text:
Relation between carbon dioxide assimilation and the ambient and intercellular partial pressures of carbon dioxide
So, water-use efficiency (and carbon assimilation rate) is correlated with ambient CO₂ concentration (Ca), and  carbon isotope discrimination Δ is correlated with Pi/Pa (partial CO₂ pressure, intercellular and atmospheric, respectively) in C3 species. If the Ca increased, would that result in decreasing Δ? In other words, would increasing ambient CO₂ levels result in less discrimination towards the ¹³C isotope, in C3 species? And if that's true, is my math sound?

After more research, I've found this to be true and the reason why. Discrimination against ¹³CO₂ isotope comes from two reasons; kinetic effects (diffusion and enzyme fractionation), and thermodynamic effects (1). ¹²CO₂ and ¹³CO₂'s diffusion rates are different, carboxylation reaction's discrimination value is 30 per million, and the diffusivity of ¹³CO₂ is 4.4 per million less than that of ¹²CO₂ (2).
When stomata are fully open

they place no place no limitation on diffusion of CO₂, C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere. When stomata are sufficiently closed that they become the sole source of limitation, the discrimination should be 4 per million. Intermediate cases give intermediate discriminations. (2)

It's known that when CO₂ is abundant in the atmosphere, stomata start to close because their job is to balance the CO₂ uptake and water loss by transpiration. This, combined with the previously mentioned information, to my understanding, means that, when they are more closed, CO₂ in the intercellular space gets consumed more. This lessens the carboxylation reaction's effect on the ¹³CO₂ discrimination because the CO₂ in intercellular space becomes more limited compared to the free diffusion of fully open stomata. In other words, carboxylation reaction has less CO₂ molecules to choose from intercellular space because free diffusion doesn't supply a constant flow of CO₂ molecules, making it use more ¹³CO₂.
(1) Farquhar et al., 1989, Annual Rev. Plant Physiol, Carbon Isotope Discrimination and Photosynthesis
(2) Farquhar et al., 1982, Aust. J. Plant Physiol, On the Relationship between Carbon Isotope Discrimination and the Intercellular Carbon Dioxide Concentration in Leaves

"C3 leaves should discriminate against ¹³CO₂ by 30 per million, with respect to the atmosphere." I don't understand the measurement.


text:
Why do baby mammals tend to play?
Why do babies of any mammal tend to play ? From humans to small dog pups, cubs of a lion, baby bears, etc.
*I am not sure if the tag I chose is correct or not. Please correct me if I'm wrong.

Because it is a way to try things and learn.

Play has been described for some birds. See also here.

If you find the book Sociobiology, by E.O. Wilson, it writes an entire section on the subject. It seems to be a preparation for adult life, simulating behaviors necessary for an adult (e.g. fight, hunt, etc). Though I don't know why it would have evolved more in mammals...

Related: Why does a housecat (or other predator) play with it's food before killing and eating it? Does it make the food taste better?

source: Stack Exchange

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

sort: votes


text:
The pBR322 convention
What is the pBR322 convention? For example in the description of the pET28a vector we can find information that the sequence is numbered by the pBR322 convention, so the T7 expression region is reversed on the circular map.

Could you please clarify the question? what do you mean by pBR322 convention? do you mean why it was named pBR322? I'm not clear what you mean by pET28a being numbered by the pBR322 convention.

pBR322 is a distant ancestor of pET28a. If you compare the two maps below you will see that they have the same replicon labelled as ori or pBR322_origin.
The map of pBR322 is shown in the conventional orientation: the single EcoRI site is at coordinate 0/4359 and numbering proceeds in a clockwise direction through the BamHI site. The map of pET28a is presented with the pBR322-derived ori element in the same orientation (note the labelling of a pBRrevBam_primer also). Because of the way that the pET vectors were built, this means that in the conventional depiction the expression region runs counter-clockwise.

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


text:
What would cause crows to be attracted to a human body?
On another SE site, there was a comment that told me something  about biology that I already know:
"A man left murdered in the fields would soon have a flock of crows mobbing his fragrant corpse."
But I don't quite understand why. Is it the "death" part,the fact that someone was injured/bleeding or just the fact the he was immobilized,that would attract the crows?
That is suppose you tied up someone and left him on the field. Would that attract the crows?
Suppose this person fell down, was bleeding, and immobile, but not seriously injured? Or is it the death part?

I think the key is "his fragrant corpse." When an animal dies and begins to rot, a number of quite smelly chemicals are given off, including putrescine and cadaverine. Crows and other carrion birds like vultures are probably very sensitive to these compounds, rather like sharks are to the smell of blood.

+1 for the etymology of "putrid" and "cadaver." The question came from the English Language site, and your answer took it back there. http://english.stackexchange.com/questions/194919/two-crows-being-an-attempted-murder

Carrion birds, such as crows and vultures, eat dead animals. As a whole, it's possible that they detect carrion by the smell or visually.
Crows specifically are omnivorous and predatory in addition to being carrion scavengers. I suspect that they will try to eat anything that doesn't fight back, especially if they are hungry enough and there is exposed flesh. I don't know if crows prefer dead meat or fresh meat, but they certainly eat both.

Suppose you tied up someone and left him on the field. Would that attract the crows?

The crows would probably be attracted because they are curious and want to check out the new, unfamiliar object. They would certainly be able to tell that you are alive by body temperature and sounds of breathing or heartbeats.
I think they will be hesitant to eat you because live humans are unfamiliar to them. They will probably find other carrion nearby and eat that instead. If you stayed unconscious for several days, the crows would get used to you, lose their fear, and eventually one would go for a taste. Once the first gets a bite or two, and you fail to retaliate, I think the others will quickly join in.

Suppose this person fell down, was bleeding, and immobile, but not seriously injured? Or is it the death part?

The fact that they can see and smell the meat, and don't have to bother piercing the skin, would make you more attractive to the crows (supposedly, they like to go for things like eyeballs even on live prey).
However, even if immobile, a conscious human could struggle (shake their head, yell, roll around) which would startle the crows and keep them at bay for a time. If you can't actually interfere with them pecking you, I'm sure they would eventually get over their fear and attack you. If you can physically swat or shake off the crows, they'd just wait for you to get tired or die, which probably won't take too long given the injuries.
In conclusion, I don't think it's impossible for crows to eat bits of a live human, whether conscious or not. However, for various reasons, it would probably take a few days for them to actually get around to it. If you are not dead by this point, larger animals would show up and attack you, and crows would end up picking at the scraps.


text:
Why do people use anti-inflammatory drugs?
Why people should take anti-inflammatory drugs, when inflammation is a physiological way to defend our organism?

You are correct in that inflammation is a physiological process. It is vital for the correct development and localisation of a strong immune response, and contributes to tissue healing.
However, the beneficial effects are replaced by dangerous processes when they are prolonged or too intense. This includes both effects of leukocyte attraction and invasion, but also deleterious consequences of the accumulated cytokines. For example, TNF-alpha originally contributes to immune cell activation but in prolonged inflammation prevents tissue healing.
Note that "prolonged inflammation" does not necessarily mean that inflammation has been apparent or noticeable for the affected person for a long time. Often by the time symptoms present, the inflammation process has been persistent and become pathological. At this point, anti-inflammatory drugs need to be used as soon as possible to minimise irreversible damage.
Aside from this, quite often inflammatory and immune processes are triggered without a need for them. Our immune system is quite prone to errors, and cases of misguided immune reactions are actually increasing. Consider for example allergies, which often manifest with skin-symptoms such as eczema that can be treated with anti-inflammatory creams.

While inflammation is a natural defensive process, it also does (sometimes severe and/or permanent) damage to tissue. Therefore, when inflammation has been caused by an injury or an auto-immune disease such as rheumatoid arthritis, anti-inflammatory drugs do more good than harm.

What really bothers me is a situation when you take a simple anti-inflamatory drug(f.e. aspirin (acetylosalicic acid(sory for misspel)) right after you feel the symptoms of inflamation. I mean, there are no reasons to suspect misguided inflammation, or prelonged inflamation but it is still the most common way to treat a lot of diseases. Wouldn't it br better to let the organism usr the inflamation to cure the diseases, and use the anti-inflamatory if the inflamation prelongs, or it is very acute?

Popping pills for minor discomfort is rarely a good idea. People do things that aren't good for them. You might as well ask why people smoke or drink, since those things are worse for them than popping the odd aspirin. Also, in most of the world, aspirin is no longer the NSAID of choice, since it has potentially severe side-effects, including gastrointestinal bleeding. The name has sort of become genericised in the US though, to the extent that people call any NSAID aspirin, when in fact, it's far more likely to be paracetamol or ibuprofen.


text:
Cloning of a sheep.. Dolly?
Dolly the sheep was a clone. When she was born she was eight years old on her 1st day of birth, her mother (from which she was cloned) was also eight years old. What is a molecular reason behind this - that Dolly was eight years old when she was born?

If you look at the replication of end of chromosomes, you will see that one of the strand gets shorter every time. To prevent the genes from being disrupted, the ends of the chromosomes have repetitive sequences called telomeres which shorten with every replication but will prevent the disruption of genes.
As you can deduce from the above information, there will be a certain limit to how many times a cell can divide.So, it has been thought that any organism ages because of shortening of telomeres.
Gametes have the enzyme telomerase which will lengthen the telomeres to full length so that the zygote formed will have unshortened telomeres. But, in the case of Dolly the nucleus was taken from a somatic cell and so the telomeres did not lengthen. The age of Dolly at the time of birth was thus the age of mother from which the nucleus was taken.
See : Telomere

Thank you so much for answering...It is really helpful.. :)


text:
Translation of mRNA?
We inserted an insulin gene from human into bacteria. Will translation of the gene (protein formation) occur in bacteria? If translation occurs then why does it occurs, give a reason for this?

In the context of this question it is useful to distiguish between the primary product of translation - a polypeptide- and a functional protein. The insulin polypeptide has to be post-translationally modified by the removal of a signal sequence, the formation of correct disulphides, and by proteolytic processing to remove the C peptide before it can be called insulin.

Yes, bacteria will produce human (or any organism's) proteins if you introduce their genetic material but there are a few things to consider.
First, the introns must be removed from the human genetic sequence. Bacteria do not have the machinery to splice out introns after transcription. This is typically done by using a viral protein to reverse transcribe mRNA, which already have the introns removed, into DNA which you can use to transform bacteria.
Second, you need to insert a Shine-Dalgarno sequence. This allows the bacterial ribosomes to bind to the mRNA they will produce, and translate the protein you desire. This sequence is not found in eukaryotic genes, so you have to make sure it was included either in the vector or in the PCR primers you used to amplify the gene sequence.

Although the genetic code is almost conserved among organisms there are some issues to take in account, among which:

Every organism has its own codon usage, i.e. the differences in frequency of occurrence in synonymous codons in coding DNA (that reflect the composition of tRNA abundances). So, for example, the codons UUU and UUC both encode for phenylalanine but - I'm making this up - UUU is common in human but rare in coli while UUC the contrary. If the coding sequence of insuline is rich of UUU, you probably need to change the codon UUU to UUC in order to avoid slow translation.
Also the aminoacid abundance can be very variable between two organisms. One of the ways you can handle the differences is by "tuning" the expression of the aminoacids. Here a table of aminoacids abundance in coli.
The regulatory sequences in coli are not the same as in human. In fact, prokaryotic translation initiation needs a purine-rich sequence upstream the (usually) AUG initiation codon called Shine Dalgarno. This sequence is complementary to the 16S RNA in 30S ribosome subunit.
Often peptide chains are subjected to various post-translational modifications. The insulin peptide, for example, once synthetized is cleaved by specific peptidases and disulfide bonds are formed. Because human and coli post-translational modification mechanisms are not the same, this can be a difficult problem to handle. Instead of trying to exactly reproduce the protein with all its modifications, often people search for functionally (and not structurally) identical proteins.
Also the folding process can be different, both assisted (by chaperones) and spontaneous (withouth chaperones). The folding can be influenced by a number of factors like molecular crowding, pH, ...
A lot of eukaryotic genes have introns: sequences removed before translation. Once splicing sites are known, this problem is easily solved by using a sequence withouth introns.

It works, and is actually done to make all the "human" insulin which is used by diabetes patients today.
This is because the genetic code is almost completely conserved (with only very few exceptions in nature), so bacteria use the same codons to code for an amino acid as in humans. So with a suitable vector (a ring of DNA which carries extrachromosomal genetic information) which has the ability to replicate independent from the cell and which has the correct promoters (start points) for initiating transcription in bacterial cells, you can basically clone and express any human gene.

Is this question have any relation with degeneracy of genetic cods..???

Sorry, but I don't understand your comment? If you are asking, if the degenerated code is important here, my answer is no.

Ok.Then the Translation occurs in bacteria, because the genetic codes are  universal.

Yes, the code is universal (for exceptions see the Wikipedia, the regulatory elements are specific for bacteria (and need to be compatible).

Thanx for the help..

All the organisms share a common ancestor and have evolved from it. So they share quite the same machinery for transcription and translation. Codons are also interpreted in the same way in almost all the organisms.
So, yes translation should happen ( Assuming that the gene has been cloned in the right way.)

It depends on the regulatory elements controlling this inserted sequence in the bacteria, isn't it?


text:
Is "tonic activity" common for neurons firing in the brain?
I've been reading about Dorsal Raphe Nucleus, a serotonin- rich part of the brain. I noticed mentioning of "tonic activity" - regular pulsing that releases neurotransmitters. On top of this "tone" the nucleus can fire bursts of spikes(action potentials?) that further increase neurotransmitter concentrations for a short time.
Is this kind of tonic firing common throughout the brain, or is it DRN specific?

Most neurons that have been studied have spontaneous activity. Tonic firing is common in sensory neurons as well as cortical neurons. However, this could be very biased since it is difficult to study neurons that are silent in vivo. In vivo studies are blind, meaning that we usually do not see which neurons we are recording from. This is known as the "dark matter" problem (ref 1).
Also, it is known that there are homeostatic mechanism for maintaining average firing rate. Basically, if a neuron doesn't fire much, then the input sensitivity of the neuron increases to produce more activity (ref 2). But we don't know how widely this can be applied.
References:

Shy Shoham, Daniel O’Connor, Ronen Segev. How silent is the brain: is there a "dark matter" problem in neuroscience? Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology, Vol. 192, No. 8. (1 August 2006), pp. 777-784  doi:10.1007/s00359-006-0117-6
Gina G. Turrigiano. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Trends in Neurosciences, Vol. 22, No. 5. (1 May 1999), pp. 221-227, doi:10.1016/S0166-2236 (98)01341-1


text:
Are serotonin levels in humans affected by light?
I'm reading this Wikipedia article on light therapy  and noticed a peculiar statement:

The production of the hormone melatonin, a sleep regulator, is
  inhibited by light and permitted by darkness as registered by
  photosensitive ganglion cells in the retina. To some degree, the
  reverse is true for serotonin, which has been linked to mood
  disorders.

If I read this correctly, when melatonin is suppressed, serotonin is released? This makes some sense. I'm interested if there is any scientific backing to serotonin being affected by light levels.

You might want to look into seasonal affective disorder which is possibly related to this.


text:
Can songbirds mimic car alarm sounds?
A silly question. A few days ago I observed a very vocal bird with impressive vocal variety. It was rapidly switching from one tune to the next. After sometime I realized that the bird might be mimicking the 6-8 tone car alarm (the one that rapidly changes). Is this my imagination, or are birds really know to mimic/compete with car alarms?

You would be amazed at the vocal abilities of the lyrebird.  A car alarm is easy for them; they can mimic much more complicated sounds.
Here's a snippet from a David Attenborough BBC documentary on YouTube (which includes the car alarm example, among others).  They are so skilled, it's hard not to think this video is fake.

Thanks, that bird does imitate car alarm, but I was really surprised at the chainsaw sound


text:
Are there tools for automatically parsing glycan names into tree structures?
My colleague and I are working on a project involving data produced at a glycan microarray facility. The array data that came back to us were a list of glycan names (in IUPAC condensed format). We would like to parse the list of 610 names into the graphical representation of the glycan.
To clarify, I wanted to take a list of glycans, written in the IUPAC condensed nomenclature, and return an image for each glycan. Here, each image would be the "graph" representation (nodes + edges). Ideally, I would like to be able to write a Python script to get this done, so we wouldn't have to do this by hand.
Is this possible? If so, what tools are available to get this done?
Thank you!

I don't know if that answers your question or not.  I think code samples on text parsing would probably be off topic here, but I could refer you to some examples.  The key would be the second KEGG table.

@AtlLED, thank you for your effort in answering. Though your response didn't give me a direct solution to what I was looking for, it was helpful nonetheless, and I up voted it. Please see my clarification in the comment there. Thanks again!

Edit: C# Functions used in our system, slightly paired down for to simplfy
using Microsoft.VisualBasic;
using System;
using System.Collections;
using System.Collections.Generic;
using System.Data;
using System.Diagnostics;
using System.Web;
using System.Net;
using System.IO;
using System.Text.RegularExpressions;

public class KEGGCaller
{
    public object ReturnKEGGgif(string GlycanMonoCode, System.Web.HttpServerUtility HTTPUtilityHolder)
    {

        string CallURL = "http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=";
        string GlycanURL = HTTPUtilityHolder.HtmlEncode(GlycanMonoCode);
        WebClient wc = new WebClient();
        System.Drawing.Image GlycanGif = default(System.Drawing.Image);
        CallURL += GlycanURL + "&mode=bfind&max_hit=1";
        StreamReader reader = new StreamReader(wc.OpenRead(CallURL));
        string Gcode = FetchGcode(reader.ReadToEnd());
        if (Gcode == "Failed") {
            return 0;
        } else {
            System.Net.HttpWebRequest Request = default(System.Net.HttpWebRequest);
            System.Net.HttpWebResponse Response = default(System.Net.HttpWebResponse);
            Request = System.Net.WebRequest.Create("http://www.genome.jp/dbget-bin/www_bget?gl:" + Gcode + ".gif");
            Response = (System.Net.WebResponse)Request.GetResponse;
            if (Request.HaveResponse) {
                if (Response.StatusCode == HttpStatusCode.OK) {
                    GlycanGif = System.Drawing.Image.FromStream(Response.GetResponseStream);
                    return GlycanGif;
                } else {
                    return 2;
                }
            } else {
                return 1;
            }

        }

    }
    public object FetchGcode(string PageBlock)
    {
        string MatchURLString = "?gl:G\d\d\d\d\d";
        Match URLMatch = Regex.Match(PageBlock, MatchURLString);
        if (URLMatch.Success) {
            return Strings.Right(URLMatch.Value, 6);
        } else {
            return "Failed";
        }
    }

}

Remainder of the Answer
Biomodels.Net is a great resource to begin with and familiarize yourself with the field and get ideas of how to tackle your qualification needs.  We used it when we were doing drug screens.
More specifically for glycans, you're going to be looking at KEGG.  Then use KEGG draw for your visual application.  If you actually just want to parse them, here is the table on the monosaccharides used (most places).
Here's a better link right to the download in case you didn't find it.  The script we wrote was pretty simple, here is the basic logic.
Start with the monosaccharide code.
Call a single return of DBGET to GenomeNet pulling from KEGG Glycan.  For example:
(GlcNAc)6 (Man)3 (Asn)1
would be called:
 http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=%28GlcNAc%296+%28Man%293+%28Asn%291&mode=bfind&max_hit=1

Where http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords= and &mode=bfind&max_hit=1 are going to be constant and the middle part is going to be your search.
You need to change your monosaccharide to standard URL ASCII Reference, concatenating each monosaccharide with a "+".  Thus (GlcNAc)6 (Man)3 (Asn)1 becomes %28GlcNAc%296+%28Man%293+%28Asn%291.
That will give you one hit with the link to your exact match if there is one.  There will be one link on the returned page in the format of http://www.genome.jp/dbget-bin/www_bget?gl:G#####, where G##### is your glycan number (in our example G00021).
Once you have the glycan number you're good to go.  All of the structure images can be found at:
http://www.genome.jp/Fig/glycan/G#####.gif
And then you just download your GIF.  The way we did our batches was to do each step for all the hits then move to the next step.
Hope that helps more.

Upvote because your answer was helpful, though I still couldn't figure out an answer to my problem. To clarify, I wanted to take a list of glycans, written in the IUPAC condensed nomenclature, and return an image for each glycan. Here, each image would be the "graph" representation (nodes + edges). I will update my original question to clarify that; in the meantime, do you know of any tool to do this? Thanks in advance!

Update: I tried KEGG Draw, but it doesn't accept glycan IUPAC names.

@ericmjl I was going to show some examples of short scripts used to call KEGG Draw, which is what I thought you would want.  If they're in IUPAC, I don't know a good way to get it graphics.  Have you asked them if they will give it to you in KEGG? Might be easy on the source side, or parsing then converting might be your only option.

Ah! I misunderstood, my apologies. Would you be kind enough to share that code?

@ericmjl are ok if they're not in Python?  KEGG is a Java program.  My Python is limited though I have a tech who's ok in it.  I'll check with my tech transfer and let you know.  Right now I'm looking for published ones, we can't be the only ones who needed to.

No problem, I can brush up on my Java (it's been 6 years since I last used it). Thank you very much!

@ericmjl actually what we have is in C# (I thought it was Java, just checked).  I added the logic of it to the answer, hope that helps.

@ericmjl I hope that points you in the right direction, maybe someone else will have a Python solution.  And there might be a way to go directly from IUPAC, I just don't know it.

I don't know if this works out for glycans but this tool converts IUPAC name to SMILES format. SMILES is a text based structure notation which can be converted to graphical structure.
You can also check these out:
http://www.openmolecules.org/name2structure
http://www.iupac.org/home/publications/e-resources/inchi.html
I am still not sure what you are really asking. It would be easy if you give a dummy example.

I tried it, but unfortunately, the tools do not work with the glycan IUPAC names that we have on hand. :-(

The CFG do not use consistent nomenclature for their glycan structures in the excel files they provide. It is human readable but not machine readable. So you'll have to curate their list first. I have bash scripts that do this.
We convert glycan array structures into CFG symbols
http://glycam.org/Pre-builtLibraries.jsp
You want to click on the cfglibs and maybe give it a few secs to load.
If you are still interested in doing this send in an email to glycam@gmail.com explaining what you would like and include my name "Oliver".


text:
How to determine whether the energy of a stem-loop fold is significant or not?
If I have a predicted RNA stem-loop of energy -0.30 kcal/mol, and another of -4.9 kcal/mol, how do I tell whether such a structure is a significantly stable structure or not? Our two competing hypotheses are that there is some structure with sufficient energetic stability to fold inside a cell, versus the one that there is not.

A predicted stem loop of what? A nucleotide chain presumably, and most likely RNA but you need to tell us.

Yes, it is an RNA. Allow me to update the original question. Many apologies for being unclear.

probably the best way is to make it and see if the sequence forms a stem loop. there are lots of energy calculations based on 3d models and sequences if you'd like to know, but i'm not clear on what is best myself.

I don't know what you mean by significant. More negative the value of folding energy more is the stability. For better predictions you can use the salt correction formulae.

@caseyr547: I am working on a substring of mRNA that is thought to fold independently of the other substring, because it is not complexed with other proteins.

You can convert the $\Delta G$ values into equilibrium constants $K$ using the formula
$$ \Delta G = R T \ln K $$
This might help you understand what those energies roughly mean.
But the more important and also more difficult part is judging how good your predicted free energies actually are. I assume you used a secondary structure prediction program like Mfold to calculate this. They typically have a several parameters you can adjust like ion concentrations and temperature, you should make sure that you have some appropriate values here.
Without knowing anything more about your system or data I'd ignore the -0.3 kcal/mole result, the -4.9 kcal/mole structure could be formed, but I wouldn't regard this as certain.
Now, in the in vivo situation the whole thing gets far more complicated. The presence of RNA binding proteins, helicases and the generally rather complex environment in the cell makes it much harder to predict which secondary structures will actually form.
If you wanted to know for sure you could e.g. do SHAPE experiments on your RNA. This is a technique that also works in vivo.

RNA folding is definitely a lot of work if you are not an RNA molecule :)


text:
Do foods with preservatives become less toxic in the gut?
Do foods with preservatives stay digestible for longer in the gut by not rotting as much (producing less toxins)?

Please note that expulsion of feces is NOT at all due to food spoiling and becoming toxic.

@leonardo thx, I edited again, hoping it's clearer now. to clarify what you requested: I mean if the food has preservatives, then maybe it prevents the food decomposing as much as it would if it didn't have preservatives, thus not becoming as toxic as fast, thus the gut doesn't expel it as soon. hope that is clearer. But in the mean time nico has said what he said, but I don't really agree, I thought it was common knowledge that the intestines expel "stuff" that is sufficiently toxic, at least certain toxins, so...

@JoRijo no, that isn't the case :-)  I think your question is interesting but you might not get the answer you're looking for as your premise is incorrect.

what a mess :P I've done some more research and it was believed that food in the gut putrified and became toxic up until early 20th century when advances in science showed no evidence of such. source:http://www.ncbi.nlm.nih.gov/pubmed/2668399.

Do foods with preservatives take longer to digest?
Food preservatives are either antimicrobials (e.g. sorbate, sulfite) or antioxidants (free radical scavengers such as butylated hydroxyanisole).
Digestion is initiated in the stomach by hydrochloric acid and pepsin. It continues in the small intestine with the action of numerous other enzymes including amylases, lipases and proteases. There is no obvious way that these digestive processes would be inhibited by preservatives.

Can you please provide any proof of this? It is by no means obvious that and antimicrobial could not have an effect say, on intestinal blood flow...

You can only exclude specific effects. And you're right in suspecting that not all is well with food additives. Lots of people have intolerance/allergies to them. In general however, the answer is correct and if it weren't, the food industry would be buried with paper by lawyers.

@rwst: not necessarily. An additive can modify absorption of food without having necessarily negative effects. For instance, EDTA is sometimes used as a preservative, and it does halve absorption of non-heme iron. http://www.ncbi.nlm.nih.gov/pubmed/818893

Absorption isn't digestion.

Hum... well the antimicrobials, if they kill some of the helpful gut bacteria then It'd be expected that they affect the absorption rate negatively, right?

Still, this does not exclude that a preservative could act as an inhibitor of an enzime (again, I can see how a calcium chelator such as EDTA could easily do that). I continue to say that this needs proper scientific sources.

If preservatives inhibit gut bacteria which aid in absorption, then preservatives could affect the body's ability to produce the digestive acids and enzymes in the first place.  That, in addition to the potential for more direct interference, it seems they are much more like to interfere in some way than to not interfere.


text:
Is warmth/temperature sensed linearly or on a different scale?
I understand that the atmospheric temperature is sensed relative to external body temperature. However, is the sensation of warmth registered linearly, or is it on a logarithmic scale, similar to sound that works on the Decibel scale? Or is it on another scale entirely?

The use of the Decibel scale is only a mathematical practicality, has nothing to do with how our brain perceives sound.

Also, related (although does not answer the question) http://biology.stackexchange.com/questions/371/how-is-temperature-sensed/372#372

Could you precise 'linearly'? In general, it is not a well-defined thing, when it comes to perception, see http://cogsci.stackexchange.com/questions/1751/what-stimulus-features-determine-the-psychophysical-power-law-exponent/1772#1772

A more general answer/comment is that technically almost nothing in biology is really linear.
In a linear relation, when one variable increases the other increases proportionally. In biological systems this typically cannot happen because of physical limits (such as the number of molecules), which tend to produce saturation at some level.
For example, when a substance is "sensed" by the receptors of a cell, sensing would become saturated as the receptors approach maximal capacity. In a similar manner, heat sensing will be limited by a maximal capacity and saturation of the nervous system. This is of course not specific to sensing but is a general characteristic of biological systems, because they are ultimately made of a finite number of components.
That said, sometimes a linear-like relation is observed at a specific range of values. For example, this is a mathematical characteristic of a class of functions called logistic functions. At ranges that are far from saturation, these functions have approximately linear behavior.
In the following example figure I marked (black box) the "linear-like" regime of a simple logistic function y=1/(1+100*exp(-x)):

The human sensation of warmth is not the measurement of static temperature.  Humans detect the rate at which heat is leaving (or entering) their body.  For instance, if you are sitting in your 0 degree car in the morning, your hand in the open air will feels warmer than your hand touching the steering wheel, despite them both being at 0 degrees.
The reason is that heat conduction from your hand to the steering wheel is much faster than convective heat transfer from the air.  So you feel "colder" touching the steering wheel, but it's really that you're losing heat faster.
Scholarpedia's article on temperature receptors:
http://www.scholarpedia.org/article/Thermal_touch#Temperature_receptors

...Cold receptors respond to decreases in skin temperature over a range
of 5-43 °C...
...In contrast, warm receptors signal that skin temperature has
increased...


text:
Are humans hardwired to continue gathering resources after the costs outweigh the benefits?
An animal will stop foraging in a berry bush if the perceived cost of searching for berries remaining is greater than the cost of finding another bush which isn't as picked over. People do the same thing on websites. We'll stay on a website searching for our information berry if we feel it costs less than jumping to another website bush.
If we had significant resources such that the cost of predatory/foraging behavior out-weighed the energy benefit from gaining more resources, would we stop? There seems to be a biological and cultural drive to keep getting more stuff. As people, could we ever reach a point where we're satisfied? The logic says yes, but common sense says we're hardwired to feel compelled to never stop gathering resources.

I really think this is so.  This has been studied by behavioral economists quite a lot - Daniel Arielly's book "Predictably Irrational" and the work of Daniel Kahneman might be a good direction to browse if you feel that interested in it.

Good edit, @DQdlM. I changed the word consuming to gather because it seems we'll never stop consuming, but would we stop hunting/foraging if we knew the cost was more than the benefit? I was the one who originally used the word "consuming" in my post. My fault. Thanks for the edit. :)

It's called "addiction", or "obsessive-compulsive behaviour". Unfortunately not every behaviour is explained by rational calculation.

There are cases where such behaviors are clearly hardwired or due to the way our brain learns.

The answer to your question is very sensitive to the time frame you are interested in.  Assuming the costs and benefits you describe are referring to fitness (i.e., survival and reproduction), then the situation you are describing is one in which a particular behavior has lowered fitness (i.e., costs outweigh benefits).
There are several possible outcomes in this case.

Evolution. If the behavior is not plastic (i.e., it cannot change in a single individual), the there would be selection pressure against those individuals that exhibit the behavior.  If the behavior is heritable then evolution would cause a reduction in the frequency of the behavior over time.
Lowered Fitness. If you are not interested in evolutionary time scales but the behavior is not plastic, then the outcome would be no change in behavior but a reduction in the survival and reproduction success of individuals with the behavior.
Change in Behavior. If the behavior is plastic (i.e., it can be changed by a single human) and the current situation provides the appropriate information about the state of the behavior, then the behavior will change.  The key here (as with optimal foraging models) is that the appropriate cues have to be present to change the behavior.  Often organisms use proxy cues to trigger behavioral shifts.  For example certain caterpillars use day length to trigger shifts in developmental pathways (diapause vs pupation) when what really matters is temperature.

So the real answer to your question lies in the further questions of whether consumption is plastic (or hardwired as you say) and if it is, whether a situation provides the appropriate cues to indicate that we have acquired enough resources.  Those are rather complex questions that, as far as I know have not been answered definitively in the general sense that your question implies.

Wow, it's so hard for me to think in all these biological perspectives. Now it's apparent I don't have a very strong foundation in biology ("schema") to put all these ideas. Thanks for your insight. :) Clearly there's lots I can learn!


text:
Have any genetically altered organisms actually become abundant in a natural environment?
Most of the things that come up in Google and Google Scholar for this question have a mostly/completely speculative tone, or at best use models instead of measurements. This report describes some actual measurements in pollen transfer to neighboring fields from GM fields, though they all seem to have been one-off measurements at some unknown time after the GM plants appeared, rather than investigations on if the genes are becoming more common over time, which might imply the ability to become unavoidably common in some environments or even a weed/pest/parasite. This doesn't seem like an obvious problem to me, because the traits associated with those genes are always meant for the context of being farmed or raised by humans and therefore probably wouldn't contribute more to fitness in wild populations relative to the wild alternatives of those genes, but a few counterexamples would smash that belief to bits.

Many organisms including plants, bacteria, insects, fishes and even mammals have been GMed. Most of them have experimental purposes, but GM crops have been released for commercial purposes. Maybe the most amazing between them is triticale, which is a hybrid of wheat (Triticum) and rye (Secale). Triticale, BT Potato, BT Tomato, BT Maize (I am not sure), BT and Golden Rice and lots of other GM crops have been released in almost all lands in world. Almost all these GM crops suppose to have higher yield and higher resistance to pathogens and physiological problems and as a result they have higher chance of surviving (specially in natural environment).
A study published in Nature in 2001 reported that Bt-containing maize genes were found in maize in its center of origin, Oaxaca, Mexico. In 2002 Nature concluded that the evidence available is not sufficient to justify the publication of the original paper.  A significant controversy happened over the paper and Nature's unprecedented notice. Also there are safety concerns about modified gene transfer during pollination in GM Rice(s). Even some scientists think that that this would not be a problem because rice is a self-pollinating plant. Any way GM crops can become abundant and release their genes by themselves or through gene transfer to other organisms.

Notice: Some of non crop GMOs also have commercial purposes but they didnt't release to environment and are restricted to laboratories.

Increased yield and higher resistance to pathogens and physiological problems don't seem like they must necessarily increase fitness in the wild. The mechanism of action behind those effects seems vitally important--for example, increased yield could be due to increased nutrient uptake from the soil, or just due to diverting nutrients from growth elsewhere. The sickle cell trait comes to mind as an analogous situation in humans; "grants malaria resistance" sounds like it wouldn't be harmful, right?
The Nature paper is what I was looking for. Are there any less controversial examples?

In India, rice is modified, resulting in the loss of almost all local varieties. It was cause of excessive cultivation of Modified rices. Then this rices can easily transfer thair genes to environment (Even local pest and deasises some times had bad attacks).

I encountered this article discussing transgenic salmon, and it says that the modified genes don't find their way into nature because transgenic salmon are bad at the salmon mating ritual. It wasn't on purpose from what I can tell, but that's still a neat way to ensure modified organisms don't spread their genes into nature.
It's a relevant counterexample to what the question sought, but not a general argument against the possibility.


text:
Does knowing the sex of each of a couple’s first N children have any marginal value in predicting the sex of child N+1?
Does knowing the sex of each of a couple’s first N children have any marginal value in predicting the sex of child N+1? By “marginal” I mean predictive power beyond other known effects, e.g., the race of the parents, the mother’s weight, season of birth (list from this presentation by Andrew Gelman).
I know that many claims that some variable can predict a child have been accused of resting on shaky statistics (see the presentation linked to above). But the sex of preceding children seems like it could be a strong predictor.
UPDATE: answering fileunderwater's question

Can you expand on why (by what mechanisms) you think that it could be a strong predictor? Male sex-chromosome bias in sperm?

Yes, sex-chromosome bias was my first thought. I almost focused my question specifically on that but the fact that I saw maternal weight listed as a predictor in the Gelman presentation made me think there might be other relevant factors that I wouldn't think of. So I broadened the scope of the question.

Can you expand on why (by what mechanisms) you think that it could be a strong predictor? Male sex-chromosome bias in sperm?

there's some evidence that there's gender based selection of sperm by the female... in snakes.  I would like to see birth records mined for patterns and statistics in people, but I've not yet seen a reference.

I remember hearing in my Genetics class in grad school that having a child of a certain gender pushes the odds (very slightly) in favor of having a second child of that gender, which then pushes the odds slightly more, etc. etc., until after the 3rd or 4th child in a row of that gender the odds are quite significantly above 50% of having yet another child of that gender. I don't have a source for that though, except this - I come from a family of 4 boys :)

For those who are interested in sex ratio bias itself, the enWikipedia article is pretty good.
As for predictive power, a Bayesian might tell you that by knowing a couple can and did have a male/female should improve, if only slightly, your belief that their next would be the same.  It's by no means predictive and probably largely indiscernible from random chance, but hey it's something!
More to the point, at the very least you might as well just guess their next child will be a son.  As the link above will tell you, the human sex ratio at birth has varied but in general males are more likely to be born - somewhere around 1.03 to 1.08 males per female.  Here's another in-depth study, from 2005, dealing with the last few decades in the US.
That study has Figure 3 (below) and Table 3, which show the raw birth ratio over successive births, and the data are pretty clear: successive births reduce bias.

Those numbers are way more clear than I thought they would - just watch those means move!  I wish there were more information on the variances - clearly there's more down by the 8th child - but that's pretty solid.  Here's another study from Denmark in 1999 doing some of the same stuff (Denmark was popular for this work).  They include the absolutely fascinating Table 2 (below), which breaks down the odds of giving birth to a male given whatever came before.  Which, in the end, is as predictive as you can get, right?

Basically, it's sort of what you'd expect: the more females you have, the more likely you are to have another female; the more males, the more likely the next is a male.  They used about 1.4 million kids but there are some interesting oddities in that table at the extremes.  The best chance for a male?  Your fifth kid, following FMFM.  Best for a female?  Your fifth, after MMMF.
There are some definite issues that can twist the data, particularly when families have another kid to try to get a child of a specific sex.  If you can tease out some of those environmental factors, you'd be better at guessing; still, I wouldn't bet the house on it.  Memorize that table but, when in doubt:

Guess male
Lotta females first?  Maybe guess another one.
A bunch of males?  Guess another male.

Probably YES.
An analysis of data from about 8 million births shows that there is positive correlation. Please see http://biorxiv.org/content/early/2015/11/16/031344

This should be converted to a comment.

@TheLastWord, why is it that this answer should be converted into a comment?

@kuzzooroo The answer is just a link isn't it?

@TheLastWord, the answer is what I've typed. The link is to the manuscript with detailed analysis and a review of previous studies


text:
How much energy does human body fat contain?
I have been reading the Wikipedia article about food energy, but as I'm not a biologist, I don't really understand it properly, so I came here to ask you guys.
My question is: If a human body needs X kcal of energy and it's taking it from the stored fat, how much fat (weight/kg) does it need to burn?
I know that 1 gram of fat represents 9 kcal of energy, but according to the food energy article, the efficiency of getting that energy isn't 100%, so the formula might be a lot more difficult.
I'm not sure what is the real efficiency value here. The article mentions more values, ranging from 18% to 40%.
P.S.: If this belongs to Chemistry.stack, please, tell me or move it there.

For your question, the body would never just burn fat - that physiologically impossible. Your question, however, is common for people trying to lose weight. Most answers are oversimplified. In the literature and on my public websites you can find values for "one pound" of fat being approximately 3500 calories. Thus, people try to make the statement - "I want to lose 5 pounds, so that means I need to burn 3500 x 5 = 17,500 excess calories". It doesn't really work that way, because they body does a great job at adjusting and conserving energy though adjustment of energy expenditure.

I am not sure if I am able to answer your question, but I will give it a try and hope that someone tells us if I'm wrong.
Biologists talk about different kinds of energy depending on where you measure it. The first measurement is the gross energy (GE) which is measured through bomb calorimetry and is basically how much heat a substance gives off when completely burnt. I have recently read in a compendium that the GE value of fat is ~9,4 kcal/g.
The next stage is digestible energy (DE), which is how much of the forage you actually can digest, which would exclude for example fibres.
Next stage is the metabolizable energy (ME), the energy which can be used in actual metabolism (DE - energy losses from transporting nutrients etc). This are the value you reported. (I don't have a source, but I've heard the same values from multiple recognized sources.)
Now is the part where it gets a bit trickier, as the final measurement of energy is the net energy (NE). This is defined as the metabolic energy minus the heat increment, which could be simplified as the energy losses through the conversion between different types of energy (ie. from long carbohydrates into glucose etc.) within the body. Even more simplified it can be said to be the difference between the heat production in a fastened person and the heat production in a fed person, thus being the heat produced by eating, digesting, absorbing and transporting food.
I argue that because the fat already is incorporated in the body it has a very efficient value, and very little transportation within the body is needed. And because the energy (ie, the fat) is internal, it is not accounted for in the heat increment and therefore the NE of internal fat is the same as ME.
And according to the wikipedia-article you linked to United Nations recommendation of the average minimum energy consumption per person is 1800 kcal/day. Thus the amount of fat required to meet the minimum energy requirements of a person would be 1800/9=200g of fat per day.
If you want to read more about the different energy-measurements and the heat increment here is a good link. And don't forget that energy alone is not sufficient for a person as we need protein, vitamins, minerals etc...

Does fat tissue contain any water? Because if it does, than you will not get 9*200 calories from 200g of fat.

Fat does contain water - just like every other cell in the body. Relatively speaking, it just has a lot less given that it's storing a bunch of triglyceride.


text:
Highly spherical Radiolaria; does this image accurately depict the organism?
If I understand correctly, Cenosphaera spp. is a type of Radiolaria, which is a type of zooplankton.  The following is an image of Cenosphaera spp. is from the supplementary material (Figure S2) of the following paper:

F. Lejzerowicz et al., Ancient DNA complements microfossil record in deep-sea subsurface sediments, Biol. Lett. (9) 2013.

Question: Does this image accurately depict the organism?

More specifically, in other images of this organism, there are numerous thorns pointing outwards.  Is this thorn-less version a natural variation (or e.g. the result of the process of imaging the organism)?  Also, is it largely a sphere with a hollow inside?
The authors give the following description of the process involved in obtaining these images.

Eighteen sediment samples were wet washed over 63 μm and 20 μm sieves. The >63 μm residua were dried and picked for radiolaria and foraminifera. From most samples all specimens were picked. Rich samples were divided with a dry microsplitter into fractions, from which at least 100 specimens were picked for each group. Specimens were arranged by taxa on micropaleontological slides. Radiolaria are classified on the generic level, according to the classification utilized by [8]. Foraminifera above the species level are classified according to [9]. In addition, for radiolaria, the 20-63 μm fractions were soaked in peroxide, then washed with tap water and propanol. For each sample, a few drops of suspended material was left on a glass to dry, covered with Durcupan ACM resin and a cover glass. The micropaleontological slides were analyzed under Olympus BX50 light microscope (electronic supplementary material, figures S2 and S3).

In terms of their hollowness, they all (at least, when they're alive) will have the actual cytoplasmic mass (the organic bits) inside. What we see in the picture, and classify them by, is the mineral exoskeleton.

According to the Marine Species Identification portal, the presence of these thorns is variable.  They also vary in size, shape, and the presence of polygonal frames.  I don't think there is anything about the imaging process described that would result in the uniform loss of spines (unless the sieve/microsplitter broke them all, but I think that would be a non-uniform loss).
Re: whether it's hollow or not, that appears to be variable too.  One species is filled with oil, while another appears to be hollow.

The genus Cenosphaera has indeed been used to qualify fossils of Spumellarians (an order of polycystine Radiolarians) that consists of a single, hollow, spherical shell. The biological meaningfulness of this definition is however unknown.
The very small external thorns that one can see on the picture you're showing are thought to be secondary growth and therefore variable with the age of the specimen, the availability of silicon in the specimen water column and the state of preservation (if it is a fossil).
When alive those species fo course are not hollow inside. The cytology of spumellarians is not as well known as the cytology of Nasselarians (read papers from Cachon, Hollande or Enjumet if you're interested or this nice review from Suzuki & Aita) but they do possess for sure a cytoplasm separated by a capsular wall into a dense endoplasm and a loose ectoplasm.
NB: The reexamination of the specimens Ehrenberg used to described his first species of Cenosphaera (Cenosphaera plutonis, de facto type-species) showed that this specimen was not actually a single-shelled spumellarian, hinting that this genus name have been probably misused in 150 years of radiolarian research.


text:
Bilayer synthesis?
If we want to design a bilayer from Myristic acid (14 carbon fatty acid). The average bond length between C-C is 1.5 A. What will be average thickness of the membrane?
Edited to include the OP attempt that was posted in a comment:
There are 13 C-C bonds in Myristic acid, 13*1.5=19.5A. 1A=o.1nm.. so 19.5A=1.95nm, so the average thickness would be 1.95nm. As membrane is bilayer it will be 3.9nm

Lewis & Engelman (1983) Lipid bilayer thickness varies linearly with acyl chain length in fluid phosphatidylcholine vesicles. J. Mol. Biol. 166: 211 - 217.
Table 1 and Figure 3 have the information that you need. For C14:0 the thickness of the hydrocarbon bilayer is given as 23 Å. Just in case this is homework, I'll leave you to convert that to nm.
added later
Just to follow up on the comments, as hinted at by Shigeta, if you wanted to calculate an estimated bilayer thickness you would have to take into account the C-C-C bond angle which for tetrahedral carbon is 109.46°.
Thus the distance between two C atoms in an extended C chain is 2 x 1.5 x sin(109.46/2) = 2.45 Å
For C14:0 the length is then 6.5 x 2.45 = 15.9 Å (from methyl C to carbonyl C).
Therefore, calculated bilayer thickness = 31.8 Å plus any distance between the two C chains in the centre of the bilayer. This is still a lot bigger than the reported 23 Å.
Clearly the bilayer does not consist of extended hydrocarbon chains. The chains are presumably partially collapsed (on average) and may also interdigitate to some extent.

I want to ask one thing that if we are not provided with the information about the thickness of membrane in any table or a graph then can we are capable to calculate the Membrane thickness according to some data that is provided in Question such as C-C bond length?                       As I have tried it tell me whether it is correct or not? :/  There are 13 C-C bonds in Myristic acid, 13*1.5=19.5A. 1A=o.1nm.. so 19.5A=1.95nm, so the average thickness would be 1.95nm. As membrane is bilayer it will be 3.9nm.

notice how your answer is ~70% longer than the actual answer?   Because the chains are flexible its not that simple. You might calculate the average length of the chain in the membrane given all the reasonable bond angles the chain might take, probably by molecular dynamics.  its not straightforward.  Even if you built a model of the molecule you'd find that the bond angles of the extended chain gave a length at least 30% shorter than your end to end number. The table cited here is the actual answer, from a measurement of membranes and so even better than that.


text:
Why isn't the phosphoglycerate kinase reaction of the glycolysis pathway irreversible?
Step 7 of the glycolysis pathway is the conversion of 1,3-bisphosphoglycerate into 3-phosphoglycerate by the action of the enzyme phosphoglycerate kinase, resulting in the production of 2 ATP molecules (per glucose).
This reaction has a large negative value of ΔG (-18.5 kJ/mol). If reactions having large negative value of ΔG are classed as being irreversible, then why is Step 7 of Glycolysis reversible?

I like to think of it as saying "there's enough 3-PG around and so little 1,3-BPG around that we do actually have to consider the reverse reaction." As @AlanBoyd points out, in erythrocytes this reaction is actually pretty close to equilibrium. So we can't call this "irreversible" because the simplifying assumption applied to "irreversible" reactions is that there is no equilibrium (K is infinitely large).

The free energy change that you quote for the phosphoglycerate kinase (PGK) forward reaction is, of course, the standard free energy change (ΔG0') for the overall reaction. The standard free energy change is defined for all reactants at a concentration of 1M. Note that this value includes the formation of ATP -  the free energy of hydrolysis of 1,3-BPG would be much larger, and some of that energy is 'captured' in the ATP product.
The actual free energy change for the PGK reaction, ΔG,  will differ from this value because of the fact that the actual reactant concentrations are very far from the idealised 1M. You can find a Table here which compares, for each step in glycolysis, the standard free energy change with a true free energy change, calculated on the basis of cellular conditions in erythrocytes (also shown). You will see that for the PGK step the actual free energy change is 0.09 kJ mol-1 rather than the -18.9 kJ mol-1 that you quote in your question.
You can also see from the Table that there are only two reactions in the glycolytic pathway with large negative values for ΔG: those catalysed by phosphofructokinase and by pyruvate kinase. These are of course the two steps that are bypassed in gluconeogenesis because they are essentially irreversible.
So - your reasoning was correct, but it was based on the wrong ΔG values.
added much later
As pointed out in the comments, the 1st step in glycolysis also has a large negative value for ΔG and is also bypassed. Not sure how I forgot to include that!

"You can also see from the table that there are only two reactions...." Isn't 1st step of glycolysis having very large -ve ∆G? So there are 3 irreversible steps, not 2.

You have to look at the complete reaction including the cofactors. In general, you can drive a chemical reaction into directions which are not favorable by:

removing products from the environment (if they are gaseous for
example or react further)
having a huge excess of substrates (and thus making the back reaction
less likely to happen)
and by coupling the main reaction to a second, which provides the
necessary energy for the main reaction to happen

If you look at the reaction of 1,3-BPG to 3-PG this looks like the following (picture from Wikipedia):

The back reaction to 1,3-BPG needs ATP as a co-factor, so that the enzyme has the necessary phosphate group to add. The lysis of  the phosphor diester bond from ATP to ADP delivers the energy to make the reaction possible.
This reaction is the control point in either generating ATP (glycolysis), when there is little ATP and much ADP present or generating glucose (gluconeogenesis) when there is much ATP and little ADP. This makes sense when you consider that ATP is a rather instable molecule with its high energy diester bonds, while ADP is more stable.

ATP is not hydrolyzed in the reverse reaction. Instead, a phosphate carboxylic anhydride is formed. If you're trying to do a Hess' law type analysis then you need to consider the hydrolysis of 1,3-BPG, which is much more favorable than -18.5 kJ/mol (in fact 30.5 kJ/mol more favorable).

I just looked it up like this. Where does the phosphate group come from then?

ATP transfers a phosphate to the 3-PG to form ADP and 1,3-BPG. Hydrolysis is when water cleaves the phosphodiester, forming ADP and inorganic phosphate.

Ahh, got your point.

Not sure why you are calling it "phosphodiester" bond (which I think is what you mean by 'phosphor diester')...there is no ester here! Its just a bond between two phosphates, not a carbon-linked phosphate and a carbon-linked hydroxide :/


text:
Do recessive alleles really exist?
This question may seem illogical to some, but I seriously have this doubt. I searched google for some proofs but they were extremely complex and I couldn't understand anything.
I was just wondering whether we really have recessive allele or not? Is it like there are only dominant allele present, and when dominant allele isn't present we consider it recessive.
Is it like there is a place reserved for dominant allele and if that place is empty it turns out to be recessive.
Although this thought is vague but then if you take this example, it probably would make sense:
Let's say there are two allele : T and t for tall and short respectively. Now, because TT, Tt, tT are tall, they all lead to the formation of specific hormone due to the presence of dominant allele. But the plant with genotype tt is short, hence the "extra" hormone for "excessive" tallness is missing in tt plant because the dominant gene isn't present. Can we say that that place for two allele (dominant allele) is actually empty in the plant with genotype tt?

A selection of related questions: what makes a gene dominant or recessive, why are some genes dominant to each other? and relative properties of alleles.

This is a good question. Firstly, let's get the terminology straightened out: The terms recessive and dominant are not actually used to describe genes, but rather alleles. The term allele is used for alternative forms of the same gene.(1) Many genes have two or more alleles, and some genes have alleles that can be described as dominant or recessive.
It is also useful to be familiar with the terms genotype and phenotype. Genotype refers to the form of the genetic material (DNA), while phenotype refers to the observed effect of the genotype.
Secondly, it's important to realize that the concept of "dominant" and "recessive" is a human-made abstraction. The concept of dominant and recessive genes were invented (or discovered, if you like) before we reached a good undertanding of how genetics works at the molecular level. Thus, genetics in the early days had a much cruder understanding of how different phenotypes depend on the genotype.
The dominant/recessive concept is useful in cases where there is a limited number of possible allele pairs and one or several alleles can mask the effect of other alleles. This is a very limited set of cases. Many genes have many different alleles, and it's hard to account for all of them. Many alleles also do not have a clear observable effect, in which case any "masking" effect is not prominent. To quote Wikipedia (2):

The most common basis of dominance and recessiveness is that the
  dominant allele codes for a functional protein and the recessive
  allele for a mutant, non-functional protein.

A further important point is made in the following passage:

Dominance is not inherent to an allele. It is a relationship between
  alleles; one allele can be dominant over a second allele, recessive to
  a third allele, and codominant to a fourth. Dominance should be
  distinguished from epistasis, a relationship in which an allele of one
  gene affects the expression of an allele at a different gene.

Let's consider your example: A single gene with two different alleles, T and t. Let's assume the T allele codes for a more powerful version of the growth hormone than the t allele, or that the t allele produces a non-functional hormone. Furthermore, we assume that production of the T hormone from a single allele is enough to make the plant grow tall, and that production of T or t from a second allele has no further effect. Then, we can say that the T allele masks the effect of the t allele. However, as you can probably imagine, one allele fully masking the effect of another is rather rare. So recessive/dominant allele pairs are rather the exception than the norm.
Thus, the that place for the two alleles in the genome of the plant is definitely not empty. Note that a mutation could in principle cause one of the genes to be deleted in its entirety from one of the chromosomes of the plant during reproduction. The "place" for the gene on that chromosome would then indeed be empty. This has nothing to do with how dominance and recessiveness usually works, except that a recessive gene could become expressed if the dominant allele is deleted.
So, at the molecular level there is no concept of recessive or dominant alleles. Some genes have allele pairs that can be described as dominant/recessive in relation to each other, most others do not. The effect of different combinations of alleles determines whether the relationship between the alleles is described in terms of dominant/recessive.

Yeah, I used wrong term gene over here. Thanks. But question still remains unanswered.

OK. I'm working on a bit more elaborate explanation.

Do we seriously have recessive allele or is it just the dominant one? Is it like when dominant allele isn't present we consider it (the allele's placeholder) to be recessive. This is want I am searching for. :)

I expanded my answer. Does it answer your question now?

Wonderful explanation Jarlemag. Thank you. :)

My pleasure. It's a concept that bugged me for a long time too, as the molecular details are often left out, and only a very simplified view of genetics is presented, when dominance/recessiveness is explained.

Great answer.  I sometimes wonder if the usual way Mendelian genetics is taught causes more confusion than it's worth.  People don't seem to get that that paradigm is only helpful for a small percentage of our observations, even though it spawns a huge number of easy-to-grade homework assignments

I'm having real difficulty understanding the original question. We know that a diploid organism has two copies of a gene because we can sequence them, and if they are different alleles we can point to the difference in their sequences. Then through genetic crosses we can follow the two alleles and look at the association between genotype and phenotype, thus deciding on the nature of any dominance.
Also we can create a mutation in a gene by inserting another piece of DNA with its own associated phenotype (drug resistance for example). In this situation we would normally see a dominant phenotype associated with the undisrupted gene, but we would know that the recessive (disrupted) allele was also present because of the associated drug resistance. Certainly this is done all of the time in yeast genetics.
I think the problem is that you are treating genes as abstract entities in some sort of 19th century theoretical framework, disregarding over a century of genetic studies and, as @jarlemag has so eloquently explained, the physical reality of genes (as DNA sequences).
Final thought: the situation that you are describing (a "space") does exist in the special case of  males for X-lined genes, where only one allele is present. This is the explanation for the genetic properties of sex-linked diseases like haemophilia.


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How are commercial steroid hormones produced?
Does someone know how oestrogens and androgens used for treatment are made? Is it with a GMO bacteria? Is it chemistry?
Thanks

Welcome to SEBiology. Before posting a question it is expected that you first try to find the answer by other means, e.g. an internet search. If the results of this are unsatisfactory then you should explain this in your question. In this case a Google search for  "Commercial production of steroid hormones" will bring up plenty of leads. You might also ask yourself when the contraceptive pill was introduced in relation to when genetic cloning techniques and how many genes would have to be expressed in bacteria to allow steroid synthesis.

In this recent review you can find fascinating information on all aspects of this topic. It's dense in sterol structures and chemical interconversions, but that's what you have to expect. This is my précis.
Direct isolation from primary biological sources This was the heroic phase of research in this area:

Androsterone was first isolated from the urine of policemen. Quickly, however, it became evident that natural isolation of hormonal steroids would not satisfy the demand, as, for instance, in 1931, 15,000 L of urine yielded only 15 mg of pure androsterone. Similarly, 4 tons of sows' ovaries were needed to isolate 12 mg of estradiol, while extraction from 625 kg of sows’ ovaries produced 20 mg of progesterone.

[edited by removal of citations]
There are still some commercial processes in this class:
Premarin contains estrogens produced from the urine of pregnant mares.
Chemical transformations starting from steroidal sapogenins of Dioscoreae (yam) These processes still make a contribution but there is a limiting availability of the starting plant material. Apparently important in China.
Direct total synthesis
This section describes chemical routes, but there don't seem to be any commercial processes
Chemical synthesis from cholesterol and phytosterols Phytosterols are plant sterols, available from e.g. soy bean oil, rape seed and paper pulp industrial waste. They can be chemically converted to steroid hormones, as described in the review, but there don't seem to be any commercial processes.
Microbial conversion of phytosterols
Bacteria can convert plant sterols into useful products. Mycobacteria seem to be particularly useful.

Today, more than 1000 tons of steroids are produced annually from phytosterols by microbial transformation, alone.


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In plants why are potassium and nitrate ions absorbed faster than any others?
Quoting my A-level biology textbook:

$\ce{K^+,  NO3^-}$ are absorbed by plants faster than any other ions. Whereas, $\ce{Ca^2+, SO4^2-}$ are absorbed with the slowest speed.

What is the reason?
My reasoning: I first though the size of ions would matter in this case. Obviously, $\ce{K^+}$ is smaller than $\ce{Ca^2+}$,  then it 'seemed to me' that smaller ions would be absorbed faster. The same reasoning can be applied to $\ce{NO3^-,  SO4^2-}$. But, there are smaller ions than $\ce{K^+}$ which are absorbed slower eg. $\ce{Na+}$. So, obviously size only does not matter here. There are other factors.

What reasons has your own research uncovered?

@James See my edit.

Since plants absorb minerals, like potassium, calcium, sulfur, etc. in their ionic form, like K+, NO3-, SO42-, Ca2+, they need to absorb them actively. Since these ions are charged, they have difficulty while passing through the plasma membrane. Hence, plants need to expend energy in order to transport them. For this, they use ATP and membrane transporter proteins. These transporters transport ions across cell membrane with an accompanying ion (H+) so as to maintain electrochemical gradient. As a result (partly), these transporters are highly selective for the ions they carry. For example, a K+ transporter will not transport SO42- or another ion. See this answer to see how transporters achieve this selectivity.
The above part explains how ions are transported in plants. Now, lets come to the main question i.e. why some ions are transported faster than others. Well, there is no definitive answer to this (at least none that I know of). But I can think of two possible reasons for this (using only the examples of K+, Ca2+, NO3- and SO42-):

Magnitude of Charge: one fact here is that both K+ and NO3- have a charge of $\pm$1, whereas Ca2+ and SO42- have a charge of $\pm$2. So what? This makes their transport a bit more difficult. For example, to transport K+ across the membrane, the transporter would antiport 1 H+ for 1 K+, whereas a similar antiporter would transport 2 H+ out to bring 1 Ca2+ in. Obviously, this does not explain the difference between ions with same charge, which the following point seems to do.
Requirement: one of the most important points to keep in mind here is the difference in requirements of different ions by the plant. This is why plant macronutrients (i.e. required in large quantities) have been divided into primary macronutrients (N, P, K) and secondary macronutrients (all others, including Ca, S, Na). As you see, nitrogen and potassium are mostly the limiting factors of crop production. This is why plants require them in large quantities, and hence try to absorb them as fast as possible. This, partly again, explains why K+ and NO3- (the only artificial nitrogen source other than NH4+) are absorbed faster by plants while Ca2+ and SO42- are absorbed slowly.

References:

Mineral Absorption - Wikipedia
Secondary Plant Nutrients: Calcium, Magnesium, and Sulfur - Mississippi State University

Great Answer. I will for some time before selecting it


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Can a hemorrhage occur after death?
Can a hemorrhage occur after death?
Specifically lung hemorrhages. Can an organ hemorrhage after death and, if so, how long for?

Under certain circumstances, yes. Can you add more detail to clarify exactly what you're looking for? Because the general answer is "no".

Hi there, thanks. I'm doing some looking over an autopsy of a celebrity for personal interest as the cause of death is uncertain. The person in question had appeared to have hung themself and CPR had been attempted around 30 minutes after the person had hung themselves. The autopsy later revealed that "the lungs had focci of hemorrhage" and if the hemmorhages were unlikely to have been caused post-death then this makes foul play more likely.

To summarise though, the person examined had been dead for a good time when CPR was attempted.

Usually,blood moves through the body by force from the contraction of ventricles, the contraction on muscles, gravity, or other forces. At death, the only force left is gravity, which is why we see lividity (or livor mortis -pooling of blood in dependent positions) after death. This continues for ~8-12 hours (depending in part on temperature).
The blood in the arterial system at the moment of death is still under pressure because arterial wall musculature has not relaxed yet. (I don't know how long this takes, to be honest.) If an artery is pierced (say, a bronchial artery, e.g. by a knife), blood will flow from a high pressure area to a lower one (e.g. into non-inflated lung tissue, the abdominal cavity, or the outside or the body) So post-mortem hemorrhage can occur until the arterial musculature has completely relaxed. After this relaxation, stabbing a corpse will produce a small amount of oozing at most, unless pressure is applied somehow, e.g. during CPR. CPR may make small petechiae larger.
Livor mortis can occur in the lungs post death as well.

as the blood accumulates in the dependent areas, the pressure of the settling blood can rupture small vesslels, with development of minute hemorrhages (petechiae)... This usually takes 18-24 hours... and is more common in (asphyxia).

Hanging is death by asphyxia, and is known to be associated with lung hemorrhages, but very small ones.
Forensic Pathology, Second Edition By Dominick DiMaio, Vincent J.M. DiMaio, M.D., pp.22-25

Thanks for the great answer! One last thing, as my knowledge of biology is limited, could the "Focci of hemmorrhage" been as a result of CPR (IE pressure on the chest causing lungs to be damaged)?

It's possible but very unlikely. CPR does cause damage: bruised muscle, broken ribs, etc., but it's not common. The petechiae in the lungs after hanging take hours to form as the blood settles in the lower parts of the lung. If the person was only hanging for 30 minutes and CPR was started, the blood is moving, not pooling. Hope that helps.

@Charlie - Here is a list of things CPR can do to screw up autopsy results: Forensic aspects of complications resulting from cardiopulmonary resuscitation.

Would it be possible to discuss this further with you in a chat? It would be great to get a knowledgeable person's opinion on the matter and look into more details the autopsy if it would be too much trouble.

that is if I can even start a chat, as I'm not entirely sure how to do it without spamming a conversation in chat for ages.

@Charlie - As I'm not a coroner, I don't think I can be of much more help. Sorry. :-/

that's fine, thanks for your help thus far anyway. Feel free to contact me if you change your mind though as any medical experience would be very valuable. :)


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Is there variation in which olfactory receptor genes are functional in humans?
According to wikipedia humans have around 400 functional olfactory receptor genes and 600 pseudo genes. Most mammals have higher numbers of functional OR genes.
My question is whether it has been studied how the number or subset of these functional ORs varies between humans.

My question is whether two randomly chosen humans have different numbers and different subsets of functional OR genes or whether they are very likely to have exactly the same subset of functional OR genes. I'm not trying to associate any characteristic to this subset, though of course one could assume that it might result in a specific range or acuity of olfactory sensing, but that's not very important to my question.

Perhaps the most dramatic example of variation in olfactory abilities in humans is anosmia, or the inability to smell. However, this isn't always due to broken olfactory receptors -- some total anosmias are due to cilia (small hairs) that don't function properly. (This paper mentions that.)
Specific anosmias, or insensitivities to particular smells, are probably closer to what you're asking about. The textbook chapter I linked to below talks about how proportions of the population lack the ability to smell certain odorants -- for example, about 1/10 people cannot detect ethyl mercaptan, which is the scent given to natural gas leaks. These specific anosmias are generally restricted to just one odorant (smell), which suggests that it is likely a receptor deficit. (EDIT: The comments below have even more examples of scents that vary from person to person.)
Interestingly, many conditions are associated with a decline in smelling ability and range, like Alzheimers, diabetes, and taking certain medications. These declines can be because of fewer olfactory receptors or because of deficits further along in sensory processing.
I couldn't find any papers assessing smell variation across all humans -- doctors rarely think to assess smell, so there isn't much data on "normal" populations. Also, it doesn't seem like the genes controlling olfactory receptors in humans have been characterized well, so it would be extremely difficult to do a comparison on the genotypic level.
In sum, there are definitely differences in the ability to smell a wide range of scents. To my knowledge, this hasn't been characterized in an especially systematic way. (If it has, I hope somebody on here knows otherwise!)
This chapter of Purves' Neuroscience gives a basic run-down of olfaction and some possible variations in it.
https://www.ncbi.nlm.nih.gov/books/NBK11032/

Hydrogen cyanide would NOT be used as a natural gas odorant, since it is highly toxic, quite aside from the fact that many people can't smell it.  Mercaptans are generally used instead.  Another instance of something smelt differently by people is the flower alyssum: to me it has only a faint grassy odor, while my ex thought it had a strong and very pleasant fragrance.

Coriander (fresh leaves, not the dried seeds), which is a common spice in asia, is percieved as 'soapy' by some people. There is an article, that also liks this to genetic variants.

@jamesqf : oops, I misread the a paper. Ethyl mercaptan is added to natural gas and some can't smell it. Some people can't smell hydrogen cyanide and that's dangerous because it could kill them. Editing now.


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What governs the size of animal bodies?
Million of years ago there lived dinosaurs up to 36 m high. About 10,000 years ago lived Machairodontinae -compared to cats today they were huge. About 400,000 years ago lived Mammuthus trogontherii: it reached over 4 m at the shoulder. And these are just some examples.
Todays biggest living creatures look small compared to previous. So my question is, why are all creatures getting smaller? Why doesn't evolution generate any big creatures with size comparable to the dinosaurs?

The blue whale http://en.wikipedia.org/wiki/Blue_whale is the largest animal that has ever existed on Earth, and it is available to ride right now.

IF you want to ride a dinosaur, ride an ostrich. :)

For the record - both my comment and that from Mike Taylor make no sense now that the question has been edited. It originally mentioned wanting to ride a dinosaur.

This question about dinosaur size might be helpful. African elephants would fit right in with many of the largest (non-sauropod) dinosaurs.

This post is so relevant to this question that it might almost be a duplicate.

It's strange that nobody has mentioned human impact. Consider the following.

There are lots of parameters that influence body size. Here is a non-exhaustive list:

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
artificial selection
etc..

Saying that today's species are smaller than previous species is maybe over generalize. For example, the largest species that is thought to have ever lived is currently extant, it is the blue whale (it can weight more than 200 tons). The tyrannosaurus is roughly the same weight that the african elephant (7 tons). However it is true that insects were typically bigger before than they are today. It is also true the the sauropoda are particularly impressive as some of them were 3 or 4 times taller than a giraffe and weight around 100 tons. [Bruhathkayosaurus](The http://en.wikipedia.org/wiki/Bruhathkayosaurus), the largest land animal that ever lived may have had a weight comparable to the blue whale!
A common argument to account for the big size of dinosaurs and especially of insects during  the triassic is the oxygen concentration in the atmosphere (ref). It is particularly relevant for insects as they have no hemoglobin, meaning that the oxygen has to be dissolved into their body liquid (mostly water) to be brought to the cells. From Henry's law, the concentration of a gas such as oxygen in a liquid is a function of the concentration of this gas in the atmosphere. Therefore, the highest is the oxygen concentration, the easiest it is to bring oxygen to all the cells of a big body and therefore the lowest is the cost of having a big body.

I agree with other commenters that we are not necessarily living in a time of small body masses.
Here is a paper on a body mass distribution. It's quite mathematical, but the first author (Aaron Clauset) is good.
For individual body masses, you can look at Kleiber's law - this says that body mass and metabolism are related by a power law.


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What is the difference between monoecious and homothallic?
In my plant reproduction book there are two distinct definitions for these two terms, but when I read them I found out that they are very much alike that I was confused and couldn't catch the difference between them. I searched on Google and found this on wikidiff:

As adjectives the difference between homothallic and monoecious is
  that homothallic is (of some algae and fungi) producing male and
  female reproductive structures in the same plant while monoecious is
  (botany) that has male and female reproductive organs on the same
  individual plant (rather than on separate individuals).

But, still, isn't this the same sentence using another words?
Thanks for answering.

Hi @Anonymous I rolled back your last edit because the text you edited is taken directly from Wikidiff and so should, I think, be left as is even though it could be better phrased.

The difference is that they come from different scientific traditions and describe the same idea for different kinds of organisms. Homothallic is applied to fungi and algae, whilst monoecious is applied to plants (and sometimes invertebrates). This use of different words to describe the same phenomena in different types of organisms is unfortunately quite common. You could also had hermaphrodite as another example for organisms with both male and female reproductive parts. One can point to crude phenotypic differences to justify the distinction in terms but the underlying concepts are the same.
I note as well that the separation into different types of organism used is usually based on older classification systems rather than reflecting any biological reality.

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Do lunar rhythms have impact on human biology, if so, how?
I'm approaching this question from the circadian rhythm perspective. A circadian rhythm is a 24 hour cycle. While doing research on deep sea circadian rhythms, I found this abstract which seemed to imply that there are some kinds of lunar rhythms (about a month long cycle). Lunar Rhythms in the Deep Sea: Evidence from the Reproductive Periodicity of Several Marine Invertebrates:

While lunar rhythms are commonly documented in plants and animals
  living in terrestrial and shallow-water environments, deep-sea
  organisms have essentially been overlooked in that respect.

What do the authors mean by the lunar rhythms? The roughly month long menstrual cycle, or are there other ways that the moon actually influences animal/human biology?

The moon doesn't have a direct effect on metabolism. Nor does it affect menstruation (an archaic theory existed which claimed so!!). The lunar effects are due to its gravitational field which is known to affect tides (Spring tides and neap tides).
Even on a daily basis if you might have observed the sea advances into the beach in the night and recedes in the day. This effect is also because of the lunar gravity.
The abstract of the article, that you mentioned, says that moonlight may have some effect on certain organisms; I am highly skeptical about that.
I think it is just the tidal patterns that might affect the behavior of marine/coastal organisms. I am also slightly skeptical about whether the currents produced by lunar gravitation would be deep enough to affect benthic life. In that case even the heating effect of the sun can produce sea currents. Perhaps it can also produce an upward current because of differential heating.

It would be great if you could add links to a few papers on the topic (am sure someone looked at that...)

@nico: i didn't refer any particular paper for this info. I'll look up and add ASAP.


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Are there neuronal firing artifacts produced by head movement?
I'm experimenting with a consumer-grade ElectroEncephaloGram (EEG) sensor and have created the image below using the device. Because the sensor on the device does not use a suction cup, there are a lot of motion artifacts when the headband contact is poor (during motion).

This got me thinking - neurons have mass and thus inertia, and they are not glued to each other.  When the person moves (actually rotates) the head around, forces of inertia are applied to neurons/axons. I'm interested if such motion produces any kind of firing artifacts within the brain or how the brain filters out such firing?
This reminded me of this article: (5-HT and motor control: a hypothesis). Could it be that some neurons stop firing in response to movement?

There are certainly head-orientation cells (e.g. in the hippocampus).  But neurons are reasonably immune to the kind of mild physical stresses that come from turning the head around; computing head orientation requires complex analysis of input from e.g. the visual system (optic flow) and vestibular system.
However, the electrical activity of muscles tends to swamp that of (nearby) neurons, so various muscle-related artifacts are often visible in an EEG if not carefully filtered out.  And, of course, if the contact is poor you'll get artifacts from that: you're just measuring the variability in resistance between the sensor and your skin, not anything interesting about what faint potential changes are visible at your skin as a result of neuronal activity.


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Is telomere length a reliable measure of health/lifespan?
Several companies are commercializing tests for telomere length such as this one here. I understand the basic mechanism for why telomeres shorten during DNA replication, but how good is the evidence that telomere length is a reliable indicator of healthspan/lifespan?

I disagree with Ctina.  So many factors go into determining loss rate, activity of telomerase, gene conversion or unequal exchange at chromosome ends, etc to ever say that length is a function of age.  There is far more variation between individuals and between cells within an individual than aging ever shows.  Here is one study:
Das B, Saini D, Seshadri M. Telomere length in human adults and high level natural background radiation. PLoS One. 2009 Dec 23;4(12):e8440.
however I've seen similar studies published elsewhere.  Telomere length as diagnostic for age is very poor at best.  Here's an article that gives a formula, but acknowledges the R2 is 0.04, which is useless: http://preview.ncbi.nlm.nih.gov/pubmed/18378481

There's no math equation processing at the moment but you can use the html  tag if you wish for things such as R-squared =)

Please note that I did never say that it is reliable.
So I don't understand in what you disagree exactly. I also referred that are many factors that alter the size of the temolere, as you did.
Just because I did not stated "It is not reliable" I also did not say "It is reliable". That was my mistake to not make this point clear.
But it is true that it gives a rough idea of lifespan (I said rough, not accurate!)

I disagree that "It would be reliable if we don't take into account the environment, and if we are comparing two genetically identical persons." There is far too much stochastic change (and non-telomerase-based repair such as interchromosomal exchange at telomeres).  Two cells from the same individual are not concordant, so your statement cannot be right. To say that it is "not 100% reliable" suggests it's still pretty good (but not perfect). It's less-than-4%, so I disagree that it can be used for "a rough idea."

Ok, what you said is true. agreed. vote up

A number of studies have compared replicative capacity of cells with lifespan.  Since Replicative capacity of cells is linked to telomere-length, these studies may provide indirect evidence for the association between telomere length and lifespan.  One interesting study in particular compared animal life spans and in vitro replicative capacity of skin fibroblasts in groupings of small, middle, large, and very large breeds of dogs of specific ages (Li et al, 1996). It was found that the life spans were inversely correlated to the frame sizes of the breeds. It was shown that all the small breeds studied have a longer life span than that of the large breeds. The replicative capacity of fibroblasts from the large dogs (Great Dane and Irish Wolfhound) was significantly decreased compared with that of the small dogs. The reasoning behind these observations may again be due to varying degrees of cell turnover between the species. Large dogs consist of more cells than small dogs and as a result more cell turnover was initially required in their development compared to small dogs. This increase in cell turnover would subsequently lead to a decrease in replicative potential (due to telomere shortening) and an increase in the rate of senescent cell formation.

It's always helpful to link to papers you reference :-)

We found that the telomere shortening rate, but not the initial telomere length alone, is a powerful predictor of species life span. These results support the notion that critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.

https://www.pnas.org/doi/full/10.1073/pnas.1902452116

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How does increased heat increase the rate of metabolism?
I have heard that taking a hot shower helps

blood circulation
metabolism.

For (2) metabolism, I think that the rate is increased since kinetic energy is given to compound to bond with enzymes to react. Is this the only reason? In addition, why is (1) true?

I don't think a hot shower has any substantial effect on body temperature, since this is carefully regulated by several mechanism to remain around 37$^\circ$C. When you expose the body to heat, you induce a response where the body increases heat loss and possibly reduces internal heat production in order to maintain the core temperature.
It is true that heating the body will increase blood circulation in the skin; this is a way for the body to carry heat from the core to the surface, where it can dissipate (radiate away). As for metabolism, I think the response to heat is less well studied than the response to cold, but presumably metabolic rate (specifically, mitochondrial respiration) will decrease in order to reduce internal heat generation, in order to maintain body temperature. Again, these are homeostatic responses that occur before there is any marked change in body temperature. Here is a review article on these mechanisms.
If you would expose the body to enough heat so that these normal responses cannot compensate, the body temperature will actually rise. Beyond 2-3 degrees (a normal fever), this is very dangerous because it will disturb a number of cellular processes. Cellular metabolism would certainly be affected, but mostly  because some enzymes have narrow temperature ranges where they can function; I don't think the actual heat energy of metabolites is an important factor here, but I don't know of any study on this. A variety of other proteins and cellular structures will be similarly affected. This will eventually affect key functions in the nervous and circulatory systems, which is life threatening. The Wikipedia page on hyperthermia is a good starting point for more information on this.


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How can I find some pieces of the genome of a microorganism?
I have figured out how to download the fasta of the genomes of microorganisms, for example the botulism bacteria and the spirulina algae. However, I want to find a fasta file for some significant extraction of those genomes - say, some important gene, some mutation, some protein that occurs in a microorganisms genome. What should I look for, and how can I find it in genbank?

You can use already available tools to extract information from available database. For finding specific genes, use this. For protein, use this. There are lot more tools. Just explore NCBI, EMBL or DDBJ sites. All information is self explanatory.
If you want specialized information for specific organism, you can use specialized database ( like Flybase for flies, SGD for common yeast, EnsemblBacteria for bacteria and archaea or HGMD for human mutations. Best way is to search in Google. You will get everything you want :D

I found these websites a bit daunting. I don't know what genes to look for - I don't know the names of any genes in, say, arthrospira. I have clicked on some genes but I get very complicated diagrams, not fasta files.

You should have little idea about what you want, else you will be lost in sequences and genes. You can look at Gene Ontology database. Here you can search genes and proteins with annotated functions. I guess that is what you want. However this will give you only reported (or annotated) genes/proteins. You can't find novel genes there. You need proper bioinformatics study to find such genes (like searching through various domains and validating them from literature)

I used GO to find the name of a mycoplasma protein, and I found mycoplasma page on NCBI: http://www.ncbi.nlm.nih.gov/genome/1028. I can't figure out how to get the FASTA from that page - do you know?

There was direct link on that page. Click on whatever sequence you want (click on replicons column )

I guess you have found the Genome entry of your favourite genomes in Genbank and got the FastA.
Dexter is completely right, you can just search your genes in the databases and filter them for your genomes of interest.
Another possibility is to get the GenBank-formated file "GenBank (full)", instead of the FastA, then use a Genome Browser (for example Artemis) which allows you to search for genes/proteins in a genome and save them as separate FastA files.
Generally it is a good thing to get the GenBank format file for an organism you are interested in, as you can extract the complete genome sequence as FastA easily, but also keep all the other information you might need later.