text:
Is it possible to get (an estimation of) reaction rates from the Michaelis constant?
I want to apply the Gillespie Algorithm to a biological system so I need to know the reaction rates for the relevant reactions. However, for all those reactions, I only know the Michaelis constant $K_M$ and the maximum rate $V_{max}$ (see Wikipedia). Is it possible to derive (an estimation of) the reaction rates $k_f$, $k_r$ and $k_{cat}$ (see image below) given $K_M$ and $V_{max}$? If so, how can it be done?

$K_M$ is a ratio and for QSSA it is $\dfrac{k_{cat}+k_r}{k_f}$ and for equilibrium approximation it is $\dfrac{k_r}{k_f}$.
It is clear from the formula that you cannot obtain all the constants simulataneously. If you know two (in case of QSSA) you can get the third.


text:
Are both B and Y ions required to determine the sequence of a protein by mass spectrometry?
I was wondering if both all b and y ions are required to determine to order of the amio acids in a peptide.

In my opinion knowing only ALL B ions or ALL y-ions is enough to determine the sequence of the amino acids in a peptide. I was also wondering how these b and y ions are differentiated in a spectrum?

I'm struggling to understand the diagram. You're asking about b and y ions, but b and y are pointing to C-N bonds. Could you expand. I'm not exactly sure what the bioinformatics tag is doing here.

In an MS/MS spectrum, difference between the successive peaks of a b or y ion series allows one to determine the amino acids making the series/peptide. Either one of them should be enough to give you the sequence. However, an MS/MS spectrum obtained from the mass spec instrument doesnt tell fragment types. Therefore it takes some expertise and tricks to spot y or b ion series. For example: if you are analysing a sample digested by trypsin, your C-term residue will either be K or R. So you can look for a Y1 ion if there is 147 indicating K or 175 indicating R. Also, Y ions tend to be highest intensity peaks in a spectrum. For more helpful tips on this there is an excellent tutorial :
http://www.ionsource.com/tutorial/DeNovo/DeNovoTOC.htm.
Also, in practice you seldom get all of the b or y ion peaks and there are often missing peaks. For this reason it is useful to have both b and y ions series so that gaps in one can be filled by the other. This is not only useful when you are dealing with denovo sequencing but also in a more typical shotgun proteomics experiment. In a typical shotgun proteomics experiment one searches their mass spec data with peptide search engines. These are software which use a protein sequence database which is in silico digested, based on the specificity of the protease used in the experiment, and from the resulting peptide sequences search engines make a library of predicted MS/MS spectra (this is done by fragmenting along the peptide backbone and listing all possible b and y ions). Then these predicted spectra are matched with the observed spectra to predict the peptide sequences that could result in the observed spectra. Again, not all of the peaks present in a predicted spectra will be found in an observed spectra. So it is best to have ions from both b and y ion series. More ions matched between the observed and predicted spectra, better is the score and confidence in identification.

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text:
Why are Natural Killer cells considered cells of Innate immunity?
Kuby Immunology says

They (NK cells) do not express antigen specific receptors and are considered part of the innate immune system.

Though
 they also have receptors for antibodies that bind to NK cells and help detect antigens or pathogenic cells that are killed by the secretions of their cytotoxic granules.
Couldn't we then call them cells of Adaptive immunity?

What edition are you using? As I mentioned in my comments to one of your other recent questions, immunologists no longer consider innate and adaptive immunity to be two entirely separate things. Cells thought to be involved in one are now seen to be involved in the other, and the processes are getting very blurred. You are quite correct that NK cells are involved in antibody-dependent cell-mediated cytotoxicity (ADCC), which is wholely an adaptive response due to the presence of antigen-specific antibodies on the surface of the target cell. Your textbook is simply incorrect.

@MattDMo It is the new edition, 7th Ed by Owen, Punt and Stranford.

@MattDMo Following your comment I have a question. I was reading Wikipedia page on Innate lymphoid cell and stumbled upon this paragraph-'The distinction between the innate and adaptive immune system focused on the innate system’s nonspecific nature and lack of memory.As information has emerged about the functions of NK cells and other ILCs as effectors and orchestrators of the adaptive immune response, this distinction has become less clear....  (to be continued in second comment)

Some suggest the definition focus more on the germline-coding of receptors in the innate immune system versus the rearranged receptors of the adaptive immune system.' What does the third line mean?

Yup! you've answered your question. The NK cells donot have rearranged receptors. Nor do they have any memory.

@Polisetty I agree with MattDMo the NK cells show immunological memory according to Wikipedia. But I don't understand the rearranged receptors. What are they?

The BCR and TCR (B cell and Tcell receptors) are formed by V(D)J recombination which accounts for their variability. This makes the receptors specific to a particular antigen. Kuby's got a whole chapter on that. Thanks for the memory thing, din't know! Anyway, found this article for nkcell memory http://www.cell.com/immunity/abstract/S1074-7613(15)00398-2

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text:
Does the string "...CATCAT..." appear in the DNA of Felis catus?
In Hofstadter's Gödel, Escher, Bach: An Eternal Golden Braid (GEB), the following claim appears:

...in the species Felis catus, deep probing has revealed that it is indeed possible to read the phenotype directly off the genotype. The reader will perhaps better appreciate this remarkable fact after directly examining the following typical section of the DNA of Felis catus:
...CATCATCATCATCATCATCAT...(OP note: truncated because, you get it)

Is this true? A cursory search for the DNA of Felis catus gives me this 1996 paper by Lopez, Cevario, and O'Brien and the given sequence does not appear – there are some instances of "CAT" but not repeated enough to make it as remarkable as claimed in GEB.
I don't know enough Biology to judge the veracity of this claim. Some points I am considering are:

GEB is full of wordplays. However, the tone of this part of the text does not sound like one to me.
GEB was written/published around 1978. The paper I linked to – which was cited by some 236 others according to Google – was published in 1996, way after GEB's time. If my impression that Lopez et al.'s work is significant because it is the first time Felis catus has been sequenced, then there is no way Hofstadter could've known of it when he wrote GEB. Then again, I don't know enough Biology that there might be some nuance to Lopez et al.'s paper that I'm missing (i.e., the results of the paper might not be mutually exclusive to the claim made in GEB).
GEB has reference notes and bibliography and there is no reference cited to back this claim. However, GEB does not attempt to be a rigorous academic thesis and the references is only called upon more when Hofstadter quotes other works directly while the bibliography is a list of readings which the reader may want to check out, regarding the main thesis of the book.

So are cats recursions with no base cases?

Welcome to BiologySE! You came with a bang! ;)

As a rule: when you find amazing scientifically impressive postulates in GEB, you better make sure whether you detected them in one of the dialogs rather than the main material. Hofstadter's dialog characters tend to take a considerable amount of poetic liberty with the underlying science. I don't know the section you found this in, but the statement about the phenotype being deducible from the genotype very much sounds like having more tongue in cheek than an average cat could hope for.

Does Lady Gaga's DNA have GAGAGA?

While I don't know the cat genome, I'm pretty sure the dog genome doesn't contain DOG.

I'm voting to close this question as off-topic because, amusing though it may be, but the relationship between the Englsih word cat and the abbreviations used for molecules can in no respect be regarded as being about biology. Perhaps it has something to do with statistics or English literature.

I’m voting to close this question because this is trivial and stupid.

I’m voting to close this question because as @David has pointed out in the past this question is trivial and has no biological relevance.

@tyersome Yet, it has been upvoted at least 92 times and favorited 22 times.

I’m voting to close this question because it is of no scientific interest whatsoever.

Interesting. I now see both @tyrsome and I voted to close this previously   Why were our close votes removed?

@David Bcoz no one else supported and your votes aged away. They age away after 14 days.

@user237650 — Thanks for the info. Well, at least the comments don't.

The Felis catus genome has been published, annotated, and updated quite a bit since 1996, including spans of so-called intergenic regions, which are basically scaffolding and other structures, along with perhaps some unidentified genes, pseudogenes, regulatory sequences, etc. Basically, pretty much the entire DNA sequence is available now, not just the gene sequence of the mitochondrial genome, which was what was published in the 1996 paper you referenced. Mitochondria are the power plants of the cell, but are just an organelle that happens to contain its own DNA; they are separate from the chromosomal DNA in the nucleus. All of this is available for free (if you know where to look) at the National Center for Biotechnology Information (NCBI), part of the National Library of Medicine (NLM) at the National Institutes of Health (NIH) in the United States. Other sites are also available, such as Ensembl, a joint project between the European Bioinformatics Institute (EMBL-EBI), part of the European Molecular Biology Laboratory (EMBL), and the Wellcome Trust Sanger Institute (WTSI). Both institutes are located on the Wellcome Trust Genome Campus in the United Kingdom.
So, to the genome. Genomic sequences can be searched in a couple of different ways, depending on what you're looking for, but the most common way is to use BLAST, the Basic Local Alignment and Search Tool. As the name implies, it takes sequences as input and searches one against the other, aligning the results as best as possible using certain algorithms that the user can define and tweak. The BLAST web interface to the cat genome is here. You don't need to worry about any of the other options here except the "Enter Query Sequence" box. FASTA format is just using the single-letter abbreviations for nucleotides (AGCT), all strung together.
The genome we're searching is of an Abyssinian cat named Cinnamon:

Cinnamon, the cat which was chosen to be the definitive genetic model for all cats in the feline genome project. Image courtesy of the College of Veterinary Medicine at the University of Missouri.
To start with, I typed in CATCATCATCAT and to my surprise got back over 200 hits, covering every chromosome the cat has. So, I doubled the length of the input to 8 CATs, and got back the same result set. Unfortunately, 12 CATs was too many (and really, it is too many), so I worked backwards.
The final results are here (sorry, link expires 10/13/16. To regenerate, go to BLAST link above and enter CATCATCATCATCATCATCATCATCATCAT). Apparently, popular wisdom is incorrect, and Felis catus chromosomes really contain 10 CATs each, one more than is needed for their 9 lives. No word yet as to why this may be, but scientists are presumably working on it.

The irony might be taken seriously, I don't think it is a good place for joking.

@har-wradim what is ironic here? The last sentence? No harm there as I'm not interested in deep research on cats, per se. I find the answer well-detailed and, limited as my biology knowledge is, Matt's explanation adds up, reproducible and verifiable. Well, NCBI Blast's UI isn't Apple-quality but it holds up as far as I can interpret it.

My question is, is felis catus the only species for which this is true? I would suppose otherwise.

@Jan: I would say it's highly unlikely. This is just pattern matching with an astronomical input set.

@JanDvorak can you come up with an animal spelled with A, T, C, and G?

THE MOAR YOU KNOW: Rumor has it that some well known pop singer has lots of "GAGA" in her DNA. In other news: every other carbon-based lifeform does too.

I heard that the entire cast of Gattaca had GATTACA sequences in their DNA.  Most of the crew did to.  I smell a conspiracy.  I think they even passed a law about large numbers to cover it up.

My background is in mathematics; I joined the Biology StackExchange in order to leave this comment. The cat genome, like our own, is about 3 billion base pairs long. The probability of matching a sequence of n base pairs starting at any given position is 1 in 4^n (since there are 4 possible base pairs), which for n=12 is about 1 in 16 million. That means you'd expect to find around 200 matches for CATCATCATCAT if all short sequences were equally likely. This won't be perfectly true, but as March points out the widespread existence of tandem repeats makes matches like this still more likely.

Reading many of the comments on this page, I get the feeling that while some of us here are having fun, others, less informed, are completely confused. My vote goes to @March Ho.

@har-wradim what exactly does that mean?

@har-wradim never mind, I see. Some people have completely missed the joke, and are taking this way too seriously.

@skytreader "NCBI Blast's UI isn't Apple-quality but ..." meaning that it cannot search apples' genomes? or.. ?

@DaniloRamirez Apple as in where Macbooks come from. A lot of scientific tools, heck even industry products, have UIs that aren't Apple-quality but are nonetheless useful and powerful.

I very much appreciate the humor at the end there :)

@skytreader Oh that Apple.... please don't...  :) the pun was intended from the initial comment, but thanks for keeping it very explanatory

@MattDMo So do I understand it correctly, could there be some other cat different from Cinnamon that can have more CATCATCAT... than her? Because we only analysed one genotype and those of other organisms of the same species can differ, right?

@nuoritoveri Yes, that is possible.

I think this is the longest one https://www.ncbi.nlm.nih.gov/nuccore/NC_018733.3?report=fasta&from=72130713&to=72130839   $(CAT)_{41}$ (reverse complemented) perphaps you forgot to uncheck 'mask low complexity regions' ?

While Matt's answer is perfectly correct, it is important to note that the sequence $(CAT)_n$ in DNA is not restricted to cats, and you would expect to find it anywhere.
For example, searching the human genome for the same 3-tandem repeat CAT sequence results in many hits as well.
This is because you are essentially searching for short tandem repeats on the DNA strand. These repeats can occur in any organism, and therefore while finding CAT substrings in the DNA of the cat may be amusing, they aren't special to cats (or any other animal) and are only the result of an artifact of naming of the bases coincidentally matching with the name of the animal.

The bases are not just 'named', they represent the four nitrogenous bases: adenine, cytosine, guanine and thymine.

@SummerEla While you are right, I don't see how it's inaccurate to call that "naming".

Well, it's more like an acronym than a naming system: those three nucleotides together (called a codon) ultimately work together in strings of codons to code for a specific protein.

@SummerEla If the bases were called adenine, bytosine, cuanine and dymine, then you would have BADBADBAD. If they were called qurine, quadrium, quitterium and quinterone, then you'd have QQQQQQQQQ. And so on. By renaming them, you can make up any short word containing only four different letters, and find it in whichever chromosome of whichever animal you want - for example you could make the human Y chromosome contains "MENS".

@immibis what?
My point was that the bases are not named arbitrarily, they actually stand for nucleotides that comprise amino acids, which when combined make up proteins.

But the naming of the nucleotides themselves is ultimately arbitrary. According to http://etymonline.com, adenine is "so called because it was derived from the pancreas of an ox", while guanine is named "from guano, from which the chemical first was isolated" and thymine "from thymic acid, from which it was isolated" (cytosine comes from cyto- meaning "cell"). Had the discoveries occurred differently, those chemicals would have very different names.

HAHAHA (no, not a remapped/renamed nucleotide sequence--really laughing). For some reason, this makes the GEB claim funnier. Thanks for the clarification!

@SummerEla Well yes, when the sequence "cytosine, adenine, thymine" encodes a particular thing. So does the sequence "quadrium, qurine, quinterone" because those are actually the same sequence, I'm just using different names to refer to the same bases.

@SummerEla  So does "thymine, adenine, cytosine" in an alternate timeline where the word "thymine" refers to the base with one ring and an NH2 subgroup, and "cytosine" refers to the base with one ring and no NH2 subgroup.

@SummerEla Also, I'm pretty sure nucleotides don't comprise amino acids, only code for them.

So as per Matt's answer (that there is a 10x sequence), can that 10x sequence be found in any other organisms?

To augment the other answers, let's compute the probability of CATCATCATCAT occurring in random DNA sequence.
Cat DNA length is 2.7 gigabases (source), and there are 4 possible bases.
For 1 CAT there are 3 bases, giving expected number of occurrences in 2.7 Gb as $\frac{2.7 \cdot 10^9}{4^3} \approx 42\,188\,000$
Repeating the calculation for longer sequences gives:

1 CAT: 42 188 000 occurrences
2 CAT:      659 180 occurrences
3 CAT:        10 300 occurrences
4 CAT:             160 occurrences
5 CAT:                2 occurrences
6 CAT:
               0 occurrences

So, indeed, there are many more CATs in cats than could be expected by pure chance alone.

It wouldn't be too surprising if repeated sequences were more likely to occur than most sequences.

DNA is not such a simple random sequence and, in particular, repeats occur above likelyhood. This is therefore not a good approach.

@JackAidley In my opinion, this is a good approach to demonstrate exactly that repeats occur more often than they would in a random sequence.

@jba: It does. But there's nothing special about the sequence 'CAT' in the cat genome. It's a general property of repeats. Perhaps you could edit your answer to make it clear the point you're making, and why?

Interpreting the expected number of occurrences as a Poisson parameter, you can interpret the occurrences of 6 CATs as a probability (through the transform $\lambda\mapsto1-\exp(-\lambda)$) of about 4% that you would have that many in a random sequence. As jpa points out, this is a good argument that STRs like CATCAT... are more likely than chance alone would suggest.

Rather, it is an argument that DNA sequences aren't random in the way this calculation supposes.

@reinierpost it's random from the CAT point of view.  The meaning we attribute to CAT is arbitrary to DNA. It's as random as the index into the number Pi that you've have to start at to find a cat video.

@CandiedOrange: That is not what this answer means by 'random'. It assumes the C, A, T and G elements are completely random in the sense that the probability of one of them appearing at a specific spot in the sequence is completely independent of what the surrounding elements in the sequence are - and that isn't the case.

@reinierpost those two ideas of random are the same idea of random is my point.

So, there are a few great answers here already, but it seems nobody addressed an interesting part of your question: GEB was published in 1978 and the genome of Felis catus was not sequenced until many years later... so how did he know?
jpa's answer shows that you'd expect to get only about five CATs - not ten, and the chance of getting ten is astronomically low. I expanded his table to show the depressingly low chance of getting ten by perfect randomness:
5 CAT: 2.5 expected per Felis catus genome
6 CAT: 0.04 expected
7 CAT: 0.00061
8 CAT: 9.54 e-6
9 CAT: 1.49 e-7
10 CAT: 2.32 e-9

That means you'd expect to find 10 CATs about 0.00000000232 times per random genome. So how on earth did the Felis catus genome end up with ten CATs in it? And how did Hofstadter know that there would be this many CATs?
As it turns out, this repeated sequence of a few base pairs is called a "short tandem repeat", or "microsatellite". This is when a 2-5 base pair sequence is repeated several times, usually between 5 to 50 times.
So at this point, to recap: we know the chance of getting this 10 CAT sequence is slightly more probable, but since we're restricted to just the Felix catus genome we definitely aren't guaranteed a 10xCAT sequence. So how did Hofstadter state it as if it was a fact?
As it turns out, one critical property of STRs, or short tandem repeats, is that mutations in these areas are far more common, and they represent a large amount of the genetic variation between individual members of a species. This discovery was made with the advent of DNA sequencing, which began only a few years before the book was published. Therefore, given a large population of nonidentical cats (which we have), we can confidently say that there is an extremely high chance for a 10xCAT sequence.
Hofstadter's genius perfectly combined math (only 2.32e-9 expected sequences per genome) with biology (microsatellites increase the chance of finding this sequence) with forensic genetics (in a population of the same species, individuals are likely to have many STR-related differences.) All of this put together gave Hofstadter what he needed to confidently say: yes, CATCATCATCATCATCATCATCATCATCAT almost certainly exists in the Felis catus DNA. Little things like this are why Godel, Escher, Bach is my favorite book of all time.

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text:
Gibbs free energy and its change for the hydrolysis of ATP
So in my book I have the reaction
$$ATP \rightarrow ADP +P_i$$
and hence $$\Delta G^0 = G^0_{ADP} + G^0_{P_i} - G^0_{ATP}$$
This is easily understood, but I have not been given any actual concentrations of values to use to calculate the result, which is given as
$$\Delta G^0 = -31.0kJ\text{mol}^{-1}$$

Where do I find the values of $G^0_{ADP}, G^0_{P_i} \text{ and } G^0_{ATP}$?

I have the formula $$\Delta G = \Delta G^0 + RT\ln \bigg( \frac{AB}{CD} \bigg)$$
where $A,B$ are the concentrations of the products and $CD$ are the concentrations of the reactants.

There seemed to be a typo in your title, which I've corrected.

You can't measure the energy of ATP itself, but you can measure the amount of energy that is released every time a P group is removed from the molecule, that is about 30 kj/mol.
Here some more details on how the deltaG is experimentally determined.
Fomr Wikipedia:
https://en.wikipedia.org/wiki/Adenosine_triphosphate
https://en.wikipedia.org/wiki/ATP_hydrolysis

Hydrolysis of the terminal phosphoanhydridic bond is a highly exergonic process, releasing 30.5 kJ mol−1 energy.
... The actual value of ΔG for ATP hydrolysis varies, primarily depending on
Mg2+ concentration, and under normal physiologic conditions is
actually closer to -50 kJ mol−1.

and

The standard amount of energy released from hydrolysis of ATP can be
calculated from the changes in energy under non-natural (standard)
conditions, then correcting to biological concentrations. The net
change in heat energy (enthalpy) at standard temperature and pressure
of the decomposition of ATP into hydrated ADP and hydrated inorganic
phosphate is −30.5 kJ/mol, with a change in free energy of 3.4
kJ/mol.[17] The energy released by cleaving either a phosphate (Pi) or
pyrophosphate (PPi) unit from ATP at standard state of 1 M are:[18]
ATP + H 2O → ADP + Pi      ΔG° = −30.5 kJ/mol (−7.3 kcal/mol)
ATP + H 2O → AMP + PPi     ΔG° = −45.6 kJ/mol (−10.9 kcal/mol)
... The values given for the Gibbs free
energy for this reaction are dependent on a number of factors,
including overall ionic strength and the presence of alkaline earth
metal ions such as Mg2+  and Ca2+ . Under typical cellular conditions,
ΔG is approximately −57 kJ/mol (−14 kcal/mol).

You can use tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$ , such as those found in Table 1 of the following reference, to calculate apparent equilibrium constants of biochemical reactions, and to calculate standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$ (at pH 7), which I think is exactly what you require.

Calculating apparent equilibrium constants of enzyme-catalyzed
reactions at pH 7 (by R. A. Alberty)

The first thing to say it that you need to include water as a reactant.
$$\ce{ATP + H2O = ADP + P_i}\tag{1}$$
Secondly, the reaction shown in Eqn(1) is used as an example by Alberty in the paper cited above, where he calculates both $\ce{\Delta _rG^{'o}}$ (at pH 7) and the apparent equilibrium constant (at pH 7).

The following values were taken from Table 1 of the Alberty reference cited above.  They refer to pH 7, 25oC, and an ionic strength of 0.1.

              $\ce{\Delta _fG^{'o}/{kJ mol^{-1}}}$
ATP             -2276.43
ADP             -1409.95
Pi              -1059.17
H2O              -156.05

Knowing these values, it is now very easy to calculate the standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$, for the reaction shown in Eqn (1) (it is merely a case of 'pluggin in' the values).
$$\Delta _rG^{\ce{'o}} = \sum v_i^{'} \Delta_f G_i{^o} = (2276.43 + 156.05 - 1409.95 - 1059.17)\tag{2}$$
$$\ce{\Delta _rG^{'o} = -36.68 kJ mol^{-1}\tag{3}}$$
In Eqn (2), $v_i^{'}$ is the stoichiometric number (positive for reactants
and negative for products)
The criterion which determines whether a reaction will 'go' in the forward direction or the reverse direction is the transformed Gibbs energy of reaction, $\Delta_rG^{'}$, (not $\Delta_rG^{'o}$).

If  $\Delta_rG^{'}$ is negative, the reaction goes in the forward direction.

We can say that under standard conditions, Eqn (1) goes to the right, and as $\Delta_rG^{'o}$ (not $\Delta_rG^{'}$) is directly related to the apparent equilibrium constant (Eqn 4), we can say that the equilibrium constant for the rection of Eqn (1) is very much to the right.
$$\Delta _rG^{\ce{'o}} = \ce{-RT ln K^{'}}\tag{4}$$
We can go a step further (Alberty,2000) and calculate the apparent equilibrium constant, $K^{'}$, for the reaction shown in Eqn (1).
$$K^{'} = e^{\frac{-\Delta _rG^{'o}}{RT}}=e^{36680/(8.3145 \times 298.15)}\tag{5}$$
$$K^{'}  = 2.67 \times 10^6\tag{6}$$
The great value of tables of $\ce{\Delta _fG^{'o}}$ it that they allow $\Delta _rG^{\ce{'o}}$ and $K^{'}$ to be calculated for many reactions, even those for which there is no known enzyme, or where the equilibrium constant has not been determined.
Notes
In Eqn (5) above, $R$ is the gas constant ($\ce{8.3145 J K^{-1} mol^{-1}}$
) and $T$ is the temperature (in Kelvin)
IMO, the Alberty reference cited above is a model of clarity that makes these type of calculations very easy. It is also an 'easy read' with many great examples.
Two other good refs, if you are 'into' such things, are

Biochemical thermodynamics (by R.A. Alberty)
Recommendations for nomenclature and tables in biochemical thermodynamics (by R.A. Alberty)

Other  tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$, may be found in

Calculation of Standard Transformed Gibbs Energies and Standard Transformed Enthalpies of Biochemical Reactants  (by R.A. Alberty)
Calculation  of Standard Transformed Formation Properties of Biochemical Reactants and Standard Apparent Reduction Potentials of Half Reactions (by R.A. Alberty)

I think the answer to your question of where you find standard free energy values is ‘nowhere’. Free energy is a concept that you can expres in equations but that you cannot measure. You can only measure the change in free energy of a process.
I cannot provide definitive support for this opinion — a chemistry list may be a better bet.

I guess you could use the boltzmann distribution or something - if you know the partition function.


text:
Gene configuration : Divergent vs convergent
I start reading a paper where they discuss the effect of the divergent promoter/gene and the convergent promoter/gene on the genetic expression of an organism.
So I want to know what is the difference between the two of them ?

RNA polymerase produces transcripts by scanning along DNA, linearly. Simplifying things, genes can thus be thought of as having a start (or 5' end) which is the main site where the polymerase begins to transcribe, and and end, where it stops. Divergent promoters are promoters oriented so that the polymerase transcribes in opposite directions, away from the two promoters (like so: <- -> ). Convergent promoters instead transcribe towards each other (like so -> <- ) . This means, for instance, that the polymerases coming from two convergent promoters could collide with one another.


text:
What plant/tree is this?
Found this in a rural area next to the road last month and I wonder what is it?

From my searches I think it is a strawberry bush but I'm not sure and any help would be appreciated, thanks!

Add the site of your pictures? It might help you get a precise answer.

I took the pictures

Your pictures are a bit vague, but I think recognize Euonymus europeus, the spindle tree. So I assume the picture comes from Europe? The fruits are encapsulated in pink capsule, the fruit itself is bright orange.
https://en.m.wikipedia.org/wiki/Euonymus


text:
Why do some tissues have insulin-dependent glucose transporters and others not?
Insulin upregulates GLUT-4 glucose transporter insertion in skeletal muscle and adipose tissue. But there are many tissues in the body that use insulin-independent glucose transporters (like GLUT-3 in the brain). Would there be any disadvantage to have the entire body use insulin-independent transporters like GLUT-3? Why involve insulin in this? Wouldn't the concentration of glucose in the blood regulate the influx of glucose via concentration gradients anyway?

I don’t understand why there has been a call to close this question as too broad. It may be naive, but it is quite specific and answerable quite simply and relatively briefly.

I have edited the title of your question to make it clearer, and removed the superfluous and generally ill-advised assertion that something is well-known. If you think I have changed your meaning do say so. Also, calling your question 'naive' was not meant in a depreciatory manner. "Basic" would have been a better term. I think my summary makes it clear why this is basic, but I still think it is a valid question, and that my answer will be useful to others.

Summary
The whole point of hormones is that they allow the organism to control the metabolism of tissues in an integrated manner, rather than each tissue acting independently. Insulin, glucagon and epinephrine are classic examples of this in relation to carbohydrate metabolism. In the fed state, the fasted state and in stress situations it is appropriate for different tissues to respond in different ways. The presence or absence of a hormone receptor — together with the enzyme complement of the tissue — achieves this. Allowing all tissues to have only GLUT-3 (or all GLUT-4) would mean they would all respond to changes in glucose availability in the same way — a totally inappropriate situation for the organism, with potentially disastrous consequences.
More Detailed Answer
Insulin is an indicator of the fed state. In such circumstances there will be a surplus of glucose and it is of benefit to the organism for it to be taken up by muscle and adipose tissue for storage as glycogen and fat, respectively. Conversely it is important that in starvation blood glucose is not so utilized, but spared for those tissues for which it is vital in any conditions. (Muscle can utilize other metabolites such as fatty acids.) Hence, for these tissue allowing glucose transport to be controlled only by blood glucose concentration would not produce a sharp cut-off and result in deny this resource to those vital tissues which cannot replace glucose by other energy sources.
The tissues you mention such as brain (and erythrocytes) depend absolutely on glucose, irrespective of whether the organism is in the fed or fasted state. If they had only an insulin-dependent transporter they would be starved of glucose during the fasted state, with lethal consequences. The insulin-independent transporter allows continued transport down the glucose concentration gradient, even as the blood glucose concentration falls.
Note that blood glucose concentration in the fasted state is maintained by the liver, so that this tissue has an insulin-dependent transporter, not to allow glucose uptake, but to allow the glucose produced by gluconeogenesis to be transported out into the blood.
Further Reading
I would hope that the logic of my answer will be sufficient convincing, but it is good practice in Biology-SE to provide references to support one’s arguments. Section 30.22 of the online edition of Berg et al. discusses the metabolic profile of different tissues and includes some discussion of glucose metabolism and glucose transporters. (The liver glucose transporter is actually different from that in nervous tissues, as is that in erythrocytes — see Wikipedia article.)


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help identify this fish

I came across this washed up fish in Panama City, Florida in November 2015. I'm guessing it's a puffer fish but I can't find anything like it online.
Thanks.

Search "boxfish". I see several in my ID book that look like contenders. I haven't seen this one in the wild so, lacking other viewing angles, that's as close as I gain get.

For real, this fish has a pattern of perfect hexagons? How cool is that!

This is a kind of trunkfish. (They have different names, this could be a smooth or spotted trunkfish.). It's really a lovely and comical little fish when observed alive in coral reefs. It has the ability to change its coloration depending on whether it's excited or calm, or to minimize its contrast to the background. It is related to puffer fish.
It has a boxy, triangular body shape, and propels itself with relatively tiny, delicate fins. Like pufferfish, they are toxin producers.

In death, the body shape and coloration are different, of course. Never saw a dead one before; sad. The juveniles are adorable:

Members of this family occur in a variety of different colors, and are notable for the hexagonal or "honeycomb" patterns on their skin. - Wikipedia

Trunkfish it is. Thanks for the help. It was around 12" in length, beautiful fish. I thought the pattern was too cool.

@Thomas - The pattern is really incredible; you can see it go from dark with spots to light with marked hexagons. Amazing fish, one of my favorites when diving. And because they are toxic and have few predators, they are not very shy at all.


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What kind of succulent is this?
I have this succulent at home and was wondering about the following questions:

What kind of succulent is this?
What will the leaf grow into?
Will there appear more leafs or just a single one?

Your plant looks like this one: https://es.wikipedia.org/wiki/Euphorbia_heteropoda. It could be this species or a close relative. I found it in the "Monadenium" section of http://succulent-plant.com/families/euphorbiaceae.html, so the exact species likely belongs to this (former ?) genus.
It seems difficult to find it on other versions of Wikipedia, which makes me think that Euphorbia heteropoda might not be its valid scientific name.
The leaf will likely fall, leaving a scar as can be seen on the older parts of the plant.
From the photos illustrating the Wikipedia article, it seems it can have more than one leaf at a same time.

Different species under the genus Euphorbia looks so many different sorts! This is really a weird genus.

As @bli writes, probably an Euphorbia (or something from Euphorbiinae), which is a large and diverse group. Maybe its the species he/she cites, but I cannot tell. The leaves will just be regular leaves though, and with enough sun and moisture it will have several of them. The "knotted" structure that the leaves sits on is the stem (which can have very diverse forms/growth patterns in Euphorbia as a whole). In my personal experience (with a small selection of potted species), they often shed their leaves quite easily when the soil dries up. Their flowers are usually very small and inconspicuous (e.g. Euphorbia leuconeura), but can sometimes be surrounded by colourful bracts (e.g. Euphorbia milii).


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Is this adaption of the Gillespie algorithm using Michaelis constants justifiable?
I would like to run a discrete simulation of a biological system as it can be done, e.g., using the Gillespie algorithm. However, the Gillespie algorithm requires you to know the reaction rate constants of each involved reaction whereas I only know the Michaelis constant $K_M$ and the maximum rate $V_{max}$ of each reaction.
Since the Gillespie algorithm only uses the reaction rate constants to calculate the reaction rate $v$ (which, again, is used to determine the probability of a given reaction), I wonder wheter it is justifiable to simply replace this calculation of $v = k * [S]$ by $v = \frac{V_{max}\cdot[S]}{K_M + [S]}$ for each reaction $S \rightarrow P$ and, apart from that, use the Gillespie algorithm as is? If not, is there any better way to run a discrete simulation of the system with the given parameters?
Note: I've already asked in a different question whether it is possible to get (an estimation of) the reaction rates knowing only the parameters $K_M$ and $V_{max}$. I hope my both questions are sufficiently distinct to justify two different posts.

The answer of @WYSIWYG is wrong in parts. (I can not comment because I have not enough reputation.) Gillespie does not make the assumption that "the reaction propensity (probability) in an infinitesimally small interval of time is same as the macroscopic reaction rate." He rather derives this statement from physical considerations about collisions of molecules. The derivation is given in Gillespies 1977 paper "Exact Stochastic Simulations of Coupled Chemical Reactions".
The derivation holds for elementary reactions only. Michaelis-Menten rate obviously does not describe an elementary reaction.

The stochastic simulation algorithm by Gillespie makes the assumption that reaction propensity (probability) in an infinitesimally small interval of time is same as the macroscopic reaction rate. (For details, you can see my answer in Chemistry.SE).
You can model and simulate every step of enzyme catalysis or you can also use the Michaelis-Menten model. In any case, you can extend the same approximations to the stochastic model.
This is also applicable to other Michaelis-Menten like (or Hill) functions of the form $$\frac{x^n}{k^n+x^n} \qquad \text{or}\qquad \frac{k^n}{k^n+x^n}$$.
There are many papers that have done this. Note that the non-linear nature of these functions results in deviation of the stochastic behaviour from the deterministic behaviour. Read about stochastic focussing. Modelling each step exactly (binding, unbinding and catalysis) may result in different behaviour depending on your parameters. Whether you should use Michaelis-Menten function to describe reaction rate totally depends on how reasonable your approximation is.

Very interesting question. People use Gillespie's algorithm for several sort of kinetic functions such as Michaelis-Menten (MM), Hill etc., no matter what the original assumptions of Gillespie's algorithm are.
Concerning MM, There was a 2011 paper by Gillespie himself that shows that the approximation is applicable in discrete stochastic models and that the validity conditions are the same as in the deterministic regime.
https://www.ncbi.nlm.nih.gov/pubmed/21261403
Remember that, because MM is derived under a QSSA, you can break down the S->P transformation as its single-step components. See for instance a comparison here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578938/


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What is the connectivity between on-center & off-center bipolar cells?

Do rod-photoreceptors only form synapses with on-center bipolar cells (and on-center ganglion cells in the next step)? If so, why is that?
Why do rod-cells only connect to on-center cells, while the cones connect to both on- and off?
Am I correct in saying that what happens in the bipolar cell as a response to light stimulus on a photoreceptor depends on i) Wether it is an on-center or off-center bipolar cell - and of course where the light stimuli is focused on the bipolar cell (periphery or center), or ii) What kind of receptors the on-center and off-center bipolar cells have? This is the part where I get really confused, because I read somewhere that what kind of receptors On/Off-center bipolar cell have, is not something set in stone? So saying that On-center bipolar cells have AMPA receptors and will, as a result of that, react in a specific way to less Glutamat release would be wrong?
How does this release of neurotransmitter works together with central / periphery stimuli. Let me try and use an example, You have an on-center bipolar cell. What will happen if light is focused on the center of this cell's receptive field? And what will happen if it is focused on the periphery? Let's just say that the light hitting the center of this cell's receptive field causes it to be depolarized. But is it really the light hitting the center which causes this effect, or is it the decrease in Glutamate release from the photoreceptor that causes this effect? If the latter, then what does it really matter if the light hits the periphery or the center of the bipolar cell's receptive field? The photoreceptor is hyperpolarized by light either way and less Glutamate will be released no matter what.
Also, in order for this to make sense, the light that enters the eye is absorbed by the photoreceptors pigmentmolecules, but some of the light also has to hit the receptive field of the bipolar cell in order to decide which signal to be transmitted? So not all of the light is absorbed by the photoreceptors then?
If the light hits the periphery of an On-center bipolar cell, you will have an inhibitory effect, is that right? And the other way around, if the light hits the center of the cells receptive field, you will get an excitatory effect? But I am curious as to how this also has to do with the kind of receptor that the on-center bipolar cell has (AMPA or MGluR6).

Please limit yourself to one clear question per post.

I suggest that you split this up into several simpler questions.

First off, the post is quite lengthy and contains various sub-questions. I will answer the first two questions in detail, but only after starting with an abstracted overview of photoreception in the retina. By the looks of it, your basic understanding of photoreceptors and secondary visual neurons is incorrect. Clearing the general neurophysiological workings of the retina up should get you on your way in understanding questions 3 - 6.
Synopsis of information flow in the retina: sensation of light
In Fig. 1 a schematic of the retina is shown. It basically consists of three layers. Layer one contains the photoreceptors, namely the rods and the cones. These primary sensory neurons absorb the light with photopigments and generate electrical signals in response to that. The photoreceptors, in turn connect to the second layer, namely bipolar cels, horizontal cells and amacrine cells. These cells are responsible for the center-surround structure of the receptive field of the last layer of cells (Fig. 2), namely the retinal ganglion cells in the front of the retina, whose axons pass across the surface of the retina and form the optic nerve (Kolb, 2017).

Fig. 1. Retina. source: Quasar Group
Note that there are no light-sensitive cells in the retina besides the rods and cones (barred the retinal melanopsin ganglion cells, but please forget that for the sake of simplicity). This one detail should basically clarify the sub-questions 3 - 6 in your post. The first two questions I will address next.

Fig. 2. ON and OFF center responses. source: McGill University
Regarding the retinal bipolar system and your first two questions:

Do rod-photoreceptors only form synapses with on-center bipolar cells (and on-center ganglion cells in the next step)?
  and
Why do rod-cells only connect to on-center cells, while the cones connect to both on- and off?

Rod bipolar cells in the mammalian retina are of the ON type. In contrast to the cone system, rod bipolar cell signals are split into ON and OFF components by amacrine cells. The cone system piggybacks then on the cone system; Rod ON signals flow from rod bipolars to amacrine cells to ON cone bipolar cells. Rod OFF signals are generated between amacrine cells and OFF cone bipolar cells (Nelson & Connaughton, 2017). See Fig. 3 for an overview of the retinal connectivity between rod and cone bipolar cells.

Fig. 3. Retinal circuitry. source: Nelson & Connaughton (2017)
References
- Gouras, Color Vision: In: Webvision: The Organization of the Retina and Visual System (2017)
- Kolb, Simple Anatomy of the Retina. n: Webvision: The Organization of the Retina and Visual System (2017)
- Nelson & Connaughton, Bipolar Cell Pathways. In: Webvision: The Organization of the Retina and Visual System (2017)

This is a great answer, I think it's worth adding that there are more than just ON/OFF Bipolar cells, about 11 according to Nelson and Connaughton. There's a bit more about specific types of OFF bipolar cells here: https://www.ncbi.nlm.nih.gov/pubmed/26500507. So it's possible that the different classes of bipolar cells have slightly different receptors, or respond slightly differently, so "not set in stone".


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When salivary amylase breaks down starch, are those substances tagged or destined for a particular use in the body
When salivary amylase breaks down starch, are those substances identified for a particular use in the body?

Salivary amylase breaks starches brown into shorter chain of sugars. In the beginning of the small intestine, this process is continued by pancreatic amylase. Other enzymes at the surface of the intestine's lining complete the process resulting in simple sugars which absorbed into the circulatory system. Some of these sugars, if there is an excess in your diet, will be converted to fat and stored.
The rest of the sugars will ultimately be taken into cells and undergo a process termed cellular respiration. The bulk of these sugars will be broken down and used to create (recharge actually) ATP, a substance that just about any process in the cell requiring energy can use for energy. The atoms in the sugars used in this process end up as carbon dioxide, which you breath out, and water. But a certain percentage of the sugars only get partially broken down. These fragments can be used to synthesize many different substances depending on what's needed in the cell at that time.


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Photoreceptors and light with mixed frequencies
I am interested in how the activation of a, say, blue cone depends on the incident light. Wikipedia tells me this:
 ,
which describes how strong the activation of the blue cone is for light with a single wavelength and a given intensity. But what happens if the incident light has several frequencies?
My question is: given the intensity i(f) of the incident light at frequency f, what is the activation of the blue cone?
(A natural guess would be that if b(f) is the activation curve in the figure, then the activation of the blue cone should be the integral of b(f)*i(f) over f. But I have not found any confirmation of this guess. For example, in the reference for the picture above, only pure light was used in the experiments.)

I'm confused. Your question seems to ask for a simple reading of the graph at a particular frequency but your comment implies otherwise. Also, what do you mean by pure light? I gather the vertical axis is fraction of maximum possible? If so, would integrating under the curve make sense?

Yes, current color models assume a linear response in the spectrum.
Given a light with mixed spectrum $\Phi(\lambda)$, the response of a cone with spectral sensitivity $\Psi_i(\lambda)$ is a (nonlinear) function of the L2 inner product:

This is how CIE XYZ color space is defined.
Reference:

M. D. Fairchild. Color Appearance Models, 3rd edition. 2013 (p.63)
https://en.wikipedia.org/wiki/CIE_1931_color_space


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What is the name of this about 10cm high, grey, "flat hat" fungus?
I found this fungus on Corsica (France). Can you please help me to identify it?

In fungi, you should always look at the underside of the hat, which gives big clues to group/species determination.

Based on the dark lamellae and the ring around the foot, I would bet on something in the Agaricus genus. The French Wikipedia gives quite some details about common species in this genus: https://fr.wikipedia.org/wiki/Agaric

Try looking up Chlorophyllum  brunneum or commonly called a shaggy parasol.
http://www.mykoweb.com/CAF/species/Chlorophyllum_brunneum.html
Hope this helps.

Thank you. I think this goes in the right direction. However, it could also be https://commons.wikimedia.org/wiki/Category:Chlorophyllum_molybdites or any other Chlorophyllum, I guess?

Most Lepiota don't have such dark lamellae.

Besides the lamellae colour, the foot seems too wide in proportion to the hat for a Lepiota, in my opinion.


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How does changing the shape of ATP synthase specifically prevent the enzyme from working any longer?
I am currently stuck on working out how to answer this question:
"A random mutation causes the enzyme ATP synthase to change shape so that it can no longer function. Describe the impact this would have upon respiration and the overall production of ATP."
My question is: How does changing the shape of ATP synthase specifically prevent the enzyme from working any longer?

That shouldn't get you stuck - just delete the word "shape" from the question (since it doesn't affect the answer).

If you look at an enzyme and its substrate you can also see this as a lock (the enzyme) and the key (the substrate). The key fits the lock and opens it, the substrate fits into the active pocket of the enzyme and a reaction takes place. See this figure for illustration (from here):

If the enzyme (or the substrate) changes its outer shape (this is what happens when amino acids of a protein are changed), this fit will not happen anymore and the reaction which is catalysed by the enzyme will not take place (the lock will not open).


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Allele frequency question
You are heterozygous at locus A. Both of your alleles, A1 and A2, have a 10% allele frequency in the population. If you are one of 22 people in a room, how many people do you expect to share a locus A allele with?
I come up with 6.8, working like so:
22 people = 44 locus A alleles in the room = 4.4 A1 alleles and 4.4 A2 alleles at 10% frequency.
I have one of each, leaving 3.4 of each allele to the rest of the room. So, looking at both alleles, there are 6.8 shared alleles out there.
My answer assumes that these alleles are all in different people - I don't know how to account for the probability of someone else having two of them. So I know I am wrong already. Is that last step all I'm missing, or have I gone wrong in a more fundamental way?
(Context: This was a question on a grad-level immunology exam. None of us students could agree on the answer afterwards, and the confused wording (I rephrased it above) made us strongly suspect the professor doesn't have the right answer either, so we wanted to see what the answer actually is for when the exams are graded.)

Gotcha, will edit it in.

Same as @bpedit but stated a little bit differently.

You are heterozygous at locus A. Both of your alleles, A1 and A2, have a 10% allele frequency in the population. If you are one of 22 people in a room, how many people do you expect to share a locus A allele with?

There are 5 possible genotypes that could share at least one allele with "you" A1|A1, A1|A2, A2|A2, A1|A3 and A2|A3, where A3 is the allele (or set of alleles) which frequency is $0.8$. Under Hardy-Weinberg assumptions, the frequencies of each of these genotypes are

$f(A1|A1) = 0.1^2$
$f(A1|A2) = 2 \cdot 0.1^2$
$f(A2|A2) = 0.1^2$
$f(A1|A3) = 2\cdot 0.1\cdot 0.8$
$f(A2|A3) = 2\cdot 0.1\cdot 0.8$

which sums to $4\cdot(0.1^2) + 2(2\cdot 0.1\cdot 0.8)=0.36$.
As the frequencies of both A1 and A2 are $0.1$, the frequencies of each of the three mentioned genotypes are all $0.1^2$. Therefore, the expected number of individuals that share at least one allele with "you" at this locus is $21\cdot 0.36 = 7.56$ people.
Why did we need Hardy-Weinberg assumption to make this calculation?
This section comes in reaction to @Atwo comment below.
To give you the intuition for why you need H-W for this calculation. Imagine all A1 where in heterozygous A1|A2 (and therefore same for A2), then the only other genotype that would share an allele with you are A1|A2 genotypes that would be present at frequency $0.2$. And therefore the expected number of people the share at least one allele with you in the room would be $21\cdot 0.2 = 4.2$ people.
For exercise, I would like to invite the reader you to repeat the same calculation for a case where all A1 and A2 alleles are only found in heterozygous A1|A3 and A2|A3.

Thanks! It looks to me like this solution requires no assumption of H-W equilibrium - is that correct?

It also require the H-W assumptions in order to calculate the genotype frequencies (in bullet points) from allele frequencies.

Gotcha. In that case can you make anything of the original exam question, which I posted as a comment on the previous answer?

Of course. Simpler and more elegant than my approach since it more easily accommodates the A1/A2 individuals.

@Atwo Please have a look at the added section that address more fully your comment about the role of H-W assumptions into the calculation.

Instead of computing this complicate sum, what about computing the expected value of the number of people $(A_3,A_3)$ : it is $21\times 0.8^2=13,44$, and the expected value of the number of people you share at least one allele is $21-13,44=7,56$

@Thomas Yes, this is the way mgkrebbs used which is computationally easier, I agree.

My first inclination for a problem like this is to address it by enumerating all the possible permutations the two alleles a random individual could have, and multiplying the two allele probabilities (frequencies) to get the combination's probability. Using the given frequencies, the remaining allele (set), call it $A3$, has freqency 0.8.  Because the two alleles of an individual are independent, there are nine possible permutations: one of $\{A1,A2,A3\}$ for the first allele and one of $\{A1,A2,A3\}$ for the second.  One can then just sum the probabilities for the cases of interest.
But for this particular problem, there is an easier approach.  What we are interested in is all individuals who have at least one A1 or A2 allele.  This is the same, though, as all individuals except those who have no A1 nor A2 alleles, or, stated another way, those having A3 and A3.  Therefore:

$f(A3|A3) = 0.8\cdot 0.8 = 0.64$
$f( not(A3|A3) ) = 1 - f(A3|A3)  = 0.36$
$expected( not(A3|A3) ) = 21\cdot f( not(A3|A3) ) = 7.56$

This is of course the same as noting that in the first exhaustive enumeration that there is just one case excluded from the group of interest, calculating its probability, and knowing that all the others must sum to the complement of this probability.  Sometimes using the complementary set out of the full enumeration is an easier way to the answer.
Note: Remi's answer shows a slightly consolidated form of the exhaustive enumeration approach.  The earlier numerical discrepancy in that answer was just due to arithmetic or typos.

Thanks for the correction (+1). Small typo is now fixed.

@Remi.b, the final result is also wrong: 7.77 vs 7.56.

And also because I multiplied the probability by 22 instead of 21 (as the question says that "you" are one of the 22 people in the room). Thanks

I've never done one like this, here goes.
First, remove yourself from the room, just 21 people to consider. You're right that you have to account for the homozygotes. Let's represent the A1 allele with p. All other allele frequencies represented by q. (Sorry I don't yet know how to format properly)
p = 0.1, q = 0.9
The genotype frequencies in the population are represented by:
p^2 + 2pq + q^2 = 1
We're interested in the p^2 + 2pq part. It represents the genotype probabilities of having either one or two of the A1 allele.
0.01 + 2(0.1)(0.9) = 0.19
That's the frequency of individuals in the population with at least one A1 allele.
0.19 * 21 people = 3.99 people
Ditto for the number of people with the A2 allele. These should be additive giving you 7.98 people. BUT, Some people would have both the A1 and the A2 allele. I think we need to subtract that from the 7.98. If this is true, the calculation is easy.
2(0.1 * 0.1) = 0.02 chance of a person having both A1 and A2
The 2 is because there are two ways of achieving this (A1/A2 and A2/A1).
0.02 * 21 people = 0.42 people
7.98 - 0.21 = 7.56 other people in the room with at least one A1 of one A2 allele.

I like it (me using A1/A2 instead of p/q shows how rusty I am), but I guess I am curious about removing yourself from the room at the start. There are, in fact, 22 people in the room. Your calculations are for a room of 21 people and produce the incorrect frequencies for a room of 22, especially given that the genotype of the 22nd is known. Or am I being led astray by my intuition here?

Can you share alleles with yourself? Sharing suggests "with others". I'd read that prof the riot act if they use 22. You said you paraphrased, perhaps the original wording makes 22 feasible.

Ouch. I edited the final answer to say OTHER people in the room.

Thanks, I understand you there. The actual question without the paraphrasing was: "The frequency of HLA-B alleles [there are 100s] ranges from <0.1% to 10% [we didn't learn any frequencies, hence the info here]. What is the maximum expected number of people in this room that share an HLA-B allele with you?" There were 22 people in the room. Can you make any headway on that (notably, no H-W equilibrium), or is it hopeless?

Ah, that doesn't seem to implicate "you" as one of the population to share. So substituting 22 for 21 seems fair.


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confusion regarding degrees of flexion and a goniometer
I have read
https://en.wikipedia.org/wiki/Anatomical_terms_of_motion#Flexion_and_extension
"Flexion ... decreases the angle...Extension is the opposite of flexion, describing a straightening movement that increases the angle between body parts"
I am clear on the directions of flexion and extension

So all agree on direction, but if I look up degrees of flexion, for example

and videos showing usage of a goniometer to measure shoulder flexion, which echo that picture, so 180 degrees is the arm up, and 0 degrees is the arm down.
What I don't quite understand, is that flexion according to wikipedia, should decrease the angle.  Whereas looking at the degrees in that diagram, and in videos of usage of a goniometer, the more flexion you have, the higher the degree.
I can think of two possible resolutions
A) that wikipedia has missed out that in fact, for the case of the arm,  flexion increases the angle. Whereas for bending movement, it decreases it.
or
B) the planes that describe degree of flexion, are different to the ones shown on a goniometer, perhaps, one field uses a gynometer, the other uses a measure with the angles going the other direction
I'm guessing that it's "A" , that wikipedia is misleading and in the case of the "shoulder"(the arm movement considered shoulder flexion and extension), flexion doesn't decrease the angle, it increases it(though wikipedia doesn't say that). But i'd be interested if that can be confirmed.

For A), it depends on how you define the angle. If 180 is directed at the floor, then it is correct. The problem is that with the shoulder "increase" and "decrease" are ambiguous, and you have to define your planes of reference explicitly.

@kmm well there's no question what planes we are talking about. One plane is the frontal plane, the other plane is the plane made by the arm straight out in front going all the way up and all the way down at angles between 0 and 180. Sagittal plane. Both wikipedia and that picture and the goniometer are using the same planes.  One could say there is a difference depending on which you define as zero and which as 180,but  clearly a goniometer uses a standard convention of goniometers.. what standard convention is wikipedia using? What other texts measure shoulder flexion the way wikipedia does?

There are two criteria to differ between flexion and extension:
1) Decreasing or increasing the angle between the involved bones. By this criteria, it should be clear that flexion means bending of the elbows and knees and lateral bending of the spine (the neck and torso) toward the bent side.
2. The anterior/posterior direction of the movement. All anterior (ventral) movements in the neck or torso part of the spine, shoulder, elbow, wrist, fingers, hip, ankle and toes are called flexion and all posterior (dorsal) movements (except in the knee) are called extension.
You should not use the both criteria at the same time, because they can contradict each other.
There are some specifics:

In the wrist, you can have palmar flexion, dorsiflexion (extension), ulnar flexion (abduction) and radial flexion (adduction) (Teachmeanatomy).
In the ankle, you can have plantar flexion, dorsiflexion (extension), inversion (inward rotation, adduction) and eversion (outward rotation, abduction). (ScienceDirect).
In the shoulder and hip, raising a limb to the same side as the limb is, is abduction (lateral extension) and raising it to the opposite side is adduction.
Moving the thumb toward the palm (in the same plane as palm) is flexion (adduction) and moving it away from it is extension (abduction).

You can read about flexion and extension and other movements here: Types of Body Movements (BCcampus)

Flexion and extension are movements that take place within the
  sagittal plane and involve anterior or posterior movements of the body
  or limbs. For the vertebral column, flexion (anterior flexion) is an
  anterior (forward) bending of the neck or body, while extension
  involves a posterior-directed motion, such as straightening from a
  flexed position or bending backward. Lateral flexion is the bending of
  the neck or body toward the right or left side.
In the limbs, flexion decreases the angle between the bones (bending
  of the joint), while extension increases the angle and straightens the
  joint. For the upper limb, all anterior-going motions are flexion
  and all posterior-going motions are extension. These include
  anterior-posterior movements of the arm at the shoulder, the forearm
  at the elbow, the hand at the wrist, and the fingers at the
  metacarpophalangeal and interphalangeal joints. For the thumb,
  extension moves the thumb away from the palm of the hand, within the
  same plane as the palm, while flexion brings the thumb back against
  the index finger or into the palm. These motions take place at the
  first carpometacarpal joint. In the lower limb, bringing the thigh
  forward and upward is flexion at the hip joint, while any
  posterior-going motion of the thigh is extension. Note that
  extension of the thigh beyond the anatomical (standing) position is
  greatly limited by the ligaments that support the hip joint. Knee
  flexion is the bending of the knee to bring the foot toward the
  posterior thigh, and extension is the straightening of the knee.
  Flexion and extension movements are seen at the hinge, condyloid,
  saddle, and ball-and-socket joints of the limbs (see Figure 1).

Now, to answer the question about the goniometer.

Again, the confusion about interpretation of this goniometer arises from two different criteria about flexion. The one mentioned in the Wikipedia and other anatomical articles says that in flexion the angle between the involved bones decreases. When you raise your arm, this criteria does not aply because the angle between the bones (humerus/scapula) in the shoulder joint does not really change (unlike in the elbow, for example), so here the criteria that all anterior movements are considered flexion applies. When you have an arm straight down, there is no flexion, so it's considered zero degrees and when it's straight up, it's considered 180 degrees, so the angle is increasing, but this is not an angle between the arm and other bones or the body but between the starting and ending position of the arm.

you write "During raising the arm, the angle is closing"  <-- the angle between what and what? between arm and torso?  I suppose you could say the angle is closing/reducing whether the arm is near fully down or fully up, depending on whether 0 is at the top or at the bottom

@barlop, I have changed the last part about goniometer. In this case, you should not think about any "body" angles, but just about goniometer angles.

So in the case of criteria 1 (bending flexion), flexion decreases the angle, and in the case of criteria 2, (direction of movement flexion), flexion increases the angle?

@barlop By criteria 1, flexion decreases the angle between the actual bones (like in the elbow or knee). But when you raise your arm, in the shoulder joint, there is no real change in angle between the humerus and scapula, so this criteria simply does not work here, so the criteria 2 (any anterior movement is flexion) applies. Now, even if by criteria 2, the "theoretical" or goniometric angle increases when you raise your arm, you can't generalize this for other movements. For example, when you bend your neck forward, by criteria 2 this is flexion...continued...

Looking from the front, the angle between the spinal vertebra decreases, but looking from the back it increases. You just need to know, which criteria applies to a particular joint and be aware that the angle that decreases can be real, physical (by crieria 1) or arbitrary by criteria 2 (forward movement is flexion). By criteria 1, flexion always decresaes the angle between the bones, and by criteria 2, it depends on the joint.

When you say that in the case of the neck, that it depends which way you look at it  and that front the front flexion decreases the angle, is that because when you look from the front you are looking at the angle between the chin and the spine with 0 at the bottom, (that angle decreases towards 0 with flexion).  But when you say that when you look from the back it increases with flexion, is that because you are looking at the angle between the top of the head and the spine with 0 at the top?  (cntd)

(cntd) It doesn't seem to me to be a front/back distinction because you can view from the front that with flexion the angle between the top of the head and the spine increases with neck flexion

@barlop OK, what I said about the neck was probably not necessary. Forward bending of the neck is considered flexion and backward bending extension.

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Can we develop a nucleos(t)ide analogue to cure rabies?
Nucleos(t)ide analogues have been successfully used to treat HIV, HBV and HCV. Since rabies virus is also a RNA virus that uses RdRp to replicate. If we develop an nucleos(t)ide against its RdRp, will it be able to save rabies victims? What would be potential obstacles?

Are you referring to RNA interference? Can you link some sources about the one used for HIV, HBV etc. ?

No. I mean this https://en.m.wikipedia.org/wiki/Nucleoside_analogue

Examples include Tenofovir to HIV, Entecavir to HBV and Sofosbuvir to HCV. Nucleos(t)ide analogues can serve as substrates of viral polymerase and incorporate into the newly synthesized nucleic acid chain. But it can prevent further incorporation, thereby terminate viral nucleic acid replication.

In theory that would be possible, as you mentioned the rabies virus does have its particular polymerase, and adequate inhibiting substrates could possibly be found.
On the other hand, the current immunoglobulin and vaccination post-exposure scheme is quite effective, and the incidence of rabies in developped countries is pretty low; so it's unlikely an inhibitor could profitably be developped to the market.  That means rabies-directed nucleoside analogues are not priority target for pharma companies, IMO the biggest obtacle.

Here are some of the technical hurdles a drug candidate would have to overcome, as a nucleoside analogue :

Affinity to the viral polymerase : too low an affinity makes competition with the native substrate difficult
Rate of conversion to triphosphate form : a low affinity of the host nucleoside kinase to the analogue can cause a inadequate concentration of active triphosphated inhibitor. Some virus (HSV) have their own kinase that may be less selective, though that doesn't seem to be the case for the rabies virus.
Selectivity for the viral polymerase (versus the host replication/transcription machinery) : a cause of cytotoxicity and, generally, adverse effects.
Pharmacokinetic problems : the analogue has to be able to be taken in through nucleoside transporters (facilitated transport into the cell), or go through other means of active transport, as that kind of compound is usually quite hydrophilic. One could also use the usual prodrug tricks to pass the membrane (see CP-4055 or sapacitabine). This may be particularly problematic for acute-stage rabies, as there would be the blood-brain barrier to pass.

Some additional perspectives on the development of nucleoside analogues
Advances in the development of nucleoside and nucleotide analogues for cancer and viral diseases -- (http://www.nature.com/nrd/journal/v12/n6/full/nrd4010.html)
Discovery and development of clofarabine: a nucleoside analogue for treating cancer -- (http://www.nature.com/nrd/journal/v5/n10/full/nrd2055.html)


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Can we call a sorbent-filled pipette tip "microcolumn"?
I came across the use of the word "microcolumn" in a Russian text. This word was used to describe a ZipTip® C18 Pipette Tip. It took me some time and some e-mailing to the author to realize that the pipette tip was the "microcolumn".
Is it okay to use the word "microcolumn" when describing such a pipette tip in English? Would the English reader understand?

The samples were applied to the MALDI plate using the dried-droplet method.
  To apply the samples, we used ZipTip C18 (microcolumns for desalting and concentration of proteins and peptides). We washed the microcolumn with 80% acetonitrile, then with 0.1% TFA in water. We next performed the binding of the sample by aspirating and dispensing it through the media multiple times (10 cycles), then washed it with 0.1% TFA in water. We eluted the sample using a 20 mg/ml solution of the matrix (2,5-dihydroxybenzoic acid) in 50% acetonitrile with 2 mM sodium acetate.


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How do cells determine what size to grow to before dividing?
How do cells determine size to grow to before dividing?

Have a look at this review.

All eukaryotic cells have 'checkpoints' during their cell cycle (1)1. They will only commit to cell division or the next phase of mitosis until all requirements have been fulfilled. The cell needs to have enough energy and the right external stimuli before it starts the irreversible commitment to cell division. The proteins effecting these changes are the cyclins and the associated CDK's. These proteins integrate a wide array of signalling inputs (e.g. DNA duplication complete or no major DNA damage) and steer the proteins actually duplicating the DNA and the other machinery needed to split a cell. You can learn more about these proteins and their signals by googling 'restriction point'
If you interfere with cyclin D modifying proteins you can get very large or very small cells. One of the best understood proteins involved is WEE1 from fission yeast. If you knock this one out, you get very small cells (2).
In mammalian cells the size of the spindle during anaphase also seems to be crucial in splitting cells equally (although some divisions are asymetrical)(3).


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What is solitary flower?
I am Just confused whether solitary means single flower in the whole plant or one flower on one branch of the plant?

only 1 flower in 1 inflorescence

Solitary flower means one flower at a specific position of a plant. It usually accompanies with another word either terminal or axillary.
Soliary terminal means a flower present at the apex of the main stem or its branches. e.g.  Trillium grandiflorum.

 Image taken from http://ohioplants.org/inflorescences/
Solitary axillary means a flower arising from the axil of a leaf. e.g. China
rose.

Image taken from https://commons.wikimedia.org/wiki/File:China_rose.JPG

 This is Sida rhombifolia. This picture is clearer.
No. It doesn't mean that a plant has a single flower.It speaks all about the position of the flower. Think of roses , they are solitary terminals and are in numbers in each plant, always growing at the apices of branches.
Source: My two years of learning Botany as an additional Undergraduate subject.

Short answer:
Solitary flower could be single or many flowers in a branch. How many flower is in a 'branch', That is not the concept of solitary flower. The concept is about 'how many flower is there in an inflorescence (branches specialized for flowers)'
Solitary flower a flower NOT in a "inflorescence" (Cluster of many flowers together). Or in another sense, Solitary flower is an inflorescence made up of only 1 flower.
The complete terminology is: "inflorescence with solitary flower".

Long answer:
To understand what is an inflorescence with solitary flower, you need to look for what is NOT an inflorescence with solitary flower.
User @SanjuktaGhosh gave beautiful examples of solitary flowers, so I gave example of only what is not that.

Brassica inflorescence (Raceme, which is racemose).

(Source http://hasbrouck.asu.edu/imglib/seinet/Brassicaceae/photos/Brassica-nigra-F-web-N1544_tn.jpg).

Foeniculum sp inflorescence (compound umbel, which is cymose)
(Source: https://upload.wikimedia.org/wikipedia/commons/thumb/a/a5/Foeniculum_vulgare_C.jpg/320px-Foeniculum_vulgare_C.jpg)

We can see now, 'inflorescence' means specialized stem axis/ branches, containing mainly flowers (and some bract leaves). In nature, flowers usually occur in such specialized stems, and look like 'cluster' (many flowers together)

But what if a flower occur NOT in such cluster? rather solitary, at clear distance, and the axis on which flower borne, is not distinctive from the rest plant-body?
We couldn't see any 'inflorescence'; however it is considered as an inflorescence with only 1 flower, and from growth-pattern it is a subset of cymose-inflorescence (since the only-bud is the top-bud of the stem going to be flower)

Reference:

what we've been taught
College Botany/ VOL-1/ Gangulee, Das, Datta/ New Central Book Agency

Feel free to write explanation behind downvote. As well, I gave picture of what is NOT a solitary flower, so that the asker can understand from-where the concept of solitary flower came.

Inflorescence itself means a group of flowers arranged on a stalk. So writing "The concept is about 'how many flower is there in an inflorescence (branches specialized for flowers)"
is wrong. Besides "only 1 flower in 1 inflorescence" is incorrect.That's why I downvoted your answer.

Probably you are considering 'Solitary flower could not be an inflorescence'. Have I understood? However, what we've been taught solitary flower as a subtype of cymose or definite inflorescence. The above mentioned textbook says "When the apical or axillary bud forms a single flower, it does not form a real 'inflorescence' but this type is better included within the 'definite' group as further development is limited. In China-rose, the stalk of the flower can be distinguished into a peduncle (axis) part and a pedicel (stalk) part with an articulation between the two".

May be you are right. I've too seen that somewhere. I'll edit my answer after referring to my Studies in Botany. Well I've removed my downvote.

Its Ok thank you very much however at any time you feel free to downvote if you found something wrong. However Colg. Bot. kept space that, it is not true-inflorescence where Studies (V1) directly classifies it in cymose. Also thanks for mentioning an example of terminal cyme. I was not aware of that.


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The pectoral fins of a whale and a shark. Are they analogous organs?
Analogous organs: Different origin, same functions,
Homologous organs: Same origin, different functions but same main structure//  right?
So, what is the case for the pectoral fins of a shark and a whale?
Are they analogous organs, because the two animals have different ancestors(shark-Some Chondrichthyes fish, Whale-some mammal) but have organs that do the same thing?
Or are they homologous organs, because the two animals have the same ancestor(A vertebrate animal) and have organs that have a similar structure?(I learned that it is alright for homologous organs to do the same function, for example the wings of a bat and a bird are homologous organs, although they do the same thing)

They are analogous at to function. Whales derive from terresterial animals that "returned" to the sea. Evolution adapted the forearms to fins. Here's a great diagram: http://evolution.berkeley.edu/evolibrary/article/evograms_03
The bat wing and the bird wing are also analogous as to function. Their functional aspects evolved independently. But as forelimbs they are homologous sharing a common ancestor with forelimbs.http://evolution.berkeley.edu/evolibrary/article/evo_09
We haven't yet answered the question of whether the whale fin and shark fin are homologous in origin: http://evolution.berkeley.edu/evolibrary/article/similarity_hs_09

There is more recent evidence they are homologous as limbs, shark pectoral fins and bony fish fins (and thus tetrapod limbs) share the same hox genes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1937022/

The ancestors of all jawed animals probably had pectoral fins [Ref]. This primitive feature is homologous to shark pectoral fins (fig. 1). The forelimbs of quadrupeds are evolved from the pectoral fins of lobe-finned fish (fig. 2), and the pectoral fins of whales evolved from the forelimbs of their mammal ancestors. Thus, these organs are homologous as one can follow the gradual changes in morphology and find continuity between the fin to leg to fin transitions.
However, the internal structure of the fins themselves are quite different between whales and sharks as they evolved from a leg structure with fingers (fig. 3 & fig. 1). The external similarity of the fins is an example of convergent evolution, not directly the result of their shared origin. Some of the internal features of the fins may be homologous (I haven't checked), but you should not assume that a shared origin for the fins means they are the same.
Fig 1. Shark anatomy

Fig 2. Lobefinned fish and amphibian homologous limbs.

(source: ftexploring.com)

Fig 3. Whale fin
Reference:
1. New study showing pelvic girdles arose before the origin of movable jaws, : Institute of Vertebrae Paleontology and Paleoanthropology, 2012


text:
Can the "Cas9"(involved on the Crispr-cas9 mechanism) be considered as a restriction enzyme?
I have many questions about the Cas9 enzyme. When the Cas9-guideRNA (crRNA and transcrRNA) complex is attached to the DNA sequence, what is the type of bond that cuts the Cas9? Does the Cas9 degrade all the sequence of DNA complementary to the guide RNA?
If the question before is "Not", then how is the sequence that is going to be cut on the DNA complementary to the guide DNA, determined? What type of enzyme the Cas9 is?

Cas9 is an endo-deoxyribonuclease (UniProt-Q99ZW2). It also has a 3'-5' exonuclease activity by which it trims the DNA a little bit, from the cut site (but not too much).
Although, Cas9 is an endonuclease and is evolved as a mechanism of immunity against viruses (like restriction enzymes), they are not considered restriction enzymes. One of the most important differences is that the restriction enzymes do not need an RNA or a DNA as a tether to identify the target sites in the DNA; their DNA binding domains can recognize the restriction sites by themselves.
Cas9 cannot just cleave any DNA complementary to the guide RNA. It needs PAM (protospacer adjacent motifs) sequences adjacent to the target site to cleave that latter.
For details check out the wikipedia page on CRISPR or read a review.


text:
Does the process of photosynthesis occur in insectivorous plants?
Does the process of photosynthesis occur in insectivorous plants?
Can you please give me a clear answer and explain to me how?
and also can you describe the environment in which they grow ?
Thank you

is this a homework question? you need to give a little more detail and effort when posting to this site... please see the help page where it discusses "how to ask a good question" - thanks!

Normally the carnivorous plants are photosynthetic and green. They need to depend on animals for nitrogen. They are adapted to regions of poor nitrogen availability in soil.

@AlwaysConfused  if you know the answer then post it as an answer. Use comments only to request clarification and suggesting something.

@WYSIWYG Ok but before that I'll have to go through some reference. However I've seen possible-answers, or where could be looked for, sometimes posted (and they helps, too). As well for unconfirmed answers sometimes it is told that "post it as a comment instead".

"Carnivorous plants are plants that derive some or most of their nutrients (but not energy) from trapping and consuming animals or protozoans, typically insects and other arthropods. Carnivorous plants have adapted to grow in places with high light where the soil is thin or poor in nutrients, especially nitrogen, such as acidic bogs and rock outcroppings."
Source: https://en.m.wikipedia.org/wiki/Carnivorous_plant


text:
Finding Regulatory Elements: How Have People Been Doing This?
First up, I am NOT asking about how to search for and match regulatory elements using a database. I'm asking about how people found what to search for and match in a genome, how they built those databases. My question is,
How did people identify regulatory proteins/nucleotide elements in the first place?
Did they first find the proteins we now call transcription factors and sigma factors, or did they tamper with the genome to find the regulatory parts and then traced them to the proteins?
Is there a book on the history of research gene regulation to recommend?
Also, I tried Googling. Every site recommended one database or the other. I would be grateful too if you could tell me what should I have searched for?
I am more interested in Prokaryotes, but answers on Eukaryotes would also be welcome.
Context: I'm a freshman doing research (yep. the experience is kinda crazy for me) and I'm interested in finding regulatory elements in Mycobacterium smegmatis and its phages.

where have you looked so far? textbooks? primary literature? can you give some specifics?

This should be covered to some extent in almost any textbook on molecular biology. One excellent book is Mark Ptashne's "A Genetic Switch". It's about regulation in lambda phage, a virus, but many of the principles cary over to prokaryotes as well. It has a full chapter devoted to a detailed analysis of the experiments used to identify the transcription factors and promoters.

This is one of the things I looked at: https://www.ibiology.org/ibioeducation/exploring-biology/molecular-biology/transcription/discovery-of-transcription-factors.html  But a lot of things I read was about the methods and discoveries, without much detail really on what people were thinking when they tried these things out.

@CharlesE.Grant Got it. I will check it out.

@CharlesE.Grant My school library has the 1986 edition, whereas the 2004 edition I have to buy. Is the chapter you were talking about in the older edition?

@CedarRen. For pete's sake, just walk down to your library and check it out. I was happy to offer a recommendation, but now you're asking strangers on the internet to do your work for you.

If your final goal is to understand how to carry out your project then you can focus on how such studies are carried out in current times. Scientific research in earlier times were limited by the technology available at that time.

Here's what one group thinks is pertinent: https://www.biostars.org/p/10596/#10749, besides @WYSIWYG... ze may have finished zer studies, and might like to contribute to the technology around zem: http://discuss.area51.stackexchange.com/users

@CharlesE.Grant, I recently ordered a copy thanks to you. It's a short book, and so far very interesting. Cheers.

As it can be seen from (more or less recent) discovery, most of the regulators were discovered through specifically designed experiment to exhibit one particular factor. Several examples include:

The discovery of Sp1, the first eukaryote transcription factor to be discovered (as described in the video linked in the comments)
The discovery of the Lac operon in E. coli.

None of these were intended to be screens for regulatory sequences in general. If you are looking for regulatory sequences of a specific gene, the technique of reporter gene, combined for instance with a random mutagenesis screening can provide you with a mapping of regulatory elements.
The following article might be of interest to perform a screen based on UV-mutagenesis: UV mutagenesis in Escherichia coli K-12: Cell survival and mutation frequency of the chromosomal genes lacZ, rpoB, ompF, and ampA.
If your question is more general: "all the regulatory sequences associated with one gene", then this question is generally unanswered, and can probably be better tackled first using bioinformatics analysis (such as promoter prediction, etc).

All this history hasn't stopped some from trying though has it? http://bit.ly/2lN7uKp


text:
Why lipophilic molecules can pass phospholipid bilayer, in spite of 2 hydrophilic layers?
It is commonly told that, hydrophobic/ lipophilic/ nonpolar molecules can quite easily pass phospholipid bilayer, and hydrophilic (polar or ionic) molecules can't pass (when no protein aid that); because hydrophobic nature of the lipid.
But in the same logic, hydrophobic molecules shouldn't pass through the bilayer. Because there are 2 hydrophilic layers in the membrane. i.e.

A and A' .
Then how the hydrophobic molecules can pass through A and A'?
I guess, it is due to thin diameter of A and A' . Is that?

Note that in a simple system like in that picture, you would find the highest concentration in the membrane, so in a way, the drugs does have difficulty getting through.

@ElianeB. you mean hydrophobic molecules ('drugs' in your example) locked inside the lipid bilayer?

Yes. https://i.imgur.com/Peuv3Lk.png (Rang&Dale 7th ed, p.100). A and A' are not that different from the water around the bilayer.

Good question. This is my take.
It's not just the surface of the membrane that's polar. There is water (polar) on both sides of the membrane. In most animal cells there is also an unequal distribution of charges across the membrane. The environment outisde of the cell is typically positive due to an excess of positive ions, especially sodium. The inside of the cell is typically negative due to an excess of negative ions such as phosphate.
This means the hydrophobic molecules aren't any more at home in the environment outside, or inside, the membrane than they are at the surface. There's no reason to suppose any more repulsion at the surface. So, just due to their random kinetic motion they will find themselves at the membrane's surface, some with the necessary kinetic energy to cross.
There's another way to view this. We shouldn't think of the membrane as allowing hydrophobic substances to enter. We should think of it as NOT allowing hydrophyllic substance to enter without a proper ID check by proteins in the membrane.

It is also worth mentioning that some lipid molecules require a carrier that will deliver them to the target tissues.