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When someone gets infected with influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?
A friend thinks that being infected with a new influenza virus means that little immunity is gained, unless you get a vaccine. But, he is forgetting that new strains can make current vaccines out-dated.
I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine.
When someone gets infected with the influenza, and gains some immunity, is that immunity just as good as getting it from a vaccine?

Hi and welcome SE isn't for settling arguments. However, generally speaking - yes.

@Andrew Perhaps I can get information, statistics or something that could convince him.

@Andrew there's no reason that someone couldn't come here with a valid question to settle an argument or debate, it happens all the time. That's what factual knowledge is for, to dispel inaccuracies.

Not really answerable, unless you define what you mean by "just as good".  If you get immunity to (a particular strain of) the influenza virus via a vaccine, you don't have to experience having the flu.  If you get it from having the flu, you do.  IMHO that makes the vaccine better :-)

@MattDMo Okay - but I've received that criticism before.

@Andrew It's all about the subject matter and the way the question is posed. If a debate is purely opinion-based, too broad, or otherwise not on topic for the particular site, then it should be closed as such. If it is on topic, like this one, it should be accepted. IMO, whether or not there's a debate or argument at the root of the question is irrelevant. You shouldn't have been criticized for that.

Yes, infection-acquired immunity is (generally speaking†) just as good as, if not better than, getting vaccinated. Remember, the whole point of a vaccine is to simulate an infection and stimulate immunity without having to suffer through the actual symptoms of a real infection, potentially getting very sick or even dying. This is regardless of whether it's a "new" strain of virus or not.
† Not all exposures lead to good immunity, whether via infection or vaccination. Many times this can be related to immunosuppression or other immune system defects, but age and other factors like co-morbidities can also play roles as well.

For your addendum, the same can be said for some exposures that produce minor illness even when the immune system is functioning well.

Natural infections almost always yield a better immunity than that acquired through vaccination. However, vaccines yield a better immune-response than getting infected with influenza. That is so to say the side effects.
I want to backtrack to part of your questions where you say I'm sure the immune system will "remember" that particular strain just as well as getting a vaccine. and add a little bit of interesting information regarding influenza.
Some Influenza (A) stereotypes that infect humans are: H1N1, H2N2, H5N1, etc...
The H stands for Hemagglutinin and N is Neuraminidase. These are important in vaccine development. The H and N are proteins located on the surface of the virus and allow for entry into a cell for infection.
Strains are classified according to their hemagluttinins and neuraminidases. Every year when the vaccine for the seasonal flu is developed we don't know with 100% certainty which strain might be the most prevalent. Rather, surveillance data is used in deciding which flu might be the most prevalent. More info on the CDC Website.
So back to the question:

Does the immune system remember that particular strain just as well as
getting a vaccine?

Yes it does and there's a paper in PNAS that looked at something similar. This is related to something called “Immunological Honeymoon”. A theory that the first infection during childhood provides stronger immunological memory than a later infection.

The paper found that people who were 28 year old were more susceptible to the Spanish Flu (H1N1) in 1918 because they had been exposed to the wrong virus as children.
The elderly, however, had been exposed to H1N1 as children and were well protected. People who were middle aged or in their teens in 1918 had been exposed to H1N8 as children and were partially protected.
This I recon is just as good as vaccine, but more to show that the immunity acquired through infection is, in fact, remembered. For how long? That's a totally different question that varies from infection to infection. Some are life-long (such as measles), other are short lived requiring re-infection, or booster shoots in case of vaccination.


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How do injected purified anti-D antibodies prevent the natural production of antibodies in order to prevent Hemolytic Disease of the Newborn?
Treatments involving Anti-D antibodies are given to pregnant women carrying Rh+ fetuses when the mother has an Rh- blood type in order to prevent Hemolytic Disease of the Newborn during the 2nd pregnancy. The anti-D antibodies are injected during later stages of pregnancy and right after birth in order to eliminate any Rh+ blood cells in the mother before D-antigen antibodies are produced naturally by the mother. If antibodies do not attack cells directly, what stops the mother's macrophages from engulfing the antibody bound Rh+ blood cells, becoming an antigen presenting cell and hence initiating the process of producing antibodies and saving the antigen in memory cells? Are the Fc receptors on the macrophages not compatible with the injected anti-D antibodies?

I think you've misunderstood some of this. The treatment doesn't involve giving someone anti-D antibodies to destroy Rh+ cells - indeed, those antibodies would cross through the placenta and potentially cause the disease in the newborn. An antibody treatment based on Rho(D) immune globulin does exist, but this functions by preventing the immune response which would otherwise cause the production of anti-D antibodies.

Hmm, it seems even I was wrong in part - the treatment involves "a solution of gamma globulin containing anti-D" according to Rudmann's textbook (p439)

@Astrid_Redfern Thank you very much for your input. Still, if the gamma globulin contains anti-D, then my question is still relevant right?

I think your question is indeed relevant. I'm doing a bit of research to see if the antibodies really are intended to destroy the Rh+ red cells, as I'm not sure if that's their purpose.

Related: https://biology.stackexchange.com/questions/35531/why-is-the-administration-of-exogenous-anti-d-not-harmful-to-the-foetus

Made a bit of progress by learning that antibodies can either be of a neutralizing or non-neutralizing nature: https://en.wikipedia.org/wiki/Neutralizing_antibody
"Neutralizing antibodies on the other hand can neutralize the biological effects of the antigen without a need for immune cells"
The anti-D antibodies in Rh Immune Globulin are of a neutralizing nature: https://www.sciencedirect.com/science/article/pii/B978012374432600035X  Could it be that sensitization is avoided because the Rh Immune Globulin does not tag the Rh+ blood cell for phagocytosis by macrophages?

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What is the purpose of co-translational transport?
During intracellular proteins synthesis, all proteins are made by free ribosomes in the cytoplasm and some, but not all ribosomes (those which make membrane or secretory proteins) move to the endoplasmic reticulum (ER) and attach to it during translation (called co-translational transport).
Why are proteins that will be exported to the outer of cell are not made in the ER directly?
What is the function of ER in intracellular protein synthesis?
What is the purpose of co-translational transport?

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The secreted proteins are not made in the ER because ribosomes cannot get into the ER. Even individual ribosomal subunits are much larger (at least 10-fold greater in volume, if not hundreds of times greater) than a typical protein, so it is much easier to translocate the protein being produced by the ribosomes across the ER membrane than to translocate the ribosomes themselves. Even the protein being produced must be at least partially unfolded as it is being translocated.
That's not even taking into account that the mRNAs would need to be translocated as well if the ribosomes were to translate them while in the ER. The mRNA is again many times the mass of the protein (a nucleotide is ~3-4 amino acids "worth" of mass, and there are at least 3 nucleotides per amino acid encoded, more if you add the untranslated regions).

Why don't secreted proteins use post-translational translocation?

Trying to translocate the protein after it has already been completely synthesized and folded would require disruption of an already stable structure, as well as presumably expose lots of aggregation-prone peptides. With co-translational translocation, only a short stretch of amino acids has been translated but not passed through the pore, and this is protected from the surrounding environment by the seal between the ribosome and the pore. This also means that the folding process inside the ER is able to act like a kind of "ratchet" that helps pull the protein through.

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@NatdanaiBoss many proteins are indeed post-translationally translocated. I am no expert on this subject, but here's a review and here's a recent paper that describes the structure of the translocation complex.

Why are proteins that will be exported to the outer of cell are not made in the ER directly? What is the function of ER in intracellular protein synthesis? What is the purpose of co-translational transport?
This is a eukaryotic cell that we are talking about.Once the mRNA is synthesized , it has to move out from the nucleus to the cytoplasm.During its exit, SRP (Signal Recognition Particle) recognizes specific signal sequences in the mRNA and forms a complex with that mRNA.then SRP complex targets ER membrane proteins for cotranslational-transport.
If the secretory proteins are not moved into the ER , disulfide bonds would not be formed from cysteine residues . Because the necessary Enzymes required for this process are found only and only in the ER (namely PDI and ERO1).
Plus, these secretory proteins often have to be glycosylated to perform their action correctly.The Enzymes are located in the ER.
Moreover I believe that these secretory proteins will aggregate and degraded later if they are not transported into the ER.
I do not know WHY this process exists this way. That is Evolution and it is just about adaptation to the environment and not necessarily based on pure logical reasons.
Further readings : Molecular Cell Biology Lodish et al 8th ed at sections 13-1
and 13-3.
In addition see : Protein translocation across biological membranes , Targeting proteins to membranes: structure of the signal recognition particle  Post-translational translocation Regarding to Ero1 and DPI
Formation and transfer of disulphide bonds in living cells

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How to do manual Saccharomyces tetrad separation with minimal equipment?
I would like to separate the four ascospores from individual asci by manual microscopic manipulation without at micro-manipulator and a basic dissecting microscope capable of 600X total magnification and a fine needle. Is this possible? My guess is that human hands would not be steady enough. But what did they do before micro-manipulators were commonplace?

Careful centrifugation can separate tetrad from individual spores. Do you mean breaking up the tetrad and isolating individual spores.

Yes, I mean breaking up the tetrad and isolating individual spores. I am trying to do this without buying much equipment. There are complete yeast tetrad separation systems that are $$$. A micromanipulator mounted to a microscope  with 600X magnification seems to be the preferred method. I'm wondering if anyone has experience doing this technique with as little expensive equipment as possible.


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Why WHO has not eliminated chicken pox like smallpox?
Chicken pox is a viral disease, so why then has the World Health Organization (WHO) not eliminated chicken pox like smallpox?
Smallpox still exists in labs.

Eliminating a virus from the world is an immensely costly undertaking. As with most things in real life, cost vs. benefit (and feasibility) need to be taken into account. Unfortunately, there is a limited amount of money available to fight disease.
The overall mortality rate of smallpox is about 30%. That's a very high mortality rate, one that shaped history significantly.
By contrast, of a yearly 4 million people who contracted chicken pox (in the US, before the vaccine), only 100 to 150 died each year.
The death rate of smallpox: 30%. The death rate of chicken pox: .00375%
Maybe someday chicken pox will go the way of small pox. But our limited monies need to be devoted to eliminating viruses that cause greater harm, e.g. polio and others.
Also, not all viruses are equally "eliminatable", e.g. H1N1, HIV, etc.
Smallpox Vaccine: The Good, the Bad, and the Ugly
Monitoring the Impact of Varicella Vaccination

As well as the risk associated with the viruses (as explained in anongoodnurse's answer), chickenpox isn't a good candidate for elimination because of its lifelong carrier state. With smallpox (like polio and measles, which are also candidates for eradication) there is no carrier state, so eliminating the virus at one time point means the virus will not return.  With chickenpox, you could eradicate every active case, and next week an adult carrier will start shedding the virus again and start new rounds of infection.  There is as yet no way of eliminating the virus from carriers, so it's impossible to eradicate chickenpox or any other virus that enters a similar long-term latent/carrier state, which includes all the herpesviruses, HIV, adenoviruses, etc.

I like the complement this answer provides but references would be important. Biologists never trust anything said without references ;)

True, but every unvaccinated generation that dies reduces the risk. Also, there is a zoster vaccine that greatly reduces the chance of shingles. Additionally, shingles is far, far less contagious (direct contact with vesicles or a surface recently in contact), so what you say is misleading. None of that is to say, however, that it would be very easy to eliminate varicella-zoster even if money were no object.

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PEGylation safety and hybridomas
PEGylation is the covalent attachment of PEG (PolyEthylene Glycol) to molecules (e.g. proteins). It states in wikipedia   ("PEGylation"):

The covalent attachment of PEG to a drug or therapeutic protein can
"mask" the agent from the host's immune system (reducing
immunogenicity and antigenicity), and increase its hydrodynamic size
(size in solution), which prolongs its circulatory time by reducing
renal clearance

It seems  to be a widely used method in phrmacology.
(Other medical uses for peg PEG - as a laxative- macrogol, and as an excipient in some drugs.)
However, there is another use for PEG which is to fuse B cells with immortalised myeloma cells in order to produce hybridoma cells for the production of antibodies. That means, PEG have the ability to fuse two cells together.
How then, it's considered safe to use it as a drug? How come it doesn't fuse cells inside the body (when taken orally or intravenously)? Under which conditions is this property (cell fusion)  of PEG observable?

Can you provide a citation for the cell fusion function of PEG? Bear in mind also that PEG is a polymer; molecules of different MW will have different activities, and those bound to another molecule will be different from PEG in free solution, etc.

wikipedia "Hybridoma technology".:  Once splenocytes are isolated from the mammal's spleen, the B cells are fused with immortalised myeloma cells. The fusion of the B cells with myeloma cells can be done using electrofusion. Electrofusion causes the B cells and myeloma cells to align and fuse with the application of an electric field. Alternatively, the B-cells and myelomas can be made to fuse by chemical protocols, most often using polyethylene glycol.

Looking at the indicated protocols, they specify the myeloma cells should be split the day before fusion so they will be in "log phase" that is, constantly dividing. Normal cells don't do this in the body so that may be a factor.


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Why does vacuum sealing of foods prevent spoilage from anaerobic bacteria?
I have noted that many purchased food items in containers only require refrigeration after they have been opened, thus eliminating the vacuum seal.  Air contains bacteria and fungus spores that enter the food container and if not refrigerated, the aerobic micro-organisms will proliferate, thus altering and rotting the food.  The air also allows any dormant micro-organisms that survived the factory sterilization process already in the food to come back to life and proliferate.
However I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers.  That plus the fact that we can leave already opened food items such as honey, jams, and peanut butter out of the refrigerator for weeks but they do not spoil.

I'm betting most of those foods are sterilized with heat either before or after being sealed in their packaging, similar to how you would can foods at home, just on an industrial scale. The vacuum seal functions to prevent microbial contamination of a sterile product, not just to prevent aerobic organisms from growing.

Honey, jams, and peanut butter each have antimicrobial properties on their own that help delay or prevent spoilage.

I think honey, jams, peanut butter antimicrobial properties isn't directly what prevents or helps with avoiding spoilage. It is their water activity being quite low. The water activity of peanut butter is typically 0.35, which inhibits the growth of spoilage and pathogenic microorganisms.

Just adding a little bit more info taking from the answer above.
You got two types of anaerobes:

Facultative anaerobe that makes ATP by aerobic respiration if oxygen is present. It can switch to fermentation or anaerobic respiration if oxygen is absent. Most common example of a food pathogen in this category: E. coli

Obligate anaerobe which are killed by normal atmospheric concentrations of oxygen. Example: C. botulinum, which is mentioned in the answer above.

I am using C. botulinum as the example here because it is widely used in making HACCP (Hazard Analysis Critical Control Point) plans. These are plans with certain steps which make sure that what you're producing is proven safe for consumption.
Now, C. botulinum vegetative cells die in the presence of oxygen. The spores allow the organism to survive when there's lack of nutrients and/or oxygen levels are too high. The spores are also heat-resistant. C. botulinum cannot grow below a pH of 4.6, so acidic foods, such as most fruits, tomatoes, and pickles, can be safely processed in a water bath canner.
If the pH is above 4.6 there's usually a CCP (Critical Control Point) in the HACCP plan to make sure the product is pasteurized. For C. botulinum that is a kill step at 85°C for 5min minimum to destroy the toxin.
Another product example would be cold brew coffee. You need a certain % of dissolved O2 so that C. botulinum doesn't proliferate since cold brew coffee has a high pH (>4.6 usually).
Another problem with Reduced Oxygen Packaging (ROP), not related to anaerobic bacteria, is mold growth. To mitigate this some products might have the air present in the bag replaced with nitrogen then flushed. Nitrogen Flushes in ROP can reduce the rate at which mold can grow.
TL;DR: They do grow but there's certain steps each company needs to take to prove safety of their product before sale. If your HACCP plan accounts for C. botulinum you're sure to knock out a wide majority of obligate anaerobes (if not all) that could grow in your product.

I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers

They do. Vacuum sealing can prevent aerobic bacterial growth but does not prevent anaerobic growth.
Botulism is a particularly dangerous consequence. If food containing C. botulinum spores is sealed without being properly treated (usually by heating) or otherwise by being inhospitable to bacterial growth (often due to acidity or salt), dangerous botulinum toxin can accumulate and be dangerous or fatal when the food is later eaten.


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Can a broken Swordfish's bill bone regrow?
The Broadbill Swordfish (Xiphias gladius) is characterized by a long bill or a "sword" which is an extension of its upper lip bone. The swordfish uses its sword in fighting, including attacking hard objects, which may cause it to break. Like all bones, it can heal after being broken but can it regrow back to full length?


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Has synthetic biology created new plants or animals as of 2013?
I've seen a Ted.com talk where the speaker suggests that modern science can create new micro organisms, like bacteria with a pre- defined new set of traits. But has anyone create a new species of plants or animals using synthetic DNA yet? If so, what are their names?

None yet as far as I know.

Can you define "new"? Is a genetically modified species "new"?

nope, only bacteria as of this time.

Answering your question
Well, considering there is a plethora of facilities that deal with the cloning of plants and animals, as well as altering specific DNA in order to create a better plant or animal. Tests have been done with rats to try and create stronger and smarter rats, and tests have been done on countless other animals to try to develop immunity to dementia and Alzheimers. In the agricultural industries of the world, new types of corn, tomatoes, rice, and other types of crops are engineered on a daily basis, and new versions of these plants are made very commonly. The problem, however, is that a vast quantity of these plants are rejected from being planted. Some plants that are engineered either taste too bad, or they are less efficient than the plant at which they were modifying. As far as inventing a new species, you have to be more specific as to what you are asking. If science creates a new animal from another animal, it is likely of the same family and genus, like breeding a dog from another dog. Creating another type of mammal or reptile or bacteria that isn't part of a specific genus would be a breakthrough, as I am sure that all types of cloning and scientific pairing have been done to the same general Genus and Species... I am assuming, however, that it will be possible to engineer lifeforms at the molecular level by the next 50 to 100 years, as science and technology is getting more and more advanced. So, by the next few centuries, it would only seem logical to assume that new species would be created. However, the practice of creating new species, or even operating a laboratory/facility that deals with the concept, is illegal in a large number of countries, and has several guidelines in others.
I am only 13, so if any of this information is to be used anywhere else, I would advise not to cite me as a credible source. All this information is from my knowledge, and my knowledge is from school studies and personal readings. This is all my information, though. If any wording sounds similar to another source, keep in mind that one human brain functions similarly to another on several accounts and coincidences are often found.  I can assure you that if the documented information above is verified by plagiarism experts as my own wording, as I have taken the liberty to scan my own work. I hope I answered your question, and I am sorry for the long disclaimer ranting of this paragraph.

If you have referred to a source, it's okay to paraphrase as long as you cite where it came from.

hey its great to see someone 13 starting to contribute here!

The answer is no.
At this moment (2016) the are only two synthetic organisms that are being constructed or have been constructed.
The first is a synthetic Mycoplasma genitalium.https://en.wikipedia.org/wiki/Mycoplasma_laboratorium Made by venter
The second is synthetic yeast, S. cerevisiae http://syntheticyeast.org/
There has been talk of building a synthetic human genome... but that is only talk.

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Why porifera is classified to have an incomplete digestive system although it has no organs?
Why are we using the term "incomplete" for digestive system only? We could have also said that for circulatory system that it is either incomplete or present as a simple system. What I mean is that, this doesn't relate to the definition of organ system. In other words, it will mean that the only organ system present in lower animals is digestive system.
Also for other organ systems, it is written that they are absent. What is the reason for this wording?

My advice would be to just learn what these labels are saying about the features the organisms have; the labels placed on them are not really important for "understanding the world", just for communicating with other people (like your biology instructors). Understand the system, then apply the label; don't use the labels to try to understand the system. The biology existed before the label.

An incomplete digestive system is one in which there is only one opening.  In our digestive system food is taken in by one opening (our mouth), the nutrients extracted and the remains are ejected by another opening (our anus).
In these lower organisms the food is taken in by one opening, the nutrients extracted and the remains are ejected through the same opening.
An absent digestive system is not having such a method of ingesting matter to be processed and ejected afterwards.  These organism absorb their required nutrients directly from the surrounding media.


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How well evolution is supported by experts? Are there acceptable scientific objection to evolution?
There are people in internet , with professional sounding voice , who claim that evolution is not scientifically possible (such as there is not enough time for evolution, or modern genetics has disproved it and what not!) or not even well supported in the scientific community. Here in Bangladesh, with a fundamentalist population, we are not even thought evolution that well, teachers avoid that and recently evolution has been forcefully removed from government textbooks. (So forgive my question is dumb) What will expert say? I am confused.

This is such a broad question that it's hard to know where to start. https://en.wikipedia.org/wiki/Level_of_support_for_evolution ; https://en.wikipedia.org/wiki/Evidence_of_common_descent

Experts say that evolution is the only scientifically valid and accepted theory that accounts for our observations of the biological world. The Berkeley Understanding Evolution website is a great resource for learning about evolution.

See also: Alternative models to natural selection, but you'll find that none of them have any traction in terms of superiority of explanatory power or consistency with the known observables. They're pre-scientific or non-scientific in approach.

As a problem in biology (the evidence for evolution) this is too broad a question for this site, as has already been said. Taken at face value, this is a question about scientists, not biology, and not appropriate for this site. I therefore think the question should be closed. But, to be kind: Regardless of whether they are right or wrong, almost all biological scientists employed in reputable universities ("experts") do not question evolution and regard the question as settled 100 years ago. It is the context in which the subject is viewed and nobody would waste time even discussing it.

the stated clearly series has some really good basic introductions to evolution. https://www.youtube.com/user/sciencestatedclearly

Those theorists are unscientific, because they trust scientific medecine for i.e. a paternity test, for a crime test, and do not trust the same science for i.e. species proximity test. They are unscientific because they don't trust fossils i.e. of hominids, early mammals, birds with teeth, and the 100% verified transition from lizards to mammals recorded in the sedimentary photographing process. In the USA the origin of species is doubted by 40% as well. There are many other logical certainties pseudscientists must deny to refute origin of species.

I’m voting to close this question because I agree with the comment: "As a problem in biology (the evidence for evolution) this is too broad a question for this site, as has already been said. Taken at face value, this is a question about scientists, not biology, and not appropriate for this site."

It's a fact.
Natural selection, adaptation and genetic changes have been observed and documented several times.
But in the end, it's not about who's right, but, who has the better explanation to describe what we observe in our world.
Evolutionist denyers will have an extremely hard time explaining ...

... the appearance of atavisms
... why humans share 98% of their DNA with chimpanzees
... why humans share 50% of their DNA with fruit flies
... why every living being (including bacteria) share the identical genetic code (genetic code = why the DNA sequence "GCC" will add Alanine to proteins, while "GTC" adds "Valine", etc.)
... the evidence described in this video

There are no explanations that explains all that without assuming that all living beings are somehow related with another, since that's how genetic information is passed on. That's why it is considered a fact that every lifeform shares a common ancestor.

Thanks. But they have "explanation" of any problem , you know that.

@Zeesan: These 'explanations' are either based on misunderstandings, religious agenda, or other things. They are not based observing nature. Because that's what you gotta do: Observe nature. Those people that want to tear out evolution pages out of school books have NOT sat in the woods and watched birds through binoculars for months. Because that's actual work. Quick 'explanations' are lazy, but doing the right thing takes hard work. And scientists do that work, because they're crazy enough to well.. doing things like watch birds for months/years/decades or inventing DNA sequencing...

if dna is accepted as evidence in criminal cases in your country you can be pretty sure they know about evolution.


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Why is the "mango fly" called a "mango fly"?

Cordylobia anthropophaga, the mango fly, tumbu fly, tumba fly, putzi
fly, or skin maggot fly, is a species of blow-fly common in East and
Central Africa. Wiki page

Why is Cordylobia anthropophaga among other names called the mango fly? I can't seem to find anything online about why they gave it this name, and I figure they don't eat mangos.


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How does Clostridium perfringens cause target hemolysis?
I am studying microbiology as a part of my course and I was studying Clostridium perfringens.
While studying its hemolytic characteristics, I came to know that it causes target hemolysis (i.e. zone of beta hemolysis due to Theta toxin surrounded by zone of alpha hemolysis by alpha toxin).
Surprisingly alpha toxin has a Phospholipase-C (PL-C) like action. Isn't PL-C supposed to be Beta-hemolytic? Since it will lyse the RBC membrane?
[Alpha-hemolysis is supposed to be conversion of hemoglobin to methemoglobin]


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Questions regarding transformation in bacterial cells
First off, in transformation the donor DNA aligns itself with the complementary bases in the recipient DNA.
Now a "perfect" alignment of the donor DNA ( Sorry if my terminologies are incorrect ) would mean that an exact replica of the donor DNA fragment already exists in the recipient DNA. If such is the case no genetic recombination will take place but genetic recombination is observed, this is the part where I get confused.
If the DNA fragment is aligning itself with the donor DNA and and causing a genetic recombination, then obviously the donor DNA fragment should contain some variation from the recipient's DNA. This would mean that the alignment of the DNA fragment isn't perfect and not every base in DNA fragment can form a complementary base pairs with the recipient DNA. ( Again sorry for usage of improper terminology as I'm a new student who just started an introductory course pertaining to microbiology ).
Now the problem is -

Shouldn't it be energetically unfavorable for the donor DNA fragment to replace the original DNA as the original one should be able to form complementary base pairs with the entirety of the recipient DNA while the donor DNA can do so only with a part of the recipient DNA.
After thinking about this, I thought of an assumption to explain this. The RecA protein involved in transformation is somehow forcing this process to happen. The thing is how? I have zero knowledge of enzyme chemistry and can't understand how this could possibly happen?
So is this assumption correct? If so is there any reference material explaining how RecA protein could be doing this?

This brings me to the second issue. This newly created DNA should now have many irregularities, how are they fixed?
After some thinking, I came to the conclusion that as RecA proteins are involved in DNA repair, the RecA protein simply fixes the irregularities. Is this line of thinking correct?

In short, I have assumed that a RecA protein is causing a DNA fragment which can not form complementary base pairs with the entirety of recipient DNA to be accepted in the recipient DNA, following which the irregularities that arise are also fixed by RecA. Is this line of thinking correct?

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly. In particular, questions must be focused enough to be answerable on this site — we cannot recreate textbook chapters! We also expect you to do research and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Your questions are both too general and based on imagination rather than looking up readily available facts. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Too many notes! Too many notes!

Transformation is done using plasmids right? So why are you concerned about recombination with the 'primary' bacterial genome?

@Roni Saiba im talking about the transformation as observed by Frederick Griffith's experiment in 1928 using virulent and non virulent strains of Streptococcus pneumoniae. Am I mistaken and does this type of transformation happen only through Plasmids?

@David im new to this website, can you please explain what are the " notes " you are referring to? ( I'm sorry if this somehow sounded rude, English isn't my first language )

Anish. Sorry for being obtuse. Welcome to the site. It's a good idea for new users to read the Help on Asking Questions. You should make sure that you are asking a single question about a problem in biology and set it out so we are clear what it is. This is a question and answer site, it is not a place to ask for comments on your general thoughts or difficulties with a topic.

@AnishKumar it is also good to have a question title that exactly states your actual question. For example you could ask "how does a completely foreign DNA recombine with genomic DNA during transformation/HGT". Also, as others suggested do not ask multiple questions (and ask one precise question) but it is good to provide a good background as you tried to do.


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Identification of butterfly from its caterpillar stage
Today I visited Bannerghatta national park's butterfly park situated in Bengaluru, Karnataka, India.
I snapped a picture of a caterpillar in butterfly park.
I inquired to caretakers over there for the identification of the caterpillar. However, They were confused and didn't give me any answer.
I tried searching with the google lens application, however, it shows parasitism and not caterpillar identification.
Please help me identify this cute caterpillar.
Below is the picture I took.

Euploea Core.
Pupates into common crow butterfly. (Aka. common Indian crow, common Australian crow, oleander butterfly (link to caterpillar)).
A common butterfly with (according to Wikipedia) 15 subspecies identified, prevalent in south Asia, and Australia - the adult is distasteful to birds as the caterpillar feeds on latex-bearing plants.
The exact mixture of colours in the caterpillar stage will depend on the diet.
It has a neat trick when attacked, it shams death and oozes a sticky fluid which when ingested by birds make them vomit they find it so distasteful. The butterfly will then "miraculously recover" and fly off, with the bird having learned to avoid that type.
Unable to post images at the moment, so put links instead.


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What is the optimal temperature for Omicron to thrive in?
I have always been under the impression that when sick, you should let a fever run its course. The accepted answer to the question Why do people take drugs to lower a fever? seems to provide some support for the theory and cites optimal temperature which says that most bacteria and viruses thrive best at 98.6 F. I was wondering how much variance there is to this optimal temperature and if some bacteria and virus infections can thrive at hotter temperatures? If so, I would think that studying the optimal thriving temperatures for various bacteria and viruses (including omicron) would be important to decide whether to treat, or let a fever run. With a quick google search I could not find any studies on the optimal temperature for omicron.

I think it's fine for this question to stand as a Biology question, but I think it asks the wrong thing if it's intending to use this as support for "should a fever be treated or not"; see https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem and https://biology.stackexchange.com/a/57974/27148

Omikron is really new, don't expect comprehensive data on it. Even with SARS-CoV2, there is still much to learn and I am not aware of any "optimal temperature" studies (and I can't even imagine a design of such a study).


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Why are green monkeys (West Africa, Barbados) green?
Melanin in fur, hair and bare skin (eumelanin, pheomelanin) does not create green colors, which is why green mammals are so rare....
Green sloths (Americas) are covered in some sort of algae, which explains their coloration....
But what about green monkeys?  I can find no explanation....


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Why are there no trees in Texas?
In Texas, there is lot of grassland and many cotton fields, which need a great deal of water. However, I have not seen any forests or areas with many trees.
Why are there no forests or heavily-treed areas in Texas?

Texas A&M disagrees. Even western Texas has some trees. The cotton farms are probably all in the east, and might be heavily irrigated, not familiar with taxes cotton farms, but I know Missouri cotton farms are in the southeast corner and get a lot of water.

I've edited the question and nominated it for re-opening. I think it's clear what the OP is asking, even if the premise is faulty.

Because the settlers cut down a lot of the trees in order to make cotton fields?

Cotton was not grown where the forests are today , too much rain. The forests were cut for lumber , became pasture , and most have regrown forests today.

A quick google image search reveals that, indeed, Texas has quite lush forests. Remember that the state is extremely large (as compared to the Northeastern states, for example), and encompasses a huge variety of terrain, climates, rainfall amounts, etc. While the stereotypical view of Texas is rugged, dusty terrain:

From: http://texasmountaintrail.blogspot.com/2013/12/big-bend-landscape.html
The eastern part of the state borders Louisiana, and is definitely not dusty and dry:

From: https://www.flickr.com/photos/horwath/2488138213/
Rainfall varies across the state from east to west:

From: http://www.worldatlas.com/webimage/countrys/namerica/usstates/weathermaps/txprecip.htm

There are many different reasons why trees are not very likely to grow in certain regions, and these may vary from place to place. There may not be enough precipitation to support trees that are not adapted to a drier environment, while some species of grass could survive just fine. Temperature changes could be too severe between summer and winter (grasses just go dormant or die during harsh winters, and regrow in the spring). Fire is a big issue, as well - prairies often burn, and while grasses can regrow quite quickly, a tree that doesn't mature for 20 years may not make it between fires. Grasslands also have very deep, tightly-intertwined root networks, with some reaching 15 feet (~5m) or more below the surface:

(Click image for higher-resolution PDF)From: http://www.conservationresearchinstitute.org/educational-offerings.html
Tree species that survive the other challenges may not be able to penetrate deeply enough to adequately take root, sustain itself, and not fall over. Also, speaking of which, grasslands tend to be susceptible to tornadoes as well, and while grasses just bend before the wind, trees get uprooted or break. So, while any one or two of these issues may be overcome by a particular tree species, when added together it translates into a very inhospitable environment for trees.

how to explain places with lots of grass but barely with trees in Texas?

@questionhang there are plenty of places like that across middle America, and around the world. Here, we call it "prairie," in Europe and Asia it's called "steppe," and in southern South America (especially Argentina) they call it "pampas." There is sufficient rain for grasses, and trees can survive if planted and maintained, but they generally do not prefer to grow there.

@That is what I ask. Why do not they like to be there? Precipitation is still not enough?

@questionhang see my edit above for some reasons.

This Texas tips his hat to your thorough and well illustrated answer. I hope the question remains up so others can enjoy it!

@Matt   Thank you. You wrote a lot. But you missed my main point. There are lots of drought-enduring trees like http://en.wikipedia.org/wiki/Populus_euphratica.  Why is there only grass?  In western Texas, you can see only grassland sometimes. Water is not a problem for many trees if  large-area grassland exists.

@questionhang my last sentence should address your question. There are drought-resistant trees, and fire-resistant trees, and flexible, tornado-resistant trees, and trees with deeply-penetrating root systems, and trees that are resistant to extreme changes in climate, but not all in the same species. It's not any one factor that prevents trees from growing, but the combination of them all together.

One more factor that needs to be considered in the reasons why some areas were grassland/prairie before European settlement is grazing.  There were herds of millions of buffalo (estimates range around 50 million) migrating around the plains, in addition to other grazers.  Trees would generally be eaten before they had a chance to grow.  Grasses and other prairie plants could have their tops eaten, yet sprout again from the roots, much as a lawn does after mowing.

Born and raised in Texas here. I think people have a hard time comprehending the size of Texas. It has every climate (except extreme cold) and terrain. The coast is tropical and humid. The west is hot and dry desert. The central part is lush hills. The east side is forest, thick forest (see piney woods and Big Thicket)

Texas has lots of trees with many varieties of native and non-native trees. Texas is almost 1000 miles across, understanding it's massive size give reason to it's various types of flora.
http://www.texasmonthly.com/the-daily-post/how-big-is-texas-compared-to-other-land-masses/
Due to elevation, temperature and the growing medium trees will grow at differing rates. Someone previously mentioned animals will eat plants so it's a balancing act in nature. I've watched squirrels propagate the seeds to have rabbit and deer eat them. In a drought most food is is up for consumption by the wildlife. Certain trees like the Dessert Willow will grow in some of the dry arid areas of Texas where you won't normally see trees.
https://plants.usda.gov/core/profile?symbol=CHLI2
Back to the question; trees can be planted and may even flourish if maintained and given the opportunity to grow. The problem is it requires investment and most people want to see a monetary return in their life time. Mankind has a hard time looking beyond 10 years and trees able to survive in a desert climate can easily take 50 years to get 3-5 feet in height.
I've noticed in the 50 years I've been alive, trees have always added to the value of land in one form or another, so keep planting!

Each part of the Earth is divided into temperate zones depending on their latitude. Texas happens to be considered a Temperate Grassland. Temperate Grasslands are usually dominated by herbaceous vegetation. Because of where Texas is located on the Earth it has high summer temperatures which encourages fires. These fires help exclude woody vegetation such as trees and usually limits trees and shrubs to margins of streams and rivers. These grassland vegetation vary from about 5 cm in dry, short grass prairies to over 200 cm in the wetter, tall grass prairies. Of course there are still going to be trees in Texas but there will not be forests like along the coasts of the Atlantic Ocean. Those are considered to be in a different temperate zone called Temperate Forest. These areas usually have more rain and temperatures are not as extreme as Texas.

Your answer is too general.  http://en.wikipedia.org/wiki/Populus_euphratica is not able to survive if we plant them with large tracts of land in western Texas?

@questionhang: Why would we want to introduce an alien species that has no obvious ornamental or food value?

@  My question is whether we should introduce them or not, but why are there no these kind of trees in Western Texas or even Africa. They can survive easily.

@questionhang: See the above answers, and also my comment re grazing.  Also, if you look at prairie regions generally, you find that people do plant drought-resistant trees as shelter belts around houses &c.

@jamesqf then why are not drought-resistant trees popular in Western Texas or even Africa? People have to plant them!

Looking at the great colored map above : Most of the area east of "green " is pine forest with some oak savanna and coastal marsh. Guessing , that area is bigger than any state east of the Mississippi. There are interesting timber museums in towns like  Nochadoches and Lumberton. I live in an east TX area that was clearcut before the 30's ; today it is mostly 100 ft ,4 ft diameter loblolly pines ( which keep me from sleeping during a wind storm.) . Much of this land is national forest because taxes were not paid during the depression because the land was worth little after the timber was gone.

Unfortunately I learned these thing over 25 years ago when i cleared pines off a homesite . Counting tree rings showed most had started growing in the mid 1920's. I also found very old barbwire in the forest from the old pastures . But I did not post it on the internet in 1995 , so for a millennial , i guess it did not happen?

In 20th Century, an overwhelming reason that few Great Plains trees survived without irrigation or wet flood plain soils, is too little rain & snow!
Historically folks used the 100th Meridian as a rough border.  From the 95th to 96th Meridians in Minnesota & Manitoba angling to the 97th to 99th Meridian in Texas then westward to the foothills of the Rocky Mtns (except the Black Hills) most upland soils are naturally treeless.

In the ustic, aridic & xeric moisture regimes, the subsoils are dry most of the year.  During rainy months the top one foot or so of the soils' profiles are recharged with available soil moisture.  Under those natural conditions most forest-sized woody plants wilt in late summers, except in wet years.  In the North American Great Plains, most tree species die, except in flood plains along streams, prairie potholes in the Dakotas & playas in west Texas & where humans irrigate their trees in yards, parks & farmsteads.
Let's research whether bald cypress, tupelo, black gum, tamarack, black spruce & others can survive along rims of playas, prairie potholes & flood plains, when humans adequately irrigate their root systems only during 1st 3 years after transplanting.  Bald Cypress does thrive in shallow water & grows "knees" to move oxygen to submerged roots.


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Is it possible to identify a particular gene sequence from next gen sequencing techniques (especially RNA-seq )?
I have to check the expression of a gene in a fish whose sequence is not known in the fish in question. Sequence is known in an another fish (zebrafish) but the gene has 10 isoforms. The genome of fish in question is not sequenced, however RNA-seq data is available. I have no knowledge of RNA seq data analysis. Is it possible to know the sequence of gene of interest from this RNA-seq information?

Okay, so you have RNASeq, but no reference genome for your fish?  Just transcript sequence from zebrafish?  Are you just trying to see if this gene is expressed, or you need to a more global view to compare it to?
If you just want to see if the gene is expressed, easy thing to do is to make a reference just made up of zebrafish transcripts, align to that.  If there are too many differences between your fish and zebrafish, that won't work.
In which case, the next thing you could try is de novo assembly of your RNAseq data, then use blast to compare the zebrafish trasncripts to your assembled transcripts.  Blast will make alignments where a short read aligner might not.

Yes, it is possible, if the gene was expressed in the cells where the RNA was harvested from.
With RNA seq basically you sequence the RNA of some cells, usually it is mRNA that you sequence, that means that the sequence you are looking for is not an plain copy of the DNA gene sequence you have. Mainly because it results from splicing and other post-transcription processing.
However, if you know the DNA sequence of the gene and you have RNA seq data (and if that particular gene was expressed in the cells the RNA is coming from), you can spot the exons of the gene in the data. If the gene is expressed in zebrafish you can find on ENSEMBL all the information about the transcripts of that gene and look for those in your RNA seq data (using BLAST for example) to confirm the presence of the expressed gene.


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Binding kinetics of 6xHis-Tag
For the planning of an experiment I would like to know the binding kinetics (kon and koff) of a 6x-His-tag to a Ni-NTA surface.
I know they should differ due to surface quality and position of the His-tag in the protein. But maybe there is some literature out there (that someone of you knows) from which one could get at least a rough estimate of the kinetics.

What sort of research have you done so far? Both Entrez PubMed and Google Scholar have very good search functions.

It seems I didn't look thoroughly enough at the results PubMed and Scholar returned yesterday. Hope it helps someone in the future…

Some more hours of literature research finally produced a result:
As published by Khan et al. 2006 6x-His-tag has two distinct dissociation constants of koff1 = 6.3 10-3 and koff2 = 1.8 10-3.


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What is a "tool strain"?
When a biologist is talking about a genetically engineered mouse strain which is a "tool strain", what does that mean? What is the exact definition of a tool strain? What is the difference between a tool strain and any other mouse strain?
Also, how are tool strains connected to recombinase techniques? Does using a recombinase automatically create a tool strain? Or are the properties "tool strain" and "recombinase containing strain" independent from each other?
If it is important, the context is mouse (and possibly other animal) strains used in cancer research.
It would help if you could keep the explanation high-level. I only have high-school biology knowledge and I am trying to make sense of the requirements for a software application for use by biologists.

It would be helpful if you could quote a section from the instructions to that software because such terms tend to depend on context.

There are no instructions. I am trying to elicit requirements from a single key user who doesn't "get" set theory. She is talking about several types of tumor models and animal strains, and when she tells me of model types A and B, she is not capable of telling me whether A is a subtype of B, B a subtype of A, both are synonyms, or unrelated. Because she is always thinking in terms of concrete data, she cannot generalize it. And when I try to pry it out with focused questions, she starts contradicting herself. Googling has helped a lot, but with the tool strains, I hit a wall.

For what it is worth, she convinced me that "tool strains" and "recombinase strains" are synonyms, and that there are other, unrelated types of strains, like "reporter strains", GE-strains without recombinase, and non-GE strains which may have spontaneous diseases like A/J, or be healthy like FVB/N. Then I found examples of reporter strains having recombinase and concluded that my understanding is wrong. Still don't know whether a strain is considered a "tool strain" in the context of a certain experiment, or whether it is a property of the strain itself.

Is there anyone else you can talk to? :) In my mind, recombinase strains could be a subset of tool strains, as a recombinase like Cre mentioned below is certainly a tool for genetic engineering, there are other "tools" that can also be used.

In extension to shigeta's answer, I could well imagine "tool strains" and "recombinase strains" to be equivalent in the sense that they mean strains of mice whose genome you can easily manipulate.
Cre recombinase is an enzyme which can recombine (effectively insert) genes from a plasmid (which you somehow delivered to the cell) into the cell's genome, if Lox-sites are present (Cre-Lox recombination). This is a very common method of integrating genes into eukaryotic model organisms (i.e. mice).
By tool/recombinase strains they could simply mean mice which express recombinase already, so that you can readily insert your genes into specific cells by delivering a plasmid with the genes on it, and then triggering Cre recombinase in the cells you want to modify in order to integrate the genes into those cells' genome.

Until a better answer shows up...
A tool strain appears to be a mouse strain that is useful for making recombinant mice.  It has genes inserted into its genome to make detection of your manipulations easier.  In this case several phenotypes (luciferase, human SMN) can be observed as well as a tetracenomycin resistance marker is in place so that offspring with the gene can be easily estimated.

These Tg(SMN2)89; Smn1+/-; Tg(SMNΔ7)4299; ROSA26rtTA; "old" Luci-TRE-SMN mice allow high levels of both luciferase and full-length human SMN expression to be regulated by the addition/removal of doxycycline. These may be useful as a fluorescent reporter and/or Tet-On/Tet-Off tool strain for doxycycline-inducible rescue of Type II (moderate) proximal spinal muscular atrophy (SMA).

I have always called those reporter mice...

its a new term to me as well.  Its a big time saver though because you never know when a recombinant mouse gene has bred into a new generation - you'd otherwise have to do a PCR and sequence from each mouse you get.  Now you only need to validate a few likely candidates.


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For how many generations does the average human have descendants?
From what pop science tends to tell us, it seems that the distribution of descendants humans have is very uneven. Mitochondrial Eve is the ancestor of all women in our present, Ghenghis khan probably also left a lot of descendants, while quite a few human beings die without ever reproducing. It seems plausible that most people from the past are somewhere between these two extremes: they reproduce, but many generations later, they are either the ancestor of only a small proportion of all living humans, or their line may have died off completely.
When trying to wrap my head around this kind of descendant ideas, I started wondering: do most people from the past still have living descendants, or does the majority of people, given enough generations, lose their lines, while a few people have many descendants? And if the second possibility turns out to be true, mathematically there must be an average time until one's line disappears. So, if we choose a generation to be generation zero, how many generations does it take on average until 50% of the people from generation zero have no more living descendants? Has this number been estimated, or if not, what is the closest concept for which estimations have been done?
This question is about the state of affairs throughout the history of homo sapiens, without modern-day complications like changed reproductive patterns, or the risk of humanity wiping itself out.

Related: https://biology.stackexchange.com/questions/115164/contribution-of-ancestors-in-a-persons-genome-david-reichs-who-we-are-and-ho

@bob1 thank you. To clarify, in this case, I'm mostly interested in the genealogical line duration, not the genetic line duration, since your link shows that they can diverge quite a bit.

the problem with such a calculation is at least part of your sample have infinity as their number, and when oyu add anything to infinity and divide it by somthineg finite you still get infinity.

for a related nmuber that may be clase ot what you want, about 15% of a humans fail to reproduce.

@John you don't have to add something to infinity. In this kind of analysis, "average" is frequently not defined as the mean, but as the median. Or, one could calculate the rate for only those people whose line ends, and also mention their proportion. I'm aware that there are all kinds of subtle details here, so the answer won't be a simple back-of-the-envelope calculation.

@John these 15% are indeed quite interesting. Do you know how they are defined? Do they refer to the modern infertility rate, to modern rate of actually not reproducing (as in, some fertile people don't reproduce by choice or circumstances), to historical rates, to prehistorical rates? Is it 15% of people who reach adulthood, or 15% of anybody born, so including child mortality of potential parents?

Its just the rate of reproduction, how many people have offspring, its enturely a modern calculation. the issue with a median or average is about how you determine it. humans use recombination so if you look back after enough generations everyone alive in the population who reproduced is your ancestor. your tree if ancestors doubles every generation. the number you are looking for does not exist becasue humans reproduce sexually.

this may help you https://biologos.org/series/evolution-basics/articles/mitochondrial-eve-and-y-chromosome-adam

@John "everyone alive in the population who reproduced is your ancestor" - this can trivially be shown to be untrue. Let's take an ancient person A, who reproduces once and has a child B. B dies young and has no descendants. Obviously, A is not my ancestor. They have a descendant line of length 1, and B has a descendant line of length 0. Some people's descendant lines diverge and they have many descendants, other peoples' lines converge and die out.

@rumtscho I think John is referring to those who reproduce and have any ancestors. Very quickly as you go down generations your number of ancestors converges to either "everyone" or "no one". So, if you ask "For how many generations does the average human have descendants?" in terms of the average, that's not a very useful number. For one, anyone you'd meet today is going to have at most a few generations because that's all there's been time for and we haven't waited long enough to see how many they end up with.

If hypothetically that weren't a problem, then most of your observations are going to be people that either have as many as you were willing to go back, plus some that are zero, some that are 1, fewer that are 2, less still that are 3, and so on.

A better way to put it would be If you have ancestors then everyone who has decendants is your ancestor once you go back a few generations.. Of course the problem is people who don't have decendants don't leave a detectable trace, they don't leave a genetic marker. and becasue relatedness goes up and down the tree we can't tell if you leave decendants or if you don't and your siblings did. We have never found a humans remains without decendants. your asking for somthing that is impossible ot determine outside modern day records.

Completely revised answer:
First let me say, “All people living today have thousands of generations of ancestors.”
To answer your question we need to look at two time periods: historical (pre-1950) and present day (post-1950).
Historically
Only a small percentage of people either couldn’t have children or chose not to have children. For most people, having children was de rigeur. Part of this was the continuation of the family name and another part was the fact that children were necessary to be able to survive old age.
People usually had several children; however, about half of children did not survive childhood to become adults. child mortality
This means that at least half of the people born had no descendants. (One generation cutoff)
If a couple had children, then they had more grandchildren and even more great grandchildren. As an example in one family I know a couple had three children, nine grandchildren and nineteen great grandchildren.
Historically a person’s line of descent would end either with them, or within two or three generations. Those whose lineage persisted longer than three generations would probably continue to thrive and grow rather than diminish. There is a report on the descendants of the Mayflower, where there were 53 people who survived the first winter. The lowest estimate gives them three million living descendants today. Mayflower descendants
I would propose that if a person has more than three generations of descendants, the probability of their line dying out dramatically decreases.
Present Day
Since the 1950’s a much larger proportion of people are choosing not to have children. Birth rates in developed countries have fallen to unsustainably low levels. For example in Japan the birthrate has fallen from 27 per 1000 people in 1950 to 7 per 1000 today. macrotrends Japan birth rate
In America "Of all adults ages 55 to 64, 19.6% were childless, compared to 15.9% of those ages 65 to 74, and 10.9% of those 75 years and older." older childless and of adults under 50 almost half of them say they are not likely to have children.  fewer children
In the family I mentioned before, from the nineteen great grandchildren there are only six great-great grandchildren.
This means that the scenario you propose, with a person’s line dying out over generations is much more likely in the future. However, as we are now at this crisis point, there is insufficient data to provide a reasonable analysis.

alot more than thousands, anyone alive today has ancestors all the way back to the origin of life.

@John You are right of course, but the OP is asking about humans, so probably some tens of thousands.


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What cell types produce immunoglobins and where are those cells found?
I know B cells found in bone marrow produce immunoglobin G.  But IgM is produced in mucosal cells at least in the gut.  Can you find immunoglobin expressing cells in other tissues in the human body?  Are B cells or IgG mRNA ever found in blood or tissues?

I think the antibodies produced in the gut are from lymphoid cells in Peyer's Patches http://en.wikipedia.org/wiki/Peyer%27s_patches , so B cells again.

First: B cells do not produce antibodies, but rather they synthesise the B cell receptor. This may sound a bit picky, but is not, since the B cell receptor is anchored in the membrane of B cells and not secreted. Its this receptor which recognizes antigens and causes the production of highly specific antibodies (including somatic hypermutation and all related processes).
Antibodies are produced by plasma cells (and that basically the only thing they do), which are differentiated from activated B cells which have undergone the selection process on the given antigen.
IgM is the first set of antibodies produced by the mature B cell, later on this often changes to IgG (different heavy chain, same antigen recognition site) by class switching.
The secreted antibody is IgA, which is found basically in all body fluids and is also secreted into the different mucosas of the body. It has two subtypes: IgA1 and IgA2 with A1 mostly present in the serum and A2 mostly secreted (see: "IgA subclasses in various secretions and in serum." for details).
IgA is made by plasma cells which are located in the lamina propria adjacent to mucosal surfaces. For details see thesetwo papers:

Intestinal IgA synthesis: regulation of front-line body defences.
The polymeric immunoglobulin receptor (secretory component) mediates
transport of immune complexes across epithelial cells: a local
defense function for IgA.

B cells (and also plasma cells) are found in the blood, they are then called peripheral cells. B cells have to be present outside the lymphatic tissues (not only bone marrow but also lymph nodes and the spleen) to be able to get in contact with antigens. Upon contact with an antigen they move into the adjacent lymphatic tissue.
You will not find IgG mRNA in the blood, as this will trigger immune responses. And it has no function outside of the cell.

thanks for the answer chris.  My immunology stopped at one lecture about clonal selection!

You`re welcome. It has at least some use that I learned this stuff. :-)

I find immunology to be particularly confusing - too many cell types doing only somewhat specified things...

@shigeta: immunology has many exceptions.. that makes it a little bit confusing

ha- i sometimes wonder if immunology has any rules! :)

Thats why I like immunology. It is not simple and you can find something new more or less every day. :-)

I know the thread is a bit old, but as per the terminology at least Kuby uses, Immunoglobulins come in two forms. The membrane form and the secreted form. The membrane form is the BCR, while the secreted form is the antibody. There is a difference in structure (the membrane one's got more hydrophobic residues) and a more interesting explanation of how they are differentially expressed. Why I bring this point up here is that, all IgA,D,M,G,E can be either secreted or membrane bound. Secreted here is from the cell and not necessarily into bodily secretions. A bit of semantics, but still.... :)

"B cells have to be present outside the lymphatic tissues (not only bone marrow but also lymph nodes and the spleen) to be able to get in contact with antigens."  This is a misunderstanding. Naive B cells come into contact with antigen in secondary lymphoid organs. Antigen is concentrated there by follicular dendritic cells, which allows for the necessary cross linking. Naive B-cells are not antigen presenting cells. In their naive state, they cannot be activated by antigen outside of lymphatic tissues.


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How compatible are mammalian digestive systems?
I'm interested in what kinds of nutrients mammals extract from food and would like to know how similar are the outputs of these systems.
For example, if it is possible to successfully replace one mammal's digestive system with another mammal's one (all the connections are correct). Would the recipient survive or experience some form of malnutrition resulting in death?

There would be a powerful immune reaction. they try to use pig valves in human hears, and those are just cartilege. AFAIK no trans specis grafts have been done.

I think this would depend entirely on the diet of the host and donor mammal.
Assuming they are of similar size and diet, I don't see any reason why this wouldn't work. The gut tends to absorb more or less everything in the food.
If the diet of the two mammals differed significantly, I could see some problems with eating the correct foods. Herbivores with the significantly shorter carnivore gut would have trouble killing and eating things without carnivore teeth/claws/what have you, and the plants would not provide enough nutrition on their own. Rabbits, for instance, have a two-pass digestive system, so in order to use a rabbit gut the mammal would have to eat their own feces regularly. (Rabbits have digestive bacteria in their colon, but grass has to travel to the colon and then back 'upstream' to the absorptive part of the gut. So this is achieved by going around again.)


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Affinity isolated peptide
What is affinity isolated peptides??(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

A peptide or protein can be purified by affinity chromatography. The principle is that the peptide has some substrate to which it will bind, retarding its progress through the column compared to the rest of the peptide population. A couple of typical examples are:

Using a His6 tag put on recombinant molecules, IIRC it binds to Ni2+ trapped in the chromatographic resin and is eluted with a chelator like EDTA.
Immunoaffinity chromatography, where you have a population of antibodies on the chromatographic resin which are specific to the protein that you want to purify (or alternatively having the immunogen bound to the resin so that you can purify the antibodies against it)

Mighty Wikipedia has a link about affinity chromatography here.

so its basically purification or extraction of peptide from a mixture using affinity chromatography...

Affinity isolated peptides/proteins are an output/product of affinity chromatography.


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Sequence based method for prediction of continuous B cell epitope
What is Sequence based method for prediction of continuous B cell epitope? What is the algorithm/procedure of this method? Can someone please explain this to me in simple language?

Why do you want to know, and do you have some background?

umm I am going through this for my research , but i have not studied biology for the last 8 years....


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What is a protective epitope?
What is a protective epitope? An epitope is basically a part of antigen. So does it mean that when the epitope combines with an antibody, it helps in the functioning of the antibody instead of going against it?

Lets define the nomenclature first: An antigen is a large structure (protein, virus, bacteria and so an) which is recognized by the immune system as foreign. The word antigen derives from the abbreviation ANTIbody GENerator. Exposure of our immune system to an antigen results in an immune response and the generation of many antibodies.
An epitope is a small part of an antigen - typically these are small structural elements or small peptides (8-11 amino acids in length) which are recognized by the binding site of an antibody. See the picture below (from here):

Here the antigen is the albumin protein. On the surface you can see 8 different epitopes which lead to the generation of 8 highly specific antibodies against the epitopes (antikörper is the german word for antibody). Every antibodies is highly specific for its epitope and will recognize no other epitope and helps raising an immune response against it. What happens after an antibody bound to its epitope can be read here.
Antibodies directed against a protective epitope are directed against (highly) conserved structures of the antigen. For example the recognize a highly conserved structure of a virus which means that even when this virus mutates (like influenza does) it will still recognize the conserved epitope and give protection against this virus (or better: antigen).

understood. But what does  a protective epitope mean?

Ah, sorry, forgot to answer that. I will updated the answer, better now?

what is a protective epitope? I still dont find the answer of y question. what exactly is a protective epitope?

It is a normal epitope. But one which is widely distributed between different strains of a virus/bacteria etc. and gives you a very good protection against these antigens.

The word protective is an adjective which describes the function of the noun epitope. It is an effective protector against infection. Like @Chris said its protectiveness is derived from recognizing a conserved region of a molecule. Recognizing a conserved region of a molecule is what merits the special adjective 'protective'.

so, we can say that all antigens have a protective epitope?

antigen receptor is epitope, am I correct??

Nope, this is the paratope. The epitope is the part of the antigen which is recognized by the antibody.


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What is MHC haplotype?
What is MHC haplotype? I did check out the wiki article, but did not understand.

(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

When you are asking these kinds of questions, please ask about specific things. Just saying "I did not understand" is far too broad. Google is your friend when trying to understand difficult words or concepts - there are many more resources on the internet than just Wikipedia.

I have an answer for this question, similar to but expanded upon the answer already provided. @user3237995 asked a basic biological question: What is a haplotype?. Why can we not provide this basic biological understanding? There are not many answers. A haplotype is a haplotype? It's not a question about the complexities of MHC. It is asking what is a haplotype. It is a simple answer. Aren't we here to help people understand biology?

@Mike Taylor Thanks a lot for your support, I hope you provide me with our answer so that I can read it and understand

A haplotype is commonly defined as

...a group of genes within an organism that was inherited together from a single parent. -- Nature Scitable

This definition of haplotype applies whether it is just a few genes or all of the genes on an entire chromosome$^1$. In the case of the major histocompatibility complex, it is a group of more than 200 genes on chromosome 6 (Janeway et al. 2001). The set of alleles$^1$ inherited together from one parent form the MHC haplotype. Thus, one offspring will inherit two different MHC haplotypes, one from each parent. The different haplotypes with so many genes helps keep genetic variation in the overall complex, which improves the immune response ability of the organism.
The term is derived from haploid, which means half of the normal set of chromosomes. Humans for example are diploid, meaning it has two copies of each chromosome, one inherited from the mother (maternal) and one inherited from the father (paternal). So, when you inherit just one half of the crhomosome pair, you are inheriting a haplotype.
For general reference, it's important to note that haplotype was not always used to reference a group of two or more genes inherited together. It was commonly used to as a term to represent a sequence of nucleotides together on the same chromosome, even if only part of a single gene. For example, Bowen et al. (1995) used mitochondrial haplotypes to study the migration of loggerhead turtles across the Pacific Ocean. They used 350 nucleotides of the mitochondrial control region. The control region is over 1000 nucleotides in size but Bowen and colleagues only used 350 nucleotides from part of the control region.  This use was very common in the 1990s and early 2000s before it became easier and less expensive to sequence entire genomes, or at least many genes.
Citaton
Bowen, B.W. et al. 1995. Trans-Pacific migrations of the loggerhead turtle (*Caretta caretta) demonstrated with mitochondrial DNA markers. Proceedings of the National Academy of Sciences USA 92: 3731-3734.
Janeway, Jr., C.A. et al. 2001. Immunobiology, 5th edition. Garland Science, New York.
Footnote

More accurately, it would be the set of alleles at each gene locus (gene location) inherited together. The same genes are inherited from either parent, but the alleles (variations of the gene) may be different between the two parents.

As stated in wiki
"The major histocompatibility complex (MHC) is a set of cell surface molecules encoded by a large gene family in all vertebrates which controls a major part of the immune system. MHC molecules mediate interactions of leukocytes, also called white blood cells (WBCs), which are immune cells, with other leukocytes or with body cells. MHC determines compatibility of donors for organ transplant as well as one's susceptibility to an autoimmune disease via crossreacting immunization. In humans, MHC is also called human leukocyte antigen (HLA)."
Basically, MHC control immune system and it work based on principle lock and key. MHC has specific cell surface that can bind to foreign materials that have compatible binding site and recognise it as pathogen or harmful compound.

functionality of MHC is understood, but what is the word haplotype ??

@user3237995 http://en.wikipedia.org/wiki/Haplotype

@user3237995 in my simple understanding, it is as follows: we have pairs of chromosomes in our genotype. The haplotype is represented by the set you get when you take one chromosome from each pair (either maternal or paternal). The genes on those chromosomes are used to build proteins (like MHC's). Therefore, an MHC haplotype would be the set of either paternal or maternal (but not both) genes used to build MHC's in an individual.


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Epitope annotated protein
What is epitope annotted protein??  The book from which I got this term is : http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1

Have a read through the wikipedia article. BTW, you could have gotten that by googling "epitope".

so basically epitope and epitope annotted protein means epitope??

Yes, they're the same thing.

First, when asking about a specific small term, it's best to check your spelling.  If you actually look at the sentience, you will note that you left out a very important hyphen:

Pellequer compared several propensity scale methods using a dataset of
  14 epitope-annotated proteins. [emphasis added]

The phrase means that the protein sequences (amino acid sequence) has the epitopes marked on them.  If you look at the cited paper, you will see the various tables and break downs of determined epitopes.  Pellequer's group did a lot of the early work when people were still working on techniques to "map" out the locations of epitopes (which are often not in linear segments of the protein sequence due to the protein structure).

authors: Дмитрий Першуков


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Are there specific non-protein substances that pathogens release into their host?
Reading research articles, I have found out that proteins called effectors get released into the host cell when a pathogen attacks a host. My question is, whether pathogens also release non-protein substances?
Have these substances been extensively studied and classified? Is there a list of such compounds? Are these compounds unique to pathogens?

Sticking my neck out (and expecting it to be bitten by a black swan) it appears that all the examples of toxins secreted by bacterial pathogens when they infect an animal host (exotoxins) are proteins.
However fungi secrete a variety of exotic (and often very nasty) small non-protein molecules (mycotoxins). It’s not clear from the question whether you would be interested in these systems as they differ somewhat from those involving bacteria. One difference from bacterial toxins is that fungal toxins not secreted inside an infected cell, but just into their environment. Thus, cercosporin is secreted onto the surface of plants on which Cercospora reside and may be taken up through lesions in the plant. However it is not clear whether the plant is the main target of such toxins, rather than bacterial ‘foes’. So the host/pathogen concept is less clear in this context.
A similarly ambiguous host/pathogen situation would appear to exists with toxins such as saxitoxin, the paralytic shellfish toxin secreted by certain marine algae and cyanobacteria.

I am not sure if mycotoxins actually are secreted by the fungi to aid its parasitic lifestyle.

@WYSIWYG No, neither am I. After reading a bit more I've edited my answer to clarify the situation a bit so the questioner can decide it the mycotoxins are relevant to her research.


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What is this wasp?
We live in central New York and these large (1.25") wasps are invading our house pretty regularly. I want to say it's a great black wasp, but the pale yellow striping makes me wonder.
A sample specimen
Edit
Confirmed the answer: these have all been female Northern Paper Wasps:

Apparently they can be almost solid black in some communities.

Do you have a better picture? It would be nice to see more details. I'm pretty sure the great black wasp is all black, but there are several other big wasps that are striped.

I'll take one next time they move into my house

If by "great black wasp" you mean Sphex pensylvanicus (the common name per the Wikipedia page here: https://en.wikipedia.org/wiki/Sphex_pensylvanicus); no.  The folded forewings visible in the picture are characteristic of the family Vespidae; I'm thinking Polistes, but bugguide.net has seven pages worth of possibilities (starting here: http://bugguide.net/node/view/572/bgpage?from=0).

This specimen is most likely a Polistes sp. from the Vespidae-family. Some Polistes species are sometimes referred to as paper wasps.
Coloring is not the primary criterion for identification here. The folded wings leave no doubt that it is a wasp from the Vespidae family (which excludes the Great Black Wasp, as suggested in the comments). Since there is only one picture, with not many details, further identification gets more difficult here. Based on my experience, I would guess that it is a Polistes sp. (no way of saying which particular species it is, based on the photo) - this would also be consistent with your observation that they invade your house frequently: Polistes, besides Vespinae (e.g. Yellowjackets), are the only 2 social Vespidae subfamilies, i.e. they live in colonies. Also, Vespinae can be excluded, they have a visible edge at the beginning of their abdomen, which the wasp in your photo doesn't have. This would leave Polistes as the most plausible option.
A detailed view of the head, the legs and the unfolded wings would be necessary for a more specific identification - there are several 100 different Polistes species alone!

We've got paper wasps around here. They seem to have stopped poking around...I just hope they're not living in my house somewhere I can't see.


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How does a smoker's finger or mustache get yellowish by nicotine?
Tobacco use is the leading cause of preventable death around the world.$\ce{^1}$

The stain is considered as a "tell-tale" sign for identifying smokers. Multiple materials stated that it's due to tar (nicotine) disposition. The colouring fades away after the smoker quits. There are also number of search results that point to "removing" these smoking stains in the skin. If it can be removed using chemicals then I wonder what sort of a chemical it utilized there as well.
Is it only nicotine that causes the yellow stains on the skin? What is the role of oxygen deprivation in this scenario? Can this be categorized under smoker's melanosis? What tissues/cells are being "transformed" in this case? What's the biochemical explanation behind the colouring of skin?
How is this staining differe from a ink stain in the skin which lasts for about about 3-4 days?

Please do not change the question significantly, especially after answers have been submitted. Instead, ask a new question.

@MattDMo I am not sure if this is a rule within Biology.SE, because there are ample of times where the original post was edited with closely related info/queries. This one from Chemistry.SE is a big example for that. Someone with moderator reps would be able to view its edit history. The answers were editted without any complain. The colouring of skin by smoking (nicotine, tar) and colouring of skin by inks are two common encounters we see day today life. So, they are related and I see it's fair enough to ask these two questions together.

This is general practice for all Stack Exchange sites, and is referred to as "moving the goalposts." Yes, of course questions may be edited to be clarified, or to add new information requested in comments, etc. However, it is bad form to add new, only tangentially-related questions to the original question, especially after answers have been submitted. Those answers may be downvoted later by users who see the expanded question, and an answer that apparently only addresses part of it. (...)

(...) Additionally, a question should be just that - a single question. Asking multiple different things in the same question makes it more broad, and makes it less likely that a single, concise answer can address all of the points.

Pure nicotine is a yellow colored liquid (although some sources say it's a clear liquid.) "Tar" is a complex sludge that is also yellow-brown. So it's difficult to distinguish 'nicotine stain' from a 'tar stain' based on visual inspection. Let's go to other considerations.
The concept of a 'stain' implies that simple hand washing doesn't remove the coloration. Since nicotine is water miscible, one would expect it's easily removed with soap and water. That implies that either a) a smoker's stain is not primarily nicotine, or b) the nicotine reacts with the skin to create the stain.
Nicotine is sufficiently functionalized that it could conceivably undergo some interesting chemical reactions with proteins, but I don't think that's what's happening. A simple observation is that transdermal nicotine patches do not contain a colored agent, and do not stain the skin. Score one point for the "mostly tar" explanation. Cigarette smoke contains far more tar than nicotine, and tar will deposit on most-any surface (at ambient temperatures), so it's parsimonious to proceed with the "mostly tar" explanation.
The picture shows that the stain occurs on both fingernails and skin. The most abundant protein that's common to those two tissues is keratin. Like other examples of protein staining, the mechanism is complicated and poorly understood, but the basic outline is that parts of keratin are greasy (the non-polar amino acids) that associate with other greasy things.  (EDIT: AliceD's answer also depicts the well-known staining of teeth, which are not keratinized, showing that the staining mechanism is likely a nonspecific adsorption of greasy things onto surfaces.)
The stain can be fixed through the involvement of free radicals and other reactive species in cigarette smoke, like formaldehyde. In this sense, reactive oxygen species are active participants. I don't think oxygen deprivation plays a role here. I don't think this can be described as a melanosis, as the skin isn't producing melanin in response to smoking but is simply being coated in tar.
Even if the stain was completely fixed, the coloring would fade away as the exterior skin cells are sloughed off, consistent with normal skin physiology. This is the explanation for the fading of any stained epidermis. The persistence of tar stains on teeth (which do not exfoliate) further evinces that the stain is removed through the replacement of skin cells.

Parsimonious does not mean what you think it means.

Nicotine is generally yellow to dark brown. While the pure chemical may be colorless, it oxidizes upon exposure to air, changing its color to brown. I added a "citation needed" template to the section of the wiki page you linked, as far more sources I checked said something along the yellow-brown spectrum than colorless.

BTW, I think you meant perspicuous. At any rate, I wouldn't use it here (maybe on [english.se]) as not many native English speakers know what it means, let alone those for whom English is a non-native language.

I have editted the question for a comparison to understand the skin staining context better. Can you take that into consideration in your answer?

That added part may be a bit vague - there are many types of ink. Permanent marker ink may stay longer than 3-4 days and washing habits may affect this too. How do you know tar persists longer? Consider asking a new question on this and specify what you wish to know. To me it looks like a different question altogether as the ink part is unrelated to the original question.

@MattDMo He/she did not use the word incorrectly. I'm not going to cite a bunch of dictionaries, but you should look at some other ones.

@MattDMo, you certainly don't know what I think 'parsimonious' means, although I do find it interesting that a dictionary of that caliber has such a limited scope. Webster-Merriam apparently needs more logicians on their usage panel!

"far more nicotine [than tar]" is an overstatement. It's about a factor 10 or so.  And tar may deposit at any surface, but will nicotine not do that? While parsimonious may be aptly used, I am not so convinced with the reasoning. For the rest, great answer +1

@AliceD, you misquote me for some reason, although you did understand my 'overstatement.' And my basic intuition is that tar will deposit at a far greater rate owing to its lower vaporization temperature...I don't have any numbers to support it (you don't provide any either.)

@Ryan - yep - I meant to say "far more tar [than nicotine]". :) I share your intuitions. I don't need any numbers to support my claims.

@AliceD, you share my intuitions but not my reasoning, making you a good person to know! Anyway, the quote is "[c]igarette smoke contains far more tar than nicotine..." so you're still misquoting! ;)

Touche :) in the end our answers are in perfect agreement :)

@Ryan do you care enough to enlighten me with the skin staining with regards to inks (fountain pen) and how it differs or similar to smoking (tar, nicotine) stains?

@Ryan Even if the stain was completely fixed, the coloring would fade away as the exterior skin cells are sloughed off, consistent with normal skin physiology. This is the explanation for the fading of any stained epidermis. Great - done. I was trying to search protein mechanism that you have mentioned but was not succesful.

Short answer
Tar deposition is the cause of the yellow cigarette stains.
Background
Both tar and nicotine cause yellow to brown staining. Although nicotine itself is colorless/white, it turns yellow upon exposure to air.
In a study on cigarette stains, the author speaks of tobacco-tar stains, implicitly acknowledging it is tar and not nicotine (John et al., 2013).
Interestingly, e-cigarettes which contain nicotine, but no tar, are reported to leave no stains, pointing to tar as the culprit, and not nicotine.
As to physiological causes of the stains I can say it is simply a tar stain and it has nothing to do with pigment or anoxic conditions, because the teeth and nails also stain yellow:

Tar stains on skin and nails. Source: John et al., 2013.

Tar staining of the teeth. Source: Identalhub.
Reference
- John et al., BMJ Open (2013); 3:e003304

That added part is a bit vague - there are many inks. Permanent marker ink may stay longer than 3-4 days and washing habits may affect this too. How do you know tar persists longer? Consider asking a new question on this and specify what you wish to know. To me it looks like a different question altogether as the ink part is unrelated to the original question.

Nice answer, @AliceD. The final link to John et al seems to point to an incorrect URL, however.

@Ryan - thanks for the appreciation and thanks for taking the time to click through the link :) I fixed it.

@AliceD see my comment on the other answer regarding the color of nicotine. I checked out a bunch of different chemical resources and vendors, and most seem to indicate that it is generally in the yellow-brown spectrum, as it is most commonly exposed to air (such as in a cigarette). I think it's only clear when freshly prepared and/or maintained in an oxidation-resistant environment, which would be the case in pharmaceutical manufacturing for nicotine replacement therapy patches. (...)

(...) Drugs.com indicates that the nicotine is sandwiched between 2 polyester backings and embedded in a matrix of various polymers, so $O_2$ likely can't interact with it.


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potency in preformed germ-line
In organism that have a preformed germ-line like Drosophila where germ cells are pre-allocated in the oocyte, are there technically no adult pluripotent stem cells since germ line cells can't be developed from somatic stem cells?

In almost all metazoa, the pro-germline cells get segregated from other stem cells at an early stage of development and they thrive and differentiate in their neighborhood. This is important in order to preserve the germline. This post provides some basic explanation.
However, even drosophila have adult multipotent stem cells and help in the formation of midgut as reported by this study.


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Screen brightness for reading in dark room
While searching online I did not find any conclusive article on whether it is good or bad for one's eyesight to read on a computer screen in a dark room. Most mention that it will cause strain that will go away after some rest (sleep).
My question is does reading in dark room has any long term effect on one's eyesight and what screen brightness setting (low of high) should one prefer if trying to read in a dark room?

This is rather close to personal medical advice, which is off-topic here. As written now, it's not really a biology question.

Not an answer, but just a suggestion:
If you are in a position where you must read off of a computer monitor without ample ambient light, I'd suggest you try setting your monitor/reader/whatever to have a dark background and light/wight text so it doesn't feel like you're staring into the sun.