硼替佐米联合丙戊酸钠对胰腺癌细胞株SW1990的生长抑制作用

目的 探讨硼替佐米联合丙戊酸钠对人胰腺癌细胞株SW1990的协同凋亡作用及其机制.方法 以浓度为100 nmol/L的硼替佐米联合3 mmol/L的丙戊酸钠干预SW1990细胞株,采用噻唑蓝(MTT)法检测细胞增殖;膜联蛋白V(Annexin V)/碘化丙锭(PI)双染法检测细胞早期凋亡;反转录-聚合酶链反应(RT-PCR)检测细胞凋亡因子生存素(Survivin)、半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3的mRNA表达水平;Western blot法检测Survivin、Caspase-3前体(pro-Caspase-3)、裂解的Caspase-3(cleaved-Caspase-3)蛋白表达水平.结果 硼替佐米单药对SW1990的生长抑制作用较弱,而丙戊酸钠单药可有效抑制SW1990细胞的增殖,硼替佐米单药组干预SW1990细胞48 h的早期凋亡率为(13.47 ±2.21)％,而丙戊酸钠单药组为(26.73±2.36)％,两药联合组为(47.06±2.76)％.硼替佐米单药组Survivin mRNA及蛋白水平表达无明显改变、而丙戊酸钠单药组及两药联合组的Survivin、Caspase mRNA及蛋白表达水平均明显下调,cleaved-Caspase-3蛋白表达水平明显上调,各项检测指标联合用药组与单药组比较差异均有统计学意义(P＜0.05),且两药联合有协同作用,可提高SW1990对硼替佐米的敏感性.结论 硼替佐米联合丙戊酸钠对诱导人胰腺癌细胞株SW1990凋亡有协同增效作用,其机制可能与下调Survivin的表达水平相关.     

Smac/DIABLO诱导胰腺癌细胞凋亡并增加对TRAIL及吉西他滨化疗的敏感性

目的 探讨外源性Smac/DIABLO对人胰腺癌SW1990细胞生物学特性和对TRAIL及吉西他滨化疗敏感性的影响. 方法 利用脂质体2000介导Smac/DIABLO基因转染胰腺癌SW1990细胞获得细胞SW1990/Smac,转染空载体为对照组(SW1990/neo);在不同浓度和时间下以肿瘤坏死因子相关凋亡诱导配体(TRAIL)和吉西他滨处理2组细胞株并分为TRAIL组、吉西他滨组和联合组.MTT法检测细胞株的生长抑制率,流式细胞仪检测细胞凋亡率及凋亡细胞形态,Western blot检测凋亡相关蛋白Smac/DIABLO、抑制凋亡蛋白XIAP、细胞色素C及细胞凋亡因子caspase-3的表达.结果 转染Smac/DIABLO的细胞生长明显落后于转染空载体的细胞.TRAIL浓度为200、500、1000、2500 ng/ml时,作用24 h对SW1990/neo和SW1990/Smac细胞的抑制率分别为11.11％、46.03％、67.08％、76.19％及22.11％、42.67％、56.63％、67.6％ (P ＜0.05).吉西他滨浓度分别为10、20、40、60μmol/L作用24 h对SW1990/neo和SW1990/Smac的抑制率分别为15.2％、34.6％、55.16％、76.4％和22.65％、36.85％、55.11％、79.99％ (P＜0.05).以TRAIL(500 ng/ml)、吉西他滨(20 μmol/L)及TRAIL(500 ng/ml)+吉西他滨(20 μmol/L)作用24 h后,SW1990/neo和SW1990/Smac细胞的凋亡率分别为5.64％、15.30％、27.27％和20.37％、23.27％、67.30％ (P ＜0.05).SW1990/Smac细胞在TRAIL及吉西他滨作用后,细胞内促凋亡蛋白Smac/DIABLO、细胞色素C及caspase-3活化片段表达均显著升高,而抑制凋亡蛋白XIAP表达显著降低(P＜0.05).结论 Smac/DIABLO可诱导SW1990细胞的凋亡、抑制细胞增殖,并增强胰腺癌细胞对TRAIL及吉西他滨的化疗敏感性,其机制可能与Smac/DIABLO、细胞色素C、XIAP及caspase-3的活性有关.     

二甲双胍对人胰腺癌细胞增殖与凋亡的影响及其分子机制的研究

目的 研究二甲双胍在体外对人胰腺癌细胞BxPC 3、AsPC 1生长增殖、凋亡的影响及其抗肿瘤相关分子机制.方法 体外培养人胰腺癌BxPC-3、AsPC 1细胞,四甲基偶氮唑盐(MTT)法检测二甲双胍在不同浓度和不同时间对于胰腺癌细胞增殖的影响,并计算IC50值.用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定(TUNEL)法检测处理后细胞的凋亡情况.RT-PCR法检测COX-2、bcl-2、Survivin的表达影响.结果 MTT法检测显示,不同浓度二甲双胍均可抑制BxPC-3、AsPC-1两种人胰腺癌细胞增殖,两种胰腺癌细胞IC50分别为68.882 mmol/L和90.984 mmol/L.TUNEL法检测人胰腺癌细胞BxPC-3,正常对照组及二甲双胍干预组(以1/2 IC50浓度处理胰腺癌细胞)凋亡率分别为(2.44±0.57)％和(17.52±0.75)％,P＜0.05;胰腺癌细胞AsPC-1在正常对照组及二甲双胍干预组凋亡率分别为(5.35±0.92)％和(45.76±1.87)％,P＜0.05.RT-PCR结果显示:人胰腺癌细胞BxPC-3在正常对照组及二甲双胍干预组COX-2的mRNA灰度值分别为0.769±0.006和0.305±0.009,P＜0.05; bcl-2的mRNA灰度值分别为0.401±0.022和0.129±0.010,P＜0.05;Survivin的mRNA灰度值分别为0.943±0.029和0.143±0.050,P＜0.05.人胰腺癌AsPC-1细胞在正常对照组及二甲双胍干预组COX-2的mRNA灰度值分别为1.232±0.011和0.831±0.022,P＜0.05;bcl-2的mRNA灰度值分别为0.400±0.053和0.129±0.032,P＜0.05;Survivin的mRNA灰度值分别为0.983±0.017和0.174±0.029,P＜0.05.结论 二甲双胍抑制胰腺癌细胞增殖、促进凋亡.二甲双胍抗肿瘤机制可能是通过抑制COX-2、bcl-2及Survivin的mRNA表达来实现的.     

小干扰RNA特异性沉默c-myc基因对人胰腺癌SW1990细胞生物学影响

目的 观察小干扰RNA(siRNA)沉默c-myc基因的表达对人胰腺癌细胞株SW1990细胞生物学影响.方法 用siRNA沉默胰腺癌SW1990细胞中c-myc基因,用实时定量反转录聚合酶链反应(RT-qPCR)及Western blot技术检测c-myc mRNA及蛋白的表达量;噻唑蓝(MTT)法检测siRNA沉默c-myc基因对SW1990细胞增殖的影响;膜联蛋白V/碘化丙锭(Annexin V/PI)双染流式细胞术检测沉默c-myc基因细胞凋亡水平;Transwell细胞迁移实验检测siRNA沉默c-myc基因对SW1990细胞迁移能力的影响.结果 靶向c-myc的特异性siRNA可以高效抑制人胰腺癌SW1990细胞c-myc基因表达,在mRNA水平(0.263±0.048)较转染对照质粒组(0.970±0.012)明显降低,c-myc蛋白质表达量及细胞增值率均较转染对照质粒组明显降低;转染后48 h c-myc siRNA组细胞凋亡率为(19.90±2.09)％,明显高于siRNA阴性对照组(4.93±0.25)％和空白对照组(4.40±0.34)％;Transwell实验结果示细胞穿膜数c-myc siRNA组[(34.3±1.2)个]较siRNA-NC组[(68.3±5.8)个]和空白组[(72.3±1.2)个]均明显降低.结论 c-myc siRNA能够显著抑制c-myc基因在人胰腺癌SW1990细胞中的表达,降低细胞的增殖和迁移能力,促进细胞的凋亡.     

吉西他滨耐药人胰腺癌细胞株的建立及其与肿瘤干细胞的相关性研究

目的 建立吉西他滨耐药人胰腺癌细胞株SW1990/GZ,并探讨SW1990/GZ和胰腺癌肿瘤干细胞的相关性.方法 应用间歇浓度梯度倍增法建立吉西他滨耐药人胰腺癌细胞株SW1990/GZ;倒置显微镜下观察细胞形态;MTT法计算耐药指数(RI);荧光定量PCR检测ABCB1、ABCC1及ABCG2基因的表达水平;裸鼠皮下种植瘤试验观察SW1990和SW1990/GZ的成瘤能力;流式细胞仪通过侧群细胞(SP)法和表面特异抗原标记法(CIM4+CD24+)检测肿瘤干细胞含量.结果 在形态学上,SW1990/GZ较SW1990发生明显改变;SW1990/GZ的耐药指数是亲代SW1990的77.2倍;与亲代SW1990相比,耐药株SW1990/GZ中ABCB1、ABCC1及ABCG2的表达水平明显增高(P<0.01),裸鼠皮下成瘤能力增强(P<0.01);耐药株SW1990/GZ中SP细胞比例为(11.0±1.0)%,亲代SW1990中SP细胞比例为(4.6±0.9)%,CD44+CD24+细胞在两者中的比例分别为(8.7±0.8)%和(1.1±0.4)%(P<0.01).结论 吉西他滨耐药胰腺癌细胞株SW1990/GZ能高效富集胰腺癌肿瘤干细胞,CD44与胰腺癌获得性耐药关系密切,可能为克服胰腺癌获得性耐药提供新的治疗靶点.     

白细胞介素6对人胰腺癌细胞上皮间质转换的影响及机制探讨

目的 应用白细胞介素6(IL-6)作用于人胰腺癌细胞株SW1990、Capan-2和沉默STAT3基因的SW1990细胞,观察细胞上皮间质转换相关基因的变化并探讨其机制.方法 使用IL-6作用人胰腺癌细胞株SW1990、Capan-2和沉默STAT3基因的SW1990细胞.MTT法检测细胞增殖.荧光定量PCR、Real-time PCR、Western blot检测STAT3、p-STAT3、Snail、Twist和E-cadherin基因mRNA和蛋白表达.体外侵袭实验检测细胞的侵袭能力.结果 100μg/L IL-6作用人胰腺癌细胞株后,细胞增殖能力增强(P＜0.05).Western blot显示P-STAT3的表达增加;荧光定量PCR、Real-time PCR、Western blot显示Snail mRNA和蛋白表达明显升高(P＜0.05);E-cadherinmRNA和蛋白表达明显降低(P＜0.05);细胞侵袭能力增强.而IL-6作用沉默STAT3基因的SW1990细胞,Snail和E-cadherin mRNA和蛋白表达均无明显改变.结论 IL-6可能通过激活STAT3信号转导通路,上调Snail和下调E-cadherin基因表达,促进胰腺癌细胞上皮间质转换,进而增强侵袭能力.     

南瓜蛋白对人胰腺癌SW1990细胞株的诱导凋亡作用

目的 探讨南瓜蛋白体外对人胰腺癌SW1990细胞株的诱导凋亡作用.方法 MTT法检测南瓜蛋白对SW1990细胞的增殖抑制作用,透射电镜观察细胞凋亡表现,流式细胞仪检测其凋亡率,Western blot法检测caspase-3蛋白的表达.结果 不同浓度(1.25、2.50、5.00、10.00、20.00、40.00及80.00 μg/ml)南瓜蛋白作用不同时间(24、48及72 h)后,南瓜蛋白对胰腺癌细胞具有生长抑制作用,并呈时间和剂量依赖性(P<0.05).40.00 μg/ml南瓜蛋白作用72 h后,透射电镜下可见细胞出现明显的凋亡改变,并可见凋亡小体;不同浓度(0、2.50、10.00、40.00μg/ml)南瓜蛋白作用72 h后,细胞的凋亡率分别为(0.30±0.11)%、(18.93±1.06)%、(28.00±2.07)%及(49.93±3.25)%,随着药物浓度的升高,细胞的凋亡率逐渐增加,呈浓度依赖性(P<0.05);caspase-3蛋白表达随着药物浓度的升高逐渐增强,呈浓度依赖性(P<0.05).结论 南瓜蛋白可能通过上调caspase-3蛋白的表达诱导胰腺癌细胞凋亡.     

胰腺癌中XIAP和Survivin的表达及其相关性

目的:研究X染色体连锁的凋亡抑制因子(XIAP)和SurvMn在胰腺癌中的表达并探讨二者之间的关系.方法:采用免疫组织化学法对26例胰腺癌组织中XIAP和Survivin的表达进行检测并积分;采用RT-PCT检测胰腺癌细胞Panc-1、AsPC-1中XIAP和Survivin基因的表达.结果:26例胰腺癌组织中XIAP和Survivin的阳性率分别为88.5%(23/26)和92.3%(24/26),其表达积分分别为7.40 4±4.12和8.53±3.83,二者共同阳性率为84.6%(22/26);表达强弱与肿瘤大小均无明显关系;分化越差的肿瘤,二者的表达越高(P<0.05).2株胰腺癌细胞中均有XIAP和Survivin的基因表达.XIAP和Survivin在胰腺癌组织和细胞中均存在相关性(P<0.05).结论:XIAP和Survivin的表达水平均与胰腺癌的分化程度有关,二者在胰腺癌组织和细胞中均存在相关性,可能在胰腺癌的转化以及耐药方面发挥重要作用.     

靶向于人端粒酶逆转录酶的miR-138增强结肠癌细胞SW480对5-氟尿嘧啶的敏感性

目的 观察miR-138对结肠癌细胞SW480人端粒酶逆转录酶(hTERT)表达的影响,探讨miR-138模拟体mimic沉默hTERT在SW480对5-氟尿嘧啶(5-Fu)化疗药物敏感性中的作用.方法 流式细胞仪检测50 nmol/L和10 nmol/L miR-138模拟体(mimic)转染SW480后hTERT的表达;5μl异硫氰酸荧光素(FITC)标记的细胞核增殖抗原(Ki-67)抗体染色转染和未转染50 nmol/Lmimic的SW480,流式细胞仪检测1 mmol/L 5-Fu处理和未处理的细胞增殖;碘化丙锭(PI)单染和膜联蛋白Ⅴ(Annexin Ⅴ)-PI双染转染和未转染50 nmol/L mimic的SW480,流式细胞仪检测1 mmol/L5-Fu处理和未处理的细胞周期和凋亡状态.结果 miR-138 mimic在50 nmol/L和10 nmol/L时,hTERT表达率分别为(30.25±1.34)％和(60.03±2.78)％,而阴性对照组为(87.50±1.63)％;转染miR-138 mimic的SW480细胞组与非转染组Ki-67阳性细胞分别为(58.18±2.90)％和(83.45±2.41)％;sub-G0期分别为(27.33±1.70)％和(1.05±0.19)％;凋亡率达(29.50±2.27)％和(5.30±1.74)％;mimic转染组、5-Fu处理组和mimic转染与5-Fu联合组的细胞增殖率分别为(61.00±1.73)％、(57.00±2.03)％和(23.00±1.24)％,sub-G0期细胞分别为(28.12±1.47)％、(34.87±2.01)％和(70.94±3.04)％;凋亡细胞比例分别为(32.15 ±2.76)％、(40.07±2.58)％和(80.84±3.06)％,差异均有统计学意义(P＜0.05).结论 MiR-138 mimic可以抑制SW480中hTERT表达并增强SW480对5-Fu的敏感性.     

胰腺癌细胞株耐药与凋亡相关基因的改变

目的探讨凋亡相关基因的改变与胰腺癌细胞耐药的关系。方法利用含有18000条人类基因的cDNA基因芯片对人胰腺癌细胞株SW1990及其耐药细胞亚株SW1990/FU和SW1990/ADM间的差异表达基因进行筛选。结果人胰腺癌细胞株SW1990与耐药细胞亚株SW1990/FU和SW1990/ADM间的共同差异表达基因有170条,其中6条与细胞凋亡相关。结论凋亡相关基因hSiah2、TIA1、CDC2、PDCD2、MAPK6及MAP4K3可能参与了胰腺癌耐药过程的发生,可能成为新的胰腺癌耐药相关基因。     

Effects of Sevoflurane and Isoflurane on Renal Function and on Possible Markers of Nephrotoxicity

Background: Low-flow sevoflurane anesthesia is associated with increasing circuit concentrations of compound A, which is nephrotoxic in rats, but the effect of compound A and low-flow sevoflurane anesthesia on renal function in humans is unclear. The authors compared the effects of high- and low-flow sevoflurane and isoflurane anesthesia on renal function and on several possible markers of nephrotoxicity in humans.

Methods: Forty-two patients without preexisting renal disease underwent either low-flow isoflurane (1 l/min, n = 14), low-flow sevoflurane (1 l/min, n = 14), or high-flow sevoflurane (6 l/min, n = 14) anesthesia for body-surface-area surgery scheduled to last at least 4 h. Twenty-four-hour urinary excretion of N-acetyl-[small beta, Greek]-glucosaminidase (NAG), [small beta, Greek]2-microglobulin, protein, glucose, blood urea nitrogen (BUN), and serum creatinine concentrations were measured before and after anesthesia.

Results: There were no differences in blood urea nitrogen, creatinine, and creatinine clearance among the three groups after anesthesia. Increased urinary N-acetyl-[small beta, Greek]-glucosaminidase excretions were seen in the low-flow and high-flow sevoflurane groups, but not in the low-flow isoflurane group (P < 0.01). Ten patients in the low-flow sevoflurane group had 24-h urinary excretion of protein that exceeded the normal ranges after anesthesia, but only one patient in the isoflurane and none in the high-flow sevoflurane groups had this.     

甲状腺素及促甲状腺素对骨转换作用机制的研究进展

甲状腺功能亢进症是引起继发性骨质疏松症的危险因素。目前关于甲亢导致的骨质疏松机制还不完全明了,但过量甲状腺素会对骨转换产生影响,促甲状腺素水平的降低可能也参与其中。本文综述甲状腺素、促甲状腺素对骨转换作用机制的研究,为以后甲亢性骨质疏松病因机制研究提供新思路。     

Effect of duodenal osmolality on gastrin and secretin release and on gastric and pancreatic secretion

We have measured the osmolality of duodenal contents in 9 dogs after a hypertonic meal, given either by mouth or directly into the stomach or perfused into the duodenum. A test meal of 2,475 mosm/kg, given by mouth, raised the intraduodenal osmolality to 700–1,500 mosm/kg over a 1-hour period. Hypertonic glucose solutions (2,000 and 3,400 mosm/kg), given into the stomach, were found to be diluted to about 700 and 1,100 mosm/kg, respectively, at the level of the mid-duodenum 30 minutes later. Hypertonic saline solutions (1,800 and 2,700 mosm/kg), perfused into the duodenum, created a stable intraluminal osmolality of 800 and 1,200 mosm/kg, respectively, (about 45% that of the perfusate) after 30 minutes. In 6 Heidenhain pouch dogs, gastric secretion and gastrin release stimulated by food were significantly diminished by administration of hypertonic sodium chloride solution (1,800 mosm/kg) into the duodenum. This hyperosmolality caused greater suppression of acid secretion (52%) than of gastrin release (28%). Stimulation of pancreatic water and bicarbonate secretion and of release of radioimmunoassayable secretin by intraduodenal HCl (pH 1.3) were significantly suppressed when the osmolality of the HCl solution was raised to 2,700 mosm/kg. Pancreatic protein secretion remained unchanged with hypertonic solutions. We have confirmed that stimulation of intraduodenal osmoreceptors inhibits gastric acid secretion in dogs, and we suggest that this is due, at least in part, to a suppression of gastrin release. We further suggest that duodenal osmolar inhibition of pancreatic secretion involves suppression of secretin but does not appear to involve cholecystokinin.

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Résumé Nous avons mesuré l'osmolalité du contenu duodénal chez 9 chiens après un repas hypertonique administré soit per os, soit directement dans l'estomac, soit par perfusion dans le duodénum. Un repas à 2,475 mosm/kg, administré per os, élève l'osmolalité duodénale à 700–1,500 mosm/kg pendant une heure. Des solutions de glucose hypertonique à 2,000 et 3,400 mosm/kg, introduites directement dans l'estomac, sont, 30 minutes plus tard, diluées à 700 et 1,100 mosm/kg au niveau de la partie moyenne du duodénum. Des solutions salines hypertoniques à 1,800 et 2,700 mosm/kg, en perfusion intraduodénale, donnent, après 30 minutes, une osmolalité duodénale de 800 et 1,200 mosm/kg (±45% de la solution perfusée).Chez 6 chiens à poche de Heidenhain, la sécrétion gastrique et la libération de gastrine provoquées par un repas sont réduites de façon significative par la perfusion intraduodénale de chlorure de sodium en solution hypertonique (1,800 mosm/ kg). Cette hyperosmolalité réduit plus la sécrétion d'acide (52%) que la libération de gastrine (28%). La perfusion dans le duodénum d'une solution d'HCl (pH 1.3), dont l'osmolalité est portée à 2,700 mosm/kg, diminue la stimulation des sécrétions d'eau et de bicarbonate pancéatiques et la libération de sécrétine mesurable par radio-immunoessai. La sécrétion pancréatique de protéines n'est pas modifiée par les solutions hypertoniques. Nous avons done confirmé l'inhibition de la sécrétion gastrique d'acide chez le chien par stimulation des osmorécepteurs duodénaux; nous pensons que cette inhibition est due, en partie en tous cas, à la suppression de la libération de gastrine. Nous estimons de plus que l'inhibition de la sécrétion pancréatique par l'hyperosmolalité duodénale résulte d'une suppression de la libération de sécrétine, mais est sans effet sur la libération de cholécystokinine.

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Supported by grants from the National Institutes of Health (AM 15241) and the John A. Hartford Foundation, Inc.

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An abstracted preliminary report of a portion of this work has appeared (Physiologist 20:93, 1977).

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Recipient of a grant from the Deutsche Forschungsgemeinschaft (Te 79/1).     

Contrasting effects on bone formation and on fracture healing of cholecalciferol and of 1 α-hydroxycholecalciferol

Summary Experimental fractures were performed on tibiae of vitamin D-depleted chicks. The chicks were divided into three groups; they were treated daily with (a) cholecalciferol or (b) 1α-hydroxycholecalciferol (1α(OH)D₃), or (c) they received no treatment. Microscopic examination of the calluses formed at the fractured sites and of the proximal tibiae of the contralateral legs showed that treatment with 1α(OH)D₃ failed to heal most of the rachitic signs seen in the nontreated chicks, despite normal plasma concentrations of calcium and of inorganic phosphorus. In a second experiment, experimental fractures were performed on tibiae of chicks that were fed a vitamin D-deficient diet, but were dosed continuously with radioactive cholecalciferol. Analysis of cholecalciferol metabolites in the callus tissue showed perferential accumulation of 25-hydroxycholecalciferol (25(OH)D₃) and of 24,25-dihydroxycholecalciferol (24,25(OH)₂D₃). Very little 1α, 25-dihydroxycholecalciferol (1α,25(OH)₂D₃) was detected in bones or in calluses. Based on the data obtained, the following conclusions were drawn: (a) that cholecalciferol is directly involved in bone formation; and (b) that 1α, 25(OH)₂D₃ is not the sole metabolite of cholecalciferol involved in this process.     

Early Effects of Parathormone and Calcitonin on the Number of Osteoclasts and on Serum-Calcium in Rats

Using succinic dehydrogenase staining of osteoclasts, the authors have studied the early effects on these cells of parathormone and calcitonin in rats. Thirty minutes after injection of the hormones the number of osteoclasts had increased (parathormone) or decreased (calcitonin), associated with inverse changes in total serum-calcium. The results confirm earlier studies showing the remarkably rapid changes in the number of osteoclasts after substances acting on serum calcium.     

Effects on calcium and phosphate metabolism and on parathyroid function of acute administration of tricalcium phosphate

The effects of the ingestion of tricalcium phosphate on calcium and phosphate metabolism and on parathyroid function were evaluated in 10 young adults. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of tricalcium phosphate containing 1500 mg of calcium and 770 mg of phosphorus. Serum and urinary calcium and phosphate and the nephrogenous cAMP fraction were measured. Significant rises in serum (from 2.32 ± 0.05 to 2.44 ± 0.08 mmol/l) and urinary (from 1.08 ± 0.65 to 3.43 ± 1.38 μmol/l GF) calcium and in serum phosphate (from 1.05 ± 0.18 to 1.28 ± 0.14 mmol/l) occurred. Unexpectedly, the acute supply of calcium in the form of tricalcium phosphate did not provoke significant alteration of nephrogenous cAMP level. In order to assess the respective effects of calcium and of phosphate, similar tests with ingestion of similar amounts either of calcium (as a glucoheptogluconate salt) or of phosphate were subsequently performed in the same subjects. Significant increases in serum total calcium were observed after calcium glucoheptogluconate as after tricalcium phosphate. However, the effects on parathyroid function differed, since a significant (p < 0.001) decrease in nephrogenous cAMP followed the ingestion of calcium glucoheptogluconate. Otherwise, a stimulating effect of phosphate on parathyroid function was observed. These findings suggest that the respective effects of calcium and of phosphate are counterbalanced when administered as tricalcium phosphate, resulting in the absence of parathyroid suppression.     

Early Effects of Parathormone and Calcitonin on the Number of Osteoclasts and on Serum-Calcium in Rats

Using succinic dehydrogenase staining of osteoclasts, the authors have studied the early effects on these cells of parathormone and calcitonin in rats. Thirty minutes after injection of the hormones the number of osteoclasts had increased (parathormone) or decreased (calcitonin), associated with inverse changes in total serum-calcium. The results confirm earlier studies showing the remarkably rapid changes in the number of osteoclasts after substances acting on serum calcium.     

手法松解结合针刺治疗膝骨关节炎临床效果及作用机制

目的探讨手法松解结合针刺对膝骨关节炎的临床效果及作用机制。 方法选取广州医科大学附属第一医院针灸门诊确诊为膝骨关节炎患者60例分为：手法松解结合针刺、机械推拿结合针刺、常规推拿结合针刺3组,分别对3组患者进行治疗,并在治疗前后行关节功能评定,关节超声及关节X线检测。另设健康对照组20例,研究结束后对收集的数据行方差分析及配对样本t检验。 结果3组患者治疗前后膝骨关节炎指数量表评分比较差异有统计学意义(t ＝8.382、5.681、5.335,均为P<0.01),胫股内侧间隙手法松解组治疗后与治疗前比较差异有统计学意义(P<0.05);髌骨外上缘至股外上髁距离手法松解组治疗前与对照组比较有统计学意义(t ＝－0.433,P<0.05),3组治疗组治疗后与对照组比较有统计学意义(F＝4.395,P<0.05);治疗前后3组股四头肌肌腱弹性与健康对照组比较(治疗前F＝5.363,P<0.01;治疗后F＝5.250,P<0.01)及髌腱弹性与健康对照组比较减小(治疗前F＝17.068,P<0.01;治疗后F＝15.064,P<0.01)。 结论手法松解结合针刺治疗方法能够对膝骨关节炎患者关节内结构、关节周围肌群力学产生作用以及能促进膝骨关节炎症状改善及生活质量提高。