text:
Experiment to show that carbon dioxide is needed for photosynthesis
In my school test, the question is as follows:

Will the experiment work satisfactorily?
What alterations can you make to obtain expected result?

What I wrote:

Yes, it will work satisfactorily. Lime water absorbs carbon dioxide and hence there is no carbon dioxide for the leaf and hence photosynthesis does not take place and no starch is prepared. Hence on iodine test, the presence of starch is negative and thus proves that carbon dioxide is required for photosynthesis.
We can put half of the leaf inside the flask and half of it outside. So, the inside part will not show presence of starch and the outside part will show presence of starch.

[Note]: It was marked incorrect by my biology teacher. It got it reviewed by another biology teacher and HE SAID WHAT I WROTE IS CORRECT and the teacher who marked it wrong gave the opinion as follows:

It will not work satisfactorily because lime water does not absorb carbon dioxide. [which to me, seems incorrect as lime water ABSORBS carbon dioxide]
The alteration is that you have to use Potassium Hydroxide instead of lime water. [which to me, seems incorrect too since both lime water and potassium hydroxide absorbs carbon dioxide and then there is no need to use potassium hydroxide when lime water works!]

Now I am confused what is correct and what should I write in my final examination??  Please help. Any help will be appreciated, Thank you.

Not an expert answer but from experience, I’ve seen limewater absorb $\ce{CO_2}$ mostly when $\ce{CO_2}$ is bubbled through the solution. However, in respirometers, KOH is used to absorb any neighboring $\ce{CO_2}$ in the chamber. Analogically thinking, it seems to me that limewater won’t be very efficient in removing $\ce{CO_2}$ from the flask in your experiment. Thus, you are correct in stating limewater absorbs $\ce{CO_2}$, but it might not work “satisfactorily,” making the teacher’s answer correct. For q2, I feel you should combine both your teacher’s and your answers. A control is needed.


text:
Is there a plant particularly suitable for absorbing Hydrogen Sulfide
I live in an area with some open sewers and in the morning I can usually can smell the gas inside my house.
There are many plants like snake plant which improve indoor air quality but I was wondering if there are any that are particularly useful for absorbing sewer gas (hydrogen sulfide)

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How does the modern synthesis theory explain the evolution of birds from dinosaurs?
The theory of evolution claims that birds evolved from dinosaurs only by mutation, genetic drift, migration and natural selection.
However, it seems to me that wings were not selectively advantageous for dinosaurs.
Would you show me a book or a paper which explains this point in detail with academic accuracy?
Level of the book or the paper should have detailed information for an advanced reader.

An introductory course to evolutionary biology such as Understanding Evolution for example might help you.

@Remi.b I'm looking for a book or a paper (or an internet site) that explains the evolution of dinosaurs to birds in detail with accademic accuracy. Does that site you mentioned have such an account?
If yes, would you please show us a link to it?
I checked the site, but I was unable to find the one.

No the site I linked is not specific to your question. But having a better understanding of evolutionary processes in general will help you to answer the specific questions you may have (such as the one you are asking in this post).

You might want to have a look at this post to avoid potential semantic issues about what a dinosaur is.

The question is unfortunately too broad. There have been many changes from the ancestors of modern day birds and modern day birds. You should reduce your question to one specific trait and also probably precise whether you are interested in knowing the phenotypic intermediate stages or the specific genes involved in the evolution of this specific trait.

@Remi.b "The question is unfortunately too broad." Why on earth do you think a question is too broad that asks for a book or a paper on a specific subject?

@MakotoKato this is broad because one would have to explain you about phylogenetic and palaeontological methods. These are not really laboratory simulations of macroevolution but inferences drawn from what is observed from the remains of these organisms.

@MakotoKato You will hopefully find this popular article interesting and useful: How Dinosaurs Shrank and Became Birds (it has also been reprinted in Scientific American)

@WYSIWYG You talk as if you know the answer.
In any case, I'm asking for a book or paper that answers my question.
What's wrong with it?

Try asking about a particular aspect such what you seem to be interested in,  the early evolution of wings and flight in maniraptorans. the entire process of birds evolving from dinosaurs would fill several large books, hence too broad.

First of all, dinosaurs did not evolve to birds. A better way of saying it is that modern birds evolved from a particular type of dinosaur. That, however, is not the same as the blanket statement "dinosaurs evolved to birds". The latter implies that dinosaurs somehow morphed into birds and stopped being dinosaurs. What actually happens is that a species starts changing and, eventually, a sub-population of that species has changed so much that we call it a new species. It is a subtle distinction but important.
As for a specific paper, no we don't have anything like that for any specific examples. What we have is a huge collection of observations all of which point to the process of speciation occurring via the processes of mutation and natural selection. It's impossible to know the precise series of mutations that led to the creation of a new species for a variety of reasons.
All we have is the current species. If we know an ancestor, we can deduce a possible path that leads from the genome of the ancestor to the genome of the target species but we have no way of knowing whether that specific path was followed. For an analogy, consider computers. If I were to give you a modern desktop PC and one of the first computers:

You might be able to guess certain changes that were made to the old ones in order to build something like the new ones but would you be able to figure out every single step along the way? How would you detect all the attempts that failed? The ideas that didn't pan out? Would you be able to infer the existence of floppy disks, for example?
The same problem applies to species. It is essentially impossible to infer the precise series of mutations that led species B to split from species A. Especially since, usually, this happens through species A.1, A.2, A.2.1, A.3 etc, and all we have is species B.
Add to that the fact that evolution is not a linear process, there are many dead ends (way more than in computers), and the story gets even harder to understand. This graphic illustrates it quite well:

Obviously, if you have the first red dot on the far left and the last blue on on the far right, it will be impossible to infer the entire evolutionary history linking these species.
So, with this in mind, given that dinosaurs and birds share a common ancestor, it is essentially impossible to get the full, true, path that led from that ancestor to either dinosaurs or birds. More importantly, as shown in the image above, dinosaurs did not evolve into birds in the first place so the question is moot.

If the "common ancestor" was a dinosaur, then it would not be incorrect to suggest that birds evolved from dinosaurs.

Could you give me a clue how reptilians(I hope the nomenclature is more accurate than dinosaurs),
for example, grew wings and lost most of bone marrows?
It seems to me that those features are not advantageous for them to survive unless they were able to fly.

@vervet as far as I know, that's not the case. I may be wrong though.

@MakotoKato well, for a clue, have a look at this answer about bats. Look at the gliding mice. You can imagine similar intermediate steps.

@terdon "First of all, dinosaurs did not evolve to birds. That is a common misconception. You might want to have a look at the answers here. What you're probably thinking of is that modern birds and dinosaurs share a common ancestor."
I beg to disagree.
http://evolution.berkeley.edu/evolibrary/article/evograms_06
"The discovery that birds evolved from small carnivorous dinosaurs of the Late Jurassic"

@MakotoKato thanks for the link. I hadn't expressed myself clearly. My main point was that while modern birds may well be descendants of certain dinosaurs, you can't say that dinosaurs evolved to birds. Only that birds evolved from dinosaurs. The first statement implies that dinosaurs were replaced by birds rather than simply that they gave rise to them.

@MakotoKato you greatly misunderstand evolution when you presuppose that all the traits that exist have to be selectively beneficial. We know that the vast majority of new mutations are near-neutral and selection can be quite weak. Also, a trait may simply piggyback on other beneficial traits - take a gene for resistance to a pathogen, for instance and a gene for fur colour in a predator free environment where the disease is selective; if the two traits emerge in the same lineage fur colour will be selected for just because disease resistance is selected for.

@AnkurChakravarthy "We know that the vast majority of new mutations are near-neutral and selection can be quite weak." Suppose wings were selectively neutral for dinosaurs. Then the probability of the evolution of birds from dinosaurs would be very very very small. It would be like a monky typing entire Shakespeare's Hamlet.

@MakotoKato perhaps, but that wouldn't mean it couldn't happen. More importantly, wings would never be selectively neutral. They immediately open up an entire new ecological niche and all sorts of new defensive options. They would most certainly not be neutral.

@terdon "but that wouldn't mean it couldn't happen."
In realty, no, it could never happen.
"wings would never be selectively neutral."
If they were selectively negative, birds would not exist.
The only option is that they were selectively positive.
But this argument is flawed because it assumes that the theory is correct.

Um no,  firstly , depending on population size even deleterious alleles can be fixed by drift.
The other thing is neutral traits can be fixed as if under selection due to chromosomal linkage with another trait that is subject to selection ; this effect is called genetic hitchhiking.
There is no evidence that wings at all stages had to be of adaptive benefit for the evolution of birds to be possible. The notion that birds couldn't have evolved if wings weren't selected for is wrong.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1459830/

That wings could be selected for, on the other hand, also enjoys support; one only needs to look at the rapid diversification of Pterosaur lineages for  a period of nearly 75 million years, and even after that Pterosaur diversity did not drop off a cliff until near the end of the cretaceous.

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Nernst equation?
I keep seeing the Nernst equation in two different forms, one using the natural log and the other using log base 10. Could someone explain why there are two different versions, and which should be used? Thank you in advance.

I see this issue calculating entropy, where the log base is chosen as a matter of convenience. With the Nernst equation, the equations of different base using either log base 10 or log base e are equal when a correction factor of ~2.3026 is applied to the log base 10 equation.

The factor of ~2.3026 comes from the ratio ln(n) / log10(n) = 2.3026... for any real positive value of n.

You will see change in constant in that case. As @Galen pointed out, you will get multiplication factor of 2.3026 in log 10 equation. And you can use any. Both are correct.

Thank you! I completely forgot about change of base when using logarithms.

Since you tagged this with neuroscience, I'm going to assume the two forms you see are these:

The top one is what you might call the "no assumptions form". Temperature is left as a variable, T, and will have to be plugged in, and one will also have to plug in the gas constant (R), Faraday's constant (F), and the valence (z) of the ion (X) in question when you solve the equation.
The bottom one could be called the "handy assumptions form", or simpler form. Temperature has already been plugged into the equation as room temperature (for early experiments, they probably measured at that...this is what is used here) or body temperature, the values for the constants are plugged in, and the valence of "X" is assumed to be +1 (such as for Na+ or K+), so the math of doing all that results in this other form, with the number 58 in it.
The conversion from the natural logarithm ("ln") to the base 10 logarithm ("log") is part of that transformation. As commenters mentioned, the conversion factor is ~2.3026 between the two. So that number is factored in, but so are all the other values.


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Gene sequence and DNA
can anyone help me with this?
It shows two gene sequences for a sheep and a goat.
   5’------C C T G A G G A G C A T G T T------3’
   3’------G G A C T C C T C G T A C A A------5’
               5         6         7         8        9
   5’------C C T G A G G G G C A T G T T------3’
   3’------G G A C T C C C C G T A C A A------5’
               5         6         7         8        9

I hope u can see it.
number 1 = goat
number 2 =sheep

what differences are there between the two gene sequences?
Decide the amino acids 5-9 for both gene sequence?

Look at the differences in the nucleotide sequences, and how those differences may change translation.

This question looks like it is from a homework assignment. What have you done to try to solve this problem on your own?

Thank you for replying. Well, as for question one, the goat has a AT meanwhile the sheep has a GC (under number 6) That may mean that there's a change in the sequence of the amino acid? Or is that thinking wrong?................. as for question 2) I find this difficult. I mean I have a table to see the amino acids, but what should i exactly do?

You're right. A change in nucleotide sequence 'may' change the amino acid sequence. To find out, use a standard translation table (https://en.wikipedia.org/wiki/DNA_codon_table) to see if a different amino acid results from the difference in codons. To translate, replace each three consecutive nucleotides (codons) with the amino acid in the table.

Amino acids can have different properties (ex. polarity) that can affect protein folding. If you find a difference in amino acids between the goat and the sheep, look up how the properties of the amino acids differ. If the properties are very different, then the resulting protein may have a different structure, and therefore may have a different function.

For translating, keep in mind that real sequences may be read by transcriptases in 1 of 3 different reading frames at a time. For each codon, you look at 3 nucleotides, but you may get a different amino acid depending on where you start.

Thank you indeed. I used the translate-table.  Now, I have to answer what difference there're between the enzyms of the organisms? How should I find that out?

As I mentioned in a previous comment, different amino acid properties can change the structure of a resulting protein, or enzyme in this case. The wiki page show some of the important amino acid properties. https://en.wikipedia.org/wiki/Amino_acid

Thank you. Now, when I'm going to use my "translate-table" to see which amino acids it's, let's take the goat, should I take the gen sequence from 5' to 3' or that from 3' to 5'  (i need to make the dna to rna)  thx

I recommend reading this article: http://www.ncbi.nlm.nih.gov/books/NBK22085/

Thank you indeed. The part with the difference between the enzyms of the organisms: I have translated my bases into amino acids, but now, when I have to find the difference, should I look at both amino acids from the goat and sheep and compare them? What should I focus on when I compare them? I find it difficult to find the difference between both enzyms.... Thx!

There is a one amino acid change, GAG encodes glutamate and GGG encode Glycine. the change from glutamate to glycine is a fairly substantial one, both in terms of polarity and also sterics, that likely effects the secondary structure of the polypeptide.


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Is the fingerprint regenerated?
Let's say you get a a cut on your finger. Will the fingerprint be regenerated to matched your original fingerprint and if so, how?

Wow! I was just searching about this :D It looks like as far as you don't damage dermal layer, you can regenerate exact same pattern.


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What is the leaf venation of a scuppernong vine leaf?
I googled around and I didn't find anything that says its leaf veination. Anyone know?

2 hours later...;-; Does no one know?

Check this

Using the link, it's netted veination, though it doesn't say if it's palmate or pinnate. So I relied on using my own judgement on looking at my scuppernong leaf and it looks decidedly palmate. It would be better if I had confirmation from some site or such, but as it has main veins and smaller veins sprouting from those main veins, I think it's palmate.
Additionally, for all other botany question confusion, I finally found this website which may be useful: http://rampages.us/fieldbotany/2014/05/23/grape-vine-3/


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When did the most recent common ancestor of all living domestic dogs live?
Wikipedia provides a very detailed page on the origins of the domestic dog, but this fact does not seem to be present there. Google searches for terms such as "most recent common ancestor (MRCA) of dogs" didn't reveal any authoritative sources.

As Remi.b points out, the where and when of the ancestor of the domesticated dog is not well known.
Based on a review by Morell (2015), the ancestor of the domesticated dog (canis familiaris) was a now extinct wolf that gave rise to Fido 11,000 to 16,000 years ago. The author bases this conclusion mainly on data from Freedman et al. (2014). Interestingly, Freedman et al.'s data indicate that it was not the Gray Wolf (Canis lupus) that gave rise to Fido, which was long thought to be the one and only ancestor. The ancestral extinct wolf is thought to have give rise to present-day dogs, Dingoes and the Chinese, Israeli and Croatian wolf. The Golden jackal split off earlier, around 400,000 years ago.
Complicating the search for Fido's ancestor is the widespread occurrence of wolves and dogs, which makes it difficult to pinpoint the location of origin. Indeed, there is indication that canids were domesticated not once, but multiple times at different places, just like the domesticated pig was domesticated twice. Moreover, there is indication of gene flow between wolves and dogs after Fido split off, further blurring the available evidence (Morell, 2015).
A recent 2015 special issue on dogs and cats in Sci Am may shed more light on this, but I have to get to that. Will update this answer if appropriate!
References
- Freedman et al. Plos Genetics; 10(8): e1004631
- Morell, Sci Am (2015): 313(1): 60-7

From the wikipedia article you linked:

The origin of the domestic dog (Canis lupus familiaris or Canis familiaris) is not clear. Whole genome sequencing indicates that the dog, the gray wolf, and the extinct Taymyr wolf diverged at around the same time 27,000–40,000 years before present.

They cite Skoglund et al. 2015.
It seems that divergence between the grey wolf and the dog started at Taymyr (northern Russia) about 27,000–40,000 years ago. Therefore, the MRCA of all dogs and grey wolf today would have lived about 27,000–40,000 years ago. Tito et al. 2013 estimated canids fossils found in Europe were 39,000 years old. We currently don't have a better accuracy and we are not able to date the MRCA of all dogs with more accuracy than the MRCA of grey wolves and dogs.

Your answer tells us about the most recent common ancestor of of the grey wolf, dogs, and the extinct Taymyr wolf. My question asks about the most recent common ancestor of all living dogs. Although related questions, I do not believe they are identical.

You are right, I was a little inaccurate in my answer. I added another study showing evidence of canid fossil found in Europe. With this (and many other findings shown in the wiki article) we understand that we don't have the sufficient fine scale to date the MRCA of all dogs more accurately than the MRCA of grey wolves and dogs.

authors: user1205901 - Слава Україні


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Why would growth hormone (somatotropin) cause both lipid AND glucose release?

GH increases lipolysis (lipid breakdown) and the release of fatty
  acids from adipocytes into the blood. Fatty acids then can be used as
  energy sources to drive chemical reactions, including anabolic
  reactions, by other cells. GH also increases glucose synthesis by the
  liver, which releases glucose into the blood. The increased use of
  lipids as an energy source accompanies a decrease in glucose usage.
  Overall, GH activates the use of lipids to promote growth and protein
  synthesis.

(From Seeley’s Anatomy and Physiology, 10th edition.)
That passage has gotten me confused. So more lipids are used by cells instead of glucose, yet the body releases more glucose into the blood in response to GH. What would be the point, or benefit, of this occurring?

The way its stated in the excerpt you have in your question could be a bit clearer. This concept can be found in any basic physiology textbook, and looking at another text may also help clarify it more.

Great question... and an important point about glucose and lipid utilization! The body can't turn fat into sugar, but it can turn sugar into fat. The more technical way to say this is that the body can't convert acetyl-CoA into glucose, but it can convert glucose into acetyl-CoA.
The enzyme that converts glucose to acetyl-CoA, pyruvate dehydrogenase, catalyzes an irreversible chemical reaction. Pyruvate dehydrogenase converts pyruvate into acetyl-CoA, which can be used in the Krebs Cycle, fatty acid synthesis, etc. Once acetyl-CoA is produced it cannot be converted back into glucose (carbohydrate) within the body. This is important because certain cells/tissues can use only glucose for energy production, while other cells/tissues like the liver can use both glucose and lipid for energy production.
This is where your question becomes very important, because the liver is the predominate organ that maintains glucose homeostasis (i.e. maintains blood glucose concentration) in-between meals or during periods of fasting. In periods of fasting, the liver uses free fatty acids released by adipose tissue for energy/ATP production in order to produce glucose through gluconeogenesis, an anabolic process that requires energy.
So, growth hormone increases fatty acid release from adipose tissue stores for uptake by the liver. The liver takes up the fatty acids from the plasma and uses them to produce glucose for release into the circulation for glucose-dependent tissues to use. During this time of fasting, tissues that can use fatty acids and glucose tend to switch to fatty acids as their energy source, while tissues that only can use glucose will continue to rely on glucose production from the liver for their energy source.
Here is a nice summary (open source) from National Library of Medicine explaining in more depth the basis for why fatty acids are oxidized to provide ATP for gluconeogenesis - "Energy Metabolism in the Liver".
Also, George Cahill, a famous physician-scientist at Harvard University who studied metabolism and starvation has an excellent review of fuel flux under fasting and starvation conditions that demonstrates the above mentioned principles as well "Fuel Metabolism in Starvation" - namely that free fatty acids released from adipose tissue are oxidized in the liver and used for anabolic processes in the liver, such as gluconeogenesis that maintains blood glucose concentrations.


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Does inorganic particles have pattern recognition receptor?
Does silica or carbon particles (inorganic substances causing silicosis and anthracosis) have Pattern Recognition Receptor (PRR) on macrophages/dendritic cells? Because phagocytic activity depends on PRR. If it doesn't have how it engulfs it?

Pinocytosis....

I think that I have posted this link for you before NIH Bookshelf: Janeway's Immunobiology. You are continually asking questions on this site about immunology that would be answered if you simply read this book (even though this edition is slightly out of date). It is a free resource and it will explain everything you are looking to find out, and then some, about the basics of immunology. The only annoyance is that in order to read you need to enter a search term, you cannot read cover to cover like a normal book.


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How do lipid-soluble substances diffuse through the cell membrane?
It’s said that water-soluble substances can diffuse through cell membrane with less ease than lipid-soluble substances because the former encounters impedance in the hydrophobic region of the phospholipid bilayer. However, does the same logic not apply for hydrophobic substances, in that they cannot traverse the hydrophilic outer/inner surfaces of the plasma membrane? How would they be able to enter or leave the cell with greater ease?

See this paragraph and image from The Cell: A Molecular Approach. 2nd edition.:

During passive diffusion, a molecule simply dissolves in the phospholipid bilayer, diffuses across it, and then dissolves in the aqueous solution at the other side of the membrane...Passive diffusion is thus a nonselective process by which any molecule able to dissolve in the phospholipid bilayer is able to cross the plasma membrane and equilibrate between the inside and outside of the cell. Importantly, only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates (Figure 12.15). Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-). The passage of these molecules across the membrane instead requires the activity of specific transport and channel proteins, which therefore control the traffic of most biological molecules into and out of the cell.

As shown in above paragraph, molecules have to dissolve in phospholipid bilayer to diffuse through it. But since the hydrophilic part is already interacting with water, so dissolving is mainly for the hydrophobic part. Now, since hydrophobic part is non-polar, so it can dissolve only non-polar substances (like dissolves like). Thus, small gases like O2, CO2 and non-polar molecules like benzene easily dissolve in hydrophobic part and diffuse through it. Also, molecules like water and ethanol can also dissolve in it in small amounts due to their small size and very less polarity. That's why only some molecules of water can diffuse passively, large amount of water would require aquaporins. Now, since bigger molecules like glucose have large size and high polarity, they cannot dissolve in the membrane and thus require transmembrane channels even for diffusion. Similar case is with ionic substances too: they require ion channels for their diffusion.
Hope this helps. Comment below if you have any further doubts.


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Disadvantage of using Drosophila for breeding experiment
What should be the disadvantage of using Drosophila for experiments?
a)small size of larva.
b)short life cycle.
c)mating soon after emergence of flies.
d)large number of offsprings.
Options (b) and (d) should be advantages.
I think that the answer should be (a) as small larvae would be difficult to maintain.
Given answer is(c).
Why is that?

All options given have advantages but become disadvantageous depending on experiment you are trying to do. Here question is asked for "breeding experiment". In these experiments it is very important to keep track of genetics. If females mates with males of some undesired genotype, it will ruin your experiment objective.
As option (c) is 'mating soon after emergence of flies' , females and males from same vial (which is generally maintained as single genotype) will start mating soon. Generally this time period is 4 hours. Drosophila melanogaster starts mating after 4 hours at room temperature. This is the precise reason in Drosophila, virgin collection is done within 4 hours of eclosion.
Imagine you want to set up cross between wild type and some mutant. You will grow them initially in separate vials. Now for crossing , assume you need females from wild type and males from mutant. In this step it is important that females should be virgin else it will be difficult to track your genotype later on. Now if Drosophila starts mating soon after emergence of flies, it is disadvantage for your breeding experiments.
Note: There is sperm competition but that is special case


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How do macromolecules (large drugs) in the eye reach the bloodstream and what are the relative significances of these pathways?
I am considering the elimination pathways for antibodies (50-150 kDa) from the vitreous humour to the blood stream. My overarching question is what is the most significant route such antibodies could take to get there?
Elimination from the vitreous humour to the aqueous humour is known to be quite a substantial route of clearance, but does drug eliminated through passage into the aqueous humour travel to the blood stream? Notably there are two routes of exit from the aqueous humour, one is directly into the bloodstream and the other is through Schlemm's canal, but where does that lead?
Also for example is the choroid directly in contact with the hyaloid membrane of the vitreous play a significant role in elimination? We also also such drugs penetrate into (and through) the retina, at that point they reach vasculature, however they have to work quite hard to get there.

Antibodies are a unique case.  I recommend reading PubMedID: 26726925 regarding the pharmacokinetics of ranibizumab (Lucentis), a Fab fragment, after intravitreal administration.
"We assume that the principal pathway for the ocular clearance of large molecules is by a first-order transfer process from the vitreous to the aqueous chambers, from which the molecule is absorbed into the circulation via Schlemm’s canal by the physiological process of aqueous humor turnover."
A comprehensive analysis of the pharmacokinetic processes are included in the mechanistic model that they have developed.  I will not copy and paste them here.


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Saturation vapor pressure effect on human body
I found this calculator:
http://www.decatur.de/javascript/dew/
It calculates the dew point based on temperature and humidity.
In the result it is mentioned the saturation vapor pressure.
I barely understand the notions of vapor pressure, but I read somewhere that divers are rising back to water surface slowly, because the vapor pressure has negative effects on blood vessels, which can pop.
My goal is to find if a similar situation  (like divers' one) can be encountered by runners who are exercising when the vapor pressure is very high.
Thoughts?
Edit:
Is it possible to experience the effects of diving 10 meters in water, at surface with the contribution of climate factors (humidity, temperature and atmospheric pressure)?

Welcome to Biology and thanks for your question. Divers encounter problems with gas bubbles, known as 'the bends', divers' disease, or Caisson disease. It has to do with gas pressures under a column of water versus those at the surface. Nitrogen accumulates at low depths, oxygen starts to accumulate at ~30 m etc etc. It has little, if anything to do with cells popping afaik. Further and quite frankly, I don't understand your question... Could you add references or sources to your claims?

If the divers then rise up back to the surface too quickly, these gases will be forced out of their dissolved form and form bubbles in the blood vessels. These gas bubbles can then cause the blood vessels to pop, causing much physical pain and serious medical issues.  << An excerpt from http://chemwiki.ucdavis.edu/Physical_Chemistry/Physical_Properties_of_Matter/Phases_of_Matter/Liquids/Vapor_Pressure .My question is, is it possible to replicate the situation of divers by a person who is running in certain weather conditions?

Your question said "blood cells." The reference you give says "blood vessels." Blood vessels are made of endothelial cells, and the gas bubbles don't rupture the cells, it breaks the junctions between the cells causing blood to leak into the surrounding tissue. If the blood vessel that bursts happens to be in the brain, then that is a stroke and there is a good chance the person will die unless the rupture can be repaired. While it is possible that a person's own (high) blood pressure could cause a small capillary to rupture, variations in normal atmospheric pressure will not do it.

Thanks @AMR So, if I understand correctly, if the atmospheric pressure is very high, maybe above 800 mmHg, the humidity is 100%, temperature above 35 degrees Celsius and a person is exercising at lactate threshold, the diver's conditions are almost similar. Is that correct?

The problem is not the pressure itself, it is a rapid change in pressure.


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How can a blood test give information about rickets?
Can we detect rickets from a blood test? What  evidence pf rickets is in the blood and how is the blood treated to detect rickets?

o one to answer :-( ?

Confirming a suspected phenotype with an emperical test helps us determine the provenance of a disease. Coincidently, here's an easy to read article about Rickets I found some time ago:

Welcome to Biology.SE. Blood is part of the phenotype. So you question (in the title) boils down to How can we infer anything about the phenotype by looking at it? The question can only be answered for a specific case (and you gave one so that's great). I would suggest to edit the title

From the Wikipedia article I linked to in your question:

Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones.

There is also a rare genetic form of rickets called Vitamin D-resistant rickets or X-linked hypophosphatemia that can be diagnosed by DNA sequencing of cells collected by a blood draw.
It should be noted that, at least in the case of rickets, blood tests alone will not diagnose the disease. There are many other possible symptoms of the disease, so a patient presenting with one or more of these symptoms may also be subjected to a blood test to confirm the diagnosis, not just make it on its own.


text:
Movement of sperm to the egg

Sperm swims through semen and reaches the haploid egg in the oviduct during fertilisation.

Once the sperm reaches the cervix, through what does the sperm swim through to reach the egg?
Is the uterus completely filled with a fluid that allows the movement of the sperm, or does the sperm only swim through the endometrium (uterine lining)?

Once the sperm reaches the cervix, through what does the sperm swim
  through to reach the egg?

It swims through the cervical mucus. Human sperm swim in a straight path in cervical mucus.

Is the uterus completely filled with a fluid that allows the movement
  of the sperm, or does the sperm only swim through the endometrium
  (uterine lining)?

Yes, the uterus is completely filled with uterine fluid. They are attacked by many leukocytes while being helped by various contractions.
I would suggest reading the Suarez 2006 review. It has very nice information of all stages of sperm moment.


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Can dermatophytes (toenail fungus) survive without oxygen?
I read that fungi in general can switch to alcohol fermentation in the absence of oxygen (https://en.wikipedia.org/wiki/Anaerobic_organism). How about dermatophytes ? (https://en.wikipedia.org/wiki/Dermatophyte aka toenail fungus) I read an interesting comment here http://gizmodo.com/cold-plasma-could-be-used-to-freeze-out-toenail-fungus-1734825446 by bra55orchid that

"Topical infections like nail fungus and warts require access to the
  open air. This is why they don't go systemic. Nail fungus progresses
  as it degrades the nail to allow air to pass through it. Pine sap is
  enough to kill them by sealing them off. Spores may survive in the
  case of fungus, so you must keep them sealed off until the spores are
  pushed out by nail growth."

PS I tried sealing off my nail, but it did not stop the fungus...

Try IPL (laser) treatment for toenail fungus, it's guaranteed to work. All other treatments never remove the entire fungae and they always come back. It will take 3-6 months for the healthy toenail to grow back nice and shiny, the fungae might be dead but the ugly nail growth will take time to be replaced naturally.

Tried laser (not sure if IPL) but it is very painful, as the laser goes deeper than the fungus, so it also hurts healtthy tissue. What worked for me is cutting out the entire affected nail as it no longer attaches to the nail bed.


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How does the "heat vision" of some snakes work?
Some snakes have an infrared sense which is used to track warmblooded animals.
How does that organ work? And would a similar organ be possible in a warmblooded animal?

https://en.wikipedia.org/wiki/Infrared_sensing_in_snakes

Vipers, pythons and boas have holes on their faces called pit organs (Moon, 2011), which contain a membrane that can detect infrared radiation from warm bodies up to one meter away (Fig. 1). At night, the pit organs allow snakes to sense an image of their predator or prey (Source: Nature).

Fig. 1. Pit organs in python (top) and viper (bottom) as indicated by arrows. Source: Wikipedia
Nerve cells in the pit organ contain an ion channel called TRPA1, which detects infrared radiation as heat. The pit organ is part of the snake's somatosensory system, which detects touch, temperature and pain. It does not receive signals from the eyes. Hence, snakes sense infrared by detecting heat, not photons of light. Infrared radiation heats up the pit membrane tissue, and TRPA1 channels open when a threshold temperature is reached, allowing ions to flow into the nerve cells and triggering an electrical signal (Gracheva et al., 2010). Rattlesnake TRPA1 is activated by temperatures higher than about 28 °C — roughly the temperature a snake would 'feel' from a mouse or a squirrel about a meter away (Source: Nature).
Hence, this organ works best in cold environments where temperatures are low so that warmblooded prey stands out. Further, warmblooded animals won't be able to use this organ, as the pit would be ~37oC and not be able to detect anything below that temperature.
References
- Gracheva et al., Nature (2010); 464: 1006-11
- Moon, Anat Cell Biol (2011); 44(1): 8–13

To my surprise, these are heat sensitive channels :o

I've just asked How do snakes determine the direction of prey from their thermal infrared sensing pit organs?

@uhoh - nice one! +1'd


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Trouble understanding how uncouplers in the thylakoid membrane increase the rates of the Electron transport chain?
I am a undergrad in a cell physiology class and just did a learning exercise involving testing rates of the electron transport chain via the reduction of DCPIP, analyzed by spectrophotometry. ( I think...  D:   )
So from what I understand, uncouplers stop the "connection" of the ETC and ATP synthase indirectly. And in our lab period we used a hydrogen ionophore(ammonia) as our uncoupler( I think... D:  ).
So for our results I obtained this graph**(The Y axis should be absorbance(600nm)) sorry**...:

Where tube 1 through 3 was a collection of thykloid membranes isolated from spinach leaves; tube 1 being kept in foil until the 10th min mark to then measure absorbance as a control. Where tube 2 and 3 were exposed to light for the 10mins, with absorbance readings being taking every 1 min. And with tube 3 having the added ammonia(from what I understand, the uncoupler).
Therefore how does the ammonia uncoupler speed up the electron transport chain?
My thoughts after googling are that since PQ( plastoquinone) is partially responsible for establishing the proton gradient for the thylakoid mebrane, since it transports H+ ions from the stroma to the lumen upon reduction, that if there was this ammonia uncoupler, that could travel through the membrane due to its lack of charge, it could then bind with the H+ ions forming $\ce{NH4+}$ in the lumen.
So then if the lumen now has less H+ ions then the high(lumen) to low(stroma) H+ gradient would be ruined/weakened.
So this is the part I guess confused with; if there is less of a H+ gradient across the thylakoid membrane, then how does that have any bearing on the reduction of the added DCPIP or the speed at which its reduced?
Since tube 3 went the fastest to clear( ~0 absorbance), this is only when it is reduced yes? This means then that in tube 3, the reduction of DCPIP  happened the fastest.
So then does this mean that DCPIP, the artificial electron acceptor, takes over for PQ somehow? Why does PQ have trouble "doing its job" in the presence of the weakened H+ gradient?
P.S: Sorry for the rambling, but I felt including my train of thought was important for others to see where I  misunderstood.


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How does the flow of ions along voltage-gated channels lead to nerve conduction along axons?
Let's say the axon lies along the x axis, and voltage-gated sodium channels lie parallel to the y axis. When a channel is opened, sodium ions will flow along the y direction into the cellular fluid. My question is, how does this flow of ions in the y direction cause a flow of electric current in an entirely different direction (i.e., the x direction along the axon)?
Both layman and technical explanation would be appreciated.

The flow of current during action potential generation is perpendicular to the axon length. The channels that transmit ions in neurons are often voltage-gated. Voltage-gated Na+ channels (VGSCs) open when the membrane depolarizes. So when excitatory neurotranmitters (e.g., glutamate) open up channels (e.g., AMPA receptors) in the dendritic region, anions (e.g., Na+) flow in. The ensuing membrane depolarization opens up VGSCs in the axon hillock, that subsequently opens VGSCs adjacently in the axon, that opens up VGSCs a little further up in the axon etc etc. Hence, while the flow of Na+ is perpendicular to the axonal membrane, the net effect is a wave of VGSCs opening up along the axon length. With some delay, voltage-gated K+ channels open that allow K+ to flow in, repolarizing the membrane, preparing the neuron for another action potential (fig. 1).

Fig. 1. Action potential mediated by step wise activation of voltage-gated ion channels. Source: Human Medical Physiology
Hence, although neuronal ion fluxes and networks can be modeled by electric currents flowing in electronic circuitry (Fig. 2), nerve conduction is not anything like it. Current flow in electronic circuits is a flow of electrons. In action potentials in neurons it is ions that carry the transported charge.
.
Fig. 2. Hodgkin & Huxley's axon model. The power sources are the electric gradients of Na+, K+ and a leak current source. The conductances are represented by those same ions. The cell membrane is modeled by a capacitor. Source: Bonabi et al. (2014)
Reference
- Bonabi et al., Front Neurosci (2014)

@Christiaan I have got a question with respect to this topic- What causes the adjacent VGSC to open? Is it the flow of Na+ along the x axis that cause conformational change in the adjacent VGSCs and thus they open ? Could we call this motion of Na+ ion, electric current?

@Tytoalba - yes, pretty much


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How to use the law of diffusion in the presence of electric forces?
Isn't the movement of ions affected by the electric field as well? For instance, when a sodium channel in a cell's membrane opens, the sodium ions are said to diffuse into the cell, from higher extracellular concentration to lower intracellular concentration. But what about the electric force fields? The negative ions within the cell attract the sodium ions outside the cell, while the potassium ions within the cell repel them, so why aren't such interactions mentioned and taken into account when discussing the direction or intensity of flow? It seems that the only factor considered by books is diffusion of sodium ions from higher to lower concentration.

Sure, the electric force matters a lot. Ions, like protons H+, follow their respective Ion Motive Force, which is the sum of two components: difference in concentration (osmosis) and difference in charge (voltage) across the membrane. You can find more details here.


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The antiquity of man
What are the oldest fossils of modern man? What is the evidence until now? I do not ask to know the evolutionary
chain that led to H. sapiens, but I wouldn't mind to hear it, nevertheless.
What are the official sources, like peer reviewed journals, confirming it?
I wish for reference and rigorous scientific analysis.

Welcome the Biology.SE! First of all, this is not a chatroom. It is a Q&A website. Second of all, from a simple web search, I have found this so I am flagging as a homework question with no research effort. Sometimes you need to learn how to make the best search. This is an example of when that is necessary. I don't know what you searched but I simply searched "oldest fossils of homo sapiens" and got many results. If you want to find peer-reviewed articles, you can use Google Scholar (probably with the same search term).

Welcome to Biology.SE. It very much depend on what you call modern man. I think this  wiki article will answer your question. Does it? The wikipedia article also contain the references you might be looking for.

Can you guys try and do better than Wikipedia?

@AMR The term modern human is slightly unclear and the wikipedia article is very complete. You did not do a better job than wikipedia.

In addition to that, understanding why the OP did not get the answer he was looking for from the wikipedia article will inform us of what was unclear to him.

@AMR the wikipedia article contains a large number of citations from peer-reviewed literature, is clearly laid out, accessible (unlike the Science paper that was your only citation), and points to a great number of other sources for reading. I see nothing wrong with it at all.

@MattDMo by removing the OPs reference to "Homo sapiens sapiens or Homo sapiens in general" you removed the fact that they understood that there are distinctions to the classifications of modern man. If you look at the Wiki article you will see that a number of the references are to Chris Stringer, the author I reference. And if you look at the title "Genetic and fossil evidence for the origin of modern humans." pretty much sounds like the right starting point for the OP, as they were not interested in other Hominids. And the 918 articles that reference that article will likely have an answer

Try this article as a starting point;
Stringer, Chris B., and Peter Andrews. "Genetic and fossil evidence for the origin of modern humans." Science 239.4845 (1988): 1263-1268.
It is old, but it has been cited 918 times to date. That should be more than enough of a breadcrumb trail to find what you are looking for. Also if you click through to the Science Magazine page, it also has a list of relevant articles below the abstract. You may need a membership to AAAS or library access to get a copy of the actual article.
Also try a Google Scholar search for Modern Human Fossil Record. The above article is the second article referenced in this search.

I am well aware of the suggested sources of info.

Then it was pointless for you to ask your question and waste people's time.

amr I am only learning this site. I have not finished my comment

When I posted for the first time my question apparently to a wrong sector, I was just explaining my frustration that there really is scant info on the web on this subject.   I mean where are your anthropology journals? Where are their guidelines and key questions regarding their field of scientific inquiry. I am not doing any homework, though my field of interest is related(health sciences).   So I ask for recent info from an established authority on the field.  Thank you for your responses anyway.

When you press enter , zoop comment posted. Do you understand now AMR?

I mean if I want to know for heart failure, or valvular heart disease, I will find authoritative info in a straightforward and open manner , from European Heart Journal, Circulation and Journal of the American College of Cardiology. I don't have even to do any googling. If I try to find info on anthropology on such a key question in their field, I don't have such luck.

And I can't help but point to the fact that though a newbie to this place I was faced from the beginning with somewhat hostile intentions; I would not be truthful if I didn't  say this.  How is a question "what is the content of water in human blood" answered and considered acceptable? Isn't this supposed to be an old knowledge and not so vague and uncertain like mine? Isn't this readily available through search engines? Does it not look like a homework question? Has that person made efforts to find answers? Please! In that sense almost any question asked in this sector has these attributes

you accuse me of

Major anthropological discoveries rise to the level of General interested, so you will often find those article going to the highest impact Journals such as Nature, Science, Proceedings of the National Academy of Sciences, The Philosophical Transactions of The Royal Society, The Royal Anthropology Institute, and so on. If you search Anthropology + those journal names, you will find resources such as http://anthropology.pnas.org and https://www.therai.org.uk. You also have museums such as American Museum of Natural History or The British Museum.

And I actually took the time to answer your question, so if you were already aware of what I gave you then you already had an answer to your question. All you really needed to do was look at the Journals that the those articles were in or look at their reference lists and the articles citing them and you could have established a pretty extensive list of the journals that cover anthropology. If I wanted to find out about Coronary Artery Diseases I might start in JAMA or NEJM, find a review on the topic, then go down the list of references to find the more specialized material. That's research.

I appreciate your answer, as pna.org was not an evident source of such material.

But, being a cardiologist I might add that trying to find an expert opinion on the heart is far easier, and done quickly and  with a greater degree of confidence. On the other hand, such info I requested, is not readily available and you have to have a fore knowledge about where to search. Anyway, I don't see why I "should" research extensively about a difficult subject(I did search and found unsatisfactory sources) , while I regularly see naive questions being posted and answered without fuss or qualms.


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If all bacteria in human gut are dead, can they be there again?
If someone likes to eat chocolate, she may have gut bacteria which like chocolate according to some articles that I have read.
http://www.theatlantic.com/health/archive/2014/08/your-gut-bacteria-want-you-to-eat-a-cupcake/378702/
If I do not eat chocolate for a long time, would their number be decreased and other (bad) bacteria dominate the gut?

I think I heard of procedures to innoculate bacteria into guts of humans.

@RoSiv - oh yeah - sterilally referred to as fecal transplantation - I will refrain from going into answering this question O.o

@AliceD From the title I totally thought they were going for Antibiotics... silly me.

@AMR - I got fooled by the title too. I also thought it was about antibiotics - and how to re-populate the intestinal microfauna. I didn't read further and commented. Luckily without answering.. It seems a bit of a twin question, and quite an unclear one too.

The article ( as far as I understood from quickly scanning over it) is more about bacteria in your gut generating cravings for different types of food. The ones "liking chocolate" are more likely to like high-sugar food. If you wouldn't eat any sugar at all, some of them might die out, but others will be able to utilise other nutrients. (Very, very basically said.)

I got a good answer from someone but he deleted it. I think this to be helpful for others, too. http://biology.stackexchange.com/questions/35887/what-are-the-most-important-factors-influencing-a-person-s-gut-microbes?rq=1

So the question your essentially asking is "Do certain types of bacteria like a specific nutrient, and if so will they dissipate or die off if I do not acquire that nutrient?"
Let's give a specific example for comparison. Lactose intolerance is a prevalent disorder among many people and those who do have the intolerance, if aware, tend to steer clear from lactose containing foods. Some studies have been shown that correlate lactose consumption to amount of lactose-containing bacteria in the gut.
So I would say if your asking if you remove a nutrient from your diet will a particular bacteria suffer i.e die then yes. Although be aware that many bacteria are able to break down a variety of different nutrients, and in the case of a cupcake which is loaded with sugars, and fats, I would say a large majority of gut residing bacteria are able to use that as energy in one form or another.
Here's an article comparing lactose-tolerant, and lactose intolerant individuals, not chocolate, but a good start. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898492/

Lactose is a better example than chocolate, thanks.


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How to measure growth of algae with colorimeter
I am doing an lab for IB Bio and don't know how to use a colorimeter to measure growth in algae. The experiment I am doing will measure the effect of pH on algae growth. The algae will be taken from a fish tank and will include cyanobacteria, diatoms, and algae bloom. I don't know how the transmittance/absorption will relate to growth. I also don't know which wavelength of light to use. Help would be appreciated, thanks!

What is the color of the algae? What is the complementary color of that?

There is/was no lab manual providing you with instructions/recipes/protocols to complete this assignment? You received no instruction or demonstration on how to use the equipment/instruments? There was no lecture material on the theory behind the experiment? That strikes me as rather unusual. What if you electrocute yourself trying to turn on the colorimeter? What if you accidentally ingest one of the solutions or the growing cells? That could potentially be dangerous.

You can measure the turbidity of water using turbidimeters, however, that would not say whether it is caused by algae or something else. Best way, IMO, is to take samples and calculate biomass but there is no straightforward way to do this optically.

The color of the algae is a brownish green.

No, I did not receive any lab manual. We must design it ourselves.

Let's be clear, you are using a colorimeter, not a spectrophotometer?
Can you provide the brand name and model number of this colorimeter?
Have you learned about the Beer-Lambert Law? It states that A = Ecl where
A is the Absorbance
E is the molar extinction coefficient
c is the concentration of the unknown
l is the length of the light path through the sample (the standard path length is 1 cm in spectrophotometers).
The first thing you need to do is measure lambda Max, the wavelength of light that is absorbed the most (or transmitted the least) by your sample. The Beer-Lambert law is linear when A is between approx. 0.1 and 1.0.
So take a dilute solution of the algae and starting at the smallest wave length of light that the device can emit (you can vary the wavelength?). Take readings of the Absorbance and then increase the wavelength by 10 nm. Starting at deep purple, and ending at far red, write down the A values. Plot this data with A on the Y-Axis and wavelength in nm on the X-axis. There should be a distinct maxima in the curve, that is the most sensitive wavelength, and is the one you should use for all your experiments. If the algae is green, then the maxima should be over in the red end of the spectrum (like chlorophyll).
Next you need to make a standard curve that correlates the Absorbance at lambda max with the number of algal cells in the cuvette (the test tube you put in the colorimeter). That means you need an independent method of counting the number of algal cells. If they were bacteria or yeast then you could plate them on agar-filled Petri dishes and count the number of cells per mL (for example). For some cells if you have a high powered microscope and a hemocytometer then you could visually count the number of cells per mL. If neither of these methods are available then you could measure the mass of algal cells by weighing them on a balance.
So by some method you will be able to plot the number of cells in the broth vs. the Absorbance (plot A on the Y-axis).
From this you can empirically determine the molar extinction coefficient of these algal cells.  Then you just need to measure the Absorbance at lambda max on  dilute aliquot of the cell culture and you will have an accurate measurement of the number of cells per mL.
With this assay working then you can inoculate a bunch of identical cultures, that vary by the pH of the growth medium. By removing small aliquots of the cultures at the same time points you will be able to plot the number of cells (on the Y-axis) versus the time they have been growing, and you will see if varying the pH alters the shape or magnitude of these growth curves.


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What is the difference between a polysaccharide and a macromolecule?
I'm having trouble understanding the difference between "Polysaccharide"
and "Macromolecule".
I know that polysaccharides are made of chains of monosaccharides.  In addition, I know that macromolecules are made of monomers.
But what is the difference?

A macromolecule is a class of biomolecules that are made of monomers. These include polysaccharides (i.e. sugars) polypeptides (i.e. proteins) nucleic acids (like DNA and RNA) and lipids (fats ans phospholipids).
A polysaccharide is one type of macromolecule made up of monosaccharides like glucose and fructose. An example of a polysaccharide is starch or cellulose.

So they can both make up each other?

@intboolstring Well a polysaccharide is a macromolecule while not all macromolecules are polysaccharide. Just like how squares  are rectangles but not rectangles are squares.

@intboolstring macromolecules is a class of molecules in which polysaccharides are included.

A polysaccharide is a long chain sugar, formed by the polymerisation of many smaller sugar molecules (monomeric units which are the monosaccharides) They have a general formula of Cx(H2O)y where x is usually a large number between 200 and 2500. For example, starch, a long chain polymer of glucose.
Defined by wikipedia:

A macromolecule is a very large molecule commonly created by polymerization of smaller subunits (monomers). They are typically composed of thousands or more atoms. The most common macromolecules in biochemistry are biopolymers (nucleic acids, proteins, carbohydrates and polyphenols) and large non-polymeric molecules (such as lipids and macrocycles)
  An example of a macromolecule is DNA, which has deoxyribose sugar, phosphate groups and many nitrogenous bases.

So, to sum up, polysaccharides are macromolecules, but macromolecules may not all be polysaccharaides
More info
https://en.wikipedia.org/wiki/Macromolecule

When you say "polysaccharides may be macromolecules," do you mean they can make up macromolecules?

No, polysaccharides may be classified as macromolecules. That means that starch can be called a macromolecule as well as a polysaccharide.


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Do scouting bees get to pass their genes to offspring?
Let's say the food-scouting behavior of scouting bees are enhanced when some particular alleles are expressed. By natural selection, the allele frequency for that "good" allele should increase because more of the scouting bees with that allele get to pass the allele to offspring generations, as more of them survive in the ecosystem.
But considering that only male bees get to produce offspring with the queen bee, do scouting bees (I assume to be females) ever get a chance to pass their genes to future generations? Or are they males? If they are males, do they get to produce offspring?

I think this question has a fundamental problem: You are using the term their genes as in regular sexual selection. In highly social collectives such as bees you better not think of the individual, but see the whole collective as one big evolving complex. The worker bee cannot reproduce itself, but here this is not a severe evolutionary problem. By raising offspring it will help the genes of her hive (and therefore also her genes to some extend) to prosper.


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Why does chlorination still work?
Chlorination has been used for over a century to disinfect water supplies. Why haven't microorganisms evolved immunity to this chlorine by now?

It's aspecific, like ethanol. A bit like humans can't evolve to sustain bullets.

Antibiotic resistance works because most antibiotics target specific sites on specific proteins. If these sites can be mutated to avoid antibiotic binding, while maintaining the proper protein function, they become resistant. Some resistance is mediated by enzymes that destroy the antibiotic, or by pumps that keep it out of the bacterial cell. Chlorination is a very harsh treatment that causes general damage to many biomolecules, it would be very difficult for any organism to develop a defense against it. TLDR, antibiotics is like picking a lock, chlorination is like breaking the door down.

@Dexter posted a nice answer on this: http://biology.stackexchange.com/questions/39931/why-is-70-ethanol-preferred-for-aseptic-techniques

It is possible for microbes to acquire resistance to non-specific agents.  Radiation resistant bacteria exist. Some bacteria can also tolerate high amount of oxidative stress (they can do that by upregulating enzymes like SOD). You may find this post useful.

@WYSIWYG You are right that there are organisms that can resist the effects of chlorine. It takes a little less than 11 days for Cryptosporidium to be killed in a chlorinated swimming pool, and given that water supplies likely use much lower concentrations of chlorine, there survival time in drinking water likely increases. http://www.cdc.gov/healthywater/swimming/pools/chlorine-disinfection-timetable.html

The reason chlorination still works is that it is aspecific, just as @AliceD mentioned.
The way chlorination works is mainly by oxidizing biological molecules. Chlorine, along with other halogens, is a strong oxidizing agent. It breaks down the phospholipid bilayer membrane, proteins and enzymes. There is no way organisms can overcome this, unless it uses none of the chemical molecules that react with chlorine, which is virtually none.
On the other hand, antibiotics inhibit particular enzymes and proteins in a particular way and by making one or two amino acids different in the protein, the microorganisms can easily overcome this.
Reference - http://www.sswm.info/sites/default/files/reference_attachments/TUE%202011%20The%20Chlorine%20Dilemma.pdf

@WYSIWYG But enzymes like SOD are mainly for tolerating oxygen radicals and reactive-oxygen species, not chlorine oxidation.

Chlorination refers to the addition of chlorate (ClO3-), not Cl2. Hence, it is not halogens being added to water - that would be bad :)

@AliceD Wikipedia doesn't back up your statement https://en.wikipedia.org/wiki/Water_chlorination

@MarchHo I'll look into it. Interesting. I must say I commented from memory. Thanks.

@AliceD technically you sre correct as the chlorine gas, when dissolved in water, forms thar ion... But I didn't include all the details. I just wanted to make it simplified.

Well, there are microorganisms that have adapted or were resistant in the first place... that is why cryptosporidium is such a problem in the potable water supply. While it is not much of an issue for healthy adults, it can be very bad for immunocompromised people. http://www.cdc.gov/healthywater/swimming/pools/chlorine-disinfection-timetable.html


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Is pathlength correction vital to be included while quantifying protein
I am trying to quantify protein in serum/plasma samples. I have carried out biuret assay for my samples using microplate reader. While performing I encountered the doubt whether I should include pathlength correction, blank subtraction steps to get accurate value. Why and how to use these factors for quantifying using microplate?

The exact way to take pathlength into account would probably depend on your platereader, though if you kept all wells at the same volume the pathlength should not be a problem. If you include blanks and a standard calibration curve on the plate, you should be able to work up the protein concentrations in your unknowns ok just using the absorption data directly from the plate reader. Just be sure to write down what well has what solution so you can do your spreadsheet correctly.


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What is the difference between sequence alignment and sequence assembly?
I read the wikipedia page about sequence alignment and sequence assembly but I have not been able to find any difference between the two. What is the difference between sequence alignment and sequence assembly? If there is no different why are the terminologies different?

Sequence alignment
It is done for checking sequence similarity between two or more different sequences. This will give information about how two sequences are different, what is their evolutionary relationship, which residues are conserved etc. Take a look at following sequence alignment between different sequences. (Image courtesy: Wikimedia Commons)

You can see conversation of different amino acid residues in variety of organisms like human, mouse, rat etc.
Sequence Assembly
It is done for creating long consensus sequence from short fragments of same sequence. Generally you would do sequence assembly after sequencing some genome or large DNA fragment. Take a look at following representative image of sequence assembly (Image courtesy: Wikimedia Commons)

Here black sequence is your original sequence which you wanted to sequence. However because of technical difficulties you can't sequence all at once. Hence you fragment and sequence different fragments which are shown in red, blue and green). Looking at overlapping region between different sequenced fragments you calculate consensus. Potentially problematic repeats are shown above the sequence (in pink) Here you are ideally sequencing only one large sequence and assembling it.

but its the same thing right? I mean both could have been given the same name...

Well, yes. Sequence assembly is kind of multiple sequence alignment ! Naming is for avoiding confusion I guess.

@Rishika As Dexter's answer shows quite clearly, it's not the same. It would be inaccurate to say that you are doing Sequence Assembly, when you are in fact comparing genomes (doing sequence alignment) from different species (e.g. as part of a phylogenetic analysis). To say that you are doing Sequence alignment when you are doing Sequence assembly could be correct (for some steps), but slighlty misleading and not very specific.

@fileunderwater is correct. I would say sequence assembly is special case of sequence alignment.

okay, understood

@Dexter Again, it is not. Sequence alignment is a part of sequence assembly algorithms, but that does not make assembly a special case of alignment.

okay, debatable nomenclature

The two tasks are quite different.
Aligning means comparing sequences to find differences between them.
Assembling means that you take a bunch of short sequences and try to stitch them back together to reconstitute the original DNA sequence.

Fig1: Screen capture from DNA Baser Assembler of an 'assembly to reference'. The reference is in purple color. The forward and reverse sequences are red and green. The contig is blue.
Note about the input of the two processes:
The sequences that enter into an alignment have (supposedly) already been cleaned up. Every base is correct/accurate.
The sequences that enter into an assembly are 'dirty' and inaccurate, because it is highly likely that the sequencing machine will generate 'bad' bases at the ends of the sequence. The user will have to manually inspect and clean up the sequences (even though today there are smart assembly programs that can fully automate the process reducing the time from 10 minutes per contig to basically nothing (under 1 second)). It is preferably that multiple overlapping sequences are used for redundancy. This way 'bad' bases are discovered and eliminated.
Once the assembly job is done, the clean contig can be used for further operations (such as alignment).
raw sequences

after reverse complement

final contig

Not necessarily. A good analogy for differentiating the two sequencing strategies (not to be confused with sequencing technologies i.e. illumina, smrt, oxford nanopore etc...) would be a puzzle. In the case of sequence alignment, you would have a bunch of puzzle pieces i.e. your reads and a picture of the finished/completed puzzle i.e. your reference genome to guide you in putting together the puzzle. In sequence assembly, you only have the puzzle pieces and no picture, no reference genome. This makes assembly a much harder task.
In the first case, you would compare the N reads against only 1 reference genome. In the second case you would compare N reads against N "quasi" reference genomes.

Both comparisons are nice, but only half of the truth. I can do alignment of two puzzle pieces (pairwise alignment) without a reference. And I can do reference guided assembly (what you describe is de novo assembly), by using alignment to a closely related reference as a guide for assembly. ( so assembly with a picture that does not show the current puzzle, but a similar one).

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


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Can mexican salamander regenerate any organ?
Mexican salamander or few other species of salamander can regenerate limbs, tail etc. Do they have HOX genes for vital organs like liver, heart, brain, kidney?
If brain is damaged, can salamander grow it's brain to normal functioning again ?

I'm going to assume you meant Ambystoma mexicanum also known as the axolotl. There are other kinds of salamanders that live in Mexico, but the axolotl is widely-studied and sometimes called the 'mexican salamander'.
The axolotl has exceptional regenerative powers, and although I suspect this ability is shared among salamander larvae(even if not the adults) there's not much research into phylogenetic distribution of regenerative capability. So in the absence of a more refined answer I'm going to hope axolotl results generalize to other salamanders.
Axolotls, as long as they don't die, can regenerate nearly any part of their brain. As a rule, as long as they don't die they can regenerate from any injury. There are a couple exceptions(it's very hard to keep an axolotl alive without a heart, so that hasn't been tested) like the eye but in general they can grow back nearly anything.
The Hox gene research I've found was done explicitly on worms and frogs, but I would feel safe concluding that axolotl regeneration relied on a similar mechanism, and that therefore they have Hox genes for internal organs. I mean, they had to grow them the first time, right?

So until he not get  killed he is immortal ?

They still die of old age, unfortunately.

They have regeneration power so they can replace old tissues ? Its stranger they become old :|

They're still subject to cellular aging as far as I know. As they age their regenerative abilities fade, until eventually they die. Similar to humans, really, but our regenerative abilities are much reduced.


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Blebbistatin effect on vesicles
Blebbistatin is a drug that specifically inhibits the assembly of myosin in the cytoskeleton. What effect would you expect blebbistatin to have on intracellular vesicles?
The formation of vesicles would cease.
The movement of vesicles within the cell would cease.
The vesicle membranes would fail and release their contents into the cytoplasm.
The vesicles would be unable to fuse with the plasma membrane.

I don't readily see how Blebbistatin would effect intracellular vesicles; I believe this ignorance comes from not knowing what myosin is and how it interacts in the cytoskeleton.

What textbook are you reading from?

Blebbistatin inhibits myosin II by blocking it's attachment with actin. Myosin II and other actin based motors have shown to be involved in vesicle budding from trans golgi network. Given this information, I think correct answer will be

The formation of vesicles would cease.

Following cartoon from (Stow et al 1998) shows proposed mechanism,

However looking at this paper, option (2) The movement of vesicles within the cell would cease, also sounds reasonable.

Option 2 is correct. Vesicles do not need cytoskeleton for their formation (it is dependent on, among others, structural proteins like COP-I/II and clathirin).

@WYSIWYG: Kinesins and dyneins do transport vesicles, and are not affected by blebbistatin. www.ncbi.nlm.nih.gov/books/NBK21710/

Blebbistatin blocks effectively the Myosin II light chain kinase (MLCK)activity, and myosin being a motor protein, plays an important role in vesicle traffciking thereby affecting the process of endo and exocytosis.
With this information, I think it would be logical to say that blebbistatin will cease the formation of vesicles, the vesicle movement and inturn will inhibit the ability to fuse with the plasma membrane.
It looks to me more like a cumulative effect of blebbistatin on the intracellular vesicles.

Vesicle formation would not be inhibited.


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Blood pH at Higher Altitudes
My Campbell's Biology Textbook says the following:

"For example, when an elk or other mammal moves up into the mountains from sea level, physiological changes that occur over several days facilitate activity at the higher elevations. The lower oxygen concentration in the air stimulates the animal to breathe more rapidly and deeply. It therefore loses more CO2 through exhalation, raising blood pH above its set point.

I was wondering if anyone could explain why blood pH increases as your altitude increases? I know that an increase in pH is a sign of less H+ ions in the blood, but what exactly causes you to lose the ions when you're exhaling CO2?
Thanks!

The following chemical equation explains why pH decreases with increased $CO_2$:
$CO_2 + H_2O \rightleftharpoons   H^+ + HCO^{-3}$
pH changes are the reason why oxygen binds to hemoglobin in you lungs and then dissociates from hemoglobin at other parts in your body where the oxygen is low because cellular respiration turned the oxygen into carbon dioxide. The binding of oxygen to hemoglobin is in turn explained by the Bohr effect.


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How does one calculate the amount of oxygen produced by trees?
I'm currently working on a project to measure the impact of tree planting.
Calculating the amount of oxygen seems harder than I imagined.
Of-course there's the type and size of the tree and the environment (soil and air consistency), but there are plenty of other variables in play of which I have no knowledge of (being an engineer, not a biologist).
From a computational standpoint I'm looking for rough and finer methods of calculation for the amount of oxygen the following produce:

A tree
A large forest
Multiple countries with their forest

The one tree can be calculated exact, given enough variables. Oxygen during the day, during the night, tracked over it's age, etc.
A large forest will be calculated more approximate. Extra relevant would be how growth and oxygen production are influenced by tree density (trees per square mile).
Calculating multiple countries would be a whole other problem. It looks like it's very hard to prevent estimations from completely destroying the accuracy of calculations.
Basically I've written down some concerns and now I'm looking for a way of actually calculating these numbers and preferably some real numbers to validate against. The internet is crawling with estimates ((1)(2)(3)(4) and many, many more), but finding decent sources to compare your calculations seems hard.
How does one usually tackle this calculation problem?

You can look into paper showing oxygen produced by non invasive and traditional method.

Apparently, we are working on the similar task regarding the measuring the impact of tree planting and decided to reach you out to ask you for help. I’ve been running a local startup project on a tree planning. We personalize trees and now our next move is to calculate amount of oxygen each baby tree produces. Surely, we take all external environmental factors in consideration. I’ve been looking for answers in internet and suddenly reached your post. What I’m asking for is to share your experience how you dealt with this issue. That would be a tremendous support.

With detailed mechanistic models. There are a huge number of variables here, and you'll need to account for nearly all of them. Here is a similar project for crops.
You could try this model for a single tree but I don't envy trying to scale that up to entire countries.
Just to ballpark some figures, you could consider photosynthetic efficiency, average insolation, and shading effects. X amount of light falls on this country on average, and of that light .1% is converted into oxygen, so that's how much oxygen is made.
You could also approach it from the other direction and estimate how much each tree weighs. Tree dry weight is going to be mostly carbon, and necessarily nearly all of those carbon atoms were once carbon dioxide and represent one O2 molecule each. This approach has the advantage of taking into account respiration, unlike the light approach. The light approach measures total oxygen produced, but the carbon approach measures total oxygen released.


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Is lowered blood pressure a primary lethal symptom of an opiate overdose?
When someone has a opiate overdose, they can have no or almost no pulse and can  have shallow breathing or stop breathing. When you stop breathing (for example) by drowning, you can survive for a long time without breathing, so it seems that stopping breathing because of the overdose won't kill very easily.
Is the lack of (detectable) pulse due to the blood pressure going really low instead of the anecdotal explanation that the heart has stopped? Can the low blood pressure be more immediately dangerous than the reduced breathing because it makes the heart's pumping ineffective and cuts off oxygen from the brain?

This is an old question, and has an open bounty so can't be closed, but I would vote to close for lack of research if it didn't. And incidentally, without particular circumstances (e.g., hypothermia), you can NOT survive for a long time without breathing.

Yeah, this is quite a puzzling question the way it is framed, I'd like to vote to close it but can't because of the bounty so I'll just downvote. This shouldn't have been bumped.

Sorry for bump then. I came across this question, thought it was a decent one and wanted an answer.

If it is vote-to-closed as unclear, wouldn't a comment highlighting exactly why it is seen as unclear be useful. At the moment, the OP hasn't gotten any comments on the contents.


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How does the brain manifest and realize the intention to resist sleep?
The question title says it all. What happens in my brain when I resist sleep? I would appreciate explanations on neurotransmitter changes, what areas of the brain activate to resist sleep, what can an EEG tell us about that condition, are there any phases to that condition..
Switching to sleep mode is very complex and automatic process and it takes over and changes the functions of the whole brain (and the whole body also), so..
What actually does the brain do to not fall asleep?


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What are the reasons which make intron detection uncertain?
Intron/exon sequence detection seems to involve statistical prediction which can at best deliver a guess (until experimentally confirmed) as to where the splice site is.
What are the reasons why there are no deterministic (rather than consensus) sequences which signal the location splice sites?
Trying to answer this myself, I guess the obvious one I can see is chromatin structure, which interacts with how RNA polymerase reads the DNA strand.  If this is the case however, isn't the current way of describing DNA as a sequence of AGCT base pairs fundamentally flawed?  If chromatin structure is actually part of the functional description of DNA, then are there any efforts being made to describe this?


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Can a cell completely lose the ability to undergo apoptosis?
What I mean is - can a super-cancer cell completely lose the ability to kill itself, losing all apoptosis-related mechanisms and becoming eternally resistant to any drug that tries to induce apoptosis directly or indirectly.

It's not so much that a cancerous cell loses "the ability to kill itself". Rather, many cancers occur because there is a relative lack of inhibition of apoptosis. Many cancer drugs try to un-inhibit these apoptosis mechanisms. I think it is unlikely that a cell would be "resistant to any drug"; the problem with cancer treatment is that the drugs often kill healthy cells too, and there is a limit on the dose that can be given while keeping the patient alive. This may give the impression that the cancer is resistant, but it may just mean that the drug dose is too low.

Try reading The Hallmarks of Cancer and The Hallmarks of Cancer: The Next Generation by Hanahan and Weinberg. Both are Cell Reviews.


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Electroporation vs gene guns

What are the pros and cons of using electroporators (left) and gene guns (right) for transformation in terms of:

Price
Target organism
Efficacy
Ease of use
Maintenance

I am not an expert on gene guns but I will try to give my answer on this question anyway.
Price-wise they are both relatively cheap. The electroporators consumables are only the cuvettes, they cost 5-10 dollar/each. The gene guns use microbeads as bullets and depending on the material they cost between 200 and 300 dollars per microgram, 10-50 dollars per shot, a bit more expensive than electroporation.
About the organisms, guns are used mostly for plant-cells and few other "hard to electroporate" organisms. I don'd have a proper list of them but roughly, if you work with bacteria, yeasts and mammalian cells, then go for an electroporator.
If you need to work with tissues or entire organisms like worm/insects/plants then go for a gun, you definitely cannot electroporate a leaf. But in general, check the literature on what is currently the best method to transfect your system of choice.
Efficacy, also in this case it depends form the cells you are working with. Electroporation reach 10^9/10^10 transform ants per microgram of DNA in case of E.coli and this is the best efficiency you can get nowadays. All other cells will be transfected at lower efficiency, how much lower? It depends from the cells!
Easy of use. They are both very easy to use, it is matter of pressing a button. For the electroporation you need to prepare electrocompetent cells, but the procedure is very easy. For the gene guns you need to coat the beads with DNA, also very easy.
Maintenance. The electroporator do not need any maintenance at all while the gun may need some care in the long run since it has pumps and pressurised chambers, this stuff usually need some attention but nothing special.
Some references:
bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf
bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf
bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf

Would you have any references to add to support your claims?

I bet instruction manuals from bio-rad should be ok as reference. Here they are: http://www.bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf ; http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf ; http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf

Great. Please add them to your answer. +1

We use both devices routinely in our lab and I have to say that I prefer electroporation over biolistic any day. The former is cheaper and faster as the only consumable is the cuvet while you have stopping screens, macrocarriers, rupture disks and helium as consumables while electroporators only need cuvettes. Cell preparation times are usually faster for electroporation as well. That being said, you often don't have a choice...

Price
Looking through Google shopping and visiting s few websites, it seems that electroporation is 3000 - 8000 dollars depending on what features you want.On the other hand, gene guns are much more expensive. The most common gene gun, the Helios model from Bio-Rad, is about $17000, including all the necessary parts. As you can see, a gene gun can be more expensive.
Also, the gene gun needs bullets, which are microbeads (or microcarriers, as Bio-Rad calls them), and those cost around 600 dollars. The electroporation cuvettes each are $90. However, they can be cleaned and reused.
Target organism
According to Wikipedia, gene guns are used for mainly for transforming plant tissues, but is also used for animal tissues. According to Bio-Rad, it is good for mainly plant systems and animal systems, but can be used for algae, bacteria, and more.
Electroporation seems to be used more for bacteria. They have used it for yeast also. It has been also used for animal tissues, but it isn't the most suitable target organism. It seems better for in vitro systems since for most electroporation systems need the tissues or cells to be transfected in a cuvette.
Efficacy
For gene guns, the efficiency depends on the environment and the type of cells being used. The transfection efficiency varies for various cell types. I can't find many estimates for the efficiency of gene guns. But some of them are 10-20% of the DNA. Electroporation is agreed to have a very high efficiency. According to Wikipedia:

Normal preparation of compentent cells can yield transformation efficiency ranging from 106 to 108 cfu/μg DNA. Protocols for chemical method however exist for making supercompetent cells that may yield a transformation efficiency of over 1 x 109.[6] Electroporation method in general has better transformation efficiency than chemical methods with over 1 x 1010 cfu/μg DNA possible, and it allows large plasmids of 200 kb in size to be transformed.

Ease of use
Both are very easy to use. They only require the press of a few buttons. However, if you want to find out how to use, you should read the manuals and protocols. The Helios gene gun system manual is available here. The MicroPulser electroporation system also from Bio-Radd has the manual here.
Maintenance
Maintenance for a gene gun is pretty simple. For example, Bio-Rad's handheld gene gun has a simple maintenance (from here):

The improved modified barrel is low in maintenance. It can be cleaned
  easily, using 70% ethanol. The tip of the barrel contains a circular
  nylon mesh, which should be replaced regularly to retain optimum
  performance. To change the mesh, simply unscrew the tip, remove
  the spent mesh and insert a new one over the O-ring. Once the tip is
  screwed back in-place, the hand-held gene gun is operational.

Electroporation needs almost no maintenance as well.


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How do large herbivores get enough protein?
The food they eat seem extremely low on protein. Do they need less protein per mass unit than carnivores? Most of them grow quite a lot in the first year, is most of that from the mothers milk?

Most amino acids can be synthesized de novo. The 'essential' amino acids in humans are mostly derived from meat. Those have to be obtained from the diet. I wouldn't be surprised when most herbivores would be able to synthesize all of their amino acids de novo

@AliceD I don't know of any animal that can synthesize all their amino acids. The good thing is that plants can make all of them, and herbivores eat the plants, and the carnivores eat the herbivores.

It boils down to the anatomy.
Herbivores are very good at digesting plant matter, which us monogastrics are not particularly good at. Many herbivores (such as ruminants) have large, highly developed gastrointestinal tracts containing symbiotic bacteria to allow them to digest plant matter. Once the cellulose in the plant cell walls is digested, the animal can then access the nutrients  contained in the plant matter to a degree we cannot. Ruminants (such as cows) are even better able to absorb nutrients in this way than monograstric herbivores (such as horses). Rumen microbes are also an important source in ruminants for production of amino acids.
There's also a reason why the GI tract of these herbivores is so big. In the cow, it's an enormous rumen. In the horse, it's a massive colon for hindgut fermentation. To get all the nutrients they need - such as amino acids - these herbivores have to consume and ferment vast quantities of plant matter. A carnivore can generally get all the nutrients it needs in a much smaller meat meal, meaning it does not need such an extensive GI tract.
Different species, of course, have different metabolic demands and corresponding nutritional needs. Cows and other herbivores cannot synthesize all the amino acids they need, meaning they have to be consumed through the diet. Though it is somewhat dated, an interesting discussion on this subject is Protein and Amino Acid Requirements of Mammals (PDF) by Anthony Albanese (1950). The author goes through in great details the different protein requirements for various species, but I will bring your attention to one interesting table on p 116 as it is pertinent to your last question:

As you can see, the protein content of milk seems to correspond with the time to double birth weight. Cats with a high protein milk grow very quickly, while cows, horses, and humans grow comparitively more slowly (and thus have lower protein milk).
All animals have to get protein or amino acids through the diet, but they just have different methods to satisfy their metabolic requirements. For carnivores, they consume small protein-packed meals. For large herbivores, they have to consume and digest large quantities of plant matter to meet their needs.

Nice, answer, though I wonder how much that table was an example of correlation not being equal to causation. Cat and Dog newborns are very small due to multiple litter mates, and doubling their weight, is less in absolute terms than larger animals. As for humans I wonder how much of the energy load goes to providing energy to brain formation and is less available to adding to muscle, bone, and fat stores.

I wonder if you could add the grass-digesting microbe to the human gut and get the same effect?

The protein RDA of another mammal, the human, is 70g every day, that's about 700g of hay if he can get 100% of the protein from it, that's 4 kilos of grass. So a 700 kilo cow would need about 40 kilos every day, and actually 700kg cows consume about 70kg  of pasture every day.
Probably energy is the most common deficit, and not protein.
Average pasture contains between 11% and 28% protein:
You can read the paragraph on protein:
https://www.teagasc.ie/media/website/animals/dairy/Whats_in_Grass_Todays_Farm_May2014.pdf
The rumen contains many organisms, funghi and yeasts, which can also synthesize their own protein. At about 10^10-10^11 cells per milliliter, ciliate protozoa at about 10^4-10^6 per milliliter, anaerobic fungi at about 10^3-10^5 spores per milliliter and bacteriophages at about 10^8-10^9 per milliliter. It should be noted that many microbes cannot be cultured in labs, so the numbers may actually be higher in reality.
https://microbewiki.kenyon.edu/index.php/Bovine_Rumen#Who_lives_there_.28Microbes_in_Rumen.29.3F
One E. coli cell has a mass of 0.95×10−15 kg, so a gram of rumen can contain 0,00001 kg of animal life, 0,01g 1%? so a 180 liter rumen can contain about 1.8 kilos of bacteria, funghi and yeast. That's a lot, especially if it can double every hour at 37'C.

To paraphrase:
Cattle don't receive their nutrients from what they consume (which, as noted, does not contain much nutrients), but rather from the various bacteria in their guts, which convert the vegetable matter into the numerous amino acids the cattle need.

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When you blow through your nose while holding it closed to "depop" you ears, why do you sometimes feel it in your eyes?
After your ears have "popped", for example on a flight, I heard you are supposed to hold your nostrils closed and blow through your nose to readjust the pressure to the normal level. Why do you sometimes feel a pop in the corner of your eye when you do this?

The sinuses connect the ear, nose and throat as well as the tear ducts of the eye. The pressure created when holding your nose and blowing is transferred to any area it can get to; in this case, the eyes and ears.


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Where I can download the genome sequence of various species of Fusarium?
I'm looking for genome sequence of various species of Fusarium (a kind of fungus!) on net, but I found no suitable information. Could you please help me out for this purpose?
Thanks in advance

The standard source for open-access nucleotide sequences is GenBank. Searching for Fusarium in GenBank gives 440421 hits, but these are shorter reads, not full genomes. Depending on your purpose, they may be useful to you.
You may also be interested in assemblies, which are collections of aligned reads stitched together, often at the scale of whole chromosomes. Assemblies with 'Fusarium' in their keywords are available here.
Genomes may be found here, but it does not appear that GenBank holds a complete assembled genome for any Fusarium species yet.

There are several strains of three different species of Fusarium available for download at the Broad Institute: http://www.broadinstitute.org/annotation/genome/fusarium_group/MultiHome.html
Follow the links to Download on the sidebar.