腺嘌呤与氢化可的松大鼠肾阳虚模型造模方法比较

目的比较腺嘌呤诱导与氢化可的松诱导的SD大鼠肾阳虚模型的优劣,从而得到临床症状、生化指标更符合中医“肾阳虚”型的动物模型,以供科研、教学使用。方法雄性SD大鼠100只,随机分成正常组、腺嘌呤造模组及氢化可的松低剂量组、中剂量组、高剂量组各20只,造模成功后检测血肌酐（Scr）、尿素氮（BUN）、尿液中17-羟皮质类固醇（17-OH）和血浆中甲状腺激素（13、T4）、睾丸酮（T）、雌二醇（E2）及模型大鼠骨密度。结果无论从症状主证方面,还是客观指标方面（除骨密度外）,腺嘌呤诱导的SD大鼠肾阳虚型动物模型在生化指标研究方面均优于氢化可的松诱导组。结论腺嘌呤诱导的肾阳虚证SD大鼠模型在症状主证方面及其相关的生化研究方面优于氢化可的松组。     

慢性心力衰竭中医证候的研究进展

慢性心力衰竭是大多数心血管疾病的最终转归,也是最主要的死亡原因之一。本文主要探讨中医对慢性心力衰竭证候的认识,从病因病机、证候分布规律、临床动态分期3个方面对慢性心衰的证候研究现状做一简要的综述,分析证候内部及证候之间的组合特点,为临床研究提供依据,推动相关证型的标准化、规范化进程。     

慢性缺氧模型与病证相关性的研究进展

长期或反复处于缺氧状态,可以影响机体组织器官的正常供氧,使心血管、呼吸和神经等系统功能紊乱,从而诱导机体多系统损伤,严重危害人体健康.随着现代人生活方式以及饮食结构的改变,生活中有氧运动不足再加上地球污染与破坏逐年加剧,人类不知不觉地处在一个慢性缺氧的环境中.因此,了解并重视慢性缺氧对生理功能的影响造成的危害,从而采取相应的防治措施具有重要的意义.国内外学者根据宏观指征与生理生化指标等微观指征变化的不同,采用不同缺氧周期与缺氧强度制备模拟不同疾病与证候的慢性缺氧模型,对慢性缺氧诱导的生理病理演变过程进行了大量的探索研究.本文综述了近5年来慢性缺氧模型与阻塞性睡眠呼吸暂停综合征、肺动脉高压、心血管疾病、神经退行性病变等疾病以及气阴两虚、气滞血瘀等证候相关性的研究进展,为遴选体现与缺氧相关病证临床特点的动物模型,并用以合理评价药物的作用特点提供参考.     

糖皮质激素诱导肾阳虚抑郁症动物模型研究进展

临床上,肾阳虚是抑郁症患者的主要中医证型之一,针对肾阳虚抑郁症患者采用温补肾阳的方法取得较好疗效,但针对肾阳虚型抑郁症动物模型的复制方法尚无明确统一的规定和标准,为肾阳虚型抑郁症的研究带来困扰,因此,为了进一步完善肾阳虚型抑郁症动物模型的复制方法,现对近十五年来采用糖皮质激素类药物诱导的肾阳虚型抑郁症动物模型的造模方法及评价指标进行系统分析,比较异同,为肾阳虚抑郁症的合理造模提供参考依据。     

应用代谢组学探讨胸痹证候分型的可行性

冠心病是严重危害我国人群健康的重要疾病之一,属中医胸痹证候.大量数据显示益气活血中药对冠心病疗效优于西药,然而胸痹的证候研究一直没有取得突破,而证是中医临床的关键.代谢组学是继基因组学、蛋白组学后兴起的又一系统生物学研究方法,目前已被广泛的用于疾病的早期诊断、代谢毒理、药物开发等领域.本文拟就把代谢组学运用于中医胸痹症候的可行性进行分析.     

基于系统生物学和病证结合模型对中医证候表征的研究

证候,作为中医临床诊治的重要依据,是中医辨证论治经验中的核心要素和学理支点,认识中医证候的现代内涵对于揭示中医辨证论治经验的科学内涵具有重要意义,也是当前中医药研究中的一个难点.本研究基于中医证候的特点和2型糖尿病的现代病理学认识,运用系统生物学原理,在建立2型糖尿病病证演变大鼠(Rattus norvegicus)模型的基础上,动态观测模型动物因时演变中跨系统多维指标群的变化,比较中医辨治经验的相关方药对模型演变不同阶段的干预效应,引入有关数理分析方法对多批实验数据进行系统分析,以探讨T2DM疾病发展中的中医证候演变特点及其现代表征.结果发现,由高糖高脂喂饲联合STZ注射复制出的T2DM大鼠模型在其发展的不同阶段表现出中医证候(气阴二虚、痰浊、瘀血)演变的特点和跨系统多指标群的组合特征,涉及现代医学糖脂代谢、神经-内分泌、氧化应激、炎症反应、血管活性等病理机制;相关方剂对于不同阶段的模型均有不同程度的干预作用,其中因证治方则表现出一定的效应优势,且与相应阶段的病证指标群具有一定的关联.该项目从证候演变的角度为论证中医辨证论治中"方证相关"经验的合理性提供了一定的科学依据,对于建立具有中医辨证论治特色的病证结合的实验治疗学平台具有重要意义.     

三黄健齿汤联合牙周局部治疗对慢性牙周炎临床疗效及炎症因子的影响

目的:研究三黄健齿汤联合牙周局部治疗慢性牙周炎的临床疗效,并观察其对炎症因子的影响,为临床诊疗提供依据。方法:选取2015年10月到2016年3月我院收治慢性牙周炎患者130例,按照随机数字表法将患者分为治疗组和对照组,每组65例,对照组给予洁治和龈下刮治、根面平整等,治疗组在对照组的基础上给予三黄健齿汤治疗,比较治疗前和治疗后牙周探诊深度(PD)、牙龈出血指数(BI)、牙龈沟液白介素-1β(IL-1β)、白介素-6(IL-6)水平变化,并比较中医证候评分。结果:治疗后两组PD和BI均显著降低,差异有统计学意义(P0.05),但两组间比较差异无统计学意义(P0.05);治疗后两组IL-1β和IL-6均显著降低,且治疗组低于对照组,差异有统计学意义(P0.05);治疗后两组中医主证候群和次证候评分均显著降低(P0.05),两组主证候群评分比较差异无统计学意义(P0.05),治疗组次证候评分显著低于对照组(P0.05)。结论:三黄健齿汤联合牙周局部治疗对慢性牙周炎具有较好疗效,能有效降低炎症因子,改善次证候评分。     

小鼠腹腔水液体积检测方法建立及肾阳虚模型小鼠水负荷的评价

目的 建立小鼠腹腔水液体积的检测方法并评价肾阳虚模型小鼠的水负荷状况.方法选取正常小鼠12 只,根据＂阿基米德原理＂改进实验方法测量小鼠的腹腔水液体积,对其腹腔水液体积测量的稳定性进行评价;选取正常小鼠5 只,利用小鼠腹腔水液检测方法对其进行线性关系考察;将SPF 级昆明种雄性小鼠30 只,随机分为正常组和肾阳虚模型组,肾阳虚模型组上午按0.08 mg/10 g 腹腔注射苯甲酸雌二醇注射,正常组腹腔注射相同剂量的大豆油,下午两组均腹腔注射1 mL 的生理盐水造成水负荷,连续15 d.结果该测量方法的稳定性和线性关系考察均取得了良好的效果;与正常组相比,造模后体重显著性降低（P ＜0.01）,肛温显著性降低（P ＜0.01）,趾温差异无显著性（P ＞0.05）;自主活动明显减少（P ＜0.05）;游泳时间明显降低（P ＜0.01）,综合评价说明肾阳虚造模成功;肾阳虚模型组的腹腔水液测量体积整体表现出下降的趋势,腹水指数显著高于正常组（P ＜0.05）.结论该检测方法可以快速、准确的测量出小鼠腹腔水液测量体积和腹水指数的变化,可以能较客观地评价中医证候的特点,为中医证候症状描述进一步提供实验数据支持.     

慢性心衰新西兰家兔某些生化指标和心功能的改变

目的：研究慢性心衰实验动物某些生化指标和心功能的变化,为慢性心衰的诊断提供依据。方法：使用阿霉素制备新西兰兔慢性心衰模型,将20只新西兰兔随机分为模型组（n=15）和对照组（n=5）,分别耳缘静脉注射阿霉素（ADR）和生理盐水1 ml/kg,每周2次,共8周。随后进行心肌酶、颈动脉压、心电和心音信号的检测。结果：经统计学分析得知,两组的各项指标均有显著性差异（P<0.05）。结论：慢性心衰导致新西兰兔心肌受损,收缩功能和舒张功能下降,心脏储备指标有助于慢性心衰的诊断。     

心气虚血瘀证动物模型的构建与评价

中医证候模型起步较晚,为推动中医现代化的发展,要求深入研究和探讨中医证候动物模型。气虚血瘀证作为心血管疾病常见的证型,其动物模型的建立是中医证候实验研究的热点问题,通过对各种心气虚血瘀证动物模型造模方法进行研究,观察实验动物的宏观体征、超声心动图、血流动力学等指标,客观评价其造模方法,同时提出当前中医证候动物模型研究中存在的问题,并对其进行了展望,为今后探究心气虚血瘀证的临床治疗提供模型支持。     

犬、猫肾功能衰竭的中西医结合疗法

本文介绍了中医的肾脏生理功能理论、阐述了目前西兽医及中兽医对犬猫急性肾功能衰竭、慢性肾功能衰竭发病原因的认识,分析了肾功能衰竭的中医辨证分型和急性肾功能衰竭、慢性肾功能衰竭的治疗原则。     

脂代谢异常对肾病的影响

肾脏疾病发展为慢性肾衰竭是个不可逆的过程,脂质代谢的异常,对肾病患者具有重要的影响。多项实验已经证实,即使在肾病的早期阶段,也会出现不同程度的脂质及脂类代谢的异常,高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、脂联素、瘦素等脂类代谢相关物质发生改变,不仅对血浆脂代谢产生影响,对于肾小球及肾小管的结构及功能也会有一定的损伤作用。肾病患者,如肾病综合征、慢性肾衰竭等疾病,多数有肾小球及肾小管间质的损伤,肾脏的脂毒性加重肾单位的破坏。随着人们对于慢性肾脏病认识的逐渐深入,降脂治疗的普遍应用,人们普遍认为改善血浆中脂类的水平,对于肾病的治疗,尤其对于慢性肾衰竭的预防具有重要作用。     

家族性肾阳虚的基因功能富集分析

在临床调查中筛选出一个典型肾阳虚证家系,选取典型肾阳虚证患者3例及家系内正常人3例进行表达谱芯片试验．芯片分析结果显示,肾阳虚证者表达上调基因106条,下调基因16条．通过基因功能分类及深入的基因功能富集分析发现,肾阳虚证与GnRH信号通路及氧化磷酸化密切相关（P≤005）,从而为肾阳虚证本质的研究提供了新的思路,但具体的机制有待深入研究．     

1982 Borden Award lecture. Nutritional, biochemical, and clinical aspects of inositol and phosphatidylinositol metabolism

Recent advances in nutritional and biochemical research have substantiated the importance of myo-inositol both as a dietary component and a constituent of cellular phosphatidylinositol. This work has indicated the importance of acyltransferase reactions for the enrichment of membrane phosphatidylinositol in arachidonic acid and the formation of the 1-stearoyl 2-arachidonoyl molecular species which commonly predominate in mammalian tissues. Inositol deficiency in animals has been shown to produce an accumulation of triglyceride in liver, intestinal lipodystrophy, and other abnormalities. Cellular functions elucidated for phosphatidylinositol in biological membranes include mediating cellular responses to external stimuli and serving as a source of arachidonic acid for the biosynthesis of prostaglandins including thromboxane. An alteration in inositol metabolism has been documented in patients with diabetes mellitus and chronic renal failure which has led to clinical interest in modulating dietary inositol levels in the prevention and treatment of human disease.     

2型糖尿病患者中医证型与糖脂代谢和甲状腺功能的关系

目的:探讨2型糖尿病患者中医证型与糖脂代谢和甲状腺功能的关系。方法:选择2016年1月-2017年12月期间武警宁夏总队医院收治的2型糖尿病患者104例,根据中医证型将其分为湿热困脾组23例、阴虚热盛组21例、气阴两虚组20例、阴阳两虚组22例与血瘀脉络组18例。检测并对比不同中医证型2型糖尿病患者糖脂代谢与甲状腺功能指标水平。结果:阴虚热盛组、气阴两虚组、阴阳两虚组与血瘀脉络组甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平低于湿热困脾组,高密度脂蛋白胆固醇(HDL-C)水平高于湿热困脾组(P0.05);阴阳两虚组TG、TC、LDL-C水平低于阴虚热盛组、气阴两虚组、血瘀脉络组(P0.05)。湿热困脾组、气阴两虚组、阴阳两虚组与血瘀脉络组空腹血糖(FPG)、餐后2h血糖(2hPPG)、糖化血红蛋白(GHb)水平低于阴虚热盛组(P0.05)。湿热困脾组、阴虚热盛组、气阴两虚组、血瘀脉络组游离甲状腺素(FT4)、游离三碘甲状腺原氨酸(FT3)水平高于阴阳两虚组,促甲状腺激素(TSH)水平低于阴阳两虚组(P0.05),各组总甲状腺素(TT4)、总三碘甲状腺原氨酸(TT3)水平总体比较差异无统计学意义(P0.05)。结论:糖脂代谢和甲状腺功能能够在一定程度上反映出2型糖尿病患者的中医证型变化,可作为2型糖尿病患者中医证型与病情变化的有效参考指标。     

An Unusual Cause of Renal Amyloidosis Secondary to Gout—the First Description of Familial Occurrence

Background: AA amyloidosis caused by the chronic inflammation accompanying gouty arthritis is extremely rare and familial occurrence has not been described so far. Case report: We present the case of two brothers (47 and 44 years old) with 7- and 10-year history of hyperuricaemia and chronic tophaceous gout with polyarticular involvement. The enzymatic assay performed in their erythrocytes proved the partial hypoxanthine-guanine phosphoribosyl transferase deficiency (Kelley-Seegmiller syndrome), the genetic defect of purine metabolism. Later on they developed proteinuria and chronic renal insufficiency /CRI/. Renal biopsy disclosed the combination of AA amyloidosis and gouty nephropathy in both the cases. Despite the standard treatment the older brother progressed to chronic renal failure. On the contrary, the younger one being longterm treated with oral colchicin have stabilized CRI. Conclusions: Only several cases of AA renal amyloidosis until recently, secondary to gout have been reported. Our case represents the first report of familial occurrence of this extremely rare disease.     

The role of insulin-like growth factor I monitoring in growth hormone-treated children

Growth hormone (GH) therapy has evolved rapidly over the past decade, and continuing research has established a clear role for therapeutic GH in a wide spectrum of disorders, including idiopathic GH deficiency (childhood- and adult-onset), Turner syndrome, Prader-Willi syndrome, small-for-gestational age children with failure of catch-up growth, AIDS-related catabolism, children with chronic renal failure, and idiopathic short stature. Although GH is used therapeutically in a wide variety of conditions, actual guidelines regarding the logistics of GH dosing continue to evolve, with data emerging regarding efficacy and safety. This review proposes a role for insulin-like growth factor I measurement in optimizing GH dosing.     

An unusual cause of renal amyloidosis secondary to gout: the first description of familial occurrence

BACKGROUND: AA amyloidosis caused by the chronic inflammation accompanying gouty arthritis is extremely rare and familial occurrence has not been described so far. CASE REPORT: We present the case of two brothers (47 and 44 years old) with 7- and 10-year history of hyperuricaemia and chronic tophaceous gout with polyarticular involvement. The enzymatic assay performed in their erythrocytes proved the partial hypoxanthine-guanine phosphoribosyl transferase deficiency (Kelley-Seegmiller syndrome), the genetic defect of purine metabolism. Later on they developed proteinuria and chronic renal insufficiency /CRI/. Renal biopsy disclosed the combination of AA amyloidosis and gouty nephropathy in both the cases. Despite the standard treatment the older brother progressed to chronic renal failure. On the contrary, the younger one being longterm treated with oral colchicin have stabilized CRI. CONCLUSIONS: Only several cases of AA renal amyloidosis until recently, secondary to gout have been reported. Our case represents the first report of familial occurrence of this extremely rare disease.     

Magnesium metabolism and its disorders

Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. Magnesium balance is maintained by renal regulation of magnesium reabsorption. The exact mechanism of the renal regulation is not fully understood. Magnesium deficiency is a common problem in hospital patients, with a prevalence of about 10%. There are no readily available and easy methods to assess magnesium status. Serum magnesium and the magnesium tolerance test are the most widely used. Measurement of ionised magnesium may become more widely available with the availability of ion selective electrodes.Magnesium deficiency and hypomagnesaemia can result from a variety of causes including gastrointestinal and renal losses. Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis. The use of magnesium as a therapeutic agent in asthma, myocardial infarction, and pre-eclampsia is also discussed.Hypermagnesaemia is less frequent than hypomagnesaemia and results from failure of excretion or increased intake. Hypermagnesaemia can lead to hypotension and other cardiovascular effects as well as neuromuscular manifestations. Causes and management of hypermagnesaemia are discussed.