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What is the purpose of the brown louver-like structure on the underside of a mushroom?
On the underside of the cap of a mushroom is a structure with many brown leaves closely spaced together like slats or a louver.
What is the purpose of this structure?

These thin, closely-spaced structures are commonly called gills (in more formal contexts a gill is called a lamella).  Our most familiar mushrooms have gills, but there are other species that do not have structures of this form.
Photo by Jason Hollinger via WikiMedia.org
The gills exist for reproduction. Mushrooms spread by producing tiny spores that disperse on air currents.  (In fact the entire mushroom structure exists for this purpose; the main part of the organism, a fungus, is a diffuse web under the ground or other substrate.)
Mushroom spores develop on surface tissues so that they can be released into the air.  The gills evolved to provide more surface area so that more spores can be produced and released (up to twenty times the area of the supporting surface).  The gill spacing is important because the spores are shot out of the surface, are slowed by air resistance, and then fall downwards from between the gills. (Source: Why mushrooms form gills: efficiency of the lamellate morphology)

The structures you're referring to are called "lamellae" or "gills". They are coated in the spores that the fungus to reproduce. Specifically you find them on Basidiomycete and Agaricomycete fungi.
By being 'vented' and hanging beneath the cap of the mushroom, it allows the wind to blow past and dislodge the spores, to fall and then be carried off and plant themselves somewhere new - in much the same way seeds would fall from plants.
https://en.wikipedia.org/wiki/Lamella_(mycology)


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Can a reservoir host act as a vector?
Is it possible to get an infection by contact with a reservoir host ?
Can a reservoir host act as a vector ?
What is the distinction between these two concepts (reservoir host vs vector) ?

Female Anopheles mosquito houses plasmodium vivax. But is not affected by the same. So reservoir host. But plasmodium is pathogen to human. So these terms are relative to perspective of viewer.

A reservoir host most obviously is a long-term carrier organism of a given pathogen that doesn't exhibit the disease caused by the pathogen.
A vector is literally any agent that transfers the pathogen to another organism. If you think about it, a reservoir doesn't have to be a vector i.e. there's no route of transmission they participate in, but a vector can certainly be a reservoir, such as bats, who often act as a vector for the pathogens they house (think Rabies). On the flip side, ticks are common vectors for Lyme disease, but small rodents actually act as the reservoir for B. burgdorferi (1).

source: Stack Exchange

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How does hydration affect digestion?
My textbook( biochemistry by Satyanarayana, 4th edition pg.no:166) says:

The polysaccharides get hydrated during heating which is essential for their efficient digestion.

(I think there is a typo , heating should be replaced with eating)
How does water add into polysaccharides? Am I right if I say it is by hydrogen bonding? It also says  that efficiency increases, is it so because the substance is now more diffused so that enzymes act on an effectively larger surface area(making colloidal solution)? Or if the added(hydrated) water plays some role in interaction between enzyme and polysaccharide?

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Who are Ursprungliche Eukaryoten?
The school textbook of my daughter (the textbook is written in German) describes the five kingdoms of life: prokaryota, plants, fungi, animals and "Ursprungliche Eukaryoten". These are defined as "single cell organisms with real nucleus and other specialized organoids, both autotrophs and heterotrophs". No Latin name is given.
I am somewhat confused, as I know that there are both multi and single cell varieties between algae, and these used to belong to even particular taxon within algae (a single cell Rhodella, for instance, not just belongs to plants but also specifically belongs to red algae). Also, there are unicellular fungi like yeast that used to be fungi (and, OK, protists used to be a separate group that probably also belongs to "Ursprungliche Eukaryoten"). Are they all pulled out of they groups into this new kingdom in this system?
The summary of the proposed classification schemes over history can be found at https://en.wikipedia.org/wiki/Kingdom_(biology)#Summary . Which scheme, if any does this taxon correspond? Is something missing in that table?
The textbook is Training Gymnasium - Biologie Mittelstufe Band 1, Harald Steinhofer (2013), ISBN 978-3-86668-709-7, seen here. The description in question is on the page 16.

It is natural to be confused because the consensus has changed over the years and is still not settled.  In part this is because knowledge has been gained but remains incomplete, and in part it is a matter of opinion and aesthetics about what is best for usefulness at various levels of detail and understanding.
The system put forth in the textbook seems to best match the system Whittaker put forward in 1969.  His Monera is the text's Prokaryota, and his Protista corresponds to the text's Ursprungliche Eukaryoten.  Essentially Protista/Ursprungliche Eukaryoten is a catch-all for all Eukaryotes not included among the Plants, Animals, and Fungi.  There may be some variations in which of the eukaryotic algae are included among the Plants versus the Protista/Ursprungliche Eukaryoten.
It should be noted that in most or all systems of "Kingdoms", at least some of the kingdom groups are not monophyletic, that is, do not include all descendants of a common ancestor, and so do not exactly reflect a true tree of descent.  The Wikipedia Kingdom article notes:

Some recent classifications based on modern cladistics have explicitly abandoned the term "kingdom", noting that the traditional kingdoms are not monophyletic, i.e., do not consist of all the descendants of a common ancestor.

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Lumpy green balls on tomato leaf
We live in central Maryland, USA, and pulled this off a tomato plant in our garden this morning (mid-summer). Any idea what these are? Not sure if they’re beneficial or parasitic, but I’d say the latter if I had to guess.

The shape of those looks more like caterpillar droppings (frass) than galls to me, though I've never seen them so green or shiny. Here's an image of tomato hornworm droppings, it looks quite similar to your picture:

If the balls are firmly attached to the leaf then they are galls, if they can be dislodged, then poop is more likely.

On closer look poop, is more likely.

Galls, the plants reaction to certain insects. Generally no action is warranted because of minimal harm to the host plant.

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Comparative cost of RNA-seq vs sequencing full length cDNAs
I am in the process of assembling and annotating the genome of a non-model organism, using almost exclusively short read (paired-end Illumina) data. Throughput is one obvious benefit of these data (high coverage for reasonable cost, error rates notwithstanding), but another benefit of RNA-seq data in particular is that they can be used in multiple ways. For example, I am mapping the RNA-seq reads to the genome to estimate transcript abundances and do some differential expression analysis, but I have also assembled the RNA-seq reads de novo to use as evidence for genome annotation.
There are, however, limitations to using RNA-seq-derived transcripts for annotation. Full-length cDNAs would facilitate much more reliable annotation. However, I have no intuition for the relative cost, time commitment, or complexity of extracting and sequencing full-length cDNAs vs next-gen sequencing. Can anyone here comment on this?

What kind of organism? Splicing makes using RNA more difficult. Is there a good existing reference genome for you organism (if lacking in annotation)? Do you have a specific goal, such as biofuels, drug production  fighting pathogenic or parasitic organism, or do you have X amount of money and want to do the best basic research? The type and depth of sequencing that is most cost efficient will vary with your goals.

"What kind of organism?" It's eukaryotic, a social insect to be precise. "Is there a good existing reference genome for you organism?" As I said, this is a non-model species, so I am the one assembling the genome. I don't know what your criteria are for a "good" genome: no physical mapping, gap filling, etc has been done yet, but the assembled sequence is close to the expected genome size and preliminary annotations have identified about the number of genes we would expect (perhaps a little bit less).

"Do you have a specific goal?" The PI of this genome project is primarily interested in the intersection of evolution, genomics, and behavior, and uses several species of social insects as model organisms for these subjects.

IMO you should do a full length cDNA sequencing (sanger) only for the doubtful cases (Small contigs/ contigs mapping with gaps/ low depth)

I would comment on this instead of an answer but I don't have the reputation to comment yet. So RNAseq is actually done on cDNA. Specifically after selecting for mRNA before making a cDNA library by its poly A tail etc... It sounds like you are thinking that RNAseq is on actual RNA molecules? Or is your question more about long sequencing of full length cDNA from RNA instead of fragmented? That comes down to an increased error rate from sequencing longer sequences (of DNA). There shouldn't be any loss of de-novo information, transcript abundance, as well as isoform abundance from alternative s

Does your organism have scaffold information on ncbi? In that case you may find the gnomon predicted cds on ncbi as well


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How to typeset gene regulatory networks
I have a relatively simply gene regulatory network I would like to visualize, complete with the common arrow and bar symbols used to show, respectively, which genes enhance or repress with other genes. Is there a way to typeset a gene regulatory network using something like LaTeX or Graphviz?
For very simple networks, I guess something like Photoshop or Illustrator would probably be the quickest solution, but these programs become very tedious as the size of the network grows even a little bit. What do people typically use for this type of task?

If you have simple 1:1 connections or can list your data in that manner, you can try Cytoscape (freely available). There are numerous plug-ins to customize what you have in mind in terms of visualization.

+1 for Cytoscape. I found it useful for looking at gene interaction networks pulled down from the yeast genome database.

Thanks. One advantage of Cytoscape is its flexibility, simply provide a bunch of A-B links. Those links can be classified - stimulating/inhibiting - but need not be.

I haven't tried it, but this StackOverflow answer suggests that you can import a GraphViz network into OmniGraffle (for Mac), which makes it very easy to produce a pretty network (much easier than Photoshop/Illustrator).

I've used the Omni suite before, it's quite well designed software =)


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Transcript(omics) terminology: cDNAs, ESTs, RNA-seq, etc
I've worked pretty frequently with genome and transcriptome data for several years now, but I'm still not 100% sure I understand the proper usage for certain terminology related to transcripts and transcriptomics. Let me give it my best shot.

cDNA: in general, this term corresponds to any DNA that is derived from an RNA template via reverse transcription (complementary DNA); however, it is often used to refer to full length cDNAs, DNA sequences that correspond to complete mRNA molecules
EST: expressed sequence tags correspond to cDNA (sub)sequences obtained from a single read of a cDNA sequencing experiment
RNA-seq: this refers to the use of high-throughput sequencing technologies to characterize entire transcriptomes, such as by transcript assembly or expression analysis

Here's my concern: I've seen ESTs described as "one-shot" or "single-pass" sequences, which I interpret to mean a single sequence read. However, they are also typically described as being hundreds of base pairs in length (Wikipedia claims about 500-800bp in length max), which (currently) limits this definition to reads derived from Sanger-style sequencing.
Does this mean that a short read derived from a high-throughput sequencing platform is not an EST? Is this distinction based on read length? platform? throughput?
Due to technical limitations, short reads are often assembled before they are used for other downstream analysis. I have sometimes heard the contigs belonging to these assemblies as ESTs, but this doesn't seem to be consistent with the previous definitions.
Is our terminology becoming inconsistent due to the rapid improvements in sequencing technology, or am I missing or misinterpreting something?

Although for historical reasons an EST is usually a longish sequence (ESTs were defined in 1991 when only Sanger sequencing was available so reads would naturally be several hundred bases in length), operationally it really only needs to be long enough to tag an expressed sequence, i.e. to provide evidence for the existence of an mRNA from a specific region of a genome.

The quick answer is that you are misinterpreting ESTs. EST stands for Expressed Sequence Tag. They are obtained by collecting and sequencing any mature (i.e. poly-A) mRNAs found in a living cell. Well, it was living until the experiment was performed at any rate :).
The term EST is not applicable to sequences derived from genomic data. It only applies to expressed sequences. You do have ESTs that are derived from cDNA libraries but these are expressed cDNAs. Short reads are not ESTs because we have no information on whether that sequence is actually expressed in a living cell.
You could apply the term to RNAseq reads (depending on the experimental procedure involved) but that is not what most people would understand by the term.
In summary, the operative term of EST is "expressed". You cannot call anything an EST if you do not have evidence that it is actively expressed in a living cell.

When I said "short reads", I was referring in that case to RNAseq reads. Of course, in general short reads can be genomic (if you're sequencing the genome) or transcriptomic (if you're doing RNAseq analysis or something similar).

Still, RNAseq can also pick up non-poly A RNAs. Personally, I would only use "ESTs" to describe sequences derived from "naturally occurring" mRNAs. Given the recent findings of the ENCODE project, most of the genome seems to be actively transcribed. Such transfrags do not, again in my personal opinion, qualify as ESTS.

@terdon: I must be missing some subtlety when you qualify ESTs as having been "found in a living cell" ... RNA-seq libraries are constructed from "living cells" as well, so what's the difference here? Capturing these reads are evidence enough that they are expressed (noise control required, obviously) Also: I suspect "mature mRNAs" are captured for "EST-ifying" much the same way they are captured for constructing a highthroughput sequencing library (via oligo-dTs to prime the polyA tail ... or even "cap trapping" if you're doing some *CAGE experiment). Can you clarify those two points a bit?

@SteveLianoglou, I was differentiating more between cDNA libraries made from DNA templates and ESTs. Yes RNAseq reads come from living cells. In my answer I just say that "most people" would not call the ESTs. Not that they are not indicative of expression. I quite agree that technically you could call RNAseq reads ESTs, its just that the term is more commonly used for the older EST type data.

My 2 cents:
To answer your main question:

Is our terminology becoming inconsistent due to the rapid improvements in sequencing technology, or am I missing or misinterpreting something?

I think what you are witnessing (being subject to(?)) is, as you say, an inconsistency of terms due to the rapid improvements in the field.
I put the caveat in that you are being subjected to this because I suspect the people referring to the "things" that a second-generation-sequencing protocol generates as "ESTs" are using a familiar word to describe something that might be unfamiliar to them.

Does this mean that a short read derived from a high-throughput sequencing platform is not an EST? Is this distinction based on read length? platform? throughput?

I guess it's (i) construction; (ii) platform; (iii) throughput; and (iv) relative "quantitativeness".

Due to technical limitations, short reads are often assembled before they are used for other downstream analysis.

You lost me here with the word "often" -- are you talking about RNAseq now or is this an EST. If you have a reference genome, I think assembling RNAseq reads before downstream analysis (alignment(?)) is an exception instead of a rule ... which is why I'm lost.

Ok, perhaps my use of "often" is biased by my own experience. I am working on genome annotation, and both the Maker annotation pipeline and some of our in-house workflows require RNA-seq data to be assembled before they can be used as evidence when predicting gene models. I understand of course when mapping short reads to a genome or quantifying gene expression, assembly is not a prerequisite.

I think RNA-Seq assembly prior to alignment is common in non-model species, where you need to first describe the features you align the reads to.


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Is there such thing as "half-life" of dopamine?
If a dopamine is released at T=0 and binds to receptor D2, what determines the time when the concentration of this neurotransmitter bound to the receptor reaches half of the original concentration? In other words, when will the effect of neurotransmitter on the intercell signalling fall in half?
Is there any time estimate of how quickly the brain thinks that neurotransmitter has "fulfilled its purpose" and is to be re-uptaken? Or is this process completely random?
Thank you for your input!

All processes involving reuptake or metabolism of biological molecules are completely random. However, when you look at a large number of molecules over time, the random events combine into a stable, predictable rate of decay. This rate is usually either exponential decay (a half-life) or, more rarely, a constant amount per second.

I don't know what the answer is for dopamine, and individuals probably vary in how zealous their brains are about dopamine reuptake.

The half life of dopamine in the extracellular space is of the order of 200 milliseconds.
Yavich,L. (2007) Site-Specific Role of Catechol-O-Methyltransferase in Dopamine Overflow within Prefrontal Cortex and Dorsal Striatum. J. Neurosci. 27:10196-10202
In Figure 1 of this paper the authors present values for the half-life (τ) of dopamine elimination from extracellular space in the caudate nucleus and prefrontal cortex of mice as:
caudate nucleus: 0.2 +/- 0.03 sec
prefrontal cortex: 1.92 +/- 0.22 sec
Apparently this is because dopamine is usually inactivated when the presynaptic cell takes it back up using the dopamine transporter, but in the prefrontal cortex uptake is instead via a lower affinity norepinephrine transporter on neighbouring neurones. Thus the value of 200 milliseconds seen in the caudate nucleus is probably more typical.

Interesting. Does this mean that upon release, dopamine has 200ms to either bind to a receptor or be reabsorbed?

If we think of release as instantaneous, we now have a pool of extracellular dopamine. This will begin to bind to receptor, setting up an equilibrium between free and bound. The free dopamine will also be taken up by DAT, and because the binding to receptor is a reversible process, as the external pool shrinks the level of DA-receptor complex will shrink. An individual molecule could be taken up without ever binding to a receptor, or could undergo multiple receptor binding/release cycles before being taken up. The half-life reflects the interaction between these processes.

If I understand correctly, the DAT cleans up extracellular and bound DA, and deposits it back within the neuron. As less and less extracellular DA is available, there's a higher chance that bound DA will be recovered. Is this correct?

Dopamine (DA) secreted by neurons is selectively reuptaken by the dopamine transporter (DAT), present on nerve terminals.

(source: inist.fr)
Image source: Plasma membrane monoamine transporters: structure, regulation and function - Torres et al. - Nat Rev Neurosci., 2003
DAT acts as a symporter, using the Na+ and Cl- gradients to generate the energy required to transport DA back in the cytosol.
The mechanism of reuptake has been investigated in vitro allowing the description of a model for DA reuptake by DAT.
In particular, from the abstract of this paper:
A multisubstrate mechanism of striatal dopamine uptake and its inhibition by cocaine. - McElvain and Schenk, Biochem Pharmacol., 1992

Dopamine uptake was found to be first order in dopamine with a Vmax of 582 pmol/sec/g wet weight and a Km of 1.2 μM. The results of experiments in which choline and isethionate were substituted for Na+ and Cl−, respectively, suggested that the uptake process is second order in Na+ and first order in Cl−. Multisubstrate analyses of the initial velocities of uptake over the concentration range of 0.025 to 1.5 μM dopamine suggested that the mechanism of binding of dopamine to the uptake carrier is a partially random, sequential mechanism where dopamine or Na+ binds first with the uptake carrier and Cl− binds last.

A transport scheme is reported in:
Dopamine Neuronal Transport Kinetics and Effects of Amphetamine

Scheme 1 is a kinetic scheme for a simple carrier adapted from that of Stein (1986) for the DAT. The subscripts o and i represent the outside and inside, respectively, of a DA neuron. Scheme 2 describes a possible mechanism for
  the cotransport of another species. All symbols are as in scheme 1 except that A corresponds to amphetamine.

From the text

This scheme describes transport as a series of steps: the competition between binding and dissociation of the substrate to the transporter on the  extracellular side, a similar process on the cytoplasmic side, and an equilibrium between the unoccupied transporter facing toward the extracellular or cytoplasmic side. The driving force for inward transport arises from the cotransport of Na1 and Cl2 as well as the membrane potential difference
  (Stein, 1986; Sonders et al., 1997). Biochemical (Krueger, 1990) and electrophysiological (Sonders et al.,1997) studies have established that DA transport is accompanied by transport of at least two Na1 ions and one Cl2 ion and that DA transport can be bidirectional in isolated preparations.

If I'm reading this correctly, then Dopamine is randomly extracted from receptors, right?

Not really "extracted"... dopamine will randomly detach from the receptor, and randomly bind to DAT. The speed of this may depend on the actual concentration of dopamine, dopamine receptor and DAT present in the system.

This is an attempt to illustrate how a system like this behaves kinetically, to help Alex visualise it. The model shown below contains external dopamine which can bind reversibly to a receptor. The unbound dopamine is subject to irreversible reuptake.

I built a quick simulation using Copasi. I haven't made any attempt to refine the parameters to fit the information in my previous answer - I'm just trying to illustrate qualitatively how the three different pools of dopamine (free external, bound external, internalised) behave in this kind of system. As @nico says, there is no question of extracting the receptor-bound dopamine - it will dissociate as the free dopamine concentration falls due to reuptake.


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Is there some branch of biology that deals with the entire organism?
I'm reading about various parts of the human body and brain and started to wander if there's a branch of biology that deals with the entire human? I know that there are branches various -biologies, from neurobiology to something like heliobiology or chronobiology. All of them look at different organ systems or parts of an organism, but from different points of view.
Then there are sciences that deal with behavior and cognition of humans.
As I read about these, I notice that there's quite a lot of overlap, particularly when neurotransmitters and hormones are involved. For example Melatonin, a hormone has functions in both the brain and the gut.
I'm wandering if there's some form of biology or science that deals with the entire organism, its behavior , as well as its parts? Am I thinking about Biology or Medicine or something else?

Organismal biology?

I was thinking of Systems/Integrative/Predictive Biology reading your question. Studying the wikipedia entry it looks like a research approach with many problems trying to understand organisms from a biochemical perspective, identifying control circuits and macro-quantities like temperature and its relation to such biochemical control circuits. Basically you have to give up reductionism and use holistic/systemic perspectives and methods. While physics was successful with such research approaches (climate simulation, many particle systems,...), biology is lacking very accurate and proven mathematical theories to implement and test reasonable models of an organism, not surprising when biological systems have so many degrees of freedom compared to something like a ideal gas in physics. The wikipedia link doesn't show a lot of proven knowledge that this field/research approach has already created.


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How animals maintain their body shape after development to maturity?
I've recently read a book on evolutionary-developmental biology for laymen, and it described how a fetus is progressively divided into more refined zones of genetic activity. These zones, kinda like GPS coordinates define which genes will be activated at which time and at which location.
What interests me is - after development to maturity, what defines how animals maintain their body shape? Is it the same "GPS" system that defines boundaries of an organism? Or is it something else within the specialized cells that tells them to grow in certain directions and avoid others?
To clarify the question with an example - lets take blood vessels - what prevents blood vessel lining from growing forever in all directions, taking up all available internal cavity space?

after development, the cells and tissues generally retain their transcriptional "memory" through epigenetic mechanisms. All they need to do is to maintain this state by replacing worn out cells etc..

Reference for the book? & possible to quote it?

@GriffinEvo.. i think any standard book on developmental biology has this topic (for e.g. Scott F Gilbert's).. It is known that developing embryo is divided into zones (governed by Hox proteins).. This is particularly well explained in case of drosophila

The laymen book is "endless forms most beautiful" by Sean b. Carroll

Normally, cells do not proliferate without a "command". The "zones of genetic activity" you mentioned are defined by gradients of morphogenic molecules (and cell interactions). In the adult organism the original "map" of concentrations of these molecules is already realized and the pattern they defined before is no longer present.
Another closely linked idea is that most cells in mature tissues are not able to proliferate, because they have already undergone the process of differentiation. In contrast, stem cells maintain their ability to reproduce. [There are still some ways to de-differentiate some types of cells, i.e. to obtain induced stem cells in vitro.] Thus, embrya are composed of embryonic stem cells, while adult organisms have several restricted pools of stem cells (for example, in haematopoetic organs, where new blood cells are produced.)


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Why is cyanide poisonous?
I know cyanide inhibits complex IV in the electron transport chain, but I don't understand why this makes it so toxic. If cyanide is bound to the complex, can't the electrons just bypass it   and reduce oxygen directly? That way fewer protons would be pumped out of the matrix, but most still would, and aerobic respiration would just be less efficient, rather than stopping entirely.
Essentially what I'm asking is what causes the electrons to get "stuck"?

But that doesn't explain why the electrons have to be passed to complex IV. My question is why can't they bypass that complex if it's deactivated and just go straight to oxygen? From what I understand, premature electron leakage toward oxygen is one of the reasons cells don't produce ATP at the theoretical maximum efficiency.

That leakage is due to the inefficiency of the complex-specificity, i.e. sometimes the highly specific requirement of substrate for these electron-transfer enzymes relaxes and it allows some electrons to leak, forming free ionic oxygen radicals. Otherwise, they are very specific in what they reduce and hence cannot bypass the predetermined chain disabling the effect of cyanide.

all these comments could be incorporated into answers - please don't answer questions in comments!

Cyanide binds cytochrome oxidase so as to prevent the binding of oxygen. Electron transport is reduced to zero, and none of the oxygen breathed in can be used. Cytochrome oxidase is one of a superfamily of proteins which act as the terminal enzymes of respiratory chains, so if the cyanide is binding to the cytochrome then it inhibits the process and making it dangerous. Another example I would give rotenone which binds competitively.

That makes sense; I think for some reason the mental model I  was using involved oxygen just floating around the complexes and magically abducting electrons when they got close enough to one of them, but your answer combined with Satwik Pasani's fixed the blight of stupidity I seemed to be suffering from for a while there. Thanks.

This answer seems to suggest that rotenone inhibits cytochrome oxidase, but it doesn't, it inhibits electron transport at complex I > ubiquinone.


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Troubleshooting SDS-PAGE of trypsin-treated BSA
I am currently working on SDS-PAGE technique having 20% acrylamide concentration for hydrolyzed BSA protein. Here I attached a gel photo for trypsin hydrolyzed BSA. I don't know , is it a good result and how do I interpreted this result?

A 20% SDS gel? How big are the fragments you are expecting? The concentration seems rather high for me.

why do you need to know (is this for a report, assignment, or research?) it may affect the type of answer, and some more detail of method might be needed & what you are testing

I am doing research on drug delivery. This my initial task to check hydrolysed protein on PAGE. protein hydrolyzed by trypsin chmotrypsin and pepsin in our stomach.

her I am using 20% because on 15% I got band at bottom of GEL, nearer to edge.

It looks like your trypsin works, at least. Is there something else you were expecting? I don't do very much SDS-PAGE(so take with a grain of salt), but I would lower the thickness of your gel and let the large blurry bands run off. The BSA and hydrolyzed protein fragments are those thin lines at the top.

What percentage is your stacking gel?

In 15% i got no any band.

At 15% did the large digested band also disappear? Again it will be great if you repeat the experiment and use a ladder, just to see how proteins of 66 kDa MW and lower gets resolved.

@kt123 Can you show an image of the 15% gel? I still doubt this makes sense based on my experiences. Your digested samples hardly enter the gel and the undigested protein doesn't enter it at all. Can you add your gel recipe? Based on my experience with similar sized proteins I would say an 7-8% gel should do the trick. Don't run it too long (until the first dye band which runs at the front is down at the bottom) to loose samples.

I'm going to treat this as a partial homework question but provide some guidance as to how you can potentially address your question and have solid theory to back it up. Chymotrypsin preferentially cleaves peptide amide bonds where the carboxyl side of the amide bond (the P1 position) is a large hydrophobic amino acid (tyrosine, tryptophan, and phenylalanine). So one solution which is often used by experimental biologists (such as myself) performing mass spectrometry (MS) is to put their protein sequence (in this case BSA) in an algorithm such as PeptideCutter (from ExPASy), which performs a theoretical digest of the protein sequence having chosen the desired enzyme or combination of enzymes) and see what peptide fragments are expected to be produced and work out their length/molecular weight and compare that to your experimental data.
Having had an initial look, I noticed that your protein marker/ladder is missing, which is quite important in figuring out the peptide sizes produced! Also what is 1-8 lanes? are they different concentration of enzymes? if so then it looks ok to me since the higher the enzyme concentration from left to right, the higher the amount of digest products you have. If the peptide sizes obtained are not the ones expected then perhaps increase or decrease the digestion time since you could have a problem due to either incomplete digest or unspecific digestion, depending. I guess since BSA MW is ~ 66kDa your gel concentration is appropriate since you have a problem with the 15% gel as the products are too small and too abundant to resolve.

I disagree on the gel percentage. I did run a lot of gels wit proteins in the 50-70 kDa range and I used 7 or 8% gels for that. The density here is ways too high, the undigested protein doesn't even enter the resolving gel, it stays at the border between stacking and resolving gel. At this position I would expect proteins around 100-120 kDa. What didn't work in the 15% gel? Can you use a marker?

I agree that 20% gel is quite high but OP in the comment section says using 15% gel fails to resolve the digested bands (which are many from the pic) as all collect at the bottom although I will be surprised if the large digested band also disappears. Hence the resolving gel (i assume) was used at 20%, which gave better results. It is important however to use a protein ladder just to see how proteins migrate as it is hard to tell at the moment what we are looking at. I personally use gradient gels 4-12% pre-made but thats ideal for proteins between 60-220kDa as I get an excellent resolution.

We don't know why the 15% gel failed as we never heard anything else about it. I see only one band per lane, the rest are the dyes used in the buffers. Additionally I wonder how he handled and stained a 20% gel, as these should be really brittle. I do 15% gels for oligo analysis from time to time and these are already hard to handle.

I expect most of BSA digestion products are to be small and various in size (smear like), which is what he is seeing, except that one band since the enzyme does not digest too specifically. Hence I do not think the smears he is seeing is non-washed stains since in between the lanes the SDS-PAGE gel is clear so he has got most of the unbound coomassie stain off although I do not know of his wash procedure. Oligos give a similar result to the above but I did not know you can run them in a SDS-PAGE as I just come across them in my agarose gel work.

It would however be nice for the OP to do an overnight wash (with a slightly modified wash buffer composition) to see if he/she gets a better resolution. Almost 100% of the times overnight washes work best and show bands, which were unresolved for me! but @Chris I agree about the general thrust of your argument specially the gel brittleness issue!


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Why do Alu repeats form secondary structures?
I've been doing a lot of research on Alu repeats and how they mediate the gene expression. I read the following article "Useful junk: Alu RNAs in the human transcriptome".
And it says that alu repeats embedded in 5'UTR makes stable secondary structure that prevents the assembly of ribosomal subunits, thus blocking the process of translation. I've been reading various articles to find out why Alu repeats form this secondary structure and why only in the 5'UTR and not in the 3'UTR. But haven't been able to find an answer.

Single-stranded RNA can easily form secondary structures, a very important example of this are tRNAs.
From a quick look at the article you read it seems that these Alu repeats work similar to riboswitches in the 5'-UTR. They can form secondary structures that block translation initiation, riboswitches commonly do this by hiding the Shine-Dalgarno sequence in a stable helix.
This kind of regulation of translation can obviously only work in the 5'-UTR as that is the place where the translation starts. The 3'-UTR can't affect translation in this way as the translation starts at the other end of the mRNA.
The Alu repeats still can form secondary structures in the 3'-UTR, and the article suggests that those might have an effect on mRNA stability.


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What was the precursor of testosterone?
Testosterone evolved about 500 million years ago (says 8fact.com). What was the precursor of testosterone (if any)? If possible, what caused the 'precursor' to evolve?

This question is very vague and I am unsure if you are really familiar with how sex hormones work. Why would testosterone prioritse sex per se? What have you already learned about the functions of testosterone in the (presumably human) organism? What hypotheses do you have based on that knowledge? Please clarify by editing your question.

Testosterone drives sex drive and has a role in starting puberty and producing sperm. How could that not encourage sex?

Organisms that do not produce testosterone do also produce sperm. Testosterone is definitely not needed for sexual reproduction at all. For me this question does not make sense.

Yes, but that is not my point. It still has a role in sex, does it not?

Just because you do not understand my question doesn't mean you should downvote it. I have put a lot of effort into editing, which by the way got rid of the question you didn't understand.

If you ask a precise and understandable question I will remove the downvote for sure. As is, I do not see any informative discussion coming out of a question as vague as this (no reference for the fact, what do you mean by precursor?, how could one - even theoretically - know what this precursor was? this is not how evolution works, the reason for evolution of a more than 500 MY old precursor is more a matter of opinion than fact, the relationship between the function of testosterone in the human body and sexual reproduction, ....) which in my view qualifies for a downvote.

If you do not know the answer, don't answer. It's that simple. No one forced you to answer so don't pull out that excuse. The word precursor is the analogue of ancestor, and only part of my question is (possibly) opinion based so there is no reason to dismiss it. Testosterone plays a major part in the sexual development of human males such as driving libido (sex drive), starting puberty and producing sperm. Just tell me how that is not related to sex. Answer my questions before you continue adding more to your argument.

Please add a citation that people can actually read. Your link simply redirects to what appears to be an advertisement for an app called Cookie, which I do not intend on even looking at, let alone downloading. There are plenty of web sites out there.

It says right on the page now linked in your question that testosterone developed from estrogen. So what's your question?

Someone else added that on and I did not know that existed so that know makes my question obsolete.

Welcome to Biology.SE
The question suggests that you have important lack of knowledge in Biology (which is fine). It will be impossible to explain everything in a post. I therefore just provide a short answer and redirect you to some source of knowledge that will be necessary to read for you to really be able to understand the basis of molecular biology and evolutionary biology.
Short Answer

Testosterone cannot 'evolve' per se because it is a hormone, right?

Testosterone is a chemical that is synthesize by our body. This synthesis is regulated by proteins which are coded in our DNA. The sequences in our DNA that code for proteins is called a gene (quickly speaking).
So, a mutation in a gene (or in a regulatory sequence) can impact the synthesis of testosterone and therefore be under selective pressures.

Was it to prioritise sex and in turn pass on your genes?

I don't understand what you mean by "prioritise sex". But yes, those individuals making efficient synthesis of testosterone and good use of this signalling molecule had/have a higher fitness.

Did the evolution of testosterone happen because of sexual reproduction?

Testosterone is directly used for sexual dimorphism, so in this sense it evolved in its current form because genders exist. However, the evolution of hormone synthesis (and related biochemical pathways) do not require sexual reproduction (asexual reproduction being the alternative).
Source of Information
I will recommend free online resources.
You should start with a basic understanding of the cell machinery. Make sure to really understand what DNA, RNA, proteins are and their relationship. I recommend Khan Academy > Biology. It is a long series of video, so I particularly recommend series on the so-called (and poorly called) central dogma.
Then you might want to have a look at Understanding Evolution (by UC Berkeley), which is a very introductory course on evolutionary biology.

I know about translation and transcription but I do not think you get what I am saying. Firstly, you did not answer my main question 'how did testosterone come to be?' and secondly, how exactly does my question demonstrate a lack of knowledge?

Maybe I misunderstood indeed. I thought you had an important lack of knowledge and you seemed to not understand the relationship between DNA and the synthesis of a hormone. Can you please further what you mean by "how did testosterone come to be?". For the moment this question is very unclear to me. Are you interested in the precursor of the current form of testosterone?

Yes, that is what I am essentially looking for the precursor of testosterone. Plus, I edited my question to make it short and concise.

I would advice that you edit the post to specifically say something like "Testosterone evolved about 500 millions years ago (citation). What was the precursor of testosterone (if any)?". For the moment, the expression "How did testosterone come to be?" is still unclear IMO.

I have edited the post now, thank you for your contribution and help. I sincerely appreciate it.

Thanks for the edit. Can you please add the link to 8fact?

Let us continue this discussion in chat.


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How do harsh conditions cause an increase in the male birth ratio?
I've heard that in harsh conditions more human baby boys are born than girls because a bigger ratio of them will die before reproductive age. But in which aspects of the random gene combination while conception can harsh conditions (and which of their characteristics) actually can make a difference?

edited - gender is a social construct

@Christiaan Yeah but now it looks like I'm talking about sexual selection.

Your last sentence doesn't make sense. Maybe improve the question somewhat.

Don't understand the question and video at all. In this video host doesn't give us any proofs that's difference (where is the source) is significant assuming we have $p_{xy} = \frac{1}{2}$.

"Why is there a male-biased sex-ratio at birth in harsh conditions?" would be a better way to express this... As someone studying the effects of environmental conditions on the evolution of lifespan in humans, I'm going to say the video wasn't great.

Nature vs Nurture. Good example is a David Reimer story. So, gender is not a social construct, is biological construct.

@chupvl I don't understand the question but I really don't see how it could relate to the very popularized nature vs nurture discussion. Also, gender is a social construct. It is not a question open to debate as gender is defined as a social construct (just have a look at its definition on wiki > gender). The fact that gender correlate quite well with sex does not change anything to the fact that gender is defined as a social construct.

an individuals gender is not defined by their sex @chupvl

Issues with the post
Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). This question has nothing to do with sexual selection.
What do you mean by random gene combination? More globally I don't understand the last sentence.
As a consequence, I don't understand the question. IMO, the post should be closed as unclear. However, I can imagine a question that I would consider interesting. I am answering to the question Is it possible that selection yield to a sex-ratio that deviates from 1:1 at equilibrium? How does it relate to environmental conditions?.
Fisherian scenario
Evolution of sex-ratio under a standard Fisherian scneario is often refered to as Fisher's Principle.
Basics
In the vast majority of strictly sexual species, every individual has exactly one mother and one father. It means that at equal sex-ratio the average relatedness of all offspring and all males in the previous generation is equal to the average relatedness of all offsprings and all females int he previous generation. When the sex-ratio is biased toward more females (for example), males have on average a higher reproductive success than females. As a consequence individuals that produce more males will increase their fitness and will increase in fecundity. As a consequence, the adult sex-ratio will always go back to 1:1 (fifty-fifty).
Adult vs baby sex-ratio
Now, it is important to understand that the adult sex-ratio is not necessarily the same as the babies sex-ratio. If typically, there is higher mortality in males than in females (could happen depending on the species and the environment), then selection would favour a bias sex-ratio toward males in babies. The adult sex-ratio will in any case be 1:1
Kin/group selection (non-fisherian scenario)
See for example the case of social spider Aviles (1993).
What is good for the population?
Thinking about the same problem but thinking about what is good for the population (rather than for the individual). For the population, the limiting factor in the number of babies produced are often the females. As a consequence, it would be good for the population if the sex-ratio were biased toward females.
When can alleles that are beneficial for the population overweight what is beneficial for the individuals
Under a standard fisherian scenario this cannot happen though selection will increase the frequency of alleles that spread the best and not the ones that are good for the population. However, typically when the relatedness within the population is high enough (you should read about group selection and kin selection) such trait that are good for the population may evolve.
Recommendation
I recommend that you take some time an introductory class to evolutionary biology such as Understanding Evolution for example. It is fast and you will learn more and faster than what you can learn here with your question. I think I already gave you this suggestion a number of times.

Oh, sorry, I let myself the second part on later and now I can see there's not much of an example of an actual non-fisherian scenario. Is there any actually found in nature? From the video I got that there is because otherwise it wouldn't be about the ratio of born males - which is the same for the fisherian scenario.

Yes, some social spider for example have a biased sex-ratio toward females Aviles (1993).

I'm grateful for that the answer contains the reason why these traits should evolve, but I didn't catch mutch about the true mechanism an organism can affect which sex will the fetus be when the gamets fuse.

@Probably The mechanism is totally different discussion and is out-of-the-scope of this post. The above answer assumes that mutations can change the offspring sex-ratio of an individual to any value between [0-1]. Before understanding this mechanism you will need to understand the sex-determination systems.

Typically for an ESD (Env. Sex Setermination), the mother can affect the sex ratio of the, say eggs by modifying the temperature of incubation (which can be modified by the characteristic of the nest or how deep they are burrowed). But manipulation of sex-ratio in pure GSD (Genetic Sex Determination) exist too such as killing the offpring very early depending on the sex or by making the sex determination under control of several loci you can reach all kind of sex-ratio in offspring.


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What happened to ProteomeCommons.org?
ProteomeCommons.org seems to once have been a resource for raw proteomics data. Thought, the website now offers gardening tools. It seems to be hacked. Does anyone know whether the data is still available somewhere?

According to Lars Juhl Jensen on a Biostars forum,

The Proteome Commons Tranche sadly shut down around 2013 due to lack of funding. It is a good example why important bioinformatics infrastructure needs dedicated funding and should not have to operate out of research grants for individual groups.

I have no quibble with your answer but feel the part of the quote regarding the need for dedicated funding is naive and simplistic. The fact is that it is difficult to get grant funding for web resources in the first place, but even more difficult to get extensions as granting bodies like to fund new projects. Thus KEGG got cut back and started charging for database access, and FlyBase likewise and is asking for subscriptions. This is a complex problem with no easy answers.

They seem to have lost the domain name. I believe all the data from that project is now on the UCSD site


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First neurotransmitter?
Cnidaria are considered to be the first phyla to develop a nervous system. Nervous systems having 1, 2 and three neurons are considered to have appeared first in Cnidaria, with 2-neuron nervous systems having already specialized neurons for sensory and motor functions.
This takes us to the first synapse, which is thought to be of chemical nature, as the sensory and motor neurons in early Cnidaria utilized a chemical to communicate. This would be the first chemical to be used as a neurotransmitter, but which was it?

the difference between neurotransmitter and any other cell to cell signalling molecule is largely semantic, multicellular organisms are full of signalling molecules, which one you co-opt for nerves may well have multiple origins.

I cannot give a thorough answer right now (if I even find one) because I'm on my phone, but here are some papers that could inform the question in the meantime (or their abstracts at least!)
One element I have gathered so far is that the evolution of nervous systems likely involved not the evolution of wholly new molecules and structures, but the cooptation of existing structures for new purposes. Meaning the first neurotransmitters would have been pre-existing with some other purpose in early proto-neurons, not new molecules evolved expressly for the first synapses. One paper talks about neurotransmitters like dopamine being common across all life, including plants (no nervous systems there!). This does not answer which of these molecules would have been the first neurotransmitters however.
The abstract of this paper doesn't say much but the title is tantalizing:
https://link.springer.com/chapter/10.1007/978-3-319-20215-0_2
"New Trends and Perspectives in the Evolution of Neurotransmitters in Microbial, Plant, and Animal Cells"
This paper shows a unicellular eukaryote reacting to various neurotransmitters. If the full paper goes into the phylogeny some more it might be interesting:
https://sciprofiles.com/publication/view/0cc41fa28399e0e366d3199c3bcc48eb
"The Phylogenetic Background of Neurotransmitters in the Unicellular Organism Tetrahymena Pyriformis"
This paper's abstract says all I was saying about the development of neurons and synapses relying on pre-existing molecules and structures:
https://pubmed.ncbi.nlm.nih.gov/2830635/
"Evolution of Neurotransmitter Receptor Systems"
What I'm looking for to find how close science is to answering your question (or if it already has) is papers looking at the phylogenetic relationships of different neurotransmitters and related molecules. That might say a lot about which ones have been used as neurotransmitters the longest. I haven't found this yet but I'll try more tomorrow when I'm not on mobile.
ETA: will re-edit this comment later, but this paper answers your question I believe, or as well as any could at present at least:
https://cichlid.biosci.utexas.edu/sites/default/files/evoneuro/files/liebeskind_et_al_2017.pdf?m=1511200627
"Evolution of Animal Neural Systems"
This paper, which is available in full and is a review paper from 2017, looks at the evolution of every aspect of animal neural systems (i.e. nervous systems mediated by neurons, a concept the paper also defines because the line is apparently blurry). One interesting aspect of it is that while you point to Cnidarians as the most "primitive" nervous systems, the paper points out the latest evidence suggests Ctenophores are the earliest branch off the animal tree, meaning nervous systems either evolved convergently, or sponges lost their nervous systems secondarily, in which case Cnidarians would lose this special status.
The paper has a section about neurotransmitters, which says the following:

Several types of molecules are used as neurotransmitters; their evolutionary deployment in different synapse types across animals is fascinating and still poorly understood. Many are used widely in eukaryotes for intercellular communication, but some of the biogenic amines may be present in animals as a result of the late horizontal transfer of synthesis enzymes from bacteria(Iyer et al. 2004). For instance, epinephrine and norepinephrine are important neurotransmitters in vertebrates but not in protostomes (but see Bauknecht & Jekely 2017), whereas the opposite is true of octopamine and tyramine (Figure 4). Cnidarians make a set of neurotransmitters similar to those in vertebrates (Kass-Simon & Pierobon 2007), but Nematostella expresses most nonpeptide types in the endoderm near the pharynx and testes—only peptide transmitters are found in neurons(Oren et al. 2014)
Intriguingly, ctenophores seem to use a much more restricted set, as glutamate is the only well-validated neurotransmitter (Moroz et al. 2014). This is consistent with the theory that neurons arose independently in ctenophores and planulozoans because vertebrates and most protostomes use acetylcholine at the NMJ [neuromuscular junction I assume -my edit]. However, arthropods use glutamate at the NMJ, just as ctenophores do ( Jan & Jan 1976), and cnidarians probably use neuropeptides (Oren et al. 2014). Although sponges do not have true synapses, they use γ-aminobutyric acid (GABA), glutamate, and nitric oxide to coordinate contractions (Elliott & Leys 2010). Trichoplax individuals also lack synapses,but their secretory flask cells label for FMRFamide, suggesting a conserved role in transmission for this peptide class (Smith et al. 2014).

This gives at least a few names of neurotransmitters that are particularly conserved and candidates for neurotransmitters the common ancestor of neurons used (glutamate, acetylcholine; they may have been peptides, whatever that covers), and I think makes it clear that it is very much not known what those first neurotransmitters were.

This is an amazing answer. Thank you.


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Is there a photobleaching-resistant, cell-permeant viability stain in the far red part of the spectrum?
I am looking for a live-cell–impermeable dye for viability. (The cells cannot be permeabilized and fixed in this experiment.)  I would prefer with excitation and emission spectra similar to Cy5, but I can be flexible here as long as the spectra are far away from Hoechst.
I have tried TOPRO3, but it seems to lose its brightness after a few exposures, so I would like something more resistant to photobleaching.

You could try SYTO Orange. Unlike SYTOX, which is a fixed-cell marker, SYTO works with both live and fixed cells.


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Are there any solitary species of ant or termite?
The social insects consist of the ants, the bees, and the termites, which live in colonies rather than living solitary.
But I've heard that there are some species of bee which are solitary and don't live in colonies.
Are there also any species anywhere of either ants or termites which are solitary?

Actually, most bees are solitary and don't live in colonies. In the UK 90% according to https://www.growwilduk.com/content/everything-you-need-know-about-solitary-bees

i.e. bumblebees and burrowing sand bees, bees that build small nests, and vespids that have gall nests.

I do not know of any solitary ants, but there are species that form very small colonies.
One such species is Jerdon's Jumping Ant (Harpegnathos saltator). They usually live in colonies smaller than 100 individuals and workers may reproduce, so the colony can survive after the queen's death.

No solitary ants have been described by scientific journals. If they had, they would be a famous exception, their ecology and survival strategy would be very interesting, to know how they rear their broods. It is mostly nectar and parasitism that makes Hymenoptera broods easy to manage alone.
velvet ants are solitary and resemble ants but they are actually wingless wasps.
Meranoplus primitive old world ants are the most likely to have solitary species, and have simpler clades, i.e. no queen, all workers may lay eggs.
Pristomyrmex punctatus also has no queen.

Carpenter ants are solitary you will see one queen in a house full of termites and other ants that live in colonies
I have spent 35 years remodeling homes infested with termites and ants the carpenter ants which are huge are never seen tohether
The queen finds termites and other smaller types of ants
She will stuff these other ants and termits into a tunnel made by the wood chewers and lay an egg and seal the tunnel
The larva hatches and eats the food left
Pupates and digs its way out of the tunnel it then either gets pregnant or looks for a mate if male
Eating the infesting ants and termites
In 35 years of remodeling and construction with many many homes torn apart i have never seen more then 1 carpenter ants at a time
There are smaller black ants people mistake for the larger cousins but ants that actually tunnel in wood are not carpenter ants
Carpenter ants invade their food's tunnels and feed them to the eggs which they abandon after sealing them into thier egg tunnels which were made by the termites or other ants
Ants are canibals by nature and eat other type of ants
Carpenter are no exception to this rule

There are no solitary termites. All the termitoides are social. You can found some clades that have small colonies like Kalotermitidae, but that is it.


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How does a veggie-less diet affect the human body?
I have some question, which I'm sure would fit better in the fitness section but proper answers should probably come from someone that knows biology.
My question is rather simple. How can a person that doesn't eat any vegetables at all be affected by such a diet? By no vegetables at all, I mean not eating any ever.

You mean something like the Anti-Vegetarian?

I don't know if it has a name. Just a person that doesn't eat any vegetables at all.

Excluding fruit. A noemal diet with fruits but no vegetables.

@ThePlan: well that renders my answer useless...

I would have thought that most nutrients that would be found in vegetables could also be found in fruits somewhere?

Yeah, the Carnivore Diet does have a name.

There is a list of several implications of not eating vegetables (references 1, 2, 3):

Weight gain (by eating fat-rich products);
Malnutrition (not reveiving enough vitamin A, C, D, K, etc);
Digestive problems (low fiber intake leads to digestion disorders, which could lead to health problems);
High risk of heart disease;
High risk of certain cancers.

I also pulled up the nutrition fact sheets for vegetables, fruits, and seafood created by the US Food and Drug Administration.
In order to obtain all the necessary vitamins, one can substitute vegetables for fruits. For example, to obtain 100% of the daily value of vitamin A, one should eat as little as one carrot a day. In order to get the same amount of vitamin A from fruits, one should eat 134g of cantaloupe, or 462g of grapefruit, or 50 large apples a day. Although this could be difficult but possible, the sugar content of the above-mentioned fruits should be taken into account.
Something else which needs to be considered is that vegetables are richer in minerals (iron, potassium, calcium), compared to fruits.
All this in mind, perhaps all minerals and vitamins could be acquired from a source other than vegetables.

FYI: this guy doesn't eat any vegetable: http://robrhinehart.com/?p=298

Weight gain? You can't possibly gain weight if you're consuming an equal amount of calories you're expending. Regardless of what you're eating.

@Memming: Almost all the people who promote meal replacement products are bogus, and so are most of the products. Even the established brands like Nestle make it clear that their meal replacement products are only to be used under guidance from medical professionals and not for long-term. Not eating real food will cause problems in the long run.

You'd be deprived of the vitamins and minerals which are found only in vegetables, but you'd live. There are vitamins and minerals in meat and other foods, plenty of them, and your metabolism would adapt to produce the proteins which are missing. Human body is a wonderful organism.
You wouldn't have a higher risk of cancer because cancer is a byproduct of life (the DNA repair mechanism and programmed cell death) and you can't get it by consuming meat or by not consuming vegetables.
You wouldn't gain weight if you're not consuming too much food. The math is simple, if you need 2000 calories, you'll gain weight if you're consuming 2050 calories of vegetables and lose weight if you're consuming 1950 calories of meat.
Your risk of heart disease wouldn't increase.
The only things which would change in this case would be the ones directly related to the nature of carbohydrates, proteins and fat. The carbohydrates in vegetables release energy slowly over a longer period of time, so if you'd eliminate vegetables you'd possibly be hungry more often. However, fat - and the glucose produced from it - would keep you going.
And you might have digestion problems because of lowered intake of fibers until your metabolism adapts.

Do you have any reference/s to support your claims?

Not saying a pure-carnivore diet is a good idea, but there are no vitamins or minerals that are only found in vegetables (assuming you include organ-meat, etc - the entire animal). There are compounds such as phytonutrients, only in plants, but those aren't vitamins. In fact, it's really the other way around, there are vitamins in meat that are, at best, extremely hard to get from plant-based diets only (no supplements).


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Do human beings have pheromone receptors?
What is the current consensus on whether or not humans have receptors that detect pheromones?
If there are purported receptors, in what anatomical areas are they located?  With what organ systems do they interact?

It would be the vomeronasal organ... I'm no expert in human brain anatomy, but I think there is a bit of a controversy on whether a functional one exists in humans...

I think it is perfume industry that knows the ultimate answer. Although some smells are sexy and attractive, there is no human pheromone as far as I remember reading (and smelling).

From reading popular science articles on the matter, it appears to be vestigal (measurable in careful studies, but swamped by other factors when looking at how it affects the relevant behaviors)

It's my personal hypothesis that pheromone receptors (wherever else they exist) also exist on the sides of the part of the nose directly between the nostrils, as well as in the ears. But I have no proof of that for you!

From what I have gathered, I would think that humans do have receptors that are able to detect pheromones.
For example, some studies that have indicated human responses to pheromones.  Of these pheromone responses, some have been traced to the olfactory mucosa and olfactory epithelium.
The trace amine-associated receptors (TAAR) for which humans have 7 genes (TAAR1, TAAR2, TAAR3, TAAR5, TAAR6, TAAR8, TAAR9) and 2 pseudogenes (TAAR4P, TAAR7P) are found in the olfactory epithelium whereas androstadienone receptors are found in the olfactory mucosa.  As suggested by the anatomical location, these receptors interact with the human sense of smell and the olfactory system
More information: http://en.wikipedia.org/wiki/Pheromone#Humans

Do you know of any specific studies on the matter?

You could take a look at http://www.ncbi.nlm.nih.gov/pubmed/9515961

While the result of the study you cite is compelling, my understanding is that the pheromone(s) and receptor(s) mediating that response have yet to be identified. As such, the jury is still out as to whether the menstrual cycle effect is really due to a pheromone response. Also, although it is true that we have TAARs, they may not be used as pheromone receptors in humans. I do not think that there is a consensus as to whether human pheromones exist.

I think that this is the most accurate information that we currently have available. As this is a science, it can be expected that results will change as new discoveries are made and old discoveries are disproven.
As far as I know, there currently isn't much evidence disproving the theory and at least some that suggests human pheromone existence, so controversy at the moment is more doubt in limited evidence than two contradicting theories

@arcyqwerty: The major evidence against human pheromone reception is that humans anatomically lack the accessory olfactory system (vomeronasal organ, etc.) that is used by other animals to detect pheromones. Is that strong evidence? That's up for debate, but I don't think either side has much stronger evidence. For what it's worth, I am inclined to believe that there are human pheromones. But that is bald opinion. The question asked for current consensus, and I stand by the statement that there is none.

Wondering if that simply boils down to the sensation of smell. So that pheromones smell good/bad (in the case of bad genetic compatibility).

This article details how man can smell ovulation thanks to testosterone: https://journals.sagepub.com/doi/full/10.1177/0956797609357733 It is also one of the base papers for one of the answers here.

Well... I'm excited that my first contribution to this site will include a study of strippers!
http://whywereason.wordpress.com/2011/06/29/menstruation-attraction-why-females-shouldnt-flirt-while-menstruating-and-why-bears-can-smell-the-menstruation/
I have read other, more detailed analysis of this (and similar) research that suggests strongly that our noses are heavily involved in all sorts of entirely sub-conscious decision making, as it pertains specifically to sexual selection.

A blind test of tshirt scents alledged that people prefer tshirts with complementing immune systems for reproduction.


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Is it purely the nervous system causing vaginal lubrication (arousal)?
My girlfriend was watching some documentary on TLC about a paralyzed woman getting pregnant. I believe that woman still has some feeling, as she spoke about feeling the effects of a bladder inflamation. So supposedly, her brain could fire up her vagina to get ready for sex (in the sense that it gets lubricated and the labia get swollen).
But suppose a woman is paralyzed so they have no nervous connection from the brain to the vagina (or vice versa). Could she still be aroused in the sense of swollen labia, etc? (Presumably via some hormonal system?)

There is a good open access review about the effects of different hormones on sexual arousal. In most instances, the hormone is acting on the brain, which signals the information to gonads and genitals via nerves (i.e., the hypothalamic-pituitary-gonadal axis). However, in a study in which I have participated, we found a more direct and probably ancient signaling pathway where the mouse liver, in response to protein intake, was sending a permissive signal to the uterus for reproduction. Whether this holds true for vagina lubrication was not investigated, but I would be optimistic that mechanisms other than nerve communication could play some roles.


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What makes humans omnivores, and not herbivores?
Some vegans claim that humans are herbivores, not omnivores, and that we are not physiologically designed to eat meat (see here: http://www.peta.org/living/food/natural-human-diet/).

"According to biologists and anthropologists who study our anatomy and our evolutionary history, humans are herbivores who are not well suited to eating meat. Humans lack both the physical characteristics of carnivores and the instinct that drives them to kill animals and devour their raw carcasses.
  Although many humans choose to eat a wide variety of plant and animal foods, earning us the dubious title of “omnivore,” we’re anatomically herbivorous."

They go onto claim that we don't have tiger claws and teeth for catching and eating meat, that our jaws and teeth are designed for grinding plants not meat, that our stomach acid is too week to break down meat, that our intestinal tract is long like a herbivore for digesting plants and that it takes so long for meat to pass through that it rots and poisons us causing cancer, that we lack a hunting drive, that meat with it's cholesterol and protein is the cause of all disease so obviously its poison that we are not supposed to eat, that we get food poisoning from meat (like that never happens with vegetables...) and that the only reason humans started eating meat was to survive in times when there was a lack of plant foods available but according to our anatomy it's clear we're actually herbivores not designed for eating meat.
Can this be debunked?

Not an anthropologist myself, but a quick web search turned up this  https://www.vrg.org/nutshell/omni.htm  which seems credible, although it does lack references.

Look at our teeth - our front teeth are the teeth of a carnivore. Compare that to the teeth (or lack thereof) of horses, sheep, cattle, etc.

"Debunk this nonsense" sounds like a cognitive bias. But that's just my opinion

Although we are omnivores (as most of the answers below explain), the main problem is the amount of meat that we consume. There is a very good chance that in the beginning of our species history, we didn't have access to so much meat. So, I would say that we need a better balance and we are naturally more herbivores than carnivores. And if you check the diet of people 100 years ago, meat was more the exception, rather than the rule.

@BioGeo: The other half of this is a sedentary lifestyle, which doesn't consume the extra calories & fats of meat.

The fundamental (no pun intended) problem here seems to be the idea that human are "designed".  We evolve, and we do that by exploiting new environmental niches.  The "eat meat when you can catch it" niche seems to be one that our ancestors moved into before they split off from the chimpanzee lineage.  A more recent example of such evolution would be the preservation of lactose tolerance into adulthood among humans whose ancestors were herders.

Just a note: PETA is a highly ideologically-charged organization that is in no way an expert on scientific facts. I would take absolutely anything they, or similar agenda-focused organizations, say with a grain of salt. Remember, not everything you read on the internet is based on facts ... -_-

Also, both "canine teeth" and the entire state of West Virginia (or, for non Americans, every rural town or village in the world that sustains a large population of game hunters) are pretty good evidence against the "facts" that PETA provides in this link.

@theforestecologist: Anecdotal evidence at most ... There is nothing to really debunk in the PETA statement. It's just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans wouldn't have evolved a really big brain without consuming animal products (which I hear over and over again, even in anthropological sciences). So far we just don't know, though it seems like human groups changed diet from vegan to omnivorous - never carnivorous for sure - and back quite frequently and opportunistically. I will give a more detailed answer in a few days.

@AlexDeLarge: I think the key there is "opportunistically".  If I would eat meat if I could get it, but  eat a vegetarian diet because "some other bugger pinches the pig", does that make me an herbivore, or just a deprived omnivore?

It is worth noting chimps also hunt and eat meat. https://www.nationalgeographic.com/science/2007/02/chimps-use-spears-to-hunt-mammals-study-says/

Recently became vegetarian, and I wanted to correct some things that I've read here. Humans by definition are omnivores, because we can eat meat. "Chimps eat meat" is a claim I've read. Great. Do you know how much meat chimps eat? 7 days out of the year chimps will eat meat, other than that they're eating fruits and veggies. So 99% of the time most omnivores are NOT eating meat.

"omnivores have canine teeth, just like us humans" - their canine teeth is drastically different than ours. And I wouldn't hold up America, especially rural America, as any bastion of good health.

As the answers given already point out, humans are generally considered omnivores that are able to use food sources available to them opportunistically. Apart from that, there actually is not much to debunk in the PETA statement - it is just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans would not have evolved a really big brain without consuming animal products. Especially the canine teeth cannot be seen as evidence for prehistoric hunting, as in great apes the size of canine teeth is ridiculously well explained not only by defensive but mostly by mating behaviour; apart from that, humans do not even have those, and that most likely is caused by the trend towards monogamy which reduces inter-male aggression.
However, coming back to the actual question, in the relative short history (approx. 200-300ky) of our species there is evidence for 'several transitions towards or away from a vegetarian diet in humans' (Nielsen et al., 2017).
And in fact, there even is a human-specific evolutionary derived haplotype (younger than the Human-Neandertal split) that shows signatures of positive selection and is associated with increased efficiency in the synthesis of long chain fatty acid from plant precursor molecules - which would not really be necessary for meat eaters, as these fatty acids are readily available in animal products (Ameur et al., 2012). More specifically, the genes lying on that haplotype belong to the FADS cluster that seemed to have had adaptive value - also for synthesising long chain fatty acids from medium chain plant precursor fatty acids - in some African populations even more recently (approx. 85 kya, Mathias et al. 2012).
This finding has been supported by a more recent study by Kothapalli et al. (2016). They investigated a 22bp-indel allele in the FADS2 gene that is associated with both higher blood levels of long chain fatty acids and exhibits high frequency (signature of positive selection) in some populations in South Asia and Africa for which they claim a long tradition for plant-based diet.

Conclusion:
Modern humans (and this is relevant, as diet varies strongly between species and therefore the species comparison does not need to be very informative) appear to have changed diet frequently but there even is evidence for human-specific molecular adaptations towards plant-based diets.

There are several claims in this that could use sourcing, like that eating meat was instrumental in human evolution is one sided, your links only confirm this view.

But you also show some adaptations AWAY from a plant based diet, so your own evidence does not support your conclusion. Also I would like to see support for your claim that South Asia and Africa have a long tradition of plant based diets, any claim about native African populations a a whole is immediately suspect.

@John: 1) My conclusion is that there appear to have been many transitions away from or towards a more meat/plant-based diet in modern humans, and I think the evidence presented shows both directions, thus supporting the conclusion. I explicitly mention evidence for only one of these transitions because of the phrasing in the OP; it was asked to debunk the claim that humans are herbivores but humans show adaptions expected in herbivores. I would have phrased it the other way around if the OP had asked to debunk the claim that humans are carnivores.

@John 2) The statement about a long tradition of plant-based diets in South Asia and Africa is taken from the Kothapalli et al. (2016) paper, it's not mine. I agree that this is definitely not a true statement for all modern human populations in South Asia and Africa and therefore edited the post to make that more clear (i.e. tone down the statement). I agree that statements about an African (meta-)population as a whole is definitely suspect and that is not what I meant. I was talking about some modern human populations in Africa and South Asia, not all of them.

The simple answer is humans are omnivores – physiologically – because we have the capability to digest both plant and animal matter. Many humans are behavioural omnivores as well, consuming both as part of their diet, although many people can and do live while consuming only plant products.
Most if not all humans can or could digest animal products in some form - a brief search doesn't bring up any counterexamples of people who cannot physiologically do this (in the same way that many people cannot digest milk well in adulthood as they are lactose intolerant). Even if some people do not have this capability, they would be exceptional and broadly speaking you could describe humans as omnivorous, at least physiologically.
The Wikipedia page for omnivore is a good starting point if you want to know more about consumption classifications.

What about B12 deficiency and anemia risk in vegans, isn't that a clear indication humans are not designed as herbivores? Vegans have to take supplements, which is a modern invention, without supplements and fortified foods vegans risk serious deficiencies which can prove fatal if untreated from a lack of animal products in their diet. We can't get sufficient b12 from plants but herbivores can because their  digestive system works differently, right? Can you explain about that please if you can?

Furthermore, fossil record shows humans have been eating meat in the last milions of years.

B12 is only sourced from dirt. Whether you are getting it from a supplement or animal meat - the source of that vitamin was found in the dirt. Humans used to get it from the dirt off fruits, veggies, etc. Now? Every bit of b12 you get comes from supplements. Even the animal meat you consume, the b12 you get from them was supplemented to them

Deer, generally considered herbivores, also have the capability to digest animal matter. https://academic.oup.com/jmammal/article/68/1/195/1041038

There are several lines of evidence.

Behavior, we regularly eat meat.

This is the one that matters most, omnivore is a behavioral classification. All humans societies eat meat, a few eat little else or nothing else. The fact that a small subset of well off people in developed countries don't does not change this. Our two closest relatives also eat meat and many of our ancestral species show direct signs of eating meat.

Gall bladders.

One somewhat useful piece of evidence is humans have well developed large gall bladders. Gall bladders function to store bile, a large one functions to be able to break down large quantities of fatty foods eaten all at once, which really only occurs in carnivores, omnivores. (there is also a weird thing ruminants do, but we are not ruminants so it can be ignored)

Dentition

Our dentition is that of an omnivore, Its not specialized for a meat or plant diet. As an example gorilla show signs of specializing in a plant diet. Our detention however does show specialization for eating cooked food. Which we do to both meat and plant products.

Digestion

We havelarger powerful livers able to breakdown toxins better than many related animals, We are also more sensitive to the smell of rot. Some have argued this is a sign of being a scavenger but this is more likely another adaptation to eating cooked food, the toxins we are best a breaking down are those that come from cooking meats and plants.
Humans are also better to digesting iron from animal sources than plant sources, and show adaptations towards this.  We also show adaptations for digesting some plant materials better supporting an omnivorous line of adaptations.
Humans lack any of the specialized gut features seen is exclusive herbivores, we have no way to breakdown cellulose nor a structure to house bacteria that could do it for us, that means you could classify us as a frugivore at best if trying to argue for herbivory. Our gut length is what is expected form an omnivore, longer than a carnivore shorter than an herbivore.

B-12

We can't make vitamin B-12. Humans and all our other great ape relatives get b-12 from eating animals.
Now some people argue humans should be classified as cucinivores (a unique classification) as well as omnivores, becasue we are specialized for eating cooked food.

We are not herbivorous because our digestive system is too short. Humans do not have many of the features required to digest plant matter efficiently. We do not have a multi chamber stomach like ruminants have. We do not have an enlarged cecum like rabbits
In fact, the human gut as a percentage of body mass is half that of a chimpanzee, (10% vs 20%). Also the composition of that gut is different, 50-60% are small intestine in human vs 20% in chimp. The human colon is also reduced: 17-23% in human, vs 52-54% in chimp.
http://www.beyondveg.com/billings-t/comp-anat/comp-anat-6c.shtml
Also gorillas, which are more herbivorous than humans, have cecum (7% of the Gut volume compared to 0% in humans.) http://huntgatherlove.com/content/human-colon-evolution-part-1-comparative-anatomy
If anything, the argument that the human gastrointestinal system is long like a herbivore's is false. It is short and reduced, and does not have the right components to ferment plant matter. However, it is longer than an obligate carnivore.
As a species, human are an ape (a fruit eating animal) that has started to evolve to eat meat. It is an intermediate species so to speak, it still doesn't digest meat well. It has many features of its fruit eating ancestor, but has already taken step to eating meat, while having lost features (like large gut size and big colon) that digest plant matter more efficiently.
Put a child on a vegan diet and the kid might die from B12 deficiency, insufficient calories, and lack of fatty acids.

Some apes eat meat as well, chimps f.e.

That is true. Estimated that Chimps obtain 6% of its calories from meat. Gorilla are more herbivorous and have larger percentage of their gut  devoted to a cecum (7% in Gorilla, 5% in Chimp and N/A in humans). http://huntgatherlove.com/content/human-colon-evolution-part-1-comparative-anatomy

I think when you say humans "digest plant matter efficiently", you are perhaps over-simplifying.  Humans seem to digest many fruits, seeds, and vegetables quite well.  We just don't have the extra machinery to digest things high in cellulose, as grazers do.  So like many other species, including some (like wolves/dogs) that are popularly supposed to be carnivores, we eat both.  Though some human groups, e.g. the Inuit, have traditionally lived on an almost exclusively animal diet.

I don't think you realize that those added machinery is required. The vegetable and fruits that we eat today are no way similar to the non domesticated versions of the same plants. It is like saying bananas are very easy to eat... only problem being the wild version of bananas are small, gummy sappy, full of large hard seeds.. and really only edible by straining out the seed and cooking the resulting pulp. The plants we are familiar today are the product of thousands of years of domestication. wheat is the product of nearly 12000 yrs of selective breeding.

@JayCkat: But there are many fruits, nuts, and vegetables that have not been subjected to that 12K years of selective breeding (and which aren't sold commercially in any large quantity), yet which sustained native populations.  Hereabouts there are pine nuts, cattail roots & pollen, camassia bulbs, elderberries, wild blackberries, and much more, all of which I eat on occasion.

Elderberry, black berries has been domesticated. Camassia bulbs show signs of domestication. The cattail... I can't find info about domestication of this plant. But it has been harvested for human consumption for over 30,000 years. I cannot imagine a plant being so heavily used not be artificially selected. Just because a plant is not commercially sold at the super market does not mean it is not domesticated.

Gut anatomy is the most swift and convincing argument that humans are not evolved to be strict herbivores. Since the OP mentioned it, there's an interesting discussion here on the evolution of stomach acidity.

Humans benefit from a plant based diet. The B12 argument is only valid at face value as domesticated animals that are raised to be slaughtered are given B12 supplements as they would to obtain enough of it through a "natural" diet. B12 is found in bacteria in the soil so washing vegetables and removing the dirt is also removing the B12. Animal products are high in saturated fats which is the main contributor to atherosclerosis and therefore heart disease which kills millions of people around the world each year. True ominovores do not have the ability to develop atherosclerosis.
 The argument that humans had always eaten animal products renders us complete omnivores is downright wrong as eating something for survival is completely different than eating for optimal health. Our ancestors had no concept of biochemistry or the effects food has on the cellular level of our body. Our ancestors also usually died at rather young ages of nutritional deficiencies.
It is not difficult to obtain protein, fatty acids, or calories for that matter as many nuts, beans, seeds, and legumes are high in unsaturated fats and flax seeds them selves are a better source of Omega 3s than fish. Lentils, dark beans especially are high in iron and, and virtually every food has some sort of minor iron content and vegans have an infinitesimal chance of becoming anemic compared to an omnivorous diet or a vegetarian who consumes dairy. Dairy products are known to hinder iron absorption.
Animal products also raise levels of a hormone called Insulin like Growth Factor 1 or IGF1. IGF1 is known to cause insulin resistance, promote cancer cell growth and release free radicals throughout the body.
The argument of what we are is really a nonsensical argument as it does not matter what the label is as opposed to what kind of diet we can optimally benefit from in the long term.

Welcome to Biology.SE. Please take a look at what is considered a good answer on this site. Some of your statements might be challenged, so please provide reference to any claims you make. Thanks!

This posting contains lots of wild claims - please add serious references for them.

B12 deficiency in livestock is due to cobalt deficiency, these animals can manufacture their own B12 ( well the bacteria in their complex gut can), they lack cobalt mostly due to human agricultural methods which prevents animals from wandering and eating a more diverse diet. Humans can't get B12 by this method. Also the nutrient content of modern crops is meaningless for our evolutionary history, since they are highly modified compared to their ancestors, more importantly most of them don't occur where humans evolved so mentioning them is pointless.

You didn't explain how Cobalt deficiency leads animals to be b12 deficient. You also didn't explain how they'd get more Cobalt if they had a more diverse diet. Humans get b12 the same way animals get b12. Bacteria in dirt.

@JustinBeagley if you want a full breakdown ask it as a question but a good summation can be found here.  https://www.agric.wa.gov.au/livestock-biosecurity/cobalt-deficiency-sheep-and-cattle. And you are wrong ruminants GUT bacteria manufacture their B12.

It is physiologically possible for a human to be an omnivore, carnivore or herbivore. It's not what we are, but what we can be or what we want to be.
Strictly speaking, it seems that humans can not be strict herbivores, because natural plant foods do not contain enough of the essential nutrient vitamin B12 and they are vegan/vegetarian websites that tell you that (Vegan Health, Vegetarian Nutrition Dietetic Practice Group).


text:
What flying insect is this? Resembles Wasp / Crane Fly / Moth?
What insect is this?
Found this in southern Bangalore, India. Looked dangerous, flew really slowly with its body upright and legs spread out and landed on a wall.
Size: about 1.5 inches tall, 1.5 inches wide, when spread.
These photos are zoomed in and rather dull colored, but the actual color was a bright orange, like #FF9050 and dark black.

The long legs suggest one of the crane fly families (Tipulidae, Cylindrotomidae, Pediciidae, Limoniidae, Tanyderidae most likely; Ptychopteridae and Trichoceridae less so); the pointed abdomen tells me your subject was female.  The patterned wings might make identification a little easeir--if India has a version of bugguide.net, that would be your next stop.

@ArthurJFrost: Thanks, you pointed me the right way. I dug it up. See my posted answer! Cheers!

Pselliophora laeta, a species of crane fly (Tipulidae) in the Ctenophorinae subfamily.
Route to discovery: Reverse image searching my own photo on Google led me to a matching image on Naturalista (Familia Tipulidae), and in-turn to iNaturalist, which showed me to Genus Dictenidia. Further Googling for "Genus Dictenidia" brought up many families of crane-fly, which I visually scanned until I spotted it -- Pselliophora! That led to Wikipedia, and to this image, which mentions its source to be whatsthatbug, where the discussion cites Pselliophora laeta on India Nature Watch.
--

Source: https://www.inaturalist.org/observations/299363
Observed: Thiruvananthapuram, India; Jul 28, 2012 5:13 PM IST
Mating Crane Flies from India

Source: https://www.whatsthatbug.com/2010/09/30/mating-crane-flies-from-india/
Observed: Mumbai, India; Sep 30, 2010 1:43 AM IST


text:
Is it possible to lose synapses over time?
I mean, what if a person is for a long time submitted to conditions in which his mental capacities are not explored, are the synapses undone? I've heard that drugs may cause such an effect, but what if the person is not submitted to drugs or any severe accident, may the forgetfulness be related to the simple lack of usage of a certain knowledge?
Is the lack of brain usage the main cause for Alzheimer's?

Regarding your question about losing synapses; yes, synapses are regularly lost in a process called Synaptic Pruning. From the Wikipedia article:

A decrease in synapses is seen after adolescence reflecting synaptic pruning, and approximately 50% of neurons during development do not survive until adulthood. Pruning is influenced by environmental factors and is widely thought to represent learning.

Synaptic pruning is most significant during development due to "excessive" Neurogenesis that creates a large number of neurons, many of which will later be pruned. It's not excessive in a bad way, it's simply the case that more neurons are generated than necessary and thus pruning is needed to keep the connections efficient. There's no "measure twice, cut once", instead pruning is used to refine connections.
Synaptic Pruning really doesn't have anything to do with forgetting; Forgetting is natural and simply happens because connections (via Recall/Rehersal) are not made strongly enough to fully encode memories into Long Term Memory.
Note that Synaptic Pruning is not the cause for Alzheimer's or other age related degenerative disorders. From Wikipedia again:

Synaptic pruning is classified separately from the regressive events seen during older ages. While developmental pruning is experience dependent, the deteriorating connections that are synonymous with old age are not. The stereotyped pruning can be related to the chiseling and molding of stone into a statue. Once the statue is complete, the weather will begin to erode the statue and this represents the experience independent deletion of connections.

Synaptic Pruning is a normal process of development and occurs in all individuals. Alzheimer's is a very visible disorder due to media focus, but not part of normal developmental/aging effects.
Instead I suggest you read more specifically about Alzheimer's disease, there's quite a bit of information on it.

+1 for a correct explanation of the fact that not only it does happen, but it is a physiological process!

This answer was very useful and instructive for me! I appreciate you so much by that!


text:
How to compare SNP from genotyping results for multiple people with a known phenotype?
I'm looking at different genotyping profiles available at opensnp.org and am trying to compare profiles for people with different phenotypes.
For example, given 10 profiles of people who can roll their tongue and those who cannot, I am trying to identify what is different between these people and what's similar.
A typical record is in this format:
Rsid, chromosome, Position on chromosome, actual 2 letter mutation

How can such records be compared to identify similarities for a given phenotype? Does RSID uniquely identify a mutation, or is it a combination of rsid and position?
In other words, if one user has rsid 123 at position 555 and another one has rsid 123 at position 666, and the mutation is the same, is this a similarity, or does position matter?

Each rsid identifies a unique SNP in the genome. Thus there should not be any entry in the files that have the same rsid but different chromosomes and/or positions. If you do find this, it is likely that you have data from different versions of the assembled genomes.
To find genetic variants associated, i.e. correlated, with your trait, you need to focus on the genotype at each of the SNPs. For example, SNP rs3094315 is an A/G polymorphism, i.e. an individual can either have the genotype AA, AG, or GG. To find if it is associated with tongue rolling, you would count the number of AA, AG, and GG individuals (alternatively you could sum the number of A and G alleles) in the group that can roll their tongue and compare those numbers to the group that cannot. You would then repeat this for each SNP that you want to test. For most SNPs, there will be no difference in proportion.
That being said, this is not a modest undertaking as this a cornerstone of human and statistical genetics. There are many issues that could strongly bias your results (e.g. population stratification, genotyping error, linkage disequilibrium, multiple testing). To learn more, you can read about the Cochrane-Armitage Trend Test and the PLINK software. If you are really serious I recommend Applied Statistical Genetics with R by Andrea S. Foulkes.


text:
What kinds of arousal can a human brain experience?
I've been reading about the new phenomenon called "arousal addiction". The context in which this term is used is Internet, Porn and/or video game addiction(cummulatively Internet Addiction Disorder - IAD). Dopamine and Dopamine receptor D2 are sometimes mentioned, as being affected by exposure to a new, novel stimuli.
I'm interested if there are other forms of "arousal" that may involve more than just Dopamine. For example, I know that there are 4 neuromodulators in the human brain:

Dopamine
Serotonin
Choline
Noradrenaline

For example, if a person likes horror movies to the point of addiction, is it Dopamine, or is it Noradrenaline that the person enjoys? If a person is addicted to comfort foods, is it Dopamine or Serotonin?
Thank you!

Depends on what you mean by "addiction": defined, addiction usually requires both psychological and physiological dependence, but conversationally we sometimes only talk about psychological dependence (as in here, your muscles won't cramp up if you NEED a horror flick).
If a person enjoys horror movies, is it the suspense? Such a rush is caused by the well-known fight-or-flight catecholamine epinephrine (also known as adrenaline). This is the short-term stress response at play. Comfort foods are a whole other story, because it depends on the food as well. Carbohydrates can contribute to serotonin levels, yes, but I read a super-interesting study a couple years back about saturated fat causing a decrease in corticosteroid levels and this sought to explain why people eat fatty foods when they are stressed (I'll try to find this article for you). Tryptophan, an amino acid, is converted to serotonin, which is why turkey, milk, and other sources of trp can make one sleepy.
Awesome question! I'm going to try to learn more about this and find that article for you. Dopamine is the primary player in most conventional addiction-talk, as it's crucial to the reward circuitry that is usually discussed.

Thanks! The way I can clarify the question is - exposure to a new arousing stimuli (ex: new sexy female) stimulates release of dopamine in response to the stimuli. I'm interested if there are other neuromodulators that are elevated or lowered in response to stimuli.