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7 results on '"Lok, Si"'

1. Nonalbuminuric Diabetic Kidney Disease and Risk of All-Cause Mortality and Cardiovascular and Kidney Outcomes in Type 2 Diabetes: Findings From the Hong Kong Diabetes Biobank

Author

Jin, Qiao, Luk, Andrea O., Lau, Eric S.H., Tam, Claudia H.T., Ozaki, Risa, Lim, Cadmon K.P., Wu, Hongjiang, Jiang, Guozhi, Chow, Elaine Y.K., Ng, Jack K., Kong, Alice P.S., Fan, Baoqi, Lee, Ka Fai, Siu, Shing Chung, Hui, Grace, Tsang, Chiu Chi, Lau, Kam Piu, Leung, Jenny Y., Tsang, Man-Wo, Kam, Grace, Lau, Ip Tim, Li, June K., Yeung, Vincent T., Lau, Eric S., Lo, Stanley, Fung, Samuel, Cheng, Yuk Lun, Chow, Chun Chung, Huang, Yu, Lan, Hui-yao, Szeto, Cheuk Chun, So, Wing Yee, Chan, Juliana C.N., Ma, R.C.W., Poo Lim, Cadmon King, Cheung, Elaine, Li, Kam-Yin, Yeung, Vincent T.F., Tsui, Stephen Kwok-Wing, Yu, Weichuan, Tomlinson, Brian, Lok, Si, Chan, Ting Fung, Yip, Kevin Yuk-lap, Fan, Xiaodan, Tang, Nelson L.S., Tian, Xiaoyu, Mai, Shi, Xie, Fei, Zhang, Sen, Yu, Pu, Wang, Meng, Lee, Heung Man, Ng, Alex C.W., Cheung, Grace, Yeung, Ming Wai, Cheung, Kitty K.T., Wong, Rebecca Y.M., Cheong, So Hon, Chan, Katie K.H., Law, Chin-San, Yuen Lock, Anthea Ka, Ying Tsang, Ingrid Kwok, Pun Chan, Susanna, Chan, Yin Wah, Chiu, Cherry, Hung, Chi Sang, Ho, Cheuk Wah, Yee Ng, Ivy Hoi, Chun Fok, Juliana Mun, Lee, Ka Wah, Candy Leung, Hoi Sze, Chan, Hui Ming, Wat, Winnie, Lau, Tracy, Law, Rebecca, Chan, Ryan, Lau, Candice, Tsang, Pearl, Chan, Vince, Ho, Lap Ying, Wong, Eva, Chan, Josephine, Lam, Sau Fung, Pang, Jessy, Lee, Yee Mui, Hong Kong Diabetes Biobank Study, Group, Jin, Qiao, Luk, Andrea O., Lau, Eric S.H., Tam, Claudia H.T., Ozaki, Risa, Lim, Cadmon K.P., Wu, Hongjiang, Jiang, Guozhi, Chow, Elaine Y.K., Ng, Jack K., Kong, Alice P.S., Fan, Baoqi, Lee, Ka Fai, Siu, Shing Chung, Hui, Grace, Tsang, Chiu Chi, Lau, Kam Piu, Leung, Jenny Y., Tsang, Man-Wo, Kam, Grace, Lau, Ip Tim, Li, June K., Yeung, Vincent T., Lau, Eric S., Lo, Stanley, Fung, Samuel, Cheng, Yuk Lun, Chow, Chun Chung, Huang, Yu, Lan, Hui-yao, Szeto, Cheuk Chun, So, Wing Yee, Chan, Juliana C.N., Ma, R.C.W., Poo Lim, Cadmon King, Cheung, Elaine, Li, Kam-Yin, Yeung, Vincent T.F., Tsui, Stephen Kwok-Wing, Yu, Weichuan, Tomlinson, Brian, Lok, Si, Chan, Ting Fung, Yip, Kevin Yuk-lap, Fan, Xiaodan, Tang, Nelson L.S., Tian, Xiaoyu, Mai, Shi, Xie, Fei, Zhang, Sen, Yu, Pu, Wang, Meng, Lee, Heung Man, Ng, Alex C.W., Cheung, Grace, Yeung, Ming Wai, Cheung, Kitty K.T., Wong, Rebecca Y.M., Cheong, So Hon, Chan, Katie K.H., Law, Chin-San, Yuen Lock, Anthea Ka, Ying Tsang, Ingrid Kwok, Pun Chan, Susanna, Chan, Yin Wah, Chiu, Cherry, Hung, Chi Sang, Ho, Cheuk Wah, Yee Ng, Ivy Hoi, Chun Fok, Juliana Mun, Lee, Ka Wah, Candy Leung, Hoi Sze, Chan, Hui Ming, Wat, Winnie, Lau, Tracy, Law, Rebecca, Chan, Ryan, Lau, Candice, Tsang, Pearl, Chan, Vince, Ho, Lap Ying, Wong, Eva, Chan, Josephine, Lam, Sau Fung, Pang, Jessy, Lee, Yee Mui, and Hong Kong Diabetes Biobank Study, Group

Abstract

Rationale & Objective: Nonalbuminuric diabetic kidney disease (DKD) has become the prevailing DKD phenotype. We compared the risks of adverse outcomes among patients with this phenotype compared with other DKD phenotypes. Study Design: Multicenter prospective cohort study. Settings & Participants: 19,025 Chinese adults with type 2 diabetes enrolled in the Hong Kong Diabetes Biobank. Exposures: DKD phenotypes defined by baseline estimated glomerular filtration rate (eGFR) and albuminuria: no DKD (no decreased eGFR or albuminuria), albuminuria without decreased eGFR, decreased eGFR without albuminuria, and albuminuria with decreased eGFR. Outcomes: All-cause mortality, cardiovascular disease (CVD) events, hospitalization for heart failure (HF), and chronic kidney disease (CKD) progression (incident kidney failure or sustained eGFR reduction ≥40%). Analytical Approach: Multivariable Cox proportional or cause-specific hazards models to estimate the relative risks of death, CVD, hospitalization for HF, and CKD progression. Multiple imputation was used for missing covariates. Results: Mean participant age was 61.1 years, 58.3% were male, and mean diabetes duration was 11.1 years. During 54,260 person-years of follow-up, 438 deaths, 1,076 CVD events, 298 hospitalizations for HF, and 1,161 episodes of CKD progression occurred. Compared with the no-DKD subgroup, the subgroup with decreased eGFR without albuminuria had higher risks of all-cause mortality (hazard ratio [HR], 1.59 [95% CI, 1.04-2.44]), hospitalization for HF (HR, 3.08 [95% CI, 1.82-5.21]), and CKD progression (HR, 2.37 [95% CI, 1.63-3.43]), but the risk of CVD was not significantly greater (HR, 1.14 [95% CI, 0.88-1.48]). The risks of death, CVD, hospitalization for HF, and CKD progression were higher in the setting of albuminuria with or without decreased eGFR. A sensitivity analysis that excluded participants with baseline eGFR <30 mL/min/1.73 m2 yielded similar findings. Limitations: Potential misc

Published
2022

2. Mutations Enabling Displacement of Tryptophan by 4-Fluorotryptophan as a Canonical Amino Acid of the Genetic Code

Author

Yu, Allen Chi Shing, Yim, Aldrin Kay Yuen, Mat, Wai Kin, Tong, Amy Hin Yan, Lok, Si, Xue, Hong, Tsui, Stephen Kwok Wing, Wong, Jeffrey Tze Fei, Chan, Ting Fung, Yu, Allen Chi Shing, Yim, Aldrin Kay Yuen, Mat, Wai Kin, Tong, Amy Hin Yan, Lok, Si, Xue, Hong, Tsui, Stephen Kwok Wing, Wong, Jeffrey Tze Fei, and Chan, Ting Fung

Abstract

The 20 canonical amino acids of the genetic code have been invariant over 3 billion years of biological evolution. Although various aminoacyl-tRNA synthetases can charge their cognate tRNAs with amino acid analogs, there has been no known displacement of any canonical amino acid from the code. Experimental departure from this universal protein alphabet comprising the canonical amino acids was first achieved in the mutants of the Bacillus subtilis QB928 strain, which after serial selection and mutagenesis led to the HR23 strain that could use 4-fluorotryptophan (4FTrp) but not canonical tryptophan (Trp) for propagation. To gain insight into this displacement of Trp from the genetic code by 4FTrp, genome sequencing was performed on LC33 (a precursor strain of HR23), HR23, and TR7 (a revertant of HR23 that regained the capacity to propagate on Trp). Compared with QB928, the negative regulator mtrB of Trp transport was found to be knocked out in LC33, HR23, and TR7, and sigma factor sigB was mutated in HR23 and TR7. Moreover, rpoBC encoding RNA polymerase subunits were mutated in three independent isolates of TR7 relative to HR23. Increased expression of sigB was also observed in HR23 and in TR7 growing under 4FTrp. These findings indicated that stabilization of the genetic code can be provided by just a small number of analog-sensitive proteins, forming an oligogenic barrier that safeguards the canonical amino acids throughout biological evolution.

Published
2014

3. Mutations Enabling Displacement of Tryptophan by 4-Fluorotryptophan as a Canonical Amino Acid of the Genetic Code

Author

Yu, Allen Chi Shing, Yim, Aldrin Kay Yuen, Mat, Wai Kin, Tong, Amy Hin Yan, Lok, Si, Xue, Hong, Tsui, Stephen Kwok Wing, Wong, Jeffrey Tze Fei, Chan, Ting Fung, Yu, Allen Chi Shing, Yim, Aldrin Kay Yuen, Mat, Wai Kin, Tong, Amy Hin Yan, Lok, Si, Xue, Hong, Tsui, Stephen Kwok Wing, Wong, Jeffrey Tze Fei, and Chan, Ting Fung

Abstract

The 20 canonical amino acids of the genetic code have been invariant over 3 billion years of biological evolution. Although various aminoacyl-tRNA synthetases can charge their cognate tRNAs with amino acid analogs, there has been no known displacement of any canonical amino acid from the code. Experimental departure from this universal protein alphabet comprising the canonical amino acids was first achieved in the mutants of the Bacillus subtilis QB928 strain, which after serial selection and mutagenesis led to the HR23 strain that could use 4-fluorotryptophan (4FTrp) but not canonical tryptophan (Trp) for propagation. To gain insight into this displacement of Trp from the genetic code by 4FTrp, genome sequencing was performed on LC33 (a precursor strain of HR23), HR23, and TR7 (a revertant of HR23 that regained the capacity to propagate on Trp). Compared with QB928, the negative regulator mtrB of Trp transport was found to be knocked out in LC33, HR23, and TR7, and sigma factor sigB was mutated in HR23 and TR7. Moreover, rpoBC encoding RNA polymerase subunits were mutated in three independent isolates of TR7 relative to HR23. Increased expression of sigB was also observed in HR23 and in TR7 growing under 4FTrp. These findings indicated that stabilization of the genetic code can be provided by just a small number of analog-sensitive proteins, forming an oligogenic barrier that safeguards the canonical amino acids throughout biological evolution.

Published
2014

4. Whole-genome bisulfite sequencing of multiple individuals reveals complementary roles of promoter and gene body methylation in transcriptional regulation

Author

Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, Yip, Kevin Y., Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, and Yip, Kevin Y.

Published
2014

5. Whole-genome bisulfite sequencing of multiple individuals reveals complementary roles of promoter and gene body methylation in transcriptional regulation

Author

Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, Yip, Kevin Y., Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, and Yip, Kevin Y.

Published
2014

6. Whole-genome bisulfite sequencing of multiple individuals reveals complementary roles of promoter and gene body methylation in transcriptional regulation

Author

Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, Yip, Kevin Y., Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, and Yip, Kevin Y.

Published
2014

7. Whole-genome bisulfite sequencing of multiple individuals reveals complementary roles of promoter and gene body methylation in transcriptional regulation

Author

Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, Yip, Kevin Y., Lou, Shaoke, Lee, Heung-Man, Qin, Hao, Li, Jing-Woei, Gao, Zhibo, Liu, Xin, Chan, Landon L., Lam, Vincent K. L., So, Wing-Yee, Wang, Ying, Lok, Si, Wang, Jun, Ma, Ronald C. W., Tsui, Stephen Kwok-Wing, Chan, Juliana C. N., Chan, Ting-Fung, and Yip, Kevin Y.

Published
2014

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