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Case study and speculations on the brain of Edward Mordake
I am very interested in the case of the man named Edward Mordake who lived in the 19th century. In particular, he had two faces. If you have not heard of this man, please, search this up as there are a very few amount of photos, but it is something very, very strange.
However, all the information on him seems to be speculation, so I am looking for a scientific look at this. I am unsure if it will even be possible seeing as how the years have passed and records may not have been accurate.
To be specific, has this condition been noted before? There seems to possibly be differing opinions onto wether the face was indeed its own individual inside, or a low functioning other half of the same man.
Indeed I am looking for any info on the biology of his brain, possibly the neuroscience and or physiology, and of course any comments and discussion.
Thank you

A similar modern case: Chang Tzu Peng. Short video: https://www.youtube.com/watch?v=ZgB0-2vb9HU

@Corvus - is that case 'true'? The wiki page has been deleted and it seems obscure fiction.

I suppose I could have been duped. I guess the lesson is the old "Don't believe everything you read in the wikipedia...."

Mordake was a conjoined twin fused at the head (Fig. 1). Twins conjoined at the heads are rare, occurring only once in every 2.5 million live births. Moreover, in Mordake's case it was a parasitic twin head with an undeveloped body that was fused with his own head. This condition is referred to as craniopagus parasiticus, or épicome / epicomus. Craniopagus parasiticus is an extremely rare teratology, of which only six cases have been recorded in the medical literature (Bondeson et al, 1989).

Fig. 1. Wax reproduction from Edward Mordakes face. Source: Bosmia et al., (2014).
The story of Edward Mordake is, however, obscure and met with skepticism. Moreover, no medical details are known as far as I know. However, he was reported to be intelligent and healthy, just depressed by the second parasitic head (Bosmia et al, 2014). To me it appears a story of a person with a normal brain and a parasitic face attached to his head. However, there are rumors that the parasitic head could talk independently, leaving open the possibility that the parasitic head may have contained a separate brain, or shared Mordake's own brain.
More is known about the double-headed Bengal of Everard Home (Fig. 2).

Fig. 2. Skull of the double-headed Bengal (museum exhibit, left) and an artist's impression of the case (right). Source: Bondeson et al, (1989)
The natural head and body were perfectly normally developed, but a number of anomalies were noted on an examination of the parasitic head, such as excessive tearing and the absence of pupil reflexes. Upon dissection the parasitic head was shown to show various anomalies, such as missing anatomical elements (e.g. auditory canal) or underdeveloped structures (e.g., small lower jaw bones).  Importantly, the brains were separate from each other and covered in individual and proper coverings. The dura mater of each brain adhered firmly and contained
many large vessels. Bondeson et al. (1989) describe the remainder of the six cases as well, which were still-borns or lived just very shortly. They had completely separated brains too.
References
- Bondeson et al, Surg Neurol (1989); 31:426-34
- Bosmia et al, Childs Nerv Syst (2014)


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Cellular Immunity Response
What response of cellular immunity would appear after complementary protein activation to keep pathogenic bacteria away from our body?
Notes: I do appreciate your explanation. Though I am facing multiple choices:
(a) wrapping the bacteria cell (b) immobilize the bacteria cell (c)    destroying the bacteria cell by enzyme (d) creating pores on the bacteria cell
The key answer is (c) but then I do not know what enzymes make this happens. Any Idea?

Your first sentence is not really a question. You want to know which mechanism of the complement is respsonsible for this protection? If so, can you please re-phrase it?

Does that has anything to do with your topic? http://en.wikipedia.org/wiki/Complement_system Then, maybe, you are looking for this mechanism: http://en.wikipedia.org/wiki/Complement_membrane_attack_complex

@aandreev so.. option (d) is actually correct then, am I getting this wrong?

that is for you to decide

The complement does d.)

As you can simply find on Wikipedia, the cellular immunity, or Cell-mediated immunity,

is an immune response that does not involve antibodies, but rather
  involves the activation of phagocytes, antigen-specific cytotoxic
  T-lymphocytes, and the release of various cytokines in response to an
  antigen.

The answer (c) (destroying the bacteria cell by enzyme) refers to the phagocytes, cells that contain many enzymes, like lysozymes. Those funny enzyme can destroy the bacteria cell's wall.
Actually, I think that the answer (d) could be right, but it's not complete. In fact not every enzymes works on the cell's wall!

After opsonization the antigen goes through phagocytosis or the complement system destroys it. The complement is a cascade of reactions, which at the end creates a hole (many holes) on the membrane of bacteria which causes lysis. http://en.wikipedia.org/wiki/Complement_membrane_attack_complex
So the right answer is d.) in your case.

source: Stack Exchange

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

sort: votes


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DNA content doubling in interphase
Why does the DNA content of a cell get doubled in interphase? Why doesn't it become tripled or quadrupled? What's stopping it from doing so?

So in mitosis, the cell has to split itself into two cells; each daughter cell has a functional genome that may again split into more daughter cells. The cell replicates the DNA before dividing, so the error in replicating 3x or 4x is that upon division, the daughter cells will have more DNA than the initial cell, and every generation will have more DNA than the last. One replication ensures both daughter cells receive one functional genome. We can see the result of extra DNA in cases like Down Syndrome (trisomy of chromosome 21).
The cell controls this process by controlling the cyclins present in the cell temporally, namely cyclin-A and cyclin-E when we talk about DNA replication in S-phase,

From wikipedia,

Cyclin A resides in the nucleus during S phase where it is involved in the initiation and completion of DNA replication. As the cell passes from G1 into S phase, cyclin A associates with CDK2, replacing cyclin E. Cyclin E is responsible for initiating the assembly of the pre-replication complex. This complex makes chromatin capable of replication. When the amount of cyclin A/CDK2 complex reaches a threshold level, it terminates the assembly of the pre-replication complex made by cyclin E/CDK2. As the amount of Cyclin A/CDK2 complex increases, the complex initiates DNA replication.
Cyclin A has a second function in S phase, in addition to initiating DNA synthesis, Cyclin A ensures that DNA is replicated once per cell cycle by preventing the assembly of additional replication complexes. This is thought to occur through the phosphorylation of particular DNA replication machinery components, such as CDC6, by the cyclin A/CDK2 complex. Since the action of cyclin A/CDK2 inhibits that of cyclin E/CDK2, the sequential activation of cyclin E followed by the activation of cyclin A is important and tightly regulated in S phase.

Source: Cyclin A

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


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Swapping genes?
So, gene therapy is to take out a gene, correct its mutation, and put the corrected one back into the organism, right?
Is it also possible to take out a gene from an organism and put in a totally different one?
I read about this study where a scientist found four genes seemingly responsible for creating high, medium, low pan sensitivities.
Genes: COMT, DRD2, DRD1 and OPRK1.
DRD1 - more common among people with low pain perception.
COMT and OPRK genes were seen more, for those with moderate pain.
DRD2 gene variant was more common among those with a high pain perception.
So for example, can we take out a DRD2 gene from a person who has high pain sensitivity and put DRD1 in him/her so that he/she can have low pain sensitivity?
Is that technically possible?

First off we don't have yet the technology to perform gene therapy in human. Will be possible in the near future and the most likely candidate is the CRISPR/Cas9 technology. For your actual question, there are a couple of approaches, for mutation correction the idea would be to directly corrected the mutation without "swapping" genes. For your question with pain, the problem is that it is very hard to predict what will happen by taking a gene "off" and putting a new one "in".

Therefore gene therapy, at least at the beginning will be used on major genetic diseases (like the Prader-Willi syndrome or Huntington's disease) rather than playing with sensitivities.

@cagliari2005 I wouldn't say we can't do gene therapy in humans yet, but it's obviously in the early stages, glybera has been approved. And CRISPR/Cas9 would only be appropriate for certain gene therapies, such as repairing point mutations. Fixing large deletions or inversions requires delivery of whole genes.

@user137 you are right. Was thinking more along the lines of the question and for actual targeted genomic modifications. Good point though.

@user137 While gene therapy to treat a fully developed human has many obstacles and technical chances, CRISPR/Cas9 can be used for targeted gene replacement through homology directed repair https://www.addgene.org/crispr/zhang/faq/#HR

It's been possible for a long time now. Take a look at this article related to trials with retroviral vectors used for gene therapy trials. A single child developed leukemia, and following that trials across the world were suspended.
The article although notes that many countries decided to proceed with trials, since as they say "for the greater good". But mainstream media articles tend to glorify the actual reasons behind such decisions, because such questions are governed by much more complex ethical considerations.
But moving on this recognised the need for targeted gene therapies, so one of the most promising techniques right now is the Crispr/Cas9 technique as noted by the comments above above.
So do we have the technology? Yes we do.
Should we go forward with it?
I would say no. But, I would also say yes.
Why such a division in opinion?
There is much that we do not understand. Until a few years ago, the non-coding part of the genome was just junk. Now, it's an essential regulatory partner. Even more recently, the understanding of chromosome architecture was not understood, now we know that Chromosome architecture has a role to play in gene expression. In 2002 epigenomics was in it's infancy, we believed "central dogma" to be a dogma, non-coding RNAs were just some junk that you tended to pick up because the transcription machinery did not know what it was doing, and chromosome architecture? that hardly mattered in the grander scheme of the cell. All in all the cell was a much simpler place. Now we know more than we did yesterday and less than we will know tomorrow, so if I was a person whose entire life is a prolonged episode of suffering I would take my current options. If I was a person who could live with a mild discomfort I would work around it.

+1 as I agree in general - but the specific example of the non coding genome being thought of as junk I think is wrong. We've known there was a lot of noncoding regulatory DNA since at least the late 90s. And the ENCODE project's 'it's all functional' line was just marketing.

When you ask:

Is it possible to take out a gene from an organism and put in a totally different one?

The answer is yes. Gene knockout technologies are available in experimental scientific fields. You can destroy your target gene by swapping the gene with a drug resistant gene.
You can swapping genes using culturing cells, however it would be almost impossible to swap genes in cells of an animal body. But there is still hope. iPS cells can be generated from human and other animals. Then the technology can be applied to culturing iPS cells. Transplantation of differentiated iPS cells may be possible to replace tissues having a problems if anatomical structures allow you to do so.
I do not know details of pain perception, but it may be not that simple. You can classified genes by sensitivities of pain, but at biochemical level, the mechanisms to gain sensitivities may be different. I might check on this, although I might not able to draw the conclusion.

It is possible to insert a new gene in another organism.
The technique is very new. I know I have done it at school where we had a colony of bacteria, and we did some things to them that some of those bacteria would 'adopt' a gene that would make them able to live on a different pertium dish.
If you are intrested in these subjects you should try to google on "Genetically modified bacteria".
Also here is a site that shows with a few images what technigue is actualy used: Link
Edit:
As for the cutting of the DNA, for some bacteria (like E-coli) there whole genetic structure is known. So there are markers available that cut the DNA of the bacteria right at a certain place.

This does not answer the question, as the question is about higher organisms and nötig bacteria. Modifying bacteria is not a really new technique, it is done for about 40 years.


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Liver - Regeneration in Cirrhosis
Liver is the most resilient of the human organ (on par with or next to skin). A very interesting experiment on liver regeneration is here. Even if two-thirds of the liver is removed, the remaining liver would regenerate to recover the full volume and function.
Cirrhosis of liver is a condition where excessive fibrosis occurs shattering the architecture of the liver. The blood vessels and the parenchymal cells of the liver get constricted into narrow spaces causing portal hypertension and fall in the Liver Function Test parameters (albumin level falls, clotting factors fall leading to spontaneous bleeding, bilirubin level rises causing jaundice, etc...). It can be either congenital or acquired. Cirrhosis is considered an end stage liver disease.
In the end stages of cirrhosis the only treatment option available is liver transplantation.
Question:
Why is partial hepatectomy (removal of part of liver) not a treatment option for end stage liver disease (cirrhosis of the acquired variety)?

The answer lies in the question. Liver cirrhosis constrains hepatocytes into small fibrous spaces limiting regeneration, hence the nodular pattern.
However,fibrous degeneration occurs in specific patterns. It can be located mostly around portal regions (centrolobular pattern) or diffusely through the whole lobule.
So basically, it is all good that hepatocytes can regenerate, but the limiting factor is not that. It is the structural impairment of the liver lobules and drainage system that will impair regeneration.
Moreover, most cirrhotic patients could not tolerate halving of their residual hepatic function. Not to mention the extensive surgery required. It would kill them swiftly.


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Transformation efficiency
I accidentally spun down the cells after heat shock treatment before adding the media into the tubes while doing transformation? will the transformation work?

The protocols for preparing competent bacterial cells all involve concentrating log phase cells and incubating them on ice in the presence of divalent cations.  There are many different recipes for the buffers, time of incubations, temperatures, etc. What could an extra centrifugation step do that would harm the experiment?

This is hard to answer since we don't know the exact conditions you chose, as these are rotation speed (or better g), how long you spun them down and also if you used a cooled centrifuge or not. It's also important how gentle you resuspended the pellet.
However, I would plate these cells, no matter what happened since you are at the last step of the procedure and have nothing to loose. Do the usual dilutions you use for plating your cells and then add another plate with undiluted transformation mix. If you have only very few surviving cells after your mistake you might get your clones on this plate. If it doesn't work, you will have to repeat the transformation.

The question is following: did you incubate cells on ice before spinning? Protocol, for example this one for $DH5\alpha$, calls for just 10 minute incubation after heat shock:

Heat shock at exactly 42°C for exactly 30 seconds. Do not mix.
  Place on ice for 5 minutes. Do not mix.
  Pipette 950 µl of room temperature SOC into the mixture.

Did you centrifuge your tubes after step in bold?
My bet is that spinning cells down (taking into account what @chris wrote about centrifugation parameters) will not dramatically decrease efficiency of transformation. DNA should be already in cells after step, highlighted in the quote.


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Where to find gene manipulation video (or photos)
I hope Im not asking a dumb question!
Where can i find video of gene manipulation in action under microscope?
Like extracting a gene from a cell, fixing gene mutations, putting the gene in a vector, that kinda stuff. Is this too small to show in video or photos?
If i look up youtube all I find is scientists using lab machines and equipments except for under miscroscope!!!

There are no videos of that, since you cannot see the DNA you are working with unless you precipitate it in large amounts.

You can find videos of microinjections, but you're not actually going to see DNA.

Like this video http://www.dnatube.com/video/5561/What-is-Blastocyst-Microinjection

Ok now I understand thanks! So how do scientists manipulate genes if they can't see what they are doing!??

The comments effectively answer the question. There is no need to close it as broad. The main question here is "Is this too small to show in video or photos?" which can be answered. I am voting to leave this open.

From the comment section:
We don't have to see the actual changes. It's like chemists who will mix compounds together and obtain a new molecule. They dont see the chemical reaction per se but can test the new molecule to make sure what they predicted would happen had happened. Finally we often use fluorescent proteins to track some of the modification performed (which could involve a microscope). For the how, well that's a bit broad and involves too many notions to make a summary here.


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Why is there only adrenoreceptors and no active adrenergic innervation in bronchus and uterus?
Our bronchus and uterus has beta adrenoreceptors, but they have no active sympathetic nervous system innervation in these organs. Was there a sympathetic innervation in trachea and uterus, earlier, that we lost it during the course of evolution, if no, why did nature gives us only adrenergic receptors and no adrenergic nerves in trachea and uterus?

If endocrine system is an alternate signalling system to nervous system. Epinephrine and Norepinephrine have endocrine roles as well apart from being neurotransmitters. In fact I had learnt about their endocrine function long before I realized that they also act as neurotransmitters.


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Can leukopenia in a person with an otherwise normal immune system lead to non-infectious diseases in the long-term?
If a person has developed leukopenia as a side-effect of long-term use of anti-convulsant medications and his/her immune system appears normal otherwise (does not get infections any more often than a healthy person, and bone marrow biopsy did not indicate anything abnormal), does the condition need to be treated? Is it even possible to treat leukopenia effectively as long as the person is on anti-convulsant medication?
Does leukopenia increase a person's chances of getting some non-infectious diseases too? I know WBC is primarily responsible for fighting infectious micro-organisms, but does it have any significant role in cleaning up body's own malfunctioning or ageing cells?

What do you mean by "non-infectious diseases"? The white blood cells are part of the adaptive immune system and play a very important role to keep us healthy.

@Chris - By non-infectious diseases, I meant chronic and potentially degenerative diseases not caused by infectious microorganisms (bacteria, viruses etc.) but due to undesirable changes happening at a sub-cellular, cellular or organ level. If WBCs have a role in eliminating malfunctioning or degenerate cells of the human body, then they may be helping prevent some diseases caused by accumulation of such cells. Hope this clarifies.

Leukopenia is just a definition. In medicine, there's a saying:

Treat the patient, not the numbers.

Numbers can mislead people, sometimes quite seriously. Definitions of leukopenia vary: some define it as less than 5,000 WBCs per µL of blood; others define it as less than 4,000.
Decreases in specific WBCs is usually described as neutropenia, lymphocytopenia, monocytopenia, etc. This, too, is important information, as each cell has a different function, and thus different results are possible.
In leukopenia, bone marrow biopsies are very informative. They reveal if the cause is a decreased production of WBCs due to destruction of precursor cells, replacement of marrow by other tissue, invasion of marrow by cancer, etc. If a bone marrow biopsy is normal, that is very comforting.

does the condition need to be treated?

Most people with anti-epileptic drug (AED) induced leukopenia are just fine. Some common-sense precautions (such as avoiding other drugs which might also cause leukopenia, and checking a white count if you fall significantly ill) should be heeded. If your doctor is a neurologist, they should be thoroughly versed in the side effects of AEDs, as this constitutes a very large patient population for them. Some of the newer AEDs have a lower incidence of leukopenia. Talk to your doctor about the potential benefits and drawbacks of switching.

Does leukopenia increase a person's chances of getting some non-infectious diseases too?

Theoretically possible, but not particularly likely.
If you are truly concerned, ask if you can get a referral to see a hematologist. They should be able to give you a real picture of the problems with long-term AED-induced leukopenia.
Remember: treat the patient, not the numbers. If you're healthy now, you're likely to continue to be so. Maybe you'll need more blood tests than others, but that doesn't mean you're not healthy. Talk to your doctors, not the internet.

Thanks for the detailed answer! Biopsy done by a hematologist some years ago didn't provide any actionable diagnosis. Since an accompanying blood test coincidentally revealed liver enzyme imbalance, was redirected to a gastroenterologist to check if liver is affected and causing low WBC as side-effect. Liver found to be normal now but WBC still low as it was years ago. Went back to hematologist who recommends repeating the biopsy to reassess bone marrow function but he was unclear as to what treatment could be given if the result is again inconclusive and only AED is the cause

Particularly appreciate you advice on taking to doctors, not the internet - hope the message reaches all internet users! Unfortunately, have to take multiple AEDs as per neurologist's advice and there doesn't seem to be a way out of these for the next few years, Even though the main AED is the latest generation one, the informational leaflet in the package mentions leukopenia as a possible side-effect.

@so2 - biopsies are necessary until there are "data points" for predictability. Also, inferno's answers is theoretical - if you had a neutrophil abnormality - that is, the ones you had didn't phagocytize appropriately - you'd know it by now. That you've not been prone to dangerous infections is evidence that you have enough neutrophils and that they're working correctly. You are likely relatively neutropenic - you have the usual complement of lymphocytes. Your WBC is low because  normally neutrophils = 75-80% of WBC count. You're probably closer to 40-50%. Again, treat the patient, not the #s.

Finally, one test you might consider is an ultrasound of the spleen, if you haven't already had one. Your hematologist will tell you why.

Thanks to you and @inf3rno! Hematologist said spleen seems normal (not through ultrasound though). Will let hematologist reassess bone marrow and advice on the next steps.

I know WBC is primarily responsible for fighting infectious
  micro-organisms, but does it have any significant role in cleaning up
  body's own malfunctioning or ageing cells?

They kill the pathogens, infected, senescent, mutated or unnecessary cells, clean up the cell fragments, clean up the oxidized LDL from the surface or arteries, etc... So I think the shortage of leukocytes can cause for example cancer, cardiovascular diseases (dependent on the nutrient composition of the food), etc... in severe cases, but it is hard to find any evidence, since these people die because of infections caused by normally harmless (or well controlled) pathogens, for example HHV8 - causes a cancer type called Kaposi's sarcoma in immunodeficient patients, saccharomycosis (S. cerevisiae, S. boulardii, etc... members of the normal flora), aspergillosis (A. niger - it is everywhere in the air), etc...
I guess there are experiments with NOD/SCID mice (which lack T-cells, B-cells, and NK cells, so a huge part of their immune system is defective), but I cannot find anything about cancer or cardiovascular diseases by them. They are usually engrafted with human cancer, etc... in the experiments, which is not the same as naturally developing cancer. Maybe if you have time to google a day or two, you can find more.
Be aware that there are many different types of leukocytes (WBCs), which have their own role in the immune system. Some of the people with leukopenia have lack only of a single type of leukocytes and not all of them. For example HIV patients have helper T-cell deficiency, people with neutropenia have neutrophil granulocyte deficiency, and so on...
I don't know anything of the treatment, I guess bone marrow transplant is involved in the severe cases. If it is caused by medication as a side effect, or you are seeking for medical advice, I think you should consult a doctor.

@inf3mo - Thanks for your response! Obviously, it is depressing to hear of these diseases, but then that seems to be nature's nature - design something very complex, make the complexity appear to be a boon, and make that very same complexity turn out to be a bane for many.
Posted the question because the previous biopsy did not lead reveal anything actionable. Was wondering if a repeat biopsy suggested by the doctor would be useful at all, especially since he could not tell if any treatment is even possible if the result is the same and AED is the only suspect. Stopping AED is not an option :(

@so2 Using another AED is your doctor's choice. There are many drugs, and I guess not all of them is immunotoxic. Your doctor should measure your WBC levels and decide what to do. I found only this article in the topic. AEDs increase the risk of relapse in patients with cancer according to this article.

Thanks for those links! Will let the hematologist do a reassessment & if he feels the condition warrants a change in prescribed AEDs then send his recommendation to the neurologist. Many specialists work in a silo-mode and don't take a holistic view of a patient's health - neurologist never ever told about the side-effects of AEDs & it was from the internet & later from medicines' informational leaflets that I came to realize they have hematologic side-effects.
Site doesn't allow me to accept 2 answers. Chose anongoodnurse's answer on 1st-come basis but your replies were equally helpful!

@so2 No problem.


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Given an EC50 value, how do I reproduce the sigmoidal curve from which this was calculated?
All-trans retinoic acid (atRA) is a potent ligand for a nuclear receptor called retinoic acid receptor alpha (RARa). The concentration of atRA at which RARa is half maximal is 19nM. The dose-response curve is sigmoidal, with concentration (log scale) on the x-axis and percentage of maximal activity on the y.
How would I use this information to reproduce the dose-response curve?
Thanks

Depends if the EC50 is given using a constant slope and a max/min that you know. If not then you cannot reconstruct it as you are missing parameters.

Basic sigmoidal curve looks like that: zero at $-\inf$ and one at $+\inf$. All in between should look like an integral of gaussian distribution. Take a look on this wiki page for more information. Now, the question, why sigmoidal curve is integral of gaussian function, I will leave out for now. My understanding is that gaussian distribution tells you how much system response will increase (say, efficiency of treatment) if you increase stimulus by $dx$. E.g., how much response changes when you go from $5$ to $5+dx$ versus from $10$ to $10+dt$.
The problem, as you might realize, that gaussian distribution has two parameters: mean value and width of the function. When you construct your fit, frist one will be 19nM, but second, $\sigma$, is unknown from your question. What you don't know is how rapidly response changes when you increase concentration by little around your EC50. So all your sigmoidal plots will go through same point but with different slope, like that:

Without knowing second parameter, $\sigma$, it makes little sense to plot your sigmoidal curve. However, if you want to, this is MATLAB code. See that cumsum() function effectively integrates gaussian distribution rendering sigmoidal curve.
c = 0:100; % range of concentrations you test
sigma = 1; % unknown parameter
m = 19; % your EC50 19 nM
g = 1/(sigma*sqrt(2*pi))*exp(-((c - m).^2)/(2*sigma^2)); % gaussian
gs = cumsum(g);
plot(c, gs)

If you want, you can plot it with log-scale of X, using semilogx() instead of plot().
NB here I started with Gaussian function and its integral just as a wild guess. You real function might very well be something like $f(x)=\frac{1}{1+e^{-x}}$. "Sigmoid" function is just description of general shape, not mathematical definition.

You answer is correct for a special case of sigmoidal curves. EC50 curves do not necessarily go from 0 to 1 in real experiments. Usually there is a baseline which is non-zero and a maxima which is not 1. To reconstruct the real sigmoidal curve you need those values.

I agree that the case is special, so OP misses even more parameters than I thought. I looked closer on EC50, it seems that it is defined as 50% increase after subtraction of background, that is after you accounted for zero-concentration efficency

Yup. He can approximate it with your method though (given an estimate of the slope). That was my upvote :)

even though I know that "sigmoid" shaped curves have various math definitions, I am a big proponent of link between gaussian distribution and most of sigmoidal relations in biology. Don't have any supporting data so far, unfrotunately

Hi Andrev, this is great, thank you... By slope do you mean the derivative at the point where the function is evaluated or the slope of the straight line bit in the middle? If you mean the latter, then I can work this out from the graph I'm looking at (since my data is from a paper). Essentially I'm trying to build a mathematical model that incorporates this data, so the values of the top and bottom asymptote will be relative - meaning I have to just make them up and see if they fit.

i'd say, 'slope of tangent to mid-point, e.g. EC50'. And yes, that might be a way to go. After that you can stretch and shift curve so it goes not from 0 to 1, but, let's say, from 0.1 to 0.9.


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Survival with only water but no food
How long can the average, healthy adult human survive with only water?

this seems to be an opinion-based question. Also, it would be better to post your research as well as question. What sites are you talking about? Any papers? what is particular side of such survival are you interested in?

@aandreev this question is not opinion based. You cannot survive forever without food, at least as far as I know.

Definitely not opinion-based, actually a great question - but a dupe

On average, it has been stated to be about five weeks however it differs from person to person based primarily on physical stats.
The process that would occur :

First food that remains in your stomach is digested
Readily available energy is then absorbed (This includes glucose, carbohydrates, anything that generally doesn't mean fat)
Your body then begins to convert fat into a source of energy. Your body would then begin to lose the resources to make protein and you would experience various effects such as night time blindness due to vitamin deficiencies
As you lose salt and other minerals the water you consume begins to build up in your cells via diffusion
You can either die of not enough energy or lack of protein or too many cells disintegrate from too much water

Source(s) : Biology book, Internet, Knowledge.


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What is the so called "hepatic glucose production"
I came across this term in my readings but I do not understand how this works. Can someone direct me to some reference as to what this "hepatic" glucose production is all about?

Hepatic refers to the liver, which is the predominant location of gluconeogenesis.

Silly me, I mixed hepatic with haptic (as in haptic feedback) and got totally confused

"Hepatic glucose production" is the gluconeogenesis process (the opposite of the gycolysis process), that is the formation of glucose primarily from lactate and amino acids. This process takes place in the liver's cells and it is regulated by hormones (insulin and glucagon).
Look here and here for a better explanation!


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When glucose production is low, the brain begins using ketoacids as energy... how does that work?
Can someone very generally describe how the brain consumes ketoacids/ketone bodies when blood glucose has been completely depleted?

Human body is a glucose driven machine which intake carbohydrates and converts to glucose. Energy is yielded from the glucose and glucose is stored as glycogen. When the carbohydrate intake is somehow reduced then body will shift its mechanism and uses the fatty acids to produce energy. Liver synthesis ketones from fatty acids in our diet or from body fat. Ketones(acetoacetate and acetone) are released into the blood, which is absorbed by the brain and synthesis energy from it through their mitochondria.

The brain gets a portion of its energy from ketone bodies when glucose
  is less available (e.g., during fasting, strenuous exercise, low
  carbohydrate, ketogenic diet and in neonates). In the event of low
  blood glucose, most other tissues have additional energy sources
  besides ketone bodies (such as fatty acids), but the brain has an
  obligatory requirement for some glucose. After the diet has been
  changed to lower blood glucose for 3 days, the brain gets 25% of its
  energy from ketone bodies.After about 4 days, this goes up to 70%
  (during the initial stages the brain does not burn ketones, since they
  are an important substrate for lipid synthesis in the brain).
  Furthermore, ketones produced from omega-3 fatty acids may reduce
  cognitive deterioration in old age.
  Reference

When the body starts using the fatty acids for energy production, one problem arises in the brain and that is the blood-brain barrier( barrier that separates the circulating blood from the brain extracellular fluid in the central nervous system )Brain cannot use long chain fatty acids because they cannot cross the blood-brain barrier due to their bondage with albumin. As ketones are medium chain fatty acids which can effectively cross the barrier. So brain uses the ketones for energy production by a process called as ketosis. The ketone bodies are then incorporated into acetyl-CoA and used in the citric acid cycle.

The citric acid cycle – also known as the tricarboxylic acid (TCA)
  cycle or the Krebs cycle – is a series of chemical reactions used by
  all aerobic organisms to generate energy through the oxidation of
  acetate derived from carbohydrates, fats and proteins into carbon
  dioxide and chemical energy in the form of adenosine triphosphate
  (ATP).
  Reference

Metabolic pathways to produce energy

I've linked to your answer in this question.

Actually there is fatty acid transport through the BBB. Maybe the rate of this transport is not enough, I don't know, I think it does not really matter.
What really happens here, that the liver prepares the fatty acids, so the brain can use them more easily in the form of ketoacids to produce energy.

fatty acid catabolism shared between the liver and the brain - ref

What you tell is astonishing: you learn about fatty acids being prohibited from being turned into glucose. With this that doesn't seem to be true: fatty acids to Acetyl-CoA and then clockwise through the TCA cycle, left hand,  to Oxaloacetate, then pyruvate, then: glucose. It looks as if it is a matter of plentitude of carbon to burn, as by being shuffled through the TCA cycle CO2 two times is being set free.  -  Should be written in all the textbooks!

@PeterBernhard Yes, in the human body there is no fatty acid -> carbohydrate biochemical pathway or it is very slow (note that this is not true for all animals). Same is true for fructose and ethanol, that's why they cause oxidative stress, fatty liver and diabetes. I think many times you can prevent diabetes by avoiding fructose (pratically most of the sweet foods and drinks) and alcohol. I think this information about carbs and fatty acids is already in textbooks, at least I learned it in the university 10+ years ago. The fructose part is a lot more recent.

Pun on "prohibition"? I mean alcohol and fructose sound icy to me, take my excuses for my strange English, by the way; the graphic has a link but the ref does not tell about which book that the graphic is from. As it occurs to me...even in wording that question could have been me. Maybe my comment truly tells - not the whole "stuory fur" sure, as you mention fructose - so how does prohibition of fructose from being turned to sweet work? Can you e-"leber"ate?

@PeterBernhard Last time I read about fructose, it was something new and very logical. Now according to new reviews it is not as certain as it was. https://www.mdpi.com/2072-6643/9/2/96/htm https://www.mdpi.com/2072-6643/9/9/981 https://www.sciencedirect.com/science/article/abs/pii/S0168827818300667 https://academic.oup.com/ajcn/article/100/3/833/4576481?login=false https://scholar.google.hu/scholar?hl=en&as_sdt=0%2C5&q=fructose+fatty+liver+review&btnG=&oq=fructose+fatty+liver

Again, thank you for clarifying what maybe is some common non having understood: e.g. medscape.com: "High levels of acetoacetate in blood may result from the following: Diabetic ketoacidosis and alcoholic ketoacidosis". As for me, I needed advice on that being the other dark side of the medal (no German) of ketose being needed. So, your shed new light on some, literally, half-knowledge. Diabetes, alcohol seem to imitate the need that must be: of calories, to starve is exhilarating.
To sum up: with your answer "ketoacidose" becomes understood, it's good, not bad, it's regular.

"Last time I read about fructose..." - Fructose, interesting to know about that..., does not seem to share any "prohibition", thus beyond topic: fructose can easily be converted to glucose by the body, ain't right? Is there any preference the link you added (not very accessible for the common people?)  is about? Fructose might be preferentially turned to ribose of DNA?

"Last time I read about fructose..." -  Fructose, interesting to know about that..., does not seem to share any "prohibition". It can easily be converted to glucose by the body.  Is there any preference the link you added (not very accessible)  is about? Fructose might be preferentially turned to ribose of DNA? Some other item is  that insuline production does not react to   fructose input, fructose heightening blood sugar in diabetic and non-diabetic in the same way.

@PeterBernhard Just use the google scholar link and you can find many similar articles. Some of them are not paywall protected. These are scientific articles published in scientific journals. You can read them in libararies or in universities. Sci-hub is another way, but it is more or less illegal, it depends on country though. https://en.wikipedia.org/wiki/Sci-Hub

Yeah, it is "fruct"(verrückt in German, dialect I use) - to chat it all up: fructose does seem convertible into glucose. 10 years ago it's use in chocolate was considered anti-diabetic. In my thinking, there is a way to store away some fructose-elevation of blood sugar if not to glycogen, then in a very regular, i.e. non-insuline way as fatty acid in adipose tissure, and in my thinking your mentioning "fatty liver" is very valuable: glucose - like "starch" seems to correlate to glykogen and maybe white fat, and fructose, just extrapolative, to "brown fat". Guess you're not German too.

@PeterBernhard Looks like normally it is converted into glucose in the small intestine, but in big quantities it reaches the liver where it is converted into fatty acids afaik. from other studies. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032988/ So consuming fructose as sweetener in big quantities (as we do nowadays with corn syrup) can cause health problems.

@PeterBernhard Another interesting thing here that it might affect cholesterol levels too. https://www.sciencedirect.com/science/article/abs/pii/0006294469900453

Mentioning cholesterol in that context seems irritating, I find it highly educating. Lately, I found myself "occuring" to me that cholesterol is either built into cell or veins' walls, however, cannot be burned, and - please help, correct me - cannot be converted into blood sugar. So, in that respect, cholesterol looks like some fat, and rightly suits this question.

@PeterBernhard The category is called lipid. It is transported with triglycerides and it is apolar, so we can call it fat. High level of blood cholesterol is problematic from atherosclerosis perspective.

I will say "lipid" not fat any more... So, I guess its trivial to know that cholsterol "cannot heat"...


text:
Common Metrics of Assessing DNA Sequence Quality
What are commonly accepted metrics for assessing DNA sequence quality (platform-specific answers are fine)? I am relatively new to this topic, and I want to either find or code (in Python or C++) algorithms for checking sequencing data quality before getting into analysis.

if you are talking about Sanger sequencing, look here: http://en.wikipedia.org/wiki/Phred_quality_score

as @aandreev pointed out Phred score is a universal metric used for denoting the quality of a sequence read. Phred is basically log transformed error probability. However, the error probabilities and their calculation procedure differs between platforms.

As mention in the comments Phred scores are the quality scores for most sequencing platforms. This value expresses the probability of a base is being called wrongly. You can find more information here. This values can be found in a fastq file coded by symbols.
For example, a phred score of 30 means that there is a probability of 1 base being wrong every 1,000 (that is 99.9% accuracy). In general values around 30 are considered good enough, but it depends on your analysis whether you want to be more more or less restrictive.
Biopython has some examples on how to plot and filter phred scores. There exits lots of other software to do QA checks, for example this one.
You can also check length and distribution of the reads, duplication levels, etc.
In case you need to trim sequences from Illumina there are several stand-alone software like this that you can use.


text:
Why didn't a concept like "pointers" in Computer Science evolve in the genome?
I see that the genome contains large regions of repeating sequences called interspersed or dispersed elements. The long dispersed elements (LINES) such as LINE-1, can reach up to 6-8 kb in length.
I'm wondering, given the amount of repetition that takes place in these regions, wouldn't a system where a pointer (such as in computer programming) existed  be more efficient? For example, instead of including a LINE, include a unique 5 base pair sequence acting as a pointer to that LINE. A separate chromosome (containing one copy of each LINE) would then be read at the correct position once the pointer was read.
Do you think that given enough time in evolution, such a system would be more sustainable? Sort of like using a proper functional language instead of Assembler in computer programming, where f(x) can be defined once, and accessed via pointers, instead of being repeated many times?

Are you sure about what pointer exactly does? As far as my knowledge goes, a pointer stores the address of an object in the RAM. I don't think your analogy is correct. And for function calls: Leave pointers to functions; there are no true equivalents of function calls in biological systems (see this post). It is imperative to understand both the subjects to a basic level before making analogies.

In the question you'll note I asked why a concept "like" pointers "didn't evolve". In this case of "like" the "object" being pointed would be a LINE. Putting semantics aside, I was curious why heavy extended chains of repeating sequences of carbon atoms would be evolutionarily beneficial when those same repeating chains could be just created once, and then activated as needed. Interestingly in the post you reference, you yourself state it's not the physical implementation, but the underlying concept that is important. It was a question regarding concept, as mentioned in the title.

There's not much point in conserving space when at least 50% of your genome doesn't do anything at all. To use a computer science analogy: Disk is cheap. (and all processing is parallel so even I/O isn't a deal)

@Resonating "50% of your genome doesn't do anything at all" is not necessarily true. A large portion of our genome does not have any currently-known function, but that is completely different from saying it has no function whatsoever.

The most generous papers have pegged maybe 80% of the human genome as functional. The average estimate is more like 15% even on the generous side. I gave a bit of a margin because much is not known, but there are ~at least~ 800 million bases that do nothing at all. I'm comfortable with my estimate given what is currently known.

Very important to be absolutely clear what "functional" means. The ENCODE estimate of 80% is based on a definition of functional that basically = "binds to something". Whether these have phenotypic consequences or not does not follow from just that fundamental property.

Short answer: Pointers already exist within the genome, in terms of transcription elements (such as repressor/activator systems). These systems can remotely activate a specific gene for transcription based on concentrations of specific chemicals within the cell.
The problem with LINEs are that they are thought to be ancient retroviruses which lost their capacity to infect other cells, instead jumping around within the genome. They are therefore parasitic in nature, and they reproduce by inserting multiple copies of themselves into the genome. It makes more sense to think of LINEs as nearly inactivated retroviruses instead.


text:
What is 'refractile' cell morphology?
I can't find a definition for 'refractile' (not 'refractory', and not explicitly in an optical context).
As in:

A tumour cell phenotype features increased proliferation, anchorage- and growth factor-independenth growth and ‘refractile’ cell morphology

It's not in any of the dictionaries I can access online, nor in the Oxford Dictionary of Biochemistry and Molecular Biology. Any help would be appreciated, thanks.

I'm not sure, but i think it refers to an actually refracting activity of those cells in phase contrast microscopy. For example, (as you can see here ) the nerve cell bodies are refractile.

Yeah, that's specifically of the 'lateral periphery'. This just says 'cell morphology', Actually I think it means they grow to a higher density

From the Biology Online Dictionary, refractile refers to:

... the ability of cellular granules to refract or scatter light.

Tumor cells can be more "dense", as they are usually rapidly dividing, and so need extra ribosomes to maintain protein production, may have a higher DNA/RNA content reflecting increased transcription and duplication, more mitochondria to power the cells, etc. This can alter the refractive index of a suspension of tumor cells as compared to organ-matched normal cells, for example.

Essentially, yes. Refractile would be of the cell itself rather than describing the solution, and they've overridden existing limits on growth (growth factor dependence etc.) It's just a term in physics, not a biological one related to granules.

Please note that this explanation may not be the actual physics definition, but it will help you to understand the concept of ‘refractile’ cell morphology.....
From the statement below by www.brittanica.com it appears that light is both partially reflected by & partially refracted or "transmitted" (think absorbed) into the object it is hitting. (Technically transmission is NOT absorption, but for this purpose it's easier to think of it as being absorbed by the cell/cell parts).
So when light hits the cells/cellular parts in a scan, some of the light is reflected back and some of the light is "absorbed" by the cell/cell parts. The amount of light "absorbed" is variable for each cellular component, and therefore, the amount of light reflected back is also variable.
In the scan or microscope, we actually "see" the reflected light. Not the refracted (absorbed) light and because the light reflected is variable, we are able to "see" the different components of the cell (i.e the different amounts of light reflected by the various parts).
So the statement ‘refractile’ cell morphology means that the cell has components which absorbs light at variable amounts and therefore, also reflects light at different amounts. Essentially, you are able to "see" the cell morphology & its differences because it refracts (absorbs) some light and reflects the rest.
Hope this helps get the concept. =)
"When a ray of light is incident upon a plane surface separating two mediums (e.g., air and glass), it is partly reflected (thrown back into the original medium) and partly refracted (transmitted into the other medium)."
https://www.britannica.com/science/radiation/The-structure-and-properties-of-matter#ref398785

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


text:
DIY storing family DNAs' samples for future uses (eg medical)
I have a question I could not get an understandable reply from Google and I am no expert in the matter, so my plead to you is if you could give me practical and relatively easy to follow advice.
With the view of the breakthroughs in DNA research and all the anticipated applications to medicine in the near-future, I am willing to build a storage of the DNAs in my family (eg 20-30 people, some at a very old age). The use may not be for cloning :) but rather, for eg to map and trace specific hereditary genes when such services become more available to the wide public; and thus, probably help with a personalized medicine for someone, or find genome problems, and probably be able to 'turn them off' at some point.
Is there a way I can extract cells (ie from inside the cheek, or hairs), and store them for a few decades while preserving the DNA (eg put them in a freezer at -18C or in some solution)?
I have only common knowledge in this area so apologies if the examples are silly, but I assume you can understand my point.
I would be grateful if you provide practical instructions as: "you buy 500ml of the chemical xx"; or "mix 150ml of xx and 200ml of zz", so me and anyone who finds the idea appealing, can follow.
Ps-the lower the costs of the procedures, the better (I found some personal "dna vaults" costing several '000$).
Thank you for your consideration!

If you have access to a laboratory (or at the very least a centrifuge and pipettes) and some laboratory experience you can extract the DNA from the cells which would be much easier to store. There are a number of commercial DNA extraction kits available that are easy to find on google and order online. I don't want to promote any particular brand but I've mostly used DNEasy made by Qiagen (really just because that's what I'm used to). All the step-by-step instructions are in the kit and all the reagents are also in the kit with the exception of 100% ethanol which should be easy to obtain.
If you have significant molecular biology experience and access to a full lab with a fumehood and appropriate safety installations you can try a manual extraction using trizol or phenol-chloroform. This would be slightly cheaper however given the toxicity of these agents I wouldn't recommend this for you. It really doesn't sound like you have these resources available to you.
Once you have the DNA extracted you can dilute it in Tris-EDTA or the elution buffer that comes in the kit. You can store extracted DNA in a regular fridge (4C) for several years. If you're looking to store for decades you may want to rent space in a -80C freezer but this would be more expensive. A fridge may be just right to suit your needs. You should be careful that this fridge has a backup power supply.
I should be clear that although extracting DNA is the easiest way to do this for somebody with experience, you should not try if you don't know what you're doing. Some of these reagents are dangerous and you are likely to ruin the samples you've taken from your family members and end up with no DNA at all. Good luck!

So cryopreservation would be the long-term mode of storage, and you'd do something like store your sample in a cryonic freezer supplied w/ liquid nitrogen at -196C. Cellgro provides some recommendations for cryopreservation here. Keep in mind, cryonic freezers are typically pricey, but broady, the idea is you need to keep your cells at the right temperature, in the right media. The source I gave you provides suggestions for media, DMSO as a cryoprotectant, and a protein source to protect the cells during the process. Also, keep in mind there are recovery issues with cryopreservation. There's some data to suggest reactive oxygen species, and apoptosis mechanisms damage/fragment the DNA in cells that have undergone that sort of freezing(1, 2, 3). These articles mainly refer to sperm storage.

I don't think OP is asking about storing live cells, but rather DNA. You certainly don't need liquid nitrogen for that, once you've purified it.

Thank you for the idea, surely it is an option one can choose. I assume the costs would be for a space in such a freezer, shippings and to hire some pro. to do the procedures you bookmarked. As MattDMo added, cryopreservation seems to be a way used mostly to preserve cells alive (we did that with our child's embryo-cord, as many parents do). I have a feeling there are even some simpler ways to preserve ONLY dna which can be analyzed after a while; I think of biologists being able to evaluate dna extracted from the remains of species long been extinct, or early humans.

You could store DNA diluted in water at -20C for a very long time. The only problem with at home storage would be the type of freezer most households have. These come standard with defrosting feature, which thaws up the freezer to remove the ice accumulation... This would affect the stability of the DNA at long term scale. Having a styrofoam box to protect the samples could however dampen the elevation of temperature around your DNA.
As for the DIY extraction, most extraction methods use either chloroform or chaotropic salts... those are very toxic and dangerous. A "dirty" extraction would be the best approach. You would still need a centrifuge, NaOH, EDTA, and Tris Base for a very simple approach (1). The referenced protocol is prescribed for rodent tissue, but could be applied to small skin snips or buccal frottis (not that I recommend ripping skin from your relatives...).
For the various reagents, Sigma-Aldrich sells pure chemicals, but I have no idea if particulars can buy on their website.
(1) http://jaxmice.jax.org/support/genotyping/dna-isolation-protocols.html

Basically agree with the other answers, but a bit of clarification. The bottom line here is that DNA is actually a really stable molecule - after all, it's evolved to be! So assuming your principal goal is 'keep enough DNA that you can read genomes and/or epigenomes'*, the main requirements for storage are low and steady temperatures. For instance ancient DNA studies regularly collect partial DNA, and even whole genomes, from organisms including humans that are thousands of years old. The key here is temperature stability.
So with that in mind:
1) I'd keep two samples, a DNA extraction** and some whole tissue. This might mean cheek swab, some blood, something like that. There's lots of material out there. Teeth are pretty good, if any of those come your way!
2) 'Cryo' stuff (at least in the UK) would be taken to mean 'very cold, something to do with cryonics, and generally aimed at preserving whole life etc'. This is way out of scope for the OP even if you agree the (contentious) claims those practitioners make.
3) Can't emphasise enough that domestic freezers won't cut it. In general you can DIYbio / hack lots of lab kit that's overpriced (water baths, gels, even PCR machines can be bodged to a degree) but as mentioned above, domestic kit will defrost periodically (even assuming you have a UPS to guard against power outages) and those temperature fluctuations will shred your DNA.
4) One final thought, bearing in mind 100yr-old DNA at -4 is probably going to be in better shape than 20yr-old DNA at -80 with periodic warming: You don't, by any chance, happen to live near any glaciers, do you? Because if so you might as well make a bio-time capsule: the ultimate backup! ;)
Either way - good luck.

*Mind you, the simplest thing to do is sequence your relatives' genomes now? Or are you waiting for costs to fall?
**The reason to keep a whole tissue sample as well as extracted DNA is this: While extracted DNA is likely to be more stable over very long periods of time, current DNA extractions have been optimised to work well with current DNA sequencing techniques but may inhibit future ones. For example, some of the well-established Tris-EDTA step https://biology.stackexchange.com/users/15594/jack mentions are contraindicated for Oxford Nanopore (MinION/PromethION) sequencing preps IIRC.

At page 12 of this pdf there is an easy protocol for DNA extraction from saliva. You just need soap and salt to do it (it works even without Chelex, but you get better DNA quality if you use it). A microcentrifuge is requested for this protocol, you can find them on eBay for less than 100 dollars. If the max speed is not high enough you can always spin for a longer time at lower speed. I tried it and it works.
Once you have the DNA, you can store it in a normal freezer (-20) for decades, just avoid to defrost it a refreeze it multiple time or it will deteriorate.


text:
How does a cell create/gain its initial ribosomes for protein synthesis?
I did some quick google searches for how a cellular organism generates or acquires its first ribosomes, but I found nothing. For instance, do the organisms initiating replication form extra Ribosomes to pass on to the created organism?

@caligari2005 Uhm...why don't you make that an answer and I'll give you the credit for it? :P

From the comment section:
Cells divide and when they do the two daughter cells will not only have copies of the DNA but also of the organelles, the cellular machineries and the cell membrane which implies that yes the daughter cells receive also ribosomes. The replication happens during the interphase.

I transferred the answer from the comments only 2 days ago so that was actually quite fast :D

Nevermind then. ;p

Each daughter cell, following mitosis, will contain some ribosomes and DNA transcription machinery already, so it can already synthesise more ribosomes.
In the case of the fertilised ovum, when the organism is only a single cell, the first ribosomes will be those already present in the unfertilised ovum.
So cells never have to start from scratch with no ribosomes.


text:
Workspace preparation and cleanup for DNA work
What steps should be taken in a molecular lab environment to help ensure that DNA samples/stocks are not contaminated, or contaminate other objects in the lab?

VTC because this question is identical to the later one, and the later one is better asked and has better answers.

From the comment section:
Mostly segregation of PCR-amplified DNA from non-amplified DNA. Typically no DNA or sample should ever enter a specific room designed to prepare the MasterMix for PCR (this is true for diagnostic labs, in the research one I never saw that). For the rest, following good laboratory practices (google that) should be enough.


text:
Software recommendation for protein in electric field modeling?
I'd appreciate a suggestion for software to compare models of two proteins in an alternating electric field. The more detail, or perhaps direction towards an existing and similar paper, the better. Right now I'm particularly interested in comparing rotation of the proteins as a result of the field. The first protein, tubulin (1TUB), will be modeled as a dimer while the second, septin (2QAG), will be modeled as a trimer.
The electric field will consist of a 200Khz field at 1.5V/m with a spatial resolution of 300Ax300Ax300A. I believe that I will only need a temporal resolution of 1.5 milliseconds for 10 solutions(?) per cycle for 3 cycles in the 200Khz field (particularly unsure of this part).
In terms of computational power I have access to two 7870 Radeon GPUs, but am also interested in cloud computing if that's not enough.

this is a tough one. Maybe you can help those, who know the field, by specifying temporal and spatial resolution, duration requirement for modeling. Molecular Dynamics approach might help, it has great resolution in t and xyz, but model duration is ~1us, as I remember.

Mathlab has many good toolboxes for many things, although it is not cheap. Good news is that there are alternatives such as Scilab that is totally free.

@aandreev I've done more searches with inclusion of "Molecular Dynamics" and have found GROMACS which, apparently unlike NAMD, allows for an alternating field. This may be the program I'm looking for... http://onlinelibrary.wiley.com/doi/10.1002/anie.200703987/full

@Timmons I am saying, you under-specified your problem. Are you looking for 1ns temporal resolution? Are you interested in how each atom moves? Or you can approximate your molecule as a sphere with uneven charge density? That kind of descriptions might be helpful.

@aandreev ahh, my mistake. I have not "picked" a temporal resolution, but I know that I'm not interested in each atom, rather, how the whole molecule rotates in the alternating electric field. A sphere might work, however, I'd like to eventually to add several of the proteins linked in a filament (realizing that's another level of complexity)

@Timmons - What structure are you using?

As in which protein structure? I'd like to look at the asymmetric units for both, if I understand the question correctly.

MD
Broadly this could be attempted with Molecular Dynamics simulations. As you discovered in your search, one of the most popular softwares is free: GROMACS. This is an atomistic approach to the problem. It also has many electrostatic parameters.
I would point out that generally MD requires careful and robust methods and often an expert lending hand if the results are to be trusted. In order to do MD at the timescales for observing rotating molecules in the field, massive amount of HPC computational time will be required. This is a full blown project to get it to an appropriate level for publication.
This is computationally intensive.
Quick Electrostatics
If a HPC is not available to you then MD may not be an option. If all you want to do is visualise the location of the charge and make qualitative predictions or visualisations, PyMol and ABPS might be a quicker combo. It is also good for quantitative analysis, but obviously is a static model.

Thanks for the additional information. I've actually just come back to this problem after finishing some other work, so your timing is serendipitous.

Your point re: the necessity of an HPC is well taken. I thought my 2 7870 Radeon GPU's might be able to handle it, but your comment suggests otherwise. Do you know whether cloud computing is a viable/affordable option? (https://aws.amazon.com/government-education/scientific-computing/)

@Timmons I've only been a part of three academic groups that were all involved in MD, but they each had their own HPCs and clusters. Whilst I can't see anything obviously wrong with cloud computing, I would email ahead and check that what you want to do is viable.


text:
Why do people in the scientific community use terminology such as renal, hepatic, cardiac instead of kidney, liver and heart?
Are there differences between renal, hepatic, cardiac and kidney, liver and heart? Is the "jargon" used more commonly because of tradition, or is there some definitive biological basis to it?

The former words have latin roots, and historically latin was the language of science. Therefore, nomenclature in different scientific fields are often based on latin roots.

I disagree with Chris. Questions on technical terminology are a perfect fit here. For example, what if the reason behind the terminology is based on historical events. Doesn't the history of biology still matter on this forum?

Also, note the answer provided by "fileunderwater". His answer makes note of the fact that there exists a specific and technical difference between the terms. If I ask why a Histone scaffold is not called a Solenoid, that is a valid question with a basis formed by the terminology set by the scientific community. In other words, it's not a matter of "english language and usage". They have essentially asked whether or not there is a difference between the renal system and the kidney.

@fileunderwater the jargon is consisted of both Latin and Greek.

Medicine is not my field, but I want to point out two things:

The former words have latin (or greek) roots, and historically latin was the international language of science. Therefore, nomenclature in different scientific fields are often based on latin.
The former words describe tissues and the related functions/processes (e.g. renal = kidney + related tissues + processes carried out by the renal system), while the latter are names of organs. Therefore, the former words are more suitable and precise when you want to describe these processes. For instance (as far as I know), Hepatic disease can be be caused by problems outside of the liver as such, e.g. blockage in the hepatic vein.

Users more knowledgeable in medicine are welcome to fill in or correct me if I'm mistaken.


text:
Online resources for entomology?
I'm going to teach a c ollege-level introductory entomology course soon, and I'm looking for free online entomology resources. Does anyone have any recommendations?
In particular I'm looking for phylogenetic resources, experiment ideas, images, topics, etc.
Ideally, I'd love to find a discussion forum consisting of other entomology instructors sharing their ideas.
Thank you!

The Entomological Society of America has dedicated page called Entomology Resources for Teachers, which might answer many of your questions. It compiles curated links to resources, universities,
Here are a couple of other entomological links/resources that I have saved from before:

Bugguide.net
Pictures, simple keys and taxonomical info. Also has a forum.
The Entomological Foundation: Education
Links, project ideas etc.
Kerbtier.de
Webpage on beetles found in Germny, but relevant for many European countries. Also has general pages on e.g. beetle morphology and a glossary that might be useful.


text:
What is this arachnid?
I came across a photo on Wikipedia depicting an Oreocereus celsianus with what looks to me like some kind of harvestman on it. The photo was taken at the San Francisco Botanical Garden.  Can anyone identify the arachnid in the photo?  (See link below for full-size image.)

Source: https://commons.wikimedia.org/wiki/File:Oreocereus_celsianus_1.jpg

It sure looks like the harvestmen I saw growing up in northwest Missouri, but I never knew their exact names.

nice photograph......it looks like harvestmen...but what is that thing it sits on ?

The latin name for this animal is Leiobunum rotundum and Nelima fuscifrons, order Opiliones.
examples:
link

Wrong continent.

@augurar. This animal is spread elsewhere, the back pattern is identical, the description is identical. I did not find any argument against this match, actually.

Several other Leiobunum species also have this pattern, see e.g. some of the photos on http://www.bio.sdsu.edu/pub/spiders/OPIL/.  But I think you have found the correct genus.  It probably would not be possible to identify the exact species without examining some microscopic characteristics.


text:
Why do people feel pleasure when using roller coasters / centrifuges?
The feeling when using an amusement park unit is usually a pleasure. Why is it not a pain instead?
Are there advantages, from an evolutionary point of view, in loving this potentially dangerous activity?
Is it related to the liking for extreme sports?

I think it works the same way as horror films, we like to fear of death, but survive.

@inf3rno, Does this "fear of death, but survive" acts (brings pleasure) the whole time or only when it ends ("survival")?

Good question, I am not expert of the topic. :-) I guess the keyword is controlled fear here. So you can take pleasure in fear when you know that you what you are doing is safe. I found this article in the topic, maybe it helps. https://www.psychologytoday.com/blog/lets-connect/201002/can-fear-and-grief-be-pleasurable

Riding roller-coasters usually (unless you are psycho) induces a release of adrenaline and other chemicals, like endorphin (your bodies pre-emptive effort to combat any possible pain and stress you may be about to experience), into your body. Endorphin is a strong chemical, specifically released to make you feel relaxed and confident. Obviously this explains the natural high you may get from riding a coaster.
However, every now and then you get that person who ruins it for everyone by having a heart-attack. This person's body was not conditioned for this type of stress, and clearly they did not enjoy their ride much. Elevated blood pressure,
erratic heartbeat and palpitations...they should have instead taken a ride on the log flume. For the rest of us thrill-seekers, this type of gung-ho, take-all-comers attitude gives us a confidence boost by wiring our brains to not be overly stressed in actual emergencies.
Imagine the people out there who have grown up in small towns. You may have heard how such people can have a difficult time adjusting to the hustle and bustle of city life, especially in larger cities. This has to do with everything from their metabolism and diet, to their sleep cycle. Their body simply needs to get used to the new environment. The same goes for new combatants. Military's try their best to simulate combat for new trainees. The better the simulation, the better prepared people will be for combat. The first few combat situations for people are obviously going to be the most dangerous, being a truly foreign experience for most peoples bodies.
Physiologically it's going to push your body to the limit. After all, you sense your life is in serious danger. But as many people deal with this stress, they can start to acclimate until they ideally stay fearful, but become extremely focused on the fight. The adrenaline rush (and again, other chems) is part of what you need to get used to. If your body has a naturally stable system when exposed to these chemicals, or you have trained it to be so, then you are at an advantage compared to your peers.
https://www.psychologytoday.com/blog/threat-management/201001/adrenaline-rushes-can-they-help-us-deal-real-crisis
http://www.faqs.org/health/topics/15/Risk-taking-behaviors.html

Roller coasters release adrenaline, a chemical that is released when your body thinks it's in danger. It strengthens your body so that you could fight or flee. However, since a roller coaster is not actually dangerous, your body just feels strong and good. Your body also releases endorphins during roller coaster which makes you feel good.

Your answer makes sense, but at Bio we press people to use and mention credible sources and scientific papers


text:
Is there a cellular mechanism that detects Ribosomal damage?
What kinds of options, if any, do cells (Eukary and Prokary) have for detecting, and repairing damage in Ribosomes (of all types)? I am curious as to
what happens when a cell sustains damage of some form, such as radiation, and the Ribosomes are damaged.

I think you should check rRNA synthesis regulation: http://www.nature.com/cdd/journal/v20/n11/images/cdd2013107f1.jpg . So it seems to be regulated by sensing stress and not the ribosome damage directly. Another possible mechanism to measure the mRNA synthesis rate and if it is too high, then build a new ribosome. Maybe there is something like that too in the background, I don't know, interesting question.

I'm unaware of any repair mechanisms. Damaged proteins and RNA are usually dealt with by degradation.


text:
Question about epinephrine
In my class we were told that adrenaline (or epinephrine) causes vasoconstriction.
My question was I had always thought that people took this via an EpiPen when they were having an allergic reaction.
So I thought it would make sense, that it would dilate vessels, because this will allow more air through. Or does the constriction help because it tightens the vessels in the throat allowing a reduction of swelling?

An allergic reaction requiring an epipen can be caused by swelling in the throat and/or bronchoconstriction (spasms decreasing the diameter of bronchioles). Bronchoconstriction can occur in the absence of soft tissue swelling in the lips, tongue and throat, and vs. versa.
Epinephrine reduces pharyngeal edema (swelling) because it is a potent vasoconstrictor in small arterioles and precapillary sphincters in most body organ systems. This is effected through alpha-1 adrenergic receptor activation. While the blood pressure and heart rate increase (due to beta-1 adrenergic effects), the permeability at the capillary level is decreased, relieving swelling.
At the same time, epinephrine relaxes bronchial muscle. It has a powerful bronchodilator action when bronchial muscle is contracted because it is a powerful beta2 adrenergic agonist.
Finally, epinephrine inhibits antigen-induced release of inflammatory mediators from mast cells, and to a lesser extent from diminution of bronchial secretions and congestion within the mucosa. Inhibition of mast cell secretion is mediated by beta2 adrenergic receptors.

Adapted from Simons. Kemp et al. World Allergy Organization Journal 2008 1(Suppl 2):S18-S26   doi:10.1186/1939-4551-1-S2-S18
Epinephrine: The Drug of Choice for Anaphylaxis--A Statement of the World Allergy Organization


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What does saying a phylogenetic tree is 'well resolved' mean?
I'm not sure what 'resolution' means in the context of phylogenies.

It means incomplete separation or a failure to split into two groups unambiguously.
There are multiple ways to estimate the resolution of a phylogenetic tree; involving an index to measure the likelihood of observing the phylogenetic tree that you derive relative to those produced by drawing species at random, for instance, or permuting species to produce a null distribution.
A badly resolved tree should show up in sets of randomly generated trees far more often than well resolved ones.
See http://onlinelibrary.wiley.com/doi/10.1111/j.2041-210X.2012.00196.x/abstract

I think PO asks what well - resolved means

My bad, well spotted, Alice.


text:
What makes a good phylogenetic tree?
How can one improve a phylogenetic tree? If one was to make the 'golden standard' of phylogenetic trees, what features would it have? Would it be highly reliable, well resolved etc? What other features are important to aim to maximise when it comes to improving phylogenetic trees?

Can you please merge your two questions into one as these are highly connected? Addtionally you may want to work on your attitude. No one here is obliged to answer, so you probably want to cut down the use of ASAP. Additionally: How does your own research look like, what have you found out?

I've found that a phylogenetic tree is an estimate of the true evolutionary relationships between species.Thus, we cannot really measure a tree's accuracy because we don't know the 'true value' i.e.what the actual pattern of evolutionary relationships is.I'm aware that trees which are well resolved,constructed using multiple genes & with high reliability/repeatability(indicated by high bootstrap values)are considered to be better than others but I'd like some references to back up my inferences since I'm doing a final year project.An objective list of what makes a good phylogeny may not exist

A 'good' phylogenetic tree would be completely refined, properly binary, have high bootstrap support for all its branches, and reconstruct clades we think exist with high support values.
Generally high support values(there are other methods besides bootstrapping but that is a question for another time) is a measure of a good tree. There are other concerns, for example a tree that has no felsenstein zones is probably better than one that has lots.
We can know a lot more about trees than you suppose, though. Through simulation studies we can create datasets with a known phylogenetic history and then see how well the methods reconstruct the history. There are still problems(errors in the model used, just random error, ILS, HGT, other things) but mostly that kind of study tells us what good phylogenies look like.
It's very easy to generate a lot of different phylogenies. Using different methods, different models or approximation schemes, different genes or sequences from each species, or simply bootstrapping "new" samples from your existing dataset. A phylogeneticist usually has dozens of trees to choose from, which is a sort of crude bootstrap method itself. If trees look similar, they're probably pretty good. If they don't, you have a problem.

Would you please elaborate on what it means for a tree to be 'completely refined'? I am interested, but unfamiliar with what you're referring to here.

Some methods represent uncertainty by producing internal nodes that have more than three connections, essentially saying "all these groups are about the same amount similar, I can't figure out their arrangement". Finding an arrangement that has fewer of these internal nodes contains more information, and is called a 'refinement' of the tree. The 'star tree' where everything is connected equally is the least refined tree, and contains no information. The 'fully refined' tree is properly binary and has the maximum information.


text:
Regarding cryonics, why can't you freeze a living body and then thaw it later, fully functional?
Cryonics is very popular in science fiction today, as a method of preserving animals, including humans, for long time storage and thawing the tissue later in the future. What is the difficulties with this method? Why can't we simply freeze living persons and expect them to be fully functional again later?
I've heard that the membrane potentials get lost in the process and thus all neural activity stops. I've also heard that freezing cells leads to cells imploding, due to the formation of ice crystals, leading to rapid necrosis. Is any of this true or just myths?


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Why do body parts sometimes get a itching and tingling feeling when falling asleep?
Just before I fall asleep I sometimes experience an itchy and stinging feeling in my body parts. It can be that the nose or neck suddenly start to itch or a tingling stinging feeling in the legs. Sometimes my fingers also start to do small uncontrolled movements.
What is this about?

This is not a duplicate.

Not a dupe of http://biology.stackexchange.com/questions/31107/involuntary-twitches-and-apnoea-during-early-phases-of-sleep

@FloriOn Why is this marked as a duplicate? My question is not about PLMD nor apnoea.

Sorry everyone, removed.

Maybe you're being allergic at something from your bed (maybe dusts). Try sleeping with clean bed clothing and pillows (and yourself too) and see if the itching persists.


text:
Mosquito physics
What are the environmental limitations of mosquitos I should know of if I want to avoid getting bitten?
For example:

How fast should I walk in order to be moving too fast for one to bite
me?
Can a fan work to blow mosquitos away from me?
If I'm looking to
buy an apartment, is there a minimum height in which mosquitos will
no longer reach?

Thanks!

Speed of mosquitoes vary from place to place and their current health status.But if there is any such problem, maybe you can run a short distance (some yards) and then they won't harass you for some time till they cope up with you.
Yeah, a fan usually at comfortable speed will be enough to blow the mosquito away. If this doesn't work then set speed at full speed and wrap yourself in a blanket
I don't think there is some height where mosquitoes can't reach but my friend who lives on 12th floor in his apartment hardly has 4-5 mosquitoes bugging him.

Could you provide some references?

I am quoting this web page http://spectrum.ieee.org/consumer-electronics/gadgets/backyard-star-wars which describe a prototype of a system to kill mosquitoes by means of a LASER, for what regard the speed:

Mosquitoes fly up to a meter per second.

This speed is compatible with 1.2 meter per second quoted in the paper
SNOW, W. F. Field estimates of the flight speed of some West African mosquitoes. Annals of tropical medicine and parasitology, 1980, 74.2: 239-242.

There was a relationship between wind speed and catches of Anopheles
  melas and Culex thalassius which attempted to bite man at ground level
  and at 4 and 8 m on  an open scaffolding tower, in cleared bush in The
  Gambia. It was expected that in winds which exceeded their flight
  speed, no mosquitoes would be able to approach  and attack men on the
  tower. Catches of mosquitoes fell off sharply in winds of 120 cm/s,
  which may approximate to their flight speed, although some insects
  were still captured at the highest wind speeds encountered.

For what regard the flying altitude:

The average flying altitude varies among mosquito species but is
  usually only about 2 meters. They will fly over obstacles when
  necessary—even into an upper-story window—but if your virtual fence is
  3 to 5 meters high, it can catch almost all mosquitoes that fly by.

The system is patented and the patent is specific about Anopheles:

For example, more than 99% of Anopheles mosquitoes (which may carry
  strains of malaria that can infect humans) fly at less than 3-5 meters
  of altitude

HYDE, Roderick A., et al. Photonic fence. U.S. Patent Application 14/255,119, 2014.

Environmental limitations of mosquitos can be:
1) Wind. Prefer a windy day for a walk in the marches! Or a large ceiling fan above you bed makes a real barrier against mosquitoes!
Mosquitoes cannot fly against the wind if the wind is more than ~1m/s as you read in your reference.
1) Temperature. Prefer the winter season or AC-rooms!
Some species hibernate during winter (but they still need to take some blood meal from time to time). If it is spring or if spring season doesnt exist where you are, prefer a cold day. It is relative to the normal temperature of the considered location. Some cold-climate species swarm very well at 12°C (Aedes communis  https://doi.org/10.1016/J.JINSPHYS.2021.104233)
2) Humidity. Prefer the dry season or dry locations!
Mosquitoes prefer humid places, otherwise they could die. Again, it depends of the species and some got adapted to arid location. However, they always need water to lay their eggs.
3) Mechanical barrier. Prefer to sleep under a bednet!
Mosquitoes are small and are very good to pass below your door in in a small holes of your window, however they cannot pass if you are in an isolate place. To keep some afresh air, use a bed net. It is a recommended by WHO (https://www.who.int/elena/titles/bednets_malaria_pregnancy/en/)


text:
Why do mushrooms grow in rings (sometimes called "Fairy Rings")?
Mushrooms disperse their spore in all direction. Then why is there a formation of fairy rings? Why do they grow in one shape and not randomly?

Welcome! I think this is an excellent question! :)

The mushrooms require a lot of nitrogen, more than grass, and they deplete the nitrogen enough that the grass withers, so they grow outwards. https://en.wikipedia.org/wiki/Fairy_ring#Necrotic_or_rapid_growth_zones

When spores germinate, they do not generate mushrooms directly, but haploid mycelium starts to grow. Only when the mycelium from spores with the other mating type is met, cells fuse and generate diploid mycelium, from which mushrooms can grow.

Fairy rings are caused by a radial outgrowth pattern of the diploid mycelium, followed by resource depletion in the oldest part (middle).

This page seems to have good additional information about hyphal growth.


text:
How to isolate host cell RNA (tRNA,mRNA,rRNA) from viral RNA?
A retrovirus with RNA genome infected a host cell. You would like to isolate the host cell’s RNA (rRNA, tRNA, and mRNA) from the virus RNA. What properties can you rely on to determine the three types of host cell RNA- for example, in terms of their size, complexity, GC content, or abundance in the cell? The undetermined RNA can be identified as the virus RNA.

This is a homework question, right?

@Chris I am a Bioengineering student preparing a presentation for the next lecture, so it kinda is a homework.

So what's your idea of solcing this problem?

Here in Germany we are at the beginning of the 2. semester and up until now what i can think of is using radioactive Uracil, but that would only 'seperate' the DNA from all RNA. Another idea would be using Polymerase-Chain-Reaction.

Does this question assume an unknown virus? So you're separating the RNA so that you can sequence and identify the virus?

@user137 no just a arbitrary retrovirus. But the question was how to seperate the Virus RNA from the hosts cell RNA? so you dont need to specify what kind of virus it is .

@Sam Well if you know the virus and know its gene sequence, you might be able to use RT-PCR to get DNA copies of its RNA. I can't think of a way to take total RNA from a cell and physically separate host RNA from viral RNA.

Thermo Fisher has a protocol for the separation of host mammalian RNA from prokaryotic RNA, optimized for E. coli vs human, mouse or rat sequences. Capture oligonucleotides bind portions of the mammalian RNA and hybridize. These hybridized oligo/RNA are then removed from solution via "oligonucleotide-derivatized magnetic beads," after which the remaining RNA assumed to be from whatever prokaryote can be precipitated out w/ ethanol. If you know enough about your virus and your host, I don't see why a similar assay can't be created. Otherwise, Thermo Fisher has additional links to RNA isolation protocol.. most of the viral assays, however, utilize serum, plasma, etc. because host DNA/RNA will elute along with the viral RNA if they're present, as in samples containing cells.

Retrovirus is not prokaryotic; so that kit may not work. But the the principle is, as you mentioned, the same: adsorb oligos that will bind specifically to viral RNA on beads and remove the viral RNA. Modified oligos such as LNA can be used for a stronger binding and longer life.

Right, i was thinking more of a modified assay based on the same principles.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

@questionhang see my edit above for some reasons.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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