Thursday, August 03, 2006

john hopkins ends in singapore

Nature 442, 493(3 August 2006) | doi:10.1038/442493a; Published online 2 August 2006

Singapore pulls plug on US collaboration

Ichiko Fuyuno

Research ties with Johns Hopkins University cut.

The Singaporean government is known for its generosity in pumping money into international research projects. But it can apparently be ruthless if these projects do not please it. The city-state is shutting down a medical research arm of Johns Hopkins University in Singapore, claiming it has not delivered as planned.

The decision has sent shock waves through other universities and research institutes, some of which are in the initial stages of collaborating with Singapore.

On 20 June, the 60 faculty members and staff of the Division of Biomedical Sciences, Johns Hopkins Medicine in Singapore, were given official notice that as of 1June 2006, the facility was being wound down. The process will take 12 months, with researchers and staff receiving salaries until the facility closes on 31 May 2007.

"We thought it unwise to continue putting money into something that is not working," says Andre Wan, director of the Biomedical Research Council at the Agency for Science, Technology and Research (A*STAR). He claims that Johns Hopkins failed to meet key requirements in its contract.

The split is the first major failure of Singapore's recent push into biomedical research, which includes building the ambitious Biopolis research centre.

Singapore and Johns Hopkins Medicine first got together in 1998, to set up Johns Hopkins Singapore as the university's base for medical research, education and clinical studies in southeast Asia. In 2003, the two parties restructured the organization, making it the first full division of Johns Hopkins Medicine outside its US home in Baltimore, Maryland.

Under the five-year contract begun in February 2004, A*STAR agreed to provide S$75 million (US$47.5 million) to cover salaries, facilities and research equipment. For its part, according to A*STAR, Johns Hopkins aimed to build a centre of immunology, experimental therapeutics and cancer research, to establish a PhD programme and to bring senior researchers with international reputations to Singapore.

Wan alleges that Johns Hopkins has failed to meet 8 out of 13 key performance indicators in the past two years. For example, it agreed to hire at least 12 full-time senior researchers with residence in Singapore by the end of the second year. So far, Wan says it has hired seven, only one of whom fulfils all the requirements.

Gary Stephenson, a spokesman for Johns Hopkins Medicine, declined to comment, saying the university plans to issue a joint statement with A*STAR soon. But on 22 July, a Singaporean newspaper reported a Johns Hopkins official as alleging that Singapore failed to meet its financial and educational obligations under the agreement; A*STAR denies those claims.

The break-up has reminded other universities not to take their collaborative projects with Singapore for granted. For instance, in 2005 Duke University School of Medicine in Durham, North Carolina, established a graduate medical school with the National University of Singapore, as part of a seven-year contract. "The major lesson I'm taking from this is to seek great clarity of how performance in our exciting new venture will be defined," says Sanders Williams, founding dean of the new school.

Wednesday, August 02, 2006

article on lab building refurbishing

http://www.the-scientist.com/2006/8/1/40/1/

"a lot of really ugly old buildings have produced some really good science over the years"

Monday, July 31, 2006

new paper

Antiviral Res. 2006 Jul 7; [Epub ahead of print]
Expression of vector-based small interfering RNA against West Nile virus effectively inhibits virus replication.

Ong SP, Choo BG, Chu JJ, Ng ML.

Flavivirology Laboratory, Department of Microbiology, 5 Science Drive 2, National University of Singapore, 117597 Singapore, Singapore.

RNA interference is one of the effective emerging anti-viral strategies to inhibit virus i nfection in cells. In this study, a small interfering RNA expressing vector (pSilencer-NS5) targeting the NS5 gene of West Nile virus (WNV) was employed to target and destroy WNV transcripts. Real-time PCR revealed drastic reduction in WNV RNA transcripts in pSilencer-NS5-transfected Vero cells. The virus infectious titre was also significantly reduced by 90% as determined by plaque assays. The resulting decrease in virus replication was shown to be specific since both scrambled and nucleotide(s) mismatch siRNA against WNV NS5 gene did not have any effect on WNV productive yields. Furthermore, Western immunoblot analysis on the expression of viral NS5 and envelope (E) proteins showed significant down-regulation on the expression of viral NS5 and envelope (E) proteins in virus-infected cells that were pre-transfected with pSilencer-NS5. These data clearly supported the notion that the expression of vector-based siRNA against WNV NS5 gene is able to exert its silencing effect on WNV-infected cells without inducing cytotoxicity, hence holding promise in therapeutic treatment of this important emerging infectious disease.