There is not some simple dichotomy of "neurons shrink and other cells swell" in response to hypoxia/ischemia.

Neuronal death can be necrotic or apoptotic or both, and at different stages different morphology is observed: generally swelling earlier, shrinkage later, though both are observed together early as well. Eosinophilia/"red neurons" tends to occur later as mentioned in this passage (after 6 hours, consistent with 12-24 hours) so that's probably why the author is referring mostly to shrinkage. Cells can also have swelling of some organelles, like mitochondria, despite shrinking overall.

Without further context of the passage you provided it's hard to say much more.

Garcia, J. H., Yoshida, Y., Chen, H., Li, Y., Zhang, Z. G., Lian, J. I. N. Y. I. N. G., ... & Chopp, M. (1993). Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. The American journal of pathology, 142(2), 623.

Jenkins, L. W., Povlishock, J. T., Lewelt, W., Miller, J. D., & Becker, D. P. (1981). The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta neuropathologica, 55(3), 205-220.

Portera‐Cailliau, C., Price, D. L., & Martin, L. J. (1997). Excitotoxic neuronal death in the immature brain is an apoptosis‐necrosis morphological continuum. Journal of Comparative Neurology, 378(1), 10-87.


Can anybody recognize this cardiac waveform?

To be conclusive, another couple of leads recorded at the same time as this event would be helpful though the fact that you do have a recognisable QRS complex and a T wave and that the QRS happens before you would expect it to based on the prior rhythm and the P wave, if that is one, prior to it is to close to the QRS complex to have caused it would suggest a premature supraventricular arrhythmia.  There are many technical texts to consult to refine this further, if this is a small animal ECG, I recommend Larry Tilley's textbook entitled ECG for the small animal practitioner.


Black bumps on the cut surface of an avocado

It looks to me (although I'd want to use a microscope to check) like the black dots are xylem. When you cut the fruit, you've severed the xylem and also exposed the flat surface. Three main things have then happened:

The increased surface area has led to the 'fleshy' part of the fruit contracting as the cells dehydrate.
The stiffer, lignified xylem tubes have retained their structure and have not contracted with the rest of the fruit, so they've become exposed.
The exposed xylem have blackened due to oxidation - this eventually happens to all the flesh but, again speculating here, the oil in the fleshy tissue might protect it from oxidation longer than the exposed xylem which don't have the oil coating.


Healing rate of cut while suffering from a cold

First of all: No, there is no connection between these two incidents, correlation does not imply a causation. Cold and flu viruses affect the respiratory system and the infection route goes via it. A cut is a local wound, which does not affect the respiratory tract.

Then: Recovering from an infection is a task for the immune system (its both, the innate and the adaptive immune system, the last involves the antibodies), which is not doing much for wound healing. The wound attracts neutrophils and macrophages which are attracted by factors released by the wound and they react to bacterial infections (when they occur). See this Wikipedia article.

The ressources of a normally healthy person are quite big. This is demonstrated by the fact that many secondary infections only occur in a opportunistic fashion (for example viruses like Herpes or certain fungi) when the body is weakened by other infections. So there is a limit, but this will certainly not be reached with a severe cold.


Given the large eyes, the almost non-existent antennae, the humped back, elongated abdomen and the wings, I'd say it is a robber fly.

It is one of many insects known to prey on wasps.

Note the description on the linked page:

  This spindly piece of nastiness is a Robber Fly in the genus Diogmites. It seems that it's members of this particular genus that are adorned with the name Hanging Thief. You may remember that this was to denote their habit of dangling from a leg or two while the other limbs held onto prey, stabbed it to death with venom and then sucked out the insides. [Emphasis mine.]


How can just random mutations explain mimicry?

/how come these animals (below) show such striking resemblance with their surroundings/

You are looking at the culmination of millions of generations of these insects.  The mutations are random, but only the helpful ones (of all the random ones) produce an advantage for the organism and so persist in the species.   If a random mutation caused an insect to look slightly more like its environment, that insect might do better at avoid predators or catching prey.   Thus it would be more likely to produce offspring which would also have its mutation.  Random mutations that caused an organism to look some other way would not confer any benefit as regards producing more offspring.

In each generation, if there is some random mutation that made the organism more similar to its environment, it could produce better fitness.  The end result, over thousands (even millions) of years, is an organism which looks very much like its environment.

Fitness is what drives evolution.  Read more at the link if you are interested.  The more offspring I have the more I pass along my DNA and the better my fitness is.  If I have a mutation that lets me have more offspring, that improves my genetic fitness.


What is the energy consumption of the brain?

I assume that you mean energy consumption.

Talking in round numbers the daily energy requirement of a sedentary human is 2,500 kcal. It's usually said that the brain uses 20% of this energy.

What does this mean in terms of power consumption?

500 kcal = 500 x 1000 x 4.2 J  -[1]
24 h = 24 x 60 x 60 s          -[2]

1 W = 1 J/s

therefore brain power  = [1]/[2] = approximately 24 W

Most of the energy consumed by the brain is used in maintaining membrane potentials so energy is used continuously. I would think that there will be very little difference between waking and sleeping.


What happen's to a virus's capsid after it injects its genetic material into the host cell?

Interesting question and actually I haven't found a real answer here yet. The phages seem to bind rather hard, since the need to be blended (subjected to relatively high forces) to shear off. This was used in the Hershey-Chase-Experiment to find out what the genetic material of the cell is. It doesn't matter though, since most of the cells which are infected get destroyed anyway. If not, they are most likely taken up and broken down inside the cell, as it happens with other membrane proteins.
This is only valid for viruses which inject their genetic material into the host cell, while the capsid stays outside. This happens mostly for Bacteriophages.

There are a few other possibilities for viruses to enter cells where this is no problem:

Viruses which have a membrane envelope can enter the cell via membrane fusion. To make the fusion happen, either the membranes have to get very close, or the virus first binds receptors on the cell surface and then fuses its membrane with the cell. This causes the interior of the virus to be released into the cell. The picture below shows the fusion (from the Wikipedia article on membrane fusion). An interesting article on this topic is: "Membrane fusion."

Another possibility for a virus to enter a host cell is via endocytosis. Here the virus uses the uptake of material from the surrounding of the cell to get inside. This can either happen together with resources inside a vacuole.
Or it happens via the binding of specific receptors, which are internalized into the cell upon binding of the specific ligand. Here the virus mimics the ligand of the receptor to get internalized into the cell.
In both cases the virus needs to escape from the vacuole before it get broken down because the vacuole is turned into a lysosome.


What's the amount of blood passing through heart every second at Max Heart Rate?

· Heart Beat Rate

  The normal heart has a rate of 72 beats per minute, but in infants the
  rate may be as high as 120 beats, and in children about 90 beats, per
  minute.

Lets say the heart beats at an average pace of 70 bpm (beats per minute)
(~100.000 times a day)

· Cardiac Output

Volume of blood pumped by the heart in a minute.

CO = HR X SV (heart rate multiplied by the stroke volume)

Cardiac output is the volume of blood being pumped by the heart in a minute. It is equal to the heart rate multiplied by the stroke volume. So if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/ minute during extreme exercise.

So for an average adult at rest the estimate is around 5 litres of blood per minute (~1.33 gallons)

· Cardiac Outout / second

There are 60 seconds in a minute so simply :
divide amount pumped per minute by 60

0,083̅3̅  L of blood per second
(83,33 mL of blood per second)

But this is just an average with specific variables defined... so maybe you have to take into account other factors that may vary this value.

· Factors Affecting Cardiac Output

  Factors affecting cardiac output in a healthy but untrained individual
  could be:

Increase/ decreased in heart rate
Change of posture
Sympathetic nervous system activity
Parasympathetic nervous system activity can also affect cardiac output.

  Heart rate can vary by a factor of approximately 3, between 60 and 180
  beats per minute, whilst stroke volume can vary between 70 and 120 ml,
  a factor of only 1.5.

You can read more here & here


I've been thinking about this question for a few days and along the lines of @ThomasIngalls comment, the simple answer is that cooperation between organisms has such a huge advantage in selection that any chance a eukaryote would become a chemautotroph would simply not adapt fast enough to compete with those that are already holding these niches.

The chemautotrophs I'm aware of are usually archaeabacteria.  They are optimized to grow slowly and have a large number of genes that can break down the unusual chemical compounds to grow in an inorganic often anoxic environment.  These bacteria have genes evolved from the chemautotrophic earliest days of life on earth.  They live deep within the earth, under ground, in volcanic vents.  There are animals that live in some of these environments, but its simply too easy for these to use the bacteria that are already growing here readily rather then re-evolve the genes to do it by themselves.

Eukaryotes are already symbiotes - they used bacteria to create ATP and photosynthetically fix carbon to the extent that they absorbed them as mitochondria and chloroplasts respectively.  If eukaryotes were under a tremendous amount of selective pressure, some of them might absorb symbiotic chemautotrophs, but without such pressure, it doesn't happen when you are competing against plants with roots and animals that eat for their energy.

Forming systems of organisms is much more stable than having individual species that can do it all.  This question is actually similar to other questions that ask why we don't have metal armor, run as fast as cheetahs, etc.  Evolution doesn't actually create super animals that are completely self contained.  The ones that reproduce the best are the ones that can actually spread out the risk of survival and contribute to an ecosystem.

It kind of makes me think of human beings - the only superorganism on the planet in this regard.  We don't really need to compete against any organism - we are in fact killing most of them out there without really thinking about it.  That might now turn out to be good for us long term.


Do genes play a role in the athleticism and shape of a person?

All these characteristics you observe (speed, ability to play cricket, belly size, height, etc…) are what what we call in biology a list of phenotypic traits. Basically, the phenotype is a characteristic of an organism that we can eventually measure or describe (physiological, behavioural, morphological, and life history are four common classes).

In a given population the phenotypic variance (the variance in height for example) can be expressed as the sum of the genetic variance (=the genetic variance underlying the phenotypic trait of interest), the environmental variance (=the environmental variance underlying the phenotypic trait of interest) and the variance due to the interactions between genes and environment (the variance due to the interaction that is underlying the phenotypic trait of interest).

Mathematically expressed it gives:

$$V_{phenotype} = V_{genetic}+V_{environment} + V_{gen X env}$$

Therefore, for each trait there is a given part of the variance that is explained by the environment and a given part that is explained by the genes. We might go a bit further and defined the concept of heritability (in the narrow sense, see wikipedia article for more info). The heritability (in the narrow sense) is the ratio of the phenotypic variance to the additive genetic variance. Mathematically expressed it gives:

$$h^2 = \frac{V_{additive}}{V_{phenotype}}$$

Each trait has it's given heritability. The heritability can be defined only for a trait in a population (which defines $V_{genetic}$) and its environment (which defines $V_{environment}$).

For example, the heritability of height in human is around 0.8 (non-peer reviewed source). Which means that 80% of the variance in height in the world-wide population is explained by the genetic variance. See this post for more info about the concept of heritability

In your question, you also used (before your question was re-edited!) the word fitness (also it is not really present in your question). The fitness is a very important concept in biology, it is the ability of an individual to survive and sire offsprings. Our phenotypic traits influence our ability to sire offsprings and therefore our genes influence our fitness. If the whole phenotypic variance is explained by the environmental variance only, then, even the the trait is under selection, there will be no change in allele frequency due to selection. Note: an allele is a gene variant. If eye color is a gene, brown eyes and blue eyes are alleles (to make it easy). This change in allele frequency is called a response $R$ to selection $S$. This link between selection, the response and the narrow sense heritability $h^2$ is given by:

$$R=S\cdot h^2 $$

So to answer your question. Yes, part of the variance in height, belly size, cricket playing ability, etc… is genetically coded. As the fitness depends on phenotypic traits, Yes, the fitness is genetically coded (otherwise there would have no response to selection). Therefore we're not all equal to playing crickets!


GST is glutathione-S-transferase, an enzyme that binds reasonably tightly to glutathione. It is often used as a tag to purify proteins of interest. In your case, GST has been fused to RhoA most likely so that you have some means to purify it by applying it to a glutathione conjugated column. See here for more information.


What would the RBCs of someone heterozygous for sickle cell anemia look like?

The peripheral smear in a patient with sickle cell trait typically appears normal (see Cecil Medicine Ch. 166). Each cell has only 30-40% HbS, and so the polymer that causes the sickling doesn't usually occur.  You can find some examples online of smears with target cells and maybe one sickled cell, but these are the exceptions to the rule. This is one of the reasons a smear is not a good screening tool for sickle cell trait.

To clarify, RBCs in the blood of a patient with sickle cell disease aren't all abnormal either. See this smear from this case published on the NEJM blog:

Again, this is sickle cell disease, not trait, and you see many normal RBCs, even from this patient (honestly, it's not clear whether this is that patient's smear, but this would be typical). In sickle cell trait, the smear would likely be normal (image from webpath tutorial at the university of utah):


How can bobcats feel the mice under the snow?

You can smell roughly where your pan is cooking, but you can hear it with more precision, in order to pin point something you would tend to use your ears, especially if it is under snow.

Cats use all their senses and experience to hunt. The mice have tunnels under the snow to get around and they mark their territory randomly, so the smell doesn't provide a very precise coordinates for tracking: it propagates via wind, through snow, and takes a lot longer than sound to be sensed by the cat. Smell can travel further amd mouse piss smells strong, and freezes. Freezing temps prevent aromatics from diffusing outwards and from reacting with other chemicals. Snow is a very good thermal and therefore airflow insulator. Wind doesnt go through snow very fast, and aromatics take a while to get through (aromatic molecules can even travel through steel and glass)

Cats can hear higher-pitched sounds than either dogs or humans, detecting frequencies from 55 Hz up to 79 kHz (a range of 10.5 octaves) and dogs hear from 67 Hz to 45 kHz, a range of about 9 octaves.

To compare the hearing of a cat to that of a bat, the most sensitive range of bat hearing is 15 kHz to 90 kHz. A human adult hears up to 16-18khz and a child up to 20-22khz.

Sound arrives at the cat nearly instantaneously and provides a direct triangulated reference to the mouse position... One sound arrives slightly later than the other depending on the position of the sound source, and the entire sound spectrum is used in the brain to construct a clear image of the mouse position... shuffling sounds and percussive grey noise generated by animal movement tends to have peaks of energy distributed over a wide range. If the mouse is out of it's den in the middle of winter, it means that it's mostly searching for food, forageing, actually quite noisy activities.

Snow dampens the propagation of sound, so in winter you may notice that ambient sound is different in snowy conditions. That cats can pin point a mouse under snow is not that suprising, given the ambient silence of mid winter, the foraging of rodents, and the olfactory and auditory faculties of felines. it's a good quesiton because you wonder what cats do near mole hills, they are probably sensing a lot of activity there that we don't think about.

https://upload.wikimedia.org/wikipedia/commons/thumb/5/5d/Animal_hearing_frequency_range.svg/512px-Animal_hearing_frequency_range.svg.png


First line of wikipedia > Immune system

  The immune system is a host defense system comprising many biological structures and processes within an organism that protects against disease

First line of wikipedia > Allergy

  Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment.

In other words, the immune system is here to defend the organism against diseases. However, sometimes this immune system misinterprets a harmless substance and start triggering an immune response against it. Such immune response against harmless substance is called an allergy. An allergy is hence a defect of the immune system. There are other defects of the immune system though, such as autoimmune diseases.


What kind of mushroom is this in central Europe?

Could be oyster mushroom. Get some books. Look up Pleurotus ostreatus; a book I found it in is primarily for US,although mushrooms often have very wide distribution. One book I have says " The worst thing you can do is pick mushrooms ,then try to decide what they are ;if they are edible". The recommendation is to learn some local editable mushrooms and then hunt for them.


Distance matrix with different length sequences

There are two possibilities:

Do not use the sequences per se but a scalar metric of sequence similarity for distance values
Introduce gaps in the alignment. You can also do an end to end gapped alignment such as the Needleman-Wunsch and use the alignment scores for the distance matrix.


One can list candidate genes based on their functions.

If a drug acts by inhibiting the expression of gene G in order to reduce process P, then, gene G, all its regulatory elements and all sequences involve in process P are good candidates for such interaction and should be investigated. If there is known genetic variation in the population at these loci and if we know this genetic variation affect phenotypic variance, then definitely, those are good candidates.

However, to my knowledge, this is the extend at which we are able to go. We can list candidates but it does not mean in the absolute that a candidate must present an interaction with the drug of interest and it does not mean that a non candidate gene would necessarily not have an interaction. Only a statistical testing for such interaction would allow one to solve the mystery.


There is of course a pathway that synthesizes NAD+ de novo, usually from tryptophan, aspartic acid  or vitamin B3, or salvaged from compounds like nicotinic acid, nicotinamide. You can read more about it here: https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide#De_novo_production
The fact that TCA works in isolated mitochondria is not necessarily the effect of de novo synthesis. The reason for that is the cycle-like fashion of NADH production in the TCA and consumption of that NADH for electron-chain reactions (which recreate NAD+) or other reactions involving oxidoreductases. Redox reactions do not change the overall amount of the coenzyme. But in a living cell, some reactions will irreversibly consume NAD+, ADP-rybosylation may be an example. Still, the cell prefers the salvage pathway over amino acid pathway, because it consumes way less energy.
ADP and NAD+ cannot pass through the membranes without channels. Both are polar molecules and only non-polar molecules such as steroids can freely pass through the cellular membrane without any help from transport proteins.


Why do humans require vitamin B12 supplementation while herbivores do not?

The bacteria in the foregut of cud chewing animals (e.g. cows) provide enough B12 and other B vitamins. Uptake of B12 happens mainly in the small intestine. There are lots of bacteria in the human intestine but most fermentation of plant matter happens in the hindgut.

Hindgut fermentation also produces B12 but since this happens past the small intestine it is not sufficient to provide enough B12. Therefore non foregut fermenting herbivores (e.g. rabbits) get their B12 when they consume their own feces, which they do anyway to obtain higher digestion efficiency of plant matter. I would not recommend this process to any vegan human though.

As mentioned by bonCodigo, these animals need to take up enough cobalt, and their requirements for this element are higher than our own.

Source:
Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients
C. EDWARD STEVENS , IAN D. HUME
Physiological Reviews Published 1 April 1998 Vol. 78 no. 2, 393-427


Why don't the female lions in a pride help their male lion to protect their children from other males?

Alright, after watching a few more documentaries, here is what I found:
Lionesses do try to expel nomadic males, even if the male lion is not in presence.  On the other hand, I am still yet to find a single video taping the male and females collaborating to expel the invading lions.
When invading a pride's territory, the nomadic brothers will usually not attack first, even if there is only one "lion-king" in the pride. The nomadic brothers might think that the females will help the lion-king to protect the territory; otherwise the brothers will just simply attack as it is a 2 to 1 odd.
The nomadic brothers will usually disrupt the pride's food-supply first. As the pride usually have many cubs to feed, it consumes much more food than the nomadic brothers, and the lion-king is then forced to launch his attack first.
The fight between male lions are usually not lethal possibly due to male lions' body structure. Most of time the nomadic brothers are expelled, but sometimes the lion-king is wounded or expelled from his own territory.
After being wounded, the lion-king cannot protect his cubs. The nomadic brothers then start to find and kill the cubs. The females do sometimes try to protect their cubs, but their attacks can only lightly wound the male lions as males are well-protected by their hairs. In contrary, the males can one-hit the youngsters.
Cubs close to 2-year-old do try to run away and the females do sometimes help them by providing them food, even if the females seem to be obedient to the new dominating males. In this video the lioness even decide to run away from the original territory to raise-up her children and half-children: https://www.youtube.com/watch?v=eMgPf83uDec.
After all cubs are killed or expelled, the females lose the motivation to fight against the invaders, and the new pride is formed.


Your understanding is correct to some extent. Tooth enamel mostly consists of a mineral called hydroxyapatite ($\ce{Ca_{10}(PO4)6(OH)2}$) (Staines et al, 1981).  Though this makes enamel the strongest material in the body, it is susceptible to degradation. In acidic environment, hyrdoxyapatite gets dissolved and leads to cavities (Brown, p. 688). The reaction is:
$\ce{Ca_{10}(PO4)6(OH)2_{(s)}~+~8~H+_{(aq)} -> 10~Ca^{2+}_{(aq)}~+~6~HPO4^{2-}_{(aq)}~+~2~H2O_{(l)}}$
To overcome this, fluoride is added in toothpastes. Fluoride ($\ce{F-}$) reacts with hydroxyapatite of enamel to form fluoroapatite via demineralization and remineralization cycle. The 3 main mechanisms through which it happens are (Rošin-Grget et al, 2013):

Iso-ionic exchange of $\ce{F-}$ for $\ce{OH-}$ in apatite:
$\ce{Ca_{10}(PO4)6(OH)2~+~2~F- -> Ca_{10}(PO4)6F2~+~2~OH-}$

Crystal growth of fluorapatite from a supersaturated solution:
$\ce{10~Ca^{2+ }~+~6~PO4^{3-}~+~2~F- -> Ca_{10}(PO4)6F2}$

Apatite dissolution with $\ce{CaF2}$ formation:
$\ce{Ca_{10}(PO4)6(OH)2~+~20~F- -> 10~CaF2~+~6~PO4^{3-}~+~2~OH-}$

Instead of preventing cavities, fluoride just controls the rate of formation of cavities (i.e. it repairs, not prevents, tooth decay), due to which its repeated exposure on enamel throughout the day is important (Cate et al, 2013). However, the effects of fluoride are minimal once it gets swallowed (Ismail et al, 2008).
Talking about fluorosis, the cause behind it is dissolution of hydroxyapatite due to higher concentration of fluoride (see the 3rd point in mechanisms, it requires higher level of fluoride to occur). Apart from this, formation of fluorohydroxyapatite is also a cause of fluorosis, the reaction being:
$\ce{Ca_{10}(PO4)6(OH)2~+~F- ~+~H+ -> Ca_{10}(PO4)6(OH)F + H2O}$
Dissolution of fluoroapatite causes depletion of enamel layer, causing fluorosis.
References:

M. Staines, W. H. Robinson and J. A. A. Hood (1981). "Spherical indentation of tooth enamel". Journal of Materials Science. 16 (9): 2551–2556. doi:10.1007/bf01113595.

Wikipedia contributors. "Tooth enamel." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 25 Apr. 2017. Web. 1 May. 2017.

Rošin-Grget, K; Peroš, K; Sutej, I; Bašić, K (Nov 2013). "The cariostatic mechanisms of fluoride". Acta medica academica. 42 (2): 179–88. doi:10.5644/ama2006-124.85. PMID 24308397. Retrieved 31 March 2014.

ten Cate FM. Contemporary perspective on the use of fluoride products in caries prevention British Dental Journal 214, 161 - 167 (2013) PMID 23429124

Ismail AI, Hasson H; Hasson (2008). "Fluoride supplements, dental caries and fluorosis: a systematic review". J Am Dent Assoc. 139 (11): 1457–68. doi:10.14219/jada.archive.2008.0071.


What do breeders call the effect when a breed resists modification?

I'm honestly not sure if one exists. They simply lack the gene/allele - the only specific term I can think of when it comes to lacking a gene is referencing Knockout variations where a researcher purposefully removes a gene from a subject in order to observe the effect.

However, "Knockout Mice/etc." imply intent on behalf of the researcher, not a result of breeding or natural lack of an allele. Perhaps "Genetically Incapable" would be a phrase meaning the same thing - but I'm not aware of any 'official' shorthand for 'Cannot because it's not in their genes.'


I have read that cohesin is one of such enzymes, but works as a
  transcription factor by binding specific DNA motifs.

Cohesin binding is not motif dependent (like transcription factors) and is also dynamic. Though sequence may have a role it is, just as in the case of nucleosomes,  mostly the overall composition rather than a sequence based motif:

From this article:

  Cohesin binding peaks correspond closely to peaks of high local AT
  composition, a base composition periodicity of ∼15 kb that is distinct
  from the ∼50 kb periodicity of base composition isochores, consistent
  with axis association of cohesins.

DNA-protein complexes can be crosslinked and subsequently the loops can be pulled down. However, this is tricky. You would need to cut the DNA at the loop ends in order to ligate them together. I don't know how to do that (Perhaps by using an antibody linked to an endonuclease).


Can we change the Eye/Hair color by knocking out the OCA2, HERC2 and MC1R genes using CRISPR in an adult human?

Let's first breakdown this question

What is CRISPR?

CRISPR is a group of DNA sequences that play a key role in the antiviral defense system of prokaryotic organisms such as bacteria and archaea.
They are derived from DNA fragments of bacteriophages that had previously infected the prokaryotes.
These sequences are used to destroy DNA from similar bacteriophages for future infections.

What is CRISPR-Cas?

The CRISPR-Cas system is an immune system seen in prokaryotes that provides resistance to foreign elements such as plasmids and phages. This is a form of acquired immunity.
Some factors allow Cas protein which is an enzyme to recognize and cut foreign pathogenic DNA making them act like a pair of molecular scissors.

What are OCA2, HERC2, and MC1R?

Now we know we can cut a specific part (Gene) of DNA. What do we accomplish by cutting out the genes which Andrew mentioned? To answer this we need to know what those three genes do.

OCA2 (P-gene): Provides instructions for making a protein called the P protein. This protein is located in specialized cells
(melanocytes) that produce a pigment called Melanin.
Melanin is a natural skin pigment. Hair, skin, and eye color in people and animals mostly depends on the type and amount of melanin
they have.
HERC2 (E3 ubiquitin ligase HERC2): Protein ligase which helps in DNA repair regulation, pigmentation, and neurological disorders.
MC1R (Melanocortin 1 receptor): Proteins involved in regulating mammalian skin and hair color.

In short, these Genes affect the Eye and Hair Colour and Andrew is suggesting to us that by removing/modifying them using CRISPR we change the Eye/Hair Colours.

Can we knock out OCA2, HERC2, and MC1R?

Yes, it has been done before and there are sequences available to target these genes within the genome. An example would be the gRNA sequences developed by Sigma-Aldrich and Genscript. I'll provide links of articles which has knocked out the respective gene and links to the gene sequences.

OCA2: (Article: https://pubmed.ncbi.nlm.nih.gov/29555241/ | Sequence:
https://www.genscript.com/gRNA-detail/4948/OCA2-CRISPR-guide-RNA.html)

HERC2: (Article:
https://jmg.bmj.com/content/early/2020/06/22/jmedgenet-2020-106873 |
Sequence: https://www.sigmaaldrich.com/catalog/genes/HERC2)
MC1R: (Article:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html
| Sequence:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html)

Can we change the Eye/Hair Colour by modifying the above genes?

An Interesting article from MIT Technology Review called Engineering the Perfect Baby gives you a nice idea of what I am going to tell you.
In Theory: It's technically possible. We can put up a convincing theory and there is a huge chance that this can be successfully done.
In Reality: Well, Reality kinda sucks cause most of the genetic engineering breakthrough starts from failures. Killing a rat for scientific purposes won't make any big difference but what about killing a fetus? It's almost impossible to get the permissions required to use CRISPR to edit the human genome even if it is to find a cure for a deadly disease that would actually improve the human race significantly. Due to its obvious ethical questions, people always stand against it. I said "almost impossible" cause there are few people who actually got the permissions and there are indeed few ongoing trials experimenting with CRISPR on Human Genome.
A popular Example would be He Jiankui who gave rise to the first-ever gene-modified human babies "Lulu and Nana". He had to forged ethical review documents, misled doctors into unknowingly implanting gene-edited embryos into two women, and many more things which haven't come out yet. What are the consequences? He's bloody missing!
The point is, there is absolutely no way they would approve the usage of CRISPR for modifying something as silly as Eye/Hair color.
I mean we all like our babies to look like Megan Fox but I totally doubt if anyone would dare to modify a human genome for changing mere appearance cause people would start protesting if they find out someone is putting all those innocent fetuses at unknown and uncalculatable risk for changing external traits.
We want people to use CRISPR for things like this - Scientists edit gene for blood disease in human embryos and not for things like this - The rise of the designer baby: Parents who paid $16,500 to choose the sex of their child.
TL;DR (Too Long; Didn't Read):

What is CRISPR-Cas?

Technique in which we can edit genes relatively more precise than before.

What are OCA2, HERC2, and MC1R?

Genes which control the color of Eyes, Hair, Skin, and has other purposes.

Can we remove OCA2, HERC2, and MC1R genes using CRISPR?

Yes

Has it been done before?

Yes

In Humans?

Nope cause we got all those ethics and stuff.

What are we trying to accomplish by removing those genes?

To change the Colour of the Eyes/Hair of a human being.

Can we change the Colour of the Eyes/Hair of a human being?

In theory, it'll work. In Reality, nobody would allow it. They'd be better off with Hair Dye and Contact Lenses than to risk the lives of innocent fetuses.


Does the NMDA antagonist, Memantine that's used to prevent Excitotoxicity cause brain damage?

Yes, it does cause lesions in rats, although I don't think it's been observed to do so in humans.

See: http://www.druglib.com/druginfo/namenda/description_pharmacology/


Multi-modal distribution for gene expression data

One trivial situation in which this can happen is when the tissue used for expression studies is heterogeneous. Different cells express different levels of the gene.

Bimodality can be observed when the system can actually occupy two stable states; i.e. a gene can either have a high expression or a low expression. When you sample the population you would get two peaks. Bistablity (two stable steady states) is a common phenomenon in biological systems and positive feedbacks generally exhibit such behavior. In bistable systems there is also an unstable steady state which lies "between" the two stable states (like a mountain separating two valleys). If the system is in the unstable state, it can fall to either of the two stable states. (See this article for an example). This concept can be extended to multistable systems but they are a little more complex than the simple feedbacks. However they can theoretically exist (I don't know of a biological example yet).

Bimodality/multimodality can be also observed in the absence of a deterministic bistability in the system. This happens because of the expression noise due to stochasticity and is observed in case of transcription bursts (See here).


120-year-old gene regulation problem independently solved by a computer. How?

The paper by Lobo and Levin is an attempt to learn a model that represents the inner workings of a biological system by fitting parameters to data. This is a common topic in "systems biology", a model-based approach to studying biology that is popular in some fields.

Even for small systems, this is a phenomenally hard problem. Unlike most machine learning problems, achieving good accuracy (on independent test sets) is not enough; the model structure itself must be correct, meaning that it should reflect the actual mechanisms operating in the cell or organism. It's like trying to identify the actual structure of an integrated circuit by only observing inputs and outputs --- not only identifying the logical rule that the system exhibits, but the actual wiring diagram that implements that rule. It is of course quite possible that alternative models exist that perfectly captures the behavior, and yet is completely different "on the inside". In other words, the system may not be identifiable from the data --- two different models may produce exactly the same behavior. So there's no way to know beforehand if these problems are even theoretically solvable (let alone practically feasible).

Lobo and Lewin claim to have accomplished this task for a small system of gene products. As far as I can tell, the central piece of evidence is that the model they come up with does capture some mechanisms previously known to exist. Whether this is just plain luck, overfitting, or a special case where (parts of) the system is actually identifiable from data is hard to tell. But it's notable that Lobo and Levin fall back on demonstrating predictive accuracy in the end, which is not enough to support their thesis. The critical test is to take a new prediction from their model and actually test it experimentally, to prove their (strong!) claim that their method can actually infer new mechanisms. Doing so is expensive and time-consuming, and much more difficult to get right than tweaking models to fit mechanisms you already knew beforehand --- which is exactly why I want to see that evidence. If the authors really believe that their method is a breaktrough, those experiments should have been done.

Finally, these type of algorithms are applied to models containing only a handful of components, and typically to systems that have been studied for decades and are very well-characterized to begin with. In most of biology, the problems are orders of magnitude more complex, and often we don't even know what the components are. So I thik there are a limited number of cases where this approach is feasible.


Where are the evolutionary "inbetweeners"?

More specifically, the lack of observable gradual change between species.

Most significant phenotype differences occur over several thousand generations, which means several thousand years on up. While we certainly can create experiments where a controlled form of evolution occurs within a very small time-frame, I'm going to assume that you're not interested in closed laboratory experiments given the nature of your question.

  It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

The data below does answer you question, but in reverse. Hammerheads are much older than most of their relatives; so their cousins have actually grown smaller heads... but there are certainly intermediates.

From Andrew Martin (1993 - mtDNA data) via Elasmo-research.org:
*The circles represent the head-width vs. body-length ratio.

Martin's conclusion: "...the hammer appeared rather suddenly and fully formed, and was later optimized along different lines to suit various selection pressures."

  I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right?

Not necessarily. Single Nucleotide Polymorphisms (a.k.a. - "SNPs" - a change in one nucleotide) can have pretty wide-ranging effects.

The vast majority of humans, for instance, are lactose intolerant in adulthood. However, lactose tolerance evolved twice from two different SNPs in two different human populations: One European and one African. One gene. One regulatory mechanism change. Massive benefits (essentially opening up a whole new resource in adulthood).

Significant differences in phenotypes (the physical appearance of something) can require more gene mutations, or not. It depends on where the mutation is in the genome and what the gene does.

  But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now?

The simple answer is because either there wasn't enough selective pressure that the rest of the shark phenotypes succumbed to that the hammerhead avoided, or that the hammerhead design doesn't give enough of an advantage to completely dominate the gene pool. An alternate, but more abstract answer, is that there simply hasn't been enough time for the hammerhead design to dominate the shark phenotype. Remember, evolution works by generations - not years. It would take unknown thousands of generations for a weakly-advantageous design to dominate an entire niche - if it ever would.

Also, it is worth it to point out that evolution doesn't only select for advantageous mutations. Mutations that aren't very detrimental can still exist within a population as long as the detriment doesn't prevent resource exploitation and offspring production. Think Huntington's Disease which severely restricts a person's survivability, but only after their mid-30's (in general) - plenty of time for the person to have sex and raise a kid into semi-adulthood. It is a genetic defect which sticks around only because it allows humans to reproduce before it seriously affects them.

  The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life.

Maybe, maybe not. Maybe it shot something else before blood, and then a mutation caused it to shoot blood instead - but the overall effect (deterring predators) was the same so it doesn't really matter.

You're correct that some traits might appear very awkward if they had evolved gradually, but the question then becomes: Did they evolve gradually? Sometimes we simply do not know.

  So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

Like I said above, just because a trait is detrimental doesn't necessarily mean it will be eliminated. As long as the being can survive long enough to reproduce successfully with the trait, the trait might not be eliminated for a very, very long time- if ever.

As for in-betweeners dying out - it's difficult to think of it like that. You're talking bout LCAs ("Last Common Ancestors") of extant (currently-living) species. While some LCAs just die out for some reason or another, it's more common that the LCA simply continued to evolve and become a genetic relative due to some sort of isolation.

Think of it like the in-betweeners coming to a fork in the road. Some choose right, some choose left. There isn't anybody left behind - merely two populations that are changing over time that were once one group until they don't really mate between each other anymore (or can't). Heck, even Biologists have trouble deciding at what point a population is considered a different "species" because of discoveries in the last 50 years - so right now a firm answer like "It takes 15% of the genome to change for a new species to emerge" isn't possible as it doesn't really work like that.

We'll get to it eventually, but for the time-being, it might be easier to say that everything currently living on Earth is an in-betweener of something else in the future. Everything in its current iteration will eventually die off, but not before something else emerges from our offspring which may or may not be significantly different from us due to however many genetic mutations our offspring have from us. It could be one that opens up a whole new realm of possibilities (like lactose tolerance) or an accumulation due to selective pressures (like Phoemelanin production and pale skin in humans [Redheads] to produce more Vitamin D3 at higher latitudes).


Do the simplest bacteria have ribosomes and helicase?

I've had a direct look at Carsonella rudii, which is I believe is the bacterial genome with the smallest number of genes so far - 184 as well as being only 160 kb in length.   It has a putative DNA helicase encoded in it.  37 of those genes encode for ribosomal components as well.

If there was ever a bacterium or any living cell (non virus that is) discovered without a ribosome, you would have heard about it.  nobel prizes all around.

So I would say that your answer is yes.


Biology is a large field of knowledge! As you give examples drawn from population biology (logistic population growth and Lotka-Voltera models), I will assume you are mainly interested in ecology and evolution.

For analytical models used in ecology and evolution, I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Day. The book assumes a relatively low level of knowledge in mathematics from the reader and walk the reader through most of the most iconic models in ecology and evolution, their analysis and interpretation. The mathematical tools used in this book include linear algebra, equilibrium analysis, analysis of cyclic behaviour, Markov chain and esp. birth-death processes, diffusion equations, probability theory and stochastic models, approximation theory, class structure models (Leslie matrix and more) and, separation of time scales among others.

For books, mainly theoretical, in population genetics, please have a look at the post Books on population or evolutionary genetics?.

As you talk about the Lotka-Voltera model, you will find an intro to this model in the post What prevents predator overpopulation?.


Do blood glucose "spikes" contribute to insulin resistance, or is prolonged elevation required?

Great Question.

The biggest problem is persistent insulin signaling from prolonged excessive high blood glucose over time. The reason being that it is this kind of signaling that results in insulin insensitivity due to down-regulation of the insulin receptors.

Any bolus of carbohydrates > ~ 25grams in a sitting is going to bump up blood sugar at a fast enough rate to warrant the release of insulin to help lower blood sugar levels.  This can be mitigated by an excessive amount of fat along with the carbohydrates, thus slowing down the spike.

  Your question: 1) Is it true that high blood glucose is normalized substantially more rapidly in people who have depleted their glycogen, or who have higher energy needs?

So this is a little confounded by several variables.  The thought process is that people that have less glycogen or higher energy needs, don't have insulin insensitivity; thus the same amount of insulin would do a better job of shuttling glucose into cells.  We know that consistent exercise increases insulin sensitivity, as does lack of persistent insulin signaling (such as comes from being in a glycogen depleted state).  So the answer to your question is generally YES for these reasons.

  2) Does repeated exposure to high levels of blood glucose contribute to IR by itself, or are high and prolonged levels of blood glucose required?

What we know from epi studies suggests that it isn't insulin spikes.  It is prolonged insulin signaling that causes insulin insensitivity through down-regulation of insulin receptors.

If you are fuel deprived, or only getting what you need from your food, insulin spikes are normal and transient and don't cause this IR.

Persistent insulin signaling causes many many side effects. Insulin is mitogenic,  has downstream pro-inflammatory cascades, and the insulin insensitivity that results is a major player in non-alchololic fatty liver disease.

Some references for these thoughts and further reading:

This one gives evidence of reduced IR activity, not
downreglation
Insulin signaling and NAFLD
Exercise and Insulin Sensitivity


How having sickle cell trait would provide resistance to malarial parasites?

I would say that there are at least 2 explanations:

Higher levels of free heme in the blood of individuals with sickle cell anaemia/sickle cell anaemia trait. Free heme is toxic to Plasmodium.sp Science. 1981 Nov 6;214(4521):667-9., detailed mechanism is described here: J Mol Med (Berl). 2008 Oct;86(10):1097-111. This effect is also observed in people with other diseases affecting stability of erythrocyte's membrane, such as thalasemia or spherocytosis.
It is also possible that, when erythrocyte's membrane is prone to disruption, Plasmodium.sp  antigenes are present in higher concentrations and may be faster presented to the immune cells.


Why doesn't yearly screening for lung cancer decrease mortality rates?

There are a number of reasons, generally, why a screening test may fail to decrease cancer mortality rates:

The screening test may not be very good. I know this seems like an obvious one, but its something of a problem - a screening test will only reduce mortality if it catches cases that are both treatable and wouldn't be detected in time to treat using other methods. For example, it may be that even if caught slightly later by other methods, lung cancer is equally treatable (or equally difficult to treat).
Mortality from false positive tests and subsequent procedures in non-cases offsets any gain in survival among cases.
Diagnosis is only one step toward treating a disease. Even if detected, if a disease is not treatable or isn't treated, knowing you have the disease doesn't change your mortality risk.

In this case it appears that a chest radiograph isn't good enough at detecting lung cancer to manifestly improve mortality outcomes. The author's of the paper don't really specify why this is - though since they're just looking at lung cancer mortality, it's likely not #2.


Effect of a doubling of the start codon in a gene

There is a basic misconception in the question you have asked, which @biogirl has explained. There is only one start Codon in any mRNA and it defines the open reading frame.

All other AUGs in the open reading frame are simply codons that encode for the Amino Acid Methionine and have no function in the start of translation. There are factors other than AUG that determine the start of translation.

So a frame shift that gives you an additional AUG only means that you will have a different Amino Acid encoded for in the resulting polypeptide. A frame shift will generally completely alter the protein product of the gene. If however the frameshift does disrupt the start codon, then it is unlikely that you will have any translation what-so-ever, as the other elements necessary for determining the start of translation will likely not be present in other areas of the coding sequence. In prokaryotes, you need a Shine-Delgarno sequence to initiate translation, and in Eukaryotes, though all of the factors for translation start are not well understood many genes carry a Kozak sequence that indicates to the ribosome the start of the open reading frame.

The more important codons to look for are introductions of stop codons. These three codons, UAA, UAG, and UGA do not have tRNAs with complementary anticodons (for the most part, as tRNA genes can also sustain mutations that change their anticodon) and therefore all result in the termination of translation if the shifted frame results in the ribosome reading one of the three stop codons in frame.


Embryonic cells, when can you detect them in vivo? (In order to do whole genome sequencing)

As usual, the answer is "it depends what you mean". There is a large existing field (prenatal genetic diagnostic testing) which trying to diagnose genetic diseases in fetuses using different technologies. These technologies are described more in points 2 and 3 below, whereas point 1 is a somewhat academic statement about the technical capabilities of genomic technology in pure research settings which are currently not really relevant for medical applications.

I can think of 3 different answers to the question as originally posed:

With currently available sequencing technology you can never know
the full genome sequence of a human well enough to see all the potentially damaging variants. The "finished" human reference genome in
fact has gaps and errors that are constantly being corrected. For
more information about what "finished" means, see here. Only one assembly of a telomere-to-telomere human chromosome exists as far as I know, and that's only the X chromosome. Even accepting that this best available technology is good enough, it also relies on things like the ability to isolate lots of high-molecular-weight DNA, which makes it very tough to do on the amount of cells you could get from a newborn without highly invasive procedures such as e.g. sampling fetal tissue in vivo. My guess is that even amniocentesis would be very hard to get good HMW DNA from.
With currently available sequencing technology you can however test
very early provided you used IVF, at least as early as the 100-cell stage
(probably earlier). This is a chancier method that will miss a lot
of information but gives you good enough info to diagnose
aneuploidies or other very obvious variants.
Alternately, you can screen cell-free fetal DNA as early as 7
weeks (or possibly earlier). However this does not involve
isolating cells so it is potentially not what you are thinking
about. It is somewhat better information than preimplantation
screening, but rather worse information than you can get from whole
cells.

Likely none of those are exactly the answer you want, but it's also a less simple question than it appears at first: a) getting cells is hard and probably not necessary for the current tech, and b) the tech isn't actually as good as generally advertised.


Did Mendel believe that proteins are hereditary substances?

The first person to directly indicate a linkage between the hereditary material and enzymes was Garrod in 1902, based on the observation of the hereditary enzymatic disorder alkaptonuria. This is after Mendel's death.
The tetranucleotide hypothesis (i.e. DNA is not informative) that you refer to seems to have been formulated around 1910. So there is no way that Mendel knew about that.
It was not even proposed that proteins were composed of amino acids before 1902. No protein was sequenced before 1950. So Mendel had no idea what sequences or amino acids were, for any biopolymer.
It is formally possible that Mendel knew at some point about Miescher's result, but I'm not aware that he was at all interested in the chemical nature of Mendelian factors (what we now call "genes"). I agree with commenter @jamesqf on this point.
It was not immediately obvious to anyone that there was a discrete mapping between phenotypes and specific agents such as proteins. The major theories of inheritance at the time came from biometricians such as Galton, who believed that inheritance was driven by a blending-like mechanism (more or less), based on phenomena such as regression to the mean. They weren't really interested in the chemical basis either.
Mendelian genetics was only rediscovered around 1900 (Mendel was basically ignored during his lifetime), after which the debate started to consider the question of discrete genetic factors.
In short, I don't think that there is any evidence that Mendel had any interest in chemistry or the chemical relations of the organismal characters he studied.


Intuitive explanation for Kin- and Group- selection

First of all, there is a very heated debate about this in the field of social evolution at present, and you aren't likely to get a conclusive answer. One theorist may give you one answer, but another will vehemently disagree. I'll start by logically answering your questions in reverse order!

Question 2: Can you please provide an intuitive explanation of why kin- and group-selection are the same thing?

The first formal 'proof' that they are the same came from a paper by Queller in 1992. Let me give you the gist of what he found without being ultra rigorous. I won't focus on relatedness, since that was answered nicely by @falsum, "Price's equation tells us that this happens when the genetic variance between-groups is higher than the genetic variance within-groups. This is equivalent to saying that altruists tend to interact with other altruists and, accordingly, that the coefficient of relatedness increases."

Queller explored the change in mean additive genetic (breeding) value for a trait over a single generation using Price's equation

$
\Delta \bar{G} = \mathrm{Cov}(W,G)
$

where $G$ is the additive genetic value, and $W$ is relative fitness. Now, the key question is, how should we define fitness? If we treat it as a random variable, we can do a linear regression of fitness on a set of explanatory variables. What should we choose for the explanatory variables? One natural choice might be to predict the fitness of a focal individual based on the phenotype of the focal individual itself, and the phenotype of the individuals the individual interacts with socially:

$
W_{i} = w_{0} + \beta_{direct} P_{i} + \beta_{social} P_{j}
$

where $w_{0}$ is baseline fitness, $P_{i}$ is the phenotype of the focal individual, and $P_{j}$ is the phenotype of the focal individual's social partner. However, another way to predict the fitness of a focal individual might be to focus on the average phenotype of individuals in the focal individual's group, and the deviation of the focal individual's phenotype from the mean phenotype of individuals in the group

$
W_{i} = w_{0} + \beta_{deviation} (\bar{P}_{group} - P_{i}) + \beta_{group} \bar{P}_{group}
$

These regression equations for fitness hold exactly (only for a single generation), independent of the 'true' form of the fitness functions (they can be as non-linear as you like). What these allow us to do, however, is partition fitness effects into those that are due to benefits of a behaviour, those that are due to costs of a behaviour (and unmodelled residuals or 'noise').

From a kin-selection perspective, it turns out that the benefit in Hamilton's rule is

$
\beta_{social} = B
$

and the cost in Hamilton's rule is

$
\beta_{direct} = C
$

From a group-selection perspective, it turns out that the benefits and costs in Hamilton's rule are distributed over deivation and group effects

$
\beta_{deviation} = C - B
$

and

$
\beta_{group} = C + (N-1)B
$

Thus, we find that it possible to write fitness equivalently in two different ways that relate the change in frequency of individuals to benefits and costs associated with a social phenotype.

Question 1 Is group selection equivalent to kin selection for any evolutionary game or exclusively for the prisoner's dilemna?

They are always equivalent no matter what game is being played or how the population is structured if you are happy use the regression methods described to define fitness, benefits, costs, and relatedness. Many people have issues with the regression methods though. See Allen et al for a discussion of this. Others argue that kin-selection holds in every case and that the problems with kin-selection stem from a misunderstanding of the methodology. See Gardner et al for a discussion of this.

Many biologists find the debates in social evolution about kin/multi-level selection unhelpful (at best), and choose either framework to work in based on the question at hand. A few are very partisan on either side. There is a great deal of misrepresentation floating around about both, so read papers making strong claims with skepticism and caution.


It is not uncommon for cells to have parallel pathways for same outcome. This ensures foolproof response and makes the system robust. E.coli also has another sensor for aerotaxis (Aer and Tsr proteins). See my answer on your previous post and the linked paper.

Also look for coherent feed forward network motifs.


Where and how is information about pathogen immunity stored in a cell?

All the body does is produce a ton of cells that can recognize single antigens. Each time you encounter pathogens, some of these naïve cells contact antigen that can activate them. The activated clone replicates itself, forming effector cells that can deal with pathogens.

As the infection is cleared and the population of effector cells begins to contract (i.e. many die off or become anergic), some of them undergo changes which alter their migratory pattern and longevity. Some can stay in the tissue that was originally infected as tissue-resident memory cells. Some home back to the lymph node and hang there as central memory cells. The lineage is affected largely by chemical signals being produced by the tissue and other immune cells in the vicinity.

Upon re-encounter of the same pathogen, if it has some of the same antigenic determinants as the original infection, these memory cells are already known to be specific to them. Encountering the same antigen will cause these memory cells to undergo another round of clonal expansion, producing more effector cells and additional memory cells so the process can repeat. These events can be limited by telomere length or inhibitory molecules, as a caveat.

The key understanding is that the immunologic memory is actually stored in the repertoire of long-lived memory cells, and in part results from recombination events at the T or B-cell receptor locus during their maturation before they're released as naïve cells.

See: Abbas (2014). Cellular and Molecular Immunology, 8th ED., many different chapters.


How do you detect a potenially positive transfection? Short fragments might have proper teriary structures which may make them behave differently than you would expect. Also, noncircular DNA and RNA is targeted much faster for degradation in most cells if the right head or tail signals are missing.

To your question: pulsed electroporation with well prepared bacteria (state, buffer,...) is usually 5-100 x more efficient than chemically competent bacteria.


What's the difference between prions and prion-like proteins?

My understanding is that the principal quality of a prion is that it behaves like a prion in cells- the logic is a little circular.

A few of these criteria for acting like a prion (in yeast, where prions are most common):

Reproduces itself by "templating" (refolding of non-prion versions of itself into prion versions)
Sensitive to protein denaturing agents (which get rid of the prion protein conformation).
Dependence on protein chaperones which reproduce prions by releasing prion oligomers from larger prion aggregates. These oligomers go on to "seed" new prion aggregates.
Forms insoluble protein aggregates consisting of many copies of the prion protein.

An important subtlety here is that proteins with identical amino acid sequence can be both prion and non-prion in the same cell. It is a biochemical consequence of a specific protein structure, rather than simply a feature of the protein sequence. Thus, a prion domain confers the ability to become a prion, not necessarily "prion-ness" itself. This Scientific American article might be helpful regarding this point.

As an example of how these criteria are applied, this paper uses some biochemical and genetic methods to screen for the presence of new prions in wild yeast.

As a review of how prions oligomerize and form their classic aggregates, this paper might be helpful.

It is certainly true that creating fusion proteins with candidate prion domains is a common way of confirming that those domains are competent to become prions (see e.g. this paper). But there is usually a higher standard of evidence to show that some protein actually is a prion- usually by demonstrating the existence of heritable protein aggregates mentioned in point (4).

Hope that helps.


How does dsDNA become ssDNA when binding to a nitrocellulose membrane?

The DNA is denatured in-gel prior to transfer using alkali conditions, most commonly a solution containing 0.5 M NaOH (buffered with 1.5 M NaCl). Following that the pH of the gel is neutralised in 0.5 M Tris-HCl, pH 7.5; 1.5 M NaCl.

I have found the Roche DIG application manual to be a well-written and reliable resource for performing Southern and Northern blots. The section on Southern blots starts at page 94 and you can modify the protocol to suit other detection systems.


Well, technically yes, but most adult dolphins do not have hair:

  Unlike most mammals, dolphins do not have hair, except for a few hairs around the tip of their rostrum (beak) which they lose shortly before or after birth. The only exception to this is the Boto river dolphin, which has persistent small hairs on the rostrum.

Whales do, and depending on your definition of "hair" - that includes Baleen - which is composed of fine keratin fibers, much like normal fur/hair, which is the distinguishing characteristic of "Baleen whales" (like the Blue Whale).


We are currently using CRISPR in the lab to modify cells. Like @AMR said, it was modified from the In Vivo immune system to be used in the lab in DNA editing field. The Addgene website features both historical background and an application guide that are very well done. To answer your questions:

The bacteria (S. pyogenes, S. aureus, etc) integrates part of the viral DNA (protospacers) inside its genome, flanked by repeats. When transcribed the RNA derived from this newly combined sequence will direct the Cas9 protein to the viral DNA, which is complementary. Another element required is the PAM (protospacer associated motif) which is on the viral DNA just besides the protospacer. By not being on the bacterial DNA, it ensures that the Cas9 does not cut its own DNA.
The only limitations are the PAM and the off-targets. The PAM is specific for every species (EG S. pyogenes is NGG). Some sequences can be repeated in the genome of an organism, meaning that if you find a sequence that would result in a cut at a desired site, it could still cut elsewhere. That would make the guide sequence a poor choice.


What is the name of the category of viruses that affect only one side of the body?

Short answer: Viruses that affect only one side of the body are not categorized by this information.

Long Answer: For people who likes details

Several types of virus classification exists:

Baltimore: Classified by the type of DNA or RNA that is carried by the virus
Holmes: Classified by the target organisms of the viruses (plants, bacteria, animals)
LHT: Classified using several physical differences (More specific and complex)

For example, Shingles would be classified as:

Baltimore: Group I (double DNA stranded viruses)

Holmes: Group III Zoophaginae (animals)

LHT:

Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genus: Varicellovirus
Specie: Human herpesvirus 3 (HHV-3)


Does the Peptide bond produce water in our organism?

The simple answer is that there are literally thousands of chemical reactions (mediated by enzymes) going on in the cell. Some produce H2O, others consume it. For example, when proteins are broken down into their individual amino acids as part of normal turnover in the cell, a water molecule is necessary to break the peptide bond. Therefore, the overall balance of water produced vs. water consumed is fairly equal, especially when you take into consideration the consumption of water and its excretion via urine and sweat.


How is it possible for the absolute fitness to be more than 1?

That definition in the wikipedia is misleading at best. Contrary to what it seems to suggest there, absolute fitness is computed across a single generation, not within a single generation. For simplicity, let's look at an example using asexual haploids with discrete non-overlapping generations. If individuals with the A genotype produce an average of 3 offspring, each of which survive with probability 0.5, the A genotype has an absolute fitness of 1.5. The key is that we've multiplied fecundity (3) by viability (0.5) and this allows us to obtain a value greater than 1.

Things get more complicated if we look at diploid sexuals. The absolute fitness of the Aa genotype is not the ratio of the number of individuals with the Aa genotype at time t+1 to the number of Aa at time t. An easy way to see this: in a population of AA and aa parents only, e.g. as produced by a cross, the ratio of Aa at t+1 to Aa at t is infinite, which would imply infinite fitness if we went this with definition. Rather, the absolute fitness of the Aa genotype is one-half the number of surviving offspring at time t+1 produced by Aa parents at time t. The one-half comes from the fact that a parent individual contributes only one-half of the genetic material of each surviving offspring. For some traits, e.g. those involved in sex ratio determination or parental care, it will not be sufficient to count surviving offspring; in these cases we apply comparable logic to counting grand-offspring.

The wikipedia seems to suggest we are to look only at viability because we are comparing before-selection numbers to after-selection numbers, within a single generation and thus without an opportunity for fecundity to come into play. That is not consistent with the common usage of the term. To be fair, I have on rare occasion seen "absolute fitness" used as a synonym for "viability"--though I cannot think of any good justification for this usage.


Inheritance patterns in individuals with triploidy

Triploids are characteristically sterile, but people with Down's Syndrome aren't triploid(they're anueploid technically). There's only one chromosome duplicated, and it's the smallest one. Women with Down's can have kids just fine, but men tend to be sterile(according to WebMD at least).

See here for a full coverage of triploid genetics and why triploids are nearly always sterile. In short: gametes formed during meiosis pair off but there's always one copy of each chromosome that chooses a daughter cell at random. If one daughter cell gets none of the extra copies, you have a haploid gamete and a diploid zygote and everything goes according to plan. If one daughter cell gets all of the copies you have a diploid gamete and you'll have a triploid zygote and everything will be fine-ish, but you'll have another triploid generation.

Statistically this happens for 2(1 for females with asymmetric gametes, but let's fudge it a little) of the possible sorting patterns, of which there are 2^n where n is the number of chromosomes. For a triploid human male(bear with me) mating with a diploid female(the best possible combination mathematically) instead of the more typical 200 million viable sperm he would produce about 50 viable sperm(About 2 in 8 million sperm have a chance.). If you account for 23-triploidy that number goes up to about 100, but that's still worse than a millionth of the fertility.

Other combinations are vastly worse. A human female only has about 2 million eggs lifetime total, so even in the best of circumstances a triploid female has maybe a fifty fifty shot at having a single viable egg in her entire life. The calculation for the probability of a two triploid humans(or any n=23 organism) breeding successfully is left as an exercise for the reader but it's very low indeed.

If you were working in some other organism with maybe n=2 chromosomes the numbers would be more forgiving and it might be worth thinking about making Punnet squares. They'd work much like Punnet squares for diploid creatures, but the sides would be a little longer to accommodate the larger number of gamete genotypes, and you'd have to adjust the probability of some of the squares to account for aneuploidy-related fatalities and other weirdness. For instance, with two triploid parents the probability of getting a successful triploid zygote from any random pair of zygotes is something like 1/2^n instead of the 4/2^2n or whatever it is for diploid or quadruploid offspring. This is counterbalanced by aneuploid gametes perhaps dying(or even being slightly less fit).

If n=1 the math is more tractable, however(surprisingly, this exists. haplodiploidy complicates triploidy considerations so I'm pretending it doesn't exist). Examples like AAaxAa give strange results(only 1/12 are recessively phenotyped) but AaaxAa produces 1/4 recessive phenotypes and 3/4 dominant ones, just like AaxAa.

In sum, I see why triploids are just declared infertile and not dealt with in the fullest, most complex sense.


What is this agglomeration of pink cells I found attached to a stone?

They are Apple snail's eggs; check the picture:

Check this.


About what percent of mutations are not adaptive?

As suggested by the McGrew comment, this is dramatically dependent on the shape of the fitness landscape. It will vary quite a bit from situation to situation.
More precisely, you are interested in the distribution of fitness effects (DFE) of mutations, and the upper tail specifically.
Wikipedia has a section on this. In there, they note one study of a virus that suggests that ~4% of mutations are beneficial. That may be an overestimate, and many of those are probably only very slightly beneficial. Probably the number is lower in non-viral organisms.
For a review on the DFE of new mutations, see here. They write in their section "Advantageous mutations":

As expected, relatively few of the mutations that are not
effectively neutral are advantageous.In three mutagenesis
experiments, the proportion of advantageous mutations was 4% in the RNA virus vesicular stomatitis virus (VSV)15 (FIG. 1), 0% in Escherichia coli(14), 0–15% in the bacteriophage φX174 (REF. 40), 0% in φ6 (REF. 13) and 6% in Saccharomyces cerevisiae (16).


can you create an offspring from ancient human's DNA?

A species is generally defined as a group of organisms that can breed and produce fertile offspring. So, if you are extracting DNA from the an ancient human that is indeed the same species as us (homo sapiens), then by definition, you will be able to combine it with modern human DNA and generate offspring.

This is just stating the theory, the actual biology behind extracting that DNA and using it to fertilize offspring will be... messy.


What is the term for all of the RNA in a cell at any given time?

Qiagen and Life Technologies call it  RNA content, total RNA, or total cellular RNA.


How many people's DNA were involved in the compilation of the reference human genome?

tl;dr: In the Human Genome Project, they used the DNA of four people (though one male provided >70% of DNA. The Celera genome was compiled from five people.

  In the [...] Human Genome Project (HGP), [...] scientists used white
  blood cells from the blood of two male and two female donors (randomly
  selected from 20 of each) -- each donor yielding a separate DNA
  library. One of these libraries (RP11 [anonymous donor from Buffalo,
  NY]) was used considerably more than others, due to quality
  considerations.

  [...]

  In the Celera Genomics private-sector project, DNA from five different
  individuals were used for sequencing. The lead scientist of Celera
  Genomics at that time, Craig Venter, later acknowledged (in a public
  letter to the journal Science) that his DNA was one of 21 samples in
  the pool, five of which were selected for use.

  On September 4, 2007, a team led by Craig Venter published his
  complete DNA sequence,[21] unveiling the six-billion-nucleotide genome
  of a single individual for the first time.)

Source: Wikipedia


I think HELA cells are edible, although from moral point of view this would be cannibalism.

Despite they are cancer cells, they are safe for foreign organism, because any ate matter is destroyed. Even if these cells were implanted into another being by surgery, they will be safe since immunity will recognize them as foreign and kill. They are much less cancerous for recipient than just foreign.

Remember, then when we are eating meat, we don't care if cow or pig had cancer. Even if we avoid eating explicit tumors, we can still eat metastatic cells from sick animals. I think this happening all the time and has no consequences.

Simultaneously HELA cells are dangerous for other cell cultures in laboratory. There were several cases, when other cultures were infected by HELA cells and crowd out. HELA cells were traveled by air and on objects unexpectedly. Scientists were not ready for this phenomenon.


What is the number of species known through paleontological evidence?

Very interesting question.

I remember reading about it in one of Stephen Jay Gould's great books (The Panda's Thumb? The Flamingo's Smile? Wonderful Life: The Burgess Shale and the Nature of History? Dinosaur in a Haystack? Probably in one of these).

He wrote exactly about this question, and the effort made by teams from many different countries to get to an "approximate" result. What really impressed me at the time (fifteen years ago) is that when Chinese scientists were invited to add material for a second analysis, the number of known fossil species doubled!

Please, if anyone find the exact source of this, I'll be glad to read it!

But maybe you can get an idea by looking at the number of fossil species for certain groups, and comparing with the number of estimated/known extant species. Keep in mind the rates of fossilization for each group, and also the fact that Nematoda and Acari might be the most overlooked groups in terms of species number (both seem to parasitize animals through most of the Animal Kingdom).


Reproductive isolation causing evolution

Reproductive isolation isn't exactly a cause of evolution, but rather a cause of speciation. Reproductive isolation allows for two cohorts of one species to be reproductively separated. In this case, evolution via random mutation or mechanisms like genetic drift allows for the differentiation of the two groups, up to the point that the two cohorts and their respective gene pools have evolved to be completely different species.

Truly defining a species is still debatable (via the Biological species definition, Morphological, etc) but reproductive isolation is definitely a mechanism involved in speciation.


what are the ethical considerations when preparing a bacterial culture for testing antibiotic resistance?

While I think the question is off-topic, I could not help but trying to answer it! It is easy to find ethical issues in every activity.

Potential ethical issues

You are killing bacteria
Your research has an environmental cost. You consume loads of plastic thingies for example.
Your research costs money as well. You consume tax payer money (depending on your source of funds)
You are selecting for anti-biotic resistance and might, by mistake, release them in nature (of even they are not pathogens, they might become, they might transfer their resistance to pathogenic bacteria as well or your experience may have all sorts of unexpected consequences)
Are you sure it is not pathogenic? We are never sure of anything, so just don't take risks.
Don't play with nature, you are not God!
Are you helping those nasty big pharmaceutical companies, huh?
You are a clever person. There are so many other things you could do for the world that would be so much more beneficial. Your time could be used for better purposes. You could work on improving sanitation conditions in India, or improve women's right around the world, or help children involved in the current civil war in Somalia for examples.

Basics of philosophy of ethics

For any question of ethics, one has to define his/her own values and from this point this person can formulate an opinion on a particular case. Of course, I personally do not feel bad about killing bacteria and consider antibiotic resistance a very important field of study to improve our everyday well-being but other people may disagree based on their own values.

I am not formally trained as a philosopher. So, please read the wikipedia articles on ethics and values I linked above and if you have any other question of Philosophy, you can ask them on Philosophy.SE


For the human head, which direction is anterior, and which direction is ventral?

Humans are are upright in their anatomical position - fig. 1 - from which all directions and terminology stems.

Figure 1: Anatomical Position

Because of this, anterior is normally the same direction as ventral and posterior normally the same as dorsal - fig. 2.

Figure 2: Normal directions in humans

Cranial anatomy is a special case, however, as the entire axis of the body bends round during embryonic development as seen in fig. 3.

Figure 3: Bending of the developmental axis

This leads to the cranium being a little odd, where dorsal is equivalent to superior and ventral to anterior in this area of the body only

Figure 4: Resultant difference in neuroanatomy conventions

However, for convenience, anterior and posterior retain their original directions even in this area.  Therefore you could eliminate a large amount of your difficulties by just using these terms instead for most of the body.

To answer your specific questions:

  So I conclude that human nose is anterior

Yes

  So I concluded that humans' top head is dorsal. Yet ...We call humans' top head anterior

The top of the head is technically dorsal, however in practice would never really be referred to as such, instead being superior.

  In humans, is humans' chin ventral from the eye too? or posterior?

The human chin is both inferior to the eye (looking straight at the face in the coronal plane) and anterior to the eye (but only marginally).  It's more obvious if we look at the tip of the nose instead, which again is both inferior and anterior to the eye.

  In humans, is the nose anterior too?

Yes, the nose is anterior.


What is the inbreeding coefficient for the female offspring of a sib-mating in a haplodiploid system?

From the same article on wikipedia:

  The inbreeding is computed as a percentage of chances for two alleles to be identical by descent.

Now let's draw a family tree for such mating and sign chances for having each allele:

You can see, that the "brother" has a 50% chance of receiving A allele and the "sister" has a 50% chance of receiving A from their mother, but the "brother" will not have the C allele that the sister certainly has. Their daughter will have the allele from her father and one of mother's alleles. Therefore, her chances of having a C allele are 50%, and for a A or a B allele each 75% (remember, she needs two copies, so we need to end up with 200%; furthermore, she may have two A alleles but not more than one C allele). Chances of her having two A or two B alleles are 56,25% $$0.75 * 0.75 = 0.5625$$

Now we have the percentage of chances for two alleles to be identical by descent, her inbreeding coefficient is 56,25%.

The son will have only one allele, 50% for C, 25% for A and 25% for B. Because he does not have two alleles, by definition there is no inbreeding possible.


Term for a prey animal's recognition that something potentially threatening is looking at it?

"Gaze" is the typical term for the direction something is looking, including head/neck and eye position. Gaze detection, gaze following, and gaze perception are used in the literature; there might be other combinations with the term "gaze", as well, I see lots of results with a more general gaze+predator search.
These are all more general terms than the specific use by prey animals, particularly in social gaze: being able to figure out what others around you are looking at, but they are to some extent the same sort of ability.


To be very brief: A gene is a sequence of DNA or RNA, which is hereditary and has a biological function. In the Saccharomyces cerevisiae genome you posted, every gene is a DNA sequence. The function of most genes is to be transcribed  to messenger RNA (mRNA), which is then translated to a protein. "Coding" DNA refers to DNA which eventually has its sequence translated into protein

Structural RNAs are encoded by genes but not translated to protein, and thus are not coding regions. They are made up of RNA, but function more like proteins. When they enable reactions, like enzymes, they are called Ribozymes. The most well known ones are the Ribosomes, which are an essential part of protein biosynthesis. Others form special structures which help molecules recognize each other. tRNAs are needed for the ribosome to recognize the right amino acids.

As David said, this is very basic molecular biology and gene regulation/expression in eukaryotes can get quite complex. The wikipedia articles provide a good introduction and the Berg biochemistry book he linked is excellent further reading. If you want to know more about yeast genomes, you can check out https://www.yeastgenome.org/. It provides a whole lot of information regarding the amount of coding/noncoding regions and their function. There is also a graphical genome browser, where you can view each region in detail and compare it with your own findings.


How much does capillary action contribute to blood flow to the human brain?

None. I have no idea what that video is talking about.

Capillary action of water happens when you have a thin tube and water likes to stick to the "edges." Blood vessels are already full of water, there is nothing for them to capillary up against: there is already water there, so there is no surface tension (there is no surface at all). Blood flow through capillaries is caused by the heart which creates a pressure gradient between the arterial and venous circulation, in the brain and everywhere else.

Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2009. Chapter 2, Anatomy and Ultrastructure. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53086/


How much of the jejunum is bypassed during gastric bypass?

One of the most used surgical technique is Roux en-Y where the small intestine is divided approximately 40-50 cm below the lower stomach outlet and is re-arranged into a Y-configuration.

The portion of intestine (jejunum) from the upper stomach is called the "Roux limb". It has a total length of 80 - 150 cm.

So the Roux en-Y technique "bypasses" only the duodenum and a small portion of jejunum - no more than 50 cm, that's about 7-10% of total length of small intestine.

"Total gastrectomy with Roux-en-Y" by ignis - Own work. licensed CC BY-SA 3.0 via Wikimedia Commons.

Reference: Wikipedia contributors, "Gastric bypass surgery," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Gastric_bypass_surgery&oldid=606081291 (accessed June 27, 2014).


You asked three questions here, so I'll answer them one by one.

Yes, you can survive with glycogen as the only source of carbohydrates, assuming that you also take other nutrients like proteins, fats, vitamins, etc. also because carbohydrates cannot supplement all of them. See this article:

There are three macronutrients: carbohydrates, protein and fats. Macronutrients are essential for proper body functioning, and the body requires large amounts of them. All macronutrients must be obtained through diet; the body cannot produce macronutrients on its own.

No, there's no way to calculate this. If we were talking about glucose, a definite range could be given. But since glycogen is a polymer with variable amount of glucose molecules linked together (at least I couldn't find an exact number),  its not possible to tell how many glycogen molecules are needed for the daily metabolism in the body.

Glycogen is an organic, non-polar polymer, insoluble in water just like starch. It does not have a specific taste, but once you eat it, an enzyme called salivary amylase will break it into glucose, maltose and limit dextrins, causing it to taste a bit sweet. See this article:

This enzyme acts on starch, glycogen and related polysaccharides and oligosaccharides producing beta-maltose by an inversion.

Source


As you may have realized, crystal violet can be replaced by a lot of dyes since the ethanol will wash out the dye from the gram negative cells. Methylene blue is a nice choice - malachite green may also work.
A weak concentration of hydrochloric acid (3%) is also a possible replacement for the ethanol. A 3% HCl solution is used in the acid-fast stain but it may be too strong for non-acid fast cells. It would be worth testing it out and trying it to see if it could replace the ethanol step.


What instances are there in which two species share the same binomial name?

There are four other instances of species-level hemihomonyms I can find:

Agathis montana can be either a critically endangered species of conifer or a parasitic insect.
Centropogon australis can be either a fish or a plant with a long red flower.
Asterina gibbosa can be either a sea star or a type of fungus
Baileya australis can be a moth or a yellow flowering plant


What network motifs or other mechanisms can make the expression of a gene invariable to the environment?

This phenomenon of being insensitive to certain fluctuations is called robustness. The fluctuations can be of two kinds for an input-output device such as a gene that is activated by a signal:

Fluctuations in the signal
Fluctuations in the intrinsic parameters

Signal fluctuations can be temporal but parameter fluctuations are not (parameters are supposed to be time invariant). Parameter fluctuation can exist in a genotypic space or a population of cells because of variation.

Some motifs are robust to signal perturbations whereas some are robust to parameter fluctuations.

Negative feedbacks and incoherent feed-forward can confer robustness by correcting the output fluctuations because of fluctuations in the input.

When an all or none sort of (binary: one state need not be smaller in magnitude than the other) behaviour is important, then positive feedbacks confer robustness to such systems because of their property of bistability.

I cannot recall any particular motif that is robust to parameters. There are certain cases though (I am still working on that!! :P).

In any case environment can be thought of as an input.  For your question "what mechanisms can make a gene susceptible to a certain environment in one cell-type but not in another":

There can be a heterogeneous population of cells which can arise because of bistability or even otherwise, due to stochastic effects. If the gene that is in one of the two states (expression levels) in these two sub-population of cells, and this gene is responsible for the expression control (the controller gene in feedback), then one sub-population will be sensitive to the environment while the other will not be.

For more information on biological robustness read this review.


Blood pressure in various blood vessels and heart

Blood vessels have "compliance": that is, they are stretchy. Mathematically, this is very similar to capacitance in electricity.

The further from the heart you go into the vascular tree, the more the oscillations are dampened and the less it makes sense to think of systolic and diastolic pressures. In the capillaries and veins, blood flow and pressure is more or less constant rather than oscillatory (except in the most proximal veins where the motion of the heart again adds some pulsatile influences).

Therefore, for those vessels, you can just stick to mean values for pressure, the oscillations around those values are small.

See another Q&A: Why do people perceive blood pressure as the force that moves the blood forwards (see details)? that has a diagram showing the dampening of oscillations in pressure.


Correlating Ki values of pesticides to bacterial growth

Ki is the equilibration dissociation constant. The smaller this constant is, the stronger (more specific) is the binding between the inhibitor and the enzyme.

If the residual concentration is now higher than the Ki, for each molecule from the inhibitor which dissociates from the enzyme a new will bind (simply because of the concentration). If the concentration is lower (or much lower), this will not be sufficient to inhibit the enzyme. This assumes that the relation between enzyme, inhibitor and substrate are linear (and we are not getting some kind of saturation here).

Under the conditions mentioned above, P1 and P4 will inhibit the enzyme. For P2 and P3 the concentration is to low.


Why is triclosan not considered an antibiotic?

I agree with @Chris that this is mostly a matter of definitions -

Greenfacts defines biocides as:

  According to the Biocides Directive (98/8/EC), biocidal products are those that are intended to destroy, render harmless, prevent the action of, or otherwise exert a controlling effect on any harmful organism by chemical or biological means. Examples include disinfectants, preservatives, antiseptics, pesticides, herbicides, fungicides and insecticides.

and antibiotics as:

  Antibiotics are widely used as medication against disease-causing bacteria. However, bacteria can acquire resistance to particular antibiotics through mutation or gene transfer.

So the key difference is that antibiotics act more specific and may induce resistance. Antiseptics such as alcohol stay active, even after repeated use, because they act broadly. Now that triclosan is argued to have a specific molecular target, it may have to be re-defined from a general biocide to antibiotic. This means that its widespread use may be alarming, and I quote from your linked article (Schweizer, 2001):

  [Triclosan is used in a] multitude of health care and consumer products [and has] germicidal properties [and has] flooded the market in recent years in response to the public's fear of communicable bacteria.

Reference
- Schweizer, FEMS Microbiol Lett (2001); 202(1): 1-7