text:
How can DNA profiling be used to determine the number of organisms from a specific species that is within a certain area?
Here is the tedious exam question that asks this: question 8(b).
https://drive.google.com/drive/folders/0B23NLD5L6099VWJya3dfLVJpbmc
The question states:

In 2007, the brown bear was a threatened species in Alberta, Canada. A study was carried out to determine the number of bears in the area. Fur wascollected from trees that the bears had rubbed against and their DNA analysed.
(i) Explain how DNA analysis would help the scientists to determine the number of bears in the area.

The answer simply states:

idea of comparing bands

idea that each bear has unique {DNA / banding patterns}

idea that the number of different banding patterns would equate to the number of different bears

My question is: How does the entire process fit into together?
I am absolutely baffled as to how the entire investigation would fit into each other, and I've been trying to articulate it for hours. It seems like if I'm just going to be collecting fur samples off trees there are going to be cells belonging to different species, then the DNA pattern produced will include a different number of bands from all of the different species. To overcome this problem, I think 'would we somehow separate the different cells into different groups with each group belonging to a specific bear by some technique that isn't DNA profiling and I don't need to know about at high school level? I then reason that we would have accomplished our task of identifying the number of different number of bears present within the sample. How would one identify the different numbers of bears?
The second part of my question is that I don't understand how the different samples from trees and fur will be used in order to estimate the overall population size within the area? The only animal sampling technique that I know of is that capture-recapture method.

Please just write the question here.

Is it okay now?

The general process of DNA profiling (I prefer calling it "DNA fingerprinting", but that's just me) generally involves developing PCR primers specific for a particular region surrounding some sort of highly polymorphic region. So in this case one would need primers surrounding VNTRs (or other polymorphic regions, have a look at the wikipedia article for an overview of some other methods). Presuming the PCR primers are specific for bears (one could blast them to get an idea of this), then regardless of what other animals were mixed in, the resulting bands would predominantly be from bears (after all, PCR results in an exponential amplification of favored species). This would be answer part (1).
For part 2, one needs to find a sufficient number of sufficiently variable regions for profiling to work. A single site might not be informative enough, but a couple of them together will be.
Part 3 is the logical outcome of parts 1 and 2. If you can amplify a bunch of mixed samples together and the repeats are of variable length (thus the use of VNTRs or similar repeats), then you'll see those as different sized bands on a gel.


text:
Why does the gc content deviate from 50% in prokaryotes
I have read quite some articles but I can't figure out the main reason for gc content deviation in prokaryotes. In eukaryotes I can understand it, because the genome isn't composed at random, like TATA boxes and CpG island, because they are important for functioning in the production of proteins.
However in prokaryotes there is such a variety, GC% is ranging from 20% up to 70%. Most of the time it depends on the environment, high temperature needs a stable genome (= high gc content).
I also read the answer to this question How does GC-content evolve? however it's still not clear to me. I hope someone can explain the deviation a little bit more.
Question
Prokaryotes have an AT drift, but what mechanism causes some of these bacteria to higher their GC% instead of lowering it.

Possible duplicate of How does GC-content evolve?

I have already read How does GC-content evolve, I even mentioned in mine question @Forest

Sorry, I should have seen that, @Rick Beelo!

I wonder whether it is just some sort of functionless drift. I don't know about bacteria, but think the example of some human viruses may be instructive. The human herpes simplex 1 virus (causes cold sores) has a very high GC content, whereas the quite closely related (in terms of gene repertoire and organization) human varicella zoster virus (causes shingles) has a bias towards AT. Now these viruses depend completely on the host cell's translational machinery, which will be similar (e.g. distribution of tRNA species) in the cells these two viruses infect (as will temperature, ionic strength etc.) (The viruses encode their own DNA replication enzymes but not the systems for transcription or translation.)
So if there is a functional reason for the differences in these alpha-herpes viruses, it is difficult to discern, and one might assume that the situation in bacteria might well be similar.
Clearly, there must be mechanisms for the accentuation in a GC bias once established. One imagines there could be a selective advantage in either replication, transcription or translation, but molecular explanations do not jump to mind (at least not to mine).

Interesting point about viral GC content, I never thought of that. As to bacteria, I could imagine a scenario, in which random drift affects DNA stability or replication/transcription efficiency, leading to a sub-population that's now better suited to some environment and in turn leading to speciation. Between genetic drift & selection pressure, though, we can paint a nice picture of evolution in general. =P

There may be other factors involved with viruses of course. Perhaps what's important there is for the DNA to be different from the host for some reason.

If we are talking about viruses, most of the time there is an bias towards A/T on the third position of the codon right? So the virus can adapt it's self to the tRNA pool of the host to speed up production of new virusses. @Forest

I don't know about the overall picture. Just those wretched herpesviruses which were such a pain to sequence. I think you need to be careful drawing conclusions as to why. Or at least recognize that a rationalization may seem plausible but have no experimental evidence to support it. And these herpesviruses show that tRNA availability need not be limiting.

@RickBeeloo - I didn't know about the codon usage bias, so thanks for the TIL. Perhaps there's an evolved mechanism for codon usage bias in bacteria that affects GC content in different species. I found this paper (http://www.ncbi.nlm.nih.gov/pubmed/14659556) on the topic, which I won't have time to really read for a day or so. Might have some useful insights, though.

Interesting question. I think that bacterial GC content diversity boils down to a mix of mutational biases, such as using different polymerase and replication/repair gene isoforms, and environmental pressures, such as temperature and salinity, that have placed different selection pressures on the various microbes.
I would read over the linked papers for more detailed info, but at least in broad strokes, I think that the two mechanisms listed above account for most of the observed variance.
NB: This isn't my main field, so you might get a more detailed answer if an actual microbiologist weighs in. :-)

You're welcome! Don't forget to vote up helpful answers. :-)

Hahahha I'm new here :) @Forest

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text:
why does the score matrix influence the E value (BLAST)
When I align two HBB protein sequences wich have 80% identity, I used two kind of score matrices: Blosum62 and PAM30, to figure out the impact on my results.
I noticed that the bit score is higher when I used PAM30 instead of BLOSUM62, which makes sense because PAM30 is based on more closely related species.
However I don't understand why the E-values differs from each other:

PAMP62: Bit score: 251, E value: 8 * 10^91
PAM30: Bit score: 258, E value: 6*10^82

Question: I don't understand why the E-value changes when using an other scoring matrix?
thankyou,

Perhaps this BLAST tutorial by Steve Altschul will be helpful:  The Statistics of Sequence Similarity Scores
There is also the BLAST book by Mark Yandell and Ian Korf.

The Altschul article is definitely what you should look at as it's on the BLAST website. There is one relevant section entitled: "The choice of substitution scores" and another entitled "The PAM and BLOSUM amino acid substitution matrices". Have fun digesting them!

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text:
What is the difference between tissue engineering and 3D bioprinting?
3D bioprinting is the modified version of the tissue engineering but when we want to describe the both terms, what are the basic criteria or points to make difference between these?

Tissue engineering is research into ways of organizing cells and cell droplet/matrix structures into a useful form, usually for medical applications. In the near future, tissue engineering could refer to rewriting or genetically modifying cells for a new purpose or to enhance their existing function. Even more into the future and tissue engineering could mean custom-building multi-cell structures from scratch on a computer.
3D bioprinting is the practical or laboratory deployment of the first technology mentioned above - a subset of tissue engineering.
In a nutshell:
Tissue engineering = "Come up with a creative way to arrange these cells and cell structures into something useful".
3D bioprinting = "Use the above-mentioned technology to build part of a synthetic organ".


text:
Can polystyrene sulfonate bind calcium or sodium in the gut? How?
Polystyrene sulfonate is used as a potassium binder to treat hyperkalemia in traumatic rhabdomyolysis, acute and chronic kidney disease. It is listed as an ion-exchange resin that can also remove sodium or calcium from solution, but is also available in sodium salt or calcium salt form. How might this work?

Are you talking about Sodium Polystyrene Sulphonate (a.k.a SPS)?
If yes, then ...
Quoting from Chaitman, Dixit and Bridgeman (2016)

Synthetic cation-exchange resins are insoluble polymers resembling a crystalline lattice. When placed in a solvent, this structure swells, allowing the exchange of ions between the reactive group on the resin (in the case of SPS, sodium) and ions dissolved in the solvent.

However, other cations like sodium and calcium ions can bind too.
As SPS moves through the intestine, sodium ions are released and exchanged for potassium ions.

References
Chaitman M, Dixit D, Bridgeman MB. Potassium-Binding Agents for the Clinical Management of Hyperkalemia. Pharmacy and Therapeutics. 2016;41(1):43-50.

Welcome to Biology SE! Please clearly attribute the sources you used if you are quoting from somewhere else. Your sentence starting "Synthetic cation exchange...in the solvent" appears to be taken verbatim from https://www.ptcommunity.com/journal/article/full/2016/1/43/potassium-binding-agents-clinical-management-hyperkalemia.

I am really sorry! I am pretty new to this!
Well it is from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699486/


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How does a decrease in free Ca2+ result in nerve/muscle overexcitability?
I have in my notes that a decrease in free Ca2+ increases membrane permeability to Na+ so that it is brought closer to threshold, but no further details. So how does this work?

The thing is that the Voltage Gated Channels,they are closed in resting state because Ca2+ is bound to it.So,in the resting stage,Ca2+ somewhat blocks the Na+ - K+ channel.But since there is low Ca2+ so there won't be much Ca2+ for guarding of channels and so it will lead to an increase in permeability.See the photo and imagine the gate being guarded by a Ca2+.I hope this helps.

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text:
Question about Racemic Mixtures in Miller-Urey Experiment
I'm studying the Miller-Urey Experiment for my Biology class, and a significant point made by my professor was that Miller made a 50/50 racemic mixture of chiral monomers.
However, life is homochiral.
I'm trying to draw some significance out of Miller and Urey's experiment. Could life have started in multiple various places (because all you need for life to start is some organic molecules), so you could have developed various chiral forms of polymers (like amino acids), but one chiral form dominated and thus natural selection favoured that one form?
Thank you!


text:
How come our thyroid glands don't suffer awful mutations (or do they)?
I was listening to a lecture by my Biology professor and he said that the thyroid gland contains radioactive Iodine which can break down and create reactive Oxygen species (because ionizing radiation from the Iodine interacts with water in the human body).
So, shouldn't the thyroid gland suffer awful double-stranded chromosomal breaks constantly? Shouldn't we be suffering mutations in the thyroid gland all the time?
Thanks!!!

Radioactive does not mean much in and of itself, your bones are radioactive (potassium), just being radioactive is not enough to do any damage.  It needs to be the right type of radiation and have high enough intensity before it can start damaging DNA and thus cause cancer. Second the amount of iodine in the body is miniscule, the aforementioned radioactive potassium in your body is orders of magnitude larger (if there is any radioactive iodine present at all which is unlikely).
On top of this remember we are surrounded by low dose radiation all the time so our bodies have evolved ways to handle minor damage.http://imgs.xkcd.com/blag/radiation.png

The thyroid gland contains iodine, but is usually not radioactive. In the contaminated area, it can adsorb radioactive iodine, which would lead to a health danger. In such circumstances, pills with non-radioactive iodine are prescribed as a preventive measure.


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How does sexual reproduction generate more genetic variation?
I'm curious as to why sexual reproduction generates genetic variation. For me, the term genetic variation is a little ambiguous. The way I understand it, it's the number of alleles at a locus in a population or "group" of organisms.
But sexual reproduction only "reshuffles" alleles, and doesn't generate new ones (most of the time, at least). So why does it create genetic variation?
Thank you for reading.

Short answer it doesn't. Sexual reproduction generates new combinations of traits and increases the difference between individuals in the same populations.
New combinations means beneficial traits have a better chance of finding complimentary traits while the opposite are also true detrimental traits have a greater chance to find combinations that make them worse. It increases variance in the sense that individual genes can disperse easier in the population, and genes can form more unique combinations, but not in the sense of actually increasing the overall variability.
Likewise it also keeps individuals from being identical which makes a population more vulnerable to parasites and disease.

There are two questions here. 1) What is genetic variance? It is actually clearly defined. 2) How does sexual reproduction generate more genetic variation?

What is genetic variance?

Assuming bi-allelic loci, just assign a value of 0 to one allele and 1 to the other allele. Then compute the variance! Average this value over all loci. Done! Have a look at any intro book in quantitative genetic for more info (see here)

How does sexual reproduction generate more genetic variation?

You are right "sexual reproduction only "reshuffles" alleles, and doesn't generate new ones". It is a common misconception that sexual reproduction generate genetic variation. The details of whether it does or it does not depends upon the detailed distribution of dominance coefficient and distribution of epistatic effects.
There has been a lot of work on the subject and it is not an easy work to summarize it. Sally Otto does a great job to summarize this misconception in her speech On the Evolution of Sex and the Advantages of Recombination. You should definitely have a look at it.
Note however, in some species that preforms both asexual and sexual selection, it happens that sexual selection is coupled with higher mutation rate than asexual selection. In such cases, sexual selection does indeed increase genetic variance but only so because of tis correlated effect on mutation rate.

Having read over, I think in "common misconception that sexual reproduction generate genetic variation"  you seem to use two different terms "variation" and "genetic variation". So there is a definition of "allelic variation" that differs from "genetic variation"?

From your question: "... only "reshuffles" alleles, and doesn't generate new ones (...). So why does it create genetic variation?"
There are no trick questions, still my answer goes:
Because genetic variation is also created by independent assortment.
There are two ways of crossing-over in meiosis.
First, there is Chromosomal crossover, or crossing over, which "is the exchange of genetic material during sexual reproduction between two homologous chromosomes' non-sister chromatids that results in recombinant chromosomes." (Wikipedia)
Second, however, there is, much lesser known  Independent assortment of chromosomes:
"The physical basis of the independent assortment of chromosomes is the random orientation of each bivalent chromosome along the metaphase plate with respect to the other bivalent chromosomes. Along with crossing over, independent assortment increases genetic diversity by producing novel genetic combinations."
Without alleles being changed (if exchanged, as a result), chromosomes from on parent are exchanged with (homologous) chromosomes of the other parent. This, too, results in genetic variation, and - as such does not involve so called crossing over of allelic genes. Exchange of alleles as a result of independent assortment must be distinguished from creating new alleles by crossing over,i.e. exchanging genes or parts of genes.
Independent assortment can be differentiated from "allelic variation". Hermaphrodite reproduction as sexual reproduction shows that in one single individual there are a million combinations of alleles. By definition, however, not all alleles existent in a population. Interestingly, this rule is not valid in respect of the rather unknown mechanism of mingling of chromosomes (not alleles). Any indivual has got the potential to find any - among all - combination of chromosomes.
From this finding results that intercourse of different individuals in contrast to hermaphrodite interchanging of chromosomes and alleles can be distinguished by potenitally combining all alleles, whereas all chromosomes can - potentially - combined by one hermaphrodite individual.
Surprising about this answer is that, in the words of your question, "new genetic variation" that is not considered allelic variation as it does not involve the changing of genes is thus produced by sexual reproduction.

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text:
What is the difference between neurotransmitters acting as neurotransmitters and hormones?
My main confusion is what differentiates the action of a transmitter substance as a neurotransmitter and as a hormone. For example, when norepinephrine is being talked about as transmitter substance that modulates brain responsiveness and information processing, it's a neurotransmitter. But when norepinephrine is involved in the functions of the autonomic nervous system (ANS), does it work as a hormone or a neurotransmitter?
Quoting from Physiology of Behavior, by N. Carlson, 2013 edition:

"Neurons in the central nervous system contain a1- and a2-adrenergic
  receptors and b1- and b2-adrenergic receptors. All four kinds of
  receptors are also found in various organs of the body besides the
  brain and are responsible for the effects of epinephrine and
  norepinephrine when they act as hormones outside the central nervous
  system."

So does that mean that whenever norepinephrine works outside the CNS, it works as a hormone?

Right.  It's nomenclature to differentiate actions and release in the CNS (neuronal) versus outside (endocrine in this case). A neurotransmitter will act locally to it's release site typically from a neuronal synapse, while hormones tend to be released into the bloodstream and can act much further away as well as at a different time scale.
Source from textbook: Principles of Neural Science (Fourth Edition), Kandel et al. 2000, McGraw-Hill Medical ISBN 10: 0071120009


text:
Why do cells in the cerebral cortex act as interacting nonlinear oscillators?
I'm not a biologist, but I'd like to know something about EEG analysis.
In particular, I have read that EEG signal derive from cells in the cerebral cortex and hippocampus. And that these cells act as many interacting nonlinear oscillators.
I'd like to understand why they are oscillators and why their behaviour is nonlinear. Many thanks for the help!

This link could probably give you your answer. Sorry that i'm too tired to read and vulgarise it at this time :)


text:
How to build a phylogenetic tree without an outgroup?
I have whole genome aligned sequences of four beetle populations of same species. I wish to construct a phylogenetic tree with the four. However, I am unable to find a suitable outgroup of the species, so I cannot use an outgroup to root the tree. Is there a particular method that one can use to construct a tree without an outgroup? I found that the MEGA software does this well. What is the theory and understanding of constructing a tree without an outgroup? what are the implications of constructing a tree without an outgroup? Ar the distances between trees measured relative to one another?

Isn't a phylogenetic tree without an outgroup just an unrooted tree?

Related.

Most classic phylogeny reconstruction algorithms root the tree a posteriori, based on the outgroup chosen by the user. The tree is actually inferred and internally represented without root.
Therefore, if you use a program that asks you an outgroup, it is likely that you can just choose an arbitrary one and later "de-root" the obtained tree.


text:
What is the relationship between the e value reported by HMMER and BLAST? (Are they equivalent?)
Both HMMER and BLAST report an e value for alignments.  Is it calculated in the same way and - assuming that default settings are used - can they be compared directly (are the equivalent)?  If not equivalent, what settings can be changed to make them equivalent?

can  you add some background information so that others less familiar with the question can at least partially follow what is being asked?

They use very different algorithms so they should not have the same E-value. BLAST uses a position-independent substitution matrix (e.g. BLOSUM) while HMMER uses a position-dependent substitution matrix that is different for every profile. Check out the "Background and Brief History" section in the HMMER's user guide. It explains the conceptual differences at a very broad level.
Therefore, I don't think there's any way to make them equivalent.

E-value, in short, is a statistical measure of how likely it is that your sequence of interest could have arisen by pure chance. This definition is 'discipline-wide', so should be adhered to by any bioinformatics software that elects to provide it.
Thus, the longer and more complex your sequence is, the better (lower) E-value it will have when conducting sequence alignments.
As far as I am aware, they should be directly comparable. I don't see why they also wouldn't be calculated in exactly the same way.
HMMERs website does state that it utilises 2 different kinds of E-Value however:

The are then two E-values for the domain:
Conditional E-value - This is the E-value that the inclusion and
reporting significant thresholds that are measured against (if defined
as E-values). The conditional E-value is an attempt to measure the
statistical significance of each domain, given that it has already
been decided that the target sequence is a true homolog. It is the
expected number of additional domains or hits that would be found with
a domain/hit score this big in the set of sequences reported in the
top hits list, if those sequences consisted only of random
nonhomologous sequence outside the region that sufficed to define them
as homologs.
Independent E-value - This is the significance of the
sequence in the whole database search, if this were the only
domain/hit that had been identified. If this E-value is not good, but
the full sequence E-value is good, this is a potential red flag. Weak
hits, none of which are good enough on their own, are summing up to
lift the sequence up to a high score.

The calculation for E-Value via BLAST can be found here:
https://www.ncbi.nlm.nih.gov/BLAST/tutorial/Altschul-1.html


text:
What type of immersion oil should I buy?
I have an old Nikon Alphaphot microscope that came with a 100x oil immersion objective, but no manual. I've seen plenty of sources that explain that you need to place a drop of oil between the slide and objective, but when I went to order immersion oil I discovered that there are several different types. There's Type A, Type B (apparently similar to Type A but more viscous), and a number of specialty types. My plan is to use the microscope for projects like looking at blood cells, pond water, and other high school science project-type investigations?
Which type of immersion oil is right for all around, general purpose use?

For the best image (where you lose the fewest photons and get less refraction), you want the immersion oil to have a refractive index as close to the refractive index of the coverslip you intend to use.  In my experience, this is not much of a consideration on the oil-side, but rather on the coverslip-side.
There is little difference between type A and B oil, although for other types of oil see here.  If I were you, I would just use some type A.
For a lesson on the impact of immersion oil on optics, see this Zeiss website (similar sites for Nikon and other scope manufacturers exist too I'm sure!)


text:
where i can download reference MSU7 rice genome?
I am working with RNA Seq data analysis. I have to download MSU7 rice genome. somehow i downloaded from
"http://rice.plantbiology.msu.edu/pub/data/Eukaryotic_Projects/o_sativa/annotation_dbs/pseudomolecules/version_7.0/all.dir/ "
. But i am not able to find Annotation (.gtf) file and reference genome (.fa) file . so how can i find and how can i download..help me

You can find this on the phytozome website. You will have to make a free JGI account to access it


text:
what is the princlple of using DMS (Dimethylsulphate) for structural analysis of rRNA?
I want to check the secondary structure of rRNA (PTC) in a particular position by using DMS footprinting. I have deleted the modified nucleotide (m5c) which is present in the PTC and it helps in the ribosomal structural stability. I am interested to know after the deletion of the modified nucleotide.
I am using DMS treated RNA with primer extension. I don't understand the basic principle of DMS reacting on RNA. can you please explain me.
I used this article for reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701642/

Here is a good explanation of the theory and chemistry behind DMS footprinting, from chapter 11 of Probing RNA structure within living cells :

In vivo chemical probing assay using dimethyl sulfate (DMS). (A) DMS methylates the N1 atom of adenosines and the N3 atom of cytosines. Both of these positions are located on the Watson–Crick face of the respective nucleotides. (B) Scheme of a structured RNA interacting with a protein ligand to exemplify residues accessible to DMS modification. (C) Mapping the modified positions by reverse transcription. The enzyme terminates the extension due to steric hindrance by the bulky methyl group at the Watson–Crick face of A and Cs. (D) The pool of cDNAs is separated on a standard denaturing gel. A and C denote the sequencing lanes, which are essential to map the modified positions. In addition, an RT control, which is prepared from RNA extracted from untreated cells, is essential to determine any natural stops of the RT (lane -). Comparison of the RT control lane with the cDNA pool created from DMS-modified RNA (lane +) reveals sites of modification. Note that the band resulting from a DMS modification migrates one nucleotide faster than the corresponding band in the sequencing lane, because the ddNTP is incorporated into the nascent cDNA, while the methyl group results in a stop one residue prior to the modification.

My take -- DMS adds a methyl group at the hydrogen-bonding face of exposed A and C bases. As and Cs protected by either proteins or base-pairing interactions are not methylated.  Methylated bases inhibit reverse transcriptase, resulting in a truncated DNA product that can be visualized on a gel.  Comparison to an untreated control allows for inference of which As and Cs of the RNA sequence are exposed and which are protected, from which the native RNA conformation can be inferred (or the possibilities greatly constrained).

Yeah..you are right but if you check in the literature apart from A and C other nucleotides also modified. It gives information about solvent exposure and
unusual chemical environment. These two factors enhance the methylation. http://ribonode.ucsc.edu/Pubs/Wells_etal00.pdf                                                                  https://www.nature.com/articles/s41598-018-30383-z


text:
How to do desalt reaction by passage through a Micro Bio-spin 6 column?
I want to perform the bisulfite sequencing on rRNA to detect the 5-mC. I followed this protocol
•    DNA-free™ DNA Removal Kit (Invitrogen)
•    Purified RNA, Treat RNA according to manufacturer's instructions.

Adjust DNAse-treated RNA to a volume of 10 μl.

2.Sodium Bisulfite Treatment of RNA EpiTect Kit (Qiagen)
•   DNAse-treated RNA preparation
•   PCR thermal cycler
•   Micro Bio-spin 6 columns (BioRad)
•   GlycoBlue coprecipitant (LifeTechnologies)
•   Cooled microcentrifuge
3.Transfer DNAseI-treated RNA solution into a PCR tube.

Add 42.5 μl freshly made bisulfite solution (EpiTect kit) and mix thoroughly by pipetting.
Add 17.5 μl DNA stabilization solution (EpiTect kit) and mix thoroughly by pipetting.
Place samples in a thermal cycler and run the following program to deaminate RNAs:

•   70 °C: 5 min
•   60 °C: 60 min
•   Repeat steps (i) and (ii) two to six times (depending on target RNA abundance and predicted secondary structures)
•   25 °C—hold
7.Desalt reaction by passage through a Micro Bio-spin 6 column according to manufacturer's instructions.

Add 1 volume (70 μl) of 1 M Tris–HCl (pH 9.0) and incubate at 37 °C—30 min for desulfonation.

9.Precipitate RNA by adding sodium acetate (pH 5.2) to 0.3 M, 15 μg GlycoBlue coprecipitant and 3 volumes of 100% ethanol and incubate at − 80 °C for ≥ 1 h.
10.Pellet RNA by centrifugation at 4 °C for ≥ 30 min at top speed.
11.Wash RNA pellet with 75% ethanol.
12.Air-dry ≤ 5 min at room temperature.

Store deaminated RNA pellet until further use at − 80 °C.

In the step-7 I got stuck. i do not know whether do I have to use flowthrough or do i have to elute from the column.
Ref. https://www.sciencedirect.com/science/article/pii/S0076687915002335?via%3Dihub

Did you read the manufacturer’s instructions?

yeah, but it is confusing for me. The Manufacture's link...http://www.bio-rad.com/featured/en/desalting-column.html

That link does explain the basis of separation, and tells you the relative order of elution. You can take a look at the manual for more explicit directions.

Since it's a desalting column, without reading the instruction manual you could guess that the column will bind the RNA while you wash it with a new buffer. You will want what you elute at the end (RNA in elution buffer). The flowthrough will be the small salt molecules that wont bind to the column.

That’s not how a desalting column works...

@canadianer perhaps you should answer the question or if you think it is trivial (or needed more effort from the user, which is what I feel), you can VTC.

Maybe you can take a look at this. I found it through google when searching for the manual as well.
http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006051.pdf


text:
When is a person declared to be dead?
From what I can tell, it is not well defined, but at least in the US it has to do with cessation of cardiopulmonary functionality. Any reliable sources that give a definition of when a human being is considered to be no longer living?

Really a legal question...

That's not true at all. Legality is different from country to country and some countries make laws based on biology or rejection thereof (ie abortion, transgenderism, etc.) The legality of it can be easily looked up (in the US it is the cessation of pulmonary and cardiac activity) but biologically (and philosophically) what do we consider as "alive?" Something that breathes? Something that has circulation? Metabolism? When you define what constitutes "alive", it is easy to define the opposite (e.g. a heartbeat means you are alive, therefore no heartbeat means you are dead).

OK, then it becomes a philosophical question :-)  Because you can be "dead" in humanly-meaningful terms (that is, no brain function but have bodily functions kept going by life support) but be legally alive.  Or if you die and your organs are harvested & transplanted, parts of you are still "alive".

I have also asked the question on the philosophy SE so I am not sure what you are getting at... We have real world, medical/biological/scientific problems to deal with such as abortion, life support, IVF, etc. that all deal with the concept of when the scientific community declares life has started or ended. It is an incredibly relevant question medically, biologically, scientifically, and philosophically. What exactly is your point in trying to argue that?

My point is that the "scientific community" has declared no such thing.  It doesn't really have a hard definition of life: are viruses alive, or prions?  Or are they just complicated chemical reactions?  With the issues you mention, it's not even a matter of defining life, but of the more complex question of personhood: that is, a fetus (or indeed, a sperm cell) is clearly "alive", but is it a person?  Or at the other end, a brain-dead body on life support, or someone who's lost all cognitive capacity?  Likewise transplanted organs, cultured cells...

Although there exist some differing opinions mostly to do with brain function, the best answer is definitely the heartbeat. Here's why:
In some ways the human body really does operate like a machine. The process of delivering oxygenated blood is THE foremost example of a time-critical activity that must occur constantly in order to maintain life. That process stops when either breathing or pumping of the heart ceases, and since the circulation of the blood is more immediately critical than breathing it makes sense to place more weight on that criterion.
Some medical conditions can lead to a person being essentially "Brain-dead" before they are biologically dead, but these situations are almost always extreme outliers to the general discussion of alive vs dead. Furthermore, the arguments surrounding that state too often and too easily cross over into philosophical/metaphysical commentary.
The only serious wrinkle to the argument above is hypothermia. This wrinkle is encapsulated quite nicely in the old medics' axiom "You're not dead until you're warm and dead." And it is well documented that hypothermic patients can sometimes be revived after long periods of time - in excess of a half hour - using special techniques and equipment (to prevent frostbite).
Bottom line: Has the subject's heart been pumping any blood (including during CPR chest compressions) in the last 10 minutes? Is the subject hypothermic with a core temperature below 95 degrees Fahrenheit? Answers of "No." and "No." mean that the subject is no longer living.

I do quite like your answer, but do you have any comments to make about a person being "brain dead" on life-support? I'm more familiar with debates about whether a person is "dead" or not when being kept on life support indefinitely.

After heavy research, I have determined that metabolism is what denotes something as alive. Obviously it is open to debate and many will disagree, but the ability to turn exterior means into nutrition (i.e. food for humans, light for plants, etc.) seems to be the core characteristic of what we consider "life"

But with modern medicine, it's possible to remove a heart and keep the person alive for hours (or even longer with artificial hearts) while a replacement is inserted.

In the United States there is the Uniform Determination of Death Act (UDDA) which defines death as either:
1.Irreversible cessation of circulatory and respiratory functions; or
2.Irreversible cessation of all functions of the entire brain, including the brain stem.
This purpose of this Act, which dates back to 1981, was to more closely align the legal and clinical definitions of death and to have a broader nationwide standard.  This act was approved by leading medical and bar associations.
source: http://healthcare.findlaw.com/patient-rights/what-is-the-uniform-declaration-of-death-act-or-udda.html


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Why is my DNA below the ladder?
I have run a gradient PCR.. and band 6 after the ladder is clearly the brightest. But all bands appear below the ladder. What does that mean? It is extracted mDNA that was loaded.
Thank you in advance!

Below the ladder means primer dimer.  You have no product.

Thank you! That explains it. I will try deciding primer amounts and hope for the best!

In my experience, altering primer concentration won't do anything.  I'd rethink the annealing temp, maybe try a more robust Taq, double-check the quality of your input DNA, and double-check that you have the right primers, and that they actually should make a product.


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what kind of bonds join the okazaki fragments
During DNA replication, the synthesized okazaki fragments adjacent to each other are joined up directly by DNA ligase-catalyzed phosphodiester bond formation. Can someone point out to me which part of this statement says it's false? All I know is that the fragments are joined together by DNA ligase, which can only mean the part about the phosphodiester bond is wrong, but arent the 2 nucleotides joined by a phosphodiester aka nucleotide bond?

This seems to be a garbled version of a trick MCQ which is of no interest to anyone. Rather than vote for the half answer, vote to close it.

I'm pretty sure the "phosphodiester bond" part is correct.
The only thing I can think of that might be questionable is the word "directly". If directly = immediately, then the sentence could be termed false, because they aren't joined immediately.
Even then, it seems like that's just grasping at straws, so I wouldn't worry too much about it. It sounds like you understand the concept, which is what matters.

The best guess I could make is "directly". Okazaki fragments also contain RNA primers, which need to be replaced by DNA fragments. This is why joining Okazaki fragments together is a bit longer process. In short, the RNA primers are first removed by Flap endonuclease I and replaced by DNA Polymerase $\ce{\delta}$, after which these fragments are joined by DNA ligase I. I would suggest you read the Wikipedia article about Okazaki fragments.

You're most welcome :) If my post really answers your question, please consider selecting it as correct. It gives points to both the answerer (me) and the asker (you) ;)

Okazaki fragments do not attach to the lagging strand adjacent to one-another, but rather, attach randomly, some distance from one-another.

My answer is correct. Okazaki fragments do NOT line up adjacent to one another. They are some distance apart, and the distance between them must be filled in. That was the error in the question.


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Clustering collection of PDB files based on 3 dimensional structural similarity in python
I have generated a set of 3-dimensional structures of the peptide AGAGAG with different structures. Total number of PDB files are 300. I need to cluster the peptide structures based on their similarity. Is it possible to do Kmeans clustering and get the total number of clusters in Python? The issue is that the RMSD-based distance matrix requires reference PDB which is not available here. Kmeans does not do clustering based on the distance matrix.

First, there are versions of k-means that can handle k-medoids from distance data.
Second, there are plenty of clustering methods that are fine with distances (see e.g. hierarchical clustering). Is there a reason you don't want to use this?
Third, is there a reason that you need to cluster them based on their similarity?
Fourth, you may be interested in approaches like FoldSeek that describe differences between structures using a structural alphabet to yield a sequence, making it a lot easier to do structural comparisons. Your example is admittedly a lot simpler than what they are trying to do with full proteins, but nonetheless may hold some points of interest. It is being used for larger-scale protein clustering tools like ProteinCartography.


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Who are humans' closest relatives, after primates?
This question here addresses the controversy of whether humans are more closely related to bonobos or chimps.
My question is - which group of animals are are closest relatives, beyond primates? Or which group of animals are all primates most closely related to?

Short answer
It is a flying lemur (there exist only 2 species). Flying lemurs and primates are together a sister clade to treeshrews.
Easy source of information
Have a look at the post The best free and most up to date phylogenetic tree on the internet?.
In short, you can have a look at onezoom.org, tolweb.org or opentreeoflife.org by yourself!
Tree of life of placental mammals
Here is a screenshot coming from tolweb.org.

In this tree, there are polytomies showing everything that is unknown. This tree was last updated in 1995 and there are also clades that we now know were misplaced including the bats (as commented by @NoahSnyder). It is not handy to make a good screenshot from onezoom.org or opentreeoflife.org so I just welcome you to explore the tree of life by yourself on onezoom.org or opentreeoflife.org to get a better representation of the reality.
Tree of Supraprimates
Supraprimates (=Euarchontoglires) include all primates and a few of the most related clades. Stealing the tree from @Gwenn's answer, here is the tree of Supraprimates
[
Here is the original tree from Janecka et al. (2007)

Here we see that flying lemurs (=Dermoptera) is a sister clade of primates (ignoring the extinct plesiadapiformes) and treeshrews (=Scandentia) are a sister clade of flying lemurs and primates together. Below I briefly talk about these three clades and about their position on the phylogenetic tree.
Flying lemurs
Flying lemurs is a small clade that contains only two extant species, both found in the family of colugos. Note that flying lemurs are not lemurs (which is confusing). Here is what a flying lemur look like

The position of flying lemurs on the phylogenetic tree has always been quite uncertain. In the tolweb.org screenshot above, flying lemurs (=Dermoptera) is a sister clade to bats (=Chiroptera) and together they are sister clade to treeshrews and primates. However, Janecka et al. (2007) placed flying lemurs as the sister clade to primates. Together flying lemurs and primates are a sister clade to tree shrews.
Tree shrews
Treeshrews is a clade of 20 species native from southeast Asia. Before, the era of phylogenetic comparisons, treeshrews were mistakenly thought to be part of the Insectivora.

Extinct clade of Plesiadapiforms
Although they are represented above as a sister clade of primates, it is possible that they the fossil we found are just individuals coming from the lineage giving rise to primates. As such, they would not be a clade aside from primates. Below is an artistic representation of what they may have looked like.

Introduction on phylogenetic trees
As the question is quite introductory, I presume you might want to improve your understanding of phylogenetic trees. You might want to make sure, you understand what a monophyletic group (=clade) is and understand why a chimpanzee and a human are both equally related to any species of treeshrews.
Here are two sources of information for you:

Understanding Evolution (UC Berkeley) > The history of life
This answer on Biology.SE

The most closely related animals to primates are colugos (order Dermoptera).
The next most closely related after colugos are tree shrews (order Scandentia).
The next most closely related after tree shrews are rodents (order Rodentia) and lagomorphs (order Lagomorpha) (rabbits, hares, and pikas).

Sources: Wikipedia's section on the evolutionary history of primates and onezoom.org.

Where did you see that Dermoptera is sister clade to primates? Do you have a reference for that? Note that colugo is a family made of two extant species only. This family is nested within Dermoptera and therefore a colugo is equally related to any primate than any other dermoptera

@Remi.b Just Wikipedia's section on the evolutionary history of primates. Wikipedia in turn cites this Science article from 2007 (which I sadly cannot read to verify because I don't have a subscription). And from what I understand, colugos are the only extant members of Dermoptera.

@Remi.b: The position of colugos (Dermoptera) in the evolutionary tree has traditionally been somewhat uncertain, but recent studies (such as the 2007 Science article by Janečka et al. mentioned by Gwenn, PDF here) do apparently support their position as the closest surviving sister clade to the primates.

Oh, I just realized that Dermoptera are also called flying lemur (which is a confusing term)! As a consequence, it is not so much an issue of definition as I suggested rather than an uncertainty about the position of flying lemurs on the tree. I will update my answer. Thanks for your help. +1 on answer and comments!


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"Most bacteria have at least one cell wall"
In the first answer to How do we find antibiotics? @Ashafix claims that

Most bacteria have at least one cell wall

Does this mean that there are bacteria with more than one cell membrane? Which are those and how does that look/work? Are there different milieus in the different compartments?
Cheers

Thanks! I will edit the original answer accordingly to make it more clear.

The phrase you quote is a little unclear, but in looking at the page you link to I believe that @Ashafix was referring to Gram-positive (one cell membrane) and Gram-negative bacteria (two cell membranes).
Each type has only one cell WALL, which refers to the structural peptidoglycan layer, which is between the two membranes in gram-negative bacteria, and is much larger in gram-positive bacteria.
The differences between these two cell types are of some interest with regard to the biology of what structures can sit in the cell membrane and how easy they are to work with in the lab, and how easy things are to get across the cell wall (w/r/t @Ashafix's original point).

Thanks, @Maximilian. Yes I got the original point of the refered to question. I was merely wondering just that which you answered. Thanks. As I'm only just signed up of this community, the only thing I can award you is the checkmark. Sorry.

great, glad that it got cleared up. no worries on votes or whatever.


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Is it possible to have a random un-mutation of genes?
According to this article:

Gene mutations can be classified in two major ways:

Hereditary mutations are inherited from a parent and are present throughout a person’s life in virtually every cell in the body. ...

Acquired (or somatic) mutations occur at some time during a person’s life and are present only in certain cells, not in every cell in the body. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.

The "random mutations in genes" appear to be called Somatic mutations. For the context of this question, these are the mutations I am asking about (not the hereditary mutations).
My question: Is it possible for there to be a random un-mutation of genes? Some sort of reverse-somatic mutation. If so, have there been any clinically proven instances of it?
After-thought: Or is it all a Somatic mutation, aka you can experience a mutation that makes you more susceptible to a particular disease, then another mutation that makes you less susceptible to the same disease... so not necessarily a reverse mutation, but a 'forward' mutation that negates the original ill effect of the first mutation.

Of course a mutation can revert back to its old state via random mutagenesis (un-mutation as you call it). Nobody has kept a track of it I guess but it is not such an uncommon thing. But think of its probability; it would be low (just a simple calculation). You may also want to look at PAM matrices.

A large part of the body of your question seems relatively unrelated to the main question which is a little confusing. I will focus on the question

Is it possible for there to be a random un-mutation of genes?

Yes, these are usually called reversed mutation. It is quite common though that a second mutation at a distinct locus may reverse the phenotypic effect of a first mutation. This is called a compensatory mutation.


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Why do obese people heal more slowly?
I recall an obese patient who was referred to a transplant clinic as his stitch wounds hadn't healed after a year. While there's a myriad of side effects caused by immunosuppressive medication after transplants, the usual healing process for patients that underwent the same procedure is around one to two months1.
It's not an isolated example, as patients with very high BMIs can be considered ineligible for transplantation because of the post-surgical complications that follow, namely, delayed wound healing and increased chance of infection. It does not seem to be dependent on diabetes or merely low metabolism rates caused by a sedentary lifestyle (some of the patients perform well in exercise tests and monitor and control their blood glucose levels) and as such, BMI tends to remain the only (imperfect?) factor.
Why does a large percentage of body fat or a high BMI delay or impair healing?
It seems counter-intuitive to me because, as I understand it, the two major parts of the healing process involve 1) a great range of proteins for the creation of new vessels, tissue etc., and 2) The energy needed for the different processes, such as the mitosis of the cells. If blood glucose levels are close to normal and there isn't much of an insulin resistance, then surely it's not a problem of availability for either of the parts to play their role?
Clarification: I restrict the scope of the examples to transplant surgical procedures as what I state is more likely to be factually correct due to  personal experience. I would expect wounds other surgical operations to follow the same patterns, but I could be wrong.

[1]: That is an extreme case, especially considering the possibility of effects of diabetes, obesity and steroids compounding. However, there's a general trend.

It's well known that obese patients have slower wound healing, but the specific cause isn't known; most likely there are multiple causes acting together.

The correlation between obesity and deficient wound healing has long been established. ... Substantial evidence exists demonstrating that obesity is associated with a number of postoperative complications. Specifically in relation to wound healing, explanations include inherent anatomic features of adipose tissue, vascular insufficiencies, cellular and composition modifications, oxidative stress, alterations in immune mediators, and nutritional deficiencies.

--Obesity and Surgical Wound Healing: A Current Review  (This is an open-access article that nicely summarizes the open questions)

Obesity has been shown in a number of studies to impair wound healing, and chronic nonhealing wounds in obesity and diabetes are a major cause of limb amputations in the United States. ... Recent evidence indicates that aberrant wound site inflammation may be an underlying cause for delayed healing. Obesity, diabetes, and other conditions such as stress and aging can result in a chronic low-level inflammatory state, thereby potentially affecting wound healing negatively.

--Exercise, Obesity, and Cutaneous Wound Healing: Evidence from Rodent and Human Studies (Also open-access, a little more recent but less wide-ranging)


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Maximum loading volume for agarose gel with 10 well comb
I want to load my agarose gel with my PCR products, which are 50 µL reactions.
I am wondering how much of those reaction I can load into one well if I use a standard agarose mini gel (10 well comb, ~8 mm thickness, 1.2%).
Should I try loading the entire 50 µL into one well or should I split it into two?
Thanks in advance
Phil

Why do you want to load so much sample?

Low concentration or for gel extraction I would assume...

Yeah, it is for gel extraction. I want to load maximum sample while using the minimal amount of gels

If this is for gel extraction, load two lanes. Or connect two on the comb with tape to make a bigger well.

How many samples have you got? You can tape neighbouring teeth of the comb together to create double- or triple-wide wells to load more sample.
I don't normally load more that about 20 µL.
You could also make the gel thicker potentially.

Thanks for the tip! Unfortunately, I only have one standard agarose apparatus, and it doesn't allow me to use wider gels. I tested with loading buffer in one well, whether or not it would fit 50 µL. It did, but I didn't take the risk of losing sample due to leakage, so I will just run more gels. Thanks a lot, though!

@Philz0rs If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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How many cells are in prophase on this onion root tip slide?
In the following image, I have to identify the cells in the different phases (not counting the cells that are too faded to see), and it's fairly easy to identify metaphase, anaphase, and telophase, but I'm not sure I'm doing it right for prophase vs. interphase.
I try to see if there's a nucleolus or not, but sometimes it's difficult. When I counted, I got 7 cells in prophase. Is this close to what you guys see or am I way off?
Thanks!

Hard call on early prophase versus interphase, especially since these are not natural distinctions with discrete boundaries but are used to articulate a continous process.
I'd say you're pretty close, I count six for sure. That includes the one in the top row on the far left that is partially clipped in the photo. One iffy possibility is in the third row just left of the obvious anaphase on the left.
Unless your teacher is far more particular than I was with students, I think you're good to go.


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Is a set of chromosomes made up of many copies of DNA, or is one complete string of DNA broken up into one set of chromosomes?
I know technically the question isn't really accurate but hopefully it gives the essence of what I'm trying to ask.
By the way I was taught in school, I was under the impression that a chromosome was made out of multiple complete copies of DNA. But, what I'm reading online makes it sound like a single complete string of DNA is broken up into sections and those sections are wound into chromosomes (so that one complete set of chromosomes would make up one complete string of DNA).
I'm assuming neither are 100% correct, but could someone explain it in a way that I can understand?

please cite what you are reading online

I agree with @tyto-alba, but over generations the separation can break down. Crossing-over occurs, even between the Y and X chromosome, duplications of chromosomes occur, crossing over between unusual chromosome pairs occurs, horizontal gene transfer/between species gene transfer occurs, etc. The genome is never fused as one entity, save for in prokaryotes, but chromosomes aren't perfectly isolated.

A chromosome is one long molecule of double-stranded DNA.  As a diploid organism, you (almost certainly) have two copies of each autosomal chromosome; one from your father, one from your mother.  You (almost certainly) inherited one copy of the X chromosome from your mother, and you either have a second one from your father, or you inherited a smaller Y chromosome instead.

Is a set of chromosomes made up of many copies of DNA?

Yes, 23 different chromosomes (discrete ds DNA molecules) form a set of the pair in human beings.

Or is one complete string of DNA broken up into one set of chromosomes?

No. No such string of DNA with all the chromosomal materials fused together exist in any stage of a cell's life.
When a cell in not dividing  it has 46 discrete ds DNA molecules.
Here's a karyotype of human male:

From: wellcomeimages.org

For this answer it might be useful to understand the different "stages" of genetic information.
The very root of genetic information is DNA. A section of DNA makes up a single gene. Genes are physically represented by loci (points) on a chromosome. What's more, chromosomes can fall into two categories: allosomes and autosomes. The former are what determines your gender, they contain all of the genetic data required to form the various proteins to eventually build your reproductive organs. The latter is everything else: your hair colour, eye colour, specific enzymes, etc are all made here.
This is useful to this question because it means that each chromosome contains sperate genes to control set functions. Thus, each chromosome is part of the same set of DNA - in the sense of the same genome (the complete genetic code in a given organism).
It would then be logical to arrive to the result that, in terms of your question, chromosomes are part of the same DNA "chain". One structure cut into chunks, if you will.
Hope that helps.
EDIT: My reference is: Genetics By, B. Guttman, A. Griffiths, D. Suzuki and T. Cullis.
EDIT: Please bear in mind that each chromosome is itself it's own module.

Very interesting! I always assumed that DNA was one long strand. I didn't know that it doesn't exist as one entity, but rather is broken up into chromosomes. And I assume the entire DNA (I guess the correct term would be "genome"?) comprises all the chromosomes and the mitochondria (I think)?

Good, I am glad! Yes genome would be the correct term. No. Whist chromosomes make up your genetic information, mitochondria are actually ancient bacteria that formed a biotymbiotic (both parties gain value from the following action) with a human cell, as ATP (energy) is formed by the mitochondria and the cell provides other necessities for the bacteria (mitochondria). So the mitochondria remains in the human. The bacteria has its own genome and is thus separate from our DNA.

-1: I'm sorry but this is just too inaccurate. To focus on the most glaring mistake, chromosomes are most certainly not part of the same DNA chain! Each of them is a distinct molecule.

That is correct, in the sense that they are completely separate from one another as distinct entities, but they are still ultimately part of the same genome, of which I think is a suitable answer the question he is asking. They are certainly not copies of the same DNA if that is the answer you are supporting.

I completely agree with @terdon. Chromosomes are not part of the same "DNA chain". You are implying that eukaryotic multi-chromosomal DNA somehow has a "natural state" where you can connect all the chromosomes together, if you wish. A genome is not a "chain" - it is composed of individual, separate elements (chromosomes), which exist independently - you cannot just splice them together and expect them to work in the same way. Telomeres are one reason, the issue of multiple centromeres and what happens during mitosis (independent assortment) is another.

MattSMo, yes I understand that. But I used the word 'chain' (with quotation marks to show that it wasn't really the correct term) to convey the idea that his second suggestion in the question itself was the correct one of the two. I apologize if my wording seemed inaccurate, for this is my first answer so I this feedback on board. I think I was just trying to convey my meaning in a way much more related to the context of the question - I didn't want to go information overboard.

Your second assumption is right. Dna is broken into various parts and then arranged into sets of chromosomes


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What is the surface area of the cardiovascular system?
In this question says:

An adult human has been estimated to have some 60,000 miles (96,560
  km) of capillaries with a total surface area of some 800–1000 m2 (an
  area greater than three tennis courts).

But the question is about the length and only mentions area in the body not the title, and the answers don't cite the area.

Does the Coastline paradox affect this?

Friction? Drag in blood vessels is much more complex than friction...

@Aron Ok, but maybe I can calculate a lower bound.

@Andrey Very interesting point. To that I can answer this: imagine a blood vessel section of 0.1 meter long, and 0.01 meter in "average diameter" (that needs to be estimated. Then you say the surface area corresponding of that section of the circulatory system is the area of the abstract cilinder we use to represent it. Also, if we specify the ruler size, the area becomes more well defined (althought still subjective a little).

Friction is a very bad word to describe it. But the simplest way to estimate the drag is to use Newton's 3rd. The drag is equal to the force on the blood, assuming the blood is at a steady speed. Figure out how hard the heart pushes.

@Aron I edited out the friction part, it wasn't part of the "question part" of the question. Indeed, it was why the doubt arised but not the doubt itself. Now the question is simpler. Thanks for your help.

@Santropedro so what is your question? Are you asking if the area estimation is correct?

@MattDMo Now the title make it obvious, the question is how much meters squared of surface does the circulatory system posses.

Even that is a difficult question to answer. It really can only be answered with "it depends on what you are asking".

@Aron To wich comment are you answering? I don't understand why it depends on what I'm asking, I'm clearly asking one specific thing. There is no variables that can't be handled in the answer that I see, if there are tell me what they are. I don't understand where the ambiguity is for you, explain please. The cardiovascualr system is a well defined closed system, and a vein for example in wich blood circulates, has a certain shape wich can be asbtractly treated as a tube cilindrically shaped that is curved, with a certain diameter.

See the first comment...the coast line paradox.


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Claim: Cat litter with different colors each son, could have different fathers
I'm newbie in biology. I can't look this in the internet and distinguish reliable sources because of this. I want to know if it's normal that a cat mother litter normally has multiple fathers, and that is the cause of cats looking very differently colored. Now, I imagine difference in coloring of the fur could happen with the same father, because sons are not necessarily genetically identical, however there are many claims in google when searching:

http://pets.thenest.com/can-cats-litter-two-different-fathers-8341.html
http://pets.thenest.com/possible-kittens-one-father-8061.html
http://www.drjeffnichol.com/?p=2277
http://animalcarebasics.com/each-kitten-different-father/

If the claim is true, does all the kids start developing at different starting times? Does that mean they could be born some more premature than others? How big is the window for female cats to be fecundated?

This might be better suited to [skeptics.se].

@MattDMo I though the same. I decided randomly.


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Catching a cold outside in winter?
We have all heard the typical “Put a jacket on youre going to catch a cold.” Usually stated by an older person typically a grandmother. Excuse the stereotype. Is there any evidence that colder weather makes one more prone to catching the flu or cold or is this simply a myth and misconception.

@Remi.b - That answer covers only seasonal flu, not colds.

This is a pretty old old-wives tale, taking many forms: don't go out into the cold while it's raining, or without a hat, with wet hair, without a warm coat or scarf, without boots, etc., "or you'll catch your death of cold."
The old wive's tale was immortalized by Jane Austin in her book, Pride and Prejudice, when the heroine's sister Jane falls ill after getting a soaking in the rain.
This has been studied extensively. A New York Times article describes one such uncomfortable-sounding study:

In the 1950's, Chicago researchers repeated the experiment on a larger scale with several hundred volunteers sitting in their socks and underwear in a 60-degree room before being inoculated with infectious mucus. Others, in coats, hats and gloves, spent two hours in a large freezer. The conclusion: all 253 chilled volunteers caught cold at exactly the same rate as 175 members of a warm control group.

In other words, being cold had no effect on catching a cold.

A survey of the medical literature shows that for more than a century, scientists have invested an extraordinary amount of time and energy in debunking this old saw, with the aid of a small army of shivering, sneezing volunteers. But despite their efforts, the link between colds and the weather still lingers and continues to inspire yet more research.

A 1968 experiment studied the effect of (among other methods of chilling) a cold water bath at several stages during and after inoculation with rhinovirus (one of the many viruses responsible for the common cold). No effect.
Yet the studies continue, because anything shown to decrease the incidence of the common cold would be beneficial to the sufferers, as in the US alone, 75 to 100 million physician visits are due to the common cold, and millions of days are lost from school and work.
But what has never been proven is that getting chilled in any way causes one to come down with a cold.
There are a lot of studies that fail to show a corellation. However...
there are a handful of small studies that show that having cold and dry nasal mucosae increases the susceptibility of infection when inoculated with rhinovirus, though. So, if these studies are accurate, then being in the cold when exposed does increase the chance of becoming symptomatic.
'You'll Catch Your Death!' An Old Wives' Tale? Well...
Exposure to Cold Environment and Rhinovirus Common Cold — Failure to Demonstrate Effect
Acute cooling of the body surface and the common cold

That 1950's study seems odd in that 60°F is not very cold at all.

Agree that 60° is balmy. Freezers less so.

How stupid of me to miss the freezer part…


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What are the abilities, sizes, and appearance of tyrannosaur rex?
Size
height 15-20ft tall
weight 7-9tons
length 40-42ft long
did the flim of jurassic park had some corrections of the reality I beilve there many things they gotten right on the trex

you really need to show some research of your own, you also need to be more specific about what you are asking, Are you just asking what is wrong with the ones in jurassic park?

I’m asking were the Trex in Jurassic Park flims were indeed right of their appearance size and abilities

You may want to change the question to reflect this.

The jurassic park rex is probably the best one ever put on film. the hands and skin are the biggest errors everything else is pretty good asinde from a few minor things.
It should probably be feathered but that is relatively recent discovery so they can be forgiven , how the feathers were distributed is anyone's guess. the weight estimates range from 5-9 tons with reality likey somewhere in between, 7-tons is a safe estimate for the largest ones.
The arms are a little too big and the finger position is all wrong. The fingers are held laterally (palms toward the midline) like a birds wing and with a lot less flex in the fingers and the arms would have been closer together. the production crew even admits they changed the arms to make it more intimidating.
They did make the rear portion of the head too narrow, it spreads out more with wide "cheeks"(jugal) improving the binocular vision and increasing the size of the jaw muscles. they did improve this in more recent movies. The base of the tail might be a little skinny too but that is nitpicking.
for scale and measurements use a scientific skeletal drawing like this.

As for behavior the only seeing movement thing is total fiction, but even the movie make it clear this is due to the genetic reconstruction not natural so no points lost. T-rex actually has a really good suite of senses with better hearing and smell than many other dinosaurs and binocular vision to boot. They would have head better vision than a human and a sense of smell comparable to a modern bloodhound. Hearing would have been good for a dinosaur but still inferior to a modern mammal.
The bite force we see on screen is light and dainty compared to what the animal could actually do, T-rex has the most powerful bite of any animal known.
40 mph is within the highest estimates of its speed but not unbelievable, 25-30 is more likely. T-rex does have some derived adaptations for speed (elongated interlocking compressed metatarsals, transverse processes on the caudals,ect) and was probably the faster and/or more maneuverable than other large theropod and it may have been faster as an adolescent. great lecture on T-rex anatomy.
Vocalization is an issue t-rex probably could not roar but it could have honked like a goose, and when you scale up a honk to T-rex size it will still end up sounding roar like, the roar from the movie is not that bad.
I am sure someone who has watched the movies more recently can recall a few other errors.

tyrannosaur rex roar could be possible since these dinosaurs were non avian birds they could roar. trex height 15-20ft tall so the height is correct and speed mostly 20mph


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What dinosaurs live during cretaceous period?
I cant find website that shows all dinosaurs that lived during this time?
Tyrannosaur rex and triceratops I know but what else?

Wikipedia has a nice summary: https://en.wikipedia.org/wiki/Category:Cretaceous_dinosaurs

cant you make list of them that lived with tyrannosaur rex please

To see which dinosaurs lived alongside Tyrannosaurus I suggest you browse the dinosaurs list here: https://en.wikipedia.org/wiki/Hell_Creek_Formation#Dinosaurs , as T-rex was found in the Hell Creek Formation. It might not be a complete list but it is the best I know.


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Advantages of Monogamy over Polygamy and Vice Versa In Nature?
Some animals take on a single partner, possibly for life, while others have multiple partners over their lifetime, possibly even at the same time. What are the advantages to each approach, and how much is conscious choice verses instinct?

This doesn't look too broad to me as an old student of the life sciences.   I might just offer an answer too.


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Why outgroups are supposed to be ancestral?
I was reading about phylogenies and found many literatures said that outgroups contain the ancestrial trait, but why is that? Aren't they also experiencing the same amount of evolutionary time and (presumably) changing their characters as well?

http://www.blackwellpublishing.com/ridley/tutorials/The_reconstruction_of_phylogeny13.asp

Yes, sister taxa are, by definition, of equal age. So they evolve independently after the two groups diverge. You are asking about character polarity, and you are exactly right. That is why multiple outgroups are better for inferring which state is ancestral. If an outgroup is state A, and a second more distant outgroup (an out-outgroup) is also state A, and the ingroup has state B, then you can be fairly confident that state A is ancestral. If you look at dozens of characters this way, you will find that any of the three taxa in any combination may have the ancestral state. Imagine the distant outgroup (the out-outgroup) is state A, and both the close outgroup and the ingroup are state B. Then again, you could not know which state is ancestral, and would need a further outgroup. These are inferences, not measurements.


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Is "Monophyly" context dependent?
I am thinking about this thought experiment: Suppose we have three taxa which are grouped into the following tree: {{A,B},C}, clearly {B,C} is a paraphyletic group. But if A go extinct in the near future, we are left with {B,C} only, then can the group be called monophyletic?

As long as you don't say A is OUT of the BC group, This is a monophyletic group yes.

To expand on Remi.b's answer, groups are defined based on all the species we know about. This includes extinct species. So in your example, the group {B,C} is paraphyletic regardless of whether A goes extinct or not.
But what if A went extinct ages ago and we don't know about it at all? In that case we would only have B and C to base a group on, and they are the only descendants of their common ancestor that we know about, so we would indeed define {B,C} as monophyletic.
The question comes when we discover A's existence, and that it is more closely related to B than to C. At that point we have a choice: expand the definition of group {B,C} to include A, in which case the group becomes {{A,B},C} and is monophyletic, or keep the group {B,C} and accept that we were wrong about it being monophyletic, it was really paraphyletic all along.
You can see these processes happen as paleontology and cladistics advance. Birds used to be classified differently from dinosaurs, but as our knowledge of how birds are descended from dinosaurs increased paleontologists chose to classify them as a subset of dinosaurs, keeping the group "dinosaurs" monophyletic.
On the other hand as our understanding of how mammals/birds are descended from reptiles and tetrapods are descended from fish increased, making both of those groups paraphyletic, the attempts to redefine them as clades have largely failed, so they are now considered paraphyletic groups. "Amniotes" has replaced "reptiles" as the name of the clade containing reptiles, mammals and birds, and "Craniata" is the monophyletic group containing various fish and tetrapods.

To be strict about the definition, a monophyletic group is a group that contains the common ancestor and all of its descendant. This means {{A,B},C} is a monophyletic group only if you consider all of the shared ancestors until the MRCA of them all.
If A get extinct, it still remain in that {{A,B},C} (and their common ancestors) are a monophyletic group. You do not remove A from the group because it is extinct.
Of course, this means that to have a monophyletic group we should be able to name every single species (or even every single individual given how messy is the concept of species; see here) that is descendant from an ancestor but we never do that. The most important is to not willingly ignore or include a species that should not be ignored/included. Here you would ignore A under the excuse that it is extinct and that would be wrong.


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Can erythrocytes Function without plasma?
my title is not very specific. So i will proceed to clarify it.
I am trying to make sure that the only blood cells in a sample are Erytocytes, since i want to evaluate their metabolism, I am aware that they don't have Mithocondria and thus catabolize Glucose into Lactate, (I belive I am not making false statements, however if any corrections pop up please give me a heads up.)
Thus a way I thought of getting rid of leucocytes was through centrifugation, erythrocytes would be at the bottom of the flask and if We got rid of Supernadant (plama and fine layer of leucocytes), we would have a much purer sample of erythrocytes.
My question is: Do they stil carry out their metabolism, so i can a posteriori evaluate it, even after centrifugation and gettting rid of the plasma. Or evaluating the lactate production afterwards would be impossible? I know there are more easier and methodic ways of getting rid of leucocytes(irradiation that destroys all nucleated cells and leucoreduction by filtracion, for example), but this is somewhat hypothetical, and i need to know the final answer in these circumstances.
Thanks in advance :)

@user1136 I apologize for my absolute statement, nothing is ever black or white, I was aware of the HMP shunt, but i failed to see the affect of it in the metabolism since it take 6 molecules of R5P to produce 5 molecules G6P, the net lactate would be bigger if there was no shunt, hypothetically. As for most of the references given about erytrocyte metabolism it was most fun reading them and I discovered things that will almost certainly help me in future studies, even if not, they were very fun to read.

@user1136 However i failed to understand one of your previous statements."And 'reserves' of 2,3-DPG can give rise to a 'burst' of ATP production, especially in stored RBC", do you mean that  the Lubering-Raport pathway will lower net ATP count, or that a considerable ammount of stored 2,3BPG will enter the Glicolytic pathway in media res are produce more ATP and lactate out of the blue?

@user1136 Thanks for the +1! The only implication of the of storage of blood I withdrew from your references was “A practical application of the DPG story was
the realization that the increased oxygen
affinity of blood during storage is due to
destruction of DPG." in the citation classic article by Benesch & Benesch. Much obliged about the information you helped me in on another question I also had! :)

Erythrocytes need more than just glucose in order to function and, they also need a extracelullar medium who shares the same osmolarity, so placing your red blood cells into a medium that solely has glucose will be problematic. If you solely want to evaluate the lactic fermentation carried out by erythrocytes on a short period of time, then you can add the blood plasm on your centrifuge tube (which will be in the superior layer) to the newly separated erythrocyte fraction. This way, we make sure your extracelullar medium not only has every metabolite needed, but is also isotonic with respect to your erythrocytes. If you're planning on evaluating this pathway for a considerable amount of time (days, perhaps), then you, most likely, will have to prepare a solution with glucose that is isotonic with respect to your red blood cells.

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

They need glucose, they absorb that from dissolved particles in water (the plasma). So if you isolate the cells, you'd have to put them in a medium with sugar and so on. It would be analogous to the medium they exist in before you centrifuge them, I think.

Thanks your answer was was most insightful!

If you're interested in what drives osmosis (really, not the "concentration gradient of water"), feel free to have a look here,
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.618.291&rep=rep1&type=pdf

Wow i did not know that, I will certainly look into it! Much Obliged!!

I discovered it just a few weeks ago, and it was published not too long ago, in 2009. Have not seen any earlier references. The short story is, the membrane is what drives osmosis, acting like a pump. That might sound weird, it does initially, but water organizes into a 4th state at membrane surfaces (or broadly speaking "contact zones"). This 4th state is analogous to ice but without the hydrogen ions to bond the lattice sheets vertically, those ions are instead excluded (ionized). Colloids affect the thickness of these gel-layers, and a concentration gradient forms for H+.


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Why is Homologous Recombination (HR) more frequent at long sequence repeats?
I'm studying plasmids in bacteria (E. coli), and trying to understand the well-cited phenomenon that recombination frequency increases with longer repetitive sequences. I think this also applies to eukaryotes.
In my (potentially misguided) current view, HR can occur between two DNA duplexes either during or after replication (?). As I imagine it, the new DNA duplex will have near identical homology to the template duplex (from which it has just been replicated), meaning that sequence homology is widespread across the entire molecule. This would mean that sufficient homology between sister chromatids can be achieved anywhere (?), negating the trend for 'long sequence repeats'.
So, why is there a focus on long repeats promoting higher recombination frequencies? Is my view on when HR happens misguided?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular it is helpful if you can provide references to reliable sources (and links) documenting that "recombination frequency increases with longer repetitive sequences". This will help provide context and lead to more focused answers. Thanks!

HR rarely occurs at all in normal somatic cells, because multiple different mechanisms try to prevent this from happening between sister chromosomes during mitosis; the implications of this recombination can be detrimental to the organism. Instead, in eukaryotes, HR normally occurs during Meiosis, in the formation of Gametes, which will recombine anyway. This actually has a beneficial effect because it increases genetic diversity of offspring, thereby promoting evolution.
As for how homologous repeats enhance HR, it is a rather simple mechanism. Basically, you have the two homologous strands side by side, and you have this extensive repeat section in the middle. The thing is, because the repeat section is so long, and because of the fact that it repeats, really any repeated sequence anywhere along that section can cross over with any repeated sequence on the other strand. This increases the availability of HR sites, as well as increases the number of possible outcomes, therefore increasing the probability that HR will occur. Plus, as the number of repeats increases, the number of possible recombinations increases exponentially, making HR on long repeats much more likely than other cases of HR
I hope that satisfactorily answers your question.

Thank you - this all makes sense. I since realised I was trying to figure out how HR occurred specifically in the context of DNA replication, and therefore wanted to make sense of 'which strands were which' in a potential HR process. Through a combination of this answer and chatting to other people I figured it out :)

I should add for those wondering where I got stuck: DNA replication can stall at any point, promting the repair machinery to get it 'back on track'. One of the ways this happens is through HR. This may require dissociating a newly paired nascent strand for it to be a potential substrate for strand invasion of the duplex on the other side of the replication fork. Reasons for homology are then as you described.

I'm not sure what you mean by "repetitive" sequences because homologous regions don't have to be repetitive, but the relation between long homology regions and increased HR efficiency is due to the mechanism. HR in yeast is achieved by strand invasion of single-stranded DNA (perhaps generated by DNA damage or self-induced in the case of meiosis) at another DNA duplex. The longer the homology region, the more complementary base pairing and the stronger the bond. Conversely if the homology region is short then the bonding is not so strong and the single-stranded DNA will probably get displaced by the other strand in the duplex thus reducing HR efficiency. I believe it's similar in E.coli.


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Does cell culturing contribute to dangerous antibiotic resistance to the same degree as livestock?
According to the CDC, antibiotic resistance is one of the biggest public health challenges of our time. The largest incubator for antibiotic resistance is the factory farming of animals where livestock are administered large antibiotic doses often and kept in infection-prone conditions.
Another area where antibiotic use is common is in cell culturing for biological research and engineering. To what degree is this use of antibiotics contribute to the public health challenge today, and moving forward as the biotechnology sector grows?
I am curious both about the impact for yeast cell culturing, and also for the culturing of meats as a future food source. I wonder how the problem differs from the antibiotic resistance problem in the livestock industry, and how this might affect the outlook of a future filled with synthetic biologic products and lab-grown meat.
I see two differences off the bat between livestock farming and cell culturing:

animals have much more powerful immune systems than cultures
culture contamination can be much more readily monitored and responded to by operators

Antibiotics are used in very different ways in cell culture and in livestock farming.
As you note, in farming, antibiotics are used to manage infection in unsanitary conditions and also to increase animal growth. Farming is essentially an inherently non-sterile environment and so there's not really any good way to keep microbes from spreading and interchanging, potentially carrying antibiotics resistance with them.
In cell cultures, on the other hand, one is typically working with a largely sterile environment, and it has to be maintained that way in order for the cell culture to work. They are far, far more delicate than farm animals---but they also can be entirely enclosed in a sealed vessel. Getting a significant contaminant into such an environment is not a "treat the sick animal" situation but a "sterilize and purge the bad batch" situation. Antibiotics are indeed often used as part of this defense, but the potential modes of infection are very different than with animals, which rules out many classes of pathogen simply because they are adapted for respiratory or gastrointestinal transmission, and a cell culture does not have these things.
Moreover, for most current industrial cell cultures, if the product is not the cells themselves, everything alive including pathogens will generally get killed off during later stages of the process (e.g., pasteurization of wine and beer).
If the cells themselves are the target of mass-scale culturing, e.g., cultured meat, however, then there will indeed be opportunities for antibiotic resistant pathogens to be developed and spread, particularly as increasing scale of operation
offers more opportunities for sloppy operations and regulatory evasion by low-cost operators.
Bottom line: antibiotic resistance is generally far less of a concern with cell culture than with livestock, but may still be at least somewhat of an issue.


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Expression of red and green fluorescences in the same tissue
In this article (https://jcs.biologists.org/content/122/14/2351), especially in Figures 1 and 2, they show the expression of GFP and red fluorescence in the same tissue, and I feel like that red fluorescence is present where GFP is expressed (though weaker than where GFP is absent), but I wonder why it's not yellow? Usually, when these two are expressed in the same cells (in this case, GFP is in cytoplasm and red indicates a membrane protein), the yellow color is observed, not like this. In this article, I feel like I see some red below green if that makes sense...
If anybody knows what this means, please give me some advice!
Thank you.

These images are not typically taken using color cameras. They are taken using grayscale cameras, using filters that allow the excitation wavelengths to hit the sample and the emission wavelengths to go to the camera.
For visualization, these black and white images are often put into the red or green channel in a digital image (TVs and computer monitors make color by mixing different amounts of red, green, and blue light: RGB). If you have red and green together that shows up yellow to a human eye, but that doesn't mean any yellow light is involved: it's just perception.
If you don't see yellow in these images it's because the red and green emission were not in the same place.


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Gene terminology - is one gene a concrete, single physical sequence?
Suppose you have two identical copies of the same, coding nucleotide sequence (e.g. two copies of BCL2 - a random gene I found on Wikipedia).
Could you say that these are two genes (i.e. the name "gene" refers to a specific, physical sequence, and where there are two of them, you have two genes, even if identical)? Or just two molecules of one gene (in the same way that when you have two molecules of carbon dioxide, you can't say that they are two carbon dioxides)?

You should familiarize yourself with molecular genetic terminology by reading some of the literature. It differs in many respects from chemical terminology, and the gene was defined in non-chemical (genetic) terms before its chemical nature was determined. Search especially for "gene duplication" to see how this is referred to. Then come back with more specific points if this does not answer your question. (And "two molecules of one gene" means absolutely nothing.)

'just two molecules of one gene'.
They are the same gene. Gene is more of an abstract concept. We say for example that humans have ~ 20,000 protein-coding  genes. It does not mean that we have only 20,000 molecules, one for each gene. We have many more molecules of course. What we mean is that we have 20,000 different entities, each coding for a specific type of protein. If you have two molecules of a sequence in a tube, it becomes questionable whether these sequences can be thought of as genes. I would say that those sequences lose their 'genicity' or their property of being genes because they are not coding for anything in a tube. They lack the cellular machinery that makes them code for something. I would just say you have 2 nucleotide sequences of the gene BCL2 but not that you have 2 copies of the gene BCL2. It's maybe just a personal difference I see though.

A gene is more a functional unit in the genome. As such if you have, say, 5 sequences of the same gene, you will say that you have 5 copies of this gene but you won't say that you have 5 genes. If you say that you have 5 genes, then we would think that you refer to 5 different loci (locus = position in the genome).
Note that if you are not familiar with the term allele, then you will want to check it out. An allele is a variant of a gene. Again, an allele is more the information in the sequence than the sequence itself (a gene is typically a coding region). Therefore, if you say that at gene BCL2, there are 4 alleles in the populations, that means that there are 4 possible variants in the population, not that the whole population is made of only 4 physical sequences of this gene.


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Resources to learn about marine life
I recently saw the documentary series Blue Planet 2 and was mesmerised by it. Can someone recommend me some resources to learn about marine life? I am particularly looking for those that detail the habits and lifestyles of marine organisms.
P.S. - Hope this is the right stack exchange for this question

There are a lot of marine documentaries out there. These are some that I know of:
Shark (2 episode series in 2015);
Deep Ocean;
Life in the Blue;
Ocean of Giants (Nat Geo);
Ocean Giants (BBC);
Humpback Whales;
Ocean Voyagers (whales);
The Polar Sea;
Swimming with Killer Whales;
Ocean Wonders (no narration, just under sea footage of animal behaviour);
Martin Clunes: Man to Manta;
Nature's Great Events: Diaries (a couple episodes of marine ecology);
Dolphins: Spy in the Pod (a view on dolphin activity using dolphin-shaped cameras);
I watched these off YouTube:
Alien Reefs;
The Giants of Rurutu (whales);
Mucky Secrets: The Marine Creatures of the Lembeh Straight;
Reef Life of the Andaman;
Secrets of the Australian Ocean;
Oceans of Contrast (spends a lot of time on life on land revolving around the ocean, but there's reef life as well);
The Incredible Glowing Creatures of the Deep Sea: Documentary on Bioluminescent Sea Life;
Documentary on Coral: African Wonderful Coral Reef
Conservation type documentaries:
Sharkwater;
Mission Blue;
Chasing Coral;
Blackfish;
Sonic Sea;
A Plastic Ocean;
Shark Men (If you like reality style television series. They capture, tag and learn about sharks to protect them)
If you want a more in-depth resource for learning, you can also YouTube search "marine biology lectures"


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Why does maintaining contraction of muscles require ATP?
So from my understanding, if I maintain the contraction of my muscle, the myosin head will be bonded to the actin. Why is ATP needed to maintain this bond?

Actually, it is not. ATP releases the myosin bonded to the actin, so when it is absent, the muscle remains contracted. This is, actually, precisely what happens during rigor mortis after death.
However, as long as you are alive, on a molecular level this is a dynamic process - actin release and bonding - and maintaining it requires energy. Moreover, muscle relaxation is not achieved by stopping the ATP flow, but incurrs additional ATP cost - it happens by actively removing calcium ions required to enable the actin to bind the myosin.


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Does cow urine have medicinal properties?
It is a common belief in India that cow urine has medicinal properties.
It is said to be anti-biotic.
It cures diabetes, cancer and many other diseases if not all.
Because this is biology I would like to focus on the anti-biotic property and set aside other claims cos they many be related to medicine and not biology.
Is it anti-biotic?
Does urine not cause infections?
Especially since it is applied the belly of new born babies by orthodox Hinuds.

it's a question for skeptics.se

there's a bunch of questions on skeptics on this topic already, for example this one : https://skeptics.stackexchange.com/questions/36282/is-there-a-hindu-cult-in-india-that-drink-cow-urine-to-cure-diseases

@gilleain Note that only asks is such a practice exists not the medical validity of it.

Don't use these medicines please. It only goes into the vicious cycle of spreading more fraud.

Interesting question anomdsgf. There are substances present in Bos taurus urine that promote antimicrobial activity. Studies like this and this have shown how the urine can inhibit the growth of certain bacterial strains.
However, with all that said, Bos taurus urine could still contain other harmful bacteria that are not inhibited simply because it was excreted out of a cows urethra and could cause infections. Read more on possible harmful effects here.


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Do animals have greater tendency to care for their opposite sex siblings due to mate competition among same sex siblings?
According to the gene-centered view of evolution, siblings have p=1/2 relatedness, thus having greater altruism between them than cousins or unrelated animals.
For species with a conventional sex binary, how does sibling sex relate to altruism? My idea is that siblings of opposite sex show greater altruism than siblings of same sex, since siblings of same sex have more to compete over. Namely, same sex siblings compete for the same pool of mates. Is this something known to be true in studies of species altruism?


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How to filter the PBD databank for "single-domain proteins with full length 3D-structures solved"
I am trying to reproduce a machine learning model that has been developed here. As one of the datasets, they use single-domain proteins with full length 3D-structures solved. Since I don't have a background in biology, I am not sure how to filter the PDB databank for these kind of proteins. Any help would be appreciated.

This question would probably be a better fit for the bioinformatics.SE. If I were you, I would take a look at the ftp/download section of the PDB and see if the documenation for that let's you figure out the appropriate filters. It may be necessary to downlaod the full pdb & filter then.

I'm voting to close this question as off-topic because it is about bioinformatics rather than biology. Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site for descriptions of what is (and is not) a good fit for this site. Thanks!