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Should I design a primer to detect virus based on NCBI genebank?
When I searched HIV on NCBI gene bank, I found 2 results from 1997: http://www.ncbi.nlm.nih.gov/genome/?term=HIV. HIV can change every day, so I think the sequence from 1997 is not useful. Is it?

Please give some more information on what you are trying to do.

I'm trying to design a primer to detect HIV so i need an up to date sequence of HIV. But the one in NCBI Genebank is from 1997 and i think it's not useful anymore.

My impression from your questions is that you're doing DIY biology and are not in a corporate or academic lab. I'd very strongly suggest you to avoid doing anything with potentially HIV-infected material, handling this requires at least a biosafety level 2 laboratory. Handling HIV without proper precautions and permits could result in infecting yourself and potentially a lot of legal trouble or even criminal charges.

Hello, thank you so much for your advised. However, i just give an example. May be i will try on other virus/bacterial , should i using the sequence from NCBI to design primer when it's not up to date ? Any other database better than NCBI ?

@ĐứcUltraSoft you can look at highly conserved sequences in viral/bacterial genome. But as told in the other comment, don't work with pathogenic microbes.

@WYSIWYG If i have more result, like 1998, 1999, 2000 ... i can compare them and know which is the highly conserved sequences. However, how i know which is the highly conserved sequences when i have only 1 result from 1997 ?

you can.. certain regions of important viral genes such as reverse-transcriptase and Nef are conserved

@ĐứcUltraSoft Try searching Google Scholar or a similar engine for "conserved sequence HIV".

Any other database better than NCBI ?

A lot of people overlook some sub-databases inside NCBI and search the main nucleotide database only.
If You never tried it, you can blast the HIV sequence which You have found, against other databases. On the ncbi blast webpage, just choose the options other than nucleotide collection (nr/nt). I tend to find new sequences in Expressed sequence tags (EST), Genomic survey sequences (GSS) or Whole genome shotgun contigs (WGS). Some of these databases cover unfinished sequencing project and should be a source of new data.
(I am a plant person, not virus person, so maybe you will find out, that different databases are worth searching for you. Or you will find it a waste of time.)
BTW, now some time had passed since your question. How did you solve Your HIV sequence problem ?


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Valves in the heart
I am confused regarding the presence of valves in the superior vena cava.
The superior vena cava does not possess valves unlike inferior vena cava, which possesses Eustachian Valve.
Then where are Haversian valves present?
Aren't they present at the opening of caval i.e., superior vena cava.
Then why is it said that there is absence of valves in superior vena cava?

The purpose of valves is to maintain blood pressure against gravity until it reaches the heart. The Superior Vena Cava (SVC) inlets exist above the heart, and any valves would only prevent gravity from helping bloodflow. The Tricuspid prevents blood from the SVC from just directly flowing into the Right Ventricle.
As a note: The Eustachian Valve either isn't present, or is very small in most individuals as it's only used during development.
Haversian Valves are also found in development, if I remember correctly, and exist when the two vena cavas have yet to separate and mediate bloodflow into the Right Auricle.

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Iron metabolism in the brain
I did an expression profiling from publicly available RNAseq data for mouse tissues. While for liver and testes I am getting expected proteins in the top highly expressed mRNAs, for brain I am getting ferritin (Ferritin heavy chain 1: Fth1) as the top expressed mRNA!
There are a few studies which report elevated ferritin and iron in neurodegenerative diseases while some others have implicated its role in ageing.
I haven't come across any study on iron metabolism in the normal brain. Does iron metabolism play an important role in the function of the brain?
PS :

The data that I am talking about, has the SRA accession number- SRR652247 (I tried all three runs submitted in SRA)
The mice used in the experiment were 11 weeks old
I used bowtie -> eXpress for quantification of RNAseq reads.

Look at the study summary - it describes expression profiling in testis. Do you think they might have mis-labeled the organ?

I don't think so.. because testes sample has high level of protamine expression which is not there in brain. Also, the highest expressed transcript (all RNAs) in brain is Bc1 - a ncRNA known to regulate translation at synapses.

As usual, association of NDD or age with Fe does not mean it's the causative agent, nor vice versa.

Many articles focus on the pro-oxidant function of iron (and globins in particular). It makes sense that levels may be higher in the CNS due to their role in respiration, which is increased secondary to the “absolute requirement” for glucose facilitated by constitutive GLUT3 expression. So perhaps ferritin is increased to maintain supply for neuroglobin synthesis?
Another thing to consider, Ferroportin1 (FPN1) (iron export protein) is expressed at relatively low levels in the brain when compared to i.a. bone marrow (HPA 2018). You could hypothesise that increased storage is required as a result of decreased transport. But I would look at expression of import proteins; TFR, DMT1, and ZIP 8/14, as that could very quickly throw this theory off.
References:
The Human Protein Atlas (HPA) 2018, SLC40A1, The Human Protein Atlas, 11 September 2018, www.proteinatlas.org

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Reasons why people say that AIDS/HIV doesn't exist
It's been recurrent when I hear people saying that AIDS doesn't exist. When I ask why, they give weird reasons like HIV is a virus created to control economy and to develop medicine, etc. Also when I try to watch videos on youtube about people that are infected with this virus, I see a lot of comments saying that AIDS is a lie and some of them base their opinions on a documentary called House of Numbers. So I would like to know scientific reasons if this a myth, or why this is true.

Ultimately I suspect that those people are just terrified of getting HIV, so they invent or accept these conspiracy theories in order to not lose the one thing in their lives that can make them happy. There's nothing scientific about it.

Well, the fact that there is an ENORMOUS amount of scientific evidence in favour of the fact that HIV is the pathogenic agent causing AIDS and that there is zero proof of the contrary seems to be a good starting point... Anyway this has been discussed here: http://skeptics.stackexchange.com/questions/10435/is-hiv-the-cause-of-aids Now, the reasons why a restrict amount of (delusional) people say the contrary are probably that they do not really understand how immunology works, but feel like they should have a say on it anyway.

@nico - despite people's efforts to the contrary, science is not a democracy (see the global warming "debate"). Just because a lot of people have an opinion doesn't mean it's right, or even deserves to be seriously discussed...

@MattDMo: I am not speaking of opinions. I am speaking of a large amount of scientific literature. Surely, in science you can never say something is true, but the current body of knowledge (see the large amount of refs in the Skeptics.SE link or this NIAID page) is in support of the current theory. So, until proof of conspiracy arise, or until a better explanation of the current experimental data is found, we can say HIV causes AIDS.

@nico - I completely agree with you - I was more speaking to the OP's mention of "opinions"

@MattDMo: oh, sorry, I didn't notice you were referring to that :)

I think no one can really deny the existence of HIV or AIDS, just a search on google scholar will show >1,500,000 hits for each of those terms, and ask (hopefully any) doctor and they will say it does, though AIDS denialists do debate whether HIV causes AIDS. This paper explains the process of HIV causing AIDS. Further, AIDS denialists have not offered up well supported alternatives as to how AIDS arises without HIV being involved.
I think however that there is more debate fuelled by conspiracy theorists as to how the disease came about. This article from TIME magazine on conspiracy theories is a short piece about it, there are two main conspiracy theories:
1) The west invented the disease to "decimate the African population."
2) The US government invented the disease in the 70's and injected gay men to stop the spread of homosexuality.
You should read this section on the critical response to the film House of Numbers, it seems to be thought that the film was driven by funding wishing to promote conspiracy theory and interviews were edited in such a way as to help portray that message.
Caution, the following is my own personal opinion ;)

To most these seem like pretty outlandish claims and most people do ignore them - apart from anything, placing blame on someone won't stop the continuing spread of this horrendously devastating disease so the conspiracies are quite pointless. I personally think these conspiracies are driven by the uneducated, the scared, and those who want to "bring down the man & corporate/capitalist western society led by a powerful minority" etc..

Back to the science: The people who discovered the disease (Dr. Robert Gallo of the National Cancer Institute and Dr. Luc Montagnier of the Pasteur Institute in Paris) along with the majority of the scientific community say:

"the virus jumped from monkeys to humans some time during the 1930s"

Molecular analysis of the genetic sequence for the virus supports the theory that the jump from apes to humans was around 1920-1930. Some other studies support the jump being made around this time though some estimate it to be a little earlier, this is due to estimated rates of mutation being used to calibrate molecular clocks.
I recommend taking a look at AIDStruth.org and more specifically start with this page (thanks for the link @MattDMo) if you have watched House of Numbers.

I seem to recall hearing recently that the jump could have been as early as the late 1800s, I just wish I could remember where. Knowing my viewing/listening habits, it was probably NPR/PBS...

@MattDMo There are a few papers which show it generally to be around the late 1800's-early 1900's. The uncertainty comes from the model used I believe, to do with rates of mutation and calibration of the molecular clock.

OK, thanks, I'll look into it further. BTW, you might want to link to this page on aidstruth.org which specifically refutes "House of Numbers" and many of the denialist claims it makes.

@GriffinEvo Thank you so much for all the references and the information. I've never been interested in biology at all but now these sort of "existencial" questions arise quite often in my head. In the overall I can deduce then that people is being mislead and confused for some reason. In my case, as an ordinary person, meaning I have almost no information about these sort of things, this documentary makes me feel totally confused and sad about manipulation of science, the government and the economical system in general.

Unfortunately there are definitely people who can deny it and believe it wholeheartedly.  Christine Maggiore is a good example.  She had AIDS, transmitted it to her infant daughter via breastfeeding, refused proper treatment for her daughter (which led to the daughter's death) then refused proper treatment for herself, ultimately leading to her own death.  It's sad, but there genuinely are people who absolutely believe that HIV/AIDS isn't real.

I'm not sure if I should be posting this as an answer, but I think a very approachable and accurate account of the history of HIV can be found from Dinis de Sousa et al..  I agree with what has been posted above.  On the theory that a picture is worth a thousands words, you might also introduce skeptics to the cryo-electron microscopy images of the virus (searching cryo-EM HIV will pull up plenty).
That said, hard skeptics would likely want discount the thousands of publications, studies, and plain old researchers who have studied the virus (myself included).
Also, for the record, viruses that are "created" by humans artificially in a lab do exist, practically by definition.  I, and a great many others, make viruses with markers that make them easier to measure or see (such as fluorescent proteins).  But given the time that HIV entered humanity, it seems highly unlikely that anyone had the technology, let alone the will, to engineer the virus as a bioweapon.  Certainly SIV predates HIV, but the technology to make such modifications (or even of the basic players and genetics) to make a recombinant/chimeric virus simply didn't exist.
It is the unfortunate truth that viruses have been used as weapons of terror and warfare against various populations (I could get into examples but that seems off topic).  But the historical examples we have of this are all surrounding existing viruses.
To the question of people made to make money (not withstanding all of the above), it is certainly not for lack of trying that we don't have an vaccine for HIV.  There are a lot of complications (extremely rapid mutation and escape mutants, reservoirs of virus, direct infection of cells from your immune system, etc etc).  And it shouldn't be seen as though HIV is the long lasting human virus we need a vaccine for (Herpes and RSV just two good examples).  You would stand to make a lot of money if you could successfully make a vaccine to any of the pathogens.  And a LOT of people are trying.  The US government alone is spending a lot of money on HIV/AIDS.  Having a successful vaccine could actually SAVE a good deal of money.


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Do apes and humans share 99% of DNA or 99% of genes? What is the difference?
I made an answer on the Scifi.SE that can be read here. It is about how the characters in the story Jurassic Park might have gotten DNA for all the species shown.
In my answer, I said this:

Apes and Humans, for example, share over 99% of their genes. That means the difference between our species is less than 1% of our genes. In fact, all life on Earth shares about 50% of it's genes.

but in the original posting (before someone edited it) I chose to use the word DNA instead of genes.
He left this comment in the section to explain the edit:

Sorry, I'm a biologist, I can't help it. Humans and apes share 99% similarity in the coding sequences of their DNA, the ~5% that codes for genes, not on all the DNA. I simplified this to genes for the answer.

I have a basic high school understanding of DNA and genes, so I'm afraid I fail to see the difference between using "DNA" or using "genes" in my statement. I understand that genes are specific sequences of DNA that are used by the cell in some way. I understand that DNA is more generic, including all of the strands, whether they are used or not, whether they seem to code for something or not.
So is it wrong then to say that apes and humans share 99% of their DNA or is it equally correct to say "genes"?

I generally trust what @terdon says, he's quite a well-rounded person. That being said, I would be a bit more pedantic and say that apes and humans share over 99% of the coding sequences (or DNA) in our genes, right in the answer, but that's just me. It is technically incorrect to say we share 99% of our DNA, for reasons I'll explain below...

@MattDMo yeah, I didn't want to use "coding sequence" since I thought that to be a bit too technical for the other site. I am just pedantic enough that I couldn't allow "99% of DNA" to stand unchallenged :).

So, a quick molecular biology lesson.

Proteins are the things that make up a good percentage of our cells (which make up a good percentage of us), and are the things that do the work of the cells - many are catalysts and are known as "enzymes".
Proteins are encoded by genes - while the statement that one gene
codes for one protein is not quite correct (one gene can code for
different variations of the same basic protein), it's a good way to
think about things in this context.
Genes are made up of DNA, a polymeric molecule that constitutes our chromosomes, the informational portion of which resides four “letters” (chemical bases).
However, now we get to the key part — although all genes are made of DNA,
not all the DNA of chromosomes makes up genes. In fact, as @terdon    mentioned in a comment, only about 5% (or less) of the 4 billion letters in the total DNA — the genome — constitute genes - those sequences that
directly code for protein.
The function of the rest of the genome is not entirely clear. Some is regulatory, some may be structural, and may be “junk DNA”. However it’s stuck      around for millions of years, so it we assume it must have some purpose. This non-coding DNA differs between species to a greater extent than the genes themselves do, so perhaps it somehow contributes to the differences between organisms.

From AndroidPenguin
Here are the links to a paper about the function of "junk" DNA from 2013.

Summary in NY Times
Abstract in Nature
ENCODE threads on nature.com

Side note, the ENCODE stuff about junk is at best controversial and more  strongly was (admitted by the consortium) pure hype; it was not in the peer-reviewed article, is considered nonsense by researchers on junk DNA, and should not be treated as a valid reference.

Since it was my edit of your question that started all this, I may as well weigh in. I will give a simplified version of genes and gene transcription, there are various details that make the process much more complicated than what I will describe but they are not relevant to the basic question here.
First of all, as others have mentioned, genes are specific sequences of DNA. A gene's job is to "code for" a protein (first big simplification). However, not all of the gene codes for protein, only those parts of it called exons (image modified slightly from here):

The take home message from the image above is that the red bits (the introns) are removed and do not affect the final protein product. So, only part of the gene codes for the protein. Introns tend to be far less conserved between different species than exons.
Not only does the entire gene not code for protein but most of the genome does not contain genes. In fact, in humans, genes represent ~5% of the total DNA and exons represent ~2%.
Another confounding factor are the sequences called repetitive elements. These are various types of usually shortish sequences that exist in many copies in genomes, In the human genome ~41% consists of repetitive elements of various types, and ~10% represents copies of a single such element (Alu), that's twice as many as genes. Such repetitive elements are usually not considered when calculating whole genome similarity rates.
In terms of their entire genome, human and chimp are very very similar. However, the exact percentages vary (I've seen estimates from ~85 to ~90something) depending on the way the sequences are studied. To be on the safe side, you should say that they share 99% similarity at the gene level and leave it at that.

Thank you for the details. Now having finished my first college level biology course I understand most of this when I understood very little when you first answered. +1 but I did not give you the selection because Matt's was better for simplicity and organization of thoughts.

Just to clarify definitions, your genome is made up of sequences of DNA. DNA is constructed pairs of four nucleic acids, or nucleotides (A,G,T,C). That DNA has many loci within it, each codes for a gene. Loci are given gene names such as SHH (sonic hedgehog) which is part of a discipline called gene nomenclature. Humans have two versions of each gene, one from each parent. These genes, such as SHH, have different variants called alleles. This is where you may have heard the terms homozygote and heterozygote, when a person has two copies of the same allele or two different ones respectively. You may remember talking about sickle cell anemia in high school.

So is it wrong then to say that apes and humans share 99% of their DNA or is it equally correct to say "genes"?

Well the similarity between humans and chimps in terms of known DNA sequence is about 98.8%, there is fairly low sequence divergence, so in my opinion you are right to say that they share 99% of their DNA. This means that in 100 nucleotides there is roughly one difference e.g. (showing 90 bases, made using random sample of four letters in R):

Human DNA strand:
atgactgtagcccatga t
gtaaacgtaccaagcctcctcggctgtcccgaaatagatacgcctggtagacgtattaatagtgagtaa...cgt
Chimpanzee:
atgactgtagcccatga c gtaaacgtaccaagcctcctcggctgtcccgaaatagatacgcctggtagacgtattaatagtgagtaa...cgt

Having said that, given that there is >3,000,000,000 base pairs in the human genome (the sequence of 4 nucleotides that make up the DNA) that equates to ~36,000,000 different base pairs (bnetween humans and chimps) which likely equates to a large difference. Sometimes even a single nucleotide polymorphism (SNP, pronounced snip), a change in just one base pair, can bring about quantifiable changes:

a single base mutation in the APOE (apolipoprotein E) gene is
associated with a higher risk for Alzheimer disease.

Here is a little reading on the humans vs chimp. You may also wish to see this similar post on biology SE.
But the editor of your original post is right... only the Euchromatic region has been sequenced.

"Humans and apes share 99% similarity in the coding sequences of their DNA"

The euchromatic region is often thought of as the protein coding part of the DNA, and makes up 92% of the genome (I think this is perhaps 92% of genes, but only a small part of the physical DNA).
The rest, the heterochromatin, contains non-sequenced information and could harbour some of the DNA variation between the two species. Some work has suggested that the heterochromatin, previously labelled as Junk DNA, actually has some effect on traits. For example in Drosophila there has been studies which show effects of the Y chromosome on traits despite the Y chromosome being mainly heterochromatic.

Further: I think a common source of confusion comes from the use of the word gene. It is often used interchangeably to mean either Allele or Genetic Locus. When someone says that humans and apes share 99% of their genes they mean they share 99% of their genetic loci. When someone says that a person shares 50% of their genes with a parent they mean that they share half of their alleles with that parent (it is only roughly half due to recombination and mutation). An individual has all (barring genetic defects such as deletions) the same loci as their parent.

Most of the answers here focus on the difference between the concepts of 'DNA' and 'genes' very well. However, the sequence identity between humans and chimpanzees is not covered as rigorously and remains unclear from what has been answered. Therefore, I will elaborate on that, so that the first part of the question is also covered.
Humans and chimpanzees differ approximately every 100 nucleotides in their total DNA sequence. This is does not mean that 98.5% of the genes are shared. It means that humans have about 98.5% (more precisely about 98.8%, The Chimpanzee Sequencing and Analysis Consortium, 2005) sequence identity with chimpanzees, disregarding indels. They treated indels and nucleotide differences separately and "calculate[d] the genome-wide nucleotide divergence between human and chimpanzee to be 1.23%" which includes intergenic regions and introns - so obviously also non-genic regions. Sequence identity at the gene level is presumably way bigger.
The Chimpanzee Sequencing and Analysis Consortium also gives information how this divergence is structured. The main part (about 85% of the 30 - 35 Mio. different nucleotides) comes from fixed differences: a fixed difference is a position in the haploid genome in which every human has, say, a G and every chimpanzee has a T. Accordingly, the site is different between the two species for every individual of the respective species. The smaller part (about 15%) comes from sites that are either variable (SNP) in humans or variable in chimpanzees, or in both (there is even a small number of very old variants, i.e. shared alleles between humans and chimpanzees, e.g. see Azevedo et al., 2015). Note that the estimates get better the more individuals of the respective species are sequenced and compared.

I just read a article that says even the 99% stat is not technically correct. To get to that number they had to ignore 25% of the human DNA and I think 18% of the chimp DNA.  I am also assuming the stat was only including the coded DNA.  Because if the what they used to refer to as junk DNA is not the same, then the 99% stat from 2005 starts to look less and less accurate and bit misleading.
https://futurism.com/watch-do-we-really-share-99-our-dna-chimps/

It's not only coding DNA but also all non-coding DNA. Additionally, the publication that mentions the 98,8% sequence identity thoroughly mentions that the this does not relate to structural differences (indels etc.) as these differences cannot be quantified as easily. However, they also cover structural differences in the article.

Humans and chimpanzees differ approximately every 100 nucleotides in their total DNA sequence.This is does not mean that 98.5% of the genes are shared.It means that human have about 98.5% (more precisely about 98.8%,The Chimpanzee Sequence and Analysis Consortium,2005) sequence identity with chimpanzees,disregarding indels.They treated indels and nucleotide differences separately and "calculate[d] the genome-wide nucleotide divergence between
human and chimpanzee to be 1.23%" which includes intergenic regions and introns-so obviously also non-genic regions.Sequence identity at the gene level is presumably way bigger.

I feel like the math here doesn't work. How can 100 nucleotides equal 1.23% of the whole sequence?


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Identification of an Insect (Hemiptera)
I found a a few of these guys on my composter, so they could have easily been eating bugs or decaying organics (or both):

To me it looks like a stink bug with oversized legs, not like the ones I'm used to seeing. His body measures just under 3cm, and I haven't pulled on his legs to get a measurement (I haven't pulled on it at all).  The legs seem to be at least 1.5 times the body length as do the antenna.  The body is grayish brown and the antenna and parts of the leg seem reddish brown.
I'm a microbiologist, so things big enough to see in a jar are not really my specialty.  That said, here's info that I've been trying to use ID it:
Wingless Normal compound forelimbs (don't seem to have any kind of   prey modification)
Segments filiform antenna (I think)
2 Tarsomeres (I think)
In the middle of South East US
Have had (unusually) heavy rains
Underside of the limbs and antenna seem red, but to seems gray
I've never seen it before! (and I usually notice such things).
Update: Despite my 4 year old putting other bugs and some leaves in with it, the bug died.  I took the opportunity to get some much better photos, and low and behold when I started manipulating it I was able to pull out a substantial rostrum that I missed!  These guys are good at hiding those.  So going back to assassin bugs, can anyone id which assassin bug it is?
More photos: [I would add more but I think this should be plenty]

I at least think it's quite a pretty specimen (to betray my mammalian aversion to bugs).

Also if anyone could rule this out as a potential threat to vertebrates, ie Triatominae, that would also be appreciated (even if not a complete answer).

Thanks for the new pictures; see ID edit in my answer below

species ID
I feel reasonably confident this is a late-instar Acanthocephala declivis nymph (that is, almost-but-not-quite-adult).
Compare your pictures with those on bugguide of a similarly-aged individual, or the bugguide ID page. Also see the key here; which gives three characters for declivis

Humeral angles of pronotum broadly expanded, extending laterally well beyond maximum lateral abdominal margin. Distal dilation of hind tibia broad until apex, then curving in at right angles to tibial shaft. Anterior pronotal lobe with 2 small shining blunt tubercles along midline

If you look at your pictures, you'll see that you're three for three here: the broad 'shoulders' (pronotum), the right-angle in the leg flange (dilated tibia) just above the the 'ankle', and the two rounded bumps on the pronotum (visible in photos 1 and 3).
original answer / working towards the ID
You're right on track, it definitely looks like a true bug (Hemiptera/Heteroptera). Possibly immature if it looks wingless. Maybe some kind of Assassin Bug (Reduviidae)? They don't all have burly forelimbs. You might also want to consider Coreidae, for instance the genus Leptoglossus (pdf on Leptoglossus in Georgia).
You could try this key to Florida bug families, it looks pretty user-friendly.

Thanks for the link, I looked at that and didn't see it.  I'm also not in Florida, but it's more fuel for the search.  I agree it looks kind of like the assassin bug, but it seems to missing some of their features.  I'd vote you up but I don't have the rep here.  I'd accept any definite answered on the species/genus with a reference to a good description on the bug.  Happy for someone with editing power to bring in the images if possible.

Added in images for you (waiting on peer review)

Lacking a rostrum: interesting. Do you have a picture? I thought most bugs had piercing mouthparts of some kind. Often they're tucked away in a special groove underneath.

Thanks! Regarding the bug-beak, I'm not saying it's necessarily a vital diagnostic character, but if you're interested it should be there see e.g. http://bugguide.net/node/view/63015

let us continue this discussion in chat

I was completely wrong, it has quite a rostrum!

Nailed it. That bug guide photo looked like it exactly!

Maybe this is a late answer, but the difference between an assasing bug (Reduviidae) and a squash bug (or leaf-footed bug, Coreidae) is the structure of the beak.  Reduviidae, being predaceous, have relative short, bended beaks, made of three segments and do not go beyond the first pair of legs.  Coreidae, herbivores, have a long beak made of four segments.  This can be see it clearly in the third and fifth picture, it is a Coreidae.

It looks very much like a squash bug, which look close too assassin bugs but don't eat insects, probably explaining what it was doing in your mulch. I have the same thing.


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How to obtain bacteria samples?
Would anyone know how to go about obtaining samples of Salmonella or E. coli for purely educational purposes?
Note: I just want to look at the stuff under a microscope.

Shopping questions are off-topic, unfortunately.

As he mentioned below, you probably don't have what you want, but that is not the point.  My point is that this question will not likely be helpful for future visitors because that vendor could go out of business leaving an obsolete answer.

It's regarding a different type of product, but this meta.Biology answer gives a general overview as to why these questions are discouraged.

@Jonsca, I'm actually ok with this type of question. The alternative way to ask how to achieve such things but not exactly from whom, which is a reuseuable question. (ie how to appropriate go about contacting certain people)

As requested I removed the request for a purchasing location and reworded the question.

Can't answer because the question is on hold. If all you wish to do is view cells, you can buy prepared slides here for example. (I have no connection with this company, I have not used their products, and I am sure that other suppliers are available.) Alternatively live yoghurt is a source of safe bacteria if the species aren't important to you. Most rods look very similar.

If you just want to look at stuff under a microscope get a sample of dirt from your garden, dilute it in some water and behold the extreme variety of microscopic critters you will find in there!

@nico I don't understand the fear of the normal man getting his hands on what he could get quite easily if he didn't cook his food long enough...

@Usman Mutawakil: I am just saying it is much easier and cheaper to go into your garden and get some dirt than to order bacteria from a company, which would probably most likely involve quite a bit of bureaucracy on top of it. On top of that, fear or no fear Salmonella should not by law be handled in a normal household.

In a litigious world no supplier will want to take the risk of supplying you, as a private individual, with something that you could claim had made you ill.

@bobthejoe As currently asked (after the edit) I have little problem with it.  "Where to buy" questions are never good SE questions, IMO.

I would be happy to update my answer with good ways to isolate microbes around your house, and prep them on slides, if we can decide if this message is to be kept or not.

@jonsca I think I have modded my answer in such a way as this can be kept.  Feel free to edit if I'm wrong.

@AtlLED: that would DEFINITELY be better IMHO, although it seems the OP is not of that opinion. However, maybe you could write a new question?

If the mods want to close this one, I'd be happy to put it in a Q/A.  As long as this stands, I'm happy for it to stay here.

@Jonsca, shall we start the reopenning process?

@bobthejoe I started another question as suggested. I'm fine with it being closed if this is re-opened.

To be honest, you really shouldn't be buying such things if you're not prepared to handle them properly.  If you work with a proper lab, you will be inindated with vendors trying to sell you these and many others.
But to answer your question, if you are looking to purchase many such items ATCC is an excellent resource.  Not only will you have to meet regulatory requirements, but you will also have to deal with a great many MTA's depending on what you are trying to get.
In response to edit: Salmonella is actually not normally a serious pathogen to a healthy adult.  It is, however, still a human pathogen and should be handled under BSL2 conditions.  So if you have the funds and time to setup a BSL2 lab at your house, by all means go to town.  And I hope you don't live with any children, the elderly, or otherwise immunocompromised individuals.
In response to further edits:
If you just want to look at things under the scope, then I suggest you get started by making your own homemade culture plates.  If you can get your hands on some Lysogeny Broth (LB), agar, and petri dishes then you can make lb plates like a researcher in a real lab (minus an autoclave but you could use a pressure cooker).  These are items the public could get, but might be harder to come by.
I however will assume that you want to make your own plates from common household ingredients (I used to do this a lot as kid, whatever that says about me).
**
Making your own culture dishes:
**
1) The "plates" themselves.

I recommend getting the smallest Tupperware like
containers your can find that are microwave safe, dishwasher safe, and
really make a good seal (water tight at the least).  They really
don't have to be big, and you will make your life easier if you buy a
bunch to match.
They need to be super clean.  After running them through your
dishwasher at home, put them all in a boiling pot of water until you
are ready to pour in your "media." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.
2) Your "Media" or Broth

I highly recommend using pectin as your gelling agent if you can't
get your hands on some agar.  After that comes plain unflavored
gelatin, but I recommend pectin.  You can get it at almost any
grocery store and my recipe is made assuming that.  You can determine
how much you want to make, just scale up the ratios.  I'm going to
list things as rough volume by volume so you won't need a scale.
i) Make the powder first:

45mL of pectin;
4 bouillon cubes ground as finely as you can (you can get different
types and results depending on if you start with vegetable, beef, or
chicken.  I recommend starting with vegetable.);
125mL of refined white sugar;
Additives (more on this later)

ii) Mix the powder into 500mL of water

Before you mix in the powder, hear the water to 50-75oC (mid low
heat), but not boiling.  Mix the powder in while stirring until
dissolved.

iii) Bring the mixture up to a boil.
Let it boil for about 2 min, stirring all the while.
iv) Cover the pot and let it cool for 4-5 min.
You by no means want it cool down to room temperature, you just want to get it a little below boiling.  If you are at 55oC or bellow it's definitely time move on.
v) Dip/fill your "plates" 1/3 full of media using clean/sterile utensils and seal while hot but not boiling.
You may have noticed this seems an awful lot like canning, and that's because it is.  Again you want to be as clean as possible in this step and of course try not to burn yourself on anything.
vi) Let your media plates set and chill over night in the refrigerator.
You really probably only have to wait a few hours if you are anxious to get going.  You are going to want to store the plates that you are not using in the refrigerator anyway.  Also if you made a bunch of plates, let the cool on a counter before you put them in the fridge so that you don't raise the temp of your fridge too much.
Remember the thing about additives?  You can play around with adding different amounts and different types of salts, vitamins, food, or other items to see how they effect the cultures you get to grow.  All kinds of fun there.  First go round, leave them all out.

Now you have your own home made culture plates!  The above recipe was empirically tested by my childhood, and repeated by my son's.  Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company).  I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.
Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate.  While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.
Leave your plate in a warm wet place, but not in direct sunlight.  Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow.  On top of our dryer is where I leave.
After a day or so you should have colonies you can streak out on a slide and look under a scope.  You will find all kinds of things this way.  If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.
You are actually quite likely to run into E.coli if you sample enough "areas" this way.  Obviously don't eat or huff the stuff that ends up growing.  Maybe you can post some fun pictures of this if you try it.

[I would comment above but I don't have the rep yet.]  It is certainly true that ATCC could go out of business, but if I were to reference Coke-a-cola to someone who was asking for a referral to a soda manufacturer, I don't think that would be on list of common concerns.  Instead, pathogens in general, select agents in particular, are by design not easy to get your hands on.  I would be interested if a member of the general public could get a pathogen from ATCC. That would let me know that there are people that need to be made aware of that fact.

Great answer! Did you ever try using food grade agar (a.k.a. agar agar)?

I have, i just found it less avalable and more expensive for what you need.  They may vary on your local market's demand for canning supplies.

I remember from my own childhood microscopy fun, that in Germany, agar agar is found even in the supermarket and it was cheap enough to make my dad buy it without him complaining once. Pectin would be harder to find. Seems to be regionally quite different.

@skymninge  In places where food grade agar is relatively available, it will absolutely work, probably getter.  You just need to get a sugar based gelling agent.  I double checked after writing the second version of this, and really couldn't find agar in our grocery stores.  Pectin is pretty cheap, ether way I don't think it should be expensive.


text:
Is there theory that connects longevity, time-scale of environmental disturbance, and adaptation?
I'm thinking here about environmental disturbance or like climate change-driven warming. It seems as if there are two macroevolutionary ways to deal with environmental change:
1) Have short generation times, and evolve fast. For instance, the mosquito Wyeomyia smithii is under selection by the warming climate in North America and it has shown an evolutionary repsonse. The response is "detectable over a time interval as short as 5 years" (Bradshaw and Holzapfel 2001).
2) Be hardy, and 'try' to wait out changes. No real-world example to cite, but imagine a long-lived tree growing in an area that has become to warm for its seeds to effectively produce seedlings.
It seems intuitively like strategy 1 is better in the case of ongoing climate warming. However, we could easily imagine a 5-year hot spell followed by a return to the normal as part of natural weather variation. Perhaps in this situation strategy 2 is better.
Essentially, having a longevity/generation time/hardiness that matches the time-scale of the disturbance would be important – if the disturbance is long (or unidirectional) compared to your lifespan, evolving fast seems best; if the disturbance is short compared to your life, it seems best to wait it out.
So the question is, is there theory that deals with this? I suspect that I just need to hit the population genetics books again or something; or perhaps there's a massive tome by Gould I should be reading?

 Bradshaw WE, Holzapfel CM. 2001. Genetic shift in photoperiodic response correlated with global warming. PNAS 98: 14509–14511.

Found this question, which seems related: http://biology.stackexchange.com/questions/378/has-there-been-any-observation-of-species-adapting-the-evolution-process

If the disturbance is short compared to a species' lifespan, then it's would be difficult for any adaptations to that disturbance to become fixed. Say an individual with a novel mutation is born during the disturbance that would impart some benefit under such conditions; since the species lifespan is much longer than that disturbance, by the time the individual reproduces, the disturbance will no longer be in effect and thus that allele will no longer be beneficial. In fact, this is seen in the thrifty phenotype in humans. When the mother experiences a period of duress during her pregnancy (say, the Dutch Hunger Winter of 1944), the fetus will undergo epigenetic changes that signal, in effect, that food is scarce and resources should be used sparingly. When those children grow up, they find themselves no longer under harsh conditions and this thrifty phenotype becomes a disadvantage, causing diabetes, obesity and so on.
If the disturbance is on the order of the lifespan of the species or slightly larger and especially if it is cyclic, polyphenism would be advantageous. This might also impart some resistance against long-term change, at least up to a certain point. For example, the butterfly Bycyclus anynana shows marked differences when born in the cool, dry season versus the warm, wet season: different body mass, different resting metabolic rate, different wing patterns and so on. This is controlled by hormonal switches in response primarily to temperature.
It seems that the best strategy in the face of long-term change would be gradual evolution due to progressive selection on traits that impart resistance to the disruption, at the cost of being vulnerable to future reversions in the conditions.
But of course, none of this can be "planned for" by the species. In the face of a new change in environmental conditions, be it gradual or sudden, the species can only work from its current genetic background. So whether there is a specific theory that deals with this (aside from the examples given above) is not clear. I would think that what we will see with strong-but-gradual climate change is a progressive loss of biodiversity (due to the inability to adapt in time) followed by rapid expansion to fill newly opened niches. To that end, I guess Gould's "Wonderful Life" would be appropriate to read. Any book on Evo Devo would lend insight into understanding how species might be able to rapidly adapt to a slowly changing environment, albeit in an indirect/abstract manner (i.e. "food for thought"); I like Sean B. Carroll's "Endless Forms Most Beautiful".

I dont understand your reasoning in the first paragraph; a trait that is advantageous under a particular environmental condition will contribute positively to fitness even if the specific conditions only occur in e.g. 10% of all years, as long as the same trait does not cause lower fitness during other/normal years. Therefore, it will be selected for and the trait is likely to increase in freq in the population, even if the disturbance events are much shorter than species' life span. Or are you only considering one-off disturbance events?

Not exactly matching your question, but I think that the idea (from stochastic demography) that life histories should be buffered against environmental variability in influential vital rates (Pfister, 1998, Morris & Doak, 2004) can be related to this issue, even if it is mainly (originally) dealing with stationary environmental fluctuations.
In general, fluctuations in vital rates cause the stochastic population growth rate to decrease. This can be described by Tuljapurkar's approximation (Tuljapurkar, 1982):
$$log \lambda_s = log \lambda_d - \frac {1}{2\lambda_d^2} \sum_{i,j} V(a_{ij})S^2_{ij}-\phi$$
where $\lambda_s$ is the stochastic growth rate, $\lambda_d$ is the deterministic growth rate based on average conditions, $V(a_{ij})$ is variance in vital rates (here matrix entires) and $S^2_{ij}$ is sensitivity in vital rates. $\phi$ represents covariances between rates, which can be important, but can sometimes be ignored for simplicity. This equation shows that the effect of variability in vital rates on stochastic growth rate (which can be interpreted as a measure of fitness) is a product of sensitivity to change and the amount of variability.
Because of the negative consequences on stochastic population growth, selection is expected to minimize variance in population growth rate. Pfister (1998) predicted (based on an evolutionary argument and the equation above) that a species should have smaller temporal variances in the life history traits it is most sensitive to. Therefore, across species, there should be a negative correlation between the sensitivity and the temporal variance of vital rates. This also means that the evolution of life histories and the tolerance of species to variability in environmental conditions are shaped by their life-history patterns.
A consequence of this is that in a long-lived species (as an example), you should find larger variabilty in juvenile survival than in adult survival, since population growth rate is more sensitive to variability in the latter. The lower variability in adult survival can then be seen as an expression of "hardiness" to variability in environmental conditions, and this theory can therefore be used to understand likely evolutionary trajectories of different species, also under a climate change scenario. The ways to minimize the negative effects of variability in population growth in this theory is to either be hardy in important traits (change in environmental conditions doesn't translate much into variability in vital rate) or to decrease the sensitivity in vital rates that vary a lot (which amounts to modifying the life-history pattern of the species). Your question mainly deals with longevity, and this is influenced by both maturation age and adult survival. Therefore, this theory can be useful to think about which species should develop a "hardy" strategy.
However, this answer completely ignores tipping-points in environmental tolerances, nonlinear responses and the genetic variation that selection can act on.
Related articles you might want to check out are Van de Pool et al (2010), Morris et al. (2008) and Doak et al 2005.


text:
Are there "multi-frequency" signals within a human brain?
I know that neurons can exhibit tonic and phasic firing, and also that a neuron is sometimes called an integrator. This makes me interested to know if there are activities in the brain that depend on two or more signals of different frequency occurring at the same time. For example, in a telephone system, two signals with a different frequencies at once(DTMF) are interpreted as 1. Is there anything similar in the human brain?

Remembering that neurons don't generate sinusoids, just spikes (mostly)....
It depends on exactly how you want to define "depend on".  For instance, a downstream neuron receiving inputs from two neurons will be more likely to fire as it spatially/temporally sums the inputs from the two neurons.  Regardless of their specific rates, if their interaction is such that an impulse from each neuron arrives within a certain timing of the other, it may be sufficient to cause the downstream neuron to spike.  In this case, particular sets of frequencies of the two upstream neurons would be more likely to activate the downstream neuron and would do so at a particular rate for the downstream neuron.  Of course, the phase delay between the two neurons would be important too.
In a more general sense, one might consider the binding problem, by which many sensory inputs are bound into a single, higher level experience, such as an object or a biographical memory, which can then later be recalled (and thus activate all the lower sensory regions that encoded the memory in the first place, nearly recreating the experience).

There is a somewhat-hypothetical phenomenon called cross-frequency coupling which has generated some interest recently. This has mostly been described in the hippocampus and in interactions between the hippocampus and neocortex.
http://www.cell.com/neuron/abstract/S0896-6273(13)00231-6
http://www.bio.brandeis.edu/lismanlab/theta.html

In general, drawing analogies of how the brain might work from engineered telecommunication/computing system can be quite misleading.
I just wanted to add Izhikevich's FM modulation theory of communication, but I would say it is controversial.

Izhikevich E.M. (1999) Weakly Pulse-Coupled Oscillators, FM Interactions, Synchronization, and Oscillatory Associative Memory. IEEE Transactions On Neural Networks, 10:508-526
Hoppensteadt F.C. and Izhikevich E.M. (1998) Thalamo-Cortical Interactions Modeled by Weakly Connected Oscillators: Could Brain Use FM Radio Principles? BioSystems, 48:85-94


text:
Who would win in a fight: an amoeba or a leukocyte?
(sorry, I couldn't resist the rhyming, silly title)
I find it facinating that humans can suffer from an amoeba infestation. Amoeba must reproduce far more slowly than bacteria. In size, they seem to be approximately the same size as the various leukocyte cell types (I see estimates ranging from 10μm to 30μm in diameter). I would assume that they are slow-moving, or, at least no more motile than a leukocyte.
How is it, then, that a population of amoeba can take up residence (and a particularly dangerous one, at that) in a human body without them being wiped out by the immune system? Do we know much about the pathology of such an infection? Do the amoeba actually consume the leukocytes by phagocytosis before they can be consumed themselves?

How can I add a Greek letter "mu" for "micrometer"?

Also, this could probably use some better tags like "protozoa", "amoeba" or "phagocytosis" but I cannot create new tags yet.

This is nothing I really know or could prove, but wouldn't amoeba be in a region where there is no blood, like the gut? Then the problem is more about surviving in this environment. Additionally I don't think the bacteria are in a way actively "running away" from an immune response. This is not about speed, it is about adaption.

Hm, that could be but according to Wikipedia, at least, advanced infestations make it into the blood stream though.

Also, I didn't mean to imply that bacteria were running away from an immune response but I was positing that amoeba, in theory, could.

Still, if the advanced infection makes it to the blood stream, the region where they grow in numbers which are dangerous for the host can be free of leucocytes. After some individuals entered the blood stream, they might do damage before found and eliminated by immune response. New individuals can enter the blood stream again and this goes on. Additionally, the wikipedia article you posted actually gives another clue: The amoebae in question are normaly commensals. So the immune system could recognise them as "not dangerous" even if they have become so.

I added the μ for you (it's easy for me, I have a Greek language keyboard layout installed).

Assuming you don't mean a single leukocyte as I doubt That a lone leukocyte could do much. Macrophages and neutrophils can release their lytic/degrading enzymes spewing them on to the amoeba. Antibodies produced by BCells, particularly the IgE type can coat amoeba and cause histamine release from mast cells recruiting more neutrophils and macrophages. Eosinophils are also important. Finally one must not forget the complement system, a series of proteins that could kill by making pores in the amoeba membrane. Amoeba have however developed many techniques for immune evasion, such as diverting the immune system via cell signalling (cytokines) such as IL10 which dampens the immune system or coating themselves or activating the "wrong" immune system.

Beat me to the punch.  The idea you are looking for/asking about is parasite immune escape/evasion.  Here is a good article on the subject.  You can find many more, but remember that pathogens evolve with the hosts they infect.  I agree that a lone leukocyte wouldn't be able to do much of anything without the rest of the immune system coordinating an interaction.  Also a successful infection of a human is unlikely to come from a single amoeba but a large group of amoebas.

Thanks for the response. I have found a rich set of literature pointing to the expression of cytokines as an immune response to amoeba, resulting in a strong and potentially damaging inflammatory response. Also, of course I didn't really mean only one amoeba and one leukocyte; that was just for my admittedly lame question/title.

I would argue against any specific evolution of amoeba in response to the human immune system, though. Amoeba are not obligate parasites of humans or mammals in general; they do just fine in their natural habitat of small bodies of water. I would argue that upon coming in contact with a human, they just find themselves in a new, cell-rich environment where they can carry on doing their usual thing. Selection for success in their natural, aquatic habitat is almost certainly far stonger than selection for success in mammalian hosts.

(Yes it is a very old question but I can't resist posting an answer here...)
Not all amoeba are parasites. The common one that cause amoebiasis is Entamoeba histolytica, which can cause diarrhea in some infested individuals. Note that infested is not equivalent to infected. There are many types of bacteria colonizing the gut without causing any problems, including those contained in probiotics. Therefore it's really not necessary for the immune system to clear E. histolytica from the gut.
E. histolytica is normally separated from the gut mucosal lining (surface) by the mucus layer, with or without secreted antibody. If it managed to penetrate that mucus layer, E. histolytica can start digest the extracellular matrix (the matrix between cells) and cause a whole lot of problem. In response the gut cells will secret cytokines e.g. IL-8 to recruit immune cells. That's when the original question's condition would occur, but it'd be more like a combined arms of immune cells against an army of amoeba...
Among the immune cells, neutrophils, the most abundant leukocyte, are the first to arrive the battlefield.
They are numerous but ain't particularly "strong" or large. They can't phagocytize (eat) the amoeba, but they can still kill amoeba by releasing reactive oxygen species (basically the action is similar to bleach). However, more virulent species of amoeba can kill neutrophils very effectively, as well as protecting themselves from neutrophils.
Before other components of the immune system are activated, neutrophils : amoeba casualty ratio may be as high as 3000:1, but with other components of immune system the host would survive...
Source:
Moonah SN, Jiang NM, Petri Jr WA. Host immune response to intestinal amebiasis. PLoS pathogens. 2013 Aug 22;9(8):e1003489.


text:
Why does the body not recycle red blood cells?
This question is out of curiosity.
The life expectancy of a red blood cell (RBC) is approximately 3 months, and then RBCs are disposed of. Why does the body opt to build new red blood cells rather than using the existing ones? Do RBCs lose functionality/efficiency as they get older?

They are recycled, the iron and other components are broken down and then absorbed. Adaptations of the RBC prevent the same RBC being used. They lack a nucleus to make them highly efficient oxygen carriers (pack as much haemoglobin as possible). Without a nucleus and other organelles they're unable to synthesise the stuff they'd need for renewal. There's a lot of wear and tear that occurs as they're constantly flowing in tiny blood vessels and getting damaged or affected by substances in the blood.

Just one additional factor worth mentioning: the haemoglobin-oxygen interaction is a source of damaging free radicals which add to the 'wear and tear'.

RBCs do lose their functionality as they get older. In addition to the free radical damage they receive, the cells also become smaller over time which increases the effective concentration of the haemoglobin which causes other problems like hemolysis or rigidity.

I didn't know this - do you have a reference?


text:
In the context of twin studies, what do 'unique environmental factors' and 'shared environmental factors' refer to?
I was reading this study on sexual behavior and they refer to both terms without clarification. Does 'unique environmental factors' refer only to the prenatal environment or does it include individual experiences with, say, illness as well? Would friends be considered a 'shared environment factor' or an 'individual environment factor?'

Shared environmental factors are those shared by the twins: uterine/prenatal environment and then the home environment and other environments both twins are raised in or remain in together. Unique environments are any environment not shared by the twins - they generally appear later in age.


text:
What is it called when one human eye is seeing brighter color than the other?
What is the name of a phenomenon where one of the human eyes is seeing brighter/more saturated color than the other? I can observe the same object from the same position while alternating which eye is closed, and there's a visible difference in the saturation of color. Like one color is more pale than the other.
Here's an example of what the difference looks like between image perceived by two eyes:

Interesting question; I've also noticed this but it's been that way my entire life. ♂

here is forum discussing similar effect ,
where as similar problem which leads to double vision is single eye is called monocular Diplopia.
There are two possible causes discussed in that forum. One is a cataract or an early indication of a cataract, for which a vision specialist visit is recommended.
Another solution is much simpler one of the pupils is more dilated than the other:

The way your eyes see colors changes throughout the day, not dependent
  only on external conditions. Try this: gently press the palm of your
  hand against one eye (closed), for about a minute; leave the other eye
  open during this time (feel free to blink, of course...). Now, look at
  the world with one eye covered (for a couple of seconds), then the
  other — the eye you help closed will see things as quite more
  saturated, partly because you've fostered its pupil to dilate in the
  time during which it was shut. I recall being confused by this when I
  first started noticing that, upon awaking, either eye would see colors
  differently from the other; simply, the eye rested on the mattress
  would be seeing colors with greater saturation.

Could you add some details to your answer useful to the questioner, in case that link goes away in the future?

I also noticed this phenomenon after laying on a mattress with one side of my head against the mattress. I don't recall which side had most brightness, but the answer sounds correct

So is it because our eye needs time to adjust back to the standard brightness or is it connecting to the "pressing"? (I suspect covering the eye is sufficient)

The phenomenon in question is anisochromatopsia, however this term is rarely used. This phenomenon is always present, however it is rarely mentioned subjectively, while objective color testing will reveal it easily.
In pathologic state, the term Color Desaturation is being used defining that the previous status of color vision has changed to "abnormal" one. The causes to this change could be multiple, for example the most common one Optic neuritis in Multiple sclerosis.


text:
Approximately how thick is a single strand of cat (domestic housecat) hair?
I did a little research to lead me to finding the general range of width for human hair, which is anywhere from around 30µm to 180µm... approximately.
I'm trying to compare this to the width of cat hair, since I have been told (and it does seem a bit evident) that cat hair is much thinner than human hair in general.
I can't seem to find any information on this.  Does anybody have any answers?
Note:  I apologize if this isn't the right Stack Exchange forum for this question.  I wasn't sure where to put it, so I did an SE site search for 'cat' and this one seemed to be the most appropriate.

Off hand I don't know, but I actually do know a few books that might have it in it (unfortunately I couldn't find open copies).  But if you really want to find out the answer of say your cat, you could do this experiment and let us know.  I will post an answer if I find one.

Google  cat hair diameter gives this as top hit (30 micrometers).

Oh Google algorithms.  That's the third hit on mine.

Thank you.  Hmmm... I didn't see that when I searched earlier...

There are a few different types of hair on a cat.  But I think you are referring to the down hair on the cat.  It will also vary on the breed of domestic cat.  As a general statement, you can find a lot of quirky characteristics of mammals by looking at early genetics papers where people where trying to find genetic elements to obvious phenotypes.
For the down hairs, you can see "The ‘rex’ type of coat in the domestic cat."
Journal of Genetics [0022-1333] Searle, A G and Jude, A C yr:1956 vol:54 iss:3 pg:506
Table 3. Thickness in µ of normal and rex down-hairs

[Type of Cat][Diameter in um][SE of Mean]

Normal          25.8;   1·32;

English rex     16·2;   0·54;

German rex      17·0;   0·50;

Ooh that's pretty.  Thanks for the edit, I now know how to make tables.

You're welcome. It's not really a proper table, but the code formatting does make it look nicer.


text:
A source for leaf architecture of different plant species/genus?
I'm currently working on extracting some features of the leaf architecture based on their images (like L:W ratio, laminar shape, ...). I use the Manual of Leaf Architecture as the reference. It is really great in mathematically describing the features and how to calculate them.
But, the problem is I am not able to find a source (a book, or a data set) to have this architecture of different leaves (plants). For example, whether the Acer genus has leaves with a certain (or a range of) L:W ratio or the laminar shape for this species is mainly ovate,....
Does anybody know any source of this kind?

I don't know of a ready-made database that's exactly what you're looking for. However, if you wanted to make your own, there's a massive number of taxonomically determined (that is, identified to species) pictures of plant leaves online in the forms of digitized herbaria. With a bit of coding, or a lot of undergrad labor, you could harvest a massive data set. Alternatively, if there's just one species you're looking for, you could do it individually / by hand.

@Oreotrephes, thanks for the comment. Currently, I am using the ImageCLEF data set for my work and it's comprehensive with all the leaves data accompanied (even location). But I was looking for a data set with more "quantitive features".

Quantitative descriptions of leaf shape used as diagnostics are hard to come by. There are numerous qualitative descriptions (lyrate, cordate, acicular, etc.), and I think this fits within the example you give that "the laminar shape for this species is mainly ovate." But actual quantitative ranges as you mention (e.g., that the L:W ratio of Acer lies within a certain range) are much more difficult to come by. Also, there are ways of quantifying leaves using all the shape variance present in their outlines, and I describe some of these methods below. By using quantitative methods such as these, you can avoid the trap of a subjective criteria that arbitrarily distinguishes leaf morphs by a particular feature. Plus, you won't be biased by using a particular shape attribute, as you will be measuring the entirety of shape. Use of these various methods though depends on the species you are studying.
Oreotrephes I think is on track saying that, if possible, you should build your own diagnostic criteria for whatever system you are working in. You mentioned certain "ranges" that can diagnose a species ... this is a critical question. Measuring intra-genotype/individual variance in shape for your system is critical. Which leaf to measure for a species? ... i.e., shoot position, developmental age of the leaf, if working with compound leaves, the placement of the leaflet along the proximal distal axis of the leaf, what about heteroblasty (changes in leaf form at different nodes), leaves from lateral vs. main branches, environmental effects on leaves (e.g. sun vs. shade leaves)?
For tomato, I measure shape quantitatively using Elliptical Fourier Descriptors, which reduces the shape of an object to a series approximation and explains variance with a Principal Component Analysis. I use the resulting Principal Component values of leaves as a trait and explain shape quantitatively that way. A very useful program to perform Elliptical Fourier Descriptors is described in Iwata & Ukai 2002 and can be downloaded here. In Chitwood et al 2012, I describe how to perform shape analysis on tomato leaves, separating components of shape based on genotype (e.g., by species), by position in the leaf series (heteroblasty), the ontogentic age of the leaf, and placement of leaflets along the proximal-distal axis.
Other easy ways to measure shape: Circularity, solidity, L:W ratio (or aspect ratio) as you mentioned. All very easy to measure in ImageJ!
You mentioned Acer leaves, which piqued my interest because I study differences in the shape of grape leaves. But like grape, many Acer leaves are palmately lobed. If every one of your samples has certain features (e.g. 5 lobes and 5 sinuses as in Acer, including petiolar sinus) then you can perform a landmark analysis using a Generalized Procrustes Analysis (The "Shapes" package in R is useful for this analysis).
Using global methods to describe shape, that is, methods to quantify the totality of shape variance, are critical to distinguish leaves. It may very well be that two leaves are so similar from different species that they are not statistically separable by shape! Be creative in the ways you measure shape, and if need be, create your own system for doing so!

 Chitwood DHD, Headland LRL, Kumar RR, Peng JJ, Maloof JNJ, Sinha NRN. 2012. The developmental trajectory of leaflet morphology in wild tomato species. Annu Rev Plant Physiol 158: 1230–1240.
 Iwata H, Ukai Y. 2002. SHAPE: a computer program package for quantitative evaluation of biological shapes based on elliptic Fourier descriptors. Journal of Heredity 93: 384–385.

Thanks for your answer and resources. About qualitative description, do you know of a good not-so-techincal source? That would help. And, about using descriptors like Elliptic FD, my work is more of an expert-system approach, so I try to use the features familiar with the botanists. That's why I'm trying to use the quantitative features that lead to describing the leaf's shape in words (L:W >10 => 'linear' leaf).

For qualitative features, you could try essentially any flora. Most of these will have descriptions like this one in Flora of China

Acer ....
  Leaves mostly simple and palmately lobed or at least palmately veined, in a few species pinnately veined and entire or toothed, or pinnately or palmately 3-5-foliolate.

The problem with using florae is that a) they're limited in geographical scope and b) they're  usually just blocks of text (not databased or usually even XML tagged). However, a big flora like FoC will have plenty of genera for you to work with, and it should be easy to manually look up the information you want for a few genera, and possible for you to automate the information retrieval with online florae.
Florae can be a pain to use for non-botanists, but I think the FoC site is pretty explanatory – you can navigate from the family list to any family, and then down at the bottom will be a link called "list of lower taxa" (or just a list, if it's a small family) where you'll seelinks to each of the genera in the family. Then you'll see the genus description page, for instance, for Acer as quoted above.


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Can Pfx polymerase add only one 3' A overhang?
I am trying to clone a PCR product that was amplified using Pfx polymerase into pGemT vector. I had to A-tail the PCR product using Taq polymerase since Pfx only generates blunt end products. My ligation reaction was successful, however when I got the sequences, there is an extra T between the 3'end-T of pGem and the start codon of my product. It only happens in the 3' end of pGemT (or 5' end of my product). Can Pfx polymerase generates PCR products with just one 3'end overhang? or Can Taq polymerase add two consecutive dATP during the A-tailing?
Please write me your thoughts ASAP, it has happened twice and it's a pain already :(
GGC CGC GGG A-T-T-T-G ATG GGA AGC ATG AAG
The two Ts in Bold belong to pGemT, the T Italic is the extra T I've got from the sequencing reaction. After the T in Italic you may find the 5'end of my insert. The second T (in bold) from pGemT is the one that ligates with the overhang A added through the A-tailing protocol.

Pfx wont add an overhang. Check this. Taq generally adds one A

Could you post sequences at the two junctions, just to make the problem absolutely clear?

Hi, Thanks for your answer! I have included above the sequences at the two junctions as you requested. Hope this helps to better understand the issue.

did you check the electrophretogram of your sequencing reaction. just to make sure that it is not an erroneous base call

Yes, I've checked every peak of the electropherograms and there is clearly an extra T there. From four clones I've sent for sequencing, all of them had this extra T. I have called promega to confirm it is not a vector issue. They said it is possible that they may have produced a wrong batch of pGemT with an extra T. I can't believe that was the case though. Anyways they will possibly send me a new batch next week. If you think that might be a vector issue, please let me know.

Just try with TOPO-TA once.. if you have it in your lab..

Ok, I am wondering if I can amplify the insert from the clone I already have into pGemT? As the coding region of my gene is fine and primers will unlikely pick that extra T, I would like to use the pGemT construct to amplify my gene, because I've ran out of PCR product.

Yeah, as far as the experiment is concerned you dont have any problem. Even with an extra T there is no problem with the current construct wrt expression. You can amplify the clone too if you want. And, it is always better if you keep some sequences ahead of start codon (such as kozak consensus sequences or restriction sites etc).

It's unlikely to be a bad batch of pGemT, as I think these vectors are generated by restriction digestion. Also, the suggestion of using TOPO-TA would be quite expensive if you do not already have it (and I suspect that s/he doesn't by the use of pGemT). Sometimes erroneous bases get added by Taq. As @WYSIWYG has said, the insertion of this extra base does not change your reading frame and won't affect expression. If you were really concerned, the easiest method is to do a simple mutagenesis, but I don't see a need for it since you will move the insert to a destination vector.

I understand the extra T won't change the reading frame of the coding region. However, I am planning to subclone this insert into pet30 expression vector. For this step, I need to digest pGemT-insert leaving the extra T in the digested fragment that is to be subcloned. When this happens, the coding region of my protein will not be in frame. Therefore, I will get another protein completely different as the reading frame will be shifted. My question is: if I use pGemT-insert as a template for another PCR, is there any chance to pick that extra T? Forward primer starts from GATG..

I am asking to run another PCR using the wrong construct (with the extra T) as a template because my gene is lowly expressed. I had to struggle a lot in order to get the coding region amplified without mutations. So, running another PCR using cDNA as a template will be a pain. Now that I have the coding region healthy into pGemT with an extra T upstream my gene, can I use it for PCR?


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Is Hydrogen gas present in biogas, and does it spontaneously ignite?
Is Hydrogen gas present in biogas? As it is highly inflammable, may it ignite the other gases like methane?

What's your question here? Are you asking why biogas with hydrogen doesn't spontaneously ignite?

first question is whether Biogas constitutes Hydrogen and if yes why doesn't then the biogas spontaneously ignite?

cf. http://biology.stackexchange.com/questions/7336/gas-from-bacteria-thats-not-methane

The constitution of the biogas depends greatly on its source and the fermenting microbe. But in general, it does contain hydrogen about 0-1%. Even if it did contain large amounts, the mixture would be inflammable, but it would not burst into flames without any external igniter, which could be any small fluctuation of heat if the mixture is too unstable. But in general, an inflammable gas doesn't start burning on its own.

The auto ignition temperature of a combustible mixture of hydrogen in air is 500 degrees C source - Wikipedia. It will not spontaneously ignite, some part of it must first reach that temperature through a spark, flame, or other heat source.  Once it ignites, the methane of course will burn too.


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Eusociality and Natural selection?
Eusociality, particularly focusing on the presence of certain altruistic sterile organisms within the social set-up creates questions as to why would the process of natural selection have favoured the persistence of such genes especially in hymenopteric species. One explanation (provided probably by Hamilton) pertains to very similar genetic constitutions of females of such species (owing to haploid nature of males), which increases genetic similarity between the female members of the social group. Thus it would be more "beneficial" (i.e., favourable for the persistence of similar genetic builds) for a female worker to help the fellow siblings, to which it bears greater genetic similarity, than its own offspring to which it bears a lesser genetic similarity. This might in a deeper way explain altruism in case of hymenopterans where the male is a parthenogenetic haploid and the female is diploid.
But why would the sterile condition of the workers in case of almost all eusocial groups be favoured by natural selection on grounds that it improves the 'fitness' of the 'genetic build' of the workers and ultimately the sterile altruists benefit the persistence of its genetic traits? Moreover the altruistic nature of the haploid males also goes unexplained.

In what way are the haploid males altruistic? In the eusocial insects that I know about (not many) they act only as drones i.e. sperm donors, making no contribution to the success of the colony.

The female workers are altruists in the true sense. The drones, though not altruists by definition, follow or rather hold a social position wherein they take a part only in the societies' development through mating with the queen and do not improve their personal 'fitness' directly. Moreover, a number of drones might not even mate with the queen but still their presence has not been eliminated by natural selection.

I might be misunderstanding, but it seems as though "mating with the queen" is best possible thing you could do to improve 'fitness'! Remember, fitness is number of children, or grandchildren, or great-grandchildren, and in that sense while it applies to an individual, it doesn't manifest except through mating.

A related post: http://biology.stackexchange.com/questions/13693/empirical-evidence-for-group-selection

I hope I've interpreted your question properly... It's an interesting question, but I think it's important to remember that evolution doesn't act on the two sexes separately. Sterile males might evolve and be maintained simply because they're good for their sisters or mothers. Sometimes genes that are advantageous for one sex are linked with genes that are disadvantageous for the other sex, leading to maladaptative traits in one sex. And of course, individuals don't necessarily forego opportunities willingly. If subordinates that attempt to mate are killed by the dominant individuals, then that trait is not advantageous. They'd be better advised to be altruistic and help their relatives, rather than be selfish and be killed (thereby depriving their colony of a worker). This would lead to selection for sterility.
It's also worth noting that while haploidy makes it easier for kin selection to evolve by increasing relatedness, it's not crucial. It all depends on the relative costs and benefits.
In these eusocial situations, nothing really makes sense until you summed the fitness of the whole lineage, not just one caste or one sex or one individual.

There are also a lot of systems where the "satellite/helper" males do just fine by sneaking in copulations when the dominants aren't looking.

True, but I'm not aware of many examples of sneaking in properly eusocial species?

Fair enough, but maybe that's just the terminology we use. There are, for instance, female cheater worker bees (they call them, I'm not joking, "anarchists") who decide to start reproducing on the sly.

+1 for anarchists. I've heard of this - I believe they get very harshly punished if they're caught!

@Oreotrephes Source on the anarchist bees?

@Alex it must have been one of the sources I ctd in this question http://biology.stackexchange.com/questions/5076/modern-reference-for-kropotkins-lazy-bees but I'm not sure which.

Try the 2001 review "Worker reproduction in honey-bees (Apis) and the anarchic syndrome" by Barron and there are also more recent publications.

Group selection, in the extreme, yields eusociality due to the shared fate of the replicators in the group.  In a multicellular sexual organism, this "shared fate" of the "group" is the shared prospect that all replicators (alleles) have for making it into the next generation via the meotic lottery that produces the gamete.  Since they share this prospective fate they have an evolutionary incentive to cooperate in the construction of specialized cells that are, in effect, "sterile caste" members of the total "hive".  Similarly, if it is possible to subject all members of a group of individuals to a shared fate through multiple generations -- they will tend to evolve highly cooperative social structures.  However, one of the confusing aspects of the eusocial insect colonies is whether they evolved to be that way through shared fate of individual organisms, or some variant on the meotic lottery's shared fate of alleles.  The answer appears to be, primarily, that it is a peculiar form of meotic lottery in which the genes of the parents have extended phenotypes in the children that, in essence, parasitically castrate the vast majority of the children to help rear more offspring for the parents -- in particular the queen.  In this respect, one can view the evolution of eusociality in the social insects as a perverse form of individual selection where the genes of, say, the queen, cooperate in constructing not just the queen's body but, also, the entire hive.  The sterile castes are simply extended phenotypes of the queen (and the  drone with which she mates).
See "The Social Conquest of Earth" by E. O. Wilson for an in-depth treatment of eusociality and its evolution as set forth by Nowak et al in their recent paper "The Evolution of Eusociality".  See also "The Extended Phenotype" by Richard Dawkins -- in particular the chapter "Host Phenotypes of Parasite Genes".


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Beginning with centrifuge experiment
This is the first time I do a centrifuge experiment with my own centrifuge machine, it's just simple made by a rotor that can rotate the tube at high speed. As I know a centrifuge machine can be using for separate biology samples like bacteria, cells, molecules ... But I need some advice to understanding more how to working with it.
As the suggestion from Alan Boyd, I'm planning to separate Lactobacillus from diluted yogurt. How do I know where the bacteria will be located in the tube after centrifugation (is it usually in bottom ?) and how do I  calculate the RPM that is suitable ? And any other interesting diy experiment to do with it ?

It would be interesting to see a picture of your centrifuge, which you appear to have built in a few days.
Centrifugation simply accentuates the effects of gravity, and since bacteria are denser than aqueous solutions they will move to the bottom of the sample to form a fairly tight pellet.
The conditions for your centrifugation will depend very much on the design of the centrifuge since as well as the rotational velocity, the radius of rotation is also important.
I found a suggestion on the internet to use a relative centrifugal force (RCF) of 12000 g for 2 minutes (I must admit that from memory I always spun slower and for longer than this suggests). Anyway...

using RCF = 1.12 * 10-5 * r *N2
r = radius of rotation
N is revolutions per minute
and plugging 12000 g into that, for a rotational radius of 10 cm, I get 3300 rpm.

Don't know if you can manage that with your machine, but as I say, a lower RCF with a longer spin will probably be ok as long as you can dilute the yoghurt sufficiently to reduce viscous drag. Of course if you have access to any microbiological growth media you could grow a standard liquid culture by inoculating some sort of broth with a small amount of yoghurt.
Try a Google image search for hand powered centrifuge to get an idea of what has been used in the past.
after comment from Mad Scientist
see here for a typical large table top centrifuge maximum RCF is 3120 g at 4600 rpm. You can certainly pellet bacteria in something like this in tens of minutes.

12.000g sounds rather high to me for a tabletop centrifuge. For bacteria I'd use 4000-6000g for 15-30 minutes.

@Mad Scientist - agreed, I have supplemented the answer, which was only intended to get the questioner thinking about his own centrifugal circumstances.

@MadScientist depending on his design, it could be closer to a microfuge, in which 12,000g is quite reasonable. I'm more worried about balance and shielding in case the thing goes off kilter (that's a technical term, by the way :)

Ok, i'm fairly new to the "g" unit because i never using it before and familiar to the "rpm" unit. But i will research more about it now, thank you so much.

@AlanBoyd thank you so much, your information is very detailed.

I certainly don't want to discourage experimentation and self-learning, but please be extremely careful. A centrifuge has to be perfectly balanced at high speed to stay stable. As an example, one of the table-top centrifuges I use has a steel jacket that's perhaps 1 cm thick or more surrounding the rotor, just in case there is a balance issue or the rotor breaks from mechanical stress. A Google image search for centrifuge accident shows what mechanical stress can do when an improper rotor was used on a high-speed centrifuge for just a few hours. Keep in mind that angular momentum increases both with the mass of the object being rotated, and with the moment of inertia, which increases as the radius of the object being rotated increases. In other words, if you tie a ball to a short piece of string (say 0.5m) and swing it around your head, you can feel a certain amount of force. Take that same ball and tie it to a 2m piece of string, and at the same number of rotations per minute the force will increase substantially. All this means is that as the radius of the rotation increases, the amount of g force increases as well, but the stress on the machine also increases, especially if the balance is off.
So, good luck with your experiments, just remember that safety always comes first. You can replace samples, and you can replace equipment, but you can't replace you. Even simple precautions like always wearing goggles or protective safety glasses should always be followed. Don't work alone, or in a situation where there is no one to call for help if you get hurt. If something doesn't feel right, don't do it.

thank you so much for your advice, i deciding to add a chip for detect vibration - automatic stop, and using a secure box to cover the motor.


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Finding a easy and cheap method for dyeing dNTP
I want to measure OD to know the concentration of dNTP. Any idea for dyeing dNTP at cheapest price and easiest way ?

There may be such a dye, but I'm not aware of it.  The standard way to measure dNTPs, and nucleic acids in general is by absorbance at 260 nm. This article has a table of molar extinction coefficients for dNTPs (Table 10.2). They are
        wavelength      molar extinction coefficient
dATP    259 nm          15,200
dCTP    280 nm          13,100
dGTP    253 nm          13,700
dTTP    267 nm           9,600

In practice for routine work with DNA you can use 260 nm and assume that an absorbance of 1 corresponds to [DNA] = 50 µg ml-1. Using an average of the values in the Table, and disregarding the fact that these are actually at different wavelengths, and using an approximate average dNTP MW of 500, I calculate an absorbance for a 50 µg ml-1 solution of all 4 dNTPs as 1.3, so that's a reasonable agreement given all of the assumptions I've made.
There are fluorescent dyes that can be used to measure DNA, but these rely upon the presence of stacked bases, so are not useful for free dNTPs.
So, bad news if you don't have a UV spectrophotometer. There are plans available for construction of simple spectrophotometers using Lego and a few optoelectronic components. These tend to use LEDs as a light source, but I don't know if UV LEDs are available.

It will be difficult to achieve the level of wavelength resolution required to differentiate dNTPs, considering that you are doing a DIY experiment. Only very precise spectrophotometers can achieve it and they are expensive.
Another technique you can try is thin layer chromatography(TLC). It is cheap and you can easily do a DIY. But you need standards in order to differentiate NTP, NDP and NMP; the latter two might arise because of degradation during the experiment. People generally use a cocktail of anti-oxidants and protectants to minimize the degradation of nucleotides.
A strategy to go about this is to remove the phosphate using phosphatase and then do a TLC with Nucleosides (which are quite stable).
You can check this review on nucleic acid TLC.


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How to refer to person-derived and place-derived species names
Are there words that categorize latin specific epithets by how they're derived? Specifically, I was wondering if there exist adjectives to refer to:
Person-derived species names as in Nothura darwini (these could be "eponymic" or "eponymous" perhaps, but that seems grammatically wrong )
Place-derived species names as in Amolops hongkongensis (would these be "toponmyous", or maybe "loconymous"?)

I think generally both could be called latinisations, as the practice with species names is to take the name and try to translate/modify it into an appropriate Latin genitive case.  As far as a word the gets specific enough to reffer to eponymic latinisations, no I don't think there is one.  I searched through the OED a few times but I don't think there is one.  Do you have reason to coin the term?  I would be excited if I was proven wrong.

This isn't a purpose-driven query – just trying to write a sentence and looking for le bon mot. As an update, I did find a few thousand google hits for "eponymous taxa", but also some criticism of that phrase; and nothing similar for place-derived names.

According to A Source-Book of Biological Names and Terms by Jaeger, the appropriate terms are the simple, obvious ones:
"Geographical" for place-derived names and
"Personal" for person-derived names.