The Monday Morning Quote #197

“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.”

Eric Zorn

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The Monday Morning Quote #196

“All the adversity I’ve had in my life, all my troubles and obstacles, have strengthened me…

You may not realize it when it happens, but a kick in the teeth may be the best thing in the world for you.”

Walt Disney

Mayan Apocalypse

From Hugh at Gaping Void

Mayan Apocalypse     

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!
apocalypse_t_shirt

#00: Podcast Test

Just testing.

[audio https://theincisaledge.files.wordpress.com/2012/12/theincisaledge.m4a]

TGBSL #10 – A New Strategy To Prevent Or Halt Periodontal Disease Suggested By Research

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

The Monday Morning Quote #195

“The best way to have a good idea is to have lots of ideas.”

Linus Paulin

220px-L_Pauling

NHS & PFI: Please do not cry!

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.

Today, I listened live to the House of Commons’ Public Accounts Committee.
Please, do not cry!
Margaret Hodge, M.P. did not shy away from pointing out that:
“Every single one of you has failed to do proper due diligence about this and no one has been brought to account.
“There is an issue of negligence here and one that I have not felt with a health report to this committee before.”
Who were they that failed?
Dr. David Bennett (not a medical doctor and seemed less confident for someone from McKinsey)), Una O’Brien, permanent secretary for the Department of Health, who looked the most confident of the lot she did not know that Hospital Trust Boards are not to be trusted and of course the Trust CEO (well there has been 5) and Head of the Strategic Health Authority.
MPs were also outraged at the apparent failure of trust bosses, the health regulator Monitor and the Strategic Health Authority to take responsibility for the crisis.
The PFI Hospital:
This is about the 611-bed Peterborough City Hospital was opened in November 2010 at a cost of £289 million with the funding being provided through the government-backed PFI scheme.
The solution: millions again! Not on nurses or doctors!
MPs were also told that over the last few years, some £14 million has been spent on a range of consultants as well as five chief executives, to try and resolve the crisis.
A further £3 million is to be spent on setting up a new team of consultants, which was announced by Monitor today, and which will go into the hospital next year also in a bid find a solution to the trust’s woes.
Free advice from Bloggers etc: why not just buy the companies that own the PFI shares and if necessary by compulsory purchase?
Allyson Pollock:
How PFI is crippling the NHS
Last year the NHS underspent its budget by £900m, returning much of it to the Treasury. This raises serious questions about stewardship of public funds, at a time when hospitals with PFI-associated deficits, such as Hinchingbrooke, have been franchised out to companies such as Circle, and other PFI hospitals in south London and elsewhere are under “special measures”. Before 1990 any hospital overspending would have been managed without recourse to closure, and failing hospitals were unheard of.
Failure is a product of successive governments’ policies since 1990: Kenneth Clarke’s introduction of capital charges and trusts, New Labour’s PFI policy, foundation trusts and payment by results, and now Lansley’s new funding regime and policies.
Since the policy was launched in 1992, report after report over almost two decades has shown how each wave of PFI has been associated with trust mergers, leading to 30% reductions in beds; staff lay-offs; and closures of hospitals, accident and emergency departments and an untold number of community services – all because of lack of affordability. PFI, once trumpeted as the largest hospital-building programme, was in fact the largest NHS hospital and bed closure programme.
Allyson Pollock again:
The debt is toxic.
However, the government will not allow hospitals to default on the debt (it would threaten all the other PFI schemes and result in the banks taking legal action). Moreover, PFI is a Treasury policy for the whole of the public sector and it is a policy that the Treasury is exporting abroad. The Treasury and health department signed off all the PFI deals in the full knowledge that affordability had been an issue from the very beginning. The Treasury stuck to the line that there was no alternative.
This is what the public needs to know and is not being told.
First, the high costs of PFI debt charges means that the NHS can only operate anything from a third to half as many services and staff as it would have done had the scheme been funded through conventional procurement. In other words, for every PFI hospital up and running, equity investors and bankers are charging as if for two. Edward Leigh, the chair of a Treasury committee report into PFI, called investor returns the unacceptable face of capitalism.
Second, we can still afford to pay for universal healthcare – but only if we stop using NHS funds to prop up banks and equity investors.
Third, it is PFI deficits that are driving service closures, not patient demand or an ageing population. Service closures have nothing to do with service redesign.Fourth, the government has now embarked on a new path, bringing in an Act that effectively abolishes the NHS, and which allows hospitals both to enter into more joint ventures with industry and to raise up to half their income from private patients. Two monsters are now unleashed – PFI and Lansley’s Health and Social Care Act 2012.
Colin Douglas
Here in The BMJ, he reviewed Allyson Pollock’s Book, NHS plc.
“Since it was Pollock’s views on the PFI that so upset its proponents, it is worth summarising them briefly. Costs are now intrinsically higher, because of capital borrowing at higher rates than those available to government, because of cash hungry consultancies and the vast transactional and monitoring costs of countless contracts, and because—for the first time on a large scale in the NHS—commercial profits must be made. To accommodate all these new costs clinical services have been scaled down, while matching assumptions about increased efficiency are only variably delivered. All this, along with the rigidity of a trust based strategy for building hospitals and the locking in effect of contracts fixed for decades, seems to Pollock and many others at best a bad bargain, at worst a naive betrayal that opens the NHS to piecemeal destruction and the eventual abandonment of its founding principles. And all over the country PFIs—greedy, noisy, alien cuckoos in the NHS nest—gobble up its finances and will do so for the next 30 years.”
Next 30 years!
The private finance initiative was devised to get schools, hospitals and roads built without swelling the government’s overdraft. Critics discerned a conjuring trick. Instead of the state borrowing, private consortiums did, and then the public paid – at a premium rate. It has often been likened to sticking a mortgage on a credit card; but Whitehall always resisted that charge.
It was just too important to flatter the books, especially to Gordon Brown. His twin obsessions were constructing temples to New Labour’s social policies and establishing his prudence: PFI appeared to further both. But the trickery was too flagrant. Friendly thinktanks were tasked with devising a rationale couched in the language of public-private partnerships. It was said that City expertise would somehow foster efficiency. Henceforth PFI was all about improving the allocation of risk. Beautifying the books had nothing to do with it.     
PFI makes me particularly angry. It is a guaranteed loan to property investors, where high-rate mortgage payments are kept off-balance to reduce the country’s declared debt. In other words, it’s the Enron of the NHS. This is money the NHS has committed to leave frontline healthcare for the next 35 years.”

Dr Helena McKeown

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