DAILY MAIL: DIRTY ICE

Ice in six out of ten restaurants has more bacteria than water from toilets

• McDonald's, Burger King, KFC, Starbucks, Cafe Rouge and Nandos tested
• Ice from branches had higher levels of bacteria in ice than toilet samples
• Experts say it could be down to toilets cleaned more often than ice machines
• Four samples contained enough microbes to be 'hygiene risk'

By Ben Ellery
PUBLISHED: 23:05 GMT, 1 June 2013 | UPDATED: 06:54 GMT, 3 June 2013

Read more: http://www.dailymail.co.uk/news/article-2334533/Ice-restaurants-bacteria-water-toilets.html#ixzz2VI2xvwnu
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OW THEY COMPARED

NANDO'S More bacteria in ice than toilets. Tests on ice water  at 22C: 2,100 organisms. Toilet water: 1,300 organisms.
BURGER KING More bacteria in ice than toilets. Ice bacteria at 37C: 260 organisms. Toilet water: Within drinking water regulations.
McDONALD'S More bacteria in ice than toilets. Ice bacteria at 22C: 1,400 organisms. Toilet water at 37C: 260 organisms.
KFC More bacteria in ice than toilets. Tests on ice water at 22C: 1,100 organisms. Toilet water: Less than 1.
CAFE ROUGE More bacteria in ice than toilets, but not above laboratory’s hygiene guidelines. Toilet water: Less than 1.
STARBUCKS More bacteria in ice than toilets but within laboratory hygiene guidelines. 
PIZZA HUT Bacteria in ice at 22C: 430 organisms. Toilet water exceeded drinking water standards.
PIZZA EXPRESS Bacteria in ice insignificant. Toilet water: 3,200 organisms  at 22C, highest in study.
GOURMET BURGER KITCHEN Bacteria in ice insignificant. Toilet water: Within bacteria count guidelines. 
WAGAMAMA Ice bacteria at both temperatures less than 10 organisms. Toilet water at 37C: 160 organisms.
All per ML

Read more: http://www.dailymail.co.uk/news/article-2334533/Ice-restaurants-bacteria-water-toilets.html#ixzz2VI3dq96q
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DEBRETTS: Dr.Simon FRADD MBBS(Lond.) FRCS(Eng.) GP-UROLOGIST

Dr Simon Fradd

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Dr Simon Fradd's Biography

Forename(s)

Simon Oakley

Sex

Male

Date of Birth

20/4/1950

Foretitle(s)

Dr

Surname

FRADD

Style

Dr Simon Fradd

Recreations

DIY, gardening, skiing, gliding

Dr Simon Fradd's Professional Career

Career

house surgn Westminster Med Sch 1977; SHO: in paediatrics Queen Mary's Roehampton 1978, in neonatology Whittington Hosp London 1979, in A/E then orthopaedics St George's Tooting 1980-81; registrar: in surgery Burton Gen Hosp Burton-on-Trent 1981-84, in urology Univ Hosp of Wales Cardiff 1984-85; GP trainee: Burton-on-Trent 1985-86, under Dr Saunders Nottingham 1986-87, Castle Donington Leics 1987; GP princ Saunders & Fradd Nottingham 1988-; chm: Hosp Doctors' Assoc 1979-82, Negotiators' Hosp Jr Staff Ctee 1986-87 (dep chm 1984-86), Jr Membs' Forum BMA 1990, Doctor Patient Partnership 1997-; dep chm Gen Practitioners Ctee of BMA 1997-; memb Med Practices Ctee 1989-93, Gen Med Servs Ctee negotiator 1993-; memb GMC 1989-; Freeman City of London 1976, Liveryman Worshipful Co of Needlemakers 1976, Liveryman Worshipful Soc of Apothecaries 1993; Hon FAMGP 1998, Hon MRCGP 2000, FRCS

Dr Simon Fradd's Publications

Books and Publications

Hospital Doctors' Association Guide to Your Rights (jtly, 1981), Making Sense of Partnerships (jtly, 1994), Nottingham Non-Fundholder Project, Members Reference Book RCGP (1995)

View the full entry on Debrett's People of Today Online

DAILY MAIL : Dr SIMON FRADD MBBS(Lond.) FRCS (Eng.) millionaire GP-urologist

GP who laughed all the way to the bank: He's the millionaire doctors' leader who destroyed out-of-hours care - while securing a bumper pay deal for his colleagues. Ashamed? No. He thinks it's a 'bit of a laugh'

By Tom Rawstorne

57 shares

69

Britain's out-of-hours health care is in crisis — and the Mail has launched a major investigative series to highlight the true, shocking scale of the problem. Yesterday, a consultant at a major A&E unit revealed the devastating knock-on effect it's having on emergency care. Today, we reveal the inside story of how GPs got a massive pay rise while opting out of caring for their patients round the clock...
With a bejewelled chain of office where his stethoscope once hung and an ermine robe to boot, Dr Simon Fradd has every reason to look as pleased as punch. This is the man who, in 2004, helped to negotiate arguably the most generous public sector pay deal in modern British history.
Representing GPs, he and his colleagues at the British Medical Association not only secured what turned out to be a 50 per cent pay rise for family doctors, thanks to new bonuses — but also managed to ditch their obligation to provide care in the evenings and at weekends.
For more than half a century that round-the-clock responsibility had been the bedrock of GPs' contract of care with patients.

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Le Monde Diplomatique: Offshore care of the old.

Diplomatic Channels

New challenges of world’s ageing population

Germany outsources elder care

It costs too much to take care of the western world’s old and frail in their own homes or care homes. German is beginning to export the work to low-wage service economies.

by Heike Haarhoff

Legionnaires' Disease secrecy at VA PITTSBURGH HOSPITAL

Department of Veterans Affairs

Office of Inspector General

Office of Healthcare Inspections

Report No. 13-00994-180

Healthcare Inspection

Legionnaires’ Disease at the VA

Pittsburgh Healthcare System

Pittsburgh, Pennsylvania

April 23, 2013

Washington, DC 20420

To Report Suspected Wrongdoing

in VA Programs and Operations:

Telephone: 1-800-488-8244

E-Mail:

vaoighotline@va.gov

Web site:

www.va.gov/oig

Legionnaires’ Disease at the VA Pittsbur

gh Healthcare System, Pittsburgh, PA

Executive Summary

The VA Office of Inspector General (OIG) Offi

ce of Healthcare Inspections conducted a

review of Legionnaires’ disease (LD) at t

he VA Pittsburgh Healthcare System (VAPHS)

at the request of the VA Secr

etary, Senator Robert P. Ca

sey, Jr., Congressmen Michael

F.

Doyle and Tim Murphy, and the Chai

rmen and Ranking Mem

bers of the House

Committee on Veterans’ Affairs

and the Senate Committee on Ve

terans’ Affairs. They

asked that OIG evaluate whether VAPHS wa

s adequately maintaining its system for

preventing LD. Additional ques

tions regarding mitigation of

risk at other VA hospitals

will be addressed in a subsequent report.

VAPHS has a long history of comprehensive

mitigation efforts for LD. Following the

recent outbreak, VAPHS instituted numerous additional measur

es. However, we found

that while employing copper-silver ionizati

on systems during 2011-12, VAPHS allowed

ion levels inadequate for

Legionella

control to persist. There was a lack of

documentation of system monitoring for subst

antial periods of time and inconsistent

communication and coordination between the

Infection Prevention Team and Facility

Management Service staff.

We also found that VAPHS di

d not conduct routine flushi

ng of hot water faucets and

showers, especially in ar

eas that are infrequently us

ed, as recommended by the

copper-silver ionization system manufactu

rer. We found that VAPHS conducted

environmental surveillance in accordance wit

h Veterans Health Administration (VHA)

Directive 2008-010. However,

VAPHS responded to positive cult

ures by flushing distal

outlets with hot water at normal operati

ng temperatures, a corrective action not

consistent with VHA or Centers for Diseas

e Control and Prevention guidance. In

addition, VAPHS did not test all health

care-associated pneumonia patients for

Legionella

as specified by VHA guidance for tr

ansplant centers with a history of

healthcare-associated LD.

We recommended that the VAPHS Director ensur

e that any disinfectant system in use

for

Legionella

prevention is monitored and ma

intained in accordance with

manufacturer’s instructions, that hot-wat

er faucets and showerheads are routinely

flushed, and that close c

oordination between the Infe

ction Prevention Team and

Facilities Management Service staff occurs

. Additionally we

recommended that the

VAPHS Director ensure that wh

en environmental cultures ar

e positive, actions taken

comply with VHA guidelines, an

d that all healthcare-associ

ated pneumonia patients are

tested for

Legionella

infection.

BMJ:GENOME SEQUENCING

Head to Head

Should we sequence everyone’s genome? Yes

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f3133 (Published 21 May 2013)

Cite this as: BMJ 2013;346:f3133

1. John Burn, professor

Author Affiliations

1. john.burn@newcastle.ac.uk

As technological prowess soars and costs plummet, is the era of personalised medicine now in sight? John Burn says sequencing everyone’s genome would give us unparalleled knowledge to prevent, diagnose, and treat disease, but Frances Flinter (doi:10.1136/bmj.f3132) thinks there are serious ethical implications

We should all have our genomes sequenced. In 1986 our 5 year old son planted a conker in our back yard. He explained that he wanted a tree house so needed a tree. The tree is now ready to receive boarders, though they will be from our family’s next generation. The Human Genome Project began at about the same time with similar high aspirations: to deliver personalised medicine to generations to come.

That time is now upon us. The cost of gene sequencing has fallen 10 000-fold in a decade, with another drop by an order of magnitude expected soon. Setting aside the considerable but surmountable challenges associated with large segments being duplicated or deleted and stretches of hard to sequence repeats, we can have a whole genome for the price of a family package holiday. Even now, bulk sequencing all 20 000 “genes,” the exome, costs less than £500 (€590; $770).

The Human Genome Project depended on British discovery, particularly the work of the Wellcome Trust’s Sanger Institute. No one can match our capacity to do “genetic medicine” in a coordinated healthcare system at scale. This is why the UK government has committed £100m to pump prime sequencing of 100 000 whole genomes in the NHS. Only by analysing sequence data and phenotypes across large patient populations will we understand which bits of genetic information are clinically relevant. We can and should lead the world in showing how to put genetic knowledge into patient care safely and effectively.

Responsible use

Genetic predisposition plays a central role in most common diseases. It is the primary cause of most of the rare diseases that collectively afflict 1 in 17 people.1 Clinically relevant discoveries are entering practice at a rate of more than 30 a month.

And the provisos? First do no harm. Our capacity for interpretation is still rudimentary so we must have explicit consent to retain sequence data linked to patients’ records. Our population trusts the health service to deliver healthcare to all in need, regardless of their genetic predispositions. We must keep that principle safe along with the sequence data. That doesn’t preclude partnership with the pharmaceutical and biotechnology industries: we need them to expand the exciting list of drugs that can target genetic subgroups and give us the gadgets and biomarker algorithms to find them.

As we leave the high ground of “single gene disease,” such as hereditary cancers and cardiomyopathies, we risk drowning in data and doing harm. Offering volunteers at risk of monogenic disorders an effective service in return for them allowing their genomes to be pooled and data mined is straightforward. Systematic gathering of genomic information where there has been no request, and any sequence variation discovered lacks clinical use, is more challenging if consent and follow-up counselling are to be effective.

Each one of us carries, perhaps, three million sequence variants, of which about 400 contribute to disease predisposition,2 and one or two would cause a severe recessive disease if both partners pass them to a child. The bioinformaticians need to know it all to develop robust diagnostic algorithms.

But patients do not. We must not dump heaps of molecular uncertainty on patients, families, and their carers. In Nijmegen, the Netherlands, teams of geneticists try to interpret exomes of patients provided by clinicians, passing on (with explicit consent) only information about variants of known relevance plus “incidental” findings of obvious importance (H G Brunner, personal communication).

Personalised treatment

Genomics is not just about rare syndromes and predisposition to disease. It underpins huge variation in our capacity to metabolise drugs, often leading to serious adverse events, but this is ignored. At the moment everybody gets the same size shoes and they are asked to hobble back next week if they don’t fit. We have known for decades many of the simple genetic variants responsible for such adverse events. We write more than half a million prescriptions for warfarin each year, knowing that three genetic variants can help quickly to reach the individual dose, cutting attendances and adverse events; yet still we just guess.3 Widespread sequencing linked to outcomes will expand such knowledge considerably.

I remain sceptical of an early transition to providing our genome as part of our electronic medical records. The sequences we can provide now are not sufficiently complete, and safe storage and access present challenges.

When it costs only £100 we can run the sequencers more than once, extracting necessary information and discarding the rest. In some situations we will be able to reduce the question to a genetic test at the point of care.

I am part of a team that’s been working for five years on using nanowires to analyse nucleic acids.4 We are about to test disposable cassettes that will extract, amplify, and perform specific tests such as drug sensitivity in under 15 minutes for under £20. The next step will be to provide whole genomes. Others are also innovating in this field. Whoever wins the race, the strong probability is a mixed economy of stored whole genomes, disposable sequencing in hospitals, and cheap, fast genotype panels in some frontline care settings. The net result will be accurately targeted diagnosis, treatment, and prevention.

Genomics extends beyond identifying predisposition to disease. Linking whole genome sequencing to clinical outcomes will influence drug discovery and development—for example, the BRAF gene inhibitor vemurafenib to treat melanoma was developed only a decade after the cancer genome project identified the target.5 And the tools developed from human genomics will transform another battlefront—routine high speed sequencing of pathogens will expose their weaknesses within hours, revolutionising response to epidemics worldwide.

Meanwhile “point of care” technology will allow drug resistance of infective agents causing diseases such as malaria to be studied in real time in the swamp. Whole genome sequencing is a technical, clinical, and societal challenge. But as Goethe said, “Whatever you do, or dream you can, begin it. Boldness has genius and power and magic in it.”

Notes

Cite this as: BMJ 2013;346:f3133

Footnotes

• Competing interests: I have read and understood the BMJ Group policy on declaration of interests and declare the following interests: I am chair of the British Society for Genetic Medicine and genetics lead for the National Institute of Health Research. I am a shareholder and director of QuantuMDx Group, which is involved in nanowire based genotyping and sequencing.
• Read Frances Flinter’s side of the debate at doi:10.1136/bmj.f3132.
• Provenance and peer review: Commissioned; not externally peer reviewed.

References

1. ↵
   Chief Medical Officer. The 2009 annual report of the chief medical officer. Department of Health, 2010.
2. ↵
   Xue Y, Chen Y, Ayub Q, Huang N, Ball EV, Mort M, et al. Deleterious and disease allele prevalence in healthy individuals: insights from current predictions, mutation databases, and population-scale resequencing. Am J Hum Genet2012;91:1022-32.

   CrossRefMedline
3. ↵
   Anderson JL, Horne BD, Stevens SM, Woller SC, Samuelson KM, Mansfield JW, et al. A randomized and clinical effectiveness trial comparing two pharmacogenetic algorithms and standard care for individualising warfarin dosing (CoumaGen II) Circulation2012;125:1997-2005.

   Abstract/FREE Full Text
4. ↵
   Cui Y, Wei QQ, Park HK, Lieber CM. Nanowire nanosensors for highly sensitive and selective detection of biological and chemical species. Science2001;293:1289-92.

   Abstract/FREE Full Text
5. ↵
   Sosman JA, Kim KB, Schuchter L, Gonzalez R, Pavlick AC, Weber JS, et al. Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib. N Engl J Med2012;366:707-14.

   CrossRefMedlineWeb of Science

MULTIPLE MYELOMA: DANA-FARBER CANCER INSTITUTE

• 
• 

• 
  

New Strategies in the Treatment of Multiple Myeloma

1. Nikhil C. Munshi1,* and
2. Kenneth C. Anderson2

+ Author Affiliations

1. ¹Medical Oncology/Hematologic Neoplasia, Dana-Farber
2. ²Medical Oncology, Dana-Farber Cancer Institute

1. ↵* Corresponding Author:
   Nikhil C. Munshi, Medical Oncology/Hematologic Neoplasia, Dana-Farber, 450 Brookline Ave, Mayer 230, Boston, MA, 02215, United States Nikhil_Munshi@dfci.harvard.edu

Abstract

Multiple myeloma (MM) is the second most common hematologic malignancy affecting terminally differentiated plasma cells. Although high-dose chemotherapy and autologous stem cell transplantation improved survival in younger patients, the natural history of MM has been changed with the availability of five new agents approved in last 10 years (thalidomide, bortezomib, lenalidomide, liposomal doxorubicin and carfilzomib). Despite this significant improvement in overall outcome, MM remains incurable in majority of patients prompting continued search for additional therapeutic options. Extensive molecular and genomic characterization of MM cells in its bone marrow milieu, which affects myeloma cell growth and survival, has provided number of novel drugable targets and pathways. Perturbation of protein catabolism at multiple levels has become an important target in MM. Similarly with improvements in monoclonal antibody generation and vaccine development along with identification of number of cell surface and cellular targets have led to development of various strategies including antibodies and antibody-drug conjugates which are under investigation both preclinically as well as in early clinical studies. We propose that eventually, molecularly-informed multi-agent combination therapies will be required to eliminate the MM cell clone for a long-term disease control.

• Received August 4, 2012.
• Revision received February 18, 2013.
• Accepted February 26, 2013.

• Copyright © 2013, American Association for Cancer Research.