text:
Names and abbreviations in biology
After one year in college, I am quite surprised with the number of different abbreviations used in biology for the same thing.
I wonder if there are any rules for naming something new in biology, for example new genes, or if it is just up to the researchers without restriction?  If there are rules, how did the confusion arise?

Can you provide examples?

What do you mean? This is not about examples mg! :D That wasnt a point of this question.

I have made some further modifications to the question to include more explicitly the obvious concern of the original poster that different abbreviations are used for the same thing. I have also extended it to the actual names, because the problem is in the name itself. In the case of gene symbols these sometimes are, in fact names rather than abbreviations, for example bacterial genes named A, B, C etc for a particular operon when their individual functions are unknown. Finally, I think the poster wished to know how the confused situation had arisen. I shall add my own answer about that.

Elsewhere on SE Biology I have answered a related question regarding enzyme names. Here I will restrict myself to genes, as it seems that this is the main concern of the poster. (In talking about ‘abbreviations’ I think he is referring to what are generally termed gene ‘symbols’.) The answer from @KarlKjer addressed current recommendations regarding gene nomenclature; mine addresses the causes of the current confusion.
Summary

Rules (actually recommendations) did not appear until a late stage in
the development of the field of genetics, when the problem was
already there and there was a need to do something about it.
Historically in animal systems the naming of new genes tended to
relate to mutant phenotypes as this was how they were discovered. The function of the gene that had been mutated was generally unknown.
Sometimes different mutants of the same gene caused different
phenotypes, either because of severity of damage to the protein, use
of animals from a different development stage, or different growth
conditions for bacteria. These mutants appeared to be of different genes, which
were given different names.
Sometimes the same gene was discovered at about the same time by
different workers and given different names in the laboratory while work was in progress and, hence, on publication.
Later it became possible in some cases to identify the products of
genes for which there was no clear mutant phenotype — perhaps just
lethality — and one method of naming was on the basis of the size of the
protein, preceded by the letter ‘p’ (e.g. p63)
The current trend is to try to rename genes according to the function
of their products, where these are known, i.e. to replace the name of a
mutant phenotype by the name of an enzyme or structural protein.
The implementation of such rules or recommendations is imperfect,
depending on the cooperation of authors and editors.

Illustration using some Drosophila genes
I shall use Drosophila melanogaster (the fruit fly) to provide some illustratations of the history of genetic nomenclature, because this was the organism used by Thomas Hunt Morgan (he of the centimorgan) to perform genetic studies after the rediscovery of Mendel’s work in 1900.  His laboratory was responsible for the discovery in 1910 of the first Drosophila mutant, a spontaneous sex-linked mutant that resulted in males having eyes that were white, rather than the normal red. The gene responsible for this mutant was named white, initiating the custom of naming genes after their mutant phenotype. (Drosophila gene names became italicized by convention.) What else could they have done? Not only was the protein product of this gene unknown, the whole idea of genes encoding proteins did not yet exist. The abbreviation (symbol) for this gene was merely w. Clearly, nobody anticipated that another 17,000 genes would follow, or suggested that a committee on gene nomenclature should be set up.
It is interesting to note that the product of the white gene was not identified until almost 90 years later. In 1999 it was established that this was a member of the ABC transporter family, responsible for bringing  into cells the guanine and tryptophan  needed to make the red pigment so characteristic of the eye of the wild-type Drosophila. The human version of white was identified roughly contemporaneously by sequence homology, and although it was initially referred to as hW (human homologue of white) is now named according to its gene product: ATP-binding cassette sub-family G member 1 (ABCG1). Its function in humans — who only have red eyes in flash photographs — is in lipid transport.
The era of of molecular genetics in the late twentieth century brought an avalanche of new genes, many not associated with a particular phenotype. The culture — accepted by scientific journals — was that if you discovered a new gene you had the right to name it as you pleased. A generation of young scientists were pleased to chose names that reflected twentieth century, rather than classical, culture. Flip through the names of Drosophila genes (try the autocomplete here) and you will find alien, bazooka, cactus, Dorothy, ether a go-go all the way to zucchini. Nor was it only the Drosophila geneticists that were responsible for this. The hedgehog segmentation gene, discovered in Drosophila, has three human homologues. One of these was named ‘sonic hedgehog’, which I am informed is the protagonist of a children’s video game. O tempora, o mores!
A couple of final points will be made to illustrate the problems of nomenclatue of Drosophila genes. Several other mutations of the white gene have been observed which have different phenotypes (e.g. result in different eye colour). This is because they involve insertions into the gene rather than its complete deletion. This also illustrates one historic difficulty that could result in several names for the same gene. The other point is that many of the genes identified by genome sequencing, at least initially, were associated with no mutant phenotype and had no known function, and were so named simply be an accession number (CG1234 etc.). As functions emerged they would be renamed. And an example of the nomenclature situation can be seen in the NCBI entry for Drosophila gene TfIIS (RNA polymerase II elongation factor):

Also known as: BG:DS00929.12; br52; CG3710; Dmel\CG3710; DmS-II; DmSII; l(2)35cF; l(2)35Cf; l(2)br52; l35Cf; RnpSII; TFIIS; TFIISA; TFS-II

Regarding the hedgehog gene, the name stems from the appearance of the larva of the mutant larva, which, like the animal, is covered with fine hairs (ZPA property of hedgehog). The original mappers of the fruit fly genes were German (Nüsslein-Volhard and Wieschaus from Tübingen). So they initially gave some genes German name, mostly from the appearance of the mutant (knirps, krüppel, and spitz) and some in English (shavenbaby, buttonhead, faint little ball). They got the Nobel in 1995 for this I believe. No, not the Nobel in Literature.

@AlainPannetier — Yes, I realize that many of the 'amusing' names were related to appearance, and that this was extremely important work. And my experience in Germany (I had a sabbatical there and speak the language) suggests that German scientists would have been unlikely to name genes after video games characters. But thanks for the comment, and I don't think it harms to have a little history for the younger scientists. Indeed my objective in posting was to show that these irritations of nomenclature arise from the way science is actually done.

There are rules. Both genes and proteins are regulated in their formats, and standardized in terms of capitalization and italics. Different species have different rules. So for example SHH is a human gene, and Shh is the homologue in mouse.
You can find these rules here: https://www.genenames.org/about/guidelines and read about them here: https://en.wikipedia.org/wiki/Gene_nomenclature
Also, amino acid abbreviations are standardized in both one and three letter forms. Also, things like restriction enzymes are given as the first letter of the genus, and then the first two letters of the species epithet, such as EcoR1 from E. coli. Note that since it comes from a Linnaean species (in Latin) it is italicized. Other enzymes like Taq polymerase, come from species names, and follow similar guidelines.

One reason why some genes have several different names is because they have been discovered several times by different teams in different species.
For instance mice Int1 being Wg of the fruit fly.  Each team name their discovered genes independently and they eventually realise they're the same (homologous).
This was quite common before biologists understood/accepted the universality of homeobox genes.


text:
Proteins folds: relation to splicing and post-translational modification?
Is the secondary structure pattern of protein folds related in any way to alternative splicing and post-translational modification?

"somehow related" is very vague - do you have some idea how they might be related?

Our prof.  in biochemistry basic seminary said, that diffrent kombinations of folds Is releted to diffrent function of protein. He didnt said anything that how Is this process regulated in Cell. So i thought that would be releted to alternative slicing. That one gene sliced to diffrent structure can have a simular pattern.

I see. So I don't think you mean 'secondary structure' - you probably mean domains. For example, see https://www.ncbi.nlm.nih.gov/pubmed/23562110 or this question https://biology.stackexchange.com/questions/13834/what-are-some-examples-of-genes-that-code-for-multiple-proteins

source: Stack Exchange

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

sort: votes


text:
Horizontal gene transfer in a bacteria
I encountered an old examination question:

Which of the following is not required in Bacteria for horizontal gene transfers?

Infection 2. Translation 3. Transformation 4. Conjugation 5. Transduction

Clearly this is aimed at testing an understanding of horizontal gene transfer. So far I have tried to think about it in the following terms:
A horizontal gene transfer is defined as “obtaining DNA” which doesn‘t stem from the original cell line.
Transformation is the intake of DNA, Transduction is the transfer between two bacteria over a phage, conjugation is like sex (?) between two bacteria. All these would seem to be needed.
However, during Conjugation, a bacterium translates/produces new DNA, so translation would also seem to be needed.
In this case all five items listed would seem to be required. Is this correct?

I have edited your question to make it of more general relevance, focusing on the process of horizontal gene transfer. Your definition of horizontal gene transfer is fuzzy, and you need to find a text book that describes it in detail, checking against the five processes in the question. You only define three of them and your implicit assumption about translation is incorrect. You can edit your question after doing more work.

There's a difference between being technically correct and getting the correct answer on an exam. Yes, theoretically transcription and translation need to occur for the formation of a conjugation pillus, but it's a stretch. That's the only answer that isn't directly related to transfer or uptake of genetic material. If you really want to be technically correct, none of the answers are "required" since that specific word choice would imply they are necessary in every instance of HGT.

Horizontal gene transfer (HGT) is the transfer of genomic information between two already living cells. It is most known in Bacteria but happens also in Fungi (look for Ug99).
In bacteria the genetic information can come from the genome, a plasmid or from random dna or rna strains.
Transformation, Transduction and Conjugation are different kind of mechanisms. You should research them for better understanding.
I guess that by infection they mean infection by a bacteriophage which is a way of HGT.
Translation is the process of synthesize proteins from mRNA
This process is independent of HGT and therefore the right answer to the question.
As far as I know all the mechanisms needed for conjugation (the genomic material, pili and other cellular apparatus) are already present in the donor cell and therefore translation isn't needed. I belive you are confusing translation with transcription (creating RNA from DNA) but that isn't needed either as the plasmids containing the F-factor already exists.

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


text:
Why does acidosis cause cells to remove hydrogen ions using the proton/potassium ion pump rather than exchange with another cation?
Many mammalian cells respond to acidosis by transferring hydrogen ions to the blood using a proton/potassium ion pump. Why is this system employed rather than one involving another cation such as sodium? I ask this because it seems to me that exchange for potassium has the disadvantage of causing hyperkalaemia and therefore potential cardiac problems?

It is hard to know what your question means — you need to reiterate what the Bohr effect is in your opinion and how potassium ions come into it. But the idea that evolution has anything to do with the exchange of ions in molecular processes is absurd — its chemistry. If you can explain your problem clearly, you might consider posting on SE Chemistry.

I meant to ask why is it only potassium that is being exchanged for protons, why not any other cation like maybe sodium or calcium be exchanged for the proton instead. I’ll try to edit the question to better explain what I wish to ask. I had mentioned evolution because I was wondering that maybe there was an advantage of having K+ instead of some other cation be exchanged for H+.
Any input regarding this would be appreciated, thank you!

I have edited your question to reduce it to its essentials, as far as I understand your intent. If I have changed your meaning do make necessary alterations. However the Bohr Effect would seem to be irrelevant and wrong as this involves the uptake of hydrogen ions by haemoglobin. Also there is no reason to refer to evolution in considering the advantages and disadvantages of a particular system, especially as the way you refer to it is very clumsy.

Can you update your question with references to whatever you are reading about the process you're talking about? What type of acidosis, which proton/potassium ion pump are you talking about, what cell type, etc. pH and ionic homeostasis is quite complex.

Isn't the premise itself incorrect, or incorrectly written, that hydrogen ions are 'transferred to the blood' from cells, in exchange for potassium?  The K+ in that case is being excreted by cells.  As for the query itself regarding the specificity of this exchange, H+ for K+ and not Na+, while no doubt complex, this must inevitably relate to the exigency of maintaining an energetically expensive Na+/K+ equilibrium across cell membranes: viz, the excessive extracellular K+ implicated in conditions of acidosis must then be restored to the cytoplasmic compartment via the Na+/K+ ATPase.

I apologise for any misunderstandings, I’m still trying to fully understand the concept. As per what I’ve read online in articles, protons will bind to deoxyhemoglobin in the Red Blood Cell and in order to maintain electrical neutrality, potassium ions will have to exit the RBC. What I meant to ask was why there was the exit of specifically potassium and not any other cation?
A similar doubt I had was regarding the shift of chloride into Red Blood Cells following the exit of bicarbonate from the cells, why specifically Chloride and not any other anion?

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


text:
Why are fatty acids synthesized in two carbon units?
Why does long-chain fatty acid synthesis involve the two-carbon precursor, malonyl CoA, rather than the one-carbon acetyl CoA (or even a three-carbon precursor).
Is this because fatty acids with an even number of carbons are somehow ‘better’ than those with an odd number, or does it reflect some aspect of the chemistry involved?

@kmm I do not think this question is about evolution except in the most tangential sense. There is a tendency of people to bring evolution into questions which just relate to functional utility. In this case there is no evidence that there were ever organisms that had a one-carbon pathway of fatty acid synthesis, so the question of a selective advantage does not come into play. In an effort to make people keep things simple, I have edited the question removing all references to evolution, and distilling it to its essentials, which now seem capable of a factual answer.

Thanks for the edit! The new question is pretty much what I'm interested in knowing about!

@kmm I did give the answer a read and I learnt something new, but it didn't help me exactly with what I wanted to know, thanks for providing the link though!

@David Now it seems more appropriate for chemistry.SE, as it is about biochem and not biology.

@kmm It is totally on-topic here as it is about biochemical pathways and metabolism, which are (molecular) biological concepts, not about chemistry per se. You will find dozens of questions in this category on the site. Please withdraw your close vote, I am in the process of answering. You will see my answer is about metabolic strategies, not pure chemistry.

The answer to this question lies in the chemistry of fatty acid synthesis — specifically the chemical energetics of the reactions. For those new to the biochemistry there is a basic concept that must be understood: that a reaction can occur spontaneously only if it involves a negative change in Gibbs Free Energy. This is discussed, among other places, in my answer to another question.
As regards long-chain fatty acid synthesis, the answer can be found in Section 22.4 of Berg et al. Biochemistry some of which I summarize here.
The reactants in fatty acid synthesis are linked to a protein during the cycle of reactions — acyl-carrier protein, ACP:
malonyl CoA + ACP ⇌ malonyl ACP + CoA
The first condensation reaction of a malonyl constituent in the elongation cycle of reactions is shown below.

The key point to note is that in this step the malonyl carboxylic acid
group is released as carbon dioxide with a substantial decrease in
free energy that makes the reaction favourable. Without it the
reaction would not proceed, which is why the synthesis of acetoacetyl
ACP from two molecules of acetyl ACP does not occur.

It is worth adding that this free energy is ultimately derived from ATP, which is needed to drive the reaction in which malonyl CoA is formed from acetyl CoA and carbon dioxide.


text:
Who discovered DNase?
I was recently studying genetics in which  DNase had a crucial role in proving DNA to be the genetic material and I tried to find who discovered DNase (like the discoverer of DNA) but in vain.
Who found the DNA-digesting DNase ?

You imply (if I’m not mistaken) that you know who discovered DNA. I wonder whether you might be confusing who discovered DNA, who showed it was the genetic material, and who elucidated its structure. If you’re interested in the history of science it might be useful to clarify that while we are about it.

@David Thanks It clarifies my doubt If you don't mind I have a question that is , In Martha Chase Experiment, It has been proposed that Since Radioactive Nitrogen is Transferred The DNA act as a genetic material but Why can't the transferred material be RNA as It also has same amount Of Nitrogen as of DNA ?

A principle of this site is that questions should be asked as separate questions, not as add-ons in comments. There are a few questions on the Hershey-Chase experiment on this site, and also a Wikipedia entry. However the short answer is that the bacteriophages studied consisted of DNA and protein, and the experiment was to distinguish between the two. You need to look at old experiments in their historical context.

There are, of course, many different deoxyribonucleases (DNase), but the question has other implicit problems. It assumes that there was a single event that resulted in the realization of the existence of a new enzymatic activity. As the Introduction to this paper by M. McCarty on the purification of one such enzyme in the Journal of General Physiology in 1946, science wasn’t (and still often isn’t) quite like that:

The enzyme which breaks down highly polymerized desoxyribonucleic (sic) acid
has been known for many years under various names. In 1903, Araki (3)
reported that crude preparations of trypsin and erepsin brought about
liquefaction of gels of a thymonucleate prepared according to the
method of Neumann (4) Although Araki interpreted the effect as being
proteolytic in nature, his experiments represent the first observations
on the enzymatic breakdown of this type of nucleic acid. Two years
later Sachs (5) demonstrated that liquefaction of the nucleate gel by
pancreatic extracts is caused by an enzyme distinct from trypsin, and
further presented evidence indicating that trypsin rapidly inactivates
the nuclease. De la Blanchardière (6) confirmed the findings of Sachs,
and made several unsuccessful attempts to separate the nuclease from
the inactivating tryptic enzymes. This writer also devised a more
quantitative method of measuring the nuclease activity by following the
fall in viscosity of a dilute solution of thymonucleate during
digestion with the enzyme.

Araki, T., Z. physiol. Chem.,1903,38, 84.

Sachs, F., Z. physiol. Chem.,1905,46, 337.

De la Blanchardière, P., Z. physiol. Chem., 1913, 87, 291

[desoxyribonucleic acid and thymonucleate are older terms for DNA and its ionized form]
Many scientists have subsequent been involved in identifying different types of DNase and their roles in DNA metabolism, and anyone wishing to know about a particular DNase would need to research the literature.


text:
Can Mung Bean Nuclease only digest a ssDNA 5' overhang?
Can Mung Bean Nuclease only digest a ssDNA 5' overhang, if the double-stranded region of DNA (20bp) is A-T rich at the ends?
Does this enzyme degrade 5' overhang (5bp or 30 bp) with 100% efficiency?


text:
Identify this insect, found in Central Vietnam, with long antennae, black wings, and red body
Last year this insect landed on my hand when visiting the My Son city ruins in Central Vietnam.
I've been trying to identify the insect, but until now without result.
Can you help me? Or do you know who could?

That is a pretty cool bug.

Upvoted for the nice photo!

This question has been asked before. It's Identify this insect, found in Central Vietnam, with long antennae, black wings, and red body
And it is Drosicha corpulenta. I'm having trouble finding a credible source.
Try these: google[http://nc.biodiv.tw/bbs/showpost.php?p=19392&postcount=1]
google[https://isabellevea.wordpress.com/2014/05/27/the-giant-scale-drosicha-corpulenta-on-uncovering-its-biology-part-1/]

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


text:
What biproducts do vinegar eels produce?
What chemicals, acids, gases or other biproducts do vinegar eels (Turbatrix aceti) produce (in raw vinegar and/or in the vinegar-creation process, which process may have them in environments including such as fruit scraps and fermented fruit scraps, sugar, alcohol, or water)? I know they're said to feed on acetic acid bacteria and apples.
I'm particularly curious if they produce acetic acid, carbon dioxide, enzymes, and/or vitamins, but I'm generally curious about everything they produce. I'm not sure exactly how many chemicals a single nematode species can produce (so, if it's a lot, you can narrow your answer down to what might be particularly useful to a nutritionist and/or someone making vinegar).
I thought this might be a better place to ask than Seasoned Advice, seeing as it's about biological processes, and as far as I know, little is publicly known in the culinary world about what they produce (I couldn't find any information on it).

If it's appropriate here, feel free to create a tag for nematology and add this to it.

Per wikipedia vinegar eels don't contribute to the creation of vinegar, rather they feed on the bacteria that are creating the vinegar.


text:
How much pollen is needed to pollinate a flower?
Assuming 100% of the pollen gets delivered to exactly the locations it needs to pollinate a female flower, how much pollen is needed to pollinate a flower? If it's more than one unit of pollen, what, if anything, prevents more than one plant's pollen from pollinating the flower?
If we need an example plant to answer this question, let's assume zucchini. For instance, if you plant a zucchini in the middle of a spaghetti squash and an orange-fleshed squash, is there any likelihood at all that you'll get a single zucchini pollinated by both in one generation (such that the next generation of cross-pollinated zucchini would be both stringy and orange-fleshed instead of just one or the other)?

A single ovule in a fruit is pollinated by a single grain of pollen. So, in theory, a fruit with n seeds can be pollinated by n grains of pollen. In reality, of course, not every pollen grain makes it to the ovules, but if we treat your assumption as true, then a flower can be fully pollinated by as many pollen grains as there are ovules in the flower.
If you plant your zucchini and cross your zucchini flower with pollen from spaghetti squash and orange-fleshed squash, you will end up with a zucchini fruit filled with seeds that are either half spaghetti squash or half orange-fleshed squash. If you planted the seeds from that zucchini, you would end up with some individual plants that have spaghetti-squash traits and some with orange-fleshed squash traits. You would not end up with any plants with both stringy and orange-fleshed fruit.


text:
Cell targets of Glybera
So we know that there is a first gene therapy drug in the market out there called Alipogene tiparvovec to address  lipoprotein lipase deficiency (LPLD) at a genetic level. Does this genetic drug target all cell types (except germline) that expresses the LPL gene in the human body or simply the parenchymal cells that process fat? I have not been able to find information specific to Glybera.

Glybera doesn't target all cells, and doesn't target fat processing cells. Glybera is adeno-associated virus 1, which normally infects skeletal muscles. Glybera is delivered by intramuscular injection, so the virus easily infects the muscle tissue. The infected muscle cells produce a variant of lipoprotein lipase that has better activity than normal LPL and secrete it into the bloodstream. Once in the blood LPL can interact with chylomicrons and make them smaller.
Here is a paper about viral gene therapy for LPL deficiency, specifically about glybera, but I don't think it's open access.

So does it mean that all muscle tissue associated cells will be targeted and test positive for the new LPL variant?

Probably not all muscle cells. The virus is given by multiple injections into lower limb muscles, most likely only the cells near the injection sites are infected. The virus is also replication incompetent, so it can't copy itself and infect new cells.


text:
How cone snail collection is done safely and legally?
I'm really intrigued by the hobby of cone snail collection. However, some cone snails are known to be venomous and dangerous to humans, so how are they freely available for purchase and traded online?

Is it just the shell of a decomposed body of a dangerous species of cone snail eg. conus geographus that are sold as collector's items?
How are the specimens safely harvested? Is there regulations apart from endangered species laws governing their harvesting? Or is it an self governing risk based approach practice by those in the collector's trade?

I’m voting to close this question as off-topic because it is not about biology as defined in the [help].

Perhaps this question would be a better fit for The Great Outdoors SE?


text:
DIYbio - CRISPR injection sites for targeting the ABCC11 gene
I've been researching into the biohacking world where people most notable Josiah Zayner and Tristan Roberts have used a CRISPR solution developed in their backyard for gene therapy.
There is even a CRISPR guide floating online for the curious, published by Zayner's startup.
However, the guide doesn't help us identify the injection sites in the human body to deliver the solution. Zayner injected Myostatin in his arm muscle.
Another biohacker's Youtube video describes making a pill for targeting stomach cells in a bid to cure lactose intolerance "Developing a Permanent Treatment for Lactose Intolerance Using Gene Therapy"
In general, how does one determine the most suitable site and or methodology for administering CRISPR in the human body that is appropriate for the gene and/or condition we are targeting?
EDIT: Personally, in my case, the gene of interest is ABCC11. I do note that most CRISPR (or any other gene therapy technique for that matter) attempts may target conditions involving more than one gene. However, why I think this gene and its associated conditions is unique is due to the fact much is written online about the effects of a single gene mutation in this particular gene. A paragraph on Wikipedia states:

Physical human traits that are controlled by a single gene are uncommon. Most human characteristics are controlled by multiple genes (polygenes) although ABCC11 is a peculiar example of a gene with unambiguous phenotypes that is controlled by a SNP. Additionally, it is considered a pleiotropic gene.

Official Pubmed documentation : A SNP in the ABCC11 gene is the determinant of human earwax type.

CRISPR biohacking sounds fun and all, but let's be real, if it was feasible for anyone to efficiently and safely engineer human cells in situ... many researchers would be out of a research project right now, and many diseases would already be eradicated. Just to emphasize the fact that things are far, far more complex than "just inject something that you brewed in your kitchen, not too far from the organ you're aiming for". But it's great to be interested, and if I were you I would look further into genetics, and molecular/cell biology books to understand the challenges at a fundamental level

Personally, I'm not targeting a disease, Im targeting a gene variant which I find isn't preferable to me. See my update

Personal medical questions and health advice are off-topic on [biology.se]. Your question is on-topic as long as it is academic or for general understanding of biology. I don't have anything against you injecting something in your body but please don't make others a part of your experiment. I'm putting this question on hold but if you remove all personal references then it may be reopened.

if you want to affect your earwax, then the cells producing the wax need transformed... gene delivery is a major hurdle. You might get lucky just dropping naked plasmid DNA into your ear with no injection/electroporation similar to these sort of results http://www.academia.edu/download/46122460/Electroporation_enhances_reporter_gene_e20160601-22062-1yqcq1x.pdf

Creating changes in the genome in order to get your favorable results is not always as easy as it looks. Expression of a particular gene is not necessarily bound to its existence. There are other factors (mainly proteins) that have to be in the cell at the right time to make that gene expressed. Yet a trait is not always the result of one gene being expressed. So basically adding one gene will never give you bigger muscles and still, this is not really why performing gene editing in your garage is absurd. (Yes those videos are just hoaxes.)
In order to have a CRISPR/Cas9 system work, you gotta send both the Enzyme Cas9 and the guide RNA into the cell. You can't inject proteins or RNA directly to a cell or expecting cells to uptake them from the bloodstream. The gene constructs for both guide RNA and Enzyme have to be added to a vector which is mostly a virus. The virus had specific receptors on its envelope which help it to target the right cell to infect then viral genome will be inserted into the infected cells and thus they receive the genes that will express CRISPR/Cas system.
Designing the gRNA, viral vector and engineering the virus for the specific target cells and applying the virus to the tissue requires precise and professional skill and a decent lab. By no means works done by those guys can lead to verified and trusted consequences. I recommend reading this if you are interested in gene therapy and CRISPR/Cas.

Besides upvoting, as you have provided more information in the second paragraph, I have edited my question to include the gene Im interested in. See if you can provide more info

Okay, I didn't want to write an answer to this, because honestly - don't do try this at home.
You have to realise that what Zayner (who does incidentally have a PhD in biochemistry) does is not risk free, very likely not having actual effects besides editing the DNA in some of his cell$^{*1}$ and definitely just barely not illegal (in the US, it's very likely illegal in i.e. the EU).
The science behind gene therapy (which this essentially is) is not easy and trials are just starting to be performed, but mostly using viral vectors, because they are much more efficient and easier to target towards specific cells. While it's possible to target muscles by injecting into them, or cells in the ear by injecting there this always targets all cells in the given area and not just a specific cell type.
Also please note that the article about ABC11 you linked is anything but an 'official documentation': it's a research article published by a japanese
research group that states they observed an correlation between earwax phenotype and a certain (SNP) genotype, which is also causative for a change in cGMP signalling of the protein it codes for.

*1 from this article (which also links to this interview)

But Dana Carroll, a biochemist and CRISPR expert at the University of
  Utah, said the experiment is unlikely to work as Zayner suggests,
  pointing out that the gene is most influential when muscles are being
  developed early in life.
“When your muscles are already developed and you’re sitting there with
  mature muscles, there’s not a lot you can do to make them bigger and
  stronger other than exercise,” he told BuzzFeed News. “So he’d be
  better off exercising than injecting himself.”

IMHO, Perhaps Zayner should have considered human growth hormone (HGH) instead. But as I understand it, he is leveraging on the activism of such acts to bring about an underlying political message. He should have choosen genes such as  ABCC11 as its more effective in targetting a condition controlled by a single genotype

@Nederealm You are mixing a lot of things up: 1) He did a CRISPR knockout experiment, so targeting growth hormone wouldn't have increased muscle growth for sure. 2) Targeting a growth hormone with gene therapy is VERY risky and could have substantial side effects (read: high risk of cancer). 3) Just because ABCC11 is linked to a clear phenotype, doesn't mean that this phenotype has a single genotype. If you'd actually read the paper you linked you would know that the genotypic analysis alone didn't allow them to distinguish between 5 different candidate genes.

Japanese researchers said that the dry (earwax) genotype is common in individuals of Asian ancestory. I fit that category. It is still possible that I might have another genotype, but highly unlikely.


text:
Where do migratory birds go when it rains?
I was reading a comic from XKCD which inspired me to ask this question: "well, where do they go when it rains?" I know that when it rains you usually don't see any birds flying through the sky.
I imagine they normally hide in trees or under other kinds of cover. But for migratory birds, I don't think it is possible to hiding under cover until the rain passes. There might not be any cover (trekking across seas) or it might stay rainy for a very long time (and therefore cold...).

I did some research, but the answers are conflicting. Some people say they do stay in trees, others say they AVOID trees (because trees can snap in a storm, plus if there's lightning then sitting in a tree will net fried birds). Then there's people saying that birds have a waterproof coating... but that's a bit contradictory with me not seeing birds when it rains.
So where do birds go when it rains?
I assume that different bird species and groups of birds will behave in different ways. I am interested in the case of migratory birds because they are likely to encounter different climates and have perhaps devised strategies to be safe. I would appreciate any well-referenced examples.

Quick point, all birds aren't likely to do the same thing.  A duck, an ostrich, a pigeon, and an hawk are likely to have different reactions.  Example, pigeons are known to rain bathe on the ground.  Would examples for common flocking birds of US cities be sufficient?

@AtlLED I'm interested in trekking birds specifically. Birds in forests or urban regions have plenty of shelter, so I'd expect the obvious answer of "they get out of the rain and under the treetops/rooftops". But there's no shelter when you're trekking... I live in Europe and I don't know enough about birds to tell you what types they have here (sure we have geese, ducks, pidgeons, owls and hawks). If you NEED a focus, european "urban" trekking birds would be it.

Examples of specific birds are also welcome as I can see each bird having its own strategy.

Nominating to reopen, since nobody has stated clearly in the comments why it should be closed as opinion-based.

Also see discussion in Meta.

Obviously, as you point out, some birds, such as waterbirds (ducks, puffins, auks, sandpipers) are perfectly fine in the rain, as they spend much of their time in the water anyhow and have oil glands that waterproof their feathers.
For other birds, rain can increase heat loss. For instance, rain increases metabolism by up to 22% in eagles (Stalmaster & Gessaman, 1984), although the actual impact on average daily metabolism was 'negligible'. However, eagles were able to feed their offspring only half as much, and therefore had only half as many eaglets, when it rained (Elliott et al., 2005). (On the other hand, the authors point out that in the Tropics, eagles actually do better when it rains because there is more food available).
Migrating birds stop migrating, hide where they can, and wait until it dries up before they continue (Erdi et al, 2002); those that don't, often end up far away from where they should be and, eventually, dead. In short, some birds don't mind the rain (e.g. seabirds), others sit it out in misery (e.g. nesting eagles) and others hunker down wherever they can find shelter (e.g. migrating birds).

Interesting. Have there been cases of significant reductions in bird numbers because of a heavy storm during migration season?

Birds can easily cover enough distance flying that they can avoid short showers entirely by not sitting right below clouds, unless they have an actual reason to stick around. Birds move around a lot more than we do.

I've frequently seen rain clouds on weather radars that cover quite a big area. How do they dodge these?

@Pimgd presumably most clouds can't move faster than birds since they can ride the same currents. So to avoid big clouds the birds could fly with (or alongside or in front of) the cloud. This would help explain Kyle's answer on why the ones that continue flying end up far away: staying out of the cloud forces them to fly off course.


text:
How are the vitreous humour and aqueous humour of the eye, connected?
My question is regarding the biological nature of the separation between the vitreous humour and aqueous humour of the human (or mammal) eye. What connects the two in terms of the passive transport of proteins between the two? Is there a single membrane?
If so what is the name of this membrane and is it the only thing separating the aqueous from the vitreous? What is the anatomical difference between the aqueous and the vitreous?
Apologies, I am far from a biologist.
Specifically what sort of transport is arrow 9 in the figure below representing? And is backward transport (from the aqueous to the vitreous) possible?
Any links to papers detailing this mechanism would be highly appreciated, I can only find references to experimental readings of concentrations, but nothing about the transport process itself.

I do apologise for that. However to me I don't really see the difference, the main body of my question asked about the transport of molecules, I merely drew more attention to that part of my question. I would say previously it was vaguely phrased, as, which I previously mentioned, this is not my field, I was attempting to make up for that, I'm sorry to have offended however.

Retracted comment - sorry! +1 had to make a slight edit before I could upvote again. Feel free to roll back :)

You have changed the question, so my answer looks unrelated. I'd suggest roll question back and ask others in separate question.

@Ilan, will do. Here is a link:
http://biology.stackexchange.com/questions/36140/how-do-drugs-or-other-molecules-move-between-the-vitreous-humour-and-aqueous-h

@Ilan Well the question might have sounded different but the OP asks if there is any connection in the sense of exchange of matter between the two "humours". This doesn't require a different question. OP just clarified their actual intention. You can edit your answer to add if there is any material exchange between them or not. Your answer is still fine.

@Freeman Keep the actual title of the question.. Add details in the body so that Ilan's answer remains pertinent.

@WYSIWYG I've added a little detail regarding the membrane. I believe IIans answer is still very useful. I would however like to know more regarding the actual process.

@Freeman edit the question.. This doesn't need a new question

@WYSIWYG Apologies for the confusion here.

@WYSIWYG I added the clarification to the answer, but I should mention that a question is too broad to answer in a format it is asked.

@Ilan You can tell that to the OP in the comments.

Don't be confused by the word "humour": the vitreous body is presented in birth and has very low "exchange" rate of its components, while aqueous is in constant turnover.
Secondly, the vitreous is an organ-like structure and is separated from other eye structures by its membrane, while aqueous is fluid produced by ciliary body processes into the posterior chamber and moves  anteriorly throughout the pupil. Aqueous can move posteriorly in a case of trauma, operations and other non-physiologic states.
ADD (after attachment of the image)
I'd correct some things in the scheme - call Vitreous as Vitreous, not Vitreous humour, change arrow pointing at the ciliary body as on the following image, depict the vitreous body membrane as I did.

In addition learn two terms: Cloquet canal and Berger's space.
Number 9 shows a vitreo-aqueous route which will follow blood, drugs injected to the vitreous (not an only route), etc.

Thank you for your answer, so are you saying that as soon as a component has managed to pass through the vitreous membrane it is quickly removed by the aqueous? Would you mind looking at this diagram in my edit? I don't understand arrow 9, what sort of transport does this represent?

This is very helpful. Thank you very much for adding details.

Since 2015, have you been able to answer your question "Specifically what sort of transport is arrow 9 in the figure below representing?"

@PeterBernhard 9 had to show drainage pass to the anterior chamber angler (number-arrow 4)

@Ian Thank you! Surely, you mean "chamber angle". I can now do my own research on this. Vitreous detachment is very common, fluid may be seen as leaving the vitreous body, maybe because the secretion of anterior - "tears" - fluid is insufficient. My own hypothesis, btw, now is that anterior fluid substituted, in eveolution, the water-part of the vitreous body (said to become more watery before vitreous detachment). Cheers!


text:
Identification of an insect found near the Rhine, Germany

It was about 2-3cm long
It has two small wings and 6 legs

Is that the only photo you have? A side view would be very helpful.

possibly larval cicada, but I don't have access right now to figure out if true.

It would be helpful to know the size.

Hey thanks for the answer and yes I have more pictures just not as good quality.

Also I wrote the size under the picture it was about 2-3 cm long

That side view is very helpful, thanks.

It is the larva of a hemimetabolous insect for sure. Considering it was close to a water body I would say a nymph of some Odonata ?
The legs are a bit bulky though, I might be completely wrong.
These are not wings yet, they will be there at adult emergence.
Maybe check these out :
https://www.pentaxforums.com/gallery/photo-dragonfly-nymph-20082/
https://www.flyfishbc.com/threads/april-2011-fly-o-the-month-dragonfly-nymph-gomphus.5843/
Edit : my colleague Dirk Mikolajewski says it is a Gomphidae larvae. He will probably tell you which species soon.

Nice links! (Not a very pretty insect, though.) +1

Odonata larvae are the only insect I am scared of. I resent them a lot for eating amphibians.

I'm relieved to read that. I thought, "That thing would scare me to death!" It looks like it could take a chunk out of someone's hand, too.

Thanks everyone for the help

I also have a short video of it Walking but can't upload here I think


text:
Use of ADP hydrolysis for driving energy-requiring processes?
The free energy of the hydrolysis of the β-γ phosphoanhydride bond of ATP is used to drive energy-requiring biological process such as chemical synthesis, movement, ion transport and production of light.
However the chemical structure of the α-β phosphoanhydride bond of ADP appears very similar, but I am unaware of instances where its free energy of hydrolysis is used in a similar way. Is this theoretically possible, and are there any actual examples?

I have edited your question as the term "potential energy" is not generally used in relation to biochemical reactions, the expression "used for energy" is imprecise, and the title poses as different question to the body of your question.: ADP can be used for other purposes (as a regulatory molecule, for example) besides driving energy-requiring reaction, but it appears that it is the latter that you are asking about.

Polynucletide phosphorylate is an example (but the only one I know of)

The story of the discovery of polynucleotide phosphorylase, which can catalyze  the reaction RNA(n) + NDP = RNA(n+1) + Pi, (where NDP is a dinucleotide diphosphate such as ADP) is told here by Grunberg-Manago. Although the enzyme appears to have a very different role in vivo,  it was of great importance historically in the elucidation of the genetic code (synthesis of poly-U, poly-A, etc)

@David I think I understand how ATP is used, but I don't understand why "used for energy" is imprecise. If it is used to drive chemical reactions, couldn't it be considered energy?

Precision is saying what specifically is the source of energy. “ATP is used” is only comprehensible to those who already know.  In this context it is important to state what is happening is the hydrolysis of a particular bond with a particular free energy change.

It is theoretically possible

The structures of ATP and ADP are shown above, with the phosphate groups designated α, β and γ. The value of the Gibbs standard free energy of hydrolysis of the α–β phosphoanhydride bond of ADP is similar to that of the β–γ phosphoanhydride bond of ATP at approx. 30 kJ per mol. Hence it is theoretically possible to couple the hydrolysis of the α–β phosphoanhydride bond of ADP to an energy-requiring process and produce an overall negative ΔG.(The reader may wish to consult an external source — e.g. this previous SE Biology answer — if unfamiliar with a chemical account of the popular but imprecise idea of ATP as a “source of energy”.)
The hydrolysis of the analogous bond of ATP is so used
Most reactions and processes for which ATP provides the driving free energy change involve the hydrolysis of the β–γ phosphoanhydride bond in the reaction:
ATP → ADP + Pi
However in several synthetic processes the energy is provided from the hydrolysis of the α–β phosphoanhydride bond in the reaction:
ATP → AMP + PPi
These include RNA synthesis (to form a phosphodiester bond) and amino-acyl tRNA synthesis (to form the aminoacyl bond, which itself provides the energy to drive peptide bond formation).
Examples of ADP hydrolysis driving energy-requiring reactions?
Although this may merely reflect my ignorance, I know of no reactions of the sort:
ADP → AMP + Pi
where the energy of hydrolysis is used to form a chemical bond etc.
So, although I may be proved wrong, my answer is NO. But…
…a possible exception — not producing inorganic phosphate — is the adenylate kinase reaction, for which the overall standard free energy change is near zero:
2 ADP ⇔ ATP + AMP
This could be considered as using the energy of hydrolysis of the α–β phosphoanhydride of one of the molecules of ADP to form the β–γ phosphoanhydride bond of ATP. This is thought to be important in the regulation of glycolysis, the AMP produced serving as a signal for the requirement of energy and acting as an activator of the enzyme phosphofructokinase.
Why — or why not?
“Why” questions are dangerous in biology, as there is a tendency to argue that the way things are are the way they must be; and there are generally no tests of hypotheses in support of such a view. Nor did the original poster ask why. But with the strict understanding that what follows is just speculation, I offer these thoughts in support of my generally negative answer:

I have argued previously that an NTP (ATP — perhaps by chance)
developed as the “universal energy currency” because it was already
involved in RNA synthesis in the hypothetical RNA world. Clearly this
requires hydrolysis of the α–β phosphoanhydride bond of a nucleoside
phosphate molecule. The argument for ATP over ADP would be that the
pyrophosphate produced in the former process is further hydrolysed to
inorganic phosphate by pyrophosphates, and the irreversibility of the
reaction (heat is produced) is important to prevent RNA synthesis
reversing. As NTPs had to be synthesized anyway, they could also be
used for other purposes, but it was energetically more efficient to
hydrolyse the β–γ phosphoanhydride bond if irreversibility was not
crucial (e.g. the product removed).
Once ATP became fixed as the energy currency, metabolism was tuned
for its production and, later regulation. Thus the development of
systems for anaerobic and aerobic synthesis of ADP would not have
conferred any advantage on an organism. When regulatory systems
developed in involving the relative concentrations of ATP, ADP and
AMP (as mentioned above), using ADP to drive reactions would have
been disruptive.

Similar, perhaps, but not identical


text:
Do Mannose and Galactose yield the same products as Glucose when oxidized?
I just started learning about sugar metabolism, when I saw how other monosaccharides enter the glycolytic pathway. Mannose enters glycolysis as fructose-6-phosphate at the expense of 1 ATP, then pretty much follows the same reactions as glucose. On the other hand, Galactose enters glycolysis as Glucose-6-phosphate then would also follow the same reactions as glucose. Does this mean that both of these monosaccharides yield the same products as Glucose? Or is there something I am missing?
I apologize if the answer to this is obvious; I can't seem to find online references that give the net yields for other monosaccharides, so I just wanted to be sure.

The answer to this question is yes. And it is obvious to anyone familiar with metabolism. I hesitated to give a formal answer, but I hate answers in comments, so let me supplement this with some ‘principles’ (in so far as there are any principles in biology) for those less familiar with metabolism (as we all were once).

To a cell, fructose 6-phosphate is fructose 6-phosphate, so its metabolic fate is likely to be the same, regardless of its source. It will be dealt with according to the activity of the enzymes that can catalyse the reactions of F6-P. (These may, however, differ in different cell compartments, as enzymes and concentrations of reactants may differ there.)

Central metabolic pathways such as glycolysis are complex and highly evolved to do their job well. They are found throughout all kingdoms of life†. It is economical to feed minor substrates into them, rather than duplicate a full pathway. Hence the additional pathways for dealing with minor sugars will be those converting them to intermediates of glycolysis, and it is these where metabolic diseases of sugar metabolism are found.

† This doesn’t mean that they are all present in every organism or in every cell type of a multicellular organism. Just that their distribution is such that that (supplemented by other arguments) we consider them to have appeared early in evolution.

Thank you for answering sir, I actually tried to examine how other sugars aside from glucose enter glycolysis and initially thought that there should be no difference in their yields as compared to glucose, but I got confused since I saw a couple of online resources that says galactose yields 0 ATP in glycolysis.

@JoshArceno — You are welcome. I imagine that you must have misunderstood the articles you mention, as galactose is half of the disaccharide, lactose. As the function of lactose is to provide nutrition for sucklings, common sense would suggest galactose oxidation would result in net generation of ATP.


text:
What is the fluid clearance rate inside the retina?
I'm attempting to model the chemical concentration between several compartments of the eye, including the retina. Does anyone have any idea what the rate of fluid removal is in the retina, or could direct me to a study of this?
EDIT: It appears that Müller cells play a crucial role in this, dehydrating the retinal tissue. I am attempting to find the rate at which they achieve this. (see link)
http://retinatoday.com/2008/11/1108_07.php/

For the best of my knowledge the structure that dehydrate the retina is Retinal Pigment Epithelium, not Muller cells.

look at the answer, do you need subsequent clarification?

As I mentioned in a comment, the RPE (retinal pigment epithelium) is in charge of absorbing the "water" from the retina and beneath it.

Water is eliminated from subretinal space by active transport by the
  RPE. The transportation rate was estimated to range from 1.4 to 11 µl
  x cm-2 x h-1.

Oh you are fantastic! Thank you very much. This is exactly what I need.

@Freeman You are always welcome %)


text:
What do arranging and assigning mean in sequence annotation?
Please could someone explain these lines to me in a simple way

These sequences were then arranged based on some overlapping regions present in them. This required generation of overlapping fragments for sequencing. These sequences were subsequently annotated and assigned to each chromosome

What do "arranging" and "assigning" mean in this context?
Source: NCERT class 12 (This text in in reference to the method developed by Frederick Sanger)

I edited the post to improve its format. Feel free to roll back if you don't like it. Would be great if you could link to the source.

Word "arranged" means simply alignment of sequence based on overlapping regions in two sequences. For example:
Seq1: AGTGTCCGTCGTAAGTCA

Seq2:GTCGTAAGTCATCGAGATACC

leading to:
Seq12: AGTGTCCGTCGTAAGTCATCGAGATACC

Maybe he used the word "arrange" as overlapping determines the direction of resultant sequence (for which word alignment is sufficient)
Assignment: Is simply dividing the genome's sequence down as per chromosomes of the species. Like for example, if it's human genome sequence and first chromosome is 2,50,000bp long (just assumption - I don't remember exact figure), then first 2,50,000 nucleotides in the sequence will be "assigned" to chromosome 1. From 2,50,001 onwards to chromosome 2 and so on..

@Felix_17 Pleasure! :)


text:
Can birds suddenly suspend in the air in one position?
I don't know if it was my eyes fooling me or if it was real. I've seen birds suddenly get suspended in the air, flapping their wings but not moving. Like making non-locomotor movement on the air. Is there an explanation for this?

Do you mean hovering?

Doing a stationary flight is called hovering (as @kmm said in the comments).
With head wind
When there is a (relatively important) head wind, many birds are able to perform stationary flights. However, in the bird's referential the flight is not stationary. It is typically common to see that for see birds.
True hovering
In absence of head wind, most birds aren't able to hover. There are a few exceptions. Hummingbirds hover while feeding on nectar. Some birds of prey are able to hover (they do so for hunting purposes) such as the common kestrel for example. While fishing, the pied kingfisher is famous for its hovering behaviour.
Anatomy and metabolic cost
Generally speaking, hovering requires flapping its wings very fast and is therefore energetically very costly. From wikipedia

Most birds that hover have high aspect ratio wings that are suited to low speed flying. One major exception to this are the hummingbirds, which are the most accomplished hoverers of all the birds. Hummingbird flight is different from other bird flight in that the wing is extended throughout the whole stroke, the stroke being a symmetrical figure of eight, with the wing producing lift on both the up- and down-stroke. Some hummingbirds can beat their wings 52 times a second, though others do so less frequently.

Videos
Here are some videos of birds hovering:

Hummingbird hovering
Common kestrel hovering
pied kingfisher hovering


text:
Is there an evolutionary basis for why women mature faster than men?
Females develop both physically and mentally earlier than males do. For example; females start puberty at an earlier age than males, and females brains mature more quickly than male brains.

Girls have always developed earlier than boys - on average the onset
  of puberty happens between the age of 8 and 12 years in girls and
  between 9 and 14 years in boys.

Is there an evolutionary basis for this? Are there theories for why females mature earlier in life?

Hi @WYSIWYG, I am not able to understand your comment. Perhaps it would be helpful if you could advise how I should clarify on the meaning of "evolutionary basis". Thank you.

You should clarify what you expect to know when you ask for evolutionary basis? Do you mean to ask "whether it has/had any evolutionary advantage wrt fitness" or something else? Moreover, the linked article does not really say that the female brain matures faster than the male brain- if I am not wrong it is about brain network reorganization. I am not also sure what you mean by brain maturation. Can you please clarify this too?

I think it's a legitimate question, there is sexual dimorphism in maturation & onset of puberty, why is a genuine and interesting question

To higher the survival rate of the species

You mix males/females and men/women. I know comparison with other species is useful, but is your question about us humans, or is it about a larger branch of the Tree of Life?

You may think about the reproductive success of a family, which depends on the reproductive success of sons and daughters.
The reproductive success of the sons is theoretically unlimited, provided they are big enough to win many competitions. To get bigger, it's good to have a larger growth period. Thus, latter maturation.
The (direct) reproductive success of daughters is limited by the duration of their fertile years. Thus, the more years of fertility, the bigger the reproductive success. Thus, early maturation.
EDIT
Somebody asked for references, so study evolutionary theory:
Darwin, The Origin of Species.
Dawkins, The Selfish Gene.
Futuyma, Evolutionary Biology.
Wilson, Sociobiology.
Wright, The Moral Animal.
I truly hope that's enough. If it isn't, just don't pretend to understand evolution, and quit trying to understand biology.

Wow, you totally stole my answer.

@BenWelborn I didn't even read your answer.

I think you are on the right track. It would be great to (1) further the answer by including references about this hypothesis and typically (1bis) report and explain a published analytical model to explain this concept and (2) eventually cite a paper (if any exists) that apply this concept to humans

@Remi.b I hope you're satisfied now.

Reproduction is kind of the definition of biological success. Logically, it works because it works because it works. Provided that the mother is responsible and healthy, there's a good chance the offspring will survive and reproduce. And since health and age are like opposing forces, the sooner a female develops and develops responsibility, the more likely they will be to reproduce and supply viable offspring to the population.
Similarly, males remain verile for many years past their prime. Since it doesn't matter (as much) whether the father survives child birth, his health is less important. More important (genetically) is the spread of his DNA. The more time a male has to do that the more his DNA will spread. So why not start earlier? Reproducing for an extra ten or twenty years will cause the spread of a much greater amount of DNA than 1 or 2 years early on, and (plausibly) since the male often has a dangerous occupation, males that develop(ed) later (when their size/strength was greater), probably help(ed) ensure the males' survival.
And there is something to say about sexual preference. It is likely that the males' disposition toward healthy females and a females' dispositon toward successful males is genetic... much like a bird who sings the best song. Why? Because it is/was a successful cascade of events.


text:
How is evolution possible in contemporary humans?
I would like to know if evolution is continuing to happen in modern humans, assuming things like existence of the nuclear family structure, fidelity to one partner, etc. It seems to me the answer would be NO because evolution depends on differential reproductive rates, but in the modern world, all male humans have roughly 2.5 (or whatever the number) kids. Add in the process of culturally modified selection pressure, and it seems to me that even an "unfit" male would end up having a couple of offspring. The fittest male (or female) is no better off than his or her contemporaries because of this "leveling" effect.
However, the impression I get from the popular science media is that scientists think evolution is continuing to happen. I would like to know what the actual scientific consensus is, and why. Thanks.

Time rate of evolution is multiple orders slower than time rate of our sociology science perception. If nuclear war will happen, which is probable, then entire humanity appear to last for 30000 years. This is zero in evolution scale. So, evolution DOES continue, but it goes so slow that we cant see it.

This might be a perverse theory, but what if what we identify today as "development disorders" like autism, is actually evolution responding to modern information age pressures

@GabrielFair you should read David Brin's Existence it suggests exactly that!

No I haven't. I will add Existence to the top of my reading list. While we are on the topic have you heard of any research or peer reviewed studies referencing a theory like this one?

cesarian sections are increasing the tendencies to have babies that are too large for the woman's hips.

It is certainly not true that "all male humans have roughly 2.5 (or whatever the number) kids". First of all, male and female humans have exactly the same reproductive rate. For obvious reasons, every time a male has offspring, a female must have had also. Last I checked neither male nor female humans are capable of parthenogenesis (certain popular religious beliefs notwithstanding).
Second, let's assume that the 2.5 number is correct. That would be the average number of children per couple. That does not mean that all couples will have 2.5, or even that most couples will have 2.5. It just means that the average will be 2.5. If, for example you have one couple with 6 children, one with 2 and two with 1, the average will be (6+2+1+1)/(1+1+2)= 2.5.
On to the main point. What does selection mean? In its simplest form, that the individual most likely to survive (the famous "fittest") is also most likely to reproduce. This is a very simple concept, the longer you live the higher your chances of managing to have offspring. If you die two weeks after birth it is going to be hard to manage to reproduce yourself. This has not changed.
So, what does "fitness" mean? It can mean many things. If you are a warm blooded creature at the beginning of an ice age for example, it could mean being better at regulating your temperature than your peers. If you are a 21st century human, it could mean being funnier on twitter than your peers. The two are not fundamentally different. They can both be selected for or against. As long as one mate is chosen over another, selection is happening and the "fittest" (in each particular context) is most often selected.

Add in the process of culturally modified selection pressure, and it
  seems to me that even an "unfit" male would end up having a couple of
  offspring. The fittest male (or female) is no better off than his or
  her contemporaries because of this "leveling" effect.

"Culturally modified selection pressure", as you call it, is still selection pressure. Cultural factors can change what it means to be "the fittest" but there is no objective gold standard of "fitness". While it may be true that in modern human society, different characteristics are selected for than was the case with early Homo sapiens, this does not mean that "evolution is not occurring". On the contrary, it is occurring but perhaps it is moving in a new direction. In fact, this is essentially a circular argument. By definition, "fittest" means most likely to survive and reproduce. It does not mean strongest or fastest or prettiest. It just means whoever is better at reproducing. If that happens to be those individuals who are best at square dancing, then it is they who are the fittest.
Take the example of a modern human with diabetes. Medicine allows diabetics to lead fully productive and largely normal lives. So, perhaps diabetes is no longer a selective criterion. This does not mean that the diabetic cannot be selected for or against based on their fitness on other scales.
Whatever the selective pressure, whatever it may be that defines a "good mate", if selection is present then so is evolution. The only way to remove a species from the process of selection would be to have all (or none) individuals of each and every generation reproducing at the same rate. This is clearly not the case with humans. Surely not everyone around you has, or will have, children? There you go, selection!

UPDATE:
In answer to your comment, yes indeed, in order for a selective pressure to make itself felt and affect phenotype (at the species level), it needs to be constant across several generations. However, even the absence of selective pressure affects evolution. As others have mentioned below, active selection is not the only mechanism of evolution.
Your main question however seems to be the following: If modern society (medicine etc) allows individuals that would not survive in the wild to reproduce, how does that affect evolution? The main points in my answer, and all others here, are:

Even if we accept that modern humans have removed themselves from the purely "biological fitness"-based selection pressure (an assumption I am not at all sure is true), and assuming that this removal is constant enough over many generations (again unclear), even if all this is true, evolution is most certainly still occurring. It may even be faster since genotypes that would not survive in the wild persist in the gene pool, thereby increasing its diversity.
As you point out in your comment below, for such social pressure to make itself felt, it needs to be constant across many generations. We are probably not there yet.
Most importantly, as I said above, there is no such thing as an absolute biological fitness. When the ecosystem changes, so does the definition of fitness. Modern humanity's ecosystem, our habitat, is intimately connected with our culture and society. If an individual is better at reproducing in that context, then that individual is more fit.

Thanks for the answer. A follow-up: It's true that not all couples have the same number of children, but it seems like whether or not they have more children than average is no longer strongly dependent on biological fitness. Therefore, given that reproductive rates are fickle from one generation to the next (due to cultural factors), the signal would not have time to develop, right? It seems to me that there should be a persistent multi-generational selection pressure for the phenotype to develop, which is missing in the modern context. Maybe evolution is occurring, but significantly slower?

Very thorough answer. +1

I doubt that the distribution of reproductive success is exactly the same for men and women.  you are assuming that women and men have the same partners all through their lives, which is not so true at least in the US. In a society where a large percentage of children are born out of wedlock men and women do not need to have the same reproduction distribution. Also in polygamous societies or where there is gender based infanticide it doesn't hold. No judging here, just saying. Overall the point holds, but not sure you needed this base assumption.

@shigeta, for every child a man has, somewhere a woman has had one also and vice versa. Wedlock has nothing to do with it, nor does infanticide or anything else. This holds true for all (exclusively) sexually reproducing species. By definition.

@joebevo "It seems to me that there should be a persistent multi-generational selection pressure for the phenotype to develop, which is missing in the modern context. Maybe evolution is occurring, but significantly slower?"
... Evolution IS a slow process which has been occurring over billions of years, gradually fumbling its way along to the many species we know & others that have existed. Selection, though not constant, will have a temporary consistent tendency over a time frame which to us is huge (possibly hundreds or thousands of generations) but in an evolutionary sense it is very short.

Can I just add here that evolution would happen even without any directional selective pressure? You're all talking about fitness and directional selection, whereas selectively neutral processes (drift, migration) can also dramatically change the allele frequencies in a population ergo evolve the populations (think asteroid and the dinosaurs).

@yotiao, you're quite right of course. That's what I mean by "active selection is not the only mechanism of evolution" and it was also mentioned in DQdlM's answer below.

"That does not mean that all couples will have 2.5, or even that most couples will have 2.5." In fact, it's safe to say that no couples have exactly 2.5 kids.

@BruceAlderman well yes, I was going to make that point but then I figured that I might be belittling someone's personal tragedy. Do you know that no one has ever given birth to, say, a fine set of legs and attached pelvis alone? :)

+1 For noting that that the average number of kids per male is insignificant

I think that it is possible that the average number of kids per male to be different from the average number of kids per female. Consider this situation: Suppose the world has only one human male and two human females. If a male has exactly one kid from each of the two females, then the average number of kids per male is 2, while the average number of kids per female is 1

Let us not forget the effect of contraceptives and family planning, which is quite new. Now evolutionary very "fit" people can decide to have fewer kids.

Evolution is defined as the change in the allele frequency of a population through time.  In other words a change in the genetic diversity of the population through time.  This change can be the result of 4 processes, known as the mechanisms of evolution:
1) gene flow - this is the movement of individuals into or out of the population.
2) genetic drift - this is the removal of individuals due to random events (such as accidents).
3) mutation - this is the spontaneous change in the DNA, which instantly increases genetic diversity.
4) selection (natural, sexual or artificial) - this is the increase in the frequency of alleles (traits) that confer a fitness advantage (i.e., those with a given trait will leave more offspring). Most adaptive changes in gene frequency are the result of selection.
Even if one presumes that your analysis is correct and natural selection is no longer operating on modern humans (although this is suspect, as is pointed out by other answers), evolution would still be occurring due to mechanisms 1 - 3.  If we go further and consider the Earth's human population as a whole (eliminating gene flow as a mechanism) you would still have evolution via genetic drift and mutation.
In other words, yes, evolution is not only possible but inevitable in modern human populations.

In the US, different races have significantly different birth rates.  Obviously race has a genetic component, though I'm guessing that the racial differences are mostly due to cultural and economic reasons.  Still in this sense, the US population is evolving: alleles associated with some populations (African Americans, Hispanics) are becoming more common, while those associated to other populations (white non-hispanic, etc) are becoming less common.  So the US is definitely evolving to become "less white".  Note that this is true even though the overall birth rate reported in the study is not much above the minimal replacement rate of 2.0.
Another example: religiosity is associated with increased fertility, and there is some evidence that religiosity has a genetic component.  In that sense, the population may be evolving to be more religious over time.
Similarly, there are genetic factors to obesity, which has a negative effect on fertility.  These genes may even have been actively selected for in the past (the thrifty genome hypothesis), but are probably being selected against now.
We are currently undergoing one of the biggest shifts in human fertility in the history of our species: in the past century, we've developed technologies which allow people to more carefully choose when to become pregnant (condoms, abortions, hormone birth control).  Any genetic factor which has an impact on use of birth control could lead to evolutionary changes: this could range anywhere from ethnicity associated with economic or religious status (poverty, Catholicism), impulse control, etc.
This is all somewhat speculative (except for the first example), but it's certainly possible for evolution to occur in modern human society, and it likely is occurring.

I just want to emphasise that "races" is more of a social construct than a scientifically strictly defined category (see Razib Khan's comment here: http://blogs.discovermagazine.com/crux/?p=1350#.UR45L1qcYVo) . So while I agree with a term "alleles associated with some populations" the other terms you use ("race has a genetic component", "less white") are more murky (unless, in the latter example, you're talking about alleles associated with skin color - but then again, they do not necessarily correlate with ancestry).

I mean that there are differences in allele frequencies among the census bureau race/ethnicity categories.  These are probably self-identified groups, but there are differences in allele frequencies between the group of people who self-identify as hispanic vs those who self-identify as white/caucasian.  Alleles common in the former group are becoming more frequent relative to alleles common in the second group. Those would presumably include some alleles for skin pigmentation, among others (like variations in lactose tolerance, renal sodium channels, sickle-cell anemia, etc).

To rephrase that paragraph in more PC language: some self-identified ethnic groups have higher birthrates than others. To the extent that allele frequencies in high-birthrate ethnic groups are different from the mean frequency for the population as a whole, the US population is "evolving" to increase the frequencies of those alleles. I added "race has a genetic component, but..." to specifically avoid an interpretation that genetics were the cause of increased birthrates.

Darwin used the term “descent with modification” to describe evolution. That means a change between generations in the characteristics, or traits, of a population. It is a process which occurs by four processes - mutation, migration, drift, and selection. The conditions for evolution are i) a population must be able to reproduce, resulting in a descendant population, ii) offspring must tend to resemble their parents and this occurs because traits are determined by heritable information, e.g. DNA, and iii) that heritable information must have the potential to change from one generation to the next. It does not require selection.

Here is a paper about evolution and adaptation in humans:

"Despite popular misconceptions, natural selection does operate in
  modern human populations. New studies even show that changes
  associated with modernization are deeply reshaping selection pressures
  and, perhaps, bits of our biological nature."

Selection is still occurring in humans too, leading to further adaptation (a subprocess of evolution) (e.g. here and here). Many people naively think and suggest that selection has been halted in humans, the fact is, it hasn't. We still have variance in reproductive success based upon the genes individuals possess, e.g. some people die from genetic diseases before reproduction.

Here are some illustrations describing the mechanisms of evolution. Note that drift and selection both cause variance in reproductive success among individuals in a population, for drift the variance is independent of the genes, while for selection it is a tendency for the carriers of one allele to have higher reproductive output than another.
Mutation:

Migration:

Drift:

Selection:

Modern humans are continuing to evolve. Let me give you an example.
Before cattle were domesticated over 99% of all adults were lactose-INtolerant (i.e., they did not produce the enzyme needed to break down lactose (lactase) and could not digest it, i.e. got diarrhoea if they drank milk). All infants produce this enzyme, but in lactose-intolerant people the gene that codes the enzyme responsible for breaking down lactose becomes suppressed after the age of 1 or so. Before domestication of cattle, lactose-intolerant people were by far the majority in any human population. Why? Because if you never consume milk, constantly producing an unneeded enzyme is a huge waste of protein, especially in conditions of limited food supply. With the domestication of cattle, people who could utilize lactose suddenly had a huge advantage - they had another source of protein and calcium. They quickly became bigger and stronger than people who could not consume dairy products in adulthood. Thus, people in Europe and Africa (where cattle were domesticated) quickly became lactose-tolerant, unlike people in Asia, where to this day most people are lactose-intolerant. The evolutionary pressure at that time was huge - people in Europe and Africa went from mostly lactose-intolerant to mostly lactose-tolerant in 10 000 years or so. Interestingly enough, in this respect cats evolved in parallel to humans and now cats in Europe are predominantly lactose-tolerant, whereas cats in Asia are mostly lactose-intolerant.
Of course, this is not the only change that has occurred within the last 10 000 years and it surely is not the last one that will take place. It is just an illustrative (and hopefully interesting) example of evolution and natural selection in modern humans. In what direction humans will evolve in the future is very speculative.
As requested, a couple of references: http://evolution.berkeley.edu/evolibrary/news/070401_lactose
http://www.smithsonianmag.com/arts-culture/lactose-tolerance-and-human-evolution-56187902/?no-ist

can you please add some references to this answer

Evolution is possible for the same reasons it has always been possible (and I'll let the other answers' details comment on the mechanics, as they have done already...
I would like to offer a *slightly more philosophical point of view on the term, however.  I think that we have arrived at a point in our evolution where our prefrontal cortex is impeding our biologically driven urges, somewhat (which would have us evolving in similar ways to all the creatures less aware of the consequence of their actions).
I think it's impossible to say to what extent our evolution will now be driven by conscious choices we make about what traits we value vs. the traits that our biology drives us towards.  Certainly innate biological drivers are incredibly powerful, but as is evidenced by our desire to promote our intellect, and our progressive urge to help even the sickly and mentally challenged to get the most out of life (up to and including procreating), rather than to evaluate our potential partners purely based on physical traits and our brute strength, these purely biological imperatives are governing our reproductive choices less and less.
There is also much (reasonable) speculation as to what our new found understanding of genetics will allow us to artificially do to ourselves in the near future.
I think it's important to consider both these factors when speculating about how we're evolving, but I think it's not even slightly controversial to suggest that we're definitely evolving in a different way now than we were 500k years ago.


text:
Evolution, self organization and neuroscience
I have rudimentary knowledge of evolution, and biology in general, so bear with me if this question is a bit naive.
Let's say we have a particular trait, like highly sensitive peripheral vision. There are two ways to go about explaining how this came about:
One is to say that evolution selected for it over time, because animals with a poor sensitivity to peripheral activity could easily become prey. So there is an advantage to having sensitive peripheral vision, and such a trait is adaptive. The picture I have in my mind is of an assembly line where there are randomly wired visual cortices and the best ones get selected for automatically. This seems to be the view of the field of evolutionary algorithms, at least to my mind.
Now, if we focus on the random nature of the wiring, we might see that there is an explosion of possibilities in terms of how the visual system can be wired together. After all, evolution is blind, and it doesn't know beforehand which physical signals are of interest.
I'm trying to think of a more plausible mechanistic explanation. Suppose we assume that given certain reliable properties of the physical world, like permanence of objects for example, evolution has found the optimal way to wire the visual cortex so that peripheral vision (and a host of other good-to-have features) is a natural outcome, then it would give us more focus in what environmental features and algorithms to look for. This can also be thought of as the idea that evolution, over time, has come to assume that certain things in the physical world will be a given and exploits these. (For example, objects in the peripheral areas of vision will tend to have different perceived velocities, so perhaps normalizing velocities across the field of vision automatically results in a need for higher sensitivity in that region. It just so happens that this could also be useful in detecting predators).
My question then is, is my assumption in the above paragraph valid? (Of course, the question then gets shifted to "Why normalize velocities across the visual field in the first place?").

I'm not sure that I fully understand the question, so I'm not answering. However the idea that adaptive evolution proceeds from a set of randomly wired visual cortices seems to me to be a wrong assumption - rather at each stage it starts from an already partially optimised wiring, with smallish changes offering some selective advantage. I think this resembles your more plausible explanation, but as I say, I'm not sure that I fully understand.

What is your assumption, I don't fully understand. You assume that given some properties of the world, evolution selects for the most optimal solution (for a given living thing to increase its reproductive success). Is this your assumption?

@Remi.b: My assumption, stated more simply, is a sort of "maximum efficiency hypothesis". That is, that evolution assumes the environment to be a certain way, and codes this into the developmental program, and therefore implicit in the developmental program are certain invariant features of the world, which the program uses to develop the brain fully. I think my question is more about developmental biology than it is about evolution.

@Joebevo See my update. let me know if it starts to answer your question! Sorry if I use some technical words that you don't know but their meaning are easily understandable from wiki articles. You might already know the concept of fitness landscape from computer science and genetic algorithm.

I recommend looking at Hoffman's interface theory of perception to help you explore some of the assumptions you are implicitly making in your question. Also, just because a fitness peak exists, doesn't mean you'll get there (for any reasonable notion of getting there).

another idea is that there are general algorithms for cognition/processing sensory data and they are reused in different parts of the brain for different sensory modalities (sight, hearing, etc) and all that is needed of evolution is that it "discovers" these algorithm(s), & incorporates them into neuron function. in other words why would peripheral vision processing be much different than "central" vision? this general idea/theme is somewhat articulated by Hawkins. see also research on visual "feature/line detectors" (possibly the basic function in play here)

fyi here is a recent blog on a candidate for such an algorithm supported by circumstantial/direct biological/computational evidence... line/feature detecting algorithm/sparse coding in visual cortex

@ArtemKaznatcheev: Thanks, that was quite an interesting video. However, I do think he's throwing the baby out with the bathwater. He's taking the so-called "bugs" in perception as evidence that perception is completely flawed. But, he does raise some interesting philosophical points about the truthfulness of perception, which is relevant to my question. (In general, I think throwing out conventional wisdom in favor of a computer simulation of evolution is dangerous).

Since the question is already answered, I will just add few points: Evolution is based on 'mistakes' (you can also call them 'experiments' or 'random-events' etc.). Experiments which are deemed useful are passed on to future generations and eventually selected. One additional point: in the context of your question, you are considering eye and brain (visual cortex) as separate, which is not the case. The eye is the sensor which sends brain all the sensory input data and brain processes it. The image you perceive, the colors etc. are your psychological response to different frequencies and inten

I don't fully understand your question. I hope the following will help a bit.
I'd like to pinpoint what seems to me to be one important mistake in your text. Reading you we have the feeling that selection acts on wires so to select the best combination. If this is what you meant, then it is obviously wrong. The thing is that the change that get inherited are alleles. An allele is a variant of a gene. For example: gene codes for eyes color. A bi-allelic gene has an allele which codes for blue eyes while the other codes for brown eyes. Assuming that there is genetic variance underlying the wire connection variance in the population, then yes selection will select for the best genetic variant. This does not necessarily mean that this best genetic variant is the most optimal possible to imagine solution. The most optimal allele might have never been created just because of the randomness nature of mutations.
EDIT:
To answer:

Do natural selection always bring a particular phenotypic (loosly speaking, phenotype = morphological) trait to its optimal state?

No! It does not.

The main reason is that the genetic variant coding for this optimal trait does not necessarily exist because of the randomness of mutational process. Also, because of the metabolic pathway bringing some variance to a trait, it is often very hard to even imagine a  mutation that would allow creating a new, more optimal, phenotypic variant. So indeed developmental biology has to be taken in account to.
Because in absence of genetic drift (infinite population), selection can only bring genotypes uphill in the fitness landscape. If a very high peak exist somewhere in the fitness landscape but in order to reach such peak, 10 mutations are needed were all of them in any other genetic background are deleterious (correspond to valleys in fitness landscape), then the optimal high will probably never be reached (except if all 10 mutations appear suddenly in the same individual).
Because selection might be weaker than genetic drift. Also, different subpopulations might be in different environments were different traits correspond to optimal traits and because of migration (gene flow) between subpopulations, it is possible that no optimal phenotypic trait can be ever seen although all the genotypic variance exist.
The seemingly most optimal trait might actually not be really optimal. For example: Peripheral vision might be limited by the brain rather than by the eye because it would be an important energy cost for the brain to process more information, a cost that might outweight the benefit of having a better peripheral vision.

Your two arguments are actually the same
The import point you are missing about the algorithm approach of optimizing a genome is it optimizes for the environment it was cycled through in the past. the laws of physics have been constant through those generations so the system becomes optimized for the laws of physics. Well optimized for physics at the scale of life at least, we are not good at handling relativity for instance.
It is much the same reason the human brain favors a desire for sweetness that is counter productive in a modern industrial world, because in the environment of our ancestors getting problematically high concentrations of sugar is simply impossible, so there is no benefit to having evolved a limiting behavior. Evolution has only had a handful of generations to select for anything else. Advantage and disadvantage are always relative to the environment, so the environment of the ancestral line effects how evolution optimizes an organism. Consider being very good at conserving heat would be very beneficial in the artic and very detrimental in a hot jungle. Retaining water would be very helpful in a hypertonic environment and very deadly in a hypotonic environment. Things are adaptive or maladaptive depending on the environment so evolution favors or disfavors the passing on of genes differently depending on the environment. A brain the predicts motion well under earth gravity has a big advantage, on earth, but since earth life evolved on earth brains can be slowly optimized for predicting motion under earth gravity, note I say can be sometimes the brain is stead simply made plastic and learns to predict motion in earth gravity because it is only exposed to earth gravity. It can be very hard to tell which is occurring.
Now it is worth noting optimization is only local not ultimate, Remi covers this quite well in his discussion of fitness landscape so I will refer you to it, I will just say optimized is not the same thing as perfect, it is only the best given what is available and given a history of X.


text:
What does the "G" and "V" in penicillin V and penicillin G stand for?
I've been looking for a convincing explanation for the designation penicillin G and V. The answers I've found includes G as in "gold standard" and "V" as in "viscus" but they're not sourced and not especially credible explanations.

The first discovered penicillins were designated I, II, III in Britain and F, G, X in America. I can't find what the letters stand for. Could it be that, as they were determining the composition of natural penicillin (which originally referred to the Penicillium culture supernatant), they designated compounds alphabetically and these letters happened to correspond to penicillins?

Penicillin V is synthetic and, according to this book, was named V for vertraulich (German for confidential).

The answer to this question lies in a reference from Ernst Chain written in 1948. The paper is titled "The Chemistry of Penicillin and is in Annual Review of Biochemistry. I don't know if it is open access, but it has a first-page of PDF available to read for free, full reference at the end of this answer.
The names derived from a recognition that there were different penicillins with different properties, but people at the time lacked understanding of what these properties might be. It turns out that the differences are side-chains on the core penicillin molecule and they are named based on their order in terms of discovery - so "A" would be first and "G" later. To quote the article:

Multiplicity of penicillins. Nomenclature. - As the work on the
degradation progressed it became clear that penicillin was not a single substance, but that there existed several penicillins, possessing very similar biological and chemical properties, though differing in their chemical composition. It was found that they
contained a common nucleus, but differed in the composition of a
side chain R (XXVIII). They were at first distinguished in England by Roman numerals (following the historical sequence of their
discovery) , and in the United States by letters.

At the time of the article being written, there were quite a few that were found as indicated by Chain's table 1, reproduced below:

Name of Penicillin
Original Designation
Formula of Side Chain*
Empirical formula*
Reference

$\Delta$-$\beta$$\gamma$-pentenylpenicillin
I or F
CH3CH2CH=CH.CH2--
C14H28O4N2S
11,12

$\Delta$-$\gamma$$\delta$-pentenylpenicillin

CH3CH=CH.CH2.CH2--
C14H28O4N2S
13

n-heptylpenicillin
K
CH3CH2CH2CH2CH2CH2CH2--
C16H22O4N2S
14, 15

benzylpenicillin
II or G
C6H5CH2--
C16H18N2O4S
16

p-hydroxybenzylpenicillin
III or X
OH.C6H4CH2
C16H18N2O5S
17, 1

* There might be some errors in these formulae as the original table is hard to read and copy/paste gives errors
Ref:
CHAIN E. The chemistry of penicillin. Annu Rev Biochem. 1948;17:657-704. doi: 10.1146/annurev.bi.17.070148.003301. PMID: 18893607.


text:
Is carbohydrate an important part of phospholipid?
My professor tells us that carbohydrate is an important part of phospholipid, but phospholipid is composed of Choline, Phosphate, Glycerol and two Fattyacid, and I don't think even one of them is carbohydrate.
What's wrong with my statements?

Question: What is a fatty acid and which elements do you find in it?

Similar question: what are the elements in glycerol?

@Chris Sir, fatty acid is a kind of lipids and I find C,H,O in it.

There you have the carbohydrate part you are looking for.

@Chris fatty acid is also carbohydrates? I don't think so. It's not in the textbook. Lipids and carbohydrates are completely different.

No, but the fatty acids have a carbohydrate tail.

@Chris do you mean hydrocarbon tail? And phosphoinositol would have something similar to a carbohydrate as its head group.

Phospholipids have lipids, of course, but those are bound to glycerol, a 3 carbon carbohydrate that is usually derived from glucose.  Glycerol is the only carbohydrate (or even carbohydrate-like) part of the phospholipid.

@JasonPatterson Thanks, that's the right answer I am looking for! Would you mind write this as an answer?

Your thinking is correct based on typical carbohydrates, but glycerol, the backbone of the phospholipid, is a 3-carbon carbohydrate that is usually derived from glucose.  It is not a sugar, but it does fall into the general class of polyols (aka sugar alcohols) that are a type of carbohydrate.
A carbohydrate definitely is an important structural part of the phospholipid, but your instructor probably should have been more clear in describing why that is the case; I can definitely understand your confusion here.

There's nothing wrong in your statements!
Maybe your professor was talking about glycolipids, that are lipids (also phospholipids) with a carbohydrate attached; they can be found on the outer surface of all eukaryotic cell membranes. They are important because they work as a recognition site for specific chemicals or for antibodies.