羟乙膦酸钠对去睾丸大鼠不同部位骨骼的影响

背景：男性骨质疏松的预防越来越受到人们的重视。 目的：建立去睾丸大鼠骨质疏松模型,通过骨形态计量学方法观察羟乙膦酸钠对不同部位骨骼的影响。 设计、时间及地点：随机对照动物实验,于2002-10/2006-09在广东医学院动物实验中心及骨生物学研究室完成。 材料：3.5月龄SD雄性大鼠40只,体质量(299±22) g。羟乙膦酸钠,成都化学制药厂生产,批号：970101。甲基睾丸酮片,广州侨光制药厂,批号：990701。 方法：将大鼠随机分成基础对照组、假手术组、去睾丸组、去睾丸加甲基睾丸酮组和去睾丸加羟乙膦酸钠组,每组8只。基础对照组在实验开始时处死。假手术组切开皮肤,暴露睾丸但不切除。其余大鼠按文献报道方法切除睾丸。假手术组和去睾丸组给予生理盐水,睾丸酮组给予甲基睾丸酮片1.8 mg/(kg•d),羟乙膦酸钠组给予羟乙膦酸钠36 mg/(kg•d),大鼠每只按5 mL/kg灌胃给药,连续给药90 d。 主要观察指标：测量胫骨上段、第5腰椎松质骨和胫骨中段皮质骨骨组织形态计量学参数。 结果：与假手术组比较,去睾丸组大鼠胫骨上段和腰椎松质骨骨小梁面积百分率、骨小梁数量或骨小梁厚度减少(P < 0.05和0.01),而骨小梁分离度、标记周长百分数、骨形成率、每毫米破骨细胞数均增加(P < 0.05和0.01)。与去睾丸组比较,羟乙膦酸钠和睾丸酮组大鼠胫骨上段和腰椎松质骨骨量均增加,而骨形成和骨吸收的参数均降低,羟乙膦酸钠组与睾丸酮组比较差异无显著性意义。各组大鼠胫骨中段皮质骨形态计量学参数均无明显变化。 结论：羟乙膦酸钠能预防鼠造成的胫骨上段和腰椎松质骨丢失,但对胫骨中段皮质骨无明显影响。     

雌孕激素联合对去卵巢大鼠骨密度和骨形态计量学的影响

背景：雌孕激素联合治疗绝经后骨质疏松症不仅能减轻雌激素的不良反应,而且能增强疗效,越来越引起关注。 目的：验证雌孕激素联合对去卵巢雌性SD大鼠骨密度和骨组织形态计量学的作用。 方法：雌性SD大鼠随机分为5组。假手术组仅行开关术;其余各组大鼠双侧卵巢切除。雌二醇组和雌二醇+左炔诺孕酮组术后给予17β–雌二醇10 μg/(kg•d) 灌饲,左炔诺孕酮组和雌二醇+左炔诺孕酮组术后给予18-甲左炔诺孕酮60 μg/(kg•d)灌饲,假手术组和卵巢切除组予等量生理盐水灌饲。实验12周后处死大鼠。采用DEXA骨密度仪测定全身骨密度,截取第4腰椎进行骨形态计量学静态参数和动态参数的测量,测定骨代谢生化指标。 结果与结论：卵巢切除组和左炔诺孕酮组全身骨密度、股骨质量低于假手术组、雌二醇组和雌二醇+左炔诺孕酮组 (P < 0.05),雌二醇+左炔诺孕酮组和雌二醇组差异无显著性意义( P > 0.05)。与假手术组比较,卵巢切除组和左炔诺孕酮组骨小梁面积百分数、骨小梁厚度、骨小梁数量下降(P < 0.05),骨小梁分离度增加(P < 0.05),骨矿化沉积率、骨表面积骨形成率、骨体积骨形成率和骨组织体积骨形成率增加(P < 0.05)。与卵巢切除组相比,雌二醇组和雌二醇+左炔诺孕酮组骨小梁面积百分数、骨小梁厚度、骨小梁数量上升(P < 0.05),骨小梁分离度降低(P < 0.05),骨表面积骨形成率和骨体积骨形成率降低(P < 0.05)。雌二醇+左炔诺孕酮组和雌二醇组上述指标比较,均差异无显著性意义( P > 0.05)。结果证实,17β-雌二醇和左炔诺孕酮联合应用可增加骨密度,降低骨转换率,且无明显抑制骨形成作用。     

仙灵骨葆治疗骨质疏松大鼠：血清学及骨组织形态计量学评价

背景：目前对于骨质疏松的治疗多为抑制骨吸收,有研究报道仙灵骨葆可促进骨形成,但具体机制不清。 目的：通过干预去卵巢大鼠骨质疏松动物模型,探讨仙灵骨葆对骨质疏松大鼠骨量、生物力学性能及骨代谢的影响。 方法：将24只大鼠随机分为正常对照组、模型组和仙灵骨葆组。除正常对照组外,其他2组行卵巢切除。6周后仙灵骨葆组给予仙灵骨葆干预,模型组给予等量双蒸水。4周后各组留取尿液、血清检测血Ⅰ型原胶原氨基端延长肽、尿脱氧吡啶诺啉排泄率和Ⅰ型胶原氨基末端肽排泄率。取各组左侧股骨行骨密度测定,取左侧胫骨制备硬组织不脱钙切片,行骨组织形态计量学检测。 结果与结论：与模型组比较,仙灵骨葆组血Ⅰ型原胶原氨基端延长肽、尿脱氧吡啶诺啉排泄率、尿Ⅰ型胶原氨基末端肽排泄率,破骨细胞数、骨吸收周长百分数显著降低(P < 0.05),而远端骨密度和骨小梁体积均显著增高(P < 0.05),结果证实,仙灵骨葆可抑制骨吸收,促进骨形成,降低去卵巢大鼠骨转换水平,进而部分阻止其骨量丢失。     

雌二醇对铅中毒模型大鼠骨组织及骨代谢指标不能产生影响**

背景：关于铅中毒能否引起骨质疏松症及雌激素对其治疗是否有效尚无共识。 目的：观察雌二醇对去卵巢大鼠和铅中毒大鼠所致骨质疏松症的治疗效果。 方法：雌性大白鼠100只等分成正常对照组、去卵巢模型组、染铅模型组、雌二醇+去卵巢组和雌二醇+染铅模型组。建模后1周雌二醇+去卵巢组和雌二醇+染铅模型组皮下注射雌二醇(100 μg/kg),2次/1周,连续12周。 结果与结论：在去卵巢模型组和铅中毒组中骨钙、骨磷、血钙及血磷均出现降低(P < 0.01),血碱性磷酸酶升高(P < 0.01),骨组织形态呈现骨质疏松的病理改变。雌二醇+去卵巢组的骨代谢生化指标血钙、磷、和碱性磷酸酶和骨组织形态均恢复正常,而雌二醇+铅中毒组的骨代谢生化指标和骨组织形态呈现骨质疏松未出现明显改善迹象。铅中毒组和雌二醇+铅中毒组的骨铅和血铅明显高于正常对照组(P < 0.01)。说明铅中毒可引起骨质疏松的病理改变,雌二醇对去卵巢大鼠的骨质疏松症有良好治疗效果,而对铅中毒所致的骨质疏松症无明显疗效。     

卵巢切除股骨骨折大鼠骨愈合中降钙素的作用

背景：降钙素可活化腺苷酸环化酶蛋白激酶A通路及磷脂酶C通路,抑制破骨细胞的活性,可能治疗骨质疏松性骨折。 目的：观察降钙素对去卵巢大鼠股骨骨折愈合的作用。 方法：构建双侧卵巢切除骨质疏松右股骨骨折SD大鼠模型,然后分别皮下注射生理盐水和降钙素(16 IU/kg),隔日1次,于骨折后3周和6周测量右股骨行骨密度,苏木精-伊红及抗酒石酸酸性磷酸酶染色,骨形态发生蛋白2及血管内皮生长因子免疫组化染色。 结果与结论：骨折后给予降钙素治疗的大鼠抗酒石酸酸性磷酸酶染色阳性细胞积分吸光度值较生理盐水治疗的大鼠显著减少(P < 0.05)。骨折后3周,两组骨折线均较清晰,骨痂体积无明显差别,骨折愈合以软骨内化骨过程为主,骨密度无显著性差异(P > 0.05)。骨折后6周,两组骨折线较模糊,骨痂体积无差别,骨小梁排列较有序,用药组股骨骨密度较对照组升高(P < 0.05)。两组在骨折后3周和6周的骨形态发生蛋白2及血管内皮生长因子差异无显著性意义(P > 0.05)。证实降钙素可以抑制去卵巢大鼠骨折部位破骨细胞活性,但无明显促进大鼠股骨骨折愈合的作用。     

不同载荷环境对去势大鼠骨组织形态计量学的影响

背景: 采用动态无损伤加载系统对去势大鼠骨组织形态计量学研究的文献报道较少。 目的：观察不同强度力学加载对去势大鼠骨组织形态计量学参数的影响。 设计、时间及地点：对比观察骨形态计量学指标,于2007-04/08在吉林大学生物医学工程研究室完成。 材料：9月龄雌性SD大鼠35只,随机分为假手术组、去势对照组、去势加载1 N组、去势加载2 N组、去势加载4 N组,每组7只。 方法：将去势对照组和去势加载组大鼠双侧背部卵巢切除,假手术组背部切口除去少量脂肪后,闭合伤口。大鼠去势1周后,去势加载组采用自行研制的动态无损加载系统对大鼠胫骨两端开始加载,加载载荷分为1,2,4 N,15 min/d,加载4周。 主要观察指标：胫骨近端骨组织形态计量学参数的变化。 结果：去势加载组骨小梁面积、骨小梁数量、骨小梁厚度均高于去势对照组(P < 0.05,P < 0.01),去势加载4 N组和去势加载2 N组大鼠骨小梁面积、骨小梁厚度高于去势对照组(P < 0.001);去势加载4 N组骨小梁分离度较去势对照组下降 (P < 0.05),随着加载载荷的增加,骨小梁面积、骨小梁数量、骨小梁厚度有增加并接近假手术组的趋势,骨小梁分离度有下降趋势。假手术组单荧光标记表面、双荧光标记表面均低于去势对照组。随着加载载荷的增加,单荧光标记表面、双荧光标记表面、双标间距、骨矿化沉积率均有增加趋势;去势加载2 N组和去势加载4 N组骨矿化沉积率均明显高于去势对照组(P < 0.05)。 结论：在1~4 N范围内,随着加载载荷的增加,去势大鼠各个骨形态计量学参数都有优化的趋势,骨组织微观结构有较大的改善,骨量丢失减少,骨质疏松进程减慢。     

葛根素联合雌二醇干预去卵巢大鼠骨组织和骨代谢的变化**

背景：用中药与雌激素治疗骨质疏松症,可能减少激素用量,进而减少不良反应和并发症的发生。 目的：观察小剂量葛根素联合雌二醇对去卵巢大鼠的骨组织和骨代谢的影响。 方法: 5月龄健康雌性大白鼠分为假手术组、去卵巢模型组、葛根素组、雌二醇组和小剂量葛根素+雌二醇组,建立去卵巢动物模型,分别皮下注射雌二醇100 μg/kg,2次/周和/或葛根素25 mg/kg,1次/d。在第4,8,12和20周,每组随机取6只大鼠取股骨切片观察骨组织,采血测量血钙、磷和碱性磷酸酶。 结果与结论：去卵巢模型组第4,8周与假手术组相比血钙、磷明显降低(P < 0.01),血碱性磷酸酶均明显升高(P < 0.01),骨组织呈骨质疏松的病理改变。3个用药组与假手术组相比骨组织和血钙、磷和碱性磷酸酶无明显差异(P < 0.05)。小剂量葛根素+雌二醇组与葛根素组或雌二醇组相比骨组织和血钙、磷和碱性磷酸酶无明显差异(P > 0.05)。小剂量的葛根素联合雌二醇对去卵巢大鼠的骨质疏松症的治疗效果与单独使用较大剂量的葛根素或较大剂量的雌二醇效果相近。 关键词：葛根素; 雌二醇;去卵巢大鼠;骨组织;生化指标     

丹参素对大鼠牙槽骨代谢的影响*

背景：有研究表明胰岛素样生长因子Ⅰ降低是骨丢失的早期标志。 目的：测定大鼠牙槽骨组织中胰岛素样生长因子Ⅰ的活性,探讨丹参素防治牙槽骨骨质疏松症的可能机制。 方法：SD大鼠随机分为对照组、去卵巢组和丹参素组,后两组行双侧卵巢切除,对照组和去卵巢组用蒸馏水灌胃,丹参素组用丹参素12.5 mg/(kg•d)灌胃。给药90 d后取大鼠牙槽骨,检测牙槽骨量、牙槽骨组织中胰岛素样生长因子Ⅰ活性。 结果与结论：与对照组相比,去卵巢组骨小梁面积百分数减少33.88%(P < 0.05),骨小梁分离度增加43.58%(P < 0.05),牙槽骨骨量明显减少,牙槽骨组织中胰岛素样生长因子Ⅰ表达变少、变弱(P < 0.05)。与去卵巢组相比,丹参素组骨小梁面积百分数增加了45.45%(P < 0.05),牙槽骨骨量明显增多,牙槽骨组织中胰岛素样生长因子Ⅰ表达增强(P < 0.05)。结果证实,丹参素能促进牙槽骨组织胰岛素样生长因子Ⅰ活性,防止去卵巢大鼠牙槽骨的丢失。     

骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化*◆

背景：有研究表明经典补肾方剂左归丸可用于治疗绝经后女性的骨质疏松。 目的：观察骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化。 方法：将SD大鼠麻醉下结扎上颌第一磨牙建立牙周炎模型、摘除大鼠卵巢建立骨质疏松模型,去势3个月后分别用左归丸和戊酸雌二醇治疗3个月。 结果与结论：左归丸、戊酸雌二醇治疗均能促进大鼠牙槽骨的新生,减轻牙周附着丧失(P < 0.05),使破骨细胞数量减少 (P < 0.05),牙周组织中骨保护素水平升高(P < 0.01),降低了血清中的碱性磷酸酶水平(P < 0.01)。结果证实,左归丸、戊酸雌二醇在改善骨质疏松性牙周炎大鼠牙槽骨结构的基础上,促使颌骨骨量增加。     

海藻酸多糖衍生物治疗大鼠骨质疏松

背景：作者既往研究发现海藻酸多糖衍生物有促进骨细胞生长的作用。 目的：探索海藻酸多糖衍生物治疗骨质疏松的效果。 方法：60只Wistar雌性大鼠随机分成对照组，治疗组和模型组，每组20只。治疗组和模型组大鼠用维甲酸诱导产生骨质疏松模型。治疗组大鼠每只每公斤每天10 mg多糖衍生物灌胃，模型组每只每公斤每天10 mg葡萄糖灌胃，持续2周。观察大鼠股骨病理形态学和骨组织形态计量学变化。 结果与结论：与对照组相比，模型组大鼠股骨骨小梁面积、平均骨小梁厚度、骨小梁密度显著降低，而髓腔质间隔宽度则明显增加；经过海藻多糖衍生物治疗后，治疗组大鼠股 骨平均骨小梁密度，平均骨小梁厚度和骨小梁面积较模型组均显著上升，同时髓腔质间隔宽度明显下降；说明海藻酸性多糖能有效促进骨细胞生长，可治疗和预防骨质疏松。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of Legislation of 1933 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -