7 results on '"Seok-Hwee Koo"'
Search Results
2. A pilot study to examine the association between human gut microbiota and the host's central obesity
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Magdalin Cheong, Collins Wenhan Chu, Seok Hwee Koo, Edmund J.D. Lee, Ngai Moh Law, Joan Joo Ching Khoo, Gaik Hong Soon, Kwong Ming Fock, John Chen Hsiang, Tiing Leong Ang, Eliza Xin Pei Ho, and Paola Florez de Sessions
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obesity ,Rikenellaceae ,Saturated fat ,Physiology ,RC799-869 ,metabolic syndrome ,03 medical and health sciences ,0302 clinical medicine ,Insulin resistance ,Diabetes mellitus ,microbiota ,Medicine ,Microbiome ,Hepatology ,biology ,Adiponectin ,business.industry ,Gastroenterology ,Original Articles ,Diseases of the digestive system. Gastroenterology ,continental population groups ,biology.organism_classification ,medicine.disease ,Obesity ,030220 oncology & carcinogenesis ,Original Article ,030211 gastroenterology & hepatology ,Metabolic syndrome ,diet ,business - Abstract
Background and Aim Perturbance in the composition of human gut microbiota has been associated with metabolic disorders such as obesity, diabetes mellitus, and insulin resistance. The objectives of this study are to examine the effects of ethnicity, central obesity, and recorded dietary components on potentially influencing the human gut microbiome. We hypothesize that these factors have an influence on the composition of the gut microbiome. Methods Subjects of Chinese (n = 14), Malay (n = 10), and Indian (n = 11) ancestry, with a median age of 39 years (range: 22–70 years old), provided stool samples for gut microbiome profiling using 16S rRNA sequencing and completed a dietary questionnaire. The serum samples were assayed for a panel of biomarkers (interleukin‐6, tumor necrosis factor alpha, adiponectin, cleaved cytokeratin 18, lipopolysaccharide‐binding protein, and limulus amebocyte lysate). Central obesity was defined by waist circumference cut‐off values for Asians. Results There were no significant differences in Shannon alpha diversity for ethnicity and central obesity and no associations between levels of inflammatory cytokines and obesity. The relative abundances of Anaerofilum (P = 0.02), Gemellaceae (P = 0.02), Streptococcaceae (P = 0.03), and Rikenellaceae (P = 0.04) were significantly lower in the obese group. From principle coordinate analysis, the effects of the intake of fiber and fat/saturated fat were in contrast with each other, with clustering of obese individuals leaning toward fiber. Conclusion The study demonstrated that there were differences in the gut microbiome in obese individuals. Certain bacterial taxa were present in lower abundance in the group with central obesity. Fiber and fat/saturated fat diets were not the key determinants of central obesity., The objectives of this study are to examine the effects of ethnicity, central obesity, and dietary components on the human gut microbiome. Asian subjects (n = 35) provided stool samples for gut microbiome profiling using 16S rRNA sequencing and completed a dietary questionnaire. The relative abundances of Anaerofilum (P = 0.02), Gemellaceae (P = 0.02), Streptococcaceae (P = 0.03), and Rikenellaceae (P = 0.04) were significantly lower in the obese group.
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- 2019
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3. Effect of Dietary Purines on the Pharmacokinetics of Orally Administered Ribavirin
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Seok Hwee Koo, Edmund J.D. Lee, Hung Hiang Quek, Lie Michael George Limenta, Khadijah Binte Hashim, Linghui Li, and Li Han
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Adult ,Male ,Purine ,viruses ,Administration, Oral ,Pharmacology ,Concentrative nucleoside transporter ,Food-Drug Interactions ,chemistry.chemical_compound ,Pharmacokinetics ,Ribavirin ,Humans ,Pharmacology (medical) ,Dosing ,Purine metabolism ,Meal ,Cross-Over Studies ,biology ,virus diseases ,Middle Aged ,biochemical phenomena, metabolism, and nutrition ,Crossover study ,digestive system diseases ,chemistry ,Food ,Purines ,biology.protein - Abstract
Ribavirin is found to be absorbed in the intestine through the human concentrative nucleoside transporter 2 (hCNT2). Cellular uptake of ribavirin was strongly inhibited by purine nucleoside in an in vitro study. This study aims to examine the effects of dietary purine on the pharmacokinetics of orally administered ribavirin in vivo. Twenty healthy participants were enrolled in a randomized, 2-period crossover study. Participants were administered a single 600-mg oral dose of ribavirin after either a high-purine meal or a low-purine meal. Serial blood samples were collected predose and over 144 hours after dosing. Ribavirin concentrations were measured by liquid chromatography/tandem mass spectrometry. In comparison with corresponding plasma values of ribavirin following a high-purine meal, C(max), AUC(0-144) and AUC(0-infinity) of ribavirin following a low-purine meal were 136% (90% confidence internal [CI]: 120%-155%), 134% (90% CI: 118%-153%), and 139% (90% CI: 120%-159%), respectively. This study indicates that dietary purines have an effect on ribavirin absorption. Dosage regimens of ribavirin might need to be adjusted according to the purine content of the meal.
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- 2009
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4. Distribution of the Fc?RIIIa 176 F/V polymorphism amongst healthy Chinese, Malays and Asian Indians in Singapore
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Peter Thompson, Kok Ting Chong, Woon Fei Ho, Seok Hwee Koo, and Edmund J.D. Lee
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Adult ,Male ,China ,Genotype ,Population ,India ,Disease ,Biology ,Asian People ,Gene Frequency ,Polymorphism (computer science) ,Humans ,Pharmacology (medical) ,Genetic variability ,Allele ,education ,Allele frequency ,Pharmacology ,Singapore ,education.field_of_study ,Polymorphism, Genetic ,Traditional medicine ,Asian Indian ,Malaysia ,Pharmacogenetics ,Female ,Demography - Abstract
What is already known about this subject • Genetic variability of the FcγRIIIa 176 F/V polymorphism has been widely studied in patients with systemic lupus erythomatosus and rheumatoid arthritis, as well as the general population of various White groups. • Its implications in disease pathogenesis and response to therapeutics have been well documented. • This study aimed to profile its polymorphism pattern in the Asian population, thus it serves as useful reference controls in disease association studies and tailoring therapy to ethnic-specific populations. What this study adds • In this study, we have established the genetic variability profile of the FcγRIIIa 176 F/V polymorphism in three distinct Asian groups (Chinese, Malays and Indians) and also supplemented existing data based on ethnic-specific healthy controls. • The polymorphism pattern of Malays was found to differ significantly from Chinese and Indians, which was also extended to almost all other healthy controls of various ethnic groups published elsewhere. • Such differences could have implications in disease susceptibility and pathogenesis, as well as response to drug therapeutics. Aims To determine and compare the distribution of the FcγRIIIa 176 F/V polymorphism across three ethnically distinct populations (Chinese, Asian Indians and Malays) in Singapore. Methods The FcγRIIIa 176 F/V polymorphism was genotyped by direct sequencing from genomic DNA samples obtained from normal healthy Chinese, Asian Indians and Malays (n = 192 from each population). Results The allelic frequencies of the high binding affinity FcγRIIIa 176 V allele for Chinese, Asian Indians and Malays were 35%, 33% and 46%, respectively (F allele frequencies were 65%, 67% and 54%, respectively). Genotype distributions were found to conform to the Hardy–Weinberg law (P > 0.05) in each group. χ2 comparisons revealed significant differences in the genotype distributions of the FcγRIIIa 176 V/F polymorphism of Malays from the other two populations (Chinese and Asian Indians). However, no significant difference in the genotype distributions of the FcγRIIIa 176 V/F polymorphism was observed between Chinese and Asian Indian populations. Conclusions The genotype distributions of the FcγRIIIa 176 V/F polymorphism in healthy Malays are significantly different from both Chinese and Indians. These observations provide the fundamentals on which future disease associations may be built and also present important implications for the design of therapeutic regimens amongst various ethnic groups.
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- 2007
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5. Genetics of Atrial Fibrillation
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Lin Yee Chen, Chee-Seng Ku, Seok Hwee Koo, and Edmund J.D. Lee
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Genetics ,Candidate gene ,Heart disease ,Genetic variation ,medicine ,Atrial fibrillation ,Genome-wide association study ,Biology ,Bioinformatics ,medicine.disease ,Penetrance ,Exome sequencing ,Genetic association - Abstract
Atrial fibrillation (AF) is the most common sustained arrhythmia with poor prognosis, reaching epidemic proportions in the ageing population. The condition affects more than five million people worldwide and is a significant clinical problem. Of particular interest is a subset of younger patients (
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- 2011
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6. Unravelling the Mystery of Sudden Cardiac Death Through Genetic Approaches
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Chee-Seng Ku, Paul Chui, Seok Hwee Koo, and Edmund J.D. Lee
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Genetics ,Candidate gene ,medicine ,Cardiac arrhythmia ,Genome-wide association study ,Copy-number variation ,Biology ,Bioinformatics ,medicine.disease ,Sudden death ,Penetrance ,Sudden cardiac death ,Cause of death - Abstract
The sudden unexplained death syndrome is a tragic and distressing event, which may arise due to an underlying fatal cardiac arrhythmia, which may be associated with a defective ion channel. These electrical abnormalities of the heart do not present with gross structural changes, rendering it a challenging task to the forensic pathologist in ascertaining the cause of death during autopsies. The attempts to identify genetic variations in the key ion channels known to cause arrhythmias have only been able to reveal the presence of putative mutations in a small percentage of the cases. It is thus imperative to look beyond the discovery of single-nucleotide polymorphisms to other forms of genetic variations (such as copy number variations and structural rearrangements), as well as alternative mechanisms that may underlie the molecular pathogenesis of arrhythmias and electrocardiographic abnormalities causing sudden death. Additionally, the various technological platforms for genetic analysis are also described in this article. Key Concepts: Sudden unexplained death syndrome is an important clinical problem. Sudden death may be the result of a fatal cardiac arrhythmia. Arrhythmias are associated with genetic mutations in ion channel genes. Genetic mutations often exhibit incomplete penetrance. Genetic mutations may have functional impact on the ion channel. Single-nucleotide polymorphisms only account for a fraction of the cases. Copy number variations and chromosomal aberrations may play a role in sudden death pathology. The role of alternative mechanisms such as epigenetics in arrhythmias/sudden death remains to be ascertained. The technology for identifying genetic variations is advancing rapidly. Genome-wide sequencing is expected to become increasingly feasible. Keywords: sudden unexplained death syndrome; arrhythmias; genetic variants; ion channels; genome-wide association studies; candidate gene sequencing; next-generation sequencing
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- 2011
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7. SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome
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Pattarapong Makarawate, Narumol Chaosuwannakit, Suda Vannaprasaht, Dujdao Sahasthas, Seok Hwee Koo, Edmund Jon Deoon Lee, Wichittra Tassaneeyakul, Hector Barajas‐Martinez, Dan Hu, and Kittisak Sawanyawisuth
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appropriate implantable cardioverter defibrillator shock therapy ,Brugada syndrome ,genetics ,implantable cardioverter defibrillator ,SCN5A R1193Q ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
BackgroundBrugada syndrome (BrS) is an inherited primary arrhythmia disorder leading to sudden cardiac arrest. SCN5A, encoding the α‐subunit of the cardiac sodium channel (Nav1.5), is the most common pathogenic gene of BrS. An implantable cardioverter defibrillator (ICD) is the standard treatment for secondary prevention. This study aimed to evaluate association of the SCN5A variant with this cardiac conduction disturbance and appropriate ICD shock therapy in Thai symptomatic BrS patients with ICD implants. Methods and ResultsSymptomatic BrS patients diagnosed at university hospital were enrolled from 2008 to 2011. The primary outcome of the study was an appropriate ICD shock defined as having non‐pacing‐associated ICD shock after the occurrence of ventricular tachycardia or ventricular fibrillation. Associations between SCN5A polymorphisms, cardiac conduction disturbance, and potential confounding factors associated with appropriate ICD shock therapy were analyzed. All 40 symptomatic BrS patients (median age, 43 years) with ICD implantations were followed for 24 months. There were 16 patients (40%) who had the appropriate ICD shock therapy after ICD treatment. An independent factor associated with appropriate ICD shock therapy was SCN5A‐R1193Q with an adjusted hazard ratio of 10.550 (95% CI, 1.631–68.232). ConclusionsSCN5A‐R1193Q is associated with cardiac conduction disturbances. It may be a genetic marker associated with ventricular arrhythmia leading to appropriate ICD shock therapy in symptomatic BrS patients with ICD treatment. Because of the small sample size of study population and the appropriate ICD shock outcome, further large studies are needed to confirm the results of this study.
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- 2017
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