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Icteric flare of chronic hepatitis B in a 95-year old patient 被引量:3
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作者 WS Wong wai keung leung Henry L Y Chan 《World Journal of Gastroenterology》 SCIE CAS CSCD 2003年第12期2876-2877,共2页
A 95-year old gentleman developed fatal icteric flare of chronic hepatitis B despite lamivudine treatment. This article highlights the atypical presentations of chronic hepatitis B in elderly patient and the need to c... A 95-year old gentleman developed fatal icteric flare of chronic hepatitis B despite lamivudine treatment. This article highlights the atypical presentations of chronic hepatitis B in elderly patient and the need to consider this possibility for acute fulminant hepatitis in endemic areas. 展开更多
关键词 慢性乙型肝炎 高龄患者 黄疸 拉米夫定 急性暴发性肝炎
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p53-independent pRB degradation contributes to a drug-induced apoptosis in AGS cells
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作者 Yan JIN wai keung leung +1 位作者 Joseph Jao-Yiu SUNG Jia Rui WU 《Cell Research》 SCIE CAS CSCD 2005年第9期695-703,共9页
The retinoblastoma (RB) tumor suppressor protein, pRB, plays an important role in the regulation of mammalian cell cycle. Furthermore, several lines of evidence suggest that pRB also involves in the regulation of apop... The retinoblastoma (RB) tumor suppressor protein, pRB, plays an important role in the regulation of mammalian cell cycle. Furthermore, several lines of evidence suggest that pRB also involves in the regulation of apoptosis. In the present study, the degradation of pRB was observed in apoptotic gastric tumor cells treated with a new potent anti-tumor component, tripchlorolide (TC). The inhibition of pRB degradation by a general cysteine protease inhibitor IDAM resulted in the reduction of the apoptotic cells. Furthermore, the survival of the gastric tumor cells under the TC treatment was enhanced by an over-expression of exogenous pRB. These results suggest that the pRB degradation of the gastric tumor cells under the TC treatment involves in the apoptotic progression. In addition, the same extent of TC- induced pRB-degradation was detected in the gastric tumor cells containing a p53 dominant-negative construct, indicat- ing that this kind of pRB degradation is p53-independent. 展开更多
关键词 眼部肿瘤 肿瘤抑制蛋白 细胞周期 药物诱导
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Metabolic memory:mechanisms and diseases
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作者 Hao Dong Yuezhang Sun +4 位作者 Lulingxiao Nie Aimin Cui Pengfei Zhao wai keung leung Qi Wang 《Signal Transduction and Targeted Therapy》 SCIE CSCD 2024年第3期1086-1114,共29页
Metabolic diseases and their complications impose health and economic burdens worldwide.Evidence from past experimental studies and clinical trials suggests our body may have the ability to remember the past metabolic... Metabolic diseases and their complications impose health and economic burdens worldwide.Evidence from past experimental studies and clinical trials suggests our body may have the ability to remember the past metabolic environment,such as hyperglycemia or hyperlipidemia,thus leading to chronic inflammatory disorders and other diseases even after the elimination of these metabolic environments.The long-term effects of that aberrant metabolism on the body have been summarized as metabolic memory and are found to assume a crucial role in states of health and disease.Multiple molecular mechanisms collectively participate in metabolic memory management,resulting in different cellular alterations as well as tissue and organ dysfunctions,culminating in disease progression and even affecting offspring.The elucidation and expansion of the concept of metabolic memory provides more comprehensive insight into pathogenic mechanisms underlying metabolic diseases and complications and promises to be a new target in disease detection and management.Here,we retrace the history of relevant research on metabolic memory and summarize its salient characteristics.We provide a detailed discussion of the mechanisms by which metabolic memory may be involved in disease development at molecular,cellular,and organ levels,with emphasis on the impact of epigenetic modulations.Finally,we present some of the pivotal findings arguing in favor of targeting metabolic memory to develop therapeutic strategies for metabolic diseases and provide the latest reflections on the consequences of metabolic memory as well as their implications for human health and diseases. 展开更多
关键词 DISEASES METABOLISM alterations
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幽门螺杆菌治疗后长期使用质子泵抑制剂与胃癌发生的风险:以人群为基础的研究
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作者 Ka Shing Cheung Esther W Chan +4 位作者 Angel Y S Wong Lijia Chen lan C K Wong wai keung leung 彭浩(译) 《英国医学杂志中文版》 2019年第7期422-422,共1页
目的质子泵抑制剂(PPIs)与胃萎缩恶化相关,尤其是在幽门螺杆菌(HP)感染者中。我们确定了在接受抗HP治疗的HP感染者中,PPIs使用与胃癌(GC)之间的相关性。设计本研究以中国香港全区健康资料库为基础。我们首先确认出自2003至2012年间接受... 目的质子泵抑制剂(PPIs)与胃萎缩恶化相关,尤其是在幽门螺杆菌(HP)感染者中。我们确定了在接受抗HP治疗的HP感染者中,PPIs使用与胃癌(GC)之间的相关性。设计本研究以中国香港全区健康资料库为基础。我们首先确认出自2003至2012年间接受过以克拉霉素为基础的三联疗法门诊处方的成年人。排除标准:使用该处方治疗失败的患者,HP治疗后12个月内确诊为GC的患者,以及治疗后发生胃溃疡者。GC排除前的6个月内开始PPIs或H2受体阻滞剂(H2RA)治疗,以避免原始偏倚。通过C。x比例风险模型的倾向分数调整,评估GC发生风险与质子泵抑制剂二者之间的关系。H2RA作为阴性对照暴露。结果共63 397名合格受试者入选,在平均7.6年的随访时间中,有153(0.24%)名发生GC。PPIs使用与GC发生风险增高相关[危害比(HR)2.44,95%可信区间(C/)1.42-4.20],而H2RA无相关性(“R 0.72,95%CI 0.48-1.07)0GC发生的风险随PPIs使用时间的延长而增高(PPIs使用时间/年22年和年的GC发生风险分别为:HR 5.04.95%CI 1.23-20.61;6.65,1.62-27.26和8.34,95%CI 2.02-34.41)。PPIs使用相比非PPIs使用,调整的绝对风险差为每10000人年超过4.29 GC(95%C/1.25-9.54)。结论即使在HP根除治疗后,长期使用质子泵抑制剂仍与GC的发生风险增加相关。 展开更多
关键词 COX比例风险模型 质子泵抑制剂 治疗失败 幽门螺杆菌 胃癌发生 H2受体阻滞剂 人群 HP根除治疗
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