延续性护理干预对降低泌尿系结石患者复发率的影响

目的探讨延续性护理干预对降低泌尿系结石患者复发率的影响。方法选择2016年2月至2017年6月250例在达州市中西医结合医院进行治疗的泌尿系结石患者,采用随机数字表法将患者分为两组,每组各125例。对照组实施常规护理,观察组在此基础上加以延续性护理。对比两组患者的复发率、自我护理能力及治疗依从性。结果对照组复发率为14. 4%,明显高于观察组的4. 0%(P<0. 05)。干预后两组患者心理、躯体活动、饮食及治疗方面自我护理能力均得到明显提升,但观察组提升幅度更大(P<0. 05)。观察组治疗依从良好率为96. 0%,明显高于对照组的88. 0%(P<0. 05)。结论延续性护理较常规护理可明显降低泌尿系结石患者复发率,提高其自我护理能力及治疗依从性。     

Inhibition of hepatic δ-aminolevulinate dehydratase activity induced by mercuric chloride is potentiated by N-acetylcysteine in vitro

Mercuric chloride (HgCl)₂ is a toxic metal that causes oxidative damage in several tissues. N-acetylcysteine (NAC) is a sulfhydryl compound with antioxidant activity. In the present study, we investigated the in vitro effects of the association between HgCl₂ and NAC in tissues of mice. For this purpose, we evaluated the in vitro effect of HgCl₂ + NAC association on δ-aminolevulinate dehydratase (δ-ALA-D) activity and on thiobarbituric acid reactive substances (TBARS) levels in liver and kidney of mice. The results demonstrate that HgCl₂ inhibited δ-ALA-D activity in both tissues. Hepatic δ-ALA-D activity inhibited by HgCl₂ was potentiated by the highest concentration of NAC. The inhibition of hepatic δ-ALA-D activity seems to be related to sulfhydryl groups oxidation of the enzyme. We observed also that HgCl₂ increased TBARS levels in kidney and liver. Hepatic TBARS levels were reduced by NAC, at higher concentration. In contrast, NAC, at higher concentration, increased renal TBARS levels. In conclusion, the inhibition of hepatic δ-aminolevulinate dehydratase activity induced by HgCl₂ is potentiated by NAC in vitro, and this effect is not related to hepatic lipid peroxidation.     

安非他酮联用碳酸锂缓释片治疗双相抑郁的对照研究

目的:探讨安非他酮联用碳酸锂缓释片治疗双相抑郁的疗效及安全性。方法:进行8周开放式前瞻性随机对照研究,将78例符合《精神疾病诊断与统计手册》第4版(DSM-IV)双相抑郁诊断标准的住院患者随机分成观察组(安非他酮联用碳酸锂缓释片治疗,n=40)及对照组(单用碳酸锂缓释片治疗,n=38),分别在基线及1、2、4、8周末应用汉密尔顿抑郁量表(HAMD-17)评定疗效,同时应用Bech-Rafaelsen躁狂量表(BRMS)评定转躁情况,用治疗中出现的症状量表(TESS)及实验室检查评定不良反应。结果:8周末两组HAMD总分(8±3,8±4)与基线(24±7,25±8)相比均明显降低(P<0.01),两组间HAMD总分比较差异无统计学意义(P>0.05)。第1、2周末观察组的HAMD总分(21±7,12±5)分别低于对照组(25±8,16±6)(P<0.05)。同时观察组第2周末的有效率(30%)及治愈率(20%)亦明显高于对照组的10.5%、2.6%(P<0.05)。第4、8周末时观察组HAMD总分分别为9±4、8±3,与对照组(9±5,8±4)比较无统计学差异(P>0.05),同时第8周末两组有效率(90%vs89.5%)及治愈率(62.5%vs60.5%)比较亦无统计学差异(P>0.05)。两组间不良反应类似,研究过程中两组均无病例转躁。结论:安非他酮联用碳酸锂缓释片及单用碳酸锂缓释片治疗双相抑郁均安全有效,安非他酮联用碳酸锂缓释片治疗双相抑郁可加快起效速度,同时并不增加转躁风险。     

Cd modifies hepatic Zn deposition and modulates δ-ALA-D activity and MT levels by distinct mechanisms

Cadmium (Cd) is a pollutant that is harmful to human and animals. The liver is a target for Cd accumulation and it can disrupt Zn homeostasis. Here we examined the interaction of Zn and Cd to determine how these two metals could affect δ-aminolevulinate-dehydratase (δ-ALA-D) and metallothionein (MT), two potential molecular endpoints for Cd hepatotoxicity. Cd exposure (0.25 and 1 mg kg1 body weight, i.p., for 10 days) caused a marked increase in hepatic Zn deposition, which was not modified by treatment with Zn (2 mg kg1 , i.p.). Cd caused a dose-dependent increase in hepatic Cd content that was not modified by Zn. Zn and/or Cd treatment increased hepatic δ-ALA-D activity, although the increase caused by Cd was less marked. Reactivation index of δ-ALA-D by DTT was decreased by Zn and Cd exposure, which indicates that Zn protects enzyme from oxidation. Hepatic MT was increased only after exposure to 1 mg kg(-1) Cd and Zn reduced the stimulation of MT synthesis. The results presented here indicate that Cd can redistribute Zn from non-hepatic tissues to liver and the increase in hepatic Zn deposition can account for the increase in hepatic δ-ALA-D activity after Cd exposure. However, Zn blocked the increase in hepatic MT levels caused by Cd. Thus, the modulation of the two molecular endpoints of Cd toxicity used here was distinct, which indicates that the mechanism(s) involved in Zn and Cd distribution, δ-ALA-D and MT regulation are not coincident.     

我院门诊口服钙制剂临床应用分析

目的评估口服钙制剂的临床应用情况。方法对医院2007年11月至2008年1月口服钙制剂的门诊处方进行统计分析。结果口服钙制剂的临床应用广泛,女性与中老年人使用尤多,补钙现象普遍。结论钙制剂有过度使用的趋势,补钙需谨慎。     

δ-氨基-γ-酮戊酸脱水酶和维生素D受体基因多态性与铅肾毒性易感性的相关研究

目的探讨δ-氨基-γ-酮戊酸脱水酶(ALAD)和维生素D受体(VDR)基因多态性以及基因-基因、基因-环境之间的联合作用对铅肾毒性的作用。方法选择233名铅作业工人,根据工人接触铅水平是否超过职业接触限值将其分为两组,分别测定血铅、尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)、尿β2-微球蛋白(β2-MG)和尿肌酐,全血提取DAN基因组,多聚酶链反应-限制性片段长度多态性(PCR-RFLP)法分析ALAD和VDR基因多态性。结果超职业限值组,ALAD1-2/2-2基因型和ALAD1-1基因型工人尿NAG的浓度分别为(2.12±0.07)U/mmol Cr和(1.73±0.03)U/mmol Cr,差异具有显著性P<0.05;VDR-Bb基因型的工人尿β2-MG浓度[(20.94±0.12)μg/mmol Cr]高于携带VDR-bb基因型工人的尿β2-MG浓度[(15.28±0.09)μg/mmol Cr](P=0.01)。多因素Logistic回归分析发现,铅接触、高血铅等环境因素以及环境-基因的联合作用都是铅作业工人肾损害的危险因素,接铅水平、血铅水平、ALAD基因型和接铅水平的联合作用引起尿NAG异常的OR值分别为6.85(2.51～10.87)、2.41(1.70～3.41)、3.01(1.10～8.19)。结论在高铅浓度接触下ALAD和VDR基因型与铅肾毒性有关,ALAD-2等位基因和高铅接触是加重铅肾毒性的危险因素。     

Long-term sucrose and glucose consumption decreases the delta-aminolevulinate dehydratase activity in mice

OBJECTIVE: This study evaluated the long-term effects of high-glucose (GLU) and high-sucrose (SUC) diets on the development of obesity, abdominal fat deposition, glucose intolerance, oxidative stress and effects on delta-aminolevulinate dehydratase (delta-ALA-D) activity in various organs. In particular, the effect of aging on these parameters was evaluated. METHODS: Mice were assigned to a baseline, control, or experimental group. The control group was provided with tap water and experimental groups with solutions of glucose or sucrose for 30 wk. To verify the effect of aging, young mice (baseline group, 8 wk old) were compared with aged animals (control and experimental groups, 38 wk old). RESULTS: Consumption of GLU or SUC diets caused increases in body weight, abdominal fat index, and fasting plasma glucose levels. A positive correlation was observed between the abdominal fat index and fasting glucose levels. There was a significant increase in levels of thiobarbituric acid-reactive species (TBARS) and a significant decrease in delta-ALA-D activity in various tissues of GLU and SUC feeding mice. Importantly, the dithiothreitol-induced enzymatic reactivation in the GLU and SUC groups was significantly higher than in the control group, and in the aged group it was significantly higher than in the baseline group. After 30 wk, the experimental groups had a decrease in delta-ALA-D activity and an increase in TBARS levels in relation to the baseline group. CONCLUSION: Alterations in the activity of the delta-ALA-D found in this work demonstrate the possible contributions of hyperglycemia and aging for protein oxidation, leading to impairment of its biologic function.     

多粘菌素B对豚鼠内耳碳酸酐酶活性的影响

为了解多粘菌素Ｂ（ＰＢ）对内耳碳酸酐酶（ＣＡＨ）的影响，用Ｈａｎｓｓｏｎ法和Ｙｏｋｏｔａ法观察豚鼠鼓室注射生理盐水或ＰＢ１万Ｕ／ｍｌ后内耳ＣＡＨ的定位。结果发现生理盐水组豚鼠内耳ＣＡＨ分布广泛，血管纹、内外毛细胞表现为极强阳性，前庭暗细胞表现为强阳性。ＰＢ组内耳ＣＡＨ活性普遍减低，电镜下外毛细胞内ＣＡＨ反应产物几乎消失，并且出现细胞水肿。推测ＰＢ破坏细胞膜的通透性后影响ＣＡＨ的活性，加重对内耳的损害     

多孔碳酸钙陶瓷修复骨缺损的实验研究

目的 探讨多孔碳酸钙陶瓷修复骨缺损的可行性。方法 取20只新西兰大白兔，采用兔桡骨干1．5cm缺损的动物模型并植入多孔CaCO3陶瓷，分别于术后2、4、8、12及16周处死后取材，行大体、X线、扫描电镜和组织切片观察。结果 植入材料4周扫描电镜显示材料的骨结合紧密、且无纤维组织界面；组织学观察12周植入材料内有较多板层骨生成、植入材料被吸收，骨缺损得到修复。结论 多孔CaCO3陶瓷具有良好的生物相容性和降解率，是一种替代自体骨修复骨缺损较理想材料。     

Short-term toxicity of 1-naphthaleneacetic acid in rats.

In a 90-day feeding study, 4 groups of 10 male and 10 female rats received in the diet 0,200, 1000 and 5000 ppm 1-naphthaleneacetic acid (1-NAA). Growth and food intake was reduced significantly only in males on 5000 ppm. Haematological examination yielded essentially negative results except for a non-significant reduction at the 1000 and 5000 ppn levels in the leucocyte count, mainly due to a reduction in neutrophils. No significant effects were observed in the renal concentration test, urinalysis, renal histochemistry or histology of a wide range of organs at any level of 1-NAA tested. Increased relative weights of thyroid, testes, brain and liver were confined to the 5000 ppm level. The increase in relative liver weight was not accompanied by histological liver damage and was associated with elevated liver microsomal enzyme activity. The loss of glucose 6-phosphatase (G6Pase) and increase in glucose 6-phosphate dehydrogenase (G6PDH) seen histochemically in the centrilobular region of the liver in males on 5000 ppm, accompanied by glycogen depletion in the liver, could however be indicative of liver damage. On the basis of conventional criteria, a no-effect level of 1000 ppm would have been indicated by this study but in view of liver glycogen depletion at all levels tested a no-effect level was not established.