Why do 6-8% of diphtheria patients do not develop natural immunity after being affected? I am thinking of why some patients do not have natural immunity after exposure to the A-B toxin of diphthria.
I think the A-B exotoxin is the key factor causing this disease and should trigger memory cells to form.

DT has both local and systemic effects.
Locally, its action on epithelial cells leads to necrosis and inflammation, forming a pseudomembrane composed of a coagulum of fibrin, leukocytes and cellular debris.
Absorption and circulation of DT allow binding throughout the body.
Local effects produce pseudomembrane.

The major impact of transduction in pathogens is the introduction and stable inheritance of virulence genes such as those coding for toxins.
C diphtheriae is lysogenic with a phage containing the diphtheria toxin gene.
Diphtheria toxin is produced by C diphtheriae only when infected with a bacteriophage that integrates the toxin-encoding genetic elements into the bacteria

The toxicity for intact cells depends on toxin binding and uptake.
In other words, the net effect of the toxin depends on the function of the target protein and the function of the cell.
B subunit binds to receptors that regulate cell growth and differentiation, thus exploiting a normal cell function.
A subunit inhibits protein synthesis.
B subunit binding determines cell susceptibility.
Absorption and circulation of DT allow binding throughout the body.
I think this uptake does not occur sufficiently with patients without natural immunity stimulation.

I think the reason for no natural immunity for some patients after toxin exposure is that the host does not stimulate enough adaptive immunity and no memory cells are built.
Again, this is because the bacteria has little invasive capacity.
Diphtheria is due to the local and systemic effects of DT with potent cytotoxic features.
The uptake of the toxin varies also among some patients.
So other patients have probably more local effects.
This would explain partially why the adaptive immunity is not triggered.

Diphtheria toxin is antigenic itself.
So it can stimulate the production of protective antitoxin antibodies during natural infection.
In those patients without development of natural immunity, A subunit fails to bind EF-2, probably.

One reason is that the toxin does not get into bloodstream in 6-8% cases, and so natural immunity is developed.
So there is too low effective dose of diphtheria for some patients to invade the epithelium and trigger the adaptive immune response and create memory cells.

Sources: Murray Microbiology, Sherris Microbiology and Jawetz Microbiology.

Why do 6-8% of diphtheria patients not develop natural immunity after being infected?

There are two other, but rather exotic possibilites which explain why people do not develop immunity after an diphtheria infection. These are unlikely to get to 6-8% of the cases which @Masi writes, but I am missing the reference here.

The first possibility are people with chronic renal failure. They have problems with their immune responses since their antigenpresenting cells do not get the necessary co-stimulatory signal by the T-cells. See this paper. People with other problems in their T-cells or the co-stimulatory signal would have this problem, too. See this article.

The other possibility would be the distribution of the antibodies. The diphteria toxin is made out of two subunits, A and B. B is important for making the way of A into the cell, A gets cleaved in this process and fully active. When the antibodies made in the process are mostly against A (and then against parts, which change their conformation after the cleavage), this antibodies are mostly useless to fight the toxin. See this paper.

One (but is complete speculative) possibility is on the toxin itself. It could be possible, that some people are more sensitive to the diphtheria toxin, so that the amounts necessary for the negative effects are too small to trigger an adequate immune response. This is known for the tetanus toxin, where even a survived infection doesn't provide immunity (except when people are vaccinated afterwards) as the toxin is so toxic, that it doesn't trigger the immune system. The caveat is, that the diphteria toxin is about 3 orders of magnitude less toxic than the tetanus toxin.


Can yeast survive without mitochondria? Some yeast cells have very low mitochondria copy number (see number of mitochondria in non budding cell, you can count mtDNA). This makes them susceptible to fluctuations, and one can conceive that some yeast cells might arise entirely without mitochondria. Would they survive? Could they reproduce?

Please, assume they have all the nutrients required, in particular excess glucose to ferment, so mitochondrial energy output is dispensable.

If you could point me to some references that would be awesome.

Basic answer: Yes, they can survive, but only if they do not need to undergo cellular respiration.  I quote from Microbiological Research, Volume 169, Issue 2-3, p. 185-195:

  Mitochondrial DNA (mtDNA) is a compulsory genetic component for encoding essential respiratory enzymes in all eukaryotic cells.

In other words, for cellular respiration to occur, the yeast must have the mtDNA.  However, the article goes on to explain,

  However, some yeast species (called rho positive) could survive without mtDNA under conditions of fermentation (a metabolic pathway alternative to respiration). In these species, partial or complete losses of mtDNA (spontaneous or induced by mutagenic factors) is associated with the formation of respiratory deficient mutants (rho− type or rho0 type) characterised by slow growth on fermentable carbon sources (e.g. glucose) and inability to grow on non-fermentable sources, such as glycerol or ethanol.

In other words, yeast can survive in the presence of correct conditions for fermentation to occur.  In the absence of those conditions, the yeast must have the mitochondrial DNA, because in order for it to survive, it must perform cellular respiration.


Which is the guideline to choose a molecular target to identify vertebrate hosts from arthropod bloodmeals? There are some molecular targets to identify vertebrate hosts from arthropod bloodmeals including the Cyt b gene and the COI gene. Which are the standards or characteristics that I have to bear in mind to choose a molecular target to identify host blood from mosquitoes? I would appreciate your help.

I have looked about the topic and I have asked experts and the best aproximation to know the vertebrate host from arthropod blood meals is targeting mitochondrial genes because you can get clean sequence data due the fact that only one allele is present rather than two.

Within the mitochondrial genome, you should select a gene which has been widely sequenced for most vertebrate species you are likely to detect in your region, other wise you will have many unknown identities among your bloodmeals. Really, there are just two choices that match these criteria: cytochrome oxidase I (COI) gene, which has been used by the Database of Life project; and cytochrome b, for which sequences are widely available (i.e. for many vertebrate species) in GenBank. If you get a negative result for one, you can try the other. Primer sequences are widely available in the literature.

In conclusion, you must be target COI and Cytb genes to assure the host identification and prevent a unidentified match in Database of Life project or GenBank.

I give you a paper example to review the metodology: Host Preference of the Arbovirus Vector Culex erraticus (Diptera: Culicidae) at Sonso Lake, Cauca Valley Department, Colombia


Whats the difference between voltage gated and ligand gated neurons? How are they similar and how are they different?

There is no such thing as voltage gated or ligand gated NEURONS. I believe what you are refering to are what is known as voltage gated and ligand gated ion CHANNELS. Each neuron has both types of channels in their cell membrane.

Voltage gated ion channels open in response to voltage (i.e. when the cell gets depolarized) where as ligand gated channels open in response to a ligand (some chemical signal) binding to them.

Both types of channels are critical for proper activation of the post synaptic neuron. The pre synaptic neuron releases neurotransmitters into the synaptic cleft, these neurotransmitters then bind to the ligand gated channels, thus activating them. The ligand gated channels open up and allow the influx of sodium, which depolarizes the cell. This depolarization activates nearby voltage gated ion channels, which open up and let in even more sodium. Voltage gated sodium channels open up one region at a time, the previous region providing enough depolarization to activate the next regions voltage gated channels. This effectively allows the action potential to propagate through the cell.


How can we determine which chromosome came from which parent? In this article there is a graph (figure 1) describing different levels of methylation in the maternal and paternal chromosomes after karyogamy.
How can the researchers identify which chromosome originates from each parent?

A straightforward way to identify which chromosome came from which parent would be to use sequences of known fragments of parental chromosomes or to use SNP arrays. I hope that I did not miss your question completely.
Regards,


Which fish did modern tetrapods descend from? Did modern tetrapods descend from Tiktaalik or Ichthyostega? While I understand that in terms of all tetrapods, the lineages of Tiktaalik and Ichthyostega both would be included, but I want to know if their lineages have continued to the modern day. Since they also have 10 million years between them, it's possible that both of their lineages have not continued to the modern day. It's also possible that neither of them have continued to the modern day and it was a later fish species altogether whose lineage has continued to this day in the form of currently living tetrapods even though Tiktaalik and Ichthyostega were the first vertebrates on land. I'm especially interested in knowing which fish pecies have humans descended from. I'd be grateful if anyone is able to shed any sorta light on this.

Your question cannot be answered.
One of the effects of how incomplete the fossil record is, is that it is impossible to say if a species was a member of a direct line or a side branch. we just do not have the resolution in the vast majority of the fossil record to tell. The answer could be both, neither or one or the other and we would not be able to tell. All we can say is it is likely they were closely related to or part of our ancestral line. But the working assumption is always that you have a related sister species and not the ancestor unless you can show extremely good evidence otherwise, (which is so rare you can assume it is impossible in extinct vertebrates).
Tiktaalik and Ichthyostega only give us a rough idea of what our ancestors would have been like. It is impossible to say with any certainty if either was a direct ancestor or merely a sister species to them. This is part of the reason cladograms are constructed the way they are, so that no fossil is ever put on the direct line.
Source.
Source 2
Note: Tiktaalik probably did not live on land, more likely it was a shallow water air breather.
Also whatever species was the ancestor of tetrapods, all living tetrapods would be its descendants. One aspect of population genetics is for a specific individual in an ancestral population, past a certain point in a linage  either every descendant is your descendant or you have no descendants.


What happens in your brain when you receive information which causes you to bristle? I'm talking about moments when you watch a film and you bristle, or when you listen to music, etc.

What kind of neurotransmitter flow changes?

One thing is that we can't control the Goosebumps. It is an involuntary function caused by the Sympathetic Nervous System which is the major part of the Automatic Nervous System. The major function of the SNS is fight to flight response along with maintaining homeostasis in which case it internally will be alert maintaining body status from the background.

Before sending any response to target tissue when there is input to SNS it has to secrete neurotransmitters but before this to the sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it.

So whenever SNS senses (message flow is bidirectional) any stress it responds it in following action mentioned:

  At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus postganglionic neurons - with two important exceptions - release norepinephrine, which activates adrenergic receptors on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system.

Once the receptors receive the information then the response flows to the target tissue via neurons with the help of the neurotransmitters. To explain goosebumps technically:

  Properly known as piloerection, horripliation or pilomotor reflex, the bumps we get are stimulated by fear and cold and they are essentially just a temporary change in the skin. These stimulants cause a nerve discharge from the sympathetic nervous system (which is an involuntary portion of nerves we have) and the nerve discharges create muscle contractions called arrrectores pilorum that raise the hair follicles in our skin. It is the elevation of the hair that causes the Goosebumps.  The name Goosebumps actually comes from the fact that plucked goose feathers resemble the human hair follicles.

Goosebumps also occur when we listen to surprise songs, sad songs or some other kind of thrilling music. Researchers have tried to explain it and they call it "Frisson".
Check out this small video which talks about it. It is nice:

http://www.youtube.com/watch?v=-EA2eWZuYDs

Also refer to this website: Goosebumps


Is there an acceptable term for 'male fox' other than 'dog'? I'm writing a lab on sexual dimorphism in Arctic foxes. As such, I use the words 'dog' and 'vixen' fairly often. In the discussion section, I compare the results from the lab with the results from research on other animals. The most relevant research I consider pertains to dimorphism among dogs (Canis lupus: the kind we keep as pets and their immediate relatives).

The term 'dog' denotes a subspecies of Canis lupus, males of that subspecies, and male foxes.

There are ways to disambiguate what I'm writing, but none of them are elegant.

I'm considering using 'tod' or 'reynard' instead. Are either preferred in biological writing? If not, is there an alternative?

In the scientific arena, stick to male and female.

The word reynard can apparently describe a male fox or foxes in general (either gender).

It is presumably derived from the French word for fox, renard.

I don't know French, but a little research suggests that la renarde describes a female fox (vixen), while le renard can refer to a male fox, or it can describe foxes in general.

I did a little work with foxes in Alaska years ago and never heard them described with any terms other than fox, male and female.


How many SARS-CoV-2 viruses in circulation at the moment? Mass? How many SARS-CoV-2 viruses are in circulation at the moment? And what is their total mass?

To clarify: if there are 10 000 viruses on average in an infected human and 100 000 humans are infected the answer would be (if all viruses are in humans, which probably isn't true) 10^4 x 10^5 = 10^9 viruses.

Of course I am only looking for a rough estimate, a number that, when multiplied with 10 or 0,1 (so two magnitudes) or so, is correct.

Based on all species of viruses, Everyday you breathe in 100 million viruses. There can be 1mn+ viruses per ml of blood of patients. Covid-19 diameter = 125 nm.

Perhaps it's wrong, the maths would go something like this:

1mn * 1000ml * 5liters * 400k patients = 2^12 - 2^13 sars2 viruses.

total volume of viruses =  2^13 viruses / 1^15 viruses per cm3 = 0.02 cm3

(10^7 nanometers per centimeter, 125nm diameter, gives, about 10^(5*3) viruses per cm3.)

Weight of all the Covid Sars 2 in the human population = a raindrop or a teaspoon of hydrocarbons/mayonnaise, probably less than a teacup.

Perhaps i am wrong, it's reasonable to think that the people with major symptoms contain about 1 ml of virus. 20k x 1ml = 20cm3


what is the exact definition of entdothelial cell fenestrae? In fact, I want to know that are fenestrae 1.holes which exist between cells or 2.they are holes in a cell( for example, a cell is like a paper we have punched it and the holes are called fenestrae). which one is true?

Fenestrae are basically holes within the cytoplasm of the squamous cell, that allow the transmission of macromolecules, therefore, according to the two options you've provided, your second example is the correct one.


Chromosomes are of different size but why do all chromosomes have similar GC percentage? When I browsed NCBI I saw a pattern: even if the chromosome sizes, number of genes, and number of proteins are different, GC% in chromosomes tend to be similar. The examples are linked below.

Yeast,
Plasmodium falciparum

If you see Mitochondria genome it is not very similar to chromosome. Why all chromosomes tend adjust their GC% near to the average of total GC%
Is there a specific reason related to metaphase of meosis?

to further clarify I have some images to help

The chromosome size or genes in an organism are not adjusting near the average of their total but GC% does. It has only 3-2% (falciparum) or 3-4% (vivax) variation in GC%. It feel like its balancing like equalizer. Why?

As @dd3 points out, average GC% indicates a need for stability and coding regions or structural regions of the genome may need to be more stable.  But the largest %GC in genomes are found in thermophiles - organisms which live in high temperature water - in hotsprings and undersea geothermal vents. This review mentions how some thermophiles can be found with 50% GC.  The extreme thermophile Thermus thermophilus can have a GC% content of 69.4%.

But you are asking how does GC content get averaged out over the length of a large genome.  The answer is variation and selection.  When a gene needs to be more stable because of genomic function or because its trying to live in a hotter environment mutations that convert A/T to G/C base pairs will convey an incremental advantage to survival and will tend to be retained in the gene pool as long as no greater disadvantage to the mutation results.  Over time and as the stability creates a greater advantage, GC % will migrate further and further away from the mean.

This works for both thermo-tolerance and because of the biofunctional constraints of being a telomere, centromere or a coding region - stability and coding constraints play against each other to converge on an optimal GC content in any given stretch of the genome.

Conversely most genomes have a GC content below 50% are migrating there because too much stability can have a cost as well.  Breaking up the DNA helix for transcription and other cellular processes must go smoothly as well for example.

Coding regions are significant for bacteria (E coli is 89% coding sequence).  For coding sequences, the genetic code is logically 50% GC on the average, but if you look at the actual codons in the diagram below you will see that except in the case of a single codon case (tryptophan, methionine) the third base always has a GC option, allowing for a GC content in the mid 60 percentiles.  The constraint of allowing coding sequences to freely vary is only an approximation - in some cases substitutions to amino acids with GC rich codons might move the cieling up a bit. And the more frequent amino acids have the possibility of making 2 or 3 bases of their codon GC bases.  Overall it would be remarkable to find a bacteria with GC% greater than 72%.  Mutations and the requirements of proteins being coded for would simply not allow it.

So: over evolutionary periods these GC mutations accumulate where they are helpful, even to the extent of 2/3 of the genome being GC pairs.  The strongest selective force to accumulate a high average GC% for a genome is exposure of the genome itself to a high temperature environment.

Note that this thermo-stability argument doesn't count for many animals because they do regulate their body temperatures.


Do lizards expand in the summer and contract in the winter? We all know that objects expand on heating and contract on cooling.

Lizards are cold-blooded animals, i.e. they become hotter and cooler depending on their outside temperature. Warm blooded animals like us however maintain a constant body temperature.

This must mean that lizards are cooler in the winters and hotter in the summers, which should mean that they expand in the summers and contract in the winters, although by a very unnoticeable amount.

Does this really happen? How does the lizard or other cold blooded animals accommodate this expansion and contraction?

I think you might be over-extrapolating your knowledge a bit. Animals are mostly made of water, and water only changes density by about 1% between 0C and 37C, so you are overestimating the effects of expansion/contraction due to temperature (and most organisms don't experience such a wide range of core temperatures, outside of special circumstances).

Because water is such an important component of organisms, size would also change with variation in hydration levels (you can easily observe this in plants because many plants use water pressure to support themselves). I would expect this variation to be as great or greater than any expansion/contraction with temperature.

Also note that just because animals are cold-blooded doesn't mean they don't regulate their temperature. Cold-blooded animals move between sun and shade, water and land, etc to regulate their temperature externally.


What kind of ribes is this? I have a plant in my USDA zone 5 garden that appears to be in the ribes genus.

Details:

The location is east of Toronto (Ontario, Canada).
The plant is currently flowering (today is May 18th, 2019).
It is approx 4 feet tall.
The plant flowers every year, but does not set fruit (not self-fruitful).

More photos here:

https://i.stack.imgur.com/coEp5.jpg
https://i.stack.imgur.com/wv0TA.jpg
https://i.stack.imgur.com/pFmtk.jpg
https://i.stack.imgur.com/KvjGe.jpg

What species is it?

I think this is Ribes americanum or wild black currant.
I'm basing this on page 306 of Newcomb's Wildflower Guide, an excellent source for the Eastern US and some of Canada.  On that page we have two main choices:

Base of flowers prickly or bristly... or

Base of flowers not prickly or bristly...

Your excellent pictures suggest that your specimen is in category 2.
From there, we have:

a. Flowers solitary or 2-3 in a cluster; branches bearing a few thorns. or
b. Flowers 5 or more in racemes.

Your specimen looks to have quite a few flowers, so in category 2b we have a choice of Ribes americanum:

Whitish or yellowish flowers, longer than wide (and fruit black, you can check later I guess),

or Ribes sativum:

Greenish flowers, wider than long (and fruit red).

Color in the white/green/yellow range is a bit subjective, but your flowers look longer than wide, hence Ribes americanum.
Of course, with this in mind you might re-inspect the plant and refine this a bit.


Effect of respiration on Arterial pressure I am trying to explain the effect of respiration on arterial pressure.
I am looking preferably some visual way to show it.

How can you show the effect of respiration on arterial pressure?

I am thinking some kind of figure which has the respiration rate and arterial pressure.

Alan's pointing picture is this

I found this picture better

but not sure if it is exactly the level respiration to the arterial pressure.


Why is duck fat less saturated than cow fat? Why does the composition of fat in animals vary?  Is there an evolutionary advantage to producing fat that is less or more saturated?

Because ducks need to float and cows don't. If there was a densely fat duck it wouldn't float or fly very well and it wouldn't survive to reproduce.

To answer your question, the composition of fat varies because of the different conditions in which the organism needs to thrive. Fur is different as well. Bear in mind nature is a cruel place and any tiny edge you can get is vital for your survival.

My answer is a bit general but I hope it addresses the question.


How can eating bacon not make me fat? This page says it won't.

This page says it's the carb again http://www.mindbodygreen.com/0-10454/in-defense-of-bacon-why-eating-fat-can-help-you-get-thin.html

I don't see how eating fat will not make me gain weight while eating carbohydrates will, since fat is made of, well, fat.

It says eating carbs will make us fat. How can this be? Is this true?

I think this question can also be said to be - how can the Atkins diet work?

Atkins and other low carbohydrate diets sound counterintuitive.  They vary in details, but the basic theme is: cut back on carbohydrates - e.g. bread, sugar, fruit, pasta, milk etc etc.  But eat as much fat and protein as you like - e.g. steak, ham, bacon, eggs, cheese etc etc.

These diets really do work.  Our metabolism allows us to draw food from two sources.  Glucose or fat. (there is also something called glycogen, but that is only used short term and not relevant for diets long term).

It was known in the late 50s that our metabolism will to switch over consuming fat, allowing weight loss, only based on the amount of carbohydrates we consume. low carb diets initiate this change from glucose to fat metabolism because our bodies make the switch based only on the amount of glucose available in the blood.  Our bodies think we are starving even if we are gorging ourselves on food which is has little or no glycemic index.

Low carb diets are not a hoax or snake oil - they really work.  They can be a shock to the system and so one should discuss with your doctor before engaging them.

The first link you have is also true though.  Eating fat will usually just make you gain weight.  The low carb response has to be induced by basically removing all carbohydrates from the diet.  If you break the low carb regime and eat a large amount of carbs, the body will switch practically instantly out of starvation mode and also take in all the fats you're eating.  Lots of people on low carb diets can gain a lot of weight rapidly if they break the diet.


Are there any substance that are more dangerous at low dose than at higher dose? It is commonly admitted that

  The dose makes the poison

which means as a person, the more I take a substance, the more risk I take for my health.

There is even an indicator called LD50 (see Median Lethal Dose), which specifies the 'lethal dose' at which 50 percent of subjects will die.

This might seems a stupid question but: are there any substances for which it is more dangerous to take at low dose than at higher dose? For example, you have to ingest at least 1µg of XXX because if you ingest less you will have health problem...

Yes. Taking antibiotics (and by extension antivirals and antineoplastics) at low doses is dangerous, as this creates an evolutionary pressure to evolve antibiotic resistance (or rather, incorporate through horizontal gene transfer). This is dangerous because an infection resulting from these bacteria will then be harder to treat.

In the paper "Experimental evolution of resistance to an antimicrobial peptide", Perron et al. gave E. coli the chance to evolve resistance against a novel antibiotic. When given a high dose initially, most bacteria died. When exposed to low doses, the bacteria evolved resistance in 600 to 700 generations.

For the same reason it is strongly advised to finish a course of antibiotics even after symptoms fade.


Two mice heterozygote and black are reproduced. Find the probability of getting the filium dark and heterozygote Well, here's what I did: P: Aa*Aa

F1: 1/4 AA, 1/2 Aa, 1/4 aa, SO the answer is 1/2, but out teacher did this:
AA(1)    Aa(2)    aa(1) and she said we divide the number of filium for the phenotypes number and get 2/3. This is the probability. I don't get it.

Okay so in your teachers answer there are four offsprings. . You used all offsprings when you made the division so 2/4 = 1/2.Your teachers 2/3 comes from the fact that 3 out of four is black, but only 2 out of that 3 black is heterozygote so 2/3 is good by this logic. I think that your teacher's logic faulty because you have to take into consideration all the offsprings. Basic genetics and Mendel's law tells us that crossing two heterozygotes with independent alleles result in a 3:1 ratio in phenotype separation in the next generation with 1:2:1 genotype separation -- that is what basically both of you have wrote. The fault is in the getting the probability - basic maths tells us that in an independent experiment, the probability variables have to sum up to one. In your teacher's logic this basic rule is not kept, because finding homozygous non-dark offspring would be one (there is only one non-dark filium and that one is homozygous). So by this logic all filium are non dark-homozygous, but then what about the others. I hope you see the problem with that logic.


Current along an axon When an action potential is induced on a neuron, the local transmembrane potential jumps from $E_{\mbox{rest}}$, the resting potential of the neuron, to $E_{\mbox{eq}}$, the equilibrium potential of an ion or group of ions in the vicinty. Current thus travels in and out of a part of the neuron's cell membrane as ions are exchanged during an action potential. This effect repeats itself as the neighboring regions of the membrane are depolarized, causing the action potential to propagate along the neuron's axon.

Take $\Delta Q$ to be the total charge exchanged locally during an action potential, $C$ to be the membrane capacitance, and $\Delta t$ to be the duration of the action potential. While we can approximate the local average current through an neuron's membrane by taking $$I = \frac{\Delta Q}{\Delta t} = C\frac{\Delta V}{\Delta t} = C\frac{E_{\mbox{eq}} - E_{\mbox{rest}}}{\Delta t}$$ Is there a way to approximate current traveling along the axon of the neuron? Is there even such a thing?

As far as I was able to find there exists two models of the action potential by using RC circuits. Do note that there is no flow of electrons per se across a tube, but rather a migration of potential. See this.

The Hodgkins Huxley model :

  The Hodgkin–Huxley model, or conductance-based model, is a mathematical model that describes how action potentials in neurons are initiated and propagated. It is a set of nonlinear differential equations that approximates the electrical characteristics of excitable cells such as neurons and cardiac myocytes, and hence it is a continuous time model

http://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model

The Fitzhugh-Nagumo model:

  The FitzHugh–Nagumo model is a simplified version of the Hodgkin–Huxley model which models in a detailed manner activation and deactivation dynamics of a spiking neuron. In the original papers of FitzHugh, this model was called Bonhoeffer–van der Pol oscillator...

http://en.wikipedia.org/wiki/FitzHugh%E2%80%93Nagumo_model

http://en.wikipedia.org/wiki/Quantitative_models_of_the_action_potential

Hodgkin, Allan L., and Andrew F. Huxley. "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo." The Journal of physiology 116.4 (1952): 449-472.

Now, I have not dealt with differential equations in quite a while, and hence may not be the best source for explaining the model itself, but I'll try and update the post with what (if anything) I understand.


Do women tend to have longer legs and shorter torsos than men? I've always heard that women tend to have a greater leg length to torso length ration than men, and I think that my anecdotal observations of pedestrians of both sexes tend to confirm that.

However, now I read that is not the case:

  If they are the same height, she’s a lot “leggier” than he is. It looks as though women really do have long legs and short upper bodies for their height. (We’ll see later this isn’t the case.)

  (...)

  This observation is purely anecdotal, though. There are studies which measure the lengths of men’s and women’s legs, arms, upper bodies, and so on. These measurements show that women have shorter legs and longer torsos than men as a proportion of their heights.

So, at least, says a bicycle designer. And I suppose bicycle designers should know anatomy.

I have a cognitive dissonance here, since again, my eyes watching pedestrians tell me otherwise.

So - what is the truth?

We seem to have a preference for proportionally longer legs (see comment here for a good summary around that study).  So when you are observing "pedestrians" they have probably tended to dress and comport themselves to skew your perception of their leg lengths.  Perhaps in your cultural environment females have a greater capacity and/or motivation to alter that perception than do men.

The reality is that adult female legs are on average proportionally shorter than those of men.  See, for example, this detailed 1977 U.S. Army study comparing body proportions in adults by gender.

For readability I would highly recommend this much broader survey of the subject, which contains not only clear illustrations of how proportions are measured but also an extensive survey of cross-cultural and historical variations: Leg Length, Body Proportion, and Health: A Review with a Note on Beauty.


Does the biosphere have infinite resources and are they infinitely renewable? Does biomass represent all of the resources of the biosphere and therefore it would be theoretically infinitely renewable (as long as we have the sun) since all the biomass is part of the carbon cycle?

Also, should I consider resources like gold to be part of the biosphere and therefore all the resources would not be infinite nor infinitely renewable?

No, it is not infinite.

The sun has not an infinite mass neither does the earth. So energy is not infinite. But we probably don't really care about that as it applies at a scale we're not really concerned with. What is important at our scale is the rate at which is the rate at which the biomass we're destroying (eating, building houses with) is produced. The rate at which we consume this biomass has to not overpass the rate at which this biomass is produced. Than, practically speaking, biomass will be produced infinitely. Of course, ecosystem stability is not that easy but it is not within the scope of the post to talk about that.


Does X-inactivation lead to expression of sex-linked recessive disorders in half of carrier females' cells? If one of the two X chromosomes in female mammals is randomly inactivated (i.e. becomes a Barr body) in each cell, shouldn't half of all cells in a female who is a carrier for an X-linked recessive disorder (say, Duchenne muscular dystrophy) express the disorder?

Yes and No... You are correct that X-Chromosome Inactivation will randomly inactivate the good X-chromosome (i.e. the one NOT carrying the mutation/disease) half of the time. However, this doesn't always seem to be associated with a disease phenotype. It likely depends on the gene and other factors, like the gene allele's function, to determine whether there is a disease phenotype that manifests with inactivation. Check out this paper that looked at Duchenne muscular dystrophy in females that is available freely on PubMed.


Coronary circulation It is said that the coronary artery that gives the posterior descending artery(PDA) determines if the heart is right dominant(most cases) or left dominant. Is there any reason to this? Why PDA?

This is purely an anatomical definition: right dominant is defined as coronary circulation where the PDA (posterior descending artery) is a branch of the RCA (right coronary artery) and left dominant is defined as coronary circulation where the PDA is a branch of the LCX (left circumflex artery). The Wikipedia article on coronary circulation is a reasonable reference for this question.

There's nothing else special about the statement "dominant" and it doesn't have any other importance for cardiac function, except that someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX.

Typical human coronary artery anatomy consists of two ostia off the aorta, right and left. The "left main" branches fairly early on into the LAD (left anterior descending) artery, which follows the septum between left and right ventricles down the anterior side, and the LCX, which follows the 'top' of the left ventricle counter-clockwise (if looking down at the top of heart and rotating the heart so the atria are on top; in an actual human heart the atria actually point towards the midline a bit more than other species). The RCA travels in roughly mirror fashion, following the 'top' of the right ventricle in clockwise fashion. The RCA and LCX nearly meet on the other side of the heart, at the posterior septum.

In a majority of people, the RCA continues and follows the septum down to the apex (kind of like the LAD but on the opposite side). In a non-negligible minority, the supply of the posterior descending artery is either shared by RCA and LCX or is completely supplied by the LCX.


What species is this blue and white bird? I want to know what kind of species this bird is

The bird in the photo appears to be a white faced "variety" of Lovebird - Genus Agapornis - mainly identified by beak and nares not being visible (cere skin and nostrils not visible). The exact species is uncertain due to ease of hybridization between species and the availability of many color varieties.  The links below may be of further help.

https://en.wikipedia.org/wiki/Lovebird#Species

https://www.agapornidenclub.be/eng/?page_id=2


Books about famous experiments in biology - 'methods of investigation' I'll explain briefly what I need (hoping to find something) :

I wanted to know if someone knew about a book that in a way or another talked about the greatest experiments in biology (Griffith, Avery-MacLeod-MacCarty, Hershey-Chase) or methods normally used to study  certain phenomena  for example, and explaining or talking about the paradigm used in biology research in such cases.

I know it might sound too vague, but I will have a kind of 'exam' essay, in which in addition to the biologic phenomena asked in terms of "notions" one will also have to suggest a 'method of investigation' to study it.

And my main problem is that in school just the theory is normally taught and not the practical approach to such topics, so I really lack knowledge in this.

So what I'm asking is whether there is a certain book or even a suggested approach that I might start using that might help me in learning what I explained above.

Thank you for your help!

Although it's not stricly about biology, A short history of nearly everything by Bill Bryson, especially chapter 5, is a good start to look for historical experiments.


How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV? How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV? Now I don't mean how long it takes for euphoria to come on but analgesia.

The opioids I would like to know this information to include:

Buprenorphine
Butorphanol
Fentanyl
Hydromorphone
Methadone
Morphine
Oxycodone
Pentazocine
Pethidine (meperidine)
Sufentanil
Tramadol

These are 'peak' values when administered via IV, with the exception of oxycodone. There will be some variation person to person depending on their opioid tolerance and any concomitantly administered medications.

Buprenorphine: 60m

Butorphanol: 5m

Fentanyl: 5m

Hydromorphone: 30-90m

Methadone: 1-2h

Morphine: 20m

Oxycodone: Not administered intravenously

Pentazocine: 15m

Sufentanil: 3m

Tramadol: 2h


If a person has a specific mutation in a gene, is it more likely he has other mutations in that gene? If a person has a specific mutation in a gene (2281 del/ins in a single copy of the Bloom BLM gene), is he more likely than the general population to have other types of mutations in the same gene?

A priori, no! Why would it? Do you have any specific hypothesis in mind you would like to discuss?

Below are some expectations from a simple model and possible reasons for why this expectation may break down under more complicated models.

Simple model

Under a simple model (panmictic population and a few other simple assumptions), the number of mutations a given individual has in any sequence considered follows a poisson distribution. Assuming that all mutations occuring have a constance selection coefficient $s$, a constant dominance coefficient $h$ and that the mutation rate for the sequence of interest is $U$, then the number of mutations an individual carry comes from a Poisson distribution with mean $\frac{U}{2hs}$ (Crow 1970).

This model is simple but is probably a pretty good approximation to reality. Below are three assumptions that are not necessarily true and that would yield to a higher variance in the number of mutations (that is a higher probability for an individual that already carry a mutation to get a second mutation).

Population structure

In reality, populations are often not panmictic. As the genetic load depends upon the population size. More specifically, the smaller the population, the higher the genetic load (or the higher the number of mutants alleles present in the population) (Kimura et al. 1963).

Past evolutionary and demographic history

Populations are not stable through time. Some population have recently gone through a bottleneck, others a quickly expanding, some are shrinking, some have recently suffered from a plague, etc... Such processes can all cause populations to differ in the number of mutations they carry and therefore would increase the variance in the distribution of number of mutations individuals carry.

Within a specific short enough sequence, physical linkage associated with specific past evolutionary process will create a relatively long lasting linkage disequilibrium.

Condition-dependent mutation rate

It has been shown in Drosophila melanogaster that individuals with poor genotype tend to have a higher mutation rate causing their lineage to accumulate even more mutations (Sharp and Agrawal 2012).


How can I compare the STRIDE and DSSP output files of a particular pdb file? I have the pdb file of H-ras protein 5P21.pdb. I am supposed to compare the output of DSSP and STRIDE files after feeding this pdb file to respective servers. My question is how to make a quick comparison between these two results?

Here a solution that does not require you to upload the files to the servers: You can graphically visualize DSSP and Stride at the Sequence Page at RCSB PDB:

http://www.rcsb.org/pdb/explore/remediatedSequence.do?structureId=5P21&bionumber=1

"add annotation" -> Stride and look at the graphical comparison between DSSP and Stride.


How much does sprayed water remove bacteria? I was quite skeptical about some company claiming that their device was able to suppress 99.99 % of bacteria.  Then I read a report testing the germicidal effect of their device, from a large and independant testing laboratory.

The device was tested against a number of bacteria, including Salmonella, Escherichia coli, Staphylococcus aureus, or Listeria.

They incubated contaminated Petri dishes, then used the device, then incubated the Petri dishes again.  It appears that the test samples had a CFU level log-reduced by 4 to 6 (i.e. the number of bacteria is reduced by a factor of 10,000 to 1,000,000) in most cases when compared to control samples, which supports the claim.

However the device implies spraying water, to which the control samples have not been subjected.  I am curious about how much this simple spraying may affect the results.

Would rinsing the dishes with sprayed water significantly reduce the amount of bacteria ?

Though conditions are not exactly the same (the water is not sprayed, the duration of water exposition is different, and samples are not Petri dishes ; I am not competent enough in biology to compare methodologies), I found two relevant papers.

Listeria innocua/monocytogenes, pure rinsing

The first paper used Listeria innocua "as a surrogate for L. monocytogenes", while the EMSL report linked in the question tested the latter.

They found the following bacterial log-reduction after rinsing for 15 s under running cold tap water at room temperature and without prior soaking :

on brocoli and lettuce : 1.41 (96.11 %) ;
on apples : 2.01 (99.02 %) ;
on tomatoes : 2.10 (99.21 %).

To be compared to the report from the EMSL which found, after spraying modified water for 10 s on an inoculated Petri dish (which surface is obviously smoother than that of a tomato) :

at 20 °C : 4.24 (99.994 %) ;
at 25 °C : 3.01 (99.903 %) ;
at 30 °C : 3.37 (99.957 %).

Note that although not mentioned, uncertainties on the EMSL numbers must be fairly large since the quantitative counts are below the detection level of the apparatus (but would actually make the numbers conservative…).

Link to the paper : Efficacy of Home Washing Methods in Controlling Surface
Microbial Contamination on Fresh Produce (open access PDF), Agnes Kilonzo-Nthenge, Fur-Chi Chen, Sandria Godwin, Journal of Food Protection, 69, 2, 2006.

(NB : it contains further testing which are out of scope for this question but may be of interest, e.g. soaking, rubbing or wiping with paper towel.)

Escherichia coli O157:H7, rinsing while thoroughly rubbing

The second paper tested Escherichia coli 0157:H7, which has also been tested by the EMSL.

The paper reports the following log-reduction after thoroughly rubbing during 15 s under running tap water (no indication of temperature, but flow of 2.0 L/min ; the values in the abstract seem wrong for tomatoes, here are the in-paper values) :

lettuce leaves (not rubbed ?) : 1.16 (93.08 %) ;
cabbage leaves (not rubbed ?) : 2.02 (99.05 %) ;
lemons : 4.10 (99.99 %) ;
tomatoes : 5.78 (99.9998 %).

Note that the same reduction is reached for tomatoes after only 8 s of washing.

To be compared to the EMSL results (sprayed "modified" water, 10 s rinsing, no rubbing, Petri dish) :

at 20 °C : 5.67 (99.9998 %) ;
at 25 °C : 5.14 (99.9993 %) ;
at 30 °C : 4.88 (99.998 %).

(Same comment about uncertainties applies.)

Interestingly, in this study they also tested the effects of alkaline electrolyzed water, which may not be too far from "ionized water" (I have yet to dig into details), which itself may not be too far from what is supposed to exit the device tested by the EMSL.  And… they found no significant difference with regard to plain tap water.  (Though they did find significant effects with acidic electrolyzed water and by applying both successively — but that's out of the scope of this question.)

Link to the paper : Reduction of Escherichia coli O157:H7 on Produce by Use of Electrolyzed Water under Simulated Food Service Operation Conditions (open access PDF), Pangloli et al, Journal of Food Protection, 72, 9, 2009.


What is the difference between rheobase and threshold? Neuronal tissues can be excited by electrical stimulation. Two commonly encountered characteristics for electrically stimulating nerve cells is the threshold and the rheobase. My question is what the difference is between rheobase and threshold? In the definitions I've read it's described as almost the same thing. The threshold, or minimal stimulus, is defined as "the electrical stimulus whose strength (or voltage) is sufficient to excite the tissue. Rheobase is defined as "the minimum strength (voltage) of stimulus which  can  excite  the  tissue". What is the difference?

Excellent question! The difference is the fact that the rheobase is an example of a threshold measure. The threshold, as you correctly suggest, is the minimal energy (typically current level and not voltage as you suggest) to excite neural tissue. The threshold applies only under the specific experimental parameter settings used. These parameters include the type of electric stimulus (for example, a biphasic current pulse), the electrode configuration (for example, bipolar stimulation) and the stimulus duration (for example 200 microseconds).

The rheobase is the minimal current level needed to excite a tissue when an infinitely long stimulus would be applied. The rheobase is typically found by plotting the threshold level (as defined above) as a function of stimulus duration. The reason for developing this measure is the fact that excitable membranes integrate the injected current, so charge builds up in the tissue. In other words, increasing the pulse duration decreases the threshold current level needed. Hence, the rheobase is a convenient threshold measure because it incorporates the duration parameter of the stimulus. It will still depend on things like electrode configuration and stimulus shape.

The function of the strength-duration relationship can be fitted with a decaying exponential:

I = Ith / ( 1-e(-t/Tsd) )

where I= Threshold current level;
Irh = rheobase
t = stimulus duration
Tsd = Tau = exponential

Here is a picture of a theoretical strength-duration curve copied from the wiki page on rheobase. [NB: I find the wiki page needlessly complicated].

The rheobase is the horizontal asymptote. An often used parameter to characterize the function is chronaxie, which is the pulse duration equivalent to two times the rheobase.

The explanation given here was adapted from the book "Cochlear Implants", chapter 5 "Biophysics and Physiology" by Abbas and Miller, two veterans in cochlear implant electrophysiology. Unfortunately I cannot give you a link to the pdf as I own the work in hard copy.


Up to date, extensive documentary about dinosaurs? I just finished reading the Wikipedia page about dinosaurs, and I very much enjoyed it. I knew that much of what I learned in the 80's as a child is (and was) incorrect, and now that I am a parent, I am excited to finally make some time to learn about this stuff.

It seems that a lot is known about ecosystems, socialization, and interactions between different species, herd behavior, and other interesting things.

Before I start reading books, I want to watch a good documentary.  A quick google search turned up some suggested documentaries, but in general they seem to be either old or focused on a particular dinosaur, and not on the era in particular.  All are short.

I watched the 10 hour documentary "The Life of Mammals" by David Attenborough a few years ago, and developed a much better understanding of how we as humans evolved, and how we are related to other mammals. I'd love it if there was something as extensive about Triassic/Jurassic/Cretaceous era dinosaurs. Is there something recent, extensive, and mostly correct?

Try Planet Dinosaur (2011) or Dinosaur Revolution (2011). Neither is as good as the original Walking with Dinosaurs trilogy, but both are relatively informative and entertaining at the same time.


Why Insect bites are itchy rather than pain? i don't understand if some thing bites or hurt we feel pain, but its differ for insect bites, why so?

You're more likely to have an allergic reaction if you're stung by an insect. The reaction can be classed as:

  Minor localised reaction – this is normal and doesn't require allergy testing, although the affected area will often be painful for
  a few days

  large localised reaction (LLR) – this can cause other symptoms, such as swelling, itching and a rash

  systemic reaction (SR) – this often requires immediate medical attention because it can cause a potentially life-threatening allergic
  reaction (anaphylaxis)

Taken from : http://www.nhs.uk/Conditions/Bites-insect/Pages/Symptoms.aspx

You can read up on this here:

http://en.wikipedia.org/wiki/Inflammation

http://primer.crohn.ie/the-inflammatory-response

For a more detailed look, I would suggest papers like this:

Loza, Matthew J., et al. "Assembly of inflammation-related genes for pathway-focused genetic analysis." PLoS One 2.10 (2007): e1035.

or a good immunology textbook.


Why do COVID19 serology tests focus on the nucleocapsid while vaccine efforts focus on the spike? When I look at the specification sheets for many of today's serology tests like the new Roche test or the Abbott test, they use a nucleocapsid antigen in the test, looking for anti-nucleocapsid antibodies. Given that these tests seem to have high sensitivities toward past infection, it suggests that recovered patients seem to reliably generate an immune response to the nucleocapsid.

At the same time, a lot of the research into vaccines focuses on the spike protein: Moderna is developing a vaccine based on an mRNA coding for the spike protein, CanSino and Oxford combine an adenovirus carrier with a SARS-CoV-2 spike, and so on. I'm having trouble finding any vaccines that target the nucleocapsid peptide.

I'm having trouble understanding this difference. Is it the case that recovered patients reliably produce antibodies to both viral components, but the nucleocapsid is better for testing due to cross-reactivity or other concerns? Or does a natural immune response target the nucleocapsid, while scientists think that the spike is a much better target because it's directly expressed on the cell surface or for some other reason?

The vaccines will be directed towards a protein/epitope of the virus that creates the most robust immunogenic response, in which the defense system will create an array of antibodies to confer immunity, those antibodies will have to NEUTRALIZE the virus upon entry.
In the case of SARS-CoV-2, the majority of research shows that neutralizing antibodies are directed towards the S1, S2 and RBD proteins which are all part of the S protein.

In this same line, the fact that the body creates antibodies directed towards other components of the virus doesn't mean that they are protective. So creating a vaccine towards those components wouldn't be useful at all.

The reason why those serologic tests target the N protein is probably due to the fact that is highly antigenic. But I'm sure I've seen tests that also target the S protein.


How can I improve efficiency of Ecoli transformation? I am an intern in biology institute. I have a 17.3kbp plasmid need to transform to Ecoli. But I have tried many time but have no or very few colony on LB plate.

I know large plasmid have less frequency in transformation, How can I improve chance of successful transformation?

Thanks everyone.

The plasmid is quite big which might explain why it is difficult to transform bacteria (is it a lentiviral vector?).
If you could give additional details you might have a chance to have improved answers to your question.

Hello, I suggest you follow this protocol:

At step 7 instead of this "Add 250-1,000 μl LB or SOC media (without antibiotic) to the bacteria and grow in 37°C shaking incubator for 45 min. "

Do this " Add 250 μl LB or SOC media (without antibiotic) to the bacteria and grow in 30°C shaking incubator for 2 hours. Do not shake too hard, gentle motion might be fine (500 rpm).

At step 9 instead of this "Incubate plates at 37°C overnight."

Try to incubate at 30°C. I would even suggest to try to grow them at lower (25°C, or 16°C) temperature if you can prepare a second plate.
It will take much longer than overnight to grow the cultures, probably more 48 hours (might be 72 hours at 16°C).

Hope that helps good luck!


Why aren't nucleic acids on Nutrition labels? All the other macromolecules are listed on the Nutrition labels and nucleic acids do have some caloric value, why aren't they on the nutrition facts?

This FAO report can tell you all about food analysis and why things are and aren't on the label: http://www.fao.org/docrep/006/y5022e/y5022e03.htm#TopOfPage

  First, not all nitrogen in foods is found in proteins: it is also contained in variable quantities of other compounds, such as free amino acids, nucleotides, creatine and choline, where it is referred to as non-protein nitrogen (NPN). Only a small part of NPN is available for the synthesis of (non-essential) amino acids.

The DNA in food would contribute to the nitrogen content. Then (using a food-specific "Jones" factor) total nitrogen content is converted to protein content. So in a way it's already there.

Listing DNA separately would require extra testing, and also the difference in daily use would be negligible. There's not that much DNA in food anyway and, like protein, DNA can be converted into new protein and energy. The Jones factor already accounts for this.


Definition of Dye- Reduction Test? Can some one give a simple explanation or definition on what a dye-reduction test is.

Dye reduction tests (and there seem to be loads of different ones) are simply assays in which a dye becomes decolourised to give you a visual indication of whether a certain process is occuring. Here you can find an example of a dye reduction test with Methylene Blue and Reazurin which indirectly measures the bacterial densities in milk and cream. See this google book for more info.


Difference between 'Orbit' and 'Globe' in eye anatomy? What's the difference between 'Orbit' and 'Globe' in eye's anatomy. Do they refer to the same ? I encountered this in this text:

  ... ciliary ganglion, which is approximately 3 mm in size, and located
  2-3 mm posterior to the globe and lateral to the optic nerve,...

I've found a rough answer myself:

  The globe of the eye, or bulbus oculi, is the eyeball apart from its
  appendages

http://en.wikipedia.org/wiki/Globe_%28human_eye%29

  ... the orbit is the cavity or socket of the skull in which the eye and
  its appendages are situated. "Orbit" can refer to the bony socket, or it can also be used to imply the contents.

http://en.wikipedia.org/wiki/Orbit_%28anatomy%29


Help ID this South Indian fruit-bearing tree So there's this fruit-bearing tree near my house in Kerala, South India. A senior neighbor of mine tells me that this fruit is edible. I tried it out, and it tastes alright. I want to ID this plant, know its botanical name, as well as whether it has any medical/commercial/culinary application.

The fruit is green when tender and red when ripe.

This looks like Muntingia calabura, the Jamaica Cherry.

pic source

pic source
It is indigenous to tropical America and often planted in Asia.
It is edible and used in jam, cake and fruit drinks. The bark is sometimes used as rope. Source: "Tropische vruchten, Nowak&Schulz 1999"


What are minerals (other than zinc) that the human body cannot store It is known that zinc is an essential mineral that the body cannot store.

What are other minerals, especially metals, that the body cannot store?

(other than water-soluble vitamins such as vitamin B and C)

Sincere thanks.

Essential "minerals", i.e., metal cations are magnesium, zinc, iron, potassium, sodium, manganese, molybdenum, selenium, cobalt, copper and even calcium, as we lose a tiny amount of it through urine and sweat. They are all "stored" in some way, but only temporally, so some amount has to be taken up daily. It would show only weeks later, however, if you have a deficiency.

Wikipedia adds phosphorus and iodine but they are not metals.


What are the effects on hearing of in ear headphones? I have been told many times by my teachers and grandparents that using in ear headphones will ruin my hearing, but I was unsure of these claims. So of course I turned to stack exchange to help me.

So really I'd like to know the effect on hearing from frequent earphone use (particularly as I listen to quite a lot of loud rock music)?

Thanks.

The main effect on hearing is the volume of the sound. Both the intensity and duration matter. However, it seems like hearing loss from personal music players is not as prevalent as from other causes like gunfire or occupational noise exposure (see also here).

The specific problem with in-ear headphones is people tend to listen to them louder than other types of headphones, here is an example study that shows this result.

So, in summary, there isn't anything wrong with in-ear headphones if you listen at a low volume, but be wary that peoples' tendency is to listen louder with in-ear headphones, and you already mentioned liking loud music. The volume is going to be your problem.

Be very wary with your hearing though: once you have lost hearing, there is no way to get it back at this time. Hearing aids only temporarily compensate for the loss. You might be okay now but regret a lifetime of noise exposure by the time you are an older adult.

References:

Clark, W. W. (1991). Noise exposure from leisure activities: a review. The Journal of the Acoustical Society of America, 90(1), 175-181.

Hodgetts, W. E., Rieger, J. M., & Szarko, R. A. (2007). The effects of listening environment and earphone style on preferred listening levels of normal hearing adults using an MP3 player. Ear and hearing, 28(3), 290-297.

Mostafapour, S. P., Lahargoue, K., & Gates, G. A. (1998). Noise‐induced hearing loss in young adults: The role of personal listening devices and other sources of leisure noise. The Laryngoscope, 108(12), 1832-1839.


Phoresis and mechanical vectors According to wikipedia and Human Parasitology
By Burton Jerome Bogitsh, Clint Earl Carter, Thomas N. Oeltmann

  Phoresis: In this type of symbiotic relationship, the phoront, usually the smaller organism, is mechanically carried by the other,usually larger organism the host.

So can the host acting as a carrier be called a mechanical vector?

On searching google.books I found some books mentioning:

Like Clinical parasitology

  Hosts that transmit parasites to man are vectors. Those that are essential in the life cycle are biologic vectors; those that are not essential are phoretic or mechanical vectors.

A mechanical vector just as biological vector transfers a parasite to its obligatory host but carrying it on the surface of its body while the host in phoresis is not necessarily carrying a phoront to an obligatory host (for parasitic interaction).

A parasite-mechanical vector relationship is possibly a kind of phoresis.


Effect of closed eyes on balance? Suppose you want to stand on one leg. Doing it eyes open is not that difficult, but doing it eyes closed seems to be difficult. Why?

Balance is tricky and depends on a lot of things, including, to some degree, your sight. Balance is achieved and maintained by a complex set of sensorimotor control systems that include sensory input from vision (sight), proprioception (touch), and the vestibular system (motion, equilibrium, spatial orientation); integration of that sensory input; and motor output to the eye and body muscles. Your vision helps you see where your head and body are in relationship to the world around you and to sense motion between you and your environment.

Very simply put, to blindfold someone is to take out the contribution of vision to balance. So, if the other systems involved in balance are off even a bit, blindfolding someone will interfere with their ability to keep their balance, even on two legs, let alone one.

Here are those systems in more detail.

Proprioception. In your joints, muscles, tendons, skin, and other areas, you have proprioceptors, that tell your brain where yoor aody parts (arms, legs, etc) are in relation to self in space. Because we live on a planet with  gravity, even if we are blindfolded, if we are standing correctly, our feet will sent our brain signals that will in turn allow the brain to judge our position in space with regard to gravity and we will keep our feet firmly planted on the ground in a way which will maintain us upright in a constantly regulated position (if we sense less pressure from the bottom of our right great toe, we will adjust by leaning forward and to the right a bit until out=r brain says, "ok, right there!" This happens from all the skin and joint proprioceptors responding at the same time. Notice that once vision is blocked, our bodies become relatively very still; we focus on our balance. We move tentatively.

As people age, they lose some of their propioceptive abilities. That's one of the reasons for falls in the elderly.

Inner ear. In our inner ear are the semi-circular canals, three on each side, which are oriented at ~90° to each other so we cover 3 dimensions. In these canals is fluid which sloshes about when we move our heads, change directions, bend over, etc. The fluid moving about is detected by fine hair-like projections on the sensory cells lining the canal called stereocilia - like a wave would be detected by your leg in shallow ocean water. These semicircular canals help us to remain oriented in space. Now, the semicircular canals are also attached to otolith organs - two chambers which are concerned with gravity. They have fine crystals in them - called otoconia - which move according to our head's position with relationship to "down", or gravity.

If we stand perfectly still (probably not possible without support), everything is read by the vestibular system (the semicircular canals and the otolithic organs) as normal, and we stay upright (there is a constant communication between our vestibular system and our brain). So, when blindfolded, we can stay upright even if we shake our heads, bend them forward or back, etc (within reason). As we age, things can degenerate in this vestibular system, which affects our balance, and results in more falls in the elderly. (Diseases in the young can also affect this.)

Vestibulo-ocular Reflex. A complicated system which reflexly coordinated input from your vestibular system and your vision in head movement. If someone suddenly turns your head, your eyes will move in the equal and opposite manner, that is, your eyes will stay focused on the object on which they were focused just before your head was moved. This system is what allows you to easily keep reading something while you shake your head from side to side (not the case if you move the print side to side).

When things start going wrong (in a very slow manner) with your vestibular or proprioception systems, your eyes can help compensate by orienting you to the horizon, etc., in a manner, correcting for some 'off' calculations in your vestibular system. Vision helps us to identify orientation with respect to gravity, determine direction and speed of movement, etc., to a much lesser degree than the other systems described but enough to have an impact. So, in people whose vision is failing, either their other systems have to be in really good working order (e.g. why young blind people aren't always falling over) or they have problems with falling.

The Human Balance System (easy)
Researchers find diminished balance in those with poor vision (easy)
Balance (easy)
Visual influences on balance
Baloh and Honrubia's Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Kevin Kerber, MD
Somatosensory Systems
Vestibular Occular Reflex


Why do the fastest runners tend to be black? If you watched the last Olympics like me you probably also observed that most medallists in running events were black. Why is that? I discussed this with university grad friends and researchers and we only came up with hypotheses but nobody had an actual explanation. Is it cultural, genetic, other reasons or nobody really know?

Update:

Sprint and distance running requiring different attributes for being the best, let separate this question in two parts: 1) Sprint (i.e. 100m) and 2) Distance running (@Forest already provided a great answer for this).

Note: I know this question can potentially bring disrespectful answers/comments, but I'm hopeful that this site and its members can answer this interesting question. Otherwise, I'll simply erase my question.

It's an interesting question and one that has been asked before. NPR did a story in 2013 on this topic, but their question was a bit more focused than just "why are so many black people good runners?"

The observation that led to their story wasn't just that black people in general were over-represented among long-distance running medalists, but that Kenyans in particular were over-represented. Digging deeper, the story's investigators found that the best runners in Kenya also tended to come from the same tribal group: the Kalenjin.

I'm not going to repeat all the details in that story (which I encourage you to read), but the working answer that the investigators came up with is that there are both genetic traits and certain cultural practices that contribute to this tribe's success on the track. Unfortunately, from the point of view of someone who wants a concise answer, it is very difficult to separate and quantify the exact contributions that each genetic and cultural modification makes to the runners' successes.

Pubmed also has a number of peer-reviewed papers detailing the Kalenjin running phenomenon, but I could only find two with free full-access and neither had the promising title of "Analysis of the Kenyan distance-running phenomenon," for which you have to pay. Insert annoyed frowning face here.

I did a quick search of some Kenyan gold medalist runners in the 2016 Olympics and sure enough, several (though certainly not all) are Kalenjin. I'm less sure about the Ethiopian runners, since most research that I found online seems to focus on the Kenyans, but I'd feel safe hypothesizing that something similar can explain their dominance at the podium.

So, the short answer to your question is that it's not just "black people" who dominate the world of competitive long-distance running, but that very specific subsets of people (who, as it turns out, are black) do display a competitive advantage and that both genetics and culture account for much of this advantage.


Using Jpred to predict secondary structure I'm trying to use Jpred to predict secondary structure for a protein sequence. When I run J-pred, I get a bunch of hits from PDB. I've also noticed these 'hits' are the same name as the templates i use when using Swiss mod. How do i interpret these hits, do I just ignore them and force jpred to predict structure anyway?

That depends on what your are trying to do. Apparently your query sequence is similar to that of proteins with a known 3D-structure. As it says on Jpred's result page (and help), in this case it might be worth looking at these homologues with experimentally determined structures for information on secondary structure. Most likely it will be more accurate than Jpred's prediction.

How much of the secondary structure you can use from the 3D-structure also depends on which parts align between your sequence and the ones in the PDB. You can show the alignments on Jpred's result page by clicking the button below 'Alignment of PDB hits to your sequence'. However, if you are going with annotations from the 3D-structure, it would probably be better to use SWISS-MODEL directly.

If you don't want to see those hits and just force a Jpred prediction, you can tick 'Skip searching PDB before prediction' in the advanced options before submitting your prediction. The hits are shown merely as a convenience, ignoring them doesn't change anything about Jpred's prediction.


Connection between genes and pathways I am reading about a paper about inferencing pathway information in cancer cells. Authors refer to ERBB2 as a gene and a pathway. I don't have solid biology background. What exactly means when we refer to ERBB2 as a pathway? Does it refer to activity of a protein encoded by ERBB2?

ERBB2 appears to be a (tyrosine kinase) receptor; that is, it lives in the cell membrane; with a part that sticks outside of the cell, and part that sits inside.  When the right molecule attaches to the outside part, the inside part changes shape, which alters its function, causing it to start phosphorylating other proteins, which alters their functions.

So the ERBB2 pathway is the set of genes/proteins whose behavior is affected by ERBB2.

Google "ERBB2 pathway" and "tyrosine kinase receptor" for more info.


difference between blastula and blastocyst What is the difference between these 2 terms. I believe that blastocyst is for animals, but structurally is there any difference? And how would you be able to identify each?

A blastula is a hollow ball of cells, while the blastocyst occurs slightly later in mammalian development and has a defined inner mass and an outer layer of trophoblast.


How does one confirm the discovery of a new species of plant/animal Hearing from the National Geographic and the news about the discoveries of new species of plants/animals, I was wondering how can a person confirm when they have actually discovered a new species of plant or animal?

How can they identify with enough certainty that it is not one of the species that has been previously discovered (out of the umpteen varieties of species)? Is there some kind of official/international database of species for plants/animals they typically look up to to confirm it? Also, how is the process of naming of a new species decided and why does it end up being a Latin name?

Basically, you have to examine as much of the relevant 'material' (preserved museum specimens) of the proposed new species and its closest relatives, and compare the diagnostic characters of your proposed new species versus those of its presumed closest relatives to confirm it is actually distinct. For example, with snakes (my field), we use counts of head and body scales, relative distances between features, relative length of tail, hemipene morphology, and even colouration, to determine species.

When combined with genetic evidence of monophyly of the new species and adequate divergence from closest relatives, it becomes a very robust species description.
Finally, names can be accepted or rejected by the ICZN based on existing names for proposed species, though it's a very confusing mess for most groups. I'd recommend checking out their website for more in-depth guidelines


Why does DNA mutate? I just read that pregnancy in space would be super dangerous because - among other reasons - of a higher risk of mutations due to radiation. This made me wonder: why does the DNA in organisms mutate? What are the main natural reasons? Is this due to the construction of DNA and would happen even in "perfect" conditions or is it due to something that is in the environment, like radiation?

So far I got two answers on reddit and also asked this question to a doctor and what I heard is along the lines of "this is how it is". I heard about "cells being worn out". But what makes the process non-deterministic, probabilistic? I guess I don't know enough about biochemistry to formulate the question, but I guess it's related to "given certain conditions, what determines at which point (and what kind of) a mutation occurs?"

If I am not mistaken, the vast majority of mutations happen during DNA replication.

DNA must replicate itself so that cells can replicate itself. The DNA polymerase is one very important protein that replicates DNA. The human genome (to consider this example) is 3.5 billions nucleotides long. Just to realize how long is 3.5 billions letters, let's make a book analogy.

Book analogy

In the Harry Potter series, there are about one million words (ref).
In the LOTR series, there are about one 400 thousands words (ref).
In the Chronicles of Narnia series, there are about 230 thousands words (ref)
In the King James Bible, there are about 788 thousands words (ref)

This sums to about 2.4 millions words. As, in english, there are 5.1 letters on average per word (ref), this lead to a total of about 12.3 millions letters. Imagine you have to rewrite all of these books almost 300 times (12.3 millions * 300 ≈ 3.5 billions)! How many typos would you make?

There are several cell divisions between a zygote and the ovule/spermatozoid produced by this individual but as most mutations happen during meiosis, I will just ignore mitotic mutations. The DNA polymerase makes about one typo every 100 millions nucleotides (Kong et al. 2012; Rahbari et al. 2016)! So really, the DNA polymerase is doing a pretty good job!

What is causing mutations?

Shit happens

I am hoping that form the above analogy, you may have a sense that mutations are just small mistakes. They happen because the replicating machinery is not perfect. Sometimes a molecule comes sideway, does not bind very well and another molecular passing by sticks to the DNA, etc.. Errors happen just like you would be making a lot of typos, rewriting books.

Mutagens

There are of course factors that can affect this mutation rate. Physical, chemical and biological agents increasing the mutation rate are called mutagens and they include radiation decay, ultraviolet radiation, ROS, benzene as well as some viruses and some parasitic bacteria.

Variation along the genome

Note also that the mutation vary along the genome too. Regions with high repeats (e.g. AATAATAATAATAATAATAATAAT) such as microsatellites for example tend to have a much higher mutation rate.

Variation among species and Drake's rule

Mutation rate also vary among species. There is a general tendency that the per nucleotide mutation rate negatively covary with the genome size, a phenomenon called Drake's rule (see for example Bradwell et al. 2013 or one of the early Drake's paper).


epitope prediction/ mapping B-CELL EPITOPE PREDICTION

Regarding this article:

"Such a molecule can be synthesized or, in case of a protein, its
gene can be cloned into an expression vector."----- is a particular
line in this article. What does expression vector mean here??
"antipeptide antibodies"---- what are these?
"immunogenic peptides"----these are basically epitopes, am I right??

An expression vector is a (usually circular) piece of DNA which is able to replicate inside a (bacterial) cell independently of the genome. Vectors can be transferred between bacteria and can express proteins from their own DNA sequence. They are used to express proteins inside of bacterial cells which can subsequently be purified. In this case the sequence for an immunogenic peptide is cloned into a vector and expressed in bacteria.
These are antibodies which are directed against a certain peptide. This is one technique of generating these antibodies. Making a (synthetic) peptide and then immunize animals against it. Then you can purify the antibodies from the serum of the animal.
Yes. You make short peptides of 8-12 amino acids (which is the length that the antibodies binds to) and use them for immunization.


How is satiety measured? I am aware of satiety only through experience, rules-of-thumb and possibly myths. For example: white bread is not filling, a pasta meal can be filling but because we "burn" carbs quickly pasta itself is not, and I personally find fruit in the melon family filling. (But that could be because I hate them ;) )

Is there a formal measure of satiety? How does it work?

Satiety is complex, and there are several kinds of satiety, all of which come into play in different circumstances. Things that decrease or halt our eating are called satiety signals. Different satiety signals are put out by different substances (carbohydrates, fats and proteins) as well as by things like gut stretching and other signals. There is also a psychological component to override satiety signals (company during meals, appearance of food, cost, etc.). The best measure of satiety may well be when a person stops eating a given meal. In lab conditions, the meals are carefully calibrated, but people (and animals) can feed as long as they desire to (ad lib).

Historically, satiety was thought to be the end product of serum glucose, available energy based on body heat, fat utilization by the liver, and the generation of ATP and other energy-rich molecules by the liver and/or brain. For the most part, these hypotheses have not withstood the test of time.

Three major signals influence food intake: satiety signals, adiposity signals, and central effectors. For the sake of simplicity, I'll deal only with satiety signals. Satiety signals (SS) arise from the GI tract and related organs during a meal, and influence eating behavior by activating peripheral nerves passing from the GI tract to the brain, or by recognition by brain receptors.[1]

As food interacts with the lining of the stomach and intestine, gut peptides and other signals that coordinate/optimize the digestive process are secreted. The signals that inform the CNS function as satiety signals. Different signals are secreted in response to carbohydrates, fats, and proteins, and it's the specific mix of signals that informs the brain as to what precisely has been eaten.[2]

Cholecystokinin (CCK) is the most extensively studied gastrointestinal satiety hormone. It is secreted by cells in the duodenum and jejunum in response to ingested fat and protein in chyme (food plus gastric fluid). Giving CCK IV decreases ad lib meal size, while blocking CCK receptor sites will increase ad lib eating per meal.[3][4]

Carbohydrates and fats as the most effective stimulators of Glucagon-Like Peptide (GLP-1) and Peptide YY (PYY). IV GLP-1 decreases meal size by promoting early satiety.[5] Within the CNS, PYY is detectable in the hypothalamus, medulla, pons, and spinal cord.[6]

Enterostatin is a protein which is broken down into a digestive lipase and a five-peptide fragment (Ala-Pro-Gly-Pro-Arg (APGPR) in humans). The appetite regulating effects of APGPR in the brain are specific to high-fat or fat diets but not towards diets rich in protein or carbohydrate.[6][7]

Amylin decreases meal size in rats, probably through the same pathway as CCK. Oxyntomodulin (OXM) and pancreatic polypeptide (PP) are also meal terminators. Pre-prandial subcutaneous administration of OXM to overweight and obese humans over a 4-week period resulted in a significant reduction in body weight of 2.3 kg, compared with 0.5 kg for the placebo arm.[9]

This is a growing field, and there is more suspected, and more to prove. But one can see that there is no one measure of satiety.

[1] That satiety signals come from the stomach and beyond was shown by "fake eating", that is, diverting swallowed food from the stomach by creating a fistula. If food is allowed to enter the stomach, satiety signals are elicited; if not, eating continues for a long time.
[2] Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake
[3] Gastrointestinal hormones and satiety
[4] Rats with spontaneous mutations of the CCK-1 receptor (called
OLETF -Otsuka Long Evans Tokushima Fatty- rats) eventually become obese
during their lifespan.
[5] Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2
[6] Introduction to Gut-Brain Interactions
[7] Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors.
[8] Amylin decreases meal size in rats
[9] Gut-Brain Interrelationships and Control of Feeding Behavior


Parsimony (cladistics) I don't understand how to sum the changes in a phylogenetic tree.

Here for example: http://www.med.nyu.edu/rcr/rcr/course/phylo-cladistic.html

How do you end up with 8 for the first and 9 for the second ?

It seems to me that they are not summing the changes correctly in this page.

They are summing the lengths of the paths to the root (and for the fig 2, they assume that the terminal branches, from left to right are of lengths 3, 2, 1 and 1). This doesn't make sense to me.

The correct way to count changes using parsimony is to consider each site in the alignment, and try to put the minimum number of mutations on the tree to explain the states observed at the terminal branches. Then, sum the number of mutations across alignment sites.

Here, for figure 1, I get:

site 1: 1 mutation, either on the left (T->A) or on the right (A->T) internal branch.

site 2: 1 mutation on the 4th terminal branch (T->C)

site 3: 0 mutations (all terminals have C)

site 4: 1 mutation on the 2nd terminal branch (G->C)

Total: 3

for figure 2:

site 1: 1 mutation on the branch leading to the most recent common ancestor of the two right-most terminals (A->T)

site 2: 1 mutation on the right-most terminal branch (T->C)

site 3: 0 mutations (same reason as for figure 1)

site 4: 1 mutation, either on the left-most branch (G->C) or on the branch leading to the most recent common ancestor of the 3 right-most terminals (C->G)

Total: 3

The trees are equi-parsimonious.

I hope I did not make any mistakes.

There exist algorithms to do this. For instance, Wagner parsimony.

Don't trust a course on phylogeny that resides on a medical center web page.


Do we know of any "species ending bugs"? Are we aware of a "bug" (virus, bacterium, prion, ...) that has completely exterminated an entire species? Either through direct observation or maybe some form of archeological evidence? If not, are there realistic scenarios where this could happen?

I am primarily interested in cases where the disease was the driving factor of extinction of an otherwise well established and healthy population, but examples of species that were in bad shape to begin with are welcome as well.

My understanding is that this is unlikely, since very deadly infections tend to burn out or evolve towards being less deadly. Killing your host is not conducive to your survival. But maybe it would be possible to reduce the number of individuals so much that reproduction became problematic. I imagine a species confined to an island or something might be susceptible.

I'm asking this because in an interview I saw, an epidemiologist said that his usual research interest are "bugs with species ending potential". The interview was on COVID-19 so he didn't elaborate on what he meant by that or give any examples.

For the special case of humans, I was able to find this article that claims such an event to be unlikely, but I suppose we are the best equipped species that has ever existed on this planet to deal with such a threat.

From the vantage point of other species, humans might be considered "bugs" in the sense that we are organisms that are causal in the ongoing extinction of numerous species. We're doing a pretty good job of it, so far:

  The included extinctions span numerous families of plants[4] and animals, including mammals, birds, amphibians, reptiles and arthropods. With widespread degradation of highly biodiverse habitats such as coral reefs and rainforests, as well as other areas, the vast majority of these extinctions are thought to be undocumented, as the species are undiscovered at the time of their extinction, or no one has yet discovered their extinction.   The current rate of extinction of species is estimated at 100 to 1,000 times higher than natural background rates.


What is the definition of a stringent/relaxed plasmid? I have found a publication which proposes some definitions, including a definition for strict and relaxed replication. The definitions are:

Relaxed control of plasmid replication. Relaxed control should be used in reference to plasmid replication that is not obligatorily coupled to chromosome-replication.
Stringent control of plasmid replication. Stringent control should be used in reference to plasmid replication that is obligatorily coupled to chromosome replication.

However, the publication is from 1976. Are these definitions current? If no, what is the current definition?

In short, yes, the definitions are still correct:

The number of copies of a plasmid in the cell is determined by the mechanism of its replication: whether it is synchronized with the replication of the bacterial chromosome or is independent of it.

In the first case, the initiation of replication is performed by the same mechanisms of replication of the bacterial chromosome. This means that the origins of replication, as well as all proteins involved in the initiation of replication, are shared between the plasmid and the bacterial chromosome. For plasmids, which replication is synchronized with the replication of the bacterial chromosome are under stringent control of replication. The stringent control of replication is characteristics of plasmids with low copy number. These plasmids contain DNA regions called par-locuses (from partition) that control the correct division of the plasmids in the two daughter cells.

Plasmids with high copy number are under relaxed control of replication. These plasmids are replicated independently of the replication of the bacterial chromosome. They have individual mechanisms for initiation of replication. The plasmids themselves encode the initiation factors for replication, which are mainly RNA molecules. Once the plasmid replication is initiated, it continues with the same machinery used by the bacterial chromosome.

Reference (Textbook): Bacterial Genetics, Margarita Pesheva (2000)


Is this a real dinosaur species? I recently got  and would like to know if this is a real species. It doesn’t look quite like a Styracosaurus, but is close. Can someone identify?

I'm pretty sure that's an Achelousaurus.

Two curved horns on top, plus hump on nose:
Front view:

Side view: (for nose)


is having more copies of gene better then having it less? if it's why is it ? I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.

so I wonder if it's better to have more copies of the gene then having 2

I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.

Where did you read that? Please always include your sources.

What you're saying is unclear but I suppose you are referring to ploidy variation among species and not to CNV (Copy Number Variation) for specific genes. It is also possible that you mistake alleles for genes but it is impossible to tell where your misunderstanding is without reading from your source. I will assume you talked about ploidy variation.

Elephants are diploids, just like humans. So, the claim appears flat wrong.

  so I wonder if it's better to have more copies of the gene then having 2

There is no general rule. Because having a single working copy is often enough, high ploidy can be a pretty good defense against loss of function mutations but that's only valid for some time just after a recent polyplodization event as the relaxation of selection pressures against such mutations will lead these deleterious mutations to higher frequencies (at mutation - drift - selection equilibrium).

Note that doubling or halving the number of gene copies often yield to issues in dosage of mRNA and protein expressed. Related to that you might to read about dosage compensation


What dictates which protein to synthesize at a given time? I understand how DNA is replicated and how it directs the synthesis of proteins from amino acids through RNA polymerase, RNA and ribosomes. Now I want to understand how it works in the big picture.

With my current level of understanding, any protein can be synthesized at any time at any rate, but it looks to chaotic to work at all.

What dictates which protein to synthesize at a given time?

Your asking how a cell or organism regulates protein synthesis. This is a complex question, with many different parts. It is well presented in Alberts Molecular Biology of the Cell, Chapter 7, on genetic switches. Here's an online section from that chapter in the 2002 edition.

There is a lot involved in regulating protein synthesis. As a general rule if you can imagine regulating it, it's regulated. Here's a figure from Alberts to get you started thinking about this:

There are some things that are required for all genes. General transcription factors, for example, and the Pribnow, or TATAAT box. The presence, absence, location, and accessibility of these things can regulate the levels of protein synthesis by the cell. Other things are going to discriminate between different genes. Under certain conditions, certain gene regulatory proteins will be produced, not destroyed as quickly, activated, allowed entry into the nucleus, etc, regulatory sequences will be exposed or not exposed, methylated or unmethylated... and transcription rates will change accordingly (increasing if those protein gene interactions stabilize assembly, binding, and transcription by the polymerase, decrease if they destabilize assembly, binding, and transcription by the polymerase).

This is just a taste of the wonderful world of gene regulation in the eukaryotic cell. As it says in Alberts, of the roughly 30,000 human genes, an estimated 5–10% encode gene regulatory proteins. And these are just the proteins that directly regulate transcription.


How do centrioles auto-locate to opposite sides of cell during mitosis? I realize that centrioles are made of 9 triplets of microtubulin wound together with a hollow core, and that they are responsible for the configuration of the spindle during mitosis. The spindle fibers attach to the kinetochores of the sister chromatids and pull, ultimately separating them in preparation for cytokinesis.

How do the centrioles recognize where to go in the cell, such that they are oppositely positioned with one another? Is the mechanism similar to how neurons "find their way" during development to forge the correct connections that give us sight, etc, but on a subcellular scale?

During cell-division centrioles move towards opposite 'poles' and finally get attached to cell-membrane. Different factors influence & drives this process, most still not discovered. So this mechanism is largely unknown. From the scientific literatures published on this  matter till recently we can say that this process should include:

A structure along which the centrioles can migrate,
Molecules associated with the movement of centrioles,
Signal molecules triggering this process,
Signal molecules determining the direction of migration.

To answer 1., Microtubules form a intra & inter-cellular network along which subcellular structures can move. Actin & Myosin are also involved in some cells. For reference read Ganong's review of Medical Physiology. (the example you stated in your question about neurons is a substantially different process. But neurotransmitters are carried with the help of Microtubules. Chromosomal structures also are arranged with the help of them.)

For points 2,3 & 4 read this paper, these parts are very clearly described there.

Thank you.


RNA interference and the former Petunias experiment > I'm having problems trying to understand how RNA interference works.

From what I understood, in simple terms there is this  dsRNA which is fragmented into siRNA by the enzyme called Dicer, and those siRNA make the RISC complex active, which leads to the degradation of mRNA which are complementary to one of the strands of the original dsRNA.

Said this (which I don't even know if it is correct), how this relates to the petunias experiment? From what I understood the researchers put into the petunias an enzyme that coded for the pigment and not strands of dsRNA which then would have created the inhibition...

What am I missing?

PS. I don't have technical knowledge about Technologies so excuse me in case I said wrong things.

Thanks in advance everyone.

They introduced a foreign gene responsible for petunia leaf colour, with the intentions of up-regulating gene expression for this colour, which was purple. What was observed however was intriguing. Rather than an up-regulation of the purple colour, the leaves were all white instead. This finding showed that the RNAi system in plants recognised the foreign gene and degraded it. Not only that, but the RNAi system also identified the endogenous equivalent of the foreign gene and down-regulated this also thinking it was foreign. This is how they discovered this miraculous finding :)