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Why does abnormal mitosis takes place in the cells of tapetum?
I know that the tapetal cells present in the anther are binucleate. I also know this means that after karyokinesis the cell does not divide itself and instead form a syncytium.  This occurs due  to abnormal mitosis, but I don't find a reason for abnormal mitosis to occur.
What is the reason for abnormal mitosis to occur?


text:
What are these (eggs?) ? ( Location - India )

The picture can be zoomed in on clicking
Description:
There are 24 of them, each ovoid, 1mm long and attached to the switch's frame by suction cups connected by tubes. They are secured to the base and couldn't be brushed off with a stick. Found them in East of India.
UPDATE
The ovoid heads have reduced in number (17) and have turned brownish (10.04.2017). The number of ovoid heads are 11 now and two of them have a black spot at the proximal end (could be the eye spots of developing embryos) (13.04.2017). The bunch has 4 of them now (24.04.2017).
Research & Question:
Assuming those are eggs (resemble those of Green lacewing and with the changes observed it is evident), what group of arthropods have such stalked eggs other than Green lacewing?

Appears to be very similar to the specimens in this SE Post

Yeah, they do look like eggs (of Green lacewing). In fact they have turned brownish and the number of ovoid structures have decreased which makes me think that they are eggs of some arthropod. @theforestecologist

The group of insects called Neuropterans have several species that lay eggs on stalks. This group includes lacewings, owlflies and antlions, however stalked eggs are not a defining trait of the group. In addition to the Green lacewing, the Blue-eyed lacewing from Australia lays stalked eggs while owlflies do not. Mantidflies also have stalked eggs which are members of the Neuroptera order, but the stalks are relatively short compared to lacewings.
This thread provides some interesting discussion.
P.S. While not an arthropod, at least one Genus of Molluscs (Nucella), lay stalked eggs too.
These are certainly eggs from this order (Neuroptera). Incubation time for these type of eggs can be anywhere from 2-7 days so you may already be having hatching if there are less eggs than what was initially there.

You may also like to include the Berothidae, beaded lacewings with those having stalked eggs.

source: Stack Exchange

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High Blood Pressure - Na or NaCl?
What is the cause of high blood pressure? or, Which foods can cause high blood pressure?
Is it just sodium, or sodium chloride? I'm confused because sodium chloride should ionise in the aqueous medium of the stomach.
It'd be great if someone could share the working details/mechanism of the same. Thanks in advance!

Welcome to Biology.SE! What research have you done before asking it here?

High blood pressure is caused by an excessive amount of fluid circulating in the blood vessels, or an excessively small mean blood vessel diameter. The later is more associated with stress situations and stressful lives, while the former is more related to the theme of your question: electrolyte balance.
An electrolyte is any molecule that produces an electrically conducting solution when dissolved in water (http://www.medicalnewstoday.com/articles/153188.php). In other words, they are or give rise to ions or charged molecules when dissolved in water. Examples are sodium, potassium, calcium, magnesium, chloride, phosphate, bicarbonate, ...
Water, even though on its own is a neutral molecule, it is still polar. This means that it has parts which are more negatively charged (in concrete, the oxygen atom) and parts that are more positively charged (the hydrogen atoms). These are called poles, and are due to different electronegativities.
The result of this is that water will form electrostatic bonds with charged molecules such as ions, or, in other words, which causes salts to be soluble in water. This also means that water is attracted to places with a lot of charged molecules - places with higher osmolarity. The travelling of water from places with lower to higher osmolarity is called osmosis.
That's what happens when the blood has an excess of ions (and thus higher osmolarity) when compared to the rest of the body and the normal, healthy values. Water starts travelling from the different parts of the body to the blood, being attracted by the extra concentration of salts, and pushing the blood volume over the healthy limits. This also makes it harder for the kidneys to excrete water from the blood, increasing further blood volume and giving rise to hypertension.
As you can see, any charged molecule in excess in the blood can increase blood volume (through higher plasma osmolarity) and create hypertension. In our bodies, the most common and impactful electrolytes are ions, being Sodium the most abundant.

Because sodium is the most abundant in the blood and the most ingested electrolyte, it is usually referred as its excess being the cause of hypertension. The common salt we use to cook comes in the form of NaCl, containing Sodium and Chloride, both electrolytes. They are very useful and fundamental to our organism, but in excess can cause diseases such as this.

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What would be a reason for a tree to have flowers of different colors?
The spring is here and the cherry trees along my street are blooming again!  Some trees have white flowers, some dark pink. But then... there're these trees which are all white yet just a few flowers are pink, just like that:

Is there a layman explanation for this phenomenon?

This is probably an example of Co-Dominance
As you may have learned according to mendelian inheritance
there exists dominant and recessive allels. However in reality there also exist phenomena like incomplete dominance and co-dominance where no specific allels are said to be dominant over the other.

There are a couple of possibilities for what's going on here:

The most likely explanation is Position Effect Variegation (PEV). Genes are, at the most basic level, organized linearly on chromosomes (very long strings of DNA). Some parts of chromosomes contain stretches of genes that are actively silenced, or turned off, by cells (large silenced regions like this are called heterochromatin). The boundaries of where this silencing starts and ends are sometimes fuzzy. If a gene necessary to produce pigment happens to be next to a silenced region, the silencing can randomly creep in and shut off that gene as well, or creep back to its normal boundary. (This is why it's called 'position' effect variegation: it depends on the physical position of a gene, in this case the pigment gene, on the chromosome, and how close it happens to be to a normally 'silenced' region.) This process is (probably) effectively random, so it won't happen in every cell, which means some cells will produce pigment whereas others won't. A famous example of this happens in fly eyes, as in the image on the left. Importantly, the difference here isn't 'genetic' (the actual content of the DNA), but 'epigenetic' - essentially, the way cells modify and read their own DNA.
Another possibility is an active jumping gene, or transposon: unlike most genes, transposons can move around in the DNA, and can sometimes carry with them a piece of DNA that tells nearby genes to be turned on or off (or are simply silenced by the cell, like in the PEV case above). If a transposon sits right near a pigment gene, it can cause that gene to be silenced. However, if the transposon up and jumps somewhere else at a random time (which active transposons do!), the gene nearby is no longer silenced, and can now cause pigment to be produced again. There's an example of this happening in snapdragons (see middle image). In this case, there is an actual genetic difference between the pink and white cells: one group has a jumping gene sitting next to the pigment gene, and the other doesn't.

Importantly, PEV silencing--like the transposon jumping--is inherited when cells divide, so if a stem cell that eventually makes a whole flower silences the pigment gene (or transposon jumps out), the whole flower will be white. If the silencing happens later in development, maybe when the early divisions forming the flower have happened, then a single petal, or just a sector of a petal, could be white, and the rest pink. Such sectoring is a telltale sign of PEV or transposon-related effects.
In your photo and description, the tree is mostly white, and individual sectors are pink, not vice versa. If the cause of the color switch is PEV, then the pigment gene's 'default' in this tree being silenced, with the silencing randomly moving away from the pigment gene in some cells. Or there could be a particularly active transposon that tends to bring gene silencing along with it at play here.


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What is the advantage of not having cytokinesis after karyokinesis?
In nature most of the cells are mononucleated, but in some cases like osteoclasts, umbrella cells of transitional epithelium, tapetal cells of another etc. are multinucleated. Wikipedia article about tapetum says that it is a strategy to increase the production of proteins. Why don't cells just up-regulate their genes for more production? What is the benefit of not having cytokinesis?

The absence of cytokinesis allows the two nuclei to remain in the same cell. If a cell has 2 nuclei instead of 1, it can transcribe DNA to mRNA at double the maximum speed, and so produce the desired proteins at double the rate. It's almost as if the cells become tetraploid, or hexaploid, and so on.
Learn more: http://www.nature.com/scitable/definition/cytokinesis-100
Why is it more desirable to have 1 cell with 2 nuclei than actually do cytokinesis and have 2 cells with 1 nucleus each (still 2 total)?
Because it is unfavorable to create two cells, which needs an extra investment in energy and nutrients to maintain, and is also harder to coordinate, and so it becomes more desirable to just have one single cell with the capacity of producing double the proteins.
Then why don't all cells adopt this strategy? What is the reason for such partiality?
First, because most cells don't need the extra transcription speed, as they don't produce a lot of proteins. Second, because of cell differentiation - to have cells doing different things they have to transcribe their genetic material differently, and so must be separate. Third, a lot of times it is desirable to have extra cells. For example, skin epithelial cells: their main purpose is to serve as a barrier or protection, and so there has to be a lot of them. That's why the basal cells are in constant mitosis.

This can happen after cytokinesis too, then why don't they ?

@JM97 cytokinesis divides the citoplasm, and thus the cell, in two, creating two separate cells, each with one single nucleus. I added an useful link to the answer.

Yes, effectively in both cases the proteins produced are doubled , then why do they undergo cytokinesis in some cases like in gut but not in other cases like osteoclasts?

@JM97 What do you mean in both cases the proteins produced are doubled?  Are you counting with both the daughter cells? Then in that case it is because it is unfavorable to create two cells, which needs an extra investment in energy and nutrients to maintain, and is also harder to coordinate, and so it becomes more desirable to just have one single cell with the capacity of producing double the proteins.

Then why don't all cells adopt this strategy? What is the reason for such partiality?

@JM97 first, because most cells don't need the extra transcription speed, as they don't produce a lot of proteins. Second, because of cell differentiation - to have cells doing different things they have to transcribe their genetic material differently, and so must be separate. Third, a lot of times it is desirable to have extra cells. For example, skin epithelial cells: their main purpose is to serve as a barrier or protection, and so there has to be a lot of them. That's why the basal cells are in constant mitosis.

Let us continue this discussion in chat.

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Are there any flowers that look like snakes?
In Rio 2, they showed a flower that almost looks like a snake head (with two fangs and a long tongue).

Are there any such flowers in real life too?

Interesting question, but I must say it looks opinion based, as different people may have very different perceptions on the shape of flowers.

The tongue could be the pistil and the fangs could be the stamens. To find such a flower, you need to search for species with two stamen and a bilateral symmetry.

There are quite a few examples of plants which look like snakes. I'll tell about them one at a time.

Darlingtonia californica: or Cobra Lily, is a type of pitcher plant which looks much like a snake. It is native to Northern California and Oregon, growing in bogs and seeps with cold running water. See this image:

Arisaema triphyllum: commonly called Jack-in-the-Pulpit, it is a type of corm which resembles cobra. It is native to eastern North America, occurring in moist woodlands and thickets from Nova Scotia west to Minnesota, and south to southern Florida and Texas. See this:

A similar and closely related plant, Arisaema griffithii, called Griffith's Cobra Lily, resembles even more. See this:

Pogonia ophioglossoides: also called Snakemouth Orchid, whose flowers resemble the face of a snake, pretty much like your image. It is a species of orchid occurring from central Canada to the east-central and eastern United States. See this:

Isotria medeoloides: named Little Five Leaves, its flower also resembles a snake's face. It is a threatened species of terrestrial orchid found in temperate eastern North America. See this:

Malacothrix coulteri (Snake's head) looks like the head of a snake.

It is an annual herb that produces a waxy, upright flowering stem. The inflorescence is an array of flower heads the yellow or white ray florets are about a centimeter long. The bracts are green, often with dark striping or marking.
It is found in sandy and coastal areas, grasslands and deserts.
For more info:
See here, and if you are interested in it's geographical locations, you can visit this page.


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Solving Hardy Weinberg problems
I really fail to understand Hardy-Weinberg equilibrium and can't find an easy enough source of information.
Can you help me to understand Hardy-Weinberg equilibrium?
My goal is to be able to solve the following kind of problem

In a population with two alleles for a certain locus, B and b, the allele frequency of B is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

Homework questions are off-topic, so I rephrased your question to make it more general and ask for a tutorial rather than asking for the answer to a specific question. Feel free to roll back if you don't like the edit but the post will likely be closed if you do

Do you want a method to solve the questions or you want to understand the mechanism?

That's perfectly fine with me!

The one thing about Hardy-Weinberg Equilibrium you should understand; this is the null-hypothesis for evolution. It's important not when it's correct, but when and how it's incorrect for a population. Deviations from HW are how populations genetics are measured. As such, it's a simple mathematical model for the random distribution of alleles.

Here is a tutorial to perfectly understand Hardy-Weinberg Rule! If you feel like you just need a brief reminder, you can skip the text until the section In short... and try out the exercises just to check your understanding.
Terms you should know a priori
I will not define the following terms, so make sure you understand them

locus
allele
(relative) frequency
Homozygosity and Heterozygosity

What is the Hardy-Weinberg rule?
Hardy-Weinberg rule (HWr) describes a relationship between allele frequency and genotype frequencies. I will present the maths later.
Alleles and Genotypes frequency
Let's assume we have a bi-allelic (two alleles) locus. The possible alleles are called A and B.
Notation for genotype frequencies
Note that I will use a slightly unusual notation on purpose.
Let $f_{AA}$ be the frequency of the homozygous individual caring the allele A on both haplotype (both chromosome). Let $f_{BB}$ be the frequency other homozygote. Let $F_{AB}$ be the frequency of heterozygote which inherited the A allele from the mother and the B allele from the father. Finally, $F_{BA}$ is the frequency of heterozygotes which inherited the B allele from the mother and the A allele from the father.
Most of the time people write $f_{AB}$ (or similar notation) to designate all heterozygotes irrespective of whether the A allele comes from the father or the mother. In this answer, I make the difference of which parent gave which allele. I will instead note $f_{het}$ the frequency of all heterozygotes. Therefore $f_{het} = f_{AB} + f_{BA}$. Similarly, I will note $f_{hom}$ the frequency of all homozygotes. Therefore, $f_{hom} = f_{AA} + f_{BB}$.
Notation for allele frequency
Unlike the above, I will use a class notation here.
Let the frequency of the A allele be $p$ and the frequency of the B allele be $q$.
All genotype frequencies must sum to 1
Of course, if you add up the frequency of all types of individuals in a population, you should reach 1 (or 100% if you prefer). Per consequence,
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
is our first important result.
Problem 1

There is 20% of heterozygote in the population, what fraction of the population is homozygote?

Answer: (hover to see the answer)

 $f_{hom}=0.8$ (or $f_{hom}=$80%)

Problem 2

There are 10% of AA individuals and 15% of BB individuals in the population, what fraction of individuals are heterozygotes

Answer:

 $f_{het} = 0.75$ (or $f_{het} =$ 75% )

All allele frequencies must sum to one
The same is true for the allele frequency, they must sum to one. This is even easier than before. Using the above notation it means:
$$p + q = 1$$
You will note that an obvious consequence of this result is that $1-p = q$ is also true. This is the second important result.
Problem 3

The frequency of alleles which are the A allele is 0.3. What is the frequency of the B allele?

Answer:

 $q = 0.7$

Hardy-Weinberg equilibrium
Let's now talk about HWr.
HWr assumptions
HWr makes a number of assumptions that I will not detail them here. Please have a look at the post Assumptions of Hardy-Weinberg rule for more information.
HWr exercice without explanations
Here are exercises that one may consider they come too early in my explanations. Don't worry too much if you can't solve them but please take the time to try solving them. Please do not try to apply known formulas about HWr, only use your logic and the above formulas (allele frequencies must sum to 1 and genotype frequencies must sum to 1)
Problem 4

In a population, one observes that 20% of the population is homozygote for the A allele and that there are no heterozygous individuals at all. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.2$

Below is a drawing of the population (assuming N=20 individuals) to help understand the answer.
AA | AA | AA | AA | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB
Problem 5

In a population, one observes that all B alleles are present in heterozygote only. The frequency of heterozygotes is 0.1. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.95$

The hard part here is to first calculate $f_{B} = 0.05$. Let's draw the population (assuming only N=20 individuals) and that will likely help you out.
AA | AB | AA | AA | AA | AA | AA | AA | AA | AA | AA | AB | AA | AA | AA | AA | AA | AA | AA | AA
HWr formula
As said above, HWr describes a relationship between allele frequency and genotype frequency
Without much explanations, here are these relationships
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$
To build your intuition, you should try to consider for yourself extreme cases where one allele is fixed (fixed=reached a frequency of one). For example, what are the expected genotype frequencies when

$p=1$ and $q=0$?
$p=q=0.5$?
$p=0$ and $q=1$?

How HWr is often expressed
Mixing up the idea of the above relationships and the fact that all genotype frequencies must sum up to one, one can also write
$$p^2 + 2pq + q^2 = 1$$
As by definition $q = 1-p$, it is also common to replace write
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
Why do these relationships make sense?
Problem 6

Imagine you are drawing alleles in a population of alleles like you would draw cards from a deck of cards! You draw a single allele. If the frequency of A allele is $p$, what is the probability of drawing an A allele?

Answer:

 $p$

Similarly, the probability of picking a B allele is $q=1-p$.
Problem 7

Ok, now. Assuming that the fact that you already drew an allele does not change the allele frequency in the population (because the population is very large), what is the probability of drawing two A alleles in a row?

Answer:

 It is $p$ for the first draw and $p$ for the second draw. The overall probability is therefore $p \cdot p = p^2$

Here we go! You just solved why $f_{AA} = p^2$. You can apply the exact same logic to find out $f_{BB} = q^2$.
Now the probability to first draw a A allele and then a B allele is $pq$. Therefore, $f_{AB} = pq$. The probability to first draw a B allele and then a A allele is $qp=pq$ as well. Therefore, $f_{BA} = pq$.
Exercise
Problem 8

In a population with two alleles for a certain locus, A and B, the allele frequency of A is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

(You will note I renamed the alleles to match my above notation)
Try to solve this problem yourself now!
Answer:

 It is a given that $p=0.7$. The question is what does $f_{het}$ equals to?
 Let's start by calculating $q$. $q=1-p=0.3$.
Then, let's calculate the the genotype frequencies.
$f_{AA} = p^2 = 0.49$.
$f_{BB} = q^2 = 0.09$.
$f_{het} = 2pq = 0.42$.
Here we go! We've got the answer. Let's make sure the answer makes sense by summing up the genotype frequencies to ensure we get 1.
$f_{hom} = f_{AA} + f_{BB} = 0.58$
$f_{hom} + f_{het} = 0.42 + 0.58 = 1$
All good!

Problem 9

At a bi-allelic locus, the allele A is dominant over the allele a. The phenotype associated with the dominant allele is present in 10% of the individuals of the population. What is the frequency of the allele A?

Answer:

 The genotypes coding for the phenotype associated with the dominant alleles are AA and Aa. Therefore, $f_{AA} + f_{Aa} = 0.1$ and therefore, $f_{aa} = 0.9$.
 The frequency of the allele a is $p = \sqrt{f_{aa}} = \sqrt{0.9} ≈ 0.95$.
 To conclude the frequency of the allele A is $q = 1 - p = 1 - \sqrt{0.9} ≈ 0.05$

Problem 10
You will find a HW problem involving selection at this post.
Problem 11
You will find a HW problem involving a population of triploids individuals at this post.
Problem 12
You will find a HW problem for sex-linked loci at this post

In short...
Here is a summary for a bi-allelic locus
Allele freqs sum up to one
$$p + q = 1$$

Genotype freqs sum up to one
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
You will note that most often when people write $f_{AB}$, they just mean $f_{het}$ and therefore don't make the distinction between $f_{AB}$ and $f_{BA}$.

Hardy-Weinberg rule
Note that Hardy-Weinberg rule holds only under a number of assumptions (such as random mating, panmictic population, no selection, ...) that I have not detailed here (see Assumptions of Hardy-Weinberg rule for more information).
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$

Putting all together
The whole thing put together is often expressed as
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$

Has anyone else explained it so nicely ever on this site? Awesome answer, +1! I read once that if allele frequency changes over time, it means evolution is taking place. And thats where this rule is used. Would you explain it a bit too? :)

@another'Homosapien'  if allele frequency changes over time, it means evolution is taking place yes, this is true by definition of evolution.  And thats where this rule is used. I don't fully understand what you mean. Actually in the assumptions for HWr to hold perfectly (and not just as an approximation), it is required that there is no selection and no drift (infinite population size) which pretty much mean no evolution. I think it would be worth to make a post on the assumptions underlying HWr. I'll be happy to start (but not tonight!).

I meant this is the application of this rule: making population studies at different times to measure change in allele frequency. I think I can ask a question about that...surely not tonight! But I'll ping you there :)

I see for the first time someone used spoil-protection (a great feature indeed ! ) out of puzzling.se :O

@AlwaysConfused Yes, I think it was the first time I used it. I kinda failed for several lines answer such as the last answer. If anyone manage to implement spoil-protection for problem 8, that'd be great!

@Remi.b I faced similar problem when I tried to include multiple paragraph under single spoil-protection. I don't know is there any command for that; but you may use an ! for each separate paragraph if that solves; but it may make understanding the answer difficult.

@Remi.b So HW's frequency is relative frequency?

Yes, it is a relative frequency, also called proportion, very often (always in population genetics) just called frequency. It indeed has nothing to do with the definition of frequency as used in wave physics.

Lets say there are 2 alleles. One of them is represented by B and other by b. Both will have some frequency at a specific time in a population. Now, frequency is number of that allele divided by total alleles. So, if frequency of B is, say X, the frequency of b is Y=(1-x). It would be because whatever alleles are not B are, for sure, b.
That gives us our first equation,
X+Y=1
Now, let us consider all the genotypes. There is BB, Bb and bb. Now, considering each of the 2 homologous chromosomes, there can be any 2 randomly selected alleles in a population. Here we are selecting an organism randomly. There can be no bias in selecting. This is one of the essential features of HW equilibrium. There is no selection pressure.
So, for B to be on the first chromosome (of the 2), the probability is x. So is for the second chromosome. So to have B on both, that is BB genotype, the probability is X x X = X^2.
Similarly for bb genotype, it would be Y^2.
Now, for heterozygous, there are 2 possible scenarios, bB and Bb.
For case 1: probability would be X x Y
For case 2: probability would be X x Y
So in both cases it is same, that is XY. So total would be 2XY.
So, lets add all the genotypes. The total should be 1 if all are included.
So,
X^2 + 2XY + Y^2 = 1
That gives our second equation. Now, whatever you have to find, you must find either X or Y first.
When you find one, you will get other by subtraction. When you have that, you can find whatever frequency is asked by putting values in second equation.
Allele B's frequency is 0.7. So allele b will be 0.3 (1-0.7).
By this you get the value of B (frequency of dominant allele) and b (frequency of recessive allele).
Now we put the values in the formula B^2+2Bb+b^2=1.
Here 2Bb is the frequency of heterozygous. So 2x0.7x0.3=0.42.

@cell0 watch the use of articles here. This does need editing, but be careful. Because "frequency" is a term in a mathematical expression, the use of articles is not going to be standard.

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text:
Why doesn't sugar spoil?
Sugar contains a lot of easily accessible chemical energy. Why seemingly nothing likes to grow on it?

lack of water. even if water is present then 2. high osmotic pressure will cause plasmolysis. Since I don't have a source I am not writing this as an answer.

Ever make bread?  Typically you'll mix a bit of sugar into warm water, add yeast, and wait an hour or to for the yeast to grow.  So the yeast is eating the sugar, but as JM97 says, it needs to be in a dilute solution.

Our food mostly gets spoiled by bacteria and / or fungi. There are 2 main reasons for sugar crystals not getting spoiled.
1- Lack of sufficient amount of water to sustain metabolic processes by microbes.
2- Even if sufficient amount of water is present , then due to high osmolality of the fluid formed, will cause plasmolysis or cell shrinkage.
Some technical data:

Microorganisms differ widely in their ability to resist salt- or sugar-induced reductions of aw. Most disease-causing bacteria do not grow below 0.94 aw (roughly 10 percent sodium chloride concentration), whereas most molds that spoil foods grow at an aw as low as 0.80, corresponding to highly concentrated salt or sugar solutions.

Source: https://www.scientificamerican.com/article/how-do-salt-and-sugar-pre/

Pop-sci reference: "How do salt and sugar prevent microbial spoilage? (from Scientific American)

@fileunderwater thanks a lot for providing source.


text:
What prevents backflow of blood from right atrium to vena cava during atrial systole
Vena cava is valve less. So,  during atrial systole what prevents backflow of blood to them?

Besides @Bryan Krause answer, there's another very important factor that prevents the blood from flowing back from the right atrium to the vena cava during systole.
Part of the muscle that constitutes the atrial walls also wraps around the site of entrance of the vena cava. Thus, during systole, the muscle contracts, closing (or almost closing) the passage and doing the job of a valve.
Nature!
EDIT: because of the high skepticism over what I have said in this answer, and having no references, I went to search for the class where I studied this, and here's the slide containing the information. Unfortunately, it is in Portuguese, but I will translate what it says, and you can check in any translator.

Venous myocardium: Cava Veins and Lung Veins
The veins that open in the heart don't have functional valves, meaning that the atrial systole could cause blood backflow through these veins.
Venous myocardium: The cardiac muscle tissue is prolonged through the vein walls that bring blood into the atrial cavities to the point of insertion of the fibrous pericardium.
Physiology: The venous myocardium contracts at the same time as the atrial wall, preventing the backflow of blood to the veins during atrial systole.

Do you have a citation? I don't believe that is accurate. If it does close at all, it certainly isn't enough to prevent blood flow in either direction.

@BryanKrause I have studied this in anatomy class, I can search later for a citation in the internet if you wish. It does close, and even if it doesn't close completely the passage, it turns it much thinner, meaning much less blood can pass through it an só the blood will go the other way - to the ventricle. It's both this system and the different pressures that you talked about that contribute to the prevention of backflow to the vena cava

@BryanKrause this is just a drawing but you can see the atrial muscle also wrapping around the entrance of the superior vens cava https://goo.gl/images/io75Jw

@FilipeRocha - I don't think hat shows what you think it shows...

@anongoodnurse what do you mean?

i dont know why the downvote, but I have edited the answer and added my "source"

Ah, thank you I found same in my book as well.

Pressure differences. Atrial contractions are much more gentle than ventricular ones, and in normal circulation the venous pressure in the vena cava often stays higher than the right atrium, even during atrial systole. If the pressure in the atrium does rise above the vena cava pressure at the peak of systole, there can be some backflow, although it is slight and brief in normal physiology.
The major veins are typically somewhat distended so they are constantly pushing blood into the right atrium. Blood continues to flow from the veins into the right atrium and from the right atrium into the right ventricle throughout ventricular diastole, including during most of atrial systole.
References:
Anderson, R. M. (1993). The gross physiology of the cardiovascular system. Robert M. Anderson.
Wexler, L., Bergel, D. H., Gabe, I. T., Makin, G. S., & Mills, C. J. (1968). Velocity of blood flow in normal human venae cavae. Circulation Research, 23(3), 349-359.

Venous pressure increases during atrial systole,  can we say it is due to backflow of blood?

@AnubhavGoel I think it's more accurate to say it's because of briefly reduced blood flow to the heart rather than from blood actually flowing backward. Maybe think about a highway, if something happens that causes some cars to slow down on a congested road, you are going to get more congestion ("pressure") behind them, but no one has gone in reverse, just slowing down is sufficient. That said, I have certainly seen this abbreviated as a "backflow" when describing venous pressure during the cardiac cycle. From a strict sense I would say this is wrong (in normal physiology).

I agree with you but regurgitation of blood do take place.

@AnubhavGoel It shouldn't happen (in the human) outside of pathology, because right atrial pressure doesn't exceed vena cava pressure. In cases of pathology, yes of course reverse flow can occur. Filipe's answer is wrong and based on a single slide with no further reference.

Look at my answer.

@AnubhavGoel Interesting, that conflicts with my source. I did a little more research and found an actual original source that indeed supports that there is backflow, albeit quite minor and brief, see here: http://circres.ahajournals.org/content/circresaha/23/3/349.full.pdf

@AnubhavGoel I updated my answer appropriately.

The atrial pressure  when equal to that in the  incoming vein will contain blood which will be propelled  into the right ventricle without  the need for any increased  pressure [as  does the ''muscular  pump' in the body. In other words  the right  atrium is ' functionally a sophisticated  valve'

Welcome to Biology.SE! Please elaborate on your answer by providing references. For more information on how to provide good answers on this site, please see: https://biology.stackexchange.com/help/how-to-answer. Thanks!


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What is the best food to eat at this type of day since it is so vey very late?
Best food to eat? In this time of the day because it's late very soon to be

Welcome to Biology. It's 20:15 in my time zone, and in the West Coast in the US it's still morning. So be specific. Further, this question may be opinion based and even if it's not, it's better suited for Health. SE. Could you improve your question such that it is clear what you define as 'late' and consider the fact that the question should be answered in a scientific fashion without a medical advice component?

Following AliceD, it is currently 1:35pm where I live. Also, note that The dose makes the poison and therefore nothing is fundamentally healthy, everything is toxic, it just depends upon your needs (and therefore a lot on a standard diet). Also, "Best" is very subjective. What are you trying to achieve?

If this question relates to evolution then everything on this website really does.

@Remi.b - If by evolution, you mean the physiology all biological organisms evolved, their genetic and environmentally adapted behaviors, etc,. then yes, it probably all does.


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Why do we feel asleep at night?
Why do we feel asleep at night mostly?
 I tried not to sleep but I could not resist my sleep at night.

You may be interested in this Q&A about the evolution of sleep. Currently your question could be a book title. It's a tad broad.

Do you mean "feel sleepy" or "fall asleep"?  Some of it is simply habit: I tend not to feel sleepy until midnight or so, but when I've shifted my sleep pattern towards early rising (which requires a concerted effort :-)), I would start to feel sleepy earlier in the evening.


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Kin selection Vs altruism (social biology)
I know that this is a contentious topic and I found conflicting explanations online which is what prompted me to put his question up. In some papers, Kin selection is mentioned based off the concept of inclusive fitness (sum of direct and indirect fitness). However, Kin selection is said to be an altruistic characteristic. That being said, altruistic genes only propagate through indirect selection (since an actor gives up its own fitness and do not generally reproduce). In that case, isn't Kin selection based off just indirect fitness and not inclusive fitness as a whole?
In a webpage, it is mentioned that "Kin selection is the evolutionary mechanism that selects for those behaviors that increase the inclusive fitness of the donor.". In that case, how can kin selection be altruistic? Can someone shed some light on what Kin selection is exactly? Also, a proper definition for indirect selection would be good as well. Thank you.

how can kin selection be altruistic?

Part of you confusion is purely semantic.
Kin selection cannot be altruistic. Kin selection is an evolutionary process. Altruism is a behaviour. Saying "kin selection is altruistic" is like saying "natural selection is flying" (when thinking of selection for flying abilities in, say, flying squirrels).
Altruism
Altruism is a behaviour in which increases another individual fitness at the expense of its own fitness. However, this definition lead to confusion of whether one is talking to lifetime fitness or only to a contribution to one's fitness that will eventually be returned. For this reason people talk about True Altruism and False Altruism
True Altruism
True altruism is a behaviour in which the actors's (the one performing the altruistic behaviour) life time fitness is decreased while the recipient (the one benefitting from the altruistic behaviour) is increased.
True Altruism can only evolve via kin selection (or group selection for the few who still view these two processes as different).
It is the indirect component of the inclusive fitness that selects for altruism indeed.
False Altruism
False altruism refers to cases where the actor performs the behaviour because he is expecting (not necessarily consciously) a return later in life. False altruism can be seen as an investment.
Such false altruism can be selected by natural selection (no need to consider indirect fitness). "Return on investment" can be caused by direct reciprocity or indirect reciprocity. In case of indirect reciprocity, some populations can use a system of reputation, where individuals are more likely to help individuals that they have seen being helpful to others before.
Game theory
All types of interaction between individuals can be modelled in game theory. One can also investigate specific type of strategy in response to a a specific game. For example, Tit-for-Tat is one type of strategy in a multiple encounter between two individuals game.


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Beetle identification - Kakadu NP, NT, Australia
I am trying to ID this beetle;

Size: not too big - approximately 2 cm (3/4 inch)
Where: Litchfield National Park, Northern Territory, Australia;
When: Southern hemisphere's spring, early September; the end of the dry season;
Time of day: night.

To my untrained eye, it looks like a cockschafer, but from the linked wiki page I understand they are a species confined to Europe. I tried a reverse Google image search and sifted through the site of Parks Australia and related pages, but to no avail.

After a hint from @fileunderwater I also think now that it is much more likely that this beetle belongs to the family of the Scarabaeidae which contains some 30.000 species worldwide. Scarabaeidae and Trogidae (what I thought was right before) are part of the same superfamily, the Scarabaeoidea.
The way the antennas are shaped as well as the body shape and the way the legs are ordered looks pretty much like this, even better than for the Trogidae. Have a look at this poster which shows a lot of different varieties (from here):

Some more information and real images can be found here and here.

Wow thanks Chris. Yes, the shape of the antennae is indeed an outstanding feature and reminded me of a May bug. I'll look into this!

I will have a further look tomorrow, when I have my experiment measuring and have idle time in front of the computer. :-)

Looks like belonging to the Genus: Anoplognathus

What makes you say Trogidae instead of Scarabaeidae (both belong to Scarabaeoidea)? The clubbed antenna with flat lamellae is typical for both families, as are the strong legs with spurs. Also, Trogidae usually have "bumpy" elytra, and there appear relatively smooth. I think it belongs to Scarabaeidae.

@Chris - You are not really trying to tell me in a lot of scientific words that my beautiful May bug is a cockroach do you ;-)


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Null hypothesis of Chi-square test for independence
My understanding of null and alternate hypotheses :
The null hypothesis is a hypothesis whose plausibility is being tested by a test statstic and is denoted by H0. It assumes that observed data follows a standard scientific theory (and the variation/deviation is due to
chance).1 Alternative hypothesis is a hypothesis that contradicts null hypothesis. It assumes that the variation in the observed data is real, not due to chance.It is usually the hypothesis that a scientist is trying to establish.
(Source: Biostatistics by Lee & Forthofer & Statistics by David Freedman)
This1 holds good for Goodness-of-fit test but not chi-square test for independence as there is no theoretical data to compare the observed data with.
So my question is in a given problem of chi-square test for independence how to determine what the null should be?

When what the scientist is trying to establish is mentioned:
Q : In a study of effectiveness of an antipsychotic drug, patients are treated with the drug and were compared to those receiving a placebo. 698 of 1068 patients were released after taking the placebo while 639 out of 2,127 relapsed after taking the antipsychotic drug.
Test the prediction that the antipsychotic drug is significantly more effective in preventing relapse than placebo.
A:  Ho : Edrug = Eplacebo  Ha : Edrug > Eplacebo
(Reasoning: Ha is the hypothesis the scientist is trying to establish and so Ho should be something that opposes the Ha that he has to disprove.)
When what the scientist is trying to establish is not mentioned (at least not clearly):
Q: Among 60 males and 50 females, 25 males and 20 females were with attached ear lobes. Statistically prove whether or not the attached pinna has any relation with sex.
Not sure what the scientist wants to establish so unable to assume a null.

What is an attached earlobe? Earlobes are always associated with the pinna right?

@AliceD It's a commonly used human trait for biology/genetics classes that was thought to follow Mendelian genetics (attached being recessive). It refers to whether the earlobe is attached to the face along its length or whether there is a portion that hangs down below the lowest attachment point of the pinna. Its better known now that it actually isn't a simple Mendelian trait but it still shows up in textbooks as an example.

@SanjuktaGhosh I don't understand what your point of confusion is. There is a theoretical null when you use chi-square test for independence. Specifically, the null is that the variables are independent. So, in a population that has both males and females and attached and unattached ear lobes you expect the proportion of males with attached ear lobes to be the same as the proportion of females with attached ear lobes.

This question looks more appropriate for CrossValidated than Biology to me. The questions are framed as biological questions but this is really a question about statistics -- nothing fundamentally "biological" about them.

@BenBolker I agree. There was a post on this matter on Meta, and in fact according to it should still stay on Bio.

@BryanKrause Is it the same for homogeneity? P.S. Thank you. Given the time constraint I'm forced to do surface reading.

@SanjuktaGhosh Yes. Maybe part of the confusion comes from the somewhat poor naming of the tests. In truth, a "test for independence" is really testing for non-independence: that is, you reject the null hypothesis if the samples are not independent. Same thing with tests for homogeneity, normality, etc: in all cases, you are rejecting the null if the data are not homogeneous, not normal, etc.

@BryanKrause Here(1st problem, a one-tailed test) the Ho: Pdrug_released>=Pplacebo_released  Ha: Pdrug_released<Pplacebo_released ? My understanding

The Chi-squared test of independence is, as the name suggests, a test of the independence of two outcomes.
Two outcomes are defined as independent if the joint probability of A and B is equal to the product of the probability of A and the probability of B. Or in standard notation, A and B are independent if:
P(A ∩ B) = P(A) * P(B)

from which it follows that:
P(A | B) = P(A)

So in your drug example, there is a probability that a person in the study is given the drug, denoted P(drug), and a probability that a person in the study is released, denoted P(released). The probability of being released is independent of the drug if:
P(drug ∩ released) = P(drug) * P(released)

Release rates can be higher for individuals given the drug, or they can be lower for individuals given the drug, and in either case, release rates would not be independent of drug. So Ha is not
P(released | drug) > P(released)

rather, it is
P(released | drug) ≠ P(released)

In your second example, there is a probability that a person is female, denoted P(female), and a probability that a person has attached earlobes, denoted P(attached). These events are independent if:
P(attached ∩ female) = P(attached) * P(female)

and Ha can be stated as:
P(attached ∩ female) ≠ P(attached) * P(female)

or equivalently:
P(attached | female) ≠ P(attached)

Not sure if you missed this. The question in the 1st problem essentially asks to test the hypothesis that the Effectiveness is more. 'Test the prediction that the antipsychotic drug is significantly more effective in preventing relapse than placebo.'

That's the reason I pointed out that a significant result on a chi-squared test of independence is not sufficient to conclude that the drug is more effective than the placebo, only that the effectiveness of the drug and the placebo are not equal. Researchers will often get a statistically-significant 'not equal', and then look at the contrast and interpret it as 'greater than' or 'less than' based on the observed direction, but that is not what the test formally tests.

Could you tell me a bit more about 'Researchers will often get a statistically-significant 'not equal', and then look at the contrast and interpret it as 'greater than' or 'less than' based on the observed direction'?

Some detailed examples are available here: https://math.la.asu.edu/~elajack/Fall14/STP231/Lecture_ch10.pdf.
Essentially, since the test only formally tests 'is response independent of treatment', a researcher who gets a significant result might then look at their data to infer directionality. e.g., a researcher has 100 trials of treatment A, and 100 trials of B. The success-rate is 22/100 for A, and 80/100 for B, so they have a significant result: success-rate depends on treatment. Since 80 > 22, they might further conclude that success is higher for B than for A, with caveats at the link.

It might help if you first ask yourself what the independence test is for in plain English, you are testing to see if one categorical variable has
an influence on another. In other words, if a person (or whatever)with attribute X (for example, is bald) are they significantly more/less likely to have attribute Y (like being allergic to penicillin) than someone who does not have attribute X.
So in your example the alternative hypothesis would be (in words): the ratio of males with attached ear lobes compared to males without is equal to the ratio of females with attached ear lobes compared to those without.


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Cytoskeleton made of only actin?
I am aware that the cytoskeleton has three structural components: actin, microtubules and intermediate filaments. I was wondering if any cell could possess a cytoskeleton made only of actin. Or made only of microtubules, for that matter. Is it possible for actin to perform the functions that microtubules ordinarily perform in a cell? Or vice versa?

If you are talking about an eukaryotic cell, I'd say no, due to the reason that the three types all have some different, irreplaceable functions. For example, microtubules form the mitotic spindle; actin filaments are greatly used for movement protrusions and cell adhesion; intermediate filaments are what convey the cell its structure, being the strongest. As the cell system is already tuned differently around these 3 types of filaments (proper linking proteins, enzymes, ...), my idea is that taking any out would probably make the cell unviable

1) Can cells survive without any of the different cytoskeletal components?
Yes, most certainly. At least for actin and microtubules (MTs) there are plenty of eukaryotic cell types that can survive without them. MTs can be disrupted by cold-shock (see for example here https://www.ncbi.nlm.nih.gov/pubmed/16505977). How well the cell survives depends on the type of cell, but the ability to survive without MTs can range from minutes to hours as far as I'm aware. Once the temperature goes back to normal, the MTs just grow back. Of course, the cells won't behave normally in the meantime, because many processes do depend on MTs. Actin can be disrupted using various drugs or genetic constructs, or they can be cut using femtosecond lasers (see for example https://www.ncbi.nlm.nih.gov/pubmed/28324605). Again, many processes are disrupted, particularly cell motility, but most cells can survive without actin for a while.
I'm not aware whether any eukaryotic cells exist that have no intermediate filaments or can survive at least for some time without them.
2) Could a cell function normally while lacking one type of cytoskeletal component?
First, to my awareness there is no eukaryotic cell without MTs or actin. We do commonly use actin and tubulin promoters for transgenes and assume that all cells will express them. So I'm taking this question hypothetically.
As with every hypothetical question, the answer then purely depends on the restrictions that you define. Can the cell possess arbitrary new proteins that currently don't exist? Then yes, definitely you could get eukaryotic cells with just MTs or just actin or just intermediate filaments. You just have to bend all the other things the cell does to fit with that filament type, and then enjoy arguing whether that's still a eukaryotic cell or not.
But I think actin would find it easier to take over the other filaments' jobs compared to the other way round.
MTs are large and rigid. They can't operate on scales below 25nm like actin can, and the individual tubulin dimers can't do anything useful until a tube of some minimal length has been formed out of many dimers. Intermediate filament monomers are pretty thin, but very long. Actin monomers are small and globular, and a supershort actin filament made of a handful of monomers can already function as a filament, branch out, form networks, pull on things etc. Actin-mediated endocytosis crucially depends on this (https://www.ncbi.nlm.nih.gov/pubmed/25675087 for example). It would be difficult to find workarounds for these small-scale functions of actin if MTs or IFs were to replace it. On the other hand, actin filaments can very easily be made into large, thick, rigid rods like microtubules. Many cell types do this constantly when they form filopodia. Actin meshworks can also provide similar mechanical support (both stable and flexible) as IF meshes. With minor shifts in the regulation of where, when and how to organise filaments, actin could probably take over the other cytoskeletons' functions. It would probably require a quite sophisticated regulatory system though to perform all the different functions at the same time in one cell.

@EliKorvigo Noted, thanks for the correction.

I think sperm is only having microtubules (axoneme) in them as a part of the cytoskeleton. Different types of cytoskeletons evolved to perform the different function so generally they will not exchange their function but are precisely evolved to carry out their individual functions.
(From textbook Molecular Biology of the Cell. 4th edition https://www.ncbi.nlm.nih.gov/books/NBK26914/)In tail section of sperm, which is a long flagellum.The core of the flagellum is composed of a structure called an axoneme.The axoneme consists of two central singlet microtubules surrounded by nine evenly spaced microtubule doublets. These dense fibers are stiff and noncontractile, and it is not known what role they have in the active bending of the flagellum, which is caused by the sliding of adjacent microtubule doublets past one another. Flagellar movement is driven by dynein motor proteins, which use the energy of ATP hydrolysis to slide the microtubules.
But I would like to correct my answer, as sperm also contains actin for capacitation and acrosomal reaction.So I think sperm is a eukaryotic cell where you can only see 2 types of the cytoskeleton.Here is the link for the paper https://www.ncbi.nlm.nih.gov/pubmed/15749953

Welcome. Can you add sources and references to your claims to allow other users to background read on your answer?

Yes ,see this link please https://www.ncbi.nlm.nih.gov/books/NBK26914/

Could you add it into the answer proper, please?

Sperm cells, like all eukaryotes (with some pretty rare exceptions), contain actin. "So I think sperm is a eukaryotic cell where you can only see 2 types of the cytoskeleton" – by virtue of having a nucleus, sperm cells also contain lamins – intermediate filaments.


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How a nerve impulse reaches the correct destination?
Say your brain wants to retract your right hand.
If there is some information coding playing a major role here, then what is the mechanism to find the correct path to reach the correct muscle?
Or is it every part has a single nerve connecting to the brain?
Any difference when it comes to withdrawal reflex comparing to brain initiating action? i.e. how the reflex round trip reaching the correct muscle?

This is a fairly basic question. Have you tried google? Do you know the difference between neurons and nerves?

Yes, tried but no avail. "how nerve impulse finds the correct path" is what I tried. But I only found results about how a nerve impulse travels, but not the mechanism on how it can select the correct path to reach the correct destination.

Here's a recent video I made in response to a similar question. It's called "Spinal cord is (not) a bus". https://www.youtube.com/watch?v=e5TRfya3FPk ---------- >! Basically, spinal cord is pretty much a labeled line!

OK, I think I can answer at the right level now.
Firstly, a nerve is a bundle of neurons, each neuron is like a fibre. So the sciatic nerve in the leg will carry fibres from the spinal cord to the muscles in the leg, like a data cable might connect many computers in an office to a server on another level.
Each neuron will form connections with a specific area on a specific muscle, at a specialised synapse called the "neuromuscular junction". When a signal travels down that particular neuron, it will release neurotransmitters that activate that particular muscle region. So by sending signals to the right neurons, the muscle to be activated and how much to activate it can be selected by the CNS.
A nerve impulse is a slightly misleading term as it refers to the collective activity of signals within the many neurons of the nerve, so an individual neuron won't register on an impulse. The signals in neurons are called "action potentials".
There is some information coding in the frequency of action potentials within neurons, but it is used to control the response of the muscle, rather than locate the correct muscle.
Wikipedia is pretty good on the subject if you know where to look:
neuron
withdrawal reflex
sciatic nerve

Right ok. The question is still there: "How to select the right neuron so that the correct destination can be reached"? Using computer terms, we have router to send signal to the correct computer and the router can look at the signal header to know which ip to send.

The motor cortex in the brain is divided into regions associated with each part of the body: https://www.memrise.com/mem/3977517/primary-motor-cortex/ so activity in the part associated with the hand will lead to movement of the hand. i.e. if you stick an electrode into someones motor cortex you can trigger twitches in certain muscle groups. It involves a massive amount of processing, and learning to generate smooth, controlled movements.

Thanks. You mean the only selection point is at the brain? And the rest is just signal propagation to the nerve end point? Isn't there some intermediate relay nodes like from the brain to the spinal cord? Or these relay nodes are also 1-to-1 mapping to the brain cortex?

Sort of, there is a relay in the spinal cord, where upper motor neurons pass signals to lower motor neurons, but yes I believe it's one to one. There is also input from other brain areas, such as the cerebellum and brainstem that helps fine-tune movements, but I can't remember much about it. Also sensory neurons (usually pain) can directly activate motor neurons in the spinal cord, e.g. during the withdrawal reflex, so no brain input whatsoever.


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Can you bleed from your bones?
I was talking to my science teacher about the body specifically the red bone marrow.
She said that blood is created in the red bone marrow. Does that mean that if you were to cut a fresh bone open it would bleed?

What research have you done before asking it here? Bone marrow is a solid spongy tissue, and won't bleed.

@another'Homosapien' but don't harvasian canals have blood vessels and nerves?

@another'Homosapien' Yes. Harvesian canal. It ought to bleed right?

@Homosapien. I looked at the  make-up of a bone.

No one really knows where the term dry as bone came from, many assume it comes from sun bleached bone which was the easy way to dry bone for other uses.

I edited your question removing the last part of the question as it was unrelated to biology and the overall question. Feel free to rollback to your original question but I believe the edits will get you more upvotes for the attention you need to award the bounty. You could also add what you already know to the question to give answerers a starting point to go from

Yes, bones too bleed if they get damaged (break or bruise). This is because bones are highly vascularised organs and breaking of bones will indeed rupture the blood vessels causing bleeding. Main artery which supplies blood to bone is nutrient artery , others are epiphyseal, metaphyseal and periosteal arteries. Skeletal system receives about 15.6% of cardiac output.
Since bones contain very low percentage of water ( about 31% ) comapred to others like skin(64%),brain and heart (73%) and lungs ( 83%). So the saying "as dry as bone " stills holds well.

Sources:
1-https://www.mananatomy.com/basic-anatomy/blood-supply-bones
2-https://water.usgs.gov/edu/propertyyou.html

You can also have bone bruises, which I believe are the result of bleeding inside the bone.

Thanks for the information. It feels good to actually "know" people that will help me with questions. If you ever need anything tell me and I'll try to help.


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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.


text:
Why do herring have fine bones
Most fish have largish bones which support the core muscles.  Around the abdomen, they act as a sort of framework protecting the organs.  With herring, the bones are really fine: almost thread like and there are lots of them: more than on any other fish I've eaten.  I would like to know why herring have such fine bones.

Most likely to assist in maintaining neutral buoyancy. Many fish have reduced weight of heavy structures (evolutionary wise)like bone to assist in maintaining nuetral buoyancy. The swimbladder struggles to maintain  buoyancy near the surface for some herring
https://www.researchgate.net/publication/231918276_The_herring_swimbladder_Loss_and_gain_of_gas/amp

I've changed your link to the actual link


text:
How much oxygen does a plant use up at night?
Given the fact that plants cannot do photosynthesis at night but need respiration for their energy needs, they use up oxygen and generate carbon dioxide. But how much is this? If I fill a room with plants thoroughly, what composition will the air in this room be in the morning? Are different plant species vastly different in this regard?

I saw this and thought, "surely this is google-able"! For me, a non-expert in plants, there seem to be different results for different plant types and this makes getting an answer tricky on the scholar, and on regular google, it's hard wading through the basic level material. I'm sure for an expert this is an easy answer.

@James: I first googled it, but I just stumbled upon answers from people not educated in the matter, who just made wild guesses. I hope to find an answer that is more fact backed than what I found out in the wild of the internet.

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

Source:
https://academic.oup.com/aob/article/94/5/647/151785/Plant-Respiration-and-Elevated-Atmospheric-CO2
Furthermore, it appears like plant respiration rates do not change much with changing temperature, and that larger plants have higher respiration rates.


text:
What happens to tube nucleus of the pollen tube after fertilisation?
Background:
Pollen tube contains a vegetative cell and a generative cell. The vegetative cell contains the tube nucleus, and the generative cell contains two male gametes. The two male gametes fuse with the egg to form the embryo and with the polar nuclei to form the triploid endosperm in angiosperms.
Question:
What happens to the tube nucleus of the pollen tube after/during fertilization?
Research:

This site says that the tube nucleus disintegrates.
This article does not mention about disintegrating nor discuss anything about the fate of tube nucleus.

Short Answer: It disintegrates.
Background: Although I was unable to find any primary reference, there were many secondary references stating that the pollen tube does disintegrate. In very short, after the pollen tube reaches the female gametophyte, the pollen tube nucleus disintegrates. For the 'why', it disintegrates to let the two sperm cells pass through, and also since its function of controlling the growth of pollen tube has finished.

For citation, you can have a look at:

Fertilization - Wikipedia
Advanced Biology -
A new mainstream text for the new specifications
Advanced Science; Michael Kent, 2000
Sexual Reproduction in Angiosperms; Kimball's Biology Pages
BIOPL 2410 Introductory Botany; KNiklas, TSilva; Cornell University
The Structure and Functions of Flowers - LeavingBio.net (image source)


text:
Why do stomata close in salt water?
Why do the guard cells of the stomata close when they come in contact with salt water?
I recognize it has something to do with osmosis and the fact that osmosis makes the water drain in some sort, following this distilled water has the opposite effect.. why?

INTRODUCTION:
The basic process by which opening of stomata takes place is by endosmosis.Endosmosis causes an increase in turgidity in the guard cells thereby causing its opening.
The closing of stomata is achieved by exosmosis which makes the guard cells flaccid.
HOW DO THE REGULATION TAKES PLACE IN PLANTS:
If you read the theory proposed by Levitt from the given [link]
,in which the theory is explained in simple steps with diagrams, you will understand that $K^+$-$H^+$ pumps is the main driving force which regulates whether endosmosis or exosmosis would take place.
When the concentration of $K^+$ increases in the guard cells there is osmotic influx of water from the surrounding epidermal cells  and thus 'endosmosis' occurs causing opening of stomata.
Similarly when concentration of $K^+$ decreases there is osmotic loss of water from the guard cells to cause 'exosmosis' and thus closing of stomata.
WHY THE STOMATA CLOSE IN SALT WATER:
When the guard cells of the stomata are open it means they are turgid due to endosmosis.However when such a turgid plant cell is placed is  in salt water(hypertonic solution) the latter having a higher concentration of salt ions than the guard cells causes the loss of water from the guard cells.
Thus the salt water is inducing exosmosis to take place in the guard cells due to which they become flaccid and close.
REFERENCE:
[link]

Osmosis. According to answers.com (and I know this is not a good site for research, but I couldn't find anything else), There are potassium ions in stomatal guard cells, and since salt water has a higher concentration of these ions than the cells, the stomata closes to retain moisture.

down voted because stomata donot close to retain moisture.They close because they loose moisture.

Yes, I feel that answers.com doesn't quite live up to it's reputation. It should not be used for research...


text:
Could a biological process organically build solid metal "organs"?
Human ingenuity has made great use of metal tools. But are there any known, or potential, biological processes that might produce sizable solid metal objects like how for example skeletons and shells are being grown? Does solid metal manufacturing require melting point temperatures beyond what biological processes can survive, or could it be grown by proteins more or less atom by atom?

i think that, even if it could be possible to "be grown by proteins more or less atom by atom", there would be two problems. First, metals are already hard to find in a proper manner for consumption, and even if it was easy, in excess they become toxic to the organism. Second, building something like a metal skeleton would mean a great loss in adaptability, as once made, I understand it would be immensely difficult to unmake without using great amounts of energy. So I don't see how metal parts could be biologically used apart from beings with a somewhat developed intelligence and means

You might have better luck on worldbuilding.stackexchange.com if this is for a story. They are more focused on finding ways to make something sound feasible if that is what you're looking for. I'm not giving an opinion either way on if it should be here. That depends on your intention.

That is an excellent question. I was a little confused at first because, without realizing it, you actually cited a perfect example of a biological process that manipulates metal: bone formation.
Bone is made of hydroxyapatite crystal, which is a mineral whose main ingredient is, of course, calcium (metal).
Now, to answer the how of your question; bone is formed, as you eluded, through protein to protein interaction mediated by cells called osteoblasts (osteo- = bone, -blast = immature cell). The osteoblast first locates a site on the bone that is to be expanded, then encases itself in a framework of collagen fibers. When this is done, calcium phosphate and hydroxide bind to the collagen and "harden" as hydroxyapatite (Ca10(PO4)6(OH)2). The osteoblast, now encased in a shell of hydroxyapatite (called the lacuna), transforms into an osteocyte (-cyte = mature cell) and projects long arm-like structures called filopodia which it uses as sensors and to communicate with surrounding osteocytes. All that adds up to look an awful lot like this (with respect to the fact that they are usually fully enclosed, but that would make for quite an insipid picture):

Finally, to put Filipe Rocha's concerns to rest, how is this fully organic and (almost) solid metal structure adapted and "unmade," should the need arise? Well, there is a third type of bone cell called an osteoclast (-clast = to break). Osteoclasts break down bone by secreting hydrogen ions to dissolve the calcium in hydroxyapatite, then cathepsin and other protease to digest the collagen network.
So there you go; a fully biological system with the capability to not only create a non-toxic, solid metal structure, but also maintain it and even manipulate and "unmake" it. Even though bone is not an organ, I'm sure this system could be modified for such an implement if we put our minds to it... :)
Edit:
If calcium isn't "metally" enough for you, you might want to check out limpet teeth, which are comprised of goethite, iron oxide-hydroxide (FeO(OH)). I can go further in depth with the biological processes necessary to produce this mineral if you want; just ask. :)

I did think about bone, but did not include it because Calcium is not a true metal. It is actually an alkaline earth metal, and its properties are somewhat different from true metals. I was going to suggest bone as being an almost perfect example of a biological process that manipulates metal, but did not want to prolong my comment. Also, bone is not a pure metal formation, which is what I think the asker was referring to, but rather a formation that includes "metal" atoms in its composition. Apart from that, your answer is nice and detailed, I just suggest you edit accordingly.

@FilipeRocha I am aware of calcium's peculiar properties, but alkaline metals are still, nonetheless, metals. You have, however, reminded me of a certain marine mollusk with iron (goethite) teeth... I also did outline the constituents of bone, so if the OP would like to specify a more restrictive definition of "solid metal," I will be happy to revise. I assume the OP is not referring to truly pure metal, as it would be necessary, obviously, for an organ to sustain cells, so including minerals such as hydroxyapatite in his research would be largely beneficial.

you interested me with those iron teeth! But not every part of the body has to sustain cells - think hair, or a seashell shell (this one I'm not sure!)

Also since you offered, I would be interested in you going into deeper details about the iron teeth! You can even make a question and answer it yourself!

@FilipeRocha They are quite fascinating! They happen to be the strongest known biological material... but this is not the time nor the place for that conversation; perhaps later :) Thank you for reminding me about them; this discussion would be incomplete without mentioning a biological structure comprised of arguably the most common metal.

Thank you too! I think hemoglobin may be angry at us for forgetting it either! And just to add, I went to reread the question, and he did say "solid metal parts"

@FilipeRocha I believe it would be inappropriate here unless the OP asks about them... If not, I will consider asking and answering a question regarding it. I will definitely tag you in it if I do.

I will be grateful

@FilipeRocha This is what I love about the stack exchange; everyone has something to add to the conversation :) You are right, we mustn't forget about metal blood! ;) I think the confusion here is coming in because of the loose term of "solid metal." Let us await clarification by the OP. If you think there is more to talk about, I believe we should start a discussion in chat... much more of this and we will effectively bogged down the comments section. :)


text:
Female mosquito fate in absence of food
What happens to female mosquitoes which want to lay egg but couldn't find mammal host for blood, will that mosquito simply die, if no mammals in area would mosquitoes will be absent too?

Interesting question. Mosquitoes are pretty much ubiquitous except in Antarctica, so lack of food evidently isn't a problem for the species as a whole. Not all mosquitoes feed exclusively on mammals - Wikipedia says "Thousands of species feed on the blood of various kinds of hosts, mainly vertebrates, including mammals, birds, reptiles, amphibians, and even some kinds of fish. Some mosquitoes also attack invertebrates, mainly other arthropods."

Usually, the function of having blood meals is to produce eggs but not for surviving. Some exceptions are for overwintering species which uses some blood-feed meals to survive during winter such as Culex pipiens.
In absence of blood host (the host depends on mosquito species and can range from fish to mammals!) and after mating, the female would just keep looking for a host (and some sugar source to stay alive) until she dies. So there is no reason for not living as long as in the case she would have found one or several hosts in her entire life (a couple of weeks usually).


text:
Can recessive alleles be expressed?
Say I have a disease that is autosomal recessive. If one was heterozygous for this trait, could the recessive gene still be expressed?
I know sickle cell anemia has a heterozygous advantage so it must be possible but what are the conditions for this to happen and also to what degree?
EDIT: This isn't asking how a gene is recessive or dominant in a molecular level.

Possible duplicate of What makes a gene dominant or recessive

I disagree that the post is a duplicate. This post has to do with the semantic of dominance interaction. I think the OP did not realize that for talking about dominance interaction one must chose a phenotypic trait of interest. The other post has to do with the molecular mechanisms yielding to dominance interactions between alleles.

Retracted my vote.

Short answer
The concepts dominance, additivity, epistasis, recessivity and others are all specific to a given phenotype. Here you are getting confused because you are considering two different phenotypes at once.
Slightly longer answer
By definition, if an allele is recessive, then in the heterozygote state, the phenotype of interest is just like the homozygous dominant. An important point in the above sentence is "the phenotype of interest". A given locus may show a pattern of simple dominance-recessivity for a given phenotype but may show a completely different pattern for another phenotypic trait.
Let's consider your example of sickle cell anemia. For the phenotype which is the disease, sickle cell anemia has a simple dominance-recessivity relationship. However, for the phenotypic trait which is fitness (yes, in quantitative genetics, fitness is often modelled as a simple phenotypic trait), sickle-cell anemia shows (environment dependent) heterozygote advantage. Also, the fitnesses of the two homozygotes differ greatly.
Note that, in reality, very few loci show cases of perfect recessivity dominance.
EDIT
You are considering two (or even three) phenotypes.
First Phenotype: Fitness
Fitness shows overdominance (with highly unequal fitness for both homozygotes).
Second phenotype: Disease
Double mutant are sick, the others aren't. Perfect dominance-recessivity (although if I am not mistaken heterozygotes individuals have some restriction when it comes to scuba diving if I am not mistaken)
Third phenotype: Shape of hemoglobin
If the heterozygote hemoglobin is shaped just like the healthy homozygote, then there is dominance-recessivity. If the shape differs (which might be causing malaria resistance, I don't know), then there is some partial dominance going on.

Ok, so the phenotype in interest (again in sickle cell anemia) is having the disease, which is having the point mutation causing hemoglobin to change shape, and this is simple dominance-recessivity like you said. What I am still confused about is why are heterozygous individuals more fit, because if the phenotype in interest is the change in shape of hemoglobin then in a heterozygote all cells should be normal, and doesn't protect against malaria.

This is a bit simplified but, in the heterozygotes the cells are not 'normal'. Both types of hemoglobin are expressed, it just doesn't result in the disease. Restated, one healthy allele is sufficient to prevent the disease phenotype. At the molecular level both alleles are expressed and that's why the recessive allele protects against malaria, it's still expressed.

@MichaelZheng See edit

Ok I get it, Disease ≠ Shape ≠ Fitness Thanks

Others have already explained. I add some clarifications. You said that you know the molecular mechanism of dominance; revisiting them will answer your queries.
Gene expression means the formation of the gene product in whatever form it is active – protein or RNA. If an allele is recessive it can:

Not form the product
Form a non-functional product
Form a hypo-active product
Form less amount of product

In all but the first case the gene is expressed although it may not give rise to the product of your interest.
Phenotypes of homozygotes and heterozygotes can differ in these different cases but in a strictly Mendelian case, the expression (or non-expression) of the recessive allele has no effect on the phenotype if the dominant allele is present.
Now, one can also dig deep on what phenotype is. Phenotype is an observable manifestation of a trait but with latest technology we can observe even the DNA sequence. In my opinion (in a contemporary perspective), an allele is strictly dominant if a recessive allele present along with it does not perturb the regulatory/metabolic/signalling network at all.

There are a couple of distinctions to make here. You can have an allele which is 'Phenotypically Expressed', that is it's visible at the organism level by some feature. In that case, no, recessive alleles by definition do not express that particular phenotype.
Now at the molecular level things can be different. You have the same two alleles and both can produce equal mRNA and protein levels, but they differ by a nucleotide/codon, which gives rise to the distinct functions and thus produce distinct phenotypes.
At this molecular level, both alleles are expressed and are co-dominant for the phenotype of measuring mRNA variants by sequencing and at the same time, the organism presents only the dominant phenotype.
So it's important to consider in which context one is discussing 'expressed'. If a research paper is about genetic disease, you'll often hear discussion of the 'recessive allele' and still have measurements of it's expressed mRNA. Everyone just knows by convention that recessive in the context of a human genetics disease paper means the particular disease the paper is on or a phenotype that is being discussed.