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Cockroaches and magnetic fields
Aloha, I live in Hawaii working with sharks and their sensitivity to magnetism but here we also have large cockroaches. Has anyone worked with cockroaches and magnetism?  I wonder if placing high magnetic fields near food and anywhere else, would repel cockroaches. Mahalo and aloha.

Adrianus Kalmijn of the Woods Hole Oceanographic Institute, In 1982, to test whether the Round Stingray (Urolophus halleri ) can orient to magnetic fields, Kalmijn set up weak magnetic fields. When the simulated field was rotated through various degrees, the rays sought food in the 'east' defined by that imposed shift. In field experiments conducted during 1987, Kalmijn set up a ring of electromagnets in shallow waters off Bimini, Bahama Islands, along the known daily route of a Lemon Shark (Negaprion brevirostris).

the pair of electromagnets which aligned with Earth's magnetic field at that location; when the shark swam by it maintained its course as though nothing had changed. Next day, as the shark swam through the ring of electromagnets, Kalmijn switched the pair of electromagnets which rotated the artificial field 90° to the weaker natural field. The shark altered its course by 90°C in the same direction as the field shift.


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why do some cells in the body prefer necrosis to apoptosis as a means of cell death?
There are many programmed cell death pathways, but some cells show a greater preference for some over the other. I'm wondering as to why if necrosis is an inflammatory response that causes damage to neighboring cells, why some cells would prefer this as opposed to a more controlled mechanism such as apoptosis or even autophagy.

Necrosis often happens in case of mechanical injuries or diseases. Apoptosis is programmed and controlled cell death. If tissue damage is too severe, however, the necessary steps can't take a place. A severed cell membrane pretty much prevents apoptosis

What makes you think some cells prefer necrosis? I think the condition leading to cell death is deterministic

There is actually no preference for apoptosis or necrosis in cells of the human body - both types can occur in all cells and they have different triggers. The main differences can be seen in this figure (from here):

Apoptosis (also called programmed cell death) has three different triggers (intrinsic, extrinsic and Perforin/Granzyme pathways), see the image below for details (from reference 1):

All three activate different components and caspases in the beginning but finally all activate Caspase 3, which finally activates endonucleases (which degrade the chromosomal DNA), Proteases (which degrade the proteins in the nucleus and the cytoskeleton) which leads to the degradation of the cell. In the end apoptotic bodies are formed from the cell. Additionally the mitochondria break down and release cytochrome c and ATP. Their release from the cell attracts macrophages which take up and eliminate the apoptotic bodies and in turn release cytokines which suppress an inflammatory response.
Apoptosis goes on in a ordered way and does not trigger any further reactions in neighbouring cells (except these receive the same signal). See also reference 1 and 2 for more details.
Necrosis is triggered by external stimuli of the cell as injury of tissues or toxins from infections. Necrotic cells swell, while there internal structures are in a state of unregulated degradation. Finally the membrane will burst and set free cytochrome c and phosphatidylserines from the membranes which cause inflammation in the affected tissue. The necrotic cells are not removed by macrophages which allows the released interior of the cell to spread further and cause problems.  See reference 2 and 3 for more details.
Necrosis is usually not as a beneficial process, but there are also publications which see
the process as a specific form of cell death (see reference 4).
References:

Apoptosis: A Review of Programmed Cell Death
Apoptosis vs. Necrosis
Cell death by necrosis: towards a molecular definition
Review Necrosis: a specific form of programmed cell death?

Necrosis basically occurs when a cell is injured beyond recovery and it does not have sufficient energy and time to undergo apoptosis

@CRags That would the TL,DR version :-)

The answer given above by Chris is correct, but does leave out one relatively recently discovered method of cell death, somewhere between the two responses of apoptosis and necrosis.
It's called pyroptosis. It's a form of programmed cell death (in immune cells, e.g. macrophages), so it is similar to apoptosis. However, instead of a neat and tidy non-phlogistic (inflammatory) death as is the case in apoptosis, the cell purposefully upregulates inflammatory cytokines, swells, and bursts, releasing the cytokines and other inflammatory mediators out into the extracellular space.

The wikipedia page on this is quite good, and for this image and more information you can check out this study.
It's a response to certain Pathogen Associated Molecular Patterns (PAMPs). These are patterns that are present on pathogens - in this case particular bacterial species - and trigger an immune response. Read more about them here. This pro-inflammatory response attracts other immune cells to the area, and helps to drive an immune response, containing and aiding in the elimination of the invading pathogens.
Edit: OP may also be interested to know that if an apoptotic cell is not cleared by a macrophage, eventually it will become "secondarily necrotic", meaning the membrane eventually falls apart and the cell releases it's contents (Source). This turns it from non-inflammatory to an inflammatory response. Neutrophils are particularly adept at keeping their membranes intact, due to the harmful nature of the cell contents. There is a pubmed entry here regarding it, but the actual book I've taken this information from isn't available without subscription.

Necrosis can be described as accidental cell death or damage, triggered possibly from external environmental factors such as exposure to radiation, toxins, excessive heat and etc...whereas, Apoptosis is a programmed form of a cell death mechanism. This process may be used to recycle unwanted cells in the body. Therefore, the particular stimulus that the cell receives may be a key determinant of the cell death mechanism observed.

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Relation between a compound's toxicity and it's concentration level
I know that ammonia is toxic for the body since it disturbs enzymes of mitochondria.
I want to know that why the ammonotelic animals don't get affected by it?
I mean that even if there is plenty of water to remove ammonia from their body, does ammonia not cause any damage till it's inside body?
Does toxicity depends on concentration level?
Can anyone tell me its evolutionary significance?
Sorry for the previous question. .
Actually it was a easy one and I got the answer.
Sorry for the unclarity.;)

I read it .   It was like this-"uric acid being less toxic,can be removed with a minimum loss of water".       Another one-"Terrestrial adaptations necessitated the production of lesser toxic nitrogenous wastes like urea and uric acid for conservation of water".   Am I interpreting it wrong or is there some relation between them?

I read it in our high school book.    I want to know that' is  there a evolutionary significance of it.'... I mean isn't it a coincident  at the same time, a less toxic and less soluble substance is formed?   I want to know how are they toxic to our body and can this TOXICITY be related to LESS NEED OF WATER FOR EXCRETION? Can there be any  structural significance of these compounds in their toxicity?

Toxicity does depend on concentration levels. If you want to know the evolutionary significance, add it to your question. And add the evolution tag to the question so that it gets attention

The article at linked at the bottom says that the marine organisms keep the concentration of Ammonia under very strict control.

pH of the ECF (Extra Cellular Fluid) is said to play a very important role.
The concentration of ammonia in the environment (ambient ammonia levels) also plays an important role.
Less importantly temperature also plays a role.
Ionic strength of water also is involved.

The NH3:NH4+ ratio seems to be more important than the abosolute value of ammonia.

Ammonia is more toxic than ammonium ion. The lipophilic (ammonia is amphiphilic - soluble in both water and lipid) nature of ammonia allows it to easily cross the cell membrane and the blood brain barrier (in organisms where BBB exist) and affect the physiologic functions. The ammonium ion on the other hand can't enter the cell as easily, as it is not as soluble in lipid as ammonia.

For ammonia and marine organisms see http://www.sciencedirect.com/science/article/pii/S1546509801200053
For more on ammonium toxicity see: http://www.ucl.ac.uk/~ucbcdab/urea/amtox.htm

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What would happen to a body in an astronaut suit over time if floating free?
I'm not sure if this is best in Biology or Physics, but on Earth we decay to skeletons and then eventually to dust.  What would happen in space in a space suit?

You are probably going to need to be more specific.  If the body is floating free for an extended period of time then it must be either in orbit around something or really far away from any gravity well.  If it's in sunlight, it will get really hot, if it's not it will get really cold.  How long will the suit stay pressurized? How much oxygen is available until then?  I'm not an expert on this site, but I doubt you'll get anything decent with this question as it stands.

@AdamPhelps. I agree. It heavily depends on where, as close to the sun the answer is very different than in a cold environment far from any heat source. Also the how matters, as the space suit characteristics also matters in terms of heat and radiation that may affect the body

Closed Duplicate. Answer here : http://biology.stackexchange.com/a/20958/8804

That's not a duplicate, though it is very close.  To answer your question Adam, by "floating free" I mean you are ejected from a spaceship between galaxies.  You're lightyears from anything.  Would a suit stay pressurized for 100 years?  Would the oxygen run out?  I don't know, that's part of the question.

@Raoul the moon has little atmosphere and gravity which is not the same as space

@CRags, thanks for that, but I think given the answers to those questions, the more important part is that it is very close to a sun, which apparently makes a huge difference.


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Does Pseudomonas aeruginosa have any common name at all?
Pseudomonas aeruginosa is the fifth most written about¹ binomial name of all species. I'm having trouble coming to terms with the possibility that such a well researched and studied organism has never been given a shorter vernacular name. I can't find one listed anywhere.
Is there any short common name for it? Even a colloquial one? Maybe a pet name common to microbiologists or students in the labs of some particular region? I'm mostly interested in English but how about in other languages?
I am aware it can be abbreviated to P. aeruginosa. I don't consider that a common name. Pseudomonas by itself refers to a genus of around 191 species.

¹ "most written about" meaning mentioned in the most books or volumes of Google Books' English corpus (ngram data), according to my own research. The top five are: Homo sapiens, Escherichia coli, Staphylococcus aureus, Candida albicans, Pseudomonas aeruginosa.

Soil bacterium?

Not as far as I know. It's sometimes referred to as Pseudomonas alone, but not more.

Pythagoras is written about a lot in Philosophy and Mathematics, yet I've never seen a shortened version of his name. Some organisms do have shortened versions, e.g. C. diff. It works. I suspect P. aerug is clumsy to say. Pseudomonas is easy to say.

In medicine, it's often shortened to just "Pseudomonas", but that's about it.

That's odd because I've never heard Pythagoras the Samian, the mathematician, not the sculptor of the same name, referred to by anything but just his first name. Shortening to just the genus "Pseudomonas" might make sense in medicine where infections by other Pseudomonas species are rare (and perhaps treated similarly to P. aeruginosa?), but for microbiologists there are 190 other Pseudomonas species to distinguish between when referring to P. aeruginosa.

I can't think of any common names given to any bacterial species. Is there an example you can give?

Golden staph is the obvious one.

Well in that case, how about "rusty pseudo"…

Staph, Strep, H. flu, Toxo, there are a few more. But partly it depends on how easy it is to say. @Qubei - yes, there are a few other Pseudomonas species that can cause trouble, but P. aeruginosa is by far the most common; if it's a different species, we'd say the whole thing.

The rule for so-called common names seems to be to abbreviate the genus names. Straightforward yet ambiguous.

I think there's a difference between a vernacular or common name ("tiger", "cat", "pigeon", "elm", "pine") and a pet name or nickname as you use it here. The former are names in human languages for a particular kind of animal or plant, while the latter are a colloquial name used by professionals to refer to a particular species, often based on its scientific name.
I can't think of many micro-organisms that have a true vernacular name -- most micro-organisms were given fancy scientific names, and those were used consistently thereafter. The only proper microscopic common name I can think of is "slipper animalcules" -- but I'd be happy to be proved wrong!
Lots of micro-organisms have pet-names -- E. coli, C. diff., "smallpox", "Ebola", "white nose", even Pelagibacter ubique -- but they're either based on the scientific name or on the disease the organisms cause. AFAIK (and based on the comments), Pseudomonas aeruginosa doesn't have one. However, of the list of species you list, only H. sapiens has a vernacular name, while the others only have nicknames based on their scientific name, so I'm not sure it's that surprising! IMO it's mostly macro-organisms that get vernacular names.

Good distinction between vernacular and pet name/nickname, but in the end I am looking for either.


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Is this a grass cell?
I found this picture online claiming it was a grass cell. Clearly it is a cross section image but I was hoping you could tell me if this is actually grass, or something else if anything.

I wonder how many people noticed a little something in this image.

Not a cell but many cells and several tissues, with artificial staining. This is a sort of xerophytic (desert-climate) grass leaf in TS (transverse section). On rain the roll get opened and absorb water.

@user1306322 Yes... Yes I did

@user1306322 Me too... :)

Matram Grass leaf Stained cross section

It's not a single grass cell, but this does indeed appear to be a micrograph of a leaf of grass—so it actually contains numerous cells. Here's another image I was able to find with a much more clear description of exactly what you're seeing:

Marram grass leaf. Light micrograph of a cross section through a closed (unravelled) leaf of Marram grass, Ammophila arenaria. The deeply grooved leaf is thrown into folds (seen here) and it uncurls when mature so that the folds do not face the centre. The folds conserve water and withstand salt, and prevent excessive evaporation. Round vascular bundles are visible inside each fold, serving to transport food and water through the leaf. Spines on the surface discourage animals from eating the leaf. Marram grass is important in coastal ecology, since it is one of the commonest grass species in Britain to stabilize sand dunes. Magnification: x22 at 35mm size. (Emphasis added)
Source: http://www.sciencephoto.com/media/30161/view

And here's another:

Transverse section of Marram Grass leaf , showing adaptations to prevent water loss; outer thick cuticle, curling by means of hinge cells to protect inner epidermis, stomata
  sunken into surface to maintain high humidity
Source: http://www.eplantscience.com/index/principles_of_horticulture/minerals.php

The coloration yielding the yellow 'happy faces' is artificial, either due to staining or direct post-processing of the image.

Happy faces... good adjective for vascular bundles TS ... :D :) :D

This is a transverse section (T.S.) of leaf blade a sort of Xerophytic (Desert-climate) grasses. such as Ammophila arenaria , Spartina sp, Agropyron sp, Poa pratensis etc. However similar-type-adaptation also seen in other (not-grass) plants.
It is T.S. of an object like this.

(highly diagrammatic, actually it is much more thinner, needle-like).
The 2 sides of the leaf develop into different structure. The adaxial ("upper") surface,  which in its underneath contain the  the soft, green tissue, and the abaxial ("bottom") surface which contains more sclerotic tissue.
Normally, when dry-period runs, the leaf remains rolled in an way, so that soft side stay inwards , concave manner, closed, protected from evaporation. The outer, convex abaxial-face acts as a shield.
When rains come; the leaf work in a manner of bimetallic-strip. The inner (adaxial) surface absorbs water and expands (the "hinge cells" help it); and the inner-face become open. Then the inner-face work as a water-absorption tissue.
When dry-period come-again, the leaves enter their original state.
In  the photograph given by you;
The Cells are:

The whole diagram (Colors not realistic. Either The specimen is stained; or image has been processed after photograph) with pointing, is like this.

Iv'e provided a textbook-diagram for it:

Ammophila arenaria , from A Textbook of Plant Ecology / Shukla and Chandel.

Reference : A textbook of Plant-ecology by Shukla and Chandel; S.Chand
College Botany, Vol-1 by Gangulee, Das, Datta; New central book agency .
Studies in botany, Vol-2, by Mitra , Guha , Chowdhuri; Moulik Library Kolkata


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Does the metabolic rate determine how fast the telomeres shorten?
In many papers one can read that telomeres may play an important role in longevity. According to Calado et al.1 the telomeres of mice are much longer than the telomeres of humans. However, mice have an average life expectancy of about 2 years and humans about 80 years.
Does the metabolic rate therefore determine how fast the telomeres shorten? Can one say that the higher the metabolic rate, the faster the telomere shorten?

Telomere dynamics in mice and humans

Note, correlation does not imply causation. In other words even if these two values are correlated, that doesn't mean that one determines the other.

The paper is freely available through Pubmed Central, I added the link for you.

@p.s.w.g I'd rather use a phrase suggested by Tufte: Empirically observed covariation is a necessary but not sufficient condition for causality. The usage of implies in this common phrase is a little dangerous, because in one way, correlation does indeed "imply" causation.

@Alex You're right, of course. Correlation does not necessarily imply causation. I was really trying to point out to OP that the title and the body of the question do not ask the same thing.

@p.s.w.g I agree with you, question does indeed to make this distinction. I just try to comment on the usage of this phrase where ever I see it because the word implies have different meanings in its logical and its common usage, and I've seen some signs if confusions in the other direction. Maybe his other suggested phrase is even better: "Correlation is not causation but it sure is a hint.", depending on the situation of course.

Thx for the feedback guys. I ve rewritten the header. Sorry, i am not a native speaker and so may be my expression is not that clear.


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Largest direct ancestor of humans
Going back the genealogical lineage from present humans to the beginning of life, what was the biggest - in terms of body size or mass - animal in this sequence?
More generally, what would a time vs. size graph look like? Obviously the first ones were tiny microbes, but do we have "deep valleys" and high peaks one after the other? I know that our ancestors at the time of the dinosaurs were very small rodents. Were there some even smaller ones earlier (not referring to the microbes)?

I would tend to think that the tallest individual of a given human lineage is just a Homo sapiens, but I am really not sure. Is there a reason why you are specifically interested in human lineage?

In the absence of fossile records, the standard method for estimating te phenotype of a given ancestor species is to take the average phenotype of the descendent. Such methods is unlikely to give a result indicating a very tall ancestor. Primates tend to be smaller than humans, first mammals were very small, amphibians (sister group) are small, fishes are smaller than humans as well. You can go over the phylogeny here

@Remi.b Because it's my lineage. Just recreationally wondering about it and connecting science to everyday life in my head. I'd like to have a better mental picture of my ancestors.
I was specifically thinking about something like the Dimetrodon. While I know it's not a direct ancestor, it's often included in illustrations because it's a mammal-like reptile. Was maybe the common ancestor of us and the Dimetrodon also quite large?

Oh well. I didn't know about the Dimetrodon. I had in mine that when the first mammals came to existence, they were quite small but that sounds totally wrong when considering the Dimetrodon and the size of the basal mammals (monotremata and marsupials).

Except among the very recent ancestors of modern humans (and there is debate even there), generally we do not consider fossil species as direct ancestors. All fossil species are endpoints, tips of the phylogenetic tree.

@Remi.b the Dimetrodon is not a mammal. I can't find it on NCBI Taxonomy oddly enough, but according to the Wikipedia link you posted: "Dimetrodon is nevertheless more closely related to mammals than it is to any living reptilian group, though it is not a direct ancestor of any mammals."

@terdon Indeed, Dimetrodon (sphenacontidae) is a Synapsida(position on tolweb). the fact that sister species of mammals are quite big suggested that the direct ancestor of mammals might have been big. Looking at the tolweb tree, again, it would be interested to know what cutleria, panetelosaurus, paleohatteria and other closely related groups look like.

We can't really say for sure, because we have insufficient information about this. We can't trace every step of evolution through fossils. We can make educated guesses for most stages of evolutionary history, but they remain guesses.
Please note: Most of what we find in the fossil record are species that are not directly our ancestors, but rather branched off our evolutionary line and then went extinct. Those fossils can still give a good indication as to what the morphological features of our common ancestor were. And a lot of this is guesswork with some evidence behind it.
Going "down" the timeline of humans, we roughly encounter these steps:
Homo
The genus Homo: appeared roughly three million years ago, includes species such as Homo erectus and Homo habilis. Fossils of Homo habilis point to a height of around 100 to 135 centimeters, fossils of Homo erectus are closer in size to modern humans with 145 to 185 centimeters. The rest of the Homo genus was smaller than modern humans (Homo heidelbergensis/rudolfensis/neanderthalis)
Australopithecus
The fossils from Australopithecus are around 3 to 4 million years old, the most famous is probably "Lucy", a member of Australopithecus afarensis. Since members of all Australopithecus species appear to be smaller than humans (afarensis: 100-150 centimeters, africanus: 115 to 140 centimeters, etc.), it is likely that our common ancestor was smaller than modern humans. (Our ancestors likely were Australopithecus, we just don't know which species)
Apes
The split between the line leading to modern humans and the line leading to modern chimpanzees occured somewhere around 4 to 7 million years ago. The clade is called Hominini. The split between those and the line leading to modern gorillas occured around 8 to 19 million years ago (yes, the dates are getting fuzzier). A fossil coming close to this ancestor may be Nakalipithecus nakayamai, however, we only have a fossil jaw from that species.
Going back, we get to the split between modern-day humans/chimpanzees/gorillas and modern-day orang-utans. This is the "ape" family, Hominidae. The largest ape that we know of, Gigantopithecus, that grew to about 3 meters, is classified as an orang-utan. Note that this is not a direct ancestor of humans. Even if our ancestors were larger than modern humans at this point it's unlikely that we are talking about anything larger than a big gorilla.
Primates
Going a bit in the reverse order here: The first true primates evolved around 55 million years ago. Fossils from that time are about the size of squirrels. Humans are "old world monkeys" who first appeared around 40 million years ago - the fossils from that clade we know, for example Apidium or Aegyptopithecus are a bit larger, some as large as a dog.
Primate-like mammals
The first primate-like mammals, called Plesiadapiformes appeared around 60 million years ago. We don't know all that much about them, but the most famous Purgatorius was the size of a rat or mouse.
Mammals / placenta mammals
Going back even further, things become even murkier, but early mammals were small. Placentalia, placental mammals appeared around 90 million years ago. They were small, arboreal (tree-dwelling) animals. Early mammals appeared around 160 million years ago and fossils we have from that time place them around the size of a shrew.
Now, is it possible that there were larger mammals in there somewhere, that then "shrunk" again? Sure. Just unlikely.
Therapsid
Therapsis are mammals and their ancestors, evolved around 275 million years ago. The most well-known fossils from around then are Tetraceratops insignis. All we have from it is a skull of about 9 centimeters size.
Synapsid
Synapsis are making things complicated. As you mentioned in a comment, there were some really big synapsids. According to the Tree of Life project:

Early synapsids were moderately large (body length between 50 cm and 3 m)

Tetrapods
Tetrapods is the name for the clade that encompasses what we now call amphibians, reptiles and mammals - those animals appeared around 380 million years ago. An example of an early fossil from that time is Dendrerpeton, which was up to 1 meter in length.
Vertebrata
Synapsids are vertebrates. Vertebrates first appeared more than 450 million years ago. The time period following that, the Silurian, is called the "age of fishes".  Those fish could get really large, some of their jaws being over one meter wide. That's really all the information I could find.
Chordates
Taking another big step back, vertebrates are chordates, a group that first appeared in the Cambrian, somewhere around 550 million years ago. Early fossils are mostly small, for example Pikaia is about 5 centimeters large. Yannanozoon lividum is around 3 centimeters.
Before chordates
Before chordates, we really don't know all that much, the fossil record is poor because the structures that usually fossilize hadn't even evolved yet. For example, Hiemalora is around 3 centimeters in diameter. Whether it is our ancestor, we have no idea.
And before that come the first multicellular animals, the first animals, the first eukyrotes, and the archae,...
In summary
In summary, while we can only make guesses, the history of animal size from unicellular organisms to us probably wasn't spectacular. We go from very small (pre-Cambrian), to small (Cambrian), large or small (fish and synapsids), around 1 meter-ish (tetrapods), smaller again (early mammals, mammals), a bit larger (primates), again a bit larger (apes), and then to "human-sized".

This is a well thought out answer +1

I believe, you wanted to put Synapsids above Tetrapods.

@EliKorvigo I believe so, too! Thanks for pointing it out.

Therapsids were the largest of the direct ancestors of humanity. Even we can't reach their sizes yet. (Yes our line was probably 6-7 feet in that stage but the largest therapsid which was not in our line, Lisowicia, was a staggering 15 feet long — higher than the tallest human (which was about 9-10 ft)!)
Extra: The time of the therapsids, which was before any dinosaur or crocodilian, was arid and savanna-like — similar to how the place where Homo had evolved. The therapsids also had larger brains, compared to all other organisms at that time, or maybe even the largest (evidence in endocast).

Welcome  Illil. Please take our [tour] and refer to the [help] as and when  for guidance as to our ways. The Therapsids are mentioned in the other answer, but do you have any reference to support your assertion that their size is that great?

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What are the differences between cancer and tumour?
What are the differences between cancer and tumour? I mean is it in the DNA or shape or something else... And how can a benign tumour turn into a malignant tumour? The body has a lot of tumours all the time, however not all of them become cancerous, why is this so?
So my main question is: What is so special about cancer cells that they can get out of control unlike an ordinary benign tumour?

please accept an answer. It is considered impolite when the question has been answered to the fullest and the OP (original poster) has not accepted an answer. It means that the OP is expecting something more. So if you feel that the question has been answered, then please accept the answer which has suited you.

What is the difference between "a car" and a "Volvo XC60"? What is difference between "disease" and "sarcoidosis"? What is the difference between "planet" and "Earth"?

A tumour is simply a space-occupying lesion (something that should not be there, that is; a "lump") caused by abnormal cell replication.
(In medicine, the word "tumour" literally means "swelling", and can sometimes refer to that instead, but that's a different story).
Cancer is a disease in which cell replication is totally out of control. What causes cancer is damage to the genes (DNA) which normally stop cell replication when it needs to be stopped.
There's no such thing as an "ordinary tumour"; all tumours are abnormal. However, what makes a benign (harmless) tumour different from a cancerous tumour is that there is still some mechanisms stopping the cells inside the tumour from replicating; they are doing it more than they should, but they are not totally out of control. When those last mechanisms are broken too, the tumour is cancerous.
(This is a simplified explanation; the actual explanation is a semester-long university course. It's mostly accurate for the layman, though)

Thanks! and where can I get the "actual explanation"? can you give me an outer source for that?(book/site etc)

Wikipedia is always a good start; the article on cancer has a "Further Reading" section down near the bottom.

Uterine smooth muscle tumors other than the ordinary leiomyomas and leiomyosarcomas: a review of selected variants with emphasis on recent advances and unusual morphology that may cause concern for malignancy. ') Just nit picking here, but I do believe many kinds of "tumors" are so common that they deserve the appellation "ordinary". Subcutaneous lipomas, for instance.

Hallmarks of Cancer: The Next Generation is a review article that'll provide a great understanding, sorry for no link, on my phone.

@Kendall here is the link to the 2011 Cell article by the same name. I could download the PDF at home, so I believe it's open-access.

@anongoodnurse You make a good point; I think it depends on your definition of "ordinary". All tumours are out-of-the-ordinary in one sense because they come about due to cellular dysfunction - cells doing what they would not ordinarily do. In another sense, though, I suppose some "ordinary" tumours do exist.

@anongoodnurse I am confused about the title, does it imply that leiomyosarcomas are also ordinary? I agree that leiomyomas are ordinary as are lipomas

Tl;dr answer, tumors are abnormal growth (or swelling, thanks to Malic for pointing out) of any kind. The kinds of tumors are benign and malignant.
Benign tumors are usually slow growing and harmless. Example would be a lipoma.
Malignant tumors are otherwise called cancers. They generally have a bad prognosis. Very few cancers are curable.
Swelling over an injury (which is also called tumor) is due to local transudation (shift of plasma from capillaries). This is temporary and usually goes down one the injury heals.

All of the tumors are abnormal?  I heard that if part of the body get hurt, the body does a tumor on purpose to fix the part that get hurt, is it true? and there is a lot of small tumors in the body at a given moment?

When a part of body swells, it is also called tumor. Thanks for pointing out! @MalicOfSdom. But that swelling is also considered pathological. As it is a deviation from physiology

haa! so every time a part of the body swells it is tumor...scary! and does a benign tumor can turn to a malignant tumor?

Yes, it can occur. Some benign tumors are more prone to malignant change while some practically never do

In general, though tumor can denote any swelling regardless of the presence of any growth, practically speaking, doctors rarely use the term tumor to denote an edematous swelling. So for practical purposes, the word tumor means abnormal growth

ha ok, and when I get hurt for example in the bone, the swell on it is benign tumor?  what is the chance that it will convert to malignant tumor?

@MalicOfSdom Tumors due to swelling in response to injury will never turn malignant. Only benign tumors due to abnormal growth has the potential to turn malignant

and how this turn from benign to malignant obtained?  is it in the genome of the tumor or something else...?

@MalicOfSdom you should post this as a new question. There are many theories in that. Searching in wiki will be of great help too.

one more thing: malignant tumor always strarts from a benign tumor?

Not always, can start from normal cells too

@CRags - you've given a number of incorrect answers here. Curable cancers are not few and far between. Malignant tumors are not always deadly (see, for example, basal cell carcinomas). You should try to stay within provable statements when answering questions.

@CRags - no, I don't agree; if I did, I would not have left that comment. I define "cure" like any normal person: it's gone and will never bother you again. It is possible, and it is done every day, to declare a cancer patient cured. Childhood leukemia is now a largely curable disease; others include some lymphomas, cervical cancer, and others if caught early. Clearly there are some that, regardless the initial response, can still come back. I'm just saying, don't make claims which are untrue. BCC is a malignant cancer with a very good prognosis, if not even excellent.

Yes, I got it. I will be more careful @anongoodnurse Thanks for helping me answer better


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Can methylation of a promoter induce gene expression in some rare cases?
Can methylation of a promoter induce gene expression in some rare cases?
I've read somewhere that methylation of an intron can induce gene expression (eg. Igf2). How is that even possible?
Thank you in advance!

Can you decide if you read this about a promoter or an intron? This makes a difference. Additionally: Do you have any idea where you read this?

@Chris: I'm intersted if a methylation of a promoter can induce gene expression in some rare cases, but I've only read about introns- if they are metilated they can induce gene expression. I really don't remember where I've read this, probably on a website but don't know which so I'll try to find it, though.

There is nothing intrinsic to DNA methylation itself that requires it to repress transcription. Simply, it affects sequence recognition by proteins. CpG methylation can prevent transcription factor binding and/or recruit proteins that inhibit transcription, either competitively or through chromatin condensation. This is why it's generally associated with transcriptional repression.
I have found some articles which describe methylation in intergenic regions and introns activating transcription but, since you're asking specifically about promoters, I'll limit the examples to methylation in the 5' flanking region. Please note that I'm grossly oversimplifying these articles, you should actually read them to get the full picture.

Bahar HK, Vana T, Walker MD. 2014. Paradoxical role of DNA methylation in activation of FoxA2 gene expression during endoderm development. J Biol Chem 289(34):23882-23892
This study reports that, during development, high levels of methylation of a CpG island in the FoxA2 promoter is present in expressing tissues and absent in non-expressing tissues. Their hypothesis is that CpG methylation prevents binding of a protein that represses transcription by condensing chromatin through histone modifications.

Hantusch B, Kalt R, Krieger S, Puri C, Kerjaschki D. 2007. Sp1/Sp3 and DNA-methylation contribute to basal transcriptional activation of human podoplanin in MG63 versus Saos-2 osteoblastic cells. BMC Mol Bio 8(20)
Here, PDPN expression was associated with CpG methylation. They hypothesize that methylation could affect chromatin state or recruit, what they term, a methylation dependent factor, which activates transcription.

Niesen MI, Osborne AR, Yang H, Rastogi S, Chellappan S, Cheng JQ, Boss JM, Blanck G. 2005. Activation of a methylated promoter mediated by a sequence-specific DNA-binding protein, RFX. J Biol Chem 280(47):38914-38922
This study describes a DNA binding protein (RFX) that can recognize and activate the methylated promoter of MHC. They suggest that RFX can competitively inhibit binding of methyl-DNA binding domain proteins that condense chromatin.


text:
Why does a tumour's genome change depending on the environment?
According to the book "Primer of The Molecular Biology of Cancer" by Vincent, Theodore and Ateven, the tumour cell is changed depending on its environment.

performed genome-wide analysis on three tumor samples: a patient's primary breast tumor; her metastatic brain tumor, which formed despite therapy; and a xenograft tumor in a mouse, originating from the patient's breast tumor. They find that the primary tumor differs from the metastatic and xenograft tumors mainly in the prevalence of genomic mutations

Why the tumour cell changing on different places?
why suddenly the breast tumour cells changes on the xenograft tumour and why the metastasis on the brain are now different from the place they came from?
How does this alteration obtained? in the DNA or microRNA or something else?

Tumor cells can have very unstable genomes, as much of the error repair machinery is damaged or missing. Since the cells are rapidly dividing and the DNA gets duplicated each time a cell splits, more and more mutations accumulate as the tumor grows and metastasizes. Just like in evolution as a whole, mutations that are either neutral or help the cell survive better in its environment are kept, whereas cells that develop deleterious mutations (perhaps killing the cell outright, making it more visible to the immune system, or just giving it a growth disadvantage as compared to neighboring cells) either die out or get outnumbered by other cells. This is why, over time, tumors can become resistant to therapies intended to kill them, as their cells accumulate mutations that help it evade the treatment and keep growing. There may be a disadvantage that the cells might grow more slowly than the original ones, but since the original ones were killed by the treatment, the resistant ones survive. So, this means that a tumor is rarely homogeneous, with all the cells having the exact same genome. Deep sequencing using next-generation methods is being used to gather information on all the different mutations throughout a tumor, which can help doctors learn which mutations are most common and prescribe patient-specific combination therapy which can kill all the various cell populations at once.
So why are metastatic and xenografted tumors different from the parent? Metastases can arise from single cells or very small clumps of cells, and xenografts are generally made with very small pieces of tumor, so both may start with a different set of mutations than is common in the original tumor. As they grow and divide, as described above, they will become different from their parents. The surrounding environment definitely affects this: the amount of oxygen present, degree of vascularization and blood supply, number and kind of immune cells present, etc. With all these and more factors, a metastasis or xenograft will evolve differently than its parents.


text:
Can people with paralyzed eye muscles see?
As far as I am aware, the saccades of the eye are central to visual perception. If the eye is held still, the human stops seeing, even if light is reaching the retina and the visual pathway is intact.
But we recently had a question on UX.stackexchange about possible improvements to a visual+EEG interface used for communication with locked-in patients. The designer asking it mentioned that eye tracking devices are unlikely to work, because the patients' eyes can't move. This surprised me, as I would have thought that the patients must be able to move their eyes if they are able to read the device's screen. But I have never had contact with a locked-in person, and assume that the asker knew more about them than I do.
So, are there situations in which a human's eye muscles are paralyzed, so the eyeballs cannot be moved in their orbits, but this human still has visual perception and can mentally process information in his/her field of view?

Why will the human stop seeing if eyes are held still?

@CRags - through adaptation (image fading). See my answer below. Good question, though.

@ChrisStronks Sorry Chris, now got it. I didn't read the full answer. It is nicely explained.

Short answer
Visual perception persists in the absence of functional eye movement.
Background
An example case would be retinal implants wearers. Retinal implants like the Argus II consist of a set of electrodes placed onto the degenerate retina of blind folks. Electrical stimulation of the electrode array elicits flashes of light (phosphenes). Visual input is provided via a head-mounted camera, and the device translates the camera images into patterned electrode stimuli. Hence, because the camera is head worn, Argus II wearers cannot use eye movements to scan the world. They have to use head-scanning techniques. Still they are able to perceive flashes of light (phosphenes) and can recognize simple shapes and perceive motion.
In fact, eye movements such as saccades are detrimental in Argus II wearers, because the oculomotor system feedbacks muscle movements to the brain when a saccade is made to stabilize the perceptual field of view. In normally sighted people the oculomotor feedback system is important, as it tells the brain to compensate the retinal image position shift when a saccade is made. Compensation occurs through a shift in the brain representation of the retinal image to the opposite direction, thereby stabilizing the image representation. However, this is detrimental in Argus II wearers, because the position of the electrode array and hence retinal position of the image is unaffected by eye position. Hence, when subjects use their implant, any saccades will disrupt visual processing, because the oculomotor system will abberantly compensate the perceived location of the object being viewed.
More importantly, perhaps, are micro-saccades. Micro- saccades are small, involuntary eye movements. When images are present stably to the retina the images fade very quickly due to adaptive processes in retinal neurons. Micro-saccades are thought to prevent fading, as they constantly produce small, involuntary fluctuations in gaze, thereby shifting the image quickly over the retina, and thereby refreshing the retinal image and preventing adaptation (Stingl, 2013). When Argus II wearers stop scanning the image, images indeed fade within seconds (Stronks, 2013).
To get back to your question and summarize:
Title question: No, eye muscles are not needed for sight, given that Argus II wearers have sight (though artificial, crude vision). However, a functional saccade system in normally sighted folks improves scanning, and anecdotally micro-saccades prevent image fading by constantly refreshing the retinal image.
Body question: Argus II implant wearers are an example of vision without oculomotor control. Although they cannot use their eye muscles for scanning, they still have functional vision.
 However image fading is a problem in Argus II users and folks without functional eye muscles alike, so head scanning techniques will be needed.
PS: Other implant systems, such as the Alpha-IMS use light-capturing methods inside the eye. Hence these subjects can use normal eye scanning and saccades for scanning. Also, albeit anecdotally, fading is reduced in Alpha-IMS wearers, because of the micro-saccades preventing adaptation (Stingl, 2013).
References
- Stingl et al., Proc Royal Soc B (2013); 280(1757)
- Stronks et al., IOVS (2013); 54(6): 3891–901.

Can add refs when needed later, I am mobile now unfortunately.

Good answer, why are saccades essential to see in a normal person?

@CRags - Thanks! Saccades are not essential, just beneficial for scanning and preventing adaptation. Answer adapted :)

Could you add some references on micro-saccades and image fading? You say "anecdotally" in your answer, does that mean no studies have been performed on it?

@MattDMo. I am still mobile. Will work on refs when possible. Anecdotal evidence is published, but as far as I can see not thoroughly investigated.

Finally - references!

Is the author of the second paper same as the Chris Stronks on this site?

@MarchHo - shush, I'm hiding behind my nick name :-)


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Why is hyper pigmentation the common aftermath of skin lesions and abrasions?
I'm aware that melanocytes produce melanin, giving color to the skin, but why are these cells recruited or overactive when healing skin abrasions, lesions and sores when T-cells and inflammatory cytokines of the immune response help with healing. I'm just wondering why the production of color is associated with the healing of the wound and if it proves beneficial, or if it just a side effect so to speak.
EDIT: In this study, it explains the recruitment of melanocytes after the initially response of innate immune cells and inflammatory cytokines, however, it does not delve into how this is beneficial to the cell.
[source]

It's considered a requisite on biology.se that at least some research is carried out and presented with your question. Otherwise it will be closed as homework. What other cells are involved in skin healing? Certainly more than white blood cells. The site tour and the help center  provide guidance on how to use this site.

I am not fully aware of the details now but I know that IFNγ signaling is involved at some step in the regulation of pigmentation.

The upper layer of the skin (or the epidermis) is formed mostly by keratinocytes and some melanocytes (about 30-40 times more keratinocytes) and also fibroblasts (although they are not shown here). The melanocytes are found in the basal cell layer at the border between epidermis and dermis as shown in the figure below (from here):

The melanocytes spread out their dendrites between the keratinocytes and transport the melanosomes (pigment containing vacuoles) to them to pigment these cells. This is a highly regulated process and depends strongly on the interaction between keratinocytes and melanocytes.
In the so-called paracrine pathway the keratinocytes secret substances which regulate the production of melanin. These are for example alpha-MSH or ACTH, which stimulate the melanocytes to produces more melanin.
This regulation is the key to the hyperpigmentation. During the proliferation or the inflammation chemokines and hormones are produced (and secreted) in the skin which stimulate keratinocytes and fibroblasts. These are for example the keratinocyte growth factor (KGF), as well as the chemokines IL1-alpha and TNF-alpha. This stimulation leads to the production of ACTH (and derived peptides) by the keratinocytes and the secretion of stem cell factor (SCF) and hepatocyte growth factor (HGF) by the fibroblasts which all induce pigmentation. The chemokine secretion is also enhanced from the keratinocytes by KGF. If you are interested in a deeper view at this topic, have a look at reference 1 (and the references in the paper). Reference 2 goes deeper into the regulation of the paracrine signalling.
In an injury (especially in larger areas of the skin) a lot of cells are damaged and need to be replaced. This functions via cell division but also via the migration of cells into the affected area. This is described by the paper you link - here melanocytes and melanoblasts (melanocyte stem cells which can divide and then differentiate into melanocytes) migrate into the injured region to replace the destroyed melanocytes.
References:

Mechanisms underlying post- inflammatory hyperpigmentation: lessons
from solar lentigo
Hepatocyte Growth Factor Establishes Autocrine and Paracrine
Feedback Loops for the Protection of Skin Cells after UV Irradiation


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Trying to differentiate between the three muscle tissues with small pictures
For an assignment I have to differentiate the three types of muscle tissues in these three pictures
.
I'm having difficulty seeing the striations and branches etc. because the pictures are so small. Am I missing something?

The first one is cardiac muscle(it has branches and anastomoses(where they join), the second one is smooth muscle(no striations, single nucleus), and the third one is skeletal muscle(striations, circular fiber structure with membranes).

Without answering the problem for you, because you have not shown work yet to try to figure out which is which, let me tell you that you have three options.

Skeletal Muscle- striated, peripherally located nuclei, same thickness along length, non-branching
Cardiac Muscle- striated, few centrally located nuclei, branches and anastamosis
Smooth Muscle- non-striated, centrally located single nucleus per cell, tapering ends

Now, hopefully, based on your pictures, which are indeed sufficient for you to figure out which is which, you can answer your own question. Good luck!


text:
What happens when the brain is no longer capable of co-ordinating or regulating the heart and breathing rates?
Does the heart no longer function? Does it go into ventricular fibrillation?
What happens?

It's considered a requisite on biology.se that at least some of your reading is presented with your question. [What caused the heart to beat? Why would the heart fibrillate? Etc.] Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

I think this answer needs specification. Total collapse of vital functions by, eg, destruction of the brainstem centers controlling breathing will lead to death. Suppression of these centers by opiates may lead to reduced cardiac and pulmonary function, but not death.  Please specify your question.

@ChrisStronks I'm sorry but I don't see what to specify?

A specific medical condition, or theoretical situation would help, but @CRags has answered already.

Damage to the brainstem - the part of the brain responsible for controlling breathing and the heart - has different effects on the heart and the lungs.
Every heartbeat is not directed by the brain. Instead, the brain has a "throttle" to the heart, by which it can regulate the heart rate up and down, but the actual heartbeat is initiated by special cells in the heart, called pacemaker cells. In the absence of signals from the brainstem, the heart will continue pumping; this is (one of the reasons) why people who need ventilators to breath for them do not also need their heart pumped for them.
Breathing, however, is directly controlled by the brain. Without signals from the brain, breathing will stop completely (the technical term is "respiratory arrest", but that literally just means "breathing-stuff stopped-ness"). Survival time without breathing depends on a number of factors, but at room temperature, without medical intervention (ie. rescue breaths or a ventilator) and barring any special circumstances, is only a few minutes. Permanent brain damage sets in a few minutes later, even if the person can be resuscitated.
Of course, without any breathing, the heart will stop beating due to a lack of oxygen before long. The general progression will be from sinus ("normal") rhythm, to ventricular tachycardia, to ventricular fibrillation, to asystole ("flatlining").

The heart beats are initiated by the pacemaker cells which are located in the heart itself. So absence of neural input will not affect heart function by much. Though heart can function without neural input, it will not be able to respond to stimuli. The human heart rate is regulated beat by beat through the vagus nerve. This would be lost. The sympathetic system would be able to influence heart rate through the adrenal gland. But even this is delayed. Plus till the levels of noradrenaline falls to normal heart rate will be high.
The contractility control also will be lost pretty much.
The respiratory centers are located in the medulla and in the absence  of brain stem outflow the person will be under respiratory arrest which is a medical emergency.

Is neural input not necessary? And "heat" should be "heart"  +1

Neural input to the heart is only regulatory→ it increases/decreases rate, contractility, etc... I will edit answer to give more info, thanks for pointing out the typo @ChrisStronks

This answer fits in well with the other +1


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Repair wrong DNA pair after ending replication?
If there are wrong DNA pair, for example A=G, is there mechanism that could repair such things - after the replication was finished?
Or it happens only during replication?

DNA mismatches and indels can be repaired after replication through an aptly named mechanism called DNA mismatch repair.
I'll briefly describe the mechanism in Escherichia coli, but it's similar in other organisms. A protein called MutS scans DNA for lesions caused by mismatched nucleotides incorporated during replication that escaped DNA polymerase proofreading. These are detected by the kink they produce in the DNA backbone. MutS recruits MutL and MutH; the former activates the latter, which is an endonuclease. MutH cuts the DNA backbone near the lesion in the newly synthesized strand (the one containing the misincorporated nucleotide). This strand can be identified because it has not yet been methylated, while the parent strand contains the original methylation. After cleavage, UvrD helicase unwinds the strand and an exonuclease digests it. The gap around the former lesion can then be filled by DNA polymerase III and DNA ligase.

[ image adapted from ]
Here's an interesting review in a Nature publication that discusses it in more depth, as well as the mechanism in humans:
Guo-Min L. 2008. Mechanisms and functions of DNA mismatch repair. Cell Res 18:85-98

Thank you! Only the link to Nature - page not found.


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Making sense of enzyme Km comparisons
I have encountered comparisons of the Michaelis-Menten constant ($K_m$) a few times. Generally speaking if the $K_m$ of an enzyme is higher, then its affinity to its substrate is lower. How does this make sense?
Maybe the maximum velocity ($V_{\mathrm{max}}$) of higher $K_m$ enzymes is higher? Then of course, $K_m$ can have a higher value. Because $K_m$ is the substrate concentration at half of the $V_{\mathrm{max}}$. But I think we cannot determine affinity with $K_m$.

Since the Michaelis-Menton constant Km is the concentration of substrate at 0.5Vmax, it is an inverse measure of its substrate affinity, because a lower Km indicates that less substrate is needed to reach a certain reaction speed. Hence, a low Km means a high substrate affinity.
Your statement

"Maybe the maximum velocity (Vmax) of higher-Km enzymes is higher? Then of course Km can have a higher value."

is incorrect. Km characterizes how steep reaction speed increases with substrate availability; it does not determine maximum speed.
Lastly, to address your title question, comparing affinities can make a lot of sense. For example, consider the case where enzymes catalyzing similar reactions in different species of organisms are compared. Very low Km means optimal use of small substrate levels, while a high Vmax shows optimized reaction speeds. This in turn may tell you something about optimal habitats and evolutionary pressure.

Am mobile, will add ref later:  http://www.ucl.ac.uk/~ucbcdab/enzass/substrate.htm

To be spesific, here is what my professor says: "Glucokinase has much higher (Km) value for glucose than hexokinase-1. The Km value of glucokinase is 10(micromolar), whereas the (Km) value for hexokinase-1 is 0,1(micromolar). Therefore glucose affinity of glucokinase is low.". Now, lets say glucokinase has 100 times higher velocity than hexokinase, then affinities of these two become about the same.. Because at the Km concentration of hexokinase, they produce nearly same amount of product. (I know that they don't in real because the graphic is not lineer, but.. could I explain myself?)

Affinity to substrate resembles the desire of reaction, which means yield of product? Why should we forget about V and speed then?

No, affinity reflects bonding. Km is measured using Vmax, but the absolute value of Vmax is totally irrelevant for Km. It merely reflects 0.5vmax, whatever the absolute value of Vmax. You are coupling Km and Vmax, while in reality Km says nothing about speed or product. It says something about substrate. Period.

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


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Which of the two mitochondorial membranes relate to bacteria according to the endosymbiotic theory?
I seached for endosymbiotic theory in Wiki and I found this about endosymbiotic theory:

Symbiogenesis, or endosymbiotic theory, is an evolutionary theory
  which explains the origin of eukaryotic cells from prokaryotes. It
  states that several key organelles of eukaryotes originated as
  symbiosis between separate single-celled organisms. According to this
  theory, mitochondria and plastids (e.g. chloroplasts), and possibly
  other organelles, represent formerly free-living bacteria that were
  taken inside another cell as an endosymbiont, around 1.5 billion years
  ago.

But I couldn't find any answer for my question, so I decided to ask:
According to this theory and differences between inner and outer mitochondria and plastid membranes, which membranes (outer or inner membranes) of mitochondria and plastids (e.g. chloroplasts) relate to bacteria?
And why do mitochondria need to have a double membrane?

The inner membrane is that of the engulfed bacteria. The bacterium would have been phagocytosed by a larger cell. Hopefully you can see in this image the smaller cell being engulfed in the membrane of the larger cell:

[ source ]

How and why is the second membrane made?

@Majid Look at the top left image. The outer membrane is from the larger cell. It surrounds the smaller cell and eventually pinches off. Read about phagocytosis for more information.

@Canadianer - yes but in the present situation (nowadays), is the outer membrane organelle-based or host-cell-based? I think that is Majid's question. +1

@ChrisStronks That is entirely unclear to me since the question is about embosymbiosis. In any event, the majority of lipids in the mitochondrial membrane are imported from the endoplasmic reticulum. Some, however, are synthesised by mitochondria in the inner membrane. Lipids can be transported between the two membranes.


text:
Relationship Between Evolution and the Increase of Entropy of Earth
I was confronted by this question:
Biological evolution of life on Earth, from simple prokaryote-like cells to large, multicellar eukaryotic organisms,

A) has occurred in accordance with the laws of thermodynamics.
B) has caused an increase in the entropy of the planet.
C) has been made possible by expending Earth's energy resources.
D) has occurred in accordance with the laws of thermodynamics, by expending Earth's energy resources and causing an increase in the entropy of the planet.
E) violates the laws of thermodynamics because Earth is a closed system.

Answer:  A
However, I do not understand. Biological evolution does cause the system (living organisms)'s entropy to decrease. So, by the second law of thermodynamics, the entropy of the universe (in this case Earth), must have overall increased.
I would answer D... Where am I going wrong?

Life (excluding chemosynthetic bacteria and such) doesn't expend Earth's energy resources, it uses energy from the sun.  So entropy increase on Earth is much more than balanced by the decrease on the sun.  (Or is it vice versa?  I forget which way it goes...)

This sounds like a question a creationist might ask.

The second law of thermodynamic states the entropy can only increases in a closed system. Life is definitely not a closed system. I think that this question would be a better fit for physics.SE

@Remi.b I think this question is a good fit here as well (even though I'm a physicist): this is the application of physics to a primarily biological problem and I think looking at and becoming well versed in this kind of thing is pretty essential for biologists, particularly of they don't want to get wiped out by well funded creationists with very big megaphones.

This area is extremely complicated and has been the subject of historical scientific disagreement, as the Wikipedia entry shows. At the best of times MCQs are, in my opinion, the antithesis of education, but to use them in this context seem to me quite absurd. It suggests to me that the so-called educators of the poor poster were force feeding him some glib line, which they then expected him to regurgitate. I feel for him, but as this was six years ago, I hope he may have recovered from the experience by now.

Related question: Is the principle of “the least energy” a fundamental principle of evolution? How does it stand with the rule “the one who replicate the most”? https://biology.stackexchange.com/questions/101626/is-the-principle-of-the-least-energy-a-fundamental-principle-of-evolution-how

However, I do not understand. Biological evolution does cause the system (living organisms)'s entropy to decrease. So, by the second law of thermodynamics, the entropy of the universe (in this case Earth), must have overall increased.

The universe and the earth are not equatable. Earth is not an isolated system. Life causes entropy of the earth to decrease. This is offset by increased entropy of the sun, which is the primary source of energy for the earth. Overall, the entropy of the universe increases.

It's somewhat disconcerting that this is my highest rated answer…

Yes, for example entropy of the sun decreases, because of nuclear reactions. I suggest to improve this answer so that it wouldn't be overrated.

What if we had no Sun and all the biological process got their energy from Earth's internal energy? There would be no evolution? Please help me understand.

@anthony You should post your own answer.

Okay, added a quick and dirty one, could use some restructuring maybe.

I would say A or D are acceptable, but A is probably the better answer: firstly, the entropy of the planet system alone is probably not increasing (indeed, it's probably near to constant) and as noted elsewhere, you need to consider a closed system to apply the Second Law, so you need to think about everything that comes to and leaves the Earth. This is the key to understanding why life on Earth doesn't violate the second law: Earth absorbs and re-radiates roughly the same amount of light, but that light's state is radically changed as this happens, and this state change and the huge entropy increase it brings about overwhelmingly offsets the decrease in Earth's organisms' entropy as they build themselve whilst making use of that light.
Let's look at the radiation balance in more detail.
The thermodynamic entropy of a system is basically the system's conditional information content (also known evocatively as equivocation in information theoretic circles) conditioned on the given macroscopic properties of a system. It's the logarithm of the number of ways a system's internal microstates can be arranged consistent with the observed outward properties. A simple explanation of the logarithm is that when you add two systems together, the number of ways that they can be arranged multiplies (think of two car number plate letters: one letter yields 26 different number plates, two letters $26^2$ number plates, three letters $26^3$ number plates, three letters and two digits yields $26^3\times 10^2$ number plates and so forth). So the entropies add when the possibilities multiply.
The entropy of a system of identical particles is proportional to the number of particles in that system. Think of each particle as like a letter in an alphabet of its states and then think of long "number plates" of concatenated particle states.
So now: let's look at the input to the Earth: around about $1{\rm kg}$ of energy in the form of sunlight per second is available to Earth systems to do work. It comes as $\frac{c^2}{h\,\nu}$ photons per second, where $\lambda = \frac{c}{\nu}$ is of the order of 500nm so $\nu\approx600{\rm THz}$. That is, about $2\times 10^{35}$ photons per second.
The energy output of the Earth is basically infrared heat: it's the same amount of energy as comes in, but it is now composed of many more photons, because now $\nu$ in the photon number $\frac{c^2}{h\,\nu}$ is of the order of $30{\rm THz}$ (corresponding to $\lambda=10{\rm \mu\,m}$). The Earth therefore radiates roughly twenty times more photons than it absorbs: about $4\times 10^{36}$ photons per second. Each photon can encode the same amount of information, so the entropy increase is roughly twentyfold. Life systems on Earth use about one thousandth of the incident Solar energy: it has been estimated that photosynthesis fixes energy for use by life systems at the rate of about $100{\rm TW}=10^{14}{\rm J\,s^{-1}}$, compared with an input of $1{\rm kg\,s^{-1}}\approx 10^{17}{\rm J\,s^{-1}}$. So, no matter how complex life organisms get, this barely makes a dint on the massive entropy "production" of the total Earth energy cycle: the nett production of entropy by the whole Earth system is still strongly positive notwithstanding the presence and evolution of life, and therefore in keeping with the Second Law.
An interesting calculation has been done on how much Solar energy is needed to evolve life on Earth to the present day. This is presented in the paper:
Emory F. Bunn, "Evolution and the second law of thermodynamics", Accepted for Publication Amer. J Phys.
Bunn calculates that less than a year of sunlight would be enough to power the evolution of all life on Earth over the last four billion years and still be in keeping with the Second Law.
I should cite where I first saw this idea for explaining the life versus second law problem: I took this line of argument from:
Roger Penrose, "The Road To Reality: A Complete Guide to the Laws of the Universe", 2004 Chapter 27, "The Big Bang and its Thermodynamic Legacy"
but I have heard it used in several lay explanations of physics since.

My 2 pennies on this discussion
Entropy in general is the total number of states a system can occupy which is also called degrees of freedom (so is with the supply of heat, the molecules vibrate and can occupy more states). Any system tries to avoid confinement and maximize the number of states it can occupy. However if the system is in a stable state and any movement would cost it energy, then it would remain in the present state at the cost of reduced degree of freedom.
This relationship is described by this equation: ΔG = ΔH -TΔS Where ΔG is change in the Gibbs free energy, ΔH is change in enthalpy, ΔS is change in entropy and T is the temperature.
Though the process of natural selection destroys the number of phenotypic states that life can occupy, thereby causing a decrease in entropy, there are other processes which lead to gain in entropy (for example population growth and migration). Note that the process of reproduction itself creates order from disordered molecules, but as the population expands and spreads entropy is again maximized. As already pointed out by bobc, catabolic processes which fuel life processes increase entropy but anabolic processes do the opposite.
So my opinion is that the process of Natural Selection reduces entropy, so is the formaton of the eukaryotic cell. A free living bacteria has more freedom than a cell-locked mitochondria. However there are other energetic benefits that balance this reduction of entropy.
For earth I would guess that the overall entropy has reduced because the earth has cooled down since its birth. Since heat is removed entropy has reduced.
There is no violation of the second law in any of these cases. It is a universal law.

The correct answer is almost D: Life on Earth has occurred in accordance with the laws of thermodynamics by consuming Earth's free energy (which is continually being replenished) and causing an increase in the entropy of the universe. Life maintains it's own low entropy by increasing the entropy of it's environment. The Earth radiates energy of lower entropy than it receives (see citation 3), thus increasing the entropy of the universe. This happens by re-radiating the short wavelength radiation received as longer wavelength radiation. Life contributes to the process of converting the former to the latter. The outgoing radiation is in the form of more but lower energy photons than the incoming higher energy photos from the Sun. Keep in mind that the energy into the Earth is approximately equal to the energy out of it.
Useful resources for looking into the subject more:

Ulanowicz, R.E. and Hannon, B.M., 1987. Life and the production of entropy. Proceedings of the Royal society of London. Series B. Biological sciences, 232(1267), pp.181-192.

Schneider, E.D. and Kay, J.J., 1994. Life as a manifestation of the
second law of thermodynamics. Mathematical and computer modelling,
19(6-8), pp.25-48.

Kleidon, A., 2010. Life, hierarchy, and the
thermodynamic machinery of planet Earth. Physics of life reviews,
7(4), pp.424-460. – Anthony 1 hour ago

The answer is A because D implies a fallacy that Earth is a closed system.

Read carefully and notice that I didn't propose D and specifically point how it is not a closed system. The closed system is the universe.

Yes but some of the other answers were much more clear on that.

Well I guess time will tell us where voters' reading comprehension is at.

Excellent reference list - at least, from a physicist's point of view!

The Second Law is one of the most misunderstood and misapplied laws of thermodynamics. It has a scope largely confined to physics, nothing more should be read into it. Simply put, it states that "Heat cannot spontaneously flow from a colder location to a hotter location". (Wikipedia) There is nothing about life that violates that, or creates "negative entropy".
When you get into the details, you need to consider closed vs systems, and equilibrium vs non-equilibrium systems.
In fact, life contributes to positive entropy, like everything else. Energy at high potential is transformed to low potential, at the same time creating useful work and waste heat. Note that "useful work" can include storing energy in a form useful for future use.

Although I agree with the broad scope of your argument, however I requires some further referencing! but still a nice response!

Sometimes the reduction of entropy is balanced by reduction in enthalpy (for e.g. RNA folding).

It is A for one simple reason the ultimate source of energy that drives evolution may be earth or the sun.
First Additionally it is arguable if a multicellular organism has less entropy than ancestral prokaryotes since there were far far more iterations of prokaryotes.
Evolution has no effect on individual organism's entropy. Evolution can only occur in a system that is consuming energy. To put it a different way if I build one car and then build a second more complex one, building the second car has no effect on the entropy of the first. So you can only be looking at the process itself, in which case the traits of the organisms are irrelevant.
Consider sorting in geology, particles can be sorted into organized patterns, but only if there is enough energy to move them in the first place. Sorting in theory might decrease entropy, but it can only occur if there is an overwhelming increase in energy to drive it. for living things ,depending on the organism, that energy/entropy may be coming from the earth or the sun, in the latter case the entropy of the planet may not be effected depending on how you define it.
That said that is a horribly written question, because sunlight could be considered part of earths energy resources, and it is written in a way to confuse different usages of entropy.

Evolution increases complexity (entropy)
e.g., developing a new citrate path way in E. coli
It does this process by of expending energy.
i.e., via lifeforms's metabolism
So to answer your question:
A,B,C are all correct (or part of a correct answer)
However D is the most correct answer (It is an all of the above type answer)
E is a none of the above answer (and most incorrect)

There is no way of breaking the second law of thermodynamics. And you "don't get away with it" by "using the the 0th and 1st". The second law is only valid for closed (energetically) systems, which the earth is not. So it is not correct to use this law here.


text:
Kinetic Vs Potential Energy in Biochemical Contexts
This question is causing great confusion in my head.
Which of the following is an example of potential rather than kinetic energy?
A) the muscle contractions of a person mowing grass
B) water rushing over Niagara Falls
C) light flashes emitted by a firefly
D) a molecule of glucose
E) the flight of an insect foraging for food
Answer:  D
A) Muscle contractions is caused by the use of potential energy in ATP used by actin and myosin.
B) This is a classic example of what potential energy means.
C) Bioluminescence is a process caused by the use of chemical (potential) energy.
D) Yes, the molecule of glucose does contain potential energy. BUT, it is not potential energy itself...
E) Flight is kinetic energy. However, you can still boil this down to ATP in actin and myosin.
How do I approach this problem? My teacher said this is the type of problem she would give us. But this is so ambiguous. Am I lost?

If you find one of the answers solving your problem accept it. Doesn't matter which!

I think you are right and many examples are ambiguous.  Even D) is ambiguous as a molecule is always in motion due to entropy except, perhaps, at absolute zero (0 Kelvin). But normally, it does contain kinetic energy.
However, as you already identified the ambiguity, look at the best, or in this case least incorrect answer; The only option without any physical movement explicitly mentioned in the question description is D). All the others mention 'emit', 'flight', 'rushing down', etc.
Also ask your teacher :)

Is emitting really a form of kinetic energy? Maybe they were referring to "light energy" and not the potential energy that was used to make the light.

A moving photon has, however small, kinetic energy

Going by the answer, the key to interpret this question seems to be the absence of kinetic energy.
Total Energy (mechanical) = Potential + Kinetic (let's ignore the pressure component as this question does not involve it).
So the key to answer this question would be a system where the full energy is represented by the Potential energy.
In a contracting muscle - let's consider gross dynamics - the muscle is in motion (the myofibrils are moving) ~ Kinetic Energy
Water moving in a falls - Definitely kinetic energy (In fact this system is one where the potential energy is constantly decreasing while the kinetic energy is increasing constantly)
Bioluminescence - Light Energy which is neither kinetic nor potential (as I understand physics, so correct me if I am wrong)
Glucose as a source of energy - In its unutilised state (only during which it is called glucose) is purely potential energy. When glucose is talked in terms of potential energy, the movement of glucose inside a medium is not what is being talked about.

Yes, well broken down answer +1

You'll find the answer glucose best fits the definition of potential energy, as in it's standard state the glucose has all of it's energy stored in it's bonds (1). Every other answer is some sort of expenditure of energy (ATP in the case of firefly luciferase reaction, see (2)).


text:
Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?
I read these two from various books, and got confused. The confusion is -
Reticulospinal tracts control gamma motor neurons. Gamma motor neurons control tone of muscle.
In decerebrate rigidity, the reticulospinal tracts are cut, so the gamma motor neurons start firing excessively, and SPASTICITY develops. I understood this part and why Decerebrate Rigidity is a misnomer as it is actually spasticity.
Question is, in decorticate rigidity, the cerebral cortex is damaged. The basal ganglia are intact. One explanation I found is that the basal ganglia keep the reticulospinal tract activated so gamma motor neuron is under control. But if basal ganglia have no direct communication with brainstem or spinal cord, and their efferents pass through cerebral cortex, then even in decorticate rigidity, the reticulospinal tract should not be working, and thus the gamma motor neurons should fire excessively, in which case the decorticate rigidity also becomes a spasticity.
Am I missing anything? I am keeping red nucleus and vesticular nuclei out of this just to make matter simple. My question is about activity of gamma motor neurons in these two conditions. I hope you got the question. Thank you.

Interesting question, and presented with nice explanation of your difficulty. +1

1)
a. Decorticate posturing means rubrospinal tract is the dominant output to the motor neurons of the body... maybe dominant is the wrong word, I am not all that knowledgable on this subject, but it is certainly altering the standard reticulospinal tract based extensor posturing.
http://en.wikipedia.org/wiki/Rubrospinal_tract
It is responsible for the strange flexion of upper limbs (aka arms). I say strange because when you think coma you think extension, not flexion. The lower limbs (aka legs), as always is extensor. Why the upper limb but not the lower limb? The red nucleus may play an additional role in controlling muscles of the shoulder and upper arm via projections of its magnocellular part.
b. In decerebrate posturing the rubrospinal tract is also cut, since the lesion is below the red nucleus. In this scenario the reticular activating system (aka reticulospinal tract) is the dominant output to the motor neurons of the body. Here you get the classic extensor pose, for both upper and lower limbs...
The point is: Rubrospinal tract was what you were missing. The red nucleus is the specific part of the basal ganglia that is involved...

2)
the difference between spasticity vs rigidity:

spasticity is an increased resistance to the passive movement of a
joint due to abnormally high muscle tone (hypertonus) which varies
with the amplitude and speed of displacement of a joint.
rigidity is an increased resistance to the passive movement of a joint which is
constant throughout the range of joint displacement and not related
to the speed of joint movement.

your supposed to test this out on patients to get a feel for what's the difference.
spaciticity is the case for upper motor neurons lesions (ex. stroke), since the spinal reflexes are not being inhibited from above...
an example of rigidity in neurology is Parkinson's disease, which is the loss of the substantial nigra, which like the red nucleus is also in the midbrain... while the the substantial nigra and basal ganglia loop do influence the motor control of the body... they are not upper motor neurons. Upper motor neuron is specific to the corticospianl tract, it is the neuron going from cortex to anterior horn of spinal cord. Basal ganglia does influence the motor cortex but it isn't part of the corticospinal tract, hence not an upper motor neuron lesion.

3)
Role of muscle spindles in spasticity from upper motor neuron lesions:
I am using this website for this part of my answer:
http://www.d.umn.edu
it's from university of minnisota, which is funny because their acronym is UMN

high resistance to stretch occurs when the spindles are overactive
  (usually due to high rate of gamma motor neuron discharge) -->
  HYPERTONIC (SPASTIC)
removing inhibitory inputs to the gamma motor
  neurons increases their discharge rate, and increases spindle output
this can happen when there is an UPPER MOTOR NEURON lesion

It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes are intact so the a/g-motor neurons should relax, since only UMN damaged and not any part of the reflex arc. I seem to be missing something here.
I'm calling for back up, someone please help!

I'm sorry but this doesn't answer my question. My question is why only in Decerebrate rigidity, we see gamma motor neuron overactivity. Red nucleus plays a part in pathogenesis I agree, but the rubrospinal tract ends on alpha motor neurons and not on gamma motor neurons. Another thing which I would like to correct, Red Nucleus is not a part of basal ganglia, but a part of extrapyramidal system. Also basal ganglia have no direct connection to brain stem, they have indirect connection through cortex.

this website has something at the very bottom of the page: http://www.d.umn.edu/~jfitzake/Lectures/DMED/MuscleReceptors/SpindlePhysiology.html It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes intact, only UMN damaged.

Not sure if this helps but its what i know after reading my class notes on reticular formation.This may not help but as I trying to learn also I will share.
Decorticate - The motor part way/Rubrospinal no longer has the influence of the higher centers such as the corticospinal - Flexor Response
Decerebrate - The lesion happens below the red nucleus therefore the rubrospinal spinal tract is not functioning - Extensor Response

Since in decorticate posture the lesion is at the level of neurons which originate from cortexand relay in the basal ganglia...but since basal ganglia are still intact they do influence in controlling increased discharge rates of gamma motor neuron. Moreover red nucleus is dominant here since no input from motor cortex flexor posture is present that too in upperlimbs since rubrospinal tract ends in cervical spinal cord.
Decerebrate means no rubro no cortex no basal ganglia...so gamma motor neuron are like "yay, i'm free now" so they keep increasingly discharging causing spastic extensor response...

Overall well-written answer... Please add some reliable references though


text:
How long can a human neuron live outside the body in a controlled environment?
Have there been any experiments that have kept neurons alive (stationary), without preserving methods such as freezing? If yes, then how long were the cells kept alive for?

Do you mean primary cultured neurons?

You can look into culture protocols. For example this one suggests 7-10 days for culture maturation, then 2 weeks harvest time (scroll down to the last step). While a protocol won't tell you the longest time, it will give you a lower limit for the longest time. This is about nonhuman neurons of course, but there are also human cultures started from stem cells.

According to this paper from 2001, they've got the survival time up to about a year on average. The trick is sealing the neuron inside a permeable membrane so you don't actually risk contamination when feeding. This paper lays out experiments that take many weeks to perform, so as far as I can tell the science of keeping neurons alive has advanced to 'as long as I keep feeding them and nothing bad happens'.


text:
Why do the proportion of predators increase at mass extinction events?

Why does predation surge with mass extinction? It is caused by extreme selective pressures over resource competition that forces certain species to adapt to predatory niches?

Interesting question. Do you know whether this pattern repeat with the 3 other mass extinctions? Can you please link to the article who produced this figure? That will probably help.

@CN7 What book/paper is the graph from, and how to they discuss the dashed ranges?

The data used in the graph you posted seems to be from Bambach. 2002. Supporting predators: changes in the global ecosystem inferred from changes in predator diversity (in Kowalewski & Kelley. The Fossil Record of Predation) - see fig 19b - and, if so, is specifically dealing with marine predators.
I don't have time to look at that paper closely (it is quite long), and paleoecology is not my field, but a couple of relevant sections are:

However, the diversity of predators and the proportion
  of total faunal diversity composed of predators have both increased over time, implying that ecosystems have
  increased their ability to support either more predators or more specialization among predators. Also, turnover
  in diversity dominance among predator groups, with more energetic predator taxa replacing or being added to a
  fauna of less energetic groups, implies that the energy available in marine food webs has increased.

and

If
  the efficiency of energy transfer between levels in
  the food pyramid has stayed nearly constant (and
  there is no evidence that it has not), then a reasonable
  hypothesis for the increased proportional diversity
  of predators is that either the biomass of prey species
  has increased or the populations of prey taxa have
  become more stable (or both), permitting greater
  specialization by predators on more reliable food
  supplies. Thus, predators could increase their
  proportional share of total diversity by specializing
  on fewer prey taxa.

So according to the author, energetics, energy flow and predator specialization seems like likely reasons for the change. However, the paper also discuss factors such as rates of fossilization and also the fact that predators are generally rarer than prey means that there is probably more stochasticity in the fossil occurence process, which could affect estimated turnover rates and maybe also the proportion between predator and prey. You'll have to look at the entire paper for a fuller picture, and maybe somebody more knowledgeable can fill in later. I also think that you need to look at radiation patterns in certain taxa to fully understand these stepwise changes, and also to consider oxygenetion events as possible underlying reasons, but these are just my speculations.
The reasons given above also in one sense echoes the "biotic" explanation for the latitudunal diversity gradient (see e.g. Gaston, 2000 and Mittelbach et al, 2007), where high levels of primary production can support more specialized predators/parasites in more complex food webs, then leading to higher species diversity. So there might be interesting connections to contemporary patterns and processes of biodiversity as well. However, I haven't seen a compilation of %predators over different biomes or latitudes to match the graph in the question. Also, the "biotic" explanation for the latitudunal diversity gradient has been criticized and is not without problems (see papers above for more).


text:
After how many generations descendant is not more related to ancestor, than to a random individual in an ancestral population?
Descendant of n generation has on average 1/2n DNA of ancestor. (For example children have 1/2 DNA of parents and 1/4 DNA of Grandparents, After 10 Generation 1/1024 DNA and after 100 Generations 1/2100 DNA).
Is there a point (value of n) when descendant is no more related to ancestor and is similarly related to random individual from an ancestral population.

Welcome to Biology.SE. Your question sounds like a Coalescent theory question. Do you assume that no mutations and no selection in your model? The answer will very likely depend on the population size.

Thank you. Answer will likely depend on effective population size. logically mutations will decrease value of n and selection will increase or decrease depending how it favors certain DNA.
I just did not thought about this and wanted to know if this is even possible, that descendant is no more related to ancestor than to random individual from an ancestral population.

There is an interesting way to look at this question. By definition, two individuals are related only if they have a common ancestor. (If you mean something else by it, please correct me. For completeness, I include the trivial case in this: that is, I regard you as one of your own ancestors.) So your question can be inverted: it is really asking after how many generations everyone in the ancestral population is your ancestor?
As indicated in the comments, the answer will depend on the specifics of the population structure, including its size. But a first stab can be taken in this way: you had 2 ancestors one generation back, 4 two generations back, ..., $2^n$ (not necessarily distinct) $n$ generations back. So you certainly cannot be descended from everyone in the ancestral population if less than $\log_2 N$ generations have passed. ($N$ = population size, which for simplicity I assume to be stable.) In a freely mixing population under the very simplest assumptions, you will eventually decay exponentially towards complete coverage with a half-time of one generation.
This is complicated by the fact that some lineages die out completely. For instance, some of the individuals in the ancestral population didn't have any children. Some had children, but no grandchildren, etc. Obviously none of them were your ancestors, so you will never be related to them (except through previous common ancestors), no matter how much time passes. In fact, as time passes, more lineages tend to die out. So, if you look back very far, you'll find that the entire current population has only a very small numbers of ancestors in the distant past. This is called coalescence, and is what people are talking about when they speak of "mitochondrial Eve", for instance.
So, in summary, it's complicated. It takes only a fairly small number of generations ($O(\log_2 N)$) before you're potentially related to most of the ancestral population. But over longer times ($O(N)$ generations) your relationship to the ancestral population actually goes down.

Thank you for answer, very interesting.
My question is slightly different, will make it more clear:
Is my DNA more similar to Mitochondrial Eve or Y Adam or it is not possible to distinguish from other individuals who live with Mitochondrial Eve or Y Adam.
I understand that Mitochondrial DNA and Y chromosome is not recombining, but they have higher mutation rates than autosomal DNA and also, they are just a small part from total DNA.

Your mitochondrial DNA is more similar to that of mitoEve than to her contemporaries. Your Y chromosome is more similar to Y Adam than to his contemporaries. Other regions of the genome will trace back to one of them, or to other humans living in the distant past. It's hard to say a lot more without making detailed assumptions about the genetic structure of the population.


text:
Can Helicobacter pylori be eradicated naturally?
This question is not to discuss whether substances that have anti-H. pylori activity work or not, or to discuss the pros and cons of such but from a medical perspective.
Assuming that one is able to control, reduce, or eliminate H. pylori via foods containing natural anti-bacterial activity targeted at H. pylori without the consumption of antibiotics, what is the possibility of reinfection or an overgrowth with H. pylori?

In this study, the bactericidal activity of Korean and Japanese wasabi roots, stems and leaves against Helicobacter pylori were examined... All parts of wasabi showed bactericidal activities against H. pylori strain NCTC 11637, YS 27 and YS 50.

My questions are:

If this method was carried out in vivo and the results were found to be consistent with the research mentioned above, what is the chance of developing resistance to H. pylori?
Will developing resistance prevent recolonization of the stomach lining with H. pylori?

Bactericidal activity of wasabi (Wasabia japonica) against Helicobacter pylori

Your sentence is quite confusing. Could you break it up in some meaningful way?

Do you have any evidence that you can clear H. pylori with foods? Can you share that?

To clarify - By eradication, I mean symptoms disappear, but not confirmed by testing.

Then you have not eradicated the infection.

Ok I tried, but here's what I've come up with http://www.ncbi.nlm.nih.gov/pubmed/15246236

So my questions is, if this method is carried out in-vivo, what is the chance of developing a resistance to h.pylori? And will developing a resistance prevent the re-colonization of the stomach lining?

+1 for showing your research. This is the response that saves a question from closure. I've edited your question to add the research and revised questions.

There is a flaw in your logic. You are saying that the foods have antibacterial properties and then say can the infection be eradicated without consuming an antibiotic. If you eating something that actually has antibacterial properties, then whether you like it or not, you are consuming an antibiotic. Just because it didn't come in a pill made by GlaxoWellcome, Pfizer, Merck, etc, doesn't mean it isn't an antibiotic, just that it hasn't been standardized, had safety and efficacy tests done, and been proven in clinical trials to be scientifically effective.

H.pylori is a bacteria that is a cause for Peptic ulcer disease of human being. It helps to create more acidic product and causes ulcer. But human body is naturally protected to H.pylore, but excess stress,irregular life style etc helps H.pylori to growth and causes ulcer. Simple measure can escape you from this infection. 1. Intake enough water 2. Maintain oral hygiene is very Imp, 3, at bed time gurgle by H2o2 ( Hydrogen per Oxyde) 3. If you are infected then triple therapy for 3 weeks is the choice of treatment

Can you please add some references for your claim?

I am a registered physician and from that respect I answered

@fazlerabbi Still best to add references.

@fazlerabbi Great to have experts here. Still references are required. If they come from your practice, there should be something available like guidelines etc.

My answer was from my own knowledge,but Here I am giving a ref. Hope it will be helpful. JOHN HOPKINS MEDICINE Health Library (p00373)

If I understand you correctly you would want to eat lots of wasabi and the likes to decrease/eliminate the bacterial load of H. pylori in your body.
Concerning your questions -

to be perfectly blunt here - The chance to develop resistance to a bacterium by temporarily eating something is close to 0. This can be explained by two factors:

1 - resistance could develop spontaneously due to mutations and the likes, however the chance is incredibly low if not 0 (nothing in biology is ever impossible ;) ).
2 - if you only temporarily consume an antibiotic substance you will only be protected as long as the substance is active in your system. Surely you could eat wasabi every day, but would you want to for the rest of your life? Additionally, resistance to bacterial pathogens seems to be a temporal situation since their "ability" to incorporate foreign DNA into their own arsenal as well as spontaneous mutations turns the pathogens into ever changing organisms and while you might have been resistant to the "old" bacterium, the newly mutated or modified version could still harm you - unfortunately (This is one of the reasons why it is so hard to develop anti bacterial vaccines).

If - and only if! - you would be resistant to the bacterium, than this should in theory protect you from further colonization of said bacterium. As previously mentioned this is a currently very unlikely scenario due to the limitations science is facing.

IF sources shall be needed just comment and I will search the web for something suitable ;) Hell, I might even get the chance to cite some of my own papers, finally ;)

Yes please add sources to allow users to background read on your answer

There is many possible antibacterial natural treatment using probiotics provided by natural product such kambucha,Baikkimchi,kefir (1,2,3).In the other side,plant oil extracts also studied in vivo and in vitro (4,5,6) ,but in  general, all result was relative that we can not be cured 100% with such therapy.
source:

http://nordicfoodlab.org/blog/2013/2/komboooucha
http://link.springer.com/article/10.1007%2Fs13765-014-4198-6
http://www.ijaaonline.com/article/S0924-8579(05)00054-3/abstract?cc=y=
http://cmr.asm.org/content/12/4/564.short
http://onlinelibrary.wiley.com/doi/10.1111/j.1348-0421.2004.tb03521.x/full
http://www.sciencedirect.com/science/article/pii/S0378874107004370

Which of those links are you claiming shows in vivo efficasy in humans?  Because as far as I can tell, none of them do.