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Meta-analysis of fruits in blocking Cytochrome family
My professor says that some drugs cannot be used with grapefruit.
I am trying to search a list of cytochromes and their effect to block members in the cytochrome family. Some in Cyt P450.
What is the main meta-analysis of fruits in blocking cytochrome family?

While I haven't found a list which is restricted to fruits, I found this page: P450 Drug interaction table. They list quite a number of substances which inhibit different isoforms of the P450 protein and also give the original references.
This list gives a large number of herbals which inhibit different P450 isoenzymes. The disadvantage is that they do not give further references so if you want to have a closer look you will probably have to spend some time with Pubmed.

Thank you! The table includes the grapefruit juice as moderate inhibitor that was emphasized by my lecturer. I did not see any other significant food there.

The second list contains a number of latin names of different plants. If you translate them into the normally used ones (Wikipedia is helpful here) you can see if there are other fruits among them.

I asked my old Latin teacher how to learn the latin names of different fruit. I think there is some logic behind the fruit names.

Add the complete latin name into the search field of the Wikipedia to get the normally used name. Works pretty well.

Any possibility of doing it for those all at once? Doing list search?


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What is the quality rate of intrinsic autoregulation in the heart?
Autoregulation is the maintenance of constant blood flow to an organ in spite of fluctuations in Blood pressure.
It involves the relaxation of myocardium and contraction.
It is local.
I know that autoregulation is best done in the brain, well in kidneys and badly in skeletal muscle.
I am interested how it is in the heart.
I think it should be at least good.
Brain can be thought more important.
However, I am not sure.
How good is the autoregulation of the blood flow in the heart?

My conjecture: Intrinsic regulation is done in the heart the second best, after the brain.
This idea is based on the fact that the brain controls heart's some autonomic functions.
It is an open research question how the autonomic nervous system affects the intrinsic functions of the heart - and the reverse is true too.
To answer this question, we need to understand the autonomic regulation of the heart better i.e. the inner-physiology of the heart's electrical activity.

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Characteristics of radius of blood vessel
Which properties do determine the radius of blood vessel?
I have these thoughts

distension,
elasticity,
contractility and
cross-sectional area of the walls.

Is there any other properties?

The radius of a blood vessel is entirely defined by only two parameters:
1.blood pressure
2.compliance of the vessel walls
Of course, active contraction can decrease the vessel radius. Physically, this is a decrease in compliance, so the above relation always remains true.

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Can SIRS occur without Sepsis from Infection?
I am thinking this figure

It suggests me that there has to be Sepsis that infection can lead to SIRS.
I am thinking particularly the pathogenesis of Cryptococcus neoformans where

respiratory tract $\to$ pulmonary infection $\to$

asymptomatic and nonspecific pulmonary signs in normal patients
progressive systemic disease in immunocompromised patients

and the last row.
Can SIRS occur without preceding or simultaneous Sepsis?

According to the classification of sepsis, it is SIRS with a suspected or known source of infection. By definition therefore, sepsis without SIRS is not sepsis but SIRS can exist without sepsis. In all fairness though, SIRS can exist if you run for a while (elevated heart rate and respiratory rate by themselves qualify for a diagnosis of SIRS).
Sepsis is however not the same as a bacteraemia which may be caused even by brushing your teeth (although the bacteraemia in this case is transient).

Very clear explanation with good examples! Thank you!


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Speed of effective lymphatic drainage?
Lymphatic drainage occurs from many portions of the body:
To venous angle:

head
axillary lymph nodes

hands
abdomen

legs (I think legs' drainage goes through abdomen)

The speed of the lymph drainage is different in each part of the body depending on the situation at hand.
Assume you have tense muscles in the hand (biceps and trieps).
The lymphatic drainage there can be lowered and be the limiting factor in the system.
I think lowered lymphatic drainage in one part of the body causes more lymph goes to other parts of the body.
What are the negative results of too high lymphatic drainage in an organ?
My intuition

edema
hypertrophy in some cases (excess of nutrients)
hypertension

Negative results of too slow lymphatic drainage are the prolonged intoxication times of

biological,
chemical and
physical factors.

I am trying to find any studies about the effective speed of lymphatic drainage.
I have an intuition that the lowest drainage of one section is the limiting factor in the whole system.
Is there any studies about how to quantify the speed of lymphatic drainage from one part of the body?
Heart pumps (blood) and sucks (lymph).
So probably some cardiovascular study relates the pumping to the lymphatic drainage.

Probably, this one: http://www.ncbi.nlm.nih.gov/pubmed/3444363 ?

Do you know any research about the normal lymphatic drainage in different organs? What is too high level and what is too low? For instance.

Oh Masi, you and I share the same interests (pharmacology and  lymphatics) and I do enjoy your questions... very old school... I wondered the same question your asking leonardo myself and I ended up buying this book: http://www.sciencedirect.com/science/book/9780120425204... the cheapest way to buy it is on google play... I've only had the time to read certain parts, usually focusing on lymphatics, but I haven't even finished that... it's an old book from the mid 80s, and the information on lymphatics is often incomplete... but it's the best I know of...

@JasandPruski We need technical tools to evaluate the speed of lymphatic drainage that is to investigate the flows of liquid phases and energy transfers. This is a part of Soft Matter Physics where the leading books are 1) Hamley - Introduction to Soft Matter, 2) Intermolecular Surface Forces by Israelachvili, 3) Giant molecules - here, there and everywhere. Still, these books do not cover the topic fully only provide some tools. You have to do the computation and visualisation yourself. I am actually doing a course about this topic called "Soft Matter Physics" in Aalto University right now.

wow, I'm jealous! I'm looking at the programs in alto and it seems they're not too focused on biology more engineering, but in a way thats great, new methods for studying things hard to study. I appreciate the book recommendations on soft matter, I'll look into them and perhaps when I have the funds I'll purchase one. It seems like theres some overlap on soft matter and rheology (not that I know anything about that either)... the word "liquid crystal is great. Also it seems like it's a meeting point for studying physical properties of cell membranes and ECM/interstitium...very interesting. :)

Leonardo's answer:

Animal study on sheep - here.

where

[L]ymphatic flow in sheep, and
  the range being very heterogeneous (virtually no flow at the lower
  bound). I would agree that, in general, this is a very heterogeneous
  effect subject to many chemical (hydration, osmotic balance, blood
  pressure modifying drugs) and physical (cardiovascular tone, posture,
  activity level) factors.


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S.pyogenes binary fission rate/speed
For my Math IA (IB SL) I want to calculate the average amount of time that one viable S.pyogenes bacteria will need to create an ID50. I cannot find the average speed for the divison of any Streptococcus anywhere.

Hi @Jakub. Welcome to Biology S.E. I would highly recommend to take the tour (https://biology.stackexchange.com/tour) to know how a Stack Exchange site works. Also, you will earn a badge for reading the tour. As you will see, research effort prior to asking a question as well as using the correct tags will make sure that you can enjoy and use this site to its full extent.

Growth rates are largely temperature-dependent. According to this study (Growth rates of Streptococcus pyogenes and derived L form at various temperatures) the growth / doubling rates for Streptococcus pyogenes are as follows:


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Inoculating agar plates with microbes suspended in sterilised water?
We were having a problem with our experiment (culturing microbes on homemade nutri agar) so we decided to change our set-up. It already cost us quite some money. So, we saw this procedure. Can anyone tell if this is legit? Thank you!

You have more chance of a useful answer if you include brief outline of your original protocol and your problems.

What kind of bacteria are you using? 2. I prefer to store my Petri dishes at room temperature. If they are contaminated at least I can see it. If contaminated Petri dishes are stored in the fridge, you'll see the contaminant only after inoculating your strain

It would be great if you could provide more information with regards to what you have done already and what the problems were that you observed. That being said, yes, the "protocol" you found should work.
I am assuming that this is some kind of homework / school project so you don't actually need to know what organisms you are inoculating with and at what levels.
One thing I would recommend is that when you take your swab sample, wet your swab by dipping it into the sterilised water first and then swab a predefined area of about 10cm x 10cm (4in x 4in) very thoroughly before putting the swab back into the test tube. Once back in the test tubes make sure that you swirl the swab around for a sufficient length of time (~30s) and press the swab against the inside of the test tube to allow as much liquid as possible to run out of the swab. The last step is important in order to maximise the yield of bacteria, yeasts and moulds that you might find in your sample.


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Why aren't there more Ash-Red pigeons?
My favorite color pigeon is Ash-Red, but I don't see a lot of them.  I figured it must be a recessive phenotype, but when I googled it, I found out it's dominant.  So why aren't there more Ash-Red pigeons around?
Edit: I'm in North America.
Edit 2: This website from the University of Utah is where I learned that Ash-Red is the dominant phenotype.

"I don't see a lot of them" is a bit of a vague statement. Have you checked whether there is some data available that shows that population levels for Ash-red pigeons are low in North America? It could simply be that the pigeons are more timid than other species or that the particular micro-enviorment you live in (it's an assumption here) is not suitable for Ash-red pigeons.

Good point!  Searching for specific numbers of Ash-Red pigeons in North America actually helped me find a book with a really good answer to my question... thank you!

Welcome to Biology.SE
Assumption
I will assume it is true that the allele causing a ash-red plumage is dominant over all other alleles. Note however that you should cite your reference when making such claim in your post.
Dominance and allele frequency
Phenotypes associated to a dominant allele A aren't necessarily more common than the phenotype of the recessive allele a. It all depends on the allele frequency. If the dominant allele is at low frequency then both AA and Aa (both displaying the dominant phenotype) are at low frequency (esp. AA individuals) and most individuals are aa and show the recessive phenotype.
Learn more
You might want to read about Hardy-Weinberg rule with this post for example.


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Prehistoric fossils
I have found very old seashell fossils (clamps) on a hill. They may be as old as a million years. Who can tell me how old they may be looking the pictures shown.

Hi @gio ! Welcome to Biology S.E. Could you please attach the pictures you mention in your question.

Fossils are dated in several ways. Radiometric dating, which we cannot do over the internet and if you're asking on the internet then you can't do it either. Identifying the fossil's species, which allows you to have a range of when the fossil could have been from insofar as other, better-dated discoveries of fossils in that species tell us when that species existed, and finally identifying the geological layer the fossil was found in. In other words, you should give a picture of the fossil so people can find the species and say exactly where you found it and what the surrounding area was like

Also the location where you found it.  If it comes from an undisturbed rock layer, that would help pin down a date.  Though perhaps not: the area I grew up in (upstate New York) had a good many rocks with fossil shells that were glacial erratics from the last Ice Age.


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Lactobacillus casei and paracasei
I am carrying out a study of lactobacilli isolated from different samples.
Genus and species are identified using a sequenced 1000pb long 16S fragment in BLASTn.  I cannot distinguish between L. casei and L. paracasei because they have same score and query coverage when they appear as a hit for a sequence.
I read somewhere (cannot remember where) that L. casei and L. paracasei both should be itnegrated in a single L. casei species and their differences should be considered at strain level.
Should I focus my discussion on this fact? Or are they really different species?

My recommendation is to find that source you mention that you forget,  check to see if it's a reputable source, and (if it is)  use it to substantiate your discussion. Check to see if  anyone else has ever cited  the work,  and if so, make sure  the newer work doesnt contradict your first source.

The definition of a bacterial species and (even worse) strain are somewhat debatable unfortunately. As far as I know there is no real single authority with a standardised decision process on what is a separate species or not. At least none that everybody agrees on.

As far as I am concerned L. casei and L. paracasei can be differentiated by the amplification of the 16S rRNA gene of the aforementioned species using PCR - please see the work done by Ward and Timmins (1999). An alignment of the V1 region of the 16S rRNA genes of Lactobacillus casei and Lactobacillus paracasei shows the bases comprising the species-specific PCR primers - screenshot taken from Ward and Timmins (1999):

So, perhaps in your study you have not amplified the correct region of the 16S rRNA gene of L. casei and L. paracasei?
With regards to the classification of these organisms. Just as @skymningen has already mentioned in the comment section, the definition of a bacterial species (not even to mention strains) is somewhat debatable and tricky.
However, here is what Mori et al (1997) suggest:

The primary structures of the 16S rRNA genes of the type strains of Lactobacillus casei and related taxa were determined by PCR DNA-sequencing methods. The sequences of Lactobacillus casei, Lactobacillus zeae, Lactobacillus paracasei, and Lactobacillus rhamnosus were different. The K nuc values ranged from 0.0040 to 0.0126. On the basis of the K nuc values and the levels of DNA-DNA relatedness among the strains of these species, the L. casei-related taxa should be classified in the following three species: L. zeae, which includes the type strains of L. zeae and L. casei; a species that includes the strains of L. paracasei and L. casei ATCC 334; and L. rhamnosus.


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Antibiotic resistance of Staphylococcus epidermidis and S. warneri
I am looking for information regarding the antibiotic resistance of S. epidermidis and S. warneri, specifically against penicillin, ampicillin and tetracycline but to no avail. Are there any good websites with databases where this information is shared?

Here some studies concerning the antibiotic resistance of Staphylococcus epidermidis and Staphylococcus warneri:
Antibiotic resistance patterns of coagulase-negative staphylococcus strains isolated from blood cultures of septicemic patients in Turkey - Koksal, Yasar & Samasti [2009]
The abstract of the study above reads as follows:

The aim of this study is to determine antibiotic resistance patterns
  and slime production characteristics of coagulase-negative
  Staphylococci (CoNS) caused nosocomial bacteremia. A total of 200 CoNS
  strains were isolated from blood samples of patients with true
  bacteremia who were hospitalized in intensive care units and in other
  departments of Istanbul University Cerrahpasa Medical Hospital between
  1999 and 2006. Among 200 CoNS isolates, Staphylococcus epidermidis was
  the most prevalent species (87) followed by Staphylococcus
  haemolyticus (23), Staphylococcus hominis (19), Staphylococcus
  lugdunensis (18), Staphylococcus capitis (15), Staphylococcus xylosus
  (10), Staphylococcus warneri (8), Staphylococcus saprophyticus (5),
  Staphylococcus lentus (5), Staphylococcus simulans (4), Staphylococcus
  chromogenes (3), Staphylococcus cohnii (1), Staphylococcus schleiferi
  (1), and Staphylococcus auricularis (1). Resistance to methicillin was
  detected in 67.5% of CoNS isolates. Methicillin-resistant CoNS strains
  were determined to be more resistant to antibiotics than
  methicillin-susceptible CoNS strains. Resistance rates of
  methicillin-resistant and methicillin-susceptible CoNS strains to the
  antibacterial agents, respectively, were as follows: gentamicin 90%
  and 17%, erythromycin 80% and 37%, clindamycin 72% and 18%,
  trimethoprim-sulfamethoxazole 68% and 38%, ciprofloxacin 67% and 23%,
  tetracycline 60% and 45%, chloramphenicol 56% and 13% and fusidic acid
  25% and 15%. None of the strains were resistant to vancomycin and
  teicoplanin. Slime production was detected in 86 of 200 CoNS strains.
  Resistance to methicillin was found in 81% of slime-positive and in
  57% of slime-negative strains. Our results indicated that there is a
  high level of resistance to widely used agents in causative
  methicillin-resistant CoNS strains. However fusidic acid has the
  smallest resistance ratio, with the exception of glycopeptides.
  Additionally, most S. epidermidis strains were slime-positive, with
  statistically significant (p<0.001) association between methicillin
  resistance and slime production.

The other two studies contain information on the aforementioned strains with regards to penicillin susceptibility.
Antibiotic-resistant Staphylococcus epidermidis in patients undergoing cardiac surgery - Archer & Tenenbaum [1980]
Clinical significance of Staphylococcus warneri bacteremia - Kamath, Singer & Isenberg [1992]
In addition, I would recommend to acquaint yourself with Google Scholar for these kind of questions. It normally makes for a good starting point.

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Fair point @Chris. I will amend my answer at the earliest convenience. I may have been lead astray/tempted by O.kth question for a website / database. However, I agree with what you say in your comment.


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Do different species of bacteria have distinct absorption bands?
Do bacteria of different species absorb different wavelengths of light? How different?
Most of my searching has lead to topics about Optical Dispertion which seems to be species independent as opposed to single species.

Did you do some research to find an answer? Please share them in your question. Low effort questions get closed on Bio SE.

Yes they do, as demonstrated by the fact that bacteria have different colors ! Moreover, some bacteria are photosynthetic and others aren't; the photosynthetic bacteria have a very specific mechanism for absorbing light that the others don't so it stands to reason they won't absorb the same wavelengths.
This page talks about it very nicely, with a list of different colors and bacteria that have them:
http://www.biotecharticles.com/Applications-Article/Colorful-Bacteria-612.html
Money quote :

Bacteria are pigmented or colored. Pigmented bacteria are also known as chromobacteria. Bacterial pigments are water soluble or insoluble; water soluble pigments are diffused in the growth medium. Chemically, bacterial pigments are pyrrole, phenazine, carotenoid, xanthophylls and quinine or quinone derivatives. The pigment molecules are synthesized in cell wall or periplasmic space. We can visualize pigmentation in bacteria in specific growth medium or my staining bacterial cells with a dye to observe under microscope. It has been proved that only aerobic and facultatively aerobic bacteria are pigmented because, molecular oxygen is essential for pigmentation. Therefore, anaerobic bacteria are nonpigmented. Pigment synthesis is also dependent on light, pH, temperature and media constituents like indicator dyes. They display all the colors from rainbow including light or dark tinges and unual colors like black, white, brown, golden, silver and fluorescent green, yellow or blue.

And the list:

Purple: Spirillum rubrum
Violet: Chromobacterium violacein
Indigo: Janthinobacterium lividum
Blue: Streptomyces coelicolor
Green: Chlorobium tepium
Yellow: Xanthomonas campestris
Orange: Sarcina aurentiaca
Red: Serratia marcenscens
Brown: Rhizobium etli
Black: Prevotela melaninogenica
Golden: Staphylococcus aureus
Silver: Actinomyces sp.
White: Staphylococcus epidermidis
Cream: Proteus vulgaris
Pink: Micrococcus roseus
Maroon: Rugamonas rubra
Fluorescent blue/green: Pseudomonas aeruginosa
Fluorescent yellow: Pseudomonas fluorescens

It appears some purposes of producing pigments, aside from photosynthesis, are to absorb UV light (i.e. absorbing a specific wavelength is the entire point) or mopping up free radicals.
An additional note, from the Wikipedia page for Rhodospirillum rubrum, the first bacterium in that list (which Wikipedia describes as "pink" but close enough):

The photosynthesis of R. rubrum differs from that of plants as it possesses not chlorophyll a, but bacteriochlorophylls. While bacteriochlorophyll an absorbs light having a maximum wavelength of 800 to 925 nm, chlorophyll absorbs light having a maximum wavelength of 660 to 680 nm.

https://en.wikipedia.org/wiki/Rhodospirillum_rubrum
And while that paragraph describes "chlorophyll a" as being a feature of plants, other bacteria do use it such as Chlorobium tepidum, so there you can see some wavelengths that are absorbed by one and not the other.

Hmm, but most bacteria will still be visible in monochromatic light, right?

I'm not sure what you mean. Most things are visible in monochromatic light aren't they ? They would have to be completely transparent to a given wavelength not to be, and bacteria are full of many different molecules so I doubt that would be the case.

Yes, they do, just as Rozenn Keribin has explained in her answer. In addition to the answer above, there is a 1954 research paper written by Shibata, Bensen and Calvin freely available from the Berkeley Lab of the University of California which should give you the theoretical background, experimental methodology as well as some data on the absoprtion spectra of different micro-organisms including bacteria:
The Absorption Spectra of Suspensions of Living Micro-Organisms


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How specimens are organized in a large biological specimens archive
In a library, (and I'm not totally sure about this, but from experience) books are organized by category/theme into sections, and then they are given a number so that, globally, the numbers are ordered sequentially. This way you can easily just look up a number and go right to it, but then you can also browse entire sections by a common theme. I'm not sure how exactly they do this, but this is roughly what I've seen how it works.
So I'm wondering how biological specimens are organized in a gigantic specimen archive like at a large museum or university collection, with hundreds of thousands or millions of specimens. I'm wondering if they just give them a random number, and then place them wherever that number falls in the sequence. Or if they do like the libraries and group them by category/theme, then by number. Or something different.

Do you mean like binomial nomenclature?

Biological specimens are ordered in museums phylogenetically. So all the birds are in one place, and the insects in another. Fossils are generally kept in their own place. Different museums may have their own standards, but most sort specimens phylogenetically as well. But alphabetical sorting also happens. So that all the members of a family are in one place, and then the genera within the family are organized alphabetically. So all the Trichoptera (Insecta), for example, at the Smithsonian are together on one of the floors with other insects, curated by a Trichoptera specialist. Within Trichoptera, the first drawers are Apatanaeidae, and the last are Xiphocentronidae. Individual specimens are often given a unique number, usually sequential, with the time of accession into the museum.

As an addition to Karl Kjer's answer
Fossils specimens are usually ordered by locality(where it was collected) or phylogenetically, but size and shape is often more important as well. its hard to keep 3000lb sauropod pelvis in the same place as 3 ounce microraptors bones, but large sauropod bones and large pieces of petrified wood might be stored together.  This is why good records are important in fossil collections, physical limitation often trump ideal cataloging. Fossil collections are often constantly growing as well which is why locality is often better than phylogeny, you don't know how many of anything you will end up with, but at least you can group things by where it came from.

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Do cells store information other than permanent (chromosome) information
The brain stores information in neurons (i.e. neural networks), and cells store information in DNA. But with DNA, this is permanent information. There is a lot of potential temporary information in the cell as well. The brain deals with temporary information in the short term memory, maybe there is something parallel in the cell. Wondering if there is any temporary or localized information cells store related to their processes such as for gene expression or their interaction with the external environment.
Maybe this looks like they have a small recombinant DNA strand that is used for creating some temporary proteins or such things to temporarily store information. Wondering if anything like this exists in cells and/or is studied.

Bacteria have plasmids that are separate from chromosomes. Although still DNA.

Well really, that’s what RNA does. RNA expression is regulated often very tightly, and its expression often responds to changes in the environment—almost like a short-term memory. A good example in c elegans—my favorite model organism—is its response to stress. Two+ generations after starving, without any change in the actual genes of the organism (they can self fertilize, thus keeping genetics a bit constant), the gene expression changes to activate some stress response genes. So it happens short term (expression changes every minute) and even across generations.

Although this question is interesting, it is also far too broad. "Temporary", for example, covers events that range from nearly instantaneous to effectively permanent. Everything from second messenger systems to epigenetic modification reflect forms of information storage, and almost every aspect of cellular biology except for DNA itself lies somewhere in between.

DNA methylation (as well as other epigenetic mechanisms) also comes to mind.


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The meaning of and standards for "specimen numbers"
I just read here:

For example, in the research collection of the Natural History Museum in London, there is a bird specimen numbered 1886.6.24.20. This is a specimen of a kind of bird commonly known as the spotted harrier, which currently bears the scientific name Circus assimilis.

I am wondering what exactly that number 1886.6.24.20 means and how to find out more information. It seems it is structured to give some significance, such as perhaps year.month.day.incremented number. Wondering if this is unique to the Natural History Museum in London, or if this is how everywhere does it. By everywhere, I mean every museum. That is, wondering if there is a standard of some sort on how to number specimens.

It is good scientific practice to utilize some sort of consistent structure for sample/specimen identification, but to the best of my knowledge there is no "standard", per se.

In this case, your suspicion of year.month.day.sequential number is correct. The NHM specimen page has an image of the collector's notes:

On line 20, that specimen of Circus assimilis is accessioned, with a note on the right that it is the type for that species.
Generally however, there are no standards for specimen numbers in museums. Many museums that I have studied in have several different numbering or ID systems in use at the same time. Importantly, each specimen is accessioned under the system used at the present time. Sometimes these are later renumbered, sometimes not.
Even in the NHM, there are different schemes in use. Megalosaurus bucklandi, the first described species of dinosaur, is specimen PV OR 2482.
The NHM has 80,000,000 specimens. I'm sure that those doing the cataloging at the start couldn't have imagined the collection would grow to that size, so planning ahead for a single numbering scheme wouldn't even have occurred to them.

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text:
List of genes across species (or just for humans)
Wondering if there is a place that has a list/table/database of all the genes in the human genome, and/or all the known genes in all the species we've studied so far. Something that contains any of this would be great.
I found this but not sure yet if that is just for humans and just for one chromosome. But I'd like something along those lines across species, or the closest thing to that that exists.

There are a number of sites that store genetic data. The most famous of all is probably NCBI

In principle there are a LOT of these databases and depending on your specific questions you may want to look into different ones. Like already mentioned NCBI hosts basically all of the available information, however it's not always easy to find the bits you care about.
The database I personally use the most is biomart (hosted by the ensembl consortium). It doesn't just contain all known for genes for pretty much all organisms, but is also able to link this to a ot of different information sources.
I usually access the database directly via the biomaRt R package, so I can't really say how good the actual website this. However, this link should allow you to download a table of all human genes with names, (unique) identifies & descriptions (I selected these from the 'Attributes' section).


text:
Is there such thing as "being aware of itself" at a cellular level, or is awareness only a multicellular thing?
It appears to me after a brief thought, that you need multiple cells to send and coordinate messages in order to have "self awareness". Basically, you need some sort of centralized brain it seems. But maybe I'm wrong there, jellyfish don't have centralized brains right? And are they considered self-aware?
What about individual cells, can a cell be considered "aware of itself"? If so, in what ways, if not, why not? I know the definition of awareness is probably ill-defined, but maybe you can pinpoint a definition and say why cells either are or are not in within that definition.
Any research in this line of thinking to link to?
I guess a related question is, if cells do not have self-awareness, is when/where in the evolutionary chain does self-awareness arise?
Trees and sponges (and algae mats for example) are networks of multiple cells, but do they have awareness of themselves? I don't know. So maybe only after a certain degree of centralized brain then self-awareness emerges? Like I would say any mammal is self-aware, maybe lizards and fish too? Anything with eyes, but maybe that is because they seem somewhat human.
But then ChatGPT and AI throw into the question what self-awareness can really be like :)

See https://en.wikipedia.org/wiki/Hard_problem_of_consciousness - It also seems you have a primarily philosophical question, rather than a biological one. People literally write entire books on this topic, as well, it does not seem to be scoped to something answerable in a StackExchange Q&A format.

I agree this is philosophical... biologically based (imo) but argued by philosophers. One measure of self awareness is recognition of self in the mirror (pigs can do this, dogs and cats can't) but blind people are self aware.


text:
What is the philosophical definition of life?
How does philosophy define life? And how does it overlap and contrast with the concepts and nuances of other sciences such as biology, chemistry, physics and mathematics?

There is no scientific definition that differs from the philosophical definition. You should ask your question on philosophy.SE. If you happen to speak french this book by Bersini is a very good overview of the diversity and difficulties of how to define life

I'm voting to close this question as off-topic because it will be better suited for philosophy.SE

But, this question equally fits in the science section. The philosophy section might argue that it belong to the pure Science section. So, I request not to close but give sometime for other to follow. I just want to hear some thoughts, and might close if it doesn't receive as much attention. Any thoughts?

Nope philosophers will not consider that this is a science question. However, they may consider the question as being too broad such as the post What are the phylosophical implications of the definitions of life?. You should probably start with wikipedia > life

I don't speak french. Hope there is an english version of that book. Also, any personal reviews on that book. I couldn't see any rating or review online. Thanks

@Remi.b: I have read about several topics on wikipedia, as a matter of fact I am an avid wiki reader. The link to the question you posted is closed and marked as broad. But, on my question I think I pointed out specifically - what overlaps and constraints philosophical concepts of life with material science? Isn't that specific?

If it is specific, then it is opinion based as it falsely assume that scientists have a clearly defined concept of life and same for philosophers.

You're asking for the philosophical definition of life. How philosophy defines life. This is very explicitly not a biology question. The philosophy section might argue it belongs in the science question but I don't know on what basis they would do so when the question is so clearly and explicitly restricted to their field.

Isn't every answer an opinion? And if the opinion is shared among large number of people that becomes an answer to that question in that circle. I am not falsely assuming if there is or isn't a clearly defined concept of about anything, not just life. Everything is clearly defined if it makes sense to comprehensive mind, weather that definition is true or not in the real world. Defining something clearly and stating a fact are two different things, isn't it. Wish we had followed on writing an answer, lol :)

Just to add to the conversation, I find the amalgamation of phiolosophy of life and maths in G.H Hardy's "A Mathematician's Apology". And, the answers are in continuum of the imagination not on the discrete elements of classifiable objects.

There is no difference along the lines of philosophy vs. science. However, there are broader and narrower definitions in biology.
The broadest I know of is "a self-replicating, chemical system (thing) with both exhibits heredity and some form of homeostasis (display internal negative entropy)", and some even argue the last part may be optional.
The narrowest also requires being made of cells, displaying growth, metabolism, adaptation, and response to stimuli. Some argue against these because they are either implicit in the other definition (homeostasis requires a metabolism, self-replication + heredity = adaptation),  that they are unnecessary (cells or growth) or difficult to define themselves (response to stimuli).

They ask different questions. Philosophy may ask what is life, is there a purpose behind it, etc. Biology asks how does it work, chemistry what are the chemical reactions that drive it, physics maybe how does physics allow for life and how life utilizes and impacts physics, and mathematics how can life and its components be described mathematically.
It is good to remember that all scientific disciplines branched off from philosophy (and religious philosophy) and that they are interconnected.
This is the answer to the part of your question that includes biology. If you want to discuss the meaning of life philosophically, you are welcome to come to do it on the philosophy page!


text:
Calculating CV for intra-assay ELISA
Sorry if this is in the wrong thread.
I have to calculate CV for intra-assay ELISA sample OD's. My problem is that i'm finding people are using sample standard deviation in their CV formula, though from what i understand as intra-assay CV reflects variability within the same assay run that to me should be considered as a whole data set and therefore population standard deviation should be used.
Am i correct in my assumption or am i missing something?

As far as I am concerned the intra-assay CV is the average of individual CVs found in an assay.
So let's assume you have a data set of 40 samples, and for each sample you have 2 replicates (results), like the one below.

You would first calculate the mean for each sample, so in the sample above that would be: $$\frac{0.132 + 0.128}{2} = 0.130$$
Then you would calculate the standard deviation for each sample, so going back to our example above, the standard deviation for sample 1 would be as follows: $$\sigma=\sqrt{\frac{1}{2} ((0.132-0.130)^2 + (0.128 - 0.130)^2)}=\frac{1}{500}=0.002$$
Next you would calculate the Coefficient of Variation, so in our case:
$$CV = \frac{\sigma}{\bar{x}}\times100=\frac{0.002}{0.130}\times100\approx1.6%$$
Afterwards you would repeat the aforementioned procedure for each sample.
In the end you would calculate the average of all individual CVs, so: $$CV_{intra} = \frac{\sum_{i=1}^{40} CV}{40} \approx 5.2% $$
I have stolen the example from Salimetrics, I think this document explains inter-assay and intra-assay CV very nicely.
Please note: The usefulness of inter and intra-assay CVs are somewhat disputed, as this Wikipedia article mentions.

Thank you for your reply, i have read this. They have 2 result sets, so it's possible to calculate the CV for each individual sample, i generally only have one. It's probably fine to use Sample Standard Deviation in their formula as they are calculating the individual sample CV from a whole data set. As i have only one set to work with i need to calculate the CV from the data set as a whole, which is why i think i should be using Population Standard Deviation in my CV formula rather than Sample Standard Deviation for my scenario instead. Though everyone seams to use Sample SD regardless.

I guess it really depends what you want to measure with the CV. It sounds to me, seeing that you have only one result per sample, that an intra-assay CV is not the measure you are looking for. Going by what you have said it sounds like you simply want to calculate the CV for your entire data set and that seems to make sense. I think it then becomes more of a question what it tells you about your data and that really depends on your study design and what you test for..


text:
Can you increase the microbiota in an insect?
I know you can suppress the microbiota of an insect with antibiotics, but I´m am looking for a way to increase it. For example, can I feed an insect with something that helps boost the bacteria like agar or something.

The answer is absolutely yes.
There are 3 main ways:

Faecal transplant: faecal sample from other insect could be
transplanted in order to colonize the gastro-intestinal tract
Injection of bacterial culture into the desired tissue
Use of functional foods to increase the abundance of specific bacterial
genus.

See this review for more detail


text:
Lactobacillales vs LAB (Lactic acid bacteria)
As far as I understand bacteria of order Lactobacillales are all LAB (Lactic acid bacteria). So often "Lactobacillales" and "LAB" are used interchangeably.
But I also thought that this is not the whole truth, because there are LAB which are not of order Lactobacillales.
Can anyone elaborate on this topic and is there a paper/review explaining the consensus on this topic?


text:
Are there any animals that are both poisonous and venomous?
From my layman understanding, animals that inject venom into the bloodstream by biting or poking are venomous. And ones that harm you when you eat them are poisonous.
Are there any animals (or plants) that fit both descriptions?
I'm guessing eating a venomous rattlesnake will give you an upset stomach but not cause enough damage to be classified as poisonous. And I'm pretty sure poisonous tree frogs don't bite into their prey and inject them with anything.

Any stomach upset from eating rattlesnake is likely to be purely psychosomatic.

What is poisonous depends on who (what species) is eating it, so you might want to specify if you are specifically interested in animals that are poisonous to humans.

Anecdotally, people consume the venom sac of cobras in cognac. Apparently this causes some mild hallucinations (and if you happen to have a cut where it enters your bloodstream before the venom is neutralized by your stomach acids, it kills you)

Eating rattlesnake is pretty common. They're not at all poisonous.

@WayneWerner - ...and now, across America, thousands of idiots will start raising cobras for their venom sacs...which should, predictably and in short order, raise the average intelligence of Americans.

If a poison kills you through the bloodstream but not through digestion, it means that it was digested, nothing more. Rattlesnake venom is a protein that denatures in the stomach long before it reaches the bloodstream - it's not really different from eating any other kind of protein. Others may be destroyed through cooking through the same basic mechanism. Contrast this to e.g. alkaloids, which pass through the stomach unhindered.

The amazonian giant centipede has a venom that is injects with bites, but it also exudes a poison that really will only give you a rash but i believe is classified as a poison.

That is certainly an interesting question!
First, to clarify definitions:
To be considered venomous the toxic substance must be produced in specialized glands or tissue. Often these are associated with some delivery apparatus (fangs, stinger, etc.), but not necessarily.
To be poisonous, the toxins must be produced in non-specialized tissues and are only toxic after ingestion.
Interestingly, many venoms are not poisonous if ingested.[1]
I know of at least three species that produce both poison and venom. One is a snake (although not a rattlesnake, which are, in fact, edible): Rhabdophis tigrinus, which accumulates toxins in its tissues, but also delivers venom via fangs.[2] The other two are frogs: Corythomantis greeningi and Aparasphenodon brunoi, which have spines on their snout that they use to deliver the venom.[3]

[1] Meier and White (eds.). 1995. Handbook of clinical toxicology of animal venoms and poisons. Boca Raton, Fla.: CRC Press, 477p.
[2] Hutchinson et al. 2007. Dietary sequestration of defensive steroids in nuchal glands of the Asian snake Rhabdophis tigrinus. PNAS 104(7): 2265-2270.
[3] Jared et al. 2015. Venomous frogs use heads as weapons. Current Biology 25, 2166-2170.

Interesting, I got different answers when I asked for the difference between "poison" and "venom" on english.SE.

But not too surprising. Try asking the definition of significant on english.SE and Cross Validated and see how disparate the answers can be. English.SE is concerned with general parlance, whereas, biology.SE is (generally) more concerned with the technical conventions. That is a good object lesson that definitions are only definite within a field.

Can you please add links to your sources? I don't know if the book is available on Google books or some other resource, but the two journal articles will be available via PubMed. This will very much help people who want to check your claims, as well as those who wish to learn more. If Wikipedia articles (or some other better resource) are available for the animals you mention, you should link to them as well.

@svick Most of the answers to your question cite no sources. Interestingly, those that do actually align quite nicely with this answer.

The answers in english.SE are not that different... Still, of course there is a difference between scientific use and regular use. But I would call it difference in the details.

@MattDMo I've added links. Luckily, Meier and White (1995) is available on Google (it is also available at any library with inter-library loan service). I think you'll find the claim you are wanting to check on page 3, first sentence.

Your definition of poison seems rather narrow. I don't think poison frogs would meet it as stated.

@CodesInChaos Can you explain why you don't think Dendrobatids conform to the definition.

Although it fits the question, isn't "To be poisonous, the toxins must be produced in non-specialized tissues and are only toxic after ingestion." a bit narrow?  After all there are animals (like some frogs and toads, as well as many insects) - as well as some plants (poison ivy) - that are poisonous to the touch (causes rash and maybe allergic reaction) or have poisons (often on the skin) that start working as soon as they're in your moth (so you spit it out).  These are not venom, since it's not injected into the blood... but nor are they toxic in the sense that the poison must be ingested.

@BaardKopperud, I think you are coming at this question from too anthropocentric a viewpoint. Organisms may produce topical reactions in human skin, but it is unlikely, in most cases, that this was the selective impetus for developing that chemical. They probably evolved those toxins in response to predation, and the topical reaction of hair-less apes (recent new comers in most cases) is just collateral effect.
Also, there are plenty of things that taste bad (e.g. sour citrus, spicy peppers, bitter greens) that evoke a taste aversion response, but are harmless to ingest (so, not poisonous).

I once read something about a type of tiger snake that was poisonous to touch and has a venomous bite.
Edit: I found the species Asian Tiger Snake, Rhabdophis Tigrinus
Rattlesnake meat is the same as any snake just don't eat the head.

authors: Bob Jarvis - Слава Україні


text:
How does HBeAg change to Anti-HBe in acute hepatitis
I am thinking this figure

which can also be drawn like this

How does HBeAg change to Anti-HBe?
There are some triggers that stimulate Anti-HBe production after HBeAg level is done.
I think they can Anti-HBc.
There must be other mechanisms too.

Can you please introduce your abbreviations? This would be a good style so people can understand the figures better.

Alan answered the question. Just standard antigens and antibodies for HBV.

I'm not sure that I have understood the question but ...
HbeAg is a secreted variant of HbcAg (the core antigen of HBV). Unlike HbcAg, HbeAg is found in the blood. I believe that it is produced as a result of a splice variant of the corresponding RNA.
The phenomenon described in these Figures is an example of seroconversion. Before seroconversion the antigen is detectable in the blood but there is no antibody directed against it; after seroconversion there is antibody but no antigen.

Thank you for your clear answer! You understood what I mean. I missed the term seroconversion. I think there are actually two windows periods and two  seroconversions in the figure. First, for HBe and then for HBs. I would like to know how these two seroconversion stages and/or windows stages differ. It would be nice to use some analogous words like "isovolumetric contraction" and "isovolumetric relaxation" just to differentiate some property between the two window periods. I do not know which property that can be.


text:
What is this abbreviation CT in female reproductive system
I have this sentence in my notes

Ovary is surrounded by tunica albuginea and the cortex keeps the primordial follicles. The medulla containing CT and blood vessels develop from mesonephros.

I have these words in my mind about CT

tunica
cyto- (maybe cytotrophoblast)
corona (no other than corona radiata so not)

What can CT be here?

Homework question and too easy. Please, close.

I think CT is an abbreviation for connective tissue. Some examples of its use in that fashion:
http://en.wikipedia.org/wiki/Connective_tissue
https://web.archive.org/web/20151024041339/http://www.vetmed.vt.edu/education/curriculum/vm8054/Labs/Lab5/Lab5.htm
http://www.pitt.edu/~sshostak/biosci1450/hislec03.html

I found this as well, and it is a fact about the ovaries.

Thank you for your fast answer! Yes, it makes sense.


text:
To understand clearly extraintestinal diseases
Extradistestinal disease seems to prefer to "bowel" diseases, I think this is about diseases outside gastrointestinal tract so stomach.
Consider diseases ulcerative colitis and Crohn's disease (enteritis) as examples.
Colitis affects to colon, outside of small intestine, I think extraintestinal therefore.
Crohn's disease (enteritis) however affects to the small intestine so I would think intestinal disease (but this clause is wrong) - it should be at least have extraintestinal manifestations.
What is the exact definition of the word extra in intestinal diseases?

Certain intestinal diseases have symptoms that appear concurrently in other systems of the body, but the bowel diseases themselves are not extraintestinal.

Extraintestinal manifestations of inflammatory bowel disease are prevalent in both ulcerative colitis and Crohn's disease. The most common manifestations involve the musculoskeletal and dermatologic systems. Other manifestations involve the hepatopan-creatobiliary system (eg, primary sclerosing cholangitis) as well as the ocular, renal, and pulmonary systems1.

One of the key differences between extraintestinal manifestations and comorbid conditions (though seemingly not a necessity, the article cites primary sclerosing cholangitis as an counterexample) is that the extraintestinal effects will subside once the disease of the bowel is treated.
1 Levine, J.S., Burakoff, R. (2011). Extraintestinal Manifestations of Inflammatory Bowel Disease. Gastroenterol Hepatol (NY), 7(4), 235–241.

Does there exist any extraintestinal disease with some type of diarrhea?

@Masi In that case, the manifestation wouldn't be extraintestinal, it would be directly related to the intestine.


text:
What is the difference between intracardiac and extracardiac reflexes in cardiac regulation?
The primary parameters of heart pumping are

strength of contractility (inotropic positive; Frank-Starling relationship)
rate of relaxation (lusitropic positive)
heart rate (chronotropic positive)

which change the secondary parameters according to the marginals

Heart rate
Stroke volume

Contractility
Starling relationship

Which of these paramecers are controlled intracardiacally and which extracardiacally?

Rate is controlled outside the heart by the Vagus Nerve having parasympathetic activity on the sinoatrial nerve.
Stroke volume (taking contractility and Starling's law as one) are factors from the cardiac tissue itself - "intracardiac".


text:
What is the benefit of using Gonoline-Euroline in combination?
I was heard that this combination first Gonoline and other culture another culture on Euroline is good one.
What is the benefit of using Gonoline-Euroline in combination?

What's the context, I've never heard of using them in combination/not sure you really mean to be asking about Euroline.

Please, close. This is too unclear to be discussed.

Looking at your other question, I think there's some serious editing that needs to be done to clarify this question.
Still I think there is a quick and easy answer to your question.  Gonoline media makes an excellent transfer media.  If you are out in the field some where and want to take a swab for further analysis, you could easily choose a gonoline media for transport.  Then you would want to follow that up with some selective blood agars that might show a pathogenic species that you were looking for.  Thus to use gonoline media with any other medium, is merely to preserve your sample for plating on your diagnostic media/agar later.
Again, looking at your related question, I could only guess that you meant chocolate agar, because you might be hunting Neisseriaceae (which you should put in the question if you are).

I'm also ok with closure


text:
What is the effect of Montelukast on the amount of IgE in blood?
I know that it decreases the amount of leucotrienes in blood.
I saw a patient with high IgE altough under Montelukast medication.
This suggests me that Montelukast does not affect the immunoglobulins, but somehow restrict the allergic reaction indirectly.
What is the effect of Montelukast on the amount of IgE in blood?

I was interested in this question because I have always been a little confused about allergic responses, so I did some rather superficial research (i.e. I looked at some Wikipedia pages). As far as I can see there is no reason to think that Montelukast will have any effect upon IgE levels.
Montelukast is a leukotriene receptor antagonist. It is used to treat allergies and asthma.
Leukotrienes are lipid signalling molecules that are used by cells to regulate immune responses. One role of leukotrienes is to promote contractions in the smooth muscles lining the bronchioles. If they are over-produced they can cause inflammation in the airways leading to symptoms of asthma. Since leukotrienes act through a receptor, an antagonist of that receptor such as montelukast can reduce their effect.
IgE is involved in allergic responses because it interacts with Fc receptors on the surface of certain cells such as mast cells. If the IgE molecules are associated with one another through Ig-antigen interactions this leads to clustering of the Fc receptors which triggers an intracellular signalling pathway leading to mast cell degranulation - the release of histamine by fusion of storage vesicles with the cell membrane (i.e. exocytosis). Histamine causes constriction of the bronchioles via effects on smooth muscle, just like leukotrienes.

Thank you for your work and clear answer! It is interesting to note that HIV virus leads to clustering of CD4+ cells so total CD4 cell count decreases. Here,  Fc receptors cluster (IgE interaction) so all total count of Fc cells decrease. - So histamine can interact with Fc receptors and cluster Fc cells, like leukotrienes.


text:
Why rectus abdominis is not proximal muscle?
I am thinking this picture which shows proximal muscles.

Why for instance pectoralis major, subclavius and rectus abdominalis are not included in proximal muscles?

It's not clear what "proximal" means in this context. It's not a standard use of that anatomical term in English. I'd also say that the figure on the left actually does show the pectoralis major.
The author of this figure might be trying to show the muscles that cross the proximal joints in the upper and lower limbs. For example:
Upper limb

Pectoralis major
Biceps brachii
Triceps brachii
Latissimus dorsi

Lower limb

Adductors (brevis, longus, magnus)
Rectus femoris
Semimembranosus, semitendinosus, biceps femoris (long head)
Gluteals (maximus, medius, minimus)

Muscles that do not cross the shoulder or hip are not included. This explains the lack of rectus abdominis or subclavius. Though it is not clear to me which the paired muscles in the posterior view are running craniocaudally from the thorax to the gluteal region.


text:
Is funnel web spider venom poisonous?
Does the venom of the Sydney funnel web spider have to be injected into the bloodstream to have an effect? If the venom was swallowed (e.g. if a spider was eaten), would it still have an effect? Or wouldn't it be able to pass through the gut lining, or be broken down in the gut?
I understand that the funnel web's venom is different to most spiders', but would this answer apply to spider venom in general?

Interesting question.

@Chris: Very interesting.

For the above reason, I'd also be interested to know if ethanol would degrade spider venom...

@naught101 Ethanol would not degrade this venom. In practice, it actually stabilizes protein by inactivating proteases (enzymes that degrade protein)

I think this question is hard to answer as toxicity will depend to a large extent on the amount of toxin ingested. Even peptide-toxins normally degraded in the gastrointestinal system may eventually become toxic when enough is ingested.

The Sydney Funnel Web Spider's venom is called δ-atracotoxin and it is especially toxic to primates. It is a peptide toxin, which means that it has the potential to be digested in the stomach before having any physiological affect. However, many peptide toxins are not inactivated by swallowing--you don't want to be eating any Botulinum toxin.
Characterization of insecticidal peptides from venom Australian funnel-Web spiders (Vonorax et al. 2006) harvested venom from Hadronyche infensa, the Darling Downs funnel-web spider. This spider is closely related to the Sydney Funnel Web spider and also produces δ-atracotoxin.

An oral ingestion activity test was undertaken using crude H. infensa venom.

The ingestion test was performed with insect larvae, which are susceptible to the venom when injected. (Aside: there's a lot of interesting research on the toxin's effect in insects). They didn't find much:

Oral ingestion activity test of crude H. infensa venom
No effect was observed in this test, even though approximately 4 times the dose required for lethality by injection was orally consumed by the larvae.

I don't think anyone has performed a study of toxin ingestion in primates (if they have, I couldn't find it). The researchers don't speculate as to why the toxin has no effect when ingested. As expected, the toxin had no effect on (non-primate) mice:

Effect of atracotoxin-Hv1 on newborn mice
All mice in both test and control groups survived without apparent toxic effect beyond 24h post injection.

Whether this is applicable to other spider venom depends on the nature of the venom. A non-peptide, low molecular weight venom able to be absorbed by the lining of the esophagus could be very toxic by ingestion.

Further reading:
Scanning Mutagenesis of ω-Atracotoxin-Hv1a Reveals a Spatially Restricted Epitope That Confers Selective Activity against Insect Calcium Channels (Tedford et al. 2004)
Isolation and pharmacological characterisation of δ-atracotoxin-Hv1b, a vertebrate-selective sodium channel toxin (Szeto et al. 2000)
(for more info on peptide toxins): Cyanobacterial Peptide Toxins


text:
What is the definition of "dry weight" and "dry cell weight"?
As I understand it, the dry weight of something is its weight minus the weight of its water content. Is this the definition? What about dry cell weight?

Why would dry cell weight be different?

dry weight is used in non-biological sense too.. thats the difference

@terdon so the definition I've written of dry weight is accurate?

http://biology.stackexchange.com/q/13692/561

According to my Henderson's Dictionary of Biological Terms, dry weight is

The weight or mass of organic matter or soil after removal of water by heating to constant weight.

So yes, your definition is correct and it is also applicable to cells. The dry weight of cells is the weight left when their water content has been removed by heating.

+1 thanks. What does "heating to constant weight" mean?

@becko heating until further heating does not result in a reduction in weight. Basically, until all the water has evaporated.


text:
what are the mechanics of sweating?
The causes of sweating aside, i.e. I'm not interested in which and how nerve signals are transmitted to sweat glands. But I would like to read a detailed account on what a sweat gland consists of, what it does when not sweating, but esp. what happens when a sweat nerve signal arrives. Is there a good free review or can you give one?

Myoepithelial cell contraction initiates glandular release from most exocrine glands developed from the ectoderm. These are the cells that exist in the glandular epithelium.
At the distal end of the glanduar coil, an isotonic plasma filtrate gets actively transported into its lumen. As you move down the coil, close to where it connects to the duct, absorptive cells remove NaCl to make sure the sweat is hypotonic when it reaches the surface of the skin. If you view these cells where staining for alpha tubulin or beta actin, you will see they have abundant levels of myofillaments, something uncharacteristic of epithelial cells. Hence Myoepithelial.


text:
Lac operon: How can lactose enter the cell in the absence of lactose permease?
My textbook states that

lactose permease...transports lactose into the cell

and

When lactose is added to the growth medium, the lactose molecules bind to the other site on the repressor protein

My question is, how can lactose enter the cell to bind to the repressor protein to allow beta galactosidase and lactose permease to be synthesised if there is no lactose permease present to transport the lactose into the cell?

Based on the questions you are asking, you have good intuition about the information you are reading. Out of necessity introductory textbooks are cursory and only cover the very basics of only the most important of topics. They basically are teaching you the vocabulary of biology and keeping the detail at arms length. Keep reading and keep looking deeper, you are on the right track.

Here's everything you need. It's called the lactose paradox:
http://sandwalk.blogspot.it/2008/10/lactose-paradox.html

Introductory textbooks will not get into the details of the lac operon.
Basically, the operon is expressed constitutively at a low level that means that Beta Galactosidase and Lactose Permease are expressed at low levels by the bacterium. This is because it takes a little bit of time to build up the concentration of LacI in the cell before it can start to bind the operator.
The LacI repressor only binds the operator in the absence of Lactose in the cell's environment due to the fact that allolactose allosterically binds the LacI repressor and affects that molecule's ability to bind the operator. So RNA polymerase can bind the promoter of the Lac operon at some low rate and continue to produce the protein.
When the cell no longer has glucose, it generates cyclic AMP, which induces the CAP protein to bind to the CAP site, just upstream of the promoter of the Lac Operon. CAP associates with RNA Polymerase, and this makes the promoter very active. Beta Galactosidase and Lactose Permease levels increase rapidly.
Where you see the full effects of the LacI repressor is when neither Glucose nor Lactose are present in the environment of the cell. At this point the repressor binds to the operator and blocks transcription by DNA Polymerase.
I hope this helps. I have an entire book that covers the Lac Operon, so even though this is a bit expanded of an explanation from a basic textbook, it is still a summary.

Thank you for your informative reply! I'm just still slightly confused; by 'the operon is expressed constitutive lay at a low level' do you mean that even with no lactose present, a repress or protein is not constantly bound and therefore some beta galactosidase and lactose permease are expressed? This seems to contradict with 'when neither Glucose nor Lactose are present in the environment of the cell...the repress or bonds to the operator and blocks transcription by RNA polymerase'. I apologise for misunderstanding and being quite slow with this, and thank you again for your help :)

@21joanna12 it is going to take me a bit of time to update my answers. But very briefly, DNA binding proteins all have a certain on/off rate associated with them. There will be certain instances where the operator is clear and RNA Pol can bind. Also proteins have half-lives and are degraded, so depending on the cytoplasmic concentration, there is a probability that the promoter will be free to be bound by RNA Pol. Cell biology is unfortunately not digital as it is often described in textbooks. I'll try to get to a better answer soon.


text:
Example Clade Names in PhyloCode
After looking through the PhyloCode, the only thing I found that looked like an example was in Article 9, Chapter 4:

A node-based definition may be abbreviated "<A&B" or "<A&B&C&D [etc.]".
A branch-based definition may be abbreviated ">A~Z" or ">A~Z∨Y∨X [etc.]".
An apomorphy-based definition may be abbreviated ">M(A)".

Then from the following lines, I assume that that is actually how the names would appear in print:

The system of abbreviations used here adopts the following conventions: > = "the most inclusive clade containing"; < = "the least inclusive clade containing"; & = "and";  ∨ = "or"; ~ = "but not"; A, B, C, etc. = species or specimens used as internal specifiers; Z, Y, X, etc. = species or specimens used as external specifiers; M = an apomorphy; () = "of" or "synapomorphic with that in"; >∇ = "the most inclusive crown clade containing"; <∇ = "the least inclusive crown clade containing". The inverted triangle meaning "crown clade" resembles the representation of a crown clade on a phylogenetic tree diagram.

I'm wondering if one could clarify what an actual real-world Clade name would be using the PhyloCode. Maybe just a few examples or even just one. For example, there is this fern Equisetidae, a subclass of Polypodiopsida. Altogether it has this set of names:
Kingdom     Plantae
Subkingdom  Embryophyta
(unranked)  Tracheophyta
(unranked)  euphyllophytes
Class       Polypodiopsida
Subclass    Equisetidae

I am wondering how you would rewrite this using the PhyloCode. If it's too complicated or requires a bunch of additional work to initialize a basic set of codes or something, then that would be good to know too. But from the documents I've seen, it seems to suggest one can translate existing Linnaean classification terms to the PhyloCode somehow. My attempt at it without having gone thoroughly through the whole document is this:
A = Plantae
B = Embryophyta
C = Tracheophyta
D = euphyllophytes
E = Polypodiopsida
F = Equisetidae

So the full name of it would be something like A>B>C>D>E>F. Or maybe it's more like this:
A = Plantae
A>B = Embryophyta
A>B>C = Tracheophyta
A>B>C>D = euphyllophytes
A>B>C>D>E = Polypodiopsida
A>B>C>D>E>F = Equisetidae

Looking for some help on better understanding how to translate existing Linnaean terms/species to PhyloCode. Wondering if you are actually renaming things like Tracheophyta, which has a descriptive Latin name, to A>B>C, which is a non-descriptive identifier. Thank you.


text:
Tree of Life in Text Format
Wondering if there is a tree of life in Text format for open data sharing.

Perhaps not though the tree of life website, but the Open Tree of Life exists to fulfil this need. You can export newicks of nodes which you are interested in.

I don't see how to export, would help if you wouldn't mind explaining.

@LancePollard if you look to the bar on the right hand side you should see a heading called "Download subtree as newick string". For large trees this will take you to the repository, but for smaller subtrees there should be an immediate tool.

Note that such a huge tree will be difficult for most treeviewers; Dendroscope is probably a good bet

The NCBI taxonomy database contains an (as far as I know most complete/up-to-date) database with information about all classified species.
I haven't tested it, but I would guess that its accessible through the E-utilities tools, which will usually allow you to query and download information in xml or raw-text format.
Additionally the whole data the taxonomy database is built on is available on the NCBI ftp-server, they also include readme files so you can figure out how the data is formatted.


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Where to find fossil databases
Looking for sites with fossil data in the following categories.

Fossil cells
Fossil invertibrates
Fossil fish
Fossil amphibians
Fossil reptiles
Fossil dinosaurs
Fossil birds
Fossil mammals
Fossil insects
Fossil plants
Fossil mushrooms
Fossil humans

I would like for the sites to be copyleft (i.e. free, public domain, or creative commons type license) if possible, not necessary though. However, some museums such as the British museum are copyleft. Also, many other sites that google brings up are not working.
The sites I have found are mostly not copyleft:

American Museum of Natural History - Paleontology (4.75 million specimens) (very restrictive, only personal/educational use)
Paleoportal (aggregated stuff from the University of California Museum of Paleontology, the Paleontological Society, the Society of Vertebrate Paleontology, and the United States Geological Survey). This may touch on all of the fossil categories above.
Paleobiodb. (top categories: Mollusca, Brachiopoda, Arthropoda, Mammalia, Cnidaria, Radiolaria)
Fossil works
Florida Museum - Natural History Collections (botany, plus others)
Bryophyportal. Unfortunately, the images are only for personal/educational use. Looking for sites that allow free use of the content (such as copyleft licences like creative commons, or as public domain).
UCMP (not copyleft, personal/educational use only)

Wondering if these are good enough, or if there is anything else that should be added to this list to cover the categories above.

No such database exists, you have already found the best that is available. there is a current effort to build one, but these are disconnected, poorly funded and in some cases dead( poor dinosauricon). Sadly wikipedia is currently one of the better websites for finding such things. Part of the issue is for many of those categories there are only a handful of scientists even studying it.


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why is cellulase not found in animals?
As it is really beneficial for all organisms, why are animals, especially mammals (I don't know about other vertebrates) unable to synthesize cellulase enzyme in their body? Is it linked to some DNA defects or have we not evolved from cellulase producing bacteria?

Doesn't the bacteria flora in some higher vertebrates (ie: cows) allow for the celluase, and therefore the digestion of cellulose? We lack the bacteria and therefore the enzyme. I am not sure I understand the last part of your question, " or have we not evolved from celluase producing bacteria".

i actually meant 'why cant mammals synthesize their own cellulase?' or 'why are cows dependent on bacteria for cellulose digestion?' and, by the last part i just meant that if we lack cellulase producing gene, then we must not have received it from our ancestors, which could thus not be cellulase producing bacteria ;-)

I think its a symbiotic relationship, so the bacteria bet something benifital, as do we(the calories).  Bacteria flora are often passed down from mother to child anyway, so why would we even need to have it in our genome? Couldn't we extend your logic to why we don't have any gene "x" that provides benifit "y"; for evolution tinkers and not engineers right?

thanks, and maybe its because of those bacteria only that mammals never needed to develop that gene (if i got you right)

Or they lost the gene. That is usually the better assumption. Think about gene duplications. Once a gene is duplicated, only one copy need be under selection, so the other one can be mutate, either becoming a nonfunctional gene or a newly functional gene. Also remember that there is a cost to maintaining and expressing a gene in the genome. If a symbiont is producing something for you, then it costs you less to maintain your own genome if you lose the gene you don't need to use.

Duplication of If a trait would be advantageous to an organism why hasn't it evolved.

@AMR your last line "If a symbiont is producing something for you, then it costs you less to maintain your own genome if you lose the gene you don't need to use." is confusing me now. How can a gene be expelled or lost just because a symbiont is already providing the resulting protein to you. Its just like you cut off your legs just because a horse is there to carry you. So I doubt "Or they lost the gene.". Maybe that gene gradually became non-functional with time or is still present, but works on feedback mechanism.

You cannot call it duplicate as that question says "This is a general question that would be applicable for any kind of trait."

These are molecules, not body parts. If you do not have a symbiont that produces the product, then you have to maintain the gene or a mutation that causes the gene to be non-functional would be deleterious and could lead to the organisms extinction. A mutation that makes the gene non-functional can occur if there is a symbiont producing the gene product and so you remove selection for that gene and it can mutate to non-function without hurting the host organism.

Substitute cellulase for any trait and that is your question which is why it is a duplicate of that question.

Why substitute? (don't mind) This question is specifically about a single trait which, according to me, has probably evolved but never showed up. Anyways, this discussion is now going off-topic, so thanks everyone for your help.

Histidine is one of the most important amino acids for proteins, but humans cannot produce it. So if I asked, Why did humans not evolve (or retain) the gene to produce histidine? then it is a duplicate of that question. That is why we have it as a community wiki.

But thats different. Humans can eat proteins and breakdown them to get histidine, but humans cannot eat cellulase and become able to digest grass.

The answer to questions like this is just a guess (Primarily Opinion Based), and I've voted to close. But some food for thought too long for a comment:

As it is really beneficial for all organisms...

Why do you think that cellulase is so very beneficial to mammals? Animals did have cellulase (some ancient invertebrates still do, like sea squirts, abalone; crayfish have it); we may well have faulty copies of the gene (as @AMR suggested in comments.) But you presume to know we'd be better off with it. That's a belief without any objective evidence.
What might happen if we could convert cellulose into sugar? This is also important to think about. If some of that surfeit glucose in out guts were fermented into alcohol (this condition does rarely occur in humans, and the living people afflicted with this are truly afflicted), because we have a gut microbiome, we would walk around drunk much of the time (ok, maybe even only some of the time), which would make escaping predators less drunk than we were difficult. Maybe the body would be incapable of handling that level of glucose ingestion, and we'd all be T2 diabetics by the time we were just out of toddlerhood.
Humans need fiber in our GI tracts. I don't know all the reasons why we developed that way, but we do. Cellulase would do away with that. Do you know for sure that this would be good for us?
The thing is, you've made an assumption (we'd all be better off with cellulase) that has no evidence to support it at all (or, at least you have not provided any.)
It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK. There are millions of reasons that they are doing OK. We don't know all of them, but the absence of the very thing you presume would be a benefit may be what allowed vertebrates to develop at all.
Ancient Origin of Glycosyl Hydrolase Family 9 Cellulase Genes
Structure and function of a cellulase gene in redclaw crayfish, Cherax quadricarinatus

"I don't know all the reasons why we developed that way, but we do" lack of cellulase might be the reason for it. As you've said, answers to such questions are, and will be, opinion based and also, as you said "It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK" one can never estimate how would something have affected our evolution. My point was that maybe having cellulase would have enabled us to live more easily in food scarcity. But, again I cannot assume this to be perfect solution.

@aayushsrivastav - gosh, you missed my entire point, entirely.

I know, I was just justifying my point.


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Interpreting SNP-in-gene associations from GWAS studies
For most SNPs identified in GWAS studies, is the underlying assumption that if it is indeed associated with a phenotype (and lets assume its associated because it affects protein function), that you don't need two knocked out copies of that gene for it to confer susceptibility risk to the individual?
In other words, is my assumption that GWAS is likely uncovering alleles that confer risk in single copy, correct?

Why would a SNP ID tell you anything about its effects? To my knowledge you couldn't say anything about phenotype from just a SNP, but I'm not professional on this.

@leonardo Of course, I wasn't saying that a SNP can't have an effect; but that you can't predict the phenotype just knowing there's a SNP [unless you investigate its effect] (cf. your answer)

In short, yes.
If a gwas study links a SNP to a particular phenotype then yes, it is an effect of a single copy. Bear in mind, however, that a SNP is not a knockout or even a knockdown. It can be, but it is not always the case.  SNPs can produce a change in the protein sequence or in the regulation of the production of that protein. Both types of variation can result in a phenotypical change.
In any case, SNP information is always about a single allele, I imagine that you can find cases where a cell is homozygous for a particular SNP but is is not necessarily, or even often as far as I know, the case.


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Why did S. serrata die?
We are interested to farm Scylla serrata which is a type of crab. We introduced the crab weighing 800 g into a environment with 22 ppt salinity with a pH of 8.2. The crab was feeding on around 12 g of chicken meat daily. However at the end of the 4th day, after flipping the crab to its back, it died shortly after. Previously it was able to flip itself back successfully. Note that salinity and pH did not vary much.
What are the possible root causes for death?

A complete species name would be better


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Find protein homologs with BLASTp
I'm trying to find homologs of a set of proteins using BLASTp. I'm working with custom databases.
I'm using evalue of 0.00001 as threshold.
I would like to filter queries having hits with >90% identities. Because BLASTp output is based on HSPs, I cannot filter by %identities/query, only by HSP.
I would like to know how to do this and also if I'm following a reasonable strategy.
Here is an alignment example: qcovs=100 but qcovhsp lower.
qseqid           sseqid         pident length mismatch gapopen qstart   qend  sstart    send   evalue bitscore qcovs qcovhsp
HPNK_01698      HAPS_0519       81.88   596     75      5       630     1225    615     1177    0.0      889    100     49
HPNK_01698      HAPS_0519       49.17   301     115     8       84      366     201     481     2e-56    214    100     23
HPNK_01698      HAPS_0519       53.64   261     61      6       436     684     616     828     6e-49    191    100     20
HPNK_01698      HAPS_0519       46.61   251     62      3       332     510     584     834     6e-46    181    100     15
HPNK_01698      HAPS_0519       53.27   214     79      4       1       194     1       213     1e-45    180    100     16
HPNK_01698      HAPS_0519       55.96   218     60      8       550     764     643     827     1e-40    164    100     18
HPNK_01698      HAPS_0519       51.56   225     61      7       516     731     642     827     1e-38    157    100     18
HPNK_01698      HAPS_0519       49.57   230     77      6       484     713     643     833     1e-37    154    100     19
HPNK_01698      HAPS_0519       57.89   76      26      1       364     433     760     835     1e-13   76.3    100     6

Code used
Make database
makeblastdb -in $Hparasuisfastadatabase -out H_parasuis_strains_gb_ALL.fna_databaseBLAST -dbtype prot -parse_seqids

Run BLAST
blastp -db H_parasuis_strains_gb_ALL.fna_databaseBLAST -query 'out_2.fasta' -out HPNK_selected_vs_H_parasuis_strainss.tblastn -evalue 0.00001 -outfmt "6 qseqid sseqid pident length mismatch gapopen qstart qend sstart send evalue bitscore qcovs qcovhsp" -max_target_seqs 50

Thanks, Bernardo

If I'm not wrong, qcovhsp is a perc_identity for ONE HSP. I would have to calculate manually for each hit as an average for all HSPs perc_identity for one hit.

I even don't like hit_perc_identity because of its reductive information assumption. Average is normally influenced by extreme values.

What species are you comparing? How distant are they? If close enough, "real" homologs should be able to form a single HSP spanning most of the target sequences.

You can calculate the average HSP coverage for the entire sequence (from all alignments). You can also calculate average score per residue. The other option is to do an end-to-end alignment with tools such as stretcher.

Check out my new question related to BLAST: http://biology.stackexchange.com/questions/23958/tblastn-and-blastp-discordance-is-that-possible

First of all, if you want 90% identity, you can discard this hit. None of the HSPs pass that threshold. What's more, since you're working with proteins, there are no splicing issues involved and you should be able to get a single HSP spanning most of the query and subject sequences. Assuming, of course, you have a true homolog.
In your output, I see many small, overlapping HSPs, most of which have low identity. I can't be sure without seeing the sequence but it's a safe bet that what you have there are low complexity/repetitive regions and that's why you have so many separate HSPs. The only half way decent one starts at position 630 of the query sequence and is only 595 residues long, less than half your query protein. Either you have a very diverged N-terminal region or your HSP is just a conserved domain. Again, I would need to see the actual sequence alignment to be sure but that doesn't look like a true homolog (assuming your species are reasonably close which they must be if you're using a 90% identity threshold).
So, always assuming that your species are close enough to expect decent homologs, I would simply ignore the shorter HSPs and deal with those that represent more than, say, 80% of my query's length at >=90% identity. Shorter hits will most often be conserved domains or repetitive/low complexity regions. The thresholds you choose depend on the species you are studying.
If your species are not that close, don't use BLASTP at all. Instead, you can use something like hmmer. Collect a set of homologs from various species for each of your query proteins, build a matrix using these and use that matrix to search your database. You could also use Selenoprofiles which uses a similar approach.

They are strains of the same bacterial specie. I agree with the thresholds you suggest. Thanks


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Comprehensive database of cell types
Wondering if there is a comprehensive list/database of cell types, similar to this wiki list of cell types in the human body. It lists probably 100+ different types, but this is just for a human. If we include all animals, and plants, and bacteria, and single celled organisms, etc. then the list would probably get larger.
Wondering if any such aggregation exists, either just as a collection of lists or as a database of cell types. Doing a search returns CELLPEDIA, but the last results are from 2011, so it looks like it never came to be. I also saw MorphoBase, but it didn't look like it was there either. But something like that would be good, otherwise just a list. Basically like a cell taxonomy.

A currently active cell database is SHOGoiN, which says it is a significant extension of the world-first human cell database, CELLPEDIA.  It focuses on human cells but also has information on mouse, sea urchin, and C. elegans.
The site says:

The database consists of several modules that store cell lineage maps, transcriptome, methylome, cell conversions, cell type markers, and cell images with morphology data curated from public as well as contracted resources, based on sophisticated cell taxonomy.

Wondering if you know of anything similar for plants/bacteria/single-celled organisms.


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Extract protein sequences from a GBK(GenBank) file without scripting
How to extract protein sequences from a GBK(GenBank) file without scripting?
I know that writting a script using BioPerl or Biopython can do this, but it is not elegant and daunting to beginners and biology persons. Any thing like
$ SOME_PKG_MANAGER install PKG
$ CMD ab.1234.gbk > ab.1234.faa

Coding is definitely elegant but not un-daunting perhaps ;)

I'm not sure what you mean by "it is not elegant". If scrolling through the file and copying and pasting sequences out is your version of elegant I'm not sure what the question is... Scripting languages like perl and python were made exactly for this situation. But I can't see the biological question here so I'm going to flag as off topic.

Yeah I agree with Good Gravy. This is like asking "I want to do cell culture but I don't want to go through the process of changing media. Is there a robot that can do this for me?"

@WYSIWYG If there is, you cannot afford not knowing that. This is the value of my question.

@FrozenFlame Extracting sequences is not very difficult. Usually most people write their own scripts to do that. Packages are generally made to deal with more complex data extractions and computations. What you want to do can be done using a one liner code.

@WYSIWYG I know that extracting sequences is not a difficult task. But why waste time writing the same script again. If you can do it in one line, show me your code; that's what I want.

@FrozenFlame That is off-topic in biology. See the meta-post that Good Gravy mentioned.

@FrozenFlame I posted my answer previously (in Perl) and it would be trivial to convert it into a one-liner, but everyone jumped all over it in the comments because they thought you did NOT want some code, and because I provided no instructions. Then Chris, a moderator deleted my answer. I guess you didn't see it in time. Oh right, as WYSIWYG mentions you cannot post answers that your so-called "peers" here have determined to be off-topic. Because being on-topic is so much more important than actually helping someone.

My colleagues and I have recently published a toolbox of command-line utilities that are modeled after GNU Textutils (e.g. grep, cut, tr, uniq) called FAST: Fast Analysis of Sequences  (cite).
To install FAST you can use:
perl -MCPAN -e 'install FAST'

Or install the current development version from github. The FAST install comes with a cookbook, sample dataset and all utilities have man pages. The cookbook is also available on the github wiki.
To convert the features annotated in a genbank file to fastA sequences you can use gbfcut. Below are examples of using gbfcut:
To convert all annotated features of a genbank file to fastA format:
gbfcut genbank-file

Output only tRNA features:
gbfcut -k tRNA genbank-file

Output all feature sequences with a "note" qualifier containing "telomere":
gbfcut -q note=telomere genebank-file


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What do the intervals between groups of arrays in microarray gene expression data images mean?
This can be a dummy question, but I am not familiar with microarray experiments at all. In this image, what does each of 16 big squares mean, and what are the black intervals between them are? I know each small square corresponds to a gene expression value, but I don't know what each separated group of expression values means. Oftentimes I see those separated expression values in microarray dataset images. I would be happy if someone can explain. Thanks!

The borders provide visual cues for the image analysis software to know which spot is which. The spots are also not printed all at once, but by a series of print heads, and the spaces allow for a small amount of error in the alignment of the print heads. It also allows for humans to more easily eyeball the results - the chip map can be printed in groups, and if you're looking to see what gene X did in your experiment, and know it's in the 2nd row, in the 2nd block, row 8, column 4, you can find it more easily than just knowing it's in row 73, column 27.


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Is there a taxonomy of species with emergence and extinction dates?
I know the NCBI has a list of each species and their place in the evolutionary tree. But do they have the dates that these species existed? Does any such database (partial or complete) exist anywhere?
For example, Adelobasileus on Wikipedia says "about 225mya", so that would be one example date. Obviously they aren't super exact, but it would be cool if this has already been collected somewhere.

for the vast majority of species those will just be question marks.


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Deletion errors with Phusion Polymerase?
I was wondering if anyone has ever seen large deletions (~40-50 bp) occur when using phusion polymerase to clone a gene.  I have recently tried using Circular Polymerase Extension cloning to clone a 200 bp insert into a 6.5kb plasmid and obtained two separate clones with 40bp+ deletions in the center of the insert.
Phusion has a 5'->3' exonuclease activity, but I didn't think it could cut in the center of a sequence.  While our inserts were created with oligo synthesis, it is my understanding that such large deletions are rare with oligo synthesis. If you have heard of this happening please let me know.

I don't think that it would be an exonuclease issue. Rather it may be an issue with hairpin formation during amplification. Are you sure you have the complete 200 bp insert?

In my own personal lab experience, I got some unexpected results using Phusion polymerase. However, I have not seen deletions, only insertions (ranging from single bases to 3 tandem copies of a primer sequence). This is not an answer to your deletion question, but it does suggest unusual things might happen.
I have seen deletions with T4 DNA polymerase during "blunting" reactions. According to the NEB website:
Q10: Is T4 DNA Polymerase active at room temperature?
A10: We suggest 12°C. The DNA ends "breathe" at higher temperatures allowing the exonuclease to remove nucleotides past blunt.


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Why do three nucleotides code for one amino acid? Why not 5 nucleotides?
We all know why there are 3-base codons, and why there aren't any 2-base codons. But why is there not a 4-base a 5-base codon?

http://biology.stackexchange.com/questions/6933/why-are-3-nucleotides-used-as-codons-for-amino-acid-mapping-in-dna

The more bases there are per codon the more information you can code for. There are only 22 different amino acids, in consequence we need minimum 3 bases per codon.

1 base-codon --> 4^1 = 4 possible codes which are:

A / T / C / G

2 base-codon --> 4^2 = 16 possible codes which are:

AA / AT / AC / AG / TT / TA / TC / TG / CC / CA / CG / CT / GG / GC / GT / GA

3 base-codon --> 4^3 = 64 possible codes which are:

AAA / AAT / AAC / AAG / ACA / ACT / ACG / ACC / AGA / AGT / etc...

4 base-codon --> 4^4 = 256 possible codes which are:

AAAA / AAAT / AAAC / AAAG / AATA / AATC / AATG / etc..

5 base codon --> 4^5 = 1024 possible codes

If we had only 2 bases per codon we couldn't code for all of the possible different amino-acids.
On the other hand there are several costs associated with carrying lots of DNA. It takes space, it takes energy and matter to get copied, it takes time to copy it (generation time might be limited by copying time), … I have just asked this question hoping to make things clear about the possible costs. If there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. Such trait (that has a cost with no benefit) are not expected to evolve (counter-selected).
You'll notice that there are 64-22=42 extra possibilities. In consequence the genetic code is redundant. Meaning that several codon codes for the exact same amino-acid. And interestingly, it is often a the last of the three bases of the codon the does no yield to any change in the coding sequence as you can see here.

This post about the evolution of genetic code might interest you.

You really helped me, thank you. But could you please clarify your statement: "that would sounds stupid to have 5-base codon if there is no gain."?

@user6318 I already changed this sentence! I meant that there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. In consequence, such trait are not expected to evolve. Hope that makes sense to you.

Warning for the uninitiated - that table is not the 'standard code' , it is the mitochondrial code (AUA is Ile in the standard code).

@AlanBoyd Whoops! Thanks a lot. I changed it, it is the "standard code" now.

I'm always bemused by arguments based upon the metabolic cost of maintaining DNA. I estimate that for E. coli less than 0.06% of ATP is used in replicating DNA, so for a 4 base codon system this would rise but would still be well below 0.1 %. This doesn't strike me as the basis of a strong selective pressure.

What about physiological issues? Space taking up by DNA and the machinery having to deal with these big sequences in bacteria? And what about timing issue? I've heard (but have no reference, I should make sure of this claim) that in some species the generation time is limited by the DNA copying time

@AlanBoyd I have just posted this question hoping to make things clear. +1 on your comment ;)

@Remi.b great! let's see what answers you get. In E coli it takes 40 min to replicate the genome, but they can grow with a doubling time < 20 min by reinitiating before the previous round of replication has ended. I was once told that the limit to growth is the exponential increase needed in ribosome number as more and more ribosomes are tied up just making ribosomes.