text:
Webtool to design guide RNA (gRNA) for use with CRISPR-AsCpf1?
My goals are to use a free webtool to:

Identify guide RNAs (direct-repeat sequence followed by the targeting sequence) appropriate for use with AsCpf1 in order to target a specific segment of genomic DNA.
Estimate efficiency and specificity of using the guide RNAs identified by the tool.

Unfortunately, when I tried to do this using the CRISPOR tool, the "Job Status" never advanced past the "Waiting" stage, even after 10 minutes. Attached is a screenshot to show what I see.
Specifically, I used the following settings in my query:
I named my sequence:
Mm Acaca block2 from BLAT alignment
In "Step 1" I submitted this sequence:
aactaaatct ccagcatctc catccccttc ttaggtttat ttattttatg ggtatgagtg
tatgtccgtg caccacatgt gtgcctggtg tctaccaagg taagtagagg tatacaaacc
cttggaattg aattatccac catgccgtca ggtgctggga gcaaattcag gtcctctttt
agagcagcaa gtatttccag ccacttagtc acctctgcag ccccttattt tcacagtctt
gagacaagaa tctcactctt tagcccatat tggcctggaa ctttaggcag tcctgccgga
gtttcagact gctgggatga caggcctgac ccattacgtc cactaaggat ggtttccttt
cctgtgagct agcagcatgt agactccaca aggctcctgg ggaagtgttg ttatagtatg
ttatagtata gttgcgaaag gaaggttttc agaagatatg ggtattacga agaaattcta
tgtaaagttt cttttggatt ctctgtttgt atAGATCCAG CATGTCTGGC TTGCACCTAG
TAAAACAAGG TCGAGACAGA AAGAAAATAG ACTCACAACG AGATTTCACT GTGGCTTCTC
CAGCAGAATT TGTTACTCGT TTTGGGGGAA ATAAAGTAAT TGAGAAGgta agttaaactt
actaaactat ttcgcttgaa gtatgtgaga tttcatgcct agatttgttg tttctgttca
aaaggatatt taggttttta gggactttgc ctttttatgc agggctatcc tttctgtctc
cctagcatgt tactaataca taatctcact gtgtacctgt gtttttacat

In "Step 2" I selected:
Mus musculus- Mouse- UCSC Dec. 2011 (GRCm38/mm10)...

In "Step 3" I selected:
TTTN-23bp - Cpf1 Acidaminococcus / Lachnospiracea

My questions are as follows:

Should I do anything differently to use the CRISPOR tool for my goals?
Are there other free webtools available for me to achieve the goals I outlined above?

UPDATE: I emailed the folks at CRISPOR, and they informed me the site had been down, but they have since restarted it. Hopefully, their restart is sufficient, but I will leave my question up with the hopes that others can point me to more webtools.

Crispr tech. is very cool. Was wondering if you wouldn't mind explaining a little bit a bout the technology and your process described above?

Most online tools will only help you to design gRNAs for Cas9 because it is the one that is most commonly used. I found an online suite called RGEN tools that also has an option for AsCpf1.
However, if you don't find it satisfactory then my suggestion is that you either design your gRNA manually or write your own script (which won't be that complex).


text:
Are casein proteins in UHT milk digestable for infants or toddlers?
As a novice cheesemaker, I have read that Ultra High Temperature prosessed milk is unsuitable for cheesemaking, as casein proteins are denatured and cannot be curdled with rennet.
I have verified that claim experimentally. Although curd has formed, its quality was poor (I managed to make whey-like cheese after further heating though).
As casein is the majority of milk protein and curdling with rennet is important component of milk digestion, I started to worry if feeding UHT milk to toddlers is a good idea. (I also wonder, whether boiling milk may lead to a similar casein denaturation.)
Unfortunately, Wikipedia addresses only the cheesemaking aspect of UHT processing. I do not know whether it is possible to digest temperature-denatured casein (without proper curdling).
Moreover, after some more research I am not sure what is mechanism of milk digestion in infants: Which enzyme curdles milk in human infants?

Why are you asking specifically about infants and toddlers? They have the same enzymes as adults and they typically digest milk better than adults.

@Jan It is exactly because they typically digest milk better than adults. I want to avoid answers based on age-related enzyme production loss. I have been taught in school that our infants produce rennet while adults don't (which I am not so sure any more). For sure a lot of adults do not produce enough lactase - thus I expect there may be similar case with rennet.
Also, because a toddler is the main milk consumer in my family. ;)

Goat’s milk is easier to digest but did you mean cows milk?

UHT treatment increases the digestibility of casein.
Ultra High Temperature Treatment, but Not Pasteurization, Affects the Postprandial Kinetics of Milk Proteins in Humans (Journal of Nutrition)

Moreover, the UHT treatment of milk causes structural changes in its
  protein system. The main change is the denaturation of whey proteins
  and their interaction with casein micelles. Consequently, it was
  expected that the behavior of the UHT milk would be similar to that of
  casein micelles, as observed with native casein. However, it has been
  shown that the interaction between casein micelles and whey proteins
  is also accompanied by a large increase in number of very small,
  soluble particles resulting from the desegregation of casein micelles.
  Consequently, by weakening the interaction forces between caseins,
  heat treatment provokes both a loss of the micelle framework and the
  formation of small aggregates. Correlatively, an increase in the
  amount of nonsedimentable casein has been observed in UHT milk
  following high-speed centrifugation (33). Two effects of these changes
  on milk properties may be softer coagulation and a higher
  susceptibility to enzymatic hydrolysis due to loosening of the
  micellar structure and the presence of small aggregates that may be
  more accessible to enzymes.

In the stomach of adult or infant, gastric acid and the enzyme pepsin denaturate whey and casein proteins from either raw or heated milk Critical Reviews in Food Science and Nutrition). The denatured proteins are then nearly completely digested by the enzymes pepsin in the stomach and by trypsin, chymotrypsin and peptidases in the small intestine (Medical Libretexts.
Humans, including infants do not have the enzyme rennin (chymosin).

Rennin, also called chymosin, protein-digesting enzyme that curdles milk by transforming caseinogen into insoluble casein; it is
  found only in the fourth stomach of cud-chewing animals, such as cows.
  Its action extends the period in which milk is retained in the stomach
  of the young animal. In animals that lack rennin, milk is coagulated
  by the action of pepsin as is the case in humans. A commercial form of
  rennin, rennet, is used in manufacturing cheese and preparing
  junket (Britannica).
Chymosin is secreted in the neonatal stomach of ruminants (cattle,
  goats, camels), pigs, cats, and rats. Animals including humans,
  chimps, and horses have inactivating mutations in their chymosin gene
  and do not secrete the enzyme (vivo.colostate.edu).

There's one study that mentions the presence of chymosin in humans, but the evidence seems to be very weak as described in another Biology SE answer. Some articles, like this one mention chymosin in humans without proper references.

Does it mean that UHT processing does not affect latter cuddling in the stomach?

UHT does not affect casein, but it does affect whey protein. I'm not sure what exactly this means in regard to milk curdling in the stomach. But stomach acid and pepsin denaturate both casein and whey; this does not prevent their digestion or absorption, but it can slow it down, which can be actually a good thing, because it results in more even nutrients supply. In general, various types of heating do not slow down the digestion or absorption of nutrients. In other words, stomach acid affects milk proteins more than heating.

From what I have read so far curdling is important to prevent proteins from leaving the stomach too early. Also, from slide #22 of this presentation on UHT treatment (no further references though) I infer that denatured whey protein may disturb casein curdling.

@abukaj, at the top of my answer, I added a quote from the ScienceDirect article, which says that heating makes both casein and whey proteins more digestible, which means they are both more accessible for pepsin, which breaks them down. So, this first phase of digestion of proteins in the stomach is increased; the second phase, which occurs in the small intestine, does not seem to be increased, but in summary, the digestion time is shorter.

Hesting milk to 90°C does not count as UHT processing. The milk is not even boiled.

@abukaj, I found another source (see in the answer), specifically about the effect of UHT treatment on milk proteins. In short: UHT increases digestibility of both casein and whey proteins. If proteins are digested easier, they will leave the stomach faster, so they will quicker come into the small intestine when they will be digested further. So, in this case, faster passage of protein through the stomach does not decrease but speed up their digestion.

source: Stack Exchange

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sort: votes


text:
Should the sum of RPKMs be constant over experiments
I have cufflinks data from 18 different RNA-seq experiments.
I've noticed that if the sum all the RPKM values for a particular experiment, are vastly different between experiments. How could this be? I was under the impression that RPKM was normalized by the total number of reads. If that is true then the sum of RPKM values for a single experiment should be the same?

I recommend that you ask this question in biostar. This is a valid question and neither biostar nor seqanswers have addressed this issue yet.

I think it might have something to do with reads that do not get aligned. unaligned reads might affect the normalization factor in RPKM, but since it is not aligned it dosen't contribute to the sum of RPKM values.

I guess this arises because of the default cufflinks option --total-hits-norm in which it normalizes the FPKMs with total reads including the ones that are not mapped to a known gene or a predicted gene from the assembly. In the genes.fpkm_tracking file the FPKM values are reported for known/predicted genes. It is certainly possible that the number of genes are different in a certain sample compared to the other and perhaps therefore the sums are different. If you are not interested in finding new transcripts then you can run cufflinks with a reference GTF/GFF file provided using --GFF along with using --compatible-hits-norm.
You can also try this:
Assemble with cufflinks, merge the GTFs with cuffmerge and run cuffquant with the merged GTF.
You can subsequently use cuffnorm to normalize the expression values. It has been observed by me and others that the FPKM value reported by cuffdiff and cufflinks are different which is most likely because of differences in default parameters (see this). The inner operations of cufflinks are not very clearly documented; so I cannot conclusively answer your question.

I fell like the --total-hits-norm must be it. but I cannot confirm either. thanks!

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text:
How much total RNA can be extracted from Drosophila brain
I am wondering how much total RNA could be extracted from a single D. melanogaster brain.
I could not find this information from the literature.
The closest hit was this paper, that claims that 16-21.9µg of total RNA can be extracted from 100 brains, which translates to at least 160ng for a single brain.
I also found in the supplementary material of this paper that 1µg of total RNA was extracted from 5-10 fly brains, which would also make > 100ng for a single brain.
I am asking the question because I am envisioning to perform RNA-seq of single Drosophila brains. The standard Illumina TruSeq library preparation protocol works with 100ng of total RNA. Thus I am wondering if this is realistic, or if I should rather target low input library preparation protocols.

In my opinion you should try low input library prep protocols because in my experience even with a decent quantity of RNA, standardizing the sequencing is not an easy job. The manual says that this kit works with 10-20ng of RNA; always assume the higher limit to be true. There is a higher chance of loss (relative) during extraction also. Try doing precipitation with 5M LiCl and a little glycogen along with alcohol; but assuming your yield is 80ng you can still run replicates for statistical comparisons.

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text:
Oxygen Uptake Rates in Microbial Cultures
Normally if air is sparged into a fermenter, the oxygen uptake rate is roughly equivalent to the oxygen transfer rate:
KLa(C* - CL) = Xμ/YX/O2.
How would this equation change if the oxygen became limiting (DO < 0.3 mg-O2/L)?

If you share with us your background research, it would be useful to the community, and also help us understand your question

I know under steady state conditions (ie when oxygen transfer is limiting) the OUR = OTR - this i know from background research. But if the dissolved oxygen drops below the critical dissolved oxygen concentration wouldn't that change the above expression?

Also, please explain the equation; explain what the symbols denote (what are the constants/variables).


text:
Are people genetically predisposed to being interested in specific fields/ideas? How does specialization occur?
I'm not sure if I formulated my question well, but I'm curious about a couple statements made by Steven Pinker and and James Heckman.
In this interview: http://www.youtube.com/watch?v=KJ9Ad6s8g7I&t=7m51s Steven Pinker says

"there'd be a wide variety of families I could have grown up with and
  had the same kinds of interests"

and in this interview with James Heckman, he says:

But anyway, Smith says people are basically born the same and at age 8 one can't really see much difference among them. But then starting at age 8, 9, 10, they pursue different fields, they specialize and they diverge. In his mind, the butcher and the lawyer and the journalist and the professor and the mechanic, all are basically the same person at age 8.
  This is wrong. IQ is basically formed by age 8, and there are huge differences in IQ among people. Smith was right that people specialize after 8, but they started specializing before 8.

Can anyone explain Heckman's statement that people "start specializing before 8"?
What do we know about genetic influence on interests? (Is this the right stackexchange to ask this on?)

I think the concept you are looking for is the one of heritability.
In short, heritability represents the part of the variance for a trait that is caused by the genetic variance only. For more information, you can refer to this, this, this or this post or to wiki.
This wikipedia article talks about the heritability of IQ in human. It has been measured to be around 0.7.
Of course, heritability in IQ is not the same as heritability of "interests". But I don't know about any measure concerning the heritability of "interests". Such measure will be highly dependent on how you classify interests together. Does a mathematician specialist of probability theory have the same interests than a mathematician specialist of non-linear algebra? Does a Mathematician have the same interests than a chemist? and of a engineer? and of an electrician? Does a butcher have the same interests than a backer? and of a waiter? and of a bricklayer? .. Does anyone who work in business have the same interests? The fewer groups you make, the higher will the correlation between parents and offsprings and the higher is the part of the genetic variance that explain the variance in interests choice.

I guess this is another nature vs nurture debate. IQ may be a heritable trait but the question is whether proclivities are also genetically heritable.

Have there been any "separated twin" studies on this? Although, speaking from informal experience, several of the twin sets I know are in completely different lines of work, if that's any measure of "interest."


text:
Is using Hidden Markov Models to find homologues sensible in abstract, short sequences?
HMM alignment tools like hhpred excel at finding subtle homologues of folded proteins that simpler scoring techniques (such those used in BLAST algorithms) would miss.
I am only looking at a small (20AA) sequence and it is helical throughout.
Is hhpred still likely to pick up on subtle similarities in the basic secondary structure as it would in a folded protein sequence, or would simpler alignment be just as appropriate?

Hi there - seems like you may get an answer from someone on BioStars or another site with more computational/statistical expertise - as this question is not really biological per se, more bioinformatic

Thanks for the tip, I'll give that a go. I think this question is right at the fringe of what is appropriate for this site, but you never know! Someone might have come across this problem before!

TMHMM is a very good standard on predicting the TMHs in the first place, so it stands to reason that predicting homologues using this approach is completely viable.

authors: نعيمة الرماح


text:
Blast output - program to count the number of hits
I have to use the old version of Blast (not Blast+) to compare DNA sequences and I have to know the number of all hits. They are not given in the header and I have to know them for many many of blast outputs and its nearly impossible to count them (or to export them in excel). I think I probably have to write a 'Perl Script' and I did my best but I am not familiar with programming and it is not working. Furthermore I had a look on the internet and they are always comparing it to BIO Search. I have e code, which for me looks pretty good,but it also done a comparison with BIO Search, what I don't need/want.
use strict;
use warnings;
use Bio::SearchIO;

Usage information
die "Usage: $0 <BLAST-report-file> <number-of-top-hits> <output-file>\n", if (@ARGV != 3);

my ($infile,$numHits,$outfile) = @ARGV;
    print "Parsing the BLAST result ...";
    my $in = Bio::SearchIO->new(-format => 'blast', -file => $infile);
    open (OUT,">$outfile") or die "Cannot open $outfile: $!";

# print the header info for tab-deliminated columns
print OUT "query_name\tquery_length\taccession_number\tlength\tdescription\tE value\tbit score\tframe\tquery_start\t";
print OUT "query_end\thit_start\thit_end\tpositives\tidentical\n";

# extraction of information for each result recursively
while ( my $result = $in->next_result ) {
    # the name of the query sequence
    print OUT $result->query_name . "\t";

        # the length of the query sequence
        print OUT $result->query_length;

        # output "no hits found" if there is no hits
        if ( $result->num_hits == 0 ) {
      print OUT "\tNo hits found\n";
         } else {
      my $count = 0;

                # process each hit recursively
        while (my $hit = $result->next_hit) {
            print OUT "\t" if ($count > 0);
                            # get the accession numbers of the hits
       print OUT "\t" . $hit->accession . "\t";
                        # get the lengths of the hit sequences
                        print OUT $hit->length . "\t";
                            # get the description of the hit sequences
       print OUT $hit->description . "\t";
                        # get the E value of the hit
            print OUT $hit->significance . "\t";
                            #get the bit score of the hit
       print OUT $hit->bits . "\t";

                        my $hspcount = 0;

                        # process the top HSP for the top hit
            while (my $hsp = $hit->next_hsp) {
                            print OUT "\t\t\t\t\t\t\t", if ($hspcount > 0);
                             # get the frame of the query sequence
        print OUT $hsp->query->frame . "\t";
                                # get the start and the end of the query sequence in the alignment
                print OUT $hsp->start('query') . "\t" . $hsp->end('query'). "\t";
                                # get the start and the end of the hit sequence in the alignment
                print OUT $hsp->start('hit') . "\t" . $hsp->end('hit') . "\t";
                                # get the similarity value
                printf OUT "%.1f" , ($hsp->frac_conserved * 100);
        print OUT "%\t";
                                    # get the identity value
        printf OUT "%.1f" , ($hsp->frac_identical * 100);
                    print OUT "%\n";
                                $hspcount++;
                            }
       $count++;

                        # flow control for the number of hits needed
            last if ($count == $numHits);
        }
        }
}
close OUT;
print " DONE!!!\n";

May someone help me, please. I need a program, which first tells me the header and then the number of hits. I am a little bit desperate and would be so happy if someone can help me. That would be so nice. Greetings Tina

Could you provide more info on how it's not working? I mean does it run but prints wrong output, or it won't run at all?

If your issue is related to your perl script then this is not on topic in biology-se. If you are interested in general procedure to get total number of hits you can see the above link.

Can you paste the output format?

Thanks for the fast answer. The script i didn't write by myself, I just found it on the internet. I don't get any output, because it works with BioSearch (you have to download). But I think with little changes it could work...but i am not sure (4th line??). Maybe there is a easier way. I just wanted to ask here, if someone has an idea how it will work or how i can reach my aim, counting the hits. In the link you posted is written, that the hits are in the header, but there are not, in my case.

@Nina Paste the first 10 lines of your output. Without knowing how the output looks, we cannot help you

The scrip won't run because it has a missing package that it wants to use (use Bio::SearchIO;) so you either download it , or use a different script

What kind of output do you have? I would recommend the XML output, because it contains all the information and not only a part like the table output for example.  Use -outfmt 5 as parameter. Example: blast -db dbname -query path/to/query -out path/to/outfile -outfmt 5

@Nina The script you posted from the Internet has an absolute dependency on the Bio::SearchIO module of the BioPerl library. The script uses Perl's object-oriented syntax to parse the blast search output file that you specify on the command line. There are a few books that may be of help. Ian Korf and Mark Yandell have a book named Blast from O'Reilly, with working examples of Perl scripts for parsing blast reports. Jim Tisdall has two O'Reilly books, Beginning Perl for Bioinformatics AND Mastering Perl for Bioinfo. One of them has a chapter on parsing blast output (as I recall)

This script, named blast2table.pl is from the code accompanying the Blast book by Korf & Yandell (there is a 3rd author whom I haven't met).
#!/usr/bin/perl -w
use strict;
use Getopt::Std;
use vars qw($opt_p $opt_b $opt_e $opt_m $opt_n);
    getopts('p:b:e:m:n:');
    my $PERCENT = $opt_p ? $opt_p : 0;
my $BITS    = $opt_b ? $opt_b : 0;
    my $EXPECT  = $opt_e ? $opt_e : 1e30;
my $START   = $opt_m ? $opt_m : 0;
    my $END     = $opt_n ? $opt_n : 1e30;

my ($Query, $Sbjct);
my $HSP = "";
    while (<>) {
        if    (/^Query=\s+(\S+)/) {outputHSP(); $Query = $1}
        elsif (/^>(\S+)/)         {outputHSP(); $Sbjct = $1}
        elsif (/^ Score = /) {
            outputHSP();
            my @stat = ($_);
            while (<>) {
                last unless /\S/;
                push @stat, $_
            }
            my $stats = join("", @stat);
            my ($bits) = $stats =~ /(\d\S+) bits/;
            my ($expect) = $stats =~ /Expect\S* = ([\d\.\+\-e]+)/;
       $expect = "1$expect" if $expect =~ /^e/;
            my ($match, $total, $percent) = $stats =~ /Identities = (\d+)\/(\d+) \((\d+)%\)/;
            my $mismatch = $total - $match;

        $HSP = {bits => $bits,
                    expect => $expect,
                    mismatch => $mismatch,
                    percent => $percent,
                    q_begin => 0,
                    q_end => 0,
                    q_align => 0,
                    s_begin => 0,
                    s_end => 0,
                    s_align => ""};
        }
        elsif (/^Query:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{q_begin}  = $1 unless $HSP->{q_begin};
            $HSP->{q_end}    = $3;
            $HSP->{q_align} .= $2;
        }
        elsif (/^Sbjct:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{s_begin}  = $1 unless $HSP->{s_begin};
            $HSP->{s_end}    = $3;
            $HSP->{s_align} .= $2;
    }
}
outputHSP();

sub outputHSP {
    return unless $HSP;
        return if $HSP->{percent}  < $PERCENT;
        return if $HSP->{bits}     < $BITS;
        return if $HSP->{expect}   > $EXPECT;
        return if ($HSP->{q_begin} < $START or $HSP->{q_end} < $START);
        return if ($HSP->{q_begin} > $END   or $HSP->{q_end} > $END);
        foreach my $field ('percent', 'q_align', 'mismatch', 's_align', 'q_begin', 'q_end', 's_begin', 's_end', 'expect', 'bits'){
        print "$field not defined\n" if not defined $HSP->{$field};
        }
        print join("\t", $Query, $Sbjct, $HSP->{percent}, length($HSP->{q_align}), $HSP->{mismatch}, countGaps($HSP->{q_align}) + countGaps($HSP->{s_align}), $HSP->{q_begin}, $HSP->{q_end}, $HSP->{s_begin}, $HSP->{s_end}, $HSP->{expect}, $HSP->{bits}), "\n";
    $HSP = "";
}

sub countGaps {
    my ($string) = @_;
        my $count = 0;
    while ($string =~ /\-+/g) {$count++}
        return $count;
}


text:
What is the purpose of DMT in plants?
N,N-Dimethyltryptamine (DMT) is found, besides humans and other animals, in many plants(50+).
In humans (in the pineal gland) it is suggested that it is used for our immune system.

Immunomodulatory activity may contribute to significant anti-inflammatory effects and tissue regeneration. [Wikipedia]

The question is, could it have a same function in plants or it has a more defending function, like other drugs that are derived from plants?

As you guessed, tryptamine alkaloid biosynthesis is generally associated with herbivore deterrence in plants (see e.g. paper 1, paper 2, paper 3), as these compounds can be toxic to animals. I wasn't able to find a reference specifically related to DMT, as it is only one of a family of tryptamine derivatives. For example, the papers just linked to shows that expression of an enzyme catalyzing the creation of the tryptamine precursor of DMT is associated with lower herbivory by insects and nematodes. The second paper also shows that this seems to have little to do with plant morphogenesis via the auxin pathway, which was an alternate hypothesis for herbivory deterrence.
The papers also include a little speculation about the mechanism by which DMT inhibits herbivory on the animal side; it seems to come down again to animal toxicity and behavioral alteration.
So, as with other cases, likely the reason that plants express many secondary metabolic compounds is the same reason that humans use them, namely that they can have strong physiological effects on animals. But I wasn't able to find literature specifically about DMT in plants.
Hope that is helpful.
Update: found an entomology paper that goes into more detail about the effects of a variety of tryptamine derivatives on leaf-cutter ants. The compounds are toxic, but also there are some interesting insights about effects on insect behavior.
Update 2: Looking at question again, realized that I didn't address immune system response.
What's important to note is that plants don't have something homologous to animal immune systems, e.g. antibodies and so forth. They instead substitute various chemical responses, many of which are mediated by signaling factors such as jasmonate and salicylate, that have strong effects and sometimes e.g. kill off pieces of infected tissue (sort of a scorched-earth strategy). This part of plant biology is quite complex and bears further reading.
So in this sense, yeah, sure, tryptamines could be thought of as an immune system, in that their production facilitates resistance to their biotic environment. But that mechanism is completely different from any immunomodulatory effect of DMT or similar compounds in humans.

Just pointing out that there is no evidence that endogenous DMT in humans is produced by the pineal gland.    There has been much speculation, but the few studies that have measured DMT in human tissues showed the same very small amounts whether or not the pineal gland was included in the sample.    The wikipedia entry for DMT expounds on this..
In any case the amount found in these human assays was far below the amount needed for psychoactive effects.   Anyway, I hope this was helpful, six years later :)

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text:
Convergence compared to genetic distance
Is there an information (preferably in the form of a chart, though anything will do) comparing convergent evolution to how closely related the 2 species are on the tree of life.
My searches for anything touching on this subject have returned nothing
Context:
I was having a discussion with a friend on how similar we should expect alien life to be to earth. The topic of high levels of convergence on earth being indicative of convergence between life on Earth and life with a seperate origin on another planet came up. However it appears to me that convergence tends to happen a lot more in more closely related species, but I have no solid data for or against this idea. For example I don't think any plantae have developed any significant ability to move, like animalia have, which I find surprising as it is a very broad ability.
Please note my knowledge of biology is only on a general level.

convergent evolution is a concept. It does not take a value. It is not a variable to be plotted. What variable do you have in mind?

I know it's unlikely I'll get a chart as convergence is qualitative rather than quantitative. If there is a way that it is measured even in a more fuzzy way, a chart would be great but it's not required.

Technically, it is not qualitative either. It is not not numerical, ordinal, nominal, boolean or whatever. It is a concept. The question of how to measure depend upon what you want to measure and I am afraid we cannot define that for you. Note that among examples of distantly related species that undergo convergence evolution, there are bats and birds, flying squirrel and flying lizards, Euphorbia and Astrophytum, vertebrates and insect legs, dolphins and ichthyosaurs.

Among highly related lineages, the concept of convergent evolution is a bit hard to define though. How differentiated two phenotype must be so as to consider that two lineages have undergone convergence evolution if their phenotype converges. Note that we would rarely be able to detect such small deviations anyway. Another semantic issue is that the concept of convergence evolution can be defined for both phenotypic trait and genetic sequence. I here assumed you were talking about phenotypic trait.


text:
When we talk of functional macromolecules (e.g. proteins as enzymes, hormones, receptors, antibodies etc), towards what are they evolving?�
Actually this is a question which is given in a book and to be honest,it has baffled me.I'm not so much well versed with molecular evolution so my guess would be,say some sort of enzyme which could catalyse more than 1 reaction maybe coz then that 1 will be sufficient enough to do much more work,like it happens at organismic level,like reduction in legs of prawns and shrimps which has happened (earlier relatives has more legs but they were less effective as compared to their modern counterparts).So,my guess would be something like that but as I said earlier,I'm not so good in molecular evolution so please help me out.Or tell me about what were the characteristics or primitive macromolecules and those that occur today and via that,this question might be explained.Also,I've written the question as such given in the book i.e without any changes.

This is a nonsensical question akin to asking you to predict the future. Sure, further evolution of proteins etc may occur, but there is no “master plan”. Whatever TBH is should be ashamed of itself. I vote to close.

I'm voting to close this question as off-topic because the question is based on a false assumption.

Your question is not clear. Can you please [edit] it? Add more relevant details if necessary.

Well,can you explain that what are the changes that anyone have observed in the macromolecules of say the Proterozoic era or Palaeozoic era and the macromolecules that occur today.I guess that the book might be asking for this.........

"I guess that the book might be asking..." is not good enough. Please edit your question with a direct quotation from the book and naming the book, author and publisher. In addition please remove the non-unicode, non-isolatin character at the end of your title and explain what TBH is quoting from that (or delete any mention of it). As I have already commented, the question as you pose it is in my opinion based on a false assumption, namely that evolution is directed "towards" something. If this was only your interpretation of a book, then we can help you if we know what was written.

I think that TBH means to be honest,Read what I've written carefully,I've expressed my view that I myself was baffeled.Also,I've written the exact question of the book as such without making any changes i.e. the question has been copied word by word.The book is NCERT Exemplar problems and the chapter is evolution.I guess that you might be able to find a PDF of this somewhere on the internet.Also, isn't evolution is directed towards making us fitter for survival as quoted by Darwin in his book survival of the fittest.

So the title of your question (complete with dodgy character) is a quotation from a book of exam questions? This was in no way clear, and should have been stated in quotes in the question. What is clear is there is no reason for me to change my attitude to your question, or for you to spend any more time on such the flawed question in the book. One word of advice if you are approaching an exam. Use standard English (“coz” is not), divide your writing into paragraphs, and do not use text abbreviations. Unless you deliberately wish to antagonise the examiners towards you.

I mean I know this seems kinda wacky but this is the only explanation I could think of.Also,I'm kinda new on this website so can you give me some advice about posting question and writing the body please.


text:
How does the symbiotic bacteria reaches a human caecum
My thought on this matter is that we have got a very high pH of about 1.8 in our stomach.So,most of bacteria who came in through food or just open mouth should be killed by it.So,how does a bacterial fauna builds up in caecum.

key word "most"

What do you mean,I couldn't quite get you.Could you please elaborate.

Your own words "most of bacteria who came in ... should be killed..." key word in that sentence is "most" Some preliminary research on your part is expected, I suggest googling "human gut flora"


text:
Is there an adjective I can use to describe body parts like hands, feet, eyes, and ears that exist on both sides of the body's sagittal plane?
Body parts like human hands, feet, ears, eyes, etc. exist on either side of the human body's sagittal plane and can therefore be specified with the adjectives left and right. Is there a special adjective I can use to describe body parts like this that a creature has a left and a right one of? Sentence with desired usage: Hands, feet, eyes, and ears are all ____ body parts.
I need this adjective to not apply to body parts like noses, stomachs, lips, lymph nodes, etc. that a creature either has one of, has more than two of, or has precisely two of but it wouldn't make sense to call one the left and the other the right (e.g. lips).
I'm specifically looking for an adjective to describe body parts that I could say "this creature has a left ___ and a right ___" for.

I think you are describing bilateral symmetry, structures with two copies, one on the right and one on the left. So to directly answer your question: Hands, feet, eyes, and ears are all bilaterally symmetric body parts.
Noses are a little tricky, because there is only one on the midline, but the nostrils are bilaterally symmetric.
Generally, if you can draw a line in the mid-sagittal plane and there is a copy of each structure on the right and left, it's bilaterally symmetric.

The exception for the nose is a dealbreaker for what I'm working on unfortunately. I'm specifically looking for an adjective to describe body parts that I could say "this creature has a left ___ and a right ___" for.

The nose is midline, but its parts aren't (left nostril, right nostril). I don't see a problem there. It's not clear what you are looking for, I guess (or why).

I guess isobilateral can also be used synonymously with bilaterally symmetric.

@kmm The problem there is the body part "nose" can't be used in the sentence I specified in my comment: "this creature has a left nose and a right nose". I don't know how to be clearer about what I'm looking for than the information I've already given. I'm architecting some software relating to the human body that could benefit from an interface that describes an object as being able to have a left or right modifier applied to it.

A structure can be unpaired but have, within it, left and right parts (nose, heart, etc.). Why do you need this rigid, one size fits all definition?

@WYSIWYG neither of those terms properly exclude the body parts I want to exclude. Please re-read the question.

@kmm "A structure can be unpaired but have, within it, left and right parts." Of course it can, but as I've said those body parts need to be excluded from the set of objects that the adjective can be applied to. Also I've explained my use case: I want to be able to call something (e.g. a shoe, hand, earmuff, etc.) a human's left or right version of that thing. A human does not have a left and a right nose, therefore I can't use the term bilaterally symmetric to describe objects in my set since it also applies to objects outside of my set. Trust me that my software needs to be this rigid.


text:
Finding RNA Loops
I was rooting through the literature, but there is too much work on the topic of detecting loops in RNA and the RNA helices that go with them.  Can anyone point to a good review on this topic or even better describe some better performing algorithms?

What exactly do you mean by loops? Just unstructured parts of the RNA (= not in any base pairs)?

A loop in this case would be the result of an RNA helix from a single stranded RNA.  The loop would be the result of the strand forming a helix by itself.

So you only need to find the helices, from there identifying  the loops is trivial. Can the loops have interactions with other parts of the RNA, e.g. pseudoknots? If not, any secondary structure prediction program like mfold should suit your purpose.

just looking for helices.  i wasn't aware that was trivial.. is mfold accurate?

as @MadScientist said mfold or RNAfold(Vienna) should work for secondary structure prediction. Anything flanked by a half-stem should be a loop. Both mfold and RNAfold have a limit on the size of the sequence. They don't take large sequences and splitting the sequence is not a great option because the local MFE may be different from the global one. There is also an experimental technique called PARS in which the RNA is digested with different RNAses (V1, S1) and base-paired regions are identified by sequencing

Recently sequencing approach has been extended to obtain RNA secondary structures in-vivo by using a soluble RNA-methylating agent (DMS).

EDIT: Anything flanked by a half-stem (which pair with each other) should be a loop

any reviews?  the last time i looked this was not a completely solved problem.

As an improvement to what @WYSIWYG mentioned, PARS is fairly low resolution since it is still enzyme based. The newer in vivo SHAPE or DMS-seq methods are much better and more informative.

I frankly don't trust Mfold or RNAfold for finding structure. There are just too many false positives and without experimental verification, it's not reliable. For finding hypothetical local structure, it's great. However to find evolutionary conserved structure MSA methods like what has been used with Rfam are a more suitable way.
Since you asked for Reviews, any of Sean Eddy's Rfam updates are good. I also suggest checking out https://www.mendeley.com/groups/545791/rna-structure/.
But for now, I think Revolutions in RNA Secondary Structure Prediction by David Mathews who developed the Turner rules and Mfold is a good start.


text:
Is oxidative phosphorylation less efficient in gram positive bacteria?
Gram negative bacteria perform oxidative phosphorylation in their periplasmic regions, between the inner and outer membrane where a proton gradient is maintained and used by the ATP synthase to make ATP.
Gram positive bacteria do not have a second membrane, but only a porous polysaccharide capsule.  Oxidative phosphorylation then would on try to pump protons to the outside of the bacterium and it could diffuse out into the surrounding environment.  Does this cause gram positive bacteria to operate less efficiency?  does it make them more vulnerable to a basic pH in their environment?

A similar question was already answered at How do Gram + bacteria use a proton gradient for F-type ATPase? . In those answers, there is a general belief that Gram negative bacteria do not have much control over their intermembrane space pH, because their outer membranes have many porins, such as OmpC, which allows free passage both ways for protons and other molecules smaller than 600 daltons. If that is true, there is not much of a difference between Gram positive and Gram negative ability to control pH just outside the inner membrane.
There is a long review at DOI: 10.1016/j.bbamem.2005.09.010 . The first two examples of pH sensitivity are E. coli (divides more slowly when pH goes from 7 to 8.7) and B. subtilis (divides more slowly when pH goes from 7 to 8.5). The first is Gram-negative, the second is Gram-positive. B. subtilis undergoes growth arrested at pH 9, suggesting it might be more sensitive, but again, the difference is just subtle.


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Why do oviparous animals not have ears?
I was chatting with my friend, and we both found that there's a relation between putting eggs and ears; we count animals and we found that if an animal is oviparous (birds, snakes, etc.), then it does not have ears. We really did our best but we did not find anyone!!
So, Is there any scientific reason laying behind this difference, I'm a little bit curious? Thanks!

Not all snakes are oviparous. For example green anaconda, boa constrictor are viviparous.

Interesting hypothesis! - all of those animals you mentioned in fact do have ears, they just don't have external pinnae. You are probably thinking of these external structures when you are thinking of ears.
Importantly, pinnae are unique to the mammals, and not even all mammals have them. Since most mammals do not lay eggs, that is probably the joint relationship you are recognizing. Monotremes (egg laying mammals) also don't have external pinnae (for example see this book). So, the scientific reason is that both non-egg laying and external pinnae evolved in the mammalian lineage around the same time.
I don't know of any shared benefit for these traits to go hand-in-hand, but you could probably come up with more traits that also largely follow these ones, again because of shared lineage rather than a particular synergy.


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Have researchers discovered how epigenetic information is passed down during cell division?
For example, how are histone code patterns passed down?
This question was asked a few years ago in this thread:
How are epigenetic marks transmitted during cell division?
However, it has been a few years now, and I'd like to know if researchers have made any progress.
Clarification:
I'm specifically interested in figuring out how chromatin modifications are epigenetically inherited. There seems to be some evidence that it can be inherited, but there doesn't seem to be a full explanation as to how.
A good source for what I'm talking about is a article published in 2010 called: "Epigenetics and the Origins of Paternal Effects", which goes into detail on experiments done on rats that show epigenetic traits being inherited across offspring. However, the article ended on a note saying that the evidence is speculative, and further research needs to be done.  Here's the link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975825/


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Can difference in the expression potential of alleles lead to dominance?
Several hour ago I was in thoughts what allele dominance really means on molecular level. As we know from basic genetics, if the organism had Aa type of some gene so trait is controlled by this gene would be equal to AA case. And we see it only when our organism is growing up. I'd like to know, how it works on molecular level, why Aa = AA in phenotype? I suggest, that expression level of A locus is greater than a locus and if so, why? Is that because of chemical structure of dominance allele that RNA polymerase interact with it more frequent?
Please, help me to understand. Thanks.
P.S. I don't consider different gene interactions as epistasis etc. just give you simplest example to describe what I want to know, but any useful considerations are appreciated.

Related posts: http://biology.stackexchange.com/q/1294/3340 and http://biology.stackexchange.com/q/20398/3340

Thanks, i've just read it, but i didn't find full answer. Would be grate if someone describes how RNA - pol chooses allel, or it can be by chance and it's not about chemical structure just depends on size of alleles (i mean, the bigger size allele has, the bigger chance to interact with RNA-pol etc.). Sorry if it sounds simple, don't have biological background.

Dominance is not commonly known to occur because of higher expression level, per se of one of the alleles. It can certainly be a factor but usually dominance is mostly known to arise because of a slight difference in function (or in other words activity) of the gene product (which may be a protein or an RNA).
Note that a change of function doesn't mean the alleles would have a totally different function. It just means that the alleles can be different in the way they function. For example two variants of an enzyme may have slightly different kinetic properties (such as Vmax Km and kcat). While change of activity may generally refer to Vmax (maximum enzyme activity), mutations can also change the other constants. Some mutations can make the enzyme sensitive to temperature by affecting the stability of the overall structure. The extreme would be a functional allele and a non-functional allele.
While concentration of the product does affect its activity, it does not change its specific activity, which may change in the presence of a mutation.
Moreover, even if one allele is actually has a higher expression than the other, the resultant trait can be differentiated from that of the aa homozygote only if the two alleles have slightly different functions or if the difference in expression level between of the gene product in Aa and aa is great enough to elicit different biological effects. In the second case there would be no change in the gene function and the effect of dominance is purely based on gene dosage. This review by Veitia and Birchler (2010) explores the possibility of stoichiometric alterations of macromolecular complexes or cellular networks being responsible for dominant phenotypes*.
Now, how can a mutation lead to a difference in expression level without changing the activity of the product?
There are three cases here:

The mutation is in the expressed region (exonic) but doesn't lead to change in activity (for e.g. synonymous mutations)
The mutation is in the transcribed region but in the intron.
The mutation is in the non-transcribed DNA regions such as promoter/enhancer etc. Exceptions: certain downstream promoter elements are actually transcribed.

Only mutations in the promoters/enhancers can affect transcription by affecting the recruitment of RNA-polymerase. However, you should note that mutations in the non-transcribed regions, especially in the distal regulatory elements are not considered a part of the gene in consideration. Since, such complex modes of regulation were unknown during the time of Mendel, the classical genetics does not explain these effects. Hence, these mutants would not be called alleles of the considered gene.
Mutations in the transcribed regions may affect the elongation rate of polymerase (especially if it leads to formation of stable DNA secondary structures). This is just a theoretical possibility and I have not come across any study that has reported something like this.
However, mutations in the untranslated regions of the mRNA can change the expression of the protein. These mutations may affect post-transcriptional regulation of the protein expression or even the RNA localization.
Synonymous mutations in the coding region can affect the rate of translation and hence the protein concentration.

*(quoted verbatim)

Good answer +1. However, you start saying Dominance is generally not because of higher expression level. I am not so sure about this generalization. Do you have a reference for saying that most often dominance is not mediated by variation in expression level? I think we know too little about the mechansims of dominance and its evolution to make such claim.

@Remi.b I didn't mean most common in statistical terms. By common I mean commonly perceived or commonly known. I'll edit the answer.


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Was Earth's atmosphere more buoyant in the prehistoric era then today?
The mass and size of the dinosaurs and prehistoric insects continues to amaze me. I read from an earlier post that oxygen was more abundant during the prehistoric era. However supporting the weight for me is still a mystery. Is it possible that the air was denser, allowing slight decrease in weight from greater buoyancy?

How much denser should the air be? Unless it's not becoming a liquid, you can forget about this.

@Chris - actually this is a question pertaining to the flight of large reptiles as well, isn't it? So it's not far fetched. Not that I buy that the atmosphere was significantly different then from now.

@anongoodnurse If you go up to 10.000m the air is getting considerably thinner. Yet still birds can fly over the Himalaya without much problem. To have a real impact, the atmosphere had to be much thicker.

@Chris - agreed. I read a couple of papers on this, and the thought was (not mine) that there was more CO2 then, maybe twice as much, which might be enough. In any case, I don't know about aerodynamics. I agree the atmosphere was not likely so very different once sources of CO2 were being sequestered and the oceans were sucking it up out of the atmosphere.

At least for arthropods, the reason for those large species during the mesozoic was simply that their maximum body size scales with the partial pressure of oxygen in the atmosphere. This is due to their relatively simple respiratory system -- they have no lungs but tubular structures that reach into each segment for passive gas exchange.

This belongs at SE Earth science

While it seems difficult to me to imagine any mechanisms that would allow significant changes to the total amount of atmosphere (and therefore density) in geologically recent times (< 100M year), it's quite difficult to find direct evidence about it.
In 2012 Nature published a paper that calculated the air pressure (and therefore the air density) by noting the distribution of sizes of puddles formed by raindrops in 2.7 billion year old ash. The conclusion was that the air was no more than twice as great as it is today.  This amount would be quite a bit for flying creatures, but would be almost completely insignificant for  supporting the weight of large creatures.
As an example, a large elephant has a volume of slightly more than $10m^3$, and a mass of over $5000kg$.  The buoyancy of the air only takes off the equivalent of about $12kg$ of that mass.  Even an atmosphere 10 times the modern density would be little help in supporting its weight.

Is the loading bearing problem still in question, or is it resolved?

This question has an answer with some references.  http://biology.stackexchange.com/questions/1018/how-did-the-huge-dinosaurs-cope-with-gravity-and-loads-on-bones-etc


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Are all pathogens parasites?
If parasites are organisms that feed on other living organisms, then aren't all pathogens parasites?
I've emphasised on 'feed' because I guess the pathogens just eat us (i.e. take nutrients to reproduce and sustain their lives), right?
But then there's another question.
If, pathogens need us (a host) to survive, then why do they eventually kill us? I mean, why did they evolve to become an organism that exploits their food to the extent that even they, themselves die? Isn't it disadvantageous for pathogens to kill their hosts, because they will eventually die?
Or I'm totally wrong, do those pathogen sustain their lives even when host has died?
Or perhaps they don't care if they, as individual organisms die, because they can survive as an species by infecting other.

Welcome to Biology.SE. Parasites usually don't kill their host, parasitoids do. Parasites don't necessarily feed on other living organisms. There are two (or three) definitions of parasitism causing the debates under the current posts. I don't really understand the relationship between the question on the first line (which is a semantic issue) and the question(s) in the last paragraph.

The post "Why do parasites sometimes kill their host?" will probably answer your last paragraph.

Not all pathogens are parasites. Many opportunistic infections can be caused by organisms that are normally commensal or even mutualistic.
For example, this paper describes how multiple bacteria species can be pathogenic as well as mutualistic.

Despite its generally innocuous nature, over the past 20 years S.
epidermidis has emerged as a frequent cause of nosocomial infections.
Several extrinsic factors contribute to the conversion of S.
epidermidis from a member of the resident microflora to an infectious
agent. The bacteria primarily infect compromised patients including
drug abusers, those on immunosuppressive therapy, patients with
acquired immune deficiency syndrome (AIDS), premature neonates and
patients with an indwelling device.
...
Recent studies can be interpreted to suggest that S. epidermidis is a
mutualistic organism, much like the bacteria of the gut. Many strains
of S. epidermidis produce lantibiotics, which are
lanthionine-containing antibacterial peptides, also known as
bacteriocins (Fig. 3). Among the several identified bacteriocins are
epidermin, epilancin K7, epilancin 15X, Pep5 and staphylococcin
1580.37–39 Additional antimicrobial peptides on the surface of the skin have recently been identified as originating from S. epidermidis.
...
The removal of S. epidermidis (i.e. through overuse of topical
antibiotics) may be detrimental to the host for two reasons. Firstly,
removing S. epidermidis eliminates the bacterium’s endogenous
antimicrobial peptides, allowing potentially pathogenic organisms to
colonize the skin more effectively. Secondly, without bacterial
priming of the skin, the host may be less efficient in warding off
infection.

When they are being pathogenic, they are parasitic. Parasitism may not be exhibited all the time. You may say that they exhibit facultative or conditional parasitism. But they cannot be pathogenic and non-parasitic. The only case where that could be true is when the microbe itself dies but also causes harm to the host (like in case of endotoxins).

@WYSIWYG Your statement is absolutely correct. I was intending to show that parasitic (or mutualistic) relationships are not fixed, and can change from time to time.

The question is a matter of definitions.

A parasite is an agent that causes harm to another agent
A pathogen is an agent that causes disease to another agent.
A disease is bad.

Therefore, all pathogens are necessarily parasites. Note that some definitions of parasites, imply that the parasite benefits from the relationship. In which case, then the above sentence (in bold) is true only if all pathogens benefit from being pathogenic.
However, it is important that classifying all living things into one or another category is not feasible. organisms from many species can sometimes be called mutualist, commensal and parasitic (to another agent) depending on the ressources and the life-cycle. For example, "symbiotic" algea are mutualistic when there is light but are parasitic in the absence of light.

As I mentioned in WYSIWYG's answer, from an Immunology perspective, while pathogenic bacteria act parasitically, the classification of an organism being a parasite is limited to Eukaryotic protists or multicellular organisms. The distinction is important as there are much different protocols for treating infections by Eukaryotic organisms than there are for Prokaryotic ones.

The Wikipedia article on parasitic disease goes into more detail. https://en.wikipedia.org/wiki/Parasitic_disease

I wasn't aware of this semantic gap between ecology and immunology. Reading fully the OP's question (I eventually just read the title before :)) I realize that there are a bunch of misconceptions. parasite vs parasitoid, species survival thing, fate of the host, etc... I am too tired to write a complete answer on that now. And I guess there's the issue of the several definitions of parasitism.

Not only active parasitism by pathogens, but any kind of interaction that leads to advantage of one species while causing disadvantage to the other species is considered a parasitic interaction. In this post, Remi has explained why even Batesian mimicry can be considered a parasitic interaction. The only case where a microbe could be pathogenic but non-parasitic is when the microbe itself dies but also causes harm to the host (like in case of endotoxins released after death of the bacterial cell).
Now, as you pointed out, killing the host is like wasting the food but killing of the host is an inevitable consequence of the infection. In fact not all successful pathogens kill their hosts (such as influenza; people die of influenza but it generally has low mortality rate). You can think of this as an optimization problem. The pathogen has to maximize the growth with a constraint on available resources. If the host population size is very large and the pathogen has a decent infectivity, then killing the host would not matter as long as the host population remains more or less stable.
Some pathogenic microbes can even grow for a while inside the corpse. Most of these pathogens are of the opportunistic types. They would thrive on the body of the host better when the immune system has collapsed (which happens at the time of death). These microbes also assist in the decaying of the body.

From an Immunology standpoint parasites are viewed as worms or protists. The discipline of Parasitology focuses on unicellular and multicellular Eukaryotic organisms, where as Prokaryotic organisms are the purview of Bacteriology. While the strict definition of the word would allow for bacteria to be considered parasitic, one could also make the argument that a fetus can also be parasitic, especially if the result of the pregnancy is gestational diabetes or the death of the mother in childbirth.

@AMR from an ecological standpoint, parasitism is any interaction that has a +/- effect. Did you have a look at the linked post?

Yes, however as the question is asked from the perspective of a pathogen, then the definitions of immunology, parasitologist, an bacteriology have more relevance and have a more specific definition of terms.

Fetus, parasitic? I don't know the definition, but my logic says that an organism using another organism of the same species can't be parasitism.. It was a consequence of an effort to continue a particular species, using the organism of same species. It was not effort made by another species, to continue living, by using another one... But this is not the case with microbes. A worm is a parasite because it's multicellular, and a microscopic pathogen is not, because it's unicellular, that doesn't seem reasonable!

@Perceptioner. I wasn't trying to make a case for fetuses being classified as parasites, I was simply pointing out that using the strict definition of a parasite, (see Remi.b's answer) then a fetus could be viewed as a parasite in a woman who develops gestational diabetes during the pregnancy or if the pregnancy results in the death of the pregnant woman.

@AMR the immunological terms, I would say, are a bit obsolete. I am not an ecologist per se but I think that the definition of parasite as mentioned by Remi is the correct one, which is also applicable in any context. Parasitism refers to a relationship and not a class of organisms. Oh yes foetus is parasitic, and I too have once mentioned this elsewhere.

Look at my comments to Remi.b's answer below. Parasitic disease are not considered bacteriological in nature, though bacteria can act parasitically. The definition of parasite and parasitism likely predates the discipline of immunology, so I would hardly say that the immunological term is obsolete. Also as I pointed out, there is an important distinction as bacterial infections have different treatment protocols that those of infections derived from Eukaryotic organisms. Modern antibiotics actually exploit those differences to kill bacteria while leaving the eukaryotic host relatively unharmed

@AMR Comments are not for suitable extended discussion; this conversation has been moved to chat.

While all pathogens act parasitically, a definitional distinction is made between Eukaryotic parasites; protists, worms, and ectoparasites such as lice, and pathogens such as bacteria, viruses, and even eukaryotic fungi.
The Center For Disease Control's resource on Parasites states:

A parasite is an organism that lives on or in a host organism and gets its food from or at the expense of its host. There are three main classes of parasites that can cause disease in humans: protozoa, helminths, and ectoparasites.

The World Health Organization fact sheet on Antimicrobial Resistance refers to parasites separately from Bacteria, Viruses, or Fungi:

Antimicrobial resistance threatens the effective prevention and treatment of an ever-increasing range of infections caused by bacteria, parasites, viruses and fungi.

The American College of Physicians makes the same distinction on its page describing the specialty of Infectious Diseases:

ID specialists have expertise in infections of the sinuses, heart, brain, lungs, urinary tract, bowel, bones and pelvic organs. Their extensive training focuses on all kinds of infections, including those caused by bacteria, viruses, fungi and parasites. Many ID physicians specialize in treating patients with infections due to human immunodeficiency virus (HIV), the cause of AIDS.

Even the Wikipedia page on Parasitic Diseases points out the distinction:

Terminology
Although organisms such as bacteria function as parasites, the usage of the term "parasitic disease" is usually more restricted. The three main types of organisms causing these conditions are protozoa (causing protozoan infection), helminths (helminthiasis), and ectoparasites.(1) Protozoa and helminths are usually endoparasites (usually living inside the body of the host), while ectoparasites usually live on the surface of the host. Occasionally the definition of "parasitic disease" is restricted to diseases due to endoparasites.(2)

In my opinion this is an important distinction to make. The treatment protocol for prokaryotic organisms and eukaryotic organisms are different. Evolutionarily, eukaryotic organisms are far closer to us than prokaryotes, and so strategies such as disrupting the ability of a ribosome to translate proteins, a method that some classes of antibiotics employ, would not only affect the protist or worm, it would more than likely affect our own cells ability to produce proteins. In bacteria, the ribosomal subunit is different enough that it can be targeted by medicines, yet similar enough that we can use them in recombinant DNA technology to reproduce mammalian genes. The closer we get evolutionarily to the pathogen, the more alike their molecular machinery is to our own.
Even our own immune system makes a distinction. Leukocytes such as eosinophils are usually only raised to combat parasitic infections. Organisms that are medically termed as parasites also pose a problem in that they are often larger, protists, or much larger, worms, and our phagocytic cells such as macrophages and neutrophils are unable to phagocytose them as a way of clearing an infection.
From your question, you ask

If parasites are organisms that feed on other living organisms, then aren't all pathogens parasites?
I've emphasised on 'feed' because I guess the pathogens just eat us (i.e. take nutrients to reproduce and sustain their lives), right?

There are a host of organisms that live in and on the human body, that feed and reproduce in us and on us that do not do us any harm, known as commensals, and might even be symbiotic, gut flora. However commensals and even symbionts can do harm if they gain access to areas of the body other than their niche locales.
In fact, immunologists often view commensal organisms as part of the bodies innate immune defenses against pathogens. Because they take up space and use resources that would otherwise be used by pathogenic organisms, then serve to limit the ability of pathogens to reproduce and to gain access to tissue that would be vulnerable to the pathogen.
Commensal organisms can become opportunistically pathogenic if they gain access to sterile environments within the body that have not evolved to live "in harmony" with these organisms. An example of this is peritonitis. We can live our lives perfectly fine when our intestinal bacteria remain within the intestines and the colon, however if those tissue are damaged and perforated, these organisms that posed no risk to our health, and actually probably provide a benefit can lead to serious infection and possible death.
There are also commensal Eukaryotes, such as mites and fungi that either do no harm or are kept in check by a properly functioning immune system.
You also ask:

But then there's another question.
If, pathogens need us (a host) to survive, then why do they eventually kill us? I mean, why did they evolve to become an organism that exploits their food to the extent that even they, themselves die? Isn't it disadvantageous for pathogens to kill their hosts, because they will eventually die?
Or I'm totally wrong, do those pathogen sustain their lives even when host has died?
Or perhaps they don't care if they, as individual organisms die, because they can survive as an species by infecting other.

I think where you might be going wrong here is that you are thinking in terms of sanitary and clean forms of death and burial that is a social construct of human primates. Through much of the evolutionary history of multicellular organisms, when organisms died, they died in place and decomposed. This decomposition allowed the pathogenic organisms a route to go on and spread to other organisms. Other living organism came in contact with the decomposition and the pathogen had a way of spreading.
Also many bacteria and viruses can survive outside of their host for extended periods of time, so they in effect are dormant in the environment until they come in contact with a new host that they have the opportunity to infect. In this case, the most important thing for them is to escape the host until another suitable host comes along that can sustain an infection.
Though there are pathogens that have evolved the ability to circumvent our social norms. The body of a victim of the Ebola virus is highly contagious and can infect those that ritualistically tend to the body for burial. The WHO has developed guidelines to try and respect the cultural customs of burial while also preventing the spread of the disease. You could also think of Cholera. Vibrio cholera reproduces extremely rapidly in the host, and the toxins that it produces cause the host to expel the pathogen at a rate that can kill. This serves cholera as it can then go on to infect a new host.
You also have to remember that there are pathogens that are pathogenic in one organism but commensal in others. The parasite that causes malaria is commensal in mosquitos. The vector for Ebola is thought to be bats, but bats do not succumb to the disease. So for pathogens like this, the strategy would be to find a reservoir vector, then find a host where they can replicate, then escape that host either to reinfect another host or find another carrier where it can survive commensally.

The sites that you have mentioned and the classification that they make is more like a layman classification. It is not in strict sense based on any particular convention. These sites may be of credible institutions but the sites themselves are not standard sources of reference. Plus, I again emphasize, parasitism is an ecological relationship and not a classification of organisms. Phylogenetics is there for the classification.

The audience for ACP is prospective physicians.... It is how Janeway Immunobiology, the textbook recommended by many graduate Immunology and medical schools refer to it. It is how Parasitologists refer to it. It is how Bacteriologists refer to it. You seem to be the only person that I can find that has a problem with it. If I go to a doctor and they diagnose me as having a parasite, they will never be referring to viruses or bacteria... If my dog' vet tells me he has a parasite, I guarantee that 100% they are referring to a protist or worm, not bacteria or a virus, not even fleas or ticks.

Yes because your doctor or vet is supposed to interact with laymen and not give scientific discourses to their patients. The very definition of a parasite as you quoted is general. If parasite means only certain organisms then the definition should say it explicitly. You seem to justify a wrong usage simple because a lot of people do it. You also seem to hold a view that textbooks are infallible.

The majority of professionals that are responsible for the definitions have made that distinction. You have three distinct branches of study, Parasitology, Bacteriology, and Virology. The Immunology professor I had makes that distinction, and she corrected me when I did not use the term renature to describe proteins refolding into their proper conformation after denaturation. The people whose careers, research, and livelihoods are in these fields make the distinction. If I was quoting one obscure source, I could see being doubtful, but you are being like The Black Knight in The Holy Grail.


text:
How do plants get their O₂ for respiration during the night?
If I am not mistaken the stomata are closed during the night. As a result I have a hard time to imagine how the plant can get the O2 it needs for respiration during the night. I thought the plant could produce the O2 internally through some chemical reaction. Such reaction might include splitting H2O absorbed through the roots in two. Or maybe the O2 diffuses well enough through the plant tissues.
How do plants get their O2 for respiration during the night?

Welcome to Biology.SE. I edited the question. Feel free to roll back if you don't like the edit. Here are a few notes on the format of your question. 1) Your title is too uninformative 2) You could use MathJax to write $O_2$ 3) No need to thank and sign at the end 4) Avoid double question marks.

Not all plants have their stomata closed during the night. A notable exception are Crassulacean acid metabolism(CAM) plants that keep their stomata closed during the day and open it during the night. This is a common evolutionary strategy with Xerophytes.
There are also 2 other types of metabolic pathways namely C3 and C4. As a consequence we get what is called a C3 and C4 plant, which aptly represent the predominant metabolic pathway it employs.
Additionally plant cells, like all life, can produce energy without oxygen by Glycolysis. Furthermore, when stomata is closed, oxygen respiration is restricted, not blocked entirely. Finally it might be important to note that plant metabolism is reduced during the night.
Full disclosure, I am not a botanist. Please let me know if there are any glaring errors.

You are not wrong. Plants can use the oxygen obtained from the photolysis (light breaking) of water to drive cellular respiration. For every 1 $C_6H_{12}O_6$ (glucose) produced, 6 $CO_2$ and 12 $H_2O$ are consumed. In addition, 6 $H_2O$ and 6 $O_2$ are produced as well. But the primary way plants receive oxygen is the same way in which they receive carbon dioxide – through their stomata.

However, I do want to emphasize on Niobe's point of CAM plants. CAM plants have adapted to hot, arid conditions by closing their stomata during the day and opening them during the night to collect $CO_2$.

"Plants use the oxygen obtained from the photolysis (light breaking) of water to drive cellular respiration." any reference?

Well, plants provide oxygen as a byproduct of light-dependent reactions. Organisms, including photosynthetic organisms, use this oxygen as an oxidizing agent in cellular respiration.

I would like to add that plants perform cellular respiration throughout the day and night; and the way they do it is by storing oxygen during the day.

Plants lack proteins to accumulate oxygen. How are they supposed to "store oxygen during the day"? I'm not saying this is impossible, but the statement definitely requires a reference.


text:
Transcription - strands, directions
I am hoping that you can help me improve my understanding of transcription. :)  I have tried searching for the answers to all of these questions online already, but I have either had trouble finding relevant information or I have had trouble understanding it (i.e. it was too high-level for me).  I have also tried to answer my questions by browsing through different maps of genes (like this one: http://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chr9%3A132847932-133136551&hgsid=709471277_W3A9vdobj2J7obkSXshDnCBnaTeK), but my questions are still unresolved.  Please note that I have come up with the following questions in my independent learning - these questions are NOT assigned homework.  In all questions, I'm referring to eukaryotic (linear) DNA.

Am I correct to believe that in a single chromosome, one strand of DNA is not the template strand for all genes within that chromosome?  For instance, let's call one ssDNA molecule "A" and the complementary ssDNA molecule "B"; together, A and B make up a single chromosome.  Am I correct to believe that in a single chromosome, the template strand for some genes will be A, and for other genes will be B?
If my statement in question #1 is correct, then does that mean that multiple genes within a chromosome can be transcribed in opposite directions?  Note that when I say direction, I do NOT mean 5' to 3' vs 3' to 5'.  What I mean by "direction" is looking from left to right.
Is it true that both strands of the double helix cannot be transcribed for a single gene in question?  Is this because the promoter will only be found on one of the strands?

Thank you in advance for your time!

I think the fourth question ought to be separate; the question block is supposed to be for only one question, but I think the first 3 are related closely enough that they could be addressed in a single answer which deals with the underlying principle.

@rotaredom thank you for your feedback!  I removed the 4th question.

I have answered questions 1 and 2  here and here. Your answer to your third question is right in principle, but there are cases of overlapping transcripts (promoters on different strands) as I mention here and you can find elsewhere.

These questions have been answered many times now. I think the closest (also with respect to the question title and body) would be, IMO, this.


text:
Probability of carrying an autosomal recessive trait given both parents are carriers
I recently came across a question that asked for the probability of having a child with an autosomal recessive trait, namely cystic fibrosis. From various parts of the question, we can conclude that the father is definitely a heterozygous carrier and that the mother's parents are both heterozygous carriers. In this situation, the only way to produce a child with cystic fibrosis is if both parents are heterozygous carriers, and this will happen with a probability of $\frac{1}{4}$.
The part that causes confusion is figuring out the probability that the mother is a carrier.
One student reasoned that a cross between two heterozygous parents will produce a 1:2:1 genotypic ratio, so $\frac{1}{2}$ of the progeny will be heterozygous carriers. Therefore, the probability that the mother is a carrier is $\frac{1}{2}$ and the probability of producing a child with cystic fibrosis is $\frac{1}{2}*\frac{1}{4}=\frac{1}{8}$
Another student also referenced the 1:2:1 ratio but reasoned that since the mother is phenotypically normal, that the ratio is actually just 1:2 because there is no chance of being homozygous recessive. Therefore, the probability that the mother is a carrier is $\frac{2}{3}$ and the probability of producing a child with cystic fibrosis is $\frac{2}{3}*\frac{1}{4}=\frac{1}{6}$
These two answers are also found at this other question.
The last solution proposed is the most interesting. This student referenced the Monty Hall Problem, which is indeed somewhat related to this problem (read more about the Monty Hall Problem). Using the same ratio as above, we can conclude that there is a $\frac{1}{4}$ chance that the mother carries no alleles for cystic fibrosis and a $\frac{3}{4}$ chance that she does. The fact that she definitely does not carry two alleles does not change this probability. Therefore, the probability that the mother is a carrier is $\frac{3}{4}$ and the probability of producing a child with cystic fibrosis is $\frac{3}{4}*\frac{1}{4}=\frac{3}{16}$.
Out of these proposed solutions, which one is correct? And why are the others incorrect?
EDIT: To be clear, the solution I initially considered to be correct was the second one.

Solutions 1 and 2 are not contradictory.  1 is appropriate if you do not know the mother's phenotype, 2 is appropriate if you know she is not affected.

Using the same ratio as above, we can conclude that there is a 1/4
  chance that the mother carries no alleles for cystic fibrosis and a 3/4
  chance that she does. The fact that she definitely does not carry two
  alleles does not change this probability.

Yes it does.
Money Hall is about 1) picking, 2) the revealer, knowing where the prize is, reveals something, then 3) you pick again with the new information.  That's not really what this question is.
Lets say there are 4 doors; one affected, 2 carrier, and one not a carrier.  You do not pick anything (which is why this isn't really a true Monty Hall).  If you know the mom's not affected, that's the equivalent of Monty opening the affected door, no mother.  Now the odds are clearly 2/3 carrier, 1/3 not, where before they were only 1/2 for carrier.  Eliminating a door changes the odds for the others, that's the point of Monty Hall.  Eliminating a phenotype does change the odds of the genotype.

Monty Hall does not apply here because there is no decision point past where information is given: the information is already known that the mother is normal phenotype, and the probability for each child of the mother's parents is independent; in the Monty Hall problem, it is known that exactly 1 of the doors contains the prize. Because this sum is known (that only 1 door has the prize), if you know the contents of one door it changes the probability of the others. That is, the occurrence of the prize/goat is sampled without replacement: the thing behind each door is dependent on what is behind the other doors.
2/3 is the correct probability for the normal phenotype mother to be a carrier. Therefore the probability for a child to be homozygous recessive is (2/3) * (1/2) * (1/2) = 1/6.

The part of Monty Hall that appears to relate is that removing a possibility does not mean the remaining possibilities are all equally likely. The way I understand it, the incorrect third solution is saying that removing the homozygous recessive case does not mean the remaining two heterozygous and one homozygous dominant cases are equally likely.

@DarinMao Monty Hall is about adding information about one of the possibilities when you are asking which contains a prize. That is, it is not only known that the probabilities behind the doors are equal, but also that the sum occurrence across all doors is also known (and equal to 1 in the standard Monty Hall problem). Therefore, knowing one door the probability of the other doors changes. That is not true for the mother and her possible sisters, however: her probability is 2/3 regardless of how many sisters she has and regardless of how many of them are or are not carriers or homozygous.


text:
What does the phrase 'background level' mean?
I was reading BIOS Biochemistry and stumbled upon a phrase 'background level' in the following excerpt $-$

The lac operon contain lacZ,lacY and lacA genes encoding $beta$-galactosidase, galactoside permease and thiogalactoside transacetylase, respectively, preceded by an operator site and a promoter. The operon is transcribed by RNA polymerase to produce a single polycistronic mRNA that is translated to produce all three enzymes. When lactose is present the background level of $beta$-galactosidase converts some lactose to allolactose, which induces transcription of the lac operon.

What is meant by background level? Does it refer to the basal level of transcription, the constitutive transcription of facultative genes?

Why do you see the constitutive transcription of a gene as wasteful? These fulfil usually important roles...

The phrase “background level” is generally used in an experimental context where you are measuring the effect on a variable of some agent or stimulus. You might expect that your control condition(s) — without the stimulus — would give you a measurement of zero, but often that is not the case, and one needs to subtract this control value — often referred to as ‘background’ — from the experimental value.
Such background values can be real — e.g. background radiation — or artefacts caused by fundamental limitations in the measuring system used. Generally the implication is that their origin is unknown or is not specific. That is why I think that the use of the term ‘background’ in the context of the lac operon is somewhat unfortunate. I would have used (and encourage you to use) the term ‘basal level’ instead*. As the text states, there is a low — but specific and necessary — expression of β-galactosidase in the non-induced situation, so that when lactose is added some of it can be converted to the inducer, allolactose, which will then result in the synthesis of the greater amount of β-galactosidase needed to deal with the rest of the lactose.
*Footnote
In fact I hate the term ‘level’ except for water in the bath tub, and I would have used ‘amount’ or ‘activity’, but that’s not the point at issue here.

Love the footnote of you answer... I also greatly dislike the word "level" because it is not very specific and can mean different things in different situations. Many individuals use the word "level" when they more accurately should be saying "concentration".

Concentration is a measure of the expression level. I, however, do concur that people use this word casually which would is likely to mislead others. "Background level" is not a suitable usage at all.


text:
Was HindII the first restriction endonuclease to be extracted?
Background:
Guided by wikipedia and pmc I found this paper by Hamilton O. Smith. and .Daniel Nathans.

A
  restriction
  enzyme
  is
  a
  component
  of
  a
  restriction-modification
  system
  of
  a
  given
  specificity
  within
  an
  organism.
  The
  R-MT
  system
  consists
  of
  two
  enzymatic
  components,
  a
  restriction
  endonuclease,
  and
  a
  modification
  enzyme
  sharing
  similar
  (or
  identical)
  recognition
  specificity.
  We
  would
  like
  to
  propose
  that
  the
  genus-species
  designation
  be
  used
  as
  an
  R-M
  system
  name
  according
  to
  the
  following
  rules.
(1)
  The
  genus
  and
  species
  name
  of
  the
  host
  organism
  is
  identified
  by
  the
  first
  letter
  of
  the
  genus
  and
  the
  first
  two
  letters
  of
  the
  species
  to
  form
  a
  three-letter
  abbre-
  viation
  in
  italics.
  For
  example:
  E.
  coli,
  Eco
  and
  H.
  influenzae,
  Hin.
(2)
  Strain
  or
  type
  identification
  follows
  the
  genus-species
  abbreviation
  in
  non-
  italicized
  symbols,
  e.g.
  EcoB
  or
  EcoK.
  In
  cases
  where
  the
  R-M
  system
  is
  genetically
  specified
  by
  a
  virus
  or
  pla,smid
  the
  italicized
  genus-species
  abbreviation
  of
  the
  host
  is
  given
  and
  the
  symbol
  for
  the
  extrachromosomal
  element
  follows
  in
  non-italics,
  e.g.
  EcoPl,
  EwRI,
  etc.
  In
  occasional
  cases
  where
  it
  might
  be
  necessary
  to
  specify the
  host
  strain
  as
  well
  as
  the
  extrachromosomal
  element
  the
  strain
  identification
  symbol
  may
  be
  inserted
  parenthetically,
  e.g.
  Eco(B)Pl.
(3)
  When
  a
  particular
  host
  strain
  has
  several
  different
  R-M
  systems,
  these
  are
  identified
  by
  Roman
  numerals,
  thus,
  the
  R-M
  systems
  from
  H.
  injluenzae
  strain
  d
  would
  be
  HindI,
  HindII,
  HindIII,
  etc.

Main question:
Now HindII was -

extracted from  Haemophilus influenzae
the strain was strain Rd, so d
and it was the 2nd enzyme to be isolated? Hence II.

So how is it the first Type II RE?

H.O. Smith, K.W. Wilcox, and T.J. Kelley, working at Johns Hopkins University in 1968, isolated and characterized the first restriction nuclease whose functioning depended on a specific DNA nucleotide sequence. (wiki)

I don't know how widely this has been accepted but Roberts proposed in 2003 that the italics should be dropped (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC152790/). I used to be a stickler for using italics, but I now prefer without.

I'm voting to close this question as off-topic because it's not about biology it's about history, and not very interesting history either. Why should you care whether it was HindIII or EcoRI for goodness sake!

I don't understand what can be wrong in getting a doubt cleared? The question (in the title which still stands unedited) was the main question behind this post. NCERT (a book back from my school) did not mention the Type II part to keep things simple. It lingered in my mind (as why an enzyme which is II yet the first) and definitely it was my silly mistake to not have observed the Type II thing even while reading it after so many years. My question wasn't which one's the 1st enzyme? But why HindII the first one?  @David

I call them as I see them. (Friendly tip: best to try to avoid Indian English "doubt" on International forums — use "question" instead.)

if the strain is Rd then instead of Hind,HinR should have been written, what is the answer


text:
Oil absorbed into human skin -- where does it go?
For example, I apply petrolatum to my dry hands twice a day as in winter I am usually in a 20-30% RH environment.  Within an hour, the petrolatum seems entirely absorbed.
According to [1], petrolatum and the other oils tested there "do not reach the viable cells of epidermis, saturating only the uppermost horny layers of the skin."
So my question is: Where does the oil go?   I do not believe I am shedding unseen skin layers fast enough nor transferring the oil to other objects fast enough that I can repeat and apply twice a day, without the oil going deeper than "uppermost horny layers" and being excreted internally. (Via lymph? blood?)  Also, I rarely wash my hands with soap.
[1] Confocal Raman microscopy for investigating the penetration of various oils into the human skin in vivo.
Choe C, Lademann J, Darvin ME.
J Dermatol Sci. 2015 Aug.
https://atlasofscience.org/oil-penetration-into-the-human-skin/
Accessed 2/8/2019