text:
Are intercellular junctions, synapses and light-capturing photosynthetic complexes mobile?
I was reading Cell Biology by Gerald Karp and came across a section which said-

Membrane fluidity makes it possible for clusters of membrane proteins to assemble at particular sites within the membrane and for specialised structures, such as intercellular junctions, light-capturing photosynthetic complexes and synapses.

I would be obliged to know more about the topic.

Not necessarily. Sometimes the membrane localized proteins/complexes are anchored to the cytoskeleton or clustered together which limits their movements. See this post.

Membrane fluidity allows reversible association of membrane compounds, which can be thought of as diluted in a two dimensional fluid; this also implies a crucial property of membrane dynamics, which is the differential association of components into more or less stable molecular groups. Once formed, the more stable will be able to cruise the membrane surface, unchanged. This tells you that certain complexes will, by their stability and membrane fluidity, be in constant motion, and thereby statistically well distributed on the cell surface, a very important feature for many infrastructures (look up "lipids rafts" as a topic for examples).
Now, the notion of localization in biology may refer to absolute location (e.g. cell pole), or simply the relative positions of certain compounds. Such is the case for cell junctions, which need to co-localize with certain cytoplasmic compounds, belonging to the cytoskeleton. Relative localization therefore, in this case. Do understand though, that both these infrastructures and photoreceptors need to be well distributed on the cell surface, each for its own reasons (mechanical strength, and optimal photo-capture, respectively).
The example of synapses is different, as the exact site of synaptic attachement in between cells plays a role in neural messaging and its regulation. This is, therefore, a different topic, which may involve absolute positioning of infrastructures. However, at these sites, protein movement along membrane surface and ocmplex forming principles remain the same; this is an example of absolute localization.

Welcome to Bio. Can you add sources or references to allow users to background read on your answer?


text:
Why does hemoglobin electrophoresis in sickle cell trait gives two bands but not three?
Electrophoresis of hemoglobin from a patient with sickle cell trait (carrier for sickle cell anemia) shows two bands. Why not three?  Since there are two beta chains in each hemoglobin, it seems to me they should have three types of hemoglobin: HBB/HBB, HBBs/HBBs, and HBB/HBBs. Does the HBB not form hybrids with HBBs? Aren't both polypeptides produced in the cell?
*HBBs signifying mutated beta chain

"Shows" as in from your experiment or as a general question on an ideal result (like ones asked in exams)?

It appears to be "shows" as in real results used for diagnosis, either with alkaline cellulose acetate or other forms of electrophoresis that separate by charge. Just do a google search for images using the term "electrophoresis of sickle-cell haemoglobin".

This is a really interesting question and again reminds of how ignorant we are about things as subtle as this which otherwise should have been an obvious question.
First of all, although there seems to be no confusion, I'd like to clarify that we are talking of the protein being separated on electrophoresis. Hemoglobin electrophoresis classically refers to the cellulose acetate/citrate agar electrophoresis where the RBC hemolysate is used as the sample. This method uses the fact that, hemoglobinopathies generally have mutated Hb which differ in charge from the original HbA. Charge is a property of separation in cellulose acetate electrophoresis unlike SDS-PAGE where separation is on the basis of mol. wt.
We can also do a DNA electrophoresis (digressing) to identify a Hbpathy after digesting with restriction enzymes which would give a different results, depending on the restriction enzyme that has been used to differentiate the mutation from the original. Here is an example using MstII for RFLPs. This isn't the topic of discussion here. Our sample is the protein, and not the DNA.
So it is important that the electrophoresis we are going to talk of, is of a protein electrophoresis based on charge.
Considering the sickle cell trait, let us clarify the terminology now. HbA is normal hemoglobin tetramer which composes of $\ \alpha_2\beta_2^A $. HbS on the other hand is $\ \alpha_2\beta_2^S $. The terminology you have used not only isn't standard but also is conveying a different meaning. Now logicaly, in a person with sickle cell trait, one should be expecting a hemoglobin with both different beta chains. And it does happen! Literature calls it the assymetric hybrid. Let us indicate it with AH which is $\ \alpha_2\beta^A\beta^S $. Let's sum this up a bit.
HbA = $\ \alpha_2\beta_2^A $
HbS = $\ \alpha_2\beta_2^S $
AH = $\ \alpha_2\beta^A\beta^S $
The assymetric hybrid that has been mentioned here is only for the sickle cell trait. There are many other hemoglobinopathies and in their heterozygous states one can obtain other assymetric hybrids with a different beta chain.
Now that we know that assymetric hybrids are formed, why do they not show up on the Hb electrophoresis?
It is generally believed that under physiological conditions, at equilibrium, hemoglobin is a mixture of tetramers ($\ \alpha_2\beta_2$) and dimers ($\ \alpha\beta $) as $$\ \alpha_2\beta_2 ⇌ 2\alpha\beta $$ The dissociation equilibrium constant for oxyhemoglobin is approximately $\ 2x10^{-6} M $ (heme) and is much less for deoxyhemoglobin. The asymmetric hybrid is generally not isolated by conventional techniques, since the tetramer-dimer dissociation constant is much lower in-vitro than in-vivo . Thus the asymmetric hybrid dissociates into dimers $\ \alpha\beta^A:\alpha\beta^S$ and reassociates into more symmetric forms during the separation process.
There are slightly modified methods to isolate the assymetric hybrids under deoxygenated conditions such as isoelectric gel focussing, cross linking the chains, etc. The amount of AH formed in proportion to HbA and HbS can be measured in these kind of experiments and has been found to be comparable to the expected binomial distribution of $\ a^2 + 2ab + b^2 $. This implies that the stability of the AH is comparable to HbA and HbS.
Hope it helped.
To delve further, here are a couple of reference that should be of use.

HF Bunn and M McDonough (1974), Assymetrical Hemoglobin Hybrids.
  An Approach to the Study of Subunit Interactions, Biochemistry,
  13(5)989-93.
MK. McCormack, TG. Westbrook, RM. Paull & S Berman (1981),
  Identification of the Asymmetric Hybrid of Human Oxy Hemoglobins A
  and S (α2βAβS) at 4° C by Cellulose Acetate Electrophoresis,
  Hemoglobin, 5(3)251-56.

Could someone help me with the reversible arrow up there?

Glad you've solved the mystery at last. When I've digested your answer I'll, no doubt, upvote it and remove my own. In the meantime I've inserted the reversible arrows from the Mac OS Character Viewer (under arrows). If you are not on Mac OS, there is an excellent online Unicode site for this sort of thing, especially for web or computer use (although for the current case a generally query is a better way to find this.)

@David A very beautiful question. My biochem proff was also intrigued and after a little search mailed me the article. Hats off to the OP for such a thought! Anyway, thanks!

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text:
Writing methods section on PCR amplication in a paper
Considering that I am writing a paper for a journal, could the following phrase be understood? or should I put the 'step-by-step' way by giving numbers?
PCR Amplification and sequencing
PCR reaction for sequencing with universal primer  ITS5: F: (5’TCCTCCGCTTATTGATATGC3’ and ITS4:R: (5'TCCGTAGGTGAACCTGCG
C3'), including 5,8S rDNA region (White et al 1990). Amplification condition  was performed in a 25 ml reaction volume and consisting of 10 µL nuclease free water, 12.5 µL Tag green master mix, 0,5 µL forward primer, 0,5 µL reverse primer, 0,5 µLDMSO, 1 µL template. Mixture solution  was amplified by PCR machine (Biorad). Thermal cycle programmed for 90 seconds at 95°C as initial denaturation, followed by 35 cycles of 30 sec at 95°C for denaturation, 30 sec at 55 °C as annealing, 90 sec at 72 °C for extension, and final extension at 72 °C for 5 min. PCR products were examined by electrophoresis  at 100 V for 30 minutes in a 1% (w/v) agarose gel in 1 x TAE buffer. The marker used DNA ladder 1 kb.  Electrophoresis gel was soaked in ethidium bromide for 30 minutes then visualized in UV light.

You should change your "Amplification..." sentence to remove the word "condition" and change 25 ml to 25 µL, but other than that it looks okay. Also, maybe spell out "Forward" and "Reverse" when listing your primers.

Is Tag meant to be Taq?

@AlanBoyd Is there any reference as a guidance for writing a journal; cases like 'mins should be min' and 'secs should s', and other abbreviation in (micro)biology term.  Should I only learn from the previous reviews/journals? Thanks.

@Des-microbiology this site looks like a reasonable place to start.

@des: according to the SI (which is the reference for these matters) the abbreviation for seconds is s not sec.

@AlanBoyd what is the abbreviation of diameter? dia Or diam? The references in my hand do not provide it. The context is: Phomopsis sp (3).
Cultural characteristic: Colony of  2-3-1-B2 isolate on potato dextrose agar after 7 d, fast growing fungus, abundant with aeral mycelium, cotton-like, white colour, 51 mm diam, serrated edges colony.

@des There isn't a "correct" abbreviation for diameter - it isn't a physical unit in the same way that seconds or minutes are. However specific journals probably have their own rules - check their Style Guide.

Here's my take, just a few minor changes which are shown in bold (I have also changed ,to . for decimal numbers and added a few spaces where needed):

PCR Amplification and sequencing
A PCR reaction for sequencing was performed using universal primers ITS5: F:
  (5’TCCTCCGCTTATTGATATGC3’) and ITS4:R: (5'TCCGTAGGTGAACCTGCG C3'),
  including 5.8 S rRNA region (White et al. 1990). Amplification condition
  was performed in a 25 ml reaction volume and consisting of 10 µL
  nuclease free water, 12.5 µL Taq green master mix, 0.5 µL forward
  primer, 0.5 µL reverse primer, 0.5 µL DMSO, 1µL template. PCR was performed using a Biorad PCR machine. The thermal cycle was
  programmed for 90 s at 95 °C for initial denaturation, followed by
  35 cycles of 30 s at 95 °C for denaturation, 30 s at 55 °C for
  annealing, 90 s at 72 °C for extension, and 5 min at 72 °C for the final extension.
  PCR products were examined by electrophoresis at 100 V for
  30 min in a 1% (w/v) agarose gel in 1 x TAE buffer. The marker
  used a 1 kb DNA ladder. The electrophoresis gel was soaked in ethidium
  bromide for 30 min then examined in UV light.

The first sentence is not a sentence.

@terdon or even better, use the correct abbreviation for seconds which is s, not sec(s). And use min for minutes (never mins)

@AlanBoyd thanks! It's 22:00 here and I'm still in my lab writing a report for a grant I received, so my mind is not at its best. I knew that sec bothered me but I couldn't put my finger on it. WHile absolutely correct, your comment about min is nicely ironic given that what I read is: "@terdon or even better, use the correct abbreviation for seconds which is s, not sec(s). And use min for minutes (not mins) – Alan Boyd 4 mins ago". :)

@kmm indeed it was not.

Tag should probably be Taq...

@terdon I use rDNA not rRNA.

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text:
How to create a collection of anonymous sequences for teaching and testing?
I am looking for a large collection (>1000) of sequence files (eg. FASTA) from any real organism or a tool to create such a collection.
The sequence files would be used for teaching and for testing automation methods.
Students would be assigned one unique sequence file and asked to look at it (eg. using gORF) and to identify it (using BLASTn).
The sequence file would thus need to contain only the sequence data (no meta data about species or gene).
I would need an associated answer sheet.

I think you need to elaborate more on what you are trying to accomplish.  Furthermore, you may get more help on biostar

This question I asked in biostar seems related - Examples of DNA sequence motif sets for testing search algorithm

Here is the approach I ended up using, in part thanks to all the contributions here.
The associated R script is below or can be downloaded from:
BOLDS SEQUENCE RECOVERY
This creates 999 unique sequence files in plain text, with each sequence being identified to species level and few species being found across more than one sequence.
It also creates the matching answer key.
You can start at a random location to so that files change every year/group.
I used R to query the BOLDS database (Barcode of Life), to download a file and to split this huge file into separate sequences.
Here is the R script
rm(list=ls())

complete<-"http://services.boldsystems.org/eFetch.php?record_type=full&id_type=sampleid&ids=(*)&return_type=text"
write(complete, file="your location on disk")

rm(list=ls())

sequences.id<-data.frame("file.name", "recordID", "genus_name", "species_name")
write.table(x=sequences.id, file="sequences_id.csv", append=F, sep = ",", row.names=F, col.names=F)

set.seed(10)
start<-sample(1:1000, size=1)

i<-start
k<-1

while(k < 1000){

  sequences<-read.delim(file=complete, skip=i, nrows=1, header=F)
  sequence.compare<-read.csv(file="sequences_id.csv", skip=k-1, nrows=1, header=F)

  if(! is.na(sequences$V24)){
    if(as.character(sequences$V24)!=as.character(sequence.compare$V4)){
      writeLines(text=as.character(sequences$V55), con=paste(k, ".txt", sep=""))
      sequences.id<-c(k, sequences[,c("V3","V22", "V24")])
      write.table(x=sequences.id, file="sequences_id.csv", append=T, sep = ",", row.names=F, col.names=F)
      print("kept")
      k<-k+1
    }
  }
  i<-i+1
  print(paste(k,"/", i))
}

There are a couple key words in this question - anonymous and teaching. Yes, NCBI is a source for sequence data, but it is not anonymous (it is annotated, which means a student could also find it and copy/paste that annotation without doing the actual analysis). Notice, I am not assuming that the request is for human data. Now, if anonymous human data are needed, most available sequence data are anonymous but there remains that annotation issue: If it is annotated already, what will they learn?
A good alternate source for some human genome data would be from Complete Genomics. They have released anonymized (de-identified) data for at least 69 subjects. The question asks about 1000 sequences, but how large? This is an important consideration. Other details are also lacking in the question.
Another source may be the 1000 Genomes data, also human. If you're interested in plants, there are sequence data out there from ~98 different Arabidopsis thaliana accessions/cultivars/strains.

This is probably not the most elegant way but you could go to NCBI and search for nucleotide sequences from a given organism (eg., txid9606[Organism:exp] gives all sequences from Homo sapiens). Then you could use the Send to dropdown to download all the results as a compiled FASTA file.

NCBI also offers some APIs, which would make the process cleaner and allow better filtering.


text:
Where can I find the pMON7124 plasmid sequence?
I need the map of the pMON7124 plasmid. As this is not easy to find, I welcome any hints.

perhaps contact these people (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC237841/pdf/jvirol00029-0122.pdf) as these seems to be one of the original papers working with the plasmid.

Addgene is a good site to find plasmids

It seems that no good map of this plasmid is around. Life technology uses it in some of its bacterial strains, the quote:

E. coli also contain the helper plasmid, pMON7124 (13.2 kb), which
  encodes the transposase and confers resistance to tetracycline. The
  helper plasmid provides the Tn7 transposition function in trans.

They link to the original publication, but the image quality in there is pretty bad:

They give some information in the text, so I would recommend reading the paper (if you have no access, let me know, I can help here):

A broad-host-range shuttle system for gene insertion into the
chromosomes of gram-negative bacteria.

If this is not enough, you could still try to get a better version from the author Gerard F. Berry (you can find his Monsanto email adress by googling for it).


text:
How to list coding/noncoding genomic regions linked to significant SNPs?
For QTL analysis in mice GEMMA was used to get P values ("p_lrt" column) for SNPs. GEMMA output (...assoc.txt) file excerpt:
chr  rs           ps       n_miss  allele1  allele0  af     logl_H1        l_mle         p_lrt
1    UNC6         3010274  45      T        C        0.753  -1.871575e+03  9.092954e+00  4.497885e-01
1    JAX00240613  3323400  12      T        C        0.766  -1.871777e+03  9.096464e+00  6.822045e-01
...

Then, drawing a Manhattan plot with qqman R package applies default suggestive/genomewide cutoffs. But if I get it right, P < 5×10^(−8) is a commonly used genomewide threshold Ref1, Ref2.
Then I have to list the relevant coding/noncoding regions linked to these significant SNP (with P < 5×10^(−8)).
How can I do this?
I found a fantastic tool called FUMA
but it seems for GWAS in humans not for QTL analysis.
Update:
In Karl Browman's presentations: pdf (p. 13); pdf (p. 23(=28), 29(=34), 30(=35)).

GEMMA should give you confidence/credible intervals no? Also please expand on what you mean by ‘gene candidates’, that’s a bit of a vague term.

thanks for the comment. I've edited the question.

I would suggest seeing what others have done when using GEMMA. For example, you can see this paper's methods:

We converted p-values to LOD scores and used a 1.5-LOD support interval to approximate a critical region around each associated region, which enabled us to systematically identify overlap with eQTLs.

They further discuss this approach in the supplementary note:

Instead we converted p-values
to LOD scores and used a 1.5-LOD support interval to approximate a critical region around each
association. The LOD drop approach provides a quick, straightforward way to gauge mapping precision
and systematically identify overlap between eQTL genes and candidate QTGs; however, it does not
correspond to a specific confidence interval (e.g. 95% confidence interval).

I would suggest trying something like this to estimate such a "critical region". For a discussion of the relationship between LOD and p-values, a quick search yielded this paper.

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text:
Are individual auto-reactive 'lymphocytes' or auto-reactive 'clones' generated in the central lymphoid organs?
Clonal deletion is a well-known mechanism of immune central tolerance. But individual lymphocytes or lymphocyte clones are subjected to apoptosis? If clones, then what is the reason to allow mitosis in auto-reactive cells? If lymphocytes, then why do we use the adjective? I mean are there several rounds of mitosis in a (potentially) harmful say B lymphocyte prior to negative selection step?

I think you misunderstood the definition of clone at this level. As clonal deletion is a central tolerance mechanism, of all the possible clones of B cells (a clone is a B cell with a particular arrangement of the BCR), those clones (not identical clones, but different clones each) that are self-reactive will undergo apoptosis. That means that self-reactive clones are deleted and they won't divide anymore.

so, 1 clone = 1 B cell, any reference?

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

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text:
Is the whole MHC haplotype expressed and so their proteins are exhibited on each nucleated cell membrane?
Am I correct if I guess the following (?):
If we inherit both maternal and paternal MHC haplotypes, the functional (non-pseudo)genes are expressed and all of their products (MHC molecules) are exhibited on the cytoplasmic membrane of any nucleated cell.
In case of MHC type I molecules our all nucleated cells bear one (or more? how many?) types of polypeptide(s) (corresponding to and) encoded by the inherited allels of each of A, B, C, E, F, G MHC-I genes.
In other words each nucleated cell expresses all MHC type I molecules encoded by our inherited MHC haplotype.
Is it true?
Thank you.


text:
Would two species of yeast with similar genome sizes have the same number of genes or chromosomes?
Similar organisms generally have similar genome sizes. Given this, would two species of yeast have the same number of genes and chromosomes?
Edit: Fixed with thanks to @daniel-standage

I'm doubtful regarding your premise. See my related comment on this thread.

This question appears to start from the premise that different species of yeast are closely related, but they aren't. Saccharomyces cerevisae and Schizosaccharomyces pombe, both Ascomycetes, are thought to have diverged at least 300 million years ago (c.f. the mammalian divergence from other vertebrates was about 200 million years ago).
S. cerevisiae has a genome size of 12.1 Mb, with 5821 protein coding genes (plus another 786 dubious ORFs) spread over 16 chromosomes.
S. pombe has a genome size of 12.6 Mb with 5124 protein coding genes on just 3 chromosomes.
Filamentous fungi have larger genomes and gene numbers. From memory, Aspergillus nidulans has 8 chromosomes and over 9,000 protein coding genes. So, the similarity in gene numbers in the two yeasts probably reflects their broadly similar lifestyles.


text:
Can scientists name themselves in the scientific name when they discover a new taxon?
There are sometimes people names in taxonomy, like Myotis keenii was names after Mr. Keen who contributed to discover the species. So, if you discover a species and someone else is constructing the scientific name and names you, it's clear. But when you discover a species and you publish it in a paper, can you propose a scientific name that contains your name? Has it ever happened, or is it considered an unhealthy practice?

The answer is that in general, self-naming is severely frowned upon in the scientific community, but the act itself is not disallowed.
There have been at least two instances of self-naming recorded in literature, as stated in John Wright's book The Naming of the Shrew, page 34, where Jules Bourguignat named a species of snail after himself as Ferussacia bourguignatiana. The naming was apparently very poorly received (being referred to as taxonomic onanism), although I was unable to confirm this by locating the original citation.
Another example was given in the book on Sigismund Hochenwarth who named a species of moth (now Syngrapha hochenwarthi) after himself (original citation here).

So, effectively, no?

@SiyuanRen Pretty much, you can if you want, but it will lead to you being ridiculed by the community.

@Tomas Isn't this answer enough for you, please mark it as accepted.

"Taxonomic onanism" is a great term.

As this example shows, it's not terribly uncommon to name a species after a family member. Linnaeus, for example, named the plant genus Linnaea after his wife.


text:
What determines testosterone exposure in womb, baby's genetics or mom's body?
I read this article which has the following quote:

The ratio between index and ring finger is believed to be linked to exposure to the male hormone testosterone in the womb.

And I wonder what determines the amount of exposure to testosterone in the womb. Is it testosterone produced by the fetus itself, in which case the baby's own genetics is the answer, or does this exposure the article speaks of more likely refer to testosterone produced by the mother and exposed to the baby?

Fetal testis produces testosterone from cholesterol. There is a peak of production around 15 weeks of gestation (the "masculinization programming window"). So the genotype of the fetus can affect testosterone levels directly via effects on the biosynthesis of the hormone, or indirectly by defective regulation of the pathway's activity.
However, exposure to chemicals in the mother's environment is also thought to play a part in determining testosterone levels. The classic example of this is the phthalate esters used as plasticizers.

Scott et al. (2009) Steroidogenesis in the Fetal Testis and Its Susceptibility to Disruption by Exogenous Compounds. Endocrine Reviews 30: preprint freely available here.

It has long been evident that human fetuses produce the hormones that dominate their development in utero.  (Ref: Robinson et. al., J Clin Endocrinol Metab. 1977 Oct;45(4):755-61. Amniotic fluid androgens and estrogens in midgestation.)
There is a baseline increase in maternal testosterone during pregnancy regardless of fetal sex, and I can't find whether that is due to production by the mother's endocrine systems vs. transfer from the fetus.  But in any case transfer from the fetus dominates: A male fetus produces so much testosterone that the serum levels detectable in the mother's blood ranges up to 4 times the amount found in typical non-pregnant women!  (Ref: Meulenberg & Hofman, J Steroid Biochem Mol Biol. 1991 Jul;39(1):51-4.
Maternal testosterone and fetal sex.)


text:
What is the mechanism of transgene integration (from expression vector to the host genome)?
How does a transgene (in vector) integrate to the host genome? (e.g. in glass bead method, neither biolistic nor agrobacterium).
I already cut some parts (NdeI-PciI) of the vector (pUC18) and wondering if it affects the integration procedure. Is there any recombination-like procedure same as gateway?

What is your host in this case? For integration into the genome of a bacterium, you would need to use an "integration" vector. Most commercial vectors (such as pUC18) will be maintained without integrating into the host genome.
Here is a description of an integration vector from the Bacillus Genetic Stock Center to give you an idea of how foreign DNA would be integrated into a Bacillus genome:

Integration vectors are plasmids that feature conditional replication
  coupled with a selectable marker. If the plasmid is transformed into
  an appropriate host under conditions that select for the plasmid’s
  presence but restrict its replication, all transformants will have
  integrated the plasmid into their chromosome (or some other resident
  DNA capable of replicating under the selective conditions). In
  practice, the selectable marker usually specifies antibiotic
  resistance. Conditional replication usually means that the plasmid has
  replication functions that work in E. coli but not in gram-positive
  bacteria, such as B. subtilis. Sometimes a temperature-sensitive
  replication phenotype is employed instead. Integration is targeted to
  a particular locus on the chromosome by including identical sequences
  on the plasmid. If there is a single homologous sequence, a single
  crossover will integrate the entire chromosome into the target locus
  by a Campbell-type mechanism. If there are two homologous sequences,
  and they are relatively close together on the chromosome, then a
  double crossover will result in a cassette integrating between the
  chromosomal targets. (source)

For most routine molecular biology labwork, there is no need to integrate genes into the E. coli genome. Integration is usually used to generate "knockout" cell lines to study gene function in the bacteria of interest.

Thanks for your time and consideration...but the host is microalgae (a eucaryote microorganism).


text:
What makes a rotator cuff tear symptomatic in humans?
The majority of   rotator cuff tears  is asymptomatic {1}. What makes a rotator cuff tear symptomatic or asymptomatic in humans?

References:

{1} Minagawa, Hiroshi, Nobuyuki Yamamoto, Hidekazu Abe, Masashi Fukuda, Nobutoshi Seki, Kazuma Kikuchi, Hiroaki Kijima, and Eiji Itoi. "Prevalence of symptomatic and asymptomatic rotator cuff tears in the general population: from mass-screening in one village." Journal of orthopaedics 10, no. 1 (2013): 8-12. https://scholar.google.com/scholar?cluster=6848408356619886538&hl=en&as_sdt=0,22 ; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3768248/

In conclusion, our survey of 664 residents in one village demonstrated that the prevalence of rotator cuff tear was 22.1% in the general population, which increased with age. Asymptomatic tear was twice as common as symptomatic tear.
[…]
In this study, “asymptomatic” was defined as having neither pain nor
  any other symptoms related to the shoulder when the survey was
  conducted including the past history of shoulder pain, whereas
  “symptomatic” was defined as having pain or any other symptoms related
  to the shoulder when the survey was conducted.

Caption: Prevalence of symptomatic and asymptomatic tears.
  Asymptomatic tear accounted for 50% of all tears in the 50s. However,
  in the 60s and over, the percentage of asymptomatic tear was
  significantly greater than that of symptomatic tear.

The underlying reason is difference in the rate of firing of torned and intact muscle in movement of shoulder joint.

Asymptomatic patients had minimal pain (<3 on the visual analog scale and no loss of active range of motion compared with the contralateral side); symptomatic patients had pain greater than 3 on the visual analog scale and decreased range of motion compared with the contralateral side (>10 degrees of motion loss). Electromyographic activity from 12 muscles and kinematic data were collected simultaneously during 10 functional tasks. Both symptomatic and asymptomatic cuff subjects demonstrated a trend toward increased muscle activation during all tasks compared with normal subjects. During the internal rotation tasks, asymptomatic patients had significantly greater (P<.05) subscapularis activity than symptomatic patients (65% maximal voluntary contraction [MVC] vs 42% MVC). During the carrying task, asymptomatic patients demonstrated significantly less (P<.03) upper trapezius muscle activation than symptomatic patients (16% MVC vs 50% MVC). During shoulder elevation tasks, symptomatic patients had significantly greater supraspinatus (52% MVC vs 28% MVC, P<.03), infraspinatus (32% MVC vs 16% MVC, P<.05), and upper trapezius (39% MVC vs 20% MVC, P<.04) muscle activation compared with asymptomatic patients. During heavy elevation (8 lb), asymptomatic patients showed a trend toward increased activation (P<.06) of the subscapularis compared with symptomatic patients (34% MVC vs 21% MVC). Differential shoulder muscle firing patterns in patients with rotator cuff pathology may play a role in the presence or absence of symptoms. Asymptomatic subjects demonstrated increased firing of the intact subscapularis, whereas symptomatic subjects continued to rely on torn rotator cuff tendons and periscapular muscle substitution, resulting in compromised function.

Source: Kelly, Bryan T., Riley J. Williams, Frank A. Cordasco, Sherry I. Backus, James C. Otis, Daniel E. Weiland, David W. Altchek, Edward V. Craig, Thomas L. Wickiewicz, and Russell F. Warren. "Differential patterns of muscle activation in patients with symptomatic and asymptomatic rotator cuff tears." Journal of shoulder and elbow surgery 14, no. 2 (2005): 165-171. https://www.ncbi.nlm.nih.gov/pubmed/15789010


text:
Do the simplest bacteria have ribosomes and helicase?
I find it interesting that all life on earth use DNA. I've seen video on how helicase and ribosomes work together to copy DNA sequences (to RNA) with helicase then recreate them using ribosomes. Does this process work the same way in the simplest life forms? Bacteria and other unicellular life that reproduce through mitosis, for example?

Although the definition of life is complicated, there’s general agreement that viruses aren’t alive. Furthermore, there seems to be a misconception about the mechanism of DNA replication: no intermediate step via RNA is involved. Maybe you could clarify what you mean here? Still, I think this is a good question.

You seem to have got confused between translation (making proteins from RNA templates using ribosomes) and DNA replication (direct DNA-DNA copying)

I'm voting to close this question as off-topic because it is based on the false premise that ribosomes are involved in transcription.

I've had a direct look at Carsonella rudii, which is I believe is the bacterial genome with the smallest number of genes so far - 184 as well as being only 160 kb in length.   It has a putative DNA helicase encoded in it.  37 of those genes encode for ribosomal components as well.
If there was ever a bacterium or any living cell (non virus that is) discovered without a ribosome, you would have heard about it.  nobel prizes all around.
So I would say that your answer is yes.

First, mitosis is a eukaryotic process where not only genome replication and cell division is involved but quite a few more processes, not the least because there is a nucleus in eukaryotes. Bacteria simply divide after replication. And yes, even the simplest bacteria (and even some symbionts) use ribosomes for protein production. Example:
The smallest bacteria are from species Mycoplasma. The Mycoplasma species with the smallest annotated proteome on UniProt is Mycoplasma genitalium (strain ATCC 33530 / G-37 / NCTC 10195, with 484 genes. I have attached links to the set, as well as to its helicase. (For the 16S gene you would look that up in a gene not protein database)
http://www.uniprot.org/uniprot/?query=taxonomy:243273
http://www.uniprot.org/uniprot/P47340


text:
What is the difference between enrichment media and selective media?

Enrichment media
These media are used to suppress commensal bacteria while allowing the pathogen to remain viable and grow.
[Source: Ananthnarayan and Paniker's textbook of Microbiology.]

There is also an example of tetrathionate broth as enrichment media given in the book where tetrathionate inhibits coliforms while allowing typhoid-paratyphoid bacilli to grow.
For selective media it writes:

As in the above case (of enrichment media), if inhibiting substance is added to a solid medium, it enables a greater number of the required bacterium to form colonies than the other bacteria.

For this selective media an example of Deoxycholate Citrate Agar (DCA) for fecal samples is given.
The question:
What's the difference between enrichment media and selective media? Some answers give quite contradictory statements to the statement of the book like stating that "...it is designed to stimulate growth of many different types of bacterial species" for enrichment media.
I am also not able to explain myself as to how selective medium enables a greater number of the required bacterium to form colonies than other bacteria since inhibitory substance is also present in enrichment media?


text:
What is the latency between paired neuronal responses in the brain?
Is there any data on how long it takes for signals to propagate from one neuron to its neighbors in complex networks, such as the brain (particularly the neo-cortex)?
If not, is there any reasonable way to estimate at least the order of magnitude (for example by considering synaptic delay, which is in the order of 0.5 ms and the firing delay)?

do you mean what the latency is in a two-neuron network? In that case, the synaptic delay is definitely the most time consuming step because it's dependent on passive diffusion of neurotransmitter.

@AliceD What I am interested in is to get some idea about the (average/lowest/highest) latency between any two directly connected neurons in a network as complex as the brain.

Are you mainly interested in the synaptic delay or the propagation delay? The later depends a lot on whether the axon is myelinated and the length of the connection.  Are you mainly interested in delays within a cortical area or between cortical areas? Note that the the brain is NOT a dense network.

@Jonathan Ok, good to know. I'm a little shaky on terminology, but propagation delay sounds fitting, if it is the correct term for the time it takes for a "signal" to propagate from one neuron to the "next", i.e. the delay between the first neuron firing and the second neuron's potential being affected.

Short answer
A rough indication of the delay in monosynaptically connected cortical neurons is 6 - 14 ms.
Background
As @Jonathan correctly states, there are many variables involved in neuronal delays. However, because you ask for an estimate of the order of magnitude of the neuronal delay between two coupled neurons in the neocortex, I will suffice by providing the latencies reported form one study that seems to meet your demands very well. In this study the latency data on horizontally connected neurons in monkey prefrontal cortex in layer III were reported González-Burgos et al (2000).
The authors inserted stimulating electrodes to evoke action potentials and used distant recording electrodes to measure the responses in cells located distally from the stimulation site (Fig. 1).

Recording setup used in González-Burgos et al (2000).
They report that delays between monosynaptic connections range between 6 - 14 ms. Fig. 1 shows that these latency estimates depend on the position of the stimulating and recording electrodes, i.e., which part of the presynaptic cell is stimulated and which part of the postsynaptic cell is recorded. Most notably in the recording setup used, longer axon collaterals will have resulted in longer latencies. The authors conclude that the conduction velocity of the horizontal axon collaterals was 0.14 ± 0.04 m/s and the synaptic delay was estimated at 2.29 ± 0.49 ms.
Reference
- González-Burgos et al., Cereb Cortex (2000); 10(1): 82-92

The conduction velocity can vary by orders of magnitude based on many factors, so more information would be needed for a useful answer. Unmyelinated axon conduction velocities range from about 0.5 to 10 m/s, whereas myelinated axon conduction velocities can reach up to 150 m/s1.
I'm also not sure what you mean by "dense network". The brain is not a dense network and it sounds like you are including networks that are not brains.
[1]: Neuroscience (Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001. 2nd edition).


text:
Why is blood pressure higher the more distal an artery is?
Why is blood pressure generally higher in more distal arteries?

Because of reflected pressure waves and the stiffness of the blood vessel.  The forward pressure wave from the heart travels much faster than the blood itself and is reflected at areas of tapering and branching.  This backward wave slows the forward flow of blood, and at the same time, when it meets the next forward pressure wave, that forward pressure wave is augmented...so higher pressures distally...And now you know, and knowing is half the battle...

The cardiovascular system is affected by three types of pressure.  These are:

Heamodynamic - caused by the contraction of the heart, which would give the view of pressure being higher closer to the aorta as in Kevin's answer and my first thought too.
Kinetic  - caused by the action of skeletal muscles in movement in squeezing primarily veins to return blood to the heart.
Hydrostatic - the combination of fluid density and gravity that leads to pressure on the vessel endothelium.  The pressure at a given point is proportional to the volume of fluid above it.  This means that pressure is highest at the bottom of the vessel.

Arteries can of course be treated as one long tube due to their lack of valves, therefore the hydrostatic pressure could be significant in contributing to total blood pressure.  If hydrostatic pressure is more significant than heamodynamic pressure then this would explain why pressure would be higher the more distal the artery is - when standing there is simply more blood pushing down on it.

Critical Care Nurse. 2002;22: 60-79


text:
How do insects such as crickets circulate blood through their antennae?
Some insects, like the crickets pictured below, have such slender antennae it seems no blood could fit. How do they get blood through their antennae?

Insects do not posses closed circulatory system, but a space where organs float in a fluid called hemolymph. They don't have blood vessels (but some arthropodes have pumps that act a like heart). The hemolymph allows nutrients and excretion products to diffuse, but usually doesn't serve as a means to transmit oxygen to the tissues.
In insects, the oxygen is pumped through a series of little tubes named tracheae. Trachae connect the tissue directly to the air, allowing gas diffusion efficiently.
Antennae and wings have very little metabolic needs, mainly because (in the first case) they're formed by some neurons. Movement is achieved by muscles located in the base of the antenna (where it doesn't have circulation issues). The nerve tissue has the neuron bodies located in the basis too, so the nutrients and oxygen can diffuse through the axon.

Insects primarily get oxygen through diffusion of air through their skin.  I doubt the antennae need hemolymph circulation.

References, please

the answer above this one? lol

"I doubt the antennae need hemolymph circulation." doesn't sound very scientific. Can you add references, or explain why a little better?


text:
Why do plants have pith and how is it useful to them?
Many plants have pith, from walnut trees to corn to ragweed, but I can't think of anything it does them. What is pith and how is it useful to them?

Strange question: did you try to google? The first entry in my search results provides more than complete answer to your question.

The pith (medulla) forms part of the ground tissue system of a plant, and specifically it is the ground tissue which lies interior to a plants vascular tissues (xylem, phloem etc.)
The ground tissue system is responsible for much of a plants metabolic functioning, and contains various specialized cell types which aid in photosynthesis and storage of photosynthesis products. The pith is made from parenchyma cells.


text:
Do immature fruits perform photosynthesis?
Most immature fruits are green: peppers, pine cones, plums, lots of them. I want to know if the green is from chlorophyll in the cells. Do the fruit cells perform photosynthesis? When you cover a green stem or leaf, it will turn pale and stretch. That is because the stems have little need for chlorophyll in the dark, which is why they are pale. They stretch because the auxins in the stems are not destroyed by the photons, and the stems stretch out and topple over. If a green fruit is covered, will it turn pale and stretch like that?

It would definitely go pale

The green pigment is indeed chlorophyll, and the fruits do perform photosynthesis.   It's not just "fruiting" plants that do this either.  Some shading experiments i saw estimated that  up to 30% of the sugars assimilated into the barley ears (basically the grain) can come from photosynthesis occurring in those organs.

it would be great if you could provide specific references rather than "some shading experiments" that would be helpful. I am also curious about how such a shading experiment is conducted, what measurements are used to estimate the "30%", and what assumptions are made.


text:
Why do pandas have a high probability of giving birth to twins?
According to the BBC documentary "Wild About Pandas", about half of panda birth result in twins.  Why do they have such a high probability compared to other mammals?  What factor(s) control that fraction in general for mammals?
Additional question about the allometry formula:
I am a little surprised that it is not the ratio between the neonatal mass and the adult body mass that enters the formula, but just the neonatal mass.  Any ideas on that?

I don't know that they have a particularly high rate for multiple births up against other mammals when you consider cat litters of up to ten and beyond?

So you are saying it is rather normal for mammals to have high rate of multiple births, and panda is just an example?  If so, why human normally have single birth?

See Kevin's great answer :D

Charnov and Ernest (2006) present data on offspring number per year and neonatal mass for 532 species of mammals. The two are related by the linear regression equation:
ln(offspring/year) = 2.4 - ( 0.3 * ln(neonate mass) )
Giant panda neonates weigh 100-200 g and are weaned at 46 weeks.
So, according to the regression, pandas should have, on average, 2.8 to 2.2 offspring per year (for 100 and 200 g respectively). With a weaning time of 46 weeks, they could have 1.13 (52/46) litters per year. If every litter were exactly twins, that would be 1.13 * 2 = 2.26 offspring per year, which is within the predicted range.
Humans (neonatal mass of 3400 g) are predicted to have 0.96 offspring/year.
Charnov EL and SKM Ernest. 2006. The Offspring‐Size/Clutch‐Size Trade‐Off in Mammals. American Naturalist 167:578-582.

Thanks for the answer based on allometry.  What's a good survey book on animal allometry? I've read Niklas' Plant Allometry for plant allometry.

I wonder why the duration of pregnancy (95 - 160 days for panda) doesn't enter the computation?  Or is it included in the weaning time?

Could you check the correctness of my reasoning in the original post, including the use of duration of pregnancy?

Good point. You should probably include gestation in the calculation. There are a lot of other regressions in the paper mentioned above. I'm not sure if neonatal vs. adult mass is included though.

Basically a summary and details-filled version of the above.
Based on

ln(number of offspring/year) = 2.4 - ( 0.3 * ln(neonate mass) )
(c.f. Charnov EL and SKM Ernest. 2006. The Offspring‐Size/Clutch‐Size
Trade‐Off in Mammals. American Naturalist 167:578-582.)
litter/year = 1 / (pregnancy duration in years + weaning time in years)

it can be deduced that

number of offspring/litter = exp(2.4 - 0.3 ln(neonatal mass in grams)) / (pregnancy duration in years + weaning time in years)

For pandas, the parameters have values

neonatal mass in grams = 150 - 200
pregnancy duration in years = (95 - 160) (days/years) = 0.26 - 0.44
weaning time in years = 46 weeks/years = 0.88

Therefore, for pandas,
offspring/litter = exp(2.4 - 0.3 ln(200)) / (0.26+0.88) to exp(2.4 - 0.3 ln(200)) / (0.44+0.88) = 1.7 to 2
This means, pandas on average have slightly less than 2 offsprings per litter, which means a high probability of having twins, and sometimes single, but rarely higher multiples. Comparing to human which has about 0.7 offsprings per litter, panda has higher probability of having twins mainly because of much lighter neonatal mass.

I think this article provides some relevant information for your question. It specifies that the rate of twins is high (50%) in captive pandas, and low elsewhere. The article mentions that there is a genetic component to twin predisposition (which is true for humans as well, see here), but that the primary reason is the technology used for captive pandas to increase breeding success:
"To increase the chances of pregnancy, technicians will impregnate a female with at least two male panda semen after natural mating, which makes twins and triplets pretty common for captive pandas."
This doesn't relate to the allometry equations or allometric theory, but provides a practical reason for the phenomenon you are inquiring about.


text:
What causes REM atonia to be lost in sleepwalking?
I understand that in normal REM sleep the voluntary muscles are in effect paralysed in order to prevent an individual acting out their dreams.  This paper indicates that there are likley to be multiple causes of this atonia. I am interested to know what are some of these methods by which natural atonia is achieved by the body in periods of sleep?
Furthermore, what causes these mechanisms to fail in individuals who suffer from sleep-walking?

I don't know if this will help you find the right answer, but a related process is 'sleep paralysis', in which a person continues to remain paralysed after waking up from REM sleep. It's happened to me once or twice (for less than a minute each time); scary stuff: http://en.wikipedia.org/wiki/Sleep_paralysis

There's an excellent, comprehensive review article on the entire process of REM sleep:

Vetrivelan,R, Chang, C, Lu,J (2011). Muscle tone regulation during REM sleep:
  neural circuitry and clinical significance. Archives Italiennes de Biologie, 149 [DOI] [Free PDF]

Projections from the sublaterodorsal nucleus (SLD) of the Pons in the brainstem are responsible for the suppression of the spinal motor output/movement (for an anatomical schematic, see the article).

Descending SLD glutamatergic projections activating the premotor neurons
  in the ventromedial medulla and spinal cord interneurons bring about muscle atonia and suppress phasic muscle twitches in spinal musculature.

Lesions in this area in rats have resulted in REM sleep without atonia.

Many studies have
  suggested that the ventromedial medulla (VMM),
  which receives glutamatergic inputs from the SLD,
  may be the relay site for the pontine inhibitory area
  on spinal motor neurons

The SLD axons relay through the VMM, but also directly projects onto interneurons within the spinal cord, directly inhibiting their activation.
Most of the knowledge we have about this subject comes from animal studies, so it will take some time to verify whether these same mechanism and relays are the same in humans.
The area that is lending the most credence to these issues of REM atonia is not sleepwalking as much as REM sleep behavioral disorder (RBD).  In this condition, sufferers act out their dreams and generally lose atonia during REM sleep.
Evidence points to the fact that such behavior is often seen decades before such conditions as Parkinson's and Lewy Body dementia.

Ferini-Strambi,L (2011) Does idiopathic REM sleep behavior disorder (iRBD) really exist?
  What are the potential markers of neurodegeneration in iRBD? Sleep Medicine 12, S43–S49 [DOI]

They summarized two studies which explored these anatomical changes:

[Diffusion tensor imaging, a type of MRI scan] changes have been reported in the
  brainstem (pons, substantia nigra) as well as the fornix, the right
  visual stream, and the left superior temporal lobe suggestive of
  brain tissue disintegrity[1]
significant decreases of [fractional aniosotropy] in the tegmentum
  of the midbrain and rostral pons and increases of [mean diffusivity]
  within the pontine reticular formation overlapping with a cluster
  of decreased [fractional anisotropy] in the midbrain [2]

So, the answer is, we don't know for sure, but we have some clues from the animal models as to what stages of the signals to suppress movement are interrupted.
[1]Unger MM, Belke M, Menzler K, et al.(2010). Diffusion tensor imaging in idiopathic
REM sleep behavior disorder reveals microstructural changes in the brainstem,
substantia nigra, olfactory region, and other brain regions. Sleep,
33(6),767–73.[FREE PDF]
[2]Scherfler C, Frauscher B, Schocke M, et al. (2011) White and gray matter abnormalities
in idiopathic rapid eye movement sleep behavior disorder: a diffusion-tensor
imaging and voxel-based morphometry study. Ann Neurol,69(2),400–7. [DOI]

Failure of maintaining atonia does not lead to sleep-walking but to REM sleep behavior disorder. Sleep-walking is a mixture of NREM and wakefulness.
Mahowald, M. W., & Schenck, C. H. (2005). Insights from studying human sleep disorders. Nature, 437(7063), 1279–85. doi:10.1038/nature04287


text:
How correlated are the lengths of tendons in different part of a human body?
How correlated are the lengths of tendons in different part of a human body?
E.g., if the we consider two humans, A, and B. Human A has a patellar tendon of length 2 cm, and human B has a patellar tendon of length 1 cm, i.e. twice shorter. Should we expect all tendons in human A to be approximately twice larger than in human B?

I couldn't find studies analysing clearly enough tendons size, but a couple of sources show that they are probably correlated:

One study found correlation between dimensions of Achilles'tendon and other ankle tendons (see table 2).
Another study found correlation between height and dimensions of some tendons (see table 2).

Anyway, since correlation is not very strong, I doubt if the effect found is just the obvious correlation of dimension of all body parts to the general dimension of body - that is, bigger people tend to have bigger tendons, bigger bones, bigger livers, and so. It would be interesting to do a regression analysis of tendons dimensions taking in account body dimensions and other tendons dimensions. This way we could be able to see if people with some bigger tendon (compared with people of the same body size) tend to have other bigger tendons.


text:
What is the difference between "hamstring tendon" and "common hamstring tendon"?
What is the difference between "hamstring tendon" and "common hamstring tendon"?  I have seen both terms being used but I don't know whether they referred to the same tendon.
For example,
Johnson, Anthony E., Robert R. Granville, and Thomas M. DeBerardino. "Avulsion of the common hamstring tendon origin in an active duty airman." Military medicine 168, no. 1 (2003): 40-42. (https://doi.org/10.1093/milmed/168.1.40) uses the term "common hamstring tendon" but I don't see any difference with the "hamstring tendon" when reading the article.
Since there are more than one hamstring tendons, I would have guessed that  "common hamstring tendon" specifies which hamstring tendon is being referred to, but I haven't seen the term of any anatomy diagram yet.

The hamstring tendons that I am aware of are:

Lateral hamstring tendon of the biceps femoris (long head) (2 tendons: distal+proximal)
Lateral hamstring tendon of the biceps femoris (short head) (2 tendons: distal+proximal)
Medial hamstring tendon of the semitendinosus (2 tendons: distal+proximal)
Medial hamstring tendon of the semimembranosus (2 tendons: distal+proximal)

(image source)

(image source)

In the paper you cite, they are talking about the tendon on the other side from the ones you've listed, at the "origin from the ischial tuberosity" (quoted from the abstract).
In this case, the word "common" is used in the dictionary sense of "same" rather than "ordinary": it's "common" because it's the same origin for the different muscles that make up the hamstrings. This terminology is used elsewhere in anatomy, too, for example the common carotid artery splits into the internal carotid and external carotid; the "common" portion is the larger proximal vessel.

Thanks very much for the information, makes sense! It seems that the semimembranosus tendon has its own attachment though, separate from the conjoined [semitendinosus tendon + long head of the biceps femoris tendon]. I've posted some details as another answer as I didn't have enough space in the comment. If you look at my answer, please let me know if it is incorrect, I'd  appreciate any feedback.

Expanding on Bryan Krause's answer:
From {1}:

The semitendinosus (ST), long head of the biceps femoris (long head, lhBF) and semimembranosus (SM) muscles
  originate from the ischial tuberosity (Fig. 1a, b). The ST and
  lhBF have a common origin on the posteromedial aspect of
  the ischial tuberosity, over its top. Tendons of the ST and
  lhBF are conjoined at a distance of 9.1–10 cm [35, 37, 58,
  81]. The SM origin is separate from the previous one and
  it is located anterolaterally from the ST/lhBF attachment.
  Fibres of the proximal SM attachment are twisted before
  forming a proper tendon (Figs. 2a, b, 3a, b, 4).
A majority of authors agree with the presence of a conjoined tendon of the ST/lhBF, but the precise description of
  its attachment area varies amongst authors. Most of authors
  observed the attachment on the posteromedial aspect of the
  ischial tuberosity as in our dissection [61, 68, 82], whereas
  others indicated it to be directly medial [10, 58] or lateral on
  the ischial tuberosity [35, 60]. Consequently, the SM attachment is also described in different ways: on the anterolateral
  aspect of the ischial tuberosity as in our dissection [61, 68,
  82, 84], but also anteriorly [35] or purely lateral [58]

Subsequently the "common hamstring tendon" = the conjoined ST tendon + lhBF tendon, but doesn't include the semimembranosus tendon as its attachment is distinct from the attachment of the conjoined ST tendon + lhBF tendon.

To visualize the attachments of the conjoined ST tendon + lhBF tendon, and the semimembranosus tendon to the ischial tuberosity:

Fig. 2 a, b Posterolateral view of the area of the proximal attachment
  of the hamstring muscles (right lower extremity). (1) Area of
  the attachment of the conjoined tendon of the semitendinosus and the
  long head of the biceps femoris; (2) the proximal attachment area of
  the conjoined tendon; (3) conjoined tendon of the semitendinosus and
  the long head of the biceps femoris—cut and rotated 180°; (4) proximal
  tendon of the semimembranosus muscle; (5) area of the attachment
  of the semimembranosus muscle; arrowheads—shape of the
  semimembranosus attachment

(image source: {1})

References:

{1} Stępień, Karolina, Robert Śmigielski, Caroline Mouton, Bogdan Ciszek, Martin Engelhardt, and Romain Seil. "Anatomy of proximal attachment, course, and innervation of hamstring muscles: a pictorial essay." Knee Surgery, Sports Traumatology, Arthroscopy (2018): 1-12. (https://doi.org/10.1007/s00167-018-5265-z)


text:
How to calculate virus titre from qPCR
I harvested some lentivirus from 293T cells and want to titre the result. I infected 293T cells on a well plate with 400,000 cells per well which I infected with virus stock, and 1 in 10, 100 and 1000 dilutions (as well as a few uninfected wells). After 72h incubation I trypsinised the cells and used FACS to titre first, but 293T do not express the promoter under which GFP is located in some samples and hence these do not appear on FACS. As an alternative, I extracted the genomic DNA from all samples using a QIAGEN DNeasy kit (also the samples which I was able to titre by FACS already) and then performed qPCR on them.
I used the ABI PRISM 7000 SDS: http://www.cgenetool.com/products/abi_prism_7000.shtml
Included on the PCR plate were:

Number standards: 1000, 10k, 100k, 1m copies
Samples in triplicate
No-template controls as well as untransduced controls

Each of those was doubled, once with primers and probe for WPRE (an element specific for the lentivirus) and once with primers and probe for beta-actin (a housekeeping gene present in all cells).
The results returned by the machine include for each well the cycle at which the threshold fluorescence was crossed - along with the automatically calculated quantity of copies (which the software calculates from the standards I assume).
Since I named the triplicate samples identically, it also automatically calculated the mean quantitiy among each triplicate (practical, eh?). I checked if there were any outliers which should have been excluded from the means but everything was fine.
So now for example I have a result of 700k for the quantity of WPRE in sample A. The quantity of beta-actin in sample A was 6.82 x 106. The transfection was 400,000 cells per well, sample A was transfected with 10uL of viral stock diluted 1:100.
How do I calculate the virus titre per mL from this?
I have been given the formula: WPRE Qty / (b-act Qty*0.5) * cells in well (400k) * dilution factor (100), but am struggling to figure out a) why b-act Qty is divided by 2, b) whether the result would be virus titre per uL or per 10uL (transfection volume) and c) how beta-actin can have almost 107 copy numbers consistently across all samples when there were only supposed to be about 105 cells...

Having gained a lot more experience with how research works, I can actually answer myself now:
a) beta-actin quantity is divided by 2 because it is a human gene and hence present twice in mammalian cells, dividing it by 2 gives an estimate of the number of cells present.
b) The result gives an estimate of how many viral copies will end up in cells from the amount of virus solution used - thus if it was 10 uL of a 1:100 dilution this represents 0.1uL of neat virus solution. So the result's unit in this case would be "viral infections per 0.1uL".
c) The number of beta-actin copies doesn't correspond to the number of cells initially seeded. 400k cells which double once per roughly 24h would make 3.2m cells after 72h (3.2x106) so that's not all too far off the copy number.

I have 2 doubts here.

You obtain your viruses from the media whereas Actb measurements can be performed only in the cell lysates.
Actb is just a reference to normalize for the cell count: higher the cell count higher will be the viral titre because of higher number of infected cells. But that is immaterial if your aim is lentiviral transduction where you are only interested in obtaining titre values and not measuring the efficiency of its formation.

You can simply do qPCR with the media sample and the standards and regress the measured Ct values of the samples to obtain titres.

Thanks for the reply. I see that I left out relevant information so I added that - have a read of the first paragraph again and let me know if that makes more sense now :)

I think it makes more sense to qPCR the lysates for copies, with all virions removed, as that should give me an idea of how many cells a mL of virus stock can transfect, which I believe is actually the important factor - I don't think I really need to know exactly how many viral particles that mL contains in order to transfect that many cells. Does that make sense?

I think it is the media that will contain the viruses and that's what you are going to use for transfection post concentrating the virions to whatever concentration you want. So you ought to do the qPCR with the media right? I might be mistaken so please let me know if that is so.

The initial prep is 293Ts in a medium with the viral plasmid as well as packaging and envelope plasmids; cells are perforated (but not killed) by adding PEI which leads to production of functional virus. That's then harvested, aliquoted out into stock vials and frozen. I was told it's not possible to just directly qPCR the aliquots - I assume the viral proteins are the problem. I used one of the vials to infect cells with decreasing concentrations of it, extracted their DNA after three days and qPCR'd that in order to analyse how many viruses actually integrated into the cellular genome.


text:
Why are some bodily fluids more of an infection risk than others?
Whilst on a recent refresher course it was highlighted that when considering risk of exposure to infection from bodily fluids we should be aware of two distinct risk levels:
High Risk:

Blood
Semen
Vaginal Secretions
Diarrhea

Low Risk:

Saliva
Vomit
Urine
CSF (Cerebrospinal fluid)

Why is it that some bodily fluids are a greater infection risk than others?  Is it related to the fluids themselves or the species of pathogen that are located within them?

I feel like sputum / mucus should be on that list.  It's the primary bodily fluid that influenza and other respiratory tract infections are spread with.

@GWW Yeah it probably should - these were just mentioned specifically by the trainer :)

I would say that diarrhea is a medical condition, not a bodily fluid. I would use the term feces instead (OK, fluid does not apply to that either, maybe "bodily secretion" would be better?)

@nico agree with that comment too, as above I was just mentally copying and pasting from the powerpoint.  I suppose it brings about a sub question as to whether more solidified faeces is a lesser infection risk than diarrhoea?

@Rory M: good point, although I have to say I wouldn't like to be the one who tested that!!! :D

This is just about where the pathogens can be found that are dangerous to people.
Vomit is highly acidic and less accommodating to microbe growth. Similarly saliva has many immune components in it as well as digestive enzymes that keep most microorganisms down.
Urine and CSF are actually quite sterile as they come from environments that are highly filtered - the kidney is an osmotic processor that essentially is a molecular filter and does not allow cells to pass, the spine is highly insulated from the blood and other direct exposure to microorganisms.
Compare that with the 'dangerous' list and you have organs that are open to human pathogens.  Venerial disease like HPV is so common that what - about 1 in 5 people under a certain age carry it.  That is a pretty high expectation of a biohazard.  most infections and viruses are blood bourne - influenza, cold, as well as any bacterial infections.
Feces is always a dangerous thing to handle as the digestive tract is rich in nutrients and essentially directly open to external bacteria and fungi.  (and its not acidified like the stomach).  Also parasites like tape worms and other multicelled animals! yum!
Diarrhea is often caused by an infection of some sort, so its just more likely a hazard, but feces is always a place where you might find a pathogen.
This is not to say that the 'safe' list is totally safe.  Its just less likely to bear disease causing agents.

Largely unrelated question:  if roughly 1 in 5 have HPV or this venereal disease in question before a certain age, wouldn't they continue to do so after that age?  Or is the mortality so high as to bring down the fraction of the (living) population that has it?  Why am I not hearing about this as one would if, say, the plague were going around?


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Do both TSG and Proto-oncogenes have to suffer mutations to cause cancer?
I'm having a conceptual nightmare trying to understand when a group of cells may become cancerous and the more resources I consult the more confused I seem to get.
In order for a cell to become cancerous, does it have to mutate to knock out tumour suppressor genes and have a proto-oncogene become an oncogene?
I'm  currently working on the basis that that is the case, or at least that a mutated TSG on its own will not cause uncontrolled division.  However wikipedia seems to suggest that an oncogene alone can cause uncontrolled division with a functional TSG in place.
It could be a flaw in the idea I have that tumour suppressor genes only trigger apoptosis once a cell has started to divide rapidly, are they actually carrying it out to a regular schedule independent of oncogene presence?

There is a nice nature paper by Dr. Micheal Stratton et al. that I think might be a good place to start.
I think answering you question is complex, because different cancers will actually have different mechanisms that trigger their onset and aggressiveness and as such some have more complex mutational landscapes than others.
A good question to ask yourself is : what is a driver mutation and what is a passenger mutation. A driver mutation is usually what is driving the cancer, and it can be a proto-oncogene or TSG. Passenger mutations don't really have as much of an impact and result from the destructive tendencies of the driver mutations.

The typical idea is that several "hits" are required. The difference between proto-oncogene and TSG is mainly in their heritability - TSG mutations are usually recessive (because a heterozygote will still express sufficient suppressor, e.g. p53) whereas proto-oncogenes are dominant (if a consitutively active agent e.g. Ras is present, it doesn't matter if the other allele is under normal control).
A single "hit" in this way (TSG or proto-oncogene) may just cause the cell to die, which isn't a bad thing (in fact, TSG such as p53 often work by inducing apoptosis because proliferative errors make them accumulute). A tumour only results when a single cell accumulates sufficient mutations and genomic damage to gain a reproductive advantage over the cells in its vicinity.
However, you are asking about cancer, which is not simply a tumour. Tumours are any sort of abnormal growth, i.e. neoplasms, but they can be benign! This means they stay in their tumour capsule, do not grow at a fast rate and do not invade or metastasise other tissues. The distinct characteristics that define a cancer are very well-known and were published in a well recognised paper by Weinberg & Hanahan, 2002, "The Hallmarks of Cancer".
The six primary hallmarks of cancer. The first two are the ones most people know, but the other ones are just as essential for

Independence from external growth signals: Cancer cells produce their on autocrine growth factors or have mutated signal pathways active without GF receptor stimulation (Oncogenes).
Resistance to anti-growth signals: Cancer cells do not respond to growth-inhibitory factors from outside or inside (Tumour suppressor genes).
Evasion of apoptosis: Cancer cells resist signals which cause normal cells to die (apoptose) (these are also tumour suppressor genes).
Limitless replication / Evasion of cell senescence: Apart from stem cells, all normal cells can only replicate their genome a certain number of times before the ends of the chromosomes known as telomeres are too short, disintegrate and cause the cell to enter senescence or die. Cancer cells express telomerase, which extends telomeres and maintains replicative potential.
Sustained angiogenesis: Tumours and cancers form massive cell heaps. Tumours may stall growth because blood vessels do not grow into the heap and supply the cells with the nutrients needed to proliferate. Cancer cells have found a way to induce blood vessel growth (VEGF) and sustain it in order to maintain nutrient supply.
Invasion and metastasis: This is the crucial, most distinguishing difference between benign neoplasm (tumour) and malign neoplasm (cancer). Cancer cells degrade the extracellular matrix around them (by secreting metallo-matrix-proteases, MMP), which allows them to move away from where they are and invade into neighbouring tissues. They can also spill into blood vessels this way (especially if the neoplasm is well-vascularised thanks to hallmark number 5), where they can travel to other sites in the body and grow new cancerous tumours in other locations.

There are four more emerging hallmarks and enabling characteristics (immune evasion, inflammation induction, modification of energy metabolism, genomic instability), which allow better cancer growth and make a cancer more dangerous if it acquires them, but these are outside the scope of this answer.


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Is it correct that the body only responds to the most painful stimulus?
I'm rather ashamed to say that this question is partly based on an episode of House.
I have previously heard that, if there are multiple simultaneous painful stimuli, the mind will only feel the sensation of pain from the most severe injury.  A large amount of googling has turned up nothing and PubMed searches are proving tricky as I cant find the name of this effect (if it exists).
If it does exist, is the mechanism solely effective for pain signals or would we for example only feel cold at our coldest points (i.e. from the face or the hands rather than both) on a frosty morning?

"House MD" is one of the best series as regards the veracity of the medical observations. Whereas many cases are normally so rare that it is just improbably that House comes accross them, they all are usually ultimately correct as regards the symptoms, the course etc. The only series with a better medical background  is "ER", but with every new season the proportion of the medical part was decreasing so dramatically that I just gave it up in the middle.

When I get hip pain, it is so excruciating that the lower back pain goes away. As soon as my hip pain is relieved, the lower back pain comes back.

Pain is an associative cortical phenomenon, not a peripheral sensation. As with any cortical associative event, the experience of pain is dependent on attention, memory and prior experience. I may write an answer to this, but I'll have to dig a bit to find the relevant references. The way I like to think about it comes from Patrick Wall. I never met him myself, but Eric Kandel and John Brust have both quoted him to me as saying something like: pain is a need state that has more in common with hunger than somatic sensation or vision.

Your question statement is a little bit incorrect or, better say, imprecise.
First of all it is not clear what you mean by the "body response" here? Pain is sensed by peripherial receptors (several types of receptors, mostly purinergic, are assumed to play role in pain preception) and then this sensation is propagated into CNS. So, the local "response to pain" (like swelling, increase of the blood perfusion) is not the response to the pain stimulus, but rather a methabolic response to the cell injures and release of many humoral factors like interleukins, "wound hormones" etc.
And this is true that out of many different pain inputs the one with highest intensity seems to "outshine" all other inputs and ultimately the pain perception is constrained to a single body part. However, if you consciously focus your perception on other parts of your body you may be able to percieve the pain originating from these parts even if this pain is lower.
This principle is known as a smaller particular case of a more general principle known as "the dominance principle of Ukhtomsky". Wikipedia has only the Russian language version about this principle (as well as about Ukhtomsky, a prominent Russian physiologist) and it seems to be not really known outside of the Russian scientific community (this is the only page I found about him in English).
The more general principle of Ukhtomsky postulates the following: one certain input may lead to the formation of the dominance center in the cortex. The domaninace center is characterized by the higher level of nerve cell excitation, whereas the rest of the cortex undergoes an inhibition so that different, even unrelated inputs converge here, helping this center to exist for longer time. The only way how this center can be ceased is to form another dominance center by a extremely high stimulus (for example a startle sound). Here the most insensive pain leads to the formation of such a center and all substantial pain stimuli just contribute to the persistence of this center: the pain is however percieved to originate from the place where the first stimulus, responsible for dominance center formation, originated from.

Is there any evidence that Ukhtomsky's postulate actually occurs?

@yamad Do you mean if the postulate has ever been proved or if it is applicable to this particular case with pain perception?

I mostly interested if the postulate has ever been shown to be true in any case. Of course, I would also be interested if it happens to be applicable to the case of pain perception.

@yamad In Russian physiology this theory is considered to be proved. There is a classical book by Ukhtomsky (last edition was published in 2002) which describes his experiments with dogs which were used to prove the theory. There are numerous publications mentioning dominance principle in pubmed, but they are mostly in Russian.

So would Ukhtomsky's principle apply for other sensations such as the feeling of cold?

@RoryM Not every input leads to the formation of a dominant center,  the input has to fulfill certain criteria -- and if those are met then every input (cold, burn etc.) can do it. Pain is an example where it is true in most cases due to the nature of this input, but Ukhmomsky showed also other inputs in his experiments on dogs.


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Effect of Ethanol on Brain Volume Measurements
I want to compare the brain sizes of two populations of fish. However, all the samples I have were fixed in 95% ethanol. As far as I know, 4% formalin is the normal fixative for soft tissues. Can I conduct my study, or do I need to obtain samples in formalin? I've scoured the literature, and I can't find any useful recommendations.

Are all the samples fixed in ethanol? Or some in ethanol and some in formalin?

I just spoke with my histological colleague about your question. He said that you should be fine for gross examination but not for microscopy. Why? He says, "When working with specimens, the higher resolution microscopy you try to achieve, the more 'potent' the fixative needs to be. A preservative will preserve what tissues are there. However, fixatives (like paraformaldehyde or glutaraldehyde) bind proteins together and, thus, are used to try to 'fix' a tissue posthumous in the manner that it was structured in life. For gross examination, a preserved specimen (without prior fixation) can act as a decent voucher for macroscopic evaluation of its internal organs; however, it will not suffice for any type of detailed histology at the light microscopy or electron microscopy level."
So, the short answer is that it depends on the type of work you need to accomplish.


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How does the Golgi Apparatus perform its function?
The Golgi Apparatus is an organelle with a great number of functions, I am particularly intrigued in the role it plays in packaging macromolecules and sending them to their target organelle or to leave the cell in exocytosis.  I would love to know more about how this process works.  How does the Golgi Apparatus recognise which molecules are which and how does the vesicle it places the molecule into navigate to where it is needed?

This is actually is an awesome story: both how it happens and how it was discovered. This is one of those stories people get Nobel Prize, and this was Günter Blobel who was awarded this highest possible prize for his discovery, which is according to his Nobel prize certificate:

"for the discovery that proteins have intrinsic signals that govern
  their transport and localization in the cell"

If you watch or read his Nobel prize lecture you will find answers to your question formulated much better than I can do it here. His Nobel lecture was opened with the following words which might already answer you question:

Imagine a large factory that manufactures thousands of different items
  in millions of copies every hour, that promptly packages and ships
  each of them to waiting customers. Naturally, to avoid chaos, each
  product requires a clearly labeled address tag. Günter Blobel is being
  awarded this year's Nobel Prize in Physiology or Medicine for having
  shown that newly synthesized proteins, analogous to the products
  manufactured in the factory, contain built-in signals, or address
  tags, that direct them to their proper cellular destination.

Still, I recommend you to read (or watch) to the end, there are some interesting points on how it was discovered and what experiments were done to do it.

07:55-10:06 is the relevant section of the video for anyone wishing to jump to it.  I read the lecture you linked to which was very interesting, however is there anywhere which goes into more detail? =)

The most complete reference for cell biology is The Cell by G. Cooper, here is the article about Golgi apparatus available online. Does this answer your question or you want even deeper overview?


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Are there predators evolved to eat puffer fish?
Puffer fish is known for having a anti-predation defense mechanism of having toxin-exuding spikes.
Are there predators which evolved specifically to prey on puffer fish? (presumably, by evolving immunity to the toxin)?
I know that sharks eat them, but I doubt sharks evolved to be immune specifically to puffer fish toxin, since their evolutionary development preceded puffer fish's.

Wikipedia has some revealing information here:

Not all puffers are necessarily poisonous; Takifugu oblongus, for example, is a fugu puffer that is not poisonous, and toxin level varies wildly even in fish that are. A puffer's neurotoxin is not necessarily as toxic to other animals as it is to humans, and puffers are eaten routinely by some species of fish, such as lizardfish and tiger sharks. Also, Japanese fish farmers have grown nonpoisonous puffers by controlling their diet.

It seems that susceptibility to tetrodotoxin varies a lot from one animal to another, and so some natural variation might allow a reasonable amount of predation to occur.  I also wonder whether the variation in the amount of toxin in the fish implies that the fish are often depleted.
There are cases of animals who have evolved a resistance to Tetrodotoxin, but for the most part its may the predators you are thinking of.  The toxin is synthesized by a symbiotic bacteria and is found not only in fugu but also blue-ringed octopus, rough-skinned newts and some sea slugs.  These animals probably all began with enough intrinsically low sensitivity to the toxin to take on the symbiont and probably evolved to be completely insensitive.  To find a predator that would have co-evolved a similar resistance you would look for a predator that particularly favors the envenomed animal.  In the case of the rough skinned newt, its suspected that the common garter snake is an example of such co-evolution. Others may be out there to discover - its probably difficult to watch marine animals to know what their typical predators are.

I'm curious if some predator evolved to be immune to the toxin. Is there some data on whether those species that pray on pufferfish evolved this way, or is that purely an accident of environment, as is the case with sharks - which decidedly did NOT evolve to deal with pufferfish?

Added a note on that...

thanks @DVK  I should add that its also possible that Fugu could be a small enough player in its environment so that no predator has selectively pursued it.  It depends on the likeliyhood that an animal can be susceptible to the toxin and how many sources of food there are for those predators in the environment.

I know there are species of sea snakes that actually aren't bothered by the puffer fish's toxins! So they will eat them easily because puffer fish are extremely slow swimmers. Besides that sharks are the only other species, in specific Tiger Sharks don't have any consequences to consuming pufferfish.

Can you provide citations for the content in this post? Otherwise it may be deleted.

It would be an excellent answer with linked references.


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What percentage of human body's cells are contained in blood?
What percentage of human body's cells are contained in blood vs. the rest of the body?

The background of the question was a (somewhat silly) theoretical question of "how much of your body's cells can you replace with blood transfusion". I realize that the exact biological answers to the two questions will be different, but I think it's a good first approximation.

You should probably edit the question to contain that background then.

When you mean "percentage", do you mean my type or by mass?

@anon by cell count

According to this answer, there are 2.63 × 10^13 red blood cells, which is 70.69% of the 3.72 × 10^13 total human cells in the estimate.

The human body has about $3.72 × 10^{13}$ cells according to Bianconi et al. 2013, although this is disputed.
It also has about 5 liters of blood, which is made approximately 40-45% of erythrocytes. Let's assume 2.5 liters = 2500 $cm^3$ of red blood cells (RBC). Assuming a mean value of 5 millions RBC per $mm^3$ there should be in total $5 \cdot 10^6 \cdot 10^3 \cdot 2500 = 7.5 \cdot 10^{12}$ RBC.
By completely taking out white blood cells and thrombocytes out of the equation, a number of ${7.5 \over {3.72 \cdot 10}} \cdot 100 = 20 \%$ of number of cells are contained in the blood (approximately).

Given the hypothetical 70 kg man, let him be separated into components:
Blood: 7% (70 kg x .07 = 4.9 kg)
Of that, 60% is plasma, so (4.9 kg x .4 = 1.96 kg blood cell weight.)
Therefore of a 70 kg male, ~ 2 kg is blood cells
Tissue and bone: 93% of body weight (70 kg x .93 = 65kg)
Of that, 27% is extracellular fluid, so (65 kg x .73 = ~ 47.5 kg cell weight)
But we need to subtract the weight of bones:
Dry bone weight = ~6.5% total body weight, (70 kg x .065 = 4.55 kg bone weight)
So, cell weight minus extracellular fluid:
Blood cells: 2 kg
Body cells (minus bone weight): 43 kg
2kg/(43kg + 2 kg) = 4.4% of the weight of cells in the body are the blood cells.

Isn't a human being about 75% other organisms though? As in, of that 70kg, about 50kg doesn't actually have the human's DNA?


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Is a raised baseline between T and QRS normal in any ECG lead?
Here are excerpts from an unknown ECG lead. I find it weird that the "baseline" changes after the T wave and doesn't return until after the following QRS complex. Is that normal/expected for any lead?

Click for better resolution. I've got another 10 minutes of the ECG, if that would be helpful.

Also, I should note that I'm quite inexperienced when it comes to cardiology, so this is probably a basic question -- so don't upvote me too much :)

What frequencies are the high pass and low pass filters set at?

@jonsca: I've applied a 5-point moving average. As there was no baseline drift I don't think I had applied any other filters, so that would be from the data acquisition tool. It was sampled at 360 Hz. Here are the non-averaged graphs for these intervals: 80-92 sec, 88-90 sec

@jonsca: Ok, looks like I had highpassed it at 0.5 Hz.

It looks like some kind of line noise or artifact on the unfiltered plot.  See if your software has a notch filter for 50/60Hz (depending on Europe or the States).  Put that on, then try your moving average, but remember a "boxcar" filter is always going to distort your plot a bit.  I'm not an expert on ECG, but I would hedge my bets on this being non-physiological.

@jonsca: Thanks a lot, I missed that! It didn't change the signal very much, but there was a clear spike at 60 Hz there before. Smoothed notched 1 and 2

I am not sure if I understand your question correct. What I can see here is a clear ST depression, that might be indicative of myocardial ischemia/infarction. The underlying mechanism is the shortage of oxygen in myocytes leading to elevation of resting potential and slowing of the depolarization -- this accounts for the elevated baseline after T.
I am not at all an ECG expert, but I have seen the misplaces T-P segment many times while at medical school. It wasn't indicative for diagnosis, whereas all other segments were.
So, why are you worrying about this segment?

Thanks! Then I know that the TP elevation is fine. About the ST depression, is it clear because there's a large vertical distance between the isoelectrical line (measured at P onset) and right after S, or also because of the horizontal ST segment?

Actually an MI often has ST elevation and strong negative QRS complexes

This is inexact. Both ST elevation or depression can happen. Please be careful when commenting/answering on subjects pertaining to acute health problems. @Andrey ST segment depression in humans is defined by a 1mm (0.1 mV) depression from the isoelectric line.

@Raoul The answer is in no way medical consultation, especially for an acute medical problem, as stated in the site rules. The question asked is different from your answer.

@Alexander I did not mean to be rude. Yes,this answer is not about a medical problem. What I meant is that we should be careful with sensitive topics on the website. Bad things sometimes happen to people reading about health on the net, and we should strive to be as exact as we can.I also make mistakes.

@Raoul I fully agree with you (and don't think your previous comment was rude in any way). At the time of this question we already had a clear site guideline stating that no medical advice can be given or sought here.I understood the question so, that it is asked about usual finding on ECG, rather than "normal" in the meaning of "healthy". Hence is my answer.


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Does body temperature affect human lifespan?
If a human body were somehow to be kept at a cold temperature (say 30C) for the entire life of the given individual. And somehow the brain could be fooled into thinking that this 30C feels nice and warm.
Would that given individual live longer as a consequence?
What effect does a tempreature have on lifespan?

A core temperature of 30°C?  That's right on the edge of severe hypothermia, I wouldn't expect it to be a survivable condition for too long.  Especially for neonates if you wanted to maintain the temperature from birth.

okey then, 32. Could even keep them a bit warmer in the beginning.

As a flypushing biologist I know that if I want my flies to live longer I keep them at 18 degrees C, rather than the normal 25. Not sure if any work has been done to understand the mechanisms and whether or not these mechanisms would apply to larger organisms.

Epic, so u just put them in the fridge like food u want to last longer? How much longer do they live at 18c compared to 25c?

A boat sank close to Icelandic shores in march 1984, all died but one who managed to swim to land, took him five hours and the ocean was around 4C. So there are people who can tolerate unbelievable drops in body temperature and suffer no long term harm.

And frogs are relatively advanced animals, there are those who can just freeze in the autumn and thaw back in the spring: http://www.youtube.com/watch?v=Fjr3A_kfspM

So advanced animals seem to be really capable of cooling.

Could you please define what an "advanced animal" is? A vertebrate? A mammal?

I don't have an exact definition at hand but humans and frogs are what I would call advanced. I might as well rephrase and say 'humans and frogs and such animals' instead of 'advanced'. The point would remain the same.

@Hermann Ingjaldsson: no, it is extremely important to define it. For instance, a frog is cold-blooded, a human is not.

Okey I changed it.

@HermannIngjaldsson re the boat thing, whilst a pretty spectacular feat his core temperature couldn't have dropped anywhere near that low, indeed not beyond the temperatures earlier mentioned in comments.  Even if the temperature did not kill him then the muscle co-ordination apparent before the condition becomes lethal would have surely resulted in his drowning.  The discussion in comments on this question is really interesting however perhaps we should all move to chat to keep things clear.

As you probably know, hibernating mammals can lower their core temperature dramatically. There are even cases with mammals recovering from core temperatures below zero., e.g. arctic ground squirrels and bats. This is clearly not the same as being functional with drastically lowered core temps, but could be interesting/relevant.

I am assuming that you are referring to a baseline human cooled to a core body temperature of 30C from birth. I am also assuming that you are ignoring the fact that the environmental temperature (and thus the temperature of the extremities) has to be much lower than 30C to cause a core temperature of 30C. Thus, I am ignoring hypothermia-based gangrene, necrosis, and extremity loss.
If you had a normal human with a 30C core temperature starting at birth, I have doubts that it would live any longer than a human at 36.8C. Unlike flies, which are ectotherms, humans need to have a more or less constant temperature to successfully complete most of their metabolic processes efficiently. Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death. Though you might be able to "fool" the brain on thinking that 30C is normal, it is unlikely that the organ functions can follow. It could be possible to breed successive generations of humans in ever-lower temperatures, but it is unlikely for a baseline human to withstand such a large temperature drop. Sensory neuron adaptation =/= bodily adaption. However, lowering the core human body temperature by 1-2 degrees (typical of sleep) may have a chance of altering a human's lifespan in a more meaningful way. Though cooling may prolong the lifespan of temperature-conformers and single-celled animals, it is unlikely that the same can be said for endotherms. Endotherms have had biological processes that run on a fixed temperature for a long time already.  One more thing: @Hermann: Their core body temperature may not have been much lower than the baseline.

Nice (up-voting that answer!), I was thinking more about this on my run this morning, and I agree with you - flies do not regulate their temperature internally and are adapted to survival within normal temperature fluctuations. Humans on the other hand use homeostasis to maintain a core temp of 37(ish) degrees, and when that drops the body actively tries to warm it self up. I think this could actually decrease lifespan because it would increase metabolic stress (more calories are required to survive).

Another argument for cold-induced longevity is that I know a person who's been working at the ER for decades, and she says people who die in extreme circumstances, such as drowning in sub zero water, can be brought back after unbelievably long amounts of time with far less damage than when in normal temperatures. Indicating the temperature is slowing things down.

I agree though that if the body is constantly trying to raise the temperature then that should increase metabolic processes and thus probably shorten lifespan. But if the brain could be fooled into thinking this lower temperature is the nice new norm..

"Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death." Are you sure about that? The Icelander who swam for 6 hours in the 5c ocean, surely had a core temperature below 30c, and he was fine.

@ Hermann Ingjaldsson. Core body temperature is maintained at all cost. Including shutting down circulation to the skin, and  limbs. The moment core temperature is affected, the brain slows down, heart beat diminishes, breathing slows, even stops.  And organs start shutting down.

In humans the optimal temperature for enzymatic action is 37 C. See the image below:

Our body temperature is set at 37 C (~ 97 F) because all our metabolic processes are most efficient at this point. Any decrease in the core temperature will cause a drop in all the metabolic processes imitating hypothyroidism. Hypothyroidism is a very unpleasant condition to live with - extreme fatigue, inability to utilize the energy stores, very poor appetite with increasing fat stores are few of its symptoms.
For humans to efficiently operate at lower temperature the DNA has to be remade to code for enzymes that would not loose their efficacy at a lower temperature - maintaining a good reaction rate. This is impossible as of now where even a single gene modification or single nucleotide correction is extremely difficult and is under experimentation.

Source:
https://sachabiochem0001.wordpress.com/2013/04/09/factors-affecting-enzyme-activity/

Movement is life. If the human body where to undergo this kind of temperature that would be below the normal temperature for the human body, we would in fact either have to move more and or do more as in eat, exercise, communicate etc. If your body did not have this mental capacity basic survival skill you would be in the process of slowing the function of your body down leading to death.
Also the person who had swam in freezing water had a better tolerance to the cold than normal, but this does not mean that if a person had the capacity to tolerate cold temperatures that this kind of treatment of the body whould be good for you.
Over a short period of time your body can undergo extream circumstamces so it was a basic survival skill that had kicked in from the metal material of that persons being telling their physicsal as in nervous system that if they were going to survive they would have to move in order to regulate their body temperature.


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What are the different, high-level programs along which a eukaryotic animal cell can follow?
What are the different, high-level, disjunct (mutually exclusive at one particular point in time) programs or pathways along which a eukaryotic animal cell can follow? Examples of programs would include growth, cell division, senescence and quiescence. Are there programs that differ between cell types?
Any I'm missing? If so, references much appreciated.

Are growth and division separable?: surely they are! Cells may change volume without change in number. Hyperthrophy vs hyperplasia

Ok. Any thing else I've missed?

I'd categorise differentiation as a subtype of division but apart from that seems pretty much complete to me. You may want to add migration to both.

I agree. Updated question accordingly.

Cells may also divide with no growth. This happens during early development.

I'm going to answer my own question with suggestions collected from the comments.
A multipotent stem cell:

Growth

Growth and clonal division
Growth, division and differentiation

Division and no growth

A differentiated cell:

Senescence (irreversible)
Programmed cell death

Apoptosis.
Autophagic cell death.
Necrotic cell death.

Quiescence (reversible)
Growth ==> Immortality (cancer cells)

Growth and division
Growth and no division (endocycles)1

Division and no growth

1:  Norman Zielke, Kerry J. Kim, Vuong Tran, Shusaku T. Shibutani, Maria-Jose Bravo, Sabarish Nagarajan, Monique van Straaten, Brigitte Woods, George von Dassow, Carmen Rottig, Christian F. Lehner, Savraj Grewal, Robert J. Duronio, and Bruce A. Edgar: Control of Drosophila endocycles by E2F and CRL4Cdt2

To see the width of your question, have a look at what the Gene Ontology considers a cellular process:
http://www.ebi.ac.uk/QuickGO/GTerm?id=GO:0009987#term=children
I don't think you can agree on what's high-level, so it's better to see them all, I think. Also, for completeness, there is a list with cell types which is admirably maintained:
http://en.wikipedia.org/wiki/List_of_distinct_cell_types_in_the_adult_human_body

I've revised my question to a search for disjunct, i.e. mutually exclusive (at one particular point in time) classes of program of roughly the same generality. I find GO is very poor on this: often there are terms that are siblings despite describing a much different granularity, e.g. cell cycle process and membrane docking are siblings.

It's just a collection of terms used in the literature, together with associated genes/proteins.