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How much DNA do humans have?
A normal human body has approximately 3 billion base pairs. Given that humans have 10 trillion cells, how is that the number of base pairs of DNA is less than the number of cells? It can happen only if most of these cells don't have DNA, or have I misunderstand the topic?
Can you give an account of why the number of cells exceeds the number of DNA base pairs significantly? Isn't it logical to have more DNA base pairs than the number of cells?

What research did you do before posting this question? Your conclusion was clearly absurd, so an attempt to identify the flaw in your argument was called for. I am voting to close this question as extremely low quality.

No, number of base pairs is not at all related to number of cells. The correct statement should be 'a normal human body has approximatrly 3 billion base pairs of DNA in every cell'. I suggest you keep studying.

1 base would code for one cell? That would make for either very simple cells, or very information dense DNA.

Answer to the question
How much DNA is there in our cell nuclei?
In humans, there are about 6 billion base pairs in the nucleus of each cell. Why 6 billions and not 3? There are 3 billions base pairs per haploid genome (see ploidy) and therefore 6 billions base pairs for the whole genome. This number may actually further double during specific phases of the cell cycle. Each single cell contains a copy of the whole genome (with a few exception such as red blood cells for example).
So the total number of base pairs in a 10 trillion cells individuals is about $6\cdot 10^9 \cdot 10^{13} = 6\cdot 10^{22}$ base pairs.
Further information for fun
How much DNA in our cells outside of nuclei
Now, in cells there is DNA outside of nuclei. In animals (incl. humans), we have DNA in mitochondria as well. there is of the order of 104104 base pairs per mitochondria (16,569 sites to be accurate) and there are of the order of 104104 mitochondria per cell, that is 108108 base pairs total per cell which is only one order of magnitude below the number of base pairs in the nucleus per cell.
There is therefore an extra $3\cdot 10^8 \cdot 10^{13} = 3\cdot 10^{21}$ base pairs in cells outside the nucleus.
How much DNA in bacteria living in the human body?
Note that by "in the human body", I also include "in the gut" even though the inside of the guts are typically considered as being the outside our body.
There are about 100 trillions of bacteria in every one of us (this number is a vague approximation; see wiki > Human microbiota). Yes, most of the cells living in us are not our cells but are bacterial cells!
Bacterial genome vary widely but as a gross and almost insulting approximation, let's consider that the average bacterial genome from our microbiome has a genome size of $10^6$ base pairs (note bacteria don't have nuclei or mitochondria).
That means that in our body we have to add to the above numbers $10^6 \cdot 10^{14} = 10^{20}$ base pairs (which is only a hundredth of $10^{22}$).
How much DNA in the viruses in our body?
Let's not forget our virome. Unfortunately, I could not find estimates of the number of viruses (and viroids) in our body.
How much DNA is outside cells and viruses in our body?
Of course, there's plenty of DNA in our body. There's DNA in everything we eat and this DNA end up in our blood stream and in our cells. I failed to find an estimate of how much DNA does that represent.

The addition of mitochondrial base pairs would not even show up on that measurement anyway, mitochondria only have a few genes.

@John Actually, there is of the order of $10^4$ base pairs per mitochondria (16,569 sites to be accurate) and there are of the order of $10^4$ mitochondria per cell, that is $10^8$ base pairs total per cell which is almost of the same order of magnitude than the number of base pairs in the nucleus. So... it may show up on these calculations. It would show up for sur if we consider an extra significant digit.

Right I forgot about multiple mitochondria per cell, my bad.

Add the mito calculation as a footnote to the answer ? Makes the answer even better.

3 billion is the size of the haploid genome. Somatic cells have 6 billion bp.

@canadianer It can go to 12 billions bp depending on the stage of the cell cycle.

@RoniSaiba Following your advice, I wrote a few more far fetched calculations.

@Remi.b: Want to do another far-fetched calculation?  Suppose you liquified a human body, and forced it through a filter that extracts DNA: how much would you have?

@jamesqf I have it at around 65 grams.


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What is the role of potassium acetate in plasmid extraction?
What is the role of potassium acetate in the alkaline lysis method of plasmid extraction?
Earlier I was thinking its role is to shield plasmid DNA (the same as sodium acetate in genomic DNA extraction). When 100% ethanol is added, it the DNA precipitates and then we remove potassium ions from the pellet using 70% ethanol.
However, I have read that potassium acetate does not have the same function as sodium acetate in genomic DNA isolation but, rather, is a neutralizing agent which helps small plasmid DNA to renature.
I am bit confused about the role of potassium acetate and why sodium acetate cannot be used instead.

The alkaline lysis method of plasmid purification involves the addition of sodium dodecyl sulfate to lyse the cells and sodium hydroxide (a strong base) to denture the DNA. Potassium acetate is then added for two reasons:

The acidic acetate buffer neutralizes the solution and allows catenated plasmids to renature.
Potassium dodecyl sulfate is poorly soluble in water. Adding potassium to solutions of dodecyl sulfate precipitates it, thus facilitating its removal.

Okay..but then...how plasmid DNA is concentrated...like in genomic dna extraction..sodium ion forming shield around dna and on adding 100% ethanol interaction getting more stonger and then pelleting it..

So isn't potassium acetate playing that role here?....then why we are adding 100%ethanol here too?

@Krishi1234 You can precipitate plasmids with ethanol and salt. You need to post your protocol in order for us to tell what the potassium acetate is being used for. I answered based on the standard alkaline lysis method, but if you’re adding KAc and ethanol at the same time then that’s a different story.

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What does (-;-) after a gene mean?
I'm using Promethease to examine genome data originally downloaded from 23andMe. Some genes I notice do not show allele information (eg. (G;G), (C;G)) and instead seem to be blank (-;-) like in the screenshot I provided. Can someone please tell me what this means? Thanks in advance.

I suggest you to take the tutorial you can found from here
Before the $(-;-)$ there is the specific location of the gene in the DNA. Between the brackets you have your specific genotypes at the location marked before. So, whatever is inside the brackets is referred to a single nucleotide polymorphism (SNP) found in your gene. If there is nothing, as the case of the screenshot that you provided, is possible that they are not able to determine the SNP (so the SNP is not found and this information is missing).

Thanks for your answer. Yes, I'll look at the tutorial.

@OGLdude You are welcome, if you think that my answer is good, mark the question as answered by accepting the answer ;)

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Why is there sperm mitochondrial suicide?
The mitochondria in the sperm are digested upon entry into the egg, making mDNA inheritance exclusively female. What is the advantage of this? Wouldn't some male mDNA be beneficial because of the advantages of (at least a little) sexual reproduction?
Reference:
"Postfertilization autophagy of sperm organelles prevents paternal mitochondrial DNA transmission" (behind paywall, here's a ScienceDaily article discussing the results).
Edit:
Both answers seem valid but it is hard to quantify the relative costs.

cant be sure about this but sperm mitochondria have the main purpose of fuelling the sperm movement. There is a likelihood that these mitochondria have developed some mutation because of this excessive respiratory load.

Maternal inheritance of mitochondrial DNA is very well conserved, although some species, such as some mussels, show paternal inheritance.  As for why or what the advantage is, some of it is due to basic logistics: sperm cells have ~100-1000 mitochondria, egg cells have 105-106, so male contributions are largely washed out.  Plus, most mitochondria in sperm are toward the tail, which does not always or necessarily get inside the egg.
For a more selection-based mechanism of the actual destruction, think about what sperm do.  They are small packets of energy that do nothing but race until they die.  That's it.  Energy production, which occurs in the mitochondria, produces reactive oxygen that can damage genomes.  The mt-genome in the egg is far less likely to be damaged.
Additionally, I might look to chromosome uniformity.  Heteroplasmy does occur now and again, and it's not usually a good thing.  Mitochondria are very important, so it makes sense to have an all-or-nothing approach, lest any deleterious genomes persist.

The mainstream theory, I believe, is that it's a way of avoiding the inevitable destructive (organismal fitness-lowering) competition that the two parents' mitochondria would otherwise be in.
From Austin Burst and Robert Trivers' book Genes in Conflict (p. 146):

Selfish mitochondrial genomes... have
  a replication advantage over normal mitochondrial genomes in
  within-organism selection, but they lose out in conventional
  among-organism selection... Therefore, if a population is polymorphic for 2 mitochondrial types, one more selfish than the other, a nuclear gene that somehow reduces the efficacy of the within-individual selection will tend to become associated with the less selfish type, and so can increase in frequency due to among-organism selection.. That is, there will be selection for nuclear genes that modify mitochondrial behavior so as to reduce the efficacy of within-organism selection (just as there is selection on nuclear genes to suppress drive at unlinked loci)...
An even better way to limit within-organism mitochondrial selection is
  to ensure that only one parent transmits mitochondria to the next
  generation - that is, to impose uniparental inheritance...

I think the implication is that uniparental inheritance on the mtDNA, is imposed by adaptations acting in the interest of the nDNA. Without uniparental inheritance, within-cell selection on mitochondria would drive them to replicate faster than is optimal from the rest of the cell's (and the nDNA's) perspective.
Apparently this theory also plays a role in answering Fisher's question, from the preface to The Genetical Theory of Natural Selection:

No practical biologist interested in sexual reproduction would be led to work out the detailed consequences experienced by organisms having three or more sexes; yet what else should he do if he wishes to understand why the sexes are, in fact, always two?

Laurence Hurst and Bill Hamilton argue, in their paper Cytoplasmic Fusion and the Nature of Sexes (1992):

Binary mating types are proposed to arise in a three-stage process through selection of nuclear genes to minimize cytoplasmic gene conflict at the time of gamete fusion. In support of this view we argue that: (i) in systems with fusion of gametes, the mating type genes are typically binary and regulate cytoplasmic inheritance; (ii) binary sexes have evolved several times independently associated with fusion, although at least twice binary types have been lost, associated with a loss of fusion; further, in accordance with the theory are findings for isogamous species that (iii) close inbreeding may correlate with less than two sexes and biparental inheritance of cytoplasmic genes; and (iv) species with more than two sexes may have uniparental inheritance of cytoplasmic genes, be rare and be afflicted by deleterious cytoplasmic genes which attempt to pervert normal cytoplasmic genetics.


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What is cytoplasmic localization?
I was studying development of chick but didn't understand what is cytoplasmic localization. My book says:

After third cleavage , the rest of the cleavages are irregular and completely delimited cells are formed all over the germinal disc which is termed as blastoderm. This outcome of cleavage called cytoplasmic localization helps seal the developmental fate of each cell's descendants.

"Cytoplasmic localization" is a very general term and it means that something is present in the cytoplasm. For instance (hypothetical but there are known examples), you can say protein-X is localized to cytoplasm or the cytoplasmic localization of protein-Y is reduced upon phosphorylation. Similarly, there are terms like "nuclear localization", "ER localization", "mitochondrial localization" etc.
The usage mentioned in your excerpt is actually unclear and misleading. There is no process called cytoplasmic localization. What it actually means is that there are proteins/RNA inside the cytoplasm of the embryo that are asymmetrically distributed. When the cell divides, these molecules are therefore asymmetrically sorted to the daughter cells. Depending on what (and how much of) molecules the daughter cells receive, different cells adopt different phenotypes. Also note that the axis of division also plays a role; if lets say the distribution of a given molecule is asymmetric only about the anteroposterior axis and the division happens along that axis then both daughter cells receive the same amount of molecule and both the cells would be similar (w.r.t that molecule). This won't be the case if the division is along left-right axis. See the figure below.

From: Berika et al., 2014

I am not sure which book you are following but Developmental Biology by Scott F Gilbert is a good book and explains these processes nicely.

That's absolutely terrible phrasing in that quote.
I think it's referring to one mechanism of cell fate determination: a transcription factor can be transported out of the nucleus (which will result in it being localised to the cytoplasm rather than the nucleus - "cytoplasmic localisation"), and thereby that transcription factor won't perform its function anymore. The resulting changes in gene expression can be involved in the developmental fate of that cell and its descendants - depending on which transcription factor it is.
In the early embryo, various factors (for example chemical gradients of a signal) cause different cells to apply this mechanism to different transcription factors, thus resulting in different cell fates. However, unlike the statement in your quote, that is not an outcome of cell cleavage.


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Do the pH and other ions affect the hydrolysis of ATP
ATP hydrolizes to ADP and phosphate in a strongly exergonic reaction and is used for energy transfer and short-term storage in cells.
ATP is stable inside a cell, so a significant activation energy must be necessary for the reaction.
However, the English Wikipedia article implies that stability of ATP is not a given, but depends strongly on the properties of the surrouding solution:

"ATP is highly soluble in water and is quite stable in solutions between pH 6.8 and 7.4, but is rapidly hydrolysed at extreme pH." and
"ATP is an unstable molecule in unbuffered water, in which it hydrolyses to ADP and phosphate."

How does the pH affect the hydrolysis of ATP?
Why is it even relevant if the solution is buffered or not? (Do the ions stabilize the molecule somehow?)
Are there other effects that influence stability in animal cells?

Welcome to Biology SE. This is a reasonable question, although perhaps more chemistry than biology. However I have altered the title to include the key factor you are concerned about — pH. That will help others know what your question is about, and thus whether they feel they may be able to help you. It is also important for archiving purposes.

Actually, It seems that both the right ph and the existance of a buffer in the solution is required, so that needs clarification as well.
Sorry I asked two questions instead of one, but it might be related.
I did not ask at Chemistry SE, as there might be something else going on inside cells that might influence stability of ATP.

I guess alkaline hydolysis will happen via a mechanism similar to alkaline hydrolysis of phosphodiester bond in RNA.

I've changed the title to the more precise hydrolysis, because that's what the Wikipedia quotes refer to. I would imagine @WYSIWYG is right about alkaline hydrolysis. I don't know about acid hydrolysis.

I'm not sure how the activation energy would be affected by pH, but it is well known that the equilibrium is shifted by pH since the various phosphates have different pKa values. See for example http://www.jbc.org/content/193/1/425.citation

Stability of ATP is largely due to Mg2+. ATP in cell is actually Mg2ATP2-
The Mg ions stability the negative charges on the phosphates. pH is also important of course, but Mg is key, hence you see Mg2+ all the time in biochemical reactions where ATP is involved.

@David. aside from the question " are there other effects that influence stability in animal cells.

Mg2+ is there as a counter-ion and is required so the ATP is in the right conformation to bind to the active site of enzymes. All this talk of "stability" is unscientific waffle. And the Wikipedia entry is of no relevance to biology talking about the need for buffers and suitable pH. That's the milieu of the cell. It's really the sort of thing a chemist would write about preparing solutions in the lab.

@ David: My question title was changed by a moderator. The answer matches my original question "Why is ATP stable in cells?".

@SciEnt: Thank you for your answer! Do you have any sources readily available?

@user25269 Any biochemistry textbook really. But one i have personally read. Lehninger Principles of Biochemistry. By Nelson & Cox 6th Ed.

@David: I'm no expert, but I don't see why Mg2+ cannot stabilize ATP in solution. Could you please elaborate?
Of course, ATP is (kinetically) stable in the milieu of the cell. However, it is unstable without a buffer and hydrolysis occurs without any enzyme or other catalyst.
I wanted to know which component/property of the cell milieu is responsible for ATP being stable in the cell, as the reason is not evident for me.
Also, please keep it civil.

@user25269 The only reason ATP would be "unstable" without a buffer is because when the free acid were  dissolved in water the solution would become acidic and (apparently) be hydrolysed. As the cellular milieu is buffered by a multitude of things ( especially bicarbonate) this problem does not arise. And stop talking about "stability". ATP does not undergo alkaline hydrolysis at cellular pH because it is only slightly alkaline and the concentration of hydroxyl ions is insufficient. You seem to be obsessed by a problem that doesn't exist.

The question is about pH. Your answer is about Mg. It basically qualifies as "insufficient explanation".

@TomD "I wonder how many of the downvoters to this answer realize the critical importance of Mg in all ATP-dependent biological reactions." I certainly do, but, as I have written, I regard it as irrelevant, because the question (not the title) was about the hydrolysis of ATP and something called its stability (degradation of the purine ring?). If you think Mg ions somehow prevent the hydrolysis or degradation of ATP, rather than just being the counter-ion required in enzymic reactions, please cite sources.

OK. Let’s answer the questions you pose:
How does the pH affect the hydrolysis of ATP?
High concentrations of hydrogen ions or hydroxyl ions (“extremes of pH” — as you quote) cause acid or alkaline hydrolysis. The mechanism of alkaline hydrolysis is presumably through a cyclic intermediate, as with the hydrolysis of RNA. Acid hydrolysis of ATP requires very low pH — for example it has been studied in 3M perchloric acid — and the mechanism is quite complex, according to work published by Hutchings et. al. in 1981.
Why is it even relevant if the solution is buffered or not?
In unbuffered solutions the pH may easily deviate from the physiological range. This is a practical consideration of work in vitro. Physiological and cellular systems are highly buffered by a variety of ions and even macromolecules so the problem does not arise.
Are there other effects that influence stability in animal cells?
You are mistaken in your assumption that there is a particular need to prevent hydrolysis of ATP within animal cells. This appears to be based on a misunderstanding of a Wikipedia entry which is more concerned with the chemistry of ATP rather than its situation in the cell.

@TomD — ATP is an important metabolite, and its generation and the coupling of its hydrolysis to chemical, electrochemical and mechanical processes is important. Whether it is “the basis of life” any more than DNA, RNA, proteins, lipids, NAD etc. is an irrelevant and fruitless question. What I maintain is that the problems Nature had to solve with respect to ATP were those already mentioned. Its activation energy and chemistry are such that there is no tendency for its spontaneous hydrolysis at physiological pH, so preventing this is not a problem and certainly not the “the basis of life”.


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Identifying type of inhibitor from $K_m$ and $V_{max}$
Apparently it is possible to identify whether an inhibitor is competitive or non-competitive from graphs of substrate concentration (x axis) and rate of reaction (y axis).
There needs to be a line for with inhibitor (constant concentration) and without inhibitor. The difference in $K_m$ and $V_{max}$ can then be interpreted to find out whether the inhibitor is competitive or not.
I know that if the effect of the inhibitor decreases with an increase in
substrate concentration then inhibitor is competitive.
However I don't understand how to tell from the graphs mentioned earlier and  $K_m$ and $V_{max}$. Could someone explain.
I have tried to google this but most of what comes up is scholarly articles which are beyond my level of understanding...

You should use the freely searchable text books at NCBI Bookshelf for questions on biochemistry and molecular biology, rather than googling. If you had consulted Biochemistry by Berg et al you would have found a carefully written, edited and illustrated section on the topic of your enquiry: https://www.ncbi.nlm.nih.gov/books/NBK22530/#A1068.

@David Thanks, this look like a very good resource.

Competitive inhibitor competes for the active site. Therefore it will interfere with the binding of the substrate thereby increasing the apparent KM.
A strictly non-competitive inhibitor does not compete for the active site. It however inhibits the catalysis by reducing the available molecules of active enzyme, E0 (if it is a perfect inhibitor), thereby lowering the Vmax.
There can be mixed inhibitors too and there can be different kinds of mixed inhibition. For example an inhibitor that interferes with catalysis and can also compete for the active site.
Depending on how you define KM, a non-competitive inhibitor may or may not change it. If such inhibitor can bind to the enzyme at non-active site and reduce its kcat, it changes the KM as well as Vmax in case of Briggs-Haldane kinetics.

@tomd uncompetitive inhibition  is only a case of catalytic inhibition. It mandates that the inhibitor binds to ES complex. If you consider my case where an inhibitor reduces kcat, where would you place it? It doesn't fit in any of the typical cases. Classification of inhibition mechanism based on LB-plot is, IMHO, quite simplistic. As you said, a non-competitive inhibitor can change Km. Also an inhibitor that does affect substrate binding may not be competitive at all. I like your answer (it is quite comprehensive), but I guess LB analysis alone is insufficient.

@tomd thanks for.the clarification. I was only aware of the popular textbook definitions which do not represent all the inhibition mechanisms.

I think it is possible to identify the type of inhibition from (initial) velocity vs substrate-concentration curves, but it is difficult. The usual way this is done is by using a linear transformation of the Michaelis-Menten equation, such as the Lineweaver-Burk plot.
But you are right: for a reversible inhibitor, the way to identify the inhibition pattern (that is, to determine whether a reversible inhibitor is competitive, uncompetitive, mixed, or non-competitive) is to inspect the changes to the kinetic constants (usually  Km and Vmax, but see below)
Before we get into how that is done, there are a few points we need to be aware of.

The following  only applies to reversible inhibitors.  Irreversible inhibition,
such as the inhibition of acetylcholinesterase by the nerve-gas sarin, is treated differently. (By 'reversible', it is simply meant that if the inhibitor is removed, by dilution for example, the inhibition goes away).  In addition, tight-binding inhibitors are not considered.
The following also only applies to single-substrate enzymes that obey the Michaelis-Menten equation. (But the analysis may be extended, without too much difficulty, to multi-substrate enzymes).
We need to be very careful about the term 'non-competitive'.  It means different things to different people. It is also often the least interesting pattern of inhibition.
When analyzing inhibition patterns, it is often easier to analyzed the effect on Vmax and  Vmax/Km (the specificity constant), rather than on Km and Vmax.
The reason for this is that Km is a complex kinetic constant and (as Dalziel and Fersht have
shown), it should be thought of as the ratio of  Vmax and  the specificity constant (Vmax/Km). In this respect, enzyme kineticists have 'messed things up' by considering the specificity constant to be the ratio of the maximum velocity and the Michaelis constant: it is the Michaelis constant that is the ratio.  However, the paradigm of considering the specificity constant as Vmax/Km is now so ingrained, I'll stick with it. But the 'trick' in analyzing inhibition patters is to think in terms of  Vmax and  Vmax/Km.
Much of what follows may also be applied to reversible activation, but I am not going to go into that at all.

1. Reversible Inhibitor Patterns
We can now define our inhibition patterns, independent of any mechanism that gives rise to them, as follows:

A competitive inhibitor has no effect on Vmax but decreases the apparent value of Vmax/Km.  We can also say, in 'old school terms', that a competitive inhibitor has no effect Vmax but increases the apparent Km value. Or, if we are going to 'visualize' things in terms of Lineweaver-Burk plots (see this wikipedia article), we can say that a competitive inhibitor has no effect on  Vmax but increases the apparent value of Km/Vmax
An uncompetitive inhibitor decreases the apparent value of Vmax but has no effect on Vmax/Km. Or, thinking in terms of reciprocals, an uncompetitive inhibitor increases the apparent value of 1/Vmax but has no effect on Km/Vmax. In many ways, 'uncompetitive' is a a very poor term. Cornish-Bowden (2004) suggests the term 'catalytic inhibitor', and Laidler and Bunting  use the term 'anti-competitive' to describe this type of inhibition.
A mixed inhibitor decreases the apparent value of Vmax and decreases the apparent value of Vmax/ Km. Or, thinking in terms of reciprocals, a 'mixed' inhibitor increases the apparent value of 1/Vmax and increases the apparent value of Km/Vmax.
A non-competitive inhibitor is best thought of as a special case of mixed inhibition where  the apparent values of Vmax and  Vmax/ Km are decreased to the same extent.  There is  an interesting consequence of this:  as the Michaelis constant may be thought of  as the ratio of these two kinetic constants, it is unchanged in non-competitive inhibition.  But  it is difficult to envisage a realistic kinetic mechanism that results in this type of behavior.   Cornish-Bowden (2004, pp 118-119) is very strong on this point (There is also a fourth edition of this great book).
We now come to a 'tricky' bit. Some authorities, notably Cleland, do not distinguish between 'mixed' and 'non-competitive' inhibition, but instead call all cases where both  Vmax and  Vmax/ Km are decreased 'non-competitive inhibition'.  We need to be very careful on this one. As someone once said, enzyme kineticists would rather use each other's toothbrushes rather than use each other's nomenclature.

So there we have it: the two cases that 'demarcate' reversible inhibition are where only the apparent Vmax is changed (uncompetitive inhibition) and where only the apparent Vmax/Km (the specificity constant) is changed (competitive inhibition). 'Mixed' inhibition is where the apparent values of both these kinetic constants are affected, and a special case of 'mixed' inhibition is where the the apparent values of both kinetic constants are decreased to the same extent, resulting in no change to the Michaelis constant.
2. Reversible Inhibitor Mechanisms
So far, I have said nothing about the mechanisms that might give rise to these inhibition patterns.
Preliminaries:

In what follows, $K_m$ is the Michaelis constant, $V_{max}$ is the maximum velocity, $s$ is substrate concentration, $i$ is inhibitor concentration, and $K_{i}$ and $K_{ii}$ are inhibition constants. Both $v$ and $v_i$ refer to the initial velocity.
Inhibition patterns are analyzed using the Lineweaver-Burk plot. This is convenient as in such a plot (see this wikipedia article), the y-axis intercept equals $1$/$V_{max}$ and the slope equals $K_m$/$V_{max}$.  Changes to the apparent value of $V_{max}$ are manifested as a y-axis-intercept effect, and changes to the specificity constant ($V_{max}$/$K_m$) are manifested as a slope effect. In addition, the x-axis intercept equals $-1$/$K_m$, so that changes to the apparent $K_m$ value, or lack of such a change, is easily recognized.
The Lineweaver-Burk plot is not the only linear transformation of the Michelis-Menten equation, or even the best one (see here).  Other plots are the Hanes-Woolf plot and the Eadie-Hofstee plot. As someone else once said, biochemists worship at the alter of the straight line. I use the Lineweaver-Burk plot because, IMO at least, it is the most intuitive.
It needs to be borne is mind that many kinetic mechanisms may give rise to an inhibition  pattern. Many kinetic mechanisms may give rise to competitive inhibition, for example. What follows are illustrative examples.
All of the plots below (generated using Mathematica) were created with $V_{max}$ = 100 and $K_m$ = 10.  When only one inhibition constant was required ($K_i$), it was set to 100. When two were required, the second ($K_{ii}$) was set to 20  (All 'arbitrary units'). The plots, of course, are very easy to generate and may be done with many software applications.

(a) Competitive Inhibition

Let's consider reversible inhibition in single-substrate enzyme described by the mechanism shown above, where both the inhibitor and substrate compete for the 'free' enzyme.
Derivation of the rate law for this mechanism using either the equilibrium or steady-state assumption, leads to an equation of the following form (nice derivations  are given in Segel, 1975):
$$ v_{i} = {
  {{{V_{max}}}\ s\ }\over{K_{m}(1 + {i\over{K_{i}}})} + s}\ \ \ \ \ (1)$$
Representative  plots of Eqn (1), showing the effect of increasing inhibitor concentrations:

Taking reciprocals of Eqn (1) followed by rearrangement leads to the Lineweaver-Burk  linear  transformation:
$${1\over{v_i}}=\frac{K_m}{V_{max}}(1 + {i\over{K_i}})( {1\over{s}}) + {1\over{V_{max}}}\ \ \ \ \ (2)$$
It is immediately obvious that the inhibitor increases the apparent value of  $K_{m}$ / $V_{max}$ but does not effect  1 / $V_{max}$.
That is, it effects the specificity constant ($V_{max}$ / $K_{m}$) but not  $V_{max}$.  Inhibition is therefore competitive
Plots of Eqn (2) predict a family of straight lines intersecting on the y-axis at $1$/$V_{max}$, and the competitive inhibition pattern is easily recognized:

In terms of the Lineweaver-Burk transformation, a competitive inhibitor causes the slope to increase but does not change the y-axis intercept.
We can also go a step further.  The slopes of the above lines are given by the following Eqn:
$$slope = \frac{K_m}{V_{max}} + \frac{K_m}{V_{max} K_{i}}{i}\ \ \ \ \ (3)$$
Thus a plot of slope vs inhibitor-concentration is predicted to be a straight line which intersects the x-axis at -$K_i$

Such replots serve two functions. Firstly, they allow determination of the $K_{i}$ value. In this case, the x-axis intercept is -100, which is not too surprising as 100 was the value of $K_i$ chosen in the simulation. Secondly, they check for unexpected kinetic complexity. A curved slope replot, for example, might be indicative of partial competitive inhibition, where the EI complex can perhaps breakdown to give product.  Such kinetic complexity is probably rare with single-substrate enzymes, but may occur in multi-substrate enzymes (and may require the rejection of a simple kinetic mechanism as an explanation of kinetic data).  Segel (1975) is very strong on partial inhibition, and the mechanisms that may give rise to it.  When the slope replot is linear we may speak of linear competitive inhibition
 (see Cornish-Bowden, 2004).
A number of points may be made about competitive inhibition:

One of the 'hallmarks' of competitive inhibition is  that the inhibitory effect may be overcome by adding excess substrate.
A competitive  inhibitor need not bind the the active site. All that is required is that it  binds to the free enzyme in a manner that prevents substrate binding.  An allosteric inhibitor, for example, may be competitive.  But, of course, competition between the substrate and inhibitor for the same active site is one way that competitive inhibition may arise (assuming that binding of inhibitor prevents substrate binding). Segel (1975) is very strong on this point.
A good example of a competitive inhibitor is malonic acid, which inhibits succinate dehydrogenase (see Segel, 1975). In the world of two-substrate kinetics, pyrazole is a competitive inhibitor, with respect to ethanol, of horse liver alcohol dehydrogenase, and a classic paper (Li and Theorell)  showing this is available here

Finally, let's reiterate this point: Eqn (1) describes one mechanism that gives rise to a competitive inhibition pattern. It is certainly not the only one.
(b) Uncompetitive Inhibition

Now let's consider a mechanism, described by the diagram above,  where the inhibitor cannot bind to the 'free' enzyme, but instead bind to the enzyme-substrate complex (to give an abortive EAI ternary complex)
Derivation of the rate law his mechanism (again by making either the steady-state or equilibrium assumption; see Segel, 1975) leads to an equation of the following form:
$$ v_{i} = {
  {{{V_{max}}}\ s\ }\over{K_{m}} + (1 + {i\over{K_{i}}}) s}\ \ \ \ \ (3)$$

Transformation to the Lineweaver-Burk  form:
$${1\over{v_i}}=\frac{K_m}{V_{max}}( {1\over{s}}) + {1\over{V_{max}}}(1 + {i\over{K_i}})\ \ \ \ \ (4)$$
In this case,  the inhibitor increases the apparent value of  1 / $V_{max}$ but does not effect $K_{m}$ / $V_{max}$
In other words, it effects the apparent value of $V_{max}$, but has no effect on the specificity constant ($V_{max}$ / $K_{m}$).  Inhibition is therefore uncompetitive.
Furthermore, unlike the case of competitive inhibition, increasing the substrate concentration does not abolish inhibition.
An uncompetitive inhibitor causes the slope of a Lineweaver-Burk plot to increase, but does not change the y-axis intercept of such a plot.
Therefore double-reciprocal plots of $1$/$v_i$ vs $1$/$s$ at different  $i$ form a family of parallel lines.

In this case, the $K_{i}$ may be determined from an intercept-replot, where the x-axis intercept is -$K_i$.
$$intercept={1\over{V_{max}}} +{i\over{V_{max} {K_i}}}\ \ \ \ \ (5)$$

(c) Mixed Inhibition

Now let's consider a mechanism where the inhibitor may bind to either the 'free' enzyme or the enzyme-substrate complex and (to keep things somewhat realistic) where the substrate may bind to either the free enzyme or the enzyme-inhibitor complex.
Under certain simplifying assumptions (see Segel, 1975) the mechanism shown above may give rise to the following rate law:
$$ v_{i} = {
  {{{V_{max}}}\ s\ }\over{K_{m}(1 + {i\over{K_{i}}})}  + (1 + {i\over{K_{ii}}}) s}\ \ \ \ \ (6)$$
In this case, there are two inhibition constants, one 'governing' the binding of inhibitor to the 'free' enzyme  ($K_{i}$) and one 'governing' the binding of inhibitor to the enzyme-substrate complex ( $K{ii}$).

Taking reciprocals, the corresponding Lineweaver-Burk transformation may be expressed as follows:
$${1\over{v_i}}=\frac{K_m}{V_{max}}(1 + {i\over{K_i}})( {1\over{s}}) + {1\over{V_{max}}}(1 + {i\over{K_{ii}}})\ \ \ \ \ (7)$$

The inhibitor increases both apparent the value of  1 / $V_{max}$ and (by not necessarily the same factor) and the apparent value of  $K_{m}$ / $V_{max}$. Inhibition is therefore mixed.
Eqn (7)  predicts a family of  straight lines that intersect at a single point:
$$({x, y})= (-\frac{K_{ii}}{K_i K_m}, \frac{K_{i} - K_{ii}}{K_i V_{max}}) = (-0.02,0.008) \ \ \ \ \ (8) $$
In this case, slope and intercept replots may be used to determine the values of $K_i$ and $K_{ii}$.  A detailed analysis of such plots is given in Segel (1975).
(d) Non-Competitive Inhibition
We now come to the case of non-competitive inhibition, which (as stated above) is best considered a special case of mixed inhibition.  When $K_i$ = $K_{ii}$, Eqn (6) simplifies to the following:
$$ v_{i} = {
  {{{V_{max}}}\ s\ }\over(1 + {i\over{K_{i}}})(K_{m} +s)}\ \ \ \ \ (9)$$

The Lineweaver-Burk transformation:
$${1\over{v_i}}=\frac{K_m}{V_{max}}(1 + {i\over{K_i}})( {1\over{s}}) + {1\over{V_{max}}}(1 + {i\over{K_{i}}})\ \ \ \ \ (10)$$

Eqn (10) predicts a family of lines where increasing $i$ affects both the slope and intercept to the same extent, and which intersect on the x-axis at $-1$/$K_m$
But why  should $K_i$ equal $K_{ii}$ in any realistic case?
Notes
Fersht now owns the copyright to his  book, and is distributing it free of charge
All issues of Acta Chem Scand (1947 - 1999), including many classic papers, are available on-line
An example of a steady-state rate law derivation is given in this Biology Stack Exchange answer
References
Cook, P. F. & Cleland, W. W. (2007). Enzyme Kinetics and Mechanism.  Garland Science Publishing (Taylor & Francis Group).  London & New York.
Cornish-Bowden, A. (2004). Fundamentals of Enzyme Kinetics. 3rd edn. Portland Press Ltd, London.
Dalziel, K. (1957). Initial steady state velocities in the evaluation of enzyme-coenzyme-substrate reaction mechanisms.  Acta Chem. Scand. 11, 1706 - 1723. [pdf]
Dalziel, K. (1975). Kinetics and mechanism of nicotinamide-nucleotide-linked dehydrogenases.  In The Enzymes, 3rd edn., Vol. 11.  Boyer, P. D., Ed. pp 1 - 60. Academic Press, New York.
Fersht, A. (1999). Structure and Mechanism in Protein Science.  A Guide to Enzyme Catalysis and Protein Folding.  W. H. Freeman, New York. [pdf]
Li, T. - K. & Theorell, H. (1969). Human liver alcohol dehydrogenase: Inhibition by pyrazole and pyrazole analogs.  Acta Chem. Scand. 23, 892 - 902. [pdf]
Lineweaver, H. & Burk, D. (1934). The determination of enzyme dissociation constants.  J. Am. Chem. Soc. 56, 658 - 666.
Segel, I. H. (1975). Enzyme Kinetics.  Behavior and Analysis of Rapid Equilibrium and Steady-State Enzyme Systems. John Wiley & Sons, Inc., New York.


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DAPI staining showing unknown artefacts?
Dear fellow researchers,
I have been facing some problem with staining nucleus with DAPI. I use the standard protocol for fixation 4%PFA+0.1% TX-100+2%BSA.
I use 0.2ug/ml conc. of DAPI for 5 minutes. Before mounting my cover slides, the nuclear staining is very specific and no artefacts were visible. However, after mounting (with Sigma-Aldrich mounting medium), I have started observing artefacts. Images are attached for your reference.
I usually keep my samples at room temperature for an hour to let the mounting medium settle down and then move samples to 4 degrees overnight and observe them the next day. I do not think that temperature here is an issue because the other marker did not show any problems.
Another issue is that the artefacts of nuclear staining are not ubiquitous. Even after mounting, some cells stained nucleus fine but others showed cytoplasmic or membrane staining.
Is there any reason that you guys can think of? Or if you have encountered similar situation before? Thanks in advance.
Why is DAPI giving artefacts with nuclear staining? - ResearchGate. Available from: https://www.researchgate.net/post/Why_is_DAPI_giving_artefacts_with_nuclear_staining [accessed Sep 18, 2016].

Hi Udesh. Welcome to Biology.SE. Can you post the images here? It would be easier for people to check them here instead of visiting other websites. Also, can you please mention what cells were these? Did you try gentle washing to remove excess DAPI?

Hello! Unfortunately I could not attach the images here. But, in my post there is a link to the same post on research gate. Could you take a look at it? It has images attached there.
Yes, I washed three times but it did not help. These were MDA-MB-231 breast cancer cells.


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Forward or Reverse Strand: Is there a difference when encoding genetic devices?
Background:
In synthetic biology, and also in nature, there are lots of examples of genes in both the forward and reverse orientation. It seems in synthetic biology/bioengineering, most genetic devices are, by default, encoded on the forward strand unless there are concerns of readthrough from one expression unit to another, in which case one of the expression units is included on the reverse strand like below:

It also seems that genes are sometimes in the reverse orientation for no apparent reason, especially in plasmid backbones:

The Question:
My question is, ignoring issues of potential readthrough, does it matter which strand a genetic device is encoded on? So in the example below, would there be any difference between A and B, or does it not matter? Also, does whether it's on a plasmid compared to a genome matter? I'm specifically interested in bacteria here.

This seems like it should be a simple question to answer and I'm sure I'm just missing something, but I can't find anything about it.

I would consider your terminology very carefully, because although your concern is reasonable, the question misuses scientific expressions in a manner that hinders communication. First, genes encode RNA and protein: neither they nor constructs are encoded by anything. Second, each gene has a forward and reverse strand, but almost no genomes do. So what you are talking about is the relative orientation of genes or constructs within a genome, plasmid etc. It would be good if you could reword your question accordingly.

Thanks for the comment, I'll edit based on your first point. For the second point, I think that my incorrect use of terminology for forward and reverse is what caused me to ask the question in the first place, because when I tried to correct them there was no longer a question, and this was also mentioned in the answer, so maybe it's best to leave that in the question so the answer still makes sense?

First, I think you have misunderstood the concept of sense/antisense. These are defined individually for each gene, with the sense strand always referring to the coding (non-template) strand of a gene, and the antisense strand to its complement, the non-coding (template) strand. So in your plasmid example above, all genes are encoded by their respective sense strand, but which of the two strands that is sense for a given gene depends on its orientation. There is therefore no biologically meaningful sense/antisense concept for entire genomes, chromosomes or plasmids. Read more in the Wikipedia article on sense, and the answers to this SE Biology question.
Having said that, it should be clear that the expression cassettes pictured in figues A) and B) are completely identical. If you ignore the context around them (e.g. readthrough), their direction is irrelevant.

It also seems that genes are sometimes encoded on the reverse strand for no apparent reason, especially in plasmid backbones

Many commonly used plasmid backbones derive from vectors that date many decades back, to a time when cloning strategies were far from as flexible as today. Researchers were generally limited by the restriction sites occurring naturally in the DNA sequences. A gene's position and orientation with respect to its neighbouring genes might therefore be the simple result of lack of other cloning options - although I honestly doubt "wrong" orientation would even have been considered an issue. For an example you could read about plasmid pBR322 in this Wikipedia article, and references therein.

Ah yes, of course, I thought I was missing something silly! Thanks for the answer!

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Succulent weed identification
There is a succulent-looking weed growing in a crack in my driveway. What is it?

Conditions: Dry, full sun, asphalt & gravel, no competition.
Date: 2018-07-16
Location: Toronto, Ontario, Canada
Size: 40cm x 40cm x 2cm

I am not familair with the flora of the New World, but this looks like Common purslane, Portulaca oleracea

@RHA is correct, it is Portulaca oleracea (RHA you should put this as an answer).  This is purslane in one of its favorite and classic environments, a driveway crack!  If this specimen has not been sprayed, you might taste a few leaves -- people put it in salads. And if don't want it around, pull it now, it is about to bloom and the seeds will be abundant.

This is Common purslane, Portulaca oleracea. It is used in salads, although it contains oxalic acid and there are poisenous plants resembling Purslane, see comment below.
https://en.m.wikipedia.org/wiki/Portulaca_oleracea

An acquaintance advised me of this: 1) Make sure you can distinguish it from hairy-stemmed spurge (which is poisonous) 2) Purslane contains oxalic acid, so those at risk of kidney stones should not eat too much! More info here: https://jstookey.com/node/214


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Trick fruit trees into flowering later in the spring
There is a common problem with fruit trees in temperate climates where the trees flower before the last frost. Generally speaking, if the tree has flowered, and the temperature drops below freezing, the flowers die and do not produce fruit.
This is certainly not a new problem. It's my understanding that the problem affects almost the entire fruit farming industry in temperate climates.
I've heard that fruit farmers have large-scale commercial techniques that they use to mitigate the issue, such as:

Covering
Fog or smoke
Wind Machines
Sprinkling
Heating

While these methods might be practical for commercial farmers, not all of them are practical for small-scale urban farmers like me.
Instead of actively protecting the open flowers, would it be possible to trick fruit trees into not flowering as early?
I'm dealing specifically with plants in the prunus genus:
Examples:

Prunus tomentosa
Prunus besseyi x prunus salicina hybrids
Prunus avium x prunus salicina hybrids

Note: I have a related question here: What triggers plants in the prunus genus to flower?

@GerardoFurtado : So, does this mean that a plant would flower on the exact same day, every single year? No other factors influence bloom time?

@GerardoFurtad: no, temperature on root is the main factor on common fruit plants (e.g. in many Rosaceae, where flowers appears before leaves). E.g. Prunus armeniaca (apricot) should be planted on colder places, to make them flower later (such plants hate cold weather during flowering). I live in a mountaneous region, and I can tell you that leaves (or flowers) on wild tree are phased out according altitude (same latitude, so same light period). Just few perennial plants in botanical gardens use the light period.

@GiacomoCatenazzi I have a related question here: What triggers plants in the prunus genus to flower?

The Principles of Fruit-Growing By Liberty Bailey 1898 (from page 92):

Thanks for this answer.  Definitely contradicts my answer.  More research needed.

You are on the right track, but snow is the wrong way.  When the snow is around it insulates the ground.  Soil surface temps stabilize at close to freezing.
Instead, do the reverse.  Remove, or firmly pack the snow.  Do so about 1.5 times the dripline radius.  (If the dripline is 10 feet from the trunk, pack out to 15.)
This allows the ground to freeze deeper.  However see other answers.  I'm not nearly as confident about this now.
Now once melt starts in earnest, cover the ground with a couple of layers of the insulated tarps used by contractors to pour concrete in freezing conditions.  This will keep the ground cold, both by reflection (most tarps of white) and by insulation, and by wind reduction.  This should slowdown bud break by at least a week, and more likely two weeks.

For a single tree, you may be able to do protection with an oscillating sprinkler (for a big tree) or a impact rotary.  Key thing with these is to start them before the temperature gets down to freezing.  The initial few minutes while it's working with dry air you can get supercooled droplets that kill your buds instantly.   Start the sprinkler when the temps are about +6

A third way that may help is to graft onto a different root stock.  The russians work with pear on cotoneaster.  This dwarfs the pear strongly, but also forces it into dormancy earlier.  I haven't read what it does to bud break, but given that pears also tend to be early bloomers, it must help.  These interspecies grafts are working in Siberia in zone 2.
Look at using prunus that tend to go into dormancy early in the fall.

Another way to experiment with would be to keep them a bit thirsty in the fall.  If the roots are slightly dehydrated, then the first moisture they get in spring will be used to rehydrate.  This may delay bud break by a day or two.

Some trees do their budding on reserves in the bud and twig itself.  I see this some years when a winter has killed roots.  The leaves break bud, inflate about to about 1/4 size, then wither.  For these guys it's a matter of enough degree days or the day length on the bud itself.
If it's degree days, you may be able to stretch things out by making the tree lighter coloured.  Many people spray dormant oil in late winter anyway.  By adding some cheap latex paint to the dormant oil mix, you lighten the colour of the twig, and so reduce sun warming.

I have a related question here: What triggers plants in the prunus genus to flower?


text:
Peach pits with two seeds: Are the seeds identical twins?
I have Prunus persica peach pits that have two seeds.
My question is simple:
Do the seeds have the same DNA? (are they identical twins?)

For what it's worth, this seems to be happening in about 1-5% of my peach pits.

Polyembryony occurs when a single fertilized egg produces more than 1 embryo. This is the process that produces genetically identical twins.
Although polyembryony is common in some plants, I found limited information about polyembryony in peaches. I decided to broaden my search into drupes more generally. Drupes or "stone fruits" are the fruits with a fleshy outside (exocarp and mesocarp) and a hard inner shell (endocarp) around typically a single seed. Peaches are part of this category, as are almonds (the almond itself is the inner seed), cherries, and coffee.
The best citations I found reach back into history a bit.
From Webber, J. M. (1940). Polyembryony. The Botanical Review, 6(11), 575-598.:

Cases of the first class of false polyembryony
  commonly occur in such drupes as almonds, plums and peaches.
  Although these drupes normally have a single seed within the hard
  seed-like endocarp, sometimes two or even three are found. ' During
  formation, each of the plural seeds develops from a separate
  ovule, provided with a separate funiculus and micropyle. Similar
  cases of such false polyembryony have recently been reported in
  Coffea (63) and Sandoricum (47, 49).

This passage would suggest that most likely what you are observing is false polyembryony. Immediately prior to this passage, the "first class" refers to:

those in which more than one ovule develops in a normally 1-ovulate seed-like structure or locule

as contrasted with the second type:

occasionally two of the developing ovules unite to form what appears to be a single composite ovule.

Another source, Zdruikovskaya-Rikhter, A. I. (1970). The phenomenon of polyembryony in the peach. Tr. Nikitsk. botan. sad, 46, 173-177. is in Russian and only available to me in abstract form in English. The abstract reads:

In a number of varieties, two and sometimes three megaspores were functional, giving rise to several embryo sacs. On fertilization, embryos develop in these, causing the phenomenon of pseudopolyembryony.

Therefore this source seems to agree with the first.
However, a more recent paper Martínez-Gómez, P., & Gradziel, T. M. (2003). Sexual polyembryony in almond. Sexual plant reproduction, 16(3), 135-139., focused on almonds, suggests that certain almond cultivars are prone to true polyembryony, though it seems like the additional seeds are often a bit stunted and have high mortality. They also reference a paper purporting to mention polyembryony in peach, Toyama, T. K. (1974). Haploidy in peach. HortScience, 9, 187-188., though I cannot find this article in anything but Japanese - the title, however, suggests that these may be haploid polyembryos, which also occur with the almonds - these are indeed from division of the same embryo, but because they are haploid they would not actually be genetically identical, since each is taking half of the diploid chromosomes.
With only these limited descriptions to go by, which seem to be mostly observational rather than backed by any systematic study, I would hesitantly conclude that most likely what you are seeing is a fruit in which two separate ovules developed together, and therefore could be as genetically different as any two different peaches from the same tree. True polyembryos seem to be possible in stone fruits, but as a mostly rare occurrence that is only common in particular strains - when it does occur, it may be via haploidy, which means the seeds will still be genetically distinct.

Paging @CowperKettle if you have anything to add from the Russian source in my answer here - I'd be particularly interested if they have anything to say on the incidence of polyembryony and if they distinguish between true polyembryony and pseudopolyembryony.

Great answer! I was looking for an answer to this question, but I didn't know the term "polyembryony" and I couldn't find anything. Now I know, thanks!

An answer provided by Washington State University:

Peach is self-pollinated.  The actual characteristic part of the fruit
  that we eat is from maternal tissue but the seed inside the pit
  results from the sexual recombination that occurs following
  pollination and fertilization.  Technically, I would not think it to
  be a “clone”.  Even in the rare case when a double flower forms and
  when both pistils are viable and fertilized ovules result, the seed
  would have both maternal and paternal DNA and sexual recombination
  could expect to result in different progeny.
An interesting example of a seeded fruit where the seed are effective
  clones can occur with citrus and it is called “nucellar embryony”.
  These seeds are of maternal origin (nonzygotic) only and, if
  germinated, they will be clones of the mother.

Of course they are.
They're both from the same peach, so they both have identical DNA. It's like when a mother has twins or triplets, all of the babies will have the same genetic code, since they all came from the same egg. So if there are two cores in a peach, since the peach and both of it's cores are from the same tree, both cores will have identical DNA. :)

Please look up the meaning of genetic code. Also, did you never meet a twin couple made up of a make and a female?https://www.healthychildren.org/English/family-life/family-dynamics/Pages/The-Difference-Between-Identical-and-Fraternal-Twins.aspx


text:
Do hornets return to the same nest after winter each year?
I have what I think is a hornet nest on the soffit of my house.

The nest has been removed, however, the hornets keep rebuilding. Also, they have started to swarm the sewer vent pipe (not shown in photo).
If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

I'm not sure if this is relevant or not:
To give you an idea of what kind of winters I am dealing with, I am near Toronto, Ontario; the temperature goes down to -25 degrees Celsius.

The picture isn't that clear and fails to show the insects involved, but based on your description and region you are probably talking about a paper wasp, not a hornet, though in common vernacular in the region 'hornet' is used. https://en.wikipedia.org/wiki/Polistes_dominula most likely.

If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

No. The nest, likely made of wood pulp (and maybe mud), will/should degenerate to unusable over the winter, though the bulk could remain for a couple of years. All wasps die, except for the new queens (fertile, mated females) who overwinter in sheltered crevices somewhere.
In spring, it is a single wasp that starts a hive: the new queen. She builds a new, small hive in which to lay eggs, which is added to initially by the queen and then by workers who have hatched.
While she will not return to an old hive, the conditions which appeared advantageous to one queen (shelter from rain, intense sunlight, winds, etc.) will also seem advantageous to other queens, which is why nests appear in the same places year after year.
Edited to add: It appears most likely that the queens that overwinter are "new queens", that is, mated female offspring of the queen. H/T @Brian Krause.

As a minor correction, I think the overwintering population is mostly young mated females, though I don't know for certain whether queens who produced nests the prior year can also overwinter.

@BryanKrause - I believe you are correct; edited. Thanks!


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Looking for Kelly Chibale's paper on Malaria cure
From National Geographic, there has been a lot of hype on Kelly Chibale's work from University of Cape Town on the aminopyridine MMV390048. Unfortunately, this was from an announcement from an internal meeting so there is very little literature on the compound.
So I ask, does anyone have good literature on the compound?

A search for "Chibale [au] AND malaria" on Pubmed returns a few results. This may be related to what you are asking for: http://www.ncbi.nlm.nih.gov/pubmed/21966980

@TomD, I believe that you have identified MMV39008. Thanks to everyone for helping me with this search!

It turns out that TomD is the winner. That particular paper is an amino-pyridine class and exhibits single-dose efficacy. Amazingly, the other two papers mentioned by Satz and Alan Boyd are leads for other classes of compounds with Satz's paper focused on an amodiaquine derivative and Alan's paper focused on an alternative 2 amino-pyridine backbone also based off amodiaquine.
3,5-Diaryl-2-aminopyridines as a Novel Class of Orally Active Antimalarials Demonstrating Single Dose Cure in Mice and Clinical Candidate Potential

I don't know anything about this topic, but I did find this recent paper:

Kamaljit Singh,Hardeep Kaur, Kelly Chibale, Jan Balzarini, Susan Little, Prasad V. Bharatam (2012) 2-Aminopyrimidine based 4-aminoquinoline anti-plasmodial agents. Synthesis, biological activity, structure–activity relationship and mode of action studies. European Journal of Medicinal Chemistry 52:82–97

The authors analyse a range of compounds for in vitro anti-plasmodial activity. The most active is named 5-isopropyloxycarbonyl-6-methyl-4-(2-nitrophenyl)-2-[(7-chloroquinolin-4-ylamino)butylamino] pyrimidine (referred to as 10r in the paper).
Although the code name MMV390048 does not appear in the paper the strategy that this group is following is discussed in detail. My guess would be that MMV390048 is a development of 10r.
This is the structure of 10r as depicted in Table 1 of the paper:

This may be the paper you are looking for:
Ongaroraa DSB, Gutb J, Rosenthalb PJ, Masimirembwac CM, Chibale K. 2012. Benzoheterocyclic amodiaquine analogues with potent antiplasmodial activity: Synthesis and pharmacological evaluation. Bioorganic & Medicinal Chemistry Letters, 22(15): 5046–5050, doi:10.1016/j.bmcl.2012.06.010.


text:
Low temperature PCR
We're trying to do emulsion PCR using HA-coated polystyrene beads and we're noticing that the beads are seeing drastic issues with thermal degradation above 90C. As PCR has an unfortunate requirement of requiring a high temperature, I was curious about what options are out there to reduce the temperature during PCR denaturation or to stabilize the beads.

Well you can change the melting temperature using additives like DMSO and betaine. Unfortunately, the beads have to be coated and the polystyrene seems to be the best for the downstream steps so we would prefer to stick with polystyrene before re-optimizing everything else.

If there was an easy solution, I wouldn't be asking it on SE.

Perhaps isothermal amplification is possible (NASBA)?
Amplification of DNA also seems possible (NASBA at biomerieux).

Look at chemical hydrogen bond breakers.  Guanadine hydrochloride is included in the buffer conventionally to compete with the the hydrogen bonds that form the double helix.  Other hydrogen bonders like Propionamide and 2-Pyrrolidone can weaken the helix and I would think lower the melting point of the bonds.
How much the Tm is affected would depend on the concentration of the breaker in the buffer.  It might not be possible to lower the temperature this much and you may loose specificity - you might be able to squeeze a few more degrees if the oligos can't get any shorter.

i think a few molar salt will also do it, or just amping up the Gu in the solution, but the paper also tries to estimate specificity and fidelity of the PCR reaction with different compounds so that you don't get as much error with increased bond breaking.  In the extreme concentrations of adding bond breakers, you get no double helix formation at all.

Update (21/09/17) as the answers are a little outdated by now:
Isothermal amplification methods are fairly well established by now and commercially available. They tend to amplify DNA at temperatures of around 56°C.

Wikipedia entry on Loop-mediated isothermal amplification.
For the more tech-savvy, an open research article on
loop-mediated isothermal amplification in Nucleic Acids Research.
Link to a commercially available product using isothermal amplification: ANSR (Disclaimer: I work for this company)


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Is autoclaving sucrose solution necessary?
I use 10% sucrose solution to feed lab mosquitoes. Until now, I mix sucrose in autoclaved water and use it directly for feeding mosquitoes. Is it necessary to autoclave the sucrose solution itself before use?

aren't there are standard protocols for feeding these lab animals? or some sort of International Mosquito Research Association

I tried my best, but couldn't find any standard protocol. They have just mentioned what percentage of sucrose solution must be used. There is no information about autoclaving or filtering sucrose before use.

Sugars usually get charred when autoclaved or at very high temperatures. Autoclaving sugars is unadvisable.

instead what you can do is add the sugar after autoclaving the remaining components, in a hood.

Or filter the solution through a 0.2µm filter.

If the sucrose is to be used as a food source for mosquitoes do either of the possible problems – charring or fungal contamination – actually matter? Also see my contribution to the charring debate in my comment on the answer from Karthik.

I found a standard protocol for the same here : http://vosshall.rockefeller.edu/assets/file/Vosshall%20Lab%20Mosquito%20Rearing%20SOP%20DEC%2012-2014.pdf
Take a look at page no.8. They suggest to autoclave the sucrose solution.

The protocol refers to a preprogrammed cycle and doesn't specify psi. I vaguely recall using a lower psi setting for sugar solutions – 6 psi/110°C? – as compared to standard 15psi/121°C so maybe that is what this refers to.

I wouldn't autoclave this solution - sucrose will partly break down into glucose and fructose. A portion of the sugars will also caramellize and color the solution yellow to brown.
If you need the solution to be sterile, I would filter sterilize it, although this can be hard because of the higher viscosity of the sugar solution. If you haven't seen any negative effects of preparing the solution fresh with autoclaved water, I don't think there is any need to change your protocol.

I routinely autoclave 20% sucrose and don't see any evidence of caramellization. Also, 10% sucrose would not be difficult to filter.

@canadianer I stopped it, after we got brown solutions back. Seems to depend on the autoclave. Our solution was to make really high concentrated solutions (and these are hard to filter), to have the osmotic pressure on our side against contaminations. Works pretty well.


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How can I calculate alpha helix content from molar ellipticity?
How can I calculate the alpha helix content (i.e. percent) in a protein from a given molar ellipticity of 222 nm, without using any software. I have tried the Greenfield-Fasman equation, but the answer doesn't seems to be correct.

You can use the information at this site, especially section 3. (https://www.photophysics.com/resources/tutorials/circular-dichroism-cd-spectroscopy)
Notice the different CD spectra for alpha-helix, beta-sheets and random coil. If your protein is measured at 222nm you need to compare your measured values to the the spectra at 222nm, this will allow you to guestimate the secondary structure of the protein, but if you want to be accurate, you will need to measure at several wavelengths to determine the distribution of alpha helix, beta-sheet and random coil. This is because all three contribute to the measure spectra and as such you need several measurements to figure out the relative contributions of each secondary structure.


text:
What will CD spectroscopy show when L- and D- forms of proteins are mixed?
What will happen if equimolar concentration of L- and D- forms of proteins are mixed and we take the circular dichroism reading? Will the positive and negative ellipticity cancel each other out or will there be positive and negative ellipticity of identical magnitude?

I’d be interested to know how you would obtain the D-form of a protein. I presume this is a hypothetical theoretical question. You might consider this clear in the question. As it has no biological significance it doesn't really belong here. It might be better on SE Chemistry, where you are more likely to get an answer.

Interesting that my answer was blocked. It gave the shortest and most precise answer possible to the question. (L and D forms are mirror images and the signal from each cancel out.) That is literally what happens! And the question contain the explanation already!


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Protein expression in K. lactis system
I am trying to express a protein in K. lactis Protein Expression Kit (E1000S - NEB) in the way that the protein is secreted into the medium. I know that I can get some protein but it is not active. As the protein is secreted into the medium, I am not sure if doing expression for 24 h at 30°Cis a good idea. I am wondering if there are people here with some experience in this protein expression kit and, if so, what are the conditions for protein expression that worked well for you? Did you use ammonium sulphate precipitation to purify the protein from the medium or some other method?


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Could a 3D Printed Plant Seed be Possible with Existing Technology?
The first genetically cloned animal was Dolly the sheep. As I understand it, this was possible because all that was needed was an embryo containing the cloned genetic material and a womb for that embryo to grow in. Would the same process also work to clone a plant?
I assume that the problem with embryonic cloning techniques and plants stems (forgive the pun) from the need to implant it into a host seed without destroying its ability to germinate. I haven't found a reference that claims this has been attempted... If anyone knows of a study related to this, I would love to read it.
Given my assumption I tried to imagine another way to achieve this goal which lead me here, to pose my question to the brilliant minds of this community:

Is it possible to implant a cloned plant embryo into a synthetic 3d printed seed that would germinate with existing technology.

I know we have successfully 3D printed living tissue using state of the are equipment like the 3d Bioplotter. If you guys don't think it is currently possible then what technological advances would need to be made to achieve this goal.
Note: The answer to my question is relevant to a number of possible applications. A hypothetical "Seed Printer" could be used in a future manned mission to Mars. Due to the logistics of shipping supplies to mars, it could be more practical (cost effective) to ship the raw material needed for printing seeds than it would to send actual seeds.
Edit*: Thanks for the comments, I feel a little foolish for not knowing about artificial seed coats prior to posting this question. In light of new information, I would like to additionally ask:

What are the current limitations of creating artificial seed coats that could possibly be enhanced with the application of 3d printing technology.

Welcome to Biology.SE! As long as you have a cloned plant embryo, an artificial seed coat would certainly work (this is quite common, but not in 3D printing). Yet, the question is very likely to get opinion-based answers.

Thank you! The hardest part of learning about a new subject is knowing what to research. I had seen the phrase "Artificial Seed Coat" but it was never used in a context that indicated that it was exactly what I was looking for.

Hint: look for plant tissue culture and you'll most likely get what you want ;)

Also note that the chances of all the raw materials, plus power supply and assorted hardware for the printer being easier to carry than <1g seeds seem very low.

You make an excellent point! I am more concerned with the effects of ionizing radiation on the seeds and the weight of the technology and materials needed to properly protect them during shipment. You may be right however and it would be more feasible simply to ship the seeds.


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Pretty Flower Fungus in Oak Tree

Found this on a nature walk in the town of Lincoln, MA, USA. Is this edible? I believe it is a type of fungus.

It is not a good a idea to take advice from the internet about things being edible. Maybe ask for the species first and see whether there is consensus.


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Which colourful insect is this?
I found it on my plant this morning while watering it. Location: Hyderabad, Telangana, India. Any ideas?


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Purple Mushroom Identification
I found a purple mushroom that looked like this on a nature walk in South Carolina, USA today. This is not my picture, but one that looks exactly like the mushroom I saw. I have searched the internet, but I could not identify it. Does anyone know what this could be?

This Q is too broad: Mushroom identification is very difficult, even with an original picture. The picture you provided is from a relatively rare mushroom. There are much more commen purple mushrooms, like Laccaria amethystina for example.

The image you used is from a Reddit Thread, where the mushroom is identified to be Cortinarius violaceous. More information on Cortinarius violaceous can be found here.
Although it could be a different mushroom, as the picture you provided is not a picture of the specific mushroom you saw.
Another picture of Cortinarius violaceous

Source: velutipes.com
All credit goes to Reddit user tubergibbosum for the identification.


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What is this viny plant in the UK?
I am in Northumberland, UK. This is growing in my veggie plot and cannot find out what plant it is....looks like a triffid!! It is one stem growing out of the ground and has many stems growing on the side of the main one which lie along the soil with no roots appearing.
I placed a couple of pea pods beside the brick to show the size. Hope someone can help. Thank you.

The closest that I can get is some sort of chicory, but I'm not confident enough to make this an actual answer.

Neither, it's a very silly title, probably composed to attract attention. I am voting to close this question until you give your question a more descriptive title.

Thank you,  Alan, I am inclined to agree that it is a Cichorium mainly because I cannot find any thing else.

Terribly sorry, David, for upsetting you and possibly it was to attract attention but it was a valid question as nobody seems to know exactly what this plant is. I am guessing you got out of the wrong side of the bed yesterday.

Alan is right to call this a Cichorium. It is  Cichorium endivia, Endive. It is a tropical plant that is widely cultivated for its edible leaves. However, when it flowers the leaves die, so you don't recognize the plant as Endive. The dying leaves can be seen on the picture below, from the Dutch wikipedia page.

https://nl.m.wikipedia.org/wiki/Andijvie

+1 Thanks for clarifying this, I couldn't find an image that convinced me like this one does.

Thank you, both, the photo does indeed look exactly like what is in my plot. I have always thought of endive as been the dense curly head of salad greens. I found this very interesting having got a google translation of The Netherlands Wikipedia. Funnily enough, I have not sown nor planted Cichoriums of any kind so probably blown in on the wind.


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DNA Analysis (AncestryDNA)
A recent1 AncestryDNA commercial highlights a customer who discovered that she was 26% Native American.

Credit: ancestry.com/dna
You can see the full commercial here.
My question is, how can this be?
What combination of parents' race lineage would dictate that a person is 26% Native American (or any other race for that matter), and how many generations back would one have to go to achieve these numbers?

1. Recent to me, I don't watch much television.

These tests don't actually tell your ancestry, there is no way for a genetic test to do that because there is too much genetic variation among populations, as well as between.
Instead, the test is reporting, based on the polymorphisms observed, an estimate of their ancestry based on sharing those polymorphisms with others from a group. How do you know what polymorphisms an Asian or Native American has? Well, you do tests on a bunch of Asians and a bunch of Native Americans and use the similarities between them compared to other groups to form a 'profile' for that group. However, even an individual with a perfect geographical pedigree can share polymorphisms with other ethnic groups.
Wikipedia has a section on this:

Many companies offer a percentage breakdown by ethnicity or region. Generally the world is specified into about 20-25 regions, and the approximate percentage of DNA inherited from each is stated. This is usually done by comparing the frequency of each Autosomal DNA marker tested to many population groups.[2] The reliability of this type of test is dependent on comparative population size, the number of markers tested, the ancestry informative value of the SNPs tested, and the degree of admixture in the person tested. Earlier ethnicity estimates were often wildly inaccurate, but their accuracies have since improved greatly. Usually the results at the continental level are accurate, but more specific assertions of the test may turn out to be incorrect. For example, Europeans often receive an exaggerated proportion of Scandinavian.[10] Testing companies will often regularly update their ethnicity estimate, changing an individual's ethnicity estimate.

In summary: ethnicity testing is at best to satisfy a curiosity. There is no way that genetic testing can identify your geneology perfectly, and in fact it is pretty meaningless to do so, because interbreeding between geographically distinct populations happens all the time.


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What fruit did I just accidentally buy?
I live in Oxford, in the United Kingdom, in a part of the city with a vibrant multicultural community. My local corner shop has an excellent selection of spices, pulses, and obscure and vegetables fruit that mostly tends to be from the region of Pakistan and India, and only labelled (illegibly) in a language that I do not speak.
I've just bought a fruit I thought at first inspection was an unripe mango -- previously they have had excellent, cheap, small alphonso mangos for sale that I'm rather partial to. I'm completely wrong, however, for I've bought something about the size of my fist with striking white seeds that taste very peppery, a green coat, and somewhat sour flesh. It floats in water, and the skin exuded a slightly sticky, partially white gummy substance when I removed it from the bag. It's not particularly soft to touch. The seeds look a bit wrinkly, and are not hard at all to touch. The flesh has a consistency of an apple.

I can't for the life of me identify it! I'd love to know any suggestions! Thank you!

Looks like a papaya that isn't ripe yet. Being said, if you already cut it in half it probably isn't going to ripen any further. A ripe papaya has pink/orange flesh and the seeds turn black.

Yep -- with a bit more googling, I think that's exactly right. I had absolutely no idea that unripe papaya had white seeds -- I had assumed that they were black from the beginning. Thank you!


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Extreme or just rare: evolution of complex life in extreme environments
Many environments are considered "extreme" (boiling hot springs, acidic/basic water, etc) and those tend to be dominated by Archaea instead of the "usual" mixture of bacteria along with complex plants and animals. But "extreme" is in-part in the eye of the beholder.
Very little of earth (in terms of total energy available) is at 100C or pH 0, etc. Broadly speaking, the more organisms in parallel trying out various mutations the higher the chance there is to come up with something useful. We can't expect a 1km^2 hot-spring cluster or the energy-starved layer of groundwater at the 100C geotherm (about 3km below ground) to evolve as much as a 1000000km^2 rainforest exposed to direct sunlight.
There are large extreme environments. There is plenty of energy available in deserts such as the Sahara or the open surface ocean (an iron desert) but the primary productivity is very low. This means that the environment is harsh enough to stop life from adapting "effectively". Here "effectively" means how much of the available energy is used, i.e. what fraction of the sunlight is absorbed by the plant/algae (the conversion efficiency into glucose is very low, at most 7% and often ~1%, but we are ignoring that). Note that in many cases a desert is actually more hostile to microbial life because larger organisms can store water/nutriants/etc more easily.
On the other hand, there is one example of an "extreme" environment that became widespread and in which life thrived: Oxygen. O2 forms reactive species in a wide variety of biochemistry, which makes it a pretty universal poison. But life found a way around with enzymes such as superoxide-dismutase and was able harness the high energy or these reactions.
To the best of our understanding, to what extent would life have evolved and thrived if the entire Earth's ocean were an extreme environment, such as 100C, pH 0, or 34% salinity?

We cannot have any "understanding" of the outcome of a hypothetical postulate. Whereas discussion of this may be of interest to you and possibly others, there can only be subjective opinions on the question and therefore I am afraid that it is off-topic for SE Biology. (see: https://biology.stackexchange.com/help/dont-ask)


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Bacterial endosymbiosis of bacteria
Endosymbiosis was crucial to the development of complex life and it continues to happen to this day. The origin of mitochondria see bacterial guests in archaea hosts, some of which later took in cyanobacteria which became chloroplasts. Modern "eukaryotes" have varying ranges of ancestry from these two domains with animals being about 50-50. More recent endosymbiosis examples include bacterial or protist guests in eukaryotic hosts.
But are there any examples of a bacterial guest endosymbiosis in a bacterial host? Bdellovibrio bacteriovorus enters other bacteria but it destroys them much like the lytic phage cycle. Bacteria inside bacteria inside mealybug cells have been found. However, this isn't an example of a bacterial symbiosis of another free-living bacterium or even of an extracellular animal-associated bacterium. Are there any examples of bacterial endiosymbiosis of bacteria that aren't intimately associated with the intracellular machinery of a eukaryote?

There is this example but no evidence of actual symbiosis.


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Was the KT asteroid a dinosaur killer or just a large animal killer?
The KT extinction event is well-known as the demise of the dinosaurs. But today we have about 10000 bird, 11000 non-avian reptiles, and 5000 mammal species. That means almost 50% of reptile species are dinosaurs and mammals are a distant third, which is still pretty good! In fact, birds refilled empty niches left behind by the extinction event as did mammals and other reptiles. So was the asteroid really a dinosaur killer?
Consider the ratio of dinosaurs:reptiles:mammal species from the Jurassic to today. I see broadly thee possibilities:

It was much more biased, such as 4:2:1, in the Jurassic era, with the asteroid evening things out.
It was similar to today, but the asteroid initially hit dinosaurs exceptionally hard, leaving it as perhaps 0.25:2:1 after which bird speciation brought it back to 2:2:1. Note that birds are very deep within Dinosauria, with every other branch extinct.
The asteroid didn't change the proportions very much, but wiped out almost every large species as most extinctions do. The pruning of the dinosaurs was more spectacular due to a small number of large species in the fossil record, but in terms of total species counts they were hit no (more) harder than other vertebrates.

(2) is the classic "dinosaur killer" we know and love, while (3) means we should instead think of the asteroid as killing off giants and leaving the meek to inherit the Earth. Is there reasonably strong evidence as to which scenario unfolded?

I think small fossils are relatively rare because they are more likely to degrade, be scavenged etc. I can't find any evidence, but at the time of the KT debate I don't know how many small species (say <2-3 kg) were known, so the demise might have seemed more dramatic.


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Vine has simple and compound leaves
What kind of plant is this?

Some leaves are compound (leaves of three). Other leaves are simple.

Located in an urban garden in the shade; east of Toronto, Ontario, Canada (July 30, 2023).

Woody vine crawling up a fence. Vine has feet that stick to the fence.

Related posts: (30 feet away on the other side of the lawn; all are different specimens)

Is this poison ivy? (Aug 2, 2022)
Is this plant in my urban garden poison ivy? (Jul 20, 2023)

Edit:
This plant/location in the garden is especially hard to photograph. It's hard to reach, dark, and surrounded by thorny brambles. And there are lots of different species of plants in the same spot; it's hard to tell what leaves are attached to what plants when viewing a photograph.
Rather than take another dark, poor-quality photo during the day, I made a video at night with a bright light. I tried to show that there are lots of differently-shaped leaves attached to the same plant. Some leaves are simple leaves. Others are compound leaves of three.
YouTube video

Does this answer your question? Is this poison ivy?

leaves in 3s is your key here. Definitely poison ivy (again)... see your other question, look at the attachment of the vine to the fence and the leaf arrangement.

As a novice, my guess is Boston Ivy (Parthenocissus tricuspidata).

Eastern Poison Ivy vs Boston Ivy
Boston Ivy: A deciduous woody vine native to east Asia, introduced in North America. Established in numerous scattered locations, mostly around urban areas. It is a close relative of the native Virginia creeper.
Middle leaflet has no stem or a short stem not much longer than that of side leaflets.

Plants can have both compound (trifoliate) and simple leaves. Some leaves have two side leaflets fused to create a two-leaflet leaf.


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Large grey bird at creek mouth (east of Toronto)
What species of bird is this?

Spotted at the mouth of Graham Creek at Newcastle Marina (Bond Head), Lake Ontario, Canada
September 9, 2023
The bird was roughly 18 inches tall; dark grey body; light grey head and neck; yellow beak

+1 for precise location. Sometimes questions here include vague locations (e.g. Canada) or no location at all, nor even a hint on the habitat, and location is often useful to discard a lot of species.

The second picture is very good (both for identification and the moment)

I'm highly confident that this is a cormorant. I'm less certain of the species, but based on the location I would bet that it is a double-crested cormorant (perhaps a juvenile based on the head color/feathering, though I don't know if this varies in adults based on season) as these are found in high numbers around the Great Lakes region, including Lake Ontario.
  photo by Jane Mann, from Macaulay Library
See also:
The rise of the Double-crested Cormorant on the Great Lakes:
WINNING THE WAR AGAINST CONTAMINANTS

Looking at the maps in my Sibley guide, there are occasionally vagrant Great Cormorants & Anhingas in the Great Lakes area.  But their coloration is different, even for the juveniles, and so I agree that it's far, far more likely to be a Double-Crested Cormorant

Anhinga can be ruled out by the bill; theirs is straight, without the hook at the end cormorants have.

A cormorant or possibly a shag. Far more common in saltwater surroundings, but can be at home in fresh water.

As mentioned by @BryanKrause, cormorants are super-common around Lake Ontario, e.g. this photo from Hamilton harbour https://ontariohunting.net/wp-content/uploads/2018/11/3-0_Super_Portrait.jpg (source: https://ontariohunting.net/nature-not-bullets-should-control-cormorants-mcmaster-biologist-says/ )

@BenBolker - Coming from UK, I wouldn't have a clue about that! But thanks anyhow.


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Please identify this bird
Please identify this bird? There are bright red feathers at the bottom of its tail. What do we call these feathers?

update:
Location is North India. Temperature is around 35° C.

Can you provide an approximate location where you saw this bird?

The bird resembles a Red-vented Bulbul (Pycnonotus cafer), a native of the Indian subcontinent but common as an invasive species in many other regions. Some location information would be very helpful in providing positive ID.

@bshane Excellent! The image is of bad quality, the bird's head can't be clearly seen, there is no location information, and yet you guessed so accurate. This should support your answer: https://yandex.ru/images/search?text=Pycnonotus%20cafer&stype=image&lr=213&noreask=1&source=wiz

Thanks, @cezar. These were briefly reported as an invasive species around my home a few years ago, and the Ministry of Primary Industries was desperately trying to track them down before they could breed and become a pest. I never saw any, but the ID appears to have stuck with me.

Location is North India. Temperature is around 35° C. I took the picture from a long distance with camera zoom to fullest. After 1st click, bird flew away.

I am hesitant to provide 'positive' ID without location information, but this bird strongly resembles a Red-vented Bulbul (Pycnonotus cafer). The species is native to the Indian subcontinent, but is a common invasive species in many other parts of the world.

Key identifying features, with features visible in the photo given in bold (description from NZBirdsOnline):
Red-vented bulbuls are slim, starling-sized songbirds with predominantly dark plumage. They are typically bold and conspicuous, with repetitive, monotonous calls. Their slim build and curved bill are reminiscent of a honeyeater (e.g. bellbird or tui), although they are not closely related. The two most distinctive identification features are a small erectile crest on the crown (giving them a square-headed Roman helmet look when the crest is raised) and the diagnostic bright red patch between the base of the legs and the undertail. The head, hindneck and upper breast are glossy black, with a circular brown patch over the ear. This dark hood becomes streaked or scaly on the lower breast and merges into the pale grey belly. The upper wings and mantle are mid-brown with pale margins when in fresh plumage, creating a scaly appearance. The rump is white, and the tail is long and blackish with a prominent white tip. The bill, eyes and legs are dark. The sexes are alike, although males are slightly larger. Juveniles are dull brown with an orange or pinkish (cf. red) vent.
The red feathers around the vent do not have a special name - you can just call them 'the feathers around the vent'.
edited for the addition of location information
As the photo was taken in Northern India, the bird is almost certainly a Red-vented Bulbul. The Red-vented Bulbul is common throughout India, and there are no similar species in the range that could easily be confused with this species.

the "bright red patch between the base of the legs and the undertail" refer to "bright red feathers"? can we refer to them as "undertail coverts" too?

On any other bird I would say yes, but 'coverts' is partially a functional term, meaning feathers which smooth the surface transition between body and flight feathers. In the case of the Red-vented Bulbul, the red feathers stand apart from the tail, rather than smoothing the transition. I may be being overly picky, but I don't think we can use the term here.


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Help on selecting 2 tests - unsure if they are paired or non-paired statistical test
I have data that measures the temperature of flowers and leaves on different plant species. These are the comparisons I am trying to make:

Comparing the flower and leaf of the same plant at the same time of day
Comparing the flower or leaf of a plant to the same flower or leaf at different times of day - on the same plant

My current interpretation is that 1 is an independent statistical test because while they are both on the same individual plant, they are separate "individuals" themselves. For 2 I believe it is a paired test as it is measuring the same flower or leaf at different times of day.
What is confusing me is that I have been taught that if it is the same "individual" then it should be paired, therefore 1 should be a paired test. However my interpretation is that "individual" means something different in the mathematical reality of the tests, where they are seen as different pools in this instance.
Am I correct in my thought? Or completely wrong?
Thank you
Edit:
Maybe some clarification to my thought: The difference between my 2 tests is that one uses the same repeated leaf or flower (referring to case 2) at different times of day (therefore it is paired as it is a  measurement of the same thing twice at different times). This contrasts with case 1 as this is comparing 2 different objects at the same time of day. The confusion for me comes in when case 2 is still on the same individual - they are related in a way, but I'm unsure if this is relevant to the test.

I'm voting to close this question as off-topic because it is a question of statistics, not biology. Have a look at stats.SE

I would argue that statistics is the core of Biology! The whole of the empirical method underlying biology is founded in statistics. Even high school level biology uses statistics. Thank you for your opinion either way.

@s33ds Welcome to Bio.SE. You are right that biology relies on statistics! Remi.b isn't trying to say this is a bad question, but you would get a much better answer on stats.SE. For me the question is missing a few details that are important for the statistical analysis. For example in scenario 1: Are you only counting one leaf and one flower per plant? This might cause different sample sizes in the data.

There may or there may not be any correlation between the flower and the leaf of a plant. If you think there might, you ought to account for that. Switching to mixed-effects (or multi-level) models will induce the change in mentality that will make the task of modelling such experimental designs easier.

I imagine that for case 1 you have data of the type:
Plant1, $t_f$, $t_l$;
Plant2, $t_f$, $t_l$;
etc.
If you are interested in comparing the mean temperatures between flowers and leaves, your data would consist of n measurements coming from flowers and n measurements from leaves. You may surely try a t-test for independent samples, especially if you have some missing data in one column or the other. However, I find it reasonable to think that the values of flower and leaves are correlated within plant (possibly because of different background exposures of different plants). If this correlation is strong, you are at risk of not registering a true effect (a significant temperature difference between leaves and flowers).
Therefore, I would opt for a paired test even for case1.

Welcome to Biology.SE!   ——— Please take the time to go through the [tour] and the help pages starting with [Answer] questions effectively on this site. Thanks!


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Herbivorous plants that consume falling leaves
I've just seen a report about specialized herbivorous plants which build special traps to catch falling leaves from trees above them.
The only thing, which I'm missing is the correct name of this plant. Do you have any idea what plant(s) could this be?

Welcome to Biology.SE. Did you try to go through the wikipedia list of carnivorous plants?

You seem to misuse either of the term 'carnivorous' or 'vegetarian' in your title! You should have a look at the wikipedia entries for vegetarinism or carnivores

The term "herbivorous" plants would be a more accurate description of the plants that you are asking about.

You say you're missing the 'correct' name of the plant - does that mean the report gives an 'incorrect' (common) name for it? If so, could you post it?

Some bromelias growing up in the trees in tropical rainforests catch falling rainwater and probably leaves to extract nutriens. See here. Is that what you mean?

@RHA: Note that Bromeliaceae only grow in South American rainforests. They do not occur in Asian and African rainforests.

@AlwaysConfused Well I would like to provide more information. But I've seen these documentation on a flight, and I just woke up a few minutes before this part of the documentation has been shown. Due to this fact, I couldn't provide much more information. Sorry :-(

After all, I found the answer myself.
The special plant I'm looking for is the Nepenthes ampullaria. It has developed away from the "normal" carnivorous plants to a more detritivorous species.
Nepenthes ampullaria has specialized her pitcher to catch falling leaves from trees above her.

Many plants do this, with varying degrees of specialization - for some it is perhaps incidental, others have evolved this strategy to gain nutrients (often water as well). You are probably thinking of bromeliads, a diverse group of plants in which many species have specialized leaves that form cups at the base to collect water and litter. These structures, a type of phytotelmata, have similarities to some carnivorous plant traps.
These tank bromeliads are able to efficiently absorb nutrients from animal or plant matter which falls into the tank:

Considerable absorbed nitrogen is mobilized in the rosette center. Tested bromeliads appear to be well equipped to utilize minerals and organic nitrogen originating from tank-impounded plant and animal debris as nutrients.

This litter catching habit occurs in other lithophytic and epiphytic plants, i.e. those which don't grow in soil, because it allows them to capture nutrients when growing on rocks or trees. Examples include the staghorns/elkhorns and basket ferns:

They form a characteristic 'basket' that collect litter and organic debris, hence the common name. The collected debris decompose into humus, providing the plants with nutrients it would otherwise not have received from being suspended above the ground.

Thank you @nicfit! But it's not a bromeliads plant. I have them on my own in my home. But the plant I've seen was definitely no bromeliads. But thanks to your post, I've found the real plant I'm looking for. Thanks a lot.


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Can one switch the DNA present in a sperm cell?
Can a donated sperm cell be stripped of its original owners DNA and be replaced with DNA of another person to make a biological child of a man who has low production in sperm?

Not with present technology. There is next to no cytoplasm in a sperm cell. You cannot suck out its nucleus. If your remove its nucleus, the whole thing will just collapses on itself.
As for you question of replacing nucleus?. One current technique (Intra-cytoplasmic sperm injection - ICSI)  is to  inject a single sperm of a man with low sperm count with minimal mobility directly into an oocyte. (Ie sperm that is so bad that they effectively cannot swim on their own)
Unfortunately there is some indication, that this technology has made an entire generation of sons, who have also inherited their father's low sperm count and limited mobility. And now have a higher than average chance of needing IVF assistance.
https://www.newscientist.com/article/2108218-male-fertility-treatment-seems-to-pass-infertility-on-to-sons/