Objectives To analyze the effect of improved oven for defluorination in coal-burning endemic fluorosis areas in China, and to provide evidence for the prevention and control of fluorosis. Methods Electronic databases including CNKI, CBM, VIP and CDMD-D (1989 to 2005), were searched. We also checked the reference lists of relevant articles. We selected relevant articles according to the predefined inclusion and exclusion criteria. The methodological quality was assessed . Data on room heat preservation and the effect of improved oven for defluorination were collected in the surveillance spots of Three Gorges Reservoir. Correlation analyses were conducted between the improved oven and its effect parameters. Results Twelve articles of low quality met the selection criteria, of which 9 were graded C and 3 were graded D in terms of the methodological quality. A negative correlation was found between the decreasing rate of normal oven use and the decreasing rate of dental fluorosis as well as of urine fluorine (Pearson correlation coefficient r = – 0.87, – 0.63, Plt;0.01, lt;0.05, respectively). Analysis also revealed a positive correlation between room heat preservation and the decreasing rate of dental fluorosis as well as of normal oven use (the two Spearman correlation coefficients and P values were the same: r = –1.00, Plt;0.01). Conclusion High-quality studies on the effect of improved oven for defluorination in China are not available. Based on the current evidence, the improved oven for defluorination and the correct use, maintenance and house rebuilding for heat preservation may help to prevent fluorosis.
Amanitin-containing mushroom poisoning is one of the most harmful and lethal types of mushroom poisoning events. Its basic medical and clinical medical knowledge has not been fully understood and mastered, so the basic and clinical diagnosis and treatment of amanitin-containing mushroom poisoning has always been a hot research field of acute mushroom poisoning. This article focuses on the new progress in the epidemiology, toxicological properties, poisoning mechanism, clinical diagnosis and treatment of amanitin-containing mushroom poisoning, in order to provide the basis for further study, diagnosis and treatment of amanitin-containing mushroom poisoning for basic researchers and clinical medical staff.
目的：探讨醒脑静注射液联合纳络酮注射液在急性安定中毒治疗中的疗效。方法：本研究采用醒脑静注射液联合纳络酮注射液治疗急性安定中毒55例并与单纯纳络酮治疗的51例进行对照。106例患者均经静脉血毒物测定为安定中毒；来诊时均有意识障碍，平均年龄（30.35±7.95）合并酒精中毒及其他疾病20例，常规给予洗胃、补液、利尿促排泄、纠正电解质失衡、吸氧及抗感染等对症处理。结果：醒脑静注射液治疗组与对照组患者比较，神志恢复时间(h),治疗组(1.73±0.98)显著短于对照组(3.22±1.38)(P＜0.01)；同组患者就诊时与清醒后的神志、呼吸、血压、心率及瞳孔等临床指标比较差异有显著性(P＜0.05)。结论:醒脑静注射液与纳络酮联合应用，治疗急性安定中毒与对照组比较起效快、疗效确定，临床应用安全可靠。
ObjectiveTo observe the prognosis index in acute arsenic trihydride poisoning patients in order to provide references for early clinical treatment. MethodsWe retrospectively analyzed the clinical data of 20 acute arsenic trihydride poisoning patients treated between July 2010 and January 2014. The patients were divided into death group and survival group according to survival situation 90 days later. The length of time from onset to treatment, urine arsenic concentration, blood routine, hepatic and renal function, electrolyte, myocardial enzyme, arterial blood gas analysis were observed by single factor analysis, and the positive indexes were analyzed by logistic regression analysis to seek the potential influencing factors for survival. ResultsCompared with the survival group, the length of time from onset to treatment, urine arsenic, serum total bilirubin, creatinine, creatine kinase of the death group were significantly higher (P<0.05), while the value of pH, HCO3-, BE of the survival group were significantly lower (P<0.05). Logistic regression analysis revealed that these indexes remarkably affected patients' survival rate. ConclusionTherapeutic time window, extent of damage of heart, liver, kidney and acid-base imbalance are closely associated with the survival rate of arsenic trihydride poisoning patients, and timely treatment for above factors can be useful for improving prognosis.
ObjectiveTo investigate the effects of leptin on the oxidative damage in human retinal pigment epithelial (RPE) cells. MethodsHuman RPE cells (ARPE-19) were cultured in vitro, and randomly divided into control group and insulin resistance group. RPE cells were treated with 0, 10, 100 ng/mL leptin for 24, 48, 72 hours respectively. Then the levels of reactive oxygen species (ROS) expression in RPE cells were detected by 2', 7'-dichlorofluorescin-diacetate (DCFH-DA), and the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) expression in RPE cells were observed by immunocytochemistry (ICC), and the levels of human 8-oxoguanine DNA glycosylase l (hOGG1) expression in lysate were measured by Western blot. ResultsAfter 24, 48, 72 hours, the level of ROS (Control group:F=37.136, 37.178, 49.634; P < 0.05. Insulin resistance group:F=9.822, 28.881, 71.150;P < 0.05), 8-OHdG (Control group:F=88.643, 390.920, 1039.276;P < 0.05.Insulin resistance group:F=273.311, 299.155, 82.237;P < 0.05) and hOGGl (Control group:F=470.062, 1073.113, 295.456;P < 0.05. Insulin resistance group:F=240.032, 592.389, 527.760;P < 0.05) expression increased significantly with the increase of leptin concentration in control group and insulin resistance group. Under the same leptin concentration, the level of 8-OHdG has a trend that it was higher in the insulin resistance group than the control group. After 24 hours, the difference of hOGGl expression between control group and insulin resistance group was not significant (F=23.392, P > 0.05). After 72 hours, the level of hOGGl expression was significantly higher in the insulin resistance group than the control group (F=129.394, P < 0.05). The level of hOGGl expression was significantly higher at 48 hours than that at 24 hours and 72 hours (P < 0.05). ConclusionLeptin could induce the oxidative damage of RPE cells in normal and insulin resistance status. With the increase of leptin concentration and time extended, the degree of oxidative damage and its repair were both increased. The degree of oxidative repair increased with the increase of leptin concentration, but decreased with time extended.
In order to explore retinal toxicity and to estimatequot;safe dosagequot;of intravitreal gentamicin 21 Dutch-belted rabbits divided into 5 dosage groups and 1 control group were investigated.The results showed that, in 3 000mu;g group, optic disc swelling and vein dilating were observed ophthalmoscopieally. Histopathologie study displayed the retinal necrolysis. In 50~500mu;g groups,the retinal pigment change was revealed within 3~14 days after the injection.Histopathologic study displayed that the retinal damages were confined in outer layers of retina in early stage. Inner layers of retina were also influenced in late stage. The results demontrated that with increasing intravitreal gentamiein,retinal damages are gradully aggravated,and even if intravitreal gentamicin was in minimum dose,retinal damages was still observed. （Chin J Ocul Fundus Dis,1994,10:167-169）
摘要:目的:探讨加兰他敏对急性酒精中毒大鼠海马神经元N甲基D天冬氨酸(NMDA)·R2B的影响。 方法:将60只大鼠分为对照组、酒精组及加兰他敏组,每组各20只。酒精组以50％(v/v) 酒精12 mL/kg灌胃两次/日,共7d。加兰他敏组酒精(浓度、剂量同上)灌胃的同时腹腔注射加兰他敏2mg/kg一次/日,共7d。对照组以等量生理盐水灌胃。实验第8天取大鼠海马区做苏木精伊红（HE）染色,观察海马区的病理学变化;免疫组织化学采用SABC法,观察海马区神经元NR2B的表达。 结果: 病理学观察结果：对照组海马区神经细胞排列整齐,胞质淡染,无变性、坏死;酒精组神经细胞层次不清、排列松散、细胞数量减少,部分细胞变性;加兰他敏组神经细胞层次较清、排列较密,细胞数目较酒精组增; 免疫组织化学结果：酒精组与对照组比较NR2B阳性表达细胞数量明显减少(Plt;0.01);加兰他敏组与酒精组比较NR2B阳性表达细胞数量明显增高(Plt;0.05);加兰他敏组与对照组比较NR2B表达细胞数量无明显差异(Pgt;005)。 结论: 急性酒精中毒与海马区神经细胞的NR2B表达下调有关;加兰他敏具有保护急性酒精中毒导致的大鼠海马区神经细胞毒性的作用,其机制可能与加兰他敏上调NR2B的表达有关。Abstract: Objective: To study the effects of galanthamine on NmethylDaspartic acid receptor 2B (NMDAR2B, NR2B) in the hippocampus (HIP) of acute alcoholism rats. Methods: Total of 60 wistar male rats were randomly divided into control group, ethanol group and glanthamine group, and there were 20 rats in each group. The rats in ethanol group were given by intragastric administration with 50% alcohol (v/v) on the dose of 12 ml/kg twice per day, in control group were given by same dose of saline, and in galanthamine group were treated by intragastric administration with the same concentration and dosage of alcohol as in ethanol group and peritoneal injection with 2 mg/kg of galanthamine once per day for 7 days. In eighth day of experiment, the rats were sacrificed under etherization, and pathological changes of HIP’s zone of rat were observed by HEstaining, and expression of NR2B in neurons of HIP’s zone by immunohistochemical SABC method. Results: The results observed by histopathology showed that in control group, neurons of HIP’s zone lined up in order, cytoplasm had faint staining, and were no degeneration and necrosis; in ethanol group, nerve cells’ layer was unclear, structure was loose, cell number reduced and part of cells degenerated; in galanthamine group, layer of neurons was comparatively clear and arrangement was comparatively dense, and the cell number increased obviously more than ethanol group. The results detected by Immunohistochemistry for NR2B showed that the cell number with expression of NR2B in the HIP’s zone decreased significantly in the ethanol group than in the control group (Plt;0.01), increased in the galanthamine group than in the ethanol group (Plt;0.05), and had no difference between the galanthamin and control group (Pgt;0.05). Conclusion: Acute alcoholism may relate to down regulation of expression of neuron’s NR2B in HIP’s zone;The galanthamin has role of protection for neuron in HIP’s zone induced by toxicity of acute alcoholism, and its mechanism may relate to galanthamin upregulation NR2B expression.