METHODS: CYP2D6 was heterologously expressed in Escherichia coli. CYP2D6-antiarthritic compound interactions were studied using in vitro enzyme kinetics assay and molecular docking.
RESULTS: The high-performance liquid chromatography (HPLC)-based dextromethorphan O-demethylase assay was established as CYP2D6 marker. All glucosamines and chondroitins weakly inhibited CYP2D6 (IC50 values >300 µM). Diacerein exhibited moderate inhibition with IC50 and K i values of 34.99 and 38.27 µM, respectively. Its major metabolite, rhein displayed stronger inhibition potencies (IC50=26.22 μM and K i =32.27 μM). Both compounds exhibited mixed-mode of inhibition. In silico molecular dockings further supported data from the in vitro study. From in vitro-in vivo extrapolation, rhein presented an area under the plasma concentration-time curve (AUC) ratio of 1.5, indicating low potential to cause in vivo inhibition.
CONCLUSIONS: Glucosamine, chondroitin and diacerein unlikely cause clinical interaction with the drug substrates of CYP2D6. Rhein, exhibits only low potential to cause in vivo inhibition.
METHODS: A randomized trial was conducted in a university hospital in Malaysia from December 2018 to May 2019. Term nulliparas with unfavorable cervix (Bishop score ≤ 5) scheduled for labor induction were randomized to Foley catheter and controlled release dinoprostone insert simultaneously or Foley catheter alone. Primary outcomes were induction to delivery interval (hours) and maternal satisfaction on birth experience (assessed by 11-point Visual Numerical Rating Scale VNRS 0-10, higher score more satisfied).
RESULTS: Induction to vaginal delivery intervals was mean ± standard deviation 22.5 ± 10.4 vs. 35.1 ± 14.9 h, P =
SUMMARY: However, epidemiology data may be misleading due to several contentious diagnostic issues. The diagnostic conundrums are due to inherent complexity of the GEJ as a functional and pathological unit. Challenging diagnostic issues in Asia include the following: nonstandardized landmark of the GEJ, misclassification of Barrett esophagus, targeted versus nontargeted tissue sampling, histopathology disagreement and challenges in screening or surveillance of dysplastic BE and early GEJ cancer. The recent Asian-Pacific survey led by the Asian Barrett Consortium (ABC) has provided useful insights into these contentious issues. A key learning point from these diagnostic limitations is that the awareness of the disease and adherence to existing recommendations or guidelines are poor in the region. Key Messages: Standardization in diagnostic methodology is vital for accurate epidemiology data, and this can only come from better awareness and adherence through educational and international efforts. Last, surveillance strategy may need a paradigm shift from a purely diagnostic approach to a combined targeted surveillance and treatment approach using novel endoscopic techniques.
OBJECTIVE: To explore self-reported confidence level of pharmacists, perceived reasons influencing their confidence and socio-demographic associated with high confidence level in the area of anticoagulation.
METHODS: A cross-sectional, self-administered questionnaire survey was carried out among fully registered pharmacists who work in selected government hospitals and clinics in Borneo, Malaysia, from January 2019 to February 2020.
RESULTS: Overall, responses from 542 fully registered pharmacists were obtained. Proportion of respondents who claimed confident in providing necessary information to patient receiving warfarin (n = 479, 88.3%) was significantly higher (p
RESULTS: In the present study, bioinformatics and cell biology were used to investigate the functions and signal pathway enrichments of differentially expressed genes. The bioinformatics analysis of three original microarray datasets (GSE73661, GSE75214 and GSE126124) in the NCBI-Gene Expression Omnibus database showed 17 down-regulated genes (logFC 0) existed in the enteritis tissue. Meanwhile, pathway enrichment and protein-protein interaction network analysis suggested that IBD is relevant to cytotoxicity, inflammation and apoptosis. Furthermore, Caco-2 cells were treated with the main oxidation products of deep-frying oil-total polar compounds (TPC) and its components (polymerized triglyceride, oxidized triglycerides and triglyceride degradation products) isolated from deep-frying oil. The flow cytometry experiment revealed that TPC and its components could induce apoptosis, especially for oxidized triglyceride. A quantitative polymerase chain reaction analysis demonstrated that TPC and its component could induce Caco-2 cell apoptosis through AQP8/CXCL1/TNIP3/IL-1.
CONCLUSION: The present study provides fundamental knowledge for understanding the effects of deep-frying oils on the cytotoxic and inflammatory of Caco-2 cells, in addition to clarifying the molecular function mechanism of deep-frying oil in IBD. © 2021 Society of Chemical Industry.
MATERIALS AND METHODS: This was a longitudinal study of eight IGHD subjects (2 males, 6 females) with a mean age of 11.1 ± 0.8 years and age-matched control groups. The pituitary gland, basal ganglia and limbic structures volumes were obtained using 3T MRI voxel-based morphology. The left-hand bone age was assessed using the Tanner-Whitehouse method. Follow-up imaging was performed after an average of 1.8 ± 0.4 years on rhGH.
RESULTS: Subjects with IGHD had a smaller mean volume of the pituitary gland, right thalamus, hippocampus, and amygdala than the controls. After rhGH therapy, these volumes normalized to the age-matched controls. Corpus callosum of IGHD subjects had a larger mean volume than the controls and did not show much volume changes in response to rhGH therapy. There were changes towards normalization of bone age deficit of IGHD in response to rhGH therapy.
CONCLUSION: The pituitary gland, hippocampus, and amygdala volumes in IGHD subjects were smaller than age-matched controls and showed the most response to rhGH therapy. Semi-automated volumetric assessment of pituitary gland, hippocampus, and amygdala using MRI may provide an objective assessment of response to rhGH therapy.