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1.
Hong Kong Med J ; 23(2): 140-9, 2017 Apr.
Article in English | MEDLINE | ID: mdl-28232642

ABSTRACT

INTRODUCTION: Apart from individual small-scale outbreaks, infections with vancomycin-resistant enterococci are uncommon in Hong Kong. A major outbreak of vancomycin-resistant enterococci, however, occurred at a large tertiary hospital in 2013. We describe the successful control of this outbreak and share the lessons learned. METHODS: In 2013, there was an abnormal increase in the incidence of vancomycin-resistant enterococci carriage compared with baseline in multiple clinical departments at Queen Elizabeth Hospital. A multipronged approach was adopted that included a 10-week hospital-wide active screening programme, which aimed to identify and isolate hidden vancomycin-resistant enterococci carriers among all in-patients. The identified carriers were completely segregated in designated wards where applicable. Other critical infection control measures included directly observed hand hygiene and environmental hygiene. A transparent and open disclosure approach was adopted throughout the outbreak. RESULTS: The infection control measures were successfully implemented. The active screening of vancomycin-resistant enterococci was conducted between 30 September and 10 November 2013. A total of 7053 rectal swabs were collected from patients in 46 hospital wards from 11 departments. The overall carriage rate of vancomycin-resistant enterococci was 2.8% (201/7053). Pulsed-field gel electrophoresis showed a predominant outbreak clone. We curbed the outbreak and kept the colonisation of vancomycin-resistant enterococci among patients at a pre-upsurge low level. CONCLUSIONS: We report the largest cohesive effort to control spread of vancomycin-resistant enterococci in Hong Kong. Coupled with other infection control measures, we successfully controlled vancomycin-resistant enterococci to the pre-outbreak level. We have demonstrated that the monumental tasks can be achieved with meticulous planning, and thorough communication and understanding between all stakeholders.


Subject(s)
Cross Infection/prevention & control , Gram-Positive Bacterial Infections/prevention & control , Infection Control/methods , Vancomycin Resistance , Vancomycin-Resistant Enterococci/isolation & purification , Adult , Aged , Anti-Bacterial Agents/pharmacology , Cross Infection/microbiology , Disease Outbreaks , Electrophoresis, Gel, Pulsed-Field , Feces/microbiology , Female , Gram-Positive Bacterial Infections/microbiology , Hand Disinfection , Hong Kong/epidemiology , Humans , Length of Stay , Logistic Models , Male , Middle Aged , Patient Isolation , Tertiary Care Centers
2.
Oncogene ; 35(50): 6378-6388, 2016 12 15.
Article in English | MEDLINE | ID: mdl-27132508

ABSTRACT

Cancer cells are known to execute reprogramed metabolism of glucose, amino acids and lipids. Here, we report a significant role of cholesterol metabolism in cancer metastasis. By using label-free Raman spectromicroscopy, we found an aberrant accumulation of cholesteryl ester in human pancreatic cancer specimens and cell lines, mediated by acyl-CoA cholesterol acyltransferase-1 (ACAT-1) enzyme. Expression of ACAT-1 showed a correlation with poor patient survival. Abrogation of cholesterol esterification, either by an ACAT-1 inhibitor or by shRNA knockdown, significantly suppressed tumor growth and metastasis in an orthotopic mouse model of pancreatic cancer. Mechanically, ACAT-1 inhibition increased intracellular free cholesterol level, which was associated with elevated endoplasmic reticulum stress and caused apoptosis. Collectively, our results demonstrate a new strategy for treating metastatic pancreatic cancer by inhibiting cholesterol esterification.


Subject(s)
Cholesterol Esters/metabolism , Pancreatic Neoplasms/pathology , Acetyl-CoA C-Acetyltransferase/antagonists & inhibitors , Acetyl-CoA C-Acetyltransferase/physiology , Animals , Apoptosis , Cell Line, Tumor , Cell Proliferation , Endoplasmic Reticulum Stress , Esterification , Humans , Male , Mice , Neoplasm Metastasis , PTEN Phosphohydrolase/physiology , Pancreatic Neoplasms/metabolism
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