text:
How do I find the sequence of the phage BxB1 gene?
Specifically, I'm trying to find the sequence of BxB1 and its att sites.  I have success finding the att site sequences, but I'm having a bit more of an issue with finding the sequence of the actual recombinase.  I've looked through Genebank, but I can't find a definitive sequence of the BxB1 recombinase.
How should I go about looking for this sequence?
EDIT: One more thing I'm concerned about is the validity of the sequences that I do find.  For example, I have seen that Addgene has this pCAG-NLS-HA-Bxb1 sequence.  However, I'm not sure how to verify that this sequence is correct.

The genome has the gene annotated. This plasmid has the gene.

http://phagesdb.org/phages/Bxb1/ here you can click "Locally BLAST this genome" it will give you the sequence in FASTA format and then you can click BLAST if you want additional information about the sequence, alignment, etc


text:
Application of Latin names for Taxonomy
The current taxonomy has family names like Canidae and Felidae. But Felidae has sub families like Felinae and Pantherinae. Roaring cats and non-roaring cats. My question is based on the fact that we can have common words for these families based in Latin: Felines, Canines, Pantherines. Can every family in the taxonomy be represented by this latter form? Is Pantherine a valid name? Is was created by dropping the a from the subfamily but caninine was created by dropping the da from the main family and replacing with in.

Is "Pantherine" a valid vernacular name for this group in English? Sure, although "panther" is much clearer ("Pantherine" in English would mean "like a panther", not "a panther"). Also, many family names are fairly obscure: even a pretty well-known group, like Apidae, would become "Apinine" in your scheme, which is less clear to me than "a family of bees".
Is it a valid family name? No. The International Code of Zoological Nomenclature (ICZN Code), which governs all scientific names for animals, says:

Article 29.2. Suffixes for family-group names. The suffix -OIDEA is used for a superfamily name, -IDAE for a family name, -INAE for a subfamily name, -INI for the name of a tribe, and -INA for the name of a subtribe. These suffixes must not be used at other family-group ranks. The suffixes of names for taxa at other ranks in the family-group are not regulated. [emphasis mine]

Family names that don't have an "-idae" suffix need to be corrected (ICZN Code Article 32.5.3.1).
Note that the ICZN Code doesn't cover other ranks in the family-group or above.

I think OP is getting at the fact that certain non-formal names are "valid" in English to refer to members of a group, hence: scarabaeid, coleopteran, neopteran, etc.

Yes I think the common English form are valid too. I would however like to know the correct forms for singular and plural in zoological and botanical names since comman names are not always obvious. I would assume all nouns there are in plural since they are talking about groups. And I assume the form is neutral. But I see words like Goniotrichum which is singular neutral so I wonder if I can change to Goniotricha ? Or is there some article I can read that would show how to convert all latin taxa names to common forms? like deuterostomia to deuterostomes.

And you say Apidae would become Apinine but in my system it would be Apeidos since wiktionary lists eidos as the singular form of idae.

Goniotrichum is a genus name, which are usually singular nouns -- a name like Homo sapiens means "[a] sapient [adjective] Human [noun]". IMO you would refer to "Goniotrichum species", rather than "Goniotrichums".

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text:
What is the scientific name of this evergreen plant?
This plant is found in India. It is an evergreen plant. Would love to know the scientific name.

In which country did you make this images?

@Chris India - it says at the top ;) ... where in India might be useful too though, it's a big country

@rg255 You're right and  I should get another coffee :-)

If you could say which part of India you found the plant in, that would be helpful. I would guess that it is a conifer, but not a pine because the needles to not seem to be clustered into fascicles.

looks like Araucaria and Cryptomeria

Araucaria sp widely used as ornamental plant in warm-regions of India

The tree in question belongs to the Araucariaceae family,
There are multiple species of Genus Araucaria,
I'd place Araucaria araucana on the first place, but there are multiple others:
Araucaria araucana

Araucaria luxurians

Araucaria columnaris

Araucaria subulata

Just FTR, the tree in question is not A. auraucana (Molina) K. Koch. A quick image search will show you that A. auracana has much larger, robust leaves.

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text:
What is it that creates that wonderful smell after a fresh rain?
I've heard that the wonderful smell of a fresh rain is actually chemicals  released from the trees and grass and other plants.

What is the process that allows these chemicals to be released?
What are the chemicals that create that smell?
How is it advantageous for the plant to release the chemicals rather than hold onto them?

The fancy word for it seems to be petrichor. It has a nice wikipedia article which might lead you to some of the relevant publications. https://en.wikipedia.org/wiki/Petrichor

Yeah, +1 and you go 2000+ :D Petrichor ;)

That molecule is called Geosmin. It is mainly produced 1 by Actinomycetes such as Streptomyces which are filamentous bacteria that live in soil. Other organisms also produce geosmin:

Cyanobacteria
Certain fungi
An amoeba called Vanella
A liverwort

It is an intracellular metabolite and cell damage is the primary reason attributed to its release. However oxidant exposure and transmembrane pressure also causes geosmin release in cyanobacteria. It seems that the release is triggered by some kind of stress.
I am not quite sure about their advantage to the host species.

1 or perhaps the most well-studied in

Interesting answer!

What about Petrichor that @skymningen suggested in the comments?

@SolarLunix I guess that is the name of the smell, not the molecule itself

The Wikipedia article on Petrichor mentions geosmin, and indicates it is a compound different than petrichor.

@mgkrebbs Yes I checked that but I did not find much info on what petrichor really is. Moreover the wiki article does not have much info.

The aerosol generation by the rain droplet impact on wettable surface being the mechanism releasing geosmin from the soil into the air completes the story. The paper is at https://www.nature.com/articles/ncomms7083, together with a PDF version of the paper.


text:
Why a striped baby is not the result of a white and a black parent?
Someone asked me:

If a striped cat is the result of a white and a black cat, why the result of a white woman and a black man is not a striped child?

I know the answer. I also know that the result of a black cat and a white one is not a striped cat. But I'm looking for a simple answer. I'm looking for an explanation without a genetics background required. I'm looking for a metaphor or something similar.

Perhaps metaphors should be sought on English.SE. I vote to close, as the question is not about the biological underpinnings. If it were, it is closable on homework grounds.

I disagree with the close vote - it's a biological question. Asking for a metaphor (perhaps analogy is a better word) is just asking for a laymans answer. Though if you can't explain it simply I would question whether you know the answer, and why you would want the answer to not require genetics training @Farzad...

@rg255 - I don't like the general tone, I don't like the fluff, and it is homework as there is no proof of any effort.

I'm not sure I really understand. "If X then why not Y?" is completely answered by "not X".  A complete answer to this question is "because that's not how you get striped cats". Everything else is "simple ways of giving basic genetics information to people".

I want an answer without genetics background required, because I want to explain it to the guy who asked me and he has no idea about genetics. I can explain it by the means of genes and alleles that the result of a pure black and a pure white cat (that's so rare) is whether a white or a black cat. But I just want to find a real-world analogue for it, and it's still science and it's still biology. @rg255

that's what I've given in my answer - also I'm one of the ones arguing that this question is biology related... You're best hope of saving this question is to edit it to show that you understand the genetics and biology of what's going on, and ask for a good layman's explanation

@Farzad your reasoning is not entirely correct. The pigmentation patterns in cats are more complex and if you do ask about them then this question would be opened. It is up to you how you explain your friend. I don't think they can understand the pigmentation patterns without knowing what neural crest cells are.

This is a good and funny question. Cats are not striped? But cats are with black parts and white parts. This can be quite pretty. What aren't humans generally like this? There is a rare case where humans do get parts of different colors: chimeras.

@Farzad you should really edit this question to make it suitable.

The reason that there are no stripes when black and white people get babies is the fact that the number of pigment cells is the same for black and white people. What is different is the amount of pigment produced, and it will be different in the kids as well (lighter than the dark parent, darker than the light parent) See references 1 and 2 for details on the melanocyte density. Skin color is a multigenic trait, so the genetic background of both parents and their effects on pigmentation come into full play here.
Besides this effect, humans do have stripes, although they are mostly not visible. They are called Blaschko's lines and look like below:

These develop from the migration pattern of the melanocytes (and their precursor cells) in the developing embryo. They can get visible in some rare genetic conditions or by diseases. See reference 3 for a more popular explanation and reference 4 for a review on this field.
References:

The Regional Anatomy of the Human Integument with Special Reference
to the Distribution of Hair Follicles, Sweat Glands and Melanocytes
General Biology of Mammalian Pigmentation
Blaschko’s Lines
Lines of Blaschko.

And aren't cat pigments controlled by one gene?

What about cats?

Skin colour is determined by additive effects. That is, the amount of pigment is determined additively by the genes. For the basic genetics of it I will give a simple example, which is just illustrative and a gross oversimplification, it's probably much more complex (many loci all acting at once).
Imaginary example:
Suppose skin colour is affected by a single locus (at one position) within the DNA, which determines the amount of pigment produced. At this locus there are two alleles within a population, that is two versions of the DNA (e.g. ACGTCCATT and GACTTAACT are different DNA sequences). Allele one ($A_1$) produces a small amount of pigment, and allele 2 ($A_2$) produces a large amount. Thus people with $A_1 A_1$ genotype (people are diploid, i.e. they get a version from each parent) have light skin, $A_2 A_2$ genotypes have dark skin, and $A_1 A_2$ have an intermediate skin colour.
Analogy
This is analogous to mixing fruit juice with water - if you mix blackcurrant cordial with water the colour is determined by the proportions. If you put out two bottles, one with cordial and one with water, allow two people to randomly choose a bottle, and use their choices to mix a glass of drink, 50% of the time you will end up with 1/2 water mixed with 1/2 cordial, while 25% of the time just a glass full of water, and the remaining 25% of the time just a glass full of cordial.
Why stripes don't occur
Note: although stripes occur in animals including humans (see chris' answer), it's not I'm the way your question insinuates
For stripes to occur you would have to have structure in the skin with two different types of skin cell, where bands/stripes of type occur - alternating between expressing the allele inherited from the mother, and that inherited from the father. That would require structure in the skin and something called genomic imprinting so parent of origin could be a factor.
The analogy with the glass of cordial is what going on in each cell, for stripes you would have to have organised and alternating clusters of glasses (cells) which get their contents determined by one individuals choice of cordial, with the selector alternating with the cluster of glasses.

Why would black and white bands require genetic imprinting? How do cats have black and white parts?

because the cells in the offspring would need to be able to differentiate between the paternally and maternally inherited allele to be able to organise them in to stripes


text:
What does the "cov" mean in a velvet assembler generated contig name?
A exmaple of a contig name generated by velvet assembler:
NODE_127_length_39203_cov_244.873016

What does cov_244.873016 mean?
It sounds like coverage. Does it mean reads coverage or other statistical description of the contig?

It means coverage

covariate perhaps?

It means k-mer coverage. From the velvet manual:

4.2.1 The contigs.fa file
This fasta file contains the sequences of the contigs longer than 2 k
  , where k is the word-length used in velveth.  If you have specified a
  min_contig_length threshold, then the contigs shorter than that value are omitted. Note  that  the  length  and  coverage  information
  provided  in  the  header  of each contig should therefore be
  understood in k-mers and in k-mer coverage (cf. 5.2 ) respectively.
  E.g.  for a 500bp contig and a k-mer length of 21, the length in the
  header will be 480.

+1 for resisting the urge to say RTFM--I guess that is one of the many reasons we elected you as a moderator: impulse control.

@mdperry Haha.. I'm working on it actually :)


text:
How do researchers map root systems of plants?
For example, here is a picture of the root systems for some prairie grasses:

(Click image for higher-resolution PDF) from: http://www.conservationresearchinstitute.org/educational-offerings.html
How is it possible to follow one root thread 15 feet down? Especially when they are so densely packed in the top foot of soil that you couldn't dig at all without destroying roots.

You originally posted this question on the Garden and Landscaping Section - that's where I'm from, and though it was moved here instead, I'll answer it anyway:
That image you've shown isn't like a photograph, its an impression of what the roots are like. Usual method of working out root patterns on plants is to remove what's known as a monolith, or a block of soil where the plant is - the soil is then either carefully removed by hand, in the manner that archaeologists use, or air blasted, or soaked off in water to reveal as much of the roots as possible. For trees or plants with very large roots, newer methods include geophysical surveying by machine, or electric resistance surveying. Even this doesn't reveal everything - many roots may penetrate too far down, or run along cracks in rocks beneath the soil. The root length and distribution pattern vary according to local conditions, so its hard to be definite about where the roots of any particular plant are in a particular position in the landscape.

Reference and further reading:
Plant Physiological Ecology (ISBN 978-94-009-2221-1; Google books link)
Especially, check the Introduction on page No.367

...why do you assume that it's non-destructive? It's effectively performing an "archeological dig style" excavation, and the particular plant is not likely to survive it.
Here's a couple links to descriptions of "an improved method" along with a description of the "usual method" it's "improved" over, circa 1938 and 1940. jstor previews as these things do mostly get discussed in academic journals.
http://www.jstor.org/stable/1930591?seq=1#page_scan_tab_contents


text:
Which ORF will be translated
I've a question about ORF and translation into protein. Say I have an RNA transcript that contains two ORFs, one in phase 1 ; one in phase2 ; as:

ORF number 1 in reading frame 1 on the direct strand extends from base 529 to base 759.
ORF number 2 in reading frame 3 on the direct strand extends from base 849 to base 1223.

So ORF number 1 comes earlier in the transcript, but ORF number 3 is longer ..
Is it always the first ORF that is translated ?
Edit >

It's in an eukaryoytic organism and same gene (it's the same transcript)

I use ORF finder (http://www.bioinformatics.org/sms2/orf_find.html) on my transcript sequence and it gives me two potential ORFs (ORF 1 and ORF 2 within two different frames)

Thanks

This is impossible to answer. Are you talking about bacteria or eukaryotic cells? Are these different genes?

There are several parameters such as presence of proximal Ribosome Binding Site in prokaryotes or Kozak sequence in eukaryotes, secondary structures etc.

Please [edit] your question and clarify. The answer could be ORF1, ORF2 or both or neither depending on the details. Is this in a species that has introns? Is the RNA spliced? Mature? Are these the same gene? What exactly do you mean by ORF? Are they both terminated by a STOP codon?

Making this even worse, is this a viral RNA that separates ORFs by IRES?

An open reading frame is one that extends for some distance without containing one of the three translational termination codons. This has nothing to do with translation initiation. Translation in both prokaryotes and eukaryotes requires an AUG initiation codon. You don't mention if there are any in-frame AUG codons in your hypothetical transcript. Without this information nobody would be able to provide a meaningful answer.

In addition, there are alternate start codons.

If both of the ORFs that the web tool predicted start with an AUG initiation codon, then the textbook answer is that the 5' cap on eukaryotic mRNAs is the first feature that is recognized by the translational apparatus, and the ribosome scans along until it finds the first AUG (it is a simplified description). However, if there are several AUGs near each other then the one that matches the best to the Kozak PWM (position weight matrix) will be preferred. The Kozak sequence can be approximated by: CCATGG which is also recognized by the restriction enzyme NcoI. Highly expressed genes tend to match most closely to the Kozak consensus.

The most common case like this is a prokaryotic mRNA, where polycistronic genes show up regularly.  In that case the ribosomes are free to attach to the RNA and both genes are usually co-translated.

The proportion of translation between the two genes does vary depending on the affinity of the ribosome to the mRNA, which is partially determined by the ribosome binding site sequence.
If there is a lot of transcription activity on the mRNA, many ribosomes at once can translate any single ORF, as you can see in the micrograph above.


text:
(How) Does the human digestive system process petroleum jelly, aka petrolatum?
Does the human digestive system processes petroleum jelly? In other words, does it pass through the digestive system without any interaction, or is it absorbed and/or metabolized?

Liquid paraffin was used as a laxative (i don't know if it still is).

There are controversial case reports about systemic absorption of paraffin used for constipation. These reports mention systemic effects of paraffin absorption and one of them report liquid paraffin accumulations in
abdominal visceral organs. (full text article about paraffin)

Liquid paraffin is indigestible and is absorbed only to a limited
  extent following ingestion.

+

As inert substances the ingested mineral oils mostly are excreted
  intact in feces and to some degree in urine. However, some absorption
  form the small intestine has been observed (Stryker 1941). Using
  radiolabeled mineral oil, it was established that the amount absorbed
  in rat was appr. 1.5 % (Ebert  et al. 1966).

  (full text article)

Is paraffin the same as petroleum jelly? I was under the impression that paraffin was a more-or-less natural wax, and that petroleum jelly is a byproduct of oil refinement.

@mHurley In the scope of the question it is the same. https://en.wikipedia.org/wiki/Petroleum_jelly


text:
What is a substance that is safe to eat, not absorbed and not metabolized?
I would like to know whether there are substances that are safe for humans to consume, are not absorbed and do not interact with any digestive process.
So, food is disqualified because although it may be safe, it is processed by the digestive system and is metabolized. I'm looking for things that go entirely unprocessed (other than passage).
One such material, or a discrete class of materials is sufficient.

Would dietary fiber count?

Dietary fiber stimulates the intestinal movements. I think the phrase '...do not interact with any digestive process' effectively kills any answer, including laxatives and dietary fibers.

This is by no way an opinion-based question.

Dietary fiber might qualify for what I was thinking about; perhaps I just asked the question poorly. Either way, it isn't nearly shocking enough ;-)

Several sugar substitutes stimulate taste buds but are [largely] indigestible. Whether they are safe in a health sense is debatable.

Simethicone is one example. It is a mixture of silica gel and dimethicone (polydimethyl siloxane); they are individually inert too.
Simethicone/dimethicone is used as antigas (they help the gas bubbles coalesce). It does have a laxative effect, though.

Do you have any reference for that?

@rg255 Wikipedia is a basic reference; added that. It is kind of a known fact. I don't know of pharmacology databases. Looking for one.

Wiki is good enough there I think

Yeah, Wikipedia is fine for my purposes.

How about gold. You can find it on foods, but it is inert and also not absorbed.

any reference to that?

[...] gold nanoparticles [...] absorption across intestinal barriers and accumulation in secondary target organs after oral administration: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267526/

So gold nanoparticles can be taken up and subsequently deposited throughout the body

I doubt there's any research on macroscopic lumps of  pure gold and digestion, but i suspect they're entirely unaffected by the process.

I can look for a ref for this, but we use gold as a tracking source that does not get absorbed/digested. But nanoparticles are a bit unique, it isn't so much the compound as it is the size that facilitates their absorption and subsequent tissue trafficking. So @AliceD, your answer is a bit misleading, because you could really say this for a large swath of materials regardless of how much they get absorbed as Resonanting says, as a 'lump'.

@TheNightman, nice one. But my comment is not an answer, its a comment only. I'm just playing devil's advocate. As I commented under the question, I think this question is all-exclusive. I'm considering close-voting it because of its opinion-based nature.

Well, this might reveal the real answer to my question, which MIGHT be "anything will be absorbed if it's small enough."


text:
Is this a crayfish hole? or wasp nest?
I'm suspicious that it might be crayfish, which I'd think was insane (I still kind of do), if I hadn't found a dead one around  my house earlier this summer.
Is that definitely what it is, or do I have to worry it might be wasps?
I'm located in Michigan.

It is indeed a crayfish hole (sometimes referred to as a "snakehole" in Michigan, even though it is not from a snake), albeit it has eroded from weather. If you have one in your yard, you likely have dozens, and they will range in their appearance due to soil and weather conditions.
Example 1 and Example 2.

I'm inclined to agree.  Is this something I need to be concerned about?  I prefer not seeing miniature lobsters in my yard, and I don't live near above ground water, so it's odd, but will they cause any problems?

Also, just to note:  we have a sprinkler system and it has been a very rainy spring/summer which could account for the soil being pressed down.  It has the right mud-like texture to match crayfish.

@user1167442 No, they are harmless, and you'll rarely see one. If you don't like the appearance of the holes, you can knock over the burrows and kill them by putting a teaspoon of lye in the hole. However, you'd be fighting a losing battle. If you consider them to be a problem, then better drainage might reduce the number of them next year.

This is the nest of a cicada killer wasp, Sphecius speciosus.

Harmless, solitary and  Cicada-killer wasp holes are ½ half to 1-inch around with thinly scattered loose soil, usually where there is no grass. Cicada-killer burrows have a U-shaped mound of soil at the entrance. Adults emerge June/July.

Source: All the Dirt on Gardening blog
According to the Wikipedia article linked above:

this species occurs in the eastern and midwest U.S. and southwards into Mexico and Central America.

so being in Michigan, you are certainly within the region in which the insect is found.
Parenthetically, also according to the blog from above:

Crayfish holes are 1-inch wide, 2-inches high and made of mud balls.

and the texture of that hole looks more even.

Related Bio.SE question:  Cicada Killer Behavior

Great answer! Perhaps I should change my last name...

The reason the texture of the hole looks even is due to the Michigan clay and erosion from rain. This is not a wasp nest.

Interestingly, I have some experience with Cicada Killers ... See http://biology.stackexchange.com/questions/9830/bee-identification.   I haven't seen any around and I suspect I would've noticed.

@vallismortis. That is smart.  I have a heavy clay based soil with sod on top.


text:
What concentration of table salt is needed to kill bacteria in sweaty gym clothes?
My gym clothes retain an unpleasant musk even after washing them with warm water and detergent. I've experimented with soaking my gym clothes in salty water before washing them. My hypothesis is that the high salt concentration will cause plasmolysis in the cells of the bacteria. It has worked with mixed results; I'm never sure how much salt I should add or how long to soak the clothes.
I've looked for answers but I can only find papers with highly technical results.
(1) Can the odor-causing bacteria be killed with a salt treatment?
(2) If so, what concentration of table salt is needed?
(3) How long does the treatment need to last for plasmolysis to occur?

Lack of water and UV are great - Always let them hang outside right after use, never let them incubate in your sports bag and sunlight is devastating to microorganisms.

Specifically, hang them outside in the bright sun. You can soak your clothes is soap water or a mild perfumed disinfectant like dettol.

@WYSIWYG - is this question answerable without knowing the exact microfauna inhabiting OPs skin/clothes?

@AliceD Can be difficult because usually normal washing is sufficient unless the clothes have taken a long time to dry (rains etc). In such cases molds also start growing on clothes. In any case I am not sure if this salt method would be effective.

I just wanted to throw in, that if you are using fancy gym cloths (made out of those nice fabrics which are supposed to help air circulation and such, I am not an expert on what they actually can do), soaking them in salt water might actually destroy your expensive gym clothes in the long run.

You should keep in mind that the odor is a mixture of stale sweat and chemicals produced by microorganisms, not necessarily the microorganisms themselves. Basically, by the time the odors appear, it's already too late. Thorough washing and immediate drying of your clothes after exercising can help mediate the accumulation of additional odors, but what's there is there. These aromatic organic compounds can bind very tightly to the fibers of the cloth, and are quite difficult to get rid of. Bleach may help, depending on the type of fabric (and color), but I doubt salt will do much of anything.

detergents containing benzalkonium chloride are very effective against bacteria in heightened concentrations or lengthened exposure time. they certainly work better than salt, plus they may also help clean your clothes of dirt, oil and sweat.

Short answer
Toxicity of salt depends on contact time. 50 g NaCl per liter kills nearly all bacteria in 2 days. 100 g NaCl/L may do a quite thorough job in 30 minutes.
Background
Body odor is caused by bacteria that feed on the fluids produced by the apocrine glands, mainly present under the arm pits and other areas with abundant hair follicles. Bacteria in the skin feed on the products of the apocrine glands and convert it into odorous compounds. Skin microfauna includes Staphylococcus, Micrococcus, Corynebacterium, Dermabacter and others. As pointed out by others in the comments, treating your cloths against bacterial growth may not be the most efficient approach, as the bacteria are residents of the skin. Nonetheless, the following studies addressed the antimicrobial effects of salt.
A study using the gut bacterium E.coli showed that survival in 5% NaCl (50 g NaCl per liter H2O) was <0.01%. In 2% NaCl survival survival was 8%. The contact time was 48 hours (Carlucci and Pramer, 1958).
Another study examined the effects of salinity on E. coli using a shorter contact time of 30 minutes, and concluded that 10% salinity killed 80% of organisms (Somani et al., 2011).
Sea water, which has a salinity of about 3.5% contains low numbers of bacteria (Carlucci and Pramer, 1958), suggestive of toxic concentrations of NaCl, the major salty constituent in sea water.
Although E. coli has been associated with skin fauna and body odor, I must note that Gram negative gut bacteria as used in the two studies above may not be representative of the mainly Gram positive microfauna found on the skin (Strauss & Kligman, 1956).
References
- Carlucci and Pramer, Am Soc Microbiol (1958)
- Somani et al., J Eng Res Studies (2011): 40-43
- Strauss & Kligman, J Invest Dermatol (1956); 27: 67–71

5% NaCl is 5g/100mL

well, approximately yes, but to be exact 5g/100mL is probably less than 5%, though the difference should be quite small.
@AliceD is it probable that skin flora have adaptations to make themselves more resistant to salt since they live on skin which easily gets sweaty?

@busukxuan good question!

@busukxuan Biologists often use w/v concentrations. 1% w/v is defined as 1 g / 100 mL. According to Wikipedia, the sodium concentration in sweat is around 15-65 mM (50 mM is ~0.3% w/v). Bacteria should easily tolerate this without special mechanisms.


text:
How bad is ethidium bromide in your plasmid for downstream applications?
I want to transfect Adipose Derived stem cells using a clone of my own. My problem is that I get a lot of contamination (not only genomic, but due to the nature of the technique, I get undesired products I haven't been able to get rid of).
So I was thinking about running a gel with my plasmid DNA samples and gel purify my desired bands. I don't know, however, if Ethidium Bromide contamination in my sample would be a problem or if a regular gel extraction kit gets rid of it.

No, there is absolutely no problem with that. And you get rid of the EtBr in the purification anyway.

Ethidium toxicity is probably not as bad as they make you think, they use it at like 1 mg/kg in cattle to prevent parasite infections.

And I should point out that it's not efficient to use plasmid purified from gel directly in a mammalian cell transfection. You should consider a larger scale prep. If its a problem of incorrect plasmids, transform your plasmid mix in bacteria, pick several SINGLE colonies and miniprep them, sequence and try again.

Possible duplicate of http://biology.stackexchange.com/questions/14047/ethidium-bromide-and-mutagenesis-on-cloning

Thanks for your insightful answers!
To answer user137:
I cannot expand my plasmid in bacteria to use a larger prep since the OriR sequence is excised and degraded from the construct after induction with arabinose. This is what I'm trying to get: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144359/
Again, thanks

@Varekai I've used minicircles before, it's a pain, but you'll probably have to go back to the bacteria step and grow up your minicircle parental plasmid in large volume and go through the recombination step to remove the bacterial elements, then gigaprep the plasmid. If you don't get 100% conversion of parental plasmid to minicircle, consult your manual's troubleshooting section and do it again.

Purification and isolation of DNA bands by cutting them from agarose gel is commonplace (Lee et al., 2012). The purification step after excision of the band gets rid of most of the EtBr and other impurities. E.g., see the websites from Isogen and Sigma-Aldrich.
Reference
- Lee et al. J Vis Exp (2012); 62: e3923


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Linear and Circular DNA
So school has taught us that eukaryotes have DNA that is linear and inside of a membrane - called the nucleus. And that prokaryotes have circular DNA that is free floating inside of the cell.
We also know the pros and cons of both linear and circular DNA.

Are there organisms with circular DNA that also have a cell nucleus?
Are there organisms with linear DNA that is also free-floating within the cell?

generally prokaryotic cel contain circular DNA with exception like agrobacterium tumefaciens that contain 3 circular & one linear DNA.

Yes there are prokaryotes with linear chromosomes (especially archaea). Eukayotic chromosomes are almost always linear but this, study reports that yeasts with a loss of function mutation in the ATM homolog genes TEL1 and rad3, form circular chromosomes as a consequence of lack of telomeres. Upon prolonged culture these yeasts were found to undergo mitosis but not meiosis.

Strictly speaking, all nucleated (eukaryotic) cells contain linear DNA. In addition to the nucleus, the mitochondria (which break down food molecules and create chemical energy) and chloroplasts (which facilitate photosynthesis) also have small stores of their own DNA and this DNA is circular. This adds weight to the hypothesis that these organelles were once prokaryotic cells that came to exist in symbiosis with early eukaryotes.
There is also cytoplasmic DNA free-floating in eukaryotic cells. These are also circular and normally contain short copies of chromosomal DNA sequences. Their function is not well understood.
In prokaryotes, some species of spirochaetes and bacteria have been found with linear chromosomes. In addition, prokayrotes contain extra-chromosomal DNA called plasmids. Bacteria are able to pass plasmids from one to another and express the genes on them: this is an important source of the spread of antibiotic resistance genes through bacterial populations. Plasmids are also normally circular, but linear structures also exist.
References:

Cohen, Sarit; Andreas Houben; Daniel Segal (2008). "Extrachromosomal circular DNA derived from tandemly repeated genomic sequences in plants". The Plant Journal 53 (6): 1027–1034.
Hinnebusch J; Tilly K (1993). "Linear plasmids and chromosomes in bacteria". Molecular Microbiology. 10(5):917-22
Finbarr Hayes (2003). "Chapter 1 - The Function and Organization of Plasmids".

"There is also cytoplasmic DNA free-floating in eukaryotic cells." Is this stated in one of your references? I'm having a hard time tracking it down.

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


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Why does my anti-ubiquitin antibody visualization not work on my PAGE gel?
I am using 2D gel electrophoresis to visualize polyubiquitinated proteins. However, while I can see actin and heat shock protein using when appropriate antibodies, I cannot visualize them using anti-ubiquitin antibody. Could it be degradation problem?
I run isoelectric focusing at 200 V overnight (at least 18 hours) and 700 V the last 30 minutes. I am worried that I am applying more volts than needed, because the standard protocol is 200 V for 20 minutes, 450 V for 15 minutes, 750 V for 15 minutes, 2000 V for 30 minutes, but due to problems with the power unit I cannot do this.
I am sure I have polyubiquitination because I use a drug that triggers polyubiquitinated protein accumulation inside the cells.
I would like to add also that cells are collected by scraping in cold PBS and then they are placed in ice and the pellet is also collected at 4 degrees to prevent protein degradation.

Do you have protease inhibitors in your lysis buffer? If so, which ones? Also, does your anti-ubiquitin antibody work when doing a straight SDS-PAGE Western blot?

MattDMo, My anti-ubiquitin antibody works doing Western blot.

MattDMo, My anti-ubiquitin antibody works doing Western blot, but I don't use lysis buffer, after collect my cells by scraping using PBS I centrifuge the eppendorf and I freeze the dry pellet (withouth PBS) in liquid nitrogen, then I resuspend the pellet directly in rehydration buffer (urea, CHAPS, ampholytes, bromophenol blue, DTT) and I add Urea and vortex until I see a litle urea precipitates at the bottom, then I centrifugate it at 10.000 rpm 5 min and I use directly the supernadant to rehydrate my strips.

Do you have a positive control you could use next to your samples?

That is what I am looking for, I am trying to show that is possible to distingue polyubiquitination from negative control, but I have never done this before, so I don`t have anything to compare as a positive control, if so, that would mean that finally the procedure works and the spots appears.

@Biomedi when addressing a comment to someone, please put an @ symbol before their username so they can be notified.

There are stable ubiquitinated proteins in mammalian cell lysates even if active proteosomes exist in cells.
First, you might want to make sure that the antibody is applicable to WB.
Then, you would ask if your WB system using the antibody works. You could optimize the condition using just 1D SDS-PAGE followed by WB.
For the condition for isoelectric focusing, when focusing is completed, you get very high electric resistance, so you might want to monitor current after you change the voltage to 700 V. Current decreases gradually, and get stable at some level. But I do not know you can see stabilization by 700 V.
You also might want to check if major proteins such as actin form spots nicely at the expected pI. That could tell if forcusing is completed roughly.

Yes, the antibody is applicable to WB because I have used it before. I use a kind of homemade circuit connecting my system to electrodes that are connected to a water recipient, so the current I think is ok. The proteosome is alterated by the drug I use, so the proteins are accumulated  in the cells. So if I put more time that the procol say, it could be that a problem because polyubiquitinated protein could be more sensitive to be destroyed or some reason?

Urea is strong denaturing effects, so you would not have protease activities in the rehydration buffer. I am not sure about proteasome activities during freeze-dry process. Maybe ok, but no guarantee. Can you directly add the rehydration buffer to cell pellets? Or you can add acetone or 10%TCA to precipitate proteins so that proteases are immediately denatured and inactivated, and proteins you are interested in can be protected from degradation.


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Design arbitrary degenerate primers (with non-binding criteria)
I would like to design a number of arbitrary degenerate primers (primers with variable bases, e.g. NGATWGCTSATNGC) for a TAIL-PCR.
I would like to be able to specify the following parameters for the design function:

Annealing temperature (ideally 44°C)
Degeneracy (how many variations of the AD primer there are (ideally 128 or 256)
Binding frequency on (mouse) genome (ideally 1/3000) - though this may be contingent on the degeneracy, and vice-versa.
Non-binding area (of course I would not like any variation of the primer to bind to the known-sequence area in between my specific primers and the unknown area which I want to sequence)

Any ideas of any tools that can help me with the above steps? For Primer design I have used eprimer3 thus far (with invariably satisfactory results) - but it seems to not support the concept of arbitrary degenerate primers.
Ideally, if I had a function which could sort out the first of the above criteria, I could use Biopython and BLAST to script the rest myself. Though the binding frequency would take hours if not a day or two, for BLAST to determine it. It would greatly help if anybody already wrote something more elaborate for this.

Do you know the sequence that you want? I mean, the degenerate places marked as N but the rest present. I don't know of a program that does it. But I can suggest you a workflow that would use simple scripts and existing bioinformatics tools.

go, ahead, suggest! As for the question, no, the sequence itself is completely irrelevant to me. what I care about are the criteria mentioned above. Any sequence that fulfills them would suit my purposes.

Regarding the 4th point: I am assuming that the exact primer is of same length as the degenerate ones. Do you want primers with variable lengths? That will be more complicated.

By the "exact" primer you mean the specific primer(s) for the TAILPCR? if so, no, they are ~20bp, the AD primers should be around ~14bp (though I guess that can be varied a bit to account for binding frequency and annealing temperature).

If you already know the basic sequence i.e. the fixed regions in the primer; for e.g. the known nucleotides in the sequence -  NGATWGCTSATNGC, then you can implement your algorithm like this:

Fix the max length of the primers. Lets say 20nt.
Generate all combinations of primers (20nt): that is pretty straightforward. You will have  4N × 2(R+Y+S+W+K+M) × 3(B+D+V+H) number of combinations, where each alphabet denotes number of such instances. Chek this site for the nucleotide codes.
Calculate the Tm of the primer-template pairs. UNAfold has a nucleotide hybridization Tm calculator. You can specify parameters like salt concentration etc. There are other such tools too. These can be run on the commandline.
Discard all primers have Tm below the acceptable limit.
For those that exceed the acceptable Tm, keep dropping a base from the 3' until the Tm reaches within the range.
If primer length goes below 14nt then discard the primer.
Now with all these selected primers check for parameters like self hybridization, GC clamp etc (OPTIONAL). You can use primer3 for these purposes by running it on the primer_check mode.
Download the nr/nt BLAST database.
Adjust BLAST parameters for short nucleotide search: Decrease the word length, increase e-value cutoff etc (See this biostar post and BLAST help).
BLAST your primers against the database in plus-minus mode.
Worry only about cases where there is significant alignment at the 3' of the primer as only these can cause extension.

These instructions can be automated using any language or shell script.

Questions on script writing would be off-topic in this site. You can ask specific doubts about coding in stackoverflow.


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Is perceived time compressed or expanded while dreaming? (or does it match reality)
I often dream long extended dreams.  Sometimes I wonder if the timeline of the story of my dream occurs compressed, in a moment, or other times extended slowly over a long duration.

Is there any way to scientifically detect this, and how would it be accomplished?
Are there any prior examples of this study being performed?

Cognitive Science SE might be a better community to ask.

I agree, this isn't really a Biology question, although it's an interesting question.

OK asked it here: http://cogsci.stackexchange.com/q/10521/8716

I'm closing this question as off-topic because it is already cross-posted in cogsci.se which is probably a better site for this question.

@WYSIWYG agreed, definitely.


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What is the name of this bird?
Does anyone know the name of the bird in the pictures? It was found in the south of Spain in the month of June. (it is certainly neither a house sparrow nor a swallow nor a robin). Thanks for the help!

It could be female "Common blackbird" (Turdus merula)

Yes, it is may be a female, but it is surely not a "Common blackbird".

what is its size? otherwise tell compared with other known birds.

Sorry I don't have its exact size. It looks like a house sparrow, but it is a little smaller than a house sparrow. Its head is also smaller than the head of a house sparrow.

Is it possible that it was a species escaped from captivity?

Sorry I don't know. Maybe.

I asked if it would be escaped because by the colors it looks like a Chestnut Sparrow but it does not live in Europe but in Africa (Kenya, Tanzania and around). Otherwise it could be another sparrow family (the shape of the beak looks it is the Passeridae family) but difficult to say like this.

Couldn't it be a juvenile of some well known species ?

http://www.king5.com/story/news/local/pets-and-animals/2015/04/05/little-brown-bird-sings-happy-easter-song/25335167/

Yes it could also be a juvenile but I do not know too much about variation of colors for these birds; it could also be so old that it just get dry and loose its original colors.

The plumage looks in-between adult and juvenile. I think it's a fledgling, which is why no one can really identify it.

Thats a difficult one but my gut feeling is a 'bunting' and maybe a Rock Bunting juv ? - the bill is definitely bunting-like and there does seem to be a black and white eye stripe going on . There arent that many buntings in the south of Spain especially with a very warm brown colouring


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Choosing the best assay for my experiment?
Which of the following assays can be used to determine whether cell death specifically due to apoptosis has occurred in a given cell sample? Choose all that apply.

WST-1 Assay
Caspase Colorimetric Assay
Trypan Blue Staining

Which of the following assays can provide direct information about the plasma membrane integrity and/or morphological features of apoptotic cells? Choose all that apply

Annexin V-FITC / Propidium Iodide staining.
WST-1 Assay
Caspase Colorimetric Assay
Trypan Blue Staining
Wright Staining

My knowledge is very limited with these assays. I know Trypan Blue is used to measure a cell's viability, with dead cells stained blue. Wright Staining is used to study the cell's morphology and makes fragmentation visible. Caspase color and the WST assay seem very similar to me. Both measure cell viability with spectrophotometry.

Welcome to Biology. Homework-type questions are welcomed, provided OP shows prior efforts to answer the question in the post. Please edit.

I'm really not provided much information on the assays and the internet is not being very consistent. As far as I know for the first one I believe Trypan Blue Staining is one but im not sure which of the other two could be considered... possibly Caspase colormetric assay? As for the second question i think it is wst and wright staining. Again my knowledge is very limited with these assays. But I would really appreciate clarification or guidance.

I know trypan is used to measure a cells viability, with dead cells stained blue. wright is used to study the cells morphology and fragmentation is visible with it. caspase color and WST seem very similar to me. Both measure cell viability with spectrophotometry. otherwise i cant differentiate.

Great additions, please edit this info in the question, as folks may not read the comments. After edits I'm happy to retract my close vote and give you an upvote too :)

I'm voting to close as homework, despite the editing it still makes very little effort to self help.

I agree with @rg255. You should at least make an attempt to read what these assays are. "Caspase color and the WST assay seem very similar to me": this is not true. Read about them. As it stand it looks exactly like a homework with a very little effort.

Necrotic cells could be trypan blue positive. WST-1 Assay could reflect cell number by measuring mitochondrial dehydrogenase, therefore, you could not know how many cells die in dishes. When you define apoptosis in your experiment as caspase dependent cell death, measuring caspase activity is the best.
PS
Trypan Blue Staining actually is a method to see membrane integrity.


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How many animal species are larger than humans?
I sometimes think about just how huge humans are in comparison to most animals. Even compared to a squirrel, which is really a pretty large organism in the grand scheme of things, humans are hulking giants.
I know humans are classified as megafauna, but we're neither the smallest nor the largest animals in that group.
How many animal species currently exist where the average adult individual is more massive than the average adult human?
Sources that cite other measures of size, like height or length, might be useful, but I would expect the focus to be on mass.
Obviously, new species are being discovered all the time, and we don't have exhaustive measurements for every species, but considering how few megafauna there are, I would expect a fairly accurate estimate to be possible.

Welcome to Biology.SE. Larger in term of distance between the two extremities of the body? Larger in weights? or in volume? Would Placentonema gigantissima (9 meters long, 2.5 cm in diameter) be bigger than a human? Are you talking only about extant species?

In the last sentence you rephrase your question "How many different species are actually larger than us", do you mean animal species (as specified in the title) or any species? In many non-animal species, the concept of individual might be hard to define. There's a fungi who covers an area of almost 9 square km in eastern Oregon.

Depending on the exact formulation of your question I think that an exhaustive list might be very long. But I guess someone could come up with a rough estimate of the number of species.

Echoing remi.b's point - unless this question is narrowed down it is very broad.

@Remi.b I definitely mean animal species, I don't know why anyone would think I would suddenly be referring to fungi. I've clarified that. I'm referring to extant species. I assumed that mass would be the implicit measure for size, but I've clarified that as well. I didn't ask for a list anywhere, just a number. Listing them would be helpful, but not necessary.

I think this question is not broad at all, there have been plenty of serious estimates of species richness ~ size relationships: http://www.life.illinois.edu/ib/451/May%20(1988).pdf

Yes, the answer is a single number. That's about as far from broad as you can get.

EOL knows about (268 species of mammals with a mass >= 80.7kg)[http://eol.org/data_search?utf8=%E2%9C%93&taxon_concept_id=1642&attribute=http%3A%2F%2Fpurl.obolibrary.org%2Fobo%2FVT_0001259&taxon_name=Mammalia&min=80.6&max=&unit=http%3A%2F%2Fpurl.obolibrary.org%2Fobo%2FUO_0000009&sort=desc&commit=Search] and (5,701 species of mammals with a mass <= 80.7kg)[http://eol.org/data_search?utf8=%E2%9C%93&taxon_concept_id=1642&attribute=http%3A%2F%2Fpurl.obolibrary.org%2Fobo%2FVT_0001259&commit=Search&taxon_name=Mammalia&min=&max=80.7&unit=http%3A%2F%2Fpurl.obolibrary.org%2Fobo%2FUO_0000009&sort=desc]

@Gaurav Well that's pretty neat. I was not familiar with that website. I don't know how exhaustive EOL's data is, but that looks like the core of an answer to me.

Looks like 80.7 kg is the average for humans in North America. Google says the average for humans worldwide is 62 kg, but EOL has it listed at 68.8 kg.

I agree the question is definitely no too broad. I first voted to close as unclear, it is now clear and I am voting to reopen.

Humans weigh 62 kg on average. According to https://www.catalogueoflife.org/col/info/totals, there are 91 cetacean species, 80 of which are larger than humans.


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Beetle with long, slender iridescent green body and orange legs
I recently saw this beetle while on a trip in central Texas, USA (in a rural area just before sundown). The body was about 2-3 inches long (compare to nearby chair leg and floorboards) and had a long body. It was very vivid green, and its upper legs were very bright orange (which made me wonder if this is aposematism). Its antennae had very uniform half-circle arcs (instead of the uneven parabolic shape often seen in cockroaches and similar common insects) and didn't seem to bend besides being rotated ~5 degrees up and down.
It carried itself pretty high off the ground, perhaps half an inch between the belly and ground-level. It seemed to move fairly fast, but not as fast as a cockroach. It didn't fly in the few minutes I observed, and didn't seem like it could fly since the shell appeared solid, but I might have mistaken well-fitting sheaths for fused ones.

What is the most likely species? Is it poisonous?

I can't see the antenna well, but they look long. Could it be some sort of longhorned beetle?

@user137 For anyone wondering, the antenna were quite long - all of the blurry blackish line is antenna. Based on my recollections, if I pulled on them and straightened, they would be between 1.25 and 1.5 times the length of the beetle's body - consistent with your answer as well!

With this image, I've had one bite me, after maybe 6 hours a blister began to form. I believe it's a blister beetle.

I'm going to guess it's an Plinthocoelium suaveolens, based on the image found here, which I show below:

I found this link through a Texas beetle page here and is the best I can do from the image provided.


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Evolution of insects, spiders and jellyfish
Well we all learned at school the classic evolutionarily theory
From:          To:
fish           amphibian
amphibian      reptile
reptile        mammal
reptile        bird

But what always interested me:
What about invertebrates?
Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?
I can roughly imagine that there are giant evolutionary gaps between an insect and a jellifish but is there any common ancestor of all of them?
So my question has essentially two parts:
1. What is the common ancester between vertebrates, arthropods and molluscs
2. Is there an evolutionary Tree for the last two like for the vertebrates

Have a look at this post

Welcome to Biology.SE
Answering your question fully will require to write a whole book. Evolutionary Biology is a big field and I would recommend that your take some time to get an introduction (slightly more advanced than what you received in school). I am suggesting you take advantage of this free online resource.
I am briefly making comments and answering your question(s) below. They may be hard (or easy, I don't know) to understand but for more info you should really get to the above free online resource.
Species A evolved from species B
Evolution did not make mammals out of reptiles, mammals are reptiles. Evolution did not make birds out of reptiles, birds are reptiles as well (I am using here the phylogenetic definition of reptiles (Reptilia), more info there). It is wrong to think of any two extant species as one having evolved from the other one. But it is correct to understand how closely related are two extant species. It is also correct to make predictions about how the most recent common ancestor (MRCA) look like and it is true the the MRCA might look more like one of its descendents than like another.
We talk about clade as a lineage including many species. In these terms both any lizard species and any given bird species belong to the same clade, the Reptilia, they are both reptiles. They are also both vertebrates (Vertebrata) and animals (Metazoa) and eukaryotes (Eukaryota).
If the statements of the kind "mammals evolved from reptiles" are very misleading the statement "amphibians evolved from reptiles" is simply wrong. The MRCA of reptiles and amphibians was not a reptile (neither an amphibian), it was a tetrapoda (vertebrate).
I can roughly imagine that there are giant evolutionary gaps between an insect and a jellyfish but is there any common ancestor of all of them?
Any two species on earth have a common ancestor. The universal common ancestor, that is the common ancestor that any living thing (bacteria, plants, lizard, human, fungi, jellyfish, Archea, etc...) is called LUCA (Last Universal Common Ancestor). So yes, jellyfish and insects have a common ancestor. LUCA is one of them. Their MRCA is the same guy as the MRCA between jellyfish and you, as insects and primates are more closely related than are insects and jellyfish. This MRCA is an animal (a metazoa) and therefore is also a eukaryote (Eukaryota).
Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?
Evolution occurs in every single living population. So yes, evolution occurs in jellyfish as it occurs in insects. The clade of jellyfish contains several thousands of species (most of them belong to the clade Hydrozoa). There are almost a million species of insects.
Here are just a few fun facts that come to my mind when I think about jellyfish:

Some species have tentacles, some don't.
Some species have alternance of generation (a given individual is either a sticking thing on the ground while its descendent is swimming).
Size of jellyfish vary wildly

And a few fun facts about insects:

Some have evolved 3 pairs of wings to fly (we think it evolved from gills but it might have evolved from the exoskeleton as well).
Some live in water, some not, some live in water in the larvea stage and not in their adult stage.
They have all sorts of diet
When flight evolved at first, they had 3 pairs of wings. All extant species (who are descendents of this species that evolved flight) have now lost at least one pair of wings, the one closest to the head.
Some species have lost flight.
Some species have lost a second pair of wings (diptera)
Some have evolved crazy mimetism and defense mechanism from the developmental pathway of the third pair of wings.
Eusociality (which is arguably one of the most mind boggling things in evolutionary biology) has evolved several times in insects.
Some species have sex that is determined the ploidy (number of sets of chromosomes) level (it is the case in many eusocial species).

1. What is the common ancestor between vertebrates, arthropods and molluscs?
You can explore the tree of life by yourself on tolweb.org. Arthropods and molluscs are more closely related than any of them are to vertebrates. The MRCA of vertebrates, arthropods and molluscs was a Bilateria (animal, eukaryote). You can see this bifurcation here on tolweb.org. I'd recommend to explore a bit this tree of life, it is pretty fun to do.
2. Is there an evolutionary tree for the last two like for the vertebrates?
Yes, see above.
BTW, I noticed that you talk about spiders in your title but not in your post. You'll find the spiders here on tolweb.org.

You have to be very careful when saying what evolved into what.
In fact you can only say that e.g. ancestors of modern amphibians evolved from the ancestors of modern fish.
Ad. 1 Have a look at this simplified picture of the evolutionary tree of life
Ad. 2 Yes all living organism including plants, bacteria, fungi, and animals can be placed on one evolutionary tree goverened by the same principles of evolution


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What is happening when we get a tan?
Almost everyone nowadays wants that nice summer tan, but what exactly is going on beneath the skin? I've heard a few different theories about tanning - such as a tan is nothing but the pigmentation in your cells burning, but is this true?
My questions:

What exactly is happening to our skin as we tan?
Are pigments being burned (like I was told in school), or is pigment being produced by the cells. ?

Bonus related question:
Why do some people burn and others tan?
Bonus related question: https://biology.stackexchange.com/questions/35719/how-does-our-tan-disappear

When our skin is exposed to the sun, this can cause some damage in the upper layers of skin. This activates DNA damage repair and also induces signalling towards the melanocytes (which produce the pigment). Signalling means the excretion of signalling molecules (mostly alpha-Melanocyte stimulating hormone, aMSH) which binds to the MC1R receptor (melanocortin 1 receptor) on the surface of the melanocyte (the cell which produces the pigment) and induces (or increases) the production of melanin. The melanin is then transferred in the melanosomes to the adjacent keratinocytes, which are then better protected from the sun. This figure (from this article) illustrates this process nicely:

Short term tans (the fast reaction) are based on the changed distribution of melanosomes (granules containing pigment) from the melanocytes to keratinocytes. Longer term suntans are caused by increased pigmentation in the skin as a reaction to the UV exposure by the accumulation of melanin and by the burning of cells. So it is no wonder that it looks like increased pigmentation, it really is. People tan differently because of their genetic background. This influences their ability to react to sun exposure.
There is relatively little known about the degradation of the melanosomes (the granules containing the melanin). What is known is that they are degraded in the lysosome, and that the melanin is most likely degraded through oxidation. There happens to be a permanent turnover of the melanosomes, and when the body is producing fewer new melanosomes than are degraded, your skin will get lighter again.
References:

Shining light on skin pigmentation: the darker and the brighter side
of effects of UV radiation.
Melanocyte biology and skin pigmentation.
Melanosome Degradation: Fact or Fiction

I have a doubt. As keratinocytes are shed off from stratum corneum then will the melanosomes that they contain also be lost with them?

@WYSIWYG This is true for the dead cells in the stratum corneum. And there will be some pigment in them. But there has to be some degradation mechanism, as freckles also get weaker in the winter (with less UV exposure) and these don't get lost generally.

Some additional details on the same lines as Chris' answer:
Coelho et al. have studied the short and long term effects of UV on human skin and they report that there are different stages of tanning:

Immediate pigment darkening: happens in a few minutes and persists for some hours. It is most probably due to melanosome redistribution and melanin oxidation by UV.
Persistent pigment darkening: happens in a few hours and can persist for days. It happens because of new melanin synthesis in the epidermis.
Delayed pigmentation: happens in a few days and persists for weeks. It results from "prolonged increases in melanin content".
Long-lasting pigmentation:  persists fore more than 9 months after the first UV exposure. The mechanisms underlying this response are not very clear.

IFN$\gamma$ signalling is involved in inhibition of melanogenesis and apoptosis of melanocytes [1,2]. This is one possible pathway of detanning. This happens in the order of days.

First, one should mention types of skin: skin type defines how the person will tan -

Second, the solar radiation (UV) absorbed by sun defines the amount of melanin produced by melanocytes of the skin to protect the skin = melanogenesis (which in turn depends on skin type).
When the solar exposure diminish, the natural repair processes causes melanocytes to remove excessive amounts of melanin.
As mention by WYSIWYG, the question too broad, you can continue your education via wiki.


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Cut-off values for LD, LOD and D-prime as algorithmic input
I created an algorithm to generate SNPs for random people of different descents - based on HapMap data. While this works good, there is something else I want to take into consideration. So if a SNP has a MAF of 0.01, with an LD of 1, the generated results will, in most cases be sufficient. This is not the case for a MAF of 0.4 and LD of 0.8.
The HapMap LD files have, besides the LD data, also LOD and D-prime. The question is, is there a set of parameters so that as much of the relevant LDs are filtered out of the total set?
I want to filter this out, since, for example, there are LDs described with a value of 0, or an LOD < 1, and problematic D-primes.
Trying to rephrase the question:
Given a huge set of LD information (250GB), which are not filtered on statistical power, I want to make a subselection of LD information that are 'relatively' descriptive of the link with respect to another SNP. So I need to have a set of parameters to filter the LD information from HapMap. Of which possible values are LD, LOD, and D-prime.
Eyeballing the LD dataset, it doesn't gives a good instinctive boundary. A problem with using the data as is, is that both the D' as LOD can be both high and low. I know the parameters have an interdependence, but not a one-to-one mapping.
Does anybody have experience in filtering non-descriptive LD values from (for instance) the HapMap LD dataset?

I don't get your question. LD, LOD and D' are not independent parameters but scores describing the heritability linkage between SNPs. For GWAS SNPs are typically pruned at an LD linear $r^2$>0.8 to ensure independence but I don't think this is really relevant for the simulation you are doing. Also I don't see why a LD value of 0 is problematic, this means that two SNPs are completely independent.

@cagliari2005 I know what LD means, but working with lower LDs make generating alleles for SNPs that were generated before harder, since the MAFs differ. Wrt D-prime, values of -1 and 1 seem good, but only if either the MAFs are similar, or the population size is big enough. LOD of 3 seem to make sense, but for certain purposes possibly to restrictive


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Why do some people burn and others tan?
Connected to What is happening when we get a tan? - Why do some people burn while other people tan?
Very pale people tend to just burn while other people tan very nicely, what causes this difference?
I assume it has something to do with pigmentation - so what is the pigmentation in our skin actually doing in order to protect us from getting a sunburn?

Also have a look at this post. It is not directly related but addresses some points on UV damage.

There are two things happening: First melanin absorbs the energy from the UV radiation and releases it as infrared energy and thus protects the cells in the skin. This happens in all people, the deeper the skin color is, the better is the protection.
What is different between people is the amount of pigment they produce, the number of melanocytes is approximately the same. This depends on their genetic backgroud and is influenced by mutations in the pigment production pathway. As this is relatively complex, there are numerous positions which can influence the ability to tan, so I will only name a few.
The rate limiting enzyme for the pigmentation is Tyrosinase which catalyzes the first step of the melanin biosynthesis and oxidizes the amino acid tyrosine into DOPA. Without tyrosinase humans are not able to make any pigment at all which causes albinism. This is pretty drastic and doesn't happen too often. See reference 1.
Other possibilities are mutation in the signalling towards pigmentation, more specifically mutations in the MC1R gene which encodes on of the receptors. These mutations affect the ability to tan and are associated with red hair color, pale skin and freckles (most of the red-haired people carry at least one mutation in their MC1R gene). See reference 2.
Then there are mutations in the tyrosinase gene, which results in an enzyme with a lower processing rate. Because of this, less pigment can be made as the amount of materials is limited. See references 3 and 4.
The diversity of the human pigmentation is influenced by all these (and much more) genes. Have a look at references 5 and 6 for details.
References:

Analysis of tyrosinase mutations associated with tyrosinase-related
oculocutaneous albinism (OCA1).
Red hair is the null phenotype of MC1R.
Mutations at Critical N-Glycosylation Sites Reduce Tyrosinase
Activity by Altering Folding and Quality Control
Mutational mapping of the catalytic activities of human tyrosinase.
Molecular genetics of human pigmentation diversity
The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model


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Which hydrophobicity scales are best for detecting transmembrane regions, and why?
There are many hydrophobicity scales for protein analysis.
Broadly, I gather the differences between them are from the experimental method to acquire the data and the normalisation (or lack thereof) of the data.
To detect/predict transmembrane segments one method is to use a window of 19-20 of these residue scales to detect a region of hydrophobicity above a threshold. The Eisenberg et al. scale is used by uniprot for example.
Uniprot don't seem to explain their choice of using the Eisenberg et al. scale.
Why might one use a certain scale over another when predicting transmembrane segments?

In addition to hydrophobicity, alpha-helices formation should be considered.

This has been studied by some of my labmates in Why is the biological hydrophobicity scale more accurate than earlier experimental hydrophobicity scales? I am not involved in their research, but here is the gist of the paper:
Different scales are, as you say, developed based on different criteria. In particular, Eisenberg scale is one of the consensus scales, that is hopefully at least as good as all of its components. It was believed that there were no big performance differences between scales. This could be why Uniprot doesn't specify their choice of scale: at the time, it didn't matter too much. A study in 2009 showed that the new UHS scale was actually better than others.
The results of the benchmark are that the differences are indeed not so big: roughly $\pm2\%$ in difference in prediction accuracy. The overall winner? Hessa, scoring $1.29\ \sigma$ over the average of the scales, but closely followed by UHS, PM1D and PM3D. Eisenberg performance, by the way, is average.
Final note: they found that a near optimal window size for all the scales was 21 with double the weight in the central third.

This is exactly what I was after. Thanks. I don't have access to the journal at the moment. Does the article comment on Kyte & Doolittle's, or von Hiejne's scale?

@GoodGravy Kyte yes, and it is similar in results to Esenberg; von Heijne no (but it is indirectly present, as it is one of the components of Eisenberg).


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At what saltiness will water simply pass through us?
If water has a low salt content, it hydrates us. When water has too high salt concentration, like sea water, it drains water out of us instead when we drink it. At what salt concentration would water leave us completely unaffected?

given the coment from anongoodnurse here http://biology.stackexchange.com/questions/24058/what-proportion-of-salt-in-water-would-make-it-not-dehydrate-nor-hydrate-someone?rq=1 - the answer is 'there is no such concentration'

@AliceD Thanks for your comment, I didn't come across that question before. However, I don't really agree with the given comment.

As I said before, if you're not dehydrated, you cannot "hydrate" with a perfect imaginary solution. The body will remove the unnecessary salts of anything added. There is no magic "solution". better to disagree with me by posting a better answer; at least then you will understand the physiology behind it.

water leave us completely unaffected Haha!!! this sounds like you are attempting to recycle water without any other recycling material :P

The short answer is that anongoodnurse and moose are correct. The long answer is study physiology. Even when water is isotonic to blood, the composition of it's ionic species differs. Blood contains a wide variety of dissolved proteins, metabolites, and minerals. Na and Cl are major constituents, but are not the only components whose levels are carefully regulated. Your body corrects for the changes in the concentrations of these molecules. Even if you transferred blood which happened to have the same composition, your body also regulates volume and would need to make adjustments for that.

And that's ignoring the key aspect of Moose's answer re:homeostasis. Staying alive requires a lot of energy. Your body is constantly producing/accumulating the waste products of existence. The kidneys, et al are never sitting idle, but always dynamically regulating their output to drive blood composition towards its homeostatic "set points."

"Unaffected" is impossible. If you meant homeostasis, where fluid ingested = fluid excreted, well that happens all the time, and all "output" is not through urine. Sweat, respiration, fluid in feces, etc. are fluid loss. The body constantly needs water. Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested. Under no circumstances would fluid ingested pass through the stomach, small and large intestine, and colon without absorption. Once absorbed from the GI tract to the bloodstream, our kidneys regulate fluid balance. For more reading, reference the renin–angiotensin–aldosterone system.

+1 "Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested."


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What is the biochemical explanation for tingling and burning sensation in brain due to certain food?
Consumption of mustard (spicy English Mustard), wasabi and horseradish based food dressings usually result in a burning, tingling or freezing sensation in the brain/scalp and nostrils as the vapour goes through the nasal cavity.
I read somewhere, the checmical which gives the burning sensation is isothyocyanates. And some of the posts roughly mention about sinuses being agitated due to this chemical vapour.
How to explain this from biochemical and biology aspect? e.g. What sort of a cell reaction, if any receptors involved etc. (Appreciate an answer that is similar to the type of explanation here.)

You are right the compounds provoking this burning/tingling sensation is called allyl isothiocyanate.
We (human) perceive these compounds in two different ways when ingested, namely via the gustatory and olfactory systems. The molecular receptor sensing isothiocyanates is called the transient receptor channel A1 (TRPA1) [ref].
Here a simplistic view of how ingredients are perceived:

Gustatory sensation
First we get a burning sensation in the buccal cavity due to TRPA1 receptors present on the surface of the sensory neurons of the trigeminal nerve. In essence isothiocyanates dissolved in the saliva will activate those neurons via TRPA1 provoking electrical impulses in the trigeminal nerve which leads to a burning sensation.
Retronasal olfactory sensation
For several food ingredients we also perceived an aroma (taste = gustation, aroma = olfaction, taste + aroma = flavor). The aroma of an ingredient is perceived by olfactory sensory neurons in the nasal cavity and because some of the ingested ingredient will be vaporized inside the buccal cavity and travel through the nasal cavity where they are perceived (retronasal perception).
Not so surprisingly, isothiocyanates will again be perceived by sensory cells of the olfaction system via TRPA1 hence a burning sensation in the nostrils.
How receptor activation leads to a neuronal stimuli
This is a very broad subject and I will only give an overview of what is happening. We first start with the activation of a receptor by an agonist (in your question, isothiocyanates binding and activating TRPA1). Upon binding of the agonist the conformation of the receptor will change from an inactive to an active state. The way the signal is transduced varies according to the type of receptor but for the TRPA1 channel what happens is that the channel opens leading to an influx of calcium ions ($Ca^{2+}$) in the cells which changes its electrical state (as calcium ions are positively charged), a phenomena called depolarization. Depolarization of specific sensory cells (here the one expressing TRPA1) start an electrical signal in the nerve which travels to the brain where it is then decoded. The exact way the brain decodes sensory signals is still under debate but a likely explanation is that only some neurons within the nerve are activated which allows the brain to decode the sensory signal based on the nerve activation pattern. As an analogy, it would be the same as having only specific wires (neurons) turned on within a bundle of wires (nerve).
Further reading
If you want to further extend your knowledge on taste perception at the molecular level read this excellent review Chandrashekar, 2006. For a in-depth review on olfaction refer to this book. For a book on signal transduction refer to this while for TRP channels activation this is a good reading.
The field is quite broad and there are many good references. Sensory perception includes two distinct and broad fields namely neurosciences and cell signalling.

I just saw the answer and you just blew my mind with that awesome image and the well referred explanation. I had no idea it is infact related to taste perception. This is the part I was hunting for: How receptor activation leads to a neuronal stimuli. With the opening of Ca2+ from TRPA1, are there any specific neurotransmitters released by  trigeminal nerve to send the signal? And now I have gotten a good direction to read further.

@bonCodigo Glad you found my answer useful! Technically it is due to the aroma perception (taste perception is exclusive to the buccal cavity).  Concerning your question yes upon activation (or more precisely depolarization) sensory neurons will release glutamate (a neurotransmitter) and start a neuronal signal which likely propagate in the nerve as any standard neuronal signals (i.e. via neurotransmitters release in synapses). I don't know enough about the subsequent events to give you a very detailed answer but I am sure you can find that quite easily if you look for olfaction signaling.

cagliari2005 I was just going through some stereochemistry revision (R/S system). The picture in this answer came to my mind. (after 2 years I still remember, hey)! Our olfactory system and everything inside the body is so fascinating, that the receptors in smell sensory system can recognise each distinct smell which comes from same molecule with a slight difference in sinical/rectus difference. It is just magnificent. I feel so naive that I am not able to understand even a 1% of it through my visible consciousness :)


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Did any dinosaur molt?
Like snakes or lizards, did any dinosaur molt ?
if yes, have we any proof of it ?

Since dinosaurs had either scales or feathers, and both reptiles and birds go through molting, then dinosaurs probably molted too. However, I doubt the skin came off in 1 piece like a snake, but came off in small parts. Since the skin probably wouldn't fossilize well, we probably have no way of confirming any of this.

Snakes and lizards are a different clade of reptiles altogether (they are Squamata i.e. scaled reptilse). Not all reptiles molt.

Richard Prum (the author of Evolution of feathers) says that ornithology is mostly a science about dinosaurs. He insists that dinosaurs were very close to birds, part of them had feathers and these feathered dinosaurs "shed (molt) them as birds of our days do".
Thus, we can conclude that dinosaurs probably possessed at least one molting-like mechanism, while others are the subjects for consecutive investigations.
sources
Moulting tail feathers in a juvenile oviraptorisaur. Nature, 2010.


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How to measure the biomass of hydroponic plants in netpot/rockwool DWC system?
I'm doing an experiment with 4 kale plants, each in their own small deep water culture (DWC) system. Each plant was transplanted in rockwool with netpots and clay pebbles. But I need to periodically and accurately measure the biomass of each plant. The roots have grown through the rockwool and netpots and I don't want to rip out the roots.
Is there an easy way to do this?

If you did enough replications in your experiment, you could harvest one or more plants and measure fresh weight, and then gently oven dry for about 48 hours at like 160 degrees F and then take a dry weight as a measure of biomass. I don't know a non-destructive way to do it. A lesser alternative would be to measure plant height and number of leaves, though this would be less accurate. There are devices that measure leaf area, and I know a simple, low-tech way to measure leaf area.

we appreciate references to all answers to allow all users a chance to try and understand the answer and go for more information - you might want to add some references as this would strengthen your response


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Spatial learning in microorganisms
Has there ever been an experiment performed that demonstrated a form of 'spatial memory' in a unicellular organism?  I'm imagining something analogous to the classic 'rat in maze' experiments, but obviously on a much smaller scale.  Possibly even something as simple as following a concentration gradient, but choosing to go either upstream or downstream based on some sort of prior reward in a similar circumstance.

Several (if not all) motile microorganisms, such as E.coli, will follow chemical traces (usually food sources) but I am not aware of them having any memory in the sense they will simply follow it until the trace disappears. Another well know example are the immune system cells like this neutrophil chasing a bacteria: https://www.youtube.com/watch?v=NN9EHZugwl8.

The closest I can get is slime moulds. They are not strictly unicellular, but they even have the ability to adapt to periodic stimulus, showing clearly that they are capable of both memory-like behaviour and some form of pattern recognition.

To build on busukxuan's answer, there are a lot of single-celled organism responses that kind of resemble memory:
Slime mold uses an externalized spatial 'memory' to navigate in complex environments - essentially, a slime mold leaves behind a trail, which it then avoids, allowing it to avoid where it has traveled in the past.
If you apply a periodic stimulus to Physarum, it will anticipate the next stimulus: Popular, openly accessible summary Paywalled journal article.
If the amoeba Dictyostelium sees an increasing cAMP gradient, it will follow that gradient - and then be less sensitive to a reversal in the gradient: Cellular memory in eukaryotic chemotaxis
In fact, even bacteria have some memory - they can figure out whether or not they are going up a chemoattractant gradient by making a comparison with the signal they observed a few seconds ago: Temporal comparisons in bacterial chemotaxis


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Efficient algorithm to calculate various population divergence statistics
Intro and description of the data
I am simulating the evolution of very long DNA sequences. The model works well, is performant and will output data in the following kind of fasta format
>it0pop0ind0locus0
ATGTTG...
>it0pop0ind1locus0
ATGTTG...
>it0pop0ind2locus0
ATGTTG...
>it0pop0ind3locus0

, where it stands for iteration (replicate of the same simulation), pop stands for population (or subpopulation of the metapopulation if you prefer), ind stands for the individual chromosome that was sampled, locus stands for locus which is defined as a very big sequence (0.1GB or 1 GB maybe).
Issues
I never had to analyze genetic data (or only during my Bachelor degree). As I know nothing about the available algorithms that exist to make this kind of analysis, I first thought I would just make my own code (in Python). It turns out that I might have a lot of data to analyse and my Python code will be way too slow. I may also experience RAM-related issues
Moreover, I want to measure a whole series of different statistics of population divergence (Fst for each site, Fst averaged over many sites following Cochramm and Weir, Gsd, absolute number of fixed sites that differ, etc..), so the algorithm would need to be quite flexible.
Question
There are a bunch of existing efficient algorithms that would eventually fit my needs. Can you please give me some recommendations and make a few comparisons of what's available out there?
An efficient algorithm that takes in input:

a description of the naming convention in the fasta file, or a list of positions for each locus and each population in the fasta file.
A description of how I want the statistics to be calculated

and that outputs those statistics. That'd be great!

Have you looked at BioPython? Specifically the Genepop module (http://biopython.org/wiki/PopGen_Genepop) looks useful. If you've already got some Python experience, it might be the fastest way to get started.

Are these sequences of equal length?

I would suggest that instead of reading and outputting fasta files, you simply store the co-ordinates and the mutation locations as a numeric matrix. Use unsigned integers for storing co-ordinates. Use 32 bit (or if possible 16bit) float for storing other kinds of data such as frequency. If <1% variation in frequency won't matter to you then you can use unsigned short integers for saving them. Or if your sensitivity is 0.1% then multiply save them as per-thousand. In any case, even using regular floats should not impose a big load on memory.

@WYSIWYG Yes, the solution was pretty obvious, yet I didn't think of that at first. Do you want to make an answer out of your comment?


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How does chromosome fusion get fixed in the population?
It's well known that one of human chromosomes is the result of fusion between two chromosomes in a primate ancestor. If we put anthropocentrism aside, it becomes clear that fusion events happened a lot of times, since chromosome count varies in different species.
Yet some people claim that while fusion event is probable, getting it fixed in the population is not, because it would require simultaneous mutation in two animals of opposite sex.
Could anyone explain in layman terms the scenario of this trait's propagation? I may only suppose that even if one parent has two distinct chromosomes and another a single fused chromosome, then two chromosomes may attach to the fused one, and then (probably) get fused themselves, thus leaving fewer and fewer specimens with distinct chromosomes in each generation. Is this a viable and likely scenario, or is some other way of propagation more likely?

Looking at this 2001 review paper by Rieseberg: http://evolution.powernet.ru/library/Scienc9.pdf (especially Box 2), drift and inbreeding are suggested ways that chromosomal rearrangements can become fixed. These forces are strongest small, isolated populations, such as populations experiencing the founder effect.
Another model discussed in that paper is the suggestion that some centric fusions (Robertsonian translocations) lead to little or no loss of fertility in the heterozygotes.


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Do butterflies pass over migration patterns to their offspring?
So, earlier, I read online (http://io9.com/butterflies-remember-a-mountain-that-hasnt-existed-for-509321799) that Monarch butterflies veer east during their southward migration to avoid a mountain that no longer exists. If this is true, how do butterflies know to continue avoiding the "mountain" after countless generations, and does it have to do with evolution? Do other animals have similar abnormalities in their migration routes?

here's the original paper - I couldn't find support for this hypothesis in the paper but that was only a quick skim read (and the manuscript only features one brief reference to lake superior) http://jeb.biologists.org/content/199/1/93.full.pdf

If you think about it, monarchs must have a pretty strong genetic component to migration since often they only make one round trip at most in a lifetime. But its not as simple as passing a map in the DNA.
If a mountain springs up on the route, the 'common sense' of the butterflies are still operational and they will tend to find their way around it.
The paper discussed here is older.  More recent Monarch butterfly migration  of some genetics that have been done shows some traits that are related to migration patterns by sampling over many butterflies whose patterns vary tremendously.
Glancing over the paper, I'd say that there may be some 'muscle' memory in migration, but probably the mechanisms encoding the route of migration are not yet discernable.  This is far from something we understand well.
The insect is following patterns of behavior but doesn't turn into a robot just because its migrating.  Migration patterns are probably linked to a series of environmental cues.
Changes in climate or shifts in magnetic fields can change migration patterns. Butterflies would be very different than say migratory birds in terms of the social and environmental markers for migration.

I think it depends on the route taken and which population you're talking about (western vs. eastern US), but my understanding is that both migration directions are multi-generational, so any individual is not necessarily covering the same ground as its parents did.

Thanks for the review @MattDMo I can't find any reference of Monarchs living longer than 8 months.  I just re-reviewed several sites. post a link?  the wikipedia article seems to refer to the fact that Monarchs have mulitple breeding waves (called generations) over the year where their lifespans can vary tremendously (4 wks <-> 8 mos).


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What is basis of multifunctionality of "master glands" in the endocrine system?
I have just started reading about the endocrine system and I am having some difficulty understanding the basis of distribution of glands and associated hormones.
I am using multifuntionality to describe the amount of relatively independent input and output that are shared through a same organ or proximal space. Many of these organs have a heterogenous mixture of endocrine cells sharing the same glandular space.
There appear to be some glands that are considered "master glands" such that they take a variety of relatively independent input, apply some control logic via a diverse set of endocrine cells and tissue and secrete a diverse hormonal output. The pituitary and hypothalamus are the best examples, however the adrenal cortex and the pancreas also fit this definition to a certain extent. Many times the diversity of hormones and cells within an organ have no obvious connection (eg thyroid). Some glands appear more specialized with a relatively straightforward endocrine axis of input and output (eg testes).
Some of this multifunctionality seems unnecessary, in that insulin secretion could occur anywhere and be effective in the manner of an insulin pump, or contain risks due to excessive centralization as in a pituitary tumor or renal artery stenosis, so there must be some advantages I do not understand.
My textbook (Headley, Levine, 6th) seems to minimally cover multiplexing, signal cross-talk and competition between diverse endocrine cells sharing an organ. Its focus on discrete pathways and axes suggests these are evolutionarily unfavorable.
Are there synergistic advantages in shared endocrine infrastructure such as vascularity or metabolic pathways?
Is there some overlying logic that can be used to explain this distribution of glands and hormones regarding multifuntionality-specialization, or is it necessary to view the distribution of vertebrate endocrine system as the outcome of evolutionary contingencies?
Thanks

In this text, Pituitary is referred to as master gland. But in one of the sessions that I participated, referred Thyroid gland and Pancreas as master glands. So I am curious to know the answer here myself. Are you referring to the shape of the particular gland by "Spoke-Like"?

No I mean centralized as in diverse endocrine cells and tissue with diverse inputs and outputs that may be unrelated sharing a same organ or proximal space. The testes appear to me to be strictly male reproductive organs with a relatively straightforward endocrine axis of androgen production of primarily testosterone based on LH input, although a role of FSH in sperm production.

@WYSIWYG "they also affect the development of the physical and metabolic characteristics that are distinct for a sex" : Totally. Specially in terms of females, these glands (ovaries) seems to be even more crucial. Isn't it?

@WYSIWYG I misspoke and meant strictly reproductive and endocrine. I then attempted to describe how that organ has a straightforward endocrine axis. Testosterone has a diverse set of outcomes in cells, however I refer to the number and diversity of testes outputs, which is primarily testosterone. Testosterone injections in castrated chickens maintains a relatively stable phenotype with regard to endocrine status.

@hkjairam Then you should not use the term "centralized" and rather emphasize on multifunctionality (and cellular diversity?). Another point: endocrine glands don't have ducts.

@WYSIWYG. True, fixed the ducts. My connotation of "centralized" conveys the structural proximity of specialized cells with unrelated tasks, better in a more network-centric fashion,  but that is my subjective opinion. I do not understand what you mean by "cellular university".

@hkjairam I had to write "diversity" and I wrote "university". I have no clue how I did that. (PhD effect I guess!!). Regarding centralization: even in a network perspective, the out-degree would denote how many tissues does a gland affect (conversely for in-degree). That will still not convey the actual question which is "In how many different ways does a gland affect the body". I hope I am understanding correctly.

@WYSIWYG I think there are flaws in the word "centrality" as a central node may also have a single input and output but is commonly traversed, but I thought the popular understanding of "central", with the idea of a hub and spokes would accurately convey the gist of my question. I thought "multifunctional" would lead to answer regarding versatility of tissue and not the endocrine pathway architecture.  I am open to changing, but I do not how widely the word choice is leading to misunderstanding.

@hkjairam If you do not mean multifunctional then I am still failing to understand what exactly you are referring to. You tagged this question as anatomy and you are talking about architecture of signalling pathway. Am I missing something here? Are you trying to ask how proximity correlates with shared signalling pathways or in other words, whether a heterogeneous gland has higher number of local signalling paths between component tissues?

You should also add a link to your text book or if it is not openly available then illustrate the topic that it minimally covers. This would give others an idea about what you are really expecting.

If I'm understanding this question correctly you're asking why we have a mix of "master glands" like the hypothalamus that regulates a bunch of different tasks uncoupled by control logic (oxytocin doesn't influence ADH or TSH) and also specialty glands like the ovary, which do "only one thing" (yes there are many inputs and many outputs to lots of different tissues, but they're all coupled). Rolling all the glands together for efficiency would make sense, but distributing them might also make sense. Why a blend? Is that right?

it would be better if you could provide us with the sources of information

It would seem to me that in the examples that you have listed that proximity to necessary input is the overriding logic behind gland geography. Take the hypothalamus as the first example. This gland receives input from diverse regions of the brain from the amygdala and hippocampus to the retina and brainstem. The brain can tweak levels of various releasing hormones entering the  hypothalamic-hypophyseal portal veins in order to produce a response that is appropriate to the situation perceived by the brain. It makes sense to have all of these co-located because they are all receiving input from the brain. Similarly, it makes sense to have all of cells that are uptaking the releasing hormones close-by to protect these vital peptides from degradation in the systemic circulation. Their collectively unique circumstance makes sharing a specialized vasculature a logical choice.
The pancreas is a good example of the importance of cross-talk within some endocrine tissue. Within the islet, alpha, beta, and delta cells are feeding back on each other to get the balance of insulin and glucagon just right. To whit, glucagon secretion provides a paracrine signal for insulin secretion. This makes sense because the body knows that once glucagon is released the blood sugar will soon rise. Ergo, it makes sense to trigger some insulin secretion as well in preparation. Their co-location makes that possible.
In short, I would say the overriding logic to the placement of each of these glands is their proximity to the necessary inputs and outputs that each of these glands interacts with.

Nice answer but one correction....The pancreas, although in proximity of the duodenum, does not sample fluid from the duodenum that is absorbed. Nutrients absorbed from the duodenum are mostly transported to the hepatic portal circulation and then back into the peripheral venous circulation via the hepatic veins. These nutrients then flow to the arterial circulation and then back to the pancreas. The liver may be a better example of being in a good 'geographic' location for your answer as it 'sees' all portal nutrient flow and can buffer nutrient levels in the peripheral blood.

Thanks for the catch. I vaguely remember learning in a physio class that elevated local levels of glucose in the ecf can stimulate glucose release, but I can't find a source for it other than my notes. Since it can't be sourced I've removed that point. I would add the liver case because it's a good example of the importance of geography, but I can't find a good link to why it's necessary for endocrine function per se.