text:
Do gibbons have a monogamous sexuality?
the question is already in the title. If possible, it might be extended to:
Have animal taxa (mammal) who tend to live in a family structure have a monogamous sexuality? Or are there cases of these taxa, where the sexual partner is not the social one.

Regarding gibbons, yes. According to National Geographic:

Gibbons are monogamous and live in family groups consisting of an adult pair and their young offspring.

There isn't a generalized answer for "family living", although specific family types are indicative of relationship type. Nuclear families (parents and children) tend to be monogamous, families with multiple males and one female tend to be polyandrous, and families with one male and multiple females tend to be polygynous. See this page on primate social structure for more information.


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Can you find malaria parasites in saliva?
Can you find plasmodium parasites (malaria) in saliva under microscope from someone who's infected? Or it's only in the blood?

No.
Although malaria is transmitted through the saliva of a female Anopheles mosquito, it stays in the bloodstream and doesn't pass over to the saliva of humans (otherwise it probably would be transmittable via humans directly). Once the parasites travel to the liver, it infects and bursts hepatocytes after reproducing (asexually). The burst cells then infect the bloodstream via red blood cells, where the parasites reproduce further and eventually burst their host cell, leading to a vicious cycle. This whole process only has to do with the bloodstream, since the parasites live in red blood cells.
However, there are certain markers present in the saliva which can be used to detect the presence of malaria the most known of which is called PfHRP2, or Plasmodium falciparum histadine-rich protein 2. This only applies to people infected by the type of parasite P. falciparum, however it is this parasite type which is the cause for the vast overwhelming majority of deaths and complications during malaria infection. The range of PfHRP2 values in malaria-positive patients' saliva ranged from 17 to 1167 pg/mL in one study.
References:

http://www.malariajournal.com/content/11/1/175
http://www.jstor.org/discover/10.2307/30086299?uid=3738432&uid=2&uid=4&sid=21104875852967

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Found a larva in my broccoli, is it a Small White (Pieris rapae)?
Found this living larva in broccoli from a store. It was about 10 mm long. It was in july this year, and I don't remember the country of origin for the broccoli. A bit of googling makes me think it could be a Pieris rapae, but I don't know if there are any similar species.

edit: Even if I don't know the origin of the broccoli, I assume (and hope) it was grown in Europe since I got it in Sweden.

It definately looks like a Pieris rapae larvae, which are distinct from larvae in closely related common species as e.g. Pieris napi and Pieris brassicae. However, I'm not a lepidopterist and there might be related rarer species I'm not aware of, especially since you don't know where the broccoli is from. However, Pieris rapae is found basically all over the world as native or introduced (native in Europe, Asia, Africa and introduced in e.g. Ameria and Australia) and is a pest species of cabbage (including broccoli) so it is a very good fit.

Tried asking in another forum, and no one had an alternative to Pieris rapae, so I'll go with that until a lepidopterist objects!

@picapica Based on your update; if found and probably grown in Sweden, it if definitely Pieris rapae. Nice gifs on your tumblr by the way. The spider-killed syrphid fly here from 18th Aug. is a Volucella pellucida (Fönsterblomfluga), and the beetle below is probably Phyllopertha horticola.

Thanks for the bonus taxonomy, much appreciated. (I don't really dare to use this place to ask about all the animals that I wonder about, that would most likely become spammy...)

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Using Canonical Correspondence Analysis on matrices with missing data
I have a matrix of sites where not all the environmental variables I want to assess were sampled. In other words, there are sites with the whole set of variables sampled, and there are other sites where just some variables were sampled. Does Canonical Correspondence Analysis work with missing data for the environmental variables? If it does, what would be the effect of not including the missing values?

this question might best be asked in cross validated (http://stats.stackexchange.com)

I had a quick look over there. I think ecologists might be more familiar with CCA than 'conventional' statisticians.

I though I should mention it since there is a chance it could get a close vote since this is still a stats/sampling based question!

I've had mixed luck posting ecologically-motivated statistical questions on CV. I was surprised that the word 'ordination' is not well known outside of ecological stats :p

First, you cannot fully analyze pair-wise correlations between your environmental variables with NA values, and therefore cannot fully discount including covarying variables. If this is the case, you will not be able to know which of the covarying variables is responsible for any trends in your data.
Second, I don't believe CCA will work with NA values -- you will either have to eliminate the observations containing those missing values or fill them in with column averages. However, both of these methods will have an impact on your results, so move forward cautiously.
Third, I wonder if CCA is even the way you want to go. nMDS (non-metric multidimensional scaling) is much less constrained than CCA. Additionally, it doesn't suffer from as many assumptions/limitations as CCA.
From McCune & Grace (2002):

The following two questions can be used to decide whether CCA is appropriate: (1) Are you interested only in community structure that is related to your measured environmental variables? (2) Is a unimodal model of species responses to environment reasonable? If, for a specific problem you answer yes to both of these, then CCA might be appropriate

However, missing environmental data is still a problem in nMDS.

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Niche differentiation in birds of prey
I'm not much of an ornithologist but I know enough to distinguish most Central European birds of prey. To me it is amazing that there are so many species that seem to occupy the same niche. Especially the two native kite species (Milvus milvus and Milvus migrans) and the common buzzard (Buteo buteo) are -- to my impression -- quite similar in terms of size, preferred prey, habitat etc. According to the competetive exclusion principle, these species would not coexist if they would exploit the exact same set of resources. So my question is:
What are the major differences between the mentioned species that allow coexistence? Are there more such examples from other geographical regions?

Note that competitive exclusion states that the species should differ at least according to one axis of their ecological niche. Meaning that if their niche totally overlap in terms of source of food, it doesn't that they necessarily can't coexist theoretically speaking. I might be wrong though!

No, you're right. I'm just asking for the axes that differ.


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Is the Hypothalamus part of the Central Nervous System or Endocrine System
Sorry for a certainly naive question.
Some references (for example https://faculty.washington.edu/chudler/nsdivide.html) seem to to indicate that the hypothalamus is part of the Central Nervous System. Others (for example http://kidshealth.org/teen/your_body/body_basics/endocrine.html) place it in the Endrocrine System. I would have said it is part of both, but then I read the two systems are distinct. Could anyone explain me to which one it belongs and why?
Thanks,
Gilles

CNS refers to the brain and spinal cord. Its a very general term. Hypothalamus is part of the CNS but its unique in a sense that it secretes many chemicals into the bloodstream like glands! so they are both correct!

If the above comment has answered your question, please let me know so I can post it as an answer so that the question does not remain unanswered.

Hi Bez, I was just waiting a little to see if anyone else would argue with what you said. Please post it as an answer as it is exactly what I was after.

CNS refers to the brain and spinal cord. Its a very general term. Hypothalamus is part of the CNS structure but its unique in a sense that it secretes many chemicals into the bloodstream like glands hence part of the endocrine system! so they are both correct!

Can you add some references to your answer? Actually it is more a comment.

@Chris Apologies for failing to reference. Hope the response references are satisfactory.

It is part of the CNS and does not secrete hormones into the bloodstream. Instead, it delivers input to the pituitary gland, which is an endocrine organ and secretes hormones into the bloodstream. Please refer to http://en.m.wikipedia.org/wiki/Hypothalamus and specifically the section "Neural Connections". Otherwise, any basic neuroscience or endocrinology textbook covers this under hypothalamic-pituitary axis or the likes. Hope this helps.

Can you add some references to your answer? Actually it is more a comment.

I have added some suggestions Gilles. Hope that helps.

Ps. Questions like these are not naive and opportunity for interesting discussions!


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What causes a polypeptide to fold into an Alpha helix over a Beta pleated sheet
I know how they fold, but what causes some polypeptide chains to preferably fold into Alpha-helix rather than Beta-sheets (or vice-versa). What force makes it fold into one conformation over the other?

look into the primary sequence and the energy minimization if you are into the computational side of things. This (http://en.wikipedia.org/wiki/Protein_folding) should help.

I don't think this is homework. This is about relative preference of structures (this is usually not explained in detail in textbooks)

I'll answer this question in a while. Meanwhile you can have a look at Ramachandran Plot

All the residues in a polypeptide chain tends to configure into their lowest potential energy state. except the peptide bond all the other bonds are free to rotate, alpha helix makes optimal use of internal H bonds. The overall structure is stabilized by H bond between the hydrogen atom attached to the electronegative nitrogen atom of peptide linkage and the electronegative carbonyl oxygen atom. The arrangement of amino acids in the peptide plays a very important role in forming alpha helix. Different combination of amino acids results in different combination of dihedral angels, hence it determines alpha helix conformation.


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How non-invasive blood glucose concentration measurement work?
Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.
Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping onto the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

Just saw a talk by Mark Arnold, who does some of this research with NIR spectroscopy. Might be a good place to start.

This is not a new thing, by checking the articles about non-invasive glucose level measurement, it started in the early 90's.

Near-infrared (NIR) spectra of the human inner lip were obtained by
using a special optimized accessory for diffuse reflectance
measurements. The partial-least squares (PLS) multivariate calibration
algorithm was applied for linear regression of the spectral data
between 9000 and 5500 cm−1 (λ = 1.1-1.8 μm) against blood glucose
concentrations determined by a standard clinical enzymatic method.
Calibration experiments with a single person were carried out under
varying conditions, as well as with a population of 133 different
patients, with capillary and venous blood glucose concentration values
provided. A genuine correlation between the blood glucose
concentrations and the NIR-spectra can be proven. A time lag of about
10 min for the glucose concentration in the spectroscopically probed
tissue volume vs. the capillary concentration can be estimated.
Mean-square prediction errors obtained by cross-validation were in the
range of 45 to 55 mg/dL. An analysis of different variance factors
showed that the major contribution to the average prediction
uncertainty was due to the reduced measurement reproducibility, i.e.,
variations in lip position and contact pressure. The results
demonstrate the feasibility of using diffuse reflectance
NIR-spectroscopy for the noninvasive measurement of blood glucose.

1993 - Noninvasive Blood Glucose Assay by Near-Infrared Diffuse Reflectance Spectroscopy of the Human Inner Lip

There are multiple approaches, mostly spectroscopy, but dielectric properties (e.g. conductivity) can depend on glucose levels too. Saliva can be used to measure glucose levels as well.

2014 - Non-invasive glucose monitoring using impedance spectroscopy

2014 - Broadband Tissue Mimicking Phantoms and a Patch Resonator for Evaluating Noninvasive Monitoring of Blood Glucose Levels

2014 - A paper strip based non-invasive glucose biosensor for salivary analysis

The details of each technology you can find of wikipedia.


text:
How non-invasive blood glucose concentration measurement work?
Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.
Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

Please don't cross-post your questions.

I am sorry! I just don't know the two sites are connected somehow.

I'm not exactly sure how it is done non-invasively in the manner you describe but suspect that it has to do with IR absorption spectroscopy. Glucose has distinct bands in the near-IR frequency range. So by illuminating the ear lobe and the capillaries in the surface, picking off the refracted light, and spectrally analyzing you should be able to determine the amount of glucose relative to some reference calibration.
I worked for a start-up company that did this semi-invasively for glucose measurements in the ICU. We drew a small blood sample and optically analyzed it in a glass cell using a scanning interferometer - then returned the blood to the patient.
The optical method that draws blood probably is the best approach with regards to accuracy - where you would like to get within 10 mg/dL - but it also has its problems including response to 'interferents' in the blood that can pose as glucose not to mention high cost for the interferometer and fouling of the blood access system.

see http://inlightsolutions.com/

Thanks for your sharing, docscience! What are the possible "interferents" in human blood if I am targeting glucose?

Other types of sugars, sugar alcohols, some more than others. I don't recall the list but remember mannitol was one of the interferents. Our experts were working on ways to eliminate interferents, I believe by utilizing multiple peak responses of glucose.


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More extreme phenotypes when parents are from diverged populations
In quantitative traits we have many loci affecting a trait. If we took a bunch of parents where all mothers and fathers were of a certain value at the upper end of a trait range, and then looked at the offspring would we expect offspring from pairs of parents from more divergent populations to be even more extreme variance in their traits?
For example: if we look at 2 men from East Africa, both 190 cm tall. They each have children with women who are 180 cm, one of whom is from East Africa and the other from Canada. We could assume that the Canadian woman is probably more unrelated to her male than the East African woman. I would therefore expect that it is quite likely that the East Africans in the example are tall because of "tall-alleles" in many of the same loci, whereas there is a greater probability that the Canadian female is tall thanks to mutations at different loci. Therefore would it be reasonable to expect greater variation in the offspring of the Canadian woman?
Is there any evidence of this phenomenon?
Note: Ignore environmental and gene * environment interaction variance, just go with a simple additive model, and assume populations have had some barriers to migration for some time

If I get you right, you might be looking for something like heterosis (http://en.wikipedia.org/wiki/Heterosis)? Although mostly described for animals and plants, the principle should basically apply to sufficiently distinct human lineages as well.

Yes, the MHC example there is quite relevant @Hav0k

If being tall is beneficial, the "tall" loci are probably (partially) dominant and therefore, two tall parents from different origin may be expected to have taller offspring than two parents from the same origin. It seems hard to me to draw such general conclusion as it really depends on the number of loci under consideration, on the pattern of dominance and on whether the parents are homo or hetero zygous (and on epistasis).

If we assume that the parents are both heterozygous (for all loci under consideration) and all loci are bi-allelic and allele are additive, and parents are of any size, then indeed I would expect that the offspring from the parents form different origin will have higher range o possible genotypes. I am not sure my comments can help :) The question is very interesting +1

Yes, it would be reasonable to expect greater variation in the offspring of the Canadian woman.
Human genetic variation is the genetic differences among populations. Populations have access a pool of genes and over-time polymorphisms may arise to create greater variation.
Human populations within a species are defined by, divergence times and rates of gene flow - From mitochondrial, X and Y chromosome re-sequencing data.
Genetic Distance is the genetic divergence between species or between populations within a species (as in your example above). Populations with many similar alleles have small genetic distances. This indicates that they are closely related and have a recent common ancestor.
E.g. Height as you use for your example is a polygene. The inheritance of many genes alter phenotypic height of offspring.
Thus, it would be reasonable to expect a difference in allelic variations pertaining to height from the Canadian woman. The offspring may have a different height profile of alleles, and thus a different phenotypical height.
I should mention that:

"individuals from different populations can be genetically more similar than individuals from the same population"

But the above example - should not be expected.


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Physiology of benign eye twitching?
About four times in my life I have experienced the feeling of my eyelid fluttering for a few minutes by itself, and then it stops.
I have talked to other people who have had the same experience so I presume there is no pathology.
Could someone please explain the physiology behind these random eye twiching experiences that I and many others have had?

Could the down-voter please comment on how the question can be improved?


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How do ants transport water?
All living things need water to survive. Worker ants can drink directly from the source. But a queen ant would need help from the colony to get its daily supply of food and water. I have seen ants carrying tiny bits of food, but I have not really seen them carrying water. Do they use their hands like how they carry food? Do they use a receptacle like us humans? Or are there some other innovative ways?

Ants are able to roll water droplets because of how small they themselves are in comparison. It seems odd but that's because different rules apply to the smaller creatures. For instance, a mouse falling from a skyscraper would be stunned, but otherwise uninjured. We, however, would break every bone in our body.

The worker ants give water to the other ants in the nest. Also, they get most of their hydration out of the food anyway.
Here is a blogpost with some references and nice humour about it.

The key word is trophallaxis.

Thank you. I love drinking water. so therefore I hate ants.


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Book recommended for neurobiology
I am looking for a good explanatory book concerning Neurobiology. I am interested on how the brain works but prior to this I believe that I have to start learning things about the biology of neurons. So I searched on the net and found a book called "From Neuron to Brain" from John G. Nicholls et. al.
Actually there are so many books out there and because I have never worked on that subject, all these results are confusing me.
So i would like someone's opinion who has dealt with this subject to help me choose a book for beginners.
Thank you.

I can highly recommend Kandel's "Principles of neural science". I have not had any biology courses since highschool, but I was able to understand it well. It is really a book meant to teach. The style is beginner friendly, and not tedious/boring at all.
It is an expensive buy and a very long read (I think the paper version is close to 2000 pages), but given the complexity of the subject matter, I find it reasonable.
If you decide to go for it (or for any other neurobiology work, actually) get the newest edition. Getting an older one is a false economy here - our understanding of how this stuff works gets better by the year, and there is lots of missing (or sometimes even not-valid-any-longer) information in the older editions.
A few examples of what might make the book hard to understand for beginners
"Principals of neural science" does not require much preexisting biology knowledge. It is sufficient to roughly know that a cell has a nucleus, plasma with organelles swimming inside, and a membrane. But you have to be comfortable with a bit of biochemistry. This is an example passage concerning the behavior of ions in solution. I found this perfectly understandable with my prior knowledge, I don't know if you need brushing up on chemistry or not.

The cell membrane is selectively permeable to K+ because the otherwise impermeable membrane contains proteins that form pores called ion channels. The channels that are active when the cell is at rest are highly permeable to K+ but considerably less permeable to Na+. The K+ ions tend to leak out of these open channels, down the ion's concentration gradient. As K+ ions exit the cell, they leave behind a cloud of unneutralized negative charge on the inner surface of the membrane, so that the net charge inside the membrane is more negative than that outside.

And then there are examples like this one:

Isoprenylation is another post-translational modification important for anchoring proteins to the cytosolic side of membranes. It occurs shortly after the synthesis of the protein is completed and involves a series of enzymatic steps that result in thioacylation by one of the two long-chain hydrophobic polyisoprenyl moieties (farnesyl, with 15 carbons, or geranyl-geranyl, with 20) of the dulfhydril group of a cysteine at the C-terminus of proteins.

Here, my own chemistry is bad enough that I could only understand that a protein is modified by attaching some molecular structure to it, and this makes it possible to attach the protein to the cell membrane. The lack of understanding of the details (what is a geranyl-geranyl?) did not stop me from understanding the rest of the section, so I don't mind, but I know that there are readers who'd have a problem with that. Sadly, I don't know of a source which does not require such knowledge, and if you feel the need to know every single word, you might need to use a reference while reading, or start with a course in biochemistry first before switching to the neurobiology.
Finally, if you don't have a life science background, there might be words outside of the chemistry you might have to look up, or understand from context, but they will be unfamiliar at first. For example, I was surprised to see the word "process" used in the meaning of a physical protrusion from the cell body. But this is not such a high hurdle, you have to either read ahead and puzzle such words out, or use a dictionary. They are not so frequent to prevent comfortable reading.

This was the book used in my undergraduate Neurology course and I thought it was wonderful.  It's one of the few textbooks I've held onto.  Granted, I try not to hold it for too long, as the thing weighs a ton.

I totally agree with Rumtscho. Kandel's Principles of Neural Science is excellent. Eric Kandel is a Nobel Laureate and one of the gurus in the field. As to the biology of neurons I can refer you to:
Part II: Cell and Molecular Biology of the Neuron, and Part III: Elementary interactions Between Neurons: Synaptic Transmission.
These sections cover the basics petfectly. The following sections bring the reader to higher level of processing in the brain, namely Part IV-IX that cover Cognition-Perception-Movement-Arousal-Development-and Language/Thought, respectively.
So it is a nice build-up to exactly the things you are looking for.
But as Rumtscho says: it's quite a buy, but worth every penny. I have been using the book for about a decade during my studies as well as beyond.

Can you please expand you answer? Actually it is more a comment.

I concur with Old Chris — some details such as what all it covers etc would be nice. New Chris, I suggest that you can slightly modify your profile name so that the name confusion can be avoided.

I added details and changed my profile name. thanks for all your patience and help guys

@ChrisStronks Thanks. I now feels less like I am talking to myself. :-)

No worries old Chris!

I have no worries about this :-) BTW: Welcome the biology.stackexchange.


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Do all species have asymmetric female meiosis?
In all the examples I can think of, (mostly vertebrate), female meiosis, or oogenesis, only haploid gamete is produced while the other cell divisions result in polar bodies. While male meiosis results in 4 haploid gametes. This difference follows the fundamental definition of female and males being defined as resources committed into reproductive cells.
I want to know if this asymmetrical gamete production is truly universal across all organisms. Are all meiosis in plants or unicellular organisms unequal between male and female?

almost two years later and I'm returning to this question because I found a interesting paper relevant to this question. Turns out gametogenesis is much more variable than I ever knew.   "No universal differences between female and male eukaryotes: anisogamy and asymmetrical female meiosis"  http://onlinelibrary.wiley.com/doi/10.1111/bij.12874/full

Plant meiosis gives rise to four megaspores but usually upto three of them die by apoptosis leaving only one megaspore. But they are symmetric and three of them need not die all the time as it seems [REF].
Plasmodium being a haploid organism undergoes meiosis after fusion of gametocytes. Sexual differentiation is initiated at some point during the merozoite stage (See here and also the cross references).
Chlamydomonas is also haploid during its vegetative phase, and produces four flagellated haploid gametocytes. Sexual differentiation is apparently stochastic.
Perhaps there are more examples of organisms that do not undergo asymmetric division as seen in metazoa. There may be some stochastic asymmetry which leads to differentiation of sexes in the haploid unicellular eukaryotes and apoptosis in plant megaspores; these stochastic events may happen later as well. For plasmodium this is not really known; others I am not sure of.


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What kind of technology is required for plant seed DNA printing?
I'm a programmer so I have little knowledge in the field of biology. However I have an interest in plants, GMOs and DNA (in terms of programming).
So, I want to know what kind of technology is necessary and what limitations there are involved in creating a DNA printer (that could print out a cell to be grown in a pot).
First, how do we print the DNA of a plant? Can we print it all from the first pair of chromosomes? I have heard we are already able to print bacteria's DNA. Is this something we would be able to achieve outside of a lab? Could it be done on commercial scale?
Second, what conditions do we need to prepare the DNA if it is not that of a bacteria but rather of a plant that would grow into a multi-cellular organism? Can we really print a plant DNA, inject it into a cell and let it grow?
Third, what is the current understanding of DNA ? Can we analyze DNA strand with digital software yet? Can we simulate how the organism will do with the DNA? And how can I start working in this field? Are there any scientific papers I can learn from?
P.S. My first goal is to make a Nepenthes Vine. I want to have a vine plant like Pothos creeping on my fence with a jugs to eat insects.

We cannot print DNA. We can synthesize relatively long fragments of it, but this is costly and relatively slow. Additionally a cell is much more than its DNA. It is a bunch of proteins, I suggest you start by reading the Wikipedia article on it.

This is far too broad for a single question. You should read up on the basics and then post several more focused questions instead.

Before I have create this post I already seen things about DNA laser printer long times ago. So I want to ask you people how this field progress. Seem like not so much. And, somehow, I have seen most of tech blog calling "DNA Synthesize Machine" as "Printer" in so I think it is standard vocab

As Chris mentioned in his comment, 'printing' DNA from scratch (i.e. synthesizing a long strand de novo) is expensive and difficult. Unfortunately, the process of GMO creation is not as simple as assembling a beautiful DNA sequence on the computer, printing it, and then inserting it into a cell. Here's a related question about de novo sequencing. Plant biologists, please correct me if I'm wrong but I don't think it's a trivial matter to grow a plant from a single cultured cell.
Your third question reminds me of DNA programming, which is an amazingly cool, developing field. Many companies (including Microsoft) are funding research into DNA circuitry and biological computing, making computers out of biomolecules. Here's an interesting paper that will tell you more. What you may be most interested in is the branch of DNA programming that seeks to identify discrete protein-coding and otherwise functional DNA that can be utilized as a sort of "programming language" to build a new organism. One of my past supervisors recently joined this field and I'm a little jealous. Overall, this is a very new field so there is much to be accomplished and very little is technically possible, although the principle of GMOs is really just an optimization of an existing organism.
In summary, the answer to all three of your questions is: No, not very well. But we're trying.
Most likely this isn't something you'll be able to pick up in your spare time in order to have a cool plant to grow on your fence. It's very expensive and very difficult (in some cases, maybe even impossible). However, there are so many unknowns in this area of research and everything you propose is reasonable in theory. Let me know if you figure it out. I would love to code my own garden.

The closest we have come to achieving this was probably when the J. Craig Venter institute made a synthetic bacteria. They produced the genome for the smallest simplest bacteria they could find and it still took a large team of researchers several years and a LOT of money. Building a plant would be exponentially more difficult.
What complicates this is that you need more than DNA. You need the proteins that read the DNA and make RNA and more proteins. JCVI not only had to synthesize the DNA for the bacteria they wanted to make, but they had to take cells from another species of bacteria, remove all its DNA, then insert the new DNA. The leftover proteins from the previous species were able to read the new DNA, and make the proteins that built the new species. This only worked because the 2 species used were close enough that the same promoters and regulatory elements on the DNA could interact with the pre-existing protein. If you could make a plant genome and insert it into a bacteria, some plant proteins might be produced, but it would not be orchestrated well enough to actually produce a plant.


text:
Nature Scientific Reports vs. BMC Genomics
I do not know if this question to suitable here or not. I posted it as I think biologists can help me in this question. If not suitable here, then I am sorry for that.
I have written paper which I spent about 3 years working on it and it has nice findings and original sequenced data (deposited in NCBI). I submitted the paper to "Genome Biology" and I got editorial rejection but they offered to transfer the paper to "BMC Genomics". However, my supervisor refused this and suggested that we submit to "Nature Scientific Report". I tried to convince him to go to BMC Genomics because it is more focused journal and it is better for my CV, however, he said the second one is better because it has better impact factor and it is Nature! (Impact factor: 5 for Scientific Reports vs 4.04 for BMC Genomics).
What do you think as I am really confused which one to select?

This might also be a good question to pose on http://academia.stackexchange.com/

Not that journal metrics is the answer, but just for the record, BMC Genomics is ranked slighty higher based on the SCImago Journal Rank (SJR rank). In short, the SJR rank is a weighted impact factor, that takes journal prestige of citations into account. Might be useful when you discuss with your supervisor.

Thanks very much @Luigi and fileunderwater for the vey useful comments. Looking forward for more comments from other experts.

Personally, I would go for PLOS ONE, just because I am a big proponent of open-access publishing. I'm not sure about the BMC family, but Nature is notorious for its closed-access policies. I think that if your work was funded in any way by public grants (such as from the NIH in the US), your research should be open for all citizens to read if they want. I'm sure this argument has gone on long tangents on Academia.SE, but that's my view of things :) At any rate, do some research on different impact factors, and their relative advantages and disadvantages, then have a chat with your PI.

@MattDMo ALL BioMed Central journals are open access, as is Nat Sci Reports.

Indeed @blmoore. Even more, the nice chart by fileunderwater shows that Nat Sci Reports is moving fast in terms of citation

@blmoore thanks for the clarification. I've been working on non-publishable proprietary projects for a number of years in industry, so I haven't kept up to the minute on which journals are open-access.

Definitely try academics se - I'd also suggest nsr because it sounds like getting to bmc genomic is a safe card  now

I've voted to close this question because it is clearly opinion based. Whilst @Chris gave a good answer, there are many things I would disagree with on a subjective level.

This is too long for a comment, so I post it here. And these are my personal views, someone else might handle this different. I would submit the paper to BMC Genomics for some reasons:

The editor offered to transfer the paper, so you get past the
editorial review. This is not guaranteed for Nature Scientific Report
(NSR). You still have to get through the peer review, but this is not
different between both journals.
Honestly: Forget about the difference in the Impact Factor. Both are
medium range impact factor journals closely located together. My most
cited paper is published in such a medium impact journal, today you
find papers by a Medline search, so this doesn't matter anymore
(besides prestige). Additionally a lot of citations will raise the
journals impact factor in the future. I would understand this
argument when you would have to choose between Nature and BMC
Genomics, there is quite a difference.
If your work fits better into BMC Genomics the chance for acceptance
is higher, so I would go there. This is of course always a point of
consideration. The same is true for your CV.

If you have the chance to do the decision for yourself without angering your supervisor too much, I would go for it. Even better would be to convince him.

I disagree somewhat with the others comments. Scientific reports has a broader audience, higher impact factor and is associated with the Nature family of journals.
The BMC family of journal family does not have the same reputation and certainly plosONE does not, and has a reputation among some as publishing almost anything. For anyone outside your specific field they will consider publication in SR a better publication. This does not mean that SR is better journal in a scientific sense but if you are looking for prestige SR is better journal for sure.

I certainly disagree with this outdated view of bibliometrics. Impact factor is a highly contentious issue that may be directing science off-track and many people want an end to JIF. I agree association with Nature is still a big deal, and for a careerist that is the one to go for over BMC, furthmore showing commitment to open access science (which there are also problems with, but that's another story) is as important for young researchers. I certainly wouldn't disregard plosONE so flippantly. plosONE has a lot of dross, and a lot of outstanding publications.


text:
Concentration of caffeine in physiologically relevant setting
Caffeine is known to overcome G2/M (and possibly other types of) cell cycle arrest through its effects on DNA repair machinery and is used as a positive control in studies of cell cycle arrest. In this paper, for example, researchers use concentrations of caffeine in the 1-4 mM range to overcome nocodazole-mediated arrest. Is this a physiologically relevant concentration?
I found a lot of interesting caffeine data including the LD50 (estimated to be around 150-200 mg/kg) but have not been able to turn up any good numbers on reasonable concentrations that might be found in a human.

To make sure I understand your question right: You are looking for the physiologically occurring caffeine concentrations in the human body? For example after consuming coffee?

Yes, that is correct

Let's figure it out. Suppose an adult with an average blood volume of 5 L (5000 mL) drinks a cup of strong coffee with 100 mg of caffeine in it. Given caffeine's formula weight of 194.19 g/mol, and assuming 100% of the caffeine is in the blood stream, its concentration (from this awesome calculator page from Graphpad, the makers of Prism) would be approximately 103 µM, or 10-40 times less than what's being used in the experiments you cite.
Of course, this is overcoming drug-mediated cell cycle arrest, so its possible that a lower concentration is needed to jump-start physiologically-arrested cells.


text:
What does the root "phyllum" mean used botanical binomial nomenclature
I often encounter the root "phyllum" in binomial names in botany, but I've had trouble finding an actual definition for this root in any Latin dictionary outside of its taxonomic meaning. From context it seems to mean "leaf":

Acer macrophyllum - Bigleaf Maple
Tsuga heterophylla - A Hemlock with distinct two-ranked needles

But the Latin for leaf should be folium. Is there any real rhyme or reason to this? I don't know if this is a question better directed towards the Latin stackexchange, but I thought a botanist might have some insight on the subject.

Binomial names often use of greek words. Phyllum means -- as you correctly stated -- "leaf", but is not derived from latin but from the greek φύλλον, 'phyllon'.
By the way, there are also lots of examples where the latin word 'folium' is used. To stick with the genus Acer from your example, there is another species named Acer gracilifolium. So don't be confused by the linguistic chaos in binomial nomenclature.

Phyllum is used to refer leaf in Botanical nomenclature. How the word "Phyllum" is derived is not known.

Doesn't the existing answer already explain it? Why do you say it is not known?


text:
What enables azacitidine to incorporate into both DNA and RNA?
I did a mini-project on the drug azacitidine for my pharmacology class, and I learned that azacitidine has the ability to incorporate into both DNA and RNA. I think this is really unique because a similar drug, decitabine, is exclusively incorporated into DNA. Are there any specific physical/structural characteristics of azacitidine that allow it to affect the structure and function of DNA/RNA? Any help would be greatly appreciated!

If you look at the very beginning of the Wikipedia page, you'll see that azacitidine is an analog of cytidine, the C letter of both DNA and RNA fame. Decitabine is a deoxy derivative, and hence would only be incorporated into deoxyribonucleic acid, or DNA.
Reading further, by structure azacitidine is ribonucleoside derivative, and is preferentially incorporated into RNA. However, it can be metabolized to 5-aza-2′-deoxycytidine-triphosphate and so be incorporated into DNA.


text:
Are all functions of a human cell known?
Please bear with me as I'm intruding into your world from a computer science background.
In programming, once you have created a program, you know all functions of that program. Thus, 100% knowledge is achieved.
My question is, in the field of Biology, how much do we think we currently know about the human cell? Are all functions known (eg. 100%)? Are most functions known (60%)? Or do we know a miniscule proportion (1%~5%) of functions of a cell.
The reason I ask is I'm interested in the concept of simulating cells via computer. If we know about a given biological function of a cell, we could convert it into a mathematical function for use within a simulation. With simulations, you could simulate the cell's reactions to drugs, viruses, cell garbage cleanup, etc, based on it's defined functions. And the more functions we know about human cells, the better the simulation.
Thanks in advance.

It's difficult to estimate this because, in cellular biology, one new discovery (be it protein-protein interaction, drug response, etc.) may reveal 20 different, novel unknowns. As a programmer who has undertaken a similar modeling project, you're going to need to focus on specific areas of interest (i.e. signalling pathways) for specific responses, and you'll have to trust that your simulation will not be perfect, nor even great. I hesitate to even put a percentage to it but I'd err on the side of "miniscule".

There is a huge difference between designing a program and attempting to reverse engineer a program, as biologists are trying to do in biological terms with cells. We are only aware of some principles but many details are yet to be discovered and explored!

Can cellular functions be 'mapped' out in such a way where with some 'subsystem' and how it 'behaves' it's functions can be 'modelled' with useful precision not in terms of an accurate description but a description adequate enough to be useful in real medicine; like Harvey's model of blood circulation in the Heart and arteries and veins. At the time a breakthrough model but now not that accurate. At least a biological model can be made and refined. Can all cell functions be modeled like this without needing to discard any 'attempted' models?

As @Bez stated there is a fundamental difference between understanding something self-contained that you've constructed and learning about something unknown. Also, knowing 100% of functions should roughly translate to prediction withour error, which is clearly not the case for biological processes. From an epistemological standpoint estimating the %-knowledge of natural systems is almost nonsensical, since it assumes that we can compare to a complete list of "truths", when all we know is what we have been able to observe so far.

As someone who has dabbled in both biology and programming, I assume you are referring to the theoritical ability  of functional programming to simulate organic behaviour from well defined input. From that point of view, our comprehension of the human cell behaviour is  currently near stone age level.
The astounding diversity of homeostatic and signaling parameters in our body makes a realistic simulation of human cell normal behaviour largely out of reach, so don't even think about patholgic states.
The more data we will acquire, the more precise our simulations will be. Currently, our data acquisition methods are too primitive, and clearly are not deterministic enough to base computed simulations upon them.
Of course, this answer reflects my own opinion, but I dare think that most of my colleagues will adhere to that view.


text:
Does trypsin strip flask coating?
Mammalian cell/tissue cultures sometimes require flasks coated with proteins. My uneducated guess is that these proteins mimic the ECM, perhaps the basal lamina, so finicky contact-dependent cells can attach to it.
For instance, I have a BEAS-2B tracheal culture which requires a coating of albumin, fibronectin and type I collagen. This is applied by incubating an empty plastic dish or flask with a solution of these proteins overnight. I give this as an example of what a "coat" constitutes. You answer should be general enough to apply to at least the most common coat types, or if it depends on the coat, you should explain how.
Likewise, there is some variation in how the trypsinization occurs. To have a starting point, let's say I am trypsinizing according to typical ATCC recommendations: 5 minutes with 0.25% Trypsin-0.53 mM EDTA, then inactivate with equal volume medium. I haven't worked with a cell that can withstand this noticeably (but then I haven't worked with any exotic cells).
My question: When I trypsinize the cells to passage, what happens to the coat?
Since trypsin is a protease that cleaves even the attachment of cells to plastic, I am guessing that it will also destroy the coat. After the trypsin and cells are removed, the flask will have a tiny fraction of the protein coat that it had before, and will not support cells that require a coat any longer.
Am I correct in thus deducing that coated flasks cannot be reused after trypsinization? Are any of the alternative detachment reagents an exception to this?

Interesting question. Since I don't have a real answer at the moment, I would say it depends strongly on the incubation time. The longer you digest, the more of the coating will be digested, too.

@Chris Good point, edited.

Generally the coating is of poly D-Lysine. Proteases act only on L-amino acids. Moreover the amide bond in PDL is between the ε-amino group & carboxyl instead of the α-amino group as in peptide bonds. So, I guess nothing should happen to the usual coated flasks. I have used the same flask for 2 rounds of trypsinization, and the cells seemed to be fine.

A small correction: PDL is not ε-amide, nonetheless the D-conformation would make it resistant to protease.

@WYSIWYG That's an interesting point. However, what about the coat I mention? Corning fibronectin is isolated from human plasma, Corning collagen I is from cow plasma, and NEB does not clearly explain where they get their albumin (they say "fraction V") but I think it's also purified from an animal product. I thought all of these would come out as L-isomers.

Generally the coating is of poly D-Lysine. Proteases act only on L-amino acids. So, I guess nothing should happen to the usual coated flasks. I have reused the flask even after 2 rounds of trypsinization, and the cells seemed to be fine.
In your case, the matrix is made of proteins isolated from animal sources. They are susceptible to proteolysis. You are right to assume that these flasks should not be reused. If you have a shortage of flasks then you can buy uncoated petriplates (which are cheaper) and coat them yourself.

You should check the composition of the coating by using trypsin, e.g. poly-L-lysine or poly-D-lysine are usually applied:

Polymers of both D- and L-lysine are used to coat solid surfaces.
  Poly-L-lysine has been reported to improve the protein coating of
  ELISA plates. 6,7 However, in culture applications, certain cells can
  digest poly-L-lysine. In this situation, poly-D-lysine should be used
  as the attachment factor so that the cells are not disrupted by
  excessive uptake of L - lysine. The lower molecular weight
  poly-D-lysine (30,000 - 70,000) is easier to use because it is less
  viscous in solution, but the higher molecular weight poly-lysine
  (>300,000) provides more attachment sites per molecul e. The molecular
  weight poly-D-lysine often preferred by users is the 70,000 - 150,000.

Poly-D-lysine Hydrobromide - Sigma

Trypsin does not seem like to hydrolise poly-D-lysine. Roughly it is specific to L-Lys and L-Arg, so if your coating contains these amino acids (in your case it does), than it will be degraded.

Trypsin (EC3.4.21.4) is part of the serine protease family. Trypsin
  cleaves lysine and arginine at the C-terminal side of the peptide. The
  hydrolysis rate is slower if an acidic residue is on either sides of
  the cleavage site and no cleavage occurs if a proline residue is on
  the carboxyl side of the cleavage site. Trypsin optimum pH is pH-7 to
  9. Trypsin will also hydrolyze ester and amide linkages of synthetic derivatives of amino acids such as: benzoyl L-arginine ethyl ester
  (BAEE), p-toluenesulfonyl- L-arginine methyl ester (TAME),
  tosyl-L-arginine methyl ester, N-α-benzoyl-L-arginine p-nitroanilide
  (BAPNA), L-lysyl-p-nitroanilide, and benzoyl-L-tyrosine ethyl ester
  (BTEE). Serine protease inhibitors that inhibit recombinant trypsin
  include TLCK (N-p-tosyl-L-lysine chloromethyl ketone), PMSF
  (phenylmethanesulfonyl fluoride), benzamidine, soybean trypsin
  inhibitor, and ovomucoid.

Trypsin Human, Yeast - ProSpec, or Sigma here

After incubation with 1mg/mL trypsin solution at 37°C for 1h, neither
  PLL nor PDL was found to be hydrolyzed, as indicated by the constant
  number of molecules found on the surface. The reason is that the
  entire polylysine chain was adsorbed to the surface, and steric
  hindrance and electrostatic repulsion prevented trypsin molecules from
  approaching the cleavange sites. To make polylysine exposed and
  available to trypsin digestion, a DSU SAM surface was created. A
  uniform coating of 5nm chromium and 30nm gold was first introduced on
  the slides. On top of that metal coating, an amine-active
  cross-linker, DSU SAM, was formed to covalently immobilize
  AF532-PLL/PDL molecules. After the free peptide molecules were
  removed, the slide was incubated with 1mg/mL trypsin at 37°C for 1h.
  The trypsin and cut polylysine fragments were then thorougly washed
  off. Intact PLL and PDL molecules had similar fluorescence intensities
  and surface number densities before trypsin was introduced. However,
  it is clear that trypsin digested PLL but not PDL. From over 30 images
  of different areas of the slides, for PLL the average numbers of
  molecules counted were 227±16 and 0 per frame before and after
  hydrolysis, respectively. In contrast, the corresponding numbers for
  PDL were 241±15 and 234±20 per frame, respectively. As explained in
  Emil Fisher's analogy of the lock and key, the L-isomer can fit the
  active site of trypsin bettern than the D-isomer. One reason is that
  only the L-isomer undergoes a coil to α-helix transition upon binding
  with the enzyme, while the D-isomer remains disordered.

2008 - Applications of single-molecule detection in early disease diagnosis and enzymatic reaction study

So the result depends on the type of the coating. Btw. I think the easiest way to decide would be to check it with an experiment. (Note that I know nothing about coatings, just trypsin.)

In case someone finds this thread and wants an answer. In this paper (J Biomed Mater Res A. 2005 Oct 1;75(1):1-13.) the authors show that trypsinization does indeed remove the protein coating from the culture vessel.


text:
To what extent is Ebola airborne? (aerosols)
Recently, CIDRAP at the University of Minnesota announced that Ebola may be more transmissible through aerosols than previously thought.
I lack the familiarity with the field to critically evaluate this release. They also seem to more interested in making the point that there is a risk of aerosol transmission, not to settle whether it does transmit by air or not.

What is the simple answer? Can Ebola really be transmitted by aerosols?
If so, how come nobody realized this before? Is this a general phenomenon allowing any pathogen to become airborne? I don't see why you couldn't aerosolize a great many pathogenic objects, not just Ebola virus.
How does the number of virions necessary for successful infection compare to what you could get from aerosols?

Related: http://biology.stackexchange.com/questions/21481/how-is-it-possible-to-even-hope-for-an-ebola-epidemic-of-this-current-size-to-re

Interesting question and hard to answer definitively. First of all: It seems still pretty clear that the major (and by far most important) infection route comes from direct contact with infected people or their body fluids and that aerosol transmission is of far less significance. Ebola is infecting cells of the immune system (mostly macrophages and dendritic cells) which are located in the skin which makes the route through the respiratory organs pretty uneffecient, but it is possible.
However, there are reports for Ebola transmissions (or at least unclear cases in which a direct contact could be excluded), which suggest that the aerosl transmission is possible. There are reports of Ebola infections which spread among experimental animals between infected and non-infected (and without direct contact) control groups. This has been observed between rhesus monkeys and pigs. It was also possible for the pigs to infect non-human primates (see references 1-4 for details).
This results should be seen with some caution: At least for pigs an Ebola infection seems to be pretty much different than one in humans. There it looks more like a respiratory disease with all what comes along with it: Extended sneezing and coughing - which makes a lot of aerosol droplets. See reference 3 for the original paper and 5 and 6 for a summary and a classification. I think it is also possible that anatomical differences to the humans make such an infection route easier or harder.
Finally there are some reports of infected people which had no direct contact to people (see reference 7). However, this is rare and mostly restricted to people which where involved in health care for infected persons. These people come in close contact to the infected people which raises their chance of getting infected by aerosols. This underlines the importance for health care workers to get the right protective equipment.
References:

Transmission of Ebola virus (Zaire strain) to uninfected control
monkeys in a biocontainment laboratory.
Replication, Pathogenicity, Shedding, and Transmission of Zaire
ebolavirus in Pigs
Transmission of Ebola virus from pigs to non-human primates
Aerosol exposure to Zaire ebolavirus in three nonhuman primate
species: differences in disease course and clinical pathology
Pig-to-monkey Ebola: is there something in the air?
New paper on Ebola–no primate-to-primate transmission seen
Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo,
1995: Risk Factors for Patients without a Reported Exposure

Nice answer but I think "spreaded" isn't a word and should be just "spread".

@Mew You're right. It's an irregular verb. BTW: If you spot errors like these, click on the edit function below an answer or question and correct it. Your edit will undergo a review until you have a certain number of credit points. This is a perfectly accepted way of improving answers.

It is not airborne, because if it had be we would have a really big problem.

Normal immunocompetent mice are not susceptible to non-adapted
  filoviruses. There are therefore two strategies available to establish
  a murine model of filovirus infection: adaptation of the virus to the
  host or the use of genetically modified mice that are susceptible to
  the virus. A number of knockout (KO) strains of mice with defects in
  either their adaptive or innate immunity are susceptible to
  non-adapted filoviruses. In this study, A129 α/β −/− interferon
  receptor-deficient KO mice, strain A129 IFN-α/β −/−, were used to
  determine the lethality of a range of filoviruses, including Lake
  Victoria marburgvirus (MARV), Zaire ebolavirus (ZEBOV), Sudan
  ebolavirus (SEBOV), Reston ebolavirus (REBOV) and Côte d’Ivoire
  ebolavirus (CIEBOV), administered by using intraperitoneal (IP) or
  aerosol routes of infection. One hundred percent mortality was
  observed in all groups of KO mice that were administered with a range
  of challenge doses of MARV and ZEBOV by either IP or aerosol routes.

2011 - Lethality and pathogenesis of airborne infection with filoviruses in A129 α/β −/− interferon receptor-deficient mice

Ebola virus disease is not an airborne infection. Airborne spread
  among humans implies inhalation of an infectious dose of virus from a
  suspended cloud of small dried droplets.
This mode of transmission has not been observed during extensive
  studies of the Ebola virus over several decades.

2014 - WHO - What we know about transmission of the Ebola virus among humans

The virulence (ID50, LD50) is unkown for humans, but ebola is considered a highly virulent disease with low LD50 based on the studies with animals.

INFECTIOUS DOSE: Viral hemorrhagic fevers have an infectious dose of 1
  - 10 organisms by aerosol in non-human primates Footnote 41.

1997 - EBOLAVIRUS - PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

Although outbreaks of Ebola virus have largely been confined to
  endemic regions, their high fatality rate, ability to transmit
  person-to-person, and low lethal infectious dose make Ebola virus a
  dangerous threat to public health and pose a great risk for
  researchers working with these viruses as well as health care
  personnel treating patients during outbreaks. Furthermore, their
  potential to be developed into aerosolized biological weapons also
  causes grave concern for their use as a bioterrorism agent ( Bray,
  2003).

2008 - Protection against lethal challenge by Ebola virus-like particles produced in insect cells

Ebola virus is a highly virulent pathogen capable of inducing a
  frequently lethal hemorrhagic fever syndrome. Accumulating evidence
  indicates that the virus actively subverts both innate and adaptive
  immune responses and triggers harmful inflammatory responses as it
  inflicts direct tissue damage. The host immune system is ultimately
  overwhelmed by a combination of inflammatory factors and virus-induced
  cell damage, particularly in the liver and vasculature, often leading
  to death from septic shock. We summarize the mechanisms of immune
  dysregulation and virus-mediated cell damage in Ebola virus–infected
  patients. Future approaches to prevention and treatment of infection
  will be guided by answers to unresolved questions about interspecies
  transmission, molecular mechanisms of pathogenesis, and protective
  adaptive and innate immune responses to Ebola virus.

2007 - Immunopathology of highly virulent pathogens: insights from Ebola virus

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal
  cavity was ~1 virion. Mice were resistant to large doses of the same
  virus inoculated subcutaneously, intradermally, or intramuscularly.
  Mice injected peripherally with mouse-adapted or intraperitoneally
  with non-adapted EBO-Z virus resisted subsequent challenge with
  mouse-adapted virus.

1998 - A Mouse Model for Evaluation of Prophylaxis and Therapy of Ebola Hemorrhagic Fever

The high virulency is compensated by low transmissibility, that's why it is not a real threat currently for western countries (it is easy to quarantine). The current strain seems to be special, because it has about 100 times higher mutation rate than the old ones. It may mutate into a more transmissable strain, but I think there is not enough data and knowledge available to calculate the risk of such an event.

Sequencing of 99 different Ebola isolates from patients in the 2014
  West African outbreak of Ebola showed the virus to be rapidly
  mutating,[15] with a mutation rate of 2.0 x 10-3 substitutions per
  site per year making it as fast changing as seasonal influenza.[16]
  This is likely to represent rapid adaptation to human hosts as the
  virus is repeatedly passed from human to human (as opposed to usually
  being passed between fruit bats and only occasionally crossing over
  into humans), and may pose challenges for the development of a vaccine
  to the virus.[17][18]

wikipedia - Ebola virus

Molecular evolutionary analyses for Ebola and Marburg viruses were
  conducted with the aim of elucidating evolutionary features of these
  viruses. In particular, the rate of nonsynonymous substitutions for
  the glycoprotein gene of Ebola virus was estimated to be, on the
  average, 3.6 x 10(-5) per site per year. Marburg virus was also
  suggested to be evolving at a similar rate. Those rates were a hundred
  times slower than those of retroviruses and human influenza A virus,
  but were of the same order of magnitude as that of the hepatitis B
  virus. When these rates were applied to the degree of sequence
  divergence, the divergence time between Ebola and Marburg viruses was
  estimated to be more than several thousand years ago.

1997 - The origin and evolution of Ebola and Marburg viruses.

Thinking that ebola can evolve to become airborne is kind of like thinking horses can evolve to fly. It's not that kind of virus. What it can do, though, is very dangerous, akin to a horse learning to run faster.

@anongoodnurse I don't know whether airborne ebola is possible, but it certainly can become a more transmissible disease, e.g. it can become more stable in vitro, more resistant to UV light, heat, etc...

But it won't learn to float on dust particles. Probably the most dangerous mutations would involve a decreased virulence, such that people will not feel as sick early on (while maintaining transmissibility) so that quarantines are rendered less effective. But it's all speculative.

@anongoodnurse Then why are we talking about it? "I think there is not enough data to calculate the risk or say something about it is possible or not."

Just trying to counter a common but unfounded fear. Is there a reason we should not?

@anongoodnurse Do you have any evidence that it is unfounded?

@anongoodnurse I don't think the current level of life science and technology is enough to decide this question. We know too few about the ebola virus and viral evolution. I will remove the airborne ebola from the post, because there is no evidence about whether it is possible.

Me personally? No. But I quote Dr. Eric Lander, geneticist, molecular biologist, mathematician, and computational biologist (among other stellar qualifications) the founding director of the Broad Institute of MIT and Harvard, a principal leader of the Human Genome Project, a professor of biology at MIT and professor of Systems Biology at Harvard Medical School who is also Co-Chair of the President’s Council of Advisors on Science and Technology. That's good enough for me to give credence to his opinion that it won't happen.

@anongoodnurse Quoting somebodies personal opinion is not an evidence. We need a viral evolutional model with all of the possible (or at least the closest) more transmissible outcomes which we can use to calculate the risk. Currently no such model is available as far as I know, and I think there won't be such a model for many decades, because we know so few.

I thought earlier you said we needed a "life scientist." Key phrase: as far as (you) know.

@anongoodnurse I don't know what you are talking about.

Although the chance of Ebola getting airborne is bigger than zero and thus be possible, it is highly unlikely. The reason for this is quite simple: To act like this it needs to change the cells it infects. For viruses which are transmitted by aerosols these are commonly the (epithelial) cells of the respiratory tract. See the flu for example. To do so ebola most likely has to change the receptors it uses to invade cells and also the way it transmit. Both has never been observed before and would probably be a new virus afterwards.

@Chris It already infects epithelial cells using NPC1 and TIM1 receptors. So the only barrier it has to break down is the new way of transmission. I don't know how hard that is, we will see in the next few years I guess. (There were several studies on animal models, in which it was proven that it is possible to infect with a small dosage of aerosol. LD50 was around 1 virion.)


text:
Fate of erythrocytes after splenectomy
The spleen is considered a graveyard for red blood cells. So in case of Splenectomy (complete surgical removal of the spleen), what would be the fate of red blood cells? Would this cause Polycythemia?

The spleen is not the only organ which removes "old" erythrocytes, this happens as well in the liver and the lymph nodes. The whole process is termed Eryptosis, the Apoptosis of Erythrocytes. During the aging of erythrocytes sialic acid on their outer membrane surface is removed. This leads to the recognition by macrophages and phagocytosis of this cells by macrophages which are located in liver and spleen. For more information see this article: "Physiology and Pathophysiology of Eryptosis"
Polycythemia is the state when you have an elevated number of red blood cells, characterized by an increased Hematokrit level. This is caused by the over-production of red blood cells, which can be caused by an overproduction of hematopietic cells in the bone marrow (so called myeloproliferative syndrome, which are basically cancers), the exposure to permanently low oxygen-levels (this is what athletes exploit when the do training at high altitudes) or malignancies (usually lymphoma). It is also possible due to the mis-use of Erythropoietin (EPO) which induces the production of red blood cells. Another possibility for having too much red blood cells is the over-transfusion during a blood transfusion. For further information have a look into the Wikipedia. The article there is pretty complete and contains a number of references.

Lymph nodes do not play a role on RBC destruction. There are no red cells in lymph. Nor does your article support it.

When you downvote, could you please make a short comment about your criticism? Only then answers can be improved. Alternatively you could write an own (and better) answer.

So in case of Splenectomy (complete surgical removal of the spleen),
  what would be the fate of red blood cells? Would this cause
  Polycythemia?

According to wikipedia none of the side effects are related to red blood cell count (just the quality of those cells).

As splenectomy causes an increased risk of sepsis due to encapsulated
  organisms (such as S. pneumoniae and Haemophilus influenzae) the
  patient should receive the pneumococcal conjugate vaccine (Prevnar),
  Hib vaccine, and the meningococcal vaccine; see asplenia. These
  bacteria often cause a sore throat under normal circumstances but
  after splenectomy, when infecting bacteria cannot be adequately
  opsonized, the infection becomes more severe.
An increase in blood leukocytes can occur following a
  splenectomy.2 The post-splenectomy platelet count may rise to
  abnormally high levels (thrombocytosis), leading to an increased risk
  of potentially fatal clot formation. There also is some conjecture
  that post-splenectomy patients may be at elevated risk of subsequently
  developing diabetes.4 Splenectomy may also lead to chronic
  neutrophilia. Splenectomy patients typically have Howell-Jolly
  bodies5 and less commonly Heinz bodies in their blood smears.7
  Heinz bodies are usually found in cases of G6PD (Glucose-6-Phosphate
  Dehydrogenase) and chronic liver disease.8

wikipedia - Splenectomy

Splenectomy can be recommended by inherited blood diseases (e.g. hereditary spherocytosis, thalassemia, etc...) which cause anaemia due to the destruction of abnormal red blood cells in the spleen. After surgery the RBC count is around normal in these cases, so removing the spleen does not cause polycythemia. If you check wikipedia - polycythemia, splenectomy or other spleen related diseases do not cause polycythemia, while polycythemia can cause enlarged spleen which may be removed.
Erythropoiesis and so red blood cell count is regulated by EPO which is regulated by blood oxygen level, so spleen does not regulate the production of red blood cells directly. Removing the spleen cannot cause upregulation of EPO and so polycythemia. Mean erythrocyte age is increased, so in long term there can be a slight increase of RBC count because of a function loss by old cells, but that is not significant enough to cause disease.

2010 - Partial splenectomy for hereditary spherocytosis: a multi-institutional review
2014 - The spleen and sickle cell disease: the sick(led) spleen
2013 - Red blood cell vesiculation in hereditary hemolytic anemia
2007 - Erythropoietin after a century of research: younger than ever
1982 - Glycosylated hemoglobins (GHb): an index of red cell survival.

To support the speculation that macrophages might also have a function
  in erythropoiesis in the context of disease and to further
  characterize their importance in erythropoiesis in vivo, Ramos and
  colleagues show that macrophages regulate erythroid development in
  polycythemia vera, β-thalassemia and anemia (Ramos et al., 2013).
  Chemical depletion of macrophages by clodronate liposome
  administration prevents mice from recovering from induced anemia,
  suggesting an essential function of macrophages in promoting stress
  erythropoiesis in vivo. Conversely, macrophage depletion not only
  improves the phenotype of polycythemia vera and reverses the
  pathological aspects of the disease, but also alleviates anemia caused
  by β-thalassemia. These results propose an important dual role of
  macrophages in physiological and pathological erythropoiesis in vivo.
  Both studies suggest that macrophages exert two seemingly
  contradictory actions on erythropoiesis. On one hand, macrophages are
  indispensable for stress erythropoiesis in vivo. In their absence
  erythroid production in the bone marrow and spleen in response to
  bleeding is impaired. However, macrophages can also be deleterious in
  the context of polycythemia vera and β-thalassemia, since depletion of
  macrophages leads to a decreased disease pathology. Moreover, ex vivo
  cultured human macrophages from polycythemia vera patients promote
  proliferation of human erythroblasts and diminish differentiation.
  This suggests a function for macrophages in disease progression since
  polycythemia vera is characterized by an overactive erythron and
  excessive erythropoiesis (Ramos et al., 2013). These findings might
  pave the way to future therapies implementing macrophage depletion in
  the treatment of erythroid disorders like polycythemia vera and
  β-thalassemia.

2014 - Review article of macrophages and red blood cells; a complex love story

Recovery after surgery is about 4-6 weeks. Liver and lymph nodes can take over the functions of the spleen partially. Every blood cell count may be elevated (esp. platelet count). The functions of the spleen are:

storing iron (in the form of ferritin or bilirubin, to protect it from pathogens)
storing blood (for the case of blood loss e.g. injury)
filtering out damaged or old blood cells (by inherited diseases abnormal red blood cells are removed from blood as well)
filtering out phatogens, infected blood cells, etc... (to protect the body from sepsis)

And ofc. a lot of immune cells live there. Therefore in rare cases sepsis can occur after splenectomy immediately, and can cause life threatening conditions.

2001 - Infectious complications in asplenic hosts
1996 - Overwhelming postsplenectomy infection
1975 - Immunological studies in the postsplenectomy syndrome
1995 - Preservation of the spleen improves survival after radical surgery for gastric cancer.
2009 - Effect of splenectomy on antitumor immune system in mice.
2012 - Thrombocytosis in asplenia syndrome with congenital heart disease: a previously unrecognized risk factor for thromboembolism.
2009 - Vascular complications after splenectomy for hematologic disorders
2014 - Review article of macrophages and red blood cells; a complex love story

Asplenic individuals are compromised not only in their ability to
  destroy infectious agents, but are at increased risk for death from
  autoimmune disease, certain tumors, and ischemic heart disease.
  Enhanced mortality is attributed to lack of phagocytes sequestered in
  spleen that efficiently engulf and destroy appropriate targets,
  although related cells are found elsewhere.

2012 - SIRPα/CD172a and FHOD1 Are Unique Markers of Littoral Cells, a Recently Evolved Major Cell Population of Red Pulp of Human Spleen
2011 - Splenectomy Associated Changes in IgM Memory B Cells in an Adult Spleen Registry Cohort

The spleen contains immune cells, from which macrophages phagocytose the senescent red blood cells. They degrade the hemoglobin into amino acids, bilirubin and iron. The iron is sent to the blood with transferrin, which can be captured and stored by the spleen or the liver or can be used to build new red blood cells in the red bone marrow. The amino acids can be used to build new proteins or they can be degraded by the liver or the kidney. The bilirubin is transported to the liver where it is conjugated and excreted into the bile. The other parts of the red blood cells are recycled as well. For the macrophages it is easier to do this kind of work if you have a dedicated organ which can help to filter out the cells for destruction, but it is not impossible without it, because macrophages live in other organs/tissues as well.
Red blood cells can get rid of damaged parts by creating microvesicles so they can elongate their lives. Vesiculation is facilitated by the spleen. These microvesicles can contain hemoglobin as well, and they are captured by the liver.

2004 - The red cell revisited--matters of life and death.
2008 - Microvesicles in haemoglobinopathies offer insights into mechanisms of hypercoagulability, haemolysis and the effects of therapy
2003 - Hemoglobin loss from erythrocytes in vivo results from spleen-facilitated vesiculation
RBC Storage
2008 - RBC-derived vesicles during storage: ultrastructure, protein composition, oxidation, and signaling components.

The macrophages of the spleen have a remarkable function that enables
  them to remove unwanted damage from the RBC membrane, leaving the RBC
  intact (Crosby, 1957; Schnitzer et al., 1972). Removal of these
  intracellular inclusions seems to occur within the open circulation
  where the RBC are also checked for their loss of deformability to
  check for age. To achieve this, RBC must pass through the endothelial
  slits of the sinus to reenter the blood circulation. During this
  course, cells that are non-deformable will be removed from the
  circulation by residential macrophages. In the mean-time all inclusion
  bodies are also being removed. In splenectomized patients or in
  patients with a non-functional spleen, phagocytosis of the inclusion
  bodies fails and results in a retention of a variety of intracellular
  inclusions within the RBC, such as Howell-jolly bodies (inclusions of
  nuclear chromatin remnants) (Wilkins and Wright, 2000), Heinz bodies
  (inclusions of denatured hemoglobin caused by oxidative damage)
  (Wilkins and Wright, 2000) siderocytes (RBC containing granules of
  iron that are not part of the cell's hemoglobin) (Wilkins and Wright,
  2000) and Pappenheimer bodies inclusion bodies formed by phagosomes
  that have been engulfing excessive amounts of iron (Wilkins and
  Wright, 2000).
The molecular mechanism that underlies the removal of inclusion bodies
  is largely unknown. In Willekens et al. (2003) presented an analogy to
  the removal of Heinz bodies when discussing RBC that lose hemoglobin
  through vesiculation. Via the process of RBC vesiculation the RBC
  loses aggregated hemoglobin, which is important to maintain the
  homeostasis of RBC, increases in density and becomes smaller (Piomelli
  and Seaman, 1993). It was suggested that this process is also
  facilitated by the macrophages of the spleen, in which older cells
  vesiculate more than younger ones. Clearly, macrophages play a pivotal
  role in the clearance of damaged content from circulating RBC (Crosby,
  1957; Willekens et al., 2003) and vesiculation is an interesting and
  plausible mechanism to explain the efficient removal of damaged
  content while leaving the RBC intact (Wilson et al., 1987). The
  molecular mechanism by which macrophages in the spleen would be
  facilitating RBC vesiculation is still unknown.

2014 - Review article of macrophages and red blood cells; a complex love story

Aged or abnormal red blood cells with exposed phosphatidylserine
  (PS-RBCs) are cleared from the circulation by splenic macrophages. In
  asplenic patients, other mononuclear phagocytic cells in tissues and
  in circulation may function in this capacity.

2010 - Activation of mononuclear phagocytes and its relationship to asplenia and phosphatidylserine exposing red blood cells in hemoglobin E/β-thalassemia patients

Suicidal death of erythrocytes (eryptosis) is characterized by cell
  shrinkage, membrane blebbing, activation of proteases, and
  phosphatidylserine exposure at the outer membrane leaflet. Exposed
  phosphatidylserine is recognized by macrophages that engulf and
  degrade the affected cells. Eryptosis is triggered by erythrocyte
  injury after several stressors, including oxidative stress.

2006 - Mechanisms and significance of eryptosis.

CD47 on erythrocytes inhibits phagocytosis through interaction with
  the inhibitory immunoreceptor signal regulatory protein alpha (SIRPα)
  expressed by macrophages. Thus, the CD47-SIRPα interaction constitutes
  a negative signal for erythrocyte phagocytosis. However, we recently
  reported that CD47 does not only function as a ‘don't eat me’ signal
  for uptake but can also act as an ‘eat me’ signal. In particular, a
  subset of old erythrocytes present in whole blood was shown to bind
  and to be phagocytosed via CD47- SIRPα interactions.

2013 - CD47 functions as a removal marker on aged erythrocytes
2013 - Mechanisms tagging senescent red blood cells for clearance in healthy humans
2011 - Physiologically aged red blood cells undergo erythrophagocytosis in vivo but not in vitro
2011 - Human red blood cell aging: correlative changes in surface charge and cell properties
2012 - Naturally Occurring Autoantibodies in Mediating Clearance of Senescent Red Blood Cells


text:
Is viral protein expression important for peptide vaccine?
I would like to know if proteins expressed in higher quantities, such as DNA polymerase, would be better vaccine candidates for a T-cell based vaccine.

To find candidate proteins which can be used as peptide vaccine, these need to fulfill some criteria:

The most important is that the peptide (or protein) used for
vaccination shall not have a closely relate sequence in the organism
in which the vaccination shall occur. Otherwise either no reaction
(due to immunologic tolerance to self) or an autoimmune reaction
might happen.
The peptide/protein need to be expressed on the surface of the
microbe (either virus or bacteria) since otherwise it will not be
recognized by the immune system. Also domains of a potential vaccine
candidate which are inside of membrane are not useful.
The epitope needs to be stable enough to be used as a vaccine and
also be present on the microbe (otherwise there is no immune
reaction).

If you want to read further on this topic, there is an interesting Paper from the WHO available, which gives a nice introduction:

Guidelines for the production and quality control of synthetic
peptide vaccines

To answer your question: No, these proteins cannot be used for this purpose, as they are relatively closely related to the same proteins in the human body. This will probably lead to no immunologic reaction at all. Additionally, these proteins are located inside of cells and thus not exposed to the immune system.

I have doubts about the second statement. If virus replicates inside the cell, virus will let some proteins located inside cells to proteasome degradation and thus will be exposed via MHC, thus revealing to CD8+ cells that has been infected.

@Bernardo When a virus infects a cell it basically takes over. In most cases the cell is lost and destroyed when the viruses are set free. Additionally you want to find and inhibit the virus when it enters the body, not when it already had time to replicate. This is something you will achieve only when you recognize the virus.

I agree that neutralizing antibodies are a good strategy to prevent a new cell infection. But, why are T cell-based epitops have that hype? http://www.ncbi.nlm.nih.gov/pubmed/22044118    http://www.ncbi.nlm.nih.gov/pubmed/24358361

I don't understand this either - this approach always needs the professional antigen presenting cells which present the antigen on their MHC-molecules. So T cells do not stand alone.

@Bernardo Chris is right, you are not able to activate CD8+ T-cells without APC. So you need a badly infected APC or an APC presenting your protein on MHC1/MHC2 and a CD4+ T-cell which verifies that it is really a pathogen. I am not certain whether it is possible to achieve T-cell response by vaccination, but it is certainly harder than to achieve B-cell response...

@Bernardo For me your link means that we need more research to create T-cell vaccines... I can agree with your point of view, I think the answer should be extended with the term B-cell vaccines. So it is just partially valid in this context.

The original question asks about vaccine development against a virus. Most effective anti-viral vaccines elicit antibody responses that presumably protect via neutralization of viruses as they enter the body. Bob Seder has a good review on this - you may find a discussion relevant to this topic in the section titled "Viral targets for the induction of humoral immunity". These vaccines would not necessarily be leading to the destruction of infected cells as this is a CTL function.
I think the hype that biotech is referring to is in relation to therapeutic vaccines against cancer, etc. that elicit CTL responses capable of destroying cancer cells. However, it is also important to keep in mind that both CTLs and B Cells need CD4 T Cell help in order to develop - nothing stands alone in the immune system.


text:
Can a human cell live indefinetely in a controlled environment?
How long can a human cell live in a controlled environment, given all necessary nutrients, temperatures, mechanisms for waste removal, and other requirements are provided for? Put differently:

Can a human cell live on indefinitely?
What's the longest known lifespan recorded for a human cell in a controlled environment?

Theoretically yes but for dividing cells they are hindered by the hayflick limit. In vivo in terms of differentiated cells, motor neurones tend to live quite long (the longest I believe) but then again you have stem cells, which through constant replication can propagate or live on. This is a fairly broad question and requires some concept clarification!

Would you count immortalised cells?  Would they need to be primary cells taken directly from a body?  Primary cells are actually quite difficult to work with/keep alive.  Double for stem cells, they differentiate if look at them funny.

The oldest cell line (to my knowledge) is the Hela cell line from the mid 50s. Cancer cells can live forever if the conditions are right (no pesky humans involved that die), but they also accumulate chromosomal damages.

This question is at least two questions.
Dividing cells
In terms of a dividing human cell line, every time a division occurs the telomeres capping the ends of the chromosomes get a little bit shorter. Once the telomeres get short enough they act as a signal that triggers apoptosis, destroying the cell. There is some human-to-human variation in the initial length of the telomeres, but the impression I've gotten from hanging around cell biologists is that the division limit is somewhere on the order of 10-100.
There are also cells in which the activity of a protein called telomerase is upregulated. Telomerase is a type of polymerase (an enzyme that synthesizes DNA) that acts to add extra length to telomeres. Telomerase+ cells are not affected by the division limit in the normal way. Some examples of telomerase+ cells are stem cells and many kinds of cancer cells.
Stationary cells
In a very real sense, a cell "dies" when it divides. Upon division a cell splits into two daughter cells, but it cannot be said that either daughter cell "is" the original cell. So a more satisfying way to answer to the original question would be to look at how long a single cell can be kept as-is and recognizably alive (i.e. in stationary phase).
If you cheat and freeze the cell at liquid nitrogen temperatures (78 K), then there are plenty of examples of cells surviving for decades, in the sense that a culture can be stored and then thawed, and normal life processes will resume at least some of the time.
Sadly, there may not be a proper answer out there to this version of the question. A quick lit search did not turn up much. It is thought that at least some cells (in particular neurons) last for decades in the human body without dividing, although this is unsurprisingly hard to prove.


text:
How is Microenvironment strictly defined?
I started to think this definition of Wikipedia:

Microenvironment (biology), a small or relatively small usually
  distinctly specialized and effectively isolated biophysical
  environment (as of a nerve cell)

and I started to think which environments can be examples of its.
Joints, synovial joints with capsule, hyaline cartilage in capsules, ...?
I would like to get more examples of environments so I can think better definition.
What is Microenvironment?

The meaning of the term microenvironment depends on the scale of the system that you're looking at. It's a sort of weasel word that loosely means "context" or "stuff in the immediate surroundings of the system of interest that has some kind of an effect on it". I've seen it used to describe everything from the chemical microenvironment of a cell (e.g. a hormone gradient) to the electrostatic microenvironment of a single amino acid residue in a protein (e.g. the field from nearby charged residues).
Conceptually it's similar to the "surroundings" in the "system and surroundings" framework from statistical physics.

What does it mean in Medicine? I have seen it been used with synovial joints like capsule in the syvovial joint.

This term is also used in cancer. Cancer cells can go into dormancy.  This is what they used to call remission. No one knows what the trigger is for them to leave G0 and start dividing again. However factors in the microenvironment,  is negativity for Ki-67 (index of proliferation), estrogen positivity are both factors but there are many others.

Is there any energy spectrum classification of these events? For instance, in Fourier spectrum and/or time-frequency joint spectrum? - - It would be very interesting to know more about them in microenvironments. - - However, I have no idea if you can get any 1D signals in such environments.

Excellent answer overall; however, wondering if you could add some references :)


text:
How did aquatic dinosaurs go extinct?
Dominant theory is that 'normal' dinosaurs went extinct from ether super volcano or meteor impact or combination of both. However there were aquatic dinosaurs that are not present at this day. Was it one of the events above that caused them to go extinct, or was it something else?
How did aquatic dinosaurs go extinct?

There is a very good answere here, which lists the reasons and the species that you asked about. https://www.reddit.com/r/askscience/comments/1nyuqs/what_caused_all_the_giant_underwater_reptiles_to/ Mososaurs and pliosaurs were technically giant reptiles, 10 meters long. Alligators and Tortoises are marine and they were the only surviving sea-reptiles. the KT extinction killed many tropical corals and ecosystems according to fossil records.

Spinosaurs (like Spinosaurus) are currently only known from 112-97 million years ago, although isolated teeth push the origin possibly back to ~150 Mya. At least now, there isn't any definite spinosaur material younger than 97 Mya.
So spinosaurs were already extinct when the rest of the non-bird dinosaurs went extinct at the end of the Cretaceous, whether by meteor impact, volcanism, a combination, or something else completely.

keep in mind spinosaurus is also nowhere near fully aquatic.

Spinosaurs and ichtiosaurs dissapeared before a great anoxic event at 90Ma. What about pliosaurs, they are reptiles strictly speaking, 10 12 meters long, fully marine, that vanished at the KT boundary. en.wikipedia.org/wiki/Plesiosauria and mososaurs.

Not a lot of people realize how extreme and how sudden the dinosaur's extinction was. Radiolab did an episode with several geologists about the extinction of the dinosaurs. Basically, when the meteor hit the Earth, a humongous amount of material was ejected into space, and most of it fell back down to the surface all around the planet. As it fell it left an incredible amount of heat in the air, raising temperatures to as high as 1200 Farenheit (650 Celsius). Anything too large to hide under dirt died (dirt is a surprisingly good insulator). Even plankton and animals near the surface of the ocean would have been decimated by the heat, destroying the food chain that supported the large mesosaurs and plesiosaurs. The whole process is thought to have taken 2 hours. The fact that anything lived through that at all is dumb luck, and even if a semi-aquatic dinosaur was deep enough to avoid the worst of the heat, the food supply would have been destroyed and they would have starved shortly after the impact.

Interesting info, but the aquatic dinosaurs went extinct millions of years before the meteor. So, this doesn't answer the question.

@rumtscho Mosasaurs didn't go extinct until the end of the cretaceous. Some plesiosaurs did too. While these are technically not dinosaurs, for all practical purposes they are close enough, and a lot more aquatic than spinosaurus ever was.

now that I read the question again, I may have misunderstood it. I have to make a pro forma edit before I can remove the downvote. But I have to wait for the peer review.


text:
Are added yogurt cultures harmful to the gut?
I have read somewhere that the live culture added to yogurt acting as "healthy" gut bacteria are actually synthetic and harmful.
Any truth to this? If so, what are some alternatives to getting good gut bacteria?

What do you mean with "synthetic bacteria"?

I have no idea what you mean by synthetic bacteria but please don't equate synthetic with harmful and natural with healthy. The most dangerous substances we know are 100% natural. Consider, for example, rattlesnake venom, hydrochloric acid and plutonium.

I'm not sure what you mean by 'synthetic' gut bacteria, so I can't address that. is yogurt harmful to the gut? I believe the answer is no.
Women (and their doctors) have long known that taking antibiotics can result in Candidia (a yeast infection). Physicians have been advising women taking antibiotics to eat yogurt with live cultures, including lactobacillus spp. and bifidus spp. In keeping with today's movement towards evidence based medicine, Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale: Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, Ineffective, and Insufficient Evidence to Rate.
The effectiveness ratings for (just) LACTOBACILLUS are as follows:
Likely effective for:

Diarrhea in children caused by a certain virus (rotavirus). Children with rotaviral diarrhea who are being treated with lactobacillus seem to get over their diarrhea about a half day earlier than they would without this treatment. Larger doses of lactobacillus are more effective than smaller ones. At least 10 billion colony-forming units during the first 48 hours should be used.

Possibly effective for...

Preventing diarrhea in children caused by antibiotics.
Preventing diarrhea in hospitalized adults. Drinking a specific beverage containing Lactobacillus casei, Lactobacillus bulgaricus, and Streptococcus thermophilus (Actimel, Danone) twice daily during antibiotic treatment and for a week afterwards significantly decreases the risk of developing diarrhea.
  -Preventing diarrhea due to traveling. Taking a specific strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle) seems to help prevent diarrhea in travelers.
Preventing diarrhea due to cancer treatment (chemotherapy). There is some evidence that patients with cancer of the colon or rectum have less severe diarrhea, less stomach discomfort, shorter hospital care, and require fewer chemotherapy dose reductions due to GI side effects when they take a particular strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle).
Colic in babies. Taking a specific Lactobacillus reuteri product seems to be more effective than using the drug simethicone.
Lung infections. Children ages 1 to 6 years who attend daycare centers seem to get fewer and less severe lung infections when given milk containing lactobacillus GG or a specific combination product containing both Lactobacillus acidophilus and Bifidobacterium (HOWARU Protect).
Treating a bowel condition called ulcerative colitis. Some research suggests that taking a specific combination product containing lactobacillus, bifidobacteria, and streptococcus might improve symptoms.
Treating irritable bowel syndrome (IBS). There is some research showing that certain strains of lactobacillus, but not others, can improve symptoms of IBS such as bloating, and stomach pain.
Treating vaginal infections caused by bacteria (bacterial vaginosis).
Treating and preventing eczema (atopic dermatitis) in infants and children who are allergic to cow’s milk.
Helping prescription medications treat Helicobacter pylori (H pylori) infection, which causes stomach ulcers.
Treating diarrhea caused by the bacterium Clostridium difficile.

Though some of the recommendations are for specific probiotic formulations, one can achieve similar results by reading yogurt packages and mixing types to assure coverage with the proper bacterial spp.
National Institutes of Health


text:
Please help me to identify this red worm
I found bunch of red worms coming out of sink.
It is rather unusual to find an overwhelmingly large number of worms. It doesn't seem like earthworm or horsehair worm. I don't know much about the worms though.
Could anyone please identify it for me.?  Notable features are

Dark red in color.
Has  a hook like structure at its rear end.
Moves in both directions front and rear.
It shrinks when it dwells in water.

I am nearly sure it's an earthworm. Location, approximate size and number of annuli (segments) would be of great help in narrowing down the circle of potential species. Also, is it characteristic for them that have no clitellum or is it just a single specimen without it?

Judging from the photo, it's an earthworm, some species of Lumbricidae. If the accident happened in India, this faunistic paper can be of some help.


text:
Does repolarization of muscle fibers mean that the muscle bundle is relaxed?
If I flex my bicep and continue to contract it does it mean that the muscle cells are in depolarizing state and not repolarizing?

No, macroscopically human muscle works by oscillation. This means that when a muscle is contracted (isometric contraction), some fibers alternatively contract through the actin/myosin process while some others relax at the same time. The end result is that the muscle as a whole keeps the same length, although it still does consume energy to stay in that state. That is why you get tired after some time of isometric contraction. To directly answer your question, it means that muscle in isometric contraction state will have some fibers depolarized, and others in resting state at any moment.