus-y, bed of vines-like plant is?

This is a cactus, and I believe it belongs to the genus Hylocereus, possibly the species H. undatus.

As for distribution, Hylocereus are quite prevalent throughout Hawaii, and can also be found scattered throughout the globe.

Hawaii is the leftmost blue dot. image source
More information about this plant can be found here.

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What determines the differences between differentiated cells?
Given two multi-cellular species with obviously different phenotypes. The reason for the different phenotypes reflects their different DNA.
However two types of cells in an adult organism may have clearly different phenotypes (e.g. morphology), but the same DNA, with a different set of genes expressed.
To explain this it would seem that there must be some molecules to modulate the expression of the DNA in different cell types. In my reading I have found one such type of molecules the presence of which is prerequisite for one type of differentiation – modification of histons – methyl, phosphate, acetyl, ubiquitin. Another class of molecules is the transcription factors.
My question:
What would one look at to tell the differentiated type of a cell (ignoring its phenotype)?

Addendum: After having delved a little bit deeper into the topic of epigenetics, I'd like to suggest as a possible answer: it's the histone code one has to look at, something like: how the DNA is wrapped around which sequence (!) of (modified) histones.

I read the question a few times but I can't understand it. What do you mean by a species [.] in the sense of Darwin? What do you mean by a species of differentiated cells?

The two following two posts will likely help you. Why is a heritability coefficient not an index of how “genetic” something is? will tell you about what causes phenotypic variation (environmental variance, genetic variance, epigenetic variance, .... and all covariances).

How could humans have interbred with Neanderthals if we're a different species? will teach you about the difficulties and subtilities behind the concept of species.

@Remi.b: Thanks a lot for having tried to understand my question. I've got to admit that I obviously didn't manage to make clear what I mean. Possibly it's not even clear to myself? Another try: "Individuals of the same species share considerable portions of their DNA (next to having the same phenotype). What do individual cells in the human body of the same cell type have in common (next to having the same phenotype as cells) but not with other cells in the same body?"

This question may seem unclear, because of the non-biological background of the poster and the misuse of "species" in relation to cells. However, it is actually a very basic and important question. Put simply to a modern biologist one could say "If muscle cells and liver cells have the same DNA, what causes them to have a different morphology, i.e. what causes them to express different genes from the DNA?" The question hints at some of the reasons in mentioning modification of histones. The problem with answering the question is that it is very broad, and there is a lot we don't know.

@David: I understand, "species" is not to be used related to cells. But I'm quite sure to have heard of "populations of cells". Is "cell type" an acceptable term for "species of cells"?

I have modified and simplified your question in an attempt to focus it and prevent it being removed as unclear. Yes "cell type" is the term used. If you don't like my changes you can revert them. The problem now is that you have (partly) answered the question yourself. Unless someone (not me) has a reference to a good review or can write a good thumbnail account, I'm not sure where we can go from here.

You saw that part in your wiki link that the "histone code" is just a hypothesis?  The development of the anterior-posterior axis in fruit flies is pretty well explained with RNA gradients, and not so much histone positioning.  Here's a hint, RNA seq is a much more common application than CHiPseq on histones.

@swbarnes2: I did. RNA seq and CHiPseq seem to be hard stuff for the novice.

Well, you are not asking a question that can be answered by a novice in biology, either.  Scientists asking "How are these tissues different" are generally not starting with CHipSeq; they do RNAseq, or 10 years ago, microarrays.


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More informative phylogenetic trees
In the presentation of phylogenetic trees, the geometric shape of the trees often seems somehow arbitrary and is more driven by aesthetics than by informative reasons.
But wouldn't it make sense to give the geometry (distances and angles) specific meanings? Or is this already done (when it's done right)?
Some basic principles:

The vertical axis represents time (on a linear, logarithmic, or "anti-logarithmic" scale).
The horizontal axis represents the amount of genetic change (measured in appropriate units).
The line of one species (= population with virtually identical DNA) goes vertically from bottom to top.
The line ends when the species becomes extinct.
A new species branches off of an existing species by a horizontal line perpendicular to the line of the latter.
The length of the new (horizontal) line reflects the amount of genetic change.
At its end the line continues vertically.
There are no other branchings along the horizontal line.

By these principles and with perfect knowledge (and a good measure of genetic change) we would have a perfect rectangular tree like this:

But our knowledge isn't perfect: we know little to nothing about lots of intermediate species which didn't leave traces. Hypotheses about these unknown species can be reflected by inclined lines whose slopes can tell for example:

a) Their have been many pronounced genetic changes in a short period of time after the new species branched off. (grey: hypothesized intermediate species)

b) Their have been few small genetic changes in a long period of time after branching off.

I'm looking for discussions/considerations of this kind of drawing
  phylogenetic trees (papers, web pages, or simply good search terms).

An interesting - and new to me - point of view is given in Joseph Ahrens' answer to this Quora question:
How do you interpret ancestry in phylogenetic trees?
What slowly becomes clear to me: It's about the interpretation of straight line segments, maximal straight lines, of horizontal vs. vertical lines, and nodes (= branching points) in phylogenetic trees, especially: which of them is to interpreted as a species?

One interesting search term would be "phylogenetic network"

Thanks, but I am not sure if this helps.

Phylogenetic trees don't tell you anything at all about species (which is a vague term anyway). I suggest you do more reading on both topics. I'm voting to close this as unclear what you're asking.

I am asking for more informative ways to draw phylogenetic trees.

Here's the issues with your well considered project:
1/ Temporal datasets to proportion trees: That's probably the most absent thing in species measurement. You'd need data sets of time for beetle species, for mammals, plants in millenia and million years. 90+% of that information is absent.
2/ Genetic proximity to arrange trees. Scientists publish their genome studies into the ToL project. There is lots of distance data to compare all animals.... Genetic distance doesn't graph easily because on the same tree, some distances can be 500 times longer than others. On a tree of 20 extant species, you will have branches 5mm long and 5 meters long, half the the species are on your screen and the other half are higher than the ceiling. It's best to represent them with another symbol, else interactive 3D trees where you can switch compact/large views and the tree zooms out crazily, it's illustrative and cool, else use a weighted proximity length which is 1+ similarity/50, that doesn't really work either. either way, I couldnt find a way of clearly displaying that info on the tree.
Phylogeny trees don't lend themselves well to being informatively measured. You start by thinking "Oh I could find a pretty way of doing that" then when you apply the datasets, your trees become uncontrollable and jumbled up because of exponential branch lengths.
I programmed phylogenetic trees based on the 81MB ToL tree of life project to represent many millions of species, to do 3D physics trees and HTTP lookups to provide wiki texts and images for all species. There is www.biostars.org a very kind and helpful bioinformatics forum for postgrads that do trees all day.
There are many (dozens) of informative tree graphics programs coded by academics, to visualizw and analyzw species data, arranged into different trees and sorting through them.


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Cell differentiation by non-identical copies
There are in principle two ways that two cells with the same mother cell can differentiate/specialize/diverge:

Because they are not perfect identical copies (= different internal influencing factors). I explictly don't mean "non-identical on the DNA level", but on the level of other cellular components!
Because they are exposed to different external influencing factors (chemical, mechanical).

Can it be said, which of these two reasons of cell differentiation is the more common, frequent, resp. "important"? Or does it completely depend on the (type of mother) cell and some general circumstances?
If internal factors (= non-identical copies) are an important source of differentiation, I have two (optional) questions:

How does the mother cell manage to cleave into two non-identical copies in a rather fine-tuned and determinstic way? Or is any kind of asymmetry enough?
Which is the first cell (starting with the zygote) that cleaves into two non-indentical cells, different enough to give rise to differentiation? (From this answer I believe to have learned that this might happen already after 1-4 divisions.)

I found a partial answer to my and this question at Quora:
What regulates initial cell differentiation?
Ian Driver says:

In many organisms the initial cell has mRNA (or protein) partitioned
  in one half of the zygote.  One daughter cell inherits most of the
  mRNA or protein and goes on to activate or repress genes in that cell,
  but not in the other.  This has been visualized and well studied in C.
  elegans: Asymmetric cell division and axis formation in the
  embryo.

This question is kind of bad. There are common internal influencing factors that are unrelated to improper replication, most commonly:
Methylation. Addition of methyl groups to DNA regions inhibits RNA transcription from that region.
Imprinting. Can't recall exactly how this works but it's another mechanism for enabling/inactivating genes.
Histone structure (wrapping/unwrapping). DNA coiled tightly around histones is more unlikely to be transcribed.
External influencing factors include cell signaling, substrate detection, and large-scale endocrine signaling. Most important are growth factors and growth inhibitors (which let the cells know if they need to replicate quickly (repairing damage/large-scale growth) or slow down replication (overcrowding). Other external factors could include metabolism (produce these digestive enzymes when exposed to these foods) or endocrine signaling.
Non-identical copies at the DNA level (mutation) are thankfully relatively rare in practice, particularly among higher-order species with longer lifespans.

I didn't mean "non-identical on the DNA level" but on the level of cellular components - and just made this clear in the question. Is the question still bad, then?

confirmed your question is no longer bad.

Puh, I am relieved.


text:
Mold identification
I poured some agar plates and tried inoculating them with mushroom spores (I don't think they germinated bc of low humidity), but noticed what looks like mold with crystals on the surface of the agar.
My question is, what are these "dew-like" structures?

Location: Near Columbus, Georgia
Incubation conditions: Indoors (room temp), covered

I initially figured it was condensation from the agar.  But it is not on your lid and you said you suspected humidity was low.
I found this here http://www.gettyimages.ca/detail/photo/mold-penicillium-vermiculatum-growing-on-high-res-stock-photography/128606087.

with this caption

Mold, Penicillium vermiculatum, growing on agar. The water droplets on
  the mold are part of the respiration process of the mold.

Those droplets do look like pure water.  And oxidative metabolism does produce water: CHOH+O2 -> CO2 + H2O.  It is interesting that the top of the mold is so hydrophobic that the water forms little balls.  Why might that be?  If you know, comment please.
Other fungi might put stuff in the exudates that collect atop them.  I read that some aspergillum species collect droplets of purple exudate on old colonies but I could not find good images.  Here is another penicillium with amber looking exudate.  These exudates can contain metabolic products.

from http://thunderhouse4-yuri.blogspot.com/2015/08/penicillium-citrinum.html

Exudates (or Extrolites): Some fungi can produce exudates as a
  by-product of their growth, many of which can be collected for
  commercial use.  Mycotoxins are by-products (secondary metabolites)
  which are potent poisons.  Penicillium citrinum produces Citrinin, a
  nephrotoxic mycotoxin which derives its name from the fungus.  It may
  also produce other extrolites such as tanzowaic acid A,
  quinolactacins, quinocitrinines, asteric acid and compactin.

If these fungi were spreading out in their natural habitat of rotten stuff, the secreted mycotoxins would be clearing a path for them, wiping out those organisms that dare compete for that rotten stuff.

thanks Will! The droplets looked a little yellow (not captured well in the pic) to be just water, and I was actually going to take a closer look under a microscope once I finished building my flowhood, but now that I know the droplets are likely to occur again, I'll take a closer look without worrying about contamination! If they are waste products, it makes sense that the mold would excrete them onto a hydrophobic surface to avoid poisoning itself! Fascinating. I will share microscopic photos of the surface structure soon.

I like that scheme about the hydrophobicity providing a dumping ground for wastes.  That would make sense.

It makes sense that the surface of the mold is hydrophobic if it needs to release spores in the air to get a good dispersion. Just my adaptive interpretation.


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Is arachnophobia connected to lower immunity against spider toxins?
Are arachnophobics more subceptible to toxical effects coming from spider toxins?

You would have to test a pair of identical twins to see.

@Charlie ?? What is wrong about classical treatment groups?

How common are toxic - that is, with sufficient venom to pose a threat to humans - spiders? Especially ones that will bite humans?  AFAIK they're common only in Australia & Latin America, extremely rare elsewhere.

This is an interesting question and may stem from the fact that spider phobias tend to run in families and thus have a genetic link - assuming susceptibility to toxin levels can be passed from parent to offspring.  However, instead a study found that the fear of spiders was caused by social learning of disgust reactions.
Source: https://www.psychologytoday.com/blog/why-we-worry/201407/why-are-we-afraid-spiders
Directly from source:

In relation to the first question, it has been known for many years
  that spider phobia tends to run in families. It has often been assumed
  that this may represent a biological predisposition caused by the
  transmission of genes between parents and offspring. However, we found
  that this relationship was considerably more complex and indirect. We
  found that the only significant predictor of a child’s spider fear was
  not the level of spider fear in the parents, but their levels of
  disgust sensitivity. One interpretation of this finding is that spider
  fear may be transmitted within families as the result of social
  learning of the nature and intensity of disgust reactions–including
  disgust reactions to spiders.

Link to study abstract: http://www.sciencedirect.com/science/article/pii/000579679390041R

As it currently stands, your response does not properly answer the OPs question. The OP is asking whether or not there is a relationship between immunity levels of spider toxin with that of the behavioral response of being afraid of spiders. Your response though only addresses the cause(s) behind arachnophobia, which completely neglects the immunity aspect of the OP. If you can also address the toxin immunity element of the question, I will consider reversing my DV.

@Charles- Is the toxin immunity element not addressed by the author when he mentions that it was long assumed that there was a 'biological predisposition' which caused spider phobia to run in families before going on to conclude that fear of spiders is a result of social learning (behavior)?  Unfortunately, the author does not go into detail of what he means by biological predisposition but wouldn't at least a portion of that include some type of increased susceptibility?  I appreciate your response and would like to see a more definitive study directly relating immunity and behavior myself.


text:
AntiTrypsin Enzyme
In a smoking patient, is the lung over digested because of a combination of smoking and a defect in the antitrypsin gene (prevents digestion from protease)? Or does smoking act the same as a patient with a defect in the gene?

Do you have any proof for this claim? Usually proteases are not active in lung tissues.

Wikipedia has a fine article on the disease.
https://en.wikipedia.org/wiki/Alpha_1-antitrypsin_deficiency
from that article

Alpha-1 antitrypsin (A1AT) is produced in the liver, and one of its
  functions is to protect the lungs from neutrophil elastase, an enzyme
  that can disrupt connective tissue.

Neutrophil proteases are active anywhere neutrophils are.  People who don't smoke can get COPD just from having the double recessive form of this disease (no active alpha-1 antitrypsin).  But if that is the case with you and you also smoke you get accelerated COPD.  COPD is already an inflammatory disease associated with mucus and neutrophil action and the damage this causes is no doubt augmented with the lack of protective alpha-1 antitrypsin.
If you suffer this condition you can get infusions of alpha-1 antitrypsin  - sort of like type 1 diabetics get insulin.


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Does the number of base pairs between the end of one gene and the start of the next gene have to be a multiple of 3?
I'm working on a project for a Coursera course where I need to scan a string of base pairs and identify possible genes, but there's something about real DNA that I need to know to design the algorithm correctly.  My question is best illustrated by example.
Suppose we have a strand of DNA like this : ATGxxxyyyzzzTAAqqATGrsssATGuuTAAvpppTAG
The lower case letters just stand for general base pairs that are not in the sequences "ATG", "TAA", "TAG", or "TGA".
"ATGxxxyyyzzzTAA" constitutes a gene for the purposes of the assignment, and my program does correctly identify that string of base pairs as a gene. What I want to know focuses on what happens after that first gene is found. Let's consider the last portion of the string:
"qqATGrsssATGuuTAAvpppTAG"
My current gene-finding program would identify "ATGrsssATGuuTAA" as a gene, but notice that this strand starts after only two base-pairs ("qq") have been searched through. Does that matter? I.e., would this happen in real DNA, or should the second valid gene be identified as "ATGuuTAAvpppTAG"?

without providing sources or getting into reading frames, I would say that bc DNA is sometimes damaged and not always cleaved at the end of a codon when digested for analysis, sometimes you can get 1 or 2 base pairs that are irrelevant for your purposes. Short answer: it's fine to ignore the "qq" like you've been doing.

I question the value of the course you are doing if it describes open reading frames (ORFs) as genes. This is biologically incorrect, so you can only be expected to follow the precise mathematical specifications given you. Thus the correct biological answer Remi gave you is less relevant than the actual spec, which you don't give. There are other pitfalls that relate to the two strands of the DNA (note that your lower case letters represent the bases of nucleotides — not base pairs), their directionality, and the possibility of overlapping ORFs. Have you considered these?

It’s a programming course, not a genetics course. The actual focus of the exercise is string manipulation, where the input is supposedly a block of base pairs read in an actual gene, like Axl2p. My intent is really more to refine an algorithm to solve a vastly oversimplified problem based on something that computer scientists would actually do on a genomics project.

There absolutely is not a rule saying that all genes on a strand should be in the same frame.
Your program is looking for ORFs (open reading frames) and it should identify all of them, in every frame.  If you were being very thorough, you should generate the reverse complement of your sequence, and search that for ORFs too.  But I guess if you were given this sequence, presuambly the professor gave you the sequence in the desired orientation.


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What is a Slurry in Microbiology?
I have been reading this article and they refer to this thing called 'slurries' that can be made from soil samples. This is in the context of being some sort of microbiological method.
"slurries can be made from these soil samples"
Does anyone know what this is? When googling it, I can not find a clear answer to what the method does.

It's not a microbiological term; it's used according to the standard definition of the word.

Apparently, microbiologist use this term to describe the process of culturing microorganisms from soil. You make a 'slurry' which has both growth media and the soil (which would fall under the english definition of a slurry) and incubate it waiting for growth. Media(Liquid) + soil = Slurry

A slurry can also be used to mean a semi-melted ice water mix. Most people would call it ‘slush’, but I’ve come across it in some protocols before (can’t think of a reference to provide though, so it’ll depend on your particular context).


text:
What are the differences between isozymes, allozymes and isoforms?
As far as I have understood

Isozymes are derived from different genes but perform similar functions
Allozymes are derived from the same gene but different loci, functionally conserved
Isoforms are a result of post transcriptional modification of the same gene, I am not sure for its functional conservation.

Are there anyother things to know about them?
Thanks

You have the basic idea:
Isozymes come from different genes but carry out the same enzymatic reaction.
Allozymes come from the same gene - i.e., the gene at a particular point on the chromosome; but chromosomes come in pairs, and the allozymes come from the 2 different chromosomes in the pair.
Isoform proteins ["protein variants"] are from the same gene, but they can have the same or different functions, depending on how they are spliced = which exons are included, and in what order. There's a nice picture in the Wikipedia article "protein isoform."
Here are Wikipedia links:
Isozyme - Wikipedia
https://en.wikipedia.org/wiki/Isozyme
Isozymes (also known as isoenzymes or more generally as multiple forms of enzymes) are enzymes that differ in amino acid sequence but catalyze the same chemical reaction.
Alloenzyme - Wikipedia
https://en.wikipedia.org/wiki/Alloenzyme
Alloenzymes (or also called allozymes) are variant forms of an enzyme which differ structurally but not functionally from other allozymes coded for by different alleles at the same locus.  ...These are opposed to isozymes, which are enzymes that perform the same function, but which are coded by genes located at different loci.
Protein isoform - Wikipedia
https://en.wikipedia.org/wiki/Protein_isoform
A protein isoform, or "protein variant" is a member of a set of highly similar proteins that originate from a single gene or gene family and are the result of genetic differences. While many perform the same or similar biological roles, some isoforms have unique functions.

Complementing Helen's answer, I can give one example of isoforms. The main production of nitric oxide in brain is driven by three enzime isoforms of the same gene: neuronal, endothelial and induced Nitric Oxide Synthase (nNOS, eNOS and iNOS). Despite de fact they have their origins from the same gene, they are quite different in terms of regulation and activity. The different isoforms are regulated by different genes and pathways, they are found in different tissues in brain, induced isoform can produce much more NO than the others and, of course, they promote different effects in body physiology, from regulating vital pathways in brain cells to regulation of blood flow.
You could not tell if we're looking at isoforms or allozymes just by analysing their effects in organisms since they both are different forms from same type of enzime, but it's important to know their origins if we want understand how they work.

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text:
Name for a set/collection of eggs which are laid and receive no nurturing of any sort by parents
OK - so, mammals have litters, and they look after their young.
Hens (birds generally) have clutches and many/most look after their young.
Octopuses have broods since the female looks after the eggs, but expires
just as they hatch!
The thing I want to know is:
What is a group of eggs laid by a creature which just lays them and
moves on called?
Also of interest would be such creatures which lay single eggs periodically (is there a difference?).
I'm particularly interested in insects and the like, but any additional
words which may apply would be of interest, and yes, I have Googled but
to no avail!

Hi and welcome to Bio.SE! This is a very broad question and likely has many thousands of correct answers. Perhaps you could help narrow things down by explaining why you want an answer to this question.

@James The reason I'm asking is because the info-graphic here makes reference to the "average litter size" of the octopus. I told my lecturer (a comp. sci. person) that mammals had litters. I could only remember the word "clutch" for eggs, but didn't think that applied. After thinking, I came up with "brood" for octopuses. However, it led to me wondering about what one calls a set/collection of eggs that are just left by the female without any further nurturing. Octopus mothers brood till hatching, then die, but there is input!

Mammals generally nurse their young at least to some degree. I can think of no examples where mammalian young are left to fend for themselves immediately after birth. The names of groups of the young of animals is incredibly inconsistent, so I doubt this answer would have any roots in biology! It would be interesting if someone could prove me wrong.

@James - I've edited the question title. Mammals don't apply. Some birds may. Many insects lay the egg(s) and play no further role in nurturing the eggs/offspring! I want to know what is the set of eggs laid called - IMHO, it's not a litter, *nor a clutch nor a brood!

Perhaps you'd have more luck over at the English language SE?


text:
When is a person declared to be dead?
From what I can tell, it is not well defined, but at least in the US it has to do with cessation of cardiopulmonary functionality. Any reliable sources that give a definition of when a human being is considered to be no longer living?

Really a legal question...

That's not true at all. Legality is different from country to country and some countries make laws based on biology or rejection thereof (ie abortion, transgenderism, etc.) The legality of it can be easily looked up (in the US it is the cessation of pulmonary and cardiac activity) but biologically (and philosophically) what do we consider as "alive?" Something that breathes? Something that has circulation? Metabolism? When you define what constitutes "alive", it is easy to define the opposite (e.g. a heartbeat means you are alive, therefore no heartbeat means you are dead).

OK, then it becomes a philosophical question :-)  Because you can be "dead" in humanly-meaningful terms (that is, no brain function but have bodily functions kept going by life support) but be legally alive.  Or if you die and your organs are harvested & transplanted, parts of you are still "alive".

I have also asked the question on the philosophy SE so I am not sure what you are getting at... We have real world, medical/biological/scientific problems to deal with such as abortion, life support, IVF, etc. that all deal with the concept of when the scientific community declares life has started or ended. It is an incredibly relevant question medically, biologically, scientifically, and philosophically. What exactly is your point in trying to argue that?

My point is that the "scientific community" has declared no such thing.  It doesn't really have a hard definition of life: are viruses alive, or prions?  Or are they just complicated chemical reactions?  With the issues you mention, it's not even a matter of defining life, but of the more complex question of personhood: that is, a fetus (or indeed, a sperm cell) is clearly "alive", but is it a person?  Or at the other end, a brain-dead body on life support, or someone who's lost all cognitive capacity?  Likewise transplanted organs, cultured cells...

Although there exist some differing opinions mostly to do with brain function, the best answer is definitely the heartbeat. Here's why:
In some ways the human body really does operate like a machine. The process of delivering oxygenated blood is THE foremost example of a time-critical activity that must occur constantly in order to maintain life. That process stops when either breathing or pumping of the heart ceases, and since the circulation of the blood is more immediately critical than breathing it makes sense to place more weight on that criterion.
Some medical conditions can lead to a person being essentially "Brain-dead" before they are biologically dead, but these situations are almost always extreme outliers to the general discussion of alive vs dead. Furthermore, the arguments surrounding that state too often and too easily cross over into philosophical/metaphysical commentary.
The only serious wrinkle to the argument above is hypothermia. This wrinkle is encapsulated quite nicely in the old medics' axiom "You're not dead until you're warm and dead." And it is well documented that hypothermic patients can sometimes be revived after long periods of time - in excess of a half hour - using special techniques and equipment (to prevent frostbite).
Bottom line: Has the subject's heart been pumping any blood (including during CPR chest compressions) in the last 10 minutes? Is the subject hypothermic with a core temperature below 95 degrees Fahrenheit? Answers of "No." and "No." mean that the subject is no longer living.

I do quite like your answer, but do you have any comments to make about a person being "brain dead" on life-support? I'm more familiar with debates about whether a person is "dead" or not when being kept on life support indefinitely.

After heavy research, I have determined that metabolism is what denotes something as alive. Obviously it is open to debate and many will disagree, but the ability to turn exterior means into nutrition (i.e. food for humans, light for plants, etc.) seems to be the core characteristic of what we consider "life"

But with modern medicine, it's possible to remove a heart and keep the person alive for hours (or even longer with artificial hearts) while a replacement is inserted.

In the United States there is the Uniform Determination of Death Act (UDDA) which defines death as either:
1.Irreversible cessation of circulatory and respiratory functions; or
2.Irreversible cessation of all functions of the entire brain, including the brain stem.
This purpose of this Act, which dates back to 1981, was to more closely align the legal and clinical definitions of death and to have a broader nationwide standard.  This act was approved by leading medical and bar associations.
source: http://healthcare.findlaw.com/patient-rights/what-is-the-uniform-declaration-of-death-act-or-udda.html


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How is chloride concentrated in nerve cells?
Bear, Connors and Paradiso describe in depth the electrical behaviour of the neuron. This depends upon a 20:1 concentration within the cytoplasm of potassium ions AND chloride ions. All subsequent activity revolves around potassium and sodium ion channels and pumps. No mention is given of how the initial chloride concentration is created and its subsequent regulation. Obviously there has to be a chloride pump but there’s no mention of it. Any help would be appreciated.

Check out the potassium-chloride cotransporter KCC2 as well as GABA Receptors as chloride ion conductances in neurons.  Maybe overkill but a nice review here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4294553/

Many thanks Louis. I’m a beginner in cell biology and perhaps I misread the diagrams in Neuroscience exploring the Brain. It makes sense to me now just to assume that the neuron gains its anions soley from those provided by the ‘original’ dissolved potassium and sodium salts that were isolated within the cytoplasm during the cell’s devolment. Perhaps I’ve got it right!

Not quite, the examples I listed show the neuron has capabilities to change its internal anion concentration (passively or actively) which has knock-on effects for it's excitability and is not just what is left over from the ionisation of salts containing chloride.  Hope that makes sense.

Wow! The abstract gets you going, eh Louis?! Thank you so much. I’ll be reading all 43 pages. Best wishes Mike Kidd.

Thanks to Louis Leung introducing me to cellular cotransportation I can now envisage how the neuron (in particular) obtains its “background” chloride base thus enabling thecreation and transmission of nerve signals. Given the presence of sodium-potassium pumps and NKCC1 sodium-chloride cotransporters we now have a mechanism for achieving the necessary chlorode base negativity in the neuron’s axon. I’m sure that Louis will correct my amateurish description if it’s in serious conflict with the science!

I think you are doing just fine @adlibber! Just be sure to keep the chloride role in action potential propagation in context since for APs, the dominant ion conductances are still Na+, K+ and Ca2+ since the reversal potential for chloride exchange is generally close to the resting potential of neurons.  If that review was still not enough to satisfy you - I think this one may be even more suitable: http://www.sciencedirect.com/science/article/pii/B9780123877383000159

My poor brain Louis, but once again I thank you!


text:
Tests for object size discrimination in mammals?
Are there common testing protocols for establishing whether an animal (mammals especially) can distinguish the size of objects? In particular, are there procedures or is there good literature on ways to determine whether a given species can recognizes a given object as enlarged in specific settings, ideally in ways that can allow comparison across species (e.g., species A sees an object as enlarged while species B does not).


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Life cycle of proteins
I try to get a picture of the life cycle of a protein (considered as a specific molecule).
This is how I can imagine it:

After the cell is born a protein molecule is synthesized by gene expression for the very first time de novo. This happens at a specific point in time and in space, typically at an ribosome, which may be located anywhere inside the cell.
From the location of its generation (combination or recombination, see below) the protein travels to its final destination, e.g. as an ion channel in the cell membrane. (But possibly it was already synthesized very close to its point of use.) Or it just floats around in the cytosol. (Possibly, it gathers some other biomolecules around it.)
Whereever it arrives or not: the protein lives and works for some time.
Eventually, it gets damaged (= looses small functional units), but gets repaired in situ. Continue with 3.
Eventually, it gets marked by ubiquitin and destructed in a controlled manner. Continue with 7.
Eventually, it decays spontaneously (= splits into some larger fragments).
Its fragments are released (in case it was bound) and start again to float around in the cytosol.
Eventually, its (or other proteins') fragments are recombined (at specific points in time and in space, possibly at "re-factories" comparable to the ribosome-"factories"). Continue with 2.

Is this rough picture of the life-cycle of a protein essentially correct?
If so: What is known about the time ranges in which these processes take place? Especially: How long is the effective life and working time of typical proteins? Are there proteins that live and work only for minutes or hours, and others that live for months or years? (Specific examples are welcome!)

One missing aspect (for Eukaryotes) is that step 5 is actively promoted by tagging with ubiquitin (https://en.wikipedia.org/wiki/Ubiquitin). You might be interested in this post https://biology.stackexchange.com/questions/46274/is-there-selection-against-long-proteins-and-long-genes

Just today - after a heavy  autumn storm - I saw trees in a nearby park marked (by some red-white stripes) to be felled. Is this how ubiquitin works?

@HansStricker pretty much. Proteins tagged with ubiquitin (i.e. ubiquitinated) are recognized and degraded by proteasomes. Wikipedia wouls surely give some nice info about this :)

@gilleain: I added ubiquitinization in the question. Thanks for the hint.

Protein half-lives range from less than 30 min (e.g., oxidoreductases) to more than 200 hr (e.g., some nucleic-acid binding proteins) and up to, at least, 2000 hr [Rahman & Sadygov, 2017, PLoS One 12(7): e0180428].
More ubiquitination sites, shorter half-life; more/larger intrinsically disordered regions, shorter half-life; more tightly coupled with the cell cycle, shorter half-life.
Note: Not all eukaryotic proteins are degraded via the ubiquitin-proteasome proteolytic pathway.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0180428

Thanks, Martin! Do you possibly know typical life times of ion channels (membrane proteins)? Or do they vary as much as for proteins in general?

Two examples (many more, i think, can be found with an ion-channel-specific literature search): BKα subunit of BK ion channel > 10 hr; Kv1.3 ion channel ~ 4 hr; Kv1.3 ion channel interacting with TrkB ~ 6.5 hr.

This means: ion channels are in a permanent dynamic equilibrium (on a rather small time range of some hours)? Isn't that thrilling (given the fact of long-term potentation)? (This means, long-term potentation is more of an epigentic effect than the result of permanent changes of long-living ion channel proteins, isn't it?


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What is this strange horned, slug-like coral reef dwelling creature?
On the first episode of BBC's Blue Planet II they visited a coral reef and showed some odd reef-dwelling creatures as part of their establishing shots, but they did not identify the creatures.
What is this odd horned, slug-like creature?
(Sort of like a slug with legs?)

I tried a Google reverse image search and it very 'helpfully' identified it as "Documentary film". So close, yet so far.

Disclaimer:
This question was split off from another question since the original was effectively two questions.

I think the OP might be referring to the black leg like things at the front. These are feeding tentacles according to Wikipedia. The tube legs are the short stubby things along the underside. I ended up here wondering about this too - thanks! Great show :)

Here is your animal in Blue Planet II trailer:

This is a sea cucumber (Phylum Echinodermata, Class Holothuroidea).
More specifically, this is a sea cucumber from the Species Pearsonothuria graeffei, the Graeffe's sea cucumber.
Here are other images of Pearsonothuria graeffei for comparison:

Sea cucumbers have an antero-posterior elongated body, as you can see in this image of the whole animal:

Those black structures you see are the tube feet, a distinctive feature of Echinoderms.
Here is a detailed image of the tube feet in Pearsonothuria graeffei:

Thank you for the interesting answer. I now realise that they did identify it later on, but from a different camera angle where the body was hidden and only the mouth was shown so I didn't make the connection. The sea cucumber is a strange animal indeed.

@Pharap Good to know. I didn't see Blue Planet II yet, but I will, I'm a huge fan of Attenborough.


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How would infection of mosquitos with sterilizing bacteria have any effect?
According to this article from the New York Post, the US just approved the mass release of male mosquitos infected with a bacteria that sterilizes them. The idea, according to the article and some inference, is that they'll mate with female mosquitos and impregnate them with non-viable eggs, causing a missing generation of mosquitos. Brilliant, right?
Well, no. Male mosquitos, from what I can gather, typically live less than a week in their adult phase, mating perhaps once while females will live for a few weeks mating, feeding, laying eggs and repeating until they die. Even if males and females both only manage to mate once, for every female you want to not produce viable young, you'd need to release one infected male. With a very conservative estimate of 10 trillion mosquitos in the United States, one generation per year, and current separation of male from female mosquitos in the lab by hand according to the article, you'd need to manually infect 10 trillion male mosquitos per year, for at least a few years, to make a serious dent in the mosquito population.
How does anyone think this is a practical idea?

I'm not an expert on this, but I think you're right that they have to release many infected mosquitoes, and repeatedly. Instead of spraying a pesticide, which might target other insects or have negative consequences for people, I think they're releasing infected mosquiotos. So you have to continue doing it, and in large numbers. But you don't need to kill all mosquitoes in country, just where people are. Furthermore, ultimately goal is to limit transmission of diseases like Zika, not to kill all mosquitoes. Having fewer mosquitoes might limit spread of things like Zika among the mosquito pops.

@rbatt Well even if you're just targeting the urban 0.1% of the country, and you're only trying to decrease the mosquito population by 10%, that's 0.01% of the 10 trillion mosquitos per year above, or one billion mosquitos, hand-separated, per year needing to be released to have the desired effect, every year. That's just as impractical as 10 trillion

Well, there are a few extra things to consider. 1) it's not 1 infected = 1 dead. If you had 50% of the population infected, then the entire pop would die in 1 generation (because 50% of pop would be ~100% of males, then 100% females dead). 2) On the other hand, they also aren't replacing wild males with infected males ... it's a dilution. That makes it even harder. 3) As you start to decrease the population size, the problem becomes more tractable with each successive generation. If you go from 10 tril to 1 tril, that 1 tril is 10x easier to dilute the next time you try


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CD4+ as Monocytes cell surface receptors
Today in class,  our teacher was discussing about the pathogenecity of the HIV virus.
He said that the binding between HIV virus and macrophages is done by the interaction between the GP120 of the virus and CD4 receptors,chemokine receptors(CCR-5 and CXCR-4) and fusin receptor present on Macrophages.
My doubt is
I think CD4 receptors are present on T-helper cells only. Are they present on Macrophages too? Do i have a wrong notion about CD4 receptors?
If not, then are there some other receptors responsible for the transfer of viral particles inside monocytes and dendritic cells?
Any extra information is appreciated.

Macrophages and monocytic cells can express CD4, CD8 or even co-express them.

@CMosychuk - what's the function of these receptors on monocytes? As in I know their function in T helper and T cytotoxic, but What are they doing on monocytes?

Macrophages and monocytic cells can express CD4, CD8 or even co-express them. The CD4 and CD8 molecules interact with MHC complexes on neighboring cells, and as you can imagine elicit varying effect in a cell type-dependent manner.
Plainly enough, Zhen et al. demonstrated that monocytic CD4 ligation to MHC-II molecules on other cells, such as activated endothelium, induced an expression pattern conducive to macrophage differentiation (1). Gibbings et al. also demonstrated that CD8 associates with FcyR on the monocyte's surface similar to CD8/TCR associations, and stimulates the secretion of cytokines (2).
I'll try to find a model source, but CD8a on dendritic cells can associate with MHC-II molecules on T cells like HLA-DR and aid in cross-priming the T cells.
Now what CD4 does on functional, differentiated macrophages is less clear to me, and I need to review the literature on that a bit more. It could just be expression imprinted because they're monocyte-derived cells, or it could also elicit an effect like CD8/FcryR above. I do not know.
There are more cases, so these serve as selected examples.

Thank you! It was helpful. But if you get any extra information related to this, please post it up too!  =)


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Why are animal mitochondrial genomes so conserved and small in comparison to those of plants?
Background
Levings and Brown (1989):

Higher plant mitochondrial genomes are much larger and
  more complex than those of other organisms. They vary
  in size from about 200 kb in Brassica species to 2500 kb
  in watermelon, which is substantially larger and more variable
  than mammalian (15-18 kb) or fungal (18-78 kb) mitochondrial
  (mt) DNAs

Boore (1999):

Animal mitochondrial DNA is a small, extrachromosomal genome, typically ∼16 kb in size. With few exceptions, all animal mitochondrial genomes contain the same 37 genes: two for rRNAs, 13 for proteins and 22 for tRNAs.

Question
Why are animal mitochondrial genomes so conserved and so small in comparison to those of plants?

Interesting question. Do you have access to this paper? I don't, but the abstract seems promising.

Here's another.


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computing relative synonymous codon usage from a coding sequence alignment while accounting for phylogenetic inertia?
I would like to compute the relative synonymous codon usage (RSCU) from coding sequence alignments. But since the coding sequences from an alignment are not independent realization, the statistics (RSCU) need to account for the phylogenetics autocorrelation present in the data. How can I do that?

It looks like you want to test a very specific hypothesis. Wether a sequence accumulates more non-synonymous changes than expected given its phylogenetic backgroun. The programme CODEML, included in the package PAML was designed specifically for this:
http://evomics.org/learning/phylogenetics/paml/


text:
What is the effect of pesticides on worm growth?
As a new semester begins, we were asked to propose ideas for investigatory projects. Our idea revolves around the effects of pesticides on non-target organisms. Since frequent use of pesticides may potentially affect the health of the soil, we chose the earthworms as our target organism. Our experimental set-up was revolves around studying their growth. Two containers (Container A-Control, Container B-Experimental) would be filled with soil and other things that are essential for worms to live. In container A, normal soil would be used. On container B, we would spray pesticide on the soil and mix them so that it really gets in the soil. After that, we would place the worms (5 each container). The allotted time for data gathering and analysis is 3 weeks. Given this situation, we would observe the behavior of the worm each day for 10 to 14 days (depending on our schedule) and their growth on the last day by measuring their length, weight, and describing their color.
I think that our set-up is logical instead of finding farms that sprayed pesticide for the last 20 or so years which is difficult in our situation. Does anyone have any feedback on the particulars of the experiment based on previous research on the subject?

I'm voting to close this question as off-topic because it is not a question in terms of SE Biology but a request for discussion and opinion. "What do you think?" Is one of the examples of this given in the help on writing questions.

But @David, this is a perfectly valid question on experimental design by a budding biologist. How does the fact that the OP is asking for the opinion of experts detract from the merit of the question? It is my impression that this is what this site is for. This question can be answered with evidence. There may be a range of things that one could suggest but one can cite reasons why an approach is or is not appropriate, or preferred over others. I, for one, would like to reward questions such as this one that show some genuine interest and effort from the part of the OP.

I have suggested some edits to make the question more general. Feel free to modify or rollback if you do not approve my changes.

To @vkehayas (and OP). Please read the Tour and the Help section on Questions to Avoid Asking and you will see why this question is off-topic for this list as it is constituted. 1. It is not a question about biology, as in the three  examples listed under “Ask about...”. 2. It is not a “questions about an actual problem”. 3. It is “primarily opinion-based... likely to generate discussion rather than answers”. 4. It is a “subjective question” having something in common with three of the examples given.

@David, unfortunately I cannot see this question violating any of the criteria. Since we've both voiced our opinion I'd suggest we now leave the community decide on this one.

"Pesticides and earthworms. A review": https://link.springer.com/article/10.1007/s13593-013-0151-z

@vkehayas If you still cannot see why the question is off topic there is no point in further communication with you. I would ask others to read the links I provided.


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How would you find and cultivate specific forms of algae?
Knowing how simple and efficient it is to grow algae, I started wondering how a person would specifically isolate and grow different strands of algae. Say I walk to the closest body of water and took a sample of water. How would I prepare it so that I only got a specific strain of algae, say a green algae?


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What's the difference between germ line and germ cells?
I'm currently reading some introductory chapters about genetics (in Campbell's book, chapter 13) and I realized that I don't really understand what is the difference between the germ line and the germ cells.
From what I read so far, I understand that germ cells are specialized cells from which gametes are produced, and I suppose that the germ line is the "set" of all germ cells + gametes, but for some reason I couldn't find a good definition of what the germ line is and I was not satisfied with what I found in books and on the internet (because it was not as clear as I thought it could be)...
So, even if I'm ashamed to ask... Could someone explain to me the difference between those two concepts? Thanks in advance!

Germ cells are the cells of germline. Germline is a lineage of germ cells from germline stem cells to gametes. Cells that do not belong to germline are called somatic cells.

...and somatic cells form the soma (which should maybe be called somatic line instead for clarity). +1


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Plant growing inside a fruit
Today after cutting open a papaya , a plant was found in it:

How is it possible for a plant to grow in a fruit? How does it gets $CO_2$ and light for photosynthesis?

That is a papaya seed showing vivipary, or premature sprouting. The plant is getting all the sugar it needs from the nutrients stored in the seed so it does not photosynthesize. If it were to run out, the plant would die.


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What does C. Elegans sense when touched?
I'm reading up on C. Elegans' touch responses.  Once touched, what is it that the neurons are sensing, specifically?  Presumably, touch deforms the body cells, and that deformation is sensed by the sensory neurons. Is that correct?  Alternately, are the neurons themselves directly stimulated due to the organism's small size? (Or am I way off?)

In short, you are correct. You touch the skin, and that compresses mechanoreceptors, which then generate a cascading neuronal response.
As far as the actual neurons, it really depends on the type of touch. For example, a well characterized type is gentle mechanical stimuli, which can involve ALM, AVM, PLMs, and PVM, depending on the response (Will Schafer's review doi:  10.1007/s00424-014-1574-3).
Those gentle touch receptors (TRNs) are in the hypodermis, and they have specialized mechanotransduction (MeT) channels along their neurites. It's the altering of those channels that causes receptor activation and the whole downstream behavioral response (summarized from the scientific reports paper below).
So, in summary: mechanoreceptor neurons are activated, and those produce a response. By "response" I mean that those mechanoreceptor neurons activate some interneuron pathways, which in turn activate motor neurons, which make the worm do stuff.

There are many other mechanosensation mechanisms, and WormBook is the place to see a ~comprehensive review of those.

The actual mechanical mechanism/way that MeT channels are activated is a great enough question that a recent paper was published in Scientific Reports to address it. That paper is DOI:10.1038/s41598-017-12190-0 (Elmi et al. Determining the biomechanics of touch sensation in C elegans).
They introduce the paper reiterating what I summarized above.

[...] touch sensation can be considered as a chain of events initiated
  by the spatiotemporal distribution of mechanical loads applied to the
  skin, which result in stresses that deform the skin’s surface,
  sub-layers and underlying mechanoreceptors. In response to the
  transmitted mechanical energy, the mechanoreceptors activate a
  neuronal signaling network that encodes the physical contact as
  information which we perceive as ‘touch’.

Elmi et al. set up a clever assay to look at how the worm's body changes. The body is pretty elastic (up to 16 micrometers) and there's some imperfect skin displacement because the body isn't perfectly cylindrical.
They used that data to build a preliminary model of the different layers of a worm body, and then they validated and tuned the model. It's a cool paper (with some math/physics, which from your profile it looks like you might appreciate).


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What would be the molar concentration of human DNA in a normal human cell?
A diploid human cell has 46 chromosomes. A haploid cell has DNA approximately 3.2 billion bases long. What is the molar concentration of DNA in the cell then? How would we calculate?

Welcome to Biology.SE! Is it a homework question?

What do you mean by "molar concentration of DNA"? Do you "molar concentration of nucleotides" or "molar concentration of DNA strands" or "molar concentration of chromosomes"?

@Remi.b Probably bases or nucleotides, that's maybe why he mentioned the base numbers...

This question seems devoid of practical relevance or any particular biological interest. Why do you ask?

I will assume that be "molar concentration of DNA", you mean "molar concentration of nucleotides".
Cell size
Assuming a cell with a radius of 0.05 nm (nanometer). Assuming a perfect sphere, the volume of such sphere is $5.24\cdot 10^{-4} nm^3 = 5.24\cdot 10^{-11} L$.
Of course, cell volume varies a lot among different cell types. The final result will drastically depend upon the cell volume considered (Thanks to @Roland fo highlighting that in the comment).
Number of nucleotides
In the nucleus
The haploid genome size is about $3.2\cdot 10^9$ nucleotides. The whole genome is therefore $6.4\cdot 10^9$ nucleotides. As there are two DNA strands at each haploid genome, we have to further multiply by two to get $1.28\cdot 10^{10}$ nucleotides. Note that this number could be lower at other moment of the life cycle. What I am computing here is the maximal number of nucleotides per nucleus
In the mitochondria
There are about 1500 mitochondria per cell. Each mitochondria contains about 16,000 nucleotides resulting in a total of $2.4\cdot 10^7$ nucleotidesin mitochondria per cell.
mitochondria + nucleus
$2.4\cdot 10^7 + 1.28\cdot 10^{10} ≈ 1.28\cdot 10^{10}$. That is mtDNA is negligible.
In the mols
The Avogadro number is about $6 \cdot 10 ^{23}$. Hence, there are $\frac{1.28\cdot 10^{10}}{6\cdot 10^{23}} = 3.2\cdot 10^{-14}$ mols of nucleotides per cell.
Molarity
Molarity is defined is defined as the number of mols per liter. It is therefore
$$\frac{3.2\cdot 10^{-14}}{5.24\cdot 10^{-11}} ≈ 0.0006M$$

Nice, but I would add that this depends heavily on the cell volume, which varies a lot between cell types. The cell volume you use (52.4 pL) would be a very large cell: typical mammalian cells range from 1--5 pL in my experience (in cell culture). For such cells, the concentration is an order of magnitude higher, around 5mM. (Of course, the DNA nucleotides are not free, so this "concentration" is artificial.) Also, the "0.05nm" must be a typo, since that would yield a sphere volume of 5.24E-28 L.

But the poster asked specifically about moles of DNA, not moles of nucleotide, mentioning the number of chromosomes. I think the question is pretty silly and best ignored, but if you are going to answer, I think you should do so properly.


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Number of alleles' variations in a mushroom that has over 20,000 sexes
I am trying to understand the mating behavior of a particular species of fungi known as Schizophyllum commune, or the split-gill.
I found a blog post that explains the mechanisms that define the mating types (or sexes) of this species (there are about 28,000 sexes):
http://www.creativewi.re/2017/11/this-fungus-species-has-more-than-23000.html
The post says that the fungus' mating type is defined by a set of two genes that are present on two loci on the chromosomes. Each of these two genes has two alleles. Again, each allele has a number of variations. For example, a fungus with the A1 allele at locus A, and the B2 allele at locus B has the A1B2 mating type. This is a simplified example that doesn't include the alleles' variations.
Now, my question is as follows:
what is the number of these alleles' variations at each locus, and how did the scientists count the total number of sexes?
Thank you!


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Can anyone explain the idea of anodic nerve stimulation?
Nerves get stimulated under the cathode, according to the conventional current direction. But in some research, it is said that anodic stimulation or anodic current stimulation can activate neurons. How does it occur physically? The picture below shows the two types of stimulation, but I can't get it.

Short answer
Both anodic and cathodic current pulses can evoke neural activity, as shown in your image.
Background
You have to be aware that the current direction is arbitrary and the 'convention' you mention depends on your discipline. In electrophysiology, the anode is generally considered to be the positive electrode, the cathode is generally the negative electrode and the anode the positive. In physics however, current is assumed to be positive (due to historical reasons) and therefore the definition of anode and cathode is opposite.
Secondly, there is no reason to assume that nerves under the cathode are stimulated (and not under the anode), as is shown in your picture - in both cases a neural response is elicited. For example in cochlear implants, biphasic current pulses are used, because these are safer than simple anodic or cathodic pulses. Biphasic pulses are charge balanced and consist of an anodic phase and an opposite cathodic phase. (Cochlear implants are arrays of electroides implanted in the inner ear that stimulate the auditory nerve directly and are used to treat sensorineural deafness).
In animals and humans, both anodic and cathodic pulses can evoke neural responses. In human cochlear implant users, the anodic phase is more effective than the cathodic phase. In contrast, in animals usually the opposite is observed. The reason for this discrepancy is unclear (Machery & Cazals, 2016).
Whatever the exact reason of their differing effectivity in evoking neural activation - both anodic and cathodic current pulses can evoke neural activity.
Reference
- Machery & Cazals, Adv Exp Med Biol (2016); 894:133-42

In both cases you generate loops of current, with current densities determined by the overall conductive geometry. So a current flowing from the cathode (negative electrode in electrophysiology), and thus imposing negative charges onto the outer surface of an apposed neuronal membrane, would create a local depolarization there, but would also at a distance draw negative charges away from the outer surface of the membrane, albeit with a lower current density, thus creating a local and weaker hyperpolarization there. Now, consider what happens when you switch to an anode. Current flowing from the anode would impose positive charges onto the outer surface of an apposed neuronal membrane, creating a local hyperpolarization there. But it would also draw positive charges away from the outer surface of the membrane at a distance, creating a local and weaker depolarization there. Crank up the current and you can make that depolarization at a distance strong enough to reach threshold. You would thus excite the membrane at that point, despite hyperpolarizing the membrane closer to the anode.
Because the conductive geometry of biological tissue, and thus the current loop pathways, can be quite complex, the effectiveness of cathodal versus anodal stimulation can vary and be hard to predict. Thus, one usually ends up choosing one over the other on purely empirical grounds.

Welcome and thanks for your answer. Answers are required to be backed up by credible sources in this community, preferably journal papers, but credible web pages (hosted by universities etc) are OK too. Wikipedia is tolerated, but I tend to downvote answers based on wiki pages only. I'm bannering this one. Cheers

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


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Is erythropoietin released when breaking down RBCs
I came across the MCQ in my physiology book, it says:

Erythropoietin.....
i) may decrease the life span of RBCs.
ii) is not released on breakdown of RBCs.
iii) may stimulate the stem cells.
iv) is formed mainly in liver.
v) is lipid in nature

I think ii) and iii) are correct answers, as when breaking down RBCs we don't get erythropoietin, and erythropoeitin stimulated stem cells to produce RBCs, am I right?
Because the book says that only one choice is correct. Help me please! Is there something I don't understand?

To simplify only a bit, EPO production is controlled by the level of oxygen in the blood. You can argue that RBC destruction causes hypoxia, but in truth, if RBC destruction does not cause hypoxia, there is no stimulus for EPO production. Like every hormone, there is more to it and more to discover. But the obvious answer is iii, and anything more is overreading.

Erythropoietin is a glycoprotein cytokine (v is wrong) secreted by the kidney (iv is wrong); it stimulates erythrocyte production (erythropoiesis, from multipotent hematopoietic stem cells through erythroblasts through reticulocytes to red blood cells; iii is correct; i and ii are wrong) in the bone marrow.

Why should II be incorrect? Epo stimulates the production of the RBC, when these are terminally differenciated, you should find it the anymore.

@Martin Klvana, you say that erythropoietin is release when breaking down RBCs?!

@Chris: Asmaa says only one choice is correct.

@Asmaa: You say only one choice is correct.

Erythropoietin can be found in mature erythrocytes. Erythropoietin inhibits apoptosis of erythrocytes by binding to erythrocytes and inhibiting erythrocyte cation channels.
http://jasn.asnjournals.org/content/14/11/2750.long

@MartinKlvana Ah, thanks for the information.


text:
Cardiac pacemaker: how can different nodes have different frequencies?
Primary SA node creates 70 beats per minute and secondary AV node 40-60 beats per minute. Is the AV node inactive (and other subsequent nodes) while the SA node is functional? If the primary, secondary and tertiary nodes are working simultaneously, wouldn't the difference in the beats per minute cause a mess?

The AV node and any other nodes are suppressed by the SA node because it is the fastest.  If the SA node is sick or slow or there is a conduction problem one of these other nodes can take over calling the beat.
http://www.cvphysiology.com/Arrhythmias/A018. bold emphasis mine.

The higher frequency of SA nodal firing suppresses other pacemaker
  sites by a mechanism called overdrive suppression. If a latent
  pacemaker is being depolarized at a higher frequency than its
  intrinsic rate of automaticity by an adjacent cell that is driven by
  the primary pacemaker, then the increased frequency of depolarizations
  leads to an increase in intracellular sodium ions because more sodium
  ions enter the cell per unit time. This increased sodium stimulates the Na+-K+-ATPase (increases its activity) to expel more sodium from the cell in exchange for potassium (see figure). Because this pump is electrogenic, increased pump activity increases the amount of hyperpolarizing currents generated by the pump. This drives the membrane potential more negative, thereby offsetting the depolarizing pacemaker currents (If) being carried into the cell. This effectively prevents the pacemaker currents from depolarizing the cell to its threshold potential, and thereby prevents the spontaneous generation of action potentials. If the cell ceases to be driven by the SA node (e.g., because of AV block), then the additional hyperpolarizing currents will be lost and spontaneous depolarization and action potential generation can occur.


text:
Can any one identify this insect from Lokhandwala, Mumbai India?

I found this insect on my bed. I have never seen such creature before. Can any one identify this?

It's looks like a Leaf-Footed Bug (Homoeocerus Sp., Coreidae).

Source: https://www.flickr.com/photos/itchydogimages/17774939209

Source: https://www.flickr.com/photos/itchydogimages/6211603956/


text:
ID Sunbird in Oman - White, Dark Grey, Yellow
Some extensive web searching has not helped me find this bird I discovered in my travels. They were flitting too fast to get a decent picture, but here is the best description I can obtain from memory:
Dark Grey from their head to their back. Their wings looked black but, as I said, they were flying about. Throat and breast were pale, probably white. Belly and vent were bright yellow. Their beak was a similar shape to the Purple Sunbird. They were taking nectar from bushes bordering a house which had small white flowers.

You should add size description as far as it is possible. To which common bird can they be compared in size?

There are 4 species of Sunbirds in Oman.
https://en.wikipedia.org/wiki/List_of_birds_of_Oman
Based on your description and how common are the different species I think they were most likely mainly Purple Sunbird (Cinnyris asiaticus) https://en.wikipedia.org/wiki/Purple_sunbird
At the moment, in fact, they are not purple at all. They are moulting their feathers and also the male have extensive yellow on breast and belly. Among the species of Oman's Sunbirds it is the only one that shows black wings (in males) contrasting with the brownish/grey upper parts precisely as you observed.
MOULTING MALE

FEMALE (left)

Is it possible for the purple sunbird to have much darker back plumage than this? The one I saw definitely wasn't this light. Also the distinction between the white/beige front and bright yellow bum was quite clear to me as it was a sunny day.
I had found that list of birds, but I was wondering if it was incomplete. It is wikipedia after all and ornithological discoveries tend to be much more advanced than what is available on the internet.

I checked the wiki list and compared with birds of middle east "Birds of the Middle East" By Richard Porter, Simon Aspinall and it is accurate. On the book https://books.google.de/books/about/Birds_of_the_Middle_East.html?id=5ctmHxc8dZcC&printsec=frontcover&source=kp_read_button&redir_esc=y#v=onepage&q=sunbird&f=false you can see the distribution of the different species. It may give further hints. And...yes if they are in a more or less advanced state of the moult the back will appear darker or lighter.


text:
Is a walnut a nut or a drupe?
We've been learning about fruits (and the various categories thereof) in class; among them we have the nut and the drupe.
My textbook differentiates between those terms as:

Nut: It is a single-seeded indehiscent, dry fruit.

Drupe: A fleshy fruit with a stony endocarp.

How here's the problem.
My textbook lists the walnut (fruit) as a nut. But Wikipedia disagrees on this point, calling it a drupe instead.

I'd like a second opinion, since both my book and Wikipedia have had reliability "issues" in the past.
Q- Is a walnut (fruit) a (botanical) nut or a drupe?

Walnut (genus Juglans) fruits are nuts, not drupes.
It is indeed a difficult fruit to classify regarding the traditional classification ("dry" vs "fleshy"), but it is easy to see what's happening here: the fleshy structure is not derived from the pericarp and, therefore, it is just an accessory fruit (just like the cashew fruit, in which the dry fruit is the nut, or strawberries, in which the dry fruits are the black "seeds", not the pinky flesh structure).
This becomes clear when we check the classification of the fruits of the Family Juglandaceae, to which the walnut belongs. According to Milliken (2009):

Fruits are nuts enclosed by fleshy or winglike fused bracts/perianth, giving a samaroid or drupaceous appearance. (emphases mine)

And, according to Manning (1940):

Whole fruit drupelike, but the husk derived from the involucre and the calyx, and the skin from the calyx alone, neither one from the pericarp, hence fruit not a true drupe. (emphasis mine)

The same Manning, in his book titled "The morphology and anatomy of the flowers of the Juglandaceae" (1926), explains it better:

The whole fruit is drupaceous, in that it superficially resembles a drupe, but is not a typical drupe (a true drupe is a fruit in which the outer portion of the pericarp is fleshy, the inner portion hard or stony).

Have in mind that in the traditional classification "dry" and "fleshy" are mutually exclusive, meaning that a given fruit can be one or other, but not both. Therefore, your textbook is correct and the Wikipedia link is wrong.

Sources:

Milliken, W. (2009). Neotropical Juglandaceae. In: Milliken, W., Klitgard, B. & Baracat, A. (2009 onwards), Neotropikey - Interactive key and information resources for flowering plants of the Neotropics.
Manning, W. (1926). The morphology and anatomy of the flowers of the Juglandaceae.
Manning, W. (1940). The Morphology of the Flowers of the Juglandaceae. II. The Pistillate Flowers and Fruit. American Journal of Botany, 27(10), p.839.

Those were some pretty heavy comments below! The comments were removed, but they were appreciated nonetheless - I was just wondering what was wrong with my answer. Reading the comments and your answer I'm still not convinced, but +1 for the 1940 reference :) And oh no I would never start a downvote war. I just often leave a note and downvote and this time I was inetersted in what was incorrect about my answer. Also, lately on every post I make, a downvote comes in. I'm just wondering if there's someone out there hating my guts :0 Anyways, I'll remove this comment shortly.

@AliceD I removed the comments because I was afraid of initiating a downvote war. Regarding your answer, it's incorrect because a fruit cannot be both A and B in that key, it's simply impossible. Walnuts are dry fruits, not fleshy fruits. Unfortunately, that Wisconsin Uni link has some mistakes. For instance, in my deleted comment (that as a mod you can probably see) I talk about the coconut, which is clearly wrongly classified in that link you provided: coconuts are dry fruits. Unfortunately, university pages do have errors!

Actually, the book is from 1926! I just edited the answer.

Thanks for all this. I might have to remove that answer, or amend it. Either way, no war on this side.

@AliceD Good to know. Since the mistake was not yours but that page, I think is unfair to you if you delete your answer. I suggest you keep it, just clarifying why the linked page suggests it is a drupe.

@Alice "*Have in mind that in the traditional classification "dry" and "fleshy" are mutually exclusive. *" <---- That sorta appealed to my plebeian knowledge of fruits/vegetables, which is what finally convinced me to accept this answer. Additionally, the lack of a stony endocarp in walnut (fruits), makes it less of a drupe (from what I gather). Yours was an interesting answer, and provides another perspective, so it got my upvote as well. Also... there was a downvote war? :O

@paracetamol No, there was no downvotes war! Let me explain to you: After receiving a downvote, Alice asked "why the answer was downvoted?", a legitimate question by the way. I left a comment saying that asking why an answer was downvoted is not a good approach at SE sites because, once the downvoter identifies himself/herself, normally a downvotes revenge war begins. But, after having left the comment, I deleted it, fearing that the very comment could start a downvotes war... that's all.

Just to make myself clear and finishing this subject, my opinion is that, the same way we don't ask "why the upvote?" when someone upvotes us, we shouldn't ask "why the downvote?" when someone downvotes us. Upvoting and downvoting are the core of SE sites, and they are pretty much self explanatory: if someone likes our answer they upvote, if they don't they downvote. The voter can, in both upvote or downvote situation, leave a criticism/comment, but only if they want to. Have a look here: https://meta.stackoverflow.com/questions/285081/am-i-still-supposed-to-explain-my-downvotes-or-not

Short answer
Walnuts are classified both as nuts and drupes ('stone fruits').
background
According to University of Wisconsin - Madison, Department of Botany , hickory and walnut can be classified both as drupes and nuts, but are best classified as nuts.
Nuts fall into the class of indehiscent fruits: dry fruits that do not open when mature to shed their seeds. Many of this group are one-seeded fruits, such as the nuts. In addition, nuts have a thickened and hardened wall. Examples are beech, chestnut, oak, hazel, walnut and hickory. Because of extrafloral bracts, or "husk", the latter two fruits are sometimes called "drupes").
As opposed to indehiscent fruits, the fleshy fruits have a wall that becomes soft and fleshy as it matures. Drupes ('stone fruits') fall into this class. Drupes one-seeded, simple fruits developed from a superior ovary in which the innermost portion of the wall (endocarp) becomes hard and stony, the outermost part (exocarp) becomes a relatively thin skin, and the middle portion between the skin and the stone (mesocarp) becomes either fleshy or fibrous. Examples are cherry, coconut (the endocarp is the thick wood shell that surrounds the fleshy and liquid-filled seed), but also walnut and hickory. The latter two are, however, best called "nuts".
Indeed, according to a popular scientific article in the Guardian, many tree nuts are also drupes, including walnuts and pecans.

Some nut who thinks he's been duped, I suppose.

Then what's the fleshy part of the walnut?

@Rob The question's about the walnut (fruit), not the kernel (which is commonly referred to as the "walnut"). I had issues wrapping my head around that too at first :3

A true nut, botanically speaking, is a hard-shelled pod that contains
  both the fruit and seed of the plant, where the fruit does not open to
  release the seed to the world. Some examples of botanical nuts are
  chestnuts, hazelnuts, and acorns.
A drupe is a type of fruit in which an outer fleshy part surrounds a
  shell (what we sometimes call a pit) with a seed inside. Some examples
  of drupes are peaches, plums, and cherries—but walnuts, almonds, and
  pecans are also drupes. They're just drupes in which we eat the seed
  inside the pit instead of the fruit!

Source: http://www.seriouseats.com/2010/04/what-are-the-differences-between-nuts-and-drupes.html

I would opt against using culinary sources as the basis of an answer.

@AliceD:  I would normally agree.  However, in this case the author is known as the "Peanut Butter Guy" and Founder and President of Peanut Butter & Co.  I understand that peanuts are a legume, but I do value his opinion on nuts too.

I've never seen "drupe" figure in a purely culinary site/blog/book (I'm not much of a cook, but still...). That this source even mentions "drupe", and then goes on to discern between a drupe and a nut, adds to its credibility IMHO.

I wouldn't underestimate the knowledge that a culinarian has with foods.  Per wikipedia experts in this field need to have knowledge of food science defined as "the discipline in which the engineering, biological, and physical sciences are used to study the nature of foods, the causes of deterioration, the principles underlying food processing, and the improvement of foods for the consuming public"


text:
Barr bodies in males?
This source states that there are Barr bodies in 0-4% of males.
Why isn't it complete 0%? why some males loose their only X chromosome? How does then their body compensates for those genes which are inactivated?

To understand how the X inactivation can occur in, it requires a bit of understanding of how Barr bodies come about.
The main key players to keep in mind are (From 1):

Xist: Xist   Required for initiation of X-inactivation
Tsix: Tsix (It's Xist spelled backwards!) Represses Xist expression by silencing the Xist promoter, also required for X-chromosome pairing, counting the number of XICs (X-inactivated chromosomes)

From 2, Here is a general diagram of how X-inactivation occurs.

X-inactivation requires first, count how many X chromosomes are present (n). Then, the (n-1) number of X chromosomes are inactivated. The choice for which gets inactivated is largely random.
Therefore, if a male has multiple X-chromosomes (as in the case of Klinefelter syndrome) then X-inactivation would occur in males. However, there is also the case that erroneous counting may lead to the inactivation of the only X chromosome in males early in a developing embryo. But this is lethal, and the embryo would die.
More about Kleinfelter Syndrome can be found here: Klinefelter syndrome

Guided by RNAs: X-inactivation as a model for lncRNA function.
Lessons from X-chromosome ina ctivation: long ncRNA as guides and tethers to the epigenome

So all males with Barr bodies are Klinefelter males?

If they only have 1 X-chromsome and is inactivated, they would not make it to full term. They can have more than XXY, however, there will always be multiple X's.


text:
Alcohol consumption and central nervous system
After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination.
My question is- why is it so? Why do they appear in that order?
Like does it have anything to do with differential rate of absorption in cells, or anything else like related to anatomy rather than physiology.

Can you give a source for your statement? There is a big difference between being affected and feeling something. I would say your oral/esophagal and gastric mucosas would be the first body part affected (hence oral cancers in drinkers who smoke.) The liver is next. Alcohol affects a lot of body parts, so this question is fairly unclear to me. Could you possibly edit to make your question clearer? Thanks.

@anongoodnurse - i didn't exactly read that in a book or anything. It's just a question which was asked in some competitive exam. Cerebrum was preferred over cerebellum as the answer. Plus, here, I'm talking about not the long term effects of alcohol drinking. I'm asking which body part is affected first just after intake of alcohol.

@anongoodnurse -I think i have made my question a little bit clearer.

The first body part(s) affected after drinking alcohol are the oral/esophagal and gastric mucosas. Have you ever swallowed whisky and felt it burn? As to cerebellum vs. cerebrum, read about which does what, and think about which is affected first when you drink. You'll figure it out.

@anongoodnurse - i do get your logic. That's true that the mucosal lining will be the first affected part, then liver since the absorbed alcohol will go through hepatic portal vein to it. Then any cerebral effects should be seen. But my question isn't about what symptoms are seen and in what order. It's rather about why cerebral related things are affected first (like vision and speech) and then later on cerebellar symtoms appear like problems in balancing and hand eye coordination? PS: i can't do the practical you said since I'm 18 and 21 is an average drinking age in india!! Hehe =)

I'll try to edit my question accordingly

After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination. My question is- why is it so? Why do they appear in that order?

It is and it isn't complicated. When you include what each does, it's an interesting question.
We know from experience (and even research, though the ethics of carrying out such research is questionable) that of the noticeable effects on the brain, the first part of the brain (that we can see the effects of) are on the cerebrum. At relatively low doses, the drinker feels more relaxed, more talkative, less inhibited. (there is also a measurable decrease in information processing and reaction time, as well as other less obvious effects.) All these are under the control of the cerebrum.
At this stage, the cerebellum is affected as well, but not grossly (in a manner that we can observe as change in behavior.) The cerebrum is critical to functioning; the cerebellum is critical to survival. Although it's presented as a teleological argument, the simple fact is that effects of alcohol and other sedatives on various parts of the brain are dose-dependent.

First, dose-dependent functional magnetic resonance imaging (fMRI) changes were revealed in orbitofrontal (OF) and motor (but not cerebellar) regions; visual and medial frontal regions were unaffected. Second, cerebellar regions were significantly associated with driving behavior in a dose-dependent manner. Finally, a global disruptive effect of alcohol on the ICA time courses was observed with highly significant differences in OF and motor regions. Alcohol thus demonstrated some behavioral effects and unique, disruptive, dose-dependent effects on fMRI signal within several brain circuits. The fMRI data also suggest that the deficits observed in alcohol intoxication may be modulated primarily through OF/anterior cingulate, motor and cerebellar regions as opposed to attentional areas in frontoparietal cortex.

If you want to know why different parts of the brain require higher doses to become impaired, that is easy in theory but very complicated in reality. In theory, the brain is no different than any other complex organ in the body: it's made up of different cells. Sure, they're all neurons (excluding glial/etc cells), but not every neuron is the same, just like not every cardiac myocyte is the same. In reality, the answer is unknown.

Neuronal mechanisms underlying alcohol intoxication are unclear. We find that alcohol impairs motor coordination by enhancing tonic inhibition mediated by a specific subtype of extrasynaptic GABAA receptor (GABAR), α6β3δ, expressed exclusively in cerebellar granule cells. In recombinant studies, we characterize a naturally occurring single-nucleotide polymorphism that causes a single amino acid change (R100Q) in α6 (encoded in rats by the Gabra6 gene). We show that this change selectively increases alcohol sensitivity of α6β3δ GABARs. Behavioral and electrophysiological comparisons of Gabra6100R/100R and Gabra6100Q/100Q rats strongly suggest that alcohol impairs motor coordination by enhancing granule cell tonic inhibition. These findings identify extrasynaptic GABARs as critical targets underlying low-dose alcohol intoxication and demonstrate that subtle changes in tonic inhibition in one class of neurons can alter behavior.

The above sounds like a reason, but it is debated still. I think it's safe to say that like so many cellular reactions, the answer will come down to receptors and their activation or inhibition, be it for GABA/NMDA, combinations or others.
Alcohol impairment of behavior in men and women
Differential effects of ethanol on motor coordination in adolescent and adult rats
Alcohol Intoxication Effects on Simulated Driving: Exploring Alcohol-Dose Effects on Brain Activation Using Functional MRI
Modulation of GABA A receptors in cerebellar granule neurons by ethanol: a review of genetic and electrophysiological studies
Ethanol affects NMDA receptor signaling at climbing fiber-Purkinje cell synapses in mice and impairs cerebellar LTD

In the fMRI part; visual and medial frontal regions were unaffected. It means that they are affected but not in dose dependent manner. Am i interpreting it correctly?

It means (sorry to be a stickler) that no activity was seen at that dose on fMRI. I can't really say more. :)

Okay, got it! Thanks! It really helped a lot  .No need to be sorry. =)


text:
Why is my DNA below the ladder?
I have run a gradient PCR.. and band 6 after the ladder is clearly the brightest. But all bands appear below the ladder. What does that mean? It is extracted mDNA that was loaded.
Thank you in advance!

Below the ladder means primer dimer.  You have no product.

Thank you! That explains it. I will try deciding primer amounts and hope for the best!

In my experience, altering primer concentration won't do anything.  I'd rethink the annealing temp, maybe try a more robust Taq, double-check the quality of your input DNA, and double-check that you have the right primers, and that they actually should make a product.


text:
How have single-celled organisms learned to survive?
Upfront: I am a computer science student trying to understand evolution and its implications.
I've been pondering the concepts of evolution for some time, especially related to neuroscience / how the brain works / how to emulate brains. I wonder how single-celled organisms evolved at all. I know, they don't "think"; but once their ATP levels get low, they know they must find food to sustain their system, aka staying alive. This is probably no active decision, more like: "The enzyme concentration tells me to find food".
Question: Was the entropy just high enough that at some point those organisms had the property that finding food somehow is preferable to death? Edit: How can an organism perform something without "knowing" it needs to perform it?
I hope, this isn't a terribly stupid question.

Do you think the following is a good reformulation of your question: Not all responses to environmental stimulus are performed consciously. How can unconscious responses be made? How can an organism perform something without "knowing" it needs to perform it?

If the above is a good reformulation then note that 1) it is rather unrelated with the field of evolution (except by the extend that everything in biology is related to evolution) and 2) Any living organisms has unconscious responses to environmental stimuli (incl. humans). The question has no reason to be specific to unicellular organisms.

@Remi.b Yes, especially the last part of your suggested reformulation is better than my own question. I will edit my question accordingly.

@Remi.b I know, that this is not specific to single-celled organisms. I hoped, that by reasoning about simple life forms, one can deduce answers for more complex ones. If simple organisms "know" it is necessary to find food or procreate, more advanced organisms should know that too, right?

"How can an organism perform something without "knowing" it needs to perform it?" -- physical & chemical laws coupled with biological stimuli & response; nothing more, nothing less.

@Charles I see you have the same point as @Remi.b; at some point those organisms must have learned, that one response is better than another response to a specific stimuli. Is it just trial and error?

@Charles For me, it's just hard to grasp, that evolutionary forces (in the sense of natural selection and mutation) or entropy were "high" enough to allow enough variation in the first and succeeding generations of organisms to "figure out" the basic (and increasingly complex) processes of survival and the corresponding actions.

You would be better off retagging this as a question about microbiology, ethology, and possibly  neurology. the organisms don't need to learn anything the simplest behavior are entirely fixed the organism does not decide anything.  Its not a bad question it is just not very clear what you are asking without the discussion.

Nothing more than physics
Simple physics
If you drop a rock, the rock will fall to the ground. If there was a table underneath, the rock would stop its fall when reaching the table. Clearly the rock response to the environment but the rock does not need to be conscious (whatever you mean by "consciousness") of anything in order to response to the environment.
Explanations for a programmer
As you are a programmer, you will agree that when you do std::cout << 3+2 << std::endl;, nothing more than physics is happening so that the value 5 followed by a newline gets printed to the screen. It is relatively complex though. So complex as it may feel quite magical before having spend many hours learning about computer engineering.
You understand that if you write a, say, boids program, all that is happening is just a bunch of addition and multiplication (eventually a power). The program does not need to be "aware" of what it is doing (nor do the individual agent) in order to respond to the change of behaviour of a predator.
You could even write a self-learning algorithm and you would still accept that there is no consciousness involved but only very simple operations.
Biology
Living things are pretty much the same. They are relatively complex (more like a computer than like a rock) but essentially the same. Also, the response tot he stimulus is often (not always) adaptive as it has been selected. But at it's core there's nothing more than physics involved!
More info
If you want to learn more about the mechanism of living things in general, you might want to just open an intro book or have a look at an intro course such as Khan Academy > Biology for example.
You can as well pick a simple response to an environmental stimulus and study its mechanism. How about having a look at chemotaxis for example!
Note that you might also want to follow a short and introductory course to evolutionary biology such as Understanding Evolution for example.

Thank you for your answer and suggested readings! Maybe you are right with your first observation, that I concentrate too much on single-celled organisms. They are really just simple, biological state machines. As a computer scientist, it's just highly interesting to find out more about biological systems and how cognition evolved.

I understand your point that "it's just physics", especially with lower life forms. However, how do things change with, say, mammals? Or probably anything that has a nervous system with a lump of neurons acting as a brain? Then, those stimuli certainly influence the behaviour of the organism, but based on experience or other internal assessments of the situation, the chosen behaviour may be different.

Of course, the brain can also be seen as a very complex state machine, where neurons fire just differently after experiencing events ("learning"). Probably I should just do some reading to figure out how to better formulate my question about life and how the sum of these basic processes forms into something we call "intelligence" for higher life forms :)