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Is it possible to induce erysipelas to treat cancer, under the condition that the patient is to be given antibiotics to control the erysipelas?
Dr.William Coley was one of the first to attempt fever therapy on cancer patients. He did this experiment: artificial erysipelas to treat cancer.
Coley injected Streptococcus pyogenes directly into the tumor.
My question is: if we repeat a similar experiment today, (under the condition that the patient is to be given antibiotics to control the erysipelas to avoid the ethical debacle), is it possible to develop this as a cancer immunotherapy treatment?

Welcome to Biology.SE. Ethics (incl. bioethics) is a subfield of philosophy. You should ask your question on philosophy.SE.

@Remi.b I very much doubt this question would be welcome on philosophy.SE

@har-wradim How about Philosophy.SE > Biology progress and bioethics.

@Remi.b Maybe, but I believe we are in a better position to address this question: see my initial attempt.

See also, wiki > ethics. Ethics or moral philosophy is a branch of philosophy that involves systematizing, defending, and recommending concepts of right and wrong conduct.. If you think users of Biology.SE are good at answering this question, then they should do so on Philosophy.SE. Note that there are already about a 100 posts tagged ethics (see here) on philosophy.SE.

My point is that this is more a procedural question: note the "considered", "standards" and "develop ... as ... treatment". The question is not whether such an undertaking would be ethical, but whether it is at all technically possible in the context of todays ethical standards as accepted in medicine and biology.

@har-wradim this is a good point, I now agree with you. I am unsure whether it is on-topic here but it would not be on-topic on philosophy.SE. Maybe Academia.SE would be a place to consider but I don't know. In the meantime I retract my close vote.

I've suggested reopening as the question is now no longer an ethical one, but is more succinctly speaking "Can a heightened immune system influence cancer treatment"? Still, the question needs further references, and perhaps a better developed explanation of the theory behind why such an idea might work.

I'd suggest that the question was closed because it was a question of ethics, I don't think suggesting the treatment is given with antibiotics to avoid ethical issues solves that, you can still just ask whether and how the treatment would work

Before any experimentation on humans, any treatment undergoes an extensive testing on animal models.
Besides, there must be some degree of confidence in the potential curative effect of a remedy in order to start experiments in the first place. An experiment like the one you describe would not be approved by your institute's animal ethics commission (there is such an unpleasant but important thing) unless you prove with some line of evidence and prior knowledge that the suffering of the animals is likely not going to be in vain.
It is now also customary to provide an official approval from the ethics commission during publication submission. [You would not need such an approval for flies or worms, but for rodents (which would likely be your first test object in the case in question) or primates you would.]


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Identification: Is this really a case of Progeria?
There are some news about a boy being born in Bangladesh that looks very aged and presumably has Progeria: http://metro.co.uk/2016/09/29/newborn-baby-who-looks-like-an-80-year-old-after-being-born-with-rare-ageing-condition-6159215/
To my knowledge, humans born with Progeria looks quite normal at first, and it's not until after birth that the associated symptoms start to develop.
Is it plausible that this actually is a case of Progeria? Is there any other syndrome that would better match the appearance of the boy?

Not that it matters, but it appears the baby was born in Bangladesh.

@SrihariYamanoor Thank you, I've corrected it.

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Conjugation in bacteria
I was studying about conjugation in bacteria, I have a doubt. In conjugation F- cell transforms into F+ cell when there is a formation of sex pilli in between the two. The doubt is if the F- cells convert into F+ cells how can F- cells form again...?
If all the F- cells convert into F+ can we expect F- cells to form again?

Within a bacterial cell exists circular chromosomes, and plasmids. During cellular division, chromosomes are always conserved - passed to both daughter cells.
As you are aware, plasmids can be passed between cells by a form of horizontal gene transfer called conjugation - whereby plasmid DNA is replicated, and passed through a sex-pilli into an adjacent cell.
When a cell divides in to two daughter cells, it is possible that one cell will not receive a plasmid. Thus, the result is one F+ daughter cell, and one F- daughter cell.

The partitioning of the F plasmid between daughter cells is tightly regulated https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gkr457. Loss of F takes place if this mechanism fails.

That's an interesting article. But regardless of mechanism, I think the important point to OP's question is the fact that reversion to F- cells can occur during cellular replication.

Agreed, I was commenting on the (now deleted) use of the word 'stochastic' which conjured up a picture of a rather random process. Clearly it isn't. I certainly wasn't suggesting that loss of F can't happen, but I haven't found any data on how frequently it does happen. Probably that is to be found in very old literature.

As extra genes generally cause increased stress to a cell, unless the cell is actively taking advantage of plasmid DNA, I believe they will get rid of them. But I do disagree with your statement that plasmid replication does not ever display stochastic characteristic. http://www.sciencedirect.com/science/article/pii/S0147619X14000559?via%3Dihub

What about the process of duplication of plasmids and the production of pilis? My understanding of comments is that it's connected: duplication of plasmids (that is not that trivial to me, should be mentioned) should be a prerequisite for sex pili transfer, so no pili without duplication? I mean,  there's more than "never get lost on you" than a very good song.

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What is the difference between Endoproteinase Lys-C and Lysyl endopeptidase?
What is the difference between Endoproteinase Lys-C and Lysyl endopeptidase?
In the text I'm translating about peptide mapping, "lysine protease" is mentioned (in Russian: лизиновая протеаза). This might be erroneous to translate word for word as "lysine protease". There must be a slight error in the original text. This "lysine protease" is mentioned there due to its use in protein hydrolysis.
I guess that the correct translation might be either endoproteinase Lys-C or lysyl endopeptidase.
I found that endoproteinase Lys-C is used in peptide mapping. Is it synonymous and interchangeable with lysyl endopeptidase, or do they differ in their function? Is endoproteinase Lys-C used more often as a hydrolysis agent in peptide mapping?
Maybe the difference is that endoproteinase Lys-C cleaves "on the C-terminal side of lysine residues", while lysyl endopeptidase cleaves on both sides?


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Genetic entropy
One day my internet acquaintance told me, that genetic entropy can be evidence in favor of intelligent design and he also provides me this waiting time problem and this simulating evolution by gene duplication. I took a dim view of that point, but because i'm not geneticist i can't answer this question and i don't know much about genetic entropy as well. I'm not an internet troll, but i don't like when religion breaks into science, so help me to understand how can we explain it using our knowledge and logic.
Thanks.

What is your question? I can't see any interrogation point!

Also, your post might be a possible duplicate of this one.

I'm afraid this list doesn't exist to help users rebut arguments from third parties that they are unable to formulate themselves. I have never heard of genetic entropy, and acceptable questions do not require me to go elsewhere to read about it. I am therefore voting to close this question as unclear.

I'm new to this idea but did a bit of searching.  The origin of this idea of "genetic entropy" appears to be a guy named John Sanford. He is also the author of the "waiting time problem" you reference. The principal author of the other reference you cite is Michael Behe. Both of these guys are ardent creationists. This means they have an agenda. Good science is the product of good questions, it does not result from attempts to support preconceived notions. This especially applies to religious ideas since they are generally strongly held.
Further research into the "genetic entropy" idea suggests that Sanford has basically repackaged an older idea but with a decidely creationist slant. That original idea is termed Muller's ratchet. https://en.wikipedia.org/wiki/Muller%27s_ratchet
The conclusion of Hermann Muller, inherient in Muller's ratchet, is that his concept supports the rise and importance of sexual reproduction. I find no mention of creationism, this seems to be Sanford's addition to bolster his agenda.
If you really want to delve deeper into the flaws in the arguments of these two creationists:https://letterstocreationists.wordpress.com/stan-4/ This site contains an extensive list of links to rebuttals to the claims of these two men.


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Should heart-to-body energy consumption ratio equal oxygen consumption ratio?
The human heart pumps oxygen to the body, and the heart itself requires oxygen.
Both the body and the heart use energy, usually expressed in calories or ergs.
If we look at the energy consumption (in Watts) of the heart as a fraction $F$ of the energy consumption of the body as a whole it is about
$F \approx \frac{1.3}{91.3}=0.014.$
Humans consume about 550L of oxygen per day per this website and the heart itself consumes about 8 ml of $O_2$ per 100g per minute at rest according to this site. Assuming an average global human heart mass of about 310g (Google) the daily total heart oxygen consumption is about  (8ml x 3.1 x 1440 min) = 35712 ml or 35.7L of oxygen. The ratio $R$ of heart to body oxygen consumption is thus about
$R \approx \frac{36}{550-36} = \frac{36}{514} =0.07$
These figures are rough at best but not rough enough to account for a discrepancy of a factor of 5 in the ratios. Can someone suggest what might account for the difference?
The calculation seems to show that the heart's proportional consumption of oxygen is a lot higher than its proportional consumption of energy. My understanding is that the respective oxygen consumption of the heart and body are a good reflections of their respective energy consumption. Is that a sound assumption?
Thanks for any insights.

This is a really stupid question from me to you. Do you mean to say 7% percent when you say factor? But then you say factor in the ratios. Do you mean the consumption of heart versus body ratio amounts to 7? If so, I am not sure the word ratio is mathematically applied, but I might just be confused.

Also, I think oxygen consumption most likely varies by cell/tissue type. Cardiac muscles may consume more per sq.m or cu.m compared to skeletal tissue and smooth tissue. You are also probably right in that resting heart rate might lead to a more steady, lower consumption rate. Other tissue, might consume even lesser than muscle tissue, etc. So maybe heart to body rate consumption is not all too meaningful. You could look at cardiac to overall muscle energy consumption, etc.

@SrihariYamanoor: I may have worded it badly. What I mean is that 0.07 is very roughly 7 times 0.014. It should be 5 and I will edit. Yes, I mean that the heart's proportional consumption of oxygen seems to be a lot bigger than its proportional consumption of energy. Does this help?

@SrihariYamanoor: Yes, yours is a possible explanation. My assumption has always been that oxygen consumption mirrors energy needs. Maybe that is wrong?

In the case of the heart, aerobic metabolism is necessary for it to work. But that's not the case for all tissues (some have significant anaerobic metabolism). The difference being only 6% that would not strike me as too much of a stretch to explain it this way, but I have nothing reliable on the subject so that's just speculation.

@ElianeB.: How do you reckon 6%? (Not saying you are wrong...)

0.07-0.014, considering the total energy expenditure/total oxygen consumption. That's ~7 times but also absolute value 6% of total expenditure.

At first glance there are a few major issues with your calculation and assumptions.

You're comparing the energy output in work (pumping action) with the energy consumption of the rest of the body in input (oxygen consumption). I don't know how efficient the heart is, but I'd guess only somewhere from 20-40% of input energy is actually converted to pumping action.
Oxygen consumption is correlated with energy consumption, and would be a good way to measure energy consumption if you know exactly what the subject is burning. However, if you have a big difference between the preferred fuels between the heart and the rest of the body, this doesn't really apply  anymore. A quick google leads me here: https://www.ncbi.nlm.nih.gov/pubmed/17081788, showing that the heart prefers to burn fat over glucose, and this creates a significant difference:

Carbohydrate oxidation typically generates approximately 120 kcal per mole of respired oxygen, whereas fatty acid
  oxidation typically generates only approximately 100 kcal per mole of oxygen.

This means that the heart needs more oxygen than the rest of the body to generate the same amount of energy.
I think combined this could explain the 5-fold difference.

You say you compare consumption, but the link you use actually has a list of outputs, based on the mechanical work of the heart. One of the lines actually reads: "The mechanical power of the human heart is ~1.3 watts. It takes a much higher rate of energy turnover (~13 watts) to provide this mechanical power, since the mechanical efficiency of the heart is very low (less than 10%)"

And the 6% of Eliane B is relating to something completely different. The difference between one calculation and the other is 5x, that this number is also only 6% of some larger number doesn't really change that.

The only thing is that 1.3 watt is not the input, it's the estimated output. You can infer this by looking at the numbers they use for their estimates: all numbers related to the output power, not input.

Come on! In the second line you cite they even write Pmech = 1.71 (Nm)/s and Pchem = 8.6 (Nm)/s. There's your 5-fold difference.

Let us continue this discussion in chat.

There is a figure from an article in Cont. Rev. in Card. Medicine that suggests your figure of 20% efficiency is quite good. I don't really trust the figure 1.3W but if we use it there is no explaining to do and it seems that the heart's proportional energy consumption is pretty much the same as its proportional oxygen consumption. Here is the link for 20% (Appendix A): http://mathscinotes.com/2014/11/heart-energy-per-day-versus-truck-energy-consumed-over-20-miles/. If you edit your first paragraph to show your comment calculation I will accept. You were right. +1

Oh--and the second paragraph is not really necessary. Since your first point seems to eliminate the discrepancy there is nothing left to explain.

Since you took the trouble to debate this I am giving the 50 pts and will also accept if you edit your answer just a bit. Don't want it to lapse before you return to the site.

You are comparing the theoretical mechanical work performed by the heart (your 1.33 W number) with the chemical energy consumed in accomplishing that in a biological system. One is theoretical and one is empirical. The heart in fact consumes about 10% of the energy of the body even though it’s only 1% of the weight, owing to the special nature of cardiac muscle tissue (which is unique to the heart organ). It’s a “design” that can go nonstop for one billion contractions or more, and which would have been ludicrously inefficient to use for skeletal musculature. Your 5x factor is in line with typical efficiency measurements of muscle work, around 20-25%.

Cites would help. Your 10% is not in line with the sources I checked (doesn't mean it's wrong).

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Tools to analyze RNA-seq data
I hope this is a good place to ask such question. I have to do some data analysis on RNA-seq data from human cells. I am currently searching for tools to help me with that. Specifically, I would need some tools to analyze the gene expression from the data. Something to help me plot the expression of selected genes in each fastq file and compare the differences in the expression with the possibility to export the results or some command line interface for scripting. Basically I need something where I can put a fastq file and perhaps also a human genome annotation file as input and get gene expression as output. I have looked at bioconductor and it's packages and on Wikipedia's List of RNA-Seq bioinformatics tools. I suppose some of these tools have to be able to do what I need, but I have been unable to find out which one and how should they be used to achieve that. Could someone please give me some advice?

I suggest you start from a good reading first - something like RNA seq Data Analysis.

You will likely need a tool to "map" the reads on the reference genome.
You may find such a reference genome, together with annotations, here:
ftp://ussd-ftp.illumina.com/.
Mapping tools such as bowtie2 or bwa take fastq files and reference genomes and output mapping results in a format called sam.
You then have a lot of options to estimate gene expression.

You can write your own algorithm to parse sam format and estimate normalized read counts on each gene.
You can combine more or less low-level tools such as samtools, pysam, htseq with some scripting to do this.
You can use tools that do the counting (like bedtools ot htseq-count) and differential expression analysis (like deseq2).

In the last case, I would advice to start from the documentation of the final tool to find out what are the tools you need to generate the output of the preceding step.
It is very likely you will use some R or Python, or use the web platform galaxy for some of the steps.
Edits
As mentioned by @scribaniwannabe in this answer, the paper about the Tuxedo suite of tools gives a good example of the steps to carry out an RNA-seq analysis using recent tools (as of October 2016).
As @Student T reminds in this answer, RNA-seq data contain reads that can come from exon-exon junctions, so the read mapper has to be set up in such a way as not to discard reads not mapping continuously on all their length on the genome. To my knowledge, HISAT2 and CRAC do this by default. Bowtie2 needs special settings.

TopHat is the part of the tuxedo suite that does splice-aware mapping.

@swbarnes2 You are right concerning the older tuxedo suite (the new one uses HISAT2). Curiously, TopHat uses bowtie2 internally, and it seems that it doesn't use the "--local" mode (look for "local" in the tophat executable, which happens to be a complex python program). I don't know how it achieves splice-awareness.

While I also agree @bli that R and Python (in particular Bioconductor) have more than enough packages for you to compare gene expression. You shouldn't align your reads with bwa or bowtie because they don't take introns into consideration. You should use TopHat or STAR.

You're right, although bowtie2 can be used with the --local option to avoid discarding reads mapping on exon-exon junctions. Other aligners that could be used are HISAT2 https://ccb.jhu.edu/software/hisat2/index.shtml and CRAC http://crac.gforge.inria.fr/.

The answer @bli gave is great. I thought I would point out that Johns Hopkins also recently upgraded their tuxedo suite. Looks promising and has great instructions for use.
Also, I've begun to grow quite fond of the GeneTrail 2 tool for my RNA-Seq secondary analysis. Gives great results for enrichment analyses.
Hope this is helpful.

Lastly, I also like to use [HOMER][3] for de novo motif finding up/downstream of the promoter regions of deferentially expressed genes.
[3]: http://homer.salk.edu/homer/motif/

Thanks for the link about the tuxedo suite. The explanations in the article seem useful.

I think that STAR is the preferred splice-aware aligner nowadays.  STAR can output counts by gene or by transcript.  Assuming you have Illumina data, you can try using the tools on Illumina's BaseSpace.  RNASeq might be one of the things that you can do for free there.

pyrpipe claims to be a one-stop python library for RNA-seq analysis. Here is an illustration from their paper:

Furthermore, I would like to draw attention to ENCODE's official RNA-seq pipeline, which is actively maintained on ENCODE-DCC's GitHub repository.

I think HTSeq does almost that. It outputs a matrix of read counts per gene given a fastq sample and annotation file


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What snake is this?

Just caught this snake today and he was really aggressive...tried to bite me but luckily I managed to kill him and I wonder what type of snake is this. If someone knows, help would be greatly appreciated.
Thanks!
Edit: the snake was found in Italy near Parma

It would be useful if you could update the question to include where the snake was found.

A zoom on the head might be useful. Scale patterns are used to identify snakes.

It looks like a Balkan Whip Snake (Hierophis gemonensis (syn. Coluber gemonensis)):

More images:

Reptiles of Crete
Reptile Database
Balcanica.info
Wikipedia image

According to iNaturalist.org:

The Balkan whip snake is a slender snake with smooth scales usually under a metre (yard) long but exceptionally reaching 130 cm (50 ins). The head is fairly distinct from the body and has prominent eyes with round pupils. The head and front of the body are olive-grey or yellowish-brown with dark spots separated by paler areas which may form irregular bars. There are often small white specks on some of the scales. Further back the dark spots are usually arranged in longitudinal lines giving a striped effect.

This snake is not endangered ("Least Concern") but there was no need to kill it, since it is non-venomous; you were certainly not "lucky" to kill this harmless animal.

I dont think so, iaork. The speckes of the snake in the question are black sploches on a light green background. The snake you have pictured has speckles which are more angular. Also, they are not in the same pattern as the ones in griffinwish's picture.They aren' on the same light green backgrown either. The colors of the individuals in many snake species  can vary a lot, I don't think that is the case here.

Considering the location and general shape/pattern I would say Green whip snake. The genus is the same as the one from the previous answer, but these inhabit the mentioned location. They can vary in the coloration from very patterned, as in the photo, to completely black.

Non venomous, not dangerous and usually only aggressive when provoked, but they do bite...
edit1: Don't kill snakes...


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

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


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Enzyme inhibitors, reversible or irreversible?
So far, I know about competitive, non-competitive inhibitors and allosteric inhibitor. Which ones are reversible and which ones are irreversible?

These modes of inhibition are reversible. They describe a particular modification of the working of the enzyme (change of affinity, of maximum velocity, of both) due to the reversible binding of an inhibitor to a particular site.
On the other hand irreversible inhibition stops the enzyme from working through an inhibitor that binds irreversibly : no more transformation of substrate occurs after that. One cannot define a velocity, affinity, or IC50, for a non-working enzyme, thus "competitive", "non-competitive", "uncompetitive" are not useful concepts in that case.

Correct. Irreversible inhibitors basically reduce the concentration of enzyme rather than changin its reaction's' kinetics.


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How do messenger RNAs regulate each other's expression levels?
I know that researchers learn gene regulatory networks from microarray experiments that measure the mRNA expression levels. However, I do not understand how mRNAs regulate each other's levels. Do they affect the transcription step or the translation step? I know that there are transcription factors which affect the transcription step, but those are not mRNAs but proteins. How does an mRNA (the product before translation) affect another mRNA's expression level? Is this regulation process very similar to the regulation by microRNAs?

You say that "researchers learn gene regulatory networks from microarray experiments". I do not believe this is true. Microarray experiments just indicate which mRNAs increase or decrease in expression in a given situation. I suggest you either cite a paper to support your contention, delete the first sentence of your question or change the question to "How do microarray experiments show..." (to which I would say the answer is that they don't).

@David: We can argue about whether folks actually learn gene regulatory networks from these experiments, but they definitely claim to!

Yes, they claim to, that is what I mean. Bu the first sentence is not really the point here. We can even completely delete that sentence if that is confusing. What I am wondering is whether mRNAs have any regulatory role on gene transcription before they are translated to proteins.

Typically, these experimenters aren't thinking that the mRNAs directly regulate each others' expression levels, but rather that the proteins they code for affect expression. They're just mRNA as a proxy for the corresponding protein.

Thanks! Don't the mRNAs regulate gene expression at all while they are mRNAs (before being translated to proteins)? Maybe there are mRNAs transcribed but that are not translated at all, and have some function in gene regulation? Do you have any ideas?

I am a beginner and I liked your question. As @Daniel Weissman pointed out, proteins are coded by mRNAs, so the proxy is such a powerful analogy here. A coding error (horror), as it seems.


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Identification of Insect found on beach in Maharashtra
 Six legs, two antennas, Neon green colour pattern with black. Had no wings.

This appears to be a Lychee Shield Bug, Commonly found in India, formerly considered a beetle, but now classified as a True Bug.

You should add some more details, maybe with some authentic images, to support your answer.

This is a Lychee Shield Bug, Chrysocoris stolli, also known as jewel bugs or metal shield bugs. See this picture from the Wikipedia:

Some more information can be found here and here.

What's wrong with the answer?

Probably that the question was already answered, only without picture and link.

@AlexDeLarge Since I don't think the other answer is very good (neither referenced, nor has it an image) I decided to write another one. And I don't expect it to get better, as it is now four weeks old.


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What prevents the human intestine from 'exploding' as a consequence of bacteria growth?
Usually bacteria grow by dividing and they can do that very fast. So after a couple of hours or days you have many bacteria in your intestines.
And we keep feeding them by eating. In some way you would expect that the growth of bacteria has been so overwhelmed that after a week our intestines would 'explode'.
Of course this doesn't happen, but what factors protects our intestines from bacteria overgrowth?

I have a feeling stomach acid is to play here, but I can't seem to find any sources at the moment

The intestine actually has specialised immune cells just for itself, much like it has a specialised nervous system. I can't provide you with a detailed overview as it's been a while since I've studied intestinal immunology, but one component that I do remember is the secretion of specialised IgA antibodies which to some extent could regulate the baterial load in the intestine (and certainly regulates the types of bacteria "allowed" to grow there).

Bacteria also regulate themselves so as to not overwhelm their surroundings. The gut microbiome is an incredibly complex place, with multi-species biofilms that signal amongst themselves to prevent the outgrowth of any one species. The host's immune system is also involved to a significant degree. Remember, these are not laboratory-grade E. coli growing in Luria broth, and they are not pathogenic. They are symbiotes with the host, and both participate to not overwhelm the other.

If you take a nutrient agar and do a lawn culture, the bacteria won't grow on forever. There's a limit to the max population. This is without considering the host's immune factors which would play a major role in the gut

Bacteria can't create mass, even when they divide. During division, you go from one "big" bacterium to two "little" bacteria, which then have to accumulate nutrients and grow bigger before they can divide again.
When nutrients are plentiful, this can happen rapidly, and you do see exponential growth. But the exponential growth phase is only valid when there is an excess of food in the environment. Bacterial growth curves follow a typical lag/log/stationary/death profile. The log (exponential) phase only applies when nutrients are in excess. Whenever some nutrient becomes limiting (because it's already incorporated into another bacterium, for example) the bacteria switch to stationary phase growth, and reduce replication or stop it completely.
So you would never get an "explosion" of intestinal bacteria - the bacterial mass is strictly limited to the amount of mass (food) input into the system. Once that's all (or mostly) converted, the bacteria will stop growing and start dying.
If you kept accumulating mass in your intestine, you're correct that eventually it would "explode". However, most people regularly (pun intended) eliminate excess intestinal contents. (Which, as bpedit mentions in their answer, contains a high proportion of bacterial cells.) This limits the total mass contained in the intestine, and keeps it from "exploding".

There are very likely other factors at work as well, I'm no expert. But the following always surprised my Biology students.
About 30% of feces is bacteria.
http://bionumbers.hms.harvard.edu/bionumber.aspx?id=108514
Peristalsis continues to move food, food waste and bacteria through your digestive system. So, as new bacteria arise, other bacteria are eliminated.


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How is 16s rRNA used to identify unknown bacteria?
How is 16s rRNA used to identify unknown bacteria?
With PCR the 16S rRNA is amplified and sequenced, but how can you identify the bacteria with this 'piece of knowledge' if the 16S rRNA is conserved and so the same in all bacteria?

Welcome to Biology SE change. The area of this question is valid, but it is very basic. We do expect people to use web resources first to try to answer questions, and I am sure you could have found something by Googling. If the articles you found were still unclear to you, then would be a better time to ask for help here.

It is not conserved, its sequence is not the same in all bacteria. Indeed, it has a slow rate of evolution (mutation) that make it perfect to build phylogenetic trees.
As correctly suggested by David in his comment, here are some references about the 16s rRNA and on how it is used to identify known and unknown bacteria.
http://www.sciencedirect.com/science/article/pii/S1369527499800526
http://nar.oxfordjournals.org/content/38/22/e203
https://www.ncbi.nlm.nih.gov/pubmed/18828852
https://www.ncbi.nlm.nih.gov/pubmed/27388368
https://www.ncbi.nlm.nih.gov/pubmed/27659439
https://www.ncbi.nlm.nih.gov/pubmed/18353221
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760787/

You are correct, but you should provide a reference, even for something so simple, so that the questioner and others can check and find more info. I imagine there is a Wikipedia article or a NCBI Bookshelf chapter you could cite.

That's fine. I've upvoted your answer now.

There are two different kinds of conserved here that people are perhaps using a bit carelessly.
The 16S rRNA is conserved, meaning that it's present in all bacteria (and archea, mitochondria and chloroplasts). However, it's not conserved in the way that the sequence is 100% identical in all bacteria, it just evolves quite slowly (it has a low rate of mutations).
https://en.wikipedia.org/wiki/16S_ribosomal_RNA

See my comment to @alec_djinn.


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On enhancers, strands, and zygosity
I came across a passage on enhancers that sounds out-of-whack to me:

...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).  This is unlike a protein-coding DNA gene, which might need to be on both DNA strands——in a so-called homozygous state, in order to surface as a phenotype——like the classic case of blue eyes.

This is what makes no sense to me, since, AFAICT, whether something is in one or two strands has nothing to do with zygosity.
The authors continue:

And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands.  The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

Is there a grain of truth in what the authors' write, despite their muddled explanation?  IOW: does the fact that enhancers "sit on just one of DNA's two strands" somehow facilitate "evolutionary tinkering"?

Firstly, the author is deviating from traditional jargon when he tries to represent different strands as paternally of maternally derived DNA. Finally does the author add some sort of example for his statement? More so, I would be very interested how you decide an enhancer sits on either the maternal or paternal DNA.

The two authors are a computer scientist and a linguist (from the Amazon description), which explains everything - they are not biologists, and don't know what they're talking about.

...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).

Yes and no. Enhancers are in fact sometimes palindromic, so they're mirrored on both strands of the DNA.

This is unlike a protein-coding DNA gene, which might need to be on both DNA strands

No. Protein-coding DNA is always on one strand only because transcription doesn't suddenly switch strands.

in a so-called homozygous state, in order to surface as a phenotype - like the classic case of blue eyes.

No. Homozygous means on both chromsomes and has nothing to do with strands or the need for an allele to be homozygous to produce its phenotype because it's recessive.

And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands. The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

This is completely all over the place and makes no sense to me. Either "strands" is used in the correct way, in which the previous statement is wrong, or "strand" is used as "chromosome", in which case there is no reason why an enhancer should only be on one chromosome. Just like the gene, it can be hetero- or homozygous. The statement about "having to wait for a change on both DNA strands" is more relevant to whether something is dominant or negative. Regardless, I don't think it's possible to make any statements here about enhancers allowing for evolution to progress faster.


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Understanding of the saturation function in the Monod-Wyman-Changeux Model
I am reading Mathematical Physiology, Sneyd. I am a undergraduate mathematician interested in pursuing the field, so forgive me if my terminology is off. In this example, the writer considers a protein with two binding sites. The subscript $i$ indicates the number of bound ligands.
This expression, called the saturation function, appears on page 18:
$$Y = \frac{r_1 + 2r_2 + t_1 + 2t_2}{2(r_0+r_1 + r_2 + t_0 + t_1 + t_2)}$$
Where, $r_i, t_i$ denote the concentrations of chemical species $R_i, T_i$ respectively.
It looks like the weighted average of the ezymes that have occupied binding sites.
The fact that $t_0, r_0$ do not appear in the numerator suggest that it is the saturation of enzyme binding sites,  the $2$ in front of the $r_2,t_2$ indicates that the enzyme with both binding sites occupied is "double concentrated". The two on the denominator indicates the number of available binding sites in the enzyme. Perhaps, if we were considering an enzyme with three binding sites:
$$Y = \frac{r_1 + 2r_2 + 3r_3 + t_1 + 2t_2 + 3t_3}{3(r_0+r_1 + r_2+ r_3 + t_0 + t_1 + t_2 + t_3)}$$

Would this description be correct?

can you give a more precise reference to the book (Sneyd has apparently authored/co-authored several books ...) ?

ISBN 978-0-387-75846-6 Mathematical Physiology Volume 1: Cellular Physiology

I don't have access to Sneyd's Mathematical Physiology, but in Wikipedia's description of the Monod-Wyman-Changeux model, they call Y the "fractional occupancy of the ligand binding site". Other references refer to it as the "fractional saturation".
In other words, it's simply the fraction of the binding sites which currently have ligands bound to them. The denominator, then, is the total number of binding sites, which is equivalent (for a unit volume) to the total concentration of the protein (i.e. the sum of every protein form) times the number of binding sites per protein.
The numerator is the number of ligand-bound binding sites. Which is equivalent (for a unit volume) to the concentration of each form, multiplied by the number of ligands bound to it. So the zero-ligand forms are multiplied by zero, the one-ligand forms are multiplied by one, the two-ligand forms are multiplied by two, etc. (This doesn't reflect "doubly concentrated", rather it reflects the stoichiometry: for each protein molecule in the 2-bound state, there are two ligand molecules bound to it.)
So the answer to your boxed question is yes: that would be the appropriate form for a cooperative protein with three binding sites.


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How is the antigen against which autoantibodies are formed, identified?
Say we suspect some new autoimmune disorder in a patient, and we collect blood for serology.
How are self antibodies differentiated from normal ones in the collected sample?
Once they are identified, how is the antigen towards which it is directed known?
Are there assays for this? Or is it identified by the structure of the variable region? Can a simple IHC be done on all body tissues using the purified isolated antibody to localise the protein?
I mean, what is the root for suspicion of an antigen? Like, what caused ANCAs (anti-neutrophil cytoplasmic antibodies) to be suspected in systemic lupus erythematosis (SLE)?

All of the above, basically. If it's a protein antigen, you can perform an immunoprecipitation with the auto-antibody and use any one (or more) of several methods (Western blot, various methods of sequencing, etc.) to identify the binding partner(s). DNA and RNA can be identified easily by biochemical means. You can also use ELISAs or similar methods like electrochemiluminescence which allow a greater degree of multiplexing.
Sequencing the autoantibodies' variable regions may give some information about the structure of the antigen, but not enough to actually identify the binding partner. Also, one key fact to keep in mind is that the antibody response in many autoimmune diseases is polyclonal (just as the T cell response often is), meaning there could be dozens to hundreds of different complementarity-determining regions (CDRs) to sequence, a very laborious process that may not yield much information.
Immunohistochemistry (IHC) can be useful for seeing which cell types the antibodies bind to, but it doesn't give great resolution on the subcellular level, and doesn't tell you anything about what the actual target is. Additionally, due to the amount of chemical processing a formalin-fixed paraffin-embedded (FFPE) tissue goes through, the antibody's antigen may not be exposed properly for the antibody to bind.
From what I can find, people suspected an association between ANCA and lupus due to the similarities in both diseases' clinical presentation. Here is a paper from 1996 talking about it, there are many others.

Thanks! How do you identify the autoantibody from the antibody chunk that's out there roaming around?


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Mitosis and Colchicine
I'm preparing for an Olympiad and while I was going through some of the old papers I found a question. I googled it but a lot of people have different answers to it. Please help.
A student treats some onion root tips with colchicine that is responsible for arresting cell division at the metaphase stage (by dissolving spindle fibres) and further prepared a slide of the root tip staining with acetoorcein (stains chromatin) and observed under high power of compound microscope. He is well aware of the cell cycle given alongside.
Question: Which of the following is not true about his observation?
a) Most cells are in Interphase
b) Most cells are in the metaphase
c) No cells are in anaphase or telophase
d) Chromosomes could be observed better than a slide prepared without colchicine
treatment.
According to me the answer should be (c) because if colchicine arrests cell division at metaphase, anaphase and telephase being the subsequent processes would not happen. But a lot of people are saying it should be (a) or (d). I'm stumped, any help would be appreciated.

Single answer question, I presume ?

The question is asking which is NOT true.  You are correct that C is true - very few cells should be found in anaphase or telophase.
D is also true.  When spindle fibres are dissolved, chromosomes/chromatin would not be tightly bundled or packed in the cell and it would be easier to see them with an acetoorcein stain.
A and B are trick answers.  In a regular tissue, most cells are in interphase at any given time.  Interphase is the regular functioning period for the cell.
However, the question is referring to onion root tips which are primarily comprised of actively dividing cells (meristem tissue). The colchicine would affect most cells and most cells would be found arrested in the metaphase.  http://w3.marietta.edu/~biol/introlab/Onion%20root%20mitosis.pdf
Therefore for onion root tips treated with colchicine, most cells are not found in interphase.  A is the correct answer.


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How close genetically is the most human-like chimpanzee to the most chimp-like human?
I understand that:

Chimpanzees are the closest species to humans genetically. Only 1%-6% of their genes are different.
Within any species there is genetic diversity, i.e. no two individuals have the same exact DNA sequence.
This variability applies to humans and chimps.
Thus, there exists a pair consisting of a human and a chimp that will have the smallest number of different (edit: genes) DNA base-pairs within the two populations. One can say that the pair forms an "inter-species genetic gap".

Question: What is the smallest estimated inter-species genetic gap between humans and chimpanzees?
Edit: I changed the last point to base-pairs instead of genes. Most of the comments seem to suggest the population genetic variabilities are much, much smaller than the genetic distance between the populations. Visually, that looks something like this:

Is this a fairly accurate picture of the human-chimp genetic distance?

This closest pair of human-chimp is probably very negligibly more related than a random pair of human-chimpanzee. (But I haven't go through any evidence it is just a gut feeling).

As far as I know, all humans have the same genes. Ditto for chimps. Variations within humans aren't due to possessing different genes, they are do to having different variations (alleles) of the same portfolio of genes. Again, ditto for chimps. Your fourth point is suspect as applied to genes. Although, it is possible for a particular chimp and particular human to share a more similar package, compared to other individuals, of alleles for the genes that are in common.

@bpedit In reaction to: Variations within humans aren't due to possessing different genes, they are do to having different variations (alleles). There is lots of copy number variation in humans (Redon et al. 2006).

I updated the last point, changing genes to base-pairs. That seems to be a more clear way to phrase the question.

Do you expect a theoretical expectation or an empirical observation? Empirically, I am afraid we have sequenced way too few chimps and sampled humans for sequencing in a way that is way too biased (96% of sequenced people are from european descent) to answer this question. One could probably draw some conclusion from theoretical work though.

I see. Right, it would basically require sequencing every human and every chimp to get the exact answer. I think even something that approximates the gap between the 95% CIs of the two populations would be acceptable.

But would you be happy with a theoretical prediction (which I could do but it would take me some time; would be a good exercise for me though) or are you looking exclusively for an empirical observation.

Yes, theoretical prediction should work as well.

You may be interested in this 2005 Nature paper from the Chimpanzee Sequencing and Analysis Consortium: Initial sequence of the chimpanzee genome and comparison with the human genome. It breaks down the most common categories of genetic variation:

Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.

So if we accept their analysis, ~1% (it says "or less", but elsewhere in the paper they estimate a lower bound of ~0.96%) of the genome difference consists of fixed single-nucleotide differences between species.

Small insertions and deletions: On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies.

So another ~3% comes from small insertions and deletions, which gives around a ~4% fixed divergence between populations. This rough estimate of the fixed genetic distance between humans and chimpanzees is probably a reasonable estimate of the distance between the nearest human-chimpanzee pair.
If you also want to know how far apart the two furthest humans are, as @Remi.b mentioned, the populations we've sequenced don't span the whole diversity of our species, but it is likely much smaller. You could look at some of the HapMap or Human Genome Diversity Project papers. For reference, when Watson's genome was sequenced, they reported around 0.1% of the sequence to be different from the reference genome, but that isn't a particularly diverse comparison.
You may also be interested in this paper comparing the human, chimpanzee, and bonobo genomes: http://www.nature.com/nature/journal/v486/n7404/full/nature11128.html.

The answer given by leekaiinthesky and partially in the comments on the question give a good general picture. I also think that the variation within the respective species is way less than between the species. Keep in mind that also archaic humans like Neandertals fall outside of the variation of present-day humans when you do a genome-wide (nuclear genome and mt-chromosome) comparison (see Briggs et al. (2009) for the mt-genome, and Green et al. (2010) for the first draft nuclear genome and Prufer et al. (2014) for the high-quality genome. Looking at Meyer et al. (2012) you see that even Denisova genomes falls outside of Neandertal variation for whole genomes); this means that looking at phylogenetic trees of either nuclear or mt-genomes, the Neandertal always forms an outgroup, independent from what present-day human populations you are looking at. This is roughly quantified to 1% difference between humans and chimpanzees, 0.2% difference between present-day-humans and Neandertals and 0.1% difference within present-day humans. The latter two seem to be fairly close, but: there are no fixed differences between present-day human populations, and this will blur the differences in intra-present-day human populations compared to the differences of present-day humans and Neandertals or chimpanzees.
However, there is one aspect that has not been discussed here which I think is very important for your considerations: trans-species polymorphisms (TSP). In the first part of my answer I was careful to always pronounce that major differences can be observed genome-wide, but genomes have a mosaic structure. When you look at specific parts of the genome, i.e. genes or haplotypes, these major differences do not hold and TSP are a very interesting special case of that. TSP are basically just gene variants, i.e. alleles, that are shared between species. This means that individuals between species might have the same variant, but individuals from the respective same species might have other variants. In simple terms this can be seen as individuals between species are more closely related at a given gene locus than individuals within species. Shared polymorphisms between species can in principal be caused by three mechanisms: (i) Genetic admixture and introgression, (ii) molecular convergence and (iii) TSP by either incomplete lineage sorting or splits in the lineage of alleles that predates the split of the species and both alleles are maintained in both species [Těšický and Vinkler (2015)]. This figure from Těšický and Vinkler (2015) shows the three mechanisms (see the green genealogy for an incompletely sorted lineage and the red genealogy for a lineage with an early allele lineage split).

The first two are fairly unlikely in our case, even though there is some evidence that admixture between humans and chimpanzees happened after the initial lineages split [Patterson et al. (2006)]. Incomplete lineage sorting or early splits in the allele lineage, i.e. the TSP variants are identical by descent, can be seen as TSP in a narrow sense. And this type of TSP has been described between humans and chimpanzees especially for immune-related regions (see Azevedo et al. (2015) for a review) that are under long-term balancing selection. You can think of this as a selective pressure that is fairly constant in time, acting on different species over a wide geographical range, and triggering a similar selective response in the species involved. Given that, it makes sense that the candidate genes are immune-related as most likely that selective pressure is mediated by pathogens. Azevedo et al. (2015) also note that maintenance of TSP variants by balancing selection is most likely mediated by heterozygote advantage or frequency-dependent selection - both make sense in a pathogen co-evolution scenario. So far, the number of reported TSP loci is really low (really just below a dozen or so), and there might be two reasons for this that are not mutually exclusive: First and obvious, there might be very few TSP. Second, these loci are very, very difficult to detect (as you want to exclude loci that are identical-by-state due to e.g. recurrent mutation) and we might simply not yet have the tools and power to find most of them.
To draw a bottom-line and come back to your question, I would suggest that your inter-species genetic gap model needs a minor modification. Even though the general picture seems to fit, i.e. there is a significantly larger difference in variation between species than within species, there also is overlap in the far tails between chimpanzees and present-day humans. These overlapping variants are not identical-by-state, i.e. due to random effects or recurrent mutations, but are signatures of polymorphisms in the ancestral population of chimpanzees and humans that are still maintained independently in both the split lineages.

I found at least one example of genes where the same genes and the same alleles exist in both humans and other primates but the frequencies of the different alleles are different in different primate species and those are the genes/alleles associated with the AB0-blood system that humans and other primates share. Citations from this site:

Of the Old World monkeys, the chimpanzee has been the most studied
  (Socha et al., 1984).  Interestingly, they have predominantly blood
  type A and in rare cases blood type O, but NEVER blood type B (Socha
  et al., 1984).  Most blood systems found in chimpanzees also exist in
  man, but there are some species specific characteristics.

.

In contrast to chimpanzees, gorillas have been found to possess ONLY
  blood type B.

Now you can use some kind of statistic tool often used to determine genetic distance within species, such as the Fixation index on the genes regulating the AB0 blood system.
Using that tool you can say that your genetic distance to gorillas are less if you have blood type B than if you have any other blood type. If you have blood type A your genetic distance to Chimpanzees are less than if you have blood type 0 and your genetic distance to chimpanzees is the largest if you have blood type B. You can do a google image search on "Cavalli Sforza" and find a lot of interesting diagrams where this method is applied to humans.
You could in principle do the same procedure on all genes that Chimpanzees and humans shares but the allele frequencies differ and try to find who has the least genetic distance to the present day chimpanzee population.
According to a study referenced here such areas in the genome are found in genes relating to fighting off diseases, where you might have an evolutionary advantage if you have a different allele than people around you that catches a disease because your allele makes you immune.

A genome-wide analysis searching for evidence of long-lived balancing
  selection -- where the evolutionary process acts not to select the
  single best adaptation but to maintain genetic variation in a
  population -- has uncovered at least six regions of the genome where
  humans and chimpanzees share the same combination of genetic variants.


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What regulates production of first transcription factors during development?
In my biochemistry class, we learned that transcription factors regulate the transcription of genes. However, transcription factors are also coded by genes, so what activates the transcription of genes that code for the first transcription factors during development?

The first transcription factors for the first transcription after fertilization are already present in the ovum (egg) before it is fertilized.
Generally, all the machinery needed for transcription, translation, and the rest of the many necessary cellular functions are already present in a cell before it divides and develops.  This chain of dependency goes back eons of time to the origin of cells and the very origin of life.


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Why are there "Old World" and "New World" families?
I've been reading on biological classification of the animal kingdom and have come across the New World and Old World terms a few times when they are applied to ranks (family, as much as I could find). Some examples of what I mean:

Old World porcupine vs. New World porcupine.
Old World rats and mice vs. New World rats and mice.
Old World vulture vs. New World vulture.

Old World X and New World X are usually not considered closely related. I assume this is because (at least partially) they evolved separately long enough to be distinct, if they were even related (at a non-trivial level) to begin with.
Is this naming scheme only thanks to convergent evolution? Researchers found families (or species etc.) in the new world that look like families in the old world and called them New World X, which prompted the other to be Old World X? I understand that a good deal of this classification was done in the 19th century when diagnosis tools were limited and conventions varied.

Yes, I think this is exactly right in the three cases you mention, convergent evolution noticed by the humans who were doing the naming. There are other cases (Remi.b mentions simians) where the "Old World" and "New World" versions are sister clades that became geographically isolated from each other.

So in some cases they weren't related and converged to look similar, and in some cases they were related and differ due to geographic isolation?

Yes, that's correct.

Lineage split due to continent drift
Due to continental drift, at some point a lineage was split into two, the afro-eurasian lineage and the american lineage. It is then common to refer to the  american lineage as the new world lineage and to the afro-eurasian lineage as the old world lineage.
Origin of the terms "New World" and "Old World"
In case you are unfamiliar with the origin of the terms "New World" and "Old World" and why for example "New World" is associated to the americas you should have a look at wiki > New World. In short, the americas was termed "New World" by europeans during the "age of dicovery". Geographers at that time (16th century) thought of the world as being limited to Africa, Europe and Asia (the old world) but suddenly europeans discovered the americas, a new world to add on their map.
New World Monkeys vs Old World Monkeys
Such nomenclature is typically used for monkeys. There are New World Monkeys (Platyrrhini) and Old World Monkeys (Cercopithecoidea). Homo sapiens for example is an Old World Monkey. Prehensile tail is a famous adaptation among New World monkeys that is absent among the Old World Monkeys.
Evolutionary consequences for these terms
These terms therefore do not result from convergent evolution or any other fancy evolutionary process. The terms refers to a specific split between lineages due to continent drift, where one (set of) lineage is found in the americas and the other is found in afro-eurasia. In the above case of monkeys, Platyrrhini and Cercopithecoidea refers to monophyletic lineages.

I don't think this is correct. The examples cited by OP are not sister clades.


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What is a good method to test the effect of gibberellin concentration?
I was just wondering what a good method would be to test the effect of gibberellin concentration on growth. I know it is prevelant in many flowering plants but am unsure as to what would be suitable. I have been looking into tepary beans as one but am unsure as to how exactly I would measure 'growth'/the effect of gibberellin.
Thanks!

Exactly, the 'good' plant would depend on how you measure the effect of gibberellin. I think you should change the wording of the question from good plant to good method.

Gibberellins cause elongation - the acids were discovered by study of rice bolting in Japan. Fundamentally measure stem elongation versus concentration of applied GAx. There would remain a question of how effectively the GAx was adsorbed that would require some further chemical analysis - of xylem water if applied as a root drench, for example.

Could you possibly direct on me on how to apply the gibberellin as I have not found a simple methodology for this. I have also read in a number of papers that it also effects root length, germination period etc. Would it also be possible to explore these? How would I also go about applying it as a root drench?

Exogenous GA can be adsorbed via foliar sprays but more usually as a root drench. With bare rooted plants, you could prune all to the same root length, dip the roots in the solution for a period of time, then pot them. Afterward bare root the plants and measure root length. With potted plants or 'planted' plants, just pour an amount of solution on the soil.at the base of each plant (no ability to measure root length in this case). With seeds see http://www.jlhudsonseeds.net/GibberellicAcid.htm


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What is meant by topology of DNA?
I couldn't find anything on internet that would give a clear-cut idea about what it could be.

Lehninger has got a good section on dna topology along with the function of topoisomerases.

Topology is the study of flexible geometries. That is, what properties do objects have when you're allowed to stretch and bend them (but not allow them to break or pass through themselves). This is the origin of the saying that to a topologist there's no difference between a doughnut and a coffee cup. Topologically, they're the same object. If the doughnut and coffee cup were made of really elastic putty, you could  remold one into the other without cutting it, or allowing it to pass through itself.
So what does this have to do with DNA? Well, while DNA is stiff on short scales (dozens of base pairs), when you get long stretches of DNA it's very flexible. You can bend and wrap the DNA up. But there's a limit on what you can do without breaking it or letting it pass through itself. (For circular DNA) You can't get knots, and the intrinsic double-helical "twist" of the DNA can't be changed.
There are various enzymes in the cells (helicases, topoisomerases) which are responsible for controlling this coiling and twisting. The way they work is to (temporarily) make a break in the DNA, pass the DNA strands through the cut, and then reclose the strands. That is, they change the topology of the DNA. This is how you get "overwinding", "underwinding" and "supercoiling"
So "the topology of DNA" is talking about the properties and geometry of DNA that it has if you treat it as an unbroken floppy noodle: how it's wrapped up and how it's twisted.


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Inward rectifying potassium channels during undershoot of action potential
My professor said that inward rectifying channels help move the membrane potential back to the resting potential during the undershoot phase of the action potential. The membrane potential would have to be lower than the equilibrium potential of potassium for this to occur (inward potassium driving force), but the membrane potential never goes below the equilibrium potential of potassium during the action potential. So, when are potassium rectifying channels actively passing ions?

I hope I can maybe shed some light on this concept for you.  Rather than complicate anything more than necessary, let's start small and build. To directly answer your question, these channels can function as leak channels (so ions are always flowing through them at some rate) or can be open at select voltages (ions will only flow upon voltage-selective opening of the channel).
Here's a little more detail.  These channels are involved in a number of physiological processes (not only in neurons, but smooth muscle and cardiac cells as well).  One such process is, as your professor pointed out, to drive the membrane potential back to rest after you hyperpolarize the cell following an action potential.  I completely understand your confusion with this concept because in order to properly answer your question, I've gone through a number of resources to make sure I give the most complete answer possible.  Here goes:
Maybe the most important part!!!  These inward rectifiers were originally called “anomalous” rectifiers because, let's face it, they're goofy.  They don't do what you expect them to do (as you have pointed out).  Part of the reason is that there are molecular mechanisms that cause these channels to be blocked and preferentially permit an inward conductance, despite what you'd expect.  There's a decent review article on these channels that might help your understanding (the introduction is the most important part).  You can find it here http://physrev.physiology.org/content/90/1/291#ref-233.
Now I'll try to get into a different explanation that kind of oversimplifies things, but I believe might help.
Remember that the gradient is not solely electrical in nature, it is an electrochemical gradient.  Now you're probably thinking to yourself "I know that, dude, don't patronize me!"  I only bring this up because it appears your biggest concern is how the electrical properties of the gradient regulate K+ flow across the membrane (heavily considering the electrical driving force by focusing on membrane potential minus the Nernst potential for K+).  However, flip that thinking for a second.  Specifically, think about what happens during an action potential solely in terms of concentration.  Your rising phase is sodium influx to the cell (you go from lots of sodium outside the cell to lots of sodium inside the cell).  On your falling phase, sodium channels close and potassium channels open.  Thanks to the good ol' Na+/K+ pump, you have a gradient of little K+ outside the cell and a ton inside.  So what happens?  All that K+ rushes out of the cell (as you would also predict from the electrical component of your gradient now!).  That means you had a lot of K+ inside and a little outside, but you now have a lot outside and a little inside.  This goes on too long and you get an undershoot/hyperpolarization, but you have to get back to your resting membrane potential.  Enter the inward rectifiers.  These K+ channels open and (again, thinking solely about concentration) the K+ is going to flow down the gradient back into the cell.  If you throw in the electrical component, remember this:  Neurons exist in a multi-ion system which complicates things like reversal potential for a single ion.  This is a complicated subject that I won't get into, but it boils down to reversal potential being a different property from equilibrium potential, which becomes important in a multi-ion system.


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Why does the side of the mebrane of a neuron with a high concentration of positive ions become electrically negative?
I am having a real hard time understanding why the side with a high concentration of positive ions becomes the negative side of the membrane (in a neuron). This website http://www.st-andrews.ac.uk/~wjh/neurotut/mempot.html says its because "...the positive ions flow away from the high concentration side". But I still don't get it. Wouldn't it make more sense to then say that the high concentration site (more positive ions) has more positive voltage?

Hmm. look that presentation once again slowly. The membrane does not allow Cl- to pass, but it allows K+ to pass (perhaps due to their ionic radius) (https://en.wikipedia.org/wiki/Ionic_radius, see table). Now on the other chamber, K+ can diffuse-out, but Cl- not. So only K+ will come out; and at the moment a K+ come out to dilute chamber;  the concentrated side would become unbalanced. Though there is + chrg enough; - charge is slight more. But that will create a back-pull on k+. The more diffusion proceed, the back pull go up and diffusion decrease. At end, diffusion stops at a max back pull

Note that your salt soln on concentrated side, at start was neutral. There were too many positive charge, but as well the same number of negative charge. If you buy 1 packet of NaCl (edible salt) from market, it is much much more enriched in Na+ (than a soln. compatible to biological system). So it should be more positive, but it is neutral, because at the same time there are too many Cl-, too, and in equal number as Cl-, so no overall charge.

If you take some + charge apart from some negative charges; the system should become more-negatively charged... whatever the total number-density of positive and negative charges at start. At end, you're getting More Cl- ions THAN the K+ ion in the same side. Count them.

The eqlb at end (due to back-pull generated from that few extra Cl-, that try to take back the K+, against diffusion), is known in the name Gibbs Donnan Equilibrium. https://en.wikipedia.org/wiki/Gibbs%E2%80%93Donnan_effect

Oh no on my 2nd comment's last line there's typing error... read "many Cl-, too, and in equal Number of Na+" (for table salt example). I had typed Cl- twice.

Q. “Wouldn’t it make more sense to then say that the high concentration site (more positive ions) has more positive voltage?”
A. No.
I know little about electrophysiology, but looking at the graphics and explanation that precede the screen from which the sentence you quote is taken the statement is justified. Where are you going wrong?
Your argument implies that the side with the high concentration should be positive because it has more positive (K+) ions. But it has (initially) an equal number of negative ions (Cl–) so it is initially electrically neutral. (The graphic indicates this by having no charge on the K — not a very satisfactory idea in my opinion.)
The important thing to note is the premise — that the membrane is permeable to K+ ions, but not to Cl– ions. So, even though there is a concentration gradient, only the K+ ions can move across the membrane (the graphic shows those moving with a +ve charge). As they do so each leaves its ‘partner’ Cl– ion behind, so a negative charge builds up at the high concentration side. At equilibrium there may be a high concentration of K+ ions at the ‘left’ of the diagram, but there is an even higher concentration of Cl– ions!
Good luck with your further reading of these pages! It looks as if it gets much more complex as it goes on.

David's answer is good.
I would also add that the resting membrane potential is not strictly because of moving K+ ions - if you were "teleporting" ions out of the cell, you would need to move a lot more ions to get a potential of ~-70mV. Instead, the resting potential is essentially given by "how much electrical force would I need to put on this membrane to get those potassium ions to disobey their tendency to flow down their concentration gradient." You should always be thinking about the Goldman equation and the relationship between concentration gradients and permeabilities, or neurophysiology will be very confusing.


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Pathophysiology of pink frothy sputum in pulmonary edema
Pulmonary edema is a condition where fluid leaks into the alveolar spaces. This can be due to to hemodynamic causes like left heart failure and pulmonary venous obstruction or microvascular injury or increased capillary permeability.
Clinically we are taught to differentiate between various types of sputum. The sputum in pulmonary edema is characteristically pink and frothy.
It is important to mention here that the fluid that leaks into the alveolar spaces is a transudate and not blood. Hence it is by no means that the pink is due to blood. Otherwise it would be called hemoptysis.
My question is, why is the sputum pink if blood has no role to play?

Please don't migrate this question to health.se since pathophysiology pertains more to biology than health. Thanks.

Even though the fluid in pulmonary edema is a transudate, there is blood in it. This is substantiated by the fact that there are microhemorrhages in acute lung congestion and hemosiderin laden macrophages or 'heart failure cells' in long standing pulmonary congestion on histology. These signify that RBCs have escaped the vasculature to enter the tissue (and failed to get back to the blood), while the macrophages have consumed them later on.
Since the blood loss isn't very high, the color is pink rather than red as seen in hemoptysis.
The reason for this is likely due to the significant differences in hydrostatic and oncotic pressures when compared with the rest of the body. In the Lung, one edge of the capillary is up against a single, extremely thin alveolar cell that provides very little pressure to counterbalance the increased forces present in pulmonary edema. Without this inward pressure to stabilize the capillary wall, you end up with a situation in which small ruptures occur at weak points in the AC membrane, unlike elsewhere in the body where pressures are more equalized and change is an osmotic process rather than one of cellular disruption.
Although hemosiderin laden macrophages can be a proof that RBCs leave the vasculature, it is important to note that they can be found in other organs too. One example is the chronic venous congestion of the liver, where the hypoxia (due to congestion) can lead to endothelial damage letting out the RBC, which later get engulfed by macrophages.


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Possible moth identification
There's a flying insect being caught indoors today in Sydney Australia. Before it is being caught, it basically flies like a moth. However googling of Tinea pellionella and other cloth moths does not suggest it is a cloth moth as hair is missing from its very small sized head.
It is also known to be very common every year when spring approaches in australia
To assist identification, the bug was caught in a plastic jar to allow multiple angles of it to be photographed

Measured body length (not including long antennae): 1.1 cm
Color: Brown an golden brown with lustre
Legs: 6 (front pair very short, middle pair is forked, hind legs have some golden brown feathery structure)
Head is black, very small and have no hair

Here one can easily see the hindlegs are covered by some bristle like golden brown feathery structures, and also its shiny golden segmented abdomen

The camera is not fast enough to capture it unblur when it is flying, but the few moments when it opened its wings can be seen here extracted from a video

And these are our best shots using the iphone camera in capturing its flight with its wings fully opened.

Is this a type of moth, is it a pest or is it neutral. What is the species?

It is a moth, so belongs to the order of Lepidoptera, and to the unoffical suborder of microlepidoptera. These are notoriously difficult, even with good literature, which i'm not sure exists for Australia (European myself).

Do you find this similar?

That might be it, as the glossiness of the wings, the feathery ends and the colors patterns matches. Strangely, I don't seemed to see any of the two dark horizontal bands that is present in all other google images of the species (except mine and the photo shown in your link)

This is a Bogong Moth,the migration point was really helpful !!
They migrate in masses around the
 1. Victorian alps
 2. southern Australia (Sydney,Canberra)
 3. New Zealand..
Agrotis infusa,
These are pests which affect many plants,they're not neutral and they
Cause some attentive damage
More on this and the site which helped me


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Why is the resonance frequency of a neuron defined by peak impedance?
I'm relatively new to the field of electrophysiology, so if anything is unclear or incorrect, please let me know.
One thing that continues to confuse me throughout my reading is the property of resonance frequency of a neuron.  Generally, I've seen resonance frequency defined as the frequency at which neurons respond best to inputs of injected current, which makes sense.  What does not make sense to me is why it has also been defined as the frequency at which peak impedance is observed because in circuit analysis, resonance frequency is the exact opposite (the value of frequency at which you have minimum impedance).  The definition for electronics is logical in my mind because that's also the value at which current is at a maximum (since the impedance is lowest).  I'm assuming that the relationship between impedance and resonance frequency is flipped in neurons because of another property I'm not considering (like driving force of ions, voltage-gated channels, etc.), but I'm genuinely curious what the reason is.  If anyone could be of assistance on this, I would greatly appreciate it.
EDIT WITH POTENTIAL RESOLUTION BY QUESTIONER:  I believe one of the pioneering texts discussing neuronal resonance was a Trends in Neurosciences paper by Hutcheon and Yarom (Volume 23, Issue 5, published in 2000).  However, after reviewing this text, I think I may finally understand the idea.  As described in the referenced article (which I would highly recommend), membrane properties of a neuron allow it to act like a band pass filter. A little more poking around the internet led me to the conclusion that it is specifically a parallel resonant band-pass filter (for a brief explanation, visit  http://www.allaboutcircuits.com/textbook/alternating-current/chpt-8/resonant-filters/).  I believe this might be the correct interpretation, but have left it as an open question because if there is something wrong in my interpretation, all you bright individuals out there can point out my mistakes or elaborate further on the concept!  Thank you!

Can you state your source, please.

My apologies, thank you for the response!  I have made that edit and hopefully resolved my question in the process.  Though I would still appreciate hearing your thoughts on this topic!


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Sexing spotted doves
I recently took pictures of Spotted doves (Spilopelia chinensis) during their courtship. The one on the right, is large with a off-white breast and the one on the left is comparatively small with dingy reddish white breast.
My professor and I presumed that the one on the right is the male and the other is the female. The larger one mounted the other during cloacal kiss.
I've checked Wikipedia and other sites which seem to copy Wikipedia, they say that the species does not show sexual dimorphism. On the other hand, this website claims that there is a difference.
Does it show sexual dimorphism?
Location: West Bengal, India

First I think that is a Western Spotted Dove (Spilopelia suratensis), now splitted from the Eastern spotted Dove (Spilopelia chinensis). In your area there should be both species but the red iris and eye-ring should indicate the Western. Sexes are alike so there are no signs you characteristics you can check (source, handbook of the bird of the world, which is the most updated and reliable source in many occasions). Males sing much more often than females (so you can observe this behaviour) and in many species, but I dunno about this one, is the male providing food to the female...so I think your guess is right!
All the best,
Have fun

I am sorry I think there is not much more information that the one provided by wikipedia. Also this specialized website, which I trust, http://www.birdforum.net/opus/Spotted_Dove  repeats the same information.

I took the liberty of adding hbw links to the two species.

I currently have a pair of spotted dove visiting my backyard regularly for feeding.  I noticed one of them has got a more blueish head top than the other, still trying to figure out which one is male.  The one with blueish head top is comparatively smaller in size, and less courageous when it comes to having me around. My best guess is that the more blueish head is female and the bigger, more reddish head is male.  In any case, this is just my best guess.

Welcome to Biology.SE. While anecdotes are potentially interesting, your answer is much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] and [Ask] effectively on this site and then edit or delete your answer accordingly.


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Is there interphase between meiosis I and meiosis II?
Is there interphase between meiosis I and meiosis II?
After 2 haploid cells are formed in meiosis I, do the cells go through a period of interphase (G1, S, G2) or do they go directly to meiosis II?

When meiosis starts it is suppose to produce a haploid so because of this there is no need for further replication or growth.

The technical name of this brief "interphase" between meiosis I and meiosis II is interkinesis.
Interkinesis is normally short (it may not even happen) and it's not divided in G1, S or G2, mainly because there is no DNA duplication, which defines the S (Synthesis) phase.
Source: A Glossary of Genetics and Cytogenetics: Classical and Molecular

spelling edit suggested. Interkynesis --> interkinesis.

Telophase I, is followed by an interphase, called interkinesis, similar
to the mitotic interphase.
During interkinesis the chromatin is partially uncoiled; however, there is no replication of the genetic material, because each chromosome already consists of two chromatids.
Furthermore, the sister chromatids in interkinesis are generally not genetically identical, because crossing over in prophase I has reshuffled genetic material
between the maternal and paternal chromosomes (i.e recombination).

According to Concepts of Genetics by Klug and Cummings; ed 7,

In many organisms, Telophase 1 reveals a nuclear membrane forming around dyads. Next, the nucleus enters into a short interphase period. In other cases, the cells go directly from the first anaphase into the second meiotic division. If an interphase period occurs, the chromosomes do not replicate, since they already consists of two chromatids. In general, meiotic telophase is much shorter than the corresponding step in mitosis.


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The best free and most up to date phylogenetic tree on the internet?
I found phylogenetic tree in wikipedia is lacks of accuracy. It actually confusing with versions. Some terms was not scientifically accurate with dna analysis anymore
So are there anyone know where is the most updated datasource on the internet?

Tree of what organisms?

@kmm All if possible. Vertebrate, Arthropod and Mollusc is most interested in

Available ressources
I would recommend oneZoom.org is probably the best ressource. oneZoom.org is based on openTreeOfLife.org (for phylogenetic relationships) and eol.org (Encyclopedia Of Life) (mainly for the pictures I think). If you do not fancy to much the display and links of oneZoom/org, then I would just recommend openTreeOfLife.org.
There is also tolweb.org but it is not as nicely updated as openTreeOfLife.org (and therefore openTreeOfLife.org) and the dates are harder to find.
Particularities of oneZoom.org
I particularly like that for each node oneZoom.org offers links to

wikipedia
encyclopedia of life
the red list
NCBI

, which makes it a very appreciable tool. oneZoom.org has the advantage of a nice display (although a bit slow to load IMO) and is easy to navigate and get time to the Most Recent Common Ancestor of a lineage.
I also like that you can just add the species name after "#" in the URL and it will jump to its node. Here is the Kagu for example.
Potential issues in oneZoom.org
Of course, oneZoom.org contain a few mistakes! Some of them are unintentional (wrong picture, misrepresentation of what is known from the literature, fail to update information), some of them are caused by lack of knowledge of true phylogenetic relationships. oneZoom.org does not say how certain we are that a given speciation event is correct or correctly dated, it just display the best estimates we have. If a specific node is of interest to you, you will need to go to the scientific literature which will give you much more information about what we know and what we roughly guess.

Open Tree of Life could be what you're after. It was updated last month according to this page. The visual interface is rather bland, but that's probably the price one has to pay for accuracy and completeness.
Vertebrates, arthropods and molluscs are all available as categories in the taxon search bar on the home page.


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How does our body produce new antibodies?
My professor said that in human body nearly 10$^9$-10$^1$$^2$  antibodies are produced by VDJ recombination and all the antigens that a person encounters in his lifetime are dealt by antibodies already present in his body. But he didn't explain what if the body in infected by a new mutated microbe(antigen) whose corresponding antibody is not present in the body.
My question is does our body have the mechanism to judge the epitope of the new antigen and synthesise an antibody with completely new paratope? If so what is it?
After reading the following I was forced to wonder whether the specificity of the antibodies improve(improve by synthesising new paratopes) after encountering antigens in the course of response.

The human immune system is capable of producing far more than 1e9 antibodies - it's more on the order of 1e12.

"Holes" in peoples' antibody repertoire are quite common -- that is, it isn't unusual for individuals to fail to make an antibody for a particular epitope.  However, pathogens generally have dozens to thousands of epitopes (many per protein) and it's rare that a person fails to make antibodies to enough epitopes to protect against the pathogen.

Sanjukta, your English is usually better than this. I don't understand what you are trying to say in the phrase "does our body have (not has) the mechanism to JUDGED the epitope". "Judged" is wrong. Can you clarify what you are actually asking. And when you say "child" and then "lifetime", do you mean "individual" (baby, child, adult) or are you talking about early life?

The simple answer is that the variant library is independent of antigen exposure, and is created before. Your body makes as many random variants as it can, specifically for cases when new antigens (e.g. new mutated microbe) are present. It's basically a very extensive and, barring immunodeficiency, constant library. Because there are so many variants present, chances are you have one to bind any foreign antigen. So once again, all these random antibodies are made without knowledge of antigens. They're always there to bind most foreign antigens.

:p @David I've corrected the mistakes and have improved the question. Go through it,if you please. I hope it makes more sense.

That's clearer. There's nothing against the rules in your question so I've cut that bit out. Accepted answer seems OK. But be clear that the immune system is not "judging" the antigen or using it as a template in any way. Those pre-existing cells the antibodies of which can bind to some extent will expand and mutate, makingit  likely that some of those produced will have higher affinity.

@MattDMo You were right. I read in Kuby Immunology that the antibodies produced by B-cells are within the range- 1e12 to 1e14.

@SanjuktaGhosh I just read your updated question, and the idea that the innate response is not highly specific is getting out of date, as is the strong dichotomy between innate and adaptive responses. Surface and intracellular receptors for PAMPs are incredibly specific for their targets, and have a broad range of effects that varies greatly from receptor to receptor, depending on the type of microbe associated with each PAMP. More understanding about NK, NKT, and γ-δ T cells (among others, such as the interaction of immature B cells with subcapsular sinus macrophages in the spleen to (...)

ferry immune complexes in a non-specific manner across the mantle zone to B cell follicles in germinal centers) is really blurring the lines between innate and adaptive responses.

In case of T-cells and Abs our organism first generates a great diversity of T- and B-cell receptor variants so that any new foreign antigen is likely to be recognized by some of them. When a B-cell encounters its antigen it begins proliferating and changes it phenotype. Additionally, B-cell (but not T-cell) receptor starts to mutate (so-called somatic hypermutation) generating new B-cell receptor variants that differ a bit from the original one. This process acts like evolution, with B-cell carrying a receptor with higher affinity being more likely to proliferate. So the specificity of antibodies improves indeed, this is called affinity maturation.

Could you please add some references?

I've added the wikipedia link to Somatic hypermutation. Hope you don't mind. Besides welcome to Bio stackexchange and thank you very much for the life-saving answer. :) Hope you have a nice experience here.

@L.B. This topic is nicely covered in Janeway Immunobiology http://www.garlandscience.com/product/isbn/9780815342434 . This book really helped me when I've transferred to the immunology field having a pure physics background.

@51102 that's not the point. We require answers on this site to include relevant citations to the scientific literature to back up non-obvious claims. Of course there's always some disagreement about what "non-obvious" means, but it's often interpreted to mean things that a person who's had a basic biology course wouldn't understand. So, you don't need to provide evidence that DNA is the carrier of genetic information, but a link to the Wikipedia pages for T cells, B cells, and antigens (maybe) would be appreciated. Somatic hypermutation would definitely need a citation.

Also, you can find an older version (the 5th edition from 2001, unfortunately) of Janeway on the NCBI Bookshelf here if you have a particular passage or figure that would illustrate your point well.

Maybe it is worth adding that B cells in the germinal centers, after having migrated their, will be nurtured in its journey between present T cells and reticular cells, where the B cells receptor's ability to bind to antigens will judge how well it will be nurtured (with various cytokines). Hence, one is able to get rid of receptors which are not sought. (With reference to Abbas' Basic Immunology)


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How is trangender female different from normal female biologically?
I have read in many places that transgender people are usually people who are born with typical male or female anatomies but feel as though they've been born into the “wrong bodies.” The thing that I am confused about is that how someone can not be considered as normal just because he thinks he should not be what he is? I met a female who looked exactly like a normal female and she was very beautiful. She didn't know that she was a transgender till her mom told her that she was transgender when she became adult. What is biological difference between a transgender and a normal male/female?

Remi gives a good introduction to the various terms and definitions you should know when learning about gender identity. However, he didn't really address your basic question:

What is biological difference between transgender and a normal male/female[?]

Except for some likely genetic differences, which we aren't even close to beginning to understand, there is no biological difference between two persons born with $XX$ sex chromosomes, one of whom identifies as female (cis-gender) and one of whom identifies as male, or somewhere on the spectrum between female and male (trans-gender). There is no difference physically - both have the same organs, including sex organs, and both have the same secondary sex characteristics. One cannot tell the difference upon gross physical examination, X-ray, blood test, etc. Gender is a social construction, and while the majority of people in the West have a gender identity that matches their biological sex, some do not, for reasons that are not yet clear.

Let's first consider the difference between the concepts of sex and gender.

The distinction between sex and gender differentiates sex (the anatomy of an individual's reproductive system, and secondary sex characteristics) from gender, which can refer to either social roles based on the sex of the person (gender role) or personal identification of one's own gender based on an internal awareness (gender identity).

Below are some definitions of the term you used (transgender) and of terms that some people confuse.

A transgender person is someone who have a gender identity that differs from its sex. For example, a man (with standard male organs) who identifies as a woman.
A transsexual is a former transgender who seeked for medical assistance to modify its sexual organs to match its gender identity (and unmatch the assigned sex at birth).

Because (1) sexual and romantic attraction are often important driver of gender identity and because (2) many people confuse the terms relating to sexual attraction with the previous ones, I wanted to add the definitions of

A heterosexual is someone who is attracted to people of the opposite gender.
A homosexual is someone who is attracted to people of the same gender.
A bisexual is someone who is attracted to people of both genders.

While all of the above definitions were referring to social gender identity (transgender), sexual and romantic attraction (homosexuality, heterosexuality, bisexuality) and medical intervention (transexual), in my list of terms, only the term intersex actually refers to a 'biological' difference.

An intersex (previously called hermaphrodite) is someone who has variation of both sex.

You should read the linked wikipedia articles who will teach you much more about the definitions and slight variations behind these terms than I could do in the such short definitions I used. There other other concepts you might want to investigate the definition such as gender non-conformity, genderqueer, third gender and pangender for example.

You will note that as only one term was referring to 'biological' variation, the question could be answered in much more depth by a specialist of gender studies (which I am not) rather than by a biologist (which I am).
Finally, note that this post is closely related.

While this is basically correct (+1), I’d say “a transgender” is a bit awkward at best, and should probably be “a transgender individual.” Also, you don’t seem to have addressed this part of the question: “I met a female who looked exactly like a normal female and she was very beautiful. She didn’t know that she was a transgender till her mom told her that she was transgender when she became adult.” I’m not totally sure what the OP is talking about here (people don’t find out their gender as adults, from their parents!), but if you can figure it out it would be worth addressing.

Indeed, transgender is an adjective and not a noun (unlike bisexual, intersex and other terms which are both nouns and adjectives....aahhh english!). I corrected it. Thank you! I don't know what the OP meant and at this point I am too lazy to ask him/her :)


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What was the first animal having fur?
Did all early mammals have fur? Is it possible to trace the origins, how early animals with fur looked like and how it evolved?

https://en.wikipedia.org/wiki/Evolution_of_mammals#Hair_and_fur

@Thaina That's what I was looking for, thank you.

Czech version: http://www.memento.junweb.cz/clanky/spzo20.htm


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What risk does the insulin pump hack carry?
Recently, a OneTouch system was hacked, potentially allowing any malicious attacks, draining the pump into someone's bloodstream:

Jay Radcliffe, a diabetic and researcher with cyber security firm Rapid7 Inc, said he had identified ways for a hacker to spoof communications between the remote control and the OneTouch Ping insulin pump, potentially forcing it to deliver unauthorized insulin injections.

If this threat is real, what is the theoretical worst-case scenario for a patient with one of these insulin pumps? Is this actually directly life-threatening?

Yes. Yes it is.

i would suggest googling: total amount of insulin in average device; insulin LD50 for these patients. Should help answering the question.