加味黄连解毒汤灌肠辅助治疗重症肺炎合并胃肠功能障碍临床研究

目的:观察加味黄连解毒汤灌肠辅助治疗重症肺炎痰热壅肺证合并胃肠功能障碍的临床疗效。方法:选取64例重症肺炎痰热壅肺证合并胃肠功能障碍患者,依据不同的治疗方法分为治疗组和对照组,每组32例。对照组给予抗菌药、胃肠功能保护药、机械通气等对症治疗,治疗组在对照组基础上联合加味黄连解毒汤灌肠治疗。比较2组临床疗效、治疗前后中医证候积分及血清降钙素原(PCT)水平,记录不良反应发生情况。结果:治疗组总有效率93.75%,高于对照组的71.88%,差异有统计学意义(P<0.05)。治疗后,2组中医证候积分均较治疗前降低,治疗组中医证候积分比对照组下降更明显,差异均有统计学意义(P<0.05)。治疗3天与治疗7天,治疗组PCT水平均低于对照组,差异均有统计学意义(P<0.05)。治疗期间,治疗组发生不良反应5例,对照组发生不良反应4例,未经处理均自行缓解。结论:加味黄连解毒汤灌肠辅助治疗重症肺炎痰热壅肺证合并胃肠功能障碍,可以有效减轻患者的临床症状,改善胃肠功能,抑制炎症反应。     

Effects of Cassava Juice (Manihot esculenta Crantz) on Renal and Hepatic Function and Motor Impairments in Male Rats

Cassava (Manihot esculenta Crantz) is a plant that contains neurotoxins such as linamarin and lotaustraline. Its long-term consumption is associated with neuronal damage and contributes to the development of motor impairment in humans and rats. We investigated the effects of the consumption of cassava juice on renal and hepatic function and motor impairments in male rats. The rats received the vehicle, non-toxic and toxic doses of cassava juice, or linamarin as a pharmacological control, over 35 consecutive days. The effects were evaluated in an open field test, rotarod, and swim test. The toxic cassava dose and linamarin resulted in motor impairments in the rotarod and swim test from day 7 of treatment. The toxic cassava dose and linamarin increased the parameters that indicate renal and hepatic damage, with the exception of total protein and albumin levels. Behavioral variables that show motor incoordination (i.e., latency to fall in the rotarod) were negatively correlated with biochemical parameters of renal and kidney damage, whereas spin behavior was positively correlated. Our data indicate that chronic oral consumption of cassava juice caused renal and hepatic damage that was correlated with motor coordination impairment in rats, similarly to their principal neurotoxic compound, linamarin.     

糖尿病肾病内热证与肾功能及炎症因子的相关性研究

目的:观察糖尿病肾病不同分期内热证与肾功能及炎症指标的相关性。方法:收集202例糖尿病肾病患者的临床资料,采用酶联免疫吸附法检测微炎症指标,包括超敏C反应蛋白(high-sensitivity C-reactive protein,HS-CRP)、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α),进行统计分析。结果:与非内热证组比较,中期、晚期内热证组24小时尿蛋白定量明显升高;晚期内热证组的血清肌酐明显升高,肾小球滤过率(glomerular filtration rate,GFR)明显降低;炎症因子CRP、IL-6、TNF-α随疾病进展均呈上升趋势;晚期内热证组与非内热证组比较,IL-6、TNF-α升高;中期HS-CRP与内热积分呈正相关,晚期TNF-α与内热积分呈正相关。结论:内热病机贯穿于糖尿病肾病的始终,与糖尿病肾病肾功能以及疾病进展密切相关;同时,内热积分与炎症因子HS-CRP、TNF-α的表达存在一定的相关性,这种相关性在疾病中期、晚期表现更加明显。     

连续性肾脏替代治疗联合中药灌肠对急性肾损伤患者尿KIM-1、NGAL水平的影响

目的:探讨连续性肾脏替代治疗(CRRT)联合中药灌肠对重症急性肾损伤患者尿肾损伤分子-1(KIM-1)、中性粒细胞明胶酶相关脂质运载蛋白(NGAL)水平和预后的影响。方法:回顾性分析89例重症急性肾损伤患者临床资料,依据不同治疗方式分为对照组43例和研究组46例,对照组采用CRRT治疗,研究组采用CRRT联合中药灌肠治疗。比较两组尿量恢复时间、重症医学科(ICU)住院时间、治疗前后肾功能、尿KIM-1、NGAL水平,序贯器官衰竭估计评分(SOFA)、急性生理与慢性健康评分表(APACHEⅡ)评分和预后情况。结果:研究组尿量恢复时间、ICU住院时间均少于对照组(P<0.05)。治疗前,两组肾功能、尿KIM-1、NGAL水平,SOFA、APACHEⅡ评分比较,差异无统计学意义(P>0.05); 治疗后,两组肾功能指标、尿KIM-1、NGAL水平,SOFA、APACHEⅡ评分均较治疗前下降,研究组低于对照组,差异有统计学意义(P<0.05)。研究组死亡率较对照组低(P<0.05)。结论:CRRT联合中药灌肠能够促进重症急性肾损伤患者肾功能的恢复,降低尿KIM-1、NGAL水平,改善预后。     

Analysis of early mortality and related risk factors in maintenance hemodialysis patients

Objective To analyze the early mortality and related risk factors of new hemodialysis patients in Zhejiang province, and provide basis for reducing the death risk of hemodialysis patients. Methods The early mortality and related factors of new hemodialysis patients from January 1, 2010 to June 30, 2018 were retrospectively analyzed using the database of Zhejiang province hemodialysis registration. The early mortality was defined as death within 90 days of dialysis. Cox regression model was used to analyze the related risk factors of the early mortality in hemodialysis patients. Results The mortality was the highest in the first month after dialysis (46.40/100 person year), and gradually stabilized after three months. The early mortality was 25.33/100 person year. The mortality within 120 days and 360 days were 21.40/100 person year and 11.37/100 person year, respectively. The elderly (≥65 years old, HR=1.981, 95%CI 1.319-2.977, P＜0.001), primary tumor (HR=3.308, 95%CI 1.137-5.624, P=0.028), combined with tumors (not including the primary tumor, HR=2.327, 95%CI 1.200-4.513, P=0.012), temporary catheter (the initial dialysis pathway, HR=3.632, 95%CI 1.806-7.307, P＜0.001), lower albumin (＜30 g/L, HR=2.181, 95%CI 1.459-3.260, P＜0.001), lower hemoglobin (every 0.01 g/L increase, HR=0.861, 95%CI 0.793-0.935, P=0.001), lower high density lipoprotein (＜0.7 mmol/L, HR=1.796, 95%CI 1.068-3.019, P=0.027) and higher C reactive protein (≥40 mg/L, HR=1.889, 95%CI 1.185-3.012, P=0.008) were the risk factors of early death for hemodialysis patients. Conclusions The early mortality of hemodialysis patients is high after dialysis, and gradually stable after 3 months. The elderly, primary tumor, combined with tumors, the initial dialysis pathway, lower albumin, lower hemoglobin, lower high density lipoprotein and higher C reactive protein are the risk factors of early death for hemodialysis patients.     

高血压与男性生殖损伤男性生殖功能的研究进展

高血压是我国常见的慢性病,随着高血压患病人群年轻化以及生育年龄的延后,高血压对男性生殖相关疾病的影响逐渐被重视。本文就高血压与抗高血压药物对男性勃起功能障碍(Erectile dysfunction,ED)和男性生育力标志物的影响进行综述。     

Adenylate cyclase activator forskolin alleviates intracerebroventricular propionic acid-induced mitochondrial dysfunction of autistic rats

Neuronal mitochondrial dysfunction increases inflammatory mediators and leads to free radical generation and anti-oxidant enzymatic alterations,which are major neuropathological hallmarks responsible for autism.Mitochondrial dysfunction in autism is associated with decreased ATP levels due to reduced levels of cyclic adenosine monophosphate.Rat models of autism were established by intracerebroventricular injection of propionic acid.These rat models had memory dysfunction,decreased muscle coordination and gait imbalance.Biochemical estimation of propionic acid-treated rats showed changes in enzyme activity in neuronal mitochondrial electron transport chain complexes and increases in pro-inflammatory cytokines,oxidative stress and lipid biomarkers.Oral administration of 10,20 and 30 mg/kg adenylate cyclase activator forskolin for 15 days reversed these changes in a dose-dependent manner.These findings suggest that forskolin can alleviate neuronal mitochondrial dysfunction and improve neurological symptoms of rats with autism.This study was approved by the RITS/IAEC,SIRSA,HARYANA on March 3,2014(approval No.RITS/IAEC/2014/03/03).     

Extracellular vesicles transmitted miR-31-5p promotes sorafenib resistance by targeting MLH1 in renal cell carcinoma

Sorafenib provides survival benefits in patients with advanced renal cell carcinoma (RCC), but its use is hampered by acquired drug resistance. It is important to fully clarify the molecular mechanisms of sorafenib resistance, which can help to avoid, delay or reverse drug resistance. Extracellular vesicles (EVs) can mediate intercellular communication by delivering effector molecules between cells. Here, we studied whether EVs are involved in sorafenib resistance of RCC and its possible molecular mechanisms. Using differential centrifugation, EVs were isolated from established sorafenib-resistant RCC cells (786-0 and ACHN), and EVs derived from sorafenib-resistant cells were uptaken by sensitive parental RCC cells and thus promoted drug resistance. Elevated exogenous miR-31-5p within EVs effectively downregulated MutL homolog 1 (MLH1) expression and thus promoted sorafenib resistance in vitro. Mice experiments also confirmed that miR-31-5p could mediate drug sensitivity in vivo. In addition, low expression of MLH1 was observed in sorafenib-resistant RCC cells and upregulation of MLH1 expression restored the sensitivity of resistant cell lines to sorafenib. Finally, miR-31-5p level in circulating EVs of RCC patients with progressive disease (PD) during sorafenib therapy was higher when compared to that in the pretherapy status. In conclusion, EVs shuttled miR-31-5p can transfer resistance information from sorafenib-resistant cells to sensitive cells by directly targeting MLH1, and thus magnify the drug resistance information to the whole tumor. Furthermore, miR-31-5p and MLH1 could be promising predictive biomarkers and therapeutic targets to prevent sorafenib resistance.