青年去势及老龄雌性大鼠骨质疏松模型比较及其临床护理意义

目的建立青年去势及老龄雌性大鼠骨质疏松模型，探讨两种雌性大鼠骨质疏松模型骨组织微观结构、骨矿及骨负荷改变情况及潜在机制．为女性骨质疏松的临床护理干预寻找相应的理论依据。方法32只1月龄雌性Sprague Dawley（SD）大鼠。同等条件下饲养，饲养至4个月按体重随机分成青年去势及假手术对照组大鼠16只、老龄雌性及对照组大鼠16只，进行去势及老龄骨质疏松造模。比较青年去势组（Ovariectomized rats．8只，OVX组）和老龄骨质疏松组（Senile Female Osteoporotic Rats．8只．SF组）大鼠骨质改变情况。结果OVX组大鼠去卵巢8周出现骨质疏松改变，SF组大鼠22月龄自然衰老出现骨质疏松改变。OVX组骨小梁宽度显著大于SF组（P〈0．05）；两组模型之间腰椎及股骨密度差异不显著（均P〉0．05），但OVX组股骨最大负荷显著高于SF组（P〈0．01）；OVX组骨钙水平显著高于SF组（P〈0.01）．但两组血钙水平差异不显著（P〉0．05）。结论4月龄大鼠去卵巢8周以及自然饲养22月龄雌性大鼠可分别作为女性绝经后及老年女性骨质疏松的模型。老龄骨质疏松模型在骨微观结构、骨生物力学特性、骨矿水平含量方面的负性改变更甚于青年去势模型。提示对女性骨质疏松症患者的护理干预措施应侧重于不同年龄阶段及骨代谢特点进行。     

老龄骨质疏松骨形态、骨密度、生物力学实验研究

[目的]观察自然衰老骨质疏松模型中雌性大鼠骨形态、骨密度、骨生物力学改变,探索老年妇女骨质疏松症发生发展的机制.[方法]选择健康纯种雌性SD大鼠10只,喂养22月后复制自然衰老骨质疏松模型,另随机选择6月龄雌性大鼠10只为青年对照组,观察其骨形态、骨密度、骨生物力学指标.[结果]与青年对照组比,骨质疏松组骨小梁面积百分比显著降低(50%,P＜0.05),股骨平均骨小梁数显著减少(65%,P＜0.05),平均骨小梁宽度显著变窄(27%,P＜0.05).②骨质疏松组股骨与椎骨骨密度(64.3±8.1 g/cm2,59.3±15.1 g/cm2)较青年对照组(81.8±7.2 g/cm2,92.2±6.1g/cm2)显著降低(P＜0.05),椎骨骨密度下降得更明显(35.7%比21.3%).③骨质疏松组股骨与椎骨的最大负荷力(134.41±23.52N,235.0±12.2N)较青年对照组(155.81±17.84N,327.1±24.8N)显著降低(P＜0.05),且椎骨的最大负荷力降低更明显(28%比14%).骨质疏松组椎骨、股骨的最大应变(1.28±0.12 mm,1.6±0.15 mm)与青年对照(1.38±0.15mm,1.81±0.21 mm)比有明显下降的趋势,但尚未形成统计学差异.[结论]老年雌性大鼠骨质疏松症中骨形态发生、骨密度明显改变,骨形态学、变化更能反映早期的骨结构的变化,这种变化发展下去可能会影响骨的力学性能.     

增龄性变化对大鼠骨质量、血清骨代谢指标影响研究

[目的]探讨增龄性变化对大鼠骨质量、血清骨代谢指标的影响。[方法]14只新生雄性Sprague Dawley（SD）大鼠，同等条件下饲养，饲养至6个月按体重随机分为老龄骨质疏松组（AO组）和青年对照组（YC组），将YC组安乐处死，AO组继续饲养至22个月，两组大鼠均取左侧股骨，测量骨密度、骨组织形态计量学指标，以及骨矿水平及骨代谢指标。[结果]腰椎及股骨密度（BMD）在老龄大鼠均下降，其中股骨密度下降尤其显著（P〈0.01）。与YC组比较，AO组大鼠骨钙素水平显著降低（P〈0.01），抗酒石酸酸性磷酸酶（TRACP）水平显著升高（P〈0.05）；骨生物力学测定发现，AO组大鼠的股骨最大受力负荷下降。骨形态计量学测定发现，AO组大鼠骨小梁体积、骨小梁宽度、骨皮质厚度显著下降（P〈0.05或P〈0.01），骨小梁间隙增大（P〈0.01），AO组大鼠骨小梁普遍变薄、变细甚至断裂穿孔。[结论]22月龄雄性大鼠发生了骨质疏松的变化，骨形成降低，骨矿含量下降，骨微观组织结构破坏。     

过量氟化物摄入对实验大鼠胫骨骺板软骨细胞分化的影响

目的：观察及分析过量氟化物对大鼠骺板软骨生长发育的毒性作用。方法：SD大鼠分为对照组,低过量氟组和高过量氟组,分别于实验10周和20周观察大鼠胫骨骺板软骨光镜,电镜下组织形态学变化。结果：与对照组比较,光镜下过量氟组大鼠骺板软骨增厚,增殖层软骨细胞和肥大层软骨细胞滞留和堆积,排列紊乱,并出现软骨半岛,软骨岛和原纤维显露,且骺板软骨损伤随染氟剂量和时间延长而明显加重,电镜下骺板软骨细胞坏死增加,存活细胞功能活跃,可继续合成和分泌胶原蛋白。结论：过量氟对大鼠骺板软骨细胞分化有明显的损伤作用,可进一步干扰软骨内化骨。     

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.     

TGF-β在大骨节病儿童及成人关节软骨中的表达

为探索转化生长因子β（TGF-β）在大骨节病儿童及成人关节软骨中表达的分布情况，应用免疫组化方法比较正常的儿童和成人与大骨节病儿童和成人关节软骨中TGF－β的表达。结果显示，（1）大骨节病儿童关节软骨表层、中层、深层TGF－β阳性细胞表达率分别为30％,24％和31％，中层、深层表达率比正常儿童明显增高（P＜0．001）；（2）大骨节病成人关节软骨表、中、深层分别为54％，46％和16％，各层细胞阳性表达率均明显高于正常组（P＜0．001）；（3）大骨节病儿童与成人比较各层软骨细胞TGF－β的阳性表达均有显著性差异（P＜0．001），表现为表、中层成人高于儿童，深层儿童高于成人。这提示大骨节病患者关节软骨中TGF－β阳性表达率高于正常对照。     

钙剂及甲基睾丸酮对老龄雄性大鼠股骨计量形态学及骨矿的影响

目的 探讨钙剂、甲基睾丸酮对老龄雄性大鼠骨质疏松的作用效果及其发生机制,为老年男性骨质疏松的临床干预寻找理论依据.方法 26只新生雄性Sprague Dawley(SD)大鼠,按体重随机分成老龄对照组、青年对照组、葡萄糖钙组(2.5 mg/kg·d)及甲基睾丸酮组(25 mg/kg·d),同等条件下饲养,青年对照组饲养至6个月,其余3组饲养至22个月后,对其中两组开始分别连续给药92 d.经处理后,取左侧股骨,用双光子骨密度仪测定骨密度;北航半自动彩色图像分析系统进行骨组织形态计量学分析,测量骨小梁体积、骨小梁宽度、骨小梁间隔、骨皮质厚度;原子吸收分光光度法及钼兰比色法检测各组大鼠骨钙、骨磷的浓度.结果 22月龄雄性大鼠可作为自然衰老骨质疏松的实验模型;与老龄对照组比较,葡萄糖酸钙组和甲基睾丸酮组大鼠股骨密度、骨小梁体积、骨小梁宽度及皮质厚度增加(P<0.05),骨小梁间隙缩小(P<0.05),骨矿化水平提高(P<0.05).结论 补充钙剂和甲基睾丸酮可增加股骨密度及骨矿化水平,促进老龄雄性大鼠股骨形态学的改善.     

中耳胆脂瘤上皮中TLR2表达的研究

目的:探讨TLR2在中耳胆脂瘤发病机理中的作用。方法:采用免疫组化SP法观察19例中耳胆脂瘤及15例外耳道皮肤中TLR2的表达及分布。结果:胆脂瘤上皮组织中TLR2的表达较外耳道皮肤上皮组织中减少,差异具有统计学意义(P<0.01)。且TLR2在表达阳性的胆脂瘤上皮及外耳道皮肤中分布不同。结论:中耳胆脂瘤上皮组织中TLR2表达下调,表明胆脂瘤局部可能存在免疫功能障碍,局部的炎症浸润也可能使TLR2表达抑制或功能障碍。     

大骨节病病区和非病区胎儿指掌骨骨干长度的发育—X线摄影图象的测量研究

我们在观察大骨节病区和非病区胎儿手指骨的组织学变化时,曾检见骨和软骨组织内有一些轻微的形态变化,并初步探讨了这些变化的意义。为了进一步检查这些变化对于胎儿骨骼生长发育有无影响以及病区和非病区胎儿的骨骼生长发育上有无差异。我们在前后位的X线手片上测量了每例胎儿右手全部指掌骨骨干的长度,进行了有关的对比分析。     

过量氟对大鼠肾肝心损害的形态学研究

目的 探讨过量氟对实验大鼠肾、心、肝脏的损害作用。方法 用光镜观察摄入不同过量氟后3个月、5个月大鼠的肾、心、肝脏的病理形态学变化,用免疫组织化学方法观察大鼠肾组织内增殖细胞核抗原（PCNA）的表达。结果 不同剂量过量氟组大鼠肾、心、肝脏的实质细胞肿胀和单个细胞坏死。肾脏损害病变严重而复杂,特别是5个月高氟组肾组织内出现多种灶状病变、肾小管阻塞和扩张;间质灶状纤维化、小管萎缩、上皮细胞增生伴单个核炎细胞浸润;肾内细胞PCNA高表达;灶状坏死伴钙化;肉芽肿和感染灶等。结论 过量氟可损害多种内脏器官,以肾脏损害最重,其病变具有多样性特征。