BREAKING MEDICAL NEWS

TRAINING CRISIS THAT IS ENGULFING THE PROFESSION

From the News Desk of Jeanne Hambleton
Source Pulse Today
Posted 22 Juy 2014 By Jaimie Kaffash

Leaked figures reveal almost 40% of GP training places are unfilled in some areas of the UK, finds Jaimie Kaffash.

This was not meant to happen. Since 2012, the Government has been saying it wants at least half of medical training places to be for general practice.

But leaked figures obtained by Pulse reveal the worst training recruitment round for seven years, with some areas seeing almost 40% of places unfilled. The figures have been described as ‘alarming’ by GP leaders, with serious implications for the profession.

They undermine one of the main pillars of the Government’s health strategy and have all but extinguished the light at the end of the tunnel for GPs in certain areas, who saw a new generation of GPs as the answer to the unsustainable burden of workload.

There can be no positive spin. The 2,630 graduates entering training in England in August is the lowest number since figures were collected in this way in 2007.

In the North East, fewer than 70% of posts have been filled, while Health Education Yorkshire and Humber has only filled 78% of its posts. Health Education East Midlands is bottom of the table, filling just 63% of its places.

Indeed, the short-term crisis is so severe that Health Education East Midlands has instigated a ‘pre-training year’, which will see graduates who failed the GP training assessments fill gaps in secondary care.

The Government has already had to extend the deadline for its target of 3,250 GPs entering training annually by 2016 in England, but even this is looking optimistic now.

Dr Beth McCarron Nash, a GPC negotiator, says the figures are ‘extremely alarming’. She says: ‘Many GPs are already feeling it on the ground. We are looking at alarmingly low numbers of people applying for partnerships and salaried jobs. These recruitment figures will only make things worse.

‘We are not training enough GPs to fill current vacancies, let alone the urgent expansion of GPs we need to help us deliver the increased workload we are seeing as a result of the complexity of care and co-morbidity as patients are getting older.’

Massive gaps

‘In three years’ time, we will have no GPs coming through to fill our vacancies.’

Doncaster LMC chair Dr Dean Eggitt.

Overall in England, only 89% of the 2,994 posts available were filled – which compares with figures of around 98% for the past four years.

There is little problem with recruitment in London, where some 99% of positions have been filled, and the Kent, Surrey and Sussex and Thames Valley regions are not far behind.

But parts of northern England and the Midlands have massive gaps in their GP training programmes. Scotland and Wales – although not under Health Education England’s (HEE) jurisdiction – are also struggling with around one in 10 places lying vacant.

In Doncaster – where Pulse reported a practice was forced to offer a £20,000 ‘golden hello’ to a new partner as a result of the ongoing GP recruitment crisis in the region – only six of the 26 vacancies have been filled, says Dr Eggitt.

Dr Eggitt says: ‘For general practice, our concerns are that the trainees are supernumerary to us now, but in three years’ time, we will have no GPs coming through to fill our vacancies.’

‘There wouldn’t be enough trained GPs to replace all those who will go even if we filled all the places’.

Dr Nigel Watson, chair of Wessex LMCs

He says the LMC has just conducted a workforce survey of around 130 GPs, which shows that around 30% of the workforce intends to retire in the next five years.

‘If we are losing 30% of our workforce in five years’ time, and only six GPs are coming through, how are we going to fill that gap?’ he asks.

This is the reality shared by GPs across the country. As Dr Watson puts it: ‘There wouldn’t be enough trained GPs to replace all those who will go even if we filled all the places. So the fact that all the places are not filled – and that those who are coming through might not want to go straight into general practice – means we are going to face a problem in the number of GPs coming through.’

Former RCGP chair, Professor Clare Gerada, who estimated last year that 10,000 additional trained GPs were needed to keep up with patient demand, says these figures will inevitably affect care.

She says: ‘GPs now make up 30% of the medical workforce, which is disgraceful. If these training numbers do not improve, we will find that our patients will see longer waits to see a GP, more fragmentation and massively increased costs.’

The coalition Government and the Labour Party both acknowledge that their plans for more care to be provided in the community, with greater continuity of care and better access, are predicated on increasing the number of GPs.

This is reflected in the Government’s mandate to HEE, which tasks the body with ensuring that 50% of all medical graduates – translating to 3,250 graduates – should enter general practice training.

Plans undermined

‘We need urgent action from NHS England’ Professor Clare Gerada.

The deadline for this target has already been pushed back from 2015 to 2016.

Dr McCarron-Nash says: ‘I don’t think they can fulfil their own target.’

Even the Department of Health admits its plans are being undermined by training recruitment being kicked into reverse.

A DH spokesperson told Pulse: ‘HEE has created more training places for GPs, but this will only make a difference if the places are filled by doctors in training.

HEE is putting robust plans in place to make sure the training places are filled over the next two years.’

But this action is slow in coming. Professor Gerada says: ‘We need urgent action from NHS England, addressing the short, medium and long term. We need a new recruitment, retention and refreshment strategy and we need this centrally, not just relying on local areas to find their own solutions because it is too important.’

There seems to be no clear strategy to solve the problem. HEE is being accused of having ‘buried’ a report on boosting the GP workforce, with no definite publication date announced.

As Pulse reported in February, the ‘GP Taskforce’ report was set to recommend a cap on the number of secondary care training posts available so that more trainees would have to go into general practice, and that practices be given grants of £20,000 for their premises so they can create more space for trainees.

Related stories:
Patients risk becoming ‘bereft of a GP service’ in some areas, GPC warns
Dr Chaand Nagpaul: ‘General practice is not just in crisis; it is imploding’

But these radical ideas have yet to see the light of day, and the BMA has accused HEE of ‘burying’ the report.
Dr McCarron-Nash says: ‘We have written to HEE asking them why it have failed to publish its own report.

‘It is unacceptable that this report has been buried. This needs implementation and not burial, and these figures underline that fact.’

Pulse understands there is concern among HEE leaders over the recommendation to cap the number of secondary care posts, but HEE refuses to say why it has not yet been published.

HEE says: ‘The GP Taskforce report was commissioned before the establishment of HEE. However, although it takes a very specific GP view, it will be helpful information to consider as part of our work with partners like NHS England around the wider primary care workforce as set out in our mandate, and it will be published on our website in due course as one of the resources for this wider work.’

But, for GP leaders, the real solutions will need to come from fundamental changes that get to the core of the recruitment crisis.

As Dr McCarron-Nash puts it: ‘It is the constant negative portrayal and media bashing we are seeing. We need to urgently get the DH to start talking up general practice.’
‘The profession is now facing a perfect storm’

These are the worst figures we have seen in GP recruitment since GP training was standardised in 2007.

Both the numbers of trainees entering general practice and the percentage of positions filled have dropped. This has particularly hit the north of England, the Midlands, Scotland and Wales.

What is worrying is that, despite highlighting the issue on a regular basis, not enough has been done to promote general practice as a positive career option for young doctors.

In the short term, we would like to see the returners scheme prioritised, to allow already qualified GPs to return to work, rather having to go into this ‘pre-training year’.

This ‘pilot’ is simply an exercise whereby GP training funds have been directed to non-training posts to fill empty secondary care rotas.

The ageing population and workforce crisis in general practice means that the profession is now facing a perfect storm.

The Government needs to pay attention to this and start looking at more short-term and long-term solutions that will actually work. We need a much more comprehensive long-term strategy, which would have been available if we had been given sight of the GP Taskforce recommendations, which have not been published despite being submitted at the beginning of the year.

Questions have to be asked about why this delay has occurred. Dr Krishna Kasaraneni is chair of the GPC GP trainees subcommittee.


PATIENTS RISK BECOMING ‘BEREFT OF A GP SERVICE’


From the News Desk of Jeanne Hambleton

Source Pulse Today
Posted 25 June 2014 | By Sofia Lind

The chair of the GPC has warned that patients are at risk of becoming ‘bereft of a GP service’ in some areas – prompting the Department of Health to accuse GPs of ‘scaremongering’.

Addressing the BMA’s annual representative meeting later today, Dr Nagpaul will say that general practice is ‘imploding’, and that continuous defunding of the service has caused a ‘tragic’ and ‘quadruple whammy’ of a crisis in workload, workforce, premises and morale.

He will say that general practice is seeing 40 million more patients annually than five years ago, the greatest rise in any sector of the NHS, that its share of the NHS budget has dwindled from more than 10% to less than 8%, and there was a 15% reduction in GP training applications last year.

But the DH has said it is ‘scaremongering’ to claim general practice is imploding.

Dr Nagpaul will tell delegates today: ‘These intolerable pressures have butchered the joy and ability of GPs to care for their patients, leading younger doctors to shun general practice in favour of a career in hospital, with a 15% reduction in GP training applications last year, and 451 places unfilled.

Ministers ignore this workforce crisis at their peril, which seriously risks leaving patients bereft of a GP service in some areas.

‘And whilst the government has announced £650m to ease winter NHS pressures, can you blame GPs for feeling aggrieved that the crisis affecting 90% of patient contacts in the NHS which is in general practice is given zilch, showing a callous disregard for the plight of a profession on its knees.’

The solution, he will say, is to ensure GP services are funded by just over £70 per patient, which he describes as a ‘bargain’ compared to hospital services.

He will say: ‘Therefore, amidst all the headline-grabbing pressures in the NHS, I urge ministers to open their eyes and wake up to the fact that general practice is not just in crisis, it’s imploding. And if the building blocks of the NHS crumble, the NHS collapses too. Not alarmist, not scaremongering. Just fact.

‘I call upon government to finally stop denigrating GPs as the problem, and to see us as the solution. That in an NHS paralysed with cash constraints, it’s logical to invest in the unarguable cost-effectiveness of general practice. GPs are a bargain at the price – just over £70 per patient per year pays for unlimited appointments, home visits, telephone advice, and so forth – a fraction of the tariff cost of a single outpatient appointment.’

But a DH spokesperson said: ‘It is scaremongering to say that GP services are “imploding”. The number of GPs has gone up by 1,000 since 2010 and we’ve taken tough decisions to protect the NHS budget so we can strengthen family doctoring, reform out-of-hospital care and improve GP access for 7.5 million people.

‘GPs agreed to be at the heart of our radical plans for more personalised community care in return for cutting their targets by more than a third to free up more time with patients. GP premises must be fit to help deliver a single, seamless service for the elderly and most vulnerable.’


‘GENERAL PRACTICE IS IMPLODING’

‘General practice is not just in crisis; it is imploding’

From the News Desk of Jeanne Hambleton
Source Pulse
Posted 25 June 2014 |

Read Dr Chaand Nagpaul’s will tell the BMA’s annual representatives meeting that it is ‘tragic’ that general practice has been systematically devalued, attacked and defunded. Read the speech in full here.


I stand before you for the very first time as chair of the BMA’s GP committee, proud to represent 46,000 dedicated GPs working tirelessly across the UK.

Today nearly a million patients will visit their GP surgery – put into perspective that’s 16 times more than those who’ll attend accident and emergency – UK general practice is truly the pulse and lifeblood of the NHS, and that which keeps it alive.

It is admired globally, independently evaluated as having highest levels of quality personalised care, cost effectiveness, and equity. We provide the totality of first point of contact services, unlike parts of Europe where GPs for example don’t see maternity, gynaecological conditions or children.

UK GPs manage demand with 19 out 20 patient contacts concluded in primary care itself.

Whilst this should be cause for celebration, it is tragic that within our own shores, NHS general practice has been systematically devalued, attacked and defunded, leaving it in a parlous state, with the quadruple whammy of a crisis in workload, workforce, premises and morale.

We are seeing record numbers of patients in general practice – 40 million more annually than five years ago, the greatest rise in any sector of the NHS, set to increase relentlessly with a growing older population, and tranches of care moving out of hospital.

Yet despite this escalating workload, we have seen brutal disinvestment, with general practice’s share of the NHS budget dwindling in a decade from above 10% to now less than eight, and a real terms reduction of £450m in 3 years, and now MPIG and PMS funding cuts which threaten the viability of many GP surgeries nationally.

We have similarly seen a relative reduction in the GP workforce, with the number of GPs as a proportion of all doctors in England reducing from 34% to 26% in two decades.

The simple fact is that demand has far outstripped our impoverished capacity, denying patients the care and access they deserve.

GPs are struggling to square an impossible circle to manage the multiple complex physical and mental health needs of patients in the barebones of a 10 minute consultation- an insensitive insult to so many of our most ill patients.

We are forced into providing conveyor belt care at breakneck speed, up to 60 times in a day, added to by an open-ended volume of phone calls, home visits, repeat prescriptions, results, reports and hospital correspondence.

This is unmanageable, exhausting and unsustainable and puts safety and quality at risk.

It is therefore no surprise that even a Government commissioned report last year showed GPs suffering record levels of stress, and a BMA survey showing that 6 out of 10 GPs intend retiring early.

These intolerable pressures have butchered the joy and ability of GPs to care for their patients, leading younger doctors to shun general practice in favour of a career in hospital, with a 15% reduction in GP training applications last year, and 451 places unfilled.

Ministers ignore this workforce crisis at their peril which seriously risks leaving patients bereft of a GP service in some areas.

Nor do we have the space to care. With no dedicated funding for GP premises in over a decade, were struggling to provide 21st-century care from dated buildings designed for a past era, without the rooms for GPs to consult, patients to wait or staff to work in.

And whilst the government has announced £650m to ease winter NHS pressures, can you blame GPs for feeling aggrieved that the crisis affecting 90 % of patient contacts in the NHS which is in general practice is given zilch, showing a callous disregard for the plight of a profession on its knees.

Therefore amidst all the headline grabbing pressures in the NHS, I urge Ministers to open their eyes and wake up to the fact that general practice is not just in crisis, it’s imploding. And if the building blocks of the NHS crumble, the NHS collapses too. Not alarmist, not scaremongering. Just fact.

There are 340m consultations in general practice annually compared to 21m in A&E – itself under pressure. The fact is that if you destabilise general practice, it would only take us to see 6% fewer patients to double the numbers attending casualty if they went there instead, with drastic consequences.

Therefore I call upon Government to finally stop denigrating GPs as the problem, and to see us as the solution.

That in an NHS paralysed with cash constraints, it is logical to invest in the unarguable cost effectiveness of general practice. GPs are a bargain at the price – just over £70 per patient per year pays for unlimited appointments, home visits, telephone advice, and so forth – a fraction of the tariff cost of a single outpatient appointment.

And that is why we have launched our campaign ‘Your GP cares’, calling for more GPs, nurses, staff and buildings. To provide us with more time and tools to care for patients, which would reduce hospital pressures, improve the nation’s health, and release cost efficiencies in a cash strapped NHS – we would all gain from this investment.

RB, in conclusion, I urge you to support us in our fight for the very survival of UK general practice and in doing so for the survival of the NHS itself.

Talk soon. Jeanne

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GPS TOLD TO AVOID REFERRING PATIENTS TO ACCIDENT AND EMERGENCY AFTER HOSPITAL PLACED ON ‘BLACK ALERT’

From the News Desk of Jeanne Hambleton

Source Pulse Daily
Posted 14 July 2014 | By Christina Kenny

GPs in Cambridge have been warned against sending patients to A&E, after one of the country’s most renowned teaching hospitals announced that it had been placed on black alert.

Cambridge University Hospitals wrote to GPs, ambulance services and four other nearby hospitals on 10 July to warn them that Addenbrooke’s Hospital was facing ‘severe’ capacity issues.

GPs have been asked to consider whether patients they would usually send to A&E can instead be assessed through an ambulatory care service and all referrals must now first be discussed with an on-call doctor, the hospital said.

The hospital has been on black alert, which indicates the highest possible level of capacity crisis, since early July.

It had been placed on the black alert several times in recent years – for 190 days in 2012-13 alone. Though figures for 2013-14 are not yet available, it is understood that they are expected to rise.

The letter, seen by Pulse, said that the trust was experiencing ‘severe’ capacity issues across all areas.

CUH’s on call director, Amanda Kahn, wrote: ‘We have planned admissions on hold. We have contingency areas open.

“We are no longer able to place patients from the Emergency Department. We have critical staffing levels.

She added: “If you do phone GP liaison to refer a patient, please be proactive to considering whether your patient can be assessed on EAU3 (ambulatory care) rather than simply sent to the Emergency Department.”

FEED BACK FROM GPs or Readers of Pulse Daily

1. It would seem referring a patient to A&E is not a simple task so GPs it seems do not take this lightly. It seems GPs do not like it any more than we do as patients.

2. So a hospital with current, and multiple past, capacity problems wants GPs not to refer to AEU. Sorry my stock of medical goodwill ran out many, many years ago and if my patient needs to go the AEU they go. End of discussion. Why has the hospital not solved their capacity problems? Just why should GPs help those who would not help themselves?

3. Admitting a patient, or sending them to A&E is not an easy thing to do. The patient does not like it unless obviously necessary. They know they will be seen by a nurse after 1 minute and them be in a corridor for 3 hours and 59 minutes before admission. It will also take me at least 15 minutes on the phone, quite apart from arranging ambulance and letter. Does anyone in secondary care really feel admissions are an easy option? What are we going to do with patients that need admitting – leave them at home?

The same alert thing happens with our local hospital. They built the hospital they could afford under PFI, so it is too small and the car parking is very expensive. Everyone told them it would be too small and yes, surprise; it is. Our local population did not go younger, and chronic illness did not become less of a burden. Now we get regular letters with “red alert” “purple alert” etc. We get them so often, they go in the round filing bin immediately, unless I get really miffed which is when I send them back a fax. “dear hospital our practice is on black alert with bells on and red stars. Please do not discharge any of our patients as our surgery has now reached full capacity”. I am certain my missive will be treated with as much consideration as it deserves.

4. It is just a matter of funding and staff patient ratios. That is all. A hundred more inquiries will not solve anything till we can compare like with like. How many beds. consultants, junior doctors, nurses per 1000 patients ?

5. Our local hospital had black alerts last year, then they turned into rainbow alerts with spots on it, as they had hours of waits for ambulances to drop off new patients! Demand management from the DOH is the only way to stop the flood of folk turning up to A&E with coughs and sore throats, drunks need to be fined for wasting NHS time.

6. Close the doors to A&E for minor non accident and non emergency care – simple decommission them so they aren’t paid to see it. See how soon it is all sent back to where it belongs. Coughs and colds – even in small children belong at home in bed with parental care and Calpol.


NICE WIDENS STATIN TREATMENT TO MILLIONS

Nice Pushes Through Decision To Widen Statin Treatment To Millions More Healthy People

From the News Desk of Jeanne Hambleton
Source Pulse Daily
Posted 21 July 2014 By Caroline Price

NICE advisors have stuck to their decision to halve the risk threshold for primary prevention of cardiovascular disease to 10%, despite calls from the BMA and other clinical experts to drop the proposal because of concerns it will lead to over-treatment.

The final guidance on lipid modification published today could potentially put millions more people on statins and has been criticised by the GPC as having ‘insufficient evidence’ for GPs to have confidence in the recommendation.

NICE has strengthened recommendations on lifestyle changes that should be tried before starting patients on a statin, saying GPs should offer statin treatment ‘if lifestyle modification is ineffective or inappropriate’.

But the final guidance is otherwise largely unchanged from the original draft publication announced in February this year, despite months of controversy.

The major new recommendations are to use the QRISK2 tool exclusively to formally risk assess adult patients up to the age of 84, and to offer high-intensity statin treatment with atorvastatin to patients with a 10-year risk of 10% or higher.

The guidelines state: ‘Before offering statin treatment for primary prevention, discuss the benefits of lifestyle modification and optimise the management of all other modifiable cardiovascular disease risk factors if possible.

If lifestyle modification is ineffective or inappropriate offer statin treatment after risk assessment.

‘Offer atorvastatin 20mg for the primary prevention of cardiovascular disease to people who have a 10% or greater risk of developing cardiovascular disease. Estimate the level of risk using the QRISK2 assessment tool.’

Guidelines group chair Dr Anthony Wierzbicki, honorary reader at Guy’s and St Thomas’ Hospital, told Pulse that BMA concerns over the evidence base for statin treatment at the 10% threshold were baseless.

Speaking to Pulse, Dr Wierzbicki said: ‘The evidence is clearly there and even at the relatively conservative risk threshold of 10% for “hard” cardiovascular outcomes, we still show this [approach] is going to be “event-effective” in terms of the best use of resources in the NHS, and it is also cost-effective in terms of how much money we would have to spend in the NHS to deliver those outcomes.’

Dr Wierzbicki added: ‘There is actually very good disclosure on safety data on statin trials. We used a huge meta-analysis of all the phase three data comprising over 300,000 patients – this is all statins, at all doses – published within the last year, which is an enormous trial database of the randomised trials against placebo.’

‘We also have data from registries – although it is always of more limited quality – and prescribing data from various countries, on the rates of side effects and these are really quite low.’

NICE advisors also dismissed the GPC’s objection that GPs would be overwhelmed by the huge increase in appointments needed to manage more patients on statins, arguing that the new recommendations have vastly simplified the approach to managing treatment with lipid-lowering therapy.

Dr Wierzbicki said: ‘We have actually taken a lot of notice of that – and what we’ve done with this guideline is simplified the protocols.’

But the GPC hit back, re-stating its concerns that NICE is ignoring the potential increased risks of harm from statin use and over-estimating the benefits from the evidence so far.

In a collective statement, GPC members wrote: ‘The GPC believe that there is insufficient evidence of significant overall benefit to low-risk individuals to allow GPs to have confidence in the recommendation to reduce the risk threshold for prescribing cholesterol lowering drugs, and that doing so might distort health spending priorities.’

Dr Martin Brunet, a GP in Guilford, Surrey, who has campaigned on over-treatment issues, told Pulse he was ‘extremely disappointed’ that the guidelines group had not given GPs more room to give patients choice on whether to start a statin.

Dr Brunet said: ‘It is so disappointing to see the lack of emphasis on patient preference in the key points summary. There is mention that a lower dose of statin might be used in patients with established cardiovascular disease on the grounds of patient preference, but there is nothing about patient preference in the area of the key recommendation with regards to a CVD risk of 10%.’

Dr Brunet also questioned the push to treat patients with CKD stage 3 with statins.

He said: ‘They now advise not to use any risk stratification, but just to start a statin in all patients with CKD. This will include a huge number of older women who are otherwise well and have what many would consider to be normally ageing kidneys.’

‘For me this is a very significant shift in favour of more treatment.’

FEED BACK FROM GPs

One GP commented “In our society , those with the best knowledge of what is happening are those who are furthest from seeing the world as it is. “ 1984 , George Orwell

Another GP said:
(1) the implication on us is , of course, more statin ‘offer’ but offer does not necessarily mean ‘offer taken’ or ‘offer tolerated’

(2) have to engage your patient and ensure that they understand fully the meaning of 10% CVD risk as well as the concept of benefit against risk. We are not living in a perfect world, my dear academic colleagues

(3) we still need a proper and sensible debate about the exact incidence and prevalence of adverse reactions/side effects , 5-10% or 10-15%? That has to be an official information given to our patients.

(4) I would predict the Read Code ‘Adverse reaction to statin prophylaxis’ and equivalents will have to be used more. In fact, also document whether the quality of life of the patient is impaired by statin or not, bearing in mind it means differently in different age group.

(5) Time , of course , more appointments, you know what I am going to say anyway.

(6) Remember shared decision with your patients is a task based on democracy , not some autocratic parenting in this Stalinisation, sorry I mean Statinisation.

Personal comment

As a fibromyalgia patient, when I was offered statins for high cholesterol and read the side effects, it meant living with a constant fibromyalgia flare. I could see no benefit in that and found other natural means of reducing my high cholesterol. Back soon Jeanne

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GOLDEN HELLOS FOR NEW ESSEX GPs

From the News Desk of Jeanne Hambleton
Released Monday 21 July 2014
Posted on 18 July 2014 by Sofia Lind

PULSE DAILY, the on-line newsletter to GPs around the country, have today published a story written by their own journalist Sofi Lind, advising that GPs moving to Essex are being offered a £10,000 ‘golden hello’ to attract doctors to move to this county.

BREAKING NEWS

Exclusive GPs moving to Essex will be handed up to £10,000 under plans for a ‘golden hello’ scheme to try to combat a recruitment crisis leaving practices ‘on the brink of collapse’.

The scheme, which has been funded via a £400,000 fire-fighting fund from health education chiefs, will see any GP moving to Essex and staying on for two years receive £5,000, with the possibility of another £2,500 depending on the level of deprivation and an extra £2,500 depending on how under-doctored the area is – with a maximum payment of £10,000.

Essex LMC, which has been heavily involved in fashioning the scheme, said it is one of a number of projects to be rolled out to try to solve the crisis which has left practices on the ‘brink of collapse’. The region is now short of the 143 full-time equivalent GPs recommended by NHS England’s primary care strategy.

Tendering and Braintree, in the north-east of the county, will be the two key priority areas to target with the ‘golden hello’ money, it said. Pulse revealed in January that the crisis in the region has seen one permanent GP having to serve more than 8,000 residents in one area in the north-east of the county.

There is no fixed overall budget for the scheme itself, but the money will be taken out of the £400,000 pot of emergency funding that Health Education England (HEE) has offered to local commissioners to spend on longer term and short term measures to plug the gaps in recruitment, including hiring more locum GPs and training more practice nurses.

Essex LMC chief executive Dr Andrew Bradshaw said: ‘GPs have to stay for two years [to earn] payments up to £10,000. We need to do it because some practices are on the brink of collapse.’

The move comes as a GP practice in Doncaster, South Yorkshire, has so far failed to attract a new doctor despite offering a golden hello payment twice the size. The Thorne Moor Medical Practice has for months been advertising a role which would pay a £20,000 bonus above earnings over the course of three years during which they would have to stay.

However, Dr Joe Firth, a partner at the practice, said: ‘Three people showed an interest, none of whom were qualified yet. Two pulled out of the interview process because they were offered jobs elsewhere. A third was a very good candidate and we offered him the job, but he decided for personal reasons that he couldn’t start until January. So we were left with nothing.’

‘The advert is going out again this month and this time we’re going to be even more obvious with the fact we’re offering this £20,000 incentive. It’s just bizarre [because] it’s a nice place to work.’
Dr Firth said the problem appeared to be that there are not enough new doctors opting to become GPs and those that were wanted to be locums or even work abroad.

He said: ‘The problem is there’s not enough new doctors coming through. For people who qualify now, there are so many jobs out there for them to choose from. I’m on a mailing list for GP trainers and trainees, and every day there’s a new email from a practice in Yorkshire looking for a doctor. They can pick and choose where they go. Lots of them want to be locums and I even hear lots are taking time out to go travelling or are going abroad to work. They see no incentive to joining a practice or staying there.’

Pulse revealed this week that at least 109 practices in the UK – including 91 in England – have already approached their LMCs about potentially closing as a result of funding and recruitment pressures.

MORE PRACTICES PLAN FOR CLOSURE AS TOTAL HITS 109

From the News Desk of Jeanne Hambleton
Source Pulse Daily
Posted by 15 July 2014 | by Jaimie Kaffash

Exclusive Around 30 practices in London alone are under threat of closing, as a Pulse investigation reveals that the number of practices across the UK considering their future has reached more than 100.

More local leaders have come forward in the wake of Pulse’s investigation earlier this month – which found that 60 practices across the UK were under threat of closure – warning they have ‘not seen anything like this’ in 20 years.

The GPC has warned that a ‘perfect storm’ has led to ‘more and more practices considering their options’, including the withdrawal of MPIG, PMS reviews and the recruitment crisis.

London is the worst affected region, but local leaders in Northamptonshire and Devon have also come forward warning they both have six practices under threat, while Doncaster, Leicestershire, Sunderland and Sussex LMCs have all reported practices are considering handing back contracts.

Pulse asked LMC leaders across the country how many practices had contacted them regarding the possibility of closing.

A spokesperson for Londonwide LMCs said ‘current indications are around 28-30.’

Dr Tony Grewal, medical secretary of Londonwide LMCs, said that the capital was particularly badly affected by MPIG.

He said: ‘NHS England (London) have explicitly stated that no money is available to support practices severely affected by the withdrawing of MPIG payments. They have offered organisational support to practices from within existing resources.’

‘Londonwide [LMCs] have made a number of other suggestions for their consideration, including temporary bridging payments to practices… and we are waiting for their considered response.’

Pulse has reported that Jubilee Practice in Tower Hamlets, east London, has already put a ‘red button date’ in place, which may see them having to close.

Virginia Patania, practice manager, said that there was now a ‘very large campaign’ called Save Our Surgeries being led by the practice to highlight the potential of closures.

She said: ‘It’s something we are looking at in a way we have never look at before. Part of it is funding, part of it is recruitment. In Tower Hamlets a fair number of us, for a collection of reasons, would say our viability is severely limited over the next year or two.’

‘There’s definitely a view from NHS England that mergers are the way of the future. But you need to get to the future to consider this. No support has been given to practices in that transition.’

In Devon, LMC leader Dr Mark Sanford-Wood said: ‘In terms of closures, we haven’t seen any yet, but we have on our radar at least half a dozen practices we are very concerned about. It is highly likely that a good number will end up closing by the end of the year.’

‘I’ve been involved with the LMC for 20 years and I’ve never seen this before. For this to start happening now is significant.’

Dr Beth McCarron-Nash, GPC negotiator, told Pulse: ‘I am certainly hearing anecdotally about more and more practices considering their options. It’s a perfect storm of problems. Some of that is the contract imposition from 2013, some is from funding swings as a result of MPIG redistribution.

‘That, along with spiralling workload and increasing demand… is having a catastrophic effect on practices and are struggling to cope.’

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ONE INJECTION STOPS DIABETES IN ITS TRACKS

Treatment reverses symptoms of type 2 diabetes in mice without side effects

From the FMS Global News Desk of Jeanne Hambleton

Embargo expired: 16-Jul-2014 1:00 PM EDT
Source Newsroom: Salk Institute for Biological Studies
Citations Nature

Newswise — LA JOLLA—In mice with diet-induced diabetes—the equivalent of type 2 diabetes in humans—a single injection of the protein FGF1 is enough to restore blood sugar levels to a healthy range for more than two days.

The discovery by Salk scientists, published today in the journal Nature, could lead to a new generation of safer, more effective diabetes drugs.

The team found that sustained treatment with the protein does not merely keep blood sugar under control, but also reverses insulin insensitivity, the underlying physiological cause of diabetes. Equally exciting, the newly developed treatment does not result in side effects common to most current diabetes treatments.

“Controlling glucose is a dominant problem in our society,” says Ronald M. Evans, director of Salk’s Gene Expression Laboratory and corresponding author of the paper.

“And FGF1 offers a new method to control glucose in a powerful and unexpected way.”

Type 2 diabetes, which can be brought on by excess weight and inactivity, has skyrocketed over the past few decades in the United States and around the world.

Almost 30 million Americans are estimated to have the disease, where glucose builds up in the bloodstream because not enough sugar-carting insulin is produced or because cells have become insulin-resistant, ignoring signals to absorb sugar. As a chronic disease, diabetes can cause serious health problems and has no specific cure. Rather it is managed—with varying levels of success—through a combination of diet, exercise and pharmaceuticals.

Diabetes drugs currently on the market aim to boost insulin levels and reverse insulin resistance by changing expression levels of genes to lower glucose levels in the blood. But drugs, such as Byetta, which increase the body’s production of insulin, can cause glucose levels to dip too low and lead to life-threatening hypoglycemia, as well as other side effects.

In 2012, Evans and his colleagues discovered that a long-ignored growth factor had a hidden function: it helps the body respond to insulin. Unexpectedly, mice lacking the growth factor, called FGF1, quickly develop diabetes when placed on a high-fat diet, a finding suggesting that FGF1 played a key role in managing blood glucose levels. This led the researchers to wonder whether providing extra FGF1 to diabetic mice could affect symptoms of the disease.

Evans’ team injected doses of FGF1 into obese mice with diabetes to assess the protein’s potential impact on metabolism. Researchers were stunned by what happened: they found that with a single dose, blood sugar levels quickly dropped to normal levels in all the diabetic mice.

“Many previous studies that injected FGF1 showed no effect on healthy mice,” says Michael Downes, a senior staff scientist and co-corresponding author of the new work.

“However, when we injected it into a diabetic mouse, we saw a dramatic improvement in glucose.”

The researchers found that the FGF1 treatment had a number of advantages over the diabetes drug Actos, which is associated with side effects ranging from unwanted weight gain to dangerous heart and liver problems. Importantly, FGF1—even at high doses—did not trigger these side effects or cause glucose levels to drop to dangerously low levels, a risk factor associated with many glucose-lowering agents.

Instead, the injections restored the body’s own ability to naturally regulate insulin and blood sugar levels, keeping glucose amounts within a safe range—effectively reversing the core symptoms of diabetes.

“With FGF1, we really have not seen hypoglycemia or other common side effects,” says Salk postdoctoral research fellow Jae Myoung Suh, a member of Evans’ lab and first author of the new paper.

“It may be that FGF1 leads to a more ‘normal’ type of response compared to other drugs because it metabolizes quickly in the body and targets certain cell types.”

The mechanism of FGF1 still is not fully understood—nor is the mechanism of insulin resistance—but Evans’ group discovered that the protein’s ability to stimulate growth is independent of its effect on glucose, bringing the protein a step closer to therapeutic use.

“There are many questions that emerge from this work and the avenues for investigating FGF1 in diabetes and metabolism are now wide open,” Evans says.

Pinning down the signaling pathways and receptors that FGF1 interacts with is one of the first questions he would like to address. He is also planning human trials of FGF1 with collaborators, but it will take time to fine-tune the protein into a therapeutic drug.

“We want to move this to people by developing a new generation of FGF1 variants that solely affect glucose and not cell growth,” he says.

“If we can find the perfect variation, I think we will have on our hands a very new, very effective tool for glucose control.”

Other researchers on the study were Maryam Ahmadian, Eiji Yoshihara, Weiwei Fan, Yun-Qiang Yin, Ruth T. Yu, and Annette R. Atkins of the Salk Institute for Biological Studies; Weilin Liu, Johan W. Jonker, Theo van Dijk, and Rick Havinga of the University of Groningen; Christopher Liddle of the University of Sydney; Denise Lackey, Olivia Osborn, and Jerrold M. Olefsky of the University of California at San Diego; and Regina Goetz, Zhifeng Huang, and Moosa Mohammadi of the New York University School of Medicine.

Ronald Evans is a Howard Hughes Medical Institute investigator and is also supported by grants from the National Institutes of Health, the Leona M. and Harry B. Helmsley Charitable Trust, the Glenn Foundation for Medical Research, Ipsen/Biomeasure, CIRM, and the Ellison Medical Foundation. Other study authors received grants from the National Institutes of Health, the Australian National Health and Medical Research Council, the European Research Council, the Human Frontier Science Program, the Netherlands Organisation for Scientific Research, and the Dutch Digestive Foundation.

About the Salk Institute for Biological Studies:

The Salk Institute for Biological Studies is one of the world’s preeminent basic research institutions, where internationally renowned faculty probes fundamental life science questions in a unique, collaborative and creative environment.

Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer’s, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, MD, the Institute is an independent nonprofit organization and architectural landmark.

NEW GENE DISCOVERED STOPS SPREAD OF DEADLY CANCER

From The FMS Global News Desk of Jeanne Hambleton

Embargo expired: 17-Jul-2014 12:00 PM EDT
Source Newsroom: Salk Institute for Biological Studies
Citations Molecular Cell

Newswise — LA JOLLA—Scientists at the Salk Institute have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body, indicating a new way to fight one of the world’s deadliest cancers.

By identifying the cause of this metastasis—which often happens quickly in lung cancer and results in a bleak survival rate—Salk scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway, detailed today in Molecular Cell, may also help researchers understand and treat the spread of melanoma and cervical cancers.

“Lung cancer, even when it is discovered early, is often able to metastasize almost immediately and take hold throughout the body,” says Reuben J. Shaw, Salk professor of molecular and cell biology and a Howard Hughes Medical Institute early career scientist.

“The reason behind why some tumors do that and others don not has not been very well understood. Now, through this work, we are beginning to understand why some subsets of lung cancer are so invasive.”

Lung cancer, which also affects nonsmokers, is the leading cause of cancer-related deaths in the country (estimated to be nearly 160,000 this year). The United States spends more than $12 billion on lung cancer treatments, according to the National Cancer Institute.

Nevertheless, the survival rate for lung cancer is dismal: 80 percent of patients die within five years of diagnosis largely due to the disease’s aggressive tendency to spread throughout the body.

To become mobile, cancer cells override cellular machinery that typically keeps cells rooted within their respective locations. Deviously, cancer can switch on and off molecular anchors protruding from the cell membrane (called focal adhesion complexes), preparing the cell for migration. This allows cancer cells to begin the processes to traverse the body through the bloodstream and take up residence in new organs.

In addition to different cancers being able to manipulate these anchors, it was also known that about a fifth of lung cancer cases are missing an anti-cancer gene called LKB1 (also known as STK11). Cancers missing LKB1 are often aggressive, rapidly spreading through the body. However, no one knew how LKB1 and focal adhesions were connected.

Now, the Salk team has found the connection and a new target for therapy: a little-known gene called DIXDC1. The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.

When DIXDC1 is “turned on,” half a dozen or so focal adhesions grow large and sticky, anchoring cells to their spot. When DIXDC1 is blocked or inactivated, focal adhesions become small and numerous, resulting in hundreds of small “hands” that pull the cell forward in response to extracellular cues.

That increased tendency to be mobile aids in the escape from, for example, the lungs and allows tumor cells to survive travel through the bloodstream and dock at organs throughout the body.

“The communication between LKB1 and DIXDC1 is responsible for a ‘stay-put’ signal in cells,” says first author and Ph.D. graduate student .

“DIXDC1, which no one knew much about, turns out to be inhibited in cancer and metastasis.”

Tumors, Shaw and collaborators found in the new research, have two ways to turn off this “stay-put” signal. One is by inhibiting DIXDC1 directly. The other way is by deleting LKB1, which then never sends the signal to DIXDC1 to move to the focal adhesions to anchor the cell.

Given this, the scientists wondered if reactivating DIXDC1 could halt a cancer’s metastasis. The team took metastatic cells, which had low levels of DIXDC1, and overexpressed the gene. The addition of DIXDC1 did indeed blunt the ability of these cells to be metastatic in vitro and in vivo.

“It was very, very surprising that this gene would be so powerful,” says Goodwin.

“At the start of this study, we had no idea DIXDC1 would be involved in metastasis. There are dozens of proteins that LKB1 affects; for a single one to control so much of this phenotype was not expected.”

Right now, there is no specific treatment for cancers harboring LKB1 or DIXDC1 alterations, but those with a deletion of either gene would likely see results from cancer drugs that target the focal adhesions, says Shaw.

“The good news is that this finding predicts that patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials,” says Shaw, who is also a member of the Moores Cancer Center and an adjunct professor at the University of California, San Diego.

“By identifying this unexpected connection between DIXDC1 and LKB1 in certain tumors, we have expanded the potential patient population that may be good candidates for these therapies,” adds Goodwin.

Collaborators included Robert U. Svensson of the Salk Institute, Hua Jane Lou and Benjamin E. Turk of Yale University School of Medicine, and Monte M. Winslow of Stanford University.

The work was funded by: grants from the National Cancer Institute, the Howard Hughes Medical Institute, the Samuel Waxman Cancer Research Foundation, and the Leona M. and Harry B. Helmsley Charitable Trust.

My comments

Well done Salk – a double whammy in new research. We wish these young researchers and learned Professors good luck with their great discoveries.

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MAJOR CAUSE OF AGE-RELATED MEMORY LOSS

Study points to possible treatments and confirms distinction between memory loss due to aging and that of Alzheimer’s

From the News Desk of Jeanne Hambleton

Source Newsroom: Columbia University Medical Center

Newswise — NEW YORK, NY — A team of Columbia University Medical Center (CUMC) researchers, led by Nobel laureate Eric R. Kandel, MD, has found that deficiency of a protein called RbAp48 in the hippocampus is a significant contributor to age-related memory loss and that this form of memory loss is reversible.

The study, conducted in postmortem human brain cells and in mice, also offers the strongest causal evidence that age-related memory loss and Alzheimer’s disease are distinct conditions.

The findings were published today in the online edition of Science Translational Medicine.

“Our study provides compelling evidence that age-related memory loss is a syndrome in its own right, apart from Alzheimer’s. In addition to the implications for the study, diagnosis, and treatment of memory disorders, these results have public health consequences,” said Dr. Kandel, who is University Professor & Kavli Professor of Brain Science, co-director of Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute, director of the Kavli Institute for Brain Science, and senior investigator, Howard Hughes Medical Institute, at CUMC.

Dr. Kandel received a share of the 2000 Nobel Prize in Physiology or Medicine for his discoveries related to the molecular basis of memory.
The hippocampus, a brain region that consists of several interconnected subregions, each with a distinct neuron population, plays a vital role in memory.

Studies have shown that Alzheimer’s disease hampers memory by first acting on the entorhinal cortex (EC), a brain region that provides the major input pathways to the hippocampus.

It was initially thought that age-related memory loss is an early manifestation of Alzheimer’s, but mounting evidence suggests that it is a distinct process that affects the dentate gyrus (DG), a subregion of the hippocampus that receives direct input from the EC.

“Until now, however, no one has been able to identify specific molecular defects involved in age-related memory loss in humans,” said co-senior author Scott A. Small, MD, the Boris and Rose Katz Professor of Neurology and Director of the Alzheimer’s Research Center at CUMC.

The current study was designed to look for more direct evidence that age-related memory loss differs from Alzheimer’s disease.

The researchers began by performing microarray (gene expression) analyses of postmortem brain cells from the DG of eight people, ages 33 to 88, all of whom were free of brain disease.

The team also analyzed cells from their EC, which served as controls since that brain structure is unaffected by aging. The analyses identified 17 candidate genes that might be related to aging in the DG. The most significant changes occurred in a gene called RbAp48, whose expression declined steadily with aging across the study subjects.

To determine whether RbAp48 plays an active role in age-related memory loss, the researchers turned to mouse studies.

“The first question was whether RbAp48 is down regulated in aged mice,” said lead author Elias Pavlopoulos, PhD, associate research scientist in neuroscience at CUMC.

“And indeed, that turned out to be the case—there was a reduction of RbAp48 protein in the DG.”

When the researchers genetically inhibited RbAp48 in the brains of healthy young mice, they found the same memory loss as in aged mice, as measured by novel object recognition and water maze memory tests.

When RbAp48 inhibition was turned off, the mice’s memory returned to normal.

The researchers also did functional MRI (fMRI) studies of the mice with inhibited RbAp48 and found a selective effect in the DG, similar to that seen in fMRI studies of aged mice, monkeys, and humans.

This effect of RbAp48 inhibition on the DG was accompanied by defects in molecular mechanisms similar to those found in old mice. The fMRI profile and mechanistic defects of the mice with inhibited RbAp48 returned to normal when the inhibition was turned off.

In another experiment, the researchers used viral gene transfer and increased RbAp48 expression in the DG of aged mice.

“We were astonished that not only did this improve the mice’s performance on the memory tests, but their performance was comparable to that of young mice,” said Dr. Pavlopoulos.

“The fact that we were able to reverse age-related memory loss in mice is very encouraging,” said Dr. Kandel.

“Of course, it is possible that other changes in the DG contribute to this form of memory loss. But at the very least, it shows that this protein is a major factor, and it speaks to the fact that age-related memory loss is due to a functional change in neurons of some sort.
Unlike with Alzheimer’s, there is no significant loss of neurons.”

Finally, the study data suggest that RbAp48 protein mediates its effects, at least in part, through the PKA-CREB1-CBP pathway, which the team had found in earlier studies to be important for age-related memory loss in the mouse.

According to the researchers, RbAp48 and the PKA-CREB1-CBP pathway are valid targets for therapeutic intervention. Agents that enhance this pathway have already been shown to improve age-related hippocampal dysfunction in rodents.

“Whether these compounds will work in humans is not known,” said Dr. Small.

“But the broader point is that to develop effective interventions, you first have to find the right target. Now we have a good target, and with the mouse we have developed, we have a way to screen therapies that might be effective, be they pharmaceuticals, nutraceuticals, or physical and cognitive exercises.”

“There has been a lot of handwringing over the failures of drug trials based on findings from mouse models of Alzheimer’s,” Dr. Small said.

“But this is different. Alzheimer’s does not occur naturally in the mouse. Here, we have caused age-related memory loss in the mouse, and we have shown it to be relevant to human aging.”

The researchers have identified a protein—RbAp48—that, when increased in aged wild-type mice, improves memory back to that of young wild-type mice. In the image, yellow shows the increased RbAp48 in the dentate gyrus.

Image credit: Elias Pavlopoulos, PhD/Columbia University Medical Center
The paper is titled, “A Molecular Mechanism for Age-Related Memory Loss: The Histone Binding Protein RbAp48.”

The other contributors are Sidonie Jones, Stylianos Kosmidis, Maggie Close, Carla Kim, and Olga Kovalerchik, all at CUMC.

The authors declare no financial or other conflicts of interests.
The study was supported by grants from the Howard Hughes Medical Institute, the James S. McDonnell Foundation, the Broitman Foundation, the Henry M. Jackson Foundation for the Advancement of Military Medicine Inc., the McKnight Brain Research Foundation, and the National Institute on Aging (AG034618).

The Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center is a multidisciplinary group that has forged links between researchers and clinicians to uncover the causes of Alzheimer’s, Parkinson’s, and other age-related brain diseases and to discover ways to prevent and cure these diseases.

It has partnered with the Gertrude H. Sergievsky Center at Columbia University Medical Center, which was established by an endowment in 1977 to focus on diseases of the nervous system, and with the Departments of Pathology & Cell Biology and of Neurology to allow the seamless integration of genetic analysis, molecular and cellular studies, and clinical investigation to explore all phases of diseases of the nervous system.

The Department of Neuroscience at Columbia University Medical Center
CUMC’s Department of Neuroscience, whose faculty includes two Nobel laureates, focuses on fundamental aspects of neural circuit development, organization, and function, using cutting-edge biophysical, cellular imaging, and molecular genetic approaches.

Its faculty have backgrounds in a range of fields, including molecular and cell biology, systems neuroscience, theoretical neuroscience, and biophysics.

Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast.

STORING MEMORIES OF RECENT EVENTS
From the News Desk of Jeanne Hambleton

Source: National Institute of Health
Citation – U.S. Department of Health & Human Services

Memories of recent events may be held by a small number of neurons distributed across the brain’s hippocampus, a new study suggests. Understanding how the brain stores memories will yield insights into memory problems that come with normal aging and dementia.

The hippocampus plays a critical role in memory. Much prior memory research has focused on semantic memory—remembering facts, such as famous people and landmarks.

Exposure to a particular face or place becomes linked to a small number of neurons in the hippocampus; these neurons then fire when the memory is recalled. But how the brain forms episodic memories—the memories of events—is not well understood.

Researchers have proposed at least 3 different ways that the brain might encode episodic memories.

In a localist scheme, an individual neuron would code for one memory, and each memory would be linked to the activity of one neuron.

In a fully distributed scheme, each memory would be coded by a pattern of activity across many neurons.

In a sparse distributed scheme, each memory would be coded by the activity of a small proportion of neurons, and each neuron would contribute to a few memories.

A research team led by Dr. Peter N. Steinmetz of the Barrow Neurological Institute in Phoenix, Arizona, and Drs. John T. Wixted and Larry R. Squire, of the University of California, San Diego, investigated how episodic memories were encoded. Their study was funded in part by NIH’s National Institute of Mental Health (NIMH) and National Institute on Deafness and Other Communications Disorders (NIDCD). It appeared online on June 16, 2014, in Proceedings of the National Academy of Sciences.

The scientists were able to explore the mechanisms of memory at the single-neuron level by studying the brains of 9 patients with severe epilepsy who were being treated at the Barrow Neurological Institute.

The patients had depth electrodes implanted into several brain structures, including the hippocampus. These tiny electrodes are used to pinpoint seizure-causing brain regions for possible surgical removal. They can also be used to gather information about how individual brain cells process memories.

The patients were first asked to study 32 target words. They then took a word recognition test with 32 targets from the study list and 32 “foils” that weren’t on the list.

They rated the words on an 8-point scale, from 1 when they were sure it was new to 8 when they were sure it was old. Each of the 64 items on the test was presented only once to ensure that the targets, but not the foils, were represented by an episodic memory.

If the items had been presented many times, the results might simply highlight neurons that respond to long-established semantic memories, rather than to words recently studied.

Together, the patients completed a total of 18 tests. The scientists found that a small percentage of recorded neurons (less than 2%) responded to any one target. Likewise, a small percentage of targets (about 3%) evoked a strong response in any one neuron. This pattern suggests that the human hippocampus uses a sparse distributed code to store episodic memories.

“To really understand how the brain represents memory, we must understand how memory is represented by the fundamental computational units of the brain—single neurons—and their networks,” Steinmetz says.

“Knowing the mechanism of memory storage and retrieval is a critical step in understanding how to better treat the dementing illnesses affecting our growing elderly population.”
—by Harrison Wein, Ph.D.

Reference: Sparse and distributed coding of episodic memory in neurons of the human hippocampus. Proc Natl Acad Sci U S A. 2014 Jun 16. doi: 10.1073/pnas.1408365111. [Epub ahead of print].

Funding: NIH’s National Institute of Mental Health (NIMH) and National Institute on Deafness and Other Communications Disorders (NIDCD); Department of Veterans Affairs, the Barrow Neurological Foundation, and the University of California, San Diego Kavli Institute for Brain and Mind.

FOOD FOR THOUGHT

I received an email with the following interesting thoughts. It does make you value what you have. I just hope by sharing this message I am not in breech of any unknown copyright. This is without payment and in the interest of education.

This is something we should all remember.

A 92-year-old, petite, well-poised and proud man, who is fully dressed each morning by eight o’clock, with his hair fashionably combed and shaved perfectly, even though he is legally blind, moved to a nursing home today.

His wife of 70 years recently passed away, making the move necessary. After many hours of waiting patiently in the lobby of the nursing home, he smiled sweetly when told his room was ready.

As he manoeuvred his walker to the elevator, the nurse provided a visual description of his tiny room, including the eyelet sheets that had been hung on his window.

‘I love it,’ he stated with the enthusiasm of an eight-year-old having just been presented with a new puppy.

‘Mr. Jones, you have not seen the room; just wait..’

‘That does not have anything to do with it,’ he replied.

‘Happiness is something you decide on ahead of time.

‘Whether I like my room or not does not depend on how the furniture is arranged .. it is how I arrange my mind. I already decided to love it.

‘It is a decision I make every morning when I wake up. I have a choice;

‘I can spend the day in bed recounting the difficulty I have with the parts of my body that no longer work, or get out of bed and be thankful for the ones that do.

‘Each day is a gift, and as long as my eyes open, I will focus on the new day and all the happy memories I have stored away.. Just for this time in my life..

‘Old age is like a bank account. You withdraw from what you have put in.

‘So, my advice to you would be to deposit a lot of happiness in the bank account of memories!

‘Thank you for your part in filling my Memory Bank.

‘I am still depositing.

‘Remember the five simple rules to be happy:

1. Free your heart from hatred.

2. Free your mind from worries.

3. Live simply.

4. Give more.

5. Expect less.

‘Please share these thoughts. Have a nice day, unless you already have other plans.’

A great philosphy I think. Wonderful if you have the will power to do this and live happily. Certainly this is food for thought.

If everyone considered other folks and understood how valuable life really is, we might not have all these recent pointless deaths and aircrash said to be through thoughtless actions. Every day I am more convinced that quite often men make war and women make love.
Talk again tomorrow. Jeanne

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THUNDER AND LIGHTING VERY VERY FRIGHTNING ME

I am back again going on about thunder and lightning which it appears is now rumbling on in the Midlands I believe. We heard a little thunder in the distance last night but nothing as worrying as the night before.

Today’s the Daily Mail has some spectacular pictures of lightning over the Isle of Wight and Brighton and London.

This was happening at 12.45am. I wonder if Jamie Russell, the photographer, who captured the Isle of Wight aerial display, had been out in is pyjamas or was he was on an all night vigil waiting for it to happen. Well done Jamie – a great picture.

These photographers are dedicated – come rain or come storm just to get the picture. I know I married a photographer. I am sure he thought so much of his camera he would have taken it to the bedroom with us but it was not my idea of privacy if you know what I mean.

The Daily Mail claims this was the night when lightning strikes were recorded as being 17,000 times over the Isle of Wight. It certainly was very noisey. Paul Harris who wrote the story claimed it was the ‘Daddy of All Storms’ with one of a most ‘breathtaking display in living memory’ with dazzling lightning….. not to mention the horrendous thunder that kept us awake.

It is said we paid the price with the storm for two of the hottest days of the year reaching 90F in one town in Kent.
We cannot say we had not been warned by the weather experts but at 1pm in the morning I was wondering why us? I think some Spanish weather had something to do with it.

But I had this lovely note yesterday from Carole who read my article almost as soon as I published it. Carole said:
“Thanks for all the information Jeanne. I also thought it was the loudest thunder I had ever heard in my life time. My Nanna was so frightened of it that apparently she hid under the kitchen table shaking. I am not frightened by it. My Auntie Doris used to tell me it was her late husband moving God’s furniture around, so I was never frightened.

“I actually like looking at the lightning, find it fascinating, and it usually clears the air, although that does not seemed to have happened today. Apparently we have some more coming tonight (Thursday), so take care Jeanne and keep under those covers. You remember Johnny’s Gun and I will see furniture being moved around. Sending hugs from Caro9le.”

Fortunately last night I think the Home Counties had the storms. I heard it in the distance but not enough to keep me awake or hiding under the covers.

I have not heard anything about the damage the storm might have done – must have missed BBC News or nodded off after a wakeful night.

More news to come tonight. Jeanne

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THUNDER AND LIGHTING

THUNDER AND LIGHTING
VERY VERY FRIGHTNING ME


From the News Desk of Jeanne Hambleton

Having been awakened by one of the loudest thunderstorm I can ever remember, I am curious to know more about it. I heard my thunderstorm rhapsody about 12.45am this morning on the South Coast.

If you have not already had some storms the chances are you will. As a child my mother always told me thunder was Johnny’s gun. Not sure where that might have come from but I did not worry about the noise after that. But last night was something different and Johnny had certainly upgraded his guns. It sounded like some faraway war.

What causes the sound of thunder – it sounded different last night to anything I had heard before.

According to Everyday Mysteries from Science Reference Services of the USA Library of Congress, thunder is caused by the rapid expansion of the air surrounding the path of a lightning bolt. From the clouds to a nearby tree or roof, a lightning bolt takes only a few thousandths of a second to split through the air.

The loud thunder that follows the lightning bolt is commonly said to come from the bolt itself. However, the grumbles and growls we hear in thunderstorms actually come from the rapid expansion of the air surrounding the lightning bolt.

As lightning connects to the ground from the clouds, a second stroke of lightning will return from the ground to the clouds, following the same channel as the first strike. The heat from the electricity of this return stroke raises the temperature of the surrounding air to around 27,000 C° (48,632 F°).

Since the lightning takes so little time to go from point A to point B, the heated air has no time to expand. The heated air is compressed, raising the air from 10 to 100 times the normal atmospheric pressure.

The compressed air explodes outward from the channel, forming a shock wave of compressed particles in every direction. Like an explosion, the rapidly expanding waves of compressed air create a loud, booming burst of noise.

Because electricity follows the shortest route, most lightning bolts are close to vertical. The shock waves nearer to the ground reach your ear first, followed by the crashing of the shock waves from higher up. Vertical lightning is often heard in one long rumble.

However, if a lightning bolt is forked, the sounds change. The shock waves from the different forks of lightning bounce off each other, the low hanging clouds, and nearby hills to create a series of lower, continuous grumbles of thunder.

Thunder Fun Facts:

To judge how close lightning is, count the seconds between the flash and the thunderclap. Each second represents about 300m (984.25ft).

Thunder is not only heard during thunderstorms. It is uncommon, but not rare, to hear thunder when it is snowing.
Lightning does not always create thunder. In April 1885, five lightning bolts struck the Washington Monument during a thunderstorm, yet no thunder was heard.

(http://www.loc.gov/rr/scitech/mysteries/thunder.html)

A government site called Ready.gov/thunderstorms-lightning, warns all these storms are dangerous and lightning remains to be one of the top three storm killers. Thunderstorms injured hundreds and have killed 51 folk in the USA.

This site warns you to unplug electrical equipment including your computer or electric blanket if you are snug in bed. Have an emergency kit – torches, blankets, enough food and water – whatever you think you might need. Get prepared if you think storms are coming.

If you know there is a risk of thunderstorms be sure to secure anything lose outside the house or likely to blow away and cause damaged. Dispose safely of loose rotting trees and dead branches.

If you are out take cover. They say you would be safer in a thickly densed wood rather than wandering about in the storm. If you are on the water get to dry land.

About 10 per cent of all thunderstorms are classified as severe. Lightning is not always associated with heavy rain and can strike as far as 10 miles away before any rainfall.

In the States your chances of being struck by lightning are estimated to be 1 in 600,000 but this could be reduced even further by following any safety precautions.

Lightning

On the Naked Scientists forum one man said some of the thunder sounds like one loud bang or clap and other thunder sounds like a long rolling sound similar to a bowling ball going down an alley. What causes the difference?

Different sounds of thunder

The difference is due to the way in which the lightning jumps from one spot to another. A vertical lightning strike from cloud to earth arrives at the ear as a bang. A cloud-to-cloud strike can sound like rolling thunder because the bang you hear comes along the length of the bolt.

Sound moves at about 300 meters a second or about 1000 feet a second. That is fairly rough, but gives you an idea of the speed. If a lightning bolt is quite long across the clouds, say 1500 meters, then you hear the bang over 1500/300 = 5 seconds. That is the rumble you hear.

Why are there different kinds of thunder?

The reason thunder rumbles is due in part to two things. The first being a lightning bolt is very rarely a straight line and is never equally distant from you at all points.

A lightning bolt on average is 4 miles long, it zigzags all over the place, and can have many limbs that branch out in many different directions separated by many miles.

As a result, the compression waves created by each part of the lightning bolt reach you at different times. The sound wave that has travelled a greater distance will be softer and arrive later than a compression wave created by a part of the lightning bolt that was closer to you.

The second thing is the compression waves (or the thunder) will bounce around and off the clouds, the ground, and other objects nearby.

Much like your voice echoes in a canyon or large auditorium, so do the compression waves generated by lightning. These two things will cause some compressions waves to arrive at the same time which is why the thunder might get loud, then soften a bit, then get loud again (the rumbling we hear).

If you have had a lightning bolt crash down really close to you, the thunder does not rumble as much and sounds more like an explosion. That is because the compression waves did not have a chance to bounce off many things before you heard it. Whereas if you were further away, you would of heard the rumbling.

For questions and more information try

http://www.weatherimagery.com/blog/facts-about-thunder/

I am glad I know that but I still will not sleep soundly when lightning strikes near my house and thunderclaps keep me awake. I cannot say I feel reassured and feel safe in thunderstorms. I will just get further under the blankets and pretend it is not happening. Maybe I will think about Johnny and his gun for reassurance.

See you soon. Jeanne

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