text:
Why is oxygen used up in eutrophication?
This probably sounds pretty dumb, but wouldn't algae blooms produce a lot of oxygen? Although they would die out and decomposers would use up oxygen, is that more than what the algae produced?

Algae produce $O_2$ in the upper layer of water but when they die they stop producing $O_2$. They sink to the seafloor and most get decomposed by bacteria on the seafloor. In this process, bacteria use $O_2$ contained in the bottom layer of water which decreases the dissolved $O_2$ concentration in the bottom water.
These concepts (and much more!) are well described in the excellent open-access paper by Rabalais et al. (2010) Dynamics and distribution of natural and human-caused hypoxia. It also includes case-studies of areas affected by hypoxia and eutrophication around the world. A must read if you're interested in this topic!

thanks for your contribution to BiologySE! Are you able to put some references to your answer? We prefer answers with references on this site, as anonymous users can claim to be an expert in anything... and having references allows other users to read more about your answer in the context of the question

@VanceLAlbaugh that's definitely an excellent idea, thanks for pointing this to me. I edited my answer with one of my favorite paper on the topic.

As you surmise, the oxygen is consumed by decomposers. From the Wikipedia page on Eutrophication:

Phosphorus is a necessary nutrient for plants to live, and is the
  limiting factor for plant growth in many freshwater ecosystems. The
  addition of phosphorus increases algal growth, but not all phosphates
  actually feed algae.[2] These algae assimilate the other necessary
  nutrients needed for plants and animals. When algae die they sink to
  the bottom where they are decomposed and the nutrients contained in
  organic matter are converted into inorganic form by bacteria. The
  decomposition process uses oxygen and deprives the deeper waters of
  oxygen which can kill fish and other organisms.

Does the oxygen produced by the algae while they are alive evaporate away or what? Is it a question of producing O2 at the surface and consuming it at the bottom of the water column, where fish live? If the algae still have carbon-containing bodies there must be surplus O2 somewhere that they made while alive. As a continuous process why isn't the oxygen produced by new algae used to decompose the old algae? Does it just escape into the atmosphere?

As the question is tagged as "marine-biology", your answer is not completely correct. Most marine ecosystems are nitrogen-limited, not phosphorus.

Much like how planes fly, a proper explanation to this question is more nuanced and complex than first appears...
The total algae lifecycle is oxygen neutral
When any plant or algae grows sunlight is stored as chemical energy (oxygen + organic compounds). After the autotroph dies decomposers consume this energy and we are back to square one.
Would burying dead biomass keep the oxygen from being used up? Doing so oxygenated Earth in the first place (and oxidized soluble iron II into insoluble iron III). However, it only took a tiny fraction of fossilization to build up oxygen over geological time. Thus we can ignore burial in most ecosystems.
Water can't store enough oxygen
Water contains very little oxygen, even less if it is warm. Freezing water which is fully oxygenated (has been well-aerated with air at sea-level) will have about 14ppm of oxygen. This compares to 20% oxygen (200000 ppm) in the air. Water holds at most 1/10000 oxygen by mass and 1/10 by volume as air! This is also probably why no fish or shark is as big as a blue whale.
During the bloom oxygen rapidly exceeds the amount water can hold. It may seem strange that water with only, say, 25 ppm oxygen will give oxygen to the air. But the rule that "solutes move down their concentration gradient" assumes that the solvent they are dissolved in stays the same. When we consider multiple solvents we need to factor in the partition coefficient.
Even if air was pure oxygen, only 40ppm would dissolve in warm water. When shallow water exceeds this threshold bubbles of oxygen appear and rise to the surface.
Algae blooms are followed by a population crash once whatever nutrient caused the bloom (usually nitrogen, iron, or phosphorus) is used up. Such crashes are common with fast-growing species. Since most of the oxygen produced by the bloom has been lost the water will end up with less oxygen than it started with. Anoxic water is quite unpleasant.
Decaying biomass sinks
Algae blooms produce oxygen near the surface. The cells then die, lose buoyancy, and sink. The whole lifecycle of growth and decay has the effect of pumping oxygen out of deeper water and into the air. This can create near-permanent dead-zones in deeper water.


text:
Carbohydrate in egg white
I looked up online to find which type of carbohydrate is found in egg white, but the only information I found is the quantity of sugar. I would like to know the exact name of the carbohydrate found in the egg white in order to draw the sugar molecule.

It's all in a glycosylated protein (as noted in the answer), the composition of which is not homogeneous. But I found: "MALDI MS of the N-glycans released from α-ovomucin by PNGase F revealed that the most abundant glycan structure is a bisected type of composition GlcNAc(6)Man(3)." (http://www.uniprot.org/citations/21484392)

The one I found is Ovomucin,though it's not a pure carbohydrate.

Ovomucin is a highly glycosylated protein and approximately 33% of ovomucin is made up of carbohydrates.

Nutritional Values of Egg White Proteins paragraph of
http://ps.oxfordjournals.org/content/92/12/3292.full
So you can see it's mostly a protein.

Ovomucin is a trypsin inhibitor found in raw egg white.
Ovomucin is responsible for the gel properties of fresh egg white and is believed to be involved in egg white thinning. Ovomucin is composed of two subunits:

α-ovomucin - carbohydrate-poor with a molecular mass of 254kDa

β-ovomucin - carbohydrate-rich with a molecular mass of 400-610kDa

Souce: Wikipedia

I'll add more info as soon as I find some.

I did some research about the ovomucin but I didn't found it molecular stucture... Have you any idea about the ccomposition of the sugar?

No sorry about that.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
The meaning of the $\alpha$ helix and $\beta$ sheets in proteins
I asked this question to my Biology teacher and he, in collaboration with a Chemistry teacher, couldn't find the answer. My question is the following: "What does the $\alpha$ and $\beta$ represent in the secondary structure of a protein? I do reference to the $\alpha$ helix and $\beta$ sheets in proteins." I had a similar question with the glucose and we concluded that it was related to the Chemistry, the $\alpha$ or $\beta$, was related with the functional groups bonded to the carbon.

Related http://biology.stackexchange.com/q/45735/3340

To add to the confusion, there is also "alpha sheet", which is rarer : https://en.wikipedia.org/wiki/Alpha_sheet and the "beta helix" fold https://en.wikipedia.org/wiki/Beta_helix

@gilleain Yes, that what I want, I would like to know why the $\alpha$-helix is not name "$\beta$-helix"? There must be a certain meaning of the $\alpha$ and $\beta$!

@Matt - Read WYSIWYG's link. It's really just an arbitrary label. The page for alpha-helix mentions William Astbury as calling the helix "the alpha-form" so presumably it's his fault!

@gilleain The problem with this answer is that it is a kind of an "easy" answer; ["They are sometimes used in science to enumerate or differentiate between a series of related things — proteins, small molecules etc."] the answer had never explained the difference, it just says that the use of the Greek letter is used to differentiate the thing, but why a specific helix can be $\alpha$ and the other one is $\beta$? Also, to admit the answer, do you have any reference?

@WYSIWYG, Would it be possible to get a reference of your answer?

The answer is very simple. As described in the accepted answer to the related question about alpha-subunits vs alpha-helices the alpha- and beta- are arbitrary names. It could easily have been 1 and 2 or A and B based on ordering of letters or numbers; indeed, there are "type I" and "type II" turns.
The history, from the wikipedia page on alpha-helices says:

In the early 1930s, ... William Astbury initially proposed a kinked-chain structure for the fibers. He later joined other researchers (notably the American chemist Maurice Huggins) in proposing that:

The unstretched protein molecules formed a helix (which he called the α-form)
The stretching caused the helix to uncoil, forming an extended state (which he called the β-form).

(Emphasis added). In other words, he named the "α-form" first, and considered the "β-form" to be an uncoiled form of the first one. These names later became "α-helix" and "β-sheet". It could easily have been the other way around.
Indeed there are other types of helix; the 310 helix and the π-helix. If either of these had been discovered first, perhaps they would be the alpha-helix. Of them all, the 310 helix has the most 'logical' name as:

the helix has three residues per turn, and ... has 10 atoms in the ring formed by making the hydrogen bond

so if we followed a similar naming scheme, the alpha helix would be a 3.613 helix. Admittedly this is a bit of a cumbersome name.
As well there are the alpha sheet - a sheet made of helical strands - and the beta helix - a helix made of strands. For both of these, the "alpha" and "beta" part of the name has been chosen because of the naming of the original structures they are related to.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Are 'high-throughput' and 'large-scale' proteomics synonyms?
I wonder if 'high-throughput proteomics' and 'large-scale proteomics' are generally used synonymously? It would make sense to me to distinguish between 'high-throughput' as in a 'large number of samples' vs. 'large-scale' as in 'big samples with thousands and more of proteins'. However, I have not found any article on this so far and it seems to me that the community uses both terms interchangeably. Are there other terms commonly used to refer to these properties?

I often see the two terms used hand-in-hand, although I'd say they're not quite synonymous. Often the term high-throughput refers to the number of features being analyzed, with high-throughput methods quantifying many features in parallel. Because of the parallelization, the time needed to quantify all features is reduced, so you can process more samples in a fixed amount of time - the method has high throughput since many features/samples can be analyzed quickly. "High-throughput" typically refers to the technology being used to analyze a sample. Different proteomics technologies may be classified as high-throughput or not, regardless of how those technologies are applied.
Since a high-throughput method can process samples quickly and cheaply, it often goes hand-in-hand with large-scale analyses, which often refers to the number of samples (but sometimes the number of features) being processed. A "large-scale" analysis typically refers to the design of the experiment.
Older experiments were generally limited to small-scale by low-throughput technology, while high-throughput technology has enabled large-scale experiments. You could use a high-throughput technology to do a small-scale analysis, but it wouldn't leverage the power of high-throughput methods to run many samples in a short amount of time. Applying a high-throughput method to a single sample would be an example of such a case. You could also theoretically use a low-throughput technology to do a large-scale analysis, but it would take a very long time and be very costly, and would likely be infeasible without significant resources. Applying a low-throughput method to many samples would be an example, although this is not commonly seen in practice.
Usually you'd use a high-throughput method to achieve a large-scale analysis, which could not be feasibly achieved with a lower-throughput method. An experiment is often both high-throughput and large-scale so the terms are often seen together, but I'd say they have distinct connotations of referring to the technology and the overall experimental design, respectively.

That is a great summary of what I see in the literature as well. Most proteomics studies that I found use high-throughput to refer to numbers of features/proteins/peptides identified. Not so much regarding processing of samples in a short time.

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


text:
Are genes known or at least conjectured to evolve cyclically ?
I observed recently that some people born the same year in not too distant areas (say, in the same country whose size is not too big, like France) share similar phenotypical features, for example they look like each other though they are not of the same family. If confirmed, this would suggest that some alleles are more common within a given period, and hence that the global evolution of the human genetic pool could be statistically determined. One can go one step further and see the considered genetic pool in a given range as a quantum-like system governed by some kind of Schrodinger's equation. I think here of a theoretical framework like Laurent Nottale's scale relativity that could explain these similarities. Have such questions been considered so far?

Welcome to Biology.SE Sylvain!

I observed recently that some people born the same year in not too distant areas (say, in the same country whose size is not too big, like France) share similar phenotypical features, for example they look like each other though they are not of the same family.

You are likely doing a confirmation or some kind of extended Barnum effect.
You will need to provide a rigorous study for this claim and not just a vague feeling you're having.

If confirmed, [..]

This piece of sentence suggests that you agree with my previous comments. We expect the OP to provide reference for a claim on which the question lies. One cannot ask "Why do elephants have such a huge genome?" without providing an evidence that they do have a huge genome.

[..] this would suggest that some alleles are more common within a given period,

If there is such effect it is much more likely caused by shared environment than by shared genetic. Have a look at this post to understand the underlying sources of phenotypic variance.

and hence that the global evolution of the human genetic pool could be statistically determined.

Sure, it can but this is not a consequence of the above supposed observation nor by the above hypothesis for the supposed observation.
Of course, specific processes could cause some cyclic process in evolution. A population overshooting carrying capacity could go under an oscillatory behaviour around this carrying capacity. As population size affects genetic diversity, such cyclical behaviour can have some impact. However, this is quite negligible. Also, there might be fluctuating selection (typically fluctuating on a seasonal basis) but this tends to be rather negligible for species of long lived individuals. I am sure you can think of some complex mechanism in structured populations would could yield to some oscillatory behaviour as well.

One can go one step further and see the considered genetic pool in a given range as a quantum-like system governed by some kind of Schrodinger's equation. I think here of a theoretical framework like Laurent Nottale's scale relativity that could explain these similarities.

I don't understand that part. I know pretty much nothing in quantum physics (have basic understanding in general relativity but not in Nottale's attempt to merge relativity and quantum physics). You might need to expand your thoughts I guess if you want biologists to understand where you're heading. However based on the above, I suspect, there is no reason to think this cross-talk would matter in any way.

Have such questions been considered so far?

I doubt so, because I don't think any of it makes much sense (no offense).


text:
Is there a conformal transformation that maps the skull of Panthera tigris to the one of Panthera leo?
While visiting the Museum of Natural History in Rouen a few months ago, I was stunned by the similarity between the skulls of Panthera tigris and Panthera Leo: the overall shapes were very similar and only distances between homologous parts seemed to vary. As I'm into math, I wondered if this similarity could be explained by some conformal transformation mapping the skull of one species to the one of the other. Are there clues about such geometric correspondences between related species?

Have a look at D'Arcy Thompson's work.

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


text:
Population-biology, migration-patterns, & ethology of the Big Five (elephants, rhinos, lions, leopards, & buffalo) in S. Africa's winter months?
I know that animals are unpredictable, but I also know that there are seasons in which the wildlife are more active. Now, August in South Africa is still their winter season, which is emerging into spring, and I was wondering what the population-biology, migration-patterns, and ethology of the Big Five (black rhinoceros, African elephant, water buffalo, African lion, African leopard) are like in August?
Now that's quite a variety of animals (some migrate, and others don't), but I'm essentially wondering: are the wildlife less active in August (because it's winter) or do they stay pretty active all-year round, even in the winter months (because of the warmer climate)? Are the migratory animals present in the winter time in Kruger National Park?


text:
How are limits determined for systotic and diastotic blood pressure?
I know that the upper limits for systotic/diastotic blood pressure are 120/80. What is the mathematics behind these numbers? I am curious because I did not find information regarding how the numbers are arrived at. I am not sure if the numbers are based on statistical study or is there a scientific basis for the same.

120/80 are not upper limits on blood pressure - many people have blood pressures far in excess of those numbers. Instead, these are numbers beyond which studies have shown connections to negative health outcomes - heart disease, for example.
There is nothing magical about the numbers 120 or 80 besides their divisibility by 10; a blood pressure of 121/81 is no more risky than 120/80 than 122/82 is over 121/81. Because of this, drawing a hard line isn't possible - it's just a suggestion.
Typically, systolic pressures less than 130-135 aren't given any special consideration beyond normal advice to exercise and eat well, unless there are other conditions/risks. Guidelines from the American Heart Association and the UK's NHS are to consider treatment only for diastolic pressures above 140mmHg. There has been some disagreement about these precise limits, with some recommendations for lower targets, for example here. Some of the disagreement seems to be the types of interventions - the guidelines to treat diastolic hypertension only above 140mmHg are mostly considering medications, whereas the guidelines to treat prehypertension are aiming for improved lifestyle: diet, exercise, etc.

Thanks. Can you point to a specific study that drew these numbers? I am not familiar with the literature around this. I am curious about the way the sampling is done and the statistical methods that helped that highlighted these number.

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.

Added references; for some of your questions about sampling etc, @randominstanceOfLivingThing, those questions might deserve their own topic


text:
Is there a possibility that medicine will affect the efficiency of natural selection?
I mean, saving sick people means that they possibly can propagate something that nature does not allow. I know that there is already something that operate at genetical level producing alteration, i.e. genetical mutation. And i am well aware that natural selection and genetical mutations take place really slowly.
p.s. i really want medicine to work!!

You might be interested in this Q&A: How is evolution possible in contemporary humans?

Slowly? On mutations: https://biology.stackexchange.com/q/19908/24354

Summary:  Yes it can, but not the way you might think.
Humans aren't under a lot of selective pressure on a large scale right now.  We have a lot of control over our environment, and you're accurate that disease (or I'd add massive, fatal natural disasters) are the biggest ways we would see a large genetic shift.  (Or genocide, which is an extremely unnatural, artificial selection, but some of our species have historically been horrific enough to try to do this.)
Small local natural selection has happened in areas where Malaria is endemic: many people die from malaria. some people die early from homozygous sickle cell anemia, but those who are heterozygous have "sickle cell trait" (because of incomplete dominance) and have deformed enough RBC that malaria isn't able to infect them well.  So the survival advantage is enough that the prevalence of sickle cell alleles in these areas is higher.  There's a similar story with Glucose-6-phosphate dehydrogenase deficiency.
But on a scale you might be thinking of, the primary mechanism would be a global pandemic infection that targets people with a specific trait.  For example, if suddenly an incurable contagious, virulent, highly pathogenic, and fatal virus/bacteria that was only fatal to those with an allele for blood type A were to emerge.  Theoretically it would cause a genetic shift to eliminate type A blood from the gene pool, and reduce prevalence of type B (by eliminating AB due to the A).  Or if it attacked only one location of the world, but that's highly unlikely due to global travel.
Medicine could theoretically catch it in time - mitigate impact and prevent a large shift by creating a vaccine or cure that is effective and easily mass-produced.  The most likely to succeed would be a vaccine (yay for public health!).
Variations on this have happened to reduce or eliminate pathogens (such as polio and smallpox because of the vaccine) and their effect on mankind, but those have little to do with selection for human traits that would cause genetic shift.

"Humans aren't under a lot of selective pressure on a large scale right now." : That is completely wrong. Of course we're under selection! We live in a specific ecosystem and changes to that system affect our survival. We are under strong selective pressure to be animals that can survive a specific range of temperature, acidity and oxygen concentrations to name just a few. Anyway, the main driver of selection is always the way that mates are chosen and that is still going strong today. Not everyone in a generation reproduces => selection. Disease is a relatively minor player in this.


text:
Strange insect identification
Tonight I have found this new friend flyng inside my home. First time ever I sea something like this here in the north East of Italy

That is an Oleander Hawk Moth, Daphnis nerii. Order Lepidoptera,family Sphigidae. https://en.wikipedia.org/wiki/Daphnis_nerii


text:
How do plants get carbon?
How do plants get carbon? From air or soil? How is it different for aquatic plants and algae?
According to https://en.wikipedia.org/wiki/Soil_organic_matter soil has 3.3 times the size of the atmospheric pool of carbon.

SHORT ANSWER
From the air
LONG ANSWER
Trees are autotrophs, which means that they create their own compounds from inorganic carbon. So, carbon comes from inorganic carbon. This carbon comes from $CO_2$ (carbon dioxide) that is present in the air. The process by which this carbon is transformed into organic matter is called photosynthesis. More specifically, the carbon get fixed through a chain of reaction called the Calvin cycle that are part of the photosynthetic process.
The great cycle of life
You'll note that while plants (and some other things) uses $CO_2$ to build their mass, animals (and some other things) exhale $CO_2$ when they breathe. In other words, respiration frees up carbon dioxide while photosynthesis fixes carbon dioxide into organic matter.
Then you may want to ask where does the carbon we exhale come from. From our food. If you eat a beef burger for example, you'll the carbon that was present in the cow. The beef got its carbon from the grass that she grazed on. The grass got its carbon from the air and there is carbon in the air because animals (and some other things) exhale carbon when we breathe. respiration and photosynthesis are two essential series of chemical reactions that explain the existence of this cycle.

The (very simplified) chemical equation for those two processes are

Introductory sources of information
Here is a video by Veritasium that answers your specific question
Here are a series of videos of Khan Academy to increase your knowledge about photosynthesis

Also found brief overview in https://en.wikipedia.org/wiki/Plant_nutrition

You're welcome. Yes, you are right, $C_6H_{12}O_6$ is the glucose.

Aquatic plants including algae acquire carbon from dissolved bicarbonates (HCO3-) [1,2].


text:
Can humans eat grass?
Can a human eat grass and digest it?
Could it be possible to use it as food just like other plants such as wheat or beans?

Note that many of our grains are grasses. We can't metabolize cellulose, but the seeds contain enough other materials -- especially after cooking or grinding to break down any cellulose barriers around them -- to be worth eating. That may not be what you intended to ask, though.

From a taxonomic point of view, wheat is a grass. So yes, we can eat it. Narrow down and clarify your question.

To elaborate on A random zoologist's answer, the problem is that the human digestive system does not contain any cellulase enzymes. Cellulases are a class of enzymes that break down cellulose, the chief structural component of plants.  You might be able to obtain a small amount of nutrition from grass or other cellulose-rich materials, but as the plant cell walls are made of cellulose, most of the plant material will be indigestible.

At the end of the linked article it is stated that cellulase is used to treat phytobezoars, which apparently are indigestible masses of cellulose stuck in the stomach. Could one take a supplement that renders the grass more digestible?

It would probably not be useful as a supplement, as the enzymes wouldn't last very long in the stomach. Fun fact: An alternative to cellulase for treating phytobezoars is coca-cola administred through the nose: http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/practicalgasto1.04.pdf

Could we cook the grass and break down the cell walls?

Not easily. To break the crystalline structure of cellulose by cooking requires a temperature of 320 C and 250 atmospheres of pressure: http://en.wikipedia.org/wiki/Cellulose#Structure_and_properties

Cellulases are generally slow, which is why mammals that have microbes that can break down cellulose also have very long transit/residence times in their guts. In the extreme case, ruminants (cows for example) have developed huge, multi-chambered guts to ensure that food stays in their digestive system long enough for the cellulases to act on a useful percentage of the food they ingest. So a human gut with cellulases is still not going to get useful amounts of nutrition out of ingested cellulose.

Also interesting and relevant: most animals that do digest grass actually host bacteria which produce cellulase, this is because the gene for producing cellulase hasn't evolved in animals, nor have many other genes for extracting maximal nutrition from plants. By farming bacteria in their guts (why cows have so many stomachs) they can get their nutrition by digesting the bacteria and the broken down plant matter.

Hi.well first of all you need to understand difference between plant and fruit.as jarlemag said grass n other green parts of plant contain Cellulases which wehuman cant digest.we dont have specific enzyme for that.also we dont bacteria that digest green plants.on the other hand fruit is nothing but a ovary of a plant containing the seed and nutrient which a seed need for development.although i said in my last we can digest some plants.

Wheat and other grasses are very significant sources for human nutrition.  Grass seeds are digestible; seeds have to digest themselves to sprout, with very little biochemical machinery.  Human civilization is founded on the ability to cultivate grass to eat.
It is due to pepsin that a cellulase supplement would not help to digest grass stems and leaves.  Pepsin is the enzyme in the stomach that breaks peptide bonds and from its perspective, cellulase is just another peptide chain (pepsin is so effective, the stomach has to prevent itself from being digested while at the same time maintaining enough pepsin to digest food — because pepsin digests pepsin).  Cellulose is a tough sugar polymer (as is chitin, which forms insect and fungus exoskeletons), so after all the cellulase was digested by pepsin only bacteria from the intestine could process the remaining cellulose.  What the bacteria convert it to might make one ill.
Humans can derive significant nutrition from bamboo shoots, which have less robust cellulose than in mature plants, and bamboo is a grass.  Pandas also cannot digest cellulose effectively, but that doesn't stop them from trying.  They might eventually develop a cellulase gene by sheer willpower and tenacity.

@jarlemag: inhaling sugar water could quickly become a very bad idea.  Encouraging microbes to colonize near the brain may result in them converting neurons into more microbes.  The Naegleria amoebae can be very aggressive.  In Pakistan and India it is somehow traditional to treat illness by putting water up one's nose; when it is not recognized how clean the water must be to do that safely, people die.

The soda is not inhaled. It's transferred directly to the stomach through a tube inserted through the nose: http://en.wikipedia.org/wiki/Gastric_lavage Anyway, it is a medical treatment and I'm no doctor - I'm sure there are proper protocols for it but I don't know anything more about it.

Also, though I do not know, it is likely that the soda is being used for its acidic properties. If so, diet soda would work just as well, and so it is as likely to be aspartame water that is being administered via a nasogastric tube (not inhaled) as it is to be sugar water.

Yes. Apparently some protocols use regular soda and some use diet soda.

Good point about the bamboo shoots.

Well, humans can eat grass, but it will not be digested. Cause to digest grass our body needs different kind of enzymes, which lack in humans so they can't digest grass directly although humans can eat grass, but not recommended.
Similarly our body has different enzymes to digest wheat and beans etc. Also remember rice, wheat and beans are fruit, not plant. Although we can digest some of the plant.

Aren't fruits parts of plants?

"Also remember rice, wheat and beans are fruit, not plant". what is meant by this ??

I think this is a beginners mistake. I think A random zoologist thinks fruits aren't parts of plants. This isn't true, I think.

I think he meant that the rice, wheat and beans that we eat are the fruits of the rice, wheat and bean plants, and thus have a different composition than the rest of the plant. The Wikipedia article on cereals says "A cereal is a grass, a member of the monocot family Poaceae, cultivated for the edible components of its grain (botanically, a type of fruit called a caryopsis)"

Even in times of famine, when people are literally dying from hunger, they do not eat grass - it is not digestible. But they eat cooked artiplex, which commonly grows by roadsides.


text:
Is it possible to correctly identify presence of Y chromosome with external physical test only?
I asked a question related to the third sex, and I came to know that its always possible to categorize a human to male or female with presence of Y chromosome.
Now, I have another question. Is there a way to say if someone has Y chromosome only with external physical test? More specifically:

Someone has a penis, can we say that s/he will have Y chromosome?
Some one has Y chromosome, can we say that he will have a penis?

No, an external physical examination would be inconclusive. The reason is the TDF
gene. To be more specific, if a person has XY and the gene is not active then the subject
would have a female appearance. Also we cannot conclude that a person has a Y
chromosome even if it has penis because that gene could be transferred on the X chromosome.
Here is a reference: http://en.wikipedia.org/wiki/Testis_determining_factor.

Isn't it the SRY gene which expresses the TDF transcription factor?

Sometimes, the area which encodes this protein is referred as TDF gene, although I am not sure if this terminology is abusive. http://www.biology-online.org/dictionary/TDF_gene . Also see here http://www.ncbi.nlm.nih.gov/gene?term=testis%20determinding%20factor  a alias for the SRY gene is TDF.

An interesting condition is androgen insentivity syndrome. In AIS, the body is unable to respond to androgens, the male sex hormone, of which testosterone is the best known. The most common cause is a defective androgen receptor, and most of these diseases are X-linked. In extreme cases, complete androgen insensitivy syndrome (CAIS) can occur. Genetic males (XY) with CAIS appear outwardly as females due to the lack of androgens that would normally lead to masculinzation. However, the SRY gene (sex-determining region Y) that encodes TDF still causes testes to develop, although they are usually internal. Individuals with CAIS generally identify as females.


text:
What insect is this? (India)
Can anyone tell me what kind of insect (if it is one) is this...!! Or is it the pupa of some insect?

Well I don't think that the whole big thing is the insect itself, it appears to be just a kind of protection or shelter which moves along with the tiny little thing that keeps on popping out and going it so as to move.
Location:  India

I think it is worth adding a few pieces of information, to aid identification: the case is grey, without grains on its surface and tufts of hairy projections present on each end of the case.

Might be useful : if the same Tineinae

Related: Identifying a creature that appears to be a worm wrapped in a cocoon, What is this black and white worm in a white case?,  Help in identifying an unknown arthropod, What insect is this? (India), Identify this smooth-cocoon worm from Southern India, Small worm living in some kind of cocoon......

Related:  What is this animal that hides in dustlike structure?, What in the world is this critter?, What is this hard shelled insect in my house?, What is this insect found commonly in coastal India?, Insect identification - pantry moth vs clothes moth

This is mostly a guess and loose suggestion, since the picture is not very clear (would need to see the larvae in more detail). However, Bagworm moths (Psychidae), Case moths (Coleophoridae) and Caddisfly larvae (Trichoptera, almost exclusively aquatic) all build similar cases. They construct their cases out if silk and often include debris, pebbles and other materials. I wouldn't be surprised if the larvae in your picture belongs to one of the first two taxa. Bagworm moths and Caddisflies generally include lots of external materials in their larval cases, which could point to Case moths for your specimen (which seems to have a weaker case mostly made of silk).
Here are two pictures of first a UK Case moth larvae (Coleophora deauratella) followed by a Bagworm moth (Dahlica triquetrella), just as comparisons. If you do google image searches of "group name + larvae" you will see many examples of what they can look like.

And just as a cool example - the larvae often use random material lying around to build their cases, which can give the following result, if caddisfly larvae are bred in a tank containing pieces if gold and pearls. For further information see this link.

I'll just comment that caddisfly larvae are aquatic and will typically only be found in clean streams, ponds, or lakes. The two moth families you mention are much more likely based on the terrestrial location of the OP's insect. I wouldn't remove your info about the caddisflies as it can be useful/interesting to others coming across this question, but the aquatic/terrestrial differences in these insects' ecologies definitively rules out caddisflies.

@theforestecologist I agree, which is also why I mention in the answer that Trichoptera are almost exclusively aquatic.

@fileunderwater Oops I missed that. Well just giving further acknowledgment to that fact then :).

It's a household casebearer, a kind of moth larva in the family Tineidae that builds this case around itself.
@fileunderwater is wrong

Can you substantiate your answer as why you thing so, ideally with citation and picture reference? Household casebearer as I'm aware of have dirt or grain covered case, when not covered in dirt, they are close to white and not grey. This species is not only grey but also has a smooth surface = no grains.

Could be, and, as I said in my answer, the ones I mention are loose suggestions, based on the rather poor picture. Could you maybe specify what makes you so sure that it is a Tineidae?


text:
What theories exist as to how self-replicating molecules organised into the first cells?
When I was a biology student in the early 90's, what I learned and read seemed to indicate a gap in theories around the origins of life. There was, of course, no real evidence about how the first self-replicating macromolecules came about, but there were plenty of reasonable theories. One that particularly stuck in my head was Graham Cairns-Smith's idea that replication began with effective competition for space between slow-growing crystal structures, for example.
Once you have something which loosely resembles a cell then, of course, we can invoke our understanding of Darwinian evolution to explain how those early cells differentiated and developed into the diversity of life we see today. But as a student there seemed a paucity of ideas as to how we could have got from macromolecules to cells. This isn't a small step: it requires our macromolecules to be localised, enclosed in a membrane and to begin to work with each other to form basic metabolic chains.
I left academia after a few years of bench work but I was struck again by this question the other day and wondered whether there were any theories or evidence about this transition that had arisen in the meantime? A quick search on Google didn't turn up anything but the same vague platitudes about enclosures of self-replicating RNA, with little explanation of how this might have happened. It also found this question on Biology SE - How did the first self replicating organism come into existence? - but that deals with initial abiogenisis, not early cells.
Are there any more up to date ideas?
EDIT: Clarification was requested. The linked question - and information elsewhere - tend to focus on the broad question of abiogenisis and seek evidence. I'm asking about a very specific step of the process, that between replicating molecules and the first cell-like structures. I am also aware evidence is unlikely, and I'm asking for plausible theory.
Not entirely sure why this isn't clear, or why I'm getting close votes.

Can you please clarify why the post  How did the first self replicating organism come into existence? does not answer your question and esp. what you mean by "initial abiogenisis" and "early cells" and the difference between these notions?

@Remi.b edited as requested


text:
Is it possible to perform selection of plants without seeds?
When a plant spread using roots or branches I believe new plants keep same genome.
Many plants don't have fertile seeds. How it is possible to improve quality of genome (perform selection) for such plants?
Should we wait for natural mutation to spread across entire plant?
Strawberry is a good example of such plant and we know large verity among this species. How was it achieved?

It is not directly related to genome and selection per se, but in horticulture, viral phenotypic changes/symptoms  are often used and transmitted, especially to obtain attractive variegation of the foliage and flowers.

Most commonly by breeding with a related plant - if there is one. Mutagenesis is an old technique that technically works.
If one part of the plant has mutated, of course you can take cuttings or plant tissue culture samples.
Strawberries can be bred and characteristics selected for.
https://en.wikipedia.org/wiki/Breeding_of_strawberries
A good example of a difficult to breed plant is bananas
See
http://www.promusa.org/blogpost363-Who-s-breeding-bananas

what technique are used for breeding if there are no pollination/seeds?

In provided article about banana researchers pollinated flowers artificially and worked with small number of survived seeds...

If you get flowers - use https://en.m.wikipedia.org/wiki/Doubled_haploidy


text:
How many proteins do all human ribosomes together produce per hour?
Very roughly how many proteins (chains) are synthesized in the human body per hour under normal conditions?
(And how many ribosomes does the human body have?)

Welcome to SE Biology. This question has multiple issues that will see it being downvoted or closed. There are two questions rather than one. Neither question is well defined. The first question is impossible to answer. This is due to the enormous error in such an estimation. There is variation at every level of a human body; starting between tissues down to translational initiation events on individual RNA transcripts. Also, every protein/polypeptide chain has a different length so every protein will take a different length of time to produce.

@Michael_A  It's not such a crazy question I think ... It should be possible to come up with at least a ballpark figure (say, correct within an order of magnitude) from bioenergetics.

@Roland, Changing the question to ask about the number of amino acids per hour would make a ballpark estimate feasible. Once that change is made I almost agree with you regarding the first question. The other issue is that there are two questions. Currently, there are two answers but each answer addresses a different question.

@Michael_A  But once we know the number of amino acids, this can be converted to number of proteins, since we know the average length of a protein in human cells. (Although we must assume that protein turnover rate is independent of protein size.) I agree it would be good to split the question in two.

@Roland, figure 3, shows the distribution of protein lengths in the genome is not normal. This is why thay specifically discuss median rather than mean length. Figure 3 highlights the fatal flaw in the assumption of an average length of the proteins in human cells, the need to take into account the expression of proteins. At any given time a cell is not producing 1 copy of every protein in its genome, it is producing the proteins that it needs. In the figure this lowers the median length to 248 aa.

@Michael_A  No, the shape of the protein length distribution is irrelevant. The key assumption is that the protein synthesis rate is proportional to its relative abundance (or equivalently, that turnover is constant). See my revised answer for a clarification.

I'm voting to reopen this question, as I think it's fully possible to answer it with some reasonable confidence.  We often overlook these quantitative questions in biology, but they are interesting and not as hard to answer as some may think --- it is not necessary to know a lot of details. I don't know the answer to the second question on number of ribosomes, but it should  be possible to figure out a rough number for this as well, by estimating ribosomes as a fraction of total protein. This has been done for yeast, see http://book.bionumbers.org/how-many-ribosomes-are-in-a-cell/

It's a so-called Fermi question. My colleagues and I found three or four different ways to answer it, all yielding similar results. I could have posted the answers if the question wasn't closed. The moderators should be more open-minded towards scientific approaches that they are unfamiliar with.

Regarding protein synthesis rate, here's an attempt at an estimate from bioenergetics:

ATP turnover in the human body is consider to be about 100 mol / day.
Protein synthesis is estimated to require about 1/4 of ATP consumption in a mammalian cell, and one amino acid elongation requires about 5 ATP, so about 5 mol amino acids are elongated per day, which translates to $1.2 \cdot 10^{23}$ amino acids per hour.
An average human protein is about 400 amino acids, which gives about $3 \cdot 10^{20}$ proteins per hour.${}^1$

I think this should be correct within an order of magnitude at least. (Unless I screwed up at some step in the calculation, it's getting late over here :) The most uncertain factor is probably the fractional ATP demand for protein synthesis.

${}^1$ The is correct with the following assumptions. Consider that the proteome has some (any) length distribution $p(n)$ where $n = 1,2,3 \dots$ is the protein length in amino acids, and $\sum_n p(n) = 1$. Let $r(n)$ be the total rate of synthesis of all proteins of length $n$. If we assume that this rate is proportional to protein abundance, $r(n) = t\ p(n)$, where $t = \sum_n r(n)$ is the total protein synthesis rate, then the total rate of amino acids per unit time is
$r_{AA} = \sum_n n\ r(n) = t \sum_n n\ p(n) = t\ \mu$
where $\mu$ is the average protein length. Hence the sought total protein synthesis rate is $t = r_{AA} / \mu$.

For your first question I think @Michael_A has explained why this question can't be answered.
And for the second one, I quote from bscb.org :

Ribosomes are found ‘free’ in the cytoplasm or bound to the endoplasmic reticulum (ER) to form rough ER. In a mammalian cell there can be as many as 10 million ribosomes (A single cell of E. Coli contains about 20,000 ribosomes and this accounts for about 25% of the total cell mass). Several ribosomes can be attached to the same mRNA strand, this structure is called a polysome. Ribosomes have only a temporary existence. When they have synthesised a polypeptide the two sub-units separate and are either re-used or broken up.

I don't like the last sentence in the quote. Very misleading. Almost everything in the cell turns over, but ribosomes have a long half-life compared to the time needed to translate a mRNA.


text:
Microscopy of moving white blood cells
Is there a way to get white blood cells to move while on a microscope slide? I want to try to get some microscope images of them moving, but so far I have only found them stationary.

Not an experimentalist, so take this with a grain of salt.  But for motility you often need some external factor, e.g. a chemokine or chemoattractant (FMLP is a common one for white blood cells).  Also some cell types may not crawl on bare glass, and might need a protein or gelatin coating.
White blood cells on slides can look like this: https://www.youtube.com/watch?v=JnlULOjUhSQ
Unfortunately, I don't know the conditions used there.  My recommendation is to look through Google Scholar for white blood cell motility or neutrophil motility, and see what turns up.  For instance, the first paper I found was: C S Spada, A L Nieves, A H Krauss and D F Woodward, J. Leuk. Biol. 1994 (PDF) which gives some details about how they got their assays to work, including a gelatin coating for the slides.  However, the details probably depend on the origin of your cells and the type of white blood cell you're looking at.

White blood cells move. As long as they're alive, they move, but they do it veeeeeery slowly.
The movements can be seen using time-lapse photography.
See: https://www.wetenschapsforum.nl/index.php/topic/199938-levend-bloed-onder-de-microscoop/
These were made at about 1,000x, anoptral contrast.


text:
How does one go from a couple of DNA sequences to a distance-matrix?
For a project we need to explain the subject of UPGMA.
We think we understand thee method itself but I fail to see how you go from a number of DNA-sequences to the distance matrix.
I understand that the lower the number, the more related two species but on what scale is this number and how to interpret the exact meaning of this number.
For example if the number between A and B is 17 what does that mean?


text:
How would one determine if an up regulation of one protein leads to an over expression of another?
Again, I'm new to biology and have a bunch of questions.
Does it depend on the proteins involved? OR are there basic co expression procedures one could implement to determine exactly how much one protein upregulation leads to overexpression of another protein ?

It might depend on what protein you are studying.

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


text:
Does SIV cause AIDS in primates... If not why
does SIV cause AIDS in primates or have they developed resistance to the virus **

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. This question can easily be answered by a Google search.

While the question doesn't show much effort, I'm not sure it looks like a homework question - and I certainly wouldn't call it a trivial question (apparently Nature agrees).

From https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus:

Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their
  natural hosts appear in many cases to be non-pathogenic. Extensive
  studies in sooty mangabeys have established that SIVsmm infection does
  not cause any disease in these animals, despite high levels of
  circulating virus. However, if this virus infects an Asian or Indian
  rhesus macaque, the animal will develop simian AIDS (SAIDS).[5] A
  recent study of SIVcpz in wild living chimpanzees suggests that
  infected chimpanzees experience an AIDS-like illness similar to HIV-1
  infected humans. The later stages of SIV infection turn into SAIDS,
  much as HIV infection turns into AIDS.

Later in the article:

Beatrice Hahn of the University of Pennsylvania and a team of
  researchers in 2009 found that chimpanzees do die from simian AIDS in
  the wild and that the AIDS outbreak in Africa has contributed to the
  decline of chimpanzee populations. Testing wild chimpanzees,
  researchers detected organ and tissue damage similar to late-stage
  human AIDS. The infected chimpanzees had a 10 to 16 times greater risk
  of dying than uninfected ones; infected females were less likely to
  give birth, could pass the virus to their infants, and had a higher
  infant mortality rate than uninfected females.

A couple of key references:
Keele, B. F. et al. "Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz" Nature 460, 515-519
Commentary on the above: Hayden, EK (2009) "Wild chimpanzees get AIDS-like illness" (DOI: 10.1038/news.2009.711)
Heeney J, Dalgleish A, Weiss R (2006) "Origins of HIV and the evolution of resistance to AIDS" Science 313(5786): 462–466


text:
Chemical inhibition of fertilization in plants
Are there any chemical compounds that inhibit fertilization in plants after gametogenesis? Simply put, I am talking about spermicide or emergency contraception for plants.
Specifically, I am searching for a compound that will inhibit fertilization of an ovum when a pollen grain has already contacted the stigma. This compound may be effective before or after the pollen tube has formed, but ideally before zygogenesis. Although, I am also interested in compounds that prevent maturation of the zygote (basically an abortive action).
The compound is effective when applied externally to the plant (via a liquid spray, for example). Alternatively, it could be absorbed via roots or some other route.
The compound may be a small-molecule or macro-molecule.


text:
What kind of snake is this?
First, we are located in Missouri. In between St. Louis and Cape Girardeau. St. Francois county to be precise.
We just walked outside and found this on the porch so we carried it off. Normally this wouldn't be a big deal, but we have a little one now and I didn't want to take any chances.
The snake, pictured below, was approximately 6 inches long. He seemed timid in nature, he didn't let us get very close to him before he started to slither away.
I assumed he was a juvenile black rat snake, from my highly deductive google searching, but I also know that snakes sometimes change color, shape and design as they get bigger. So I wanted to find out if my guess was correctly or completely mistaken. Thanks for you help!

Great find!
I'm pretty certain that is actually a Prairie Kingsnake (Lampropeltis calligaster - likely the subspecies L. c. calligaster).  The biggest indicator to me are the two alternating rows of dark spots on sides, with some blotches fusing.  They are distributed all over Missouri, although pretty rarely seen due to their microhabitat:

They tend to be fossorial, spending much of their time underground and
out of sight. As a result, there is little known about the biology and
status of these secretive snakes. Most [prairie] kingsnakes are observed
hiding under boards or other debris or crossing roads on warm
evenings.

I actually used to study herpetology in St. Louis, and we caught a few of these.  The juveniles tend to have well defined spots that fade in time, although there is some degree of polymorphism here.  Looks like yours is somewhere in between.  See pictures below for reference.
Juvenile:

Adult:

Worth mentioning these snakes are nonvenomous, and typically docile.
Photo cred: Edward Prenzler


text:
How long do human egg cell grow up?
I read article about alcohol harm where written that child may bear with birth defect cause mother used to drink alcohol 10 years ago so egg cell stay damages that long.
I don't believe that human egg cell wait for such long time until activated.
How long human egg cell grow up until sperm fuse it?

https://en.wikipedia.org/wiki/Ovarian_follicle Eggs are paused in their development until released during the menstrual cycle.

Thanks for suggestion! It is unclear from wikipedia article (I am not biologist) but as I understand reading that number of Ovarian follicle from beginning of puberty is limited (near 300'000 - 400'000) and decreased. So I may say that human egg cell live as long as human age except childhood development time.

@gavenkoa any article that make "scientific" claims that you read that is not peer-reviewed or does not accurately reference peer-reviewed findings is at best suspect... Even articles in a source as respected as The New York Times can and do often write their articles base solely on the abstract. The problem is that abstracts to journal articles don't always tell the complete picture of the study which can lead to false assumptions that end up as articles in popular publications.

Fetal Alcohol Syndrome tends to affect the developmental process of the fetus and is not associated with actual genetic change. Ethanol is not a known mutagen, so it is not likely that it has an effect on oocytes. Oocytes are also mitotically inactive, so short of ionizing radiation, it isn't likely that any change will be made to the chromosomes of the oocytes. It is very possible that toxins such as chemotherapeutic and possibly ethanol (though unlikely) could damage or destroy oocytes, but this would likely only affect the woman's fertility and not the outcome of a pregnancy.

How long human egg cell grow up until sperm fuse it?

Ovules are made while the female is still in the uterus of her mother. The ovules (in the form of ovarian follicles) are kept in the ovaries for a long time, and just a month before leaving the ovary (ovulation), the ovarian follicle (and the future ovule) gain in size. In other words, the ovules are slightly older than the age (counting from birth/labour) than the person carrying them. You'll find more information on wikipedia > ovule > ovule Development, oogenesis, and ovarian follicle.
Does it address your interest about alcohol consumption?
Now, I don't think this question/answer address your interest about alcohol consumption. Whether or not the ovule is create by a division that happen just a day before ovulation  or many years earlier doesn't change anything to the fact that this ovule has experienced alcohol consumption (either directly or in the lineage) before.
Where to ask the question that I suspect interest you the most
If you want to question the article you read about alcohol consumption, the best you could do is to go on Skeptics.SE, link the article, quote something from the article and ask "is it true?"

Please consider editing your answer. It is incomplete from the perspective of human developmental biology. Also, I would personally question the use of "belly" over uterus on a forum on biology.

@AMR I changed "belly" into "uterus" (don't think it is quite a big deal but I guess it indeed look better this way). I realize the answer is a bit weak but it boils down to 1) the fact that the question implicitly assume a moment when an ovule is "born" which is quite an unclear concept and 2) wiki says it all. Would you think it is worth making a full description of oogenesis on this post?

No, but then don't go into partial details. Say, unlike males who do not produce sperm until puberty, and then produce them constantly for the rest of their lives, human females are born with their full complement of sex cells, which are, for the most part dormant until ovulation. You could also explain that a toxin that does not cause mutagenesis would at worst kill the cell before it could be fertilized, so it is unlikely that alcohol use outside of pregnancy would pose a risk to fetal development. It is possible that there could be diminished fertility, but that would require citation.

I wouldn't say that I am very proud of the formulation of my answer (and globally, I realize that I am not a great writer and english is not my mother tongue which probably doesn't quite help). If you don't have anything to say about the content but only about the right choice of details (and about the formulation), maybe the best is just to make your own answer, with your own formulation. Thanks for the suggestions though.

I am suggesting that an answer has a higher standard than a comment on SE sites. I gave the response I wanted to give in the comments as I did not want to get into the detail or citation necessary to answer properly. While you may not respect the OPs question or its validity for the forum, you need to remember that SE Q&A on topics rank highly on Google search, so others with the same question will be directed here. Give an answer that is representative of your training as a scientist, or leave a comment to point OP to further research. The answer represents you as much as the OPs question.


text:
Am I a lobe-finned fish?
I really wish this question only contained the title and tags, but the website forces me to write some text.

@Gyro How does that make him a lobe-finned fish? I've never met lolmaus-Andrey Mikhaylov, so you could be right, in which case I'd be intrigued to know how he used his little fins to type this post.

The answer depends on whether you want to know in the common sense or in the modern scientific sense.  The phrasing of the question suggests you want to know in the common sense, but the choice of the phylogenetics tag indicates you want a scientific answer.
In modern biology, the term lobe-finned fish would be formally taken as (an imprecise) convenient term for the clade Sarcopterygii.  Presuming you are not an alien or computer but are human, yes, you are a lobe-finned fish (a member of the class Sarcopterygii).
In the common sense, no, you are not a fish, lobe-finned or otherwise. This would also be the answer under the old tradition of zoological taxonomy, which was based on taximetrics (measurement of an organism's form) rather on the modern phylogenetic (evolutionary relationship) basis for biological taxonomy.

I would add "ecological sense" to "common sense". Ecologically, humans are not lobe-finned fish: they do not live in water, and don't use fins for swimming. But their body structures are inherited from animals that did so.

@mgkrebbs, thank you for your answer. It explicitly covers my short question. ♂

@bli So? Beavers live in water and have flappy tails. Does it make them fish? Medieval monks believed beavers to be fish, which was a loophole allowing eating meat during fasting. Very convenient, but meaningless otherwise.

@lolmaus-AndreyMikhaylov That's a very good illustration of the fact that classifications may have a purely practical goal!

A practical goal of fabricating a rule by neglecting the true nature of things?


text:
Do compound eyes exist in nature that have multiple "pixels" per ommatidium?
If yes, which species? What is the terminology for such eyes?

Have you performed some research yourself? What brought a Google search?

Uhm, I just got curious about it when thinking about fake pupils of crabs.

I thinkt it's a good question, yet we require folks to show some evidence of previous research efforts; a simple wikipedia search can do the job. Adding your own preliminary findings is a great way to bring focus and clarity to your post. You can also see that the answerer below had difficulty to answer your question because of a lack of information in the question

This question is the subject of this meta post.

OK, I've researched a bit and found this:

In apposition compound eyes each lens with its associated photoreceptors is an independent unit (the ommatidium), which views the light from a small region of the outside world.
In superposition eyes the optical elements do not act independently; instead, they act together to produce a single erect image lying deep in the eye. In this respect they have more in common with single-chambered eyes, even though the way the image is produced is quite different.

Source: https://www.britannica.com/science/photoreception/Compound-eyes
So superposition eyes are not exactly multiple "pixels" (rhabdoms) packed into a single ommatidium, but rather each rhabdom served by multiple ommatidia! In this regard, superposition compound eyes work similar to microlens array cameras sans the main lens!

This details two general classes of compound eyes, but doesn't answer the question. Perhaps the original question should have been edited with this information, rather than posting it as an answer.

@JiminyCricket. Karl Popper says it is scientifically impossible to prove that something does not exist, because it could exist where you weren't looking.
Also, why doesn't this answer answer the question? The question was about multiple "pixels" per ommatidia, and every ommatidium in superposition eyes does illuminate multiple pixels.

My comment wasn't philosophical in nature, just pragmatic. It's just the sort of background research that would have been great in the question's body. Perhaps you are unaware that there is a definitive answer to the question, and that this isn't it.

@JiminyCricket. How can any person definitevly know that no species in the world has compound eyes with multiple species per isolated ommatidium? All you can say is that you haven't learned about any such species so far, which is not a definitive answer.

@JiminyCricket. Also, you didnt explain why you believe that superposition eyes do not match the original phrasing of my question (still in the question's title).

You're making an incorrect assumption about the answer to the question in your comment that you can't prove a negative - why would anyone need to do that when they can cite a positive? Regarding your answer; omatidium is the singular of omatidia, you've answered a different question - or rather you've shown background research to the original question which should be edited to include it, rather than posting it as an answer.


text:
Has the most recent common ancestor of all living birds lived after dinosaur mass extinction?
I wonder if one or more phylogenetic threads of dinosaurs survived the mass extinction.
In other words, are all living birds equally related to any given ancient dinosaur, or do some birds relate more to some ancient dinosaurs while other birds are more related to other ancient dinosaurs?

Birds are theropod dinosaurs

@Chinmay Kanchi: No, they're not.  They're DESCENDED from theropod dinosaurs.  Saying they are is like saying mammals are synapsid reptiles, or that all of them are really just fish :-)  And we can see this by noting that there were many different orders of birds in existence long before the K-T extinction event.

Fish is paraphyletic, but the rest is true. Mammals ARE synapsids when strict taxonomy is respected. Scientifically speaking, Donald Trump is a reptiliomorph, and Vladimir Putin is an eupelicosaur. If you deny that you'll also have to deny that you're a mammal.

I suppose that by the mass extinction, you are referring to the Cretaceous–Paleogene extinction event that happened 66 mya. The Most Recent Common Ancestor (MRCA) of all birds lived about 113.3 mya (early Cretaceous, according to this in oneZoom.org).
So yes, the MRCA of all birds is definitely older than the Cretaceous–Paleogene extinction event. As you said, this also mean that some ancient dinosaurs are/were more related to some extant birds than some extant birds are related.

You (the OP) might not need it but some other readers might need clarification about phylogeny with the post If dinosaurs could have feathers, would they still be reptiles?

That's awesome! According to OneZoom, the following groups independently survived the Cretaceous-Paleogene mass extinction INDEPENDENTLY: ostriches; [cassowary, tinamou, moa, etc]; [waterfowls, magpie geese]; screamers; gamebirds; [sunbittern, kagu]; oilbirds; potoos; nightjars; frogmouths; [hummingbirds, swifts]; tropicbirds; [flamingos, grebes]; [sandgrouses, hoatzins]; [pigeons, doves]; [cranes, rails]; [bustards, floricans]; [some cuckoos, roadrunners]; [other cuckoos], turacos, [herons, shearwaters, pelicans, penguins, albatrosses, etc].

That's absolutely amazing! Earlier I thought that a single Jurassic Park-like feathered dinosaur survived the extinction and evolved into birds, but it turns out that before the dinosaur extinction birds were already very diverse!

Of course, I enumerated the groups using names of modern representatives of the groups, and 66M years ago their ancestors might have looked differently and maybe more primitively, but they were already birds (almost?) as we know them today! All those monophiletic groups of dinosaurs-birds were already established, whereas ALL human ancestors were tiny lemur-like creatures. O_O

What was the largest bird that survived the KPG boundary and did any flightless birds do do? cool topic Remi and Andrey. From the other topic Remi, i didn't find evidence that less compact genomes can evolve more efficiently. It was an logic from lessons prior to sequencing.

I've read that all modern flightless birds are relatively young groups. All of them used flight to spread across the globe before they decided to walk. It could have happened before K-Pg, though.

I'm not sure I follow the conclusion: "this also mean that some ancient dinosaurs are/were more related to some modern birds then some modern birds". What do you call "ancient dinosaurs"? If you mean that every lineage of birds that got extinct during the C/T crisis should be called "ancient dinosaur", why not, but I find this a bit unusual.

By "ancient dinosaur" I meant any member of the clade dinosauria who went extinct before/during K-Pg.

@lolmaus-AndreyMikhaylov By your definition, there indeed are lineages of birds more related to some "ancient dinosaurs" than others, but we would probably call these particular ancient dinosaurs "birds" without much hesitation. I find it not particularly notable that some lineages of birds got extinct before the crisis. This does not make things that we intuitively call "birds" non-monophyletic, for instance.

@bli of course, as you say is right. Bird is still a monophyletic clade. The only point is that some of the birds lineage already existed before the K-P extinction. You can call them ancient dinosaurs if you want. As all birds are Dinosauria, all modern birds as well as those ancient birds are all Dinosauria. That's all. See eventually If dinosaurs could have feathers, would they still be reptiles?


text:
An online tree of life with extinct species present?
There are awesome online phylogenetic trees such as OneZoom.
But they all only list living species.
I want to see dinosaurs between birds and crocodiles.
I wanna see that humans are reptiliomorphs and eupelycosaurs.
species.wikimedia.org seems to contain this info, but it's not presented in a navigable tree structure.

The tree of life project is your best bet, its not 100% complete but it is more complete than any other project I have ever seen, and unlike most actually includes many if not most extinct taxa. http://tolweb.org/tree/phylogeny.html
It also includes citation and brief descriptions of links and groups to make it easier. Some extinct lineages suffer from unresolved phylogenies but many of those are in constant flux or are actually unresolved in the fine scale so I can't blame them, especially considering they were originally based entirely on genetics, and is updated constantly.

Had this same question, and after a lot of digging, came up with this http://lifemap.univ-lyon1.fr/explore.html
Very cool tool!!

cool but dinosaurs are not included other than a footnote.

A link is not an answer in terms of SE Biology. Please finish the [Tour] and read the help on answering questions.


text:
Restriction enzymes
Why are those restriction enzymes which cut the DNA strands a little away from the centre of the recognition sequence more useful in the construction of recombinant DNA?

Why do you think? What would be the use of overhanging (hint: sticky) ends vs a blunt cut?

I've read this and there should be and is a reason behind it

Yes, there is, and I'm trying to help you answer your own question. So, we're constructing recombinant DNA, which means we're splicing a linear piece of double-stranded DNA into a spot (most likely) in a plasmid. Why would you want sticky ends, and where would you want them?

Also important - would you want the same sticky ends everywhere, or only certain places?

I'm Confused*****

There is two main ways to cut DNA, creating Blunt ends or Sticky ends.
Blunt end example of SmaI recognition site:
("|" is the cutting site)
5'---CCC | GGG---3'
3'---GGG | CCC---5'
Sticky end example of EcoRI recognition site:
5'---G  |   AATTC---3'
3'---CTTAA    | G---5'
In blunt end example, the only way you can attach both pieces of DNA is one after the other, which is harder to do and not specific at all since any bases can go one after the other.
5'---CCC --> <-- GGG---3'
3'---GGG --> <-- CCC---5'
In the sticky example, the sequences will recognize its homologous sequence and attach to it (The TGGG will attach to the ACCC part, making a strong bond). When attaching one strand of DNA on the other, the bases must be homologous (A-T, G-C), this gives specificity since the strand can only be attached with specific sequences.
5'---GAATTC---3'
3'---CTTAAG---5'
Here is some good references on restriction enzymes:

Wikipedia(Complete informations with strong references)
Biotech Learning Hub (Basics easily understandable)


text:
How many mutated genes from a complementation test?

With 1, 3, and 5 being defective together, that means they are on the same gene. 3 and 5 are defective together too, meaning they are on the same gene as 1. Why does this slide say that there are 3 mutated genes? I must be missing something, I don't think I understand something.

There are 5 mutations being tested in these complementation test.
The first gene, carries mutation number 2.  In other words, mutation number 2 complements mutations, 1, 3, 4, and 5, and fails to complement itself.
The second gene, carries mutation number 4. In other words, mutation number 4 complements mutations 1, 2, 3, and 5, and fails to complement itself.
The third of the three genes, carries mutation 1, in one strain, mutation 3, in a second strain, and mutation 5, in a third strain.  In other words, mutations 1, 3, and 5 all fail to complement each other, yet all three complement mutations 2 and 4.
There are 5 different strains in this experiment, and there are five different mutations (one in each strain), but the five mutations only affect three different genes.


text:
Is Richard Dawkins's interpretation of the theory of evolution circularly?
I think we are all familiar with the basics of Dawkins's theory of evolution. In a nutshell: All creatures are nothing but vehicles of genes with the sole purpose of passing through these genes, and in the case of human beings besides genes also memes are involved.
Isn't this interpretation of evolution circularly:
"Why do all organisms exist? Because the purpose of organisms is to pass on genes which have the ability to develop new organisms, thereby creating new organisms under all kinds of environmental pressures". In short: "Life exists to produce new life", which is a circular expression because, in the reason we search for life, the term "life" (for which we try to find a reason) is used.
I think there are more "friendly" interpretations of evolution, of which I have no doubt that it took place.You can interpret evolution for example from a less egoistic perspective, and say evolution takes place to give new organisms a chance to live. Ande, in the case of human beings, create memes to let other people enjoy them (and not just to let your memes live further in other human beings).
If we follow Dawkins's interpretation then the scientific meme is self-undermining because the way we use science is damaging the earth to such an extent that it's the question if the earth will face a long-term future.

I'm voting to close this question as off-topic because it has nothing to do with science but with the philosophical question of what is the purpose of life.

I second that and fully support @Remi.b's claim.

descheleschilder you are confusing scientific questions with a pseudo philosophical one. "organisms exist becasue they are the most successful means by which genes make more genes" is a completely legitimate scientific answer. If you ignore this becasue you feel life needs deeper meaning you are no longer using science.

Why should they make more genes in the first place?

chemistry, Its one of the things certain sequences of RNA do becasue of the structure and the interaction of their charges, in the same way salts dissolve and phospholipids form micelles. Ones that are better at produce more thus increasing in number.

For the question Why should they make more genes in the first place?, you might want to have a look at How can the number of genes increase through evolution?.

You are definitely confused as you don't seem to be able to tell the boundary between science and philosophy. You should work out on that. You likely make a strong misrepresentation of what evolution theory is saying. You might want to have a look at a short and easy intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

Who says I am the one that is confused? I definitely believe in evolution, but my interpretation of it (like there are many interpretations of quantum mechanics or Christianity)  is radically different from the one of  Dawkins

I understand how evolution works and how genes and RNA can make copies of themselves, And I think this process started blindly, but I think that when evolution evolved the more complex creatures could steer in some way the direction the newly formed genes took, which is to say that it wasn't an evolution by accidental mutations in the genes.

@descheleschilder: You really need to stop believing in evolution.  It's not a religion, and doesn't need belief, any more than believing or not believing in gravity will keep you from falling.

You can ignore gravity and don't pay attention to it, or don't even invent the term gravity, but your keys will still fall on the floor. Likewise, you can ignore evolution and all flora and fauna will still be around and invent another story how all life came into being (to which your reply, of course, is that evolution isn't a story, but how it really is). But I think I'm gonna ask the same question in the philosophy department because we're drifting off.

The following is more an extended comment than an answer...
Why the question is off-topic
Your question has actually nothing to do with biology. You are looking for a purpose behind the existence of organisms. Science does not care about purpose, nothing has a purpose, everything just happen mechanically. If the theory of evolution gives you a bad feeling, then I am sorry for you that it does but that point is not to be discussed on a science forum. I am voting to close for this reason.
Tautology
Please note that evolution is the science that has for goal to explain the change in allele frequency through time. The process studied is a continuous succession of reproduction and therefore in some respect a repetitive process but it does not make the explanation of how change in allele frequency occur a tautologic explanation. You will note by the way, that evolution does not explain the origin of life, this is the role of another of field of biology that we call abiogenesis.
Did you say Dawkins's theory of evolution?!
I often get a little mad when people write Darwin's theory of evolution thinking this is a modern concept. But writing Dawkins's theory of evolution is even worst. Dawkins is foremost a popular science communicator, so there is really no such thing as Dawkins's theory of evolution. Dawkins was also a researcher before and he brought some knowledge that allowed to grow our theory of evolution which we call the modern evolutionary synthesis (some argue that we should rename it Extended evolutionary synthesis in the light of recent discoveries).

Eh, I mostly agree with you (and definitely about the off-topicness), but I think if we reinterpret what the OP said as "Dawkin's ideas regarding evolution" (because that's what OP is referencing, not any of Dawkin's scientific contributions), which I think is what OP means rather than giving Dawkin's credit for the whole theory of evolution, the point that Dawkins emphasizes is essentially that there need not be a purpose. The existence of, and evolution of, organic life does not need to have a purpose to exist.

Thanks @Bryan. I read the selfish gene a while ago and I don't remember such saying but maybe he says that. Dawkins is known for mixing up philosophy, science and politics in its public speech. In which case, the question is of course still off-topic as the saying that 'there is no need for a purpose' is not a scientific claim but one that is to discussed in philosophy of knowledge (incl. philosophy of science).

I always get a little mad when people say that everything just happens mechanically. That means that everything they say also happens mechanically, so we can attach no meaning or purpose to the things they say. Which in turn means the evolutionary theory (which also developed mechanically) doesn't have a purpose or meaning. So what use is it discussing it? All the discussion develops mechanically too, depriving the discussion of purpose or meaning. I on the other hand can discuss the various interpretations of evolution, because I don't believe everything happens in a mechanical way.

I am sorry you don't like it but welcome to science anyway, where ones emotional response to an evidence should not alter the nature of this evidence. All of this is really a matter of philosophy of knowledge. Please consider having an intro course to philosophy of knowledge and consider asking your questions on philosophy.SE

I might be putting words in Dawkins mouth here, too, so maybe I should check that. @descheleschilder I think what someone like Dawkins would argue about purpose is that there is actually a lot of freedom in an approach to life that says there is no set purpose: it means that, as a human who has the fortune (and burden) of having a decent amount of intellect, you have an opportunity to choose your own purpose, to find your own meaning in your own life. It's a different "type" of purpose than some sort of guiding principle for the universe, but a purpose nonetheless.


text:
Does one memory cell take part in different memories?
Does one memory cell take part in different memories? For example, both in the visual memory of a bird and a monkey?

According to engram theory: Yes.
However, you need more than one cell to encode a memory engram.
The idea is that the combination of cells encodes the memory, not the cells themselves.
I am most familiar with the hippocampus, in which cells participating in the encoding of "concepts" like Jennifer Aniston, Bill Clinton or the Sydney Opera House have been found in humans Quiroga et al. (2008)


text:
How is the Guide RNA created for Crispr?
It seems that to modify DNA a guide RNA and Cripr are introduced.
But I'm unable to understand how the Guide RNA is made or created.
Is it a simple method which can be done with simple lab equipment or is it complicated?
What is the equipment need to create it?


text:
How are vaccines and inoculations different?
If so are vaccinations more safe? If so how? And how is the vaccine a magical invention?

First: Inoculation and vaccination are synonyms. So what is your question after that? If vaccinations are safe? Yes, they are.

@Jill I've added a possible definition of what you meant by inoculation. If it is not what you meant, feel free to revert back.

Vaccination has nothing to do with magic. Please clarify what you are asking, and what previous research you have done.

If you became infected before the advent of vaccination, you would either live or die. You would also probably die with really good odds. Being said, someone who lived a disease developed immunologic tolerance to the causative agent, that much you could begin to understand. To expose someone to smallpox was to really endanger their lives, so they found that a similar virus known as Vaccinia, which would normally cause cowpox, could be administered to a patient and they would catch cowpox, but now they were resistant to catching smallpox. You can read about all this on the wiki page for vaccination.
Inoculation generally differs because in the case of inoculaton, you could hope for a less virulent strain of a pathogen but you weren't guaranteed it. You ended up with vaccination methods that increased the safety of the process: On one hand, you could infect someone with related pathogen that causes a milder disease for protection from a more dangerous, related pathogen. On the other, you could find a way to disable the agents pathogenicity, such as heat-killing.
Modern vaccinations are much more refined in that we know so much more. Attenuated strains, for example, you take a virus that grows well in human cells and infect monkey cells just as an example. After many generations the virus grows well in the monkey cells, but no longer the human cells. The strain should still retain it's antigens, however, so when you inject a human now, the virus doesn't cause a disease but you produce antibodies to the virus.
In short, you can protect a population from a disease that would normally devastate it with a dramatically improved efficacy.


text:
Why do mammals produce more carbon dioxide than insects?
I understand that mammals produce more carbon dioxide than insects on a gram per gram basis, but why is that? I'm thinking it might be because mammals are warm-blooded, which require more energy consumption. Could it also be due to the fact that insects are less active than mammals? AKA they do less work?

From where do you understand this? Could you provide a source?

Source and context, please. For example, it doesn't seem likely that a resting mammal will produce more CO2 than an insect running for its life. Could be, though

As you said, endothermic animals such as mammmals or birds consume more energy and therefore expelmore CO2 not only because of a higher betabolic rate or to keep warm, but also because they are more active. Even taking all that into account you are missing the biggest difference between them: size. The consumption of energy is not directly related to the size, in fact, the energy requirements drop exponentially with the reduction of size. The same phenomenon explains why they are far stronger, fall-resisting...

The answer seems to be okay, but please provide references to your claims so that people can check and read further.

oxygen consumption endotherms vs ectotherms http://advan.physiology.org/content/31/1/97


text:
How fast can a panda run?
Pandas are going extinct, mostly due to habitat destruction. This leads me to the question:  How fast can an average adult panda run? (more specifically Giant Panda)

How does panda's habitat destruction lead you to wonder about their top speed?

@Remi.b habitat destruction -> pandas dying  -> animals dying -> being prey -> escaping predators -> running -> running speed

Adult pandas don't have predators. But anyway. The question is valid without needing justification for your interest :)

I think that in comparison to a North American bear species, giant pandas would not give chase for very long as they prefer to move slowly.  Recent research into giant panda biology indicates that the foraging speed of a giant panda is 50 feet an hour.  Their metabolism is very slow, lower than a three toed sloth.  Their entire way of life is slow movement so considering all that, I would say that you might be able to outlast them in a run.
http://www.livescience.com/51505-giant-panda-metabolism.html


text:
Purifying large amounts of PCR product
I have had trouble purifying very large quantities of pure PCR product. We are using these as templates for the reconstitution of nucleosomes and I require hundreds of micrograms to milligrams of template.
Here are some methods I have tried:
1) QiaexII slurry--typically I use the entire slurry for one purification then regenerate the resin by washing in 1M HCl then re-equilibrating with water. This way has worked best for me so far but the yield tends to be fairly low (~100 ug from 100 PCR reactions).
2) Phenol-chloroform extraction. This method seemed to work great, however I believe I have phenol contamination at the end--the yields are often much higher than they should be even if I chloroform back extract before the ethanol precipitation. When I run it out on a gel it looks like the apparent concentration I get is off. I have not tried this too many times so perhaps it could be optimized.
3) Spin column purification. I've used the DNA Clean and Concentrator from Zymo and the yields seemed quite low, even for the columns with an apparent 100 ug capacity.
Another option I have explored is large scale purification of the parent plasmid followed by digestion to liberate the small insert. However I still run into the issue of purifying away the parent plasmid. I've seen a few protocols using FPLC and/or size exclusion but I'm not sure how effective this would be.
Anyone have any ideas?

We had to do this frequently. What I would first recognize is that all of your current methods only work for at the small scale and that for you to purify mg quantities of DNA, you need to work with mg scale equipment.
First of all, you should examine your "upstream" process. Are you doing your PCR at scale? Typically, we have scaled out by going with multiple PCR reactions rather than one large PCR reaction. Generally the reactions max out at 50uL depending on your thermocycler. If you're getting around 1ug/10uL, scale up to a 96 well plate with 50 uL reactions and get ~500 ug of material. Make sure that you mix your dNTPs! Scale-up accordingly.
To start, the DNA Clean and Concentration is designed for really small reactions. It's much better to use the next level of purification by maxiprepping everything. The  The binding capacity of those columns go up to 1 mg. Using the QIAEX II slurry works but you should make sure that you scale up correctly. Make sure that you complete your regeneration. This protocol works well.
Alternatively you can ignore the column and just ethanol precipitate everything to remove your nucleotides. I suggest following Ethanol precipitation of nucleic acids from OWW. We had to make a lot of linear template and for most applications this works great.
As with all things related to molecular biology, there is a lot of voodoo. Some things that supposively work is to chill your ethanol mixture at -20C for at least an hour (or overnight), generally, you'll see your DNA fall out of solution and that's your sign that things are working. At this scale you should be seeing your DNA pellet; that's a good sign if things are working. While eluting anything from the columns, we would warm up our elution buffers. Thermodynamically this would make sense since it would reduce the barrier for unbinding. You would also get away with a lower residence time.
I would frankly avoid using FPLC unless you're working with gram quantities of DNA. You're not Moderna.

Thanks for the advice. I am doing 50 uL PCR reactions in a standard thermocycler and usually do 96 at a time--I'm honestly not sure what my yield is per reaction since I've never purified from a single reaction. For the ethanol precipitation--are we sure this is going to remove the polymerase entirely? Also--do you have a specific protocol for maxiprep-ing from PCR reactions? Zymo has a DNA clean and concentrator with 500 ug capacity, so I am considering using that; however I've found the yields to be much lower than anticipated with other "large-scale" type column kits.

Cooling the reagents (or the complete reaction) is not necessary. See this answer which fits perfecty with my experiences.

What do you guys think about just doing a large phenol-chloroform extraction/EtOH precipitation then simply dialyzing or buffer exchanging to dilute any contaminants?


text:
Are bronchioles and alveoli covered by respiratory epithelium?
Which parts of respiratory apparatus are covered by respiratory epithelium and which are covered by other kinds of epithelium?

What do you mean by respiratory epithelium ? Do you mean squamous epithelium ?

From the nose to the pharynx and larynx: stratified squamous epithelium
From the end of larynx to the bronchi: pseudostratified columnar ciliated epithelial cells.
From the small bronchi cartilage is being replaced by elastic tissue.
Bronchioles: ciliated simple epithelium with club cells (known as Clara cells). Also they lack cartilage and glands.
Alveoli are covered with squamous alveolar cells which form the wall (also known as type I pneumocytes). They also contain great alveolar cells (which produce surfactant) or type II pneumocytes and macrophages.
From http://en.wikipedia.org/wiki/Respiratory_tract , http://en.wikipedia.org/wiki/Pulmonary_alveolus and http://en.wikipedia.org/wiki/Pharynx


text:
Plant part adaptation vs animals
I have seen nurseries selling plants that grow to trees bearing different fruits. Eg: A single plant that produces fruits of peach, plum, apricot,etc. Here is one website that advertises such trees. So in conclusion any tree could be grafted to live in a trunk of a similar kind of tree. How come animal parts cannot be transplanted with other animals of the same kind. Why is it not possible to use any animal organs for humans using transplants.

Because humans have an immune system.

Can you elaborate?


text:
Detecting Calcified stones and cracks in tooth
I had a dental problem when my first molar broke some months ago and after some decay and pain I am undergoing a dental treatment. The doctor was performing a root canal and kept on talking about calcified stones being formed and looking for a 'tak' sound inspite of having x-rays. Doctor did not point to the calcified stones earlier and suddenly came out with this new issue. In the mean time when looking for stones doctor actually managed to break my tooth and has blamed grinding and clenching for a crack that caused the tooth to break.
I am shocked that neither the calcified stone nor the crack showed up in x-ray and the preliminary examination. With current technology, can the cracks in tooth and calcified stones not be detected.

Cracks on your teeth are hard to detect if they are cracks on the mesial or distal surfaces (surface of the tooth closest to and farthest from the midline respectively) through x-rays. Please check this link for illustrations and very good explanations from the University of Maryland dentistry department. The different methods on the detection of cracks as well as the uses of radiographic evidence can be found in this link.
Now pulp stones can be identified through x-rays unless they are too small or not too dense. There has been researches done specifically using radiographs for detection like "A radiographic assessment of the prevalence of pulp stones in Australians". It could also be human error that your doctor was unable to detect it. A small explanation on pulp stones can be found here.