益气血补肝肾中药对再次体外受精-胚胎移植妊娠率的影响

[目的]探讨辅助生育技术结合益气血补肝肾中药对再次体外受精-胚胎移植(IVF-ET)妊娠率的影响.[方法]将82例行周期标准长方案垂体降调节IVF-ET患者随机分成中药组(41例)及对照组(41例),中药组在第2次IVF开始前3个月经周期及IVF周期中均给予益气血补肝肾中药辨证治疗,对照组则不予中药,IVF周期开始后2...     

益气温经通络中药在膝骨性关节炎关节镜清理术后的应用

目的：观察益气温经通络中药在膝骨性关节炎关节镜清理术后应用的临床疗效。方法：选择早、中期膝关节骨性关节炎患者141例,随机分为治疗组和玻璃酸钠对照组,进行临床疗效评价和TNF—α、IL-1检测。结果：两组临床疗效比较,差异无统计学意义（P〉0．05）。治疗组治疗前后比较,TNF-α和IL－1含量变化有统计学意义（P〈0．05）;但治疗后治疗组与对照组间TNF-α和IL－1含量变化比较,差异无统计学意义（P〉0．05）。结论：膝骨性关节炎关节镜清理术后应用益气温经通络中药有较好的疗效,与玻璃酸钠疗法疗效相当。     

益肾通治疗肾虚瘀滞型前列腺增生的临床疗效观察

[目的]观察应用益肾通胶囊治疗肾虚瘀滞型良性前列腺增生的临床疗效.[方法]将门诊符合纳入标准的56例前列腺增生患者随机分成2组,治疗组30例应用益肾通胶囊(肉苁蓉、北芪、王不留行、泽兰等)口服,每次4粒,每日3次;对照组26例应用泽桂癃爽胶囊,每次2粒,每日3次;2组均以30 d为1个疗程,共治疗3个疗程,观察治疗前后...     

中药关节康治疗膝骨性关节炎的临床研究

[目的]观察具有补肾活血功效的中药复方关节康(主要由熟地、牛膝、杜仲、枸杞、丹参、红花、木香、补骨脂等药物组成)对膝关节骨性关节炎的治疗效果,为其进一步临床推广运用奠定基础.[方法]参照美国风湿病协会膝关节骨性关节炎(1995)的诊断标准及膝关节骨性关节炎Ⅱ期临床试验方案选择病例,入选病例随机分为关节康治疗组和西乐葆对照组,分别予以关节康片和西乐葆胶囊口服,连续治疗6周.按改良的膝关节骨性关节炎病情评分标准及疗效判定标准,从症状体征(膝部疼痛、膝部功能)及中医证候两方面进行疗效观察.[结果]关节康组与西乐葆组的疗效比较无显著性差异(P＞0.05),西乐葆改善疼痛的效果较好(P＜0.01),关节康改善中医证候的效果较好(P＜0.01).[结论]关节康治疗膝关节骨性关节炎的疗效与西乐葆相当,且在改善患者全身状况上具有一定优势,值得进一步开发研究和推广应用.     

补肾活血中药对子宫内膜异位症的影响

【目的】观察补肾调经汤内服加活血散结栓塞肛对子宫内膜异位症(简称内异症)体液免疫及异位子宫内膜的影响。【方法】SD大鼠130只,随机分为10组,分别为正常对照组、模型组、丹那唑阳性对照组及不同剂量补肾调经汤灌胃或加用和单独使用活血散结栓塞肛治疗7个组。除正常对照组外,其他组均复制大鼠子宫内膜异位症模型,然后分别给药,治疗4周后检测血清IgG、IgM、IgA抗体和补体C3、C4及谷丙转氨酶(ALT)水平,进行胸腺、卵巢、子宫、异位移植物及肝、肾组织的病理学检查。【结果】大鼠内异症模型手术4周后,异位的子宫内膜生长良好,IgG、C3水平升高,IgM下降,子宫、卵巢增大;中药及丹那唑治疗后均可使异位的内膜萎缩,3倍人用剂量中药灌胃加塞肛或5倍量组IgG值下降,5倍量中药塞肛或加灌胃组C3值下降,5倍量中药灌胃加塞肛组子宫和卵巢缩小;丹那唑对模型动物的性周期有抑制作用,而中药组均无此作用;各给药组均对大鼠的ALT无明显影响。【结论】补肾调经汤内服加活血散结栓塞肛可使内异症模型大鼠的子宫内膜萎缩,改善其体液免疫功能。     

鹿角方逆转充血性心力衰竭大鼠心肌纤维化的机理研究

【目的】观察鹿角方 (由鹿角、补骨脂、淫羊藿、山萸肉、女贞子、沉香等中药组成 )逆转压力负荷增加造成的充血性心力衰竭大鼠心肌纤维化的作用及其机理。【方法】 36只雄性Wistar大鼠随机分为假手术组、模型组、鹿角方组。建立腹主动脉狭窄所致充血性心力衰竭大鼠模型 ,观察左室质量指数 (LVMI) ,采用免疫组织化学染色方法观察心肌Ⅰ、Ⅲ型胶原的改变 ,采用RT PCR方法观察心肌Ⅰ型和Ⅲ型胶原mRNA的表达 ,并采用放射免疫分析方法检测血浆和心肌血管紧张素Ⅱ (AngⅡ )、血浆心钠素 (ANF)、血清醛固酮 (ALD)水平。【结果】模型组LVMI明显高于假手术组 (P <0 0 0 1) ,鹿角方组与模型组比明显下降 (P <0 0 1)。模型组Ⅰ型胶原和Ⅲ型胶原较假手术组显著升高 (P <0 0 1) ,鹿角方组较模型组明显下降 (P <0 0 1)。模型组Ⅰ型和Ⅲ型胶原mRNA的表达较假手术组显著升高 (P <0 0 5 ) ,鹿角方组较模型组显著下降(P <0 0 5 )。模型组血浆AngⅡ和左室心肌AngⅡ水平较假手术组显著升高 (P <0 0 0 1) ,鹿角方能明显降低血浆AngⅡ和左室心肌AngⅡ水平 (P <0 0 1或P <0 0 0 1)。模型组血浆ANF明显高于假手术组 (P <0 0 1) ,而鹿角方组血浆ANF较模型组明显下降 (P <0 0 1)。模型组血清醛固酮水平较假手术组显著升     

肾虚与脾虚动物甲状腺轴功能的比较

采用醋酸氢化考的松致肾虚模型和大黄致脾虚模型探讨两者甲状腺轴功能的改变，结果显示，肾虚造型使Ｔ３、Ｔ４分泌减少（Ｐ＜０．０１），ｒＴ３也明显下降（Ｐ＜０．０５），推测Ｔ４向ｒＴ３转化减少，尽管如此，ＴＳＨ无反馈性升高，说明其甲状腺轴已有明显的受抑。脾虚造型组Ｔ３（Ｐ＜０．０５）、Ｔ４（Ｐ＜０．０１）也有所降低，但幅度不如肾虚造型组大（Ｐ＜０．０５），ｒＴ３保持正常，而ＴＳＨ反馈性升高，显示甲状腺轴功能尚未完全受损。肾虚造型后补肾治疗以及脾虚造型后补脾治疗均能使上述改变恢复（Ｐ＜０．０５）。     

Disturbances in Bone Largely Predict Aortic Calcification in an Alternative Rat Model Developed to Study Both Vascular and Bone Pathology in Chronic Kidney Disease

Because current rat models used to study chronic kidney disease (CKD)‐related vascular calcification show consistent but excessive vascular calcification and chaotic, immeasurable, bone mineralization due to excessive bone turnover, they are not suited to study the bone‐vascular axis in one and the same animal. Because vascular calcification and bone mineralization are closely related to each other, an animal model in which both pathologies can be studied concomitantly is highly needed. CKD‐related vascular calcification in rats was induced by a 0.25% adenine/low vitamin K diet. To follow vascular calcification and bone pathology over time, rats were killed at weeks 4, 8, 10, 11, and 12. Both static and dynamic bone parameters were measured. Vascular calcification was quantified by histomorphometry and measurement of the arterial calcium content. Stable, severe CKD was induced along with hyperphosphatemia, hypocalcemia as well as increased serum PTH and FGF23. Calcification in the aorta and peripheral arteries was present from week 8 of CKD onward. Four and 8 weeks after CKD, static and dynamic bone parameters were measurable in all animals, thereby presenting typical features of hyperparathyroid bone disease. Multiple regression analysis showed that the eroded perimeter and mineral apposition rate in the bone were strong predictors for aortic calcification. This rat model presents a stable CKD, moderate vascular calcification, and quantifiable bone pathology after 8 weeks of CKD and is the first model that lends itself to study these main complications simultaneously in CKD in mechanistic and intervention studies. © 2015 American Society for Bone and Mineral Research.     

Neonatal Iron Deficiency Causes Abnormal Phosphate Metabolism by Elevating FGF23 in Normal and ADHR Mice

Fibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed onset following puberty or pregnancy. We previously demonstrated that the combination of iron deficiency and a knock‐in R176Q FGF23 mutation in mature mice induced FGF23 expression and hypophosphatemia that paralleled the late‐onset ADHR phenotype. Because anemia in pregnancy and in premature infants is common, the goal of this study was to test whether iron deficiency alters phosphate handling in neonatal life. Wild‐type (WT) and ADHR female breeder mice were provided control or iron‐deficient diets during pregnancy and nursing. Iron‐deficient breeders were also made iron replete. Iron‐deficient WT and ADHR pups were hypophosphatemic, with ADHR pups having significantly lower serum phosphate (p < 0.01) and widened growth plates. Both genotypes increased bone FGF23 mRNA (>50 fold; p < 0.01). WT and ADHR pups receiving low iron had elevated intact serum FGF23; ADHR mice were affected to a greater degree (p < 0.01). Iron‐deficient mice also showed increased Cyp24a1 and reduced Cyp27b1, and low serum 1,25‐dihydroxyvitamin D (1,25D). Iron repletion normalized most abnormalities. Because iron deficiency can induce tissue hypoxia, oxygen deprivation was tested as a regulator of FGF23, and was shown to stimulate FGF23 mRNA in vitro and serum C‐terminal FGF23 in normal rats in vivo. These studies demonstrate that FGF23 is modulated by iron status in young WT and ADHR mice and that hypoxia independently controls FGF23 expression in situations of normal iron. Therefore, disturbed iron and oxygen metabolism in neonatal life may have important effects on skeletal function and structure through FGF23 activity on phosphate regulation. © 2014 American Society for Bone and Mineral Research.     

A single-dose study of denosumab in patients with various degrees of renal impairment

This 16-week study evaluated pharmacokinetics and pharmacodynamics of denosumab in 55 subjects with renal function ranging from normal to dialysis-dependent kidney failure. Participants received a single 60-mg subcutaneous dose of denosumab. Kidney function groups were based on calculations using the Cockcroft-Gault equation and U.S. Food and Drug Administration (FDA) guidance in place when the study was designed. Renal function did not have a significant effect on denosumab pharmacokinetics or pharmacodynamics. These findings suggest denosumab dose adjustment based on glomerular filtration rate is not required. Rapid decreases in serum C-telopeptide in all groups were sustained throughout the study. The most common adverse events were hypocalcemia (15%), pain in extremity (15%), and nausea (11%). Most adverse events were mild to moderate in severity. Calcium and vitamin D supplementation was not initially required by the study protocol, but was added during the trial. No subject who received adequate calcium and vitamin D supplementation became hypocalcemic. Seven subjects had nadir serum calcium concentrations between 7.5 and <8.0 mg/dL (1.9 and <2.0 mmol/L), and 5 subjects (4 with advanced renal disease) had nadir serum calcium <7.5 mg/dL (<1.9 mmol/L). Two subjects (1 symptomatic, 1 asymptomatic) were hospitalized for intravenous calcium gluconate treatment. At the recommended dose, denosumab is a useful therapeutic option for patients with impaired renal function. Supplementation of calcium and vitamin D is strongly recommended when patients initiate denosumab therapy, particularly in patients with reduced renal function.