镓盐对维甲酸致大鼠骨质疏松模型影响的实验研究

目的 研究镓盐对维甲酸致骨质疏松大鼠骨代谢的影响,为镓盐治疗骨质疏松提供实验依据。方法 用维甲酸建立大鼠骨质疏松模型,并通过氯化镓灌胃给药治疗两个月,应用生化、病理等方法研究其对反映骨质疏松相关指标的影响。结果 维甲酸可导致大鼠骨结构改变,密度降低,骨有基质含量下降,血清抗酒石酸酸性磷酸酶（TPAP）上升。应用氯化镓后,可增加骨密度,增加骨皮质厚度和骨小梁百分比,降低TRAP活性和碱性磷酸酶（AKP）活性,从而降低骨转换率。结论 镓盐是一种有效的降低骨转换率的药物。     

胰岛素样生长因子-Ⅰ对软骨细胞移植修复关节软骨缺损的作用

目的：观察胰岛素样生长因子－Ⅰ（insulin-like growth factor-Ⅰ,IGF-Ⅰ)对关节软骨缺损修复的作用。方法：采用组织工程方法制备骨基质明胶（BMG）－软骨细胞移植物。40只4－5个月龄的新西兰兔均分为软骨细胞实验组及软骨细胞对照组,BMG对照组,空白对照组。实验组兔膝关节注射IGF－Ⅰ,各对照组均注射等渗盐水。术后行大体,组织学观察及免疫组化检测。结果：实验组软骨细胞生长较快,术后24周修复的软骨组织Safranin-O染色,Ⅱ型胶原染色与正常关节软骨一致,软骨细胞呈柱状排列,软骨细胞对照组术后24周修复软骨组织Safranin-O染色较淡,部分软骨细胞呈柱状排列,BMG,空白对照组未修复。结论：IGF－Ⅰ能促进关节软骨缺损修复。     

携EGFP基因的逆转录病毒包装细胞的分选和滴度测定

目的 探讨利用荧光激活细胞分选技术获得有效重组逆转录病毒包装细胞系的方法。方法 用脂质体介导pLEGFP转染PA317细胞,用荧光显微镜观察转染结果;依据EGFP荧光利用流式细胞仪的分选技术获得多克隆和单克隆源性的包装细胞,并利用PCR、RT-PCR对其鉴定;以NIH3T3为靶细胞,对其滴度进行测定。结果 荧光显微镜显示用脂质体介导的方法成功的转染PA317细胞,在4次连续流式细胞仪分选后得到了稳定表达的多克隆和单克隆源性的包装细胞。PCR和RT-PCR分别从多克隆和单克隆源性的包装细胞细胞基因组DNA以及多克隆和部分(6/8)单克隆源性的包装细胞培养上清中的重组逆转录病毒RNA中扩增出了插入的EGFP片段。滴度测定显示得到的包装细胞能够产生有效的病毒滴度。结论 荧光激活细胞分选技术是获得有效病毒滴度的包装细胞的有效方法。     

钙缺乏与老年性痴呆症及其它神经性疾病

钙是人体的一个必需元素,适量的摄入钙对健康来说是必不可少的。钙缺乏可能是老年性痴呆的病因之一,在某些老年性痴呆病人中伴有继发性甲状旁腺机能亢进而导致钙代谢异常。本文从流行病学、临床语气和细胞生物学方面说明了钙缺乏与老年性痴呆症及其它神经性疾病的关系。     

T-2毒素对软骨Ⅱ型胶原蛋白和蛋白聚糖合成的影响以及硒的保护作用

目的探讨T-2毒素对软骨细胞主要间质成分Ⅱ型胶原蛋白和蛋白聚糖合成的影响和硒的保护作用。方法采用MTT法检测T-2毒素对软骨细胞存活率的影响;用TB染色法检测人软骨细胞蛋白聚糖表达;免疫组织化学检测人软骨细胞胶原蛋白Ⅱ表达;RT-PCR检测人软骨细胞Ⅱ型胶原蛋白和蛋白聚糖mRNA表达。结果T-2毒素在浓度为0．001～2mg／L的范围内．对软骨细胞的作用呈较典型的浓度依赖关系和时间依赖关系,而且随着作用时间的延长,浓度依赖关系更加明显。T-2毒素（10～20μg／L）可以抑制软骨细胞Ⅱ型胶原蛋白和蛋白聚糖的合成及其mRNA表达。而加硒能较明显刺激软骨细胞蛋白聚糖mRNA表达,部分减弱T-2毒素的这种抑制,有一定的保护作用,但不显示对T-2毒素引起的Ⅱ型胶原蛋白及其mRNA表达的保护作用。结论T-2毒素对软骨细胞Ⅱ型胶原蛋白和蛋白聚糖合成有明显的抑制作用,微量元素硒对T-2毒素引起的软骨细胞蛋白聚糖改变有一定保护作用。     

饮食加硼治疗维甲酸诱导骨质疏松模型大鼠的效果观察

目的观察饮食加硼治疗维甲酸诱导的骨质疏松模型大鼠的效果,为硼临床治疗骨质疏松症提供实验依据。方法SD大鼠32只,随机分为正常组(n=8)和骨质疏松模型组(n=24)。以维甲酸80mg.kg-1.d-1灌胃15d,诱导骨质疏松模型。模型复制成功后,骨质疏松模型组又随机分为无措施对照组(n=8)、饮食加硼治疗组(n=8)和雌二醇治疗组(n=8)。治疗30d后,测定大鼠血清钙、磷、硼含量,及碱性磷酸酶(AKP)和酸性磷酸酶(TRAP)活性,测量大鼠全身、腰椎和胫骨骨密度,并观察大鼠股骨形态计量学变化。结果四组大鼠血清Ca和P含量无显著性差异,而硼含量硼治疗组明显高于其它三组。对照组大鼠血清AKP和TRAP活性增加,股骨松质骨和皮质骨骨量减少,破骨细胞数量增加,腰椎、胫骨骨密度下降,呈现骨质疏松变化。饮食加硼和雌激素治疗组大鼠血清TRAP活性显著下降,股骨平均骨小梁数、平均骨小梁宽度、骨小梁面积百分比、皮质骨面积百分比和全身、腰椎、胫骨骨密度等显著增加,松质骨区破骨细胞数明显减少,与正常组大鼠骨质无明显差异。硼治疗组大鼠血清AKP活性及松质骨区活跃成骨细胞数显著增加。结论饮食加硼可提高大鼠血清硼含量,增加骨形成,减少骨吸收,对骨质疏松有明显的治疗作用。     

钙与骨骼肌和肌营养不良

PHT过量分泌可能是甲旁亢时肌肉异常的原因。钙浓度的增高可影响肌营养不良和以细胞钙内环境不稳定为特征的其他疾病的病理生理过程，因此肌营养不良也属于钙反常疾病。从流行病学、临床证据、实验模型和细胞生物学介绍了钙与肌营养不良的关系。     

大骨节病关节相关软组织损害的临床诊断意义

通过不同时期儿童手指关节体征（下简称指征）与Ｘ线的检出情况，指征与Ｘ线的对比，指征的Ｘ线监测，踝关节功能障碍所致下蹲不全与踝关节Ｘ线间关系的研究看出：引起关节功能障碍的主要原因是关节相关软组织损害：骨软骨和关节相关软组织损害可各自单独发生，可同时发生，也可先出现一种组织后再相继出现另一种损害，出现次序无固定关系；单独关节相关软组织损害也可导致关节畸形和功能障碍。故骨软骨和关节相关软组织损害是大骨节     

微量元素锌与大骨节病关系初探

环境中的硒和大骨节病的关系已有较多的研究报道确认我国大骨节病分布于由东北向西南的低硒地带。但是经调查表明低硒环境下并不都有大骨节病的发生,这种低硒非病区在云南、四川、陕西等省均有发现。为了探讨硒以外的因素,对西南低     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.