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metabolism preference by the body
What I know about metabolism is that,during exercise body uses carbohydrate first then fats and then protein,so my question is why does body prefer glucose first as fuel for energy and what makes glucose biochemically preferred molecule to be metabolized first

None of them can be directly use for energy. We all talk about aerobic oxidation, which is the major process for metabolism.
They all need to go into the tricarboxylic acid cycle (TCA cycle) and oxidation phosphorylation to produce ATP, which is the energy used in organism.
For glucose, they can break down into two pyruvate and enter the TCA cycle. That is the fastest pathway organism use to produce energy.
For fat, since they have long carbon skeleton chain, they cut off 2 carbon compounds from the fatty acid every time. And under a series of process, it become pyruvate and go into the TCA cycle. So it really takes long time and complicated pathway to oxidate the whole fatty acid molecules.
For protein, it is much more complicated. Since protein is not energy store form, it need to become a energy store form first. First it need to be degraded into amino acid, and different amino acids takes different procedure to go into the TCA cycle. Here is the picture I found on the book  by John L. Tymoczko, Jeremy M. Berg and Lubert Stryer.

In sum, glucose is the fastest energy form that body can use to take metabolism, oxidate fatty acid or proteins take much more complicated pathway.

I already forget all of the structure of carbohydrate, fat and also protein. But I still remember the reason for body using order of these compounds is related to the structure.
None all of carbohydrate can be directly used, only simple carbohydrate, like glucose, can be directly used.
For fat, it can be turn by carbohydrate for storage, and of course they are storage form, then they won't be easy for using. Even fat need to be used, they will turn to be carbohydrate again then using.
For proteins are another story, they aren't storage form, but they have some ability to form carbohydrate. So if the body is very starving and there is no other resource, the body will begin turn the protein to carbohydrate for using.


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Genomic DNA isolation from wheat
Can I use dry seed, wheat for example, in place of young leaves for isolation and purification of genomic DNA for PCR amplification?
The goal of my experiment is to validate a novel gene which is either absent or present at a particular chromosome.

That depends a lot on what you want to do in later analysis, especially if you need high molecular weight DNA or not. Please include all relevant details in you question, especially what you already found in your own research. One paper that is very easily found by google would be this one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131572/

I want to validate a novel gene which is absent or present at particular chromosome.

Yes sure I tried this and give good result. But you most chose the best protocol and need to be do this manually. I recommend that use CTAB-PVP (which is use 3 buffers EBA EBB SDS %10) extraction method from "Integrated DNA technologies" and if you cant find this I will tell You.

source: Stack Exchange

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

sort: votes


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How protein denaturation affects digestion?
Which one of these is a) easier to digest, b) more nutritious (in whatever sense):
1. scrambled egg,
2. raw egg.
Bascially is "denatured protein are worse than not denatured" a myth, or not?

This article specifically looks at the question you're asking.  Just jump down to the conclusion if it's too technical.
To summarize, cooking the egg (or heat pre-treatment as they call it in the paper) leads to a significant increase in protein uptake.
I'd call that myth busted via radiolabeling.

For some proteins denaturation can make them insoluble. This is not so in the case of egg albumin though.

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


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Typical neuronal firing rates across the human cerebral cortex
I would like to find a scientific article (or articles), which would summarize typical neuronal firing rates in different parts of the human cerebral cortex.
Any good references on this?

Here's a good reference to start you off where you can access an atlas of different properties of neurons.
Cell types from the Allen Brain Institute
Remember that when you say typical firing rates you have to specify what kind of cells you are talking about because interneurons can fire faster for example than pyramidal cells. Also there are differences in basal vs active firing rates.


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Bradford Reagent Disposal
I am a graduate student volunteering in a professor's lab being tasked with finding out how to dispose of certain hazardous materials. I have encountered a problem with disposing of Bradford's Reagent. I have checked online, but am running into problems due to the methanol component of this compound. Can someone help me with the proper disposal procedure? Thank you in advance.

I would strongly suggest to ask someone in your lab about this, they will have a better idea about the different waste disposal methods you have available.
In general you would dispose anything that contains organic solvents like methanol in a waste container for generic solvent waste. You should have something like that somewhere in the lab.
One thing you always have to keep in mind is to never put anything still reactive into your waste container. A popular example would be a strong oxidizing agent, putting that into a solvent waste container is dangerous and could e.g. ignite the waste. This is not an issue in this case, but you should always keep that in mind.
Another aspect is the pH of the waste, in many cases the waste disposal facility will only accept reasonably neutral waste, so you should neutralize your waste before putting it into a container. Neutralizing it inside the container can be much more annoying. This might not be necessary if you have a dedicated acidic waste, you'll have to ask someone in your lab about that. The Bradford reagent is strongly acidic, so you'll have to pay attention to this aspect.

@wingsfan1340 If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.


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How can E. coli affect C. elegans expression?
Plasmids can be transferred to E. coli. These transformed E. coli can be fed to C. elegans to silence its gene expression by RNAi.
How can E.coli release RNAi to C. elegans? Even if we assume E. coli could enter cells of C. elegans for being intracellular Bacteria, it is hard to imagine that RNAi will exit E.coli directly and enter C.elegan's cells? Normally, no cells or bacteria will release RNA or genomic material outside of their cells?

@Chris Is there a way of merging this question with this one http://biology.stackexchange.com/questions/38586/how-c-elegans-is-used-for-siliencing-genes/38597#38597 ? While they are duplicate questions, this one asks the question in a clearer, more precise manner?

"Normally, no cells or bacteria will release RNA or genomic material outside of their cells?" Horizontal Gene transfer in Bacteria. Human immune system Neutrophils and Neutrophil Extracellular Traps...

This post provides some additional information on how dsRNA is taken up by C. elegans

Yes, as bizarre as it may seem, that is what happens. The E. coli express a double-stranded RNA hairpin (under the regulation of an inducible promoter), and the RNA contains a sequence derived from a C. elegans gene.  When the worms eat the bacteria they grind them up in their pharynx, and release the cell contents (including the induced RNA) into the worms' gut. The gut cells are able to absorb the dsRNA  and transport it to other cells as well. The RNAi pathway processes the inhibitory RNAs to down regulate the target gene.

Now that is surprising! +1. I tried to edit the question. Could you check if it's OK? It's not really my expertise.

You can also add a note on RNA transporters in C.elegans (Sid1/2). Though I am not sure, I guess that C.elegans (or perhaps related organisms) expresses these transporters more than other organisms that we know.

@WYSIWYG Ilan amd you had given similar answer to a question of mine about c.elegans. I think my question cud be merged with this one. ( amnt able to provide the link.... using app)

First of all, gut cells can absorb the dsRNA, but we are talking about the whole body's cells in C.elegans! If we transform RNAi of EGFP, it will silence the whole body's EGFP... or not?
Second, RNAi is made by E.coli or C.elegans? I am not talking about dsRNA. If RNAi is made by C.elegans, it means C.elegans must absorb the dsRNA releasing from E.coli. As far as I know, dsRNA might be bigger than proteins... is it possible to absorb the dsRNA directly? And also, back to the first question, how can dsRNA expend to the whole body of C.elegans to silence most of cells' gene in the whole body?

@RogerL. You are confusing the term RNAi, which is a biological regulatory mechanism that degrades mRNA, with small dsRNA, which can trigger the RNAi pathway. The bacteria synthesize the dsRNA, and this is released when the bacteria die. The C. elegans cells absorb, or incorporate those bacterially synthesized dsRNAs AND contain transporters that spread the dsRNA between adjacent cells. So yes, EGFP expressed in bodywall muscle will be silenced by dsRNA ingested in the gut. The RNAi complex exists in all worm cells.

Two worm genes that regulate other worm genes using this pathway are let-2 and lin-4. They do not encode proteins; they encode small interfering RNAs that bind to mature mRNAs from other genes--protein coding genes. Once the lin-4 transcript binds to its complementary target that dsRNA triggers the RNAi degradation pathway.  You can also inject dsRNA into worms (but is is labour-intensive), or you can synthesize dsRNA in vitro and just soak the animals in it for the same effect as feeding them engineered bacteria.


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Walkthrough Illumina Genotyping
I would love help outlining a basic walkthrough of the wet-lab techniques for processing blood samples from patients, all the way to loading a BeadChip, to the part just before Next Generation Sequencing takes place. Here is my basic understanding so far, that I am not 100% certain is accurate. I am not a biologist - I just communicate with them, so I do not need any confusing assay names/specifications that are important only for wet lab biologists.
Steps:
1. Collect blood from patient.
2. Purify DNA by isolating DNA
            (Procedure (?): lyse/sonicate, bind using ethanol, centrifuge,
            wash with buffer, centrifuge again, rinse with water, centrifuge
            again)
3. Cut DNA into 100-150 bp read fragments
            (Procedure (?): with restriction enzymes? how do you determine
            read length with restriction enzymes?)
4. Separate double stranded reads into single stranded reads
            (Procedure (?): denature with heat)
5. Amplify reads via PCR, leaving you with many single stranded reads
6. Disperse sample evenly into all cells on a BeadChip. The BeadChip
      contains bountiful DNA polymerase and fluorescently tagged single nucleotides.
7. Submit the BeadChip to the Next Generation Sequencer for processing.
8. You end up with a BUNCH of images which you can transcribe into sequences
      based on the color illuminated in each photo capture, in each position
      on the BeadChip.

Here's what doesn't make sense to me:
Step 6. You either have to only put one PCR read product in each cell at a time - which would take FOREVER, if you wanted to sequence someone's whole genome... Or you have more than one light going off per cell, per BeadChip, in each photo. If the latter is the case (which it would have to be for high throughput wet lab experiments), how do you determine between photo captures of a given cell in a BeadChip that the nucleotide going off in photo 2 is a part of fragment n or n+k?
Does this make sense? Basically, how are BeadChips loaded with sample reads for NGS genotyping? I know that reads are "anchored", but are they anchored in each cell of the BeadChip? This is the only way this makes sense to me.
Thanks for any insights!

Genotyping and Next Gen Sequencing are two entirely different applications.  If you are using BeadChips, you are genoptying.

The BeadChip is literally a silica chip that holds beads in an array. Each bead contains many copies of a specific oligonucleotide that bind and capture genomic DNA fragments.

@swbarnes2, isn't the input of NGS a beadchip? What is the difference between sequencing and genotyping? NGS is a sequencing technology that gives you the nucleotide sequence of sample DNA. Is this not genotyping?

Nope. NGS puts prepared DNA fragments on a flow cell, and gives you millions of short reads.  Genotyping gives you a single letter at a single pre-determined position, or in this case, the single base at a few million chosen locations.  BeadArray technology is genotyping, not sequencing.


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Common genes and enzymes involved in pathogen entry into host
Many microbes like Salmonella, E.coli, Legionella pneumophila etc. enter host cells via cystoskeleton remodeling of the host cell. Do all microbes follow the same path or there are any other ways for the microbe to enter the host cell. What are the most prominent and significant enzymes involved in these and what are the genes involved in the same. It's a general question as I am looking for the common genes and enzymes that most microbes employ the mechanism of cytoskeleton remodeling.

Passing through plasma membrane by remodeling host cell seems reasonable choice but actually most of pathogen use cell's normal functions like endocytosis, phagocytosis, pinocytosis etc to enter (well, indirectly you need actin remodeling for this also but pathogen is not doing it actively. ). Check this review for some 'simple' mechanism pathogen use to enter cell. As far as your question about enzymes, there are lot of common enzymes (specially manipulating kinases) which are important in these pathways.Pathogens use lot of other factors to exploit host. Cytoskeleton remodeling is indirect output of many of these signaling events. Just to put into perspective, recently hiked on social media, Ebola virus use micropinocytosis like mechanism to enter into host cell. Some other representative examples in following figure (Source :Gruenberg and Goot 2006 )


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Why is there a size limit on inserts that a plasmid can accept?
Throughout my undergraduate education I have been taught that plasmids can't carry very large inserts, but I have never been told why. Any insight would be greatly appreciated.

Transformation efficiency and the bacteria's ability to maintain the plasmid is reduced as the plasmid size gets larger. Bacterial (300kb) and Yeast (1000-3000kb) Artificial chromosomes can be pretty big, but it is more difficult to get them to work. Also most of what you are working with won't be that big. Inserts usually come from cDNA produced by PCR from mature mRNAs. Without introns, the majority of genes you will see won't be more than a few KB, so plasmids do not need to be that large.


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Is it possible for a person to eat so many carrots that one turns orange?
I once read that Jerry Rubin (a famous 1960s activist) ate so many carrots that he turned orange. (This was in the East Bay Express, around twenty years ago.) I assumed it could be true, though he would have to eat hundreds or thousands of carrots; while a close family member thinks it's ridiculous. Is it medically/biologically plausible?
(I hope this question is appropriate to ask here--I'm new to this forum.)

@TanMath: As I said, this claim was from an article in the East Bay Express, around 20 years ago. The article was about history/politics/ "where are they now" about Jerry Rubin, or the Yippies (a hippie group that included Rubin and the more famous Abbie Hoffman).

Beta-carotene, the pigment that gives carrots their orange colour, can accumulate in the skin if taken in excess amounts. This condition is called carotenosis. Since beta-carotene is a lipohilic (fat loving: dissolves in lipids), its absorption is facilitated by dietary fats [1].
There is one report that says that excessive consumption of beta-carotene containing fruits and vegetables can lead to carotenosis [2].
Also have a look at this Scientific American blog.

Prince, Martin R., and Joan K. Frisoli. "Beta-carotene accumulation in serum and skin." The American journal of clinical nutrition 57.2 (1993): 175-181.
Wageesha, Nekadage Don Amal, et al. "Studies on hypercarotenemia due to excessive ingestion of carrot, pumpkin and papaw." International journal of food sciences and nutrition 62.1 (2011): 20-25.

Thanks. But how many carrots would an adult need to eat?

@user24353 That I am not sure of. It may vary between person to person and would also depend on the kind of diet one is having.


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Are progenies factually half-clones of the parents?
Given that a "clone" (if anything, in the context of human cloning) is taken to be, as far as I have understood, a specimen possessing the same genome as his "father/mother", aren't all "non-cloned" organisms born out of inter-individual, heterosexual reproduction (i.e. "standard" sons and daughters), effectively "half-clones", under that same definition?*
Are "normal" sons and daughters "half-clones", as a matter of fact?

A progeny is not a half clone of its parents.

Each cell expresses both maternal and paternal genes. There are no parts of the body or even a cell for that matter that is identical to one of the parents.
When haploid gametes form, chromosomes are randomly segregated. So the gamete receives either paternal and maternal chromosomes (grandparents of the progeny) randomly. This technically means that the gamete is not an exact half of the parent's genome.
During gameteogenesis (production of sperm/ovum), genetic recombination happens between nonsister chromatids of homologous chromosomes (meiotic crossover). This mechanism creates a small shuffle in the haploid genome that the gamete is carrying.

I see now that my question was pretty unimaginative in the first place. If sons and daughters were half-clones, then there'd be no differentiation between female and male offspring and siblings would all be the same. Thank you

@Giuliano Yes. Now you know what is the mechanism behind that difference.

@AMR thanks for the correction. I nonchalantly wrote sister chromatids instead of homologous chromosome.


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Why are so many spermatozoa produced when only one of them fertilises the ovum?
During fertilisation only one sperm can fertilise the ovum. So why so many millions of sperms are produced?? Isn't this a waste of energy?

Short answer : Sexual selection with sperm competition
However this answer will vary depending on which species you are referring to. When female mates with multiple males (like in many insects), sperm competition increases male's chances of getting his genes forwarded to next generation. When there is not much rival competition with other males (like in humans) this has correlation with mate guarding behavior and quality of sperm.


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How does kinesthetic work and with what do we sense this?
I know that kinesthetic and proprioception are different things but, in contrast to proprioception, I don't know how kinesthetic works.
A broad explaination as well as very specific(but explained for 17 year olds) would be nice.


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Why does ALS start in middle age?
Amyotrophic lateral sclerosis (ALS) often starts at middle age, but I didn't find any suggestion why. Something seems to trigger the symptoms in middle age.
If I am not mistaken, the sporadic ALS is not genetic, but there are genetic variants. So these genes are with the person all his life. But why do the disease symptoms often start only in middle age?

Short answer
The causes of ALS are not well known. Some familial types are associated with toxic proteins, susceptibility to toxins and defective protein metabolism. My personal 2-cents is that metabolic and toxicologic defects tend to cause cumulative tissue damage over time, perhaps explaining the delayed onset.
Background
Amyotrophic lateral sclerosis (ALS), is a progressive, fatal disease characterized by the gradual degeneration and death of motor neurons.
In 90 to 95 percent of all ALS cases, the disease is sporadic, meaning that it appears apparently at random. Individuals have no family history of ALS, and their family members are not considered to be at increased risk for developing it.
About 5 to 10 percent of all ALS cases are inherited. About one-third of all familial cases result from a defect in a gene known as “chromosome 9 open reading frame 72,” or C9orf72. The function of this gene is still unknown. Another 20 percent of familial cases result from mutations in the gene that encodes the enzyme copper-zinc superoxide dismutase 1 (SOD1). In case of mutations in the SOD1 gene it is though that mutant SOD1 protein is toxic.
Other inherited forms are believed to change in the processing of RNA, that may lead to ALS-related motor neuron degeneration. Other gene mutations implicate defects in protein recycling. And still others point to possible defects in the structure and shape of motor neurons, as well as increased susceptibility to environmental toxins.
Source: NIH - ALS Facts Sheet

Thank you, Alice. Also for editing my question. I read this source before. If we talk about familial ALS - it's looks more clear. Accumulation of toxic mutant protein, for example. Some sort of accumulating defects. But what about sporadic? ~90% of the ALS. And also - sometimes ALS starts in young people.

@VGranin - no worries, happy to help. The disease etiology of the sporadic cases are, as far as I understand and as stated in my answer, often unknown. Because they, seemingly, don't have a genetic background, it is probably very hard to pinpoint what is at fault in these folks. In other words - I don't know and as far as I can see, no one really does. That is, implicitly, what 'sporadic' means - random occurrence / cause unknown.

Yeh I know that I will not get some proved reason. But maybe there is some studies that have some good suggestions based on some evidence ...  Also about the genetics -  I think that in all cases there must be some genetic background. The environment could trigger it - but must be something wrong in the genes from the beginning. And in middle ages the body gets weaker - so thinks go wrong more easily. It's only my suggestion.


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Is NZT-48 real?
NZT is a fictional compound in a movie called limitless, basically it's a brain booster, it gives access to more simultaneous neuron activity.
are there any real cognitive enhancers out there?

As others have said, this compound is fictional. Leaving illegal compounds aside, I would vote for nootropics. And from them I find pramiracetam to be the best fit. I have found its action to be rather similar to the one described in the movie, although with no side effects. One of the most notable mechanisms of it is the highly selective potentiation of acetylcholine and improvement of brain blood flow. Papers on this chemical are easily accessible through Google, so I won't provide lnks.
However, no cognitive enhancers will do any good without proper motivation and conscious efforts. It is pointless to eat pills and hope that something will come and change who you are for the good. Cognitive enhancers need something baseline to enhance.
UPDATE
Looks like this question really belongs to CogSci SE, but I feel that I should complement this answer with some more information that is important to take into account.
Cognition/mind enhancement can be a double-edged sword for some people. Instead of giving pleasure directly, it actually enhances mind and calls for much more self-discipline and responsibility. For example, I practice meditation and some other mental disciplines for a long time already, and it came in handy to control and direct my mind. However, some people who tried pramiracetam reported that the intensity of their own mind was too much for them, they simply did not know what to do with it for they had no real task, motivation or big plan formed before administering the compound, and it could happen that they got themselves overwhelmed by many long-forgotten memories that rejuvinated in all their lucidity at the same time when the present day reality became much more integral and whole, without many pieces comfortably forgotten.
These memories could not necessarily be negative, but what about a super-fine image of the wallpapers pattern you were looking at when you were 3 years old, standing as bright as a day before your eyes when you try to sleep, eat or mate? And I am not even saying about the fact that recent events are perceived in much greater detail and integrity, senses sharpened greatly... Personally I was able to control my mind because I also practice it in daily life (without the enhancers), but this may not be easy for people who are not used to that.
Another issue such an enhanced mind could face is that people around remain as they are. The perceived difference can render them much less intelligent and almost dumb. A person with an "enhanced" cognition can find himself living in a world of dense people. This is in no way an offense, a similar condition can be observed when one with a body "enhanced" by a stimulant can run 3 miles and still feel not even slightly tired, while an average untrained person will extinguish in under a mile. It is true that there are lots of smart people in this world, but one has to be ready for a sudden shift of perception that could occur. I remember reading reports of piracetam users who say that while they became more effective in integrating knowledge, people around did not, and situations occured when "obvious" things were not immediately understood by the surrounding people which caused irritation and conflicts. One has to be careful as this may lead to social disadaptation.
This again calls for discipline, ability to love and appreciate other people, and actually rises many unusual ethical questions. As with any gain, one must always remember that love and understanding are essential.
Another example of a two-fold effect is piracetam - an older, less potent but nevertheless useful nootropic. While it has an effect which may with high probability result in enhanced cognition, it also rises agression due to stimulating the secretion of the thyroid gland. So again, this calls for enhanced discipline. (do not mix the terms "piracetam" and "pramiracetam" in this text, they mean different compounds).
In any way, it is always important to apply conscious approach to your own behavior and thinking, be it with or without enhancers. But with enhancers, the responsibility is times greater.
One more point to notice. While nootropics do not exhaust body in any way (they are not stimulants), it is very important to provide oneself with sufficient nutrition and sleep, and avoid drug usage such as nicotine, alcohol and other psychoactive drugs. Failing on any of that may significantly reduce the useful effect and in case with illicit drugs cause unpredictable consequences. Dietary supplements such as omega-3, lecitine, vitamins can also provide some support.
Disclaimer: aside from compiling information available online, what I am saying is also supported by personal experiences of 2 courses each 6 months long, taken with a pause of 1.5 years between them, 600mg pramiracetam 2 times a day. I don't smoke or drink alcohol. Both times the experience was life-altering.

Totally, without motivation, all that is excess energy without a proper outlet. still interesting though, that we're nearing a future where we could have more access to our thoughts, more control over our lives.

@AlyShmahell I thought that I should build up on your position and express some more concerns directly related to the issue and possibilities

I'm glad you did. it's both such an interesting subject and a sensitive one. it requires as much care and planning as pushing forward into research and application. now it's my turn to build up on your information, I'll be researching what you provided in the update. and next question it's going on CogSci ;)

Yes there are a few out there, though the mechanism is quite different to the film. Things that increase the activity of dopamine and norepinephrine particularly in the prefrontal cortex where a lot of your higher functions like decision making seem to be. Things that do this can include amphetamines (ritalin and other adhd medications) along with things like modafinil.

That's very interesting, but isn't dopamine responsible for reward-driven-motivation? is that to say even intelligence is increased by increasing the promise of reward?


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Genetics of Hybrids

I'm working on this problem, but I'm not sure I've done it correctly. My initial thought was that the answer was $D$, but I don't see anything in the above graph that indicated the Hybrid species is,in fact, less fit for survival. Moreover, I cannot see why any of $A,B,C$ would need hold.

The number of off springs produced by the Generation 0 and 4 is almost the same in case of Hybrids. This indicates that the rate of production in the Hybrids is almost the same among different generations.In this case option D will be the best one to choose.


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Does a microwave oven disinfect food?
Imagine I am preparing food -- just about to put it into a microwave oven --  and some of it falls on the floor. Assuming it got some bacteria or other organisms (viruses?) on it, will the microwave processing disinfect it? What about worm eggs? As I understand, any living organism, given enough exposure to microwaves, degenerates. Is this true?

That amount of usual pathogen does not matter unless you clean up the floor with food... Yes microwave will disinfect the food, it is used for pasteurization.

http://cooking.stackexchange.com/questions/32055/why-microwaves-do-not-kill-harmful-bacteria-as-well-as-boiling

A little off topic, but I'll share anyway I have some old artifacts of wood with evidence of active worms. After putting them in a 1200 watt oven for 10-12 minutes all evidence of wood worms disappeared, that was several years ago. My assumption was that the water in the live worms was heated to a lethal temp. Obviously size was a constraint, although a commercial oven should be easy to find. Not for painted objects probably.

Microwave ovens can indeed kill bacteria in food by heating them to high temperatures. For example, this article found that microwave heating could kill all of the Salmonella bacteria in a chicken thigh sample:

The effect of microwave heating on Salmonella Enteritidis inoculated
  on fresh chicken was investigated using a microwave oven (800 w) to
  determine the destruction of Salmonella Enteritidis isolated from
  chicken carcasses, in relation to the time of heating at two power
  settings: high (power level 10) and medium (power level 6); The
  relationship between heating time and temperature was also been
  studied. The destruction was 6.4 log cycles at time 95 sec for the
  high power level, and 5 log cycles at time 140 sec for medium power
  setting. After 110 sec for higher power level, no survival of
  Salmonella Enteritidis was detected in samples (100g), but at 140 sec
  for medium power level, these food pathogens were still present.

However, the main issue is balancing the amount of microwave exposure. Heating the food for too long will result in the food becoming dehydrated or burned, and heating it for too short a period of time will result in food poisoning.
This paper shows that insufficient microwave exposure can and will lead to food poisoning if there is a large amount of bacteria inside the food:

Leftover samples of a savoury rice dish consumed by all six ill
  persons contained 6×103/gm Salmonella enteritidis PT4. The rice salad
  comprised boiled rice, raw carrots, eggs, cheese and curry powder. The
  curry powder and remainder of the pack of six eggs were negative on
  microbiological analysis. The rice dish had been prepared by heating
  in a 500 W microwave oven with a rotating turntable on full power for
  5 min.

So in essence, microwaves don't kill bacteria / viruses. Heating does.

I'm no expert, and this is more of a physics answer rather than biology. The microwaves will not reach all of the food. This is why you get hot and cold spots. The rotating plate mitigates this to some extent, but not all of the food will receive a blast. However heat will slowly spread throughout the food. If the contaminated bits are hot enough for long enough it should be OK, but I wouldn't rely on this.

Yeah, the warming of the food is extremily non-uniform, but I thought that at least the surface area gets enough radiation. And still - how much does it take to kill a bacteria? A colony of them? Is that heat that can kill them, or do microwaves affect them? ...and I bet if I asked this on Physics SE, they'd said, this one is for Biology :D.. Somehow my questions always fall in between SE sites :/ funny thing..

Not even the surface will be covered. The microwaves don't have a problem penetrating the surface, the problem is due to the wavelength only some areas get their molecules excited by the waves. This explains it better than I can: https://what-if.xkcd.com/131/

Can you provide citations to back up your claim?

Keep in mind that microwaves kill organisms via heat, and in particular, heating mainly water.  This is contrast to ionizing radiation, for example as obtained from the cobalt used in commercial food radiation.
If the pathogen does not contain, or is not sufficiently adjacent to liquid water, or is not sensitive to heat, it may persist.
As an explanation, a microwave generates heat because microwave oven peak frequency emissions (~2.45 x 10^9 Hz) (reference) are able to excite water molecules.  The physics of that are actually quite complex, but at a high level, water doesn't really exist appreciably as H20.  Rather, it is better described at STP as HOH (hydrogen hydroxide) or more accurately, H3O+ OH- (hydronium hydroxide).  All those ionic and van der Waals' forces (reference) allow water to have a high specific heat (i.e. a small bit of water can contain a lot of heat).  That water heat (via predominantly conduction) heats the rest of the food.
The importance of this is that in order for a microwave oven to sterilize anything, including food, both of the following must be true:

The target must be raised to a sufficiently high temperature.
That temperature must be maintained long enough to adequately disrupt the homeostasis or (in the case of a virus or prion) structure of the pathogen.

And these predominantly depends on water being present (though some fats and sugars can also efficiently absorb microwaves).  If there is insufficient liquid water present, the microwaves would inefficiently heat the dry food, and as a consequence could fail to achieve a sufficient kill temperature.  (In contrast to liquid water, ice has a much lower resonance with microwaves, which is why the defrost cycle of a microwave uses lower energy and switches on and off to allow heat conduction to even things out and minimize hot and cold spots).
Some pathogens would not likely be killed by a consumer microwave oven:

Bacteria which form spores often require very high heat, above the boiling point of water, so in a microwave, those spores (e.g. Bacillus anthracis, Clostridium botulinum) would be unlikely to reach those temperatures (as additional microwave energy would convert the water to steam at STP, rather than raise its temperature).
Prions are also notoriously difficult to destroy.  In fact, when a patient with CJD has neurosurgery, typical hospital policy is to throw away the entire surgical instrument tray, because there is no adequate sterilization procedure available, period.  (You're unlikely to find prions in your kitchen unless your name is Hannibal Lecter, but I include them for completeness.)

Finally, there are two main routes by which pathogens in food make you ill.  The first is an active pathogen (e.g. live bacteria or replicating virus) acting within your body.
The second mode is that of preformed enterotoxins. While the OP asked about food on the floor (presumably of short duration), the title is directed to disinfecting food.  From a food safety perspective, many common bacteria (most classically Bacillus cereus) produce toxins which persist even after they have been killed and the toxins can survive high heat.  Microwave radiation and the expected heat produced would not destroy these molecules, and would not render the food safe.  This would also apply for many chemical substances potentially present on a typical kitchen floor.
All that said, in 2014 microbiology research done at Aston University suggested that there is actually a decreased risk of eating food dropped on the floor if you follow the five-second rule.

Yes, you are right. If the food just fall on the floor and you microwave it, maybe that could kill most of bacteria or disinfect virus. bacteria are living organism, normally can't tolerate over 100 ℃, and virus' protein coats are not stable too.
However! maybe there are Spores which are generated from gram positive bacteria, the power of microwave or oven can't disinfect all of them. And also, the toxic chemicals on the floor, which might from your floor cleaners or be generated by bacteria, maybe microwave or oven are not strong enough to denature them. In biological lab, we use autoclave, 121℃ and 1.2 kg / cm² pressure over 15 mins, to kill bacteria spores. And it can't clean toxic chemicals. To be noted, there is not pressure function in normal housse using oven and microwave!

What do you mean by "spot"? Did you mean "spores"?

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


text:
Genome Sequencing
Is Genome sequencing used to determine the relationship between two species that are believed to have a common line of descent? How accurate is this method if so?
Are there more accurate methods for determining if two species have a common line of descent?

Yes, genome sequencing is one of the least subjective means used to infer common descent. It is still to some degree subjective, because we target specific parts of the genome that we think are useful - e.g. either conserved or variable across species.
It is impossible to say how accurate this method is, because we do not know the truth. We have no reference value. It is impossible to determine (i.e. prove) the relationship between species unless we observe the speciation; we can merely collect evidence that supports or refutes a theory of common descent.
There is a fairly comprehensive page on Wikipedia that describes the various types of Evidence of common descent.


text:
ATP to disassembly of nucleotide ratio
DNA Helicase, the enzyme that is responsible for tearing apart the strands before DNA replication, requires ATP to rip apart nucleotides. I have asked this question to several professors and they couldn't give me a clear answer. My question: What is the ATP:nucleotide bond breakage ratio? In other words, how many nucleotide  bonds can be broken from a single ATP through helicase.

This paper should interest you, though it likely varies between different helicases.

I think requirement of ATP also depends on the arrangement of oligonucleotide that mean bound between A and T(u) or G and C, and it could be calculate but how I cann't say yet.

All helicase is doing is opening up the DNA double helix by disrupting the hydrogen bonds between the nucleotides. The bond in hydrogen bonds is a misnomer as it is a van der Waals interaction and not a bond between atoms, so there are no bonds being broken, which would require significantly more energy to break than disrupting H-bonds. Topoisomerases on the other hand do need to catalyze breaks in the phosphate backbone in order to relieve tension from supercoiling. This is not to say that ATP is not consumed, just that bonds are not broken in the process as you are stating.

The answer to this is perhaps not as simple as you may think, in part because there are many different helicases in the human body. There is also some passive activity of a helicase that does not require ATP.
It is not clear exactly whether ATP is just involved in the translocation of the helicase or the actual unwinding.
For a RecQ helicase in E. coli, one study found that "The determined tight mechanochemical coupling of 1.1 ± 0.2 ATP consumed per nucleotide traveled indicates an inchworm-type mechanism." For more information see Sarlós et al. (2012).
Another study (Donmez and Patel, 2008) notes that "As compared with non-ring-shaped helicases such as PcrA (Dillingham et al, 2000) and UvrD (Tomko et al, 2007) that move on an average 1 nt for every ATP hydrolysed, the ring-shaped T7 helicase is three times more fuel efficient." This shows how there can be quite a bit of variation.
Bottom line - you can count on your fingers the number of nucleotides unwound by a helicase per ATP.


text:
Why we have to damage our muscles to build them?
I know that new muscle cells are made when actin fibers are disrupted. My hypothesis is that muscle mass is limited, from birth, and that nutrients (protein) are only directed to grow muscle when those muscles are actually used. Is this hypothesis true?

I edited the question in an attempt to clarify. I do not readily see where evolution comes into play. Please add when necessary. The current question is an open goal - the 'use it or lose it' principle applies.

@AliceD Thanks for your edit. I think you got it right, evolution is quite universal reason for asking for anything we have - so I saw it just like a possible contra-argument for this hypothesis (like "gene for weaker kids may not fix in population")

First, it may not be true that you have to actually damage existing muscle fibres to promote muscle growth, see http://jeb.biologists.org/content/214/4/674.full
I do not find papers on the optimality of muscle remodelling, but maybe you'll be interested by a comparison with bone remodelling. Bone faces indeed similar constraints as muscle: it has to be sufficiently strong to resist the forces that we face in everyday life. Astronauts e.g. have paralleled bone and muscle mass decrease if they don't train during flights.
Bone remodelling now is not just reinforcing the bone where it is needed: it also involves bone resorption in places where there is less mechanical stress. E.g, people having a bone implant may lose bone because the implant bears more stress than the implant ! See this paper. Why decrease the bone mass? Well, this is a matter of optimality: just as in engineering, you want the lightest structure that will be able to perform its function. See this thesis and references therein.
Muscle has every reason to perform equivalently. You want each muscle to grow according to its usage in your usual activities, so you need to regulate growth and loss. This is likely to be more important than limiting protein demand—at least as long as food is abundant enough.
A personal anecdote to finish: a friend of mine was a hardworking racing cyclist. He once wanted to take part in a multisport raid, involving some hill running—and couldn't run the way down, because of his overgrown thighs. A little of diversity in his personal training would have allowed him a better balance in muscular weight!

Muscles are developed as required by the surrounding environment. This means your body is constantly physically stimulated to grow muscles according to the external forces it experiences (e.g. gravity).
When you train your body, e.g. with weights, you are applying an unusual amount of pressure to your muscle cells, damaging them in the process. In the process of healing your muscle cells, your body will strengthen them in order to adapt to the new physical stimuli, but only when a vast amount of required elements through nutrition is available (proteins).
Quite an impressive feature, right. :-)
I know this from researching personal training/weight training.

Yeah, I wrote that in description. My question was whether it was developed evolutionary to get the nutritions only to the used organs.

+1. @Probably - I think your question was unclear. I edited to clarify.


text:
Do reptiles hunt?
I encountered the following passage in the book The Art of Interactive Design by Criss Crawford (bold formatting is mine):

[...] From stalking and evasion to the chase, the [interaction between mammalian predator and mammalian prey] is loaded with complex mental twists and turns as each tries to anticipate the opponent’s move and counter it. By contrast, the mammalian hunter’s relationship with reptilian prey is much simpler: the prey’s defense lies in venom, camouflage, inaccessibility, or speed. There’s nothing like the death dance between coyote and jackrabbit. And reptiles themselves don’t hunt in the formal sense; that’s too sequential. They wander around looking for an opportunity, and when they come across one, they strike; that’s all.

How accurate is the claim in bold font?

Welcome to Biology.SE. The answer very much depend on the definition of hunting. I don't think there is any good way to answer this question. I am voting to close. Intuitively I would say that the claim is quite wrong. I suppose that the best you can do to satisfy you intuition of how reptiles forage is to go on youtube and looked at a bunch of videos. Here is one for example showing a caiman who is foraging on snails.

Note also that the term reptiles has two different definitions (see this post). You are probably referring first definition on the post I linked. Knowing what you mean by reptiles will allow you to see how different clades of reptiles are foraging and you can decide if you can call their behaviour hunting or not.

I don't think there is much truth to this statement. It's certainly not true that "They wander around looking for an oppurtunity". Snakes follow trails of scent and heat, crocs wait in ambush at likely crossing points along rivers, and there are surely more examples than that. It's true that having legs underneath the body makes for a more agile/less stable running style and thusly a more interesting race for TV documentaries, but I can't think of any reason why a mammalian brain could cope with that running style better than a reptilian one.

A definition of hunting is required - for example, a crocodile, in my opinion, hunts; food doesn't simply fall in to its mouth. (Voting to close because clarity is needed).

Short answer
I think the author is mostly right, but there are exceptions.
Background
The author is probably referring to hunting as being an "active foraging" strategy, while he ascribes the foraging behavior of reptiles to be a "sit-and-wait" strategy.
Active hunters include the classic, and dramatic high-speed, long-distance pursuit strategies deployed by cheetahs and lions, which are indeed mammals. Lions and dolphins are well-known examples of pack hunters that use consorted team effort to catch prey.

Sources: Dreamstime and OMG facts
Reptiles, on the contrary, indeed often wait silently for passing prey, instead of deploying active hunting strategies. Well-known examples are crocodiles that lurk silently below the water surface to swiftly grab passing prey, and Komodo dragons that patiently wait for hours at a time to take down passing prey.

Source: Deposit Photos
However, there are exceptions. A study performed by Eric McElroy from Ohio State University reports that lizards use two basic foraging techniques. In the first approach which they dubbed sit-and-wait, lizards are basically waiting for their prey to pass. Then, with a quick burst of speed, they run after their prey, snatching it up with their tongues.
In the other form known as wide or active foraging, lizards move constantly but very slowly in their environment, using their chemosensory system to stalk their prey.
Source: Science Daily

Great response. However, there is evidence that Komodo dragons actually do perform a more active form of hunting. See this video of Komodo hunting water buffalo. They 'attack' the buffalo by biting it to inflict infection and then sit and wait! :p

@theforestecologist - the komodo in the video basically uses the active foraging technique mentioned in the last sentence of the answer. The waiting for the infection to kick in is as passive as it gets.

As expressed in the comments, the answer to this question depends on how you define 'hunting'. However, using common definitions in biology, hunting is almost used as a synonym to predation (see quoted definitions below). In that sense, the statement in your question is clearly incorrect, since it is describing the the foraging behaviours of predatory reptiles.
The description of reptile hunting in your quote is also too simplistic, and there is a range from sit-and-wait strategies to active pursuit of prey, see e.g. the section Foraging models in Pianka & Vitt (2006).
A couple of useful definitions can be found below.
From Encyclopaedia Britannica:

Predation, in animal behaviour, the pursuit, capture, and killing of animals for food. Predatory animals may be solitary hunters, like the leopard, or they may be group hunters, like wolves.
The senses of predators are adapted in a variety of ways to facilitate hunting behaviour.

www.thefreedictionary.com:

predation (prɪˈdeɪʃən) n
  1. (Zoology) a relationship between two species of animal in a community, in which one (the predator) hunts, kills, and eats the other (the prey)

Wikipedia: predation:

predation is a biological interaction where a predator (an organism that is hunting) feeds on its prey (the organism that is attacked).[1] Predators may or may not kill their prey prior to feeding on them, but the act of predation often results in the death of its prey and the eventual absorption of the prey's tissue through consumption.

Even if 'hunt' is often defined in terms of active pursuit, it can also include broader and more passive elements, for instance "seek out; search for", see www.thefreedictionary.com:hunt:

hunt  (hŭnt)
  v. hunt·ed, hunt·ing, hunts
  v.tr.
  1. To pursue (game) for food or sport.
  2. To search through (an area) for prey: hunted the ridges.
  3. To make use of (hounds, for example) in pursuing game.
  4. To pursue intensively so as to capture or kill: hunted down the escaped convict.
  5. To seek out; search for.
  6. To drive out forcibly, especially by harassing; chase away: hunted the newcomers out of town.

I can see the point by @AliceD that 'hunting' is often (in every-day language) used in reference to "active foraging". However, in my eyes this is too restrictive. Also note that the main use of 'hunting' is in reference to hunting by humans, and some of these hunting methods mimic the sit-and-wait strategies of reptiles (see e.g. some methods for big game hunting and the use of traps). If sit-and-wait strategies are not considered hunting, then you are also excluding some human hunting practices from 'hunting'.

Nice systematic analysis of the question. +1. The author is indeed not a biologist, but a physicist now active in the gaming industry. I linked some pages to the author and the book in the question.


text:
Bacteria Replication
I learned this at a lecture, but somehow I have trouble in understanding this. It is said that the bacteria such as E.coli need 20 minutes to divide, but its chromosome require 40 minutes to multiply. It is explained that the E. coli will have copied half of it, which will spend 20 minutes and after divided, it will continue another 20 minutes to complete the chromosome copy. However, it is said that each daughter cell will have one complete and half copy after they divide. I am confused that if the bacteria only spend 20 minutes to copy half of it, how  can each daughter cell could have one and a half?

Referring to the six stages in your diagram as Stage 1 through Stage 6, let's look at Stage 3: At that point, there is one bidirectional replication in progress, having made it about halfway around the chromosome. So it has 2 copies of the first half of the chromosome, and 1 copy of the rest, which is yet to be copied.  To get to this state of replication took 20 minutes.
Now the cell starts two new replications, one at "origin of replication" on each of the two copies of the first halves of partially replicated chromosome.  This is the state shown in Stage 4.  There are now three replications going on: the original, which is working on the last half of the chromosome, and two replications, which are working on (their own copy of) the first half of the chromosome.  All three replications will continue working for about 20 minutes.
We then get to Stage 5: the original replication has finished and the septum forms to separate the daughter cells.  The two replications started in stage 4 are continuing, and are about halfway down the chromosome.
The cells separate, and we are at Stage 6.  But stage 6 is the same state for each daughter cell as we had in Stage 3: a chromosomal replication that is halfway through (thus having one and a half copies).  It took 20 minutes to get from Stage 3 to Stage 6, where we are ready to double again.  During that 20 minutes, only one half of a chromosome had time to be copied, so it takes twice that (40 minutes) for replication of the whole chromosome.  This works out because the cell is doing three replications at once.

Your question has already answered reasoning behind it. Just remember this happens only in rich media. Now I tried to build simple model of this to illustrate how DNA levels are changing over the period of time in given scenario. I will assume very simple (but reasonable) numbers for model. Rules are very simple,

Cell division in 20 min ( Cell will lose half DNA )
DNA replication in 40 min ( Cell will double DNA copy )
Firing of origin of replication in 10 min ( Cell will have one more origin of replication )
At each time point, cell will have DNA replication depending on number of origin of replications

I wrote simple code in python and simulated,
import math
import numpy as np
import matplotlib.pyplot as plt
import matplotlib
cell_division_time = 20 #min
full_DNA_replication_time = 40 #min
firing_of_new_Ori = 10 #min
origin_of_replications = 1
total_DNA = 1 #initial condition
time_for_simulation = 400 #min
time_coordinates = range(time_for_simulation)
DNA_number_coordinates = [] #This will be updated at each time step
for t in time_coordinates:
    if (t%firing_of_new_Ori) == 0:
        origin_of_replications = origin_of_replications + 1  #Add more origin of replications
    total_DNA = total_DNA + (1.0/full_DNA_replication_time)*origin_of_replications #Add total DNA accordingly
    if (t%cell_division_time) == 0:
        total_DNA = total_DNA/2.0  #At cell division, total DNA will be half
        origin_of_replications = 1  #We will reset origin of replication to 1
    if (t%full_DNA_replication_time) == 0:
        total_DNA = total_DNA + 1 #DNA will be double when you complete one full replication
        origin_of_replications = origin_of_replications -1  #Remove that origin of replication
    DNA_number_coordinates.append(total_DNA)  #record amount of total DNA in cell
plt.plot(time_coordinates, DNA_number_coordinates,linewidth=2, label='DNA copies')
plt.axvline(x=40,linestyle='--', color='red',label='Cell Division')
plt.legend(loc=0)
plt.axvline(x=20,linestyle='--', color='red')
plt.axhline(y=1,linestyle='--', color='red')
plt.axhline(y=1.5,linestyle='--', color='red')
plt.xlabel('time (min)')
plt.ylabel('Total DNA copies in single Cell')
plt.show()

This simple game can give you intuition, check how DNA levels are changing in following image

At steady state, these will be sustained oscillations,


text:
Why is the neuronal plasma membrane more permeable to potassium ions than sodium ions?
From what I understand, the greater permeability of the neuronal plasma membrane to K+ ions (which diffuse out) than Na+ ions (which diffuse in) helps to maintain the -60 mV resting membrane potential. However, I am not sure why. After all, K+ ions are larger so should the membrane not be less permeable to them? Could it be to do with the greater charge density of Na+ ions or is there another reason altogether? Does it have something to do with the 'leakiness' of ion channels?
Also, why is it that the resting potential is maintained and does not become increasingly more negative? Should it not be that because 3 Na+ ions are pumped out and 2 K+ are pumped in continuously, and more K+ ions are diffusing out than Na+ is diffusing in, that the potential is becoming increasingly negative? Is movement of other ions also involved in maintaining this potential?

The cell membrane is inherently quite impermeable to any ion, because it is made of hydrophobic fatty acids. Ions are hydrophilic because of their charge and small size. Metal ions are relatively small and, indeed, have therefore a high charge density. They gather a lot of water around them and hence, they are hydrophilic.
Therefore ions, including Na+ and K+ are transported via dedicated ion channels, which form specialized pores in the membrane. They consist of vast families with many members and a host of different characteristics. Hence, the size of the ion does not matter, because they are transported through channels.
There are indeed leaky K+ channels, but not leaky Na+ channels. And exactly this feature is the reason cells are negative on the inside, because positively charged K+ leaks from the cell.
There is just so much the Na+,K+-ATPase can do. In the end  it burns ATP to fuel each cycle to pump out Na+ and pump in K+. At a certain point it cannot transport anymore Na+ out (K+ diffuses relatively freely) because the concentration gradient of Na+ and the electrical gradient (inside negative) gets too steep.

Sal Khan says at the end of this video that leaky Na+ channels do exist. This site also claims that. Are they both wrong?

@OrenMilman afaik, they may exist, but in the standard Hodgkin&Huxley model Na channels are assumed to be non-leaky


text:
Rampant low Vitamin D
Why have people inadequate vitamin D status? Is it just (the lack of) sun exposure, or is it related to hormone and thyroid function?

@MarchHo - how about this edit?

As far as I know by  inadequate vitamin D the thyroid must produce more thyroid hormone to compensate. I don't think the vitamin D status depends on the thyroid function. I'll look for references.

Here in Australia there are more cases of vitamin D shortage than in England. Given the double amount of sun hours per annum here in Down Under, that's quite counter intuitive. In fact, an estimated 31% of adults in Australia have inadequate vitamin D status, increasing to more than 50% in women during winter–spring and in people residing in southern states (Nowsen et al., 2012).
It turns out that in Australia people are, rightfully, careful of sun exposure due to the thin ozone layer and the resulting high incidence of skin cancer. As a result, people here wear long-sleeves on the beach, use high-factor sunscreens, wear sun hats, use umbrellas to evade the sun etcetera. The Australian  Cancer Council supports the famous "slip, slop, slap" slogan:

Slip on a shirt, slop on sunscreen and slap on a hat, Slip, Slop, Slap! You can stop skin cancer [..]!

Hence, folks here in fact often take vitamin D supplements, despite the large amounts of sun hours.
Reference
- Nowsen et al., MJA (2012); 196(11): 686-7

Vitamin D deficiency is most probably the cause of the thyroid disfunction and not the result. So the cause of vitamin D deficiency is the lack of UV exposure.

To  conclude,  the  results  of  the  present  study  suggest  that
  moderate  to  severe  vitamin  D  deficiency  is  a  risk  factor  for
  hypothyroidism. As vitamin D deficiency is highly prevalent in north
  Indian  population,  these  findings  may  ha ve  some  public health
  implications. Further, large  scale  clinical  trials  and prospective
  studies  will  be  required  to  establish  a  cause  and effect
  relation  of  vitamin  D  deficiency  in  pathogenesis  of
  hypothyroidism.     Supplementation     of     vitamin     D     in
  hypothyroi dism  may  ameliorate  its  symptoms  and  prevent further
  deterioration of thyroid function, so, for the ease, safety and   low
  cost   of   treating   this   modifiable   risk   factor   we
  recommend its screening in all hypothyroid patients.

2014 - VITAMIN D LEVELS CORRELATED WITH HYPOTHYROIDISM IN INDIAN POPULATION: A PILOT STUDY

In the present study, we demonstrated that serum vitamin D levels were
  significantly lower in female GD patients without remission than in
  those with remission.

2013 - Serum vitamin D levels are decreased in patients without remission of Graves’ disease


text:
What makes diffculty to make a human bio-tooth compare to a mouse's?
Some time ago I read a news article that said a bio-engineered tooth based on a mouse's would be available around 2015. There was some research about it at King's College in the UK, and many other institutes.
Now, I haven't heard any news that such a thing is available. It seems to be a basic result of stem-cell research, how much difference can there be between a human's tooth and a mouse's?

So what is your question - When will a bionegineered tooth be available? or What is the difference between mouse's tooth and human's? These two questions should be asked seperately in different posts

@TanMath - these two questions are likely very much related, as preclinical animal work typically precedes human stuff. This seems fine.

@AliceD but I find that asking about the difference of two animal's teeth and when bio-teeth are available as two questions that should possibly put in two seperate posts..Plus, this question seems opinion-based as well...

Thanks AliceD, anyway I will write more clearly next time.

I believe you're referring to this 2013 announcement from King's College, Biological tooth replacement -- a step closer. So called "BioTeeth" are sought after because

Current implant-based methods of whole tooth replacement fail to reproduce a natural root structure and as a consequence of the friction from eating and other jaw movement, loss of jaw bone can occur around the implant.

However, Professor Sharpe identified the following obstacle:

What is required is the identification of adult sources of human epithelial and mesenchymal cells that can be obtained in sufficient numbers to make biotooth formation a viable alternative to dental implants.

For some background, consult Biological tooth replacement (2006; Sartaj, Sharpe)
Unfortunately the 2013 article was the last I heard of it - possibly for the aforementioned reason. If you're really interested, you might consider attempting to contact Professor Sharpe yourself.

Thanks for your link and information about obstacle, jzx.

I don't think there is necessary for making "Bio-teeth". It should be more expensive and without any advantage comparing the ceramic teeth or others...
The different between mouse and humans teeth is that mouse' teeth, like toenail, will keep growing, thus they need to shave their teeth all the time. That is the reason they are always eating, and like to bit some stuffs even are not food. But humans teeth stop growing and cannot grow back once broken. There is no point to make a Bio-tooth for mouse. But for human, for the economy point too, there is no reason to make a Bio-tooth..... I can't image any advantage for making Bio-teeth

Thanks for your great explanation about the difference. I wanted to know why the research was difficult even though it was successful on mouse long time ago. Because the bio-tooth has a root structure, I believe that it can be on the ligament instead of directly connecting to jawbone like an implant. At least, wouldn't it reduce the pain when an implant is being installed in gum?


text:
Abbreviations for molecules: What are CheW, CheA, CheY?
I've encountered the abbreviations such as "CheW" and "CheA" for certain organic molecules.  For example:

Proteins associating with the Tar complex include the autophosphorylating protein kinase CheA, the transducing protein CheW, the methylating enzyme CheR
  and perhaps the protein phosphatase CheZ.  (Morton-Firth et al. 1999, p. 1060; available here)

What does "Che" stand for?  What do the capital letters at the ends of the abbreviations mean?
Let me know if this would be a better question for chemistry.SE.

Here is the paper that first defined them:
Armstrong JB, Adler J. 1969. Complementation of nonchemotactic mutants of Escherichia coli. Genetics 61:61-66.
Che is an abbreviation of chemotaxis. In this paper, complementation studies revealed three different loci that, when mutated, result in defective chemotaxis. These were termed CheA, CheB and CheC. Originally they were thought to be genes, but the following paper refined the definitions when the CheA locus was found to contain CheA and CheW genes while the CheB locus contains CheB, CheX, CheY and CheZ genes:
Silverman M, Simon M. 1977. Identification of polypeptides necessary for chemotaxis in Escherichia coli. J Bacteriol 130:1317-1325.
I'm not going to search for the discovery of every Che gene, but hopefully you have an idea of where the letters come from.

These are name of proteins.
CheA stands for Chemotaxis protein A


text:
How long a dog can remember its owner's smell?
Can dog remember multiple smells? and how long it can remember a smell?

There are a lot of misconceptions about dogs memories. They have short attention spans but they do form long term memories. If my partner has been out for the day and they return home several minutes before I return home for a walk with our beagle, he will excitedly alert to their scent. He does not do that otherwise, so he is picking up on the particular chemical signature that they produce.


text:
Is lung size/shape a factor in long-continuous running of animals?
Apart from other factors, does lung shape/structure/size play any role in long-continuous running animals.
Is there any similarity in lung structure between different long-continuous running species?


text:
How could humans have interbred with Neanderthals if we're a different species?
To be clear, I'm not doubting that Homo sapiens and Homo neanderthalensis did interbreed: of that much I'm convinced.
Within the past few years I've seen an upcropping of pop-sci articles discussing the interbreeding between pre-historic species of humans. In everything that I see in these articles, as well as in scientific literature (my college Bio textbook, among others), I see these different human groups being referred to as separate species.
This conflicts with my understanding of a species. Given the following definition, wouldn't Homo sapiens and Homo neanderthalensis be the same species?

A species is often defined as the largest group of organisms where
two hybrids are capable of reproducing fertile offspring, typically
using sexual reproduction.  ~Wikipedia

Is this definition incorrect?
Are the publications using "species" colloquially, as opposed to scientifically?
Is "species" still a poorly defined concept? (see Ring Species)

Thanks!

Short answer
The concept of species is poorly defined and is often misleading. The concepts of lineage and clade / monophyletic group are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.
Note that Homo neanderthalis is sometimes (although it is rare) called H. sapiens neanderthalis though highlighting that some would consider neanderthals and modern humans as being part of the same species.
Long answer
Are neanderthals and modern humans really considered different species?
Often, yes they are considered as different species, neanderthals being called Homo neanderthalis and modern humans are being called Homo sapiens. However, some authors prefer to call neanderthals Homo sapiens neanderthalis and modern humans Homo sapiens sapiens, putting both lineages in the same species (but different subspecies).
How common were interbreeding between H. sapiens and H. neanderthalis
Please, have a look at @iayork's answer.
The rest of the post is here to highlight that whether you consider H. sapiens and H. neanderthalis to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.
Short history of the concept of species
To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see Aristotle and Plato's thoughts). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.
Charles Darwin already understood that as he says in On the Origin of Species (see here)

Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.

You might also want to have a look at the post Why are there species instead of a continuum of various animals?
Several definitions of species
There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".
I will below discuss the most commonly used definition (the one you cite) that is called the Biological species concept.
Problems with the definition you cite

A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.

Only applies to species that reproduce sexually
Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.
In practice
In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.
How low the fitness of the hybrids need to be?
One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?
Type of reproductive isolation
We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see wiki). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:

Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?

Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?

Under what condition is the hybrids survival and fertility measured
Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?
Ring species in space
As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post Transitivity of Species Definitions). Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
Species transition through time
Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.
Practical issue - Renaming lineages
How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.
Time
Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.
Special cases
When considering a few special cases, the concept of species become even harder to apply.
The Amazon molly (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (Kokko et al. (2008)).
In an ant "species", males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (Fournier et al. (2005)).
Bias
It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this TED).
So why do we still use the concept of species?
Naming
IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.
The alternative use of the concept of lineage
It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.
In consequence
In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).
Homo lineages
I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the Homo sapiens and the Homo neanderthalis lineages. The issue is a matter of the definition of species.
Video and podcast
SciShow made a video on the subject: What Makes a Species a Species?
For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at podcast.unil.ch > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon

Here is a related answer

Might also be worth mentioning the flip-side of this, that just because two animals are considered the same species does not guarantee they are capable of producing offspring.  For example, all domestic dogs are generally considered a single species, but a female Chihuahua would be unlikely to be able to produce a viable litter with a male Great Dane.

@DarrelHoffman however a female Great Dane could produce a litter with a  male Chihuahua. On a chromosomal level, they are pretty much the same. Pure bred French Bulldogs have to be delivered via Caesarean, as even the females of the breed are not able to birth the heads of their offspring.

In reaction to your comments I added two sections: In consequence and The bias of Humans. Let me know if this seems good enough and whether I should develop it further. Thanks

Although the discussion on problems with the species concept is interesting, I find this answer to be quite strongly worded/controversial (against "species", for "lineages"), but still basically lacking references (except a couple of tangential links). I would like to see a clearer separation between personal opinion and scientific consensus and/or ongoing scientific discussions.

@fileunderwater I agree with you! I have discussed a good part of these ideas with colleagues and also with Pierre-Henri Gouyon after a talk he made about the detrimental effect of the concept of species in conservation biology. If you speak french, you can find a podcast here under "La biodiversité - plus qu'une simple question de conservation" Sorry, I can't cite any papers.

Given the inherent subjectivity of the terminology surrounding species, do you think it's feasible to use the concepts of lineage and/or clade in everyday conversation in the same way that species is? I frequently have discussions with my friends that would strongly benefit from more accurate language in reference to historical biological lineages, but actually using lineage in conversation has proven to be extremely complicated compared to the more inaccurate species identifier. Is there a better way?

The definition of species is open for debate, and this is especially the case when you try to define it from a paleontology perspective.
Homo neanderthalensis was first discovered and defined in the 1860's, long before we were able to sequence their genome, which was published in 2010. There genome was different enough that most scientists would still say that they are distinct from modern humans, but that doesn't necessarily mean that those distinctions were enough that it affected the ability to produce fertile offspring between sapiens/neanderthalensis matings.
In fact on the wikipedia article I linked to the alternative Homo sapiens neanderthalensis is suggested as a synonym making us Homo sapiens sapiens for anatomically modern humans. This is similar to distinctions made in the wolf lineages where you have Canis lupus for grey wolves, Canis lupus familiaris for Domestic dogs, Canis lupus dingo for the wild dogs of Australia, and on and on for many other sub species of Canis lupus. Wolf/Dog hybrids are known to be fertile.
Female Horses and Male Donkeys can breed to create sterile offspring, Mules. The sterility is likely due to the fact that there is a greater phylogenetic distance between Horses and Donkey than there is for sapiens/neanderthalensis and also due to the fact that Horses have a different number of chromosomes to Donkey's , where as sapiens/neanderthalensis have the same number.
Another thing you have to remember is that the discovery of Homo neanderthalensis occurred about 5 years after Darwin created an uproar about Humans being evolved primates. Now you were faced with a skeleton that clearly was different from modern human but was clearly hominid. The closely held view that humans were special and therefore held dominion over all other creatures made it difficult to accept the fact that we may actually have evolved.

I am confused by your last paragraph. Was Homo neanderthalensis not regarded as part of human evolution?

In addition to @Remi.b's answer on the species concept, and the perils of using human definitions to try to encompass biological reality, you need to understand what "interbreeding" meant to humans and neanderthals.  Fertile crosses between sapiens and neandertalis were very rare, probably less than one successful cross per generation, and there's some evidence that male hybrids were almost all sterile (or that this was a fatal condition).  This is probably less successful interbreeding than horse-donkey crosses, where the two partners are unambiguously different species by just about any definition (they have different chromosome numbers!).  So it's not like sapiens and neandertalis could effortlessly hybridize; it was very rare and generally unsuccessful.
References:

We find that observed low levels of Neanderthal ancestry in Eurasians are compatible with a very low rate of interbreeding (<2%), potentially attributable to a very strong avoidance of interspecific matings, a low fitness of hybrids, or both. These results suggesting the presence of very effective barriers to gene flow between the two species are robust to uncertainties about the exact demography of the Paleolithic populations, and they are also found to be compatible with the observed lack of mtDNA introgression. Our model additionally suggests that similarly low levels of introgression in Europe and Asia may result from distinct admixture events having occurred beyond the Middle East, after the split of Europeans and Asians.

--Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression. Currat M, Excoffier L. Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15129-34

Our results indicate that the amount of Neanderthal DNA in living non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability.

--Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans. Neves AGM, Serva M PLoS ONE 2012 7(10): e47076

These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.

--The genomic landscape of Neanderthal ancestry in present-day humans Sankararaman et al Nature 2014 507:354–357

"Fertile crosses between sapiens and neandertalis were very rare, probably less than one successful cross per generation, and there's some evidence that male hybrids were almost all sterile (or that this was a fatal condition" This is interesting. I would like to read more about it... could you provide references to this?

Among others - Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression. Currat M, Excoffier L. Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15129-34;
Neves AGM, Serva M (2012) Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans. PLoS ONE 7(10): e47076;
The genomic landscape of Neanderthal ancestry in present-day humans Sankararaman et al  Nature 507, 354–357 (2014)

Hi, I have one dumb question about this answer: why was human-neanderthal interbreeding probably less successful than horse-donkey crosses? Haven't horses and donkeys been crossed more often, with $0$ recorded instances of fertile offspring, while humans and neanderthals interbred less often, with nonzero instances of fertile offspring?

@Will - it's not true that there are no recorded instances of fertile donkey/horse offspring.  This article and this one list several well-documented examples in the past century, quite possibly more instances than all successful sapiens/neandertal crosses over the thousands of years they co-existed.

@iayork Oh cool I never knew about that, thanks! I guess to be fair though the descendants of human-neanderthal hybrids seem to have been able to make some contribution to the human gene pool, while even the rare fertile mules don't seem able to produce offspring capable of living long enough to contribute to either the donkey or horse gene pools. But I might be misunderstanding.

@Will Human/Neandertal hybrids almost certainly had some selective advantages that counterbalanced their strong disadvantages and led to some of the Neandertal genome being maintained -- speculation includes immunological advantages from Neandertal genes.  But also, it's likely that some Neandertal genes were carried along simply because of the general expansion of H. sapiens, even where those genes were neutral or even weakly harmful.

+1 for pointing the rareness of sapiens-neanderthal interbreeding. That is a very needed complement to the accepted answer since it seems to be misunderstood in the question.

The same way lions and tiger are different species but can interbreed. They do so poorly, not very often, and the male hybrids are infertile, although the female hybrids retain some fertility. Gene flow between the two species is possible but very limited. We call lions and tigers two species because gene flow between the two is limited. Free flow of genes between the two species is not possible.
If we look at the papers coming out it is obvious that the flow of genes between Homo Sapiens and Neanderthals was limited. It was so limited that we can say that two species were on the verge of cutting all ties between each other.
Firstly, there are no Neanderthal mitochrondria, meaning successful mating involving Neanderthals was mainly between human females and male Neanderthals. Next there are no Neanderthal Y chromosomes, meaning male hybrids were sterile.
Although there are Neanderthal gene in autosomes, there are no Neanderthal genes on X chromosomes, which house many of the genes regulating intelligence and fertility. So natural selection has selectively weeded out Neanderthal genes in those two areas, probably because they don't play well with their human counterparts (i.e. they cause a fitness disadvantage).
Also, the Neanderthal gene segments, although found in all non-Africans, are in small pieces. Individual have less than 2% (although as much as 35-60% of the Neanderthal genome remains in the non-African human population). So it means that the hybridization event occurred rarely and far in the past — probably when the first Homo sapiens left Africa.

There is a lot of conjecture in your answer and no evidence at all. Even though the notion of your answer might be correct, your conclusions are - given the data - way too strong and some of the information are even wrong (there is introgressed Neandertal DNA on the X, just about 5 times less then on autosomes). You will not find references to support most of your claims. -1

Really? I would think anybody would has read the literature would have said the same. All i am doing is repeating what has already been said. I am not adding anything new. Even my conclusion are just repeating the what has been concluded. The hottest thing is how many other species have been added to our genome. When and where. Latest news indicate that the how Neanderthal gene got into the human population is far more complicate that a single one off event.

No, you are putting it way too strongly. There is indicative evidence to support some of your claims, but nothing shows that the admixture events occurred only once or only far back in the past or even that male hybrids in fact were sterile. And just because we have not found Neandertal mitochondria or Y-chromosomes does not imply that there are none - absence of evidence is not evidence of absence. Remember that a mitochondrial genome is just one locus and how efficient drift is in populations with small effective sizes. The evidence is far from decisive.

I'm not really educated into the scientific community's mindset very much, but as a person who is interested in taxonomy to one degree or another, as well as plant breeding, I can give you some perspective to help you decide on an answer.
Lots of different species can hybridize (interspecies hybrids): e.g. some different pepper species, some different tomato species, some different toad species, cows and bison, lions and tigers, different species of strawberries, etc. Interspecies hybrids sometimes even become invasive species. For instance, collared doves invaded my area years ago, and hybridized with the native doves (which native doves were quite a bit different: much smaller, much different behavior; they made different sounds, and had no collars); we've had the hybrids ever since (although they took some years to stabilize much--which was a fascinating process to observe), and the other two species appear to be gone, for the most part. In my personal opinion, interspecies hybrids (perhaps^ driven by changes in habitat: for instance, if the magnetic fields of the earth change, maybe because of a disturbance caused by a solar storm, animals might migrate different places than they used to, because some animals migrate via their ability to detect magnetic fields; if they migrate different places than usual, they might find new animals to hybridize with) are a very significant driver of new forms of life, which often gets overlooked.
^That's a hypothesis of mine, anyway. I don't claim it's a proven fact.
There are even hybrids between different genera, although they're pretty rare (sheep and goats have been known to cross, for instance; hybrids can also supposedly be made between goji and tomatoes--although I have yet to see plants or seeds of the hybrid for sale).
My impression from things I've studied isn't that species differentiate sexually incompatible groups, but rather that they differentiate sexually compatible groups that tend to stick together. (You're probably not going to see llamas and camels hanging out very often, or horses and zebras, or donkeys and zebras, but that doesn't mean they can't reproduce. They are not the same species, however, and some--not all--interspecies hybrids have infertile offspring^.) It seems that other traits are also important for defining species: such as structure and lifestyle, but it's a work in progress (and they move things around taxonomically sometimes).
^It should be noted that you can have diploids and tetraploids (or greater) of the same species of plant (thanks, in part, to chromosome doubling chemicals), and their offspring aren't fertile (but if you doubled the chromosomes of the offspring, they would be).
None of the higher ranks guarantee sexual compatibility (even if it sometimes can happen). However, chromosome doubling and such aside, you can generally expect members of a species to be compatible with confidence.
In summary, it sounds like members of the same species tend to reproduce with each other over another species when given the chance (but there's no guarantee they can't and won't breed with other species, generally speaking; you can evaluate that on a case-by-case basis, however). Each species tends to have a certain set of traits (and habits) that set it apart. But, we're still figuring everything out.
That's what I gather, anyway.

A microbiology professor once told us "The Russians have about 14 times more species than the English"
The word species (Greek εἶδος¹) begins in greece. According to St. Thomas Aquinas (Summa Theologica, ca. 1265-1274 A.D.),  used as the scientific way of referring to different types of living things.
It's a notable buzzword in english owing to it's rhyming syllables, it focuses attention, and my... It isn't more precise than referring to colours... Espèces in French doesn't warrant the same obsessive buzz. Genetics is a spectrum and we divide them as best we can a bit like we divide colours of the rainbow.
Neanderthals came about only half a million years ago, and we diverge from them perhaps a million years ago.
Dinosaur species usually live for about 3 to 10 million years before changing two new species according to scientists, and their generations are closer together than humans...
So they are closer than bonobos and classical chimpanzees, perhaps something like the northern and the southern white rhino.

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


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Rushed publications based on flawed data
In 2014 BICEP2 made a very controversial press release. It was rushed, given before any papers where published, because they feared they would be scooped by another similar experiment. In the end it turned out that their analysis of their data was flawed. It was particularly dramatic because if they had been correct it would have been a significant development.
Are there any similar cases in biology? Not necessary an identical situation, but a high profile result that was released in a hurry that later turned out to be incorrect.

This should probably be posted to http://academia.stackexchange.com.

There are many publications on severely inappropriate usage of statistics in lots of biological papers driving the results unreproducible. Google something like "wrong statistics in biology".


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Resolution of gel electrophoresis
My professor mentioned the resolution of the gel in gel electrophoresis. He stated that agarose has large pores and thus low resolution whereas polyacrylamide has the opposite.
I don't understand what resolution has to do with this. Can someone explain?

Resolution size of the gel simply means the distinction that can be made between molecules very close in size.
If you were looking to distinguish between a 100bp fragment and a 200bp fragment, then agarose will give you that level of differentiation.
But if you were looking to distinguish between a 190bp fragment and a 200bp fragment then you would likely want to us polyacrylamide. The PA gel has a higher resolution because you can distinguish between smaller differences on molecule length.
Think of it in terms of a simplified idea of a microscope, at 100X, you can probably distinguish between cells, maybe make out a well stained nucleus. where as at 1000X you can start to discern other organelles. You are seeing a finer degree of detail at the higher magnification. There are many factors that go into the resolving power of a microscope and the example based on magnification is simplistic and doesn't really address optical resolution, but it is an illustrative example of resolution in a gel. You can think of agarose as the 100X and PA as the 1000x, if that helps.


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Symbiosis of Pseudomonas Fluorescens
Have a modest background in molecular biology and presently considering a project that requires some knowledge of botany.  Specifically, I seek details on the epiphytic relation between the microbe pseudomonas fluorescens and flowering plants such as the orchid and rose.
    * What would be the relationship?  Commensalism or Mutualism?
    * What is the nutrient source for Pseudomas? Life Span?
    * What becomes of the metabolic end products from Pseudomonas?
    * Does the plant alter its surface properties to accommodate Pseudomonas?


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Can people with AIDS get a fever?
It's my understanding that fevers are an immune system response to infection. Like the body's cells can take more heat than most viruses or bacteria.
So if that's the case then can you even get a fever if you have a non-functioning immune system due to AIDS?

With AIDS, the whole immune system is not non-functional. The condition results in a severe drop in CD4+ T-cells, which is what primarily predisposes AIDS patients to secondary infections.
Fever can be an immune response to infection, but it is not directly affected by the loss of CD4+ T-cells. Rather, fever occurs due to a complex cascade of events triggered by pyrogens, which causes a release of prostaglandin E2 (PGE2). In the hypothalamus, PGE2 signals a systemic response for the body to generate heat. More on the pathophysiology of fever can be read here.
AIDS patients still produce PGE2 in response to pyrogens (such as compounds produced by bacteria). Therefore, AIDS patients can certainly get fevers. In fact, AIDS patients may be more likely to get fevers because they may produce more PGE2.


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How can rapid growth cancer get nutrients in vivo?
When I was little, before I get into biological studying, I read a news talking about cancer would be totally cured after decades. I still remember that researchers had a theory to claim if they could limit the blood vessel generation near to tumor, then the rapidly growing cancer cell couldn't get enough nutrients and would kill them. However, this theory seems not to work well. Cancer cells or tumor still have another way to get enough nutrients to live, or at least, maintain themselves to survive and endanger the host. So, my question is how can rapid growth cancer get nutrients without blood vessels in vivo?

Long back in 1971 Falkman and others put forward new therapeutic implications of targeting blood vessels supplying nutrients to tumors.   Treatment you are mentioning is called 'Anti-angiogenic therapy '. However current challenges in this therapy are resistance to antiangiogenic agents and non specificity. Plus there was huge 'normalization effect' which was actually helping other blood vessels around tumor. To answer your question, Cancer cell makes their own blood vessels instead relying on host machinery. There are many other factors also why this kind of treatment is not successful yet.

Now, I do remember this saying... So there is impossible way to give "Anti-angiogenic therapy" to limit tumor growth? cuz it is so logical...

It is not impossible. This therapy needs more research :) Even in review which I cited in answer talks about how to tackle these problems.