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Diazepam with Aluminum Hydroxide
Some common medicinal preparations contain diazepam with aluminium Hydroxide, there may be other compounds [e.g. magnesium trisilicate and polydimethylsiloxane with Aluminum Hydroxide and Diazepam as ingredients of Tablet Peptica ( Geno pharmaceuticals)]. These drugs are commonly used as antacids. We can see in the drug Peptica that Aluminum Hydroxide and Magnesium Trisilicate were included for neutralizing the acidity (HCl) of stomach.....thus serving their purpose as antacids. Polydimethylsiloxane is a carminative preparation ('Carminative' means preparations that expulse gas from the gastrointestinal tract or prevent its formation). But what is the need for adding Diazepam here?

Diazepam is a very-much restricted medicine. It is sedative-tranquilizer (sleeping pill) also used in severe anxiety.  I've never seen any antacid-preparation containing diazepam. Maybe a sedative-tranquilizer preparation (maybe in mouth-dissolvable form) using some amount of antacid in it. or maybe in that tranquilizing preparation those antacid-materials just being used as a tablet base, with no functional role.

I'm not a doctor or medical professional however web search tells this particular brand is used to treat peptic ulcer. Maybe they're using it to calm-down the nervous-system of patient suffering from ulcer-pain. This question is more appropriate for a medicine or health community, than a biology community. Take professional Doctor's advice (not any web advice) for medicine use, and especially when it contains a restricted chemical.


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Why is the "worm" body shape so prevalent in Eumetazoa?
What is the selection advantage, of this incredibly common body form? (long, cylindrical tube-like body with no limbs)
Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it? I.e. is it a neutral adaptation? Or is it actually a positive one?
Examples of "worms":
- Platyhelminthes
- Nematoda
- Annelida
- many kinds of insect larvae
- sea cucumbers
- lancelets, lampreys, eels, snakes, caecilians, ...
- Chaetognatha
- Hemichordata
- Acanthocephala
- Gastrotricha
- Gnathostomulida
- Nematomorpha
- Nemertea
- Priapulida
- Sipuncula

Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it?

Pretty much.
You can see some animals which precede the emergence of this plan, like sponges. They apparently do alright, so there's nothing precluding different body plans. However sponges also have a fairly limited niche, and perhaps there's a good reason. Similar things can be said for other non-bilaterians like jellyfish.
One could speculate that the "tall-donut" shape is the key innovation. When food moves in only one direction, it is much easier for the digestive tract to specialize and digest food much more efficiently in stages. Animals, after all, are things that survive by eating things and digesting them - the faster they can digest, the faster they can eat, the better they can survive.
Animals which have no separate anus seem to have more trouble eating things and digesting them: It's slower, and they can't eat as varied a diet.
A worm, being essentially a long tube, is a simple way of accomplishing accomplishing the one-way GI tract. If you think in an evo-devo sense, it also doesn't take a lot to progress from a "basket" to a tube (the two layers after gastrulation just have to meet, fuse, and form a second hole). If you consider the so-called higher animals, like humans, cats and dogs "worms", then we can stop there. Otherwise, we can remark that the "worm" shape also allows easy movement in water and on soil by wriggling.
Past the "pure worm" you can see a large variety of body plans, such as among arthropods, but they're really just worms with a few specialized segments, including, say, humans. This does have a fundamental reason: During early development, patterning of the body (deciding which organ or limb will grow where) relies on Hox genes, which are typically top-level transcription factors that determine a segment's identity. So the "worm" also happens to be a nice developmental "base" from which more complicated embryos can develop.

is it a neutral adaptation? Or is it actually a positive one?

This is very hard to answer:

There are necessarily many confounds, and we cannot easily find two animals which are otherwise the same, but one is a worm and the other is not. We cannot artificially generate such animals yet either.
The obvious way to infer fitness is to look at whether the trait came to dominate the population. But with since body plan establishment is something that did not evolve independently many times, it is hard to say whether it dominated due to a genuine fitness advantage or purely out of being fixed. Perhaps there are other, yet more efficient body plans, but they have not yet arisen due to random chance.

This is a really good answer -- sorry for the slow upvote, I had already maxed out on them yesterday when I got your answer, so I had to wait until my limit refreshed.

source: Stack Exchange

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Determine whether aromatics originate from polyketide or shikimate pathway
Is there a way to determine whether an aromatic compound  originates from the polyketide or shikimate pathway by looking at its structure? If so, how?

I've modified your question. They are pathways not ways.

Aromatics that stem from the Shikimat Pathway result in a structure like this

Whilst aromatics originating from the Polyketide Pathway have an alternativ structure in the distribution of the OH groups.

If both pathways produce the same molecule, you can't tell: It's the same molecule.
You could knock out some enzymes on either side and see which ones affect output. Or you could spike the cells with a radiolabeled precursor of only one pathway, and then see if the output is also labeled.
However, you say "by looking at its structure", so I'm assuming no additional experiment can be done - then no, except for the trivial case where only one of the pathways produces the molecule (in which case it obviously came from that one).

It's no real world scenario. To clarify, let's say you have an arbitrary aromatic, look at its Fisher Projection for example. Is there a way to deduct from that the origin? Are there some unique properties that originate from the pathway that was used for synthesis. I remember something like that from our lecture. Maybe I'm able to find out what exactly the lecturer meant with that.

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Does the octopus have an anus? What does it look like?
Octopuses are cephalopods, which have separate anal and oral openings. Indeed, descriptions of the cephalopod GI tract clearly depict an anal opening.
However, I am very confused about how this applies to the octopus. I don't think I've ever seen the anus depicted - where is it? What does it look like? Does anything much come out?
My first instinct would be to simply do a google image search for this. Unfortunately, those results are flooded with unrelated hits (apparently the octopus is a popular motif for tattoos... in a certain part of the body).

The anus of Octopus is channeled into its siphon.

Image taken from Carina M. Gsottbauer
Note:

Siphon is a tube that leads from the mantle to the outside. Octopuses use their siphon to force water out in jets for propulsion and to flush waste products from the anus.

From Encyclopedia of the Aquatic World, Volume 6
By Marshall Cavendish Corporation

And here I was thinking that the siphon just ejects clean, harmless water... I'll keep this in mind next time I encounter an octopus!

I would imagine that you'd probably have to worry more about that poison gland than the highly-diluted waste that is ejected from the siphon.

@RobertHarvey Isn't the poison of Octopus injected through a bite? http://www.thecephalopodpage.org/octobite.php

@SanjuktaGhosh please add citations to your answer on where the image and quote originated. If you use images and/or text that are not your own words, you need to cite the sources.


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Estimate of total number of oncogenic mutations
So there are a number of ways point mutations can hyperactivate or inactivate genes. But realistically there are only some small number of point mutations ever observed for a particular gene in cancers. An example is the JAK2 mutation: c.1849G>T p.V617F chr9:5073770 which is almost the only JAK2 base substitution observed in leukemias.
Is there some estimate of the number of substitution loci ever observed in cancers?

you can visit the TCGA website, but be warned navigating that mess is a giant pain

@KoustavPal yeah I've played with TCGA a lot, but that I can find there is no sum total estimate of this.


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How to tell if/how allele frequencies change (USABO question)
This is question number 34 from the 2014 USABO Open Exam:

Black and white mice live on an island and have allele frequencies of B=0.20, b=0.80. On the continent, there is a much large population of mice with allele frequencies B=0.80,b=0.20. Ships begin moving back and forth between the island and the continent. Occasionally, a mouse finds its way onto the ship and leaves the ship and breeds with
the mice of the other population. Equal numbers of mice ride in each direction. If the ships move continuously between the island and the continent, will the allele frequencies
ultimately stabilize? (Assume that no other forces are affecting allele frequencies.)

A. Both populations will end up at approximately B=0.80, b=0.20.
B. The island and continent populations will stabilize with an allele frequency of B=0.50, b=0.50.
C. Black mice will move to fixation in both populations, because the B allele is dominant.
D. Both populations will end up at B=0.20, b=0.80.
E. The continent's allele frequencies will not change; the island will settle at an equilibrium that is somewhere between the continent's and the island's original states.
The correct answer is A.
I guessed E, because I thought the difference in allele frequencies on the continent meant that the B allele was selected for there, and since the population was so big, I thought that the immigration and emigration wouldn't affect the allele frequency there so much, while the island's allele frequencies would change a little because of the smaller population.
Why is the answer A, why is E wrong (besides that A is right), and is there a math way or some sort of rule to solve this problem (or are you just supposed to reason it out)?
Thanks! :)

Just think about it logically.


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What is this (seed/berry)-like object and where is it coming from?
I've been finding these little green (seed/berry) like objects in my garden for three years now.

This picture shows either a large variant or simply  a later lifecycle stage of development.
At their smallest, they look artificial - kind of like nerds candy - almost too green to be natural.  In the picture above, it is obvious that the item is a berry, but at the smallest sizes, my first thought was that it was fertilizer.  And indeed, I would've continued to think that if not for two things:

We re-mulched our garden two years ago, and didn't fertilize (nor have we ever, but this house is only 3 years old).
When you squeeze even the smallest sized objects, they squirt juice or water.

When the larger berries are crushed, many little seeds come out along with liquid; and it looks almost like a miniature pickled tomato.
There is nothing in my garden that produces any kind of visible berries; and I've never seen one of these attached to a plant.  That is part of what makes them so odd (and part of what made me think they were fertilizer); I always find them mixed (sometimes deeply) in soil or mulch.
If no one knows after a couple days, I'll go take a picture of one of the baby ones to help.  Any thoughts?
Location: Brighton, MI (USA).
Update:. Here are some other shots.  These are both flash shots because it is overcast today.  These are also of the younger variant because I couldn't find any  of the mature berries today.  Hope this helps.

Other photos that would help: close-up of where the 'stem' joins the 'fruit' (assuming that's what it is); sectioned (sliced in half with a razor) rather than squished, and maybe an 'in situ' shot of one where you found it in the surroundings of your garden?

Barring further details or photos, your fruits remind me of the drupe  from a hackberry (Celtis spp.)  tree.

Hackberry drupes are relatively small, often being only about 6-10mm in diameter.
Examples:
1,
2.
Do you have any warty looking trees nearby?
(like this).
Do you ever see the fruits in a different color? (purple, black, red, orange)?

I think you are right.  In response to your questions:  Different color: maybe purple - though I wouldn't necessarily realized they were the same with other colors.  We have a nearby golf course with warty trees, though it's quite a long stones throw away.  But my sense is that you are likely spot on

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If a promoter region of a gene is transcribed, can it get methylated?
Deletion of a transcription termination site can lead to a downstream gene's promoter region being transcribed. What if that portion of the mRNA acts like an siRNA methyltransferase recruiter?


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Did vertebrates diverge from other deuterostomes via neoteny?
Question: Is there any research corroborating my suspicion that vertebrates diverged from other deuterostomes via neoteny (the attainment of sexual maturity while still in larval stage)?
Context: Most echinoderms have pelagic, bilaterally symmetric larvae, while the adults are not bilaterally symmetric (except for sea cucumbers) and live on the sea floor. The same is true for tunicates, which are supposed to be the sister group to vertebrates.
Adult echinoderms also have very reduced nervous systems, although I am not sure whether the larvae have more advanced nervous systems than the adults. For tunicates, which are more closely related to vertebrates, the nervous system definitely does degenerate when transitioning from pelagic larvae to sessile adults.
Echinoderms are also one of the few clades of bilateria, except for vertebrates, which have endoskeletons. And of course, echinoderms, tunicates, and vertebrates are all deuterostomes.
In contrast to tunicates and echinoderms, the MRCA of vertebrates is thought to have resembled a lancelet, which is pelagic and which has a more advanced nervous system than adult tunicates or echinoderms. In other words, it seems like ancestral vertebrates retained larval features into adulthood, and then just grew bigger in size.

Based on morphology some hold a conceptually related - but opposing -suspicion that ( within protostomia ) caterpillars evolved from onychophorans by hybridogenesis ( rather than being larvae ) http://www.pnas.org/content/106/47/19901.full

@tsttst This is a very interesting article and concept, which I had never heard of before -- thank you for the reference! I am looking forward to reading all of it

echinoderms are sort of bilaterally symmetrical, imagine if you took a velvet worm and then twisted it around in a big loop with the legs sticking out until the head was stuck to the tail end but still pointed away from each other. That is basically how echinoderms went from bilateral to radial. of course in practice this is done by rearranging hox genes but it is a good way to visualize it.  https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-5-22
as for chordates look at hemichordates (which also have endoskeletons) and you can see why the general belief is that tunicates evolved that life stage after branching off(kinda like barnacles) instead of vertebrates losing that life stage.

Thank you for the interesting reference - I look forward to reading it later! The point about hemichordates is a good one which I failed to consider previously.


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Is post-transcriptional regulation of gene expression an epigenetic process?
Is post-transcriptional regulation of gene expression (for example regulation by microRNAs) a type of epigenetic gene expression regulation?
I think we can categorize it as epigenetic since the DNA sequence is not changed, but I have never come across that terming in any papers. Does someone have any idea, or know of any papers that categorize post-transcriptional regulation as epigenetic?

miRNAs and other post-transcriptional regulators are very well "genetic". They are encoded by genetic elements, are expressed and are affected by mutations. Just because this mode of regulation was not well known previously, it should not be classified as an epigenetic mechanism while the traditional protein based transcription factors (TF) are not.
Epigenetics, as it is originally defined (the "formal definition") is about mechanisms that can perpetuate the state of a cell to its next generation. Inheritance of gene expression programmes is therefore epigenetic. Although the gene expression programmes themselves can be implemented via different factors including protein and RNA based regulators, they would not necessarily constitute the epigenetic mechanisms that lead to inheritance of this state.
rg255's point of view is that any mechanism that causes a variation in the functional aspects of the genome without altering the genome sequence itself, would be epigenetic. This is technically correct but in that case all gene expression regulators including TFs should constitute epigenetic mechanisms.

Now, the main issue is where to draw the line between gene regulation and epigenetics?
In my opinion, the epigenetic mechanisms are one of the ways to regulate the gene expression. Although histone modifications and DNA methylation regulate gene expression and also confer heritability to the gene expression programme, the heritability can be implemented without them as well.
You can imagine a cell as a vessel which runs a system of biochemical reactions. This system can have multiple steady states (for e.g. multiple fates of a stem cell). To perpetuate a state, the new cell just needs to have the right initial conditions. This can be proved mathematically too. Such a system can be implemented via the traditional transcription factors as well. So what is epigenetic?
IMHO epigenetic was a loose term to denote something that people were not fully aware of, at that time. Anything that was not directly mediated by transcription factors was termed as epigenetic, including long distance regulators, non-coding RNA etc.

BOTTOMLINE
I would not classify non-coding RNAs as "epigenetic" for the very reason that they are encoded by genes and have more or less a direct effect on the target genes, just like TFs (which are apparently not epigenetic). As for the papers, there were many papers that used to assign these under epigenetic mechanisms, but that is IMO just too vaguely arbitrary. (Ironically, I happened to come across miRNAs and lncRNAs while I was doing a summer project on epigenetics and was reading relevant papers.)
What should be considered epigenetic would be a subject of another debate.

How can you implement functionally non-fatal heritable mechanisms without the presence of histone modifications and methylation? The conservative epigenetics definition revolves around heritable mechanisms (not loose), the contemporary epigenetics definition is now loose encompassing fields which we understand better than we did in previous years (noncoding RNAs, chromatin architecture included).

How can you implement functionally non-fatal heritable mechanisms without the presence of histone modifications and methylation?... It is theoretically possible and there are examples too but I cannot remember them at this moment. The point is that you are thinking from a top-down point of view (looking at the world from a human/animal/eukaryotic point of view). A self sustaining system does not need histone modifications. Look at the cell cycle, for example.

I meant an experimental system. I would be very interested in seeing such an implementation in a eukaryotic system where the mechanisms have been completely removed (not cases such as ipsc where the marks are procedurally removed and re-established by the system) and the system is able to propagate without these mechanisms.

@KoustavPal That would be very difficult to implement because the cells have evolved to be dependent on that complexity and it would not be possible for the cell to survive if you strip that off from it. However, a self sustaining system can exist without these mechanisms (exist just because of the GRN). It is likely that histone modifications etc came later in the course of evolution. Prokaryotic organisms don't even have typical histones!

GRN?. Ofcourse they had to come later, you might find this on prokaryotic memory interesting, I read something similar or this one a long time ago (http://www.nature.com/nature/journal/v460/n7252/abs/nature08112.html), my point with the original question was a system which has evolved a regulome around these features would find it very hard to survive without them, although a system without them wouldn't need them at all. So that sort of makes the statement moot. We are talking about very different systems altogether, with entirely different contexts, the statement to me implies

that a system which has these mechanisms may still have them taken out and yet survive and lead to fully functional progenies

@KoustavPal GRN = gene regulatory network. We can talk in chat. Getting too long for comments.

I think WYSIWYG's explanation and mine are more in tune with the consensus than that of rg255. I highly doubt you will find many molecular biologists who think of miRNA's as epigenetic

@WYSIWYG Thanks for the reply. Could you please explain a little more why it is apparent that TFs are not epigenetic?

@user5054 People somehow don't consider them epigenetic. It is just arbitrary. There is no logic.

On epigenetic and genetic effects:
Changes to the genome can be of two key types: genetic and epigenetic. Genetic changes are those which cause changes in the nucleotide sequence. Epigenetic are changes to the genome that do not involve making changes to the nucleotide sequence, e.g. post-transcriptional processing.

"Functionally relevant changes to the genome that do not involve a
change in the nucleotide sequence. Examples of mechanisms that produce
such changes are DNA methylation and histone modification, each of
which alters how genes are expressed without altering the underlying
DNA sequence".

Epigenetics is also generally used to refer to the study of variation induced by heritable non-genetic factors that affect the genome, such as maternal and paternal effects. The two subtly different definitions are responsible for some of the common confusion.

"Today, epigenetics refers to the study of heritable changes in gene
expression without the change in gene sequence. ".

On microRNA
There is some contention around whether miRNA is specifically an epigenetic mechanism - you've used it as an example - post transcriptional modifications would generally be considered epigenetic effects. See the paper from which the following extract comes which covers "classical" mechanisms too:

"Whether miRNA regulation is an epigenetic mechanism in its own right is unclear"

Also see whatisepigenetics.com:

"At least three systems including DNA methylation, histone modification and non-coding RNA (ncRNA)-associated gene silencing are currently considered to initiate and sustain epigenetic change."

And part of the conflict is perhaps because miRNA's are seemingly involved in the control of epigenetic processes:

"Epigenetics is defined as mitotically and meiotically heritable changes in gene expression that do not involve a change in the DNA sequence. Two major areas of epigenetics—DNA methylation and histone modifications—are known to have profound effects on controlling gene expression. DNA methylation is involved in normal cellular control of expression, and aberrant hypermethylation can lead to silencing of tumor-suppressor genes in carcinogenesis. Histone modifications control the accessibility of the chromatin and transcriptional activities inside a cell. MicroRNAs (miRNAs) are small RNA molecules, ~22 nucleotides long that can negatively control their target gene expression posttranscriptionally. ....
Taken together, miRNAs can be considered important players in the epigenetic control of gene expression."

From a quantitative geneticist standpoint, if it affects phenotypic variation by altering genomic properties but there is no variation in the DNA sequence, then miRNA based post-transcription modification is a source of epigenetic variance. It seems that, for molecular biologists, post-transcription modification by miRNA falls outside of the classical definition of epigenetic effects, but I've not seen any literature explaining why nor classifying it as a genetic effect.

The point is not that the field of molecular biology has a different definition. What I want to point is that if miRNAs are considered epigenetic then why not TFs? As per your definition TFs/spilicing regulators/RNA binding proteins/riboswitch/protein kinases etc should also be considered epigenetic.

I disagree with rg255 on this. Most if not all of posttranscriptional modification is encoded in the actual DNA sequence. Those microRNAs for example can be determined by reading the DNA bases or finding the encoded enzymes that do RNA editing (like C to U by TPR enzymes). The DNA sequence already encodes all the information that will determine if it will get modified or not.
Epigenetic regulation on the other hand are encoded on the histones and other proteins associated with DNA and can by definition not be understood by reading the sequence (e.g. acetylation and methylation). This information does not code for proteins or transcripts.
EDIT:
A quick Pubmed search underlines what most scientists think is epigenetic Pubmed search. You see loads of methylation/histone research but miRNA or transcription factors are nowhere to be seen.

the regulation of a gene's expression is an epigenetic process, regardless of whether the ability to do such regulation comes from genetic information

The expression of a gene is modified post transcription, not because a nucleotide was changed elsewhere in the genome, but because that nucleotide exists

e.g. expression of gene X may be regulated to be differently expressed in two cell types, each cell has the same sequence of DNA, but one part of that DNA gives instructions about regulation of gene X in specific cells - there are no differences in sequence between the cells, but there is a difference in expression, therefore it is epigenetic

@rg255 then the TFs are also epigenetic. Every gene expression regulator is epigenetic that way.

if it creates variance in the genome, but does not come from variance in the sequence, it's epigenetic

the genomic variation is not generated by sequence variation - the machinery to create that variation can be coded within the sequence, but the genomic variation is not created by the existence of that segment of sequence

@rg255 Your point of view is correct but then that would mean that any mechanism of gene expression regulation arising because of the network dynamics should be considered epigenetic. I would agree with you on this definition but the very scientific community that works on these aspects considers only a few cases.

Just to note on your pubmed search, methylation research has a considerable headstart on miRNA regulation research having been discovered decades earlier.

Let us continue this discussion in chat.

You should check out this article by Adrian Bird, titled Perceptions on Epigenetics
Excerpts from the article:

Should heritability be mandatory in a contemporary view of epigenetics?

...

To explain why, it is necessary to introduce a third, somewhat informal, ‘definition’ of epigenetics that has crept into widespread use. This incarnation of epigenetics encompasses the biology of chromatin, including the complex language of chromatin marks (see page 407), the transcriptional effects of RNA interference (see page 399) and, for good measure, the effects of the higher-order structure of chromosomes and the nucleus (see page 413)

Finally he goes on to propose a new definition:

The following could be a unifying definition of epigenetic events: the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states

If we consider that this definition might also be a possible definition for what epigenetics is, then yes RNAi would fall under the broader bounds of epigenetics


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Derivation of discrete replicator dynamics
Related: Discrete vs Continuous Replicator Dynamics
I am trying to perform a derivation of the discrete time replicator dynamics, but I am unable to get through Cressman's derivation in "Evolutionary Dynamics and Extensive form games" on page 21

Basic notations:

$S = \{e_1, \ldots, e_n\}$ are pure strategies
$\pi(e_i, e_j)$ payoff of player using strategy $e_i$ versus strategy $e_j$
$p \in \Delta^n = \{(p_1, \ldots, p_n) | p_i \geq 0, \sum_i p_i = 1\}$ mixed strategy
$\pi(p, \hat p) = p \cdot A\hat p = \sum\limits_{i,j = 1}^n p_i a_{ij} \hat p_j$ is the payoff of strategy $p$ versus $\hat p$

Derivation of the discrete replicator dynamic:

Let $n_i$ be the number of individuals using $e_i$ at generation $t$.
Then $n_i' = n_i (e_i \cdot Ap)$ be the expected number of individuals at generation $t+1$
Let $p_i = \dfrac{n_i}{\sum_j n_j}$ and $p'_i = n_ie_i \cdot \dfrac{Ap}{\sum\limits_j n_j e_j} \cdot Ap = (\sum_j n_j)p_ie_i \cdot \dfrac{Ap}{\sum\limits_j n_j}\sum_j p_je_j \cdot Ap = p_i(e_i \cdot \dfrac{Ap}{p}\cdot Ap)$
Then the standard discrete time replicator dynamic is
$p'_i = p_i \dfrac{e_i \cdot Ap}{p\cdot Ap}$

Questions: There are numerous moving parts in this derivation and little explanation as to where each item came about

Just to make sure, $n_i' = n_i(t+1)$ right?
Why is that $n_i' = n_i (e_i \cdot Ap)$ is the expected number of individuals at the next generation? This is just the number of individuals at the current generation times the payoff to pure strategy $e_i$, is there a derivation for $n_i'$?
I understand $p_i$ is the fraction of players using $i$ versus all the other strategies. But can someone explain how $p_i'$ came about, where are all its pieces? I am especially confused about the part where it says $Ap/p$, because $p$ is a vector and you can't divide it...
Is there another derivation of the discrete time replicator dynamic?

Any help is appreciated.

I think you misunderstood some of the nominators/denominators in the text you cited. In the cited text, the whole stuff after the / sign is the denominator of the fraction. So there is no division by p, but division by (p \cdot Ap), which is a scalar.


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Help to recognize spider
It is unusual to see such size spiders in Lithuania, so I was wondering what kind of spider it is and if it is strong enough to bite through humans skin.
I've googled for biggest known spiders in Lithuania, but mentioned few species don't look alike - mine has way thinner legs, but I'm not an expert.
I've placed 1 euro cent coin for size - it's diameter is 16.25mm

The long hairy legs make me think that this might be a spider belonging to the Tegenaria genus, or something related.

I agree it's a Tegenaria spider, probably Tegenaria parietina.

So Tegenaria helped me search further and it looks like it is Tegenaria atrica - turns out it is not so rare in Northern Europe, male leg span can be up to 75mm, mine was shorter, but still amazing to watch how fluently those long legs move.

Yes it looks like Tegenaria. We have plenty of these trying to get in the houses in autumn in Switzerland (not as North as Lituania but cold winter time)


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Are glands in human made up of muscles?
I came across this idea while reading an excerpt of my textbook $-$

Muscles move eye lid , tongue, beat the heart, popel food through gut, discharge wastes, squeeze out secretion from the glands etc.

But I don't understand how this happen ? Does glands really squeeze out hormones?

No they are not made of muscles. Glands are modified epithelial tissues. Glands are basically of two types Endocrine and Exocrine glands.

Endocrine gland

It is a gland that lacks a duct system. The secretions are directly
   poured into the bloodstream. They secrete hormones through exocytosis mostly.

Exocrine gland

It is a gland with a duct system. The secretions(sweat, sebum,saliva
   etc) are transported onto a surface of the body (e.g skin or lumen of GI tract) by
   ducts.Exocrine glands may be controlled by muscles at the duct level.
There are three types of exocrine glands based on the process of secretion of chemical substance at a cellular level$-$

Apocrine gland

It is a gland in which the apical portion of the secretory cells are distintegrated to release the chemical. e.g- Apocrine sweat gland

Holocrine gland

It is a gland in which the secretory cells are completely disintegrated to release the chemical.e.g.- Sebaceous gland

Merocrine gland

It is a gland in which the secretory cells remain intact and the chemical is
released through exocytosis.e.g.- salivary gland

Reference:

Wikipedia
ncbi


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What is this hummingbird-like insect?
I just saw this insect collecting polen from bougainvillea blossoms on the Greek island of Skyros, in the Aegean sea. For future reference, this is in the middle of August and the sighting was at around 17:00.

I posted all 4 photos I took since the rude little thing didn't have the decency to sit still to let me get a clear shot. I'd say it was about 2cm long, certainly no more than 3.

Had you asked this earlier, you would have gotten 40 points: http://biology.stackexchange.com/q/50432/3340

@WYSIWYG aww, dang! :P May as well close as a dupe then.

Related one: http://biology.stackexchange.com/questions/50592/please-help-to-identify-this-insect

Hummingbird hawk-moth (Macroglossum stellatarum). For what it's worth, there are also a variety of sphinx moths around the world.
Here's a photo from the linked Wikipedia page. As you can see, it looks very much like the one in yours:


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Why do boys sweat more than girls during exercise?
I noticed that boys sweat more than girls in the PE class performing same physical activity. Is there any other specific reason except muscle mass?

I've often assumed something similar, but when you look at athletes, they sweat buckets irrespective of sex! I'm starting to think that boys are just more willing to throw themselves into a sport and will therefore appear to sweat more. The study cited by @rrirower has N=37 which is incredibly small after stratification and is essentially anecdotal evidence with statistics applied! Also note that muscle mass difference applies only to mature adults, not children.

Your assumption seems to be true that Males sweat more than Females, but, not necessarily because of muscle mass.  The jury is still out as to the reasons.  However, in a 2010 study, it was concluded that…

… training improved the sweating response, and a sex difference was
  observed in the degree of improvement in the sweating response due to
  physical training. This sex difference became more pronounced with
  increasing exercise intensity. A sex difference was observed in the
  control of sweating rate to an increase in exercise intensity, i.e.
  the maximal activated sweat gland responses of untrained females
  required a higher body temperature or work intensity than the other
  groups.

So, there does seem to be something different in the way males and females sweat.  Recent research suggests

that when we're under heat stress from high temperatures or an intense
  workout -- regardless of what shape we're in or how much body fat we
  have -- women consistently sweat less than men but tend to have a
  higher skin temperature.

(http://health.howstuffworks.com/wellness/men/sweating-odor/men-sweat-more-than-women.htm)
In a nutshell, the cause(s) for the differences in how men and women sweat is still unknown.  Some think it may have to do with body composition.  While others think more research is required to determine

how efficiently we use the sweat we produce, but also to our capacity
  for making sweat, hormonal fluctuations, sex hormone differences and
  how our bodies regulate water as possible reasons why men sweat more
  than women.


text:
What is the name of this berry producing tree?
I live in Middle Tennessee (USA) and came across this tree while I was hiking through the woods. I'm curious as to what type of tree this is and if the berries have any uses or are poisonous.
The tree is rather short, and I was unable to see any more distinctive features given that the tree was surrounded by other brush. I can supply a better picture in a day or two if necessary.

This is some type of Sumac in the genus Rhus. Probably either Rhus glabra (Smooth Sumac) or Rhus typhina (Staghorn Sumac). The berries of those two species are supposedly not poisonous. But they are closely related to other poisonous plants such as poison ivy and poison sumac. Poison ivy and poison sumac are in the genus Toxicodendron, but used to be in the genus Rhus.
A photo of Smooth Sumac


text:
What causes drone bees to die?
... when not killed by other members of the hive.
Is it always a consequence of exile (denial of some resource, etc) or does some organ fail regardless of circumstances?

The number of drones in a colony may be hundred-thousand , i.e 15 % of the total population. The drones lack wax glands, pollen collecting-appartus and sting which is present in worker bees which make them completely dependent on the workers, transferring its genes to the next generation is the only contribution of the drone bees. Usually the drones do not mate with the queen of the same hive. The drones that are able to mate with the queen die shortly after mating due to breaking of bulb of endophallus(penis) inside the queen.

The rest, the survivors of the mating flight (mostly drones that could not participate in  mating) are not allowed to reenter the colony. They remain in the vicinity of the hive and eventually starve to death.
In hours of crisis when the colony needs to drop the expenditure of resources(food) the workers eat up larval drones or drive out the matured drones from the colony that eventually die due to the same reason.
Information taken from:

Wikipedia
Bees
The Backyard Beekeeper

But don't most drones never mate? Do the ones not mating have a normal lifespan or also die of some reason earlier than their sisters in the hive?

Thanks for pointing out I have edited my answer. @skymningen

@skymningen  I did write "when not killed or exiled".   As for "the only contribution", though, I am told that drones, when still welcome, do help with hive temperature regulation (shivering of fanning) same as workers do. I guess that would also make them no less useful than a worker against a hornet.

@kaay: You wrote "when not killed by other members of the hive". In my understanding you asked exactly what they die of in exile. Because even those who mate are in exile after they leave for the mating flight.

@skymningen (not killed) -> (exile) was not obvious to someone who did not already know the answer to the question. In my last comment I did not mean I wrote "when not killed or exiled" word for word, I meant that I did mention two other known reasons for death - being killed and exile-caused denial of resources (which, again, did not obviously need to be starvation - for all I knew they may have just dropped dead in the prolonged absence of some pheromones, etc).


text:
Which cells release inflammatory mediators?
Wikipedia says

Inflammation is stimulated by chemical factors released by injured cells and serves to establish a physical barrier against the spread of infection, and to promote healing of any damaged tissue following the clearance of pathogens.

then it mentions

The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells, and mastocytes. These cells present receptors contained on the surface or within the cell, named pattern recognition receptors (PRRs), which recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). At the onset of an infection, burn, or other injuries, these cells undergo activation (one of their PRRs recognizes a PAMP) and release inflammatory mediators responsible for the clinical signs of inflammation.

From this we can clearly deduce that the inflammatory mediators are released by Pattern recongintion receptor producing cells. But while studing this topic from different sources some, books on nursing and Pharmacy. They keep repeating that inflammatory mediators are released by injured cells.
What is correct?

There are several kinds of inflammatory mediators. You can broadly classify them as cytokines (including interferons) and chemokines.
Cells which sense antigens (or pathogen associated molecular patterns) do secrete cytokines, as you said but infected cells also secrete some cytokines like interferons- α and β. Infected/injured cells also secrete chemokines that attract leukocytes to the site of infection/injury (Saiman and Freidman, 2012).


text:
How do you compare unpaired biological replicates?
I have done proteomics and I have obtained genes with ratios. As an small example you can see my data below
Gene    Control1     Control2   Control3    Treated1    Treated2    Treated3
pps-1   324680000   211350000   356350000   269770000   258080000   292830000
R11A8.7 477490000   610780000   539550000   533590000   530810000   578290000
ugt-21  105080000   103430000   74137000    78915000    42381000    31415000
spp-18  1042800000  615030000   332720000   538340000   448280000   412310000

Now My question is that I have Three controls and Three Treated, Control has two biological replicate and Treated has two biological replicate
I am trying to find the pathways which the list of my genes activate it. I use IPA which is a tool for pathway analysis
How can I calculate the fold change for it? If I use the 6 values, IPA will give me 6 different results and then interpretation will lead me to hell.
I appreciate any help.

Fold change is usually defined as the ratio of the mean values for the two groups. It's pretty trivial to compute in any langauge. I think you're mainly after the R code for doing this on each row of the matrix?  I don't think this question is suitable for Biology SE, but check this page: http://stackoverflow.com/questions/9490485/how-can-i-get-the-average-mean-of-selected-columns  Do that for you two groups and then simply take the ratio.

@Roland I am pretty good at few languages including R. I don't have problem with how to do it, I want to know if I do it in this way is right or not. If I had only one control and one treated, I knew how to calculate the fold change but when I have replicate, I don't know what is best to do

I posted a question here http://stats.stackexchange.com/questions/230484/how-to-calculate-fold-change-when-we-have-replicate

How does your data extraction method work? If it produces compositionally constrained data, then everything is far more complicated.

@Eli Korvigo what do you mean with compositionally constrained datacan you please explain ?

@NikBernou basically it means that if your method samples $n$ observations without replacement from a population of size $N$ (where $n << N$, i.e. there are orders of magnitude more proteins/transcripts than the number you can pick and analyse), then in abstract terms you perform sampling without replacement from an infinite population. Suppose you have $m$ classes of observations ($m$ distinct proteins/transcripts), then $\sum_{i=1}^{m}{{x}{i}} = n$, where ${x}{i}$ is the number of times class ${m}_{i}$ was observed...

... Let $\mathbf{p} = ( {p}{1}, \dots, {p}{m} )$ be the vector of relative abundances of each class in the original population. Since you sample without replacement from an infinite population, you perform multinomial sampling with probabilities $\mathbf{p}$. The counts from a multinomial distribution are negatively correlated and constrained by definition. This means that you can only operate in the space of joint-counts distributions.

Comments are not for extended discussion; this conversation has been moved to chat.

Calculating fold change is pretty straightforward but you cannot do one on one comparison because they (control and treated) are not really paired (same sample). That's why IPA gives you six results (FC for each pair). However, you can calculate fold change between two genes because they are from the same sample. Note that fold changes are quite dangerous and can lead to misinterpretation of data (for example 1/2 would be same as 100/200). You should use them cautiously.
I think, in this case, you can simply apply a t-test. This will tell you if your two groups i.e. treated and control are significantly different from each other. You would not be calculating fold changes here. If you had more number of groups then you can go for one-way ANOVA.
I am not sure what output you really want after the analysis but I think the main goal is to say that control is different from treated.
Since you have multiple genes (variables) you can either go for a multivariate t-test, which will tell you if the control is overall different from treated, or many univariate tests which will tell you how each gene differs between the two groups. There are some methods such as Bonferroni correction which can be used to improve the prediction of multivariate tests.
When you have established that a certain gene is differentially expressed, using t-test, you can report the fold change of the averages.

♦ I agree with gene set enrichment you explained. when you say  you can report the fold change of the averages. do you mean that I should take average of my replicate over control and take average of my replicate over treated? then divide them together ?

@NikBernou You can calculate FC but you'll get 6 because of the different pairs which would not tell you anything meaningful. To work around that you can calculate the average of the replicates and report the FC between them (divide). However, before doing that make sure that this is meaningful by doing the statistical test. For the others that were not different as per t-test, just leave them or report an FC of 1 (since they are there is no significant difference between them). Am I clear?

♦ I am really sorry for asking too many questions. what you try to say is I select the upregulated genes (those that are statistically significantly different from control than treated. Then I discard the rest. Then I take average between group and average between treated and then divide treated to control. Is it what you are telling me?

@NikBernou yes. Take average of control, take average of treated and divide them (only for cases that are statistically significantly different).

♦ I see, what will happen if I do this for all? I think replicate suppose to be more or less the same value but taking into account the environmental changes during measurement, no?

@NikBernou It will be just meaningless. You can do that. As I said fold changes are dangerous and can often be misinterpreted. The statistical test takes into account of the random errors (environmental changes, if that's what you mean) that you may expect.

While I do not have any experience with IPA, I routinely face this problem.
How do you analyse separate biological replicates?
One way to approach the problem is to merge the biological replicates.
There are several methods,
To do this, you can show a pearson or spearman correlation. If you have experience in R, it is a simple task of applying the function cor.
I do not use excel for such tasks, but you can check out this excel tutorial which covers correlation in Excel.
The second and harder method is to show the clustering of the replicates, using one of the many clustering methods out there. For this the easiest way I know is heatmap2 from the gplots package, which uses hclust for hierarchical clustering. This method will produce a heatmap with a dendogram specifying the relation between the replicates. Check the package link for the pdf containing details on the heatmap.2 function and how to use it.
I would go with correlation since it hardly takes 10 minutes. Having shown the correlation between replicates, you can then merge the replicates by taking the average of the replicates.
I do not know if IPA has a way for dealing with replicates

Hi dear, thanks for your comment. Actually you don't need to know IPA. what i want is to be able to calculate FoldChange. is it possible to make an example in R ? you can use random values to generate 6 columns of data ? is it possible ?

Having shown the correlation between replicates, you can then merge the replicates by taking the average of the replicates, what will happen to those that are not highly correlated ? why should I do that ? can you please give me details explanation so that I understand your mythology ?

correlation shows you how well the samples/replicates correlate among themselves, before merging replicates this step is required to show that you are not introducing variations within the merged dataset. If you introduce a bias by merging that will lead to false statistical inference. You do not want to do that, if the replicates correlate well then values corresponding to genes can averaged between replicates.

I got your point , you have one like already thanks for highlighting it !!!! would you mind to give me an example in R?


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What is the difference between the cellular affix -cyte and -blast?
The affix -blast means an immature cell, and -cyte indicates any cell. So how do we define if a cell is mature (-cyte) or immature (-blast)? How does this apply to odontoblasts and ameloblasts? Why are they not simply called odontocytes and amelocytes, respectively?
What are the criteria for using the affix -cyte versus -blast?

Because they have different meanings? Wikipedia says, -cyte means "vessel, jar" while -blast means "germ, sprout". Those are quite different things. The -blasts usually have some function in being precursors or "generators" of something else, while the -cytes are often the result of such precursors.

@skymningen.   So odontoblasts are precursor for which cells?

@JM97 Odontocytes: http://amigo.geneontology.org/amigo/term/CL:0000140

I'm actually not convinced odontocytes even formally exist. I think this is a great question! +1

Short answer
 - The affix -cyte means cell;
 - The affix -blast means a germ (bud) cell or a cell that produces (building) materials.
Background
Cells are denoted as -cytes. There are many of them, e.g. melanocytes in the skin and chondrocytes in the cartillage.
Germ cells are denoted as -blasts. These cells typically are precursor cells such as the lymphoblasts that are undifferentiated precursor (stem) cells situated in the bone marrow that produce leukocytes.
Blast cells may also be cells that produce materials. Your examples are of that category; odontoblasts generate dentine, the main hard tissue of the tooth; ameloblasts deposit tooth enamel, which is the hard outermost layer of the tooth forming the surface of the crown. in that sense, also progenitor cells produce something, namely new cells. Hence, blast cells are cells with a chief building function, either materials or new cells.
There are also -clast cells - cells that destroy something. Fig. 1 below gives an overview of these cells as present in the bone, namely osteoblasts (bone builders that secrete the matrix), osteocytes (osteocytes are osteoblasts that are embedded in bone; they stop secreting matrix and only maintain it) and osteoclasts (different class of cells that mediate bone resorption).

Different cells in the bone. source: University of British Columbia
Why then do not call odontoblasts odontocytes? - Because it would mean loss of information. It would be the same as calling a car and a bike both transport vehicles. Moreover, the example in Fig.1 is quite convincing, as osteocytes and osteoblasts are considered to be different cells altogether (although the former is derived from the latter).


text:
Organisms with one, two, or more than two biological parents
I am interested in the generic names of organisms with one, two, or more than two biological parents. I don't know if the latter possibility is possible in nature, but if it could be, it would certainly be interesting.
Thank you for your answers.

Do you mean terms for referring to "species where reproduction mode leads individuals to have one, two or more parents"? Main cases will be roughly covered under the terms "sexual reproduction" and "asexual reproduction".

Can you please point me to a Wikipedia article with some pictures. I was wondering whether three, or more, is possible, or purely fictional. Thanks.

You might first want to read about asexual reproduction and sexual reproduction. I am not aware of a case where an individual has properly more than two parents. However, double fertilization in angiosperm might more or less be considered as such.

Very interesting Remi, I was not aware of double fertilization. Thanks for the pointer. :-)

@Remi.b I wouldn't consider double fertilization in angiosperms to be more than two parents because both sperm cells are coming from the same parent plant. Of course, self-pollinating flowering plants can undergo double fertilization as well -- in those instances, there is only one parent.

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


text:
Are viruses technically organisms, or not?
Are viruses technically organisms or not?
A quick Google search query for the term; are viruses organisms?, reveals various conflicting and somewhat inconclusive arguments & opinions from a range of sources. (Examples provided below).

Note: These answers are mostly opinion-based and inconclusive; falling short of the Stack Exchange community's quality control standards.

Let me be clear: I am not seeking opinions, or debate; but rather definitive answers supported by facts.

Wikipedia | Organism.
  The most common argument in support of viruses as living organisms is their ability to undergo evolution and replicate through self-assembly...
  Some scientists argue that viruses neither evolve, nor self- reproduce.
~ https://en.m.wikipedia.org/wiki/Organism
Encyclopedia of Life | What is a Virus?
  A virus is a microscopic organism that can replicate only inside the cells of a host organism...
Viruses infect all types of organisms, including animals and plants, as well as bacteria and archaea.
~ http://eol.org/info/458
Virology Blog | Are Viruses Living?
  Therefore, viruses are not living things...
  So technically speaking they are non- living organisms.
~ http://www.virology.ws/2004/06/09/are-viruses-living/
Popular Science | Are Viruses Alive? New Evidence Says Yes.
Viruses seem to carry out only one life process, reproduction, but even then, individual viruses don't carry translational machinery, namely, the proteins needed to read their DNA and RNA and build new viruses. They invade a cell and hijack its genetic tools to do it for them...
  But within the last decade, developments in virology have started to reveal more and more that viruses might in fact be alive...
One was the discovery of mimiviruses; giant viruses with large genomic libraries that are even bigger than some bacteria. (To put this in perspective, some viruses, like the Ebola virus, have as few as seven genes.) Some of these giants have genes for the proteins that are required for translation—those readers of DNA and RNA that in turn build new viruses...
  This throws the lack of translational machinery argument for classifying them as nonliving on its head.
~ http://www.popsci.com.au/science/medicine/are-viruses-alive-new-evidence-says-yes,409690
Science Daily | Virus.
  A virus is a microscopic particle that can infect the cells of a biological organism...
  At the most basic level, viruses consist of genetic material contained within a protective protein coat called a capsid; the existence of both genetic material and protein distinguishes them from other virus-like particles such as prions and viroids...
  It has been argued extensively whether viruses are living organisms...
Most virologists consider them non-living, as they do not meet all the criteria of the generally accepted definition of life...
  They are similar to obligate intracellular parasites as they lack the means for self-reproduction outside a host cell, but unlike parasites, viruses are generally not considered to be true living organisms...
  A primary reason is that viruses do not possess a cell membrane or metabolise on their own - characteristics of all living organisms.
~ https://www.sciencedaily.com/terms/virus.htm

@Remi.b Thankyou. It is worth linking, however; not the same question. Please don't report it as a duplicate. Cheers.

@tjt263 Can you explain how this question is different?

it is the same question, hence you've linked to sites that ask are viruses alive?

If you consider the definition of an organism to be 'something alive', they're the same question; if not, they're not.

So, if you think about where organism actually came from, organization, the virus is actually quite a very organized little compartment of stuff (without going into details). There are elements that have to cooperate within the actual virus to get anything done, thus, I would qualify that yes viruses are organisms. You wouldn't consider something like a prion or a viroid an organism, however, because on their own there's really just one part with no interdependencies.

Definitive suggests by definition. By definition, no. Fact- a virus is not an organism by definition. If the definition changes to include viruses, then yes. But for functional purposes, we speak english- which means utilizing the definition of words. The reason why a virus is not an organism is because it requires a host organism for replication. DNA is also not an organism.


text:
Where can I find clinical trial data published in JAMA?
Data in the paper:
http://jama.jamanetwork.com/article.aspx?articleid=336799
is cited in the statistical analysis in the book Clinical Trial Data Analysis using R. Can anyone help me find it?

Are trying to access the paper (question answered by @BenWelborn) or are you trying to get the data (spreadsheet;question I tried to answer to) used for this paper?

The full article: Effects of Treatment on Morbidity in Hypertension.

Data, spreadsheet would be nice.

Can you give a more precise pointer to where (chapter/section/page number) in the book they're discussed?  I couldn't find it in a quick skim through the Google books version ...

page 33, chapter 3 "treatment comparisons in clinical trials"

which edition? In the preview on Amazon, p. 33 is in section 1.6.1 - 1.6.2 ??

Is this data something that is not already given in the article? I think the author of the book must have compiled the data given in the tables in the form of an excel sheet (or other modern formats) and re-analysed them.

I'm kind of stumped -- I've searched through the available previews of all three editions on Amazon and can't find the section you're referring to ...

Raw data is not in the article.

I have edited your question so that the title gives a reader an idea of what "this" is, and the question can be read independently of the title. Please try to emulate this style in any future questions you may ask.

Online repository
Today, most journals (although t may depend on the field) require author to upload their data. The paper you are interested in was published in 1967 (internet was invented in 1969). It is very likely that the data have not been uploaded. It is also possible that the data have never been compiled numerically but is only on paper.
Ask the authors
Your best chance is to contact the authors directly and politely ask if they can give you their data. The author might be hard to contact as well as they may have changed university, be retired or even dead.
Possible loss of data
If you can contact the authors, then it is not unlikely that the data have just been lost. The loss might be due to a flood, to a technical issue or just because they don't know where it was placed.

alternatively you could try contacting the book authors. Sometimes data used in a book are available from a web page associated with the book, but this is the only associated web page I could find, and it doesn't appear to have any associated supplementary materials.  You could also try asking on http://opendata.stackexchange.com/ , although I don't think your chances are very good.


text:
Can anyone identify this spider?

I was hiking and saw this spider in the mouth of a cave in the Ozarks in Arkansas (USA). I believe it is some kind of wolf spider. I have never seen a spider in the wild this large, except for tarantulas in Texas (USA). The approximate size from the tip of back leg to front was 7-8 inches. It was bigger then my hand and I am 6'1" tall man. The spider did not have anything to reference size and did not want get too close, though I am sure it was harmless. I can go back to cave and take same picture holding a ruler to the rock if needed.
I believe my initial guess was off mark. I am thinking this may be a fishing spider. I only say this due to it being on a vertical surface and having banded/striped legs. I have never heard of one attaining this size before. Any info on this spider is greatly appreciated.

Harmless to humans? All spiders are venomous, just some more than others, so I suspect you were wise not to get too close to something this size.

The clues that point to a Fishing Spider (probably Dolomedes tenebrosus) are the nice stripy long legs and the very large size.  I've seen numerous big females slightly less than hand-sized, and one memorable one which was just about as big as my hand (about 7" tip-to-tip the longest way).  The abdomen looks a bit bulgey for a Dolomedes, but presumably she's nearly ready to lay eggs.

looks most like a Meta ovalis with a span of about 10 CM.

The spider in the question does not appear to be in the Araneoid superfamily at all (i.e. it is not a web-dwelling spider like Meta ovalis).


text:
What is the state of actin-myosin in my biceps after I have flexed my arm?
When I'm starting to flex my arm, the myosin and actin slide over each other in a ratchet like mechanism. When I've totally flexed my arm, are the actinomyosin left in this contracted state? Since there is a visible decrease in length of the muscle, muscle fibres should have contracted.
So do they remain in this contracted state? Does the myosin head attach to the actin all this time? If it leave the actin, does the myosin snap back to its original position and relieve the tension/comeback to original length? Does it require any energy expenditure? Because I can keep my arm flexed throughout the day without getting fatigued. Also, What is the state of the actinomyosin if left in a half flexed state?
By state, I mean, the stage of the cross-bridge cycle

When I've totally flexed my arm, are the actinomyosin left in this contracted state?
Yes, the sum of the length of all sarcomeres in series determine the length of the muscle.
So do they remain in this contracted state? Does the myosin head attach to the actin all this time?
Yes, it stays attached.
If it leave the actin, does the myosin snap back to its original position and relieve the tension/comeback to original length?
It doesn't really 'snap' back, it 'walks' back over the actin.
Does it require any energy expenditure?
Yes, the myosin heads require ATP to 'walk' back as well. If ATP is depleted cannot walk back, as is the case with rigor mortis (https://en.wikipedia.org/wiki/Rigor_mortis).
What is the state of the actinomyosin if left in a half flexed state? By state, I mean, the stage of the cross-bridge cycle
Myosin will partly overlap with the actin, but not completely. But this has nothing to do with the cross-bridge cycle. The myosin heads need to complete several cross-bridge cycles to fully contract the sarcomere.
For further reading, the Wikipedia page on the sliding filament model is a good start: https://en.wikipedia.org/wiki/Sliding_filament_theory

Thanks! Once it is contracted, ad you say, the myosin remains attached to the actin, is ATP required then??


text:
Parasite - host equations
The Lotka–Volterra equations describe how predator–prey interactions affect population growth. Do these equations describe parasite-host interactions? If not, how would they change by adding these interactions as well?

Parasite vs predators
In terms of ecological interaction, a parasite is essentially a predator. As such, of course the Lotka-Volterra equations apply to host-parasites interactions.
Lotka-Volterra equations
However, Lotka-Volterra equations are very simple and very general. So much so, that in order to make good prediction about the real world, one most often have to build more advanced models.
Host-parasite interaction models
There exist a whole set of models specific to host-parasite interactions. You should have a look at the wikipedia entry for epidemic model which is a pretty good overview and introduction.
Most models of host-parasite interactions fall into the category of the SIR (or SIRS and other derivatives) model. The term SIR comes from Susceptible-Infected-Recovered. The whole point of the SIR models is to categorize host individuals on whether they are Susceptible, Infected of Recovered (hence the abbreviation SIR).
The SIR models are very much used by national and international centers for epidemiology and underly many of the decisions of vaccination and other methods of disease control.
Host-parasite co-evolution
Of course, the Lotka-Volterra model and the SIR models assume absence of evolution and only track changes in population size (within each category for the SIR models). There are models that also take into account that populations also evolve in response to the interaction and demographic events that the interactions are causing. Such models are much more complicated to keep track of and we often (I think) make use of technics such as separation of time scales. These models are essential though typically for to control viral epidemic but not only. But these models are outside the scope of your question.


text:
Where do I purchase this Trypsin?
I am currently on the lookout for Trypsin, but I have some trouble finding something that is fairly cheap, ships to Europe and is equivalent to this Trypsin:

http://www.emsdiasum.com/microscopy/products/chemicals/tannic.aspx#22200
Trypsin powder 1:100 from Porcine Pancreas, 25g
Activity >100 NF units/mg
Used for whole cell preparation

I've found Trypsin on Sigma:

http://www.sigmaaldrich.com/catalog/product/sigma/t4799
Trypsin powder from Porcine Pancreas
Activity 1,000-2,000 BAEE units/mg
Suitable for cell culture

However I am not sure how to compare the activity between the two types and ultimately which concentration I should then use in my experiment if I go with the Sigma one (the protocol I am following uses the EMS Trypsin in a 1g:100ml fashion).
Can anyone shed some light on this? Or perhaps show me the way to some affordable Trypsin that can be shipped to Scandinavia?
Cheers!
/Patricia
*The trypsin will be used for diaphonization (see comment)

Could you update your question to explicitly state what you will use the trypsin for. Trypsin has a number of uses and the use alters which trypsin is appropriate.

Hi Michael. Sure! I will use the trypsin for diaphonization (aka. clearing and staining), which is basically a way of dyeing a whole specimen. Trypsins role is to digest the specimen enough so it becomes transparent, but not so much that it falls apart... If that makes no sense there is a nice video about it here: https://www.youtube.com/watch?v=haopSRCuPdo... I have experience with use of Trypsin with cells - but diaphonization is completely new to me, and the protocols I have give no clue to what type of trypsin they are using.

According to Sigma-Aldrich,

1 USP Unit = 3.0 BAEE Units
  1 NF Unit = 1.1 USP Units

So 1 NF unit is roughly equal to 3.3 BAEE units. You can then directly compare the two trypsin powders, since they are preparations of the same enzyme.

Yeah, I did see that, but the thing that bothered me is then that I need to compare unspecific units like >100 NF and 1,000-2,000 BAEE, and so I am left with questions like "How much is >100 NF? 101 NF? 500 NF?" and "Do I calculate with 1.000 or 2.000 BAEE?"

But I guess the best solution is to note that 100 NF ~ 330 BAEE and so if I end up buying the Sigma one, I can start out with trying a 1:300 solution and see how that goes :)


text:
Absorption of digested food in small intestine
My book says

glucose , galactose and amino acids are transported into cells of villi via secondary active transport(sat). Fructose is transported by facilitated diffusion(FD) .short chain fatty acids , vitamins diffuse into cells of villi. From there all these are transported to blood by FD.

This site says the reason for using SAT: http://www.phschool.com/science/biology_place/biocoach/biomembrane1/glucose.html
But I want to know why fructose, vitamins and short chain fatty acids do not need S.A.T. and travel via FD (or just diffusion)?dont they get reabsorbed into small intestine ?

In general:

Hydrophilic/polar/charged molecules require some kind of assisted transport across a membrane
Hydrophobic/nonpolar molecules can easily diffuse across a membrane

Glucose, galactose, and amino acids are hydrophilic. Fructose, fat-soluble vitamins, and short-chain fatty acids are hydrophobic.
Glucose and galactose have similar structures (aldose/pyranose) and are both hydrophilic. Fructose has a slightly different structure (ketose/furanose) which affects the way it is transported. Basically, it has a ketone (rather than an aldehyde) so it is relatively less reactive/polar. Because it is hydrophobic, it can diffuse across a membrane more easily.

"Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins." (Wikipedia) Based on this statement, it seems that the lumen maintains a higher [fructose], relative to the enterocytes.
As explained in your link, glucose is mediated via SAT to ensure one direction of transport: we want glucose going only INTO our bloodstream. The [glucose] in lumen decreases after a meal, but we want glucose to keep being absorbed (hence SAT).. Also, unlike fructose, glucose and galactose are highly regulated for use in glycolysis, so it is important to keep glucose in the appropriate cells. In particular, because of its structure, fructose enters glycolysis after the "rate-limiting" phosphofructokinase step in glycolysis.
Quick notes on fat-soluble vitamin and short-chain fatty acids: they're both relatively small and hydrophobic. Short-chain fatty acids can easily diffuse across a membrane, which is also made of lipids. (I recommend reading about hydrophobic effect if you want to know more about this).. Larger fatty acids require shuttles because of their size.
Regarding "reabsorption" into the small intestine:
Diffusion is the result of the random motion of particles. The more collisions in a higher concentration region eventually leads to a net movement "down a gradient." Using this logic: at some point, yes, the molecule may go back out into the lumen or go back in ("reabsorb") because it basically follows the gradient.
(I may come back to this post after learning more about it in a few months.. I used most of my answer based on what I learned in nutrition, o-chem, biochem)
Read more here about fructose metabolism


text:
How to tell if something is an organ or apparatus?
An apparatus is defined as

Physiology. a group of structurally different organs working together in the performance of a particular function.

An organ is defined as:

Biology. a grouping of tissues into a distinct structure, as a heart or kidney in animals or a leaf or stamen in plants, that performs a specialized task.

The below shows the Juxtaglomercular apparatus (JGA). Without knowing its name, how would I tell if it is an apparatus or an organ?
There is a question in my book (which asks: which organs are necessary for the continuation of the Renin-Angiotensin-Aldosteron-System) and to answer it correctly requires that we know that JGA is an apparatus and not an organ.
Is there any giveaways that show it is an apparatus and not an organ, based on the diagram alone?
I can't really tell based on the definitions above e.g. based on the diagram, I cannot tell if JGA performs "a specific task" or a "particular function".

It seems like a largely semantic argument and a poorly reasoned question from your book.

Thanks. I thought it was a bit dodgy too, but I haven't done biology before and am trying to learn it at home, so wanted to double check I didn't miss something obvious.

how-much aggregation makes an organ, and how-much doesn't make, doesn't have a clear-cut boundary. Its quite like "fuzzy logic". On certain contexts, a finger could be considered as organ whereas in some-other context the whole-hand could be considered as an organ. Sometimes, skin is described as an organ. So if you consider skin as an organ and hand as an organ, then, hand minus skin would be = organ minus organ=0. So clearly, the terms "organ" (and similar-terms like tissue and tissue-system), vary highly from context to context, and not very clear-cut.

Usually apparatus is used to group some components that together do a specific work, but as said by @kmm and AlwaysConfused it's a syntactic question. I'm not completely sure about that (will check that asap) but the word apparatus (generally speaking of the animal/human body but not limited to that) etymologically (Latin) was considered as a group of organs that are involved in a specific function of the organism.


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General anaesthesia and brain cell damage
Do we lose brain cells when we undergo prolonged surgery under general anaesthesia?

You are asking two distinct questions. You should decide which one you want answered.

These are conditions which can cause decreased oxygen supply to brain.I have asked so in that context.Want to know about both situations

Surgery, sneezing, strangulation. You ask a lot of anyone trying to research an answer. It's your question but I would vote to close as overly broad.

Okay .I understood.I just related these situations.Sorry for the inconvenience it created for answering

I think this question is fine now. The system won't let me change "loose" to "lose" or "anaesthesia" to "anesthesia." This would be an improvement...+1.


text:
Difference in variance of Cys in protein sequences
Suppose I have got two sets of proteins (amino acid sequences). In one set, I find that the variance in the percentage concentration of the Cys is way more (65.34) than the variance of Cys in the other group (0.456). Does it mean anything? Does this have any sort of biological implication?
The concentration has been calculated by dividing the total number of Cys found by the size of the protein sequence.

It may or may not mean anything. Without additional information no inference can be drawn.

What additional information is needed in this case?

A lot: mean cysteine density, other structural and biochemical properties of the protein etc. Basically just the variance in cysteine content won't tell you anything.

This question would be more answerable with an introduction to the biological context, a description of how each dataset was generated (included the sample sizes), and the relative percentages of other amino acids.

No, because it's extremely likely your sets are not a representative sample of the true distribution in proteins.
Your bias might be caused by an effect on the functionality of the protein, but it might as well be a bias in which organisms are sequenced or something caused by the alignment or the way you are searching for your sets.

If there be is a hint towards functionality of protein, what is that functionality? Any sort of hint is what I want to know

I'd say this is 99% biased searching / sequence collecting.

What would be the bias? What is the biological factor that creates this bias?

"a bias in which organisms are sequenced or something caused by the alignment or the way you are searching for your sets"


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Potential between endolymph/cytoplasm and endolymph/perilymph
I am studying for an exam and there is something I can't seem to understand. My textbook says that the endolymph contains 150mM potassium, 2mM Na+ and 130mM Cl-. The perilymph contains 5mM potassium, 140mM Na+ and 110mM Cl-. "Thus" the electric potential between perilymph and endolymph is +80mV (endolymph being positive).
I can see that there are chemical gradients but why is the endolymph so much more positively charged than the perilymph?

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

Marina - @MattDMO is right that you should provide more information. Most importantly, are you referring referring to 'why' (functional aspect to the workings of the inner ear) or to the 'how' (mathematical underpinnings of membrane potentials). If the latter, you should find your answer in this site - there have been many questions on potential differences and their mathematical grounds (search for Nernst or Goldman equations). If the former, then it would be a more interesting question imo. Either way, try to edit your question to make it specific where the bottleneck is.


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How can an enzyme favor even chained fatty acids?
If we look at text books for the human fatty acid metabolism (FA synthesis or β oxidation), they typically shows even length fatty acids (C8, C10, etc). Now, from a chemical perspective, I am wondering how the involved enzymes recognize that the fatty acid is an even number of carbons.
Can someone point me to (historic) experiments that have been done that show that these human pathways indeed only apply to even chain length fatty acids? Or do they also act on odd length fatty acids?

The first experiment which showed that fatty acids are oxidized in C2-units has been done by Georg Franz Knoop and been published 1904 as "Der Abbau aromatischer Fettsäuren im Tierkörper.". The paper in reference 1 states:

Georg Franz Knoop discovered fatty acid β-oxidation. In 1904, he
  published his classical experiments using odd and even chain ω-phenyl
  fatty acids such as ω-phenylvaleric acid and ω-phenylbutyric acid
  (Knoop 1904). Knoop fed these compounds to dogs and analysed their
  urine. In dogs that had been fed the odd chain fatty acids, he found
  hippuric acid (conjugate of benzoic acid and glycine), whereas, the
  dogs that had been fed even chain fatty acids excreted phenaceturic
  acid (conjugate of phenylacetic acid and glycine). From this he
  concluded that the metabolism of fatty acids proceeds by the
  successive removal of two carbon fragments. The remaining fatty chain
  had to contain a carboxylic acid. He postulated that oxidation took
  place on the β carbon atom, an oxidation unknown to organic chemistry.

If the fatty acid chain has an uneven number of carbon atoms, the resulting propionyl-CoA is modified into succinyl-CoA which is then used by different processes.
During the breakdown of the chain, Acetyl-CoA groups are released (at the end of each step), which can then be further metabolized by the body. Acetyl-CoA is fed into the Krebs cycle and then oxidized.
References:

A general introduction to the biochemistry of mitochondrial fatty
acid β-oxidation
Fatty Acid Oxidation

Good answer, which can be summarized as "they don't". I would add that for synthesis, there is also no specific odd/even check, they are just synthesized two atoms at a time. Though there are fatty acid modifying enzymes that have a particular length preference (that's why we tend to see particular chain lengths)

Victor, indeed, it shows they do not. OK, that's half of the answer. What about the FA synthesis pathway? Does that also not have a preference?

The basic answer is that the synthesis enzymes start with a 2-carbon molecule and then build the chain 2 carbons at a time. If you introduce unusual enzymes that can start with a 3-carbon molecule, you can get odd-chain fatty acids. However, the terminating enzymes do have some specificity in terms of chain length preference. https://en.wikipedia.org/wiki/Fatty_acid_synthesis


text:
What does "substoichiometric amounts" mean in the context of molecular biology?
Recent paper:

PRC2 is composed of the histone methyltransferase EZH2, EED, SUZ12,
  and the histone binding proteins RBBP4 and RBBP7. JARID2, AEBP2, PHF1,
  MTF2, and PHF19 are also present in PRC2 in substoichiometric amounts.

Does this have a more specific meaning than "very little" or "very small amounts", which I presume is what it means?
Paper (paywalled): http://genome.cshlp.org/content/26/7/896.abstract

It possibly refers to fractional stoichiometry i.e. less than a molecule of these proteins per molecule of PRC2. Obviously, you cannot have half a molecule and this statement means that in a gross sample, the concentration ratio of these proteins with respect to PRC2 is less than 1:1. At a molecular scale, it would mean that these proteins may not be always associated with PRC2.
This is also in agreement with the known fact that PRC2 core components are EZH2, EED, SUZ12 (along with RbAp46/48) and the others are accessory factors (Margueron and Reinberg, 2011).


text:
Nature of sight/ color perception?
I am wondering how we perceive color and whether that is dependent on the wavelength of the light, or on something manufactured in the brain.
For instance, if we evolved on a planet orbiting a red dwarf star, would we see colors differently than we do now, given that our sunlight has another wavelength composition?
I know that there have been experiments where volunteers have worn glasses that make them see the world upside-down and eventually the brain corrects this and they see right-side-up again (and have to re-adapt when removing the glasses). I wonder if something similar would happen with color perception.
Does anyone know of any studies done that have tested this?

I'm voting to close this question as off-topic because it is primarily opinion-based, as it is asking about a hypothetical situation. This question may be more on-topic at the [worldbuilding.se] Stack Exchange.

@MattDMo - I think it boils down to whether we can test color perception, or only color sensation. It's an OK question imo. +1 I've refined it a bit.

The color you perceive is ultimately dependent on the relative contributions of the color photoreceptors in the retina, namely the red, green and blue cones. The sensation of color, therefore, is physically determined by the wavelengths in the light source and the absorbance spectra of the cones. Thereafter, the neurophysiological wirings of the retina and the brain take over and these paths are pretty well defined too. However, one cannot say anything about the qualitative perception of someone observing a light source. This is the big difference between sensation (peripheral processes including the retina) and perception (central processes).
To quote the late Bach-y-Rita: 'You see with your brain, not with your eyes.'
Everything we perceive ('see') is a subjective construct devised by our brains. No red dwarf star is necessary to pose the possibility that you perceive my perceived red as green, or vice versa. No experiments can be conducted to prove or disprove a hypothesis like this.
In terms of experiments: we can test stuff like 'up' versus 'down', as with the prisms mentioned in the question. This, because a subject can qualitatively point out where an object is perceived relative to others, and that can be objectively measured. However, we cannot test the subjective quality of color. We can test relative color contributions through color matching experiments (Kalloniatis & Luu, 2012). These experiments will tell you which contributions the red, green and blue cones have in a certain color mixture, but they will not tell the researcher anything about the subjectively perceived color by the test subject in a qualitative way.
Reference
- Kalloniatis & Luu. Color Perception. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)

Thank you for taking my question seriously even though it seems kind of silly at first. I thought that maybe if a person was in a different (more mono-chrome) "light environment" that he/she might eventually see more diversity of color as our brains reinterpret the information that the light cones of our eyes gather. I thought that this may be something that could be tested.

@JackR.Woods now I understand your question better, thanks for that. Although I doubt I can add much relevant info,  I can try to edit my answer. If you don't mind I can re-edit the question too and see if anyone else has ideas?


text:
Is the glucose produced from photosynthesis considered an aqueous solution when written as a chemical reaction?
In the very simplified reaction for photosynthesis, the states of the reactants and products are clear to me except for glucose. Inside a plant, it would be dissolved in water, so would it be an aqueous solution or be considered a precipitate in some way? In the reaction
$$\ce{6CO_2 {_{(g)}} + 6H_2O{_{(l)}} \rightarrow C_6H_{12}O_6{_{(?)}} + 6O_2{_{(g)}}}$$
what would I put in the place of the question mark?

Yes, immediately after synthesis, glucose is dissolved in water. However, it is later used by the plant to build more complex sugars as well as starches and celluloses, which are not necessarily water-soluble.

I’m curious as to why you ask this question — what you will do with this equation when completed. You do realize that what you have written is not ‘a reaction” but a partial summary of a whole series of reactions, which, in addition, involve other substrates that you have not included.


text:
Why are there few four legged bugs?
I may be biased, and will delete if I'm wrong, but why are there so many more insects when compared to quad bugs?

What is the question exactly? Afaik, there are no invertebrates with 2 pairs of legs only. Is the question why, while we see that 2 pairs of legs is a successful bodyplan in vertebrates?

By "bugs" you mean insects, right? All insects have six legs (some may be reduced). Arachnids have eight legs. You can see this answer for some explanation on why six legs may be favourable to many insects. In general, it is not easy to reason out "why" something happened. Many times evolutionary choices are just random.

@Joce I wanted to know why six legged invertebrates are more successful than their four legged counterparts

@WYSIWYG Insects have six legs, and I want to know why is four not evolutionarily better for them

I don't see how this is a dupe


text:
How to explain the colour of these scots pines?
I would like to know why the trunks of scots pines have a particular colour, at least in Estonia, as shown here.

The bottom part of the trunks is darker than the upper part. What could explain this?
Thank you for your help!

Let me know if I can improve my question, add relevant tags, and so on. I'm new on this SE site, so I may not ask suitable questions…

Looks like they've lost a good deal of their bark on the upper trunks. Could be a result of a severe weather event, but more likely it's some sort of disease or insect infestation.

Or maybe that's just the way it looks in the wild. I'm from the northeastern US, and we generally only see Scotch pine on Christmas tree farms, where they are tended to grow well, but don't grow that high, for obvious reasons. If you do see them in the wild, they're often stunted and twisted, as they're not adapted to our soil that well. I've also heard from tree farmers that they're susceptible to some fungal or insect infestation (I don't remember which) that can kill them pretty quickly, so you have to keep a close eye on them and treat them with various chemicals to keep them healthy.

Could be squirrels...

This seems not a species-identification question. Rather it seems a plant-anatomy (bark) question.

I'm fairly sure it's intrinsic, not extrinsic causes (i.e. not squirrels etc. just something that the tree does) because the pattern is observed so ubiquitously across the species and its range.

The bark of some pinus species, like pinus sylvestris and pinus pinaster naturally turns orange when they are a bit older. Other species stay grayisch black, like pinus nigra (hence the name).
By the way: I have never seen pinus sylvestris grow so straight. Is it possible this is another species, for example P. pinaster?
Sources: Den nya nordiska floran (Mossberg&Stenberg 2003) and Heukels' flora van Nederland (van der Meijden 2005).

I'm not sure this answers the question - the question asks why the pattern is present, you've simply stated that some species do this. I also think the original species ID is correct, they often grow straight, especially in managed forests.

@rg255 It depends if you think the question aks for a fysiological explanation or that the question (and some responses) seem to assume the colour is caused by some external factor. I think it asks for the latter, in which case my answer is valid. And from your comment i see we agree on the intrinsic nature of the colour.


text:
Why is a screening process required in selection from a genomic DNA library?
After the process of construction we go for screening process of selecting a recombinant host. Which includes:

DNA hybridisation
Colony hybridisation
Random primer labeling
Nucleotide autoradiography

These techniques are very tedious. So instead of all these tedious process why cannot we just grow them in a minimal media to get the recombinant host and to check which protein is formed?

I have edited your title, first because you should avoid abbreviations in titles and second to improve the English. However I must say I don’t understand what you mean by “recombinant host”. By host we usually mean the organism (bacterium etc.) in which we are propagating some vector (plasmid, phage etc) carrying the DNA. I advise you to set out the problem in more detail, step by step, and this will clarify the question and perhaps provide the answer.

1.) What organism are you referring to? A genomic DNA library from E. coil would be much smaller (have far fewer unique genomic fragments) than a genomic library from a vertebrate (all other things being equal).  So the genomic library you wish to screen for your favourite gene may have between thousands, and millions, of unique inserts. Screening those for protein production, as you suggested, could also be tedious. 2.) Are you dealing with a prokaryote or a eukaryote genome? Many eukaryotic genes contain introns, which need to be removed by splicing, so a library of genomic clones

from a eukaryote would be quite unlikely to produce a protein during propagation in a prokaryotic host. If, on the other hand, you are dealing with a cDNA library, then there are expression vectors designed to express the foreign recombinant proteins. But how do you propose to identify the protein or interest?

The protocol makes sense, if you require to have access to a physical copy of the genomic DNA sequence - and you do not have sequence information about the genomic DNA (or even your probe of your interest). While sequencing service provides will nowadays likely use fluorescence rather than autoradiography, it is wrong to consider the protocol tedious, as you screen many different colonies at the same time with few experimental steps. Selection through media would only make sense, if you already knew what your gene is doing, and you had introduced a cognate inducible mutation in the host.

Actually my question was,  in g dna library we do alot of screening process just to find if the transformation process is successful or not. Instead of that why we cannot grow the sample in a minimal media, we can quickly find the transformed bacteria.


text:
Why is it that I can only detect smells if I breathe, and not when I hold my breath?
At school we're told that the receptors for smell (olfactory receptors) are present in the Schneiderian membrane. But I've noticed that I'm only able to detect smells only while I breathe and not when I hold my breath.
I even tried an experiment to confirm my observations and the results were positive. I placed an open bottle of really strong perfume fairly close to my nose, and lightly inhaled. I could easily detect the smell. But as soon as I hold my breath I'm not able to smell it anymore, even though I placed the bottle right under my nose I wasn't able to smell anything. Immediately I moved the bottle away, walked into another room and took a breath, and the smell of perfume was so strong it made me choke.
I guess this 'experiment' of mine contradicts what we've been taught. That Olfactory receptors present in the nasal passage simply pick up traces of molecules (in this case, perfume) and this is perceived as smell, since by keeping the bottle right under my nose the perfume would've already diffused into the air in large quantities and would've already entered the nasal passage, yet I was unable to detect it.
So my question stands, 'Why is it that I can only detect smells if I breathe, and not when I hold my breath?'

if you are breathing it is actively moving the air, containing the scent, in to your nose, otherwise you have to rely on diffusion which doesn't work well with such a narrow passage

@rg255 I suppose you can make an answer out of your comment

Once upon a time I suffered from a bad-type pharyngitis, and when I EXHALED, or blew the mucous out, I could perceived the ugly smell produced by microbes.

The olfactory epithelium is located in the highest part of the nasal cavities, overlying the cribriform plate of the ethmoid bone.  In order for you to smell something, the odoriferous molecules have to travel the length of the nostrils (which are a pair of very narrow passages which also happen to be filled with hair) and up though the full height of the nasal cavities, having to pass three sets of baffles (known as the nasal conchae) on the way.
When you take a breath, your lungs and inspiratory muscles form a suction pump which pulls air through the nostrils up into the nasal cavities; some of this air, along with any odoriferous substances contained therein, is swirled up to the top of the nasal cavities, where the olfactory epithelium is located.
In contrast, when you're holding your breath, there is no significant air movement through the nasal cavities, and even airflow contained entirely within the nasal cavities is considerably obstructed (thanx to the aforementioned hairs and baffles); therefore, for any odoriferous substance (such as the perfume you're probably sick of smelling by now) to reach the olfactory epithelium, it has to diffuse all the way from the tips of the nostrils to the top of the nasal cavities on its own.  This is a much slower process, and, therefore, it takes rather a while to notice anything smelly when you're holding your breath - even if it's, literally, right under your nose.