Yu Min Ho

National Cancer Centre Singapore

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Ann S. G. Lee

National University of Singapore

Yong-Jiang Sun

Tan Tock Seng Hospital

Sin-Yew Wong

Singapore General Hospital

Lili Yan

China National Petroleum Corporation (China)

J S Lin

Maxwell Technologies (United States)

Siti Noor Khadijah Othman

Tan Tock Seng Hospital

Peter A. Rice

University of Massachusetts Chan Medical School

Sin Yew Wong

University College Dublin

Cooperative Institutions

Tan Tock Seng Hospital

National University of Singapore

Singapore General Hospital

National Centre for Infectious Diseases

Gleneagles Hospital

National Cancer Centre Japan

Boston University

Harvard University

National Skin Centre

Bioprocessing Technology Institute

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Contribution of dfrA and inhA Mutations to the Detection of Isoniazid-Resistant Mycobacterium tuberculosis Isolates

Antimicrobial Agents and Chemotherapy (2009)

Yu Min Ho Yong-Jiang Sun Sin-Yew Wong Ann S. G. Lee

Screening of 127 isoniazid (INH)-resistant Mycobacterium tuberculosis isolates from Singapore for mutations within the dfrA and inhA genes revealed mutations in 0 and 5 (3.9%) isolates respectively, implying that mutations in dfrA do not contribute to the detection of INH-resistant M. tuberculosis and that mutations within inhA are rare. Thirty-seven (29%) of the 127 isolates had no mutations in any of the genes implicated in INH resistance (katG, kasA, and ndh; inhA and ahpC promoters), suggesting that there are new INH targets yet to be discovered.

INHA

10.1128/aac.00433-09

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Novel Mutations within the embB Gene in Ethambutol-Susceptible Clinical Isolates of Mycobacterium tuberculosis

Antimicrobial Agents and Chemotherapy (2004)

Ann S. G. Lee Siti Noor Khadijah Othman Yu Min Ho Sin Yew Wong

Genetic analysis of the embB gene revealed mutations in 17 (68%) of 25 ethambutol (EMB) resistant isolates (M306I, M306V, M306L, Q497R) but also in 4 (20%) of 20 EMB-susceptible isolates of Mycobacterium tuberculosis, namely, an ATG-->ATM substitution resulting in M306I, G406N, and the novel alterations M423I and A659T.

Pyrazinamide

10.1128/aac.48.11.4447-4449.2004

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Early complement components enhance neutralization of Chlamydia trachomatis infectivity by human sera

Infection and Immunity (1992)

J S Lin Lili Yan Yu Min Ho Peter A. Rice

Immunoglobulin G in human serum neutralizes chlamydial infectivity in vitro. Complement-intact, C5-depleted, and C8-depleted human serum all have significantly more neutralizing activity than serum heated to inactivate early components of complement. Cobra venom factor, an analog of human C3b, enhances neutralization of antichlamydial immunoglobulin G in the absence of early complement components.

Infectivity

Immunoglobulin M

10.1128/iai.60.6.2547-2550.1992

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Citations (20)