How is the cell membrane protective? Generally in biology books, it is written that the cell membrane is selectively permeable and that it has a protective function, as in here
It says that the cell membrane protects the cell from its surroundings. However the selective permeability is only for the hydrophilic substances, and not for any foreign antigen which may be dangerous for a cell.
So how does this count as protective?
Also for hydrophilic substances, carrier proteins are present, ready to take the ionic substances inside the cell.
Hence my only question here is how is the cell membrane protective?

You are right that the membrane doesn't stop everything.  Its main purpose is to separate the inside of the cell from the outside so that you can accumulate resources in it.  Your potassium ions, proteins, sugars, RNA (and DNA, behind another membrane) have to stay inside the cell because they can't dissolve through it.  There are indeed channels and transporters from some hydrophilic substances as you say, but they are usually very specific about what chemicals they will transport.*
The membrane is actually very delicate but it is reinforced by a cytoskeleton, and proteins are embedded in it to transmit force to features outside the membrane (such as desmosomes and hemidesmosomes connecting to other cells or extracellular matrix) so that the membrane itself is never put under strain.  Think of it like a thin plastic bag that can hold water because you put it inside a much stronger container - even though the stronger container is not waterproof.
Many harmful chemicals would not be harmful if they could not get into your cells, so you should not be surprised if they are often hydrophobic and dissolve freely through the membrane.  Some cells have other defense mechanisms (pumps to try to expel the toxins or enzymes to try to break them down), but ultimately any true toxin is defined as the one for which nothing works well enough.
Many pathogens have evolved methods of crossing the cell membrane.  Bacteriophages famously break a hole in the membrane with a special injection apparatus, while many human viruses fuse a cell membrane section they carry around themselves with the victim cell membrane, using proteins that have evolved the right hydrophobic features.  It is hard to defend against such things because our cellular membranes need to be able to fuse with themselves for purposes such as releasing vesicles of neurotransmitter.  The same "no true pathogen..." argument applies - we only get sick from the pathogens that can infect us.  If we lacked these protections, we would be even more vulnerable than we are.

Exceptions, perforins and granzymes, prove the rule:  they are meant to kill the cell affected.


Does scratched Teflon coated frying pans contain carcinogens which can cause cancer? Is it true that using scratched Teflon-coated pans contain carcinogens, and if so, can they be consumed through the food cooked in them?

E.g.

The deadly toxins from non-stick frying pans

Teflon is a polymer of perfluorooctanoic acid (PFOA) and related compounds.  PFOA is thought to be a carcinogen.

I think there's an urban legend that if you really heat teflon up or burn it (it doesn't burn as flouroxides are not stable in air) that you might get some of the constituent chemicals out into the air.

Once the flourocarbons are polymerized into fibers and surface coated a metal pan, they are chemically inert and aren't carcinogenic.  Teflon can be made to burn and some noxious fumes produced, but they are not especially carcinogenic.

Even after all this, this paper reviewed PFOA exposure and points out that most people in industrialized countries have some PFOA in their blood and this does not seem to be related to a strong incidence of cancer as the level of exposure is so low.

Flouro-carbon compounds are terribly inert - thats why teflon is so tough.  If PFOA is dangerous, then Teflon is > 10 million times less dangerous.  If PFOA is dangerous, crossing the street is many more times dangerous.

Even PFOA will be eliminated from Teflon production, supposedly next year (2015).


Significance of synthesis of D-glucose in plants..? why plants can only synthesize D-glucose why not L-glucose along with D glucose. I know it very well that plants have only enzymes which can synthesize D-glucose but Why not they have enzymes which can also manufacture L-glucose. So that we could have mixture of L and D glucose molecules? What is the significance of synthesis of only D-glucose by the plants ?

Synthesis from chemicals in organisms is fundamentally different from laboratory synthesis of chemicals. In the latter, more than one chemical species or other unwanted byproducts are usually formed, whist living organisms use enzymes, that are often stereo-specific. This means that they usually can bind, in the case, produce, only one stereo-isomer.

To produce both forms they would need double sets of enzymes.

It makes sense for animals, bacteria, protozoa, etc. to digest whatever comes, so less specific enzyme, but since plants will only access the glucose they themselves formed use of a stereo-specific enzymatic pathway probably enables a more efficient metabolism.


Why don't restriction endonucleases digest transformed plasmids? In the textbook that I'm using, it explains that bacteria does not digest its own chromosomal DNA because the sites that would be cut by its own endonuclease are methylated. Is there a similar mechanism involved for protecting its own plasmids? If so, how are plasmids cut while serving as vectors?

Laboratory strains used for the purposes of cloning have been genetically engineered to address this issue, typically by deleting genes of the various restriction-modification systems. There are four broad classes of restriction modification systems, which I will discuss individually. Unless individually referenced, most information below is based on the following supplier technical notes:

Promega: What are the effects of the bacterial DNA restriction-modification systems on cloning?

New England Biolabs: Restriction of Foreign DNA by E. coli K-12

Type I

In Escherichia coli, this system consists of the hsdR, hsdM and hsdS genes and is capable of both restricting (digesting) unmethylated DNA and methylating hemimethylated DNA. Knockout of hsdR and/or hsdM prevents restriction and methylation, respectively. This allows engineering of strains for specific purposes. For example, a common E. coli strain used for cloning, DH5α, has the genotype hsdR17 (rK–, mK+) which abrogates restriction activity but maintains methylation activity. This means that exogenous DNA will not be restricted, but will be methylated and therefore able to be subsequently transformed to r+ strains without worry of degradation, if the need may arise.

Type II

This is the class of restriction enzyme commonly used in the lab to cut DNA because they generally recognize short, palindromic sequences and cut within or near the recognition site. The E. coli background strains K and B, from which most lab strains are derived, do not contain Type II enzymes. The Type II enzyme EcoRI, for example, was isolated from the E. coli RY13 strain (Yoshimori, 1971; PhD thesis).

Type III

Similarly to Type II, the K and B strains do not possess this restriction-modification system, which was first characterized in E. coli 15T-.

Type IV

This system differs from the others in that it cleaves methylated and hemimethylated DNA, though it does not recognize methylation by Type I or Type II modification systems, nor Dam or Dcm methylation. In E. coli, this system consists of the mcrA, mcrBC and mrr genes and is most problematic when attempting transformation of DNA from organisms with ubiquitous cytosine or adenine methylation (eg plants and mammals). For example, the lab strain T7 Express, which is derived from the common strain BL21, has the genotype Δ(mcrC-mrr)114::IS10 which deletes mcrBC, hsdRMS and mrr.

Note on Dam and Dcm Methylases

These bacterial enzymes methylate adenine and cytosine residues, respectively, but are not directly involved in the restriction-modification systems discussed above. However, some Type II enzymes used for cloning are sensitive to this methylation and so lab strains are available with these enzymes deleted.


Using exogenous genes to reduce the set of essential amino acids? Various organisms have sets of essential amino acids that they cannot synthesize themselves, but rather that they must obtain from food. Humans have 9 of these amino acids. However, obviously certain organisms like plants contain the necessary genes to synthesize all of their amino acids. Also, the set of amino acids for various organisms differs. For example, arginine is essential in dogs but not in humans.

Have there been any attempts at taking cells from an animal or other organism with essential amino acids and providing them with the necessary genes to synthesize that amino acid, thereby reducing the cell's set of essential amino acids?

I am not asking this specifically referring to human cells, nor do I have any particular motivation for asking this other than curiosity.

Decreasing the number of essential amino acids is frequently used as a selection marker during molecular biology experiments: An organism (usually yeast) that cannot synthesize a certain amino acid is first grown in the presence of said amino acid in the media. Then it is transfected with a gene of interest together with the gene that enables it to synthesize the amino acid. Now being grown in a culture medium that does not contain the amino acid, only individuals that were successfully transfected can grow, the others will starve.

A similar approach was also used in  Beadle and Tatum's Nobel prize-winning work on the one gene-one enzyme hypothesis.


When are neuropeptides loaded into vesicles? It is well known that small neurotransmitters like monoamines (dopamine, serotonin, etc), acetylcholine, glutamate, etc are loaded into vesicles at the axon terminal. Stated differently, synaptic vesicles,SVs (which are the name of the vesicle type that store small neurotransmitters), are made locally within the axon terminal, and then ultimately loaded with small neurotransmitters.

However, I cannot seem to find when larger molecules, like neuropeptides, are actually loaded into their vesicles. I know that neuropeptides are made in the soma, but I am unsure of when they are loaded into their vesicles.

Are neuropeptides loaded into their vesicles at the synapse?

" Small-molecule neurotransmitters are synthesized locally within the axon terminal" https://web.williams.edu/imput/synapse/pages/I.html

"As a rule, the synthesis of small-molecule neurotransmitters occurs within presynaptic terminals" https://www.ncbi.nlm.nih.gov/books/NBK11110/

"SVs are made locally at the terminals and are regenerated after exocytosis"  https://www.sciencedirect.com/science/article/pii/B9780080450469013929

Neuropeptides are packaged in the soma via the Golgi into dense core vesicles, similar to how other types of secreted proteins are packaged.

These vesicles are transported to axon terminals where they await release signals.

Sossin, W. S., Fisher, J. M., & Scheller, R. H. (1989). Cellular and molecular biology of neuropeptide processing and packaging. Neuron, 2(5), 1407-1417.

Wong, M. Y., Zhou, C., Shakiryanova, D., Lloyd, T. E., Deitcher, D. L., & Levitan, E. S. (2012). Neuropeptide delivery to synapses by long-range vesicle circulation and sporadic capture. Cell, 148(5), 1029-1038.


Why are there inverted repeats in response elements? The following picture shows an inverted repeat sequence in a response element. Response element sequences for glucocorticoids, estrogen, and thyroid hormone show that they all contain inverse repeats. Why do these inverted repeats exist in so many response sequences? In other words, what advantage do they pose to the function of the response element?

Starting with prokaryotic (i.e., bacterial) transcription factors--which were the first to be characterized in depth, this type of pattern was noted.  Even for the "classic" Type II Restriction Endonucleases used for molecular cloning have palindromic recognition sequences.  In all three cases the answer is that the sequence-specific DNA binding protein binds as a dimer, and so each monomer is recognizing a "half-site" (one of the inverted sequences).


identifying which SNPs sit in TFBS (Yeast) i have a set of ~11k SNPs for Saccharomyces cerevisiae, baker's yeast and i would like to identify which ones of these sit in transcription factor binding sites and if they do information on the relevant TFBS.

i've scoured this site and the internet and i couldn't find a downloadable database that would give me locations of all known/verified TFBS for yeast. i've studied the YEASTRACT website thoroughly but didn't find such database to download information about TFBS for all the ORFs/genes in one go.

moreover, when i tried getting the information manually through YEASTRACT search on-line i found results confusing. for example: searching for TF for ORF "YOL166W-A" returns a list of 4 TFs. clicking on one of them, say Sok2p, takes you to another page which says, amongst other things, that the corresponding TFBS is "acMTGCAKg"... what does it mean? (i know the ACTG alphabet but what are the 'a', 'c', 'K' and 'g' symbols?) and what does this tell me about the actual location of the binding site? do i have to BLAST the whole genome to identify it? (shouldn't there be a database with this info for yeast already?) if so, how do i BLAST for symbols like 'K' and 'g'?

i have background in stats but currently work in genetics applications, hence extracting relevant bioinformatics data is very confusing for me on occasions. any help will be appreciated.

I agree it can be extremely confusing sometimes to find the right data.

Do you know RSAT (Regulatory Sequences Analysis Toolkit) ?
If you go in "help & contact", and "motif databases", you'll find the Yeastract database: http://rsat-tagc.univ-mrs.fr/rsat/motif_databases/Yeastract/

I thought it would also be on JASPAR, but couldn't find it.

Then for your analysis where you look for SNPs in the motifs, there is a tool on RSAT, that unfortunately works only with the Metazoa database right now, but you might be interested to check it out, and the corresponding paper: http://rsat-tagc.univ-mrs.fr/rsat/variation-scan_form.cgi


Should the length of the electrodes in the electrophoresis chamber be proportional to chamber's size? I am trying to build a small horizontal electrophoresis chamber from scratch. I want to use it for comet assay and I will be using only 1 slide, so it's going to be about 3cm wide, 10cm long and 4cm high, just enough to fit the slide and a small amount of buffer. As far as I know such thing is not commercially available, so before I make it I want to make sure that it's going to work. The main issue is the cost of the electrode (has to be platinum wire). I don't want to spent that much money just to realize that it doesn't work.
My question is: is a 3cm electrode in a 60-70cm3 enough? Basically, are there any physical restrictions on the size and the position of the electrodes and the shape of the chamber?
Since I am a biologist and my knowledge in physics are quite limited, I would greatly appreciate any information about this.

These instructions for building an electrophoresis chamber don't comment on the minimum length of wire, but on the other hand they suggest using something called Monel Seizing Wire (Ni/Cu alloy - £8.95 for 10 m in the UK) or 20-gauge copper wire, so if you follow their advice you probably don't need to worry about cost.

I imagine that alloy electrodes won't last as long, but they would be cheap to replace - in fact you would be looking for opportunities to use up all of your excess wire!


Why are nosebleeds easier to get in the winter? I understand it probably has to do with the dry air, but what does dry air do to make nosebleeds so easy to get? For example, even gently blowing your nose can cause a nosebleed for some people during the winter.

The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side): Kiesselbach's plexus.

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma.

Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.

Have you noticed that your lips chap more in the winter? Dry air and cols temperatures do that. The mucosa of your nose also dries out and suffers some damage. Not like your lips, but damage none the less. Damaged nasal mucosa is more susceptible to tears/trauma/erosion. If it happens in an area of rich blood supply, you get a nosebleed.

Anything that helps with the integrity of the nasal mucosa is going to help reduce nosebleeds. One can

run a humidifier in dry weather
avoid irritating by touching the nose or blowing nose too often
apply a very light layer of petrolatum or Bacitracin ointment to the inside of the nose covering Kiesselbach's plexus at night so the nose-breathing doesn't dry out your nose
use nasal saline spray to moisten and soothe the nasal membranes (don't rub the tip of the spray bottle against the nasal membranes, though)

*more serious or recurrent bleeding needs medical attention to rule out  other conditions that are associated with frequent nose bleeds.

Epistaxis


What's the real meaning of "brain shrinkage"? It is known that some pathologies cause brain shrinkage, for example, it is said that depression causes shrinkage in the hippocampus.

My problem to understand the statement, is that I don't undestand exactly how a brain region shrinks, or what they mean when they say that some pathology causes a brain region to shrink. Does the neurons and everything in them become smaller? Do the cellular membranes become shrink somehow and make the intracellular space smaller? or is it just that a large part of neurons stop firing and they say the brain has "shrinked" because the activity region has become smaller.

Basically, I want to know what happens or what is required in order to have a brain region shrink.

Brain shrinkage = brain atrophy, which means a decrease in volume of the brain tissue, which involves different types of degeneration on the cellular level.

Here is a Wikipedia article about cerebral atrophy with a list of ~30 causes, such as Alzheimer's disease, stroke, cerebral palsy, malnutrition, AIDS, etc. Mechanisms can involve: loss of cytoplasmatic proteins, loss of complete neurons or connections between them, etc.

Alcohol consumption and frontal lobe shrinkage: study of 1432 non-alcoholic subjects (BMJ):

  The brain tends to shrink physiologically with age. Heavy alcohol
  consumption seems to exaggerate this shrinkage in social drinkers.
  Moderate alcohol consumption does not seem to affect brain volume.

Vitamin B12, cognition, and brain MRI measures (Neurology):

  Methylmalonate, a specific marker of B12 deficiency, may affect
  cognition by reducing total brain volume...


Are transgender people born physically different from others? Are all children born with only either male or female body parts (other than exceptions), or is there actually a natural third gender with the physical characteristics of both genders, e.g. the child has the genitalia, or reproductive organs, of both sexes?

According to Wikipedia they are only either male or female when born. They only feel different later on in life.

The concept of transgenders has nothing to do with sexual organs at birth. Transgenders is a concept that has to do with sociology, not biology. See the wiki link.

intersex (previously called Hermaphroditism) has to do with biology. The wiki link makes a great job at defining intersex.

In short: A transgender person is born anatomically either male or female (with eventually exception of intersex who go on to become transgender) and they then identify themselves to the opposite sex (or a third sex) rather than identifying themselves to their actual anatomic sex.

Note that this post is closely related.


What is the source of the electrons generated in the Krebs cycle? In the Krebs cycle, where do the hydrogens and electrons that NAD+ and FAD accept come from? It seems that citric acid only loses two hydrogens because it starts out with eight hydrogens and then becomes oxaloacetic acid, which has four hydrogens.

The two electrons and a proton of NADH comes from a H$^-$ ion of a Krebs cycle intermediate during Isocitrate dehydrogenase reaction and Malate dehydrogenase reaction.

In the following reaction, Isocitrate is oxidised to Oxalosuccinate and in the process two Hydrogens are lost one as H$^-$ and the other as H+. This H$^-$ is accepted by NAD+ to form NADH.

Note: Oxalosuccinate is an intermediate formed during oxidative decarboxylation of Isocitrate.

Now coming to FADH$_2$ $-$

During oxidation of Succinate to Fumarate, Succinate looses a H$^-$ and a H+ ion which constitute the two protons and electrons of FADH$_2$  . Here's an image that illustrate the mechanism:

The alpha-ketoglutarate dehydrogenase complex reaction is similar to pyruvate dehydrogenase complex reaction(PDC).
PDC reaction is an oxidative decarboxylation reaction of Pyruvate in which the 2e$^-$ of NADH are derived from the electron shared between COO$^2-$ and C=O groups of Pyruvate.

The Hygrogen (H+) of NADH is either derived from the H+ of CoA-SH or from the medium. There's a series of complex reactions which need to be studied to fully understand the source of H of this NADH.

So you can understand that the 2 e$^-$ of NADH produced in Alpha-ketoglutarate dehydrogenase complex reaction are the electrons between COO$^2-$ and C=O groups of Alpha-ketoglutarate and the H is either from the medium or the H+ of CoA-SH.

Reference: Biochemistry by Berg


Difference between crossover rate and recombination rate? I am not a biology student and therefore, need clarification if crossover rate and recombination rate are the same thing. So if the text says 'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing? And if not then what is the difference? Also, is 'per base pair' and 'per locus' the same thing?

Let's start with the second question.

  Is 'per base pair' and 'per locus' the same thing?

No, not necessarily. A locus (plur. loci) is a location in the genome. It can be of any size. A locus can be a single base pair or it can be 10 base pairs, or a whole gene or anything you want.

  'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing?

Recombination rate and crossover rate are not exactly the same thing!

Let's define two loci. Here is a drawing of two haplotypes (the maternal one and the paternal one). Let's represent the loci on the maternal haplotype with capitalized letters and the loci on the paternal haplotype with lower case letters

---A---------B---

---a---------b---

Let's Let's say that between these two loci there are on average 0.2 crossover per reproduction. The crossover rate is therefore 0.2.

Let's draw the two haplotypes after crossover(s) in a case with...

... 0 crossover

---A---------B---

---a---------b---

... 1 crossover

---A---------b---

---a---------B---

... 2 crossovers

---A---------B---

---a---------b---

... 3 crossovers

---A---------b---

---a---------B---

... 4 crossovers

---A---------B---

---a---------b---

You might see a pattern here! If the number of crossovers is even (including 0), then the association between the two loci is unchanged. If the number of crossovers is odd (including 1), then the association between the two loci is changed.

The recombination rate is the rate at which the association between the two loci is changed. Let $P(n)$, be the probability that there are $n$ crossovers betwee our two loci. The recombination rate is therefore $P(1) + P(3) + P(5) + P(7) + P(9) + P(11) + ...$.

To make a long story short, the recombination rate is the rate at which the number of crossovers is odd.


Dominance/recessivity of new mutations What is the distribution/probability density function (PDF) of recessivity/dominance of new mutations?

I very welcome any partial answer that does not give the whole PDF but just some information about the expected value or the variance of this distribution.

Here is a related question

I don't believe you can produce a general function for this. It will depend on the exact gene and organism you are considering.

From a molecular point of view, the vast majority of recessive mutations result from a change producing either a non-functional protein product or a truncated product that is cleaned up by the cell. We can reasonably assume that most modifications significant enough to produce a phenotype will be of this class since there are more mutational sites which can produce a non-functioning product than can produce a product of changed function but the exact ratio of one to the other is not going to be equal across different genes and organisms.

Note as well that the whole notion of recessive and dominant traits is probably an over-simplification and, in fact, there are subtle differences between homozygotes and heterozygotes in many, perhaps most, cases so I'm not sure how useful an estimate would be even if you had one.


Will humans and animals be harmed by frequencies outside their hearing range? The human ear (for example) is sensitive to frequencies from 20Hz to 20kHz. Any sound beyond that limit would not be heard by us naturally.

Will it harm us (effect our ability to hear) when we hear sound more than 20kHz continuously?
Or...

Will it harm when we hear a 19,999Hz sound (which is upper limit) continuously?

The only sensible answer to these questions is "sometimes".

The reason: even a simple monotone must be described by both frequency and amplitude. Any frequency can cause harm with enough amplitude, and any frequency can be harmless when the amplitude is low enough. If you want to actually quantify the damage, you'll need something like an equal-loudness curve, but for damage rather than loudness. As a proxy, you could use the pain threshold of the equal-loudness curve.

As for the second question, there is nothing magical about 20kHz: physical damage will always fall on a spectrum, there is no single frequency and/or amplitude at which damage begins. If you set an oscillator to constant amplitude and slowly turn up the frequency, you'll notice that the sound slowly dies out around 20kHz. The damage threshold will behave the same way.


What exactly happens during the crossover My knowledge of biology is rather limited, but I think I have a grasp of some basic concepts. For me (as a person close to math) a chromosome is a sequence of elements from the set {A,C,T,G} of some (arbitrary?) length. In humans, there are 23 pairs of chromosomes, and during meiosis each of these pairs produces a singe "mixed" chromosome.

Q1 In each pair, do chromosomes have to be of the same length? If yes, does it mean that this length is the same for all humans? Do chromosomes in different pairs have different lenghts?

Now, we have two chromosomes from the first pair and they get mixed during the meiosis.

Q2 In which exactly place do they get mixed?

if chromosomes are same length, I expect they exchange pieces of the same length only as well; however, if they are of different length, do they exchange pieces of different lengths? e.g. suppose first chromosome in a pair has length 100, second is 105 (I do understand that in reality the numbers are much bigger). Can that happen that the new chromosome is created using the first 10 elements of the first, and the last 80 of the second (so the first 10 of the first replace the first 25 of the second), with the total length of 90?
how many exchanges may happen in a single meiosis, namely can that happen that chromosomes exchange several separated pieces from the middle?

I guess, that this process may not be understood completely yet, so I'm rather looking for an answer either "No, it can't happen at all, we know that for sure", or "this we don't know yet, perhaps it may happen".  Thanks.

Q1 In each pair, do chromosomes have to be of the same length?

Yes, approximatively.

  If yes, does it mean that this length is the same for all humans?

Yes, approximatively.

  Do chromosomes in different pairs have different lenghts?

Yes. E.g., in humans, chromosome 1 is 294 millions nucleotides long while the chromosome 22 is only 50 millions nucleotide long.

  Q2 In which exactly place do they get mixed?

These crossover can appear pretty much anywhere. The probability of a crossover to happen at a given locus (locus=location on a chromosome) is not a constant throughout the chromosome though. In any case, the crossover always (almost always) happen at the same locus for each pair of the chromosome. In other words, if ~3 millions nucleotides goes from the paternally inherited to the maternally inherited chromosome, then ~3 millions nucleotides goes from the maternally inherited to the paternally inherited chromosome.


Selective breeding and Mutagenesis I am writing an argumentative essay in which I claim that GMOs are safe. I know, it is not proved, but for the sake of my course I want to prove it. The counterargument that my professor said to me is that genetic modification is not like selective breeding. GM brings changes faster and most of the cases it is inevitable. We don’t know the consequences and they can be bad. On the other side selective breeding is changing the organism slowly and something bad can be prevented in the start of its development. What are disadvantages of selective breeding to compare with genetic modification? Can I use the mutagenesis as the example of selective breeding and use its cons?

Yes, GMO are safe to consume! See Is Genetically Modified food safe to consume?. Now, there are other (potential or real) issues related to the use of GMOs such as for example a loss of genetic diversity if every farmer plant the exact same strain. Talking about such issues will require talking about ethics, economy and sociology and it can therefore not be answered in a science website only.

Your teacher's argument does not make much sense (although a direct quote would have been helpful). GM plants also have to develop. They are organisms too!

  [W]hat are disadvantages of selective breeding to compare with genetic modification?

Keep in mind that it is practically impossible to define GMO. Many of the things that we would call GMO actually don't result from much more than just selective breeding. Following this logic corn, wheat, sunflower oil, lettuce, broccoli, cauliflower, peanuts and pretty much everything else you eat is a GMO.

Attempting to let aside the semantic issue a comme argument is a lack of lack of familiarity and this is why extra precautions and testing must be done. See What risks exist with GMO, but not with selective breeding?

  can I use the mutagenesis as the example of selective breeding [..]?

Mutagenesis and selective breeding are two different processes (although often used together). One is not an example of the other.


Ways to cause membrane damage to microalgae and yeast? I am researching a way to monitor the membrane damage of cells. To do that I fist have to have reference points, namely, cells with damaged membranes.

I am working with Dunalliela, Hematococcus (both microalgae), and common yeast. I have been using mostly ethanol to damage the membranes so far.

What other ways are there to cause the most possible damage to microalgae (or yeast) membranes?. The idea is not total cell obliteration, but rather membrane damage (death is expected).

To get to the membrane of these species you first need to get past a formidable cell wall. The methods listed below are therefore more aimed at making cells permeable but the membranes must sustain some damage in the process.

At our lab we regularly use glass bead transformation for microalgae
transformation. The microabrasion allows DNA to go in so I imagine
the membranes must be damaged somehow.
I've also used hypotonic media (depending on the strain) to swell
cells close to their bursting point. I imagine they become rather
permeable at this point since they let several dyes in that are
otherwise excluded.


Why do doctors use a new thread for each stitch? Why do doctors use a new thread of the same kind for each stitch instead of using a single thread for the entire stitch?

Using a single thread for a suture also known as continuous stitching has a major con that it has higher risk of failing if the suture is cut in just one place. So it is generally avoided eventhough it is very easy to do.

On the other hand interrupted stitching ( one thread for each stitch) is favoured because of lesser risk of failing, eventhough it is time consuming than continuous stitch.

Source:https://en.m.wikipedia.org/wiki/Surgical_suture


Is organ transplantation race dependent? I watched (IMHO canibalistic) movie "Seven Pounds" where protagonist donated many of his organs to other people and I noticed, that most recipients were black also as protagonist was.

Is race really taken into account when organ transplanting?

UPDATE

The question is not just about if interracial transplantation really good or bad. I can imagine, that transplantation is done same-race just in case, in favor of "do not harm" principle.

No, race is not a factor taken into account. However, due to higher genetic similarities between people of the same race, it is usually easier to find a match within a race.

Source 1

Source 2


what is the poison in chinaberry? I was trying to look up what the poison in Chinaberry is, however, with the exception of a couple related compounds was able to find no information on the poison. What chemical makes up the Chinaberry poison, and what is this chemical's concentration and LD50, if known?

Edit: The Chinaberry I am referring to is Melia azedarach

The toxin is Meliatoxin, in a class of toxins called tetranortriterpenes.
I found this here.  Bold emphasis mine.
https://wagwalking.com/condition/chinaberry-tree-poisoning

What is Chinaberry Poisoning? The chinaberry tree is a member of the
mahogany family that is native to Australia, China, and India. These
deciduous trees sprout delicate light purple flowers in the spring,
which develop into yellow, berry-like fruits in the summer. They were
transported to North America in the early 1800’s as an ornamental
plant, but has escaped into the environment and is considered an
invasive species in several southern states. It produces a potent
insecticide which utilizes a tetranortriterpene neurotoxin known as
meliatoxin. This insecticide is found throughout the plant’s bark,
leaves, and flowers but is found in the highest concentrations in the
ripe fruit. If you suspect that your pet has consumed any of this
plant, contact your veterinarian immediately. The chinaberry tree, or
Melia azedarach, is a deciduous tree that produces a potent
insecticide which utilizes a neurotoxin that can prove detrimental to
your pet if ingested. Symptoms of Chinaberry Poisoning in Dogs
Symptoms of chinaberry tree poisoning occur most often from eating the
ripe fruit, however, the bark, leaves, and flowers also contain
smaller amounts of the toxic substances. Symptoms usually begin within
just two to four hours from ingestion. Abdominal pain Blood in stool
Colic Constipation Death Depression Diarrhea         Excessive
drooling Heart attack Hyperactivity Lack of coordination Loss of
appetite Muscle rigidity Seizures Slowed heart rate Stupor Vomiting
Weakness Types
The scientific name for the chinaberry tree is Melia
azedarach, and it belongs in the mahogany family.

From another source
http://www.sciencedirect.com/science/article/pii/0031942283830398

Toxic tetranortriterpenes of the fruit of Melia azedarach . .Peter >B.Oelrichs. Michael W.Hill. Peter J.Vallely. John K.MacLeod. .Tadeusz >F.Molinski
Show more https://doi.org/10.1016/0031-9422(83)83039-8Get rights and
content Abstract Four new tetranortriterpenes, meliatoxins A1, A2, B1
and B2 have been isolated and identified as toxic constituents of the
fruit of Melia azedarach L. var. australasica. Toxicity and
pathological results confirm that the meliatoxins are responsible for
most but not all of the symptoms resulting from the ingestion of whole
fruit.


Telomere and its effect on aging The cloned sheep, Dolly, was said to have died very soon because the cells used to create it were taken from an adult sheep with an aged telomere. Why doesn't this happen with humans? Why aren't we born with 25 years less lifespan?

Broadly speaking there are two classes of cell in an organism:

Somatic cells

These are by far the most numerous in your body, and are the differentiated cells including everything from retinal cells to liver cells to neurons.

Stem cells and germ cells

Stem cells reside in tissues and replenish the somatic cells as they are damaged or removed, or as the organ grows,
Germ cells - in particular oocytes in women's ovaries - are pools of immature eggs that are generated when a women is still a foetus in her own mothers womb!

The difference between these two types that relates to your question is that somatic cells have a limited replicative lifespan - a limit to the number of times they can divide - because their telomeres (caps to the ends of chromosomes) erode during cell division, whereas stem cells are able express the enzyme telomerase which extends the telomeres and allows cells limitless replicative potential (excluding other factors). Replenishing telomeres is a major step in cancer progression [1].

Embryonic cells have 'complete' telomeres when they are fertilised and begin to proliferate into a new organism. Interestingly the telomere length of the germ cells is not at all related to fertility [2], suggesting to me that telomerase is expressed for a while post-fertilisation, so the length prior to fertilisation is not important.

Dolly was produced by a process called Somatic Cell Nuclear Transferase, where the nucleus from a somatic cell from an adult organism is transplated into an embryo with its nucleus removed [3]. A study found that she had consistently shorter telomeres corresponding to the fact that the original donor was 6-years old already [4]

You might also be interested in my answers to these questions

Are human bodies programmed to die?
Cell proliferation limit and senescence of embryonic stem cells and fibroblasts
Do trees age on a microscopic level?
Difference In Telomeres Between A Thale Cress Plant And A Methuselah Tree

Shay, 2001, Human Molecular Genetics. Telomerase and cancer. http://hmg.oxfordjournals.org/content/10/7/677.full
Turner, 2013, Mol Hum reprod. Telomere lengths in human pronuclei, oocytes and spermatozoa. http://www.ncbi.nlm.nih.gov/pubmed/23519357
http://learn.genetics.utah.edu/content/cloning/whatiscloning/
Shiels, 1999. Cloning. Analysis of telomere length in Dolly, a sheep derived by nuclear transfer. http://www.ncbi.nlm.nih.gov/pubmed/16218837


Beetle (?) on Acacia (Senegalia) greggii? I was working on my botany skills and took a photo of Acacia (Senegalia) greggii.  When I reviewed the photos, I saw a beetle (I think it's a bettle) that I had not noticed in the field.  I'd say its body is about 2 cm long.  This plant was growing in a dry wash in Phoenix Arizona USA, and the flowers on the plant were just maturing.  Observed around 9 am and the temperature was about 75-80 F. What species is this insect?

Looks to me like the Longhorn beetle (Schizax senex), possibly a female, but it is hard to judge the length of the antennae. This beetle has long antennae (hence the longhorn name), with the male having antennae that are nearly twice as long as the female. S. senex is the only species of the genus.
They are hirsute with a pale margin to the wing cases. The species was described in 1873 by LeConte, with the description being rather wonderful (in my opinion):

Niger opacicus, pube breve minus subtili cinerea vestitus, prothorace fortus, elytrus subtilius punctatus, his marginae suturali laterali apicali et scutello fulvo-pubescentibus

My very rough translation - better Latin scholars please fix:

Black opaque, hair short with subtle grey arrangement, prothorax strong, wing cases with subtle dots, and the join margins and edges pointed and scutes fawn-coloured and very hairy.

Note that I found this with a very quick google of "beetles arizona" and scanning through the linked arizonensis beetles page, which was at the top of the links provided by google. I am not from the USA or in the USA, so please anyone with a better identification, feel free to chime in.


How many generations does it take for one species to become a new one? First lets consider that a species is a group of individuals that can reproduce by breeding fertile offsprings.

It's usually said that evolution takes a very long time. Lets say that 1000 generations are required for species A to evolve into species B.

Which species would generation 999 belong to, A or B ?
If A then it means that there was no evolution in 999 generations and that the entire evolution is going to happen in a single generation from 999 to 1000.
If B then which specie does generation 998 belong to ?
etc etc

In the end it seems to me that if there is evolution it can only be instantaneous, but that requires many improbable things, one of them being that the spermatozoids and ovules of species A contain DNA of species B !

How does that work ?

EDIT this is not a duplicate I'm not asking what a species is I'm asking what is the genetic process of evolution, how do we move up in the evolution tree.

Your question is like asking about the color spectrum. A wavelength of 530nm is green; a wavelength of 580nm is yellow. So let's say it takes 60nm of wavelength change to go from green to yellow. What color does a wavelength of 579nm have, green or yellow? If it's green, then does the color shift in a single nm difference of wavelengths? If it's yellow, what color is 578nm, etc?

The answer in this case is, 579nm is yellow; so is 578nm. 570nm is more ambiguous; some people might say it's yellow, others think it's greenish-yellow, in some contexts it might look clearly green. And so on along the spectrum; the reality is that there is no hard boundary between "green" and "yellow". There are colors that are clearly green, colors that are clearly yellow, and there is a difference between those two, but there are also plenty of intermediates that are a bit like green and a bit like yellow, and those intermediates are what you go through when you go from green to yellow. There is no definite point everybody can agree on where a single shift happens.

It is the same thing with species. A species is a group of organisms that interbreed to produce fertile offspring, but "interbreeding to produce fertile offspring" isn't a on/off thing. Organisms are more or less fertile. What if organisms from two groups interbreed and produce offspring, and only half of those offspring are fertile? Or they have half as many offspring as couples within the two groups have?

The reason species are an important concept, and can be distinguished visually as being like each other and unlike members of other species, is that within a species there is widespread sharing of genes over the generation, as individuals breed with each other, but they don't share genes with other species. Meaning species will evolve as a unit; changes that happen within a species will spread between individuals of that species, but won't spread outside of it.

But because sharing genes isn't an on/off thing, you could have 100% of genes being shared from one population to another (then they're clearly the same species), or 0% (then they're clearly not), or 90%, or 70%, or 10%... That's where you find the fuzzy boundaries. The races, strains, varieties, sub-species, all those different words to describe populations that are different but aren't outright different species. And the debates on whether different groups are different species or not in the first place, in the cases where it's really ambiguous.

And the same thing is true of evolutionary change in general. You don't have a mammalian carnivore that isn't a cat, and then bam! a cat. You have a mammalian carnivore that isn't a cat (or dog, or weasel... but kind of like any of those in various ways. Like generic carnivore-ish), then a mammalian carnivore that's a bit more like a cat or a dog (and another one next to it that's a bit more like a weasel), then a mammalian carnivore that's even more like a cat (and others that are even more like a dog, and even more like a weasel), then a mammalian carnivore that's clearly feline but isn't a cat, or a lion, or a tiger; it's a different species of feline that doesn't exist today, and also looks more generic-feline-ish than any modern feline. Then there's a feline that's more like a cat (and others around it that are more like a lion, and a tiger), but also clearly isn't a modern cat. Then there are felines that are really like cats but a bit different from modern ones and it's hard to tell, maybe we should extend the definition of "cat" to include them? And then bam! a cat. But that cat isn't clearly a Jungle Cat, or a European Wildcat, or a domestic cat, or any modern species; it's its own "archaic cat" species. And then there are cats that are more like Jungle cats, or more like domestic house cats...

Also don't confuse the creation of new species with evolutionary change in general. Over the long term they are related, because once two groups are different species then they will change through evolution in independent directions, and they will end up looking different from each other as well as from their common ancestor. But over the short term you can have speciation with very little morphological or genetic change (you just need two groups that used to interbreed, to no longer do so), or morphological/genetic change without speciation (if all the change happens within one group).

Both speciation and genetic/morphological change can happen within a single generation, but usually happen over much longer timescales. But there is no hard rule for how long that is; as far as speciation goes, if groups aren't prevented from interbreeding in some way then they will keep breeding with each other and can stay a single species indefinitely (whether individual from generation 10,000 could interbreed with individual from generation 1 is a different question, but it's not like it's a situation that happens). As far as evolutionary change goes, natural selection means species change to adapt to their environment. Once they're adapted to it, if it happens their environment never changes then natural selection will push them to stay the same as they are, again indefinitely. In the real world most environments change over time so organisms do change more often than not, but just to illustrate that the timelines are a product of circumstance, not an intrinsic feature of evolution itself.


Cloning two fluorescent proteins with different promoters in the same plasmid? I want to clone two fluorescent proteins both driven by different promoters in a plasmid to be used to transform B. subtilis at the amyE locus. For this I want to use plasmid pSG1729 (Lewis and Marston, 1999), because this plasmid can be used for homologous recombination at this specific locus.

Now the problem is, because of a few reasons (i.e., the locations of the restriction sites, keeping the spc resistance gene and deleting the current GFP gene), if I want to clone two genes into this plasmid, they will be very close to each other (~10bp). Will this be a problem either technically or biologically after transformation? I don't think that possible read-through will be bad, as I want one of the fluorescent proteins (pHluorin) to be continuously expressed. Maybe an option would be to clone the two genes in opposite directions?

This is the current genotype of the plasmid:

Ori amyE5' currentGFP Spc amyE3' bla

If you want to express them in an operon, make sure you have an RBS at the 5' end of each coding sequence. If you place one 10bp downstream without it having an RBS, it will be transcribed, but not translated... If you want more help, paste the DNA code of each as a comment.


Are abrasions considered closed wounds? A closed wound is one where skin is intact and underlying tissue is not exposed to the environment.

Abrasion is an erosion of skin usually due to sheering force. In most cases the dermis is intact and the injury is superficial limited to epidermis. Abrasions heal without scarring by epithelialization.

Are abrasions considered closed wounds? I would think they are open wounds as the underlying tissue (which would be dermis in this case) are exposed to the environment. Please state the reason why they are classified into whatever group.

The definition of closed and open wounds is variable. In histopathological terms (i.e. looking under a microscope) it is usually defined that a wound where the dermis is affected is open. In this case an abrasion is an open wound. This puts it in the same class as cuts (incisional/lacerations), tears and punctures. Closed wounds on the other hand are when the dermis isn't affected, such as in a haematoma (blood collection under the skin) or crush injury (extreme force typically for a long period of time) and contusions (i.e. bruises).

Medically they may be divided by management. Where open wounds are wounds which are likely to be contaminated and need thorough cleaning and may need antibiotic cover whereas closed wounds are ones that are very unlikely to be. In this case, abrasions may be considered a relatively closed wound as not all the protective layers of the skin have been breached (the dermis is not completely breached). Thus the physical barriers are relatively intact and continue to offer us defense against bacteria and organisms.


Is it possible to process electrical signals from the brain and interpret the results as exact thoughts? If the brain uses extremely low voltage signals to communicate (from what I understand around 100 mV), what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts? I know we interface with the brain's electrical field through already at a much higher level, but what is stopping us from being able to interpret it more precisely?

The brain activity is electric and chemical. The male adult human brain contains about 86 billion neurons (Azevedo et al). There is about 100 trillion connections between them. Solving a puzzle like that is not easy..

  what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts?

What you are referring to would be called solving the neural code in neuroscience. With today's methods, it is probably not possible.

Consider electroencephalography (EEG). It records the electrical activity of the brain. Ag/AgCl sensors are placed along the scalp (typically 64-256 in research settings). When about 50,000 parallel neurons fire simultaneously, a change in a recorded signal can be seen. While the time resolution is about 1 ms for EEG, the spatial resolution is several centimeters (it is not easy to find which areas produced the recorded signals; it is an inverse problem). A newer technique, called magnetoencephalography (MEG), is becoming more and more used but is expensive. It records the magnetic fields related to the electrical activity and allows better localization.

Is there other complications? Well... lot's of them. Blink your eyes during the recording and there will be a major artefact masking the brain signals in most channels (10-100x greater in amplitude than the brain signals).

Anyway, you would probably be interested in the new research involving the use of machine learning techniques: it has been possible to decode the contents of dreams, reconstruct what a subject is seeing, etc. The best papers have been published by Science, Nature, and PNAS, so using their search engines with the keywords decoding and brain should allow you to explore the topic easily.

PS. I did not have time discuss fMRI; someone else can may be do that..


Why warfarin is given as racemic mixture? Warfarin is administered as a racemic mixture of S- and R- warfarin.
S- warfarin is 3 to 5 times more potent than R- warfarin.

So, what's the logic behind giving a mixture of it? Isn't administration of only one form gives more predictable results?

In general, it's more difficult to produce a specific stereoisomer of a compound than it is to produce the racemate. Producing a pure S- or R- sample of a particular compound requires either enantioselective synthesis, or racemic synthesis followed by a purification step such as chiral chromatography. This tends to be expensive - especially for an older drug like warfarin where it would likely imply either chiral purification (throw away half your product) or redesigning the synthesis to be chiral.

For some drugs it makes sense to do this - some reasons might include adverse effects of the undesired stereoisomer, or taking a drug that's about to go off-patent and re-branding an enantiopure preparation for further patent protection. I think the latter is what happened with Citalopram -> Escitalopram (Lexapro) although this is speculation.

Most likely in the case of warfarin there is no strong argument for producing a pure enantiomer. It has been off-patent for a while, there likely aren't major adverse effects related to the less potent isomer, and most likely economics dictate that producing and selling the racemate is cheaper / more profitable than retooling to produce and sell an enantiopure version. That latter option would only make sense if they could sell the pure S-warfarin for enough to recoup the development / purification costs, and this is unlikely for a drug with such a long history of use in its racemic form.


Does a higher body temperature slow the corona virus down? The corona virus appearantly does not like high temperature:
High Temperature and High Humidity Reduce the Transmission of COVID-19
Also it seems that higher body temperatures helps the immune system to work better: Elevated body temperature helps certain types of immune cells to work better, evidence suggests

Should therefore someone who suspect they may have the corona virus or possibly another cold virus and do not experience fever try to elevate their body temperature slightly (say 0.5-1 degrees celsius) by dressing extra warm?

This is postulated here.

Does this sound plausible to you?

SARS-CoV-2 is believed to have spilled over into humans from a Rhinopholus (horseshoe bat) reservoir. During flight, bats' body temperature is maintained at levels associated with fever in other mammals. Rhinolophus bats are reported to reach skin temperatures of 41 C during flight. (From this review which describes why bats might be special sources for zoonotic viruses)
So, this virus is likely adapted to survive higher temperatures than a human host.


Can all biological processes be understood as computations and studied as such? Can we understand a cell as an organic computational device? In that case the whole organism can be considered an ensemble of a large number of interacting computational devices?

If this is the case, biology can be studied using methods of graph theory, network theory, computation theory and complex systems theory.

If you abstract enough, anything cam be considered as a computational device. The issue with doing this with cells is the sheer number of variables.

For any given cell, the following internal variables exist:

Internal ion concentrations for dozens of ions of importance importance
Internal concentrations of hundreds or thousands of various simple organic molecules, including "raw" internalised molecules, various steps in dozens or even hundreds of metabolic processes, and metabolic end-products and by-products.
Internal concentrations of hundreds or thousands of different proteins and other complex biological "mechanical parts", as well as the states of these "parts".
The physical state of the cell - stretched, contracted, relaxed, hot, cold, etc.

This list is not exhaustive.

It's also worth noting that the above variables may also exist for multiple separate "compartments" within the cell; vesicles, the endoplasmic reticulum and the golgi apparatus being three which come to mind immediately.

The other issue is that cells do not exist in a vacuum; the external environment plays an important role in their functioning. The human body is at any one moment existing in direct contact and interaction with the following extracellular environments:

The atmosphere (Mainly, but not only, temperature exchange)
The air within the respiratory system, including nose and mouth
Stomach contents
Small intestine contents (which would need to be considered in several segements, since the nature of the interaction changes along the path of the small intestine.
Large intestine contents
Blood
Cerebrospinal fluid (Fluid found "inside" the brain)
Extracellular fluid, or "tissue fluid" (A separate compartment for each small swatch of tissue in the body)
Lymph
Pleural fluid (Fluid surrounding the lungs; a separate compartment for each lung)
Pericardial fluid (A small amount of fluid surrounding the heart)
Joint capsule contents (A separate compartment for each joint)

...and the list goes on. Each of these compartments requires tracking of the same variables as individual cells.

This is yet further complicated by the fact that some of these compartments can't easily be considered as one big compartment, because of the importance of spatial relations. For example, the oxygen and carbon dioxide concentrations of blood (as well as the concentrations of other substances like alcohol) change centimeter-to-centimeter. Yet another issue is the fact that cells are not static in terms of their relations to each other; red blood cells move with blood flow, and experience turbulence and other effects, and other cells (like macrophages) are capable of "deliberate" movement in the blood and in tissue.

You would also have to account for physical disturbances - things like a stab wound or even a pinprick are ludicrously complex at a cellular level.

Of course, human beings are very complex organisms, and there exist much simpler organisms. You might be interested in OpenWorm, which is an attempt to computationally simulate Caenorhabditis elegans, a species of roundworm, at a cellular level. Doing so even for an organism as simple as C. elegans is a massive undertaking, as evidenced by the fact that even with the contributions of dozens of experts in their fields the project has been ongoing for some time and is yet to reach stage one.

The short version: Is it possible? Perhaps. Is it easy? Definitely not.


What would cause proteins to get stuck in the stacking layer of a SDS-Page gel Typically when proteins aggregate, they will get stuck at the top of the well. However, we're seeing some protein aggregate in the stacking layer even when we're treating the loading volume with DTT.

One peculiar attribute of this experiment is that we're trying to carry out a Cu(I) catalyzed Azide-Alkyne Click rxn. Without the Cu(I), the proteins run normally. However, after Click rxn, we do see some of our expected clicked product, one of our proteins is disappearing into the top band. Hypothesis is that either the copper(I) is changing the migration or oxidative damage from the Cu(I)-> Cu(II) transition is altering the protein.

Returning to the original question, what would cause a protein to stop at the stacking layer vs. at the combs?

[edit]
According to my labmate who was having this problem, the protein was crosslinking with itself to create fairly sizeable polymers. We also saw ladders of the protein with ascending size. Spinning the clicked reaction removed the issue but also resulted at a lost of the protein. It sounds like he wasn't treating with a sufficient amount of DTT to break up the mixture.

This unfortunately still doesn't differentiate between proteins stuck at the combs vs stuck at the stacking layer.

At the interface of the stack gel and resolving gel is a pH change and a change in gel density.  If you feel certain that your protein is not crosslinking so much that it can not enter the gel than I would think about the pH of the sample and the effect of Cu ions on the stacking effect of the stacingk gel.  Is your sample the normal blue color (indication of pH) when you load it (compared to other samples you load)?  Are you overloading the gel?  I have seen overloading cause the effect you describe because the proteins get concentrated to a very high degree before entering the resolving gel.  Could the Cu ions be affecting stacking itself?

Read http://en.wikipedia.org/wiki/SDS-PAGE.  Specifically the section on buffer systems.  You might want to try a different buffer system.

Finally, you could try an acetone precipitation to try to remove the Cu ions and other chemical and see if that helps.


Definition of "essentially diploid" While researching the F12 cell culture medium (Ham, 1965), I came across the term "essentially diploid Chinese hamster ovary cells". The terms "subdiploid" and "near diploid" were also used to refer to the same cells.

Attempts at searching Google Scholar and regular Google failed to turn up a definition of the phrase.

What exactly is meant by "essentially diploid", and how is it different from regular diploid cells?

I think that the rest of the paragraph that you left out of your quotation helps to clarify. The CHO have 21 chromosomes, while the somatic lung cells have 23.

Neither case is exact for Chinese Hamsters, 2n = 22. So they have almost the complement of chromosomes that a diploid Chinese hamster somatic cell would have but they are missing one or have one extra. For the most part they will behave like normal somatic cells in culture, but it is an important fact to note as you can have cases where dosage dependence of a missing chromosome in a pair or an additional chromosome (trisomy) can affect the outcomes of research.

In the back of your mind you always need to be thinking how does the missing/extra chromosome affect the data I am collecting.

This Nature article may also be of interest.


A request for an overview of the cranial nerves Is there any resource that contains motor and sensory innervations, or pathways of all the twelve cranial nerves (i.e., cranial nerve I to XII)?

I have found this book chapter on the cranial nerves, but it is too broad for me -  I'm still at high school.

I am not entirely sure what you are after, but I (as have others that commented on this question) interpret your question as "The linked chapter contains too much technical information". Quite frankly, after scanning the book chapter, I have to agree with you. Therefore I have sought for a quick overview image of all the cranial nerves including their sensory and motor targets.

Encyclopedia Britannica has published all the cranial nerves and their sensory and motor innervations in a single comprehensive figure:

Cranial Nerves and their targets. Source: Encyclopedia Britannica

I can highly recommend this online encyclopedia. Their articles are more concise and better accessible than similar topics on wikipedia. Moreover, this encyclopedia is not freely editable by everyone on the planet, and everything I have seen so far on their website is credible.


How are two species with similar phenotypes identified as different? How are two species with similar phenotypes identified as different? Have two different individuals  that were thought to be different species ever been determined  to be from the same species ( or one a subspecies of the other's species ) ?

Species are difficult to define. This is because they form over a gradual continuous spectrum via evolution, one species does not suddenly become two, but lineages diverge (perhaps because there is some kind of barrier - like a mountain range - in the way) eventually reaching a point where we class them as separate species. How we define species is debated but the most generally accepted definition is the Biological Species Concept (BSC). Roughly the BSC defines a species as "a group of individuals that do, or could, successfully breed." Other species concepts do exist, some have their merits, but the BSC is most widely accepted and normally taken with a pinch of salt - it's not always possible to perfectly define a species because evolution and speciation are ongoing processes. Therefore, according to the BSC, two groups can be called different species even if the individuals look identical as long as there is true reproductive isolation.

Reproductive isolation can occur because of physical barriers such as rivers, oceans, mountains, environmental change. This is the cause of allopatric speciation. One species could become split when a subpopulation forms on an island (e.g. if humans take them to an island). If enough time passes without migration they will become reproductively incompatible. Another mechanism is sympatric speciation, when two species form without geographic isolation. This could be by the evolution of new behavioural, morphological or physiological forms which create division within the initial meta-population in to distinct sub-populations which over time become more reproductively isolated. Traits related to reproduction are amongst the fastest evolving and can quickly reinforce speciation (e.g. sperm morphology is extremely varied between species, see Sperm Biology: An evolutionary perspective, chapter 3).

The higher up the tree of biological classification you go the easier it becomes to classify things in to distinct groups, e.g. An oak tree is clearly a plant, and a whale is clearly and animal; further towards species definitions a whale is a mammal and a sparrow is a bird and both are animals; and perhaps less clearly, carrion crows and hooded crows are two different bird species in the Corvus genus. (Formerly these two were considered the same species!)

Obviously problems begin to occur when we consider species that reproduce through means other than sexual reproduction - e.g. bacteria which clonally reproduce. Traditionally this has been done by phenotypic information. We are now in the genomics era which opens new possibilities. This article discusses modern techniques by which utilise genetic similarity & difference between cells to define species and they suggest it to be a good method. However, this article seems to suggest that genomic methods need some refining first before we start classifying species with them.

  Currently, it appears more pragmatic and efficient to preserve the current species definition than to replace it, because it is serviceable as a first level of screening and current phylogenetic knowledge is too limited for a universal and sound change in the definition.

As for whether two species have been reclassified in to one I know there are examples but Google is not throwing up anything and there's nothing I can remember off of the top of my head - if I remember correctly the male and female mallard were once considered separate species because they look so different but I can't find anything to back this up. Species formerly described as one have been split in to two as well - gorilla's are one such example.


Can butterflies still fly after their wings are touched? When I was a kid, I was told not to ever touch a butterflies wing, as it would lose its ability to fly. This was because of some dust which was supposed to be in place on the wings and when disturbed it had the described consequences. I doubt at least the story about the dust, which sounds a bit too much like "fairy dust", but am I right?

What damage will be done by touching a butterfly?

Both the Forewing as well as the Hindwing of Butterflies are made of thin chitin structures which are pretty thin and sensitive. If you touch the wing with to much force, it may break.

Then the upper side of the butterfly wing is covered with small scales - what you called the "dust". This can be seen in this figure (from here):

and also in this electron microscopy image (from the Wikipedia):

The scales have a number of functions, they are responsible for the butterflies color and pattern (which are important for finding mating partners as well as for camouflage) and they also seem to play a role in insulation and thermo regulation (see here for more details).

The scales play also a role in making the wings stronger and help improving the flight characteristics. When flying upwards the get pressed to the wing and act aerodynamically, what the wings are in downward motion, they help stabilizing the flight. See here for more details: "Butterfly wing scales : pigmentation and structural properties".

Some of the scales get lost during flying and collecting nectar, so taken together, loss of a big number of them will influence the flight characteristics of a butterfly. However, I think it is much more likely that such a rude treatment will damage the wings, which is obviously more harmful. So light touches will not do harm, more severe will.


What happens to a virus SARS-CoV-2 on an object? Many articles say that "the coronavirus" — they probably speak of the SARS-CoV-2 — can "remain alive" for so many hours on some surfaces, so many days on some other surfaces. For example, "the virus lives 5 days on glass".

I think that this is a bad choice of word. All these articles speak about the virus SARS-CoV-2 as if it were a living being. But I think it is not a living being. The virus SARS-CoV-2 does not "live" on a glass surface. It just is there.

When a virus SARS-CoV-2 is on an object, what happens to it? If it is not there anymore after 5 days, why? What does time do to a virus?

Those articles simply refer to the viability of the virus, i.e. whether it can still infect a host thereafter. (Sometimes this is referred to as "survival" of the virus.)
A unviable virion is not quite the same as it being "not there" at all, although it is so from the perspective of a host that doesn't get infected.
Those viability [in the environment] studies use a quantitative measure of how much of the virus (i.e. how many virions) are still viable after some time on some surface (or even in "the air"), e.g.

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. [...]
SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces [...], although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel).

So they are measuring the time to some [chosen] statistical threshold of viability. For reference as to their particular method:

The TCID50 (Median Tissue Culture Infectious Dose) is one of the methods used when verifying viral titer.
TCID50 signifies the concentration at which 50% of the cells are infected when a test tube or well plate upon which cells have been cultured is inoculated with a diluted solution of viral fluid.

Which part of the virus machinery breaks first might depend on the environment. On copper, for example, it has been found that for "common cold" coronaviruses (e.g. HuCoV-229E):

Exposure to copper destroyed the viral genomes and irreversibly affected virus morphology, including disintegration of envelope and dispersal of surface spikes. Cu(I) and Cu(II) moieties were responsible for the inactivation, which was enhanced by reactive oxygen species generation on alloy surfaces, resulting in even faster inactivation than was seen with nonenveloped viruses on copper.
[...]
Coronavirus was exposed to metal surfaces and recovered, and the positive-stranded viral RNA genome was extracted and purified. A one-step reverse transcriptase real-time quantitative PCR (RTqPCR) was performed to detect a 139-bp region of ORF1 within nonstructural protein 4 (nsp4). Virus that had been exposed to copper and brass surfaces demonstrated reduced copy numbers of this fragment with increasing contact times. [...] . Comparison of the entire viral genome by agarose gel electrophoresis confirmed that nonspecific fragmentation occurred on copper and brass, with fragments becoming smaller with increasing contact time.

See also related q here on virus survival in small droplets, where a different inactivation mechanism is suspected.
In general, all viruses start to degrade outside their hosts at temperatures above -20C, even in the absence of some more specific environmental stressors (like unfavorable humidity, reactive surfaces like Cu, etc.) In suitable hosts, this temperature-based degradation is more than offset by the virus' multiplication.


Why E.Coli get bigger if they replicate faster? When E. Coli divide faster, they tend to have larger volumes. If the same cells are grown in a poorer medium, they'll have longer replication cycles and shrink. What is the explanation of this phenomenon?

Refs.

http://book.bionumbers.org/how-many-ribosomes-are-in-a-cell/
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0023126

Rapidly dividing bacteria contain more than one bacterial chromosome, and often more than two. The chromosomes take large amount of space in the cytoplasm and also attach to the cytoplasmic membrane. More chromosomal DNA requires larger cytoplasmic surface area; larger surface, larger volume.


What's the explanation for those shivers/shudders that happen at random times? They happen at any time, presenting as a sudden urge to shiver/shudder all at once. It originates in the neck and shoulders, feels like instant gooosebumps then out of total reflex shoulders roll back and neck cringes. Happens every couple of months and comes out of nowhere, then gone without a trace.

I have read about myoclonic jerks but this doesn't sound the same.

Where do these impulses come from and what's the physiological explanation?

It is just like a muscle spasm but generated from your nervous system. If the problem persist you are lacking in a certain vitamin that your body needs to function correctly.


Are there humans which the brain sends signals to the limbs faster than the average? I have done some researches on the time taken by the brain to send signals, but I didn't find whether that time is the same amongst all humans or there are some differences, and I have based my question on an article which mentioned that Messi(one of the best players in soccer history)'s brain send signals to the limbs faster than the normal human (https://www.ncbi.nlm.nih.gov/pubmed/27010676), so is this possible to happen.

Assuming that the time it takes for a signal to travel from the brain to the limbs follows a normal distribution (which is reasonable), then certainly there are people who fall at the upper and lower ends of the distribution. In fact, it's relatively improbable that someone would fall right at the mean.

Consider the normal distribution below. If the mean for all humans is at the center of the distribution, then almost all fall above or below that mean. Whether Messi falls in the lower tail is a separate question.


Is designing alien life still just science fiction? As we continue to search for life in very different environments than the earth, it would make sense to me to think about and design lifeforms (theoretical) that could work in these environments. I know that we are searching for life in extreme environments, but are we thinking about lifeforms that could have evolved in such environments? (Even if we dont find any)

The idea of the atom comes from ancient greek philosophers long before one could find any evidence for it. Although their views on what atoms look like and how they behave were incorrect, one could later refine this model through evidence and experimentation.

I think some good thought could makes us learn what to look for in the first place.

Is this still just a field that science fiction thinks about, or are there any serious publications on this topic? If not, why not?

Clarification: I mean the theoretical design of lifeforms. Not just manipulating and editing existing lifeforms, I mean designing completely new theoreticaly plausible lifeforms, within the constraints of a given environment. On paper or simulation etc, not actually making them physically.

If you find any scientific papers on how and what kind of life could exist for example on Titan, Europa, below Earths crust etc... or any other environment, please link to them in your answer. Thanks!

The answer to this question can go as far as anybody's imaginations. So I'll just tell why the answer is what it is, and try to include scientific facts (possibly with references) wherever possible.

Simple Answer: Designing alien life forms on the basis of current theoretical and practical knowledge of science (if this is what you mean) is still, and seems to remain, a field of science fiction only.

Why? Because, simply, the proposed organisms can be as many as you can count. The point is that, even if this field comes under the category of science, it will remain as large as the universe itself, because there are literally no boundations and limitations to speculation and imagination. Only recently have researchers agreed that discovering organisms similar to humans is much much less than any layman thinks. Actually, there is even a formula for it, known as the Drake equation after Frank Drake who proposed it. The equation is:

$N = R^* \times f_p \times n_e \times f_l \times f_i \times f_c \times L$

where:

$R^* =$ the average rate of star formation in our galaxy
$f_p =$ the fraction of formed stars that have planets
$n_e =$ the average number of planets per star that can potentially support life
$f_l =$ the fraction of those planets, fl, that actually develop life
$f_i =$ the fraction of planets bearing life on which intelligent, civilized life has developed
$f_c =$ the fraction of these civilizations that have developed communications i.e. technologies that release detectable signs into space
$L =$ the length of time over which such civilizations release detectable signals

Obviously, this answer comes out to be very small, meaning that intelligent life is very difficult to find. But that doesn't mean finding life is difficult. And this claim gets even more support when scientists find water on mars and even mercury! Now, to give a bit of knowledge, this field is not really limitless; there are (at least) two limits (i.e. I'm not including more). The first limit is source of liquid water$^*$. Now, knowing that water is easy to be found almost anywhere, this does not seem quite a difficult one. Another one is source of energy. Now this is a difficult one. The problem with discovering life (in near future at least) is the area in which we are searching. Most of the searches (by telescopes of course) are being conducted near red dwarf stars. There are quite some reasons for it:

red dwarf stars are quite stable
they have very long life
they are pretty less shiny (making observations easier)
they may be home for many super-Earths

But being less shiny also poses a problem: too less energy for life. Red dwarf stars emit most of their radiation in the infrared portion of spectrum, which is pretty useless for plants (on Earth at least). Now, to survive in a red dwarf system, plants need to capture infrared light. Thus, the speculated plants in red dwarf systems will be pitch black just to absorb more energy. Also, red dwarf stars are pretty lightweight, as less as 7.5% of sun. This means they have less gravitational pull i.e. they will have much lighter planets in their Goldilocks zone. Now, much lighter planets means much less gravity on planet's surface. Thus, the speculated plants in red dwarf systems will be a lot higher than plants on Earth. But, less gravity also means much less density of air even on surface. Now, you can interpret it yourself. And, not just to surprise you, there would be absolutely no surprise if in future a satellite discovers silicon-based life, because it is really possible for life to emerge from silicon instead of carbon!

$^*$why I am continuously saying liquid water has a reason. Water is actually one of the very few candidates that can serve the purpose of maintaining life forms. Its one of a handful of liquids which are liquids at desired temperature. As one might think, life cannot survive below a certain temperature, simply because below that temperature, the liquid itself would absorb all the metabolic heat from organism and evaporate. So, it is quite relevant to say liquid water here.

What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe. So, this does not really count as science. After all, if you search science definition on Google, you get this:

  the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.

This does not include imagining alien life forms in any way. So, I do not think this subject would ever be considered as scientific by the scientific community. Mostly, scientists are not indulged in this kind of work because they like to observe and interpret natural phenomena rather than imagining them. Scientists make laws from nature rather than applying laws on nature. Still, there are some scientists who take this matter seriously and publish scientific papers about it. I could find only one (PDF) related to this point. You might get some more on the internet.

In the end, if you think about how plants would look on a planet in a red dwarf system, you might end up with this:

Bonus: Dawn space probe from NASA has detected organic materials on Ceres(!) Now, what kind of organisms would you expect to see there based on our current knowledge about Ceres?


Why does a distraction cause a longer reaction time? Does it have something to do do with the fact that the individual isn't concentrating on reacting to the stimulus, so it takes longer for it to be processed? How can this be out in terms of neurones and neurological pathways? what is happening for there to be a delayed reaction time?

I am not sure which sort of answer is expected. The minimal answer to that would be that the more distracted you are the longer it needs to sample the stimulus space of interest as you are sampling another distracting stimulus simultaneously with your limited sensory capabilities.

Cognitive tasks get just more complex with distraction as the brain cannot know which features (of the full stimulus space from all the sensory modalities) to take into account and therefore needs to sample more data to find out which of the inputs matter for the specific task.  In most of natural situations the inputs match together in terms of experienced stimulus combinations (visual field and sound while walking for example) except for surprising situations that require to alter ones attention (a sound that does not match to the visual scenery is unexpected and might be important to check for danger). To decide whether the system can ignore such parts of the input requires computation and computation takes time. I don't think it is useful to tackle the question in terms of delayed signaling along specific neurons or pathways. The signaling itself is more or less of constant speed and not directly altered by distraction. Of course on a very basic level an increased adrenaline level or similar due to distraction might affect the "weights" of certain basic pathways as one is pushed into another state. In such cases therefore it requires the system to compensate those changes with respect to the actual task of interest as it might be biased to different reaction scheme that is not useful for the specific task.

Actually our brains are very good in focusing on specific parts of the inputs that are important for a task (i.e. cocktail party problem) but still it needs more time to correct the erroneous parts in the presence of distraction. In terms of a simple Hopfield network that does pattern completion distraction would be like an increase of the noise level which leads to a higher number of iterations required for convergence while the speed of signal transmission from neuron to neuron was not altered.


How did mosquitoes expand their habitations to a place they never lived before? So, in the region I live, we have some sort of like a "mosquito zone", spanning for thousands of Kilometres, this is the place where you will normally find lots of mosquitoes, and this has been so for years and years. But last year, we were surprised to see that the mosquitoes have "invaded"a village which has never experienced them even once. The village though, is at the border with what I call "mosquito zone" but never has these insects "visited" this village. So I became curious to know, what has happened so that the mosquitoes said "now let's invade this village and live there"? I can't see anything suspicious that has changed. Do we have any explanations?

It could be a number of things. Mosquitos need standing water. Look for that. Any changes? Was last year particularly rainy?  One group of mosquitos lays its eggs at the waters edge. They lie dormant until the water reaches them again. If the water was high when the eggs were laid, then recedes, it may be years before the water reaches them again and the eggs hatch, resulting in a bloom of high numbers. Also, other mosquitos breed in containers. Things like tires, or coffee cans, or flower pots in cemeteries. Even a small amount of stagnant water in a container can result in mosquitos. Any changes there? The obvious change is the warming climate, but I would look first to changes in the water.


Has any research lab done serious work to engineer new bacteria which assemble graphene wafers? I was thinking about crazy uses for engineered bacteria. Nano-assembly of Graphene seems like a potentially excellent target for the technology. Have any research/full-blown labs worked on this? Any papers on it?
What would be some of the difficulties?

Surprisingly, the answer is yes. In 2012 Tanizawa et al published a paper titled Microorganism mediated synthesis of reduced graphene oxide films. The gist of it is that most of the steps (including the structuring of the graphene sheet) were carried out with chemical synthesis, but a final reduction step from graphene oxide to graphene was carried out using bacteria from a local river.

Probably not quite what you were thinking of, but I imagine this is the closest you'll get for right now.


Why does crying lead to a running nose and reddened nose tip? Why do we have a running nose for quite some time after crying? It persists even after we stop crying. Why is it so? I have faced this always. Also, why does our nose redden on crying for long?

When you cry, you produce tears, which come out of your tear ducts. These are not only open to the eyes but also have a connection to your nose, see the image below:

A part of your tears runs through this connection and mixes with the mucus which is present in your nasal system making it thinner and allow it to flow more easily. If the tear flow is prolonged, the nose will produce more mucus and make your nose running for a longer time. The nose appears redder because the blood flow is increased. This is partly due to the production of more mucus and also because you repeatedly touch the nose when using a handkerchief.


How to detect Single Nucleotide Variants (SNVs)? This image is obtained from this paper.

The description of this image is as follows:-
DNA-sequence reads from a tumor sample are aligned to a reference genome
(shown in gray). Single-nucleotide differences between reads and the reference genome indicate germline single-nucleotide variants (SNVs; green
circles), somatic SNVs (red circles), or sequencing errors (black diamonds).
(a)
In a pure tumor sample, a location containing mismatches or single
nucleotide substitutions in approximately half of the reads covering the location indicates a heterozygous germline SNV or a heterozygous somatic
SNV - assuming that there is no copy number aberration at the locus. Algorithms for detecting SNVs distinguish true SNVs from sequencing errors by
requiring multiple reads with the same single-letter substitution to be aligned at the position (gray boxes).
(b)
As tumor purity decreases, the fraction
of reads containing somatic mutations decreases: cancerous and normal cells, and the reads originating from each, are shown in blue and orange,
respectively. The number of reads reporting a somatic mutation decrease
s with tumor purity, diminishing the s
ignal to distinguish true somatic
mutations from sequencing errors. In this example, only one heterozy
gous somatic SNV and one hetererozygous germline SNV are detected
(gray boxes) as the mutation in the middle set of aligned r
eads is not distinguishable from sequencing errors.

This is my understanding below. Am I correct?

There are multiple reads that are aligned such that for a given location in the reference genome,(here fourth), if approximately half or more of the reads covering that location has a single nucleotide mismatch with the reference genome,then it is a heterozygous SNV.
Eg:-

Your link doesn't link to the paper, and you seem to be ignoring half of what the image is trying to get across.

The point is that since tumors are heterogenous, you very well might have only 40% of the cells heterozygous for a particular SNV, which means it would only be observable in 20% of the reads.  But if multiple reads with different start sites show the same SNV, it's likely to be real.  If coverage is so low that you only get one read showing a real SNV, you won't be able to distinguish it from noise.


How does better sperm result in more viable offspring? Quoting wikipedia:

  Greater choice and variety of mates increases a female's chance to produce more viable offspring.

This led me to the question: "How sperm parameters are connected with entity parameters?"

Actually, sperm parameters are usually: motility and morphology. I am speaking about a single sperm, therefore any parameters involving their count or parameters of semen are not included.

On the other hand, what helps a particular entity to survive is determined by many parameters. Some of them are: speed, endurance, strength, agility, stealthiness and savvy. It is hard to find out how strength of being is connected with motility or morphology of sperm it has been conceived. And even less obvious is the connection of stealthiness with such sperm parameters.

But since sperm competition exist, it helps in natural selection, therefore there must be a connection. But how does it really work? How are stronger/faster/stealthier/etc. entities are the product of more motile or better in morphology sperm?

After some thinking about it I think that if there is some correlation between sperm parameters and genome, it can answer the question. E.g. presence of gene that increases fitness of organism makes sperm faster.

Greater choice and variety of mates increases a female's chance to produce more viable offspring.

The claim is a little hard to address because it is vague. However, one can give a simple example to give you a feeling of why this could be the case.

This example is based on Zaahavi handicap principle. Spermatozoids aren't free to produce. A male that can produce more and stronger spermatozoids can do so because he is a healthy males. As many of the traits that determine health, in a general sense are heritable, healthier males tend to have healthier offspring.

  On the other hand, what helps a particular entity to survive is determined by many parameters. Some of them are: speed, endurance, strength, agility, stealthiness and savvy.

You are mainly listing traits that are very specific to human's sport ability. In reality, there are loads of other traits that are much more fundamental such as the efficiency of the potassium pump or of the mechanism to produce ATP.

  [..] it helps in natural selection [..]

I don't understand what you mean by this sentence.


Can Nanodiscs be used to study membrane energetics? Nanodiscs have changed they way we can study the structures, insertion, and functions of transmembrane proteins. Below is an image of a nanodisc bilayer.

The key difference, as far as I can tell, over traditional liposome studies are that one can alter the lipid composition more easily.

Have any studies been achieved on quantifying energetics in these nanodiscs ie energy transfer upon insertion, or stability of the protein in the nanodisc etc?

Nanodiscs are very powerful technology for membrane protein invented in Stephen Sligar's lab at the University of Illinois.
A nanodisc is composed of a membrane protein, lipids and two monomers of a "scaffold protein". The most used scaffold protein is an N-terminal truncation of apolipoprotein A-1 (apoA-1), which is the primary protein component of high-density lipoprotein (HDL) particles. But because the size of the scaffold protein defines the size of the nanodisc, membrane proteins with different size could require different type of scaffold protein.

The reconstitution of a membrane protein into a lipid disc is a self assembled process. The reaction consists in mixing the membrane protein solubilised in detergent with lipids (that can be chosen according to the protein) and the scaffold protein. Removal of the detergent (using for example Bio-Beads™ SM-2 Resin) starts the self assembled process and the nanodiscs are created.

Nanodiscs provide an environment where membrane proteins are stable and compatible with aqueous environments in a native-like phospholipid bilayer. The aquesous environment makes membrane proteins compatible with analytical methods that have primarily been limited to investigating soluble proteins. The lipidic environment, that can be chosen and optimised, keeps the membrane protein stable, monodisperse and active. The stoichiometry of the protein can also be controlled.
Compared to nanodiscs, liposome are large, unstable and difficult to prepare with precisely controlled size and stoichiometry.

Several membrane proteins have now been reconstitued into nanodiscs and used for different type of studies, for example for studying ligand affinities  and kinetics, for NMR, for studying protein association state, signalling properties, and ion channels (http://molsense.com/applications/trubind-at-work/ion-channel-inhibitors/).

http://www.sciencedirect.com/science/article/pii/S0014579309007960


0.1 M sodium citrate in 10% ethanol and DNA solubility I understand how DNA precipitation works in the presence of salt (such as 0.3 M sodium acetate or 0.2 M sodium chloride) and alcohol (30 ~ 50 % isopropanol or 60 ~ 75% ethanol)

However, in the Trizol kit manual, DNA could be washed and precipitated in 0.1 M sodium citrate in 10% ethanol

At only 10% ethanol and 0.1 M sodium ion, how can DNA be in a "compact/insoluble" form so it can be precipitated by a low speed centrifugation (2000 x g for 5 mins)?

The sodium ions will bind to and neutralize the (-) charge on the phospho backbone of DNA. This reduces hydrogen bonding sites for water, which then results in less solubility.

Edited for clarity and because I didn't answer the question the first time. Sorry about that.

The extraction of DNA is from the interphase layer, which is a very small fraction of the original sample. The extraction of the interphase layer is then mixed with 100% EtOH (300 ul per 1.0 Trizol used in that sample). This should actually be 60% or more EtOH based on my experience using this method.

That is the precipitation step.

The fact that the wash has only 10% EtOH and 0.1M sodium citrate and that is still sufficient to keep DNA precipitated revolves around 0.1M sodium citrate is usually 0.3M sodium ions (sodium citrate can be mono-, di- or tri-sodium, but unless specified..sodium citrate implies tri-). Remember for the wash, you don't need to do a quick precipitation, you just need to prevent it from solubilizing again.

I am removing my comments that contained the same information.


Identification of a small flat bug So for the last few days I have been noticing these small bugs in my bathroom -- they don't appear frequently, and I see them once or twice a month.
The characteristics and behavior I observed are as follows :

They RARELY move around.
They are extremely flat, like totally flat
Some are small, some are big (but still the overall size is small)

Below are the pictures :

I cropped this picture since the original size was 5mbs and the limit was only 2. If anyone wants the original image I can inbox them .

Appreciate any help or suggestion with this :)

EDIT 2
I am adding another image for greater clarity , hope this helps

Edit 3

Location: Karachi Pakistan.

Size: 0.2-0.4 cm

As for nearby animal populations: No not much, just the usual street cats.

For a few months these bugs were gone until recently they have started to appear in the bathroom, like I see them 2-3x a month just sitting still for hours and hours.

Definitely an arachnid and mite (subclass Acari), and very likely a member of the order Parasitiformes, of which there are more than 100,000 species!!

Your specimen brings to mind the family Argasidae (the "soft ticks" -- so called because they lack a hard scutum).

Specifically, your specimen reminds me of Argas reflexus, the pigeon tick. (which has been found to be an increasing pest and human concern in urban settings).

 Credit: Milan Kudlička

Based on the size of your specimen, I would guess you're looking at a non-adult stage.

However, this is just a guess, and I will try to explore other species in this general group to see if I can come up with a better-supported guess.

(By the way: any pigeons living nearby??)