text:
What is the most appropriate way to normalize gene expression data?
This question comes because reading a paper about normalization of gene-expression data, is not clear if the method for normalize the data is just for RNA-Seq data or could be applied also for microarrays.
For RNA-Seq data, there are methods of normalization which adjust for GC-content effect or other gene-level effects. It make sense consider these effects in the normalization of microarray gene-expression data?

These methods correct for the biases during the sequencing experiment. Since microarray is a different technique, the biases it suffers from would be different. There are bias correction techniques for microarrays as well, but they are different from the ones used for RNAseq. They cannot be used interchangeably.

Normalization of expression data is a big topic with new methods being published regularly. When approaching something like this you generally want look at people who have done similar things to what you've done, and then once you understand why they did what they did, you can ask what you need to do to answer your questions. Always keep your biological question in mind. For instance if you're measuring QTLs, you'll need to be a lot more careful than if you're just looking for genes effected by a knockout mutation.
In general you want to use quite different methods for RNAseq and Microarray data. The two data types follow completely different distributions (RNAseq gives you count data, microarray data gives you continous signals) and have different types of technical noise effecting them (GC content will effect both, but in a different way). Some methods can be used on both, but usually involve coercing the data into a different form (e.g. mapping counts to a normal distribution). The limma package for R can handle both, using different distributions, and is a good start. Newer, purportedly better methods exist for RNAseq, which I haven't personally used.

Generally speaking for RNA-seq data, you don't want to correct for GC content or other gene level effects (e.g. length) because you compare expression values between conditions WITHIN a gene. For this reason, it is recommended to use raw counts and not normalized values such as FPKM. See Section 2.7 of the edgeR user manual.
This recent benchmark comparing RNA-seq quantification methods may be worth a look.


text:
What is the difference between natural selection and adaptation?
From what I've read it seems that the only actual difference is that creationists use adaptation and people who believe in evolution use natural selection. But otherwise, from my understanding, the two terms are synonymous. Is that correct?

No offense but I would love to down vote @InstructedA 's comment. (A) There are plenty of religious believes but (1) it is not our job on a science website to make a review of such beliefs and (2) your view of creationist believes is unclear and IMO wrong in the same time. (B) While believing in god (theist) or not (atheist) is correlated in accepting the theory of evolution, one can accept the theory of evolution and be theist or refuse to accept the theory of evolution and be atheist as one domain is about science while the other depends on an ideology.

Always for @InstructedA  (C) It is very obvious from your comment that your understanding of evolutionary processes is very limited. (D) Point "B" above is a discussion of philosophy and not biology. Point "A" above is a matter of religious studies and not biology. These topics are interesting, please open a post at the convenient location to discuss such topics.

The down vote is not a punishment but a help for other's to recognize good from bad info. Scientists don't believe in "absolute facts" whatever that means. Natural science does not "prove facts" anyway but only offer series of evidences congruent with a hypothesis. Anyway, this is not a place to discuss that. You might want to have a watch a short introduction to philosophy of knowledge and philosophy of science. I am not going to answer further comment in this inappropriate place.

I am glad that it is not a punishment, as I see and recognize massive amount of inconsistencies in the theory of evolution the way it is being presented. When I was young I was like you, but then the 'church' presented me with a much better theory. Things are so consistent. I have always hoped that the 'scientists' can provide their alternative remedy, but all I got was 'you are stupid, you are empty'.

Natural selection is a mechanism that is used for adaptation. With only selection and no generation of variation the adaptation is highly limited.

Natural Selection
Natural selection is the differential in survival and/or reproductive success among different individuals. As such, natural selection also refers to the process by which genotypes associated with greater fitness increase in frequency in the population through time.
More information on wikipedia > Natural Selection
Adaptation
An adaptation (or an adaptive trait) is a trait with a functional role that evolved (and is maintained) by means of natural selection.
More information on wikipedia > adaptation
Usage
Both the terms adaptation and natural selection are extensively used in science (and none of them come from the creationist religious belief). Their definitions are related as one is causing the other but these terms are not synonyms.
Further information
As the question is very introductory in the field of evolutionary biology, you might want to have a look at an introductory course to evolutionary biology. Evolution 101 (a.k.a. Understanding Evolution) by UC Berkeley is short, concise and very accessible even for those that have little a priori knowledge in biology.
Side Note
You said "believe in evolution". It is of course a common phrasing from the creationist ideology. Evolution is a theory (a theory is very different from a hypothesis see this answer for more information) and therefore, the phrasing "to believe in evolution" sounds quite wrong as it wrongfully suggests evolution is a thing on which we could legitimately have different opinion about its existence.

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text:
Why and where do red blood cells die?
Textbooks commonly state that red blood cells are removed by the liver and spleen. Do those organs destroy the red blood cells within capillaries that course through those organs or are they transported into the liver/spleen cells to be broken down into their constituents? What causes them to be destroyed/removed from the circulation?

RBC's lifespan is about 120 days. RBC's don't have a nucleus or endoplasmic reticulum, but they do have enzymes in the cytoplasm, capable of producing ATP from glucose. This energy is used mostly to maintain the structure and flexibility of the cell. The erythrocyte is a biconcave disc, that is ~7 micrometers in diameter, but the cell is pliable and it should be able to squeeze trough narrow spaces without breaking the cell membrane. Over time these metabolic systems become less effective and damaged, and the cell slowly becomes more fragile and prone to rupture. Spleen has special trabeculae (bands of connective tissue) in its red pulp, that the blood passes trough. The spaces between them are narrow and "old" RBC's tend to rupture while trying to squeeze trough. Then macrophages "catch" any cell fragments down the stream. This can happen anywhere in the body, but spleen and liver are kind of filters for blood contents.

References
Guytons physiology textbook
Ross histology textbook

To take the easiest bit first: Red blood cells are destroyed because lacking a nucleus, they aren't quite as powerful as other cells when it comes to self-repair and longevity.
As for where; it really is all over the body. They are swallowed up (literally) by macrophages lining the blood vessels, which are particularly concentrated in the liver, spleen and bone marrow, but present everywhere.
As they age, they deform, and the macrophages are capable of recognising this deformation and reacting to it (by eating the red blood cells).
When the macrophages have eaten and destroyed the red blood cells, the nutrients they contain are returned to the blood plasma, and captured in the bone marrow for production of new blood cells.
(This pattern is common in a lot of systems, by the way: Even though the liver is the primary organ to break down toxins, for instance, most cells in the body has some limited capability for doing so; this is true of many functions.)

Ref:

http://bril2002.narod.ru/bllod56.html
https://en.wikipedia.org/wiki/Drug_metabolism#Sites

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Coefficient of Inbreeding - implementation issue
The formula for the coefficient of inbreeding is as follows...

I have a family tree going back 9 generations. Say I find a common ancestor X in the 4th generation on the mothers side and in the 5th generation on the fathers side. I can work out that constituent of F... but what do I do about all the ancestors of X (they will all also be common ancestors). Do I also work out their values and add them to F?... or do I ignore them? The descriptions of the COI I have seen do not make this clear.

The $F_i$ term is the term that accounts for inbreeding of your common ancestor X. If that common ancestor is not inbred then the term is 0 and the calculation is a little easier. Using the example you have given:
 X ─┬─ Y
    │
 ┌──┴──┐
GGGF  GGM
 │     │
GGF    │
 │    GM
GF     │
 │     │
 F ─┬─ M
    │
   Mick

In this case, the common ancestors are not inbred so the $F_i$ terms go away ($1+F_i = 1$). There are two paths of common ancestry (via X and Y), therefore the calculation of the two paths from the father (F) and mother (M) to X and Y is:
$F_{Mick} = \frac12^{n_{F,X}+n_{M,X}+1}(1+F_X)+\frac12^{n_{F,Y}+n_{M,Y}+1}(1+F_Y) $
$F_{Mick} = \frac12^{4+3+1}(1+0)+\frac12^{4+3+1}(1+0) $
$F_{Mick} = \frac{1}{256} + \frac{1}{256} = 0.0078 = 0.78\% $

In a more complex case, such as where ancestor X was inbred, $F_i$ cannot be ignored. In the following example, X's parents were first cousins:
  U ─┬─ V
     │
  ┌──┴──┐
 XGF   XGM
  │     |
  XF─┬─XM
     │
     X ─┬─ Y
        │
     ┌──┴──┐
    GGGF  GGM
     │     │
    GGF    │
     │    GM
    GF     │
     │     │
     F ─┬─ M
        │
       Mick

For this, we must first calculate $F_X$ (i.e. how inbred X is):
$F_X = \frac12^{n_{XF,U}+n_{XM,U}+1}(1+F_U)+\frac12^{n_{XF,V}+n_{XM,V}+1}(1+F_V) $
$F_X = \frac12^{2+2+1}(1+0)+\frac12^{2+2+1}(1+0)$
$F_X = \frac{1}{32} + \frac{1}{32} = 0.0625 = 6.25\% $
Then we can input this $F_X$ into the same calculation as done before for the simple case:
$F_{Mick} = \frac12^{n_{F,X}+n_{M,X}+1}(1+F_X)+\frac12^{n_{F,Y}+n_{M,Y}+1}(1+F_Y) $
$F_{Mick} = \frac12^{4+3+1}(1+0.0625)+\frac12^{4+3+1}(1+0)$
$F_{Mick} = 0.00415 + \frac{1}{256} = 0.0081 = 0.81\% $

A good explanation of these calculations with further examples can be found here: The Coefficient of Inbreeding (F) and its applications. The calculations can get quite complicated even with relatively simple inbreeding.

Thank you for your explanation - but I still don't think you've answered my question. Say we are considering child C and we find a common ancestor A in the family tree of both the mother and father of C. Let us say for simplicity that A is not itself inbred. I know how to calculate all the terms to the right of the sigma in the COI equation for A, so I can add that to the summation... but what about the mother (or father) of A? That will be a common ancestor too. Do I work out everything to the right of the sigma for that too and add that to our summation?

@Mick No, if A is not inbred, then you do not need to add anything for the mother or father of A (because the inbreeding coefficient for A is 0). This is what the first simple example in my answer illustrates (neither X nor Y are inbred).

Ok, I see. I will assume you are correct and give you the green tick. Thank you.


text:
50:50 sugar/fat mixture
A couple of years ago I saw a BBC Horizon television documentary about sugar and fat. One section mentioned three experiments in which rats were given their ordinary rat food plus and unlimited supply of:
Experiment A. Unlimited sugar
Experiment B. Unlimited fat
Experiment C. Unlimited sugar&fat mixed together (50:50)
The stated results were that in experiment A the rats did not put on any weight, in experiment B the rats put on weight but not much and in experiment C they put on loads of weight and would eat the 50:50 mixture to the exclusion of their ordinary food. I also remember the documentary said the 50:50 ratio was critical and if the ratio was shifted too far in either direction then the weight gain effect reduced sharply.
I have two questions. 1. What was the original research paper. and 2. Have there been any related new results with other mixtures like sugar/salt fat/salt?
EDIT: I have just found this related paper. I don't know if its the exact one relied upon by the documentary, but it's certainly close... perhaps the documentary employed the results from multiple papers.
EDIT: You can see the whole documentary here: https://www.dailymotion.com/video/x1arpze - the rat experiment discussion begins around 46 minutes in.
EDIT: years later... I found this and this.

Are you interested in other studies about sugar/fat mixtures or in other foodstoof mixtures?

@Jan: I am interested in any food group mixtures where the combination induces greater calorie consumption than either one in isolation.

OK, you may also make clear what is your exact question. I guess, you are asking for a mechanism by which certain food/combination leads to increased food consumption. Or you just want to stick with the basic facts: this and this food combination --> greater food consumption.

@Jan: Ultimately I am looking for followup research along the same lines. If I knew the exact paper(s) the results presented in the documentary were based on then I could search for papers that referenced the originals.

@xusr: you should put that as an answer rather than a comment - so far it's the best answer I've seen.

1. What was the original research paper?
This one appears close: Hyperphagia in rats produced by a mixture of fat and sugar (PubMed, 1990)

Experimental groups were fed sugar (sucrose), fat (corn oil), or a
  sugar-fat mixture as an option to chow; options were in the form of
  water solutions or emulsions. The control group was fed only chow. The
  sugar-fat group displayed a robust hyperphagia (greater than 36%),
  relative to the control group; the hyperphagic response was greater
  than that observed in the fat group but not in the sugar group. The
  sugar-fat group selected more calories from the option than the other
  two experimental groups. Body weight gains were also greater in the
  sugar-fat group than in the fat and sugar groups. Addition of
  saccharin to the fat emulsion increased fat and total intakes to
  levels close to those of the sugar-fat mixture. In a second
  experiment, the relative palatability of the plain and sweet fat
  emulsions was assessed with two-bottle preference tests. The sugar-fat
  mixture was preferred to the saccharin-fat mixture, which in turn was
  preferred to the plain-fat emulsion. These results suggest that the
  sweetness of the sugar-fat mixture contributed to the pronounced hyperphagia and obesity obtained with this diet option.

2. Have there been any related new results with other mixtures like sugar/salt fat/salt?
A free-choice high-fat high-sugar diet induces changes in arcuate neuropeptide expression that support hyperphagia (PubMed, 2010) (a study in rats)

Our data suggest that the specific combination of saturated fat and
  a 30% sugar solution results in hyperphagia-induced obesity.

Snack food intake in ad libitum fed rats is triggered by the combination of fat and carbohydrates (PubMed Central, 2014)

Thus, it can be concluded that the combination of fat and
  carbohydrates is a major molecular determinant of potato chips
  triggering hedonic hyperphagia.

Fat/carbohydrate ratio but not energy density determines snack food intake and activates brain reward areas (PubMed Central, 2015)

We conclude from our behavioural data that the ratio of fat and
  carbohydrates, but not the absolute energy density, is the major
  determinant of the palatability and intake of snack food during
  short-term two-choice preference tests in rats.

Which Foods May Be Addictive? The Roles of Processing, Fat Content, and Glycemic Load (PubMed Central, 2015) (a human study)

In summary, the current study found that highly processed foods,
  with added amounts of fat and/or refined carbohydrates (e.g., sugar,
  white flour), were most likely to be associated with behavioral
  indicators of addictive-like eating. Additionally, foods with high
  GL [glycemic load)] were especially related to addictive-like eating
  problems for individuals endorsing elevated symptoms of “food
  addiction.”

In conclusion, it can be either a combination of fats and sweetness (due to sugar or non-sugar sweeteners) or a combination of fats and high glycemic carbs (sugar, white flour, potatoes) that can induce overeating.

Thank you. That's exactly the kind of thing I was looking for.

It is easier for the body to use carbohydrates as energy source rather than lipids.
When the food is full of fat, the mouse will use fat as a source of energy and only a little part of it is stored.
Furthermore, when the food is full of sugar, the mouse will use the sugar as source of energy and as above, only little part of it is stored.
When the food ratio is 1:1 sugar and fat, the mouse uses sugar as energy source and stores fat so it gains more weight than the other two.
Salt is not an energy source and cannot be stored in the way sugar and fat is stored.

I think the comments that applied to rocc's answer, also apply to this.

I have to apologize at first, we had that phenomena in a lecture but I am not a native speaker and some of the processes are maybe wrong translated.
Despite the other answers, I have learned that the primary cause has a chemical reason :
Your adipose tissue is made out of triglyceride. When you eat Triglyceride your body won't use them like this. Your body breaks them down and is synthesizing its own triglyceride to be saved as fat tissue. Triglyceride synthesizing  needs glycerol - this is where the phenomena appears : Your body can not use glycerol from food,  it has to use its own synthesized glycerol  from sugars and amino acids. So only if you consume fats and sugars/proteins simultanously your body can transform it into fat tissue.
Short way of fat when you eat it : Triglyceride > Monoglyceride+2 fat acids > if energy is needed those fat acids will be used for metabolism, if no energy is needed your body wants to save those acids for a later moment by resynthesizing them to triglyceride. Your body needs sugar or amino acids for this process.
It seems worthful to mention that other factors propably play a role like  preview answers already mentioned. But the biochemical principle is this one. Another aspect is the efficiancy - it is not mentioned where the amino acids or sugars come from, if they are saved ressources or fresh molecules from food. But if the phenomena doesnt appears - like my professor said - when you seperate those, it seems reasonable to assume that the body won't use stored sugars.
Edit/Sources:
I was trying to get some sources due to request in the comments: The problem that appears to me is that the medicine books,  where this pathway is described,  are not in english at our local library. Since this is a common known pathway in medicine you should be able to find it in every standard biochemistry book for  medical students. But I can give you some keywords:
Lipogenese on Wikipedia, in the introduction the pathway is already mentioned https://en.wikipedia.org/wiki/Fatty_acid_synthesis?wprov=sfla1
This is the pathway in form of a picture from a great german publisher for medical books

I have mentioned that aminoacids can also be used for synthesizing glycerol for triglyceride : https://en.m.wikipedia.org/wiki/Glyceroneogenesis?wprov=sfla1
this is an article I havent read but it seems accurate
https://www.sciencedirect.com/science/article/pii/S1043276008001379
hope these keywords help :)

It would be great if you had some even more official sources that you could reference for further reading.

is the Bounty Still on?

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text:
What does it mean to "map the human genome"
I know some elementary chemistry and biology. I also think I know what a gene is (it's a sequence of DNA which encodes a particular protein). I also know that on a chromosome there are sections of DNA which are kind of junk and do nothing. But being armed with this information, doesn't seem enough for me to understand what it means to "map the human genome".
Some possibilities:

a. It tells me the entire sequences of nucleotides that make up a particular human's chromosomes (it could not possibly do this for humans in general because of course the sequence is different from one human to another).
b. It tells me the entire sequences of nucleotides that make up a human's chromosomes... with some annotations along the lines of "at this point in the molecule, we could optionally have nucleotides A, B or C".
It tells me the start and stop points for each of the genes along the chromosome.
It tells me the function of every gene.
Something completely different!

Suggested edit changing molecules/atoms to nucleotides for accuracy/clarity, DNA is composed of nucleotides, a very specific subset of molecules which are composed of atoms. Molecules are composed of bonded atoms, atomic structure is not of particular interest, but would be inferred from the nucleotide sequence (and could vary for a given Dna sequence depending on pH and DNA modifications).

"Mapping" the genome is ambiguous. Originally it meant making a genetic map, which involved finding the ordering of various genetic markers but not the sequence of nucleotides. Mostly these days people are interested in a genome sequence which is seldom described as "mapping" by researchers.

So, the very first map of the human genome was of a few pooled samples with a single nucleotide called at each position.
This is basically okay, though, because humans are 99.9 (with possibly a few more 9s) % similar to one another. So you can get a lot of broadly-applicable information out of a single individual's DNA.
Further genome-mapping efforts brought data from new individuals and started to give us information about variants, like in your option 1b. At this point, there are projects like the 1000 Genomes Project that are trying to get 1000 full human genomes from a variety of ethnic groups sequenced and to characterize all the common variations.
Your point 2 was a different project, but was also part of mapping the genome. It's mostly complete now-- in that we know almost all of the RNA sequences that are produced by most cell types and mostly where they come from on the genome, with a few mysteries left around the edges.
Point 3-- no. Lots about the genome we still don't know. We're pretty good about where genes are encoded, but how they're regulated, how they interact... and remember that the part of the genome that codes for genes is a very small percentage of the overall sequence. Something like the the ENCODE Project is trying to figure out the various biochemical interactions present at every position of DNA, but even if that data were complete and reliable, which it's not, it still wouldn't tell us the "purpose" of all DNA.
So, when we say we've "mapped" a genome, we generally mean (A) we have (something pretty close to) full sequence of at least one individual's DNA (or a consensus sequence from a pool) and (B) we know where genes are on it. That's a huge step but only the beginning of understanding genetics. In the case of humans, we're adding on to that understanding by learning where variants are and how common they are.

As this answer suggests, mapping the location of known genes to their location in the genomic sequence is a specific (but important) example of genome mapping. More generally, mapping is identifying the location or locations of a sequence or sequences of interest in the genome. This can be genes, transcription factor binding sites, mapping variations in sequences associated with different human populations or with certain diseases, etc.

The sequence from the International Human Genome Sequencing Consortium was actually a mosaic of DNA different donors, not one individual.

Good point, I'll edit. I was thinking of the Celera DNA, which I thought was Venter's, but it turns out that they were using a pool, too. (Venter was just in the pool.)

The Celera genome is indeed mostly from Craig Venter, but this is not true for the HUGO project and today there is more data in it anyways.

InactionPotential raises a very important point. Mapping does not necessarily involve sequencing. There were maps of the human genome long before it was sequenced. There were also maps of other organisms long before sequencing was even invented. Like geographic mapping, genome mapping establishes spatial relationships between "interesting" loci.


text:
Can heritability be deduced from a correlation coefficient?
I am trying to understand the concept of heritability and from what I can gather, the heritability of a factor (say birth weight) must be closely related to the correlation coefficient of that factor when you do a linear regression of the factor between parent (say mother) and child.
So my question is this - is it possible to calculate the heritability from the correlation coefficient, and if so, what is the formula.

No. But a strong correlation may nevertheless be an indicator for heritability (it makes it more likely).
The reason is, that the correlation in the phenotype (birth weight) is not only due a correlation in the genotype but also a correlation in the environment of the child and its mother (culture, economical situation, genes, etc of their respective mothers).
If you were able to remove the association of the environments and of the genotypes and the environments by an intervention (eg. shuffling the zygotes (ideally of parents who were shuffled as zygotes as well)) then the correlation coefficient of the phenotype between one of two parents and the child would be half the heritability. $corr=\frac{1}{2} H^2$

Phenotype ($P$), Genotype ($G$), Environment ($E$)
$P_{parent}=G_{parent}+E_{parent}$
$P_{child}=G_{child}+E_{child}$
$
\begin{eqnarray*}
corr(P_{parent},P_{child}) &=& \frac{COV(P_{parent},P_{child})}{\sqrt{VAR(P_{parent})}\cdot \sqrt{VAR(P_{child})}} \\
&=& \frac{COV(P_{parent},P_{child})}{ VAR(P)}\\
&=& \frac{COV(G_{par}+E_{par},G_{chi}+E_{chi})}{ VAR(P)}\\
&=& \frac{COV(G_{p},G_{c})+ COV(G_{p},E_{c})+ COV(E_{p},G_{c})+ COV(E_{p},E_{c})}{VAR(P)}\\
&=& \frac{\frac{1}{2}VAR(G)+ COV(G_{p},E_{c})+ COV(E_{p},G_{c})+ COV(E_{p},E_{c})}{VAR(P)}\\
&\overset{(1)}{=}& \frac{\frac{1}{2}VAR(G)}{VAR(P)}\\
&\overset{(2)}{=}&\frac{1}{2}H^2
\end{eqnarray*}
$
$(1): \,\,\,$if you managed to get $COV(G_{p},E_{c}), COV(E_{p},G_{c}),COV(E_{p},E_{c}) = 0 $
$(2): \,\,\,H^2=\frac{VAR(G)}{VAR(P)}$ - the definition  of heritability

In other words, the answer is Yes, if you manage to get rid of confounding variables (just like with any correlation)

@Remi.b: so if I could guarantee that the environments were the same for all the animals, then what would the relationship be, between the correlations coefficient (call this cc) and the heritability (call this H2). Would H2 =cc? or H2 = cc squared, or H2= sqrt cc or something else?

Heritability is the slope of the parent-offspring regression. Have a look at wiki > heritability > regression.


text:
Lifetime of secondary messengers such as Calcium or IP3
Can anyone suggest me literature on the lifetime of secondary messengers such as calcium or IP3? A book would be preferred. What I am specifically looking for is a validation that secondary messengers have a certain lifetime and undergo degradation. I need not know specifically how long their lifetime is but rather interested in the fact that they do undergo biodegradation.
[EDIT]: Replaced the word 'biomolecule' by 'secondary messengers' as per the suggestion of @WYSIWYG to narrow down the answer.

The lifetime of Calcium can be considered infinite in biological time scales, it is not a real biomolecule. The half-life time of other biomolecules like IP3, PIP2, receptors, hormones, etc. is species-dependent and within the species strongly depending on the cell and its metabolic state.
Short answer: There is no overview for lifetimes of biomolecules. It is easier to search for a specific molecule in a specific cell. Perhaps you are lucky and somebody measured it.

Update to the comments:
All known second messengers, like Ca2+, IP3, PIP2, change their concentration in response to a stimulus, e.g. activation of muscarinic receptors causes activation of phospholipase C which cleaves PIP2 in DAG and IP3. IP3 causes release of Ca2+. Ca2+ never gets degraded or synthesized but the intracellular concentration changes. PIP2 gets degraded, i.e. its concentration becomes lower, while the concentration of its cleavage products, IP3 and DAG, increases. Those changes are temporary, after removal of the stimulus the 2nd messengers get degraded as well or e.g. Ca2+ is taken up into intracellular compartments.
A general overview about second messengers.

Thank for the info. But is there any book that talks about the lifetimes of biomolecules in general.

I doubt that there is a book in general. There are specific works, e.g. for IP3 and tables for drugs (can be found in most pharmacology books) but I don't recall any table for biomolecules in general. You might be lucky to find info on lipids or hormones in a review but it will require quite some work to compile a table for all biomolecules.

Not a single book that would say that biomolecules have a lifetime. I do not need to know how long the lifetimes are, but just a confirmation that any biomolecule would have a limited lifetime

I think the OP is referring to lifetime of Ca in active levels during a signalling event. Similarly with IP3 (related post). @nashynash clarify the question if that is the case.

If biomolecules would mean second messengers, then the question would be a lot easier to answer :)

@WYSIWYG  Like I stated, I want to know for the general case. I mentioned calcium and IP3 as an example. However, what you pointed out is true. But I still require the general case- lifetime of biomolecules. So I think my question stands correct to what I want.

@Ashafix what is the difference between a biomolecule as a secondary messenger and otherwise. Yes, like wysiwyg pointed out, more specific is about the secondary messenger type of molecules but I was hoping to find a general reference

A second messenger, like Ca2+ or IP3, is produced/released/degraded after a primary messenger, like a hormone, activates a receptor which is usually in the cell membrane. Biomolecules are all types of molecules produced by living organisms.

@nashynash Technically, Calcium can never perish. So your question does not make a lot of sense unless you narrow it down to a situation.

@WYSIWYG Okay. Thanks for the correction. Will narrow down the question.

@Ashafix okay. Thanks for providing the clarification and the update. However, besides the link you provided, can you suggest other sources from where you may or may not have referred to for the update?


text:
Difference between pulse coupling and diffusive coupling In biological oscillators

What are the differences between pulse coupling found among neuron cells and diffusive coupling found in cells that exhibit calcium waves?
Moreover, in both methods, is it a strict requirement that the cells have to be adjacent to each other or at a distance from each other.

I know this is not a mathematical forum, but can anyone answer the next question or at least point out some books/article where I can learn them.

How can we represent pulse and diffusive coupling mathematically?

I don't know what you are referring to in Q1. What calcium waves? Can you give us a reference?

@Memming Intracellular calcium waves. For example

Partial answer:

As for a book on the topic of mathematical modeling of coupled neural oscillators, you can start with:

Wilson, H. R. (1999) Spikes, Decisions & Actions: Dynamical Foundations of Neuroscience, Oxford University Press, Oxford UK. author's copy, amz


text:
DNA strand displacement and Branch migration- the same or different or interrelated?
So, recently I have begun studying DNA strand displacement and then I come across the term 'branch migration' (p.s. I am not a biology major student). What I understand is that branch migration is part of the strand displacement process.
Or is it not? If branch migration is not a part of strand displacement, then what is it?
First, does strand displacement refer to the case where a single-strand
(floating freely) is competing with the incumbent strand to pair with the complementary pair, resulting in the displacement of the incumbent strand?
That means we have one DNA complex and one single-strand in the input and output. And second, does branch migration refers to the case where two DNA complexes exchange strands, resulting in two DNA complexes both in the input and output?
To me, both processes are involved in the displacement of strands (but I can't seem to find their differences).
Can someone kindly explain to me their difference, if there are any?

@MartinKlvana So this confirms to my second statement on branch migration. Will this apply to the first statement as well?


text:
What is delayed compliance in blood vessels?
What I understand is it is a permanent stretch of the vessel wall. Is this true or does it mean something else?

Please start with the tour: https://biology.stackexchange.com/tour and the help section: https://biology.stackexchange.com/help with particular emphasis on asking questions.

First let's consider what compliance means:

C = compliance
ΔV = change in volume
ΔP =  change in pressure

Delayed compliance
The response of a blood vessel to a sudden change in pressure. When the volume and so the pressure highers in the blood vessel the vascualar wall will stretch. As the wall of the vessel stretches the pressure inside the vessel will fall. So an increase of compliance is the result(look at the formula ΔV will get higher because the wall stretching will make the vessel larger at so the volume bigger and the pressure less). this change in compliance is what they call delayed compliance.

I don't really think you can speak about permanent because it's a dynamic process.


text:
Function of the alpha subunit in mitochondrial ATP-synthase?
Within the catalytic core of mitochondrial ATP-synthase there are two different types of subunits; $\alpha$ and $\beta$. From what I have read, the catalytic sites occur only in the $\beta$ subunit so clearly it is in these where ATP is synthesised.
However, I can't find what the function of the $\alpha$ subunit is. A source would be appreciated.

Wikipedia tends to answer your question by this (emphasis mine):

In F-ATPases, there are three copies each of the alpha and beta subunits that form the catalytic core of the F1 complex, while the remaining F1 subunits (gamma, delta, epsilon) form part of the stalks. There is a substrate-binding site on each of the alpha and beta subunits, those on the beta subunits being catalytic, while those on the alpha subunits are regulatory. The alpha and beta subunits form a cylinder that is attached to the central stalk. The alpha/beta subunits undergo a sequence of conformational changes leading to the formation of ATP from ADP, which are induced by the rotation of the gamma subunit, itself is driven by the movement of protons through the F0 complex C subunit.

For above information, wikipedia cites this. I have put some info from it below.
From Introduction:

There are three regions to which ATP is hydrogen bound. First, the so-called Walker or P-loop (residues β-Gly-159-β-Val-164) at the beginning of helix B. Second, the beginning region of helix C, namely β-Arg-189. And third, the residue α-Arg-373 from the α-subunit (see Fig. 1, c–e) (Abrahams et al., 1994). Sequential formation of these 15–20 hydrogen bonds ensures nearly constant force generation throughout the whole duration of the binding transition. This “binding zipper” sequence would lead to the smooth closing motion of the pocket and continuous conformational changes throughout the β-subunit (Oster and Wang, 2000a; Elston et al., 1998; Oster and Wang, 2000b).

In Results:

Fig. 4, a–d provides four representative snapshots of the equilibrated closed and open binding pockets according to our simulations. These show that, in the closed pocket, the ATP molecule is surrounded by all three hydrogen binding regions. By contrast, in the open pocket a space has formed between the P-loop on one side and the helix C and the pocket's α-subunit region on the other side, with a gap between the ATP molecule and the P-loop so that ATP stays close to the α-subunit and helix C regions. An equilibrated intermediate structure where the pocket is half open is shown in Fig. 4 b. In that state the α-phosphate oxygen of ATP is still close to the P-loop, but the distance is already increasing between the β/γ-phosphate oxygens and the P-loop. The phosphate axis has rotated ∼30° and ATP is bridging the pocket. At the end of our simulations (Fig. 4 d), the ATP molecule is located between the two subunits as expected after its primary movement into the binding pocket. In that weak binding state, a newly docked ATP is expected to have contacted the ATPase, but not yet have induced conformational changes. Our simulations are consistent with this expectation. Further, we see that contacts are formed mainly between ATP and Mg2+, and between Mg2+ and the binding pocket.

In Discussion:

The importance of β-Lys-162, β-Arg-189, and α-Arg-373, for example, was connected to their formation of hydrogen bonds with ATP. In our simulations, these residues form the strongest and the last to break hydrogen bonds with the γ-phosphate oxygens. In addition, α-Arg-373 forms a hydrogen bond with one of the α-phosphate oxygens, acting as a restraining force for ATP during the movement of the P-loop and therefore facilitating the migration of the α-phosphate oxygens along the P-loop.

You can find further information here or here.

It's interesting that this source seemingly conflicts with the uniprot and interpro records from @JordiZambrino. I must say I can't find anywhere in that article that explicitly says it acts as a regulator specifically - the α-subunit still sounds to be intimately involved in catalysis.

@James I too couldn't find explanation for alpha subunit's regulatory role. The article justs points out that it helps in stabilising ATP but doesn't say a word about regulation. But since wikipedia clearly states this, so I quoted it to them. Maybe the author of wikipedia article cited wrong article for that line or misinterpreted the conclusion.

Why the downvote??? Please tell me so that I could improve any mistake in the post.

Would you agree that the article you have linked to is basically saying that the $\alpha$ subunit's role is to increase the efficiency of ATP-ase by allowing more locations for hydrogen bonds to form with? (btw the downvote wasn't me :) )

@Quantumspaghettification It seems so from what it (article) says, but it seems to me more that α subunit is for stabilizing ATP inside ATPase. I am continuously searching more details on this.

@Quantumspaghettification http://www.uniprot.org/uniprot/P0ABB0 alongwith many other links, clearly states "The alpha chain is a regulatory subunit." but gives no detail/citation for it. It seems like we don't exactly know its function yet, but someone just said its regulatory and everyone agreed on it. ;)

From: Uniprot

Mitochondrial membrane ATP synthase (F1F0 ATP synthase or Complex V) produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain. F-type ATPases consist of two structural domains, F1 - containing the extramembranous catalytic core, and F0 - containing the membrane proton channel, linked together by a central stalk and a peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F1 is coupled via a rotary mechanism of the central stalk subunits to proton translocation. Subunits alpha and beta form the catalytic core in F1. Rotation of the central stalk against the surrounding alpha3beta3 subunits leads to hydrolysis of ATP in three separate catalytic sites on the beta subunits. Subunit alpha does not bear the catalytic high-affinity ATP-binding sites.

From: InterPro

There is a substrate-binding site on each of the alpha and beta subunits, those on the beta subunits being catalytic, while those on the alpha subunits are regulatory. The alpha-subunit contains a highly conserved adenine-specific non-catalytic nucleotide-binding domain, with a conserved amino acid sequence of Gly-X-X-X-X-Gly-Lys. The alpha and beta subunits form a cylinder that is attached to the central stalk. The alpha/beta subunits undergo a sequence of conformational changes leading to the formation of ATP from ADP, which are induced by the rotation of the gamma subunit, itself is driven by the movement of protons through the F0 complex C subunit [PMID: 12745923].

Sources:

http://www.ebi.ac.uk/interpro/entry/IPR005294
http://www.uniprot.org/uniprot/P25705
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278611/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1679692/

The α- and β-subunits have a similar fold, as would be expected from
  their sequence similarity. All of the α- subunits are bound to the ATP
  analogue AMP–PNP, and the three subunits adopt very similar
  conformations. The three β-subunits, however, are in three
  nucleotide-bound states: the first, termed βTP, has AMP–PNP in the
  catalytic site (FIG. 3c); the second (βDP) has ADP; and the third (βE)
  has no bound nucleotide (FIG. 3c–e). So, the native structure of F1
  looks like a snapshot of the working rotary engine, with three
  reaction chambers representing the moment just after exhaust and
  intake (βΕ), ignition (βDP) and compression (βTP) (BOX 2). The lower
  part of the slightly bowing, asymmetric coiled-coil structure of the
  γ-subunit is displaced towards the βE , forcing the carboxy-terminal
  domain of this β-subunit to swing ~30° downwards. Thus, the βE adopts
  the ‘open’ (O) form, whereas βTP and βDP have the ‘closed’ (C) form.

Yoshida, M., Muneyuki, E., & Hisabori, T. (2001). ATP synthase--a
marvellous rotary engine of the cell. Nature Reviews. Molecular Cell
Biology, 2(9), 669–77. http://doi.org/10.1038/35089509


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IC50 calculation
I am a computer science student and I'm in an internship at a genomics and biotechnologies research institute. My current task is to calculate the IC50 and the EC50 given a set of data as a table.

The thing is, I am required to find a way to automate these calculations, currently working in excel. Which proves to be really difficult for me having no biology background. I have asked around and the people there kindly explained to me what the IC50 is and why it is needed, how the data is gathered, what tools they use to gather it and so on.
My problem though, is that what I need is a way to calculating it. A mathematical way, something I could use to write a formula in excel, or preferably a software I could write.(Once I know how to calculate it)
During my research I found this video on how to calculate the IC50 using an excel macro function, but I do not know if it actually works, having been provided a limited ammount of test data. (I am not sure on how reliable that algorithm is either)
https://www.youtube.com/watch?v=ynMcHziZhvs
Can someone please help me with an actual mathematical way to calculate the IC50/EC50?
My reading seems to not be of very much help no matter how much I try to use the internet's free resources to gather theoretical information about the topic.
Ok the question seems to have been marked as off-topic homework because I didn't present my way of solving it. First of all, it's not homework, it's a work problem I've encountered and need help with. Second, here is my attempt at solving it using an excel Macro

Function HalfWay(Ys As Range) As Double
    Dim pMin As Double, pMax As Double
    pMin = WorksheetFunction.Min(Ys)
    pMax = WorksheetFunction.Max(Ys)
    HalfWay = pMax - (pMax - pMin) / 2
    End Function
Function ECIC(X As Range, Y As Range) As Variant
    Y50=HalfWay(Y)
    Dim iRow1 As Integer, iRow2 As Integer, Asc As Integer, X1 As String, Y1 As String
    If Y.Cells(1, 1) < Y.Cells(2, 1) Then Asc = 1 Else Asc = -1
    iRow1 = WorksheetFunction.Match(Y50, Y, Asc)
    iRow2 = WorksheetFunction.Match(Y50, Y, Asc) + 1
    X1 = X.Cells(iRow1, 1).Address & ":" & X.Cells(iRow2, 1).Address
    Y1 = Y.Cells(iRow1, 1).Address & ":" & Y.Cells(iRow2, 1).Address
    ECIC = WorksheetFunction.Trend(Range(X1), Range(Y1), Y50)
    End Function

This code basically draws a line in memory between the points that are before and after the IC50/EC50 point on the graph and calculates the EC/IC's corresponding concentration based on its actual effectiveness. I am not sure how reliable this method is though.

Hm... Does it answer your question - https://www.youtube.com/watch?v=fMghQw2Ry2c

I'm voting to close this question as off-topic because it is poorly researched. Formula's can be found o'plenty by a simple google search. As a computer-science student, implementing a few numbers into a regression based on a known function should be peanuts.

See wiki pages on  IC50 and EC50.

I have been through that, Ilan, but there's the IP and the SP there that I cannot gather from my data so that's a dead end for me aswell. And thanks for the links AliceD, but I've already gone through them with no significant breaktrough. I mean seriously, who doesn't look at wikipedia first...

Problem with question is that you should ask about biology here, and about programming on StackOverflow. It is two different issues: biological -- how to model, programming -- how to implement.

Again, if you have a model, you should be able to ask how to fit data. Or learn on your own. These are two different issues: fitting/math and model/biology. Is that clear?

I am not voting to reopen - the homework vote to close is not just used for homework (http://biology.stackexchange.com/help/how-to-ask), but those showing poor research effort. You ask for a "mathematical way to calculate the IC50/EC50" - the script you've posted doesn't really show an attempt of self help, try finding the calculations for yourself, then show the maths - not a computer script, and tell us what you don't get. Also as it stands the question is only accessible to those familiar with excel macros

You don't seem to understand me. I have done my fair share of research, meaning 2 days with no actual results. The thing is, I can read all the articles I want, I don't get what they're saying though. Because I have no biology background. And all I can research is following that path which again, yields no results for someone who wants to calculate not know in theory. The reason I'm not posting on Stack overflow is because programming is not my problem here. I don't know what to implement. I know what they all mean, but not how to process the data, what to do with it.

Also, the script uses a virtual graph which is geometry which is math... I don't have what calculations to show besides that, as that's exactly what I'm asking here. How do I calculate. I need to be able to solve it on paper. My mind isn't able to comprehend a process of calculating something just by knowing what it's used for or what it means. I need formulas, statistics, something palpable... Only from there am I able to build my way to the result.

You don't have to post the excel macro. By effort we mean the basic idea or an approach that you have tried or you think is reasonable. The macro would be of no help if you do not explain what approach or analytical methodology are you trying to implement. First step is to understand what IC50 really is. I had answered a similar question in chemistry.SE; you can have a look there.

As I understand, what you really asking is:

What is the mathematical model one can use to fit drug lethality/efficiency data?

With answer to that you can go to stackexchange and bug them for fitting solution in language of your choice.
However, answer to that is quite complicated, it depends on your system and experiment. And also, how well you want to model your observation.
I'd suggest start with something like 4-parameter sigmoid, which in your case will degrade to two-parameter sigmoid: LD50 (shift along X) and steepness (how fast you transition from life to death) with edge cases that are either 0 or 1.
Now, this paper discusses one model (4-parameter sigmoid). It looks roughly like $y=\frac{x}{1+e^{\alpha(x-LD50)}}$, where $\alpha$ is steepness parameter
Another way to do such fit is to use error function. That is an integral of gaussian distribution. I do like that approach (theoretically) because normal distribution is important in data analysis of independent observations, and many random values in biology behave normally.
Let me reiterate. You have to have a model for your data in the first place. Maybe lethality drops down a little after LD50. Maybe you have some other weird stuff. What you can do is to pick a model and then see how well it describes your data.

The drfit and drc packages in R provide tools for such fitting of dose-response curves. Working with these R tools may be more efficient than writing new code or trying to force Excel to do things it really isn't meant to do.

@EdM It is not about what software you are using to implement the model. What is important is to understand or formulate a model and aaaaaa is talking about an example model.

@WYSIWYG : agreed, but the OP seemed so focused on the implementation that I hoped that knowing tools were available would allow more focus on the model.

that is useful, also those pages discuss models.


text:
Can bigger persons generally resist g-forces better?
I've seen a claim that bigger persons generally resist g-forces worse than smaller in an undergraduate biology book. However this claim was supported by the argument that blood has to travel a longer way form the head to the heart.
However, I think this is not the only factor that matters. They generally should have a larger heart, but may need to pump more blood, so perhaps this cancels.
Questions:

Has it ever been tested whether bigger persons generally resist g-forces better? If so, what were the results?
If we only take scale factors in considerations, i.e. we take identical persons, but the one is 1.2 times as large as the other in all dimensions, what conclusion will we reach? What factors should we take into consideration?

You also need to include factors like Muscle/Fat ratios. Like you wouldn't wanna test a small athletic person against an overweight giant,

Has ever what been tested? And which scale factors?

@AliceD I have tried to clarify the question.

There are some good points on high G-forces in this discussion of launch-abort systems [http://space.stackexchange.com/questions/8155/how-hard-is-it-on-the-crew-to-go-through-the-14-gs-of-a-launchpad-abort-of-the]. It is safe to say that within the size range of adult humans, the size of the person is not a very important concern compared to which way (s)he is facing.
In general, though, larger-scaled things fail under lesser forces than smaller-scaled things because strength increases as a square function of linear measurements, whereas masses increase as a cubic function.

What is "g-forces"?? Can you please use standard terminology?

@WYSIWYG G-forces. Feel free to edit the question to add in a more biological correct term.

@wythagoras I don't think the term "g-force" is used in any scientific literature. I am not sure if I am getting too old for this but I have always seen and used "Gravitational force" or "acceleration due to gravity" in such contexts.


text:
Will someone with a double mutation in the allosomes be normal?
Normally a female human has an X allosome from her father and an X allosome form her mother. What if an double mutation happened, which causes that someone has two X allosomes form her mother and no allosomes form her father? Will this person be a normal female?
Note that it is both possible that there are no allosomes form the father or mother (known as Turners syndrome, (45, X)) and that there are two X allosomes form the mother (known as (47, XXX) and (47, XXY) respectively).
Since the Turner syndrome happens for 1 in 5000 births, and the Triple X syndrome happens for 1 in 1000 births, I estimate that this would happen once in 5 million births.

Is your question Can a female (human) be "normal" if her two Xs are exactly the same, that is if she is homozygous at all sites on the allosomes??

@Remi.b I somehow didn't realize that would imply it. Yes that is basically the question, however, I am not sure if there wouldn't be other consequences.

It does not necessarily imply this. If the two Xs come from the mother, then with probability 0.5, she may receive the two different chromosomes (let's assume no recombination for ease). In which case, she wouldn't be any different from her mother for the sex chromosomes. If the two Xs are the exact same then, she will likely suffer from some level of inbreeding depression but she might be fine.

Causality is not causation.  Be careful with 'estimates' like that.

Turner syndrome occurs in about 1 in 2,500 female births.

I agree that there is a theoretical possibility. This post (Chris' answer) should answer this question.


text:
Can plants feel pain?
I was wondering whether plants could feel pain, for example, does grass feel pain when you mow the lawn? Or do the plants and trees that grow vegetables and fruits feel pain when you harvest them?
The internet is very vague about it. There are several articles on the internet, but they just say that plants do not feel pain, they only send out a chemical substance. Others say that almost all multicellular organisms feel pain, because pain is defined as any signal of having impaired tissue.
I think that plants can't feel pain because they have no nerves or central nervous system. However I'm not sure whether this means that plants can't feel pain.
Since the question is clear when pain is defined as any signal of having impaired tissue, I think it would be more interesting in the case that pain is defined as actual discomfort, like humans and animals (maybe it should be restricted to Eumetazoa) feel it.

You'll have to define what you mean by "pain". If you define it as "a signal informing the organism of damage", then yes, they do. If you refer to pain as your or I would feel it, that's a different matter.

Welcome to Biology.SE. The whole issue is around the definition of pain. Tell us what pain is and we'll tell whether plants do have this sensation. I am voting to close as primarily-opinion based.

@terdon I have added the definition.

@Remi.b I've added a definition of pain, but I'm unsure what you mean by primarily-opinion based. Can you clarify?

@wythagoras the Stack Exchange network of sites (to which this site belongs) doesn't do opinion. We're "just the facts, ma'am". A question where multiple answers are valid ("What's your favorite flower") is a bad fit for this site and will be closed as "primarily opinion based". For more on the type of question we deal with, see http://biology.stackexchange.com/help/dont-ask

@terdon No, I mean: Why is this question primarily-opinion based?

I think @Remi.b meant that it was, when it lacked a definition of pain. Now, it's just virtually impossible to answer :). Can anything with no CNS feel pain? Perhaps not but everything alive (just about, and including plants) will try to move away from harm. Does that mean they feel pain?

see here for some more: http://biology.stackexchange.com/questions/29776/how-can-we-know-or-measure-pain-in-animals/29803#29803

I am not quite sure the close vote "primarily-opinion based" is a good fit to this specific case. I definitely meant that the whole question circles around what you mean by pain. It is like asking "is a squirrel a big animal?", it depends on what you mean by big.

You suggest to define pain as any signal of having impaired tissue. This seems like a perfectly valid definition to me. It seems a bit counter-intuitive but it is valid. I'd suggest to restrict your last paragraph to this specific discussion instead and to get rid of the term pain to say "sensing impaired tissue" instead. It might interest you to open a post on Philosophy.SE to ask for definitions of pain that would be easily apply to any living things.

I think before discussing "pain", we'd probably have to discuss whether plants actually can "feel".
This is also down to how one wants to define this (hence "opinion based"), but I assume most people (?) would equal the lack of a brain/neurons with the lack of the capability to feel. And I presume so do you, as you show by using the tag "neuroscience".
In which case the answer to your question "Can plants feel pain?" is "no", regardless of whether plants react to damage through the release of chemicals or not, and whether one would like to classify this as "pain" or not.


text:
Formula for number of divisions required to form x number of cells (Mitosis and Meiosis)
In case of Mitotic Division, we say that if the total number of cells formed by mitotic divisions are $x$, then counting from the first cell onwards, we get $x-1$ divisions ($N$)
$N = x-1$
This is fairly logical to me

However, to find total number of meiotic divisions for $x$ cells, we use the formula
$x/4$ (In questions where we are supposed to find total number of divisions required for forming some number of seeds or pollen grains)
Shouldn't the formula be $N = (x-1)/3$ (Using the same logic as used for the mitosis formula)?

there will always be even number of cells unless a daughter cell has not divided. Binary fission/continuous mitosis will yield 2^n cells after n divisions

For a male, one primary spermatocyte produces two secondary spermatocytes through meiosis I, which in turn produce two spermatids each through meiosis II. So one primary spermatocyte produces four spermatids. That means that $x$ spermatids are produced after $x/4$ meiotic divisions consisting of once meiosis I and twice meiosis II.
However, we don't count the first cell here because a primary spermatocyte is fundamentally different form a spermatid. So in meiosis, the first cell isn't counted, and four new cells are produced.
In mitosis, we do count the first cell. Note that there are two cells produced form one, so there is only one new cell. Hence we get the formula $x-1$.


text:
Missing 4 $\ce{H_2O}$ (per glucose) in Cellular Respiration... Where can they be?
I having trouble understanding the equation of the cellular respiration. The thing that bothers me is the number of $\ce{H_2O}$ molecules. Generally, cellular respiration is written thus :
$\ce{C_6H_{12}O_6 + 6O_2 + 6H_2O -> 6CO_2 + 12H_2O}$
Yet studying the reaction on a molecular level, I realized that the water molecules just don't add up to be six! (on the left side) What I obtained from my textbook and Wikipedia is that (per 1 glucose molecule)

(Glycolysis) (in the reaction that 2-Phosphoglycerate(2PG) forms Phosphoenolpyruvate(PEP)) 2 molecules of $\ce{H_2O}$ are out of the reaction
(TCA cycle) (in the reaction that combines Oxaloacetate and Acetyl-CoA to form Citrate) 2 molecules of $\ce{H_2O}$ are into the reaction
(TCA cycle) (in the reaction that Citrate form Cis-Aconitate) 2 molecules of $\ce{H_2O}$ are out of the reaction
(TCA cycle) (in the reaction that Cis-Aconitate form D-Isocitrate) 2 molecules of $\ce{H_2O}$ are into the reaction
(TCA cycle) (in the reaction from Fumarate to Malate) 2 molecules of $\ce{H_2O}$ are into the reaction

These sums up to a net of (only) 2 molecules of $\ce{H_2O}$ into the process of glycolysis and TCA cycle... additional 6 molecules of $\ce{H_2O}$ comes from oxidative phosphorylation. Then, where can the remaining 4 molecules of $\ce{H_2O}$ possibly be?

Can you point to a source that uses the equation in that form? Everywhere that I have looked has no water on the LHS and 6 water on the RHS, and that is the equation that I'm familiar with. Incidentally in your accounting you missed the loss of 1 water at the aldolase step I believe.

My (possibly) outdated school textbook states the equation like what I wrote before... but I don't think it's trustworthy.(It's weird in many ways) I think the equation with only 6 water molecules is correct. So,(may I ask) is there a water molecule used in the aldolase step? two of them?

@AlanBoyd, I don't think H2O is involved in the aldolase reaction. Aldolase is a lyase, not a hydrolase; see  http://www.chem.qmul.ac.uk/iubmb/enzyme/EC4/1/2/13.html

First thing to make clear is that net $6 \, \ce{H_2O}$ go out of the reaction.($12 \,\ce{H_2O}-6\,\ce{H_2O}$)
Let me tell you my calculation, you should then be able to figure out what went wrong.
For the Left hand Side, $6\,\ce{H_2O}$ are accounted here :

$2\,\ce{H_2O}$ go in conversion of 2-Phosphoglycertae to phosphoenolpyruvate.
$2\,\ce{H_2O}$ in TCA from conversion of Oxoloacetate to Citrat by combining with Acetyl CoA.(One for each Acetyl CoA molecule)
The aconitase -cis-aconitase-isocitrate water molecules cancel out. Equal no go in and out.
$2\,\ce{H_2O}$ in TCA from conversion of fumarate to Malate.

For the right hnd side, if we calculate the no. of NADH formed = 10 and assume that each participates in respiratory chain, we have $10\,\ce{H_2O}$ from there. The other $2$ will be from the $2$ FADH produced.
So we have 6 on the LHS and 12 on the RHS. Hope this makes sense !

I'm afraid that per a NADH or a FADH2, these yield only 2 electrons, reducing only 1/2 water molecule. So, only 6H2O produced at the respiratory chain

@ChanheeJeong, No, 2 electrons reduce 1/2 O2 molecule, so forms 1 H2O. So this answer is correct I think.


text:
What is topological crossover?
I read about "topological crossover" in this paper, Table 1. What does this refer to?

The link is currently dead. Can you add a full reference, explain what the article is about and exactly how you find it unclear.

@fileunderwater - The link is functional

@ChrisStronks Not for me: "Error: Sorry, your request can't be processed due to a system problem.". Questions must be more self-contained either way, and not depend on a single link to be understandable.

ScienceDirect has accessibility issues lately. The table is rather large and the captions totally uninformative. I scanned the article link and I really dunno what topological crossovers are. It seems to be some sort of aminoacid inverted tandem repeats. I think it's an interesting question actually.

The DOI is doi:10.1016/j.ijmm.2014.12.010. For those with access issues (it's an open-access article), I put a PDF in my Dropbox here.

You may not want to know. It really depends on how good your math background is.

A topological crossover is a class of representation independent operators that are well defined once a notion of distance over the solution space is defined [1].

Let's first start with the definition of Topology.

Topology is the mathematical study of shapes and topological spaces. It is an area of mathematics concerned with the properties of space that are preserved under continuous deformations including stretching and bending, but not tearing or gluing. This includes such properties as connectedness, continuity and boundary [2].

Later on in the paper they start to mention transverse topology which leads to Differential Geometry.

In mathematics, transversality is a notion that describes how spaces can intersect; transversality can be seen as the "opposite" of tangency, and plays a role in general position. It formalizes the idea of a generic intersection in differential topology. It is defined by considering the linearizations of the intersecting spaces at the points of intersection [3].

To understand the underlining math concepts of this paper, you may need a rigorous background in mathematics. I would check the authors backgrounds to see if they are Physicists or Mathematicians.
Most students in mathematics generally take two courses in introductory real analysis and at least one course in abstract algebra before taking topology. The standard book for a first course in topology is by Munkres.
A book you may want to look into is Topology in Molecular Biology. However, the author is a mathematician, so if you are not, you may need to start with courses in analysis, topology, differential geometry before you tackle this book. I have never seen the book so I don't know how difficult it will be but here is the about the author from amazon:

M.Monastyrsky is a professor of mathematics and theoretical physics
  at the Institute of Theoretical and Experimental Physics, Moscow, Russia,
  graduated the mathematical department of Moscow state university(1967),
  author of numerous papers in diferent fields of mathematics and
  theoretical physics including the monograph :Topology in Gauge Fields
  and Condensed Matter (Plenum,1993 ) and two other books:Riemann,Topology
  Physics, Birkhauser, Boston, 1999, 2nd ed. and Modern mathematics in the
  light of Fields medals, AKPeters, 1997.I gave invited plenary talks on
  many conferences and was the visiting professor of many universities
  and institutes including IAS(Princeton), Harvard, Princeton and Yale
  Universities (USA), Cambridge and Oxford Universities (Great Britain),
  IHES and Universite de Paris (France).

Helpful answer. Seems I would have to invest some time trying to understand this.

authors: 24 ณิชานันทน์ อภิพัฒนะมนตรี


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Identify ~6-7mm long green creature

Here is the creature I found on the glass lid of my light bulb. I guess they are attracted to light as they all concentrate on the light source. I live in Hong Kong. The brown things aren't moving (those might be eggs). The green creatures are about 0.6-0.7 cm long in body length (excluding appendages and antennae). They are sluggish in movement.
Can you help me to identify these tiny creatures?

Welcome to Biology.SE. Can you please try to add some information. For example: Where do you live? What size are those? Can you tel us more about their behaviour? Are the browns things alive or is food or is it just stain on your light bulb?

I don't have much information about it. My mum fear it will spread and so I clear them away immediately after I take the photo. I live in hong kong. They are about the size in the original photo here (no magnification). And the brown, oval things I suppose are their eggs. They are sluggish in movement and I clear them easily. The eggs are kind of sticky.

I edited your post to include those info and make few other modifications. Feel free to rollback if you don't like my edits. +1

This is the first time I use this platform to post question. Thanks for your kind help.

Yep, I know that feeling! This is all good! Thanks for the extra info. I personally have no idea what it could be but I am not a good naturalist!

I see 14 eggs and 14 individuals They must have just hatched, which will make identification very difficult.  Maybe Miridae ?

Good observation. So one likely possibility is their adult form can fly and it reach the light bulb to lay the eggs. The larvae hatched and it seems it was an unsuitable environment for them and so they appear sluggish.

Based on its morphology, it should be evolutionarily adapted to living in aquatic environment I guess.

I have no idea what they are, but they are fascinating looking and rather beautiful in their way. Thanks for sharing.

This is an insect (6 legs) and a seems like a nymph (hatchlings that are not larval); if they really are hatchlings. There are a few family of insects that hatch this way. You may have a look at them. Seems like green mirid but could be baby crickets too (I am not an expert in this area).

Let's take a look at the magnified body of the insect (it is a nymphe btw) - we can see 2 brown dots one above the other along the body line. This pattern is very suggestive to Chelinidea species (the most common is Chelinidea vittiger aequoris):

I stop my search at Coreidae family, because multiple species (a lot of bugs actually) of this family have similar appearance, for example:
Gonocerus acuteangulatus:

But other enthusiasts can start from here (Coreidae family) and trace it down more precisely - I am sure they will succeed.

Thanks for your answer. It is very helpful. I will research on it further to evaluate this possibility.


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Can virus survive dessication (and come back functional after rewetting)?
I am thinking of ideas for disinfection that can be done by the average person. So, this is one question I have: Can a material/surface be effectively disinfected (I am more interested in virus) by drying using low/medium heat + wind (or any other less thermally-intensive means)? Would the virus be only temporarily inactivated and is able to come back functional?

Viruses that are protected by a protein shell (non-enveloped) like adenoviruses, rotaviruses, and hepatitis A virus can survive dessication for a while. This paper showed adenovirus remained clinically infectious after 28 days on smooth surfaces, and this paper found around 1% of human rotavirus and hepatitis A virus survived after 60 days.
Other viruses might survive dessication even longer, these are just the ones I looked into.
Regarding rewetting, any test for virus survival will re-wet the virus.

No exactly related to surfaces, but in terms of killing viruses via heat, a study from a few years ago looked at the time required for inactivation of various Alphaviruses in blood serum samples at 56°C, finding that it could take anywhere from 20 min to 2 hrs [1]
If you're looking for ways that the average person can disinfect surfaces, some fairly common consumer disinfectants are actually already capable of killing certain types of viruses (e.g. Dettol claim that some of their products kill influenza, coronavirus, RSV, etc. [2])
[1] Park, S.L., Huang, Y.-J.S., Hsu, W.-W., Hettenbach, S.M., Higgs, S., and Vanlandingham, D.L. (2016). Virus-specific thermostability and heat inactivation profiles of alphaviruses. Journal of Virological Methods 234, 152–155. https://doi.org/10.1016/j.jviromet.2016.04.004
[2] https://www.dettol.com.ng/products-old/see-all-products/

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


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What is the most readily usable form of nutrients/energy source for heterotrophic microorganism in general?
Consider a nutritious mixture containing abundant soluble sugars, soluble lipids and soluble protein etc. Would heterotrophic microbes preferentially use sugars first > lipids > proteins > insoluble polymer such as cellulose (please propose your own order if this is wrong)? If appropriate, you can further differentiate these compounds into e.g. sugars into monosaccharides and oligosaccharides. Is there a general trend or is it highly variable depending on the particular microbe concerned?

Thx, I edited the question


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Can microbes become "overweight"?
Just out of some weird thoughts, can a microbe (any single-celled organisms, accepting answers for both prokaryotes and eukaryotes) ingest too much food (e.g. via absorbing too much involuntarily because the surrounding has too much of it,or via phagocytosis) and retain part of it somehow?
Being "overweight" can be characterized by larger than average cell size/mass, presence of numerous intracellular food reserves (like glycogen?). I am guessing these (increasing cell mass and food reserves) would likely happen to some extent. But do these changes affect reproductive fitness (readiness to cell division) of the microbe? (In humans, we can safely say that being overweight is detrimental to reproductive fitness.)
For instance, What would happen when microbes are over-supplied with energy-rich and carbon-rich molecules but not the other nutrients (e.g.NPK)? And once it is switched back to a "stoichiometrically/nutritionally normal" diet, would it likely have a higher/lower reproductive fitness (compared to microbes normally-fed the whole time)?

what have found yourself? That will help focus your question and guide answers

Well, it is hard to find any relevant experimental information (if that's what you meant) because studies of stoichiometric imbalance in microbes are mostly done in the sense of "lacking" rather than "surplus". This question is rather "unusual" as such so it warrants a more "exploratory attitude". I welcome theoretical answers that explore possibilities and not having concrete evidence as well.


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Has there ever been an approved viral infection treatment method based on the physical/mechanical properties of virus?
I imagined that typical cells and viruses could have very different physical properties or reactions to mechanical stresses, which makes selective targetting possible. For instance, some  major differences between viruses and animal cells:

Difference in size/mass
Difference in elasticity (lack of cytosol in virus)
Difference in structural composition results in a different reaction in response to different vibrational frequencies

Preliminary search found something related to microwave absorption induced oscillation mode fracturing airborne virus, taking advantage of the (structural) core-shell charge separation in virus (not sure if I described the principle right, to be honest). However, though looks exciting, it is more like a disinfection rather than a treatment method. So the question goes: Has there ever been an approved viral infection treatment method based on the physical/mechanical properties of virus?


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Examples of healthy lifelong asymptomatic carrier of a severe infectious disease?
I am curious, is there any known disease/infection that is very severe normally (patient suffers greatly and die easily without medical treatment), but ends up having little to no effect on the lives of asymptomatic carriers? I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

I think this question is probably strongly misguided. For now I've given it a downvote; better research and focus might encourage me to change my mind on that. But as-is, it seems too contaminated with misunderstanding of both evolution and disease.

Research needed aside, in what way it is misguided? Isnt it just asking for a possibility (a possible example and possible reason behind)? And I am not quite sure I like the way you are judging it by "probably" and "seem", without giving any actual reason.

@ychung What I meant is that there are underlying assumptions, not contained in the question, that are wrong. One important one is how evolution works, which has now been covered a bit in the answer by user1850479. Another is the relationship between symptoms and transmission. An asymptomatic individual may carry a disease longer, but that doesn't mean they transmit it more than someone symptomatic, even if that person dies.

You are generalizing my view, fighting a strawman. I said "certain" symptoms (in response to a particular infection/pattern of infection) that make an individual suffer and die, could have evolutionary advantage in stopping an infectious disease that could harm the greater good of the species.

@ Bryan I really dont get why you guys are saying my understanding of evolution is wrong? So, how are you disproving that it is not possible certain mechanism could develop within the population to stop infectious disease while sacrificing individuals (as a consequence I insist)?

@BryanKrause, I think you misunderstood the question.  The OP is suggesting that there may be an evolutionary advantage to displaying symptoms of severe infectious disease, (presumably because it would alert and thus benefit close relatives of the sick individual).

The current Covid19 plague may be an example: it appears that most carriers in certain slices of the population may be asymptomatic (young people in particular) but able to transmit the virus.

@Dirigible Please don’t answer questions in comments. There is a specific injunction against it in every comment box on every Stack Exchange site because doing so breaks the model on which Stack Exchange was founded.

I am curious, is there any known disease/infection that is very severe normally, but ends up having little to no effect on the lives of asymptomatic carriers?

HIV is an obvious example, where so-called "long-term nonprogressors" successfully suppress HIV replication sufficiently that they do not develop AIDS but are unable to clear the infection entirely [1].

patient suffers greatly and die easily without medical treatment

Since the comments below seem to suggest that HIV does not cause death without medical treatment, I'll point out that this is incorrect.  Over 30 million people have died from HIV infection.

I am asking this as I am thinking whether this means certain disease symptoms are evolutionarily wired to protect the "greater good"

It does not.  Selection happens on individuals and not whole species, so the greater good is irrelevant.  Asymptomatic infection is a point on the spectrum of possible responses to infection between sterilizing immunity and death. Individuals who are chronically infected mount enough of an immune response to control the infection but not enough to completely clear it.  In the case of HIV, they are typically people who have exceptionally strong immune responses to a normally lethal virus.
Edit
The comments below suggest a deep misunderstanding of evolution. Since I think these are really the core of your question, I'll address them here.

If traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today.

Which individuals reproduce is the sole determinant of which genes are passed down to the next generation.  This is because the genetics of each individual are determined at conception, and cannot be changed.  Hence, reproduction alone determines the traits of the next generation.
To quote wikipedia[2]:

Evolution is change in the heritable characteristics of biological populations over successive generations. These characteristics are the expressions of genes that are passed on from parent to offspring during reproduction. Different characteristics tend to exist within any given population as a result of mutation, genetic recombination and other sources of genetic variation. Evolution occurs when evolutionary processes such as natural selection (including sexual selection) and genetic drift act on this variation, resulting in certain characteristics becoming more common or rare within a population

Evolution is the process by which some traits are passed down to the next generation while others are not though the mechanisms of selection (e.g. individuals with harmful traits dying) and genetic drift (e.g. random chance).

Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

This is exactly what happens if you put a lot of fast reproducing bacteria in a closed environment with limited resources.  They will all eventually die.
You seem to be thinking of evolution as something that intelligently looks out for the wellbeing of species.  This is not the case.  Evolution is a random process by which different amounts of reproduction and survival between individuals alters the composition of the succeeding generations. As a random, emergent process it has no goals, no intelligence, and no sense of "good".  Rather, it simply happens as a result of individuals reproducing.  This frequently does lead to extinction, as evidenced by the fact that the vast majority of species no longer exist.
(1) https://academic.oup.com/cid/article/51/2/239/303856
(1) https://en.wikipedia.org/wiki/Evolution

Thank you for the answer! HIV is an interesting case definitely. However, the severity of AIDS as I understood come from accumulating infections from other pathogens, not the immune response/symptoms to HIV itself which is kind of chronic (I may be wrong). I also disagree with the notion "Selection happens on individuals" makes greater good irrelevant. Even if a stressor act on individuals apparently, it could produce a trait that improves greater good. You can argue the evolution of "dying" is exactly for the greater good. In some diseases, acute symptoms can definitely make you "die faster".

@ychung Long-term nonprogressors are so called because they do not progress to AIDS.

@ychung The greater good is irrelevant to selection.  Traits may or may not improve whatever you consider to be "good", but selection does not care about that. Some more reading about what selection is may help you understand that point better.

My first point is trying to say that HIV/AIDS is not really what I am looking for in the question (thank you for the answer tho). Second point I disagree. Just think about it, traits can definitely be selected in the direction to preserve greater good in the face of large-scale and amplifying stressor (based on population size). Whether "selection does not care about" or not is not important, the consequence is.

@ychung Edit your question to clarify what you're looking for.  Second point: selection is the process by which individuals either reproduce or do not reproduce. A trait might act on the greater good by accident (see genetic drift), but such traits cannot be selected for. Since you have questions, what selection can and cannot do may be a good topic for a second question.

Typhoid Mary is a good example I am looking for. 2) By-product/ accident or not etc., it is the result that matters. You are not quite understanding what I am trying to say. Think large-scale, think density-dependent stressor, if traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today. Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

Similar things can be hypothesized for a hypothetical infectious disease, the denser the infected individuals (which without the "immune reaction" would otherwise die slowly and able to infect many more people), the higher chance the population will go extinct in the long-run.

I dont think any of the point about evolution disprove what I say (I have never said  evolution as something that intelligently looks out for the wellbeing of species), I said it could happen as a consequence. So, how are you disproving that it is not possible certain mechanism could develop within the population to stop infectious disease while sacrificing individuals (as a consequence I insist)? I dont really get what you are trying to disprove me and saying I misunderstood evolution.

I meant HIV/AIDS patient die not because of things arise from HIV infection solely, it is complicated from infection of other pathogens. (Which makes it not exactly what I was trying to ask for.) Thanks for the answer but you seem to be misinterpreting me all the time...

@ychung If you don't want to be misinterpreted, you can edit your post above to reflect your intended question.

@user1850479, there are many, many examples to contradict your statement that " Selection happens on individuals".  Evolution of altruistic and cooperative behaviors are examples.  Warning colors on toxic butterflies and amphibians are also examples.  Yes, the bright colors of a poison frog deter predators from eating the frog.  But that didn't directly help the first frogs to display those colors: they were eaten and killed by predators who were not repelled by those colors.  It "trained" predators to avoid that frogs' close relatives.

@S.McGrew Selection is one process that can change the traits of an organism, but it is not the only one. Consequently, pointing out the existence of any particular trait doesn't disprove the existence of natural selection.

Where did you get the idea that anyone is arguing against the existence of natural selection?

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.  You listed examples that you believe "contradict" this such as the evolution of cooperative behavior. My point is that other processes can change phenotype besides selection, and so your examples are not necessarily inconsistent with natural selection.

"Yes" is the simple answer to the first part of your question.  HIV, "Typhoid Mary", maybe Covid19, and other examples have been given.
The second part of your question,

I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

is good, but doesn't have a definite answer as far as I know.  However, your idea is certainly plausible.  Although displaying symptoms (e.g., a rash, cough, odd behavior, or bad odor) will not benefit the individual, it will benefit individuals who are repelled by those symptoms.  In cases where individuals who have a tendency to be repelled by the symptoms also have a tendency to display those symptoms (and those tendencies are encoded genetically), close relatives of those individuals have a distinct selective advantage over other individuals in the population who do not have a tendency to be repelled.
A lot of literature relating to this idea can be found by searching "evolution of altruism" and "kin selection".

Thank you for your answer! Displaying horrible symptoms to repel other individuals in the species is definitely one plausible mechanism that can reduce the transmission of pathogens.

Take note though that the two (displaying symptoms and being repelled by the symptoms) need to become coupled through selective processes, of which kin selection is the most effective.

Here is an example of the opposite: tuberculosis apparently evolved the ability to enhance its own spread by inducing symptoms: coughing. https://m.medicalxpress.com/news/2020-03-tuberculosis-bacteria-trigger.html

Yeah, that's why I said symptoms killing the patient (which in itself constitute a severe warning to other members of the species) is a more "direct" mechanism to stop transmission.

That's not quite what I meant.  It can be a co-evolutionary process.  A microbe can evolve to cause symptoms that help spread it; a species can evolve to respond to a microbe by displaying scary symptoms;  it's even possible for a species to respond to the microbe by suppressing the symptoms that help the microbe spread.

Yes, I know what you are saying. There are many different possibilities indeed.  For all the different immune response-pathogen combinations possible, it is the end result of a co-evolutionary arm race with some trickery and mimicry mixed within.

But I tilt it to humans as the main subject of evolution here because I think early humans evolve mainly by being killed and survival given that prehistoric humans live in tribes or isolated populations, only the tribe that has the right traits perpetuate. Whereas virus evolution has a whole lot of other mechanisms (like its inherent high mutation), many cases a virus may just be an opportunist capitalizes on a human trait when it hasnt even co-evolved with humans that long. (that's why I insist it is the pattern of infection, not the actual virus that matters)

It's plausible.  You should put together a mathematical model (that's "falsifiable") and see how well it fits.  The model should allow for other answers too, and compare how well they fot relative to each other.  And, just to complicate things, all of the varoius evolutionary processes are probably going on simultaneously!

Well I can only hope I have the required expertise :( Unfortunately, I do biogeochemical modeling instead. Maybe someday an evolutionary biologist will stumble upon this thread :)

It might be a fun and educational exercise for you anyway, even though you don't have experience in this field.  Important contributions to a field are often made by smart people who come in from another field with a fresh perspective.


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Why babies cry after they are born?
Well I have noticed that almost all of the babies cry after birth, but some of them (1 to 1,000,000? births) don't cry. So, we have:

Why is this happening (the cry after birth)?
Also why animals babies don't cry when they are born, but human babies cry? I have noticed that many mammals such as giraffes or chimps don't cry at all (The chimp only makes it's ordinary sounds).
Are there any special genes that humans have and animals not?

Lots of baby animals "cry" after they are born, everything from puppies to calves often vocalize when born

Crying keeps lungs dry by increasing alveolar air pressure, which otherwise is fatal.

I don't know if you have ever witnessed one, but childbirth is a rather extreme and violent expierence, were the child is pushed through something that is a bit to small for its head. That alone would be reason enough to cry. And crying has indeed a function for the lungs, as explained by JM97

Mouse pups chirp to communicate with their dame. However most of the they make are at frequencies far higher than a human ear can hear.

Having delivered at least a hundred babies, I guarantee you that your statistic is wrong. As long as the baby is breathing, the fluid in the lungs will be resorbed. Still, usually they are cold and wet and under bright lights when delivered. The more you mitigate this harsh new environment, the more peaceful the birth can be. Some babies don't cry at all. If everything else is ok (color, muscle tone, heart rate, etc.), it's no biggie.

So, you believe that they cry because of that change?

Just saw a water delivery, and the baby spoke briefly to say hi, he didn't cry. https://www.youtube.com/watch?v=U2AIRNxTFjk Depends how tight the bird is too. sometimes it's only like going down a airplane escalator for the baby.

I don't disagree with answers that talk about lung function. But a scream would do the same thing. About whether humans are unique, in terms of care they are among the most helpless of animals. Crying in babies is a form of communication that calls the parents into action when care is needed. In the first moments of life in the light and air, besides the shock of being squeezed through an opening so small that the skull is squeezed into a different shape (ouch), an infant urgently needs care.

This water  baby delivery did not cry, it practically only spoke. https://www.youtube.com/watch?v=U2AIRNxTFjk

I'm answering this question (mostly) based on prior knowledge.
Inside the womb, the foetus relies on the mother for oxygen i.e. it receives oxygen from the mother's bloodstream via the umbilical cord.  A foetus doesn't use its lungs for breathing inside the womb. Ever.
Besides, lungs of a foetus are considered fully matured no earlier than the 36th week of pregnancy. (Though there are exceptions to this)

During fetal life the baby's lungs are filled with fluid and they do not perform any respiratory functions. [1]

At birth, the baby is forced to breath on its own for the first time. Hence, the baby cries - or more precisely - gasps for air.
This 'cry' of the baby is actually a strong respiratory effort, thereby aiding the baby in its first breath. This is also why newborns don't produce tears on their first cry. Because it's not really a cry, it's a gasp for air.
Now the reason why such a considerable effort is required for the newborn to breathe is because:
A) Lungs are being used for the first time, and
B) The lungs of a foetus are filled with amniotic fluid when it's inside the womb. Effort is needed to push this fluid out from the lungs after birth.
I'm not aware if there's any genetics involved in this. I don't think there is.
Source: [1] http://www.thehindu.com/todays-paper/tp-features/tp-sci-tech-and-agri/babys-first-cry/article2267767.ece


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What is the resting human stomach pH?
This article in ThoughtCo.com claims we have a resting stomach pH of 4-5.
Unfortunately, there are no references, so I can't verify what it says.
I am slightly confused, however. The study says
"Results are given as medians and interquartile ranges: fasted gastric pH, 1.3 (1.1-1.6); gastric pH during the meal, 4.9 (3.9-5.5)"
This other one says
"In the fasted state, the median gastric pH was 1.7"
This article in UCSB Scienceline says "The normal human stomach has a pH which can range from approximately 1-3 but is usually closer to 2.". Unfortunately, they too don't provide any references, so I can't check their claim.
So what is the pH of a human stomach at rest? If it is about 2, then did the article in ThoughtCo.com get it wrong? If it is about 4-5, then what did I misunderstand in the two studies I cited?

It feels to me like your two papers answered your question. The pH of fasted stomach as around 1.1 - 1.8 and it is around 3.9 - 5.5 during a meal.

What confuses me is why the ThoughtCo article says we have a resting pH of 4-5

It is not a peer review document so they might as well say anything 2. I don't where they got these numbers from but it actually match well with the 3.9 - 5.5 estimates of Russel et al. 1993 that you found.

true, but I thought ThoughtCo was a generally respected website, so I was surprised to see them get something wrong. 2. yes, they match well, but seem to be reversed: Russel et al. says our stomach pH is approx 1-2 fasted and 4-5 during a meal, while ThoughtCo say it's 4-5 at rest (I guess they mean 'fasted'?) and 1-2 after a meal.


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Why are the shells of birds' eggs fragile but not those of other creatures?
In my limited  understanding, eggs of oviparous creatures other than birds have a flexible outer membrane.
Is there any obvious reason that bird eggs should have fragile shells?

Notes

I'm asking why birds seem to be a special case. If all other oviparians manage perfectly well without shells, what is it about being a bird that requires the extra resources to form a shell?

I believe birds are considered to be modern-day dinosaurs. Didn't dinosaurs have leathery eggs?

Well, the birds have to be able to get out of them, don't they?  Can a leathery egg withstand an adult bird sitting on it?

@swbarnes2 - (1) All oviparous species have to get out of the egg (2) I don't know if a leathery egg will withstand being sat on. However, birds are not very heavy and I don't think they put all their weight on the egg - they also use their feet and legs  to support themselves.

Bird egg shells are actually pretty strong.  Although they can break from a concentrated blow (cracking an egg) they resist distributed pressure, as from the parent sitting on eggs, quite well.  Do any of the other creatures with leathery/flexible egg casings actually sit on their eggs?

I don't understand the question. How e.g. frog eggs are more resistant?

@Exocytosis - (1) A table-tennis ball is easily squashed and will not recover its shape. A hollow rubber ball can be squashed and recover its shape. Similarly with eggs. Both types of squashing may or may not damage the embryo, however the hard shell, once broken, will allow the ingress of bacteria and viruses. (2) Frogs survive as a species, so their eggs must have sufficient resistance.

I am not sure their deformability really makes frog eggs less fragile than birds' ones. There are clearly a lot of factors involved in an egg durability. And your second statement seems irrelevant to me since birds survive as a species too "so their eggs must have sufficient resistance". Feel free to clarify though.

@Exocytosis - I'm asking why birds seem to be a special case. If all other oviparians manage perfectly well without shells, what is it about being a bird that requires the extra resources to form a shell? Does it help the hen to fly better?

https://en.wikipedia.org/wiki/DDT#Eggshell_thinning may be relevant.

@chasly - supports Monica: The difference between frogs and birds is that most frogs lay many more eggs - up to 10,000 or more at a time, for some species.  So it really doesn't matter if some of them get squashed.  Birds lay relatively few eggs, and incubate them.

Your question is, I think, based upon a false presumption: that avian eggs are more fragile than those of other oviparous animals.
The paper Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds1 suggests that increased calcification of the avian eggshell is an evolutionary response to protect against predation and microorganisms, particularly in soil. The trade off was less permeability and water absorption. To offset that "cost," birds' eggs evolved the albumen or "egg white" which adds liquid content.
This is discussed more (and referenced) in Frank B. Gill's Ornithology2, which goes on to further explain that the shells additionally protect eggs from the weight of incubating parents.
Other functions, such as that of oxygen exchange, are permitted by the calcium shell due to microscopic pores. Also, crystalline calcite (the main ingredient of the shell) can be used by the embryo to form calcium in development of its bones.
1 Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds by Gary C Packard and Mary J Packard; American Zoologist, Volume 20, Issue 2, May 1980, Pages 351–362
2 Gill, Frank B.. Ornithology. United Kingdom: W. H. Freeman, 2007.