“Making resolutions is a cleansing ritual of self assessment and repentance that demands personal honesty and, ultimately, reinforces humility.
Breaking them is part of the cycle.”
From Hugh at Gaping Void
The end is nigh. Media reports state that 700,000,000 people know the world will come to an end this Friday, December 21, 2012. The Guardian reports that Chechens are hoarding staples, including apparently lots of salt. Can they all be wrong? All we can say is that it’s looking like 85F and sunny from Miami Beach.
You may be a prepper, or a non believer, but either way, you need to look sharp the day after. That is, of course, if there is a day after.
So for the remaining 6,300,000,000 folks out there who think that there will be a December 22nd, then you’ll want that tribute to your longevity, intellect and survival instincts. And yes, before you ask, it DOES come with a money back guarantee.
So waste no time and head over to Teespring, a really neat crowd sourcing start-up, to order your limited edition “I Survived The Mayan Apocalypse” tee shirt before it’s too late!
From MNT – full article here
A New Strategy To Prevent Or Halt Periodontal Disease Suggested By Research
Periodontitis, a form of chronic gum disease that affects nearly half of the U.S. adult population, results when the bacterial community in the mouth becomes unbalanced, leading to inflammation and eventually bone loss. In its most severe form, which affects 8.5 percent of U.S. adults, periodontitis can impact systemic health.
By blocking a molecular receptor that bacteria normally target to cause the disease, scientists from the University of Pennsylvania have now demonstrated an ability in a mouse model to both prevent periodontitis from developing and halt the progression of the disease once it has already developed.
The study, published in the Journal of Immunology, was led by Toshiharu Abe, a postdoctoral researcher in the Department of Microbiology in Penn’s School of Dental Medicine. Abe works in the lab of George Hajishengallis, a professor in the department who was a senior author on the paper. The co-senior author was John D. Lambris, the Dr. Ralph and Sallie Weaver Professor of Research Medicine in the Department of Pathology and Laboratory Medicine in Penn’s Perelman School of Medicine. Kavita B. Hosur and Evlambia Hajishengallis from Penn Dental Medicine also contributed to the research, as did Penn Medicine’s Edimara S. Reis and Daniel Ricklin.
In previous research, Hajishengallis, Lambris and colleagues showed that Porphyromonas gingivalis, the bacterium responsible for many cases of periodontitis, acts to “hijack” a receptor on white blood cells called C5aR. The receptor is part of the complement system, a component of the immune system that helps clear infection but can trigger damaging inflammation if improperly controlled.
By hijacking C5aR, P. gingivalis subverts the complement system and handicaps immune cells, rendering them less able to clear infection from the gum tissue. As a result, numbers of P. gingivalis and other microbes rise and create severe inflammation. According to a study published last year by the Penn researchers, mice bred to lack C5aR did not develop periodontitis.
Meanwhile, other studies by the Penn group and others have shown that Toll-like receptors, or TLRs – a set of proteins that also activate immune cell responses – may act in concert with the complement system. In addition, mice lacking one form of TLR called TLR2 do not develop bone loss associated with periodontitis, just like the C5aR-deficient mice.
In the new study, the Penn team wanted to determine if the synergism seen by other scientists between the complement system and TLRs was also at play in this inflammatory gum disease.
To find out, they injected two types of molecules, one that activated C5aR and another that activated TLR2, into the gums of mice. When only one type of molecule was administered, a moderate inflammatory response was apparent a day later, but when both were injected together, inflammatory molecules increased dramatically – soaring to levels higher than would have been expected if the effect of activating both receptors was merely additive.
This finding suggested to the scientists that the Toll-like receptor signaling was somehow involved in “crosstalk” with the complement system, serving to augment the inflammatory response. Turning that implication on its head, they wondered whether blocking just one of these receptors could effectively halt the inflammation that allows P. gingivalis and other bacteria to thrive and cause disease.
Testing this hypothesis, the researchers synthesized and administered a molecule that blocks the activity of C5aR, to see if it could prevent periodontitis from developing. They gave this receptor “antagonist,” known as C5aRA, to mice that were then infected with P. gingivalis. The C5aRA injections were able to stave off inflammation to a large extent, reducing inflammatory molecules by 80 percent compared to a control, and completely stopping bone loss.
And when the mice were given the antagonist two weeks after being infected with P. gingivalis, the treatment was still effective, reducing signs of inflammation by 70 percent and inhibiting nearly 70 percent of periodontal bone loss.
“Regardless of whether we administered the C5a receptor antagonist before the development of the disease or after it was already in progress, our results showed that we could inhibit the disease either in a preventive or a therapeutic mode,” Hajishengallis said.
This is significant for extending these findings to a potential human treatment, as treatments would most likely be offered to those patients already suffering from gum disease.
Because not all cases of periodontitis are caused by P. gingivalis, the research team also wanted to see whether C5aRA could effectively prevent or treat the disease when it arose due to other factors. To do so, they placed a silk ligature around a single molar tooth in a group of mice. The obstruction not only blocked the natural cleaning action of saliva, but also enabled bacteria to stick to the ligature itself, resulting in a massive accumulation of bacteria. This microbial build-up rapidly leads to periodontitis and bone loss, within just five days in the mice.
The researchers then injected the gum tissue adjacent to the ligated molar tooth with C5aRA in some of the mice, and gave the other mice a control.
“These mice that got the C5a receptor antagonist developed at least 50 percent less inflammation and bone loss compared to an analog of C5a receptor antagonist which is not active,” Hajishengallis said.
This result gives the researchers greater confidence that the C5aRA treatment could be effective against periodontitis in general, not just those cases caused by P. gingivalis bacteria.
The team is now working to replicate their success in mice in other animal models, an important step toward extending this kind of treatment to humans with gum disease.
“Our ultimate goal is to bring complement therapeutics to the clinic to treat periodontal diseases,” Lambris said. “The complement inhibitors, some of which are in clinical trials, developed by my group are now tested in various periodontal disease animal models and we hope soon to initiate clinical trials in human patients.”
TGBSL #10 for an explanation go to TGBSL #1
I am no apologist for private medicine, the little bit of the NHS with which I am most familiar – dental practice – is very efficient and mostly responsible. This is because the people who are taking the risk and providing the resources are the business owners or their direct employees. Frequently the larger the organisation – and I see this time after time when dentists try to grow their empires – the less the performance. Performance being measured by taking into account a number of measures including profitability, staff morale and the quality of care – there are many more.
So I believe that private funding can provide great service and benefits to health; but healthcare isn’t like producing tractors nor even the widgets that make the tractors. Nor is it like retailing or banking.
I’m interested in this story in particular because of my association with Peterborough, I spent 7 years working as a GDP in the city and met my wife there. I know a few people who are struggling to make the system work – these are the same people whose opinions will have been ignored when they built the last new hospital. During the time that I worked in Peterborough there was just one hospital Peterborough District centrally positioned typical of its time with lots of expansion on the one site. The city’s population grew significantly during the 80s and a new hospital was needed to cope with the increased population, so they built the Edith Cavell Hospital opened in 1988, closed 2010 and is due to be demolished – great planning guys.
It has been replaced by Peterborough City Hospital (inevitably part of the Edith Cavell Healthcare Campus). What’s happening in this corner of North Cambridgeshire is repeated across the country and not just in health.
Now read on…..
From Am An Zhang aka The Cockroach Catcher.