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Old 08-27-2012, 10:55 AM   #226
William Gaatjes
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Quote:
Originally Posted by Gibsons View Post
It's kind of like asking why not have an armed SWAT team kicking in doors through the neighborhood all the time.

An real life example of where immune suppression is a very good thing (there are many)
http://en.wikipedia.org/wiki/Onchocerciasis
The example is not a fair one.
Quote:
It is not the nematode, but its endosymbiont, Wolbachia pipientis, that causes the severe inflammatory response that leaves many blind.
The reaction of the immune system damages the cornea because the surrounding tissue is infected by the bacteria.
It is the "chronic" extreme inflammation that causes the blindness.
Thus a temporary infection causes damage but not blindness. A chronic infection causes blindness. Would that not account as an inability of the immune system to get rid of the pathogen ?
I can understand that an immune suppression might be handy here, but only with a treatment to get rid of the bacteria.
Nevertheless, that is quite an interesting bacteria indeed.

Quote:
Adult worms remain in subcutaneous nodules, limiting access to the host's immune system.[citation needed] Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. Dying microfilariae have been recently discovered to release Wolbachia surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity.[10] Wolbachia species have been found to be endosymbionts of O. volvulus adults and microfilariae, and are thought to be the driving force behind most of O. volvulus morbidity. The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response
Microfilariae are simply put, the "baby" nematodes.

Quote:
Ocular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve.[11] The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms.
I meant more that instead of suppressing the immune system, we should figure out why it is that it is so reactive. Of course suppression is a good thing. But your example reminds of pushing the brakes while also flooring the gas pedal at the same time. It is better to find the reason why the gas pedal is down then just to hit the brakes and hope that it works. Too many side effects will happen.






Oh lord, i used a car analogy...
I am doomed forever...
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Old 08-27-2012, 11:17 AM   #227
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The example is not a fair one.
It's completely fair. Why is it that some people go blind from the infection, and some don't?
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Old 08-27-2012, 02:53 PM   #228
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It's completely fair. Why is it that some people go blind from the infection, and some don't?
That is a lot of variables. I will have to think about that.
Normally a lot of those variables would just pop up in my mind. The big picture and i could "zoom in" on all details of "the big picture". But not for a while anymore...

All will go well, i will have my new house soon, outside the city.
I can have proper night sleeps again, not interrupted every 2 to 3 hours because of my mentally challenged paranoid sociopath neighbors and their mentally challenged kids. And that means i will be able to use lucid dreaming (conscious dreaming) once again.
I am tired.
At the moment, i cannot answer your question besides giving standard variables...

Difference in genetic make up.
Difference in environment.
Difference in amount of pathogens received and difference in order of acquired infections .
Difference in acquired immunity and difference in the order of acquired immunity.
Difference in feeding habits.
Difference in exposure to toxins (high doses acute exposure and low doses chronic exposure).
Having multiple infections simultaneously but different in amount and type of pathogens.
Difference in epigenetic background.
Difference in character or personality (susceptibility to stress).
Difference in the family gut bacteria.

Some are related yet different.
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Old 08-28-2012, 08:36 AM   #229
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That is a lot of variables. I will have to think about that.
Normally a lot of those variables would just pop up in my mind. The big picture and i could "zoom in" on all details of "the big picture". But not for a while anymore...
It's all about immune suppression. A strong inflammatory reaction to the infection = blindness. A suppressed, less inflammatory reaction = no blindness.

My recollection is that the people who don't go blind show a large increase in IL-10 at the crucial time. IL-10 inhibits a lot of immune processes. I don't think anyone knows why people show different IL-10 responses though.
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Old 08-28-2012, 10:39 AM   #230
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It's all about immune suppression. A strong inflammatory reaction to the infection = blindness. A suppressed, less inflammatory reaction = no blindness.

My recollection is that the people who don't go blind show a large increase in IL-10 at the crucial time. IL-10 inhibits a lot of immune processes. I don't think anyone knows why people show different IL-10 responses though.
That is interesting. There are parasites that are able to also suppress the immune system but i have no idea if the Inter-leukine 10 mechanism is used.
Most use a mechanism where the parasite is recognized as if it is a normal body tissue. I think by expressing something on the outer shell ?
After some quick look up, i get the impression that IL-10 is a sort of main suppressor switch. Very powerful and versatile it seems.
I think it makes sense that the people who have a lot of IL-10 at the moment of requiring the river blindness disease, already carry some sort of infection from a pathogen. Or acute at the same time or chronic.
It makes sense that a pathogen would produce as much IL-10 as possible or at least is able to influence some process required to produce IL-10 for survival benefits. Is there not some problem with death of b cells or some type of immune cell that produces large amounts of IL-10 as side effect or as deliberate action ?

Perhaps the advantage in the cases of people with massive amounts of IL-10 is an inverse effect. An infection of pathogen X induces large amounts of IL-10 and thus prevents massive inflammatory reactions produced by dying baby nematodes and releasing the wolbachia bacteria.

The big question is, what happens when the wolbachia bacteria can roam around freely when the immune system is suppressed to much ?
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Old 08-28-2012, 11:22 AM   #231
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Originally Posted by William Gaatjes View Post
It makes sense that a pathogen would produce as much IL-10 as possible or at least is able to influence some process required to produce IL-10 for survival benefits. Is there not some problem with death of b cells or some type of immune cell that produces large amounts of IL-10 as side effect or as deliberate action ?
Pathogens don't make IL-10, it's a human gene. EBV encodes BCRF1, which is an IL10 mimic. Maybe to suppress Th1 responses, also maybe just to extend its host cells (B cells) life.

Quote:
The big question is, what happens when the wolbachia bacteria can roam around freely when the immune system is suppressed to much ?
People would die in that case. That's AIDS level suppression, not high levels of IL-10 suppression.
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Old 08-28-2012, 12:37 PM   #232
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Pathogens don't make IL-10, it's a human gene. EBV encodes BCRF1, which is an IL10 mimic. Maybe to suppress Th1 responses, also maybe just to extend its host cells (B cells) life.
You are right. I meant indirectly but wrote it wrong. I was thinking more in the idea of that the pathogen itself does not produce IL-10. But invokes by infection and hijacking cells and the cells biomolecular machinery to produce large amounts of IL-10, purposefully or as side effect.

Quote:
People would die in that case. That's AIDS level suppression, not high levels of IL-10 suppression.
Hm, ach so.
Maybe there is something you know and could tell me about it.
From addiction and ratmodels and i assume research on humans, it is known that in the brain certain receptors are reduced in number when exposed to and activated often with large amount of neurotransmitters or chemicals that can also bind to these receptors.

It is just a wild guess, just an idea. This is not proven or researched for as far as i know, i had to think about it while in public transport.
But assume this scenario :
Because of some acquired pathogen (possible chronic infection without apparent illness or symptoms), the cells are constantly exposed to large amounts of IL-10. Thus the amount of IL-10 receptors on immune system cells would become reduced over time to prevent extreme suppression reactions, the opposite effect of auto immunity.
What would happen is that the immune system becomes to aggressive and is not controlled the right way. Because of the reduced numbers of receptors.
And that is perhaps what we now see as auto immunity. The down regulation of the strength of a given amount of IL-10.

The other cells start to produce more and more IL-10 needed to create the same response. Now that is a paradox. The amount of receptors have been reduced thus more of IL-10 would not have the desired effect. Unless it is specific for certain locations and tissues in the body.

Somewhere there is a control system that monitors the amount of receptors and the correct molecules that bind to it. For some reason, i am sure, that there is the problem of auto immunity. That is, if the immune system also has the ability just as neurons to control the amount of receptors for given cytokines.

What do you think about such a scenario ,Gibsons ?
Has there ever been such research ?
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Old 08-28-2012, 02:49 PM   #233
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You are right. I meant indirectly but wrote it wrong. I was thinking more in the idea of that the pathogen itself does not produce IL-10. But invokes by infection and hijacking cells and the cells biomolecular machinery to produce large amounts of IL-10, purposefully or as side effect.



Hm, ach so.
Maybe there is something you know and could tell me about it.
From addiction and ratmodels and i assume research on humans, it is known that in the brain certain receptors are reduced in number when exposed to and activated often with large amount of neurotransmitters or chemicals that can also bind to these receptors.

It is just a wild guess, just an idea. This is not proven or researched for as far as i know, i had to think about it while in public transport.
But assume this scenario :
Because of some acquired pathogen (possible chronic infection without apparent illness or symptoms), the cells are constantly exposed to large amounts of IL-10. Thus the amount of IL-10 receptors on immune system cells would become reduced over time to prevent extreme suppression reactions, the opposite effect of auto immunity.
What would happen is that the immune system becomes to aggressive and is not controlled the right way. Because of the reduced numbers of receptors.
And that is perhaps what we now see as auto immunity. The down regulation of the strength of a given amount of IL-10.

The other cells start to produce more and more IL-10 needed to create the same response. Now that is a paradox. The amount of receptors have been reduced thus more of IL-10 would not have the desired effect. Unless it is specific for certain locations and tissues in the body.

Somewhere there is a control system that monitors the amount of receptors and the correct molecules that bind to it. For some reason, i am sure, that there is the problem of auto immunity. That is, if the immune system also has the ability just as neurons to control the amount of receptors for given cytokines.

What do you think about such a scenario ,Gibsons ?
Has there ever been such research ?
afaik, few or no immune receptors work like that - the receptor isn't downregulated in response to its ligand. There might be an exceptions.

More likely is that a problem with (a lack of) IL-10 production or IL-10 signalling would lead to autoimmunity. Autoimmunity is still poorly understood, though there's mountainous amounts of data on it. There are genetic and environmental factors in play for many of them.

My prediction is that someone who produced too much IL-10 over a long time would be mostly normal, but very sensitive to viral and some other infections. They might have severe allergies too, but I'm unsure on that.

Gross overgeneralization: Immune signalling often involves positive feedback loops, e.g. cell x activates cell y, which in turn activates cell x to better activate cell y. There's some mechanism(s) in place to put the brakes on this. IL-10 would be one of those brakes.
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Old 09-16-2012, 01:21 PM   #234
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Something about biotin shortage.
I was making a potato recipe , (will post pictures later in a off topic thread).
And was reading about if i had to peel a potato. Because i know that under the peel of the potato amounts of solanin are produced. And solanine is a poison to humans and even deathly in large amounts (more then 100mg).
Thus i did a little background reading and found out that i only have to worry about potatoes with green spots on the peel and when the potato starts to develop. Then the amount of solanine is something to worry about.

But this thread is really about biotin.
In a potato, biotin can also be found. And biotin is very important.
Make sure you have sufficient production of biotin.
If not, you may end up going bald, end up with dermatitis or end up with nervous system issues.

A healthy person has enough biotin. But when the flora and fauna inside the gut is not balanced, in a rare situation biotin deficiency may occur.
Our little friends inside the intestines, the bacteria produce biotin in large quantities. Unless something is going wrong.
Or when you start to consume large amounts of raw eggs. Avidin is a protein that...
Well, read it for yourself if you are interested...
I have to look at my potatoes and i am busy packing.



http://en.wikipedia.org/wiki/Biotin
Quote:
Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids. It plays a role in the citric acid cycle, which is the process by which biochemical energy is generated during aerobic respiration. Biotin not only assists in various metabolic reactions, but also helps to transfer carbon dioxide. It may also be helpful in maintaining a steady blood sugar level.[3] Biotin is often recommended as a dietary supplement for strengthening hair and nails, though scientific data supporting this usage are weak.[4][5] As a consequence, biotin is found in many cosmetics and health products for the hair and skin.[6]

Biotin deficiency is rare because, in general, intestinal bacteria produce biotin in excess of the body's daily requirements.[7] For that reason, statutory agencies in many countries, for example the USA[8] and Australia,[9] do not prescribe a recommended daily intake of biotin. However, a number of metabolic disorders exist in which an individual's metabolism of biotin is abnormal, such as deficiency in the holocarboxylase synthetase enzyme which covalently links biotin onto the carboxylase, where the biotin acts as a cofactor.[10]
http://en.wikipedia.org/wiki/Avidin
Quote:
Avidin is a tetrameric or dimeric[1] biotin-binding protein produced in the oviducts of birds, reptiles and amphibians deposited in the whites of their eggs. In chicken egg white, avidin makes up approximately 0.05% of total protein (approximately 1.8 mg per egg). The tetrameric protein contains four identical subunits (homotetramer), each of which can bind to biotin (Vitamin B7, vitamin H) with a high degree of affinity and specificity. The dissociation constant of avidin is measured to be KD ≈ 10−15 M, making it one of the strongest known non-covalent bonds.[2]

In its tetrameric form, avidin is estimated to be between 66–69 kDa in size.[3] Ten percent of the molecular weight is attributed to carbohydrate content composed of four to five mannose and three N-acetylglucosamine residues.[4] The carbohydrate moieties of avidin contain at least three unique oligosaccharide structural types that are similar in structure and composition.[5]

Functional avidin is found only in raw egg, as the biotin avidity of the protein is destroyed by cooking. The natural function of avidin in eggs is not known, although it has been postulated to be made in the ovaduct as a bacterial growth-inhibitor, by binding biotin the bacteria need. As evidence for this, streptavidin, a loosely related protein with equal biotin affinity and a very similar binding site, is made by certain strains of Streptomyces bacteria, and is thought to serve to inhibit the growth of competing bacteria, in the manner of an antibiotic.[6]

http://en.wikipedia.org/wiki/Solanine
Quote:
Symptoms
Solanine poisoning is primarily displayed by gastrointestinal and neurological disorders. Symptoms include nausea, diarrhea, vomiting, stomach cramps, burning of the throat, cardiac dysrhythmia, headache and dizziness. In more severe cases, hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils, hypothermia and death have been reported.
In large quantities, solanine poisoning can cause death. One study suggests that doses of 2 to 5 mg per kilogram of body weight can cause toxic symptoms, and doses of 3 to 6 mg per kilogram of body weight can be fatal.[2]
Symptoms usually occur 8 to 12 hours after ingestion, but may occur as rapidly as 30 minutes after eating high-solanine foods.
The lowest dose to cause symptoms of nausea is about 25 mg solanine for adults, a life-threatening dose for a regular-weight adult ranges about 400 mg solanine.[citation needed]
[edit]
Mechanism of action
One study suggests that the toxic mechanism of solanine is caused by the chemical's interaction with mitochondrial membranes. Experiments show that solanine exposure opens the potassium channels of mitochondria, decreasing their membrane potential. This in turn leads to Ca2+ being transported from the mitochondria into the cytoplasm, and it is this increased concentration of Ca2+ in the cytoplasm that triggers cell damage and apoptosis.[3]
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Old 09-26-2012, 12:27 PM   #235
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A lot of people suffer from diabetes mellitus type 2. Now researches have found that an unbalance of the bacteria in the intestines might also be a cause or maybe even the cause. Unfortunately, it is not mentioned which bacteria are the cause of such problems. Also, the question arises if these bacteria are naturally present but in a certain amount and that a bad high sugar diet could cause certain bacteria species to expand to much in numbers. Creating the unbalance of life inside the intestines. I do wonder if there also live fungi inside the intestines. I do remember we carry fungi with us, that is normally taken care of by the immune system. But i could be mistaken...

http://medicalxpress.com/news/2012-0...-diabetes.html

Quote:
Studying gut bacteria can reveal a range of human illness. Now, new research shows that the composition of a person's intestinal bacteria could play an important role in the development of type 2 diabetes. These results, from a joint European and Chinese research team, have just been published in the journal Nature.
The number of people suffering from type 2 diabetes world-wide has risen rapidly in recent years, and scientists estimate that just as many people could be suffering from the illness without realising it. New research now indicates that your gut bacteria can reveal whether you suffer from the disease.
"We have demonstrated that people with type 2 diabetes have a high level of pathogens in their intestines," says professor Jun Wang from the University of Copenhagen's Department of Biology and Novo Nordisk Foundation Center for Basic Metabolic Research.
Studying gut bacteria can reveal a range of human illness. Now, new research shows that the composition of a person’s intestinal bacteria could play an important role in the development of type 2 diabetes. A team scientists from the University of Copenhagen and the Beijing Genomics Institute (BGI) are behind the results published in the journal Nature. Credit: University of Copenhagen.

Important intestinal bacteria
The 1.5 kilograms of bacteria that we each carry in our intestines have an enormous impact on our health and well being. The bacteria normally live in a sensitive equilibrium but if this equilibrium is disrupted our health could suffer. In the new study, scientists examined the intestinal bacteria of 345 people from China, of which 171 had type 2 diabetes. The team managed to identify clear biological indicators that someday could be used in methods that provide faster and earlier diagnosis of type 2 diabetes.
The research, which was recently published in the scientific journal Nature, also demonstrated that people with type 2 diabetes have a more hostile bacterial environment in their intestines, which can increase resistance to different medicines.
Similar studies carried out on sufferers of type 2 diabetes in Denmark also discovered a significant imbalance in the function of their intestinal bacteria and composition. Future Danish studies will examine whether intestinal bacteria is already abnormal in people that are deemed to be at risk of developing diabetes.
"We are going to transplant gut bacteria from people that suffer from type 2 diabetes into mice and examine whether the mice then develop diabetes," says another of the lead scientists behind the project, professor Oluf Borbye Pedersen from the University of Copenhagen and centre director at LuCamp, the Lundbeck Foundation Centre for Applied Medical Genomics in Personalised Disease Prediction, Prevention and Care.

International research team investigates gut bacteria
By working together, a team scientists from the University of Copenhagen and the Beijing Genomics Institute (BGI) was able to make to several breakthroughs in the field of 'metagenomics'.
Scientists working on the EU research project MetaHIT have uncovered more than 3.3 million genes from gut bacteria found in people from Spain and Denmark. These genes could play a key role in understanding and treating a range of serious illnesses. According to Professor Karsten Kristiansen from the University of Copenhagen's Department of Biology, the recent discovery is an important step in the comprehensive international research that is currently underway to investigate the interplay between intestinal bacteria and health.
"The European and Chinese working on the MetaHIT project were able to make important new discoveries about the relationship between intestinal bacteria and health. The new discovery indicates a possible connection between type 2 diabetes and the intestinal bacteria in Chinese people," Kristiansen says.
"It is important to point out that our discovery demonstrates a correlation. The big question now is whether the changes in gut bacteria can affect the development of type 2 diabetes or whether the changes simply reflect that the person is suffering from type 2 diabetes."
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Old 10-01-2012, 01:23 AM   #236
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More news from the research front of epigenetics :


http://phys.org/news/2012-09-scienti...etic-code.html



Mouse embryonic stem cells (blue, green) lose DNA methylation (red) in the absence of UHRF1. Credit: Strahl Lab, UNC School of Medicine


Quote:
Over the last two decades, scientists have come to understand that the genetic code held within DNA represents only part of the blueprint of life. The rest comes from specific patterns of chemical tags that overlay the DNA structure, determining how tightly the DNA is packaged and how accessible certain genes are to be switched on or off.

As researchers have uncovered more and more of these "epigenetic" tags, they have begun to wonder how they are all connected. Now, research from the University of North Carolina School of Medicine has established the first link between the two most fundamental epigenetic tags—histone modification and DNA methylation—in humans.
The study, which was published Sept. 30, 2012 by the journal Nature Structural & Molecular Biology, implicates a protein called UHRF1 in the maintenance of these epigenetic tags. Because the protein has been found to be defective in cancer, the finding could help scientists understand not only how microscopic chemical changes can ultimately affect the epigenetic landscape but also give clues to the underlying causes of disease and cancer.
"There's always been the suspicion that regions marked by DNA methylation might be connected to other epigenetic tags like histone modifications, and that has even been shown to be true in model organisms like fungus and plants," said senior study author Brian Strahl, PhD, associate professor of biochemistry and biophysics in the UNC School of Medicine and a member of UNC Lineberger Comprehensive Cancer Center. "But no one has been able to make that leap in human cells. It's been controversial in terms of whether or not there's really a connection. We have shown there is."
Strahl, along with his postdoctoral fellow Scott Rothbart, honed in on this discovery by using a highly sophisticated technique developed in his lab known as next generation peptide arrays. First the Strahl lab generated specific types of histone modifications and dotted them on tiny glass slides called "arrays." They then used these "arrays" to see how histone modifications affected the docking of different proteins. One protein – UHRF1 – stood out because it bound a specific histone modification (lysine 9 methylation on histone H3) in cases where others could not.
Strahl and his colleagues focused the rest of their experiments on understanding the role of UHRF1 binding to this histone modification. They found that while other proteins that dock on this epigenetic tag are ejected during a specific phase of the cell cycle, mitosis, UHRF1 sticks around. Importantly, the protein's association with histones throughout the cell cycle appears to be critical to maintaining another epigenetic tag called DNA methylation. The result was surprising because researchers had previously believed that the maintenance of DNA methylation occurred exclusively during a single step of the cell cycle called DNA replication.
"This role of UHRF1 outside of DNA replication is certainly unexpected, but I think it is just another way of making sure we don't lose information about our epigenetic landscape," said Strahl.

Journal reference: Nature Structural & Molecular Biology

Provided by University of North Carolina Health Care
It becomes more and more clear, that there are some serious implications that ultimately will ask society to make some changes to ensure health. But the less sick people are, the higher the efficiency. Just a simple headache can make the difference in having a "eureka" moment and finding a novel solution to a problem when needed or working days at an end with overtime trying to solve a problem that seems just so hard because of concentration problems...
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Old 12-23-2012, 03:53 AM   #237
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Yay. I am slowly starting to adapt to my new surroundings.
Thus, slowly i am posting into this forum again.

The article is an interesting find, it is from march this year but i forgot to post it. Has anybody read about the research conducted after to confirm the results from this research ?

http://medicalxpress.com/news/2012-0...er-tumour.html

Quote:
March 8, 2012 (Medical Xpress)
Cancer genes differ in different parts of a tumor in Cancer. Taking a sample from just one part of a tumour may not give a full picture of its ‘genetic landscape’, according to a study published in the New England Journal of Medicine.

The findings could help explain why attempts at using single biopsies to identify biomarkers to which personalised cancer treatments can be targeted have not been more successful. The researchers carried out the first ever genome-wide analysis of the genetic variation between different regions of the same tumour using kidney cancer samples. They found that the majority, around two thirds of gene faults (63-69%), were not found in other biopsies from the same tumour. Lead author Professor Charles Swanton of the UCL Cancer Institute and Cancer Research UK’s London Research Institute, said: “We’ve known for some time that tumours are a ‘patchwork’ of faults, but this is the first time we’ve been able to use cutting-edge genome sequencing technology to map out the genetic landscape of a tumour in such exquisite detail. “This has revealed an extraordinary amount of diversity, with more differences between biopsies from the same tumour at the genetic level than there are similarities. The next step will be to develop drugs that limit this diversity by targeting key driver mutations that are common throughout all parts of the tumour.” The tumour samples analysed in this study were donated by patients treated at the Royal Marsden Hospital under the supervision of Dr James Larkin. Dr Larkin said: “The idea of personalised medicine is to tailor treatments to suit individual patients. This study in kidney cancer has shown significant molecular changes between different parts of the same tumour. We have also seen differences between primary kidney tumours and cancer cells that have spread to other organs. This may be relevant to how we treat kidney cancer with drugs because the molecular changes that drive the growth of the cancer once it has spread may be different from those that drive the growth of the primary tumour.” The researchers – funded by Cancer Research UK, the Medical Research Council and the Wellcome Trust – compared the genetic faults in samples taken from different parts of four separate kidney tumours, and also from sites where the cancer had spread to other organs. This allowed them to identify 118 different mutations – 40 of which were ‘ubiquitous mutations’ found in all biopsies, 53 ‘shared mutations’ that were present in most but not all biopsies and 25 ‘private mutations’ that were only detected in a single biopsy. By analysing the location of shared mutations in relation to the whole tumour, the researchers were able to trace the origins of particular subtypes of cancer cells back to key driver mutations. This allowed the scientists to create a ‘map’ of how the pattern of faults within the tumour might have evolved over time. Professor Swanton added: “For the first time we’ve been able to use the pattern of genetic faults in a tumour to trace the origins of certain populations of cancers cells, much in the same way as Darwin used his ‘tree of life’ theory to show how different species are related. “This underscores the importance of targeting common mutations found in the ‘trunk’ of the tree as opposed to those found in the ‘branches’, which may only be present in a relatively small number of cells. It may also explain why surgery to remove the primary kidney tumour can improve survival, by decreasing the likelihood that resistant cells will be present that could go on to re-grow the tumour after treatment.” Dr Lesley Walker, Cancer Research UK’s director of cancer information, said: “These findings highlight important differences that exist within tumours and suggest a way to improve the success rate of personalised cancer medicines. Crucially, they emphasise the need to build capacity within the NHS for in-depth genetic analysis of tumours to allow researchers to identify the markers that best predict who will benefit from targeted treatments. “We are now planning to see if these results can be replicated in larger groups of patients as part of Cancer Research UK’s Genomics Initiative - a set of groundbreaking projects using the latest high-tech gene sequencing machines to track down the genetic faults driving different types of cancer.” Journal reference: New England Journal of Medicine Provided by University College London
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Old 12-23-2012, 11:01 AM   #238
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That's actually really interesting, because in med school we were always taught that all the cells in a particular cancer were clones of each other. That obviously had implications in terms of treatment: as the article points out, we assumed that a single biopsy would be representative of all the cells in the tumour, and therefore that a treatment for one cell would be effective in general against all cells in the tumour.
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Old 12-31-2012, 02:52 AM   #239
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Quote:
Originally Posted by Mr. Pedantic View Post
That's actually really interesting, because in med school we were always taught that all the cells in a particular cancer were clones of each other. That obviously had implications in terms of treatment: as the article points out, we assumed that a single biopsy would be representative of all the cells in the tumour, and therefore that a treatment for one cell would be effective in general against all cells in the tumour.
It sure is interesting. With hindsight, it makes sense that the cells comprising a tumor (with mutated dna for whatever reason) keep mutating, since the whole regulating mechanism to correct the dna and apoptosis (programmed cell death) no longer functions. But i am happy that this kind of research keeps continuing. Also, read the next post. It is most interesting.
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Old 12-31-2012, 03:02 AM   #240
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When it comes to becoming fat, there might be another reason to watch the diet. It seems that we have bacteria in our intestines that help us absorb fats. Firmicutes is the bacteria family.
http://en.wikipedia.org/wiki/Firmicutes

This article is about zebrafish, but humans also carry Firmicutes in the intestines. Of course it is a large family and it says nothing about specific bacteria families.
It is an interesting idea, that consuming a lot of fat, will also increase the amount of bacteria that help consume fat more easy. This will lead to an increased absorption of fats. This might very well be a part of the puzzle why some people gain weight quickly to a higher fat percentage, while others seem to be unaffected. A sort of avalanching effect. Might be an epigenetic effect here as well. Might also explain why some people seem so muscled but cannot stand the cold while others seem to increase weight quickly because of increasing fat storage. Might be an evolutionary / epigenetic effect against a cold environment.
The only problems is there are many different kinds of fat.

Well, read for yourself...
http://medicalxpress.com/news/2012-0...bsorption.html

Quote:
Gut bacteria increase fat absorption September 12, 2012 in Medical research Enlarge This confocal microscopy of intestinal epithelial cells (red) in zebrafish shows that the presence of microbes stimulates dietary fatty acid uptake and accumulation in epithelial lipid droplets (green).



Credit: Ivana Semova, Ph.D.

You may think you have dinner all to yourself, but you're actually sharing it with a vast community of microbes waiting within your digestive tract. A new study from a team including Carnegie's Steve Farber and Juliana Carten reveals that some gut microbes increase the absorption of dietary fats, allowing the host organism to extract more calories from the same amount of food. Previous studies showed gut microbes aid in the breakdown of complex carbohydrates, but their role in dietary fat metabolism remained a mystery, until now. The research is published September 13 by Cell Host & Microbe. "This study is the first to demonstrate that microbes can promote the absorption of dietary fats in the intestine and their subsequent metabolism in the body," said senior study author John Rawls of the University of North Carolina. "The results underscore the complex relationship between microbes, diet and host physiology." The study was carried out in zebrafish, which are optically transparent when young. By feeding the fish fatty acids tagged with fluorescent dyes, an approach originally developed in Farber's lab, the researchers were able to directly observe the absorption and transport of fats in live animals. The Rawl's lab pioneered methods to grow zebrafish larvae in the presence or absence of gut microbes. By combining approaches, they determined that one type of bacteria, called Firmicutes, is instrumental in increasing fat absorption. They also found that the abundance of Firmicutes in the gut was influenced by diet. Fish fed normally had more Firmicutes than fish that were denied food for several days. Other studies have linked a higher relative abundance of Firmicutes in the gut with obesity in humans. The findings indicate that bacteria in the gut can increase the host's ability to absorb fat and thereby harvest more calories from the diet. Another implication is that a high-fat diet promotes the growth of these fat-loving Firmicutes, resulting in more fat absorption. Although the study involved only fish, not humans, it offers insights that could help inform new approaches to treating obesity and other disorders. "The unique properties of zebrafish larvae are helping us develop a better understanding of how the intestine functions with the goal of contributing to ongoing efforts to reduce the impact of diseases associated with altered lipid metabolism, such as diabetes, obesity, and cardiovascular disease. Our collaboration with the Rawls lab is now focused on how specific gut bacteria are able to stimulate absorption of dietary fat. We hope to use that information to develop new ways to reduce fat absorption in the context of human diseases," Farber said. The research team also included lead author Ivana Semova and co-author Lantz Mackey, both of UNC, as well as co-authors Jesse Stombaugh and Rob Knight of the University of Colorado at Boulder.
Journal reference: Cell Host & Microbe
Provided by Carnegie Institution for Science
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Old 01-12-2013, 04:19 AM   #241
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This is interesting research. Is there also not a possibility that MS is a pathogen derived disease ? The Epstein-Barr virus ? There has been research going on linking the EBV virus to MS. Could this also not be a very complex effect where the cause is molecular mimicry ?

http://en.wikipedia.org/wiki/Molecular_mimicry

http://medicalxpress.com/news/2013-0...ler-cells.html







Quote:
Multiple sclerosis study reveals how killer T cells learn to recognize nerve fiber insulators

(Medical Xpress)—Misguided killer T cells may be the missing link in sustained tissue damage in the brains and spines of people with multiple sclerosis, findings from the University of Washington reveal. Cytoxic T cells, also known as CD8+ T cells, are white blood cells that normally are in the body's arsenal to fight disease.

Multiple sclerosis is characterized by inflamed lesions that damage the insulation surrounding nerve fibers and destroy the axons, electrical impulse conductors that look like long, branching projections. Affected nerves fail to transmit signals effectively. Intriguingly, the UW study, published this week in Nature Immunology, also raises the possibility that misdirected killer T cells might at other times act protectively and not add to lesion formation. Instead they might retaliate against the cells that tried to make them mistake the wrappings around nerve endings as dangerous. Scientists Qingyong Ji and Luca Castelli performed the research with Joan Goverman, UW professor and chair of immunology. Goverman is noted for her work on the cells involved in autoimmune disorders of the central nervous system and on laboratory models of multiple sclerosis. Multiple sclerosis generally first appears between ages 20 to 40. It is believed to stem from corruption of the body's normal defense against pathogens, so that it now attacks itself.
For reasons not yet known, the immune system, which wards off cancer and infection, is provoked to vandalize the myelin sheath around nerve cells. The myelin sheath resembles the coating on an electrical wire. When it frays, nerve impulses are impaired. TIP dendritic cells, stained to show their physical features.Depending on which nerves are harmed, vision problems, an inability to walk, or other debilitating symptoms may arise. Sometimes the lesions heal partially or temporarily, leading to a see-saw of remissions and flare ups. In other cases, nerve damage is unrelenting. The myelin sheaths on nerve cell projections are fashioned by support cells called oligodendrocytes.
Newborn's brains contain just a few sections with myelinated nerve cells. An adult's brains cells are not fully myelinated until age 25 to 30. For T cells to recognize proteins from a pathogen, a myelin sheath or any source, other cells must break the desired proteins into small pieces, called peptides, and then present the peptides in a specific molecular package to the T cells. Scientists had previously determined which cells present pieces of a myelin protein to a type of T cell involved in the pathology of multiple sclerosis called a CD4+ T cell. Before the current study, no cells had yet been found that present myelin protein to CD8+ T cells. Scientists strongly suspect that CD8+ T cells, whose job is to kill other cells, play an important role in the myelin-damage of multiple sclerosis. In experimental autoimmune encephalitis, which is an animal model of multiple sclerosis in humans, CD4+T cells have a significant part in the inflammatory response. However, scientists observed that, in acute and chronic multiple sclerosis lesions, CD8+T cells actually outnumber CD4+ T cells and their numbers correlate with the extent of damage to nerve cell projections. Other studies suggest the opposite: that CD8+T cells may tone down the myelin attack.
The differing observations pointed to a conflicting role for CD8 + T cells in exacerbating or ameliorating episodes of multiple sclerosis. Still, how CD8+T cells actually contributed to regulating the autoimmune response in the central nervous system, for better or worse, was poorly understood. Goverman and her team showed for the first time that naive CD8+ T cells were activated and turned into myelin-recognizing cells by special cells called Tip-dendritic cells. These cells are derived from a type of inflammatory white blood cell that accumulates in the brain and the spinal cord during experimental autoimmune encephalitis originally mediated by CD4+ T cells. The membrane folds and protrusions of mature dendritic cells often look like branched tentacles or cupped petals well-suited to probing the surroundings. The researchers proposed that the Tip dendritic cells can not only engulf myelin debris or dead oligodendrocytes and then present myelin peptides to CD4 + T cells, they also have the unusual ability to load a myelin peptide onto a specific type of molecule that also presents it to CD8+ T cells. In this way, the Tip dendritic cells can spread the immune response from CD4+ T cells to CD8+ T cells. This presentation enables CD8+ T cells to recognize myelin protein segments from oligodendrocytes, the cells that form the myelin sheath.
The phenomenon establishes a second-wave of autoimmune reactivity in which the CD8+ T cells respond to the presence of oligodendrocytes by splitting them open and spilling their contents. "Our findings are consistent," the researchers said, "with the critical role of dendritic cells in promoting inflammation in autoimmune diseases of the central nervous system." They mentioned that mature dendritic cells might possibly wait in the blood vessels of normal brain tissue to activate T-cells that have infiltrated the blood/brain barrier. The oligodendrocytes, under the inflammatory situation of experimental autoimmune encephalitis, also present peptides that elicit an immune response from CD8+T cells. Under healthy conditions, oligodendrocytes wouldn't do this. The researchers proposed that myelin-specific CD8+T cells might play a role in the ongoing destruction of nerve-cell endings in "slow burning" multiple sclerosis lesions. A drop in inflammation accompanied by an increased degeneration of axons (electrical impulse-conducting structures) coincides with multiple sclerosis leaving the relapsing-remitting stage of disease and entering a more progressive state. Medical scientists are studying the roles of a variety of immune cells in multiple sclerosis in the hopes of discovering pathways that could be therapeutic targets to prevent or control the disease, or to find ways to harness the body's own protective mechanisms. This could lead to highly specific treatments that might avoid the unpleasant or dangerous side effects of generalized immunosuppressants like corticosteroids or methotrexate.


http://en.wikipedia.org/wiki/Epstein–Barr_virus


P.S.
There is also research suggesting a link between oligodendrocytes and EBV infection.
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Old 01-14-2013, 08:04 AM   #242
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With respect to the link of obesity and pathogens in post240...

The adenovirus AD36 seems to be able to increase the amount of bodyfat. Antibodies against the virus has been found in obese individuals.
However, this is not solid evidence of course. The host must still consume more calories than needed. Or can the virus cause an effect where already present body tissues are converted to fat ? Interesting ?

http://en.wikipedia.org/wiki/Infectobesity

http://en.wikipedia.org/wiki/AD-36
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Old 01-17-2013, 02:18 PM   #243
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Bacteria are amazing. Using laws of nature to their advantage.

This particular bacterial family has the ability to form magnetite and are called magnetotactic bacteria.
And use these magnetite crystals to find their way through their surroundings by use of the Earth magnetic field.


On the left side of the bacteria, you can see the magnetic particles.

http://en.wikipedia.org/wiki/Magnetotactic_bacteria

Quote:
Magnetotactic bacteria (or MTB) are a polyphyletic group of bacteria discovered by Richard P. Blakemore in 1975, that orient along the magnetic field lines of Earth's magnetic field. To perform this task, these bacteria have organelles called magnetosomes that contain magnetic crystals. The biological phenomenon of microorganisms tending to move in response to the environment's magnetic characteristics is known as magnetotaxis (although this term is misleading in that every other application of the term taxis involves a stimulus-response mechanism). In contrast to the magnetoception of animals, the bacteria contain fixed magnets that force the bacteria into alignment — even dead cells align, just like a compass needle.[1] The alignment is believed to aid these organisms in reaching regions of optimal oxygen concentration.
http://phys.org/news/2012-11-video-a...-bacteria.html

Quote:
Magnetotactic bacteria, like Magnetospirillum magneticum, have evolved cellular processes that allow them to take up iron molecules to produce magnetic nanocrystals like magnetite. Since they were first discovered and isolated in 1975 by Robert Blakemore, scientists continue to be fascinated by these unique bacteria, whether as a means to isolate biogenic magnetite or to understand the evolutionary advantages of producing these minerals. A new video-article in JoVE (Journal of Visualized Experiments) details a procedure to purify and enrich samples of magnetotactic bacteria from aquatic environments, developed in the laboratory of Dr. Brian Lower at The Ohio State University.

Magnetotactic bacteria are microorganisms, typically found in stratified water columns or aquatic sediments all over the world. Though many of these bacteria tend to thrive in environments with low levels of oxygen, the defining characteristic they share are small, magnetic, membrane bound nanocrystals of either the iron oxide magnetite or the iron sulfide greigite.

"These nanocrystals allow the organisms to align themselves with the earth's magnetic field and swim up or down based on the geomagnetic field to find their microenvironments," Dr. Lower explains. "These bacteria are fairly ubiquitous. They can be found all over the world, and interestingly they can be found in sediment samples from millions of years ago." These bacteria are a valuable anomaly to the scientific community. Their fossil record gives geologists accurate representations of the Earth's past magnetic field, when combined with carbon dating, and could potentially provide other clues about earth's geological history. The magnetotactic minerals may also have medical or other novel applications. "You can coat these minerals with antibodies and target specific cancer cell lines or heat the magnets with an alternating magnetic field to kill a cancer cell line," says Dr. Lower. "We decided to publish in JoVE because it will allow a wide variety of scientists to see how easy it is to isolate and enrich these species. We hope the video-protocol will spur other collaborations or new research," Dr. Lower said. The article will be published on November 15, 2012 in JoVE's General section. JoVE acquisition editor Rachelle Baker stated, "We are very excited for this article not only because it is our first featuring magnetotactic bacteria but we believe it will lay a foundation for other groups to build expand upon this work and share their methods with the community, which is the founding principle of JoVE." More information: Lower et. al. http://www.JoVE.com/video/50123/coll...-magnetotactic
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Old 01-17-2013, 03:00 PM   #244
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For those interested, humans also seem to have a tiny amount of magnetite in the Ethmoid bone. a bone structure between the eyes and behind the nose.
http://en.wikipedia.org/wiki/Ethmoid_bone






http://www.theregister.co.uk/2006/11..._nose_compass/
Quote:
Some years ago scientists at CALTECH (California Institute of Technology in Pasadena) discovered that humans possess a tiny, shiny crystal of magnetite in the ethmoid bone, located between your eyes, just behind the nose.
Magnetite is a magnetic mineral also possessed by homing pigeons, migratory salmon, dolphins, honeybees, and bats. Indeed, some bacteria even contain strands of magnetite that function, according to Dr Charles Walcott of the Cornell Laboratory of Ornithology in Ithaca, New York, "as tiny compass needles, allowing them [the bacteria] to orient themselves in the earth's magnetic field and swim down to their happy home in the mud".
It seems that magnetite helps direction finding in animals and helps migratory species migrate successfully by allowing them to draw upon the earth's magnetic fields. But scientists are not sure how they do this.
In any case, when it comes to humans, according to some experts, magnetite makes the ethmoid bone sensitive to the earth's magnetic field and helps your sense of direction.
Some, such as Dr Dennis J Walmsley and W Epps from the Department of Human Geography of the Australian National University in Canberra writing in Perceptual and Motor Skills as far back as in 1987, have even suggested that this "compass" was helpful in human evolution as it made migration and hunting easier.
Following this fascinating factoid, science journalist Marc McCutcheon entitled a book The Compass in Your Nose and Other Astonishing Facts.
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Old 01-29-2013, 09:51 AM   #245
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Default "electron eating" bacteria

Scientists have developed an amazing way to trick iron oxidizing bacteria to consume electrons (and CO2) to replicate.
But what is really interesting, is the ability to harvest the electrons from the electrode. I do wonder if the material, the electrode itself is made of, also plays a part in the whole process.


http://phys.org/news/2013-01-scienti...electrons.html

Quote:
January 29, 2013

Scientists have developed a way to grow iron-oxidizing bacteria using electricity instead of iron, an advance that will allow them to better study the organisms and could one day be used to turn electricity into fuel. The study will be published on January 29 in mBio, the online open-access journal of the American Society for Microbiology.

The method, called electrochemical cultivation, supplies these bacteria with a steady supply of electrons that the bacteria use to respire, or "breathe". It opens the possibility that one day electricity generated from renewable sources like wind or solar could be funneled to iron oxidizing bacteria that combine it with carbon dioxide to create biofuels, capturing the energy as a useful, storable substance.
"It's a new way to cultivate a microorganism that's been very difficult to study. But the fact that these organisms can synthesize everything they need using only electricity makes us very interested in their abilities," says Daniel Bond of the BioTechnology Institute at the University of Minnesota – Twin Cities, who co-authored the paper with Zarath Summers and Jeffrey Gralnick.
To "breathe", iron oxidizers take electrons off of dissolved iron, called Fe(II) – a process that produces copious amounts of rust, called Fe(III). Iron-oxidizing bacteria are found around the world, almost anywhere an aerobic environment (with plenty of oxygen) meets an anaerobic environment (which lacks oxygen). They play a big role in the global cycling of iron and contribute to the corrosion of steel pipelines, bridges, piers, and ships, but their lifestyle at the interface of two very different habitats and the accumulation of cell-trapping Fe(III) makes iron oxidizers difficult to grow and study in the lab.
Scientists think these bacteria must carry out the iron oxidation step on their surfaces. If that's true, Bond reasoned, the outsides of the organisms should be covered with proteins that interact with Fe(II), so you should be able to provide a stream of pure electrons to the outsides of the bacteria and get them to grow.
Bond and his colleagues added the marine iron oxidizer Mariprofundus ferrooxydans PV-1, along with some nutrient medium, to an electrode carefully tuned to provide electrons at the same energy level, or potential, as Fe(II) would provide. The idea, says Bond, was to "fool the bacteria into thinking they're at the world's best buffet of Fe(II) atoms."
It worked. The bacteria multiplied and formed a film on the electrode, Bond says, and eventually they were able to grow M. ferrooxydans with no iron in the medium, proof that the bacteria were living off the electrons they absorbed from the electrode to capture carbon dioxide and replicate. And since the electron donor is a solid surface, say the authors, it's pretty likely that the bacterial electron-harvesting machinery is exposed on the outer membrane of the cell.
It's this capture of carbon dioxide that could enable electrochemical cultivation to create biofuels or other useful products one day, Bond says.
"Bacteria are experts at the capture of carbon dioxide. They build cells and compounds" with the carbon, he says. They might one day be exploited as microscopic energy packagers: bacteria like M. ferrooxydans could capture electricity from an electrode, combine it with carbon dioxide, and package it as a carbon-rich compound we could use as fuel. This would take the energy in electricity, which is ephemeral, and convert it into a tangible product that could be stored in a tank. But that kind of work is a long way off, cautions Bond.
"If there are 100 steps to making this work – this is step one," he says.
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Old 01-29-2013, 10:53 AM   #246
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Speaking of, I thought you might be interested in this.
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Old 01-30-2013, 01:57 PM   #247
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Quote:
Originally Posted by Mr. Pedantic View Post
Speaking of, I thought you might be interested in this.
Ah thank you. I will read it with a lot of interest. Unfortunately, the link to the video in the first post is no longer working but the documentary is available on youtube.

More revealing news how viruses can play a role in developing cancer.
And how a virus might play a role in developing fetuses and epilepsy during childhood.

http://medicalxpress.com/news/2013-0...potential.html

Quote:
Scientists find cancer-causing virus in the brain, potential connection to epilepsy January 24, 2013 in Neuroscience Researchers at Shriner's Hospital Pediatric Research Center at the Temple University School of Medicine, and the University of Pennsylvania have evidence linking the human papillomavirus 16 (HPV16) – the most common cause of cervical cancer – to a common form of childhood epilepsy. They have shown for the first time that HPV16 may be present in the human brain, and found that when they added a viral protein to the brains of fetal mice, the mice all demonstrated the same developmental problems in the cerebral cortex associated with this type of epilepsy, called focal cortical dysplasia type IIB (FCDIIB). The findings suggest that the virus could play a role in the development of epilepsy.

The results also mean that doctors may have to re-think their approach to treating this type of epilepsy, and perhaps consider other therapeutic options related to HPV, an infectious disease. "This is a novel mechanism, and it fills a gap in our understanding about the development of congenital brain malformations," said Peter Crino, MD, PhD, Professor of Neurology at Temple University School of Medicine, and a member of Shriner's Hospital Pediatric Research Center, and the senior author of a recent report in the Annals of Neurology. "If our data are correct, future treatment of cortical dysplasia could include targeted therapy against HPV16 infection, with the goal of halting seizures. Identifying an infectious agent as part of the pathogenesis of brain malformations could open up an array of new therapeutic approaches against various forms of epilepsy." FCDIIB is a developmental malformation in the cerebral cortex, the area of the brain that plays key roles in thought, perception and memory. It is a common cause of both pediatric and adult epilepsy – especially difficult-to-treat forms of epilepsy – and it is thought to occur in the womb during early brain development. The condition is characterized by a disorganized cellular structure and enlarged, "balloon cells." Current treatments include surgery and medication. Balloon cells contain a signaling cascade called the mammalian target of rapamycin complex 1 (mTOR1), which is important for cellular growth, proliferation and division, particularly in brain development. Other scientists have recently found the mTOR pathway is activated by the HPV16 E6 oncoprotein. While there had never been any studies indicating that HPV16 could infect the brain, Dr. Crino saw a potential connection. "This is a sporadic, congenital brain malformation associated with mTOR signaling with no genetic predisposition," he said. "Based on various cellular and cell signaling similarities between cervical dysplasia and focal cortical dysplasia, this led me to a hypothesis that the HPV protein could be detected in FCDIIB." To find out, the investigators first examined FCDIIB tissue samples from 50 patients for evidence of the HPV16 E6 protein. They found that all of the samples were positive for the protein in the balloon cells, but not in regions without balloon cells or in 36 control samples from healthy individuals. They next examined the samples' genetic material by several sophisticated molecular techniques to look for evidence of HPV16 E6, and compared the findings to tissue from healthy controls and tissue from patients with different types of brain malformations and epilepsy. Again, every sample of FCDIIB was found to contain HPV16 E6 protein, whereas the control specimens and tissue from other types of dysplasia and conditions did not. Finally, in a series of experiments, the scientists painstakingly delivered the E6 protein into the brains of fetal mice. "If E6 is the causative element for HPV cervical dysplasia and focal cortical dysplasia, putting the protein into a fetal mouse brain should disrupt the cortical development," Dr. Crino explained. When the scientists did this, they found that the fetal mouse brains did indeed develop brain malformations. Dr. Crino plans to investigate other forms of cortical dysplasia to see if HPV or related viral proteins can be found. He and his team aren't sure how the virus gets into the brain, but their results suggest that an HPV infection in the placenta could be one possible path. The exact mechanism by which HPV16 might cause a malformation and epilepsy remains to be determined. He acknowledged several potential implications from the findings. "We are going to have to think about this epidemiologically as an infectious disease, not a genetic disorder. In terms of prevention, with current HPV vaccination, we have a potentially modifiable disease," he said. "In addition, if in fact this type of epilepsy represents a disorder of mTOR signaling, then one strategy could be, rather than treating the patients with anti-epileptic drugs, is to perhaps use mTOR inhibitors. "The million dollar result would be to show it is possible to induce a brain malformation with an E6 infection, and the animal develops epilepsy," Dr. Crino said. "It would be even better if we showed that it is preventable."
A TED talk about bacteriophages and applied aspects.
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Old 01-30-2013, 02:01 PM   #248
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More news about epigenetics and how it affects onset puberty in females.
It becomes more and more clear how the environment can alter the development of humans by influencing the activity of genes that are "executed" in parallel. Thereby having significant effects "under the hood" .


http://medicalxpress.com/news/2013-0...y-females.html

Quote:
New research from Oregon Health & Science University has provided significant insight into the reasons why early-onset puberty occurs in females. The research, which was conducted at OHSU's Oregon National Primate Research Center, is published in the current early online edition of the journal Nature Neuroscience.

The paper explains how OHSU scientists are investigating the role of epigenetics in the control of puberty. Epigenetics refers to changes in gene activity linked to external factors that do not involve changes to the genetic code itself. The OHSU scientists believe improved understanding of these complex protein/gene interactions will lead to greater understanding of both early-onset (precocious) puberty and delayed puberty, and highlight new therapy avenues. To conduct this research, scientists studied female rats, which like their human counterparts, go through puberty as part of their early aging process. These studies revealed that a group of proteins, called PcG proteins, regulate the activity of a gene called the Kiss1 gene, which is required for puberty to occur. When these PcG proteins diminish, Kiss1 is activated and puberty begins. PcG proteins are produced by another set of genes that act as a biological switch during the embryonic stage of life. The role of these proteins is to turn off specific downstream genes at key developmental stages. OHSU scientists found that both the activity of these "master" genes and their ability to turn off puberty are impacted by two forms of epigenetic control: a chemical modification of DNA known as DNA methylation, and changes in the composition of histones, a specialized set of proteins that modify gene activity by interacting with DNA. Using this new information, researchers were then able to delay puberty in female rats. They accomplished this by increasing PcG protein levels in the hypothalamus of the brain using a targeted gene therapy approach so that Kiss1 activation failed to occur at the normal time in life. The hypothalamus is a region of the brain that controls reproductive development. "While it was always understood that an organism's genes determine the timing of puberty, the role of epigenetics in this process has never been recorded until now," said Alejandro Lomniczi, Ph.D., a scientist in the Division of Neuroscience at the OHSU Oregon National Primate Research Center. "Because epigenetic changes are driven by environmental, metabolic and cell-to-cell influences, these findings raise the possibility that a significant percentage of precocious and delayed puberty cases occurring in humans may be the result of environmental factors and other alterations in epigenetic control," said Sergio Ojeda, D.V.M, who is also a scientist in the Division of Neuroscience at the OHSU ONPRC. "There is also much more to be learned about the way that epigenetic factors may link environmental factors such as nutrition, man-made chemicals, social interactions and other day-today influences to the timing and completion of normal puberty."



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Old 01-30-2013, 03:17 PM   #249
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More news about plasmids and a very special enzyme named : "Nicking enzyme or NES". In this article, it is described how the researchers have discovered how one of the most antibiotic resistant bacteria performs it's magic...


What is a nicking enzyme ?
http://en.wikipedia.org/wiki/Nicking_enzyme
Quote:
A nicking enzyme (or nicking endonuclease) is an enzyme that cuts one strand of a double-stranded DNA at a specific recognition nucleotide sequences known as a restriction site. Such enzymes hydrolyse (cut) only one strand of the DNA duplex, to produce DNA molecules that are “nicked”, rather than cleaved.
http://phys.org/news/2013-01-scienti...-superbug.html

Quote:
(Phys.org)—Worldwide, many strains of the bacterium Staphyloccocus aureus, commonly known as staph infections, are already resistant to all antibiotics except vancomycin. But as bacteria are becoming resistant to this once powerful antidote, S. aureus has moved one step closer to becoming an unstoppable killer. Now, researchers at the University of North Carolina at Chapel Hill have not only identified the mechanism by which vancomycin resistance spreads from one bacterium to the next, but also have suggested ways to potentially stop the transfer.

The work, led by Matthew Redinbo, professor of chemistry at UNC's College of Arts and Sciences, addresses the looming threat of incurable staph infections – a global public health problem that has mobilized scientists across disciplines to work together to identify the Achilles heel of these antibiotic-resistant bacteria. "We used to live in a world where antibiotics could readily cure bacterial disease," said Redinbo. "But this is clearly no longer the case. We need to understand how bacteria obtain resistance to drugs like vancomycin, which served for decades as the 'antibiotic of last resort.'" In his work, Redinbo and his team targeted a bacterial enzyme known as Nicking Enzyme in Staphyloccoccus, or NES. The enzyme has long been known to interact with plasmids, circular pieces of double-stranded DNA within bacteria that are physically separate from the bacterial chromosome. Plasmids commonly contain antibiotic-resistance genes, and can make the machinery necessary to transfer these genes from an infected bacterium to an uninfected one. By revealing the crystal structure of NES, the researchers found that this enzyme nicks one strand of the plasmid at a very specific site—and in a very specific way. It turns out that NES forms two loops that work together to pinch one strand of the plasmid at a particular groove in the DNA to cut it. This strand is now free to leave its host and transfer to a nearby bacterium, making them resistant to vancomycin. Moreover, Redinbo was able to capture a snapshot of the enzyme bound to the plasmid. "As a structural biologist, it's all about the pictures for me," said Redinbo. "And it was this picture that confirmed the precise location on which NES works." With this information, Redinbo knew the groove on the DNA that the enzyme recognize and could design a small synthetic molecule that would sit on this groove and block NES. Teaming up with colleagues at the California Institute of Technology, Redinbo did just that. The molecule prevented NES from nicking the DNA, which could prevent the resistance genes from spreading. According to Redinbo and colleagues, this small synthetic molecule could help guide future research aimed at developing effective therapies for strains of antibiotic-resistant S. aureus. "This is really exciting for us," said Redinbo, who is also a professor at UNC's School of Medicine and a member of the Lineberger Comprehensive Cancer Center. "It opens the door for potentially stopping the spread of antibiotic resistance—and that's exactly what we need in this post-antibiotic era." The work was published this week in the online early edition of the Proceedings of the National Academy of Sciences.

More information: Molecular basis of antibiotic multiresistance transfer in Staphylococcus aureus, http://www.pnas.org/content/early/20....full.pdf+html

Journal reference: Proceedings of the National Academy of Sciences Provided by University of North Carolina at Chapel Hill
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Old 01-30-2013, 05:35 PM   #250
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The 'nicking' enzymes are also called "relaxases," because the nick causes a plasmid, normally supercoiled, to move to the open circle/relaxed state. They've been known about for decades (see: F', F+ etc).

Pretty cool they've solved a structure, but don't hold your breath waiting for a specific inhibitor.
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