You could place part of the mould into a cut in a piece of citrus fruit to continue its growth. Citrus can also host P. italicum, the below website is one mentioning how to differentiate between them.
http://www.pestnet.org/fact_sheets/citrus_storage_moulds_197.html
Hazards.
Aspergillosis: (fungal spores growing in the lungs) which is uncommon.
Asthma: penicillium spores have been associated with increased chance of onset of asthma, and problems with breathing in people with asthma.
There may be other hazards.
I just cite one paper below, but a search using terms of penicillium and asthma shows lots more.
"Household airborne Penicillium associated with peak expiratory flow variability in asthmatic children"
published in :
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
by:
Kemp W. Bundy, MD, MBA, Janneane F. Gent, PhD, [...], and Brian P. Leaderer, PhD
doi: 10.1016/S1081-1206(10)60139-1


I'm assuming you mean the distinct architecture and regular hexagonal shapes in bee honeycombs?

In fact, Charles Darwin spent a good bit of time with honeycombs.

First of all bees and wasps have a common progenitor and wasps also build combs and nests, albeit of paper/celluose as opposed to wax.  He was interested in how the perfect hexagonal lattice formed in the wax.

  Darwin tried three different experiments with bees’ cells at Down that he reported in Origin. In one, he put a thick block of wax into the hive. ‘The bees instantly began to excavate minute circular pits in it: and as they deepened these little pits, they made them wider and wider until they were converted into shallow basins, appearing to the eye perfectly true or parts of a sphere, and of about the diameter of a cell. It was most interesting to me to observe that wherever several bees had begun to excavate these basins near together, they had begun their work at such a distance from each other, that by the time the basins had acquired the above stated width (i.e. about the width of an ordinary cell), and were in depth about one sixth of the diameter of the sphere of which they formed a part, the rims of the basins intersected or broke into each other. As soon as this occurred, the bees ceased to excavate, and began to build up flat walls of wax on the lines of intersection between the basins, so that each hexagonal prism was built upon the festooned edge of a smooth basin, instead of on the straight edges of a three-sided pyramid as in the case of ordinary cells.’ (Origin, p. 223.) The cells were built up in a hexagonal shape when their bases intersected with those of other cells; but the pyramidal bases were apparently not built, since there was no pressure to accommodate cells on the other side of the wax, which was a thick block.

This seems to have a built in burrowing behavior in how the lattice forms that eventually turns into hexagonal shapes.

BTW this topic is very similar to the evolution of spider webs, which is also fascinating.


CRISPR/Cas9: What are the main differences between sgRNA and the Cr:TracrRNA ?

You are correct about the components of the sgRNA.
However the truncation of the tracrRNA does not enable gene editing. Rather it is all that is required.
In bacteria the crRNA and tracrRNA are distinct molecules which must pair through the complementary palindromic repeat sequences. This is not the case in gene-editing as the crRNA and tracrRNA have been fused with a synthetic stem loop. Thus the palindromic repeat sequence is not required and the tracrRNA is shorter.
Check out Cong et al. (2013) in Science.


How to DIY preserve pet DNA today so that it can be used in 20 years

For the impatient, I'm going to say that probably if you only have a regular home freezer, its unlikely that you will be able to do this. If you have access to a -80C or liquid nitrogen storage its possible, but also less likely.

Cloning an animal typically starts with the transplantation of a nucleus into an egg cell whose nucleus has been removed.  So unless things change drastically in the next 20 years, just purifying DNA and keeping it in a tube of the fridge is not enough - you need to preserve epithelial (skin cells) or some other tissue in a state which can be revived to produce a live and intact cell when you want to do the cloning.

Its possible that we will have machines that can take DNA from a DNA prep and produce a living cell - this is what we hope to do with the mammoth and other extinct animals from fossil tissue some day.  But whether that will be the case in 20 years is just a guess, whether it is affordable is also just a guess.

So from what we know now, you will need to preserve a piece of tissue from the animal when it is alive.  I'm not an expert on how to do this, but you might be able to get the skin cells to sort of turn into a cell line and then freeze them for not too much money.

If you do this, regular freezers are not cold enough to prevent freezer burn.  This is what happens when you put a steak in to the freezer, wrapped in plastic even it will shrivel up and start to dry out as the water in the ice starts to sublime out of the package (the dry air in the freezer basically sucks the water out of the food).  If this happens to your animal tissue, its probably not going to revive.

Scientific labs use -80C freezers and liquid nitrogen storage because the water turns into a glass and all biochemical reactions are basically stopped. (besides drying out, the enzymes like DNAse are still nominally functioning in the cells at -20C and even simple bacterial cells don't live for more than a year at -20C, much less mammalian cells).  For preserving cell lines, liquid nitrogen is much more preferred.  I would say that properly produced cell lines can theoretically revive after indefinite liquid nitrogen storage.

So that's a quick answer.  Sorry to be a party pooper - things could change quite a bit in the next 20 years, but we just don't know how much.  popping a paw in a baggie or some DNA extract into the freezer might work, but its hard to say for sure.

As far as the choice of where the DNA comes from in the animal, its true that skin cell lines are often producing imperfect animals - the DNA may be modified in the skin in various ways that cause the animal to be smaller, weaker, or even deformed compared to the donor.  At this time all the protocols I see (and i could be wrong) are skin cells.  I would expect that there is a better tissue to preserve, but that might be just a guess at this point.  Its likely that in the next 20 years the choice of cell line from the donor will change quite a bit as well.


What are the reactions in the body that triggers dizziness after cigar(nicotine) smoking in non-smokers?

It's all about the synapses, the places where separate neurons connect to one another. All psychoactive drugs act in some way so as to modulate the signals that are passed from one neuron to another. Nicotine acts by increasing the effect of signals that pass through a particular type of synaptic receptor called nicotinic acetylcholine receptors (they're named after the fact that they're affected by nicotine). The dizziness and other effects of nicotine are caused by this interference with normal neuronal communications.

The reason why regular users of nicotine don't get dizzy is because they've gained a tolerance to the drug. Tolerance isn't super well understood at the molecular level, but it has been associated with long term changes in the quantities and types of receptors that are present at synapses in certain regions of the brain, it particular the nucleus accumbens.

Marijuana is similar to tobacco, only its main psychoactive component, THC, acts on the cannabinoid receptors.


You're right, according to standard rules of nomenclature it would be called glycerol 1-phosphate. It comes back to the outdated D/L configuration nomenclature. A more thorough explanation is quoted below.

  When the R/S system (sequence rule) is applied, substitution of one of the primary hydroxyl groups often leads to changes in the configurational prefix, thus obscuring chemical and biogenetical relationships; it is generally inapplicable to the steric description of such mixtures as occur in triacy1glycerols isolated from natural sources. The stereospecific numbering of glycerol and its derivatives as proposed by Hirschmann [9], described above and in 1, avoids these difficulties; it has proved useful and is widely accepted.

Source.


In your example, yes the two strands do code for different proteins. However, biologically this generally doesn't occur. I say generally because I don't want to rule it out definitively but I don't know of an instance where both strands at a given locus code for a protein and, where it does occur, it is often used as a criterion for annotating one of the elements as dubious. Along with that, there would be no promoter immediately 5' to one of the strands. Even if it does occur biologically, each strand would code for a different protein and would be a different gene.

In any gene, one of the strands is identical to the RNA transcript (before processing and with T instead of U). This is called the coding or sense strand and runs 5' -> 3'. The other strand is used as a template by RNA polymerase (RNAP) to polymerize the RNA transcript. It runs 3' -> 5' and is called the template or antisense strand.

Also, a note on promoters: promoter consensus sequences by convention are given on the sense strand. However, as far as I know, transcription initiation factors recognize the base pairing between both strands in the major groove of dsDNA because they must bind before promoter melting occurs. Thus, I wouldn't say that a promoter exists only on the template strand.


According to wikipedia, there have been drugs targeting CCR5 coreceptor approved for treating HIV. These drugs work by binding to CCR5, thereby prevent binding of HIV and CCR5.

However, drug resistance can still develop. Some HIV can bypass it by shifting tropism to CXCR4. While others can increase its affinity to CCR5.

And some receptors are vital for the functions of cells. If we design drugs to these targets, we should make sure that the drugs only prevent binding of viruses specifically without disrupting their normal functions.

  Maraviroc was approved for use by the FDA in August 2007.It is the
  only one thus far approved by the FDA for clinical use, thus becoming
  the first CCR5 inhibitor. A problem of this approach is that, while
  CCR5 is the major co-receptor by which HIV infects cells, it is not
  the only such co-receptor. It is possible that under selective
  pressure HIV will evolve to use another co-receptor. However,
  examination of viral resistance to AD101, molecular antagonist of
  CCR5, indicated that resistant viruses did not switch to another
  coreceptor (CXCR4) but persisted in using CCR5, either through binding
  to alternative domains of CCR5, or by binding to the receptor at a
  higher affinity.
  https://en.m.wikipedia.org/wiki/CCR5

http://www.ncbi.nlm.nih.gov/pubmed/11782552
http://www.sciencedirect.com/science/article/pii/S0042682206008245


How can a sequence be downloaded from UCSC genome browser

Yes. Table browser allows you to do that.

In the dropdown box called output format select sequence and click the button named get output. You'll get the sequence.

If you don't think it works then this is the output that I am getting. (Fist few lines):

>hg19_gold_AL096773.6 range=chr1:115207623-115347729 5'pad=0 3'pad=0 strand=- repeatMasking=none
GATCTGCCAGCGTCCACCTCCCGAGGTGCCGGGATTGCAGACGGAGTCTG
GTTCACTCAGTGCTCAATGGTGCCCAGGCTGGAGTGCAGTGGCGTGATCT
CGGCTCGCTACAACCTCCACCTCCCAGCCGCCTGCCCTGGCCTCCCAAAG
TGCCGAGATTGCAGCCTCTGCCCAGCCGCCACCCCGTCTGGGAAGTGAGG
AGCATCTCTGCCTGGCCGCCCATCATCTGGGATGTGAGGAGCCCCTCTGC
CTGGCTGCCCAGTCTGGGAAGTGAGGAGCGCCTCTTCCCGGCCGCCATCC

Actually Table browser is quite useful as you can get different kinds of data for a given genomic region which include annotations, variation, transcription factor binding sites etc.


I think any domestic animal that reverts to the wild is going to experience some genetic change given an evolutionary timescale. As you probably know, dingoes are descended from dogs introduced to Australia by early human migrants. Their ancestors were thus presumably domesticated or at least semi-domesticated.

Also, the Indian wolf is a subspecies of Canis lupus, which ranges across Eurasia and North America both.

I think this article may shed some light on your question:

It sounds like the dingo may have developed some traits that distinguish it from wolves and domestic dogs both.


In the periphery (e.g. on our fingertips), our body senses external temperature through nerve terminals, expressing certain TRP channels. These are ion channels that are sensitive to temperature (note that TRP channels can be sensitive to several things, such as pH, light, and stretch) and allow entrance of cations in the cell when the temperature is higher or lower than a certain threshold.

Six TRP channels have been described as been involved in sensing different temperature ranges1,2:

TRPV1 is activated at >43 °C
TRPV2 at >52 °C
TRPV3 at ~> 34-38 °C
TRPV4 at ~> 27-35 °C
TRPM8 at ~< 25-28 °C
TRPA1 at ~< 17 °C

Not surprisingly, TRPV1 and TRPV2 are also involved in nociception (=pain perception).

The exact molecular mechanisms by which different temperatures open different TRP channels are unclear, although some biophysical models have been proposed.3

I am not sure of the exact "format" in which sensory fibers encode different temperature, but I would assume that the neuron would fire faster the more the temperature is distant from the specific threshold (hot or cold).

1 Thermosensation and pain. - J Neurobiol. 2004 Oct;61(1):3-12.
2 Sensing hot and cold with TRP channels. - Int J Hyperthermia. 2011;27(4):388-98.
3 - Thermal gating of TRP ion channels: food for thought? - Sci STKE. 2006 Mar 14;2006(326):pe12.


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

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

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

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

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


Why are there N's after Sanger sequencing?

Typically Sanger sequencing will run into a few errors. Sometimes the traces will overlap as below in red and the computer will call N. If you truly wanted to figure out the correct basepair, you can look at the trace.


Are all single-celled organisms Bacteria?

No, many unicellular organisms are not bacteria. Examples include (but certainly not limited to); some fungi, chlorella algae, and archaea.

Bacteria are one of three domains in the classification of life. You can find more about the bacteria domain at the wikipedia page (It's a long and complex history which is hard to summarise here) and about the domains here. This last defines bacteria loosely consisting of "prokaryotic cells possessing primarily diacyl glycerol (DAG) diester lipids in their membranes and bacterial rRNA, no nuclear membrane, traditionally classified as bacteria."

The composition of lipids in their membrane (DAG-esters) differentiates them from another major class of prokaryotes — Archaea, which have isoprenoid lipids in their membranes.

Initially Archaea was called Archaebacteria. Because of significant differences, including the membrane composition, they are now grouped into a different kingdom.


What is an interaction motif with respect to protein sumoylation?

A motif means a pattern. Since nucleotides and proteins have a sequence, they can have some patterns of sub-sequence that may serve some kind of function. For example TATA box in DNA serves as a promoter element. Similarly proteins can have some sequence motifs that can serve as recognition sites for binding partners (amongst other functions). Similarly there can be structural motifs in proteins, network motifs in big networks etc.

In this case the motif is a sequence motif.

From Gareau and Lima (2010):

  Many SUMO-modified proteins identified contain an acceptor Lys within a ψKX(D/E) consensus motif, where ψ is a large hydrophobic residue

This motif serves as a recognition site for the SUMO-Ligase.

Here,

K=Lysine
X=Any amino acid
D=Aspartic acid
E=Glutamic acid

From the below figures (Rodriguez et al., 2000), you can observe that ψ can be leucine (L) (original residue in Ran GAP1), isoleucine (I), phenylalanine (F) or valine (V).

I am not sure about the effect of double hydrophobic residues on rate of SUMO conjugation.


Can we say that microevolution and macroevolution is fundamentally the same thing over different time scales?

You are mixing up two different things in your question:

the mechanisms (processes) that cause micro- and macroevolution, and
the genetic basis for different types of traits.

The processes of evolution (selection & drift acting on genetic variation) are the same for both micro- and macroevolution, and this what the Wikipedia article is stating. The second question is dealing with the amount of cumulative genetic change that is needed for different types of traits. This naturally differs dramatically between traits (the accumulated genetic change that is), and is also reflected by the different scopes of micro- and macroevolution. Macroevolution is usually studying problems above the species level, and therefore often larger morphological changes, while microevolution is dealing with smaller changes within species and populations. The macro/micro division is also artificial and should be seen as a continuum.


If I squash an insect and it produces red "juice", does it always mean it is a blood-sucking type?

No - invertebrates don't have "blood" though they do have hemolymph. Hemolymph flows around the body cavity, rather than through vessels such as veins and capillaries, and comes in to direct contact with tissues and generally it is not red.

Hemolymph fills all of the interior (the hemocoel) of the animal's
body and surrounds all cells. It contains hemocyanin, a copper-based
protein that turns blue in color when oxygenated, instead of the
iron-based hemoglobin in red blood cells found in vertebrates, thus
giving hemolymph a blue-green color rather than the red color of
vertebrate blood. When not oxygenated, hemolymph quickly loses its
color and appears grey. The hemolymph of lower arthropods, including
most insects, is not used for oxygen transport because these animals
respirate directly from their body surfaces (internal and external) to
air, but it does contain nutrients such as proteins and sugars.
~ http://en.wikipedia.org/wiki/Hemolymph

The red you see from squashing, depending on the insect, could come from blood of other animals or (eye) pigments produced by the insect. For example, in my lab we have some Drosophila melanogaster with red eyes and some with white eyes (they carry a genetic mutation which represses the production of pigments in the eye) - if I squash the red eyed fly red "juice" is left on the desk, this doesn't happen with the white eyed flies.


(Reposting my comment as an answer since it seems to be what was required.)

A DNA molecule that replicates independently of chromosomal DNA is an episome. By this definition a plasmid is (usually) an episome. If a plasmid integrates into a chromosome by some mechanism (as for example in Hfr strains of E. coli where the F plasmid is integrated) the plasmid loses its episomal status.

The term "episome" was first coined by Joshua Lederberg to describe the nature of the F element in E. coli.


Is there a term for the opposite of intergenic?

It seems to me that "genic" is a perfectly good word.
This paper uses "genic" directly as a contrast to "intergenic", so that seems like a reasonable precedent:

‘Noncoding DNA’ can be found both surrounding genes, and within genes (see schematic Figure 1). We will call the first type ‘intergenic’, and the second type ‘genic’, a ‘gene’ referring here to a transcribed DNA sequence.


Can cfDNA testing distinguish results in the case of twins?

I think you are overestimating how these cfDNA tests work.  Maybe I read the paper wrong, but from what I read of one technique (Sequenom's MaterniT21 test) there is no purification of fetal DNA.  They do restriction digests to assess the percentage of fetal DNA,  but I don't think they enrich for the fetal DNA when they sequence.  The library they make is mostly maternal, they are just looking for slight deviations in how many reads come from each chromosome, if too many come from chromosome 21, they conclude it's because the fetus has too many copies.

And as for SNPs, coverage is way to low for that.  We're talking about 40 million reads, even if that were mostly fetal DNA, which I don't think it is, that's not enough coverage to call SNPs.

So if there were two fetuses, and they were not identical, then the signal from each would be half what would be expected based on the restriction digests assay. So maybe you would have enough counts that you could tell that the Y chromosome counts were too low, and the X chromosome a bit too high, but since these tests almost certainly have not been clinically tested on multiple fetuses well enough for verify their accuracy, no company is going to report results.


I imagine that their breathing is controlled in the same way as ours. During a dive, oxygen will be used up and carbon dioxide will be produced, dissolving in the blood as bicarbonate and tending to decrease the pH of the blood.

Peripheral chemoreceptors in the circulatory system detect all of these changes and signal the need to breathe. This would tell the seal that it is time to head for the surface.

Diving mammals have various adaptations for prolonged diving, most importantly large reservoirs of blood containing haemoglobin which is oxygenated before a dive, as well as high concentrations of myoglobin in muscle which can also act as an oxygen reservoir.


How do we know which Eulerian path corresponds to the DNA sequence?

If the DNA sequence contains repetative elements, and your reads are not long enough to resolve them, you won't know if you have the right path.  Usually you split your results into contiguous regions whose sequence you are confident in.


I see no reason why it would precipitate chemically. Besides, you need to dissolve the agar via heat. Hence, auclaving is fine.

If you do not believe me these protocol allow for autoclaving of seawater agar 15min cycle 121 degrees:
1. https://www.dsmz.de/microorganisms/medium/pdf/DSMZ_Medium246.pdf
2. http://himedialabs.com/TD/M592.pdf


It is some type of boletus. You would need a spore print and a few more examples to decide which one. They are commonly found under conifers.The books say most are editable and good taste. The couple kind I have eaten had no flavor , not worth collecting. The tubes instead of gills on the bottom of the cap are an indicator of boletus group.


Meaning of "optical" in "Optical cap, 8X Strip" (used in qPCR)

Does the word indicate the the cap is fully transparent? Or that the cap creates no visual distortion (it is flat)?

Yes and yes. As an example of the different kinds of PCR tube caps, refer to the cap options available from Thomas Scientific:

Available with a domed, flat frosted, or flat clear caps for qPCR. [emphasis mine]

For most lab plastics, "optical" refers to the surface between the camera/detector and the sample.  Another example: for plate-based fluorescence assays where the plate reader takes measurements from below  the plate, one might use a Nunc MicroWell 96-Well Optical-Bottom Plate from ThermoFisher. Usually, such plates also have opaque walls to prevent signal bleed from adjacent wells.


Do ectotherms think slower when they are cold?

I would assume as the temperature decreases, even as an ectotherm organism that the neuro processes would decrease. From my experience in chemistry, the colder the temperature the slower the molecules vibrate. As a result, it would take a longer time for the sodium and calcium molecules to move from the end of the neurons to the synapses resulting in delayed thinking. If they are absorbing the energy necessary, then their neuro processes should be functioning normally.


Why do cell membranes let small non-polar molecules through but won't let small polar molecules through?

The plasma membrane consists of hydrophobic and hydrophillic characteristics. Towards the outsides, they are hydrophillic, so they can create bonds with water. The insides are hydrophobic, allowing no water inside and keeping them tight together due to the polar forces.

An non-polar particle (if small), can pass through this because it does not interfere with the hydrophobic/hydrophillic (polar) nature of the plasma membrane. However, polar particles would not have the opportunity to move in, because the insides (hydrophobic) are literally afraid of water, or charges, don't allow polar substances to pass through.

So only hydrophobic (nonpolar), gases, and small particles (nonpolar) can pass through. There are exceptions of $H_2O$ passing through the membrane in small amounts because their electric charge is very minor.


Pet allergy is an allergic reaction to proteins found not only in the
  animals' fur or hair but also in saliva, urine, mucous, and hair roots
  and in the dander sloughed from the animals' skin. Thus, the
  widespread idea that "hypoallergenic pets" are those that have less
  hair or shed less is a myth.

  Most often, pet allergy is triggered by exposure to the dead flakes of
  skin (dander) a pet sheds. Any animal with fur can be a source of pet
  allergy, but pet allergies are most commonly associated with cats,
  dogs, rodents and horses.

  Some dog breeds have been promoted as hypoallergenic because they do
  not shed their hair, shed very little, or have the same pH as human
  hair. However, no canine is known to be completely non-allergenic.

  Some cat breeds, especially females are likely to have low levels of
  Fel d 1, the main allergenic protein.

  There is only one known hypoallergenic horse breed. The Bashkir Curly
  horse has a uniquely textured coat that lacks the protein (present in
  all other horse fur) believed to be the source of allergic reactions
  to equines.

via


Why is beta-mercaptoethanol often added to cell culture media

2-me is a reducing agent necessary to be added to help keep free radical oxygen from affecting mouse cells.  It is generally not necessary for human cells.

Also from S Bannai and Ishii et al., 2-mercaptoethanol improves tumor cell uptake of cystine by creating a reducing environment.


Are there humans which the brain sends signals to the limbs faster than the average?

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.


How would one determine if an up regulation of one protein leads to an over expression of another?

To demonstrate a causal relationship where protein A leads to increase in protein B, you need to experimentally increase the level of A and measure if B increases. Over-expression is typically done with overexpression of protein A from a plasmid containing the coding sequence, driven by a strong promoter that causes high levels of protein synthesis. See this Wikipedia page for some pointers. Relative protein levels can be quantified by western blotting. The experimental details depend a lot on what cell type and protein you are studying, of course.


Do apes and humans share 99% of DNA or 99% of genes? What is the difference?

So, a quick molecular biology lesson.

Proteins are the things that make up a good percentage of our cells (which make up a good percentage of us), and are the things that do the work of the cells - many are catalysts and are known as "enzymes".
Proteins are encoded by genes - while the statement that one gene
codes for one protein is not quite correct (one gene can code for
different variations of the same basic protein), it's a good way to
think about things in this context.
Genes are made up of DNA, a polymeric molecule that constitutes our chromosomes, the informational portion of which resides four “letters” (chemical bases).
However, now we get to the key part — although all genes are made of DNA,
not all the DNA of chromosomes makes up genes. In fact, as @terdon    mentioned in a comment, only about 5% (or less) of the 4 billion letters in the total DNA — the genome — constitute genes - those sequences that
directly code for protein.
The function of the rest of the genome is not entirely clear. Some is regulatory, some may be structural, and may be “junk DNA”. However it’s stuck      around for millions of years, so it we assume it must have some purpose. This non-coding DNA differs between species to a greater extent than the genes themselves do, so perhaps it somehow contributes to the differences between organisms.

From AndroidPenguin

Here are the links to a paper about the function of "junk" DNA from 2013.

Summary in NY Times
Abstract in Nature
ENCODE threads on nature.com


Brazzein is not even a sugar - its a protein that comes from Oubli, a West African climbing plant.

While I think nearly every living thing from bacteria up to large animals can perceive some carbohydrates as a food source, the mechanisms vary over the tree of life.

Because of this the taste of sweetness in animals varies a lot.  Aspartame, a non carbohydrate sweetener does not register as sweet in all the primates.  Brazzein and aspartame as capable of activating one or more of the human taste receptors.  Receptors are just proteins which sense a stimulus.  They can be activated by other compounds - this is how most pharmaceuticals work.  Sweeteners which are not glucose/sucrose can bind more tightly or affect the structure of the receptors, causing them to send a sweetness signal. Often these compounds also register with other sense receptors and so the sweetness is accompanied by other tastes as well.  It sounds like Brazzein is a clean taste, less likely to have such side effects.

I've not dug fully into this - its clear that some human sweetness receptors are known, but I'm not sure they are all known.


How's the membrane potential restored to resting state after hyper polarisation?

The Na,K-ATPase restores negative membrane potentials.  When a cell is hyperpolarized, leaky K+ channels take care of that. Leaky K+ channels are always open. Generally, K+ has the tendency to diffuse back out of the cell along its chemical gradient through leaky K+ channels, after been pumped in, making the cell's inside more negative. However, in the reverse situation, where the cell is hyperpolarized, they may flow inwards, along the electrical gradient.

Note that while the Na,K-ATPase is indeed the driving force behind the membrane potential, it is not the direct consequence of the ratio of Na+ being pumped out and K+ being pumped into the cell. It is the leaky K+ channels that determine the membrane potential largely, together with the Na+ channels being permanently closed, except when an action potential is generated.

Suggested further readings
- What keeps the resting potential of neurons constant at -70 mV?
- If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?


Are cells electrically neutral or charged to setup the membrane potential across them?

It isn't neurons that are charged, it is their membranes. From the distance of other cells, they "see" both the charges inside and outside the membrane, so there isn't any substantial repulsion on that scale.

The charge across a membrane comes mostly not from the Na+/K+ pump directly, but due to differential permeability of the membrane to different ions. Ions normally tend to flow down their concentration gradients, but that flow can be influenced by an electrical potential. From the perspective of just Na+ and K+, there is more K+ inside the cell and more Na+ outside, and more permeability of the membrane to K+ than Na+. Therefore, the inside of the cell will be negatively charged at equilibrium where the net flow of ion charges is equal. At a negative resting potential, the negativity of the inside of the cell equalizes the net flow of potassium out with the net flow of sodium in. However, the actual concentration changes involved are miniscule. From the perspective of ion counts, there are basically as many positive ions inside as there are negative ions inside a cell; it's the very minute imbalance (fractions of a %) that gives a potential of ~-70mV.


First it needs to be said that coconut trees are not true trees, but palms, whose trunks are made of stems which grow in a cross woven pattern.

That being said - its true for any plant that no plant grows from the bottom up.  If you make a mark on any plant that mark will not rise much as the plant grows.

Plants grow from buds at the end of their stems.  As the plant grows taller  its because the tissue adds from the ends of its branches/stems.

In this illustration you can see the terminal bud, which is where the plant is growing up and also out into branches.  The palm is more like a bundle of grass stems, so the terminal bud is not obvious, but the leading edge of the grass will grow here.

A tightly wound core of stems in the crown of the palm, called the Heart of Palm is where the palm grows (see "growth point" in picture below).  It is also a terminal bud, but it is not as exposed and is not as obvious.

(figure from The Food and Agriculture Organization of the UN, fao.org)


How can homosexuality evolve despite natural selection?

Several years back, results of a twin study (Zietsch, et al., 2008; popular press in The Economist) suggested that genes associated with homosexuality make heterosexuals who carry the same genes more reproductively successful. This would explain the observation that, for example, sisters of homosexual males have more offspring.

  We show that psychologically masculine females and feminine men are
  (a) more likely to be nonheterosexual but (b), when heterosexual, have
  more opposite-sex sexual partners.

So if more sexual partners in heterosexuals is correlated with more offspring, then the genes associated with homosexuality may lead to more offspring in heterosexuals that carry them. So these "homosexuality" genes could easily be maintained in the population by conferring a reproductive advantage to siblings.

The authors conclude:

  Taken together, these results suggest that genes predisposing to
  homosexuality may confer a mating advantage in heterosexuals, which
  could help explain the evolution and maintenance of homosexuality in
  the population.


How much penicillinase is needed to deactivate 125mg of amoxicillin?

As March Ho has pointed out, we could do with a bit more information on this one.

I am going to attempt the calculation for penicillin G, and the necessary information seems to be available.

From here, A Levy Unit (LU) is the amount of penicillinase that inactivates 593 IU (International Units) of Sodium Penicillin G  per minute at 25°C and pH 7.0
From here and here, the specific activity of penicillin G is about 1667 Units/mg
I am assuming your concentrate is 20,000 Levy Units/ml (not 20,000 Levy Units/ml/min, which does not make sense to me)
Therefore 1 Levy Unit will inactivate (593/1667)mg, or 0.356 mg, of penicillin G per minute, pH 7.0 and 25oC
2.81 Levy Units will inactivate 1 mg penicillin G under identical conditions
351 Units will theoretically inactivate 125 mg penicillin G in 1 min under the conditions stated.
Your concentrate is 20000 Units/ml, or 20 Units per microliter.  So you will need (351/20) microlitres, or about 17.5 ul.
This assumes that the enzyme continues at a constant rate given by the specific activity right until the end.  This might not necessarily be the case, as one would expect the rate to slow down as the substrate concentration falls below Km.  Personally, I would use at least a 10-fold excess. 176ul - Seems a lot?

Please feel free to provide further information, or to edit the answer in any way you feel is necessary


20-30 seconds is all it takes to reach the brain, then levels continue to increase with a peak at around 15 minutes and normal levels by about 2 hours (hence the craving). Smoking increases your heart rate directly and also indirectly through reducing the oxygen levels in your blood so your body compensates by increasing heart rate as well as makes each beat stronger, so it pumps more blood with each beat. Nicotine itself is really soluble, it goes straight through the lungs (alveoli) because the lungs get an incredible amount of blood (which they need to do their job) so massive surface for the nicotine to go through so enough nicotine gets into the blood and concentrations are really rapidly high enough for you to feel the nicotine. Carrying on from that, the blood rapidly gets back to the heart and around the body with the brain being practically a direct connection away. Consider the classic cyanide capsule death seen often on TV. The reason people seem to lose consciousness within 30 seconds is because they inhale the cyanide.

Nicotine replacement therapy used to stop smoking uses similar mechanisms to give the same speedy delivery of satisfaction without the massive risks of smoking, stopping cravings and really improving one's quality of life.


How is achieved the loss of heat through vasodilation?

Sweat evaporation is the most correct answer you have mentioned.  Vasodilation increases blood flow, allowing for more blood to be cooled be vessels closer to the surface of the skin.  It's increasing the surface area the blood interacts with, which always allows for faster heat transfer.


How and why did mammals go back to the oceans?

I'll focus on whales and dolphins (cetaceans) as you mention them by name and they are representative for other marine mammals such as seals or manatees. The evolution of cetaceans was one of the fascinating evolutionary mysteries. Clearly, they were mammals, but which mammals were their closest relatives? Clues to solve this mystery began to appear in the 1980s and 1990s.
During the 1980s and into the 1990s, paleontologists discovered several fossils that were clearly land-based mammals but shared many skeletal features with cetaceans. These fossils, including Pakicetus [(Gingerich et al. 1983)] and Rodhocetus (Gingerich et al. 1994), shared skeletal features that are unique to whales and to the Artiodactyla, commonly known as the even-toed mammals. Artiodactyls includes deer, sheep, pigs, bison, and hippopotamuses. Artiodactyls and the fossil whales share a unique skeletal feature of the ankle called an astrogalus, shown in the picture below. The astragalus is a "double pulley" structure that contributes to the ankle joint. This picture is taken from an excellent summary of whale evolution, provided by the Understanding Evolution site hosted by University of California at Berkeley. The astragalus is not present in other mammals.

The fossil whales and modern cetaceans also share unique features of the skull around the area of the ear, called a tympanic bulla. Although all mammals have bullae (plural of bulla), the bullae of cetaceans and the whale fossils is unique compared to other mammals. For more on the bulla, see this Talk Origins page. More on fossil whales can be found at the Berkeley Comparative Museum of Paleontology. The many fossils that have been found are transitional forms that link artiodactyls and modern cetaceans.

Source
Around the same time as the fossil discoveries, genetic analysis added additional evidence supporting a relationship between the artiodactyls and cetaceans (Milinkovitch et al. 1993). Although early genetic analytical techniques were not as robust as they are today, many genetic studies have since supported and refined the conclusions of Milinkovitch et al. Current evidence shows that the closest living relative of cetaceans are the hippos (see, for example Price et al. 2005 and Agnarsson and May-Collado 2008). The relationships are shown below in this figure from the Agnarsson and May-Collado paper. The dark lines are the artiodactyls and cetaceans, formally called the Cetartiodactyla.

The question remains: why? The most likely explanation is that cetaceans evolved to exploit an unfilled ecological niche or adapted to new niches that formed as a result of plate tectonics or other types of environmental changes that occurred 50-55 million years ago. The niche describes all of the living and non-living resources needed by an organism to survive. Although land-based mammals were increasing in diversity, few or none were present in the oceans. The basic hypothesis is that the early whale-like artiodactyls, like Indohyus and Pakicetus were land-based (terrestrial) mammals that spent most of their time near the water's edge. Over time, they adapted to the niches in the ocean. Fossils like Ambulcetus and Rodhocetus showed clear evidence of swimming ability, with flattened tails and the enlarged rear feet. In addition, the nostrils shifted from the front of the face to the top of the head, which we recognize as the blowhole.
The shift to the aquatic habitat allowed these species to exploit resources that were not available to land-based mammals, thereby reducing competition for the resources. Reduced competition allows more individuals to survive and reproduce.
Similar scenarios are very likely for other marine mammals, such as seals or manatees. They evolved to take advantage of ecological niches that were not filled by other organisms. This basic concept, evolving to fill available niches, is a common outcome of the evolutionary process.
The of adaptation of cetaceans and other mammals to the oceans may be similar to that of the hippopotamus. Hippos spend most of their time in the water, and they show many adaptations that allow them to live in the aquatic environment.  The eyes and nostrils of the hippo are high on the head, which allows them to remain almost entirely submerged but still see and smell, as shown below.

(Hippo photo by Johannes Lunberg, Flickr Creative Commons.)
Hippos feed underwaters, they are heavy enough to walk on the bottom of the river, and the mate and give birth underwater. The young can suckle underwater. Clearly, hippos seem to be another mammal that is "returning to water." Similar types of processes must have occurred in cetaceans for them to adapt to the marine habitat.

Citations
Agnarsson, I. and L.J. May-Collado. 2008. The phylogeny of Cetartiodactyla: The importance of dense taxon sampling, missing data, and the remarkable promise of cytochrome b to provide reliable species-level phylogenies. Molecular Phylogenetics and Evolution 48: 964-985.
Gingerich, P.D. et al. 1983. Origin of whales in epicontinental remnant seas: New evidence from the early Eocene of Pakistan. Science 220: 403-406.
Gingerich, P.D. et al. 1994. New whale from the Eocene of Pakistan and the origin of cetacean swimming. Nature 368: 844-847.
Milinkovitch, M.C. et al. 1993. Revised phylogeny of whales suggested by mitochondrial ribosomal DNA sequences. Nature 361: 346-348.
Price, S.A. 2005. A complete phylogeny of the whales, dolphins and even-toed hoofed mammals (Cetartiodactyla). Biological Reviews 80: 445-473.


Think about say the left side of a shoot growing more than the right side. That way the left side will be longer and will be pulled back by the right side. This causes the shoot to turn to the right. By controlling the differences in the rates of growth in the two sides (using plant hormones) the plant can control exactly how much the shoot will turn.

Most nastic movements however, are not directional. For example, in Thigmonasty, or the movement due to touch, of the Mimosa pudica (or the touch-me-not), cells at the base of the leaves pump out K+ ions and Cl- ions, while taking in Ca+2 ions, thus create a osmotic gradient and lose water. This loss in water results in a drop in turgor pressure of the leaves and they droop.

https://en.wikipedia.org/wiki/Thigmonasty#Thigmonasty_in_the_Fabaceae


Does all the citrus fruit contain Citric acid and Ascorbic acid?

Whatever the colloquial/vernacular/etymological meaning of "citrus"; when it comes about scientific names; Citrus is a particular genus. It do have many species.

  "Amla being a citrus fruit"

No. Amla (Phyllanthus emblica) is not a member of genus Citrus; not even allied.

Ascorbic acid is just another name for Vitamin C. It is also present in common edible citrus fruits.


Need for -70 degree temperature for Corona vaccine

This is the temperature at which RNA is stored for long term storage without the occurance of degradation. It is also standard lab routine to store RNA at this temperature. Conviniently, this temperature can be reached by dry ice (-78°C), which makes shipping a lot easier.
However, there are indications by Biontech themselves that the vaccine will be stable at refrigerator temperatures between 2-8°C for five days and probably even for prolonged times (see here). This is actually being tested, storing below -70°C is simply the safeguard to ensure nothing bad happens. For injection, it will have to be warmed anyways.


Is there any documented case in which floating substances led to the introduction of a new species?

There is a number of reported cases of marine species reaching new locations through "hitchhiking" in recent times. However, it seems harder to find reports of species actually becoming established in a new location through this.

The following articles describe examples of species transported with ocean debris:

In an early study on the dispersal of plastic pellets (3), it was suggested that pellets encrusted with the bryozoan Membranipora tuberculata was transported to New Zealand across the Tasman Sea from Australia. Barring one exception, this was the first time the species was observed in New Zealand waters.

Appendix A of a later article by the same author (1) contains 13 examples of species transported by sea (not necessarily through debris, or invasive), including the previous example. Of it, the author writes that

  Later, L. M. Stevens (1992, unpublished data) was to report that [Membranipora tuberculata]
  was abundant on both eastern and western shores around northernmost
  New Zealand.

Thus, this is possibly a case of a species transported on floating debris and subsequently becoming established in a new habitat.

Jose Derraik also deals with the topic in a review (4):

  Plastics floating at sea may acquire a fauna of various encrusting
  organisms such as bacteria, diatoms, algae, barnacles, hydroids and
  tunicates (Carpenter et al., 1972; Carpenter and Smith, 1972; Minchin,
  1996; Clark, 1997). The bryozoan Membranipora tuberculata, for
  instance, is believed to have crossed the Tasman Sea, from Australia
  to New Zealand, encrusted on plastic pellets (Gregory, 1978). The same
  species together with another bryozoan (Electra tenella) were found on
  plastics washed ashore on the Florida coast, USA, and they seem to be
  increasingtheir abundance in the region by driftingon plastic debris
  from the Caribbean area (Winston, 1982; Winston et al., 1997). Minchin
  (1996) also describes barnacles that crossed the North Atlantic Ocean
  attached to plastic debris. Drift plastics can therefore increase the
  range of certain marine organisms or introduce species into an
  environment where they were previously absent (Winston, 1982).

Finally, the book Marine Pollution: New Research (2) contains the following passage which ends with the observation that conclusive proof is difficult to obtain:

  Drift plastics are known to have introduced exotic marine species to
  several areas (Winston et al., 1997; Deraik, 2002). Winston et al.
  (1997) reported that the non-indegenous oyster Lopha cristagalli was
  fond on plastics wshed ashore in southern New Zealand, and that the
  exotic bryozoan Thalamoperella evelinae was found on plastics washed
  ashore in Florida. Barnes and Milnder (2005) fond the exotic barnacle
  Elminius modestus on plastic debris in the Shetland Islands (Atlantic
  Ocean). The bryozoaen Membranipora tuberculate is believed to have
  crossed the Tasman Sea from Australia to New Zealand rafting on
  plastic pellets (Gregory, 1978). M Tuberculate and the bryozan Electra
  tenella seem to be increasing their abundance on the Florida coast by
  drifting on plastic debris from the Caribbean sea (Winston, 1982
  Winston et al, 1997). Maso et al. (2003) (...) However, attributing a
  marine biological invasion to floating marine debris and not to other
  mechanisms is very difficult in most cases, and available data are
  generally insufficient.


Great idea! It seems that this research has been done before and your hypothesis is correct, but testing a wide variety of alcohols and testing your hypothesis for each one of them would be a great project.

Now, to do this, I would expect you would need to check the growth of the cells after certain periods of time. How would you do this? Well, the best device would be a hemocytometer. It looks like the price varies from 10.00 - 400.00 which is pretty cheap. Of course, there would be mitosis if there is growth during periods of time, which means there would be more cells after certain periods of time.

What cells to choose? I would choose something easy to work with, such as E.coli. It is safe and easy to work with. It needs minimal resources. Here's a link to a simple culture you can probably make at home:

http://makezine.com/projects/how-to-make-bacterial-brothagar/

Later, however, when you get good data, you can use mammalian and human cells to show that the research is relevant to human beings. However, mammalian cells are harder to grow because mammalian cells grow slower than bacteria and fungi and moreover contamination can cause problems. You would also need biosafety cabinets or laminar flow hoods and learn of aseptic and sterile technique.


Which matched normal(s) to use when computing CNAs from exome data with a Read-Depth approach

For the detection of somatic copy nuber alterations it is best to compare each tumour sample with its matched normal. If you want to call CNVs for all your tumour samples and some don't have matched normals, then pooling together all the normal BAMs to create a reference may be the best way to standardise your calling.


Which enzymes degrade dynorphins and what drugs inhibit these enzymes?

This paper was looking at inhibition of dynorphin converting enzymes and their importance. Although they don't seem to know if it is a single enzyme, or if it is multiple enzymes.

This paper looked at bikunin as an endogenous inhibitor of dynorphin convertase in human cerebrospinal fluid.

This paper looked at several inhibitors (some of which are known to irreversibly inhibit other enzymes), like N-peptidyl-O-acyl hydroxylamines and their effects on hCSF-DCE, the enzyme that cleaves dynorphin A, dynorphin B and alpha-neoendorphin to release Leu-enkephalin-Arg6. However, it is known to inhibit serine and cysteine proteinases.

However, I don't see any actual medications that are meant to inhibit Dynorphin enzymes. Instead I found Al-Fayoumi et. al were actually looking to identify stabilized dynorphin A derivatives instead of just inhibition of enzymes.


How exactly can a drug affecting squalene epoxidase affect the methylation cycle, necessitating the use of 5-MTHF?

Preamble

I have tried to follow the logic of the rationalization of the clinical case described in the report of Trachtman and Pagano, but have failed. I suspect from the quality of their biochemical illustration (arrows leading from compounds to enzymes, and talk about ends of cycles) that they do not have a clear idea themselves. However, having done the literature search, let me set out the picture as I see it, in the hope that this may enable someone else to see a connection I may have missed.

Anti-fungals inhibit the erosterol biosynthesis pathway in fungi

As the poster states, anti-fungals such as terbinafine do act by inhibiting the synthesis of ergosterol, which is a cell-membrane steroid, unique to yeast. Of relevance to this analysis, there is a methylation reaction in this pathway, that lies after the target of terbinafine, squalene epoxidase:

Methylation step in ergosterol synthesis (from Uniprot)

Inhibition of ergosterol synthesis can affect S-adenosyl methionine in yeast

The only experiments that I can find linking ergosterol synthesis with the methylation cycle in yeast do not involve anti-fungals. Rather, they involve yeast with mutations in the genes encoding enzymes of ergosterol synthesis. In a study performed by Shobayashi et al. (2006), mutants of the gene, Erg6, encoding the methyltransferase, resulted in the accumulation of S-adenosyl methionione (SAM). Clearly there are other methylation reactions in the cell which utilize SAM, but this suggests that the ergosterol synthesis pathway is so active in yeast that its disruption affects the concentrations of intermediates of the methylation cycle.

What is the relevance of this to methylation in humans?

Although the situation described above confirms a connection between the methylation cycle and ergosterol intermediates in yeast, as mentioned in the original clinical report, it is difficult to see how it relates to human metabolism. This is because, although squalene epoxidase does exist in man, the ergosterol synthesis pathway and the methylation step catalysed by the methyltransferase (the erg6 gene product) do not. In any case, inhibition of a methylation step would result in an increase in SAM, whereas just the opposite appears to be the case in the patient.

Final observations

The clinical report is of one patient with a mutation (MTHFR) in the methylene tetrahydrofolate reductase gene, which would reduce his ability to regenerate the methionine and S-adenosyl methionine needed for methylation. L-methylfolate greatly reduced his symptoms. Nevertheless, this report is for a single patient, whereas “The gene mutation known as the MTHFR affects approximately 45% of the US population”. If MTHFR were the only factor involved in this case one would expect other reports of adverse reaction to terbinafine. In the apparent absence of such reports one suspects that in this patient the affect of terbinafine — whatever it may be — involves some other, yet undiscovered metabolic interaction.


Can DNA be used directly to determine the age of a mutation?

Yes, you are right.  Proteins are specified by DNA sequences, so DNA sequencing is a more direct way to obtain essentially the same information.  Note that mutation dating via DNA or proteins is approximate.  It involves a lot of assumptions about continuous rates of mutation, but in fact mutation is a stochastic process and does not have a knowable continuous rate.  The sequence of mutations can be determined with high confidence, but the rate can only be determined approximately.


Why to choose a grammar from a lot of grammars that can describe structure of proteins?

I did not understand your question completely but this is what I guess you want to know:

Why genetic code evolved to be what it is ?
How the sequence of the protein coded by a mRNA give rise to a particular structure ?

Answer to first question cant be definitive. The textbook explanation for why a 3-letter code exists is because a 2-letter code cannot describe all the 22 amino acids, with all its permutations. But then comes another question: why only 22 amino acids. I can't even speculate the answer to this question; the simple amino acids are fine but for an example why lysine and not a similar amino acid with a shorter side chain - no idea.

So, given 22 amino acids, a 3-letter code and 4 nucleotides, the multiple codons for an amino acid are similar in sequence (usually the first two bases are conserved in accordance with the wobble hypothesis. The last base usually doesnt base pair strongly with the tRNA and is of minimal importance).

The answer to second question is somewhat straightforward. The sequence can give rise to infinitely many structures but in a given environment (consisting of the solvent, other solutes etc), the sequence adopts a particular structure in accordance with the free energy minimization principle. There is a possibility that given an environment a protein can have two different optimal structures and can switch between these two structures.


Are humans hardwired to continue gathering resources after the costs outweigh the benefits?

The answer to your question is very sensitive to the time frame you are interested in.  Assuming the costs and benefits you describe are referring to fitness (i.e., survival and reproduction), then the situation you are describing is one in which a particular behavior has lowered fitness (i.e., costs outweigh benefits).

There are several possible outcomes in this case.

Evolution. If the behavior is not plastic (i.e., it cannot change in a single individual), the there would be selection pressure against those individuals that exhibit the behavior.  If the behavior is heritable then evolution would cause a reduction in the frequency of the behavior over time.
Lowered Fitness. If you are not interested in evolutionary time scales but the behavior is not plastic, then the outcome would be no change in behavior but a reduction in the survival and reproduction success of individuals with the behavior.
Change in Behavior. If the behavior is plastic (i.e., it can be changed by a single human) and the current situation provides the appropriate information about the state of the behavior, then the behavior will change.  The key here (as with optimal foraging models) is that the appropriate cues have to be present to change the behavior.  Often organisms use proxy cues to trigger behavioral shifts.  For example certain caterpillars use day length to trigger shifts in developmental pathways (diapause vs pupation) when what really matters is temperature.

So the real answer to your question lies in the further questions of whether consumption is plastic (or hardwired as you say) and if it is, whether a situation provides the appropriate cues to indicate that we have acquired enough resources.  Those are rather complex questions that, as far as I know have not been answered definitively in the general sense that your question implies.


Can genetically modified genes jump to bacteria in the eater's intestine?

No.

There is nothing special about a piece of GM DNA when compared to any other random piece of DNA. If this phenomenon happened at any detectable level, we'd have found eukaryotic DNA in bacterial genomes/plasmids long before the introduction of genetically modified crops. And that would be front page news in the field of horizontal gene transfer! Which has many talented people in it!


Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?

Answer
No. There is ample evidence that:

Most non-extremophilic bacteria grow over a broad range of external pH values, from 5.5 – 9.0, and maintain a cytoplasmic pH that lies within the narrow range of pH 7.4 – 7.8.

The explanation for this is another matter, but, before discussing that question there are two points of possible misunderstanding in the question that require a note of clarification.
Clarifications

What the electron transport chain establishes is an electrochemical proton gradient, or proton-motive force (PMF). This consists of two components§: the hydrogen ion concentration difference, ΔpH, and the electric potential gradient, Δψ.

The source referenced in the question shows hydrogen ions being pumped from the cytoplasm, across a membrane, to a space labelled “outside”, which, according to the figure legend represents hydrogen ions “pumped out of the cell”. This is incorrect. The hydrogen ions are pumped into the space between the inner and outer membranes of gram-negative bacteria, or the space between the inner membrane and cell wall of gram-positive bacteria. It cannot necessarily be assumed that this space has the same pH as the external milieu.

How is the proton motive force maintained?
A possible explanation of why a constant or, more striking, alkaline pH does not destroy the proton motive force relates to the two-component nature of the latter. Bacteria appear to be able to compensate for any decrease (or even inhibition) of either ΔpH or Δψ by a reciprocal increase in the other (Bakker and Mangerich,1961). One mechanism that illustrates how this can be achieved in certain cases is the use of an alternative terminal oxidase, cytochrome bd:

Cytochrome bd generates a PMF by transmembrane charge separation, but
does so without being a proton pump.

However there is a complex set of anion co-transporters involved in cytoplasmic pH homeostasis which may influence the membrane potential. The situation is neither simple nor, as yet, completely resolved, as far as I am aware (but it’s not my field).

§ The treatment of electric potential gradient, Δψ, tends to be downplayed in biochemistry text books. This may be because the generation of a hydrogen ion gradient is easier to understand than that of a membrane potential, or because the texts deal with the latter in sections on nervous tissue. There is a quantitative treatment of the free energy changes involved in Chapter 18 of Berg et al. online.


How do cone cells underneath capillaries receive light?

1) The photoreceptors in fact don't receive all the light because some of it is absorbed by the blod vessels and nerve cells above the photoreceptors. The Wikipedia article on the retina states:

  Although the overlying tissue is partly transparent, and the accompanying glial cells have been shown to act as fibre-optic channels to transport photons directly to the photoreceptors, light scattering does occur.

Here is the direct link to the article describing the fiber-optic effects.

The red blood cells in the capillaries do absorb some light but the brain corrects for the color distortion. The most notable effect of the capillaries is that you can actually see white blood cells moving across your retina when looking into the skye:

  The white blood cells in the capillaries in front of the photoreceptors can be perceived as tiny bright moving dots when looking into blue light. This is known as the blue field entoptic phenomenon (or Scheerer's phenomenon).

However, our eyes are still extremely sensitive:

  A rod cell is sensitive enough to respond to a single photon of light.

Furthermore, the inverted retina actually protects the light sensitive cells from overexposure and damage by UV light.

Interestingly, cephalopods (e.g. squid, octopus, nautilus) have their photoreceptors on top of the retina, making their eyes more sensitive and better adapted to the low light conditions of the deep sea.

2) While blood circulation is necessary to maintain nutrient concentrations in large tissues, small distances can be covered pretty well by diffusion of the nutrients through the tissue. The fovea is only 5.5 mm in diameter which is small enough for diffusive nutrient supply.


Is there a practical upper limit to ploidy?

Note that it is customary to restrict posts to a single question, which is easier to answer for these complex topics. I'll do what I can here. I'm going to deal with everything at once and then reference pieces in direct reference to your 3 questions.

MECHANISMS OF CONSTRAINTS ON PLOIDY

I think that it's worth separating out some of the different mechanistic ways in which a practical limit can be set for how many chromosome copies you could have.

Another point is that the examples you give in flies and silkworms are organs with high ploidy, rather than whole organisms. It's a lot easier for an organism to have a few weird snippets of tissue with weird ploidy than to maintain that ploidy in the germ line.

Ciliates are weird and instructive:

As another totally insane example of how some organisms have evolved to reconcile this somatic desirability of lots of DNA with a stable germ line, you should look into the nuclear organization of the ciliates, which have a germ-line micronucleus (which is just passed on to future generations) and a somatic macronucleus (which is generated by amplification of the micronucleus and does all the cellular work of DNA). The macronucleus is of extremely high "ploidy" (it's more complicated than that but that's close enough), but the germ line is of a more sensible ploidy.

Some constraints I could think of:

Physical limits:

DNAs are basically huge polymers. Packing polymers into a cell imposes a physical constraint, in the sense that you need to 1) fit all that polymer into the cell/nucleus, and 2) need to still be able to use the DNA for all of the necessary cellular processes. These constraints will vary vastly from organism to organism, based on cell volume, plasticity, morphology, etc.

Metabolic limits:

DNA is expensive to make, energetically and physiologically. It ties up a lot of sugar and nitrogen that you could use to do other more interesting things, like the rest of cellular metabolism. Silkworm silk glands are obviously eye-popping, but I assume that there is some theoretical limit above that million-ploid amount (for silkworms) that would be too much DNA to support. For a little more information see this Mike Lynch paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697398/

Chromosome segregation limits:

Moving homologous chromosomes to daughter cells is not a perfect process; cells mess it up frequently, leading to aneuploidies and cancers. Some ploidies such as triploid, and presumably higher numbers with 3 as a smallest common denominator, are particularly unstable in meiosis. However, any high ploidy leads to errors at a higher rate than lower ploidies. Look at the ciliate example also. This is I believe the main reason for the "collapse of high ploidies into lower ploidies that you mention.

UPPER LIMIT TO PLOIDY IN NATURE

See all above answers.

UPPER LIMIT TO SYNTHETIC PLOIDY

See all above answers. Synthetic increases should behave the same as natural ones, as we are honestly much worse at getting making things happen than nature itself. Nature will have gotten higher already than we ever will, in all probability.

PURPOSE OF HIGH PLOIDY

See the cost/benefit of ploidy article from above.


Are non-lytic viruses reproducing themselves in the host cell?

You are conflating production of infective viral particles with lysis of the host cell. While true for some well-characterized bacterial viruses, like lambda, or T4, there are other bacterial viruses that can produce infective particles without lysing their host cell (e.g., M13, and related viruses).

Likewise, in mammalian cells there are plenty of examples where either an RNA virus (like the RNA-tumour viruses, also called retroviruses) where the viral genome integrates into the host genome, but can also produce infective viral particles. These viruses have external coats that include both proteins and lipid bilayer membranes (the viruses pinch-off, or bud, from the host cells' surface).

Many DNA viruses also integrate a copy of their genome into the host cells' genome following infection (e.g., Epstein-Barr Virus (it can cause mononucleosis), and members of the Herpes Simplex virus family that infect neurons and can cause chicken pox, or genital herpes).  Once you are infected with these DNA viruses your body is never rid of them, rather your immune system and cellular defence mechanisms "fight" the infection such that the titre of infectious viruses drops to nil, but you still have a reservoir of circulating antibodies that can be detected--and used if you are exposed again.


Significance of upper-case, lower-case and Ns in UCSC DNA files

Lowercase letters indicate repeat-masked regions. N's represent gaps.

See:
https://groups.google.com/a/soe.ucsc.edu/d/msg/genome/S4Sx8UdJAwM/tLTpVVzdhFMJ


Short answer
All mutagens are potential carcinogens unless the mutagen is highly specific to a site. As noted in the question, carcinogens need not be mutagenic.

HPV causes oncogenic transformation of a cell because of certain proteins that it expresses. HPV is considered a carcinogen by the IARC. Some retroviruses are oncogenic: they might carry an oncogene or insert randomly near an endogenous proto-oncogene and cause oncogenic transformation; this phenomenon is called insertional mutagenesis (Coffin JM, Hughes SH, Varmus HE, editors. Retroviruses). They can also integrate within a gene and knock it out. Many of these viruses are considered carcinogens by IARC.
Hepatitis viruses (B & C) can also induce carcinogenesis but insertional mutagenesis is not the sole mechanism (Cougot et al., 2005; Fung et al., 2009; Lemon & McGivern, 2012). Hepatitis viruses are considered carcinogens by IARC.
Ethanol in alcoholic beverages is considered carcinogenic by IARC. There are many substances listed as carcinogens by IARC but they are not mutagenic. The general mechanism of carcinogenesis by these substances may be prolonged inflammation or ROS generation.
Loss of function of the tumour suppressor gene p53 leads to cancerous progression (Chiche et al., 2016; Venkatachalam et al. ISBN:978-1-59259-100-8). So an siRNA that targets p53 should be called a carcinogen. It would however not cause any mutations and is hence not a mutagen.
If you consider the tools developed for genome editing, such as ZFN, CRISPR-Cas and TALEN as mutagens then they are not carcinogenic. However the term mutagen is not used for these molecules. Mutagen almost always refers to a molecule that causes random mutagenesis thereby making it a potential carcinogen.


The ice crystals that form tear and shear the bacterial cells, unless you add a cryoprotectant (for example, glycerol) to the cells beforehand.

Remember, when water freezes its volume increases.  This is why a closed soft drink can that you put into your freezer to chill faster, will burst if you leave it in until the contents are frozen.

Exactly the same thing happens to cells (animal cells, plant cells, yeast cells, etc.) if they are frozen without a cryoprotectant.


Why does our eyes got wet when we feel emotional or whenever we are hurt?

The lacrimal gland, the major source for tear production, is situated just above the eye. It sends it's secretions to the eye via the lacrimal duct. Tears secreted collect in the conjunctiva of the upper lid. There is also a nasolacrimal duct which drains the tears from the eye into the nasal cavity. Hence the sniffles when we cry.

How is it controlled? The lacrimal nucleus in the brain is the major source for innervating the lacrimal gland, is a subnucleus of the superior salivary nucleus in the tegmentum of the pons (part of the brain stem). The lacrimal nucleus is connected to the lacrimal gland by the facial nerve (more specifically the greater petrosal nerve). This is parasympathetic (meaning it is part of the autonomic nervous sytem) and the neurotransmitter transmitting the signal from nerve to gland is acetylcholine (the receptor is muscarinic subtype of the cholinergic... though strangely wikipedia says nicotinic subtype is involved as well, but maybe this is simply poorly worded and is just refering to the ganglia stopover between pre/post ganglionic parasympathetic neurons), this information helps explain how some drugs affect lacrimation (tearing up).

Taken from source (1) [I do not know how reliable this website is]: How is the lacrimal nucleus told to start lacrimation? The lacrimal nucleus receives projections from the autonomic nervous system as well as from various brain structures, including the frontal lobe, globus pallidus, thalamus, and hypothalamus. The projections from the frontal lobe are thought to be important in human psychic lacrimation (crying because of emotions).

What I know: Another brain area called the limbic system is involved in production of basic emotional drives, such as anger, fear, etc. The limbic system [in the case of sympathetic nervous system it would be the hypothalamus specifically, but this is irrelevant here since parasympathetic nerves cause lacrimation] also has a degree of control over the autonomic system. As I under stand it, the frontal lobe usually inhibits the limbic system.

Again from source (1): While humans across the world produce psychic tears in response to both positive and negative emotions, and while similar emotions have been identified in other animal species, no reports exist of other animals showing psychic lacrimation.

according to wiki (3): Compared to tearing for physical reasons,  tears for emotional reasons have s different chemical composition. They are composed of more protein-based hormones, such as prolactin, adrenocorticotropic, and leucine enkephalin (a natural pain killer), which is suggested to be the mechanism behind the experience of crying from emotion making an individual feel better.

sources:

(1) http://carta.anthropogeny.org/moca/topics/lacrimation-tearing

(2) http://en.wikipedia.org/wiki/Lacrimal_gland#Innervation

(3) http://en.wikipedia.org/wiki/Tears


How much oxygen does a plant use up at night?

Roughly, half of the CO2 assimilated annually through photosynthesis
  is released back to the atmosphere by plant respiration (Gifford,
  1994; Amthor, 1995).

Source:

https://academic.oup.com/aob/article/94/5/647/151785/Plant-Respiration-and-Elevated-Atmospheric-CO2

Furthermore, it appears like plant respiration rates do not change much with changing temperature, and that larger plants have higher respiration rates.


Did spiders respond to light for building webs before artificial light was invented?

New Answer, following discussion in comments below.

Spiders are capable of choosing habitats based on the specific requirements of the species (reviewed by Riechert and Gillepsie 1986). Spiders move within and among suitable habitat for a number of reasons, including damage to existing webs, and life history changes that require new habitat types. They point out that spiders are probably choosing the proper habitat based on various cues from the habitat. How the spiders respond to the cues would have been shaped by natural selection. The specific cues used will vary among the different species of spiders but may include wind speed and direction, thermal regime (which affects dehydation foraging time), odor cues, density of competing spiders, and more. The many options are reviewed by Riechert and Gillepsie, which is freely available and not too filled with technical jargon.

Many species of spiders do select their habitat based on prey availability. Gillespie (1987)  lists a number of references. She also studied the long-jawed orb weaving spider, which lives along streams and rivers.  She found that this spider tends to build nests in open areas near water, which prevented dehydration, but the exact site chosen was determined by prey availability. Enders (1973) studied a different orb-weaving species. He found that the juveniles were most often in densely vegetation areas but that the adults were in more open areas at the edges of woods. He suggested that web site selection of adults is driven by light.

Heiling (1999) performed an interesting study on a nocturnal orb-web spider. The spider lives near the water so it will sometimes build its orb webs on the bridges crossing the water. She found that more spiders build their webs near the lights on one particular bridge compared to unlit parts of the bridge that were otherwise built the same. She found that there was more insect activity around the lighted area (no surprise there) and that the spiders that built near the lights caught more of those insects compared to the spiders that built away from the lights.

Perhaps the most interesting result is when she studied the behavior of these spiders in the lab. Spiders that were born and raised in the lab preferentially went to the artificial light source. These had never before been exposed to the artificial lights. She argued that the light-seeking ability of the orb-web spiders she studied is genetic.

These studies suggest that light may have functioned as a visual cue for web location long before humans lit up the night sky with house and street lights, at least for spiders that build webs in open areas. Spiders may identify open areas by light cues (lighter vs darker), perhaps along with other cues such as air movement and humidity. Lighter areas would presumably be more open and thus favorable to large numbers of flying insects. Natural selection would favor spiders that responded to light for web construction. Artificial lights may present a very strong visual cue that attracts spiders, as well as insects.

However, other cues such as olfactory cues (mentioned by Riechert and Gillepsie 1986) may attract spiders. If insect prey are found in high abundance in open areas or near artificial lights, then you would expect higher concentrations of chemical odors emitted by the insects, thus drawing more spiders.

Clearly, more studies similar to that of Heiling (1999) but across a broader range of web-building spiders are necessary to determine whether many web-building spiders are responding to light and if the response is genetically determined.

Citations

Enders, F. 1973. Selection of habitat by the spider Argiope aurantia Lucas (Araneidae). American Midland Naturalist 90: 47-55.

Gillepsie, R.G. 1987. The mechanism of habitat selection in the long-jawed orb-weaving spider Tetragnatha elongata (Araneae, Tetragnathidae). Journal of Arachnology 15: 81-90.

Heiling, A.M. 1999. Why do noctural orb-web spiders (Araneidae) search for light? Behavioral and Ecological Sociobiology 46: 43-49.

Riechert, S.E. and R.G. Gillespie. 1986. Habitat choice and utilization in web-building spiders. In: Spiders: Webs, Behavior, and Evolution (W.A. Shear, ed). Stanford University Press, California, USA.

Legacy answer

Spiders evolved long before street lights were invented. The oldest known spider fossil dates back to between 374-380 million years ago (Coddington and Levi 1991.  Street lighting of any type only goes back a few centuries. So, spiders were spinning webs long before humans evolved, and before we humans began lighting our streets and homes at night.

The spiders are simply taking advantage of the situation. The lights draw insects, the food for the spiders. Webs constructed near light sources may catch more insects than webs constructed away from lights.  Could this affect the current or future evolution of spiders? Perhaps. The spiders that build webs near the lights may get more food, which allows them to obtain more energy, and potentially produce more offspring. This would increase their fitness relative to spiders that do not build webs near lights, which could lead to evolutionary change occurring over the next several thousands of years. However, it may be that so many insects flying around the web end up damaging the web much more often than the spiders away from the lights, so the spiders near the light expend much more energy maintaining the web and removing insects they don't eat.  This is one extremely hypothetical example (of many; see comments) to illustrate the point. We can't actually predict what evolutionary changes might occur, or even if they will occur.

Some of the hypotheses stated in the comments below could be tested to determine whether natural selection is possibly occurring on spider species that build near lights, or if the observation is simply observation bias as noted by @Oreotrephes.


What exactly are genes, DNA and chromosomes. How do they relate to each other and what is their function?

Your understanding of DNA is correct. DNA is a heteropolymer of monomers called nucleotides and each nucleotide is made up of a sugar (deoxyribose), phosphate and a "base" (A, T, G, C).

As you already know, DNA is organized as a double helix with the Watson-Crick pairing rules.

A chromosome contains a single DNA double helix. Many organisms have multiple chromosomes which are very different in their DNA sequence. In diploid cells (such as the somatic cells in humans), each chromosome has two copies. The two copies are almost identical and are called "homologous chromosomes". As you know each parent contributes to one of the homologous chromosomes.

During eukaryotic cell division, each chromosome is duplicated. The duplicates (or sister chromatids), are joined at a region which is called the centromere. Centromere is an attachment point for spindle fibres that pull the sister chromatids apart.

Each chromosome has multiple genes. A gene is a region of DNA that is transcribed i.e. it can give rise to an RNA (which can either be a mRNA that in turn codes for proteins or a non-coding RNA). There are other regions of DNA that are not transcribed and these are generally referred to as intergenic regions. In many eukaryotic genes some parts of the transcribed RNAs are removed as a result of splicing. The retained parts are called exons and the removed parts are called introns.

Some organelles like mitochondria and chloroplasts also have a unique genome within themselves. A genome is the entire set of chromosomes including the homologous chromosomes and the organellar chromosomes.

However, when talking about a reference genome, which is just a bioinformatic information and not an actual genome, we just have one sequence for each unique chromosome (for example, in humans, chromosomes 1-22, X-chromosome, Y-chromosome and the mitochondrial DNA). A reference genome is used as a basal set and in a population genomics study, differences from the references are highlighted instead of presenting the entire sequences.

  Picture source: https://cnx.org/contents/9TxHOD3O@4/The-Nucleus-and-DNA-Replicatio  Note that paired chromosomes (X shape) are found only during replication. Usually the chromosome is like a single thread. Chromatin is the name of the assembly (for e.g., we don't say chromatin-21).

Bottomline: We have 46 chromosomes then it means we technically have 92 DNA sequences. However you should consider the double helix as one entity (or a metamolecule) because the strands always stay together. For more details you should read a book. Genes by Benjamin Lewin and Molecular Biology of the Gene by James Watson et al. are good books on this topic.


Transcription occurs in a special structure known as transcription bubble. Inside the bubble are present the mRNA, template DNA being transcribed and the RNA Polymerase. Upstream of bubble is the DNA already transcribed and downstream is the DNA to be transcribed. There is not enough space in cell to have completely unfolded DNA for transcription, so transcribed DNA has to be re-annealed as soon as it is transcribed, giving a bubble-like appearance to the RNA polymerase-bound DNA. Hence it is called a transcription bubble. See this image for illustration:

Source

The mRNA formed quickly leaves the bubble and hangs behind like a thread coming from RNA polymerase.

Source


Short answer
The number of eyes are not always even-numbered. In fact, many present-day lower vertebrates feature an uneven number of eyes.

Background
Eyes can be generally defined as photosensitive organs. Besides the regular paired eyes, lower vertebrates such as fish, amphibians and reptiles feature an unpaired (single) brain structure called the pineal gland, or parietal eye. It is primarily a photoreceptor organ, and its electrical activity changes in response to environmental lighting (Fig. 1). The pineal does not mediate vision, and it is mainly involved in regulation of circadian rhythms (Deguchi, 1981).

Hence, many lower vertebrates can be considered to have 3 eyes. In fact, the blind cavefish Astyanax mexicanus undergoes bilateral eye degeneration during embryonic development. Despite the absence of light in the cave environment, cavefish have retained a structurally intact pineal eye. Hence, cavefish can be said to have a single eye (Yoshizawa & Jeffery, 2008).

Fig. 1. Reptilian parietal eye. Source: review of the Universe.

The mammalian pineal gland is a secretory organ only, and no longer responds to direct illumination. In mammals it is situated deep in the brain and the mammalian skull does not admit light into the brain. Instead, the mammalian pineal needs input from the eyes to regulate the circadian rhythm.

References
- Deguchi, Nature (1981); 290(5808):706-7
- Yoshizawa & Jeffery, J Exp Biol; 211:292-9


What is the difference between Regulatory Gene and Modifier Gene?

Different terms in different fields

I think that the two concepts are very similar but are used in different fields. The term "modifier genes" is often used in quantitative genetics and in evolutionary genetics while the term "regulatory gene" is often used in molecular genetics.

Example of a modifier gene that is not a regulatory gene

The concept of modifier gene can also be used in modelling when considering genes that "modify" the recombination rate (e.g. Otto and Barton, 2007; or other properties of the genome) in a quantitative manner. As such, a modifier gene is not really a regulatory gene (as it does not regulate the expression of another gene). As such I consider definitions like this one from ndsu as being too restrictive.

What I think about when I hear these terms

I would tend to think as a modifier as a more general concept than the concept of regulatory gene. Also, when I think of a regulatory gene, I think of this gene by the mechanism by which it affects other genes while when I think of a modifier gene, I think of the statistical effect of this gene on genetic properties of the organism.


Please always link to where you found this equation. It might well have been an equation that is not common enough to be recognized without the original reference. By chance, it is a very easily recognizable equation, one that has nothing to do with biology.

What your showing is an equation to compute a variance. It is not omicron but sigma ($\sigma$). In statistics, $\sigma$ is the standard deviation and hence $\sigma^2$ is the variance. $\mu$ is the mean and $n$ the number of elements from which these statistics are being computed.


Do sulfate reducing bacteria ingest their sulfate as solid, or as dissolved in water?

Sulfates in water would not be liquid. Their melting points are far to high. When a sulfate dissolves into sulfate ions and some cation such as potassium, we say it is solvated, not liquid. Sulfates would also not be present as gasses due to their ionic nature as well as high molecular weights. So that leaves solvated sulfate ions and solid sulfates that have not completely dissolved.

To be ingested in bulk as a solid would require endocytosis which is not performed by prokaryotes: http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/proeu/proeu.html

Further research indicates sulfate, as ions, enters the cell through permeases: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.532.943&rep=rep1&type=pdf

Edit: Here's some files to help with the idea of how ions and other molecules enter cells. Again, bacteria do not engulf substances whole, in the process of endocytosis, such as eukaryotes are capable of. Here is an image of a nitrate ion within a transport protein. Only a few amino acids of the protein are shown here, the actual protein is much larger and spans across the entire membrane creating a channel for the ion to enter. http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=4U4W&preset=ligandInteraction&sele=[NO3]

Here's another channel, aquaporin, which allows transport of water across the membrane. http://pdb101.rcsb.org/motm/173 The top left image shows the channel in the protein leading to the interior. The third image down shows the interaction between the water and the amino acids (backbones only are shown) which facilitate the water's passage.


Does it really contain a capsid?

Yes. Coronaviruses have a capsid, but it's not reminiscent of the polygonal (icosahedral) capsid depicted in the Research Gate picture you referenced. Icosahedral capsids form a sort of shell around the viral genome, where helical capsids actually bind the viral nucleic acids, holding them in a more rigid shape.

  Is it SARS-CoV2 lacking a capsid, and thus special exception from general description of coronavirus?

SARS-CoV-2 is not an exception. In fact, its nucleocapsid is a target for diagnostic tests.

  What is the actual/ realistic shape of coronavirus capsid?

It is actually depicted in Goodsell animation you referenced. The nucleocapsid proteins are the squigly bits in and around the genomic RNA (labeled "N", for Nucleocapsid). The actual capsid is the complete complex of N proteins bound to genomic RNA, so it doesn't have that polygonal outline that maybe we're used to when we see depictions of viruses. If you want a more detailed look at the actual capsid protein structure, there's a depiction of its crystal structure in this New York Times piece co-authored by Carl Zimmer.


Can you consider a human as alive, or is it the cells on the body that are alive?

The definition of life is the main issue here. That is one of the great philosophical questions in Biology (and not only Biology) and is way beyond the simple Q&A format of this site. However, most definitions of life can be boiled down to1:

  A self replicating entity that interacts2 with its environment.

Or, even more simply [1]:

  Life is self-reproduction with variations

In both cases, the answer to your question depends on which level you are focusing on, your resolution if you like. If you take a human cell and apply either of the definitions above, it is alive. A cell is capable of autonomous reproduction, and metabolizes substances harvested from its environment. The same holds true of you look at the human body. However, the definition will not hold for a part of the human body, for example an arm or kidney.

Consider also that a human cell is capable of making more copies of itself, more individual cells. A human body is also capable of making more copies of itself, more human bodies. They can, therefore, both be taken as alive.

There are even more complex examples like Dictyostelium discoideum an amoeba that can exist (and be alive) either as a single cell or as a colony sporting different cell types and rudimentary organization. However, the organism is alive in both of these stages. In one case, you would consider the cell to be the fundamental unit of D. discoideum life, and in the other you could consider the colony.

So, to answer your question both a human cell (as long as it is alive, actively metabolising and capable of reproducing) and the entire human body can be taken as alive. That my cells are alive does not lessen the fact that I am too. It is just a matter of perspective.

References

Trifonov EN., Vocabulary of definitions of life suggests a definition. J Biomol Struct Dyn. 2011 Oct;29(2):259-66.

1 Yes, I know this is a simplification, I just don't want to be drawn in to a long winded discussion on what the definition of life is. My answer is applicable to any of them really.
2 Metabolism can be seen as a form of interaction.


Why do bananas turn black after some time?

Banana skin consists of plant cells and cellular tissue. This tissue contains phenolic compounds. On getting old, the cell membranes of the banana get weak. When the membranes weaken, the phenolic compounds mix with polyphenol oxidase (an enzyme present in the cells cytoplasm). As a result of this interaction, the phelonic compounds oxidize and produce a brown compound called melanin which results in the colour of the peel turning black. Also, the green skin of banana contains a gaseous plant hormone, ethylene, which diffuses into the fruit and hastens the process of ripening. It is yellow when the fruit is ripe and turns black with the production of more and more ethylene.


Effect of sex-ratio on the effective population size

The reason that an unequal sex ratio affects the effective population size is because offspring are produced by one male and one female parent, and an unequal sex ratio increases the rate at which genetic drift will occur.

  "...the smaller number of males still contributes half of the genes in the next generation..."

In other words, assuming the male population is smaller, the genes passed on by the males/fathers are sampled from a smaller population than that of females/mothers. As you know, smaller populations are more prone drift.

Imagine the classic drift example with a bag of blue and red marbles, but have the parental generation with an unequal number of marbles in either bag.

Hartl & Clark illustrate (see figure 4 here) the relationship between sex-ratio and effective population size, where a sex ratio of 1:9 gives an effective population size of around 36% the actual size (given by $100 \times (N_e/N)$). This means that the rate of inbreeding and drift in the focal population is equivalent to that of an idealised population which is 0.36 times the census size of the focal population.

$$N_e = \frac{4N_mN_f}{N_m+N_f} = \frac{4 \times 1 \times 9}{1 + 9} = 3.6$$

The population is diploid and dioecious; each parent carries two genes, and each parent must be replaced within the population so each pair must produce two offspring. Consider the case where $N_m = N_f = 1$ (and thus $N = N_e = 2$). The number of genes in this population is four. Therefore, to maintain the same population size, four genes must be drawn from the ancestral population.

Further reading:

Hartl & Clark (Page 123-124, Random Genetic Drift: Unequal Sex Ratio)
Conner & Hartl (Page 62, Chapter 3)

While (personally) I can't prove this mathematically, I can demonstrate it using simulation. I've written up a simulator of genetic drift in R, which can cope with unequal sex ratios.

The first four graphs are populations with $N_E = 360$ at various sex ratios ($N_M / N_F$ = 0.11, 0.33, 0.67, 1.00), for 100 replicate populations simulated over 80 generations, with an initial allele frequency of 0.2. The four simulations have different census population size, but equal effective population size, because of the sex ratio. The four groups of populations behave similarly (rates of drift are similar for the simulated populations under the various conditions).

These four use larger populations ($N \times 15$), at the same sex ratios, where $N_E = 5400$ in all cases simulated over 400 generations. Again the groups of simulations behave similarly.

Update:

I've added histograms to ease viewing of the pattern, using $P = 0.5$, for 1000 populations simulated over 25 generations, where $N_E = 360$ and census population size/sex ratio varies between simulations. This distributions are similar despite the different census population sizes.