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Guangzhou, China

Gao R.,Chinese Academy of Sciences | Yang Y.,Chinese Academy of Sciences | Han Y.,General Hospital of Shenyang Military Command | Huo Y.,Peking University | And 12 more authors.
Journal of the American College of Cardiology | Year: 2015

Background The everolimus-eluting bioresorbable vascular scaffold (BVS) is designed to achieve results comparable to metallic drug-eluting stents at 1 year, with improved long-term outcomes. Whether the 1-year clinical and angiographic results of BVS are noninferior to current-generation drug-eluting stents has not been established. Objectives This study sought to evaluate the angiographic efficacy and clinical safety and effectiveness of BVS in a randomized trial designed to enable approval of the BVS in China. Methods Eligible patients with 1 or 2 de novo native coronary artery lesions were randomized to BVS or cobalt-chromium everolimus-eluting stents (CoCr-EES) in a 1:1 ratio stratified by diabetes and the number of lesions treated. Angiographic and clinical follow-up were planned at 1 year in all patients. The primary endpoint was angiographic in-segment late loss (LL), powered for noninferiority with a margin of 0.15 mm. Results A total of 480 patients were randomized (241 BVS vs. 239 CoCr-EES) at 24 sites. Acute clinical device success (98.0% vs. 99.6%; p = 0.22) and procedural success (97.0% and 98.3%; p = 0.37) were comparable in BVS- and CoCr-EES-treated patients, respectively. The primary endpoint of in-segment LL at 1 year was 0.19 ± 0.38 mm for BVS versus 0.13 ± 0.38 mm for CoCr-EES; the 1-sided 97.5% upper confidence limit of the difference was 0.14 mm, achieving noninferiority of BVS compared with CoCr-EES (pnoninferiority = 0.01). BVS and CoCr-EES also had similar 1-year rates of target lesion failure (cardiac death, target vessel myocardial infarction, or ischemia-driven target lesion revascularization; 3.4% vs. 4.2%, respectively; p = 0.62) and definite/probable scaffold/stent thrombosis (0.4% vs. 0.0%, respectively; p = 1.00). Conclusions In the present multicenter randomized trial, BVS was noninferior to CoCr-EES for the primary endpoint of in-segment LL at 1 year. (A Clinical Evaluation of Absorb Bioresorbable Vascular Scaffold [Absorb BVS] System in Chinese Population - ABSORB China Randomized Controlled Trial [RCT]; NCT01923740) © 2015 American College of Cardiology Foundation. Source


Mok T.,Chinese University of Hong Kong | Yang J.-J.,Guangdong General Hospital | Lam K.-C.,Chinese University of Hong Kong
Journal of Clinical Oncology | Year: 2013

First-line epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) is a standard treatment for patients with activating EGFR mutations. Six randomized studies have demonstrated consistent improvement in tumor response rate and progression-free survival over platinum-based combination chemotherapy. The only reason to consider EGFR TKI as second-line therapy is that none of the six comparative studies has shown improvement in overall survival, which can be explained by the high proportion of patients from the chemotherapy arm crossing over to the EGFR TKI arm on progression. It is true that patients with EGFR mutations may benefit from second-line EGFR TKI therapy, but we cannot conclude that the benefit is either equal to or inferior to first-line EGFR TKI therapy. To date, there are no direct comparative data between first- and second-line EGFR TKI in patients with activating EGFR mutations. Tumor response rates to second-line EGFR TKI have been inconsistent, which could potentially be explained by the impact of first-line chemotherapy on the abundance of tumor cells with activating EGFR mutations. However, numerous arguments, including assurance on drug exposure, improvement in quality of life, better tolerance by patients with poor performance status, and deferral of whole-brain radiation therapy for patients with brain metastasis, support the general application of first-line EGFR TKI. © 2013 by American Society of Clinical Oncology. Source


Wang X.-B.,Guangdong General Hospital | Tian X.-Y.,Hong Kong Baptist University | Li Y.,Sun Yat Sen University | Li B.,Sun Yat Sen University | Li Z.,Sun Yat Sen University
Journal of Neuro-Oncology | Year: 2012

Macrophage migration inhibitory factor (MIF) plays a critical role in tumorigenesis. We aim to examine the association of MIF with tumor recurrence and survival of gliomas, and to determine whether MIF is a valuable prognostic predictor for glioma patients. The expression of MIF and interleukin 8 (IL-8) was evaluated in 36 high-grade gliomas (20 glioblastoma multiforme, 13 anaplastic astrocytoma, and 3 anaplastic oligoastrocytoma) and 32 low-grade gliomas (18 fibrillary astrocytoma, 5 pilocytic astrocytoma, 5 oligodendroglioma, 3 ependymoma and 1 pleomorphic xanthoastrocytoma) by immunostaining. Intratumoral microvessel density (IMD) of tumors in relation to immunostainings and clinicopathological factors were analyzed statistically as well as the follow-up data of patients. High expression of both MIF (58.8%) and IL-8 (52.9%) was significantly associated with high-grade gliomas and increased microvessels in tumors, but only high expression of MIF was closely related to tumor recurrence (P = 0.001). High expression of IL-8 exhibited a close correlation with high expression of MIF in tumors (P = 0.001). Histological grading, high expression of MIF and IL-8 correlated with patients' overall survival in univariate analysis. However, only histological grading and MIF expression exhibited a relationship with survival of patients as independent prognostic factors of glioma by multivariate analysis; the hazard ratios were 28.012 (P = 0.001) and 11.782 (P = 0.001), respectively. Elevated production of MIF in glioma tumor cells may contribute to tumor recurrence and a worse prognosis. MIF may serve as an independent predictive factor for prognosis of glioma patients. © 2011 Springer Science+Business Media, LLC. Source


Li L.,Guangdong General Hospital
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2011

Adefovir dipivoxil is commonly used for treatment of chronic hepatitis B. The renal toxicity of adefovir dipivoxil is dose- and time-related, occurring often in patients with a daily dose over 30 mg and those with impaired renal function. We report a case of chronic hepatitis B with a history of taking adefovir dipivoxil at 10 mg/day for 4 years. The patient complained of lumbosacral and joint pain and had the diagnosis of ankylosing spondylitis (AS) or spondyloarthropathy in several hospitals before admission in our hospital. A diagnosis of acquired Fanconi syndrome and hypophosphatemia osteomalacia associated with progressive muscular weakness was made eventually. We reviewed the literature and found reports of only fewer than 10 similar cases. Clinical attention should be given to kidney damage induced by adefovir dipivoxil. Source


Zhou G.B.,Guangdong General Hospital
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2011

To investigate the effect of COX inhibitors on pain threshold and spinal N-methyl-D-aspartate (NMDA) receptor subunit 2B (NR2B) expression in a rat model of neuropathic pain. Thirty-six male SD rats were randomly divided into sham-operated group, chronic constriction injury (CCI) of the sciatic nerve group, indomethacin+CCI group, and parecoxib+CCI group with corresponding treatments. All the rats were tested for mechanical withdrawal threshold, and at day 13 after the surgery, the rats were decapitated for detection of NR2B expression in the spinal cord at the L4-6 levels. The mechanical withdrawal threshold were lowered significantly after the operation in CCI, indomethacin+CCI and parecoxib+CCI groups (P<0.05). Parecoxib alleviated the hypersensitivity of CCI model rats but not affected spinal NR2B expressions (P>0.05). No significant differences were found in the mechanical withdrawal threshold or spinal NR2B expression between CCI group and indomethacin+CCI group (P>0.05). Parecoxib can alleviate neuropathic hypersensitivity in rats, but this effect may not be associated with NR2B expression in the spinal cord. Source

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