text:
Are all animal species prone to cannibalism induced prion infection?
Humans have the tendency to get certain prion diseases when eating human flesh. It's known animals can get prion diseases as well.
Does cannibalism among other animal species also make them more susceptible to get a prion disease, and are there distinctions between mammals doing so and other orders like reptiles, birds, fish etc.?

Perhaps worth noting that BSE wasn't caused by cannibalism, but rather because cattle were fed with material derived from sheep.

I'm not aware of prion diseases in non-mammals. It isn't clear whether this is because of differences in their PrP homologs or for some other cause.

It is perhaps worth looking into more historically established prion diseases in noncarnivorous animals, like sheep. If prion diseases were only transmitted by consuming prion-rich brain tissue, then they should be extremely rare (produced via unique misfolding events or mutations in affected individuals) or completely absent in wild herbivores and domestic herbivores which are not being fed meat meal.
In fact, I mention scrapie because it predates the practice of supplementing livestock feed with meat-derived protein. (The first documented mention of the disease dates back to about 1772 and mentions that the disease is about 40 years old at that point.) As it happens, the earliest mention of livestock feed or feed supplements being composed of meat and bone meal I can find dates to about 1890. Prion diseases also appear in wild populations of elk and deer in the form of Chronic Wasting Disease, currently a big problem in the northern US and Canada, as well as in cattle and sheep.
So how did scrapie come to be such a problem for European sheep farmers?
Well, for one thing, scrapie (and CWD) can be transmitted via ectoparasites. But the most common culprit probably lies in the soil. It turns out that infectious prions can survive for years in soil once they're deposited. Not only is the decomposition of a carcass a way to infect the soil with the misfolded prions, but CWD proteins are also present in the excreta of infected animals and even antler velvet.
This is a problem, because both scrapie and CWD can be acquired simply by consuming infected soil or grazing on grass containing it. This is most likely the most common way that these prion diseases are acquired naturally--not cannibalism at all, or at least not the sort we commonly think of! It's a simple fecal-oral route of transmission, albeit one with an alarmingly long potential incubation period.

Dr. Dean O'Del was on radio with a syndicated health show in the 1990s during the BSE/Mad Cow scares, where he cautioned that the use of bone meal on roses or plants as the heat of making bone meal did not destroy the prions until it was burnt to charcoal carbon.
Given scant evidence for  grass from contaminated soil might also have the prions in the grass for how sheep might get and transmit it, lowering the odds of eating prions still would require a totally plant based diet given the vast numbers of animals mixed into processed meat products like Pink Slime and deviled meat or ham, & a  organic diet given that,  only a spontaneous and rare mis-folded protein would start the 40 year incubation towards Alzheimer's and vCJV.
Both scrapie and CWD can be acquired simply by consuming infected soil or grazing on grass containing it. This is most likely the most common way that these prion diseases are acquired naturally--not cannibalism at all, or at least not the sort we commonly think of! It's a simple fecal-oral route of transmission, albeit one with an alarmingly long potential incubation period.

It would be handy to get some supporting references or even wikipedia links in this post, though it looks like it might be somewhat informative. Note that the other answers, which contain similar messages, do have such links.

This non-answer blatantly plagiarises the existing accepted answer and the external source without citation. Whilst this is an incomplete explanation on how non-cannibalistic and indeed non-carnivorous species could come into contact with prions it does not address the question about if those animals might be prone to infection from such contact. The first 2 paragraphs should really be a supporting comment on the accepted answer, or a community edit.


text:
How do birds decide which branch to land on?
What factors do they weigh on? Shape, position of branch within the tree body/structure, fatigue, nearness to current position, etc.
And how fast does a bird's brain and nervous system decide on this?
Narrowing it down to a bird of prey, say the Harpy Eagle.

I think that the question is too broad. There are over 10000 species of birds and the majority of them uses branches to perch. The reasons/ motivation can be so many that your question should be targeted to more specific situation to be able to provide an answer.

I agree it is fairly broad question, but, nevertheless, I'm sure the OP would benefit from a brief discussion (or the very least a list of potential sources to read) examining/reflecting on this question for any species. I wonder myself if anyone has tried to model/determine these behaviors. I vote to keep this question open.

@theforestecologist thanks for the upvote. I understand that the question is too broad in a sense. But my question was directed towards the basic premises of a bird's cognitive decision making. Let me narrow it down to a certain species within the wide classification of birds of prey in that case.

Btw, I found this for a start.
http://asifg.mycpanel.princeton.edu/publications/pdfs/TeufelGhazanfarFischer2010.pdf

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text:
How to convert FASTQ file format into GTF file format?
I have a plenty of FASTQ files (FASTQ is a standard for storing the output of high-throughput sequencing instruments such as the Illumina Genome Analyzer) and need to convert them to GTF format (gtf - file format used to hold information about gene structure which significant feature is that it is validatable: given a sequence and a GTF file, one can check that the format is correct. This significantly reduces problems with the interchange of data between groups).
I assume that (if those formats are popular files' standards) there must exist some software that easily converts information from FASTQ files to GTF file.
Did anyone hear about any such (is possible open-source) software? I am familiar with R statistical package and SAS and can learn Python on a fly.
Thanks for any help.

A quick Google search yields many hits, not to mention the feedback from below. Please [edit] your question and include more about what you have, what you don't have, what you're trying to do, what resources you have to work with, what your time constraints are, what your ultimate goals are, etc. There is absolutely no guarantee that anyone here will be able to answer it, or that it will be on-topic here, as "Too Broad" questions will get closed.

You should really read about both these file formats. As swbarnes mentioned, FASTQ and GTF hold different kind of information. GTF stores the annotation of a reference sequence. For example a GTF for a genome sequence will have the information about the locations of features such as genes, transcripts, exons, start codon etc.
FASTQ stores the sequence of a read obtained from sequencing along with the quality scores corresponding to each position.
As mentioned by others, asking for interconversion of these file formats, makes no sense.

I guess what you are asking for is "How to obtain novel annotations with a FASTQ file at hand?"
This also depends on what you want to annotate.
The sixth column in a GTF file refers to a score; you can assign expression values to different features. You can calculate expression using the read counts. If these are RNAseq reads then expression can be measured using packages like tophat-cufflinks, RNAstar or some others.
If you are doing ChIP-Seq then you can generate a GTF with a new feature called TFBS (transcription factor binding site) and annotate the locations. A popular package used for ChIP-Seq analysis is MACS, which takes your reads and outputs the TFBS in the form of a BED file which also stores co-ordinates. You can convert BED to GTF. You can also assign scores based on the read counts at different TFBS.
If you do not have a reference genome or if the annotation of the reference genome is incomplete, then you should first assemble your reads. If you have a reference genome then you can go for a reference guided assembly of the transcripts to obtain novel transcripts or splice variants; Cufflinks does this.
If you do not have a reference genome then you should go for de-novo assembly of your transcriptome and annotate the transcriptome for start codons or other features of processed transcripts. Velvet and Trinity are popular packages that do de-novo assembly.

Your question is not very clear. What should the contents of your GTF file be? Typically, GTF files contain information about where exons are located in a set of DNA sequences. Determining the location and exon/intron structure of genes is no simple technical task (i.e. a "conversion" as stated in your question), but rather a large area of active research. Annotating genes involves the use of statistical modeling (ab initio gene predictors), aligning experimental evidence (ESTs, cDNAs, and potentially Illumina RNA-Seq reads), and in some cases manual refinement of computational predictions. If you're working with a model organism like human or mouse or fruit fly, reliable GTF files are readily available for download from public databases. If you're not working with a model organism, then you many have quite a lot of work cut out to annotate a genome from scratch.
Or perhaps you want to annotate new alternatively spliced isoforms for known genes?
Without more information, it will be difficult for us to help you understand how to process your raw data (Illumina reads in FASTQ format) into a GTF file that addresses some biological question you're interested in.

The Tuxedo Suite (Tophat, Bowtie and cufflinks) used to to process RNA_seq data, assuming that is the origin of your .fastq files, should work for you.
https://ccb.jhu.edu/software/tophat/index.shtml

A fastq contains sequences.  A gtf contains coordinates of where features like exons fall in a reference sequence.  You can't interconvert them, that makes no sense.

So it is impossible to create a gtf file when I have information only from fastq file?

If this is an novel organism, and you have a very nice large set of RNAseq reads, you could in theory align it to your reference, and make a gtf from that.  But in general, no, you want to download an appropriate gtf for your organism, not make your own.

No, I want to create my own file. I do have a very nice large set of RNAseq reads and the gtf file does not exist. That's the question :)

You can't just convert.  You have to align to your reference for starters, as Daniel says, making a gtf from scratch is a big project, to do it right will be a lot of work.  But if that's what you need to do, then that's what you need to do.

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How does trees know to balance themselves so that they never fall down
Well i was flying kites today I saw a tree and its branches were spread around in random directions... I would like to know that how do these trees know to nourish their branches in some direction so as it doesn't fall off due to gravity. I know it can get its strength from the roots inside the soil so that it does not fall. But if this strength were not enough the tree may fall due to weight of its own branches. Can this happen??
I am new to this site I don't know much about the rules here. Feel free to edit if I have done any mistakes(especially about tags)

tree's do fall down, there may be a benefit, in terms of stability, to growing in a more "balanced" spread of branches but other factors also influence the direction the branches grow e.g. prevailing sun and wind conditions

I think the strength of the tree's roots are more of a factor in holding it up than the symmetry of its branches


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Why are there both stop and start codons?
Based on my understanding from wikipedia, there is the (RNA) start codon AUG and the stop codons UAA, UGA, UAG.  AUG can also encode Methionine, I'm assuming if it appears in the middle of a mRNA sequence.
But is there a chemical reason there are both start and stop codons?  Eg, if I only had a stop codon, would that also imply the next codon was start? Are there cases where there is a stop codon and the next codon isn't start?

Start and stop codons are instructions for the ribosome to start and stop protein synthesis, respectively.
The region between the start and stop codon (inclusive of them) is called ORF (open reading frame) or sometimes CDS (Coding sequence).
Why does ribosome need explicit instructions for start and stop?
Ribosome recognizes an RNA as a mRNA if it has certain features. In bacteria and other prokaryotes there is a region on the mRNA called the Ribosome Binding Site (RBS) that helps in initial recruitment of the ribosome. In eukaryotes there are Kozak consensus sequences that help in identification of a start site. When the ribosome encounters an AUG codon then the initiation reactions take place (there are some proteins called initiation factors that help in this process). The ribosome just keeps moving along the mRNA and producing a polypeptide unless it encounters a stop codon. When it does other proteins called release factors come into play and they dislodge the ribosome from the mRNA.
What about a second AUG codon?
If the ribosome encounters another AUG codon after the start then it would consider it as a codon for methionine. However there are situations when the second AUG can act as an alternative start site. You can see this paper for details.
Why is stop codon essential?
You can imagine a situation where ribosome just goes till the end of mRNA — why stop it? The reason for this is that the mRNA 3' terminus usually has regulatory regions and most importantly poly-A tails (in eukaryotes) that should not be translated. Moreover stop codon also signals the ribosome to dislodge from the mRNA. If such processes didn't exist then ribosome will remain attached to the RNA.
If I only had a stop codon, would that also imply the next codon was start?
No. Because stop codon works only when translation has already started. However it is not essential that the stop codon should be followed by the 3'UTR. Usually in bacteria a single mRNA codes for multiple proteins. There are many ORFs that are lined one after the other; such mRNAs are called polycistronic mRNAs. In these cases there is another start codon a few distance ahead of a previous stop codon.

It is important to have start and stop codons so that the molecular machinery of the cell (ribosome etc.) "know" where the actual transcript starts and ends. This is especially important, since mature mRNA contains untranslated regions which are of regulatory importance. These regions occur on both sides of the coding sequence called 5' and 3'UTR (untranslated region), then you also have the CAP-region and the poly-A tail, see the illustration below (from here):

You only want the coding sequence between the start and stop translated into a protein and to recognize these borders you need a specific marker. Behind the stop codon is untranslated sequence, not directly the next gene.
Additionally there is a large number of non-coding RNA species, like miRNA, siRNA, lnRNA and so on which fulfill regulatory purposes, play a role in splicing, replication etc. These shall not be translated into a protein (this would probably block the ribosomes and would also cost immense amounts of energy) as they wouldn't give useful proteins.

Not all the RNA is to be translated into proteins. Actually most of it is for regulation and sometimes unknown use. There are non coding regions before the start codon and after the stop codon. Hence the need for both.

Next to helping to define the region for translation on the mRNA, the stop codon also prevents transcripts that have been frame-shifted by a mutation from translating into big proteins, and also helps flagging the mRNA for destruction (nonsense-mediated RNA decay). This is because in random sequence, a codon has 3/64 chance of being a stop codon, so in a frame-shifted gene sequence there suddenly are many. The premature stop codon will prematurely end the first round of translation, but if any machinery for the splicing of the mRNA is still present (it is not at the normal stop codon), the mRNA will be destroyed so it can not generate additional mutated proteins.

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Which is the reference 16S rRNA?
Recently, I've stumbled upon a fact, which hasn't bothered me for many years. The fact is that all universal 16S primers are written as "[FR][0-9]+" (in regex notation), that is they have a position with respect to a reference. I've read through many papers, wherein these primers were introduced, and most of the time the authors say nothing but "E. coli 16S". Anyway, in one case I've found that it is in fact the reference K12 E. coli. But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB, rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a particular operon used for the 16S position notation?
Edit

Figure 2. Hypervariable regions within the 16S rRNA gene in Pseudomonas . The plotted line reflects fluctuations in variability amongst aligned 16S rRNA gene sequences of 79 Pseudomonas type strains... (Bodilis et al., 2012)

Are you sure they differ in sequence at the primer? The sequences of the structural parts of the genes are apparently almost identical. Have you checked GenBank?

@David I haven't checked that myself, but here is a relevant reference ... or the same strain may have multiple copies of the 16S rRNA gene that differ by 5% for some regions (such as Escherichia coli K12 [12])... (Nguyen et al., 2016)

@David while the primers are indeed located in short conservative regions between hypervariable regions, the latter are extremely variable. I've added a figure depicting this variation across several Pseudomonas strains. Therefore, it doesn't matter, whether the primers are located in conservative regions or not, what's important is that they target regions that can vary in both sequence and length.

As you correctly point out, designing an optimal primer pair for 16S-rRNA sequencing is a tricky affair because even the less-variable regions are not same between different strains and species. Sambo et al (2018) have even developed a bioinformatics software for optimal design of primers for 16S-rRNA sequencing for multiple bacteria.

We propose here a computational method for optimizing the choice of
  primer sets, based on multi-objective optimization, which
  simultaneously: 1) maximizes efficiency and specificity of target
  amplification; 2) maximizes the number of different bacterial 16S
  sequences matched by at least one primer; 3) minimizes the differences
  in the number of primers matching each bacterial 16S sequence. Our
  algorithm can be applied to any desired amplicon length without
  affecting computational performance.

There is diversity in the 16S-rRNA genes within the same species i.e. the different copies are not exact duplicates (Větrovský & Baldrian, 2013).

Větrovský & Baldrian (2013)

Interestingly, the different rRNA operons in E.coli have different promoters and are even differentially expressed during stress conditions (Kurylo et al., 2018).
However, Kitahara et al. (2012) found that 16S-rRNA genes isolated from soil samples, in place of the original E.coli gene, could support its growth. In other words E.coli is highly robust to mutations in its 16S-rRNA.

After counterselection, ∼200 clones of KT103-derivatives (carrying
  pRB103 whose 16S rRNA gene was substituted with foreign genes) were
  obtained, from which 33 nonredundant 16S rRNA genes (A01–H03) were
  identified. Through multiple alignment of E. coli 16S rRNA and our
  metagenomically retrieved 16S rRNA sequences, it was found that at
  least 628 (40.7%) of the 1,542 nucleotides were variable, indicating
  marked mutational robustness of the 16S rRNA. Strikingly, the
  functional 16S rRNA sequences (except A10 and F02, which were 99.0%
  identical to E. coli 16S rRNA) obtained in this study showed only
  80.9–89.3% identity to E. coli 16S rRNA, which was well below the value reported thus far (Proteus vulgaris 16S rRNA, 94% identity to E.
  coli 16S rRNA)

For your question

But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB,
  rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a
  particular operon used for the 16S position notation?

I don't think any one of them is considered the reference. The complete E.coli 16S-rRNA sequence reported in NCBI seems to consider a "consensus" of different reported sequences:

[5], [7] contain updated sequence data for the original work by the
  same laboratory [4]. There were too many discrepancies between [4] and
  [5], [7] to list each revision in our sites table. The sequence shown
  is from [7]. [4], [5], [7] point to a number of cistron
  heterogeneities. There is uncertainty, however, with regard to
  assigning these various heterogeneities to specific cistrons. The RNA
  method used by [4], [5], [7] gives the average of all the cistrons
  present in the cell [7]. The heterogeneities are classified by their
  relative proportions into major, minor and undetermined species. The
  sequence shown corresponds to the major species. The heterogeneities
  were annotated as variations in the sites table. It is not known which
  of the residues 'c' (base 633) or 'a' (base 641) undergoes a deletion,
  giving rise to the minor component 'atctg'. [7] suggests the existence
  of one or two mutated cistrons among the known seven cistrons of
  ribosomal RNA. With the exception of a single base deletion, this
  sequence is identical to the current 16S rDNA sequence for the E.coli
  rRNB gene.

The NCBI page also lists different polymorphisms and base modifications in the 16S-rRNA within and between different strains/"species".
NCBI has several partial sequences as well. When I checked for P.aeruginosa and B.subtilis, I could find only one or two complete sequences (rest were partial). Moreover, each entry indicated the strain that it was obtained from. Therefore I assume there is no single reference sequence.
I guess that people do consider the different variants while doing phylogenetic analysis (or simply just look for conserved "signature" sequences for a given species). I am sure that there are computational algorithms for doing the classification in an optimal manner (see Chatellier et al., 2014). Since, I don't have an expertise in this area I cannot say anything conclusively about the routine practice. In fact there is still ongoing research in improving the analysis (for example, Yang et al., 2016 and Sambo et al., 2018).

While I don't have access to the original paper by Ehresmann et al. (1972) that seems to be the source of that sequence, the preview does suggest that their methodology can only produce a consensus sequence.

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How can I get the coding region from gene sequences?
So, I have a file with 600+ sequences of a gene, each one from a different population. This file was obtained after blasting the chromosome sequences against the gene sequence. However, I need the coding regions as well. Should I do the same and blast the chromosomes against the exons, or should I blast the gene sequences against the exons?

Just to be clear, you want the coding region, not the mRNA transcript right?  if so swbarnes2 answer to use blastx should suffice

Not all the exonic sequence is coding. The ends have 3' and 5' UTRs.
Can you find gtfs for your organism?  Those would be easier to work with.
Or, I'd do blastx against the protein, that should pull out just the sequence that codes for protein.


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How to get the file of a published phylogeny of a taxon
If an article has a published phylogeny, is it common to get the newick file with branch lengths from the authors? In order to do further research with the tree.

Look at the R script related to this article. rotl: an R package to interact with the Open Tree of Life data
http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12593/full
install.packages("rotl")
library(rotl)
studies <- studies_find_studies(property = "ot:focalCladeOTTTaxonName",
                                    value = "Caesalpinieae", exact = TRUE)
tree <- get_study_tree(study_id = studies[["study_ids"]][1],
                           tree_id = strsplit(studies[["tree_ids"]],", ")[[1]][1])

# Example 2
cat_studies <- studies_find_studies(property = "ot:focalCladeOTTTaxonName",
value = "Felidae", exact = TRUE)
cat_tree <- get_study_tree(study_id = cat_studies[["study_ids"]][1],
tree_id = cat_studies[["tree_ids"]][1])
cat_tree
##
## Phylogenetic tree with 38 tips and 37 internal nodes.
##
## Tip labels:
## Neofelis_nebulosa, Panthera_tigris, Panthera_uncia, Panthera_pardus, ...
##
## Rooted; includes branch lengths.

It is standard practice for authors to publish their trees on TreeBase for other people to use. They'll usually list the link in the supplementary material of the paper. Some journals made this a requirement for authors.

@Ferroao I'm not sure what you mean, most of the trees on TreeBase have branch lengths

I haven't seen much with branch lengths, as the ones i needed


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If your body can slow down your metabolism, why doesn't it do that all the time?
I've read that in cases such as in anorexia or a lack of food, the body slows down the metabolism to preserve the little food it does get. If it can do this, though, why doesn't it keep your metabolism slowed, preserving energy? Are there effects to slowing down your metabolism?
Edit: I read it in various realistic fiction books about anorexia, which claimed to have accurate medical information. One was Wintergirls, by Laurie Halse Anderson, where the girl with anorexia says she has a slow metabolism, and her doctor mother says something to the effect of "your body's slowed down your metabolism because it thinks you're in a famine."

Low metabolis-> Low ATP. ATP is needed for activity so more activity-> Need of more ATP. Since we didn't need to be very slow like a sloth , therefore our metabolism is not less always.

If I have time to answer I will... but the short answer is that when your body "slows down" metabolism in times of starvation or famine, that also halts growth and reproductive functions as well. Maximal growth and reproduction require an individual with sufficient energy stores.


text:
Are Asian people genetically predisposed to be shorter than Europeans?
People in different countries have different average heights. For example, Wikipedia's article on human height states that Australian men have an average height of 177.8 cm, and Australian women 163.8 cm, whereas Japanese men have an average height of 170.7 cm, and Japanese women 158 cm.
Are these differences in height due to environmental differences between people in different countries, or does genetic differences play a role?
In particular, are Asian people (people from Far East countries like Japan) genetically predisposed to be on average shorter than people who are of European descent?

Related: Height and natural selection in humans?

I would advise against the use of the term "genetically programmed". "Genetically predisposed" would probably be a better term

Note: This is too long for a comment, so I will post it as an answer, even though it is merely an example and not a full answer to your question.

An example of the environmental influence on human body height can be found in the statistics assembled by the Swedish conscription service from 1840s to 2010 (when general conscription ended). During this time the average height of Swedish men (aged between 18-21) increased from 167.4 cm (in 1841-45) to 180.2 (in 2004), an increase of 12.8 cm or 7.6% (Werner 2008, unfortunately in Swedish, but tables 2 and 3 should be understandable). Here is a graph of the data found in the paper:

During this time Sweden has gone from what would have been a bottom-20 position in the wikipedia list of average human heights (close to contemporary India or Mexico) to a top-10 position. This is clearly not due to changes in the genetics of the population, but to changes in the environment (probably mainly due to nutrition). I know that many countries have gone through a similar development, and this is usually refered to as a secular change or trend in body height and weight (see e.g. Roche, 1979 and Loesch et al., 2000 for further examples).
Nothing of this naturally contradicts that genetics is a powerful determinant of human height. However, it shows that the average height in two countries cannot be compared in a meaningful way (at least if you want to infer genetic differences) without knowing something about the nutrition status and the average living conditions in both countries. The situation is rather that genetics is setting the limits of potential height, but that environmental factors will determine the actual outcome. This is also discussed in the paper above, but there are certainly better references to be found in English. In the reference list (#9, #10) you can also find examples of how there are also well-known genetic determinants of e.g. short stature in some human populations (in this case decreased insulin-like growth factor I receptor expression and function in African Pygmys, see ref #10)

Why is it clear that the height change in Swedish men is not due to genetics?

@canadianer Because we don't expect such dramatic changes to happen in frequencies of gene alleles in a human population of that size given the shortness of the period, absence of severe bottlenecks or strong directed selection and polygenic nature of the trait.

See @har-wradim answer. Remember that 150 years is only a couple of human generations, and this drastic change is would require an extremely strong selection pressure. For the most part, this increase in height is caused by the shift from a poor mostly agricultural population to an industrialised, well-fare nation. Also remember that a similar shift has been observed in many industrial countries.

This also doesn't disprove that there is a correlation between genetics and height, it only proves that there are other factors besides genetics. For this, we should analyze a group of Japanese living at least since the second generation in a Western country.

@vsz Agree, and this is also what I'm saying in the last paragraph.


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How to determine the primary Uniprot accession number from a list of accession numbers?
Given a list of UniProt IDs that are linked to an Ensembl ID, is there a way to systematically determine which is the primary accession number with no other information?
According to ExPasy

Researchers who wish to cite entries in their publications should always cite the first accession number. This is commonly referred to as the 'primary accession number'. 'Secondary accession numbers' are sorted alphanumerically.

But what if the order has been jumbled or compiled from a different source and resorted.
For example:
Ensembl:
ENSMUSG00000035642
Uniprot:
Q8R0P4, Q8CF11, D6RJK8, D6RJJ4, D3Z442, D3Z1Q3, D3YZD8, D3YY39, D3YX09, D3YWY5
This question is cross listed on the Bioinformatics stack-exchange.

You might get a better answer to this at the [Bioinformatics.SE] site. Perhaps you should select the curated entry?

I think there is an issue with the terminology. The "primary" accession number, is the first accession number in cases where an entry has more than one accession number, as described in http://www.uniprot.org/help/accession_numbers:

Entries can have more than one accession number. This can be due to
  two distinct mechanisms:
a) When two or more entries are merged, the accession numbers from all entries are kept. The first accession number is referred to as the

‘Primary (citable) accession number’, while the others are referred to
  as ‘Secondary accession numbers’. These are listed in alphanumerical
  order.
b) If an existing entry is split into two or more entries (‘demerged’), new ‘primary’ accession numbers are attributed to all

the split entries while all original accession numbers are retained as
  ‘secondary’ accession numbers.
Example: P29358 which has been ‘demerged’ into P68250 and P68251.

Both reviewed and unreviewed entries can have primary accession numbers.
What you probably mean, as previous posters understood, are accession numbers of reviewed entries as opposed to unreviewed ones.
In that case, you can indeed add "reviewed:yes" to your query, e.g. when you are using the UniProt ID mapping, http://www.uniprot.org/help/uploadlists

Swissprot is the reviewed section of Uniprot's holdings. TrEMBl contains everything else.
Q8R0P4 or Mth938 domain-containing protein (AAMDC_MOUSE) is the reviewed Swissprot, aka reliable, identifier.
When searching in Uniprot you can filter to only see Reviewed/Swissprot identifiers; see the top-left corner of the link above.


text:
Do pyrosomes reproduce by ways other than cloning?
I know that Pyrosomes are large colonies of floating tube-like animals that live in the sea, particularly in the tropics. They are just like any type of free floaters
I know  that pyrosomes can reproduce by cloning, but are there any other ways that they can reproduce?

What research have you done before asking it here?

Please provide a link reference in your question where I have inserted [reference required]. "I know for a fact" is not appropriate here, because it does not provide the means for readers (such as myself) to check the background to a question.

Yes. sexual reproduction. From a <1min google search: "Pyrosomes make both eggs and sperm... alternating asexual and sexual reproduction results in giant swarms of pyrosome colonies." We ask that you do your own research before asking questions on Bio.SE. Please update your question with some indication you've done prior research to avoid having it downvoted/closed. See here for tips on writing good questions. Thanks.

Indeed pyrosomes use a very interesting form of reproduction. They actually use both sexual and asexual form of reproduction each time they reproduce. Pyrosomes, which are colonial tunicates, produce both egg and sperm. In each pyrosome of a colony, a single egg is fertilized and develops into a 4-staged animal. This form leaves the parent body and starts forming its own colony. It does so using the process called budding, which rapidly develops a new colony of pyrosomes. You can see here, here or here for more information.
source (in french though ;)


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Cows milk protein transferability through breast milk
I understand that cow's milk protein(casein) transfers through breast milk via the mother's diet.
I'm looking for the process as in what hormone does it bind to to allow this process in some women and not others?

Can you please show some of the research you have put into this question?


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Is it genetically possible for these to be the parents?
In a human, assuming no mutations, is it possible to have a child with this phenotype, given the phenotype of the parents?
The mother, Alice, has black hair and brown eyes. The father, Bob, has red hair and green eyes. The child, Clare, has green eyes and black hair.
From what I know of genetics, and experimentation using a simplified model, called the 'Genetic Heredity Calculator', this should not be possible.
Being green eyed is apparently a 10%. chance, however resulting in a black-haired child isn't supposed to be possible.
Of course, my understanding of genetics is far from complete. Is it possible, and if so, what is the likelihood that this is the result, knowing nothing else of the parents' genetics, aside from them being caucasian British?
My question revolves around Alice, who has hair well within the commonly perceived range of 'black', which I here define as <7 lightness in HSL, having a child with Bob, a redheaded man, which I shall define as a man whose hair colour in hex is greater than 3:2 r:g, and >30 Lightness in HSL.
Such precision is not required, but exists to put the question in context.

I don't think our understanding of the genetic basis of hair and eye colour are good enough to give you probabilities for offspring to have certain combinations or shades of colours. The possible phenotypic range for these traits always contains at the very least the two parental phenotypes. One parent has black hair - why would it be impossible for a child to have black hair?

I think I found the tool you refer to and it's certainly not to be taken seriously. It output 100% brown hair colour for children of one black-haired and one blonde-haired parent. My parents are that exact combination, and they have one blonde, two brown-haired and one black-haired child.

many genes code for hair color and eyes, not just one. and the chromosomes can be split into 2-3 pieces and jumbled.

unlikely but possible
Eyes. As you already indicated green eyes are possible just through recombination, in fact lighter color eyes are always possible due to mutation. All the major eye colors use the same pigment anyway, it is just amount and depth that varies, so it is not discrete genetic trait meaning ballparking is the best you can do.
Hair. All the necessary genes are present in the parent pool so it is possible. Brown and black hair are just different levels of the same pigments not due to the absence of a pigment like red hair. There is also more than one combination to get both black and brown hair.  If both parents lacked the same pigment (both redheads) it would prevent black or brown hair but this is not the case so black hair is indeed possible, unlikely but possible. Worse hair color genes can be hidden by dominate ones so you can't even guess the parents genes so any estimate will be just guesswork.

Do you have any kind of rough estimate as to how likely it would be?

not aa good one the genetics of hair color is not well understood the physiology of it allows for it however. black and brown are caused by the same pigments so for a really rough back of the envelop you could say half the chance of brown hair, so around 25%,

The genetics of eye colour and hair colour is not easy enough so that we can answer. There are two main issues. 1) The traits in question are quantitative (takes continuous values) and not discrete which makes the expression "brown eyes" a little inaccurate and undefined. 2) Those traits are polygenic traits. In other words, there are a lot of loci that affect eye colour and hair colour and pretty much everything end up being possible.
So, yes it is possible, although it would be more likely that Claire has brown eyes.

Updated for precision

Is it possible for Claire to have 'black' hair?

@Armatus Yes, definitely. Sorry that was a mistake. Thanks for pointing that out

Roughly how likely is having the correct hair colour?

Your follow-up question is partly undefined. We would need an exact measurement of what you call "black" and "red" 2) I would not know anyway and I don't know if there is any study on that.

I did exactly that! Read the question.


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What are the chances that the contraceptive pill will cause death of human zygote?
The preventative pill, as I understand it, can cause zygotes to fail to attach to the uterine wall, or pry them off of it.
Ignoring any and all ethical implications, what are the chances that this will occur, provided the woman in question has taken the pill regularly preceding sexual intercourse, comparing with and without barrier method as well, the latter taking into account if it fails.

You should know that there is controversy on when to even define the beginning of pregnancy, therefore there is a really big assumption (and a lot of politics, whether or not you realize or intend that) in your statement "assuming that this qualifies as abortion." I would suggest rewriting your question to "what is the probability that preventative contraceptive pills will interfere with attachment of a zygote to the uterine wall?"

@BryanKrause Done.

Second comment, which I missed at first glance, is in your second paragraph: Why are you referring to a barrier method? I mean, if fertilization doesn't occur (due to a hormone pill or any other method) it doesn't make biological sense to even evaluate the question.

Which pill? What dosage? All barrier methods? Does that include 'soft' barriers like foam and gel? If you don't know what I'm getting at, it's: this is way too broad, unclear, and shows no research whatsoever.


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Evolutionary advantage of consciousness
What possible theories are out there, regarding the evolutionary benefits of having consciousness? Why is not all information processing done subconsciously?
Can it have something to do with language and communication? But then, a lot of animals can be considered to be communicating without "qualia".
EDIT:
Some background. Philosophy student here. Recently ventured into reading a bit of genetics. Every aspect of life seems to be slowly evolved out of need, either survival or atleast survival till reproduction occurs.
Consciousness, according to me, would be the constant "subjective experience" of our lives, the inner movie as they would say.
My question, then, is why would a part of the brain be dedicated to generating an integrated coherent experience when zombie-like information processing could suffice? Did the ability of movement, along with certain cognitive skills, really make the upper mammalian habitat so unpredictable that genes had to adapt to "every-situation-might-be-a-new-situation" level of brain capacity?
Has any biologist written about the evolution of intelligence (which is a precursor to the consciousness I'm talking about) corresponding to early humans?

I find it hard to disantangle evolutionary advantage of counsciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness. Can you please try to explain in what way is your question different from just asking What are the evolutionary advantage of high cognitive abilities in humans??

Although there is no mention of consciousness, you might want to have a look at wikipedia > Evolution of human intelligence.

Machiavellian intelligence and advanced communication can be categorized as reactions to situations. Or tools for problem solving. But the "subjective nature of experience" develops in the more advanced animals. I suppose the constant self awareness in conscious stream of thought, is what I meant by consciousness.

To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

This has the possibility to be a very good question but it needs to be fleshed out a bit. Your first problem is defining what you mean by consciousness.

DISCLAIMER
I know little on the subject. I want to first express my personal views of the existing difficulties at answering this question and then I will attempt to give a short overview of the potential answers I could find.
ISSUES WITH THE QUESTION
Consciousness vs higher cognitive abilities
I personally find it hard to disentangle evolutionary advantage of consciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness.
So, a very important issue with the question is that 'consciousness' is not well defined.
Only few peer-reviewd papers on the subject
While there are a number of ressources in the non-peer reviewed literature (mainly books or popular articles) on the question, I could not find a lot of papers in the peer-reviewed literature. I suppose again that part of the issue that prevents much discussion in the subject is the absent of a commonly agreed upon definition of consciousness. Some of what I'm about to quote is not peer-reviewed and some are not written by biologists but philosophers.
Evolutionary psychology remains very theoretical
One would note as well that most work in evolutionary psychology remains mostly theoretical as it is often hard to perform meaningful empirical testing for the existing hypotheses.
Quoting for safety
As I often failed to make sense of what I just read(!), I will try to quote quite  a bit to avoid misinterpreting other authors.
ANSWER
Definition of consciousness
I recommend having a look at Perlovsky (2007) for a semantic discussion (and opinion) on the concept of consciousness. Quoting their full abstract

The knowledge instinct is a fundamental mechanism of the mind that drives evolution of higher cognitive functions. Neural modeling fields and dynamic logic describe it mathematically and relate to language, concepts, emotions, and behavior. Perception and cognition, consciousness and unconsciousness, are described, while overcoming past mathematical difficulties of modeling intelligence. The two main aspects of the knowledge instinct determining evolution are differentiation and synthesis. Differentiation proceeds from and unconscious states to more crisp and conscious, from less knowledge to more knowledge; it separates concepts from emotions, Its main mechanism is language. Synthesis strives to achieve unity and meaning of knowledge; it is necessary for resolving contradictions, concentrating will and for purposeful actions. Synthesis connects language and cognition. Its main mechanisms are emotionality of languages and the hierarchy of the mind. Differentiation and synthesis are in complex relationship of symbiosis and opposition. This Leads to complex dynamics of evolution of consciousness and languages. Its mathematical modeling predicts evolution of cultures. We discuss existing evidence and future research directions.

Consciousness as a by-product
To my personal experience, consciousness is in general viewed as a by-product of the selection for specific cognitive abilities. Again, without much of a definition of consciousness it feels to me that selection for specific social skills, such as those requiring the Theory of Mind (ToM) would yield to increase consciousness.
If consciousness and ToM (and other related cognitive skills) are the same thing, then we got our answer, otherwise, the standard view is to consider consciousness as a by-product of the selection for those higher cognitive skills.
On the topic, see for example Judd (1910) (did I really cite such an old paper?) or Dennett (1980) (Dennett is a philosopher, not a biologist).
In the comments the OP said

To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

I would note that, if taken as an argument, then it would be a logical fallacy called argument from incredulity.
Consciousness as a result of higher social abilities
This opinion seems quite related to the previous one. Quoting from Ingold (2005)

Becoming a person is thus a matter of gathering social relations into the structures of consciousness: the movement in development, as Vygotsky put it, is ’not from the individual to the socialized, but from the social to the individual’
[..]
as relationships unfold in the course of purposive social action, they are
  enfolded in the consciousness of persons, that is, in the structures of the self.
  The connection between social relations and consciousness should thus be
  understood in terms of unfolding and enfolding, rather than in terms of cause
  and effect
[..]
This view of sociality, and the theory of direct perception on which it is
  founded, suggests that it is possible for persons to engage with one another on
  the basis of shared perceptual experience prior to the objectification of that
  experience in terms of collective representations encoded in language and
  validated by verbal agreement. Thus sociality is possible in the absence of both
  language and the kind of objective self-consciousness that (probably) depends on language

Conscioussness as result of the logistics of decision making
Quoting from Merker (2003)

Consciousness will be interpreted as a biological
  function evolved by mobile animals as a solution to neural logistics problems inherent in the
  control of orientation to their surroundings. The interpretation is motivated by the conspicuous
  absence from the contents of consciousness of two significant classes of information known to be
  present in brains, one on the afferent and the other on the efferent side of neural function. In fact,
  the thoroughness of their exclusion from consciousness suggests that their absence represents a
  design feature of consciousness providing important clues to its nature and biological function.
  This in turn helps constrain conceptions of its neural implementation as well as the search for its
  origin in the phylogeny of life forms

The problem with the question is that 'consciousness' is not well defined. +1

I'd note that the way most neuroscientists use the term "consciousness" it has little or nothing to do with theory of mind. Theory of mind requires consciousness but not the other way around; theory of mind is a much higher bar to achieve.

You put a lot of effort into answering a terribly unclear question!

I agree. However, 1) this type of question has already popped up several times in the past (and having said somewhere on an SE post that a big part of the issue lies in the definition of consciousness may be helpful in the future) 2) there is some literature on the subject 3) the question has already received 3 upvotes (non of them being mine).

Also, I have received this question twice myself and it is always unsatisfying for someone asking a question to just get a "your question is unclear" kinda answer especially in a personal setting so I thought I would give it a shot, also to educate myself a little bit. But.... I agree with you @anongoodnurse


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Is it possible that by mutation a human could see infrared or other 'colours'?

Incoming light reacts with the several types of cone cells in the eye. In humans, there are three types of cones sensitive to three different spectra, resulting in trichromatic color vision. Each individual cone contains pigments composed of opsin apoprotein, which is covalently linked to either 11-cis-hydroretinal or more rarely 11-cis-dehydroretina.
The opsins (photopigments) present in the L and M cones are encoded on the X chromosome.  A very small percentage of women may have an extra type of color receptor because they have different alleles for the gene for the L opsin on each X chromosome. X chromosome inactivation means that only one opsin is expressed in each cone cell, and some women may therefore show a degree of tetrachromatic color vision. Tetrachromacy is also demonstrated among several species of birds, fish, amphibians, reptiles and insects.
Humans cannot see ultraviolet light directly because the lens of the eye blocks most light in the wavelength range of 300–400 nm.
So, besides above mentioned exceptions, is it possible due to mutations or genetic engineering to see UV or infrared. What kind of mutations should be made or are the changes to be made in the opsines to big to create 'alien' eyes?

It might be easier to embed a microchip and a camera, though.

I seem to remember that kids can generallybsee farther into the UV range than adults typically do, perhaps because their lenses are smaller... but don't take my word for it.

UV sensing is possible and some animals do have UV-sensitive opsins. IR cannot cause electronic transitions. They can only affect vibrational states. Therefore the mechanism of IR perception would be totally different from that of the UV-visible spectrum.

@keshlam: afaik this is because the lens filters UV and the older you are the more it filters. People without a lens (or artifical lense) are indeed able to see UV, just not as a further colour, more like an overall white glow.

You might be interested in tetrachromates (https://en.wikipedia.org/wiki/Tetrachromacy) there seem to be some humans that are able to it.

Yes.
Far-red vision (>700nm)
The ability for retinal-binding proteins to absorb far-red (between 700nm-850nm) light has been experimentally confirmed in this paper. While the authors did not attempt this in vivo in an animal model, they managed to use directed mutagenesis to induce a significant shift in the absorption peak of the chromophore of the retinal binding protein.
The authors show the shifts induced by these mutant proteins in the figure below. The mutants have significantly different absorption peaks, and assuming that the proteins do not lose their ability to transduce signals via optic nerves, they would allow vision in different wavelengths.

Ultraviolet vision (300-400nm)
It is known that humans lacking a lens (aphakia) are able to see ultraviolet light. As noted in the question, the lens blocks out long-wave UV, and its removal or absence results in ultraviolet vision (although with low sharpness due to the lack of a lens).

However, aphakic patients report that the process has an unusual side effect: they can see ultraviolet light. It is not normally visible because the lens blocks it. Some artificial lenses are also transparent to UV with the same effect. The receptors in the eye for blue light can actually see ultraviolet better than blue. Military intelligence is said to have used this talent in the second world war, recruiting aphakic observers to watch the coastline for German U-boats signalling to agents on the shore with UV lamps.

I am not too sure about IR absorption. IR does not have enough energy to cause electronic transitions. Moreover I could not find a mention of "IR" or "infrared" in the linked paper. The wavelengths mentioned there correspond to far red.

Many animals that "sense" IR use thermoreceptors for it. The mechanism is totally different from that of opsins.

@WYSIWYG I don't get what you mean by "doesn't have enough energy". There is an entire field dedicated to absorbances caused by electronic transitions in the infrared region. Furthermore, thermoreceptor-based IR sensing works for far longer wavelengths from 5-30µm. I edited the answer to say "near-infrared" instead, since the M11 mutant has significant absorbance over 700nm (the rightmost boundary of the graph).

IR spectroscopy measures vibrational transitions as clearly mentioned in the first line. I meant that IR does not cause electrons to be promoted to an excited state (that is what I mean by electronic transitions). They cause stretching and bending of bonds (which are vibrational transitions). What you are referring to is called far-red.

Far red (such as 780 nm) is indeed not the same thing as true infrared (beyond c. 800 nm) which can’t activate the normal human red-sensitive opsin. Ī̲ have some mild sensitivity to far red—that is, see a dim red light where some other people see nothing—but it’s IMHO not really “infrared sensitivity” even if LEDs which emit some amount of far red light are labelled as “infrared” for some reason.

March Ho's answer is quite good.  A few extra tidbits:

The population of humans contains DNA encoding for two substantially different M receptors.  (differing by more than normal variation) See tetrachromacy in humans.  (This doesn't produce IR vision except ...)
The population of humans contains DNA encoding for several different L receptors.  Two well studied variants have very similar peak absorbances at $555\,\text{nm}$ and $559\,\text{nm}$.  Although one variant has a slightly fatter "tail" out into the IR, this doesn't normally result in significant IR vision, except ...
People who work with intense near-IR lasers do report seeing a variety of "weird pink" from sufficiently intense lasers.  This happens with scotopic adjusted eyes and seems to be a "hard to interpret" mixture of rod+L excitation.  Also, some people report seeing the Wood Effect (intense IR scatter of sunlight from grass and leaves) when visible wavelengths are filtered out after scoptopic adjustment.  One theory for IR vision in humans is that detection is via a two-photon process in the rods.  Given that only intense sources are perceived, this isn't too far fetched.  (... and is quite cool -- nonlinear optics in your own eye ...)

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


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How exactly is the wood fossil process?
I would like to know in deep how exactly is the wood fossilisation process. I am fascinated how after millions of years the fossil wood preserves its microscopic characteristics. Look at this cross section where you can see clearly differences in the cellular tissues as parenchyma, vessels, and rays.

I know that in the fossilisation process the wood was replaced by mineral particles, but I don't understand how the organic material went outside to stay only the minerals.

there are actually more than one process, but in the case of high detail wood fossils the process is the slow filling in of all the spaces in the wood (filled with water in life) with dissolved minerals from the groundwater. this is called permineralization. Of course this only works is the wood is buried so it cannot rot while this is happening. Since permineralization happens on the molecular level is can preserve great detail as the minerals form around the remaining hard tissue.
This video is a decent representation,


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Will a completely removed cat whisker grow back?
I just accidentally pulled out, while playing, my cat's whisker entirely, follicle and all. I feel terrible as I know she is a kitten and whiskers are rooted deep in a place rich in nerves. I'm wondering if the whisker will grow back and if it will cause a lot of pain as it regrows.

If you're concerned about the pain aspect, approach your vet, as I'm sure they would be able to tell you how to treat it.

The short answer is that yes, they will grow back. Cats do regularly shed their whiskers and grow them back in time (reference). The thing is that if damage has been done to the root of the whisker, it may grow back in an irregular manner (reference). Wish for the best and by now I think the whisker should be back just fine.


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Is there any bank of animations for Embryology?
I am trying to find animations which can anonymous or generalised for Embryology.
However, I have not find any single good source.
Is there any bank of animations for generalised embryos?

I don't know of any database, but a short search brought up a few candidates. Depending on what you would like to see, they should be a good start:

Human Embryology Animations
Simbryo (Flash based)
UNSW Embryology
Embryological Development of the human
Embryodynamics


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Recovering Coma patient with theoretical full knowledge of heart function
In coma, there is the medullary depression (stage of agony).
Spontaneous respiration and circulation cease i.e. vasomotor center.
There is no full circulatory and respiratory support.
Assume you could stimulate and coordinate fully the autonomic nervous system of the heart.
You know exactly which pacemaker cells and pathways are blocked in the particular coma patient.
I have in mind Schumacher's case - where you have head injury.
I think you should consider, in his case, the pressure of the head also if you can restore circulation and respiration artificially.
Some neurologists say that it is practically very difficult to wake a person if he has been in coma for six months.
I would like to understand this.
I think it is because of atrophy of muscles and probably something with atherosclerotic changes.
However, I am still interested in your opinion about the theoretical situation - if you can restore heart and respiration centre, can the recovery start?
What are the limitations of restoring the function of the body by restoring the circulation and respiration i.e. vasomotor centers after long stay in coma?


text:
How does the sticky ends of foreign gene bind with its counterpart in the plasmid DNA if positions are not matching?
Consider  a foreign gene with recognition sequence as GAATTC  for EcoR1. Now suppose that it is being cut at two palindromic sequence  to form sticky ends.
Here the sticky ends are formed such that its position is parallel to each other around the axis of DNA.
The plasmid DNA has a recognition sequence and is  being cut at a  site and as obvious would be  cut with the sticky  ends as  counterparts. If we join the foreign DNA to this vector DNA the problem of combining the DNA arises. How will we cope with this problem  or if I am going wrong can someone tell me where?

I am having trouble understanding your question. Inserting a fragment of DNA into a plasmid is pretty standard procedure, especially if the restriction sites are the same, just cut, purify, mix, and ligate. Can you clarify where you don't understand?

@user137 Let us consider a two dimensional case for this where the DNA is represented by two parallel lines where only one of the lines extended represents the strand with two sticky ends.In the plasmid DNA this would not be the case as the sticky ends are counterparts therefore opposite to each other at the site where it is cut off.This position of sticky ends of the plasmid DNA is not allowing the combination of sticky ends of the foreign DNA.

A drawing would help I guess. I can't visualize the issue.

yeah it would certainly help.But I have some complications in doing so.I am not able to upload the image.I hope some symbols would help.

Now as shown above the question is how would one be able to make the recombinant when the position of sticky ends of both the the plasmid DNA and of the foreign DNA are located in different positions such that when combined only one of the sticky ends gets its complementary while the other doesn't gets it.Think of it in 3 dimensional view, no such change is being observed.

Instead of the ridiculous characters, try and use standard molecular biological notation. Sticky ends will either be a 5' overhang or a 3' overhang. EcoRI cuts between the G and the A and produces a 5' overhang of 5'-AATT...-3'. And what do you mean by "parallel to each other around the axis of DNA" If you are saying that your target gene has two EcoRI sites that flank it then the cut at the 3' end will still produce a 5'-AATT...-3' overhang, but on the complementary strand. If you cut your plasmid with EcoRI then it will pair complementary to those ends.

Assume this is your plasmid (N-Ñ denotes any complementary pair):

And you have an insert which has EcoRI site at its 5' end.
When you do an EcoRI digestion of the insert and the plasmid you'll get these products.

Digested insert:

Digested vector

During ligation, insert will pair with the vector in this manner (black is the vector and blue is the insert):

If you now want to ligate the other end you can use the HindIII site. However, if you have same restriction sites on both the ends (for instance EcoRI) of the insert then you will get two ligated products which will have opposite orientations of the insert.
I hope this clarifies your doubt.

let us take a plastic model of DNA with sticky ends which are also complentary.I take another foreign plastic model of DNA with varying lengths which also have same sticky ends to combine with the former one.Now every length of DNA may not combine with it because of different orientation? We cannot twist it forcefully to combine.

@Sikander I can't really understand what you mean. Are you saying that there is a ssDNA region but only the first few residues are sticky. Ligation would happen only in the situation I mentioned above. You can draw a diagram to illustrate what you are asking. Use powerpoint to make a diagram, save the diagram as a picture and then post it in the question.

In a test tube, where you have added two different pieces of DNA--with complementary sticky ends, if the DNA fragments are too short to circularize--like your plastic model, then what happens is that you form random multimers of the fragments, that all get ligated in a line. Eventually, when their cumulative length allows the two free ends to reach around and find each other, you will achieve intramolecular circularization.  This can all be assayed be gel electrophoresis and electron microscopy.

@mdperry yeah! that is the possible answer  I was looking for.You mean that there are many foreign fragments which will linearly combine till they get such orientation that their sticky ends are able to combine with their complementary in vector DNA.

@Sikander Yeah they can form multimers. Typically you should get a distribution of number of multimeric repeats. It also depends on concentration. In any case it would be great if you can add an illustration in your question to clarify the exact point that you are interested in.

In the Google search engine I entered "ligation of sticky ends"; then I selected the "Images" tab. Here is the first result, which addresses your question exactly:

This originates from this website:
AddGene
Based on your question it sounds like you understand the basic rules of forming Watson-Crick base pairs; but your diagram and question omits the innate polarity of the sugar-phosphate backbone in DNA and RNA. The convention in depicting double-stranded DNA is that the "top" strand (sometimes referred to as "Watson") is written in the 5'-to-3' direction, reading from left to right. Since the two DNA strands are anti-parallel, it follows that the "bottom" strand (maybe nobody refers to it as "Crick" any longer?) is written in the 3'-to-5' direction -- if you are reading from left to right.  If you want to decode the biological information encoded in the bottom strand then you need to read it from right to left.
This is a long-winded way of saying that I usually note the 5' and 3'-ends on a drawing of DNA to emphasize this, and if I can figure out how to do so I will update the image.
Here is a slightly better version from Google:

Which is from this site: A WordPress Blog

my question is different.Now consider the one Watson strand of some foreign DNA. As one move from 5' end  we get the sticky end 5'-AATT.After some locations let the sticky end start again as 5'-TTAA.Now when we combine this foreign DNA piece to the plasmid DNA it is not necessary that the sticky ends of foreign DNA just fall above their complimentary cut counterparts of the plasmid DNA to complete the helical structure.

You may be confused about palindromic DNA sequences. Perhaps the simplest explanation is this: The Eco RI enzyme recognizes and cuts this double-stranded sequence: 5'-GAATTC-3' This sequence is the same on the top strand AND on the bottom strand--if you read the sequence in the 5'-to-3' direction. All of the sticky ends generated after digestion will have the sequence 5'-AATT-3', and will therefore form Watson-Crick base pairs with each other. There is no such thing as a 5'-TTAA-3' sticky end generated by Eco RI. That would require a completely different enzyme.


text:
What is the silencing mechanism of AGO1,AGO3 and AGO4?
I read that this proteins lack of slicer activity, so what mechanism do they use to perform gene regulation?

Just the presence of a large protein complex in the 5'-UTR of an mRNA can prevent ribosome binding and therefore translation. I'm not saying that that is the actual mechanism, but it's plausible.

Ago(s) of what organism? I presume you are talking about mammalian Ago. I am asking this because Ago proteins with same name may not be orthologs; for e.g. Drosophila Ago3 (along with Piwi and Aub) belongs to the Piwi family which in vertebrates includes Piwi, Piwi-like and Piwi-2. Also, there are differences between Ago1&2 of Drosophila and mammals. Plants have many Ago proteins (even C.elegans)

Paper by Zinovyev and colleagues in the paper "Mathematical modeling of microRNA‐mediated mechanisms of translation repression" find that there are reports to 9 different mechanisms of miRNA-regulation.

Here we are reviewing available experimental data on all reported mechanisms of microRNA action, grouping them in a way which elucidates the main details supporting each of these proposed mechanisms.

Here is a list of the mentioned mechanisms:

M1: Cap-40S Initiation Inhibition
M2: 60S Ribosomal Unit Joining Inhibition
M3: Elongation Inhibition
M4: Ribosome Drop-Off
M5: Co-translational Nascent Protein Degradation
M6: Sequestration in P-Bodies
M7: mRNA Decay
M8:  mRNA Cleavage
M9: Transcriptional Inhibition Through microRNA-Mediated Chromatin Reorganization Following by Gene Silencing

Also here is a link to the Pubmed entry of the article:

Perhaps you could briefly summarize the mechanisms.

And could you add a proper citation with a web link? -1


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Time lapse between fresh blood's exposure to air and that same blood turning darker red-brown
For investigative purposes, I'm searching for a tool that can be used as a quick visual assessment of the the length of time that blood has been exposed to air after the blood flow has stopped.. Let's say that you walk into a room and see someone unconscious. Where blood appears, it had already stopped any fresh flow & has already dried to a dark brown similar to mahogany wood.  That person has been there longer than how many minutes? Please understand that I'm not asking how long the person has been lying there but for at least how long?
You come upon a dazed person unsteady on their feet with an injury to the face. The blood flow has stopped: the person may have smeared the blood when touching their face but you  see that the blood has not changed to a deep brown and still retains a bright red color..approximately how much time has likely elapsed between the injury occurring and your encounter with the injured person?
I know there's no exact time estimate possible without testing but simply for quick field assessments, is anyone willing to hazard an opinion?
In summary: How can I tell the age of a blood stain?

It appears you are asking about blood clotting time. You should clarify your question to prevent misunderstandings on what the question is about.

I don't think it's unclear at all what's be asked; it's not about clotting necessarily.

If the coloring process is gradual, then the question needs specification as to what the PO regards as the end point

Is this what you are wanting to know about?

Good Gravy - thanks so much ...while not the answer I seek, very interesting none-the -less

I edited this... Y'all see what he wants now?

In comments it been discussed that clotting is partial answer to OP. I would say, that is is somewhat tangential to the original question.
If I may re-phrase, OP asks: how one can estimate age of blood that has been exposed to air? Problem is that you will have to have a starting point to solve that backwards, like having an initial condition for solving differential equation.
One example that can be used is measurement of $pCO_2$ content in blood serum. If it is available, someone already collected this data. In 2 hours $pCO_2$drops 30% and total $CO_2$ drops about 6%.
Moreover, it seems that during hemorrhagic shock RBC shape changes, which means that sampling patient you will be able to approximate time since bleeding started. However, you will need an electron microscope at your disposal...
Finally, and I'll leave it like that, cellular death is a powerful process that leaves a lot of traces. Apoptotic cells have mitochondria bursting (except in RBC there are no mitochondria) and releasing, for example, cytochrome C. In case of bleeding probable cause of cellular death is necrosis, so different biochemical changes will occur. Point is that you can measure time since necrosis/apoptosis started by careful measurement.


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Proteins: Post translational modification
I am a physicist and trying to understand some protein chemistry for a small project. Basically, amino acids combine to form proteins and after forming the primary structure, some chemical modification may occur, such as phosphorylation or glycosylation (post translational modification). In case of the enzyme carbonic anhydrase a zinc ion is added post-translationally as a cofactor. (The amino acid sequence can be seen here (scroll down to 'sequence' title).

Is the attachment of zinc regarded as a type of post-translational modification?
When carbonic anhydrase is denatured, is the zinc ion released in the medium?
Will the amino acid sequence (primary structure) be changed after denaturation? If yes, are amino acids removed after denaturation, if yes, which?
I guess Zinc will be removed after denaturation. Is the remaining structure the primary protein structure?

1) Is the attachment of zinc regarded as a type of post-translational
  modification?

It is not really considered a post-translational modification because the zinc atom is not covalently bound to the protein. Binding to zinc is adsorption.

2) When carbonic anhydrase is denatured, is the zinc ion released in
  the medium?

Yes, but it depends on the extent of denaturation too. Metal ions can be removed using chelating ligands like EDTA, without actually denaturing the protein.

3) Will the amino acid sequence (primary structure) be changed after
  denaturation? If yes, are amino acids removed after denaturation, if
  yes, which?

Denaturation does not include cleavage of covalent bonds. There won't be change in the amino acid sequence.

4) I guess Zinc will be removed after denaturation. Is the remaining
  structure the primary protein structure?

Yes; just the polypeptide.

So how the protein sequence will look like after denaturation (the sequence given in the link in my question)? How I know the letter corresponding to the Zinc (is it M?)?

@aneps It will look the same. M is methionine


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Database of medically validated SNPs
I'm looking for all possible sources of clinically tested human SNPs. There is a handful of databases that store SNPs (like dbSNP), but I only need those that have validated presence/absence of phenotypic effects with some additional metadata. Thank you in advance.

Any type of disease, or just a subset?

@mdperry any Mendelian disease will do.

@EliKorvigo Did you not find the desired information in the GWAS databases that I mentioned below?

@WYSIWYG I'm struggling to find true negatives. I've already found plenty of true positives though. Thank you for your answer. I'll wait a couple of days before accepting it in case someone else comes up with a valid way to find true negatives.

@EliKorvigo I think for that you may have to check the original study and get the statistics

@EliKorvigo - Be wary of the statistics for GWAS studies. Clinically we don't get too excited about them because the cost-effectiveness of doing a study has surpassed the ability for appropriate statistical analysis - the sample sizes are almost always much too small - too much noise to signal - there are several reviews to discuss this, e.g. [http://www.ncbi.nlm.nih.gov/pubmed/18464043] (review)

@VanceAlbaugh Thanks for pointing that out. Yes, at this moment we have a lot of data but we should be careful before making inferences. There have been a lot of discussion about doing the right statistical analyses.

@VanceAlbaugh exactly. That's the whole point of this question - I can't rely on available bioinformatic GWAS studies to come up with a set of true negative SNPs due to statistical issues. Hence I desperately try to find something that was clinically validated.

@EliKorvigo - yeah, good luck with that - I don't know of any GWAS studies that have reproduced externally in a statistically sound way and have been published. If someone did that it would be a big deal because the analysis of the data hasn't been perfected. We have similar questions in metabolomics, proteomics, and RNAseq. Too much noise, not enough signal.

I've added some references to the data I've managed to collect.

You can search by traits (mostly diseases) for genome wide association, in these databases:

Gwasdb2
Human genome variation Database: it also links to a Copy number Variation (CNV) database.

Just to make this post a tiny bit more useful, I must add that there are several additional sources I've found:

UniProt has an open dataset called humsavar
ClinVar database
HGMD database
OMIM
A paper with a manually collected database based on recent publications in Nature Genetics.

Different datasets intersect to some extent, but all in all you get over 200k somewhat validated SNPs.


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Can recessive alleles be expressed?
Say I have a disease that is autosomal recessive. If one was heterozygous for this trait, could the recessive gene still be expressed?
I know sickle cell anemia has a heterozygous advantage so it must be possible but what are the conditions for this to happen and also to what degree?
EDIT: This isn't asking how a gene is recessive or dominant in a molecular level.

Possible duplicate of What makes a gene dominant or recessive

I disagree that the post is a duplicate. This post has to do with the semantic of dominance interaction. I think the OP did not realize that for talking about dominance interaction one must chose a phenotypic trait of interest. The other post has to do with the molecular mechanisms yielding to dominance interactions between alleles.

Retracted my vote.

Short answer
The concepts dominance, additivity, epistasis, recessivity and others are all specific to a given phenotype. Here you are getting confused because you are considering two different phenotypes at once.
Slightly longer answer
By definition, if an allele is recessive, then in the heterozygote state, the phenotype of interest is just like the homozygous dominant. An important point in the above sentence is "the phenotype of interest". A given locus may show a pattern of simple dominance-recessivity for a given phenotype but may show a completely different pattern for another phenotypic trait.
Let's consider your example of sickle cell anemia. For the phenotype which is the disease, sickle cell anemia has a simple dominance-recessivity relationship. However, for the phenotypic trait which is fitness (yes, in quantitative genetics, fitness is often modelled as a simple phenotypic trait), sickle-cell anemia shows (environment dependent) heterozygote advantage. Also, the fitnesses of the two homozygotes differ greatly.
Note that, in reality, very few loci show cases of perfect recessivity dominance.
EDIT
You are considering two (or even three) phenotypes.
First Phenotype: Fitness
Fitness shows overdominance (with highly unequal fitness for both homozygotes).
Second phenotype: Disease
Double mutant are sick, the others aren't. Perfect dominance-recessivity (although if I am not mistaken heterozygotes individuals have some restriction when it comes to scuba diving if I am not mistaken)
Third phenotype: Shape of hemoglobin
If the heterozygote hemoglobin is shaped just like the healthy homozygote, then there is dominance-recessivity. If the shape differs (which might be causing malaria resistance, I don't know), then there is some partial dominance going on.

Ok, so the phenotype in interest (again in sickle cell anemia) is having the disease, which is having the point mutation causing hemoglobin to change shape, and this is simple dominance-recessivity like you said. What I am still confused about is why are heterozygous individuals more fit, because if the phenotype in interest is the change in shape of hemoglobin then in a heterozygote all cells should be normal, and doesn't protect against malaria.

This is a bit simplified but, in the heterozygotes the cells are not 'normal'. Both types of hemoglobin are expressed, it just doesn't result in the disease. Restated, one healthy allele is sufficient to prevent the disease phenotype. At the molecular level both alleles are expressed and that's why the recessive allele protects against malaria, it's still expressed.

@MichaelZheng See edit

Ok I get it, Disease ≠ Shape ≠ Fitness Thanks

Others have already explained. I add some clarifications. You said that you know the molecular mechanism of dominance; revisiting them will answer your queries.
Gene expression means the formation of the gene product in whatever form it is active – protein or RNA. If an allele is recessive it can:

Not form the product
Form a non-functional product
Form a hypo-active product
Form less amount of product

In all but the first case the gene is expressed although it may not give rise to the product of your interest.
Phenotypes of homozygotes and heterozygotes can differ in these different cases but in a strictly Mendelian case, the expression (or non-expression) of the recessive allele has no effect on the phenotype if the dominant allele is present.
Now, one can also dig deep on what phenotype is. Phenotype is an observable manifestation of a trait but with latest technology we can observe even the DNA sequence. In my opinion (in a contemporary perspective), an allele is strictly dominant if a recessive allele present along with it does not perturb the regulatory/metabolic/signalling network at all.

There are a couple of distinctions to make here. You can have an allele which is 'Phenotypically Expressed', that is it's visible at the organism level by some feature. In that case, no, recessive alleles by definition do not express that particular phenotype.
Now at the molecular level things can be different. You have the same two alleles and both can produce equal mRNA and protein levels, but they differ by a nucleotide/codon, which gives rise to the distinct functions and thus produce distinct phenotypes.
At this molecular level, both alleles are expressed and are co-dominant for the phenotype of measuring mRNA variants by sequencing and at the same time, the organism presents only the dominant phenotype.
So it's important to consider in which context one is discussing 'expressed'. If a research paper is about genetic disease, you'll often hear discussion of the 'recessive allele' and still have measurements of it's expressed mRNA. Everyone just knows by convention that recessive in the context of a human genetics disease paper means the particular disease the paper is on or a phenotype that is being discussed.


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Can a dog run 150 km non-stop?
In Werner Herzog's 2010 documentary Happy People: A Year in the Taiga, a dog is reported to run 150 km from the Taiga back to the owner's village, without any stop and seemingly at full speed as it is running next to a snowmobile.
I am skeptical of this. I cannot find any reports of dogs running a distance even close to this. This article on super-distance dogs does not mention any distances over 40 miles (64 km), which is still less than half the distance, and together with the owner running, so at much lower speed.
Can a dog really run 150 km at full speed?

There are 100, 200 and 1000 mile races for huskies, we can check the speeds of the winners of the races: http://www.eaglecapextreme.com/index.php/the-race/race-times
97 miles run in 17.23 hours, gives 5.6 miles an hour, 10 km/h, on a cold day, 12-16 dogs towing the musher and the sledge. without a sledge, a husky can probably run 150km at 15km/h average, so that's 10 hours of running.
there have been studies about husky mitochondria and their biology.


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Does vaccination make the immune system "lazy"?
I was having this discussion with a friend over vaccination against the flu. Although he agrees that vaccination against almost all diseases is necessary, he said that flu shots are not. He argued that the immune system is like the muscular system. It constantly goes through training. Flu shots deprive the body from "natural exercise" since, he believes, we need to train our immune system by getting "the right amount" of the real viruses from the environment. In other words, if we do too much vaccination (and flu shots are "too much") we make our immune system lazy.
Is this true? I know that there is a difference between natural immunization and vaccination, is it correct though to say that the latter makes your immune system lazy? I was under the impression that vaccination's function resembles more the way we learn and memory and less the musclar system which can get lazy.

Vaccines are intended to provoke the exact same immune response as the actual pathogens they're derived from. There is not a fundamental difference between natural immunization and vaccination. I'm not sure what "lazy" would even mean in this context.

@ Harris Weinstein: He argued that flu shots will lead the body to a state of complacency . I believe this is false but I am no expert therefore I could not convince him.

In your friend's language: vaccination means infection by dead viruses. Thats it for the difference.

@ David: I had this discussion and could not convince my friend because of my lack of expertise. I thought I might ask the experts. Sorry.

I feel the same way. From the very little I know vaccination helps a lot in the recognition of an agent. It does not prevent "a fight" (or "training", in my friend's terminology  ) of the immune system when the virus comes into the body. This fight will happen anyways every time. Therefore there is no harm in any vaccination.

Please ready about the hygiene hypothesis; there is a lot of evidence that not being exposed to pathogens weakens our immune systems. Vaccines are boosters of the immune system, not suppressors. We rarely get tetanus any more (quite common once) because our bodies, thanks to vaccines, have been given an immunological boost to fight it. Ask your friend if his mind is stronger if he uses it or if he doesn't.  The answer is obvious. It's similar for the immune system (up to a point.)

Hi Welcome to Bio.SE. I'm +1-ing this question simply because this might be a misconception shared by others, and we should try to properly address it in the answers. Your friend's theory, however, is way off. As @anongoodnurse mentions: vaccines are boosters of the immune system, not suppressors.

Contrary to many beliefs our immune system needs no "training". It is permanently active and confronted with dozens to hundreds of antigens in our food, from dust we inhale and so on. This all happens to protect our body from the environment and the immune system is pretty efficient with that and certainly it is not getting lazy.
By vaccinating against a certain disease, you generate immunogenic memory against this disease. When you then get exposed to the disease, this memory helps to speed up the immunogenic reaction against the disease - ideally you are not getting sick, in some cases the progression of the disease is much milder.
Further reading:

Wikipedia on adaptive immunity
The front line of host defense from Janeway at the NCBI Bookshelf

although there is evidence that lack of exposure may contribute to atopic immune reactions (allergies). The fact these reactions involve the adaptive immune system supports this. Immunization would have nothing to do with this one way or the other though. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)06252-3/abstract


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Trying to understand a scientific text about neurons and dopamine
I'm in the process of reading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564381/ and I'm trying to understand how the predicting is done in the neuron.
What I distilled so far: A cell gets an input, it calculates a probability of reward(bliss potential i like to call it), if it could cause a reward it releases dopamine in a quantity of expected reward.
So right now I'm wondering,  what is the process that goes on to make that calculation. Which input variables does the neuron use to calculate the probability of a reward and how much dopamined to release?
Does it take account which synapses provided the input signals? Or is it the type of input signals? Or a combination of both? Is it the frequency inputs occur?
II need an explaination how the neuron calculates its "bliss potential" as i like to call it, in normal peoples english instead of academia english.
P.s. I don't have an academic background.  I'm just interested in science related things without having a formal education.


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Was there a flu season in paleolithic times?
In temperate climates, flu viruses rise and recede with winter. This is for a number of reasons, including lack of vitamin D production in darkness (which weakens the immune system), dry air (humidity causes viral particles to become trapped in water droplets and fall), and people huddling together inside when it's cold (increasing the likelihood of spread).
So, was there a flu season in prehistoric times, specifically the paleolithic (i.e. before 10,000 BCE)? The first two causes would still apply for prehistory, but the last one might not, since people didn't have houses to live inside back then.
Also, in modern times, flu strains are reintroduced to the northern hemisphere at the start of flu season by travel from the southern hemisphere, but that did not occur in prehistory, which might have stunted the spread of the flu. Another factor is the low population density of prehistory, which may have prevented the formation of viral reservoirs in human populations. There may also have been significant variance by region, considering this is still a factor today. For example, the flu follows a more complex and less predictable seasonal pattern in tropical climates versus temperate.

Edited, focused version of an old closed question that went unanswered.

Looks pretty much the same to me. What did you change? How do you know that migration from the Southern hemisphere didn't occur? Humans have been building shelters (wood houses even) for hundreds of thousands of years. So many suppositions stated as "facts".

I removed mentions of cold viruses (which are several hundred viruses, many distantly related) to focus on the flu, and limited the timeframe to the Paleolithic (which is more narrowly defined than prehistory). There was obviously no transcontinental air travel in prehistory, preventing flu viruses from spreading between hemispheres the way they do today. Houses were much less common before the Neolithic, when humans began farming.

The first transcontinental flight (non-stop) was in 1923, 5 years after the terrible Spanish flu of 1918, which went around the globe twice, almost 30 years before transcontinental flight actually started with three airlines flying (only the North Atlantic, btw.) Houses were far from uncommon; the ancient Pueblo people on North America had multistory-dwelling villages before 10,000 BCE. I think you might be making a lot of unfounded assumptions. People huddled in tents a million years ago. A cough in a tent is pretty significant.

This question is about flu season, not the Spanish flu. Even if there was not transcontinental flight in 1918, there was rapid long-distance travel by ship and rail which obviously was not occurring in prehistory. This would certainly have an effect on the circulation of flu strains. The Pueblo people absolutely were not making multistory-dwelling villages before 10,000 BCE; they did not even exist as a culture back then.

The flu (HnNn Type A variants) is the flu; it spread before air travel; that was my point. The Spanish flu was only a particularly virulent-for-the-young variant. You're mistaken about the ancestral pueblos, and the city of Jericho was a city before 9000 BCE (some scholar date it to pre-agriculture.) Why don't you add some evidence of research to support your claims? You're more likely to get an answer that way.

I'll wait until others add cited evidence of research to support their claims. I added reference links in the previous discussion, but no one else (including you) bothered to, which made it seem pointless. Where is your source that the Pueblo people had multistory-dwelling villages before 10,000 BCE? That is a remarkable incorrect claim.

Overall, to me, this question doesn't appear on-topic for this site. This question seems like it might fit on [history.se], as the question is primarily about history, as opposed to a theoretical discussion of transmission and virulence under specified, or assumed, conditions. However, I'm not familiar with the History site, so I strongly recommend reading that site's on-topic page to verify that this would be on-topic. I'm also not a significant participant on this site, so my judgement that this is off-topic here may be wrong.

@frеdsbend - Human influenza most likely was passed to us by birds, including migratory water fowl. Here's an article for laypersons.

@anongoodnurse I still wonder about the importance of 1) domesticated animals (chickens, pigs, etc.) in transferring the virus from infected wild birds to humans vs 2) humans hunting and touching infected wild birds vs 3) those darn infected wild birds not wearing their masks and coughing on us in closed spaces and giving it to us directly.

@frеdsbend H1N1 was around before the name "swine flu", which AFAIK was coined for the 2009 H1N1 outbreak in USA/Mexico (before this it was known as as swine-origin). The 1918 + 1977 influenza pandemics were H1N1. Some variants of it are endemic in humans and some in birds too. Swine are not the only sources of this influenza strain. Phylogenetics tells us avians are the source of all influenzas (though C/D??); and you can easily isolate virions from water where birds concentrate, so not to dismiss agriculture, but catching it from the wild is certainly possible.

@frеdsbend - I read a fair number of scientific papers on the origin(s?) of human influenza virus(es). The phylogenetics bob1 mentions is the study of the genetic material of the viruses in order to determine the lineage of viruses, i.e. the where and when of a virus. Human influenza virus is an extremely old virus genetically, is most closely related to the influenza viruses affecting the Class Aves, predating pig and chicken farming, predating agriculture, predating any written history. The confidence you have in your (erroneous) opinion is unearned.

@uhoh - your comment is funny and thoughtfully put. The evolution (happening now) of influenza viruses is very heavily studied because of the worldwide morbidity and mortality of the virus, and because of the terrible consequences of a novel avian-to-human mutation that has a high degree of infectivity (the nightmare scenario: a deadly pandemic like that of 1918). While I have no doubt our close contact with birds has resulted in the deaths of some, it has not (to my knowledge) contributed to any serious epidemics. Bat influenza is also a threat, just fyi.


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Public Pacemaker database online?
I am looking for any database about pacemakers with the leads

atria A
right ventricle VR
left ventricle VL

I did not find any in Physionet.
Is there any anonymous data about different situations online or accessible by request?