Primary biliary cirrhosis in female subjects with sicca-associated antibodies

Abstract

The aim of this study is to clarify the time course of primary biliary cirrhosis (PBC) in subjects possessing anticentromere antibodies (ACA), anti-Ro, and/or anti-La antibodies, and who used alkaline phosphatase (ALP) as a serological marker for PBC. Female subjects (n = 165), who had at least one of ACA, anti-Ro, and/or anti-La, were enrolled in this study. Groups A (ACA alone, n = 44), B (anti-Ro alone, n = 54), E (anti-Ro and anti-La, n = 52), and DFG (ACA with anti-Ro and/or anti-La, n = 14) were analyzed. Healthy females (n = 65) were used as a control. The frequencies of the PBC in groups A (13.6%) and DFG (14.3%) were higher than those in groups B (1.9%) and E (0.0%). The ALP levels increased with age in groups A and DFG and slightly increased with age in groups B and C, and the control group. After correcting for age by analysis of covariance, a comparison of ALP levels among the groups not having anti-M₂ was as follows: group A ≒ group DFG > group B ≒ group E ≒ the control group. The subjects with ACA might thus have PBC more frequently than either those with anti-Ro and/or anti-La, or the control subjects.     

退变椎体周边关节软骨产生碱性磷酸酶与骨赘形成的关系

目的：研究椎体骨赘形成的机理。方法：通过切除免颈棘上韧带及棘间和分离颈椎后旁两侧肌肉引起动物颈椎力学上的失衡,经３个月的时间的发展而造成免颈椎间盘退变模型。用生物化学方法分别测定每个动物颈椎间盘纤维环和髓核、椎体关系软骨、周边关节软碱性磷酸酶性结果：颈椎间盘退变动物椎体周边关节软骨中碱性磷酸酶活性明显升高。结论：研究结果在生物化学上支持椎体骨赘来自于周边关节软骨增殖、化生、钙化和骨化的组织学观察。     

用筛选抗性突变株法选育碱性脂肪酶的高产菌

以圆弧青霉白色变株ＰＢ２２７ 为出发株⒙通过多次诱变⒙筛选抗真菌抗生素的抗性株和抗底物、底物结构类似物或分解产物的抗性株⒙获得一株己酸抗性突变株ＰＧ３７⒙其产酶水平比出发株ＰＢ２２７ 菌株提高了１．５ 倍⒙达到５５７ μｍ ｏｌ／⒉ｍ ｉｎ·ｍ Ｌ⒕．ＰＧ３７ 所产脂肪酶的最适作用ｐＨ 为１０．０⒙最适作用温度为２５ ℃⒙在ｐＨ ７．０～１０．５ 范围内稳定．     

T—2毒素诱发哺乳动物细胞DNA单链断裂效应

用总洗脱时间为2h 的碱洗脱技术测定不同剂量~(60)Co-γ线照射后 L_(1210)细胞的 DNA 单链断裂,能获得与照射剂量呈直线关系的洗脱动力学曲线,剂量效应关系 r=-0.9986。0.1、1、10和100μg/ml 的 T-2毒索与哺乳动物细胞(L_(1210)和 HEL)作用3或24h均诱导轻度 DNA 单链断裂,相对 DNA 单链断裂度为11%～19%。     

MK2 plays an important role for the increased vascular permeability that follows thermal injury

We previously reported Rho kinase is involved in vessel hyper-permeability caused by burns. Here we further explore the Rho kinase downstream signaling, it is found that its specific inhibitor Y27632 significantly diminishes the activation of JNK and p38 MAPKs but not ERK that induced by serum from burned rats (burn-serum). JNK activation was found involved in the expression of HUVEC adhesion molecules following thermal injury, although not in the process of stress fiber formation. Inhibition of various MAPKs by specific inhibitors showed that SB203580 (inhibitor of p38), but neither SP600125 (inhibitor of JNK) nor PD98059 (inhibitor of ERK), abolish activation of the p38 downstream kinase MK2. Demonstration of stress fibers by fluorescent-labeled phalloidin showed that inhibition of MK2, either by its specific inhibitor or by dominant negative adeno-viral-carried constructs, significantly reduced burn-serum-induced HUVEC stress-fiber formation, while inhibition of another downstream p38 MAPK kinase, PRAK, had no such effects. Transfection of dominant negative adeno-viral MK2 (Ad-MK2(A)) significantly inhibited thermal injury-induced blood vessel hyper-permeability in rats and, moreover, prolonged the survival of burned rats beyond 72 h following thermal injury. One of the mechanisms behind these phenomena is that Ad-MK2(A) causes a significant depression of burn-serum-induced HSP27-phosphorylation, while the adeno-viral transported dominant negative PRAK (Ad-PRAK(A)) does not block. Although the effect of blockade of MK2 through its adeno-viral approach requires further study and investigation of alternatives to know for sure, we may have found a new pathway behind thermal-injury-induced blood vessel hyper-permeability, namely: Rho kinase > p38 > MK2 > HSP27.     

骨碎补总黄酮对颅骨缺损修复大鼠血清碱性磷酸酶、钙、磷的影响

目的:探讨中药骨碎补总黄酮(assemble flavone of rhizome drynaria,AFDR)在修复大鼠颅骨缺损过程中对血清碱性磷酸酶、钙、磷及肌酐、谷丙转氨酶水平的影响。方法:60只6周龄雄性SD大鼠,饲养1周后Excel表随机分为两组(对照组和AFDR组),每组30只。用电动磨钻在大鼠左右颅骨钻孔建立颅骨缺损模型,右侧缺损可注射骨修复材料(injectable bone regeneration vomposite,IBRC)。术后第1天AFDR组中药灌胃,对照组去离子水灌胃。分别于术后2、4、8周采血,检测血清中碱性磷酸酶、磷、钙、肌酐、谷丙转氨酶指标,并进行统计学处理。结果:2周时碱性磷酸酶AFDR组高于对照组,4周时血清钙、磷及钙磷乘积AFDR组高于对照组。血清谷丙转氨酶各时间点两组差异无统计学意义。8周时血清肌酐AFDR组低于对照组。结论:骨碎补总黄酮在大鼠颅骨缺损修复过程中,于2～4周可影响碱性磷酸酶及血清钙磷水平,对肝肾无毒性。     

老年糖尿病女性骨质健康状况及干预情况分析

目的探讨60岁以上老年女性2型糖尿病（type 2 diabetes mellitus,T2DM )患者与非糖尿病患者骨量、骨代谢标志物骨钙素和骨碱性磷酸酶和血清钙、血清磷及其他骨量相关指标的差异,对糖尿病骨病目前的治疗状况进行分析,为糖尿病骨量异常的治疗提供依据。方法 用超声测量40例60 岁以上老年女性非糖尿病患者及46例老年女性糖尿病患者的跟骨骨密度,并检测两组人群的血清 钙、血清无机磷、骨质疏松生化标志物骨钙素和骨碱性磷酸酶。结果 糖尿病组的跟骨骨密度,血清钙均低于非糖尿病人群,骨钙素和骨碱性磷酸酶高于非糖尿病组,二者比较有统计学意义。结论 60 岁以上老年女性糖尿病患者骨量丢失显著重于同龄非糖尿病人群,对糖尿病性骨量减低的干预和治疗应给予足够重视,以期尽量减少和避免骨折等严重并发症的发生。     

茵陈提取物对糖尿病大鼠肾组织中PTEN蛋白表达的影响及其肾脏保护作用

目的：探讨茵陈提取物（HACE）对糖尿病大鼠肾组织中第10号染色体缺失的磷酸酶及张力蛋白同源基因（PTEN）表达的影响,阐明HACE对糖尿病大鼠肾脏保护作用的药理学机制。方法：采用链脲佐菌素（STZ）制备糖尿病大鼠模型。30只Wistar大鼠随机分为对照组（6只）、模型组（12只）和HACE组（12只）,HACE组大鼠每天1次灌胃给予HACE（5 g·kg^-1）,对照组和模型组大鼠每天1次灌胃给予等量生理盐水。给药4个月后检测各组大鼠尿白蛋白排泄率和尿总蛋白排泄率,HE染色观察大鼠肾组织病理形态表现,PAS和Masson染色检测肾小球细胞外基质（ECM）分布情况,免疫组织化学染色法检测大鼠肾组织中PTEN蛋白表达分布情况,Western blotting法检测各组大鼠肾脏组织中PTEN蛋白表达水平。结果：与模型组比较,HACE组大鼠肾小球系膜区扩大、PAS及Masson阳性染色物质聚集和基底膜增厚等现象明显减轻,24h尿白蛋白排泄率明显降低（P<0.05）,尿总蛋白排泄率差异无统计学意义（P>0.05）。免疫组织化学染色检测,对照组大鼠肾组织PTEN蛋白表达量较高,模型组大鼠肾组织中PTEN蛋白表达量降低,HACE组大鼠肾组织中PTEN蛋白表达量趋向正常。Western blotting法检测,与对照组比较,模型组大鼠肾皮质中PTEN蛋白表达水平明显降低（P<0.05）;与模型组比较,HACE组大鼠肾皮质组织中PTEN蛋白表达水平明显升高（F=5.06,P<0.05）。结论：HACE提高大鼠肾脏组织中PTEN蛋白的表达可能是其对糖尿病大鼠肾脏保护作用机制之一。