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How can the following data regarding flower phenotypes be explained?
$$\begin{array}{c|c|c} \hline
\text{Parents} & F_1 & F_2\\ \hline
\text{Blue}\:\times \text{white} & \text{All blue} & \text{196 blue, 63 white} \\
\text{Blue}\:\times \text{pink} & \text{All blue} & \text{149 blue, 52 pink} \\
\text{Pink}\:\times \text{white} & \text{All blue} & \text{226 blue, 98 white,
77 pink} \\ \hline
\hline
\end{array}$$
From the above data, it is likely that this is more complex than simple Mendelian inheritance. My guess is that there is epistasis at play here, but I can’t figure out what is really happening. What are the phenotypes of the parents? What genetic loci are involved and which traits are dominant?
(I was thinking blue ($B$) was the dominant epistatic flower color allele—$BB$ or $Bb$ would give blue regardless of the other color allele, and $bb$ would allow the expression of color dictated by the other gene, which has pink ($P$) as its dominant allele. This doesn’t work, as seen in the third row.)
Can anyone lend their aid here?
(The data was taken from here, question 32 in the sample multiple choice.)

Because it seems you might be studying for a test, I will try to not answer directly but show the beginning of a chain of logic that might be more useful.
Let's review the very plain evidence. blue crossed against other colors leads to 3:1 ratios of blue:other. So it seems that blue is dominant in those cases. But when you cross those colors against each other, you get silly nonsense, a 3:1.2:1 ratio or something.
So, based on the linked answers, you are justified in thinking that genetics determines flower color, just because of the simple Mendelian pattern of the first 2 crosses. But things don't work for a straightforward monogenic trait in the pinkxwhite cross.
Let's now analyze your explanation. You say: "I was thinking blue (BB) was the dominant epistatic flower color allele—BB or Bb would give blue regardless of the other color allele, and bb would allow the expression of color dictated by the other gene..."
But look at the parents and offspring of the third cross. You say blue is dominant- but it is in fact expressed in the offspring of non-blue parents! So blue can't both be dominant and be the "controlling" epistatic gene. So now: let's consider some other similar possibilities:
1) blue = dominant and is controlled by another locus (recessive or dominant?)
2) blue = recessive and controls another locus (recessive or dominant?)
Do any of those hypotheses match the data?
A final observation: I find it always helps to add up all the combinations of phenotypes (if possible; for example the ratio of (blue+white) : pink, etc.) to see if anything looks like a familiar ratio.
I hope that is useful (and not too late to be helpful in studying, if that is your goal).

This is an example of recessive epistasis
In short, flower color is controlled by two genes. A recessive mutation can happen in either of those genes. In one gene, the recessive genotype (pp) results in pink flowers. In the other, the recessive genotype (ww) results in white flowers. If neither of genes are homozygous recessive, the resulting phenotype is blue.
When you cross a white flower (ww PP) with a blue flower (most likely WW PP) you get offspring that are homozygous dominant at one locus and heterozygous at the other (Ww PP) and the resulting phenotype is blue. The next generation will have 1/4 white offspring (ww PP) and the rest are blue (1/2 wW PP, 1/4 WW PP). The same pattern is seen for pink flowers.
When you cross a white flower (ww PP) with a pink flower (WW pp), you get offspring that are heterozygous in both genes (Ww Pp) and the resulting phenotype is blue. The second generation shows all possible phenotypes and genotypes.
You do not need to know this much detail to answer that multiple choice question, however. All you need to know is that this is a genetically controlled trait, even if the pattern of inheritance is complicated.


text:
Oncotic (Osmotic Pressure) in the blood pressure
I just wanted to ask, why is the oncotic pressure more negative in the blood plasma even though the hydrostatic pressure is higher since the blood comes from the pumping of the heart?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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What is the P in LogP?
How does this value actually get calculated?
Logarithms are usually written as
log(base 10) of x
So what is the 'P' equivalent of 'base 10'? I know it stands for octanol/water, but what does that actually mean in a computational context?
I've found many explanations of LogP online, but they usually just say the same thing, which is what LogP is used for. How does one actually calculate it?
Sorry if this is a ridiculously simple question. Bridging the gap between chemistry and math is not my strong suit.

If it's a bridge between Physics and Chemistry than either of those SE sites may be better than Bio.

If the base isn't specified it is usually assumed to be base 10. So you could write it as log10(P). see https://en.wikipedia.org/wiki/Partition_coefficient

Would be much easier to show a particular example.

It means the following:
$$\log P = \log(P) = \log_{10}(P) = \log_{10} \left(\frac{C_{\mathrm{octanol}}}{C_{\mathrm{water}}} \right) $$
With $C_{\mathrm{octanol}}$ being the concentration of the solute in 1-octanol and $C_{\mathrm{water}}$ the concentration of the solute in water.

$C_\text{water}$ is not concentration of water but the concentration of the solute in water. Similarly for octanol.

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text:
How does glucose delivered intraperitoneal (i.p.) get into the peripheral circulation?
Intraperitoneal delivery of drugs or fluids is something that occurs much more frequently in veterinary medicine than clinical medicine. In veterinary medicine or scientific studies using animals, compounds are frequently given via this route that it is typically referred to as "i.p. injection" or "i.p. delivery".
When glucose is delivered via this route (by injection or catheter directly into the peritoneal space), how does the glucose actually get into the systemic circulation? That is, where does it actually go anatomically?
I can't find much data on this or an explanation that is collectively agreed upon. In particular for drug studies, some people say that the drugs or metabolites get into the portal circulation of the liver, while other people say that the drugs are absorbed by the peritoneum and enter the systemic circulation via the lymphatic system? Some individuals would argue that substances diffuse across the peritoneal membrane and then make their way into the interstitial fluid first, and then passively diffuse into the body's fluid compartments. Could it be another route? Could it be an active process or is it completely passive? Or, alternatively, could it be a combination of several of these processes?

Just a guess (which is why this isn't an answer), but I would suspect that the mechanism strongly depends on the compound(s) being injected. For example, small molecule drugs may be much more likely to diffuse across membranes than to require some sort of active transport mechanism. However, some proteins such as antibodies can usually get into the peripheral circulation fairly easily, whereas other proteins cannot (personal experience).

@MattDMo most definitely and worthy as an answer. This question is too broad imo. By adding a compound, or class of chemically related compounds will make it better answerable other than with an "it depends" answer. As of now MattDMO 's comment makes a fine answer.

@MattDMo agree with your comment above... but I want to find evidence of the actual route that a compound like glucose would take to get into the peripheral circulation - like when we inject mice i.p. with a glucose solution for a glucose tolerance test - the glucose molecule diffuses across the peritoneal membrane, but then where does it go? Does it just diffuse into the capillaries and then diffuse into the hepatic portal circulation? I don't know where to find that information - a lot of people refer to that as "common knowledge" - but that must be cited somewhere

@Christiaan - thanks for your comment - will change to glucose specifically  to address your concern.


text:
How can I make sure my UV-purificator kills bacteria?
I'm going to show a UV-purificator for water on science fair. How can I easily check if purificator kills most of the bacteria? I need a quick and possibly easy method.

How did you use to test for whether your UV-purificator works? Did you just assume it works?

Well... I will also check if it works using this method. It's a student project so we can just follow the descriptions on the internet and hope that it will kill bacteria. And even if it won't work with 100% efficacy, we just want to show killing effect of UV.

There are not many quick inexpensive methods that can show the number of dead/viable cells. Staining+microscopy is a quick method but I am not sure if you can obtain a microscope and the stain (whether the school will fund you for that). Moreover counting bacterial cells directly would require some patience and expertise. Colony based methods (plating) are convenient but would take time.

Not having the equipment needed to actually count bacteria, you can use things you know bacteria does to find out how much they were affected.
My approach would be thus:

Select a model bacteria. There are a few candidates, but probably the most readily available is lactobacilli, which can be found in yogurt and (loosely translating terms of art) is a Gram-stainable fermentor-sometimes-breather.
Infect the water with a known quantity of bacteria and a food source (lactobacilli eat lactose - ie from milk) and equally divide it into a control and experimental group...
You'll need to find an alternative way to estimate the bacterial content in the volume of water used compared to a control colony. Since lactobacilli produce lactic acid, you could use the pH value of the water (either with an indicator or a meter) to detect bacterial metabolism, compare that to the control's pH value.
Record the UV exposure time from the experimental group, and isolate the control group from any potential UV light source, such as the sun.

Even if you find that, for example, your particular strain of lactobacilli is not sensitive to your UV light source, that's a perfectly scientific result! How did you obtain it? The source likely knows what kind of bacteria it is. Perhaps the UV light merely interferes with bacterial metabolism, and doesn't kill it. Unanswered questions are wonderful, you may have provided a place for further research to take place. You could then use the two groups to infect a food source (ie milk) and compare post-exposure growth, depending on how much time is available.

I think the main point that is left unaddressed is regarding the technique that can be used to quantify viable cells in the sample after treatment. Your answer as of now focusses only on how to set up the experiment properly.

OP is looking to "check if purificator kills most of the bacteria" - viable cell count is probably overkill for that. I suggest a simple comparative approach. Dead bacteria don't behave like live bacteria, so one only need compare the chemical content of the water containing "possibly dead" and "known live." Say there's no difference - it wouldn't make sense to do a cell count at all. You would expect the known live bacteria to do more than a dead one, thereby changing the chemistry of the water.

OP asked whether most bacteria are killed. So you count the live ones remaining to determine that. That's how it is usually done. The dead ones can also possibly cause harm because of endotoxins. Even in that case an explanation of an existing methodology to quantify the "chemical content" is, IMO, essential.


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codon optimization / enzyme active site improvement
Does one necessarily have to use de novo synthesis of DNA when attempting protein expression improvement by codon optimization? Or are there other ways?
e.g. Say the gene coding for the enzyme needed to synthesize a certain secondary metabolite is known & sequenced already. The standard cloning approach is to extract mRNA from (say) plant tissue, then construct a cDNA library & express it in E Coli using a suitable plasmid.
Now if the neucleotide sequence needs to be modified (to increase expression) does one have to start de novo or is there easier ways that can start from the mRNA / cDNA?
A variant of the same question is when I'd want to modify the gene because a protein docking study shows some ways to modify the active site of the enzyme by changing a residue or two in the amino acid sequence.

Kind of an old post, I'm surprised it doesn't have an answer yet.
There's no reason why you couldn't modify the RNA or cDNA directly, you just have to splice the gene correctly to make the changes you want. You're absolutely right that even a single amino acid change can have a huge difference if it's in the right spot.

Some questions are unclear and the best interpretation of them is that they are trivial and could be answered by the poster with a little research. In such cases As the Help on answering questions says, "Not all questions can or should be answered here". But if you do insist on answering I suggest you read that help, because your answer only expresses an opinion which, though it may be correct, provides no supporting references or explanation of why it is correct. Thus, neither the poster nor anyone else can tell whether it is so.


text:
Computer Models of E Coli / Saccharomyces cerevisiae metabolite pathways
Are there mathematical models one can use to predict the expression levels of a foreign gene inserted into a well studied host organism like  E Coli or S cerevisiae?
I'm not, obviously, looking for some magical, accurate in silicio model; but even an approximate heuristic. e.g. Before starting a cloning experiment to estimate levels of a secondary metabolite expression in different organisms that both contain the substrate natively but may have it in different levels.
Alternatively, can the math models help in estimating which other competing pathways may be draining away a precursor of interest so that a rational attempt can be made to block such pathways to promote selective expression of the metabolite of interest.
Of course, the cloning experiment is the gold standard but are there ways to simulate a part of this and reduce the dead ends of experiments. Is there standard software I ought to be looking at?

Yes there are Flux Balance models but you would have to incorporate your gene into the metabolic network..

@WYSIWYG Thanks! Can you offer any pointers on where  / what software to start with? What sort of parameters would one need to introduce an ad hoc gene into an existing flux balance model?

I don't actually know a great deal about this but you would have to introduce new reactions in your metabolic network which might consume some primary metabolites and produce your desired secondary metabolite and by-products. You can then calculate the flux balance that can maximize the secondary metabolite production. This is basically a linear programming problem. There are some optimized programs for this but I don't have much idea. You can start by reading some basic books on flux balance analysis.


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What is the difference between the glycolate pathway and photorespiration?
I came across the definition of photorespiration as a process that forms CO2 from O2 in the presence of light. However, the CO2 is released only when the plant cell undergoes the conversion of glycolate to PGA, i.e in the glycolate pathway.
Most textbooks seem to use the term photorespiration and glycolate pathway interchangeably, but then they seem to say that the glycolate pathway evolved to regain the energy lost in the formation of glycolate, whereas photorespiration is wasteful. How is this possible?
Shouldn't photorespiration be a conservation pathway as well? It is trying to regain lost energy from glycolate, isn't it? or Have I got the two terms completely confused?
Please Explain

I don't even think that photorespiration is wasteful. It seems to me like plants generate CO2 for photosynthesis when amount of CO2 in environment is less.

Can you actually describe what process according to you is photorespiration?

As per what I have studied, I can define photorespiration as the process in which RuBisCO uses O2 and produces CO2 when amount of Oxygen in environment is higher than that of CO2. But, though it uses more ATP and also produces ammonia,  it seems to me like plant is generating CO2 for its own benifit i.e. photosynthesis. So it does not seem totally wasteful.

That would actually make some sense as the feedback for that would be less photorespiration and more photsynthesis due to increase in CO2 concentration. So in those terms glycolate pathway is just a pathway for photorespiration, right?

From http://plantsinaction.science.uq.edu.au/book/export/html/64 "Wang and Waygood (1962) had described the ‘glycolate pathway’, namely a series of reactions in which glycolate is oxidised to glyoxylate and aminated, first to form glycine and subsequently the three-carbon amino acid serine." So, it says that glycolate pathway is just a part of photorespiration in which glycolate is metabolized.

I appreciate the attraction of the idea that Nature is too smart to allow wasteful processes, but the suggestion made by @another 'Homo sapiens' just won't wash. I know of no evidence that the concentration of CO2 in the atmosphere varies appreciably, and if it did I can't see that the production of CO2 by plants would affect it significantly. And I imagine there have been many previous attempts to rationalize this inconvenient truth.

@David Amount of CO2 doesn't vary appreciably, but that of O2 does. Because RuBisCO cannot choose O2 instead of CO2 just because % of O2 has risen by 0.001% or something. By photorespiration, plant not only produces CO2, but also consumes O2 i.e. it increases amount of CO2 two-fold, which might affect it significantly. Also, when it comes to smartness of nature, there can be a long debate about why evolution gave rise to photorespiration and why plants still use C3 cycle.

The simple answer to the question posed in the title of the question is as follows. The glycolate pathway is the series of reactions converting phosphogycolate to reusable carbon intermediates + CO2. Photorespiration is the combination of two processes:

The oxidation of the enodiolate intermediate on Rubisco to phosphoglycoate + 3-phosphoglycerate.
The processing of the phosphoglycolate produced by the glycolate pathway.

You cannot use the two interchangeably as there is no respiration (use of oxygen) in the glycolate pathway. The glycolate pathway is just the latter part of photorespiration. I'm not sure what the text books are that confuse the two, but Stryer presents this quite clearly in Figure 20.6 and 20.7 at http://www.ncbi.nlm.nih.gov/books/NBK22344/#A2795.
I am not familiar with the term "conservation pathway" in your final question. I would call the glycolate pathway a "salvage pathway" (although this term is more commonly used for recycling the skeletons of the products of macromolecular, esp. DNA, degradation). It does not salvage all of the carbon skeleton of phosphoglycolate as some carbon is lost to the atmosphere as CO2.


text:
Why is HIV so large compared to other viruses?
The HIV-1 virus is about 120-150 nm in size and has a genome only about 10,000 base pairs long.
Other viruses are far more efficient, for example lambda phage has something like a tenth the volume and a genome five times longer. In other words, while half the volume of a lambda phage is taken up with DNA, in HIV it's more like 1%. Why is HIV so space inefficient?

One point is that lamba infects bacteria, which are more simple than eukaryotic cells.

There are many other things inside the HIV capsid besides RNA. The ssRNA is bound to the p7 nucleocapsid protein, the p6 late assembly protein, as well as integrase and reverse transcriptase, both of which are vital for infectivity. Also enclosed within the virion are Vif (Viral Infectivity Factor), protease, Nef (Negative Regulatory Factor), Tat (HIV Transactivator), and Vpr (Viral Protein R). Surrounding the capsid is a matrix formed by the p17 viral protein, and finally the lipid membrane envelope (taken from the host cell upon budding), which contains host cell proteins as well as the vital trimer of gp120/gp41 heterodimers, which bind to the target cell.

From Wikimedia
HIV (and many other viruses) depend on binding to certain cell surface receptors, and a larger total size increases the chances of binding to multiple receptors and potentially triggering receptor-mediated endocytosis, if that is part of the virus's entry strategy.
The naked λ phage binds to the lamB porin of single-celled prokaryotic E. coli by way of the phage's J protein and injects its DNA load into the bacterium, where host factors circularize and supercoil it, allowing for transcription to begin. While the phage's genomic material can be integrated into the host's chromosome, it is not required. Additionally, there is no nuclear barrier to cross.

From Wikimedia, numbers in parentheses are copies per virion.
On the other hand, HIV is a highly complex enveloped lentivirus that targets very specific cells in its multicellular eukaryotic host HIV requires reverse transcription and the assembly of a large pre-integration complex to transport the viral DNA into the nucleus and integrate it into the host's genome, all before it can even start producing new viral proteins.
Trying to compare the "packing efficiency" of HIV to the λ phage isn't just comparing apples to oranges, it's comparing apples to goats. The two viruses are completely different, with the only essential similarities being that they are viruses that infect cells.

First, your idea that "efficiency" has some relation to "genome size" divided by "diameter" is odd. You end up with arbitrary numbers that are not any kind of measure of "efficiency".
Second, HIV is an enveloped virus, while lambda phage is not; the internal viral core, less than half the size, is a better comparison.  Other enveloped viruses like influenza (100 nm, 14000 bp) are in the same ballpark.  Even many non-enveloped viruses, like Tobacco mosaic virus (40x300 nm, 6400 bp) have similar or "worse" ratios than HIV.
But the most important point is that it doesn't much matter.  It's not a measure of any kind of "efficiency" in the biological sense.

First, that's not my idea. My idea is that "efficiency" could be related to cell volume dividing by genome volume. That's called "packing efficiency". If you think DNA packaging is weird and biologically meaningless, you're simply wrong. See any number of references that immediately come up when searching for DNA packaging

@MarkE can you clarify what you mean? Everything that comes up for me when searching for "DNA packaging" has to do with chromosomes and how that interacts with protein production - but viruses by themselves don't produce any proteins in that state.

Obviously DNA packaging is important.  But obviously your measure of "efficiency" is meaningless.  Why?  Because so many viruses violate it.  You've created a hypothesis ("DNA:Volume ratio is important"), facts don't match it (phage to HIV have a huge range), so your hypothesis is wrong.  Facts always beat hypotheses.

I created no such hypothesis. You read the word "efficiency" and put meaning into it yourself that I did not imply. Regardless, see "Cell Biology By the Numbers", pp 9 "the viruses show strong economy of size, minimizing the required volume to carry their genetic material". If some viruses do show this economy of size and some do not, there must be reasons for that based on what the viruses do. Figuring out what those reasons are would be an excellent answer to the question.


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H3K36me3 role in RNA polymerase II elongation
I found a paper describing the association of RNA polymerase II with the histone methyltransferase Set2 that methylates H3K36.
At the end they say:

While our results strongly implicate K36 methylation as having a direct role in RNAPII elongation, the precise role is currently unclear. We propose three possibilities: (i) K36 methylation generates a chromatin structure that is more permissive for RNAPII passage. In this scenario, the loss of Set2/K36 methylation would result in a chromatin structure that is more difficult for RNAPII to pass, which might appear as an increase in RNAPII occupancy along the gene through increased pausing. (ii) K36 methylation generates chromatin structure that is less permissive for RNAPII passage. In this case, K36 methylation acts as a negative regulator of RNAPII elongation, and the loss of this “mark” permits increased RNAPII passage.

I am a bit confused about the (ii) point. If the loss of this mark permits increased RNAPII passage we would not see the H3K36me3 pattern in the active genes. Why is then H3K36me3 said to mark active genes?

We have a more recent study, Histone H3 trimethylation at lysine 36 is associated with constitutive and facultative heterochromatin and they seem to suggest that in accordance with your '05 paper, H3K36me3 in part contributes to the formation of tightly packed, inaccessible chromatin. You'll see there's a lot of crosstalk, but you would also think that transcription in heterochromatin might be poor.
Looking at yeast studies, though, it would seem that RNA Pol II is capable of transcribing through heterochromatin anyways so long as specific cofactors are present (Acetylation of H3 K56 Is Required for RNA Polymerase II Transcript Elongation through Heterochromatin in Yeast)


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Tool for translating chomosome, index numbers to sequence information
Is there a tool which allows me to transform information in the form (chromosome number, start index, end index) to sequence information? For example, something like (6, 43770819, 43770841) should yield GACCCCCTCCACCCCGCCTCCGG as this is the relevant bases on the 6th chromosome.
A command line executable is preferred, although a web-based service is also fine. Thanks a bunch in advance.

I think this should be possible with Biomart.

You can write a small script to do that. Basically you just have to print a string from position-x to position-y. Explaining how to do that is not really on-topic here.
From available tools you can use getfasta from the bedtools package. This requires a BED file, or a GTF file  as an input. The three column format as in your question will also work but usually the orientation (+/-) is also important to fetch the right sequence; otherwise all sequences would be fetched from the + strand only. GTF format is a bit different: the three columns in your question would be the first fourth and fifth column in the GTF. Seventh column holds the orientation.
bedtools getfasta [OPTIONS] -fi <input FASTA> -bed <BED/GFF/VCF> -fo <output FASTA>

(or):
getFastaFromBed [OPTIONS] -fi <input FASTA> -bed <BED/GFF/VCF> -fo <output FASTA>

There is another one called gffread which comes with the tophat package.
gffread takes a GTF/GFF file as an input and gives you a fasta file of sequences corresponding to the positions listed in the GTF file. The third column (feature) should be exon or transcript as this tool was actually designed to extract transcript sequences.
gffread -w transcripts.fa -g /path/to/genome.fa transcripts.gtf


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Does the hepatic portal system form capillary beds?
Does the hepatic portal system form capillary beds?  If so, is the capillary bed coordinated with that of arterial capillaries?
What review paper might I look in?

In anatomy, a "portal circulation" is simply when you have a capillary bed that is interposed between two venous circulations BEFORE blood flows back to the heart. There are a couple of places in the body where this occurs, including the liver (hepatic portal system) and the pituitary (hypophyseal portal system).
To answer your question... yes, the hepatic portal circulation drains into the liver sinusoids, which is one large capillary circulation.
The hepatic arteries and portal vein give off branches that make up the portal triad which delivers blood (both arterial and venous blood) to the functional units of the liver which are the hepatic lobules.
The hepatic portal system drains into the liver and forms a highly fenestrated network of capillary beds within the liver parenchyma. In the case of the hepatic portal circulation, the flow through the liver sinusoids is considered this capillary bed. In humans, the flow of blood that makes up the hepatic portal circulation is mostly venous blood from the gastrointestinal tract.  This allows blood to flow through the liver for clearance of substances like drugs and hormones before those substances reach the peripheral circulation. Specifically, arterial blood flows to the majority of the stomach, small intestine and colon from the celiac, superior and inferior mesenteric arteries. This arterial blood flows through the capillary beds in the mesenteric circulation (i.e. the capillary beds around the intestinal enterocytes) and then into the major veins that drain the intestinal tract. There are two major veins that drain the intestinal tract, the superior and inferior mesenteric veins. The inferior mesenteric vein drains into the splenic vein and then the splenic vein and superior mesenteric veins merge to form the portal vein of the liver. Once blood flows into the portal vein it flows through the hepatic sinusoids (another capillary bed) before flowing out of the hepatic veins into the inferior vena cava, and then back into the heart.

The figure below is a picture of the intestinal veins from Gray's Anatomy  (wikipedia) that form the hepatic portal vein, the superior and inferior mesenteric as well as the splenic vein. In the figure the older term lienal vein is used instead of splenic vein. The latin word for spleen is lineal.

The picture below is a schematic of the hepatic lobule that receives its blood from a portal triad. In the center of the lobule is the "central vein". The blood flows from the portal triad to the central vein, and then the central veins coalesce to form the hepatic veins (which then drain into the inferior vena cava). The picture below is available from this website, along with some other text and picture for more information.

And another nice picture from wikipedia on "hepatic lobules".
.

As for a "freely available review" that you asked for, I can't find any with better pictures from PubMed that what is already in this answer.

This picure is from Junqueira histology book:

as it shows a branch of hepatic portal vain and a branch of hepatic artery form hepatic sinusoid which is some sort of capillaries.
hope it helps :)


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Why are vertebrae, specifically, so important in classification?
A fundamental level of animal classification is the distinction between vertebrates and invertebrates.  The vertebrata are, arguably, often classified as higher life forms than the invertebrata.  But why is the presence of the spine so important?  Why not use the simpler concept of internal bones as a classifier?
I might be missing something, but I can't think of any creature that has an endoskeleton but no spine.  Do any such creatures exist?  If not, why does classification focus on the spine and not the endoskeleton?

"If you have a spine, you're a higher form of life than things that don't." This is not true. Terms like "higher form of life" are meaningless

@CactusWoman You could say these stratospheric bacteria are literally higher forms of life!

@CactusWoman - I edited the question to make it less emphasizing on the higher/lower aspect

Short answer
The term vertebrata stems from grouping animals according to obvious gross anatomical distinguishing features as typically used in the early days of taxonomy. However, from a phylogenetic point of view, the presence of the neural crest during embryonic development, which is unique to this subset of animals in the phylum chordata, is a much more important distinguishing feature than the presence of vertebrae.
Background
Vertebrates belong to the phylum chordata, but share some characters that make them unique. Chordates, with a few exceptions, are active animals with bilaterally symmetric bodies that are longitudinally differentiated into head, trunk and tail. The most distinctive morphological features of chordates are the notochord, nerve cord, and visceral clefts and arches.
Vertebrates feature neural crest cells, which sets them apart from any other group. These cells appear early in development, and only vertebrates have them. Neural crest cells form the skull and jaw bones.
The neural crest has sometimes been called the fourth germ layer because of its importance (Fig. 1). The neural crest cells produce a variety of  cell types, including (1) the neurons and glial cells of the sensory, sympathetic, and parasympathetic nervous systems, (2) the epinephrine-producing (medulla) cells of the adrenal gland, (3) the pigment-containing cells of the epidermis, and (4) many of the skeletal and connective tissue components of the head (Gilbert, 2000).

Fig. 1. Regions of the neural crest. The cranial neural formt the bones and cartilage of the face and neck. It also produces pigment and cranial nerves. The vagal neural crest (near somites 1–7) and the sacral neural crest (posterior to somite 28) form the parasympathetic nerves of the gut. The cardiac neural crest cells arise from the neural crest by somites 1–3. Neural crest cells of the trunk (about somite 6 through the tail) make the sympathetic neurons, and a subset of these (at the level of somites 18–24) form the medulla portion of the adrenal gland. Source: Gilbert (2000)
In all, the term vertebrates is just a reflection of an apparent and obvious marker of this group of animals, namely the presence of vertebrae, but their distinguishing most important feature is the presence of the neural crest during development.
Reference
- Gilbert. Developmental Biology, 6th ed. Sunderland (MA): Sinauer Associates (2000)


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Does variation in human gut length vary predictably with diet of ancestors?
Background: Numerous online searches, textbooks and other sources seem to pin the average length of the human gut from mouth to anus (oroanal) between about 5-10m in length. To pick a reputable example, this page from Harvard suggests that the small intestine is typically 2.91m and the average large intestine is 1.90m. The paper they cite (Helander & Fändriks, 2014) suggests this makes up most of the ~5m of the average human gut. Helander & Fändriks (2014) performed a lit review to come to these numbers, so their average lengths are probably some of the best estimates we have. (Other sources can be seen here and here, and Raines et al. 2014 seem to suggest that intestines of living people are much longer).
Regardless, Helander & Fändriks (2014), similar to Raines et al. (2014) and other sources, comment that there is "considerable variation between individuals" throughout the literature they reviewed.
My question: is the length of a given human gut predictable by the diet of their ancestors? In other words, are gut lengths between individuals more similar between family members and their ancestors than for others whose ancestors lived elsewhere in the world (and presumably had an alternative diet)?

For example: Are the guts of people of western European descent more similar to each other than the gut lengths of those of East Asian descent (or Sub-saharan descent, etc.).

Reasoning: Gut length (& complexity) of different animals varies based on digestive needs (which are a result of the typical diet of the animal). The general assumption (with support) is that diets high in food with indigestible material results in increased gut dimensions.

See Naya et al., 2009 for a general discussion about "gut flexibility", list of review citations, and results indicating correlation of population (diet) with gut length in toads.
Davis et al. (2013) found strong evidence that diet and intestinal complexity were linked in terapontid fishes -- specifically, more complex guts seemed to be associated with shifts away from carnivorous diets.
Gut plasticity does not seem to be immediate. For example  Ferraris & Diamond (1993) found (unsurprisingly) that intestinal length was independent of diet in a week-long mouse study.
Discussion of variation in human diet can be found here.

I haven't been able to find any sources discussing this "gut flexibility" phenomenon in humans.

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


text:
How do geneticists compute the percentage of DNA shared between species?
It's not exactly clear to me what is meant when people say that humans and bananas share 50% of their DNA.

There is a good question in here I think. Currently it's hard to tell exactly what you're asking. Could you provide a citation for the 50%?

My source is MythBusters: https://www.facebook.com/MythBusters/posts/10150466971768224

That is atrociously irresponsible science journalism. The link they provide just takes you to some flashcards. I have no idea how they came up with that number. To get an idea of how people attempt to quantify homologous genomic material, checkout this article.


text:
Why are mice with a single X chromosome and no Y chromosome males?
I was searching online and I read this article Mice can be male without Y chromosome and this is a part of it:

The experiments demonstrate that there are multiple ways to make males, says Richard Behringer, a developmental geneticist at MD Anderson Cancer Center in Houston. “They’ve done it without any Y chromosome gene information,” he says. “There’s not even a sniff of the Y around.”

I know that mouses are separated to males and females, and they both necessary for reproduction. Can someone please explain to me how could this possibly be? there's a lot of biology specific terms that i did not understand well

Welcome to Biology.SE! You might want to change your title into Why are mice with a single X chromosome and no Y chromosome males?. For the moment the title is really vague.

Definitely, not a duplicate but you might want to read Do males of all sexual species have Y chromosomes? out of curiosity.

might be good to note that in fruit flies the ratio of X to autosomes determines sex, females can carry a Y if they have two X's as well and males can be XO

@Remi.b I change it as you said

@rg255 is that really possible! i didn't know that before

as seen in the methods on this paper for example

This is also true for drosophila. (Though sex determination in it is slightly more complicated.)

Almost all mammals (including mice and humans) have two sexes where the males have a Y chromosome and an X chromosome (whereas females have two X and no Y chromosomes).  This is not the only way organisms can determine sexes, but it's the way mammals evolved to do it.
So how does having a Y cause an individual to be male?  The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y.  One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics.  It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form.
In the experiments reported by the article mentioned in the question, they managed to cause mice without a Y chromosome to develop many male characteristics.  They did this by faking one or two of the actions of SRY.  One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.
So the experimenters found a way to turn on Sox9 without using SRY or anything else from a Y chromosome.  This got them mice that looked male, but didn't produce sperm.  So they did something further that substituted for a Y chromosome, and caused a weak gene on the X to work at many-times strength to do the job that a strong Y gene normally does.  This caused the special "male" mice to produce sperm.  But these sperm were not fully functional (they couldn't swim and enter the egg), so they showed they were essentially sperm by simply using a tiny needle to inject the semi-functional sperm into mouse eggs and have those eggs develop into viable baby mice.
Bottom line, if you use artificial methods to do what the Y chromosome does, you can make male mice which do not have a Y chromosome (and learn some things in the process).

perfect answer for me! @mgkrebbs thank you s much.


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Strange Striped Insect identification (Northern Indiana)
These bugs are coming out of some wood that I cut and burned in Northern Indiana (USA) . I am not sure if it is coming out of a white ash, cherry or oak.  We did have the emerald ash boarer come though the area -- is this an ash boarer?
Thanks.

It's not an ash borer. You can learn more about Banded ash borers (Neoclytus caprea)  that are sometimes confused for this borer species here. See here for information on the more commonly recognized emerald ash borer

This is actually a Painted hickory borer (Megacyllene caryae).
According to the Virginia Cooperative Extension (and here), this species is frequently misidentified as a Locust Borer beetle (Megacyllene robiniae).
Here are their pictures side-by-side (M. robiniae on the left and M. caryae on the right):

Pretty similar, right? There are some differences though:

Appearance:

M. robiniae description (from Virginia Cooperative Extension):

Both males and females have black bodies with bright yellow markings. These markings are most notable in the "W" on the first pair of wings.  Legs are red and antennae are black. These long antennae place it among the "long-horned" beetles.

The distinction for M. caryae is the white 'W' stripe. From OSU Extension:

The first marking from front-to-back on the elytra is also a yellow horizontal band; however, the second marking appears as a distinct "W" that is light yellow to cream-colored.

The following image from the Ohio State Extension better demonstrates the white W markings of M. caryae (similar to the OP's picture):

These two insects also differ in Behavior ( this is important).

From OSU Extension:

Painted hickory borers emerge from cut wood in the spring and locust borers emerge from live trees in late summer to early fall.

Since the OP found this in the spring coming from firewood, it further points to the painted hickory borer.

Finally, they differ in the species they infest:

From the Virginia Cooperative Extension:

The locust borer is a native insect that attacks black locust (Robinia pseudoacacia L.) and its ornamental cultivars... Unlike locust borer adults, painted hickory borer adults...attack stressed or recently cut hickory and other hardwoods.

M. caryae is named for it's preferred wood, the hickories (Carya spp.).

According to OSU Extension, M. caryae also commonly infests the recently dead wood of ash, black locust, hackberry, honeylocust, oak, Osage orange, walnut, and butternut trees.

M. robiniae, on the other hand, gets it name from the larvae living in and eating their typical host tree, black locust (Robinia pseudoacacia). Adults are also often found eating goldenrod species.

Should you be concerned? Not according to the OSU Extension page:

Fortunately, painted hickory borers only infest dead wood that has been cut for less than one year. ... The beetles will not infest older dead wood; they will not infest wood that has been dried or processed into home furnishings, or used as structural wood.  So, beetles that emerge from infested firewood in or around a home are only a nuisance pest.

A quick search for M. caryae turns up few other sources, but you can find additional fact sheets for M. robiniae here, here, and here.

For those that don't know trees: here is a link to learn more about the common North America hickory species, and below are some images of common hickory species. More info about black locust (Robinia pseudoacacia) can be found here.

I updated this answer with the correct ID and the often misidentified look-alike (which I originally fell for). As a result, you get a two-for-one beetle lesson for the day :p

Thank you for the well described and documented answer, as well as answering my follow up question: "Should I be concerned".

For fun: Mating Frenzy of painted hickory borers on youtube!


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Creation of healthy genetically modified crops
GM crops are huge at the moment, and the noticeable 'counter movement' is for people to continue to purchase organic foods (please note I am specifically talking of GM crops and not meats, etc).
The argument as fair as I am aware is that some of the GM crops actually contain poisons to the human digestive system that cannot be broken down, and we have yet to find out their effects on long term health.
However, my question is: What can be achieved, if anything at all, in terms of creating GM crops which do not incur health issues? Is there a specific way of going about this?
EG:

Could crops be made larger?
Could crops become more pest-resistant?
Could a 'uniform shape' be created?
Would this be done with genes from other plants? Or artificially?

Thank you for your time.

Yes, yes, ...maybe, yes. What do you mean by "artificially"? I don't think this question is opinion based. It's just unclear at the moment. Perhaps read a specific example in which GM crops have been used to enhance yield and come back with some more targeted questions.

The "poisons" used in GM crops affects insects and not humans. This can pose an ecological problem but there are no known health issues. Many other GM crops are engineered to have longer shelf life and higher nutritive value. Your question has few issues: 1.You are assuming that all GM crops have the poisonous insecticidal protein. 2.You are assuming that this is actually toxic to humans. 3.You are asking multiple questions about how to make safe GM crops. For first two issues you should support these claims/hypotheses with some reference. And, you should ask a single precise question.

Welcome to Biology.SE.
What are GMOs?
The term 'GMO' can mean a vast array of different things and there is no objective way to distinguish what most people would call GMOs from what most peopel would not call GMOs. Humans have made 'GMO' for thousands (or even tens of thousands) of years. The detailed definition of 'GMO' will not impact the answer to the question Are GMOs safe to eat?.
Are GMOs safe to eat?
Yes, GMOs are safe to eat. There is no health risk when eating GMOs. Every scientist agree on that. Arguments saying that GMOs cause health risks have no foundation and are not based on evidence. Have a look at the Skeptics.StackExchange.com > Is Genetically Modified food safe to consume?.
Note that I am not saying that there is no discussion or debate to have around GMOs. I am only saying that these discussions have no reason to be around health risks for the consumer.
Your questions

Could crops be made larger?

Yes. We already did that.

Could crops become more pest-resistant?

Yes. We already did that.

Could a 'uniform shape' be created?

I do not understand what you mean.

Would this be done with genes from other plants? Or artificially?

The term 'artificially' has no good definition and it makes your question unclear. Most would consider pretty 'artificial' to take a gene from a species and insert it into another species (even though it occurs in nature).


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Is there a resource that has quantitative data about cell proteins?
I am a MSc student working in mathematical biology. In my thesis I am modelling diffusion of a protein that can bind to cell surface receptors. In order to simulate this I need some rough figures about the binding rates, degradation rates, diffusion rates etc. of components involved in this system. I have managed to find some information about these things, but they have all come from reading papers - biology papers where I only barely have enough knowledge to grasp the key concepts and (lets face facts) barely have the patience to read.
Is there a better way to find this quantitative data? Ideally I would love to come across a database that had this kind of data in it, but I'm not holding my breath.
What techniques do people in my position use to find this kind of information?(short of trawling through incredibly dense biology papers)

I'll list the papers that I obtained these parameters from. BioNumbers is a very useful resource and some of these papers that I cite have been obtained from the reference mentioned in BioNumbers. So BioNumbers should the first place to look for things like this. If you are not satisfied then start googling around :)
You should, however, keep in mind that simulation using exact parameters may not be very helpful. You can try varying the parameters in some given range and see the effects. Some parameters actually vary a lot.

Protein translation rate: 11 amino acids per second. Assume some steady state concentration of mRNA. This parameter is highly variable as there can be multiple ribosomes per mRNA [1]. Also see Schwanhäusser et al. (Supplementary excel sheet) [2]
Protein degradation rate: Take an average or one of the values reported by Schwanhäusser et al. (2011) [2]
Association/dissociation rates: See table shown by Zhou (2003). It lists different known interactions.[3]
Protein diffusivity: This differs for cytoplasm and water. You can assume diffusivity in ECF to be same as that in water. See Arrio-Dupont et al. (2000) [4]. They report it for specific proteins. You can extrapolate for other proteins using the Stoke-Einstein relation which says that diffusivity decreases inversely with the radius of the particle.

[1] Siwiak, Marlena, and Piotr Zielenkiewicz. "Transimulation-protein biosynthesis web service." PloS one 8.9 (2013): e73943.
[2] Schwanhäusser, Björn, et al. "Global quantification of mammalian gene expression control." Nature 473.7347 (2011): 337-342.
[3] Zhou, Huan‐Xiang. "Association and dissociation kinetics of colicin E3 and immunity protein 3: convergence of theory and experiment." Protein science 12.10 (2003): 2379-2382.
[4] Arrio-Dupont, Martine, et al. "Translational diffusion of globular proteins in the cytoplasm of cultured muscle cells." Biophysical journal 78.2 (2000): 901-907.

Thanks for the references and +1 for bionumbers! That is exactly the kind of thing I was looking for


text:
How to get the correct RefSeq Protein transcript for a given RefSeq Nucleotide transcript?
How to get versioned Protein Accession Number for a Refseq Accession Number?
I have some versioned RefSeq Accession numbers and I would like to know their corresponding Protein Accession Numbers.
According to the RefSeqFAQ   http://www.ncbi.nlm.nih.gov/books/NBK50679/#RefSeqFAQ.what_causes_the_version_number there is not a 1-to-1 mapping between these numbers.

Also, nucleotide (NM_, XM_) and protein (NP_, XP) records for the same
  transcript may not have the same version number after an update. For
  example, an update to the 5’ UTR of a RefSeq nucleotide record would cause a version number change for the updated nucleotide record but not for the corresponding protein record. Conversely, a change in the annotated start site of the coding sequence without a change in the underlying nucleotide sequence would cause a version number update for the NP_ but not for the NM_.

I have tried this, but it gives me a huge
>>> from Bio import Entrez
>>> Entrez.email='email@example.com'
>>> f = file('entrez_NM_005529.5.txt', 'w')
>>> print >>f,  Entrez.efetch(
...     db="protein",id="NM_005529.5", rettype="native", retmode="xml").read()

The XML results contain the Protein Acc No, <Textseq-id_accession>NP_005520</Textseq-id_accession> but there is no version specified. Is there a simple way to get obtain the matching protein transcript version?

Are you always dealing with the latest nt version, or do you need to get previous ones?

There is another simple way for human sequences.
Go to RefSeq FTP and download the LRG_RefSeqGene file. This file contains updated mappings between the gene, mRNA and protein sequences (latest versions).
From README:
    Tab-delimited file reporting, for each Gene, the accession.version
      of the genomic and RNA and protein RefSeqs the RefSeqGene/LRG
      project treats as reference standards.

    The columns are:
      NCBI taxonomy id (all 9606)
      GeneID
      Symbol of the gene (official from HGNC when available)
      Accession.version of the standard RefSeq
      Term describing the RefSeq
         RefSeqGene              genomic sequence
         Ref Std, nucleotide     RNA sequence
         Ref Std, protein        protein sequence

      The LRG equivalent of the RefSeq standard
         LRG:                    genomic sequence
         t1                      locations for transcript 1
         p1                      CDS from transcript 1

         NOTE: t values can be > 1 ,  the integer assigned to t
               is matched by the integer assigned to p

Some few lines from the file:
9606    3329    HSPD1   NG_008915.1     NM_199440.1     NP_955472.1     reference standard
9606    3329    HSPD1   NG_008915.1     NM_002156.4     NP_002147.2     aligned: Selected
9606    3336    HSPE1   NG_008914.1     NM_002157.2     NP_002148.1     reference standard
9606    3339    HSPG2   NG_016740.1     NM_005529.6     NP_005520.4     reference standard

It is not that easy for other organisms. For them, you should either parse the mRNA page to find the RefSeq protein id or go to their specific designated databases (such as FlyBase for Drosophila) and obtain information on the gene to protein mapping.
For obtaining RefSeq records from NCBI using parsing you should first obtain the GI accession number corresponding to the mRNA.
Example: NM_007393 (mouse beta-actin)
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=nucleotide&term=NM_007393

which would give the GI accession number: 930945786.
Then fetch the protein GI using this accession number:
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=nucleotide&db=protein&id=930945786

which gives the GI accession number: 6671509
Finally get the RefSeq id (if available) corresponding to this GI accession. You can download the feature table and look for the RefSeq i.d:
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=nucleotide&db=protein&id=930945786&rettype=ft

For more information on how to use Entrez E-Utilities see here.

Thanks for a very comprehensive answer. Fortunately I'm only dealing with humans, but this will serve as a very useful explanation for others.


text:
Is the thecal sac ectoderm?
The thecal sac, or dural sac, is the membranous sheath of dura mater that surrounds the spinal cord and the cauda equina. The thecal sac contains the cerebrospinal fluid in which the spinal cord 'floats'.
Is the dura matter ectoderm? I know neural crest and such is ectoderm. But the meninges, in particular the dura, where do they come from?

The dura mater is formed by the mesoderm. The mesoderm is the middle layer of the early trilaminar embryo. The three germ layers are the ectoderm, mesoderm and endoderm, formed by gastrulation. The middle germ layer forms connective tissues and muscle throughout the body, with the exception of the head region, where some of these structures have a neural crest (ectoderm) origin. Connective tissues include cartilage, bone, blood, blood vessel endothelium and dermis, but also the dura mater. The muscles include cardiac, skeletal and smooth muscle (fig. 1).

Fig. 1. Germ layers. Source: UNSW
Source
- UNSW


text:
At what temperature do human bones disintegrate?
I know, the human skin can get damaged as quickly as 2 seconds, when exposed to temperature above 80 Celsius.
However, what about human bones, say the skull?
For example, when you cook a meal, at great temperature, the chicken bones, still stay hard and intact, that's why I am asking.

Boiling point of hydroxyapatite is around 1500°C so you will need this temperature to make bone literally evaporate.
Prolonged exposure to lower temperature (like reference in other answer 220°C) will break collagen and make bones weak and extremely fragile.

The mechanical properties of bone (like Elastic modulus) are generally dependent on a protein called collagen and its cross links. According to this paper, collagen denatures at temperatures around 220 degrees Celsius in a dehydrated environment after gradual heating at transitional temperature intervals.

When you cook a meal, at great temperature, the chicken bones, still stay hard and intact.

The typical (and of course recommended) temperatures for cooking poultry (like chicken) are below 100 degrees Celsius. I think this is why chicken bones are usually still hard after cooking as they normally become fragile after collagen denatures.

While this answer shows that collagen denatures at 220°C under dry heat, it is possible to break down the collagen in bones at much lower temperatures by means of hot hydrolysis.
This hydrolysis can be accelerated by use of either strong bases or acids (as shown in this paper), which help to break down the peptide bonds between the collagen and release the calcium phosphate deposits. Once the matrix is destroyed, the bone quickly loses its strength.


text:
Anatomy of the ear canal
When you insert your finger into your ear, you hit a dead end. You can't insert your finger into the auditory canal. What's this dead end called, the medical term for it?

I think its because auditory meatus is curved, not straight to prevent direct entry of large substances (insects, finger) inside to the tympanum.

Short answer
There is no dead end from the entrance of the auditory canal to the tympanic membrane. The diameter and shape of the object inserted rather determine whether it can reach deep enough.
Background
The above statement can be proved by following examples:
ENT doctors use an otoscope on a regular basis to directly examine the tympanic membrane (eardrum), meaning the emitted light entering the meatus from the otoscope, and the reflected light from the tympanic membrane exiting the auditory meatus are following straight paths.
Another practical example is the use of tympanic temperature to quickly measure core temperature. Again, the infrared light emitted by the tympanic membrane has to follow a straight path out of the meatus, otherwise it would be absorbed.
Lastly, see below picture that graphically shows the relative straightness of the meatus. There is some curvature, but certainly no dead end. A dead end, or hooked region with a sharp angle would be disastrous for hearing sensitivity, as it would block the passage of sound waves to the middle ear.

structures of the ear. source: WebMD.
The finger is simply too wide to enter the meatus to the tympanic membrane. In contrast, cotton buds do readily enter the meatus up until the tympanic membrane and ENT doctors sadly see quite a lot of cases where folks turn in with ruptured tympanic membranes due to excessively deep insertions of cotton buds.


text:
Can a Turner syndrome patient develop male characteristics artificially?
From an answer to the question Can stem cells from male convert to cells of female-only organs, and vice versa?

Y chromosome is the sex determining chromosome with SRY gene that determines testes development. Absence of the Y chromosome leads to female development by default. That is why XX forms women and there are people with only one X chromosome which are women. (Turner's syndrome)

and Why are mice with a single X chromosome and no Y chromosome males?

The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y. One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics. It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form... they managed to cause mice without a Y chromosome to develop many male characteristics. They did this by faking one or two of the actions of SRY. One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.

My question: Is it possible to make a Turner syndrome patient develop male characteristics by artificial stimulation? Has it ever been tried?

After a lot of research, I've finally found an answer.
In the case of humans, it is practically impossible. See this article from wikipedia:

During gestation, the cells of the primordial gonad that lie along the urogenital ridge are in a bipotential state, meaning they possess the ability to become either male cells (Sertoli and Leydig cells) or female cells (follicle cells and Theca cells)...Once proper SOX9 levels are reached, the bipotential cells of the gonad begin to differentiate into Sertoli cells.

This part is just to clarify why it is not possible. In embryonic stage in turner syndrome patients (and females), since SOX9 is not expressed (due to absence of SRY), the bipotential gonad cells in the urogenital ridge (Müllerian/paramesonephric ducts) of embryo develop into female reproductive system i.e. become mature into that state. After this has happened, any amount of SRY cannot develop male reproductive system as all bipotential cells have differentiated into female reproductive system.
It is practically impossible, but virtually it can happen if you can insert Y chromosome or TDF in the bipotential cells of embryo. Practically, doing such experiments on embryo might not be possible (at least for now).

Source

Source
However, it only means that they can't develop primary sexual characters. Secondary sexual characters can, obviously, be developed by efforts as small as hormone injections. In fact, hirsutism is a condition in which females devlop hairs on chest, face, etc. and even beards! Its causes are as common as obesity. See this article:

Some medications can cause hirsutism. These include danazol, which is used to treat women with endometriosis; systemic corticosteroids and fluoxetine (Prozac) for depression...Being obese causes increased androgen production, which can worsen hirsutism.

So, if a Turner syndrome patient wants a moustache or beard (just in case), it can be achieved by androgen injections too.


text:
Lookup for transporter locations in humans
I am interested in several transporters and cotransporters (eg SLC12A1/2 and many others), more precicely, in (human) organism that are made of cells containing those transporters. So does anyone know a lookup table or database where I can find information about that? My google search unfortunately left me in the dark :/ So I am thankfull about any hint!

Welcome to Bio. It's unclear what information you are after; cell types? transporter proteins? What characteristics in the latter case you wish to know?

It seems to me like the OP just wants a database of all the types of transporters (especially proteins as he mentions 'cells') to get information about them.

Ah, sorry if my question wasnt clear... Basically I am looking for a database containing the transporter proteins linked with a list of human organisms where they occure. For example the transporter NKCC1(resp SLC12A1)  would be linked with the Inner ear, sensory neurons, the distal colon, salivary gland epithelial celss, etc...
So I would be happy about anything like, or just similar to this  :)

This site can help you locate RNA expression of a particular gene (if you know the gene for the protein in context) in various tissues. Its called biogps.
http://biogps.org/#goto=welcome
Hope it helps :)

Cool, this already is a good step forward :)

Update: So yes, the source helps a lot! Also I found another similar source which seems very nice: the EMBL-EBI expression atlas.
Just one confusing thing I don't understand about either of the sources: I cannot find any gene expressions for the inner ear, corti, or cochlea... Is there a reason for this?

Haha! I got no clue. I don't use these stuff. All I knew is, while i look up proteins and all on wiki, it shows up this colorful bargraph on the right. Which happens to be an RNA expression thing from the site. I just pasted the link :)

BioGPS and related sites stem from research projects where RNA from a number of tissues and cell types are obtained, and (relative) mRNA abundances were measured (using microarrays or RNA-sequencing). See literature references on these sites for the primary papers. But not all tissues are easy to get enough RNA to measure accurately; cochlea would be a very small amount of material. Also they may not have found anyone willing to part with their inner ear for the sake of research ...

Ah, that explains a lot! thanks for that explanation :)


text:
Is complete linkage found in all four chromosomes or only Y-chromosome of Drosophila?
Male Drosophila shows complete linkage. Is it observed for all four chromosomes or only the Y chromosome?

All chromosomes. There is no crossing over in males in Drosophila. Check out the related question Why doesn't recombination occur in male Drosophila? for sources and context.

Hi @Christiaan, could you clarify your comment? I thought the OP was asking if the complete linkage in male Drosophila was for all chromosomes or just the Y, to which the answer is "all".

I don't question the validity of the answer, but the norm at Bio is to elaborate on your answer. For example, where did you obtain your answer from (references, sources)? Why is it all the chromosomes and not one? How do you know? As of now, it's a one-liner and this is generally not suitable as an answer, but more as a comment.

+1. However, it makes me wonder if this question is a dupe from your linked post?

Probably? Not sure how these things work.


text:
What's the explanation for those shivers/shudders that happen at random times?
They happen at any time, presenting as a sudden urge to shiver/shudder all at once. It originates in the neck and shoulders, feels like instant gooosebumps then out of total reflex shoulders roll back and neck cringes. Happens every couple of months and comes out of nowhere, then gone without a trace.
I have read about myoclonic jerks but this doesn't sound the same.
Where do these impulses come from and what's the physiological explanation?

You should remove all personal references (and the line about ghosts). Everyone experiences these random shivers so you can edit your question to make it general. Also, we would highly appreciate if you can add some of your own research on this question.

Nice question, I'm curious too. Lets see what answer do you get. ;)

It is just like a muscle spasm but generated from your nervous system. If the problem persist you are lacking in a certain vitamin that your body needs to function correctly.


text:
Do eukaryotes assimilate DNA that is floating in the extracellular membrane?
Prokayotes, which replicate primarily using binary fission, don't get much genetic diversity. For this reason, they take in any genetic material they encounter, in a gambit to help them better adapt to their environment.
However, Eukaryotes, most plant or animal cells that contain a nuclei, have great diversity from crossing over during meiosis, not to mention genetic materials from two parents.
Due to other means of genetic diversity, it seems that eukaryotic cells wouldn't need to take in foreign DNA as prokaryotes do. But sometimes life has redundancy, so:
Do eukaryotes assimilate DNA that is floating in the extracellular membrane?

+1 Horizontal Gene Transfer occur in eukaryotes too, therefore it must be somehow possible for a piece of DNA to enter a eukaryotic cell and nucleus.

@Remi.b while true, as of my understanding horizontal gene transfer between eukaryotic cells occur only by accident, not by a coded structure like https://en.wikipedia.org/w/index.php?title=Sex_pilus

@GyroGearloose the transfer of DNA via sex-pilus occurs from one bacteria to another and not from the environment. Perhaps you mean type-IV pilus.


text:
When streaking microbes on a plate to test growth after uv exposure, does how I streak make a difference?
I've been working on what I think might be a special strain of E. coli, I've been streaking it on LB agar plate and exposing it to varied times of UVC via the germicidal hood.
I'm wondering if how I streak, as in too heavily, vs very lightly, or diluted culture, etc would make much effect in survival.
If I'm putting too much onto the plate, the e coli could be self-shielding, or some ecoli dying off, but the rest underneath being protected from the light.
I've done several generations of surviving colonies, I'm now comparing to wild type to see if my streaking method results in survival in both.
This test will also rule out if the lamp is failing and my surviving colonies are just the tougher ecoli compared to the growth on the control.
tldr
Should I lightly streak or dilute my culture to ensure all ecoli are being hit with the UVC?

What about using a suspension in liquid broth. Put it in a shaker, put it under UV light.

Wouldn't dilution be more quantifiable for replication purposes?

I work with e. coli myself though I do not know if your special strain has anything drastically different than my own so I'll just give advice that I've gotten from post docs and other PhDs on how to handle cultures.
(Note: This is methodology that I can't really find a "source" for so take with a grain of salt and change for your needs)
Typically when streaking I try to ensure that I make the streaks light enough so there aren't colonies within vicinity of each other. It's hard to really give a quantitative answer on how to do this so you will have to experiment on your own so your streaks aren't laden with massive amounts of colonies next to one another. It should look like consecutive "beads" on a string. This is generally what I try to accomplish with my colonies. Keep in mind I am focused on cloning plasmids so I'm not really concerned about experimenting on the e. coli themselves, just getting individual populations that do not have mixed variations of my plasmid. This is why having colonies with good separation is important for my particular project.
As for making sure they are all being affected by the UVC, I'm not entirely sure if having them to heavily grouped together would "shield" from UV. I feel as though UV can easily penetrate through e. coli colonies but I guess its not out of the question. Best bet is to keep your colonies well spread out, enough so you can pickup a single colony with a pipette tip and nothing else. This will make any genetic experiments you may want to do a lot easier as well. Which I think would be interesting if you are interested in the mutations occurring.
Is there something about your project that requires you to streak these out on agar plates? I saw comments suggest liquid broth. Maybe that's easier to do to make sure everything is exposed and then streak them out on a plate to see growth and/or test for mutations.


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Enzyme immobilization: Factors that help or hurt success
Are there any factors to consider that can help / hurt the chance to get a successful immobilized enzyme catalyst?
i.e. The relative attractiveness of a live host synthesis vs an immobilized enzyme.
Specifically, the product of interest is a secondary metabolite of MW approx. & the host of choice is S. Cervesae. The transformation is a single step, catalyzed by a single, known enzyme with the gene coding for it approx. 2000 base pairs.


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If birds are dinosaurs, then are mammals reptiles?
I'm just curious - it seems generally accepted that birds are dinosaurs. If that's the case, then can we call all mammals reptiles? Can we go even further and call humans amphibians? And since single-celled bacteria were the precursor of all life, isn't just anything a bacterium?

The simple answer is: Yes (in the sense that one is descendent of the other). More complex answer would involve the definitions of paraphyletic, monophyletic etc., which are more or less arbitrary names given by consensus of the scientific community (in a way, like if pluto is a planet or a dwarf planet). Doesn't change any facts,  just the names we call it. (And the school marks you get for hitting recently changed keywords.)

Can't cite it, but I've heard of recent doubt if mammals are descendants of dinosaurs or rather of some other reptiles.

You might want to have a look at If dinosaurs could have feathers, would they still be reptiles?.

@GyroGearloose The simple answer is "no". Birds are not dinosaurs, but the descendants of dinosaurs after at least 65 million years of evolution. This distinction is used so that we all know what each other are talking about. I'm voting to close the question because at the minute the question is a mixture of semantics, rhetoric, and reductio ad absurdum; it's subjective.

Why would birds being dinosaurs mean mammals are reptiles??

It has as much logic as saying if carrots are potatoes, are foxes then plants? Carrots aren't potatoes, foxes aren't plants, and even if carrots were potatoes, would that have any bearing on the relationship between foxes and plants?

Then you can as well say we are all amoeba !

The title has substantially changed (to the worse), so my first comment does not make sens to the question in the current title.

The most primitive mammals are platipus and echidnas. Oldest placental are shrews.

Reptile is not a clade - it is a paraphyletic group because it does not contain all descendants (i.e. birds) of a common ancestor. Humans are amniotes like birds and reptiles but while birds and reptiles are sauropsids, mammals are synapsids. Humans are not amphibians either because amphibia is another paraphyletic group which is distinct from amniotes. Possibly some amphibians and amniotes share a common ancestor. Amphibians, sauropsids and synapsids can be grouped together under tetrapoda. So both humans and frogs are tetrapods but humans are not amphibians.
However, birds are dinosaurs and belong to a very specific sub-clade of dinosaurs called theropods. Both dinosauria and theropoda are monophyletic groups - i.e. they contain all the descendants of a common ancestor.

Extending this to bacteria. Yes you would group all living things (eukaryotes and prokaryotes) and can call them cellular living organisms.
However, animals (or any other eukaryotes) are not bacteria (they have diverged a lot). Moreover, extant bacteria are not precursors for all life. The precursor is called Last Universal Common Ancestor but we don't know much about it (at the moment it is a hypothetical organism). Eukaryotic evolution itself is a big mystery. So it would be  preposterous to call all lifeforms as bacteria.

Well Reptilia and Reptiliomorpha are clades (which contain mammals if I am not mistaken).


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How can space-time affect ageing?
I recently watched the movie -"interstellar" and I came through the question that how can ageing be affected by space-time? Wherever I look, I get it as a fact that it's kind of ageing slows down in space, but I don't understand why.
How can space-time affect internal cellular metabolism? And if it is related to our biological clock, then can it be a sufficient explanation for this kind of drastic ageing changes?

This is a physics question related to the time dilation explained by the special theory of relativity, and is therefore off-topic in [biology.se].

See this

@WYSIWYG- I was just trying to get some kind of biological explanation on the slowing down of the chemical processes occurring in our cells. I had earlier read on wiki about time dialation and there was just this that wrt earth ageing slows down. I wasn't able to get the feeling of it ... that's why I asked it here...in biology... but as "Christiaan" explained that even the rates of reactions can slow down ....even though I don't get the feeling ....I am trying to grasp this idea....

There is no change in mechanics as you can note in the linked Physics post and wikipedia. This is just a property of the spacetime itself. As noted by someone in the [physics.se] post, the theory of relativity is not very intuitive.

According to Einstein's Special Theory of Relativity, moving objects measure shorter in their direction of motion as their velocity increases until, at the speed of light, they disappear. It also tells us that moving clocks run more slowly as their velocity increases until, at the speed of light, they stop running altogether.
Hence,  astronauts traveling at great speeds for long periods of time return to earth younger than had they stayed on earth.
Technology, however, limits the velocities of astronauts, the differences are hence minuscule: after 6 months on the International Space Station (ISS), the astronaut crew had indeed aged less than those on Earth, but only by about 0.005 seconds. Hence, your notion that there are drastic changes do not find solid ground in the light of current technology. The effects would be greater if the astronauts were traveling nearer to the speed of light (299,792,458 m/s).
It is the mere physics behind it. Everything slows down relative to a slower moving observer. Not just metabolism, but time itself.

@Christiaan- so you mean everything slows down ... like  rate of any chemical reaction occurring in our cells?

@anamikaSingh - everything slows down


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Is a bone marrow transplant limited by sex?
Can a female patient get transplanted with bone marrow of a male donor and vice versa?

Well, I guess it's possible because graft rejection/acceptance is based on MHC/hla which are not dependent on sex.

Short answer: Yes. Because in almost all cases of organ transplant, the organ recipient will be administered immunosuppressive drugs.
There is some literature on the effect of sex on the outcomes. I have included two hints here.
from: http://www.nature.com/bmt/journal/v35/n6/full/1704861a.html
The impact of the donor gender on outcome in HLA-identical sibling donor hematopoietic stem cell transplantation for multiple myeloma was studied in a retrospective registry study of 1312 patients (476 male to male (M → M); 334 female to male (F → M); 258 male to female (M → F); 244 female to female (F → F) reported to the European Group for Blood and Marrow Transplantation (EBMT). The best overall survival (OS) from the time of transplantation was found in F → F (median 41 months) with no significant difference between other groups (median 25 months in M → M, 18 months in F → M, 19 months in M → F) despite a significantly higher nonrelapse mortality in F → M. This was due to a significantly lower relapse rate (REL) in F → M compared to all other groups. Before 1994, OS was poorer in F → M than in M → M, which improved to similarity from 1994 onwards (median 29 months in M → M and 25 months in F → M). The reduced REL contributed to this improvement in F → M indicting a sex-specific graft vs myeloma effect. Therefore, a female donor is as good as a male one for male patients, while for female patients gender disparity is a negative factor for outcome.
from: https://www.broadinstitute.org/news/1386
"It's been clear for some time that bone marrow transplants involving a female donor and a male patient pose a higher risk of GVHD," said Bradner. "This ‘sex mismatch' arises from genes that are carried on the male-specific Y chromosome and are therefore present in males but not in females..."

Anyone can be a donor ir recipient in hla markers are same or a close match. A female donor over 45 who has had 2 or more kids is the worst donor choice. This is because when a woman is pregnant the blood cells get good at attacking foreign blood from the baby. When the blood is given to the recipient there will be higher likelihood of gvh bc the blood will attack the host. By bone marrow, it’s really stem cells, baby blood cells. Once transplanted they replicate and are the new blood and immune system. My donor was my brother. 15+ years ago.

Thank you for your contribution.  It could be improved by adding a reference to a source for the donor pregnancy-history effect.


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Why do shed and brown poplar (Populus) leaves get an iridescent blueish colour when wet?
When the brown leaves of poplars shed on the ground stay for a while under wet conditions (e.g. like in a puddle), they become a fascinating iridescent blueish colour, which is best seen when light shines on it. I tried to look this up, but did not get any results... any ideas?


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How can a mutator gene can cause a mutation when it is shut off?
defination of "Mutator" - a gene that increases the rate of mutation of one or more other genes.
However, in the book "Molecular Biology of the Cell" (bruce alberts) it states that when a mutator is shut down, then that shut down increases the rate of mutation. How does that process work? It seems to contradict its definition? If the mutator is shut down, then how can it create mutations?

Please give a reference of that textbook. In a general way, I can say that it works like Trp Operon https://en.wikipedia.org/wiki/Trp_operon


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What is the name of the property of viruses that can go dormant in the host for 30 years?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.
My question is: What is the name of the property of viruses that can go dormant in the host for 30 years?

What do you mean with property? The place, where these viruses hide?

As far as I know dormancy in viruses like the above stated chicken pox virus is known as virus latency which wikipedia defines as:

The ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle.


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Cross section through the right arm question
Is the largest drawn vein on first attached pictue v. brachialis or did they make a mistake and it's actually v. basilica?
Picture 1: Cross section through the right arm (source: Thieme, General Anatomy and Musculoskeletal System, p. 296)

Location of sectional plane (picture 1):

Picture 2: A similar drawing from Sobotta (source: Sobotta, General Anatomy and Musculoskeletal System, p. 240) :

do you have better quality images? its very unclear

@rg255: I've added a better quality of picture 1, but I don't have a higher quality of picture 2.

@inferoanteriorly for that top figure, how far proximal on the arm are they? In my opinion – that should say basilic vein. However, the question isn't very clear as there's no cephalic vein on that image (like the lower image) – is that picture just more proximal than the lower? Where does the book indicate that that slice is through on the arm?

@VanceLAlbaugh: I've added a picture, which shows location of cross section from picture 1.

Based on the location of that cross section in the upper arm the vein in question appears to be the basilic vein. The basilic and cephalic veins are the largest veins (most of the time) in the upper arm. Here is a nice diagram from wikipedia that shows both. The cephalic vein is much more superficial than the basilic vein, as you can somewhat appreciate in the diagram below.

I think the label "brachial vein" is probably an honest case of mislabeling.
This is another figure that supports that vein in the image in the question as the basilic vein as well:

From this image (Gray's Anatomy), you can appreciate that the basilic vein is the large and deeper vein that runs near the brachial artery. In the case of many arteries and veins there are similar names, but that does not appear to be the case in this instance.

Clinical Correlate: In vascular and/or transplant surgery, when making an arteriovenous fistula for dialysis access (for kidney failure), there are a number of common routes of access. Two of the most common are the (1) brachiocephalic fistula, which is formed by surgically connecting the brachial artery to the cephalic vein, and (2) brachiobasilic fistula, which is created by connecting the brachial artery to the basilic vein. Some additional information and a picture can be found in this open access article from Maya et al entitled Outcomes of Brachiocephalic Fistulas, Transposed Brachiobasilic Fistulas, and Upper Arm Grafts .


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Is it possible to create a restriction map using python?
I have some fragments of DNA from single and double digests using three different restriction enzymes. I'm trying to construct a restriction map of a linear fragment of DNA. The map needs indicate the relative positions of the restriction sites along with distances from the ends.
Can this be done using python at all?
DNA Sizes of Fragments (bp) - uncut DNA = 900
DNA cut with EcoRI = 500, 350, 50
DNA cut with HindIII = 600, 300
DNA cut with BamHI = 400, 300, 200
DNA cut with EcoRI + HindIII = 350, 300, 200, 50
DNA cut with EcoRI + BamHI = 300, 250, 200, 100, 50
DNA cut with HindIII + BamHI = 300, 200, 100

I've updated the description so hopefully it is more clearer

Perhaps pointing in the right direction? Like where to find possible modules that do this? We're not all experts.

I'm voting to close this question as off-topic because this is about programming in python and not really about biology or bioinformatics.

First I'll answer this question on the assumption that you are learning or about to learn python (perhaps because you have heard it's become popular in bioinformatics) and you wish to know whether it can be applied to this problem. The answer is: almost certainly, yes. Python is a programming language of the type that can be used to automate the solution of this sort of problem, just as C, C++, Java, Perl could.
How would you go about it? You would first solve the problem by hand, analyse the logic of your solution and then try to devise a general algorithm based on this logic that can deal with a variety of cases. Then you would code this in python (or whatever). The program would have to deal with inaccuracies in real values of fragment lengths (your data are obviously contrived) and the possibility of more than one fragment of the same length (see below).  If you used python and wanted graphic output you would need to use a library that provides graphics as python does not come with graphics like Java does. I gather there are some. However this is certainly not the easiest of programming tasks for a beginner, as you'll see when you try to analyse the logic of manual solution. And of course the data might be insufficient to provide a unique solution.
However as this is a homework assignment you may also be wanting to find a program to check your answer and perhaps be unsure of how to go about it. I don't know of any packages to do this — it's perhaps not 'cutting edge'. So how to go about it?
What I would do is start with the single digests and draw a set of diagrams for each of the possible arrangements of the restriction sites in each case (pencil and paper work well here). Then I'd look at the simplest double-digest, identify unique fragments that were also present in the single digests and thus not cut by the second enzyme, and again draw diagrams of the possibilities for the pairs of restrictions sites. Be careful; the HindIII/BamHI double-digest doesn't add up to 900, so there must be two fragments of the same size here. When you have all the possibilities drawn out, there is presumably only one final restriction diagram that is consistent with all the data.
On second thoughts, devising an algorithm for solving this general case would be quite a demanding task. If you are starting programming I'd tackle easier algorithms first. And an effective algorithm might adopt a brute force approach rather than the semi-intuitive way we solve these by hand. For example your algorithm might generate all possible maps for each of the the three single digestions, and then generate all possible maps for the double-digestions, together with a calculation of the size of fragments the double-digestions would generate. These would be compared with the size of the actual fragments from double-digestions, eliminating those possibilities that don't fit. Coding it would involve writing methods/functions (or whatever they are called in python) to generate these maps, storing the coordinates of the sites in a data structure such as an array, and writing other methods to make comparisons etc.

Thanks for the advice David. It was a homework assignment and I did manage to figure it out. My inquiry to whether it was possible using python is one of interest as I've just started learning it

OK. I'll edit my answer to take account of that.

Python has good string functions, as do Java and C++. You could make a list of restriction enzymes, probably a map or hashmap. Then you load your DNA sequence as a string and iterate through the list of enzymes, searching for the restriction site in the DNA string, and returning the position of the site in the DNA sequence. If the strings do not match, a -1 will be returned. So if you just want a list, you can print to console or a text file. If you want an image, you need to make a list of restriction sites, with enzyme type and cut location, then use pygame or something to draw the map.

Drawing the map isn't hard either. If linear, the DNA of B bases is a line of P pixels long. So the restriction site at position b is drawn at pixel p where p = P * b/B. When circular, you'll need to calculate the pixel from an angle, where the angle is 360 * b/B.

I agree with the previous answer. You can certainly write a solution in python, but have to formulate it as an algorithm first. Doing so will enable us to suggest an actual solution.
Also, I wanted to suggest that posting this questions on a forum with bioinformatics focus (biostars.org) may yield better feedback.


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What tool to use to map reads (samtools, sequencher,...)?
I am a beginner in Bioinformatics. I have 4 files:
2 fastq files (aln1.fastq and aln2.fastq)
2 bam files (aln.bam and aln.bam.bai)
I know that:

the raw file is aligned to hg19 human genome.
The sequenced file is pair-ended from Miseq sequencing platform.
This file is the result of an amplicon sequencing design.

I also have sequence information about the primers (4 forward and 4 reverse) and 2 adaptors.
And I have to answer these two questions:

What is the constitution of each read, for example (adaptor + primer + amplified
region) ?
Which gene region did those reads mapped to ?

My question is what kind of tool do I have to use to respond to these questions? samtools? sequencher? FastQC? Can anybody help me just to start because I am totally lost.
Thanks

The aln.bam file is likely a binary and compressed version of a file in SAM format, indicating where reads have aligned. I guess it has been generated by some alignment program using the two fastq files.
For a start, you might use a program to visualize where the reads have mapped.
For instance, you may use IGV and load your aln.bam file to see where in hg19 they aligned. IGV will also use the aln.bam.bai file to help it find the aligned reads in the aln.bam file.
As far as I know, sequencher is used to clean and assemble Sanger sequencing data, but my experience with that program is almost 10 years old.
Samtools is a command-line program that can help you extract information from the aln.bam file. You may use it to count how many alignments are present in a given genomic region, for instance, using option -c of samtools view. See the manual for more details: http://www.htslib.org/doc/samtools.html

thanks. I opened my bamfile with IGV but how can I know which chromosome to choose and which region to zoom in?

If you don't see the reads at large scale, then I'm afraid you cannot know, just using IGV, where to zoom to see them. You need to identify regions of interest with other means. For instance, samtols view -c aln.bam chr1 should give you the number of alignments in chromosome 1 (provided it is named chr1). samtools view -H aln.bam should give you, among other information, the list of chromosomes that you can query (preceded with "SN:").

Samtools is not an aligner; it is used to analyse alignments. FastQC is for analysing the read qualities and average composition. You can get to know the adaptor sequence by running FastQC.
The next step is adaptor trimming. There are many tools that do that. Trimmomatic is currently popular. You can find the adaptor composition of each read by subtracting the read length post trimming from the read length pre-trimming (this would be same for all reads).
Then you have to align your trimmed reads to a reference, using an aligner. Again, there are many aligners available; Bowtie, STAR and now a new one called HISAT. STAR and HISAT are faster than Bowtie.
Since you already have the alignments (aln.bam) to hg19, you do not need to perform alignment. You want to know, to which genes do these reads map to. This information is not available unless you have the genome annotations. The annotations are available in the form of GTF/GFF files. You can obtain the association between genomic locations and the reads using the BEDOPS toolkit as mentioned in this Biostars post.
I don't have much experience with this tool. What I would do is convert the BAM to SAM (using samtools) or to BED (using bedtools:bamtobed) and parse the columns of the SAM/BED file describing the read locations with the GTF file. See this link for the details on the SAM format. You can use any scripting language like awk or perl to parse.
Samtools does have an option to filter the reads according to regions specified in the BED format but it will not automatically annotate them.
samtools view -hL regions.bed aln.bam > aln_filtered.sam


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Construct a restriction map of a linear fragment of DNA using the following data?
I've attempted to do the single digests, and the double digests, but cannot complete the map.... I've attached what I've done so far

DNA Sizes of Fragments (bp)
uncut DNA 900
DNA cut with EcoRI 500, 350, 50
DNA cut with HindIII 600, 300
DNA cut with BamHI 400, 300, 200
DNA cut with EcoRI + HindIII 350, 300, 200, 50
DNA cut with EcoRI + BamHI 300, 250, 200, 100, 50
DNA cut with HindIII + BamHI 300, 200, 100

Why are you listing only one of the possible fragment orderings for each cut result?  (e.g. only 500, 350, 50 and not the other five arrangements, like 350, 50, 500 and 50, 350, 500)

^This. You need to list all arrangements possible. It is equally possible for the enzymes to cut in any order (theoretically). Unless specified in which order they are used.


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When there's a wound, the end result is a thrombus or thrombosis?
When there's a wound, the blood vessels are damaged. To stop the loss of blood, the clotting cascade starts off and forms a clot. This clot is a thrombus, right? Seems like perfect physiology. Where does the clot occur? As in, if we consider the vessel to be a pipe, the clot is formed at one end to block the flow or is attached to the wall of the vessel on one side?
This doubt arises because thrombosis (considered pathological) is defined as a clot within a blood vessel. Is the same not happening when there is an injury? If we consider the clot formed at one side of the vessel wall, doesn't it become thrombosis? Even if the clot is like a plug, it has to be attached to the wall, right?
In short, what is the difference between a clot due to a wound and one thrombosis (due to the Virchow's triad)? Where are the clots attached in either cases?

Thrombosis is formation of clots without injury due to reasons like ineffectiveness of heparin. Yes, clots are formed on the side of blood vessel, so they prevent blood leakage, not blood flow.

Here are a couple of distinctions,
1) The thrombus is the actual blood clot
2) Thrombosis is the condition of having a clot form in the blood vessel.
3) If the thrombus breaks away and becomes capable of traveling to some distant site, we refer to that as an embolus.
4) If the embolus lodges somewhere disrupting blood flow, we call that embolism, or in the case of a thrombus, thromboembolism.
So referring here, a protein called tissue factor is expressed on the outside of blood vessels, and when ruptured, is exposed to the blood stream that carries Factor VII. This initiates the coagulation response, and through the action of these factors you get platelets sticking to the endothelium, thrombin cleaving fibrinogen to fibrin that sticks to the platelets, and the fibrin/platelet plug forming over the wound is like a gel and RBCs become mired in it. So really, the thrombus is stuck to the endothelial wall.

so thrombosis is a thrombus occurring without an injury?

With or without, there are blood pathologies that can cause clotting without significant injury, such as A-fib, which is particularly dangerous because those thrombus tend to embolise.


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How do CD 8+ Tc cells reach the site of tumors?
In normal humoral immunity, dendritic cells present antigens to the Th cells by arriving at the Lymph node. This is fine. But consider a tumor cell. How does the Tc cell sitting in the lymph node know that there is problem out there? Consider there is a single cell which has undergone mutations and is expressing altered proteins. This wouldn't cause much inflammation to attract the Tc cell there.
So, is there continuous surveillance by the Tc cells? Where exactly do the Tc cells reside? Do they roam around like Th cells? How about the NK cells? do they too roam around in the tissues?
Cases of viral and intracellular pathogens, there may be some inflammation which draws the Tc cells there. Maybe. This can not be in tumors. So how do the Tc cells reach there?

T cells are not only present in the circulation, they are also present in the tissues.

I'd read through Trafficking of T Cells into Tumors.

Depending on tumor type, there can be plenty of inflammation inside it.

I do not remember enough details to share a mechanistic insight.
However, chemotaxis is a likely answer, which basically means moving along concentration gradient of certain ligand of interest.
Also relevant to your question: a hypothesis called 'immune surveillance' gaining support over the past few years.
http://www.biolegend.com/cancerimmunoediting

So if immunosurveillance is actually occurring, in the case of humoral immunity, why do the dendritic cells have to travel all the way to the lymph node? If there is surveillance, the Th cells themselves will be at the site. Doesn't movement of both Th and Dendritic cell reduce the probability of contact?