| 1 | The role of autophagic and lysosomal pathways in ischemic brain injury显示文摘Autophagy is involved in neural cell death after cerebral ischemia. Our previous studies showed that rapamycin-induced autophagy decreased the rate of apoptosis, but the rate of apoptosis was in-creased after the autophagy inhibitor, 3-methyladenine, was used. In this study, a suture-occluded method was performed to generate a rat model of brain ischemia. Under a transmission electron microscope, autophagic bodies and autophagy lysosomes were markedly accumulated in neurons at 4 hours post brain ischemic injury, with their numbers gradually reducing over time. Western blotting demonstrated that protein levels of light chain 3-II and cathepsin B were significantly in-creased within 4 hours of ischemic injury, but these levels were not persistently upregulated over time. Confocal microscopy showed that autophagy was mainly found in neurons with positive light chain 3 signal. Injection of rapamycin via tail vein promoted the occurrence of autophagy in rat brain tissue after cerebral ischemia and elevated light chain 3 and cathepsin B expression. However, in-jection of 3-methyladenine significantly diminished light chain 3-II and cathepsin B expression. Results verified that autophagic and lysosomal activity is increased in ischemic neurons. Abnormal components in cells can be eliminated through upregulating cell autophagy or inhibiting autophagy after ischemic brain injury, resulting in a dynamic balance of substances in cells. Moreover, drugs that interfere with autophagy may be potential therapies for the treatment of brain injury. | Zhaohua Gu Yinyi Sun Kangyong Liu Fen Wang Ting Zhang Qiang Li Liwei Shen Ling Zhou Liang Dong Nan Shi Qian Zhang Wei Zhang Meizhen Zhao Xiaojiang Sun | 2013 | Neural Regeneration Research2013，8，23： | 2 |
| 2 | Recommendations for the diagnosis and treatment of paroxysmal kinesigemc dyskinesia: an expert consensus in China显示文摘Paroxysmal dyskinesias are a group of neurological diseases characterized by intermittent episodes of involuntary movements with different causes.Paroxysmal kinesigenic dyskinesia(PKD)is the most common type of paroxysmal dyskinesia and can be divided into primary and secondary types based on the etiology.Clinically,PKD is characterized by recurrent and transient attacks of involuntary movements precipitated by a sudden voluntary action.The major cause of primary PKD is genetic abnormalities,and the inheritance pattern of PKD is mainly autosomal-dominant with incomplete penetrance.The proline-rich transmembrane protein 2(PRRT2)was the first identified causative gene of PKD,accounting for the majority of PKD cases worldwide.An increasing number of studies has revealed the clinical and genetic characteristics,as well as the underlying mechanisms of PKD.By seeking the views of domestic experts,we propose an expert consensus regarding the diagnosis and treatment of PKD to help establish standardized clinical evaluation and therapies for PKD.In this consensus,we review the clinical manifestations,etiology,clinical diagnostic criteria and therapeutic recommendations for PKD,and results of genetic analyses in PKD patients performed in domestic hospitals. | Li Cao Xiaojun Huang Ning Wang Zhiying Wu Cheng Zhang Weihong Gu Shuyan Cong Jianhua Ma Ling Wei Yanchun Deng Qi Fang Qi Niu Jin Wang Zhaoxia Wang You Yin Jinyong Tian Shufen Tian Hongyan Bi Hong Jiang Xiaorong Liu Yang Lu Meizhen Sun Jianjun Wu Erhe Xu Tao Chen Tao Chen Xu Chen Wei Li Shujian Li Qinghua Li Xiaonan Song Ying Tang Ping Yang Yun Yang Min Zhang Xiong Zhang Yuhu Zhang Ruxu Zhang Yi Ouyang Jintai Yu Quanzhong Hu Qing Ke Yuanrong Yao Zhe Zhao Xiuhe Zhao Guohua Zhao Furu Liang Nan Cheng Jianhong Han Rong Peng Shengdi Chen Beisha Tang | 2021 | Translational Neurodegeneration2021，10，1： | 1 |
| 3 | 血清胱抑素C、内生肌酐清除率及尿微量白蛋白在恶性肿瘤含顺铂化疗患者肾功能评价中的地位(英文)显示文摘Objective:Chemotherapy drugs such as platinum may cause damage to the renal function,creatinine clearance(Ccr),as a 'golden standard' indicator in clinical evaluation of renal function,was limited in application due to complicated detection steps.By detecting the expression of serum Cystatin C(Cys C),Ccr and urinary micro-albumin(UMA),this study was designed to analyze and discuss their roles and status in renal function evaluation for cancer patients before and after chemotherapy with platinum.Methods:We retrospectively reviewed 110 patients who receiving platinum-containing protocols or non-platinum-containing ones,and got the expression of Cys C,Ccr(was calculated by Cockcroft-Gault equation) and UMA,then analyzed whether there were differences for Cys C,Ccr and UMA in those patients;for patients with mildly impaired renal function(Ccr between 50-75 mL/min),whether there were differences for Cys C and UMA before and after chemotherapy with platinum.Results:There was statistical significance for Ccr,Cys C and UMA in patients who receiving platinum-containing protocols(85.01 ± 28.40) vs(76.79 ± 26.63) mL/min,(1.49 ± 0.50) vs(1.80 ± 0.84) mg/L and(14.30 ± 9.15) vs(16.90 ± 10.95) mg/L,P = 0.00,0.00 and 0.01),and no statistical significance for those receiving non-platinum-containing ones(89.45 ± 29.69) vs(86.78 ± 27.96) mL/min,(1.51 ± 0.78) vs(1.63 ± 0.73)mg/L and(17.31 ± 10.46) vs(16.59 ± 8.33) mg/L,P = 0.45,0.07 and 0.57);and there were also significant differences for Cys C for patients with mildly impaired renal function before and after chemotherapy(1.68 ± 0.55) vs(2.04 ± 0.68) mg/L,P = 0.03),while no statistical significance for UMA for the same ones(21.11 ± 10.06) vs(21.22 ± 8.81) mg/L,P = 0.93).There were statistical significance both for Cys C and UMA before and after chemotherapy in platinum-containing group,but the AUC for Ccr and Cys C is greater than that for UMA(P < 0.02).Conclusion:Cys C and UMA can both access renal dysfunction early after chemotherapy,but Cys C is more sensitive than UMA in reflecting early renal dysfunction,so Cys C can replace Ccr and become a reliable indicator in the assessment of renal function for cancer patients before and after chemotherapy especially with platinum. | Xun Cai Peng Xue Meizhen Gu Jiong Hu Hongli Gu Haiyan Yang Liwei Wang | 2011 | The Chinese-German Journal of Clinical Oncology2011，10，4： | 1 |
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