Mazabraud’s syndrome in female patients:Two case reports

BACKGROUND Mazabraud’s syndrome(MS)is a rare and slowly progressive benign disease characterized by the concurrent presence of fibrous dysplasia of bone and intramuscular myxoma,and is thought to be associated with mutations of the GNAS gene.To date,only about 100 cases of MS have been reported in the literature,but its standard treatment strategy remains unclear.CASE SUMMARY We report two cases of MS in young women who underwent different treatments based on their symptoms and disease manifestations.The first patient,aged 37,received internal fixation and intravenous bisphosphonate for a pathological fracture of the right femoral neck,excision of a right vastus medialis myxoma was subsequently performed for pain control,and asymptomatic psoas myxomas were monitored without surgery.Genetic testing confirmed a GNAS gene mutation in this patient.The second patient,aged 24,underwent right vastus intermedius muscle myxoma resection,and conservative treatment for fibrous dysplasia of the ilium.These patients were followed-up for 17 months and 3 years,respectively,and are now in a stable condition.CONCLUSION Various treatments have been selected for MS patients who suffer different symptoms.The main treatment for myxomas is surgical resection,while fibrous dysplasia is selectively treated if the patient experiences pathological fracture or severe pain.However,given the documented instances of malignant transformation of fibrous dysplasia in individuals with MS,close follow-up is necessary.

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

AIM: To investigate the influence of high dose of dexamethasone on inflammatory mediators and apoptosis of rats with severe acute pancreatitis (SAP). METHODS: SAP rats were randomly assigned to the model group and treatment group while the normal rats were assigned to the sham operation group. The mortality,ascite volumes,ascites/body weight ratio and pancreas pathological changes of all rats were observed at 3,6 and 12 h after operation. Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor (TNF-α),phospholipase A2 (PLA2) and IL-6 in serum were also determined. The microarray sections of their pancreatic tissues were prepared,terminal transferase dUTP nick end labeling (TUNEL) staining was performed and apoptotic indexes were calculated. RESULTS: There was no marked difference between treatment group and model group in survival. The contents of amylase and endotoxin in plasma and contents of TNF-α,PLA2 and IL-6 in serum,ascite volumes,ascites/body weight ratio and pancreas pathological scores were all lower in treatment group than in model group to different extents at different time points P < 0.05,58.3 (26.4) ng/L vs 77.535 (42.157) ng/L in TNF-α content,8.00 (2.00) points vs 9.00 (2.00) points in pathological score of pancreas respectively; P < 0.01,0.042 (0.018) EU/mL vs 0.056 (0.0195) EU/mL in endotoxin content,7791 (1863) U/L vs 9195 (1298) U/L in plasma amylase content,1.53 (0.79) vs 2.38 (1.10) in ascites/body weight ratio,8.00 (1.00) points vs 11.00 (1.50) points in pathological score of pancreas; P < 0.001,3.36 (1.56) ng/L vs 5.65 (1.08) ng/L in IL-6 content,4.50 (2.00) vs 7.20 (2.00),4.20 (1.60) vs 6.40 (2.30),3.40 (2.70) vs 7.90 (1.70) in ascite volumes,respectively. The apoptotic indexes of pancreas head and pancreas tail were all higher in treatment group than in model group at 6 h P < 0.01,0.00 (2.00)% vs 0.00 (0.00)%,0.20 (1.80) vs 0.00 (0.00) in apoptosis indexes,respectively. CONCLUSION: The mechanism of dexamethasone treatment in acute pancreatitis is related to its inhibition of inflammatory mediator generation and induction of pancreatic acinar cell apoptosis.

Chronic stress causes protein kinase C epsilon-aldehyde dehydrogenase 2 signaling pathway perturbation in the rat hippocampus and prefrontal cortex,but not in the myocardium

Chronic stress is strongly associated with the occurrence and development of depression and cardiovascular disease.Stress can induce altered mitochondrial function and activation of apoptosis in the cardio-cerebral system.However,it is unknown whether the protein kinase C ε（PKCε）-aldehyde dehydrogenase 2（ALDH2） pathway is altered under chronic stress,and this study sought to address this question.A rat model of depression was established using a chronic unpredictable mild stress（CUMS） protocol.After experiencing CUMS for 4 weeks,the sucrose preference test and the forced swim test verified depressive-like behaviors.Enzyme linked immunosorbent assays showed that ALDH2 activity was decreased in the rat hippocampus and prefrontal cortex,but was not altered in the myocardium.Western blot assays demonstrated reduced levels of ALDH2 and PKCε,but increased levels of 4-hydroxy-2-nonenal（4 HNE） adducts.Caspase-3 expression did not obviously alter,but active forms of caspase-3 were increased in the hippocampus and prefrontal cortex.In the myocardium,expression of ALDH2,PKCε and 4 HNE adducts did not remarkably alter;while caspase-3 expression was reduced and the active forms of caspase-3 were upregulated.Pearson＇s correlation test demonstrated that expression of 4 HNE adducts was positively correlated with levels of the active forms of caspase-3 in the hippocampus and prefrontal cortex,but not in the myocardium.In conclusion,chronic stress can damage the PKCε-ALDH2 signaling pathway in the hippocampus and prefrontal cortex,but not in the myocardium.Moreover,4 HNE is associated with active forms of caspase-3 in the hippocampus and prefrontal cortex.

Photo-induced Alignment Behavior of Azobenzene-containing Polymer Films with Different Cross-linking Degree

与各种各样的取代者和交叉连接的某些数量包含偶氮苯组的非结晶的共聚物的三个系列有能力的丙烯酸的组被准备。cross-linked 聚合物电影被丙烯酸的组的热聚合在共聚物，由控制 cross-linking 反应的时间，这些电影能与不同 cross-linking 度在期间被做获得(从 0 ～ 32% ，它被英尺红外系列测量监视) 。这些电影的导致相片的排列过程在 442 nm 与线性地极化的光在照耀下面被执行，并且导致相片的排列率上的 cross-linking 度的效果被调查。导致相片的排列的动力学与双性人一起被分析指数的曲线试穿。因为 cross-linking，导致相片的排列率和这些电影的最大的发射度减少了。为 cross-linked 样品，在重复了“写”并且“擦掉”周期以后，而且，他们发射度的浸透的价值保持不变，这被发现。调查结果表明电影罐头的 cross-linking 有效地由极化的光在照耀期间制止偶氮的聚合物的趋光性的集体运输。在 cross-linking 度和偶氮的聚合物的导致相片的排列行为之间的关系详细被讨论。

Protective effects of Salvia miltiorrhizae on the hearts of rats with severe acute pancreatits or obstructive jaundice

Objective:To investigate the therapeutic effects and mechanisms of Salvia miltiorrhizae(Danshen) in the treatment of severe acute pancreatitis(SAP)-or obstructive jaundice(OJ)-induced heart injury. Methods:A total of 288 rats were used for SAP(n=108) and OJ-associated(n=180) experiments. The rats were randomly divided into sham-operated,model control,and Salvia miltiorrhizae-treated groups. According to the difference of time points after operation,SAP rats in each group were subdivided into 3,6 and 12 h subgroups(n=12),whereas OJ rats were subdivided into 7,14,21,and 28 d subgroups(n=15). At the corresponding time points after operation,the mortality rates of the rats,the contents of endotoxin and phospholipase A2(PLA2) in blood,and pathological changes of the hearts were investigated. Results:The numbers of dead SAP and OJ rats in the treated groups declined as compared with those in the model control group,but not significantly(P>0.05). The contents of endotoxin(at 6 and 12 h in SAP rats and on 7,14,21,and 28 d in OJ rats,respectively) and PLA2(at 6 and 12 h in SAP rats and on 28 d in OJ rats,respectively) in the treated group were significantly lower than those in the model control group(P<0.01 and P<0.001,respectively). Besides,myocardial pathological injuries were mitigated in SAP and OJ rats. Conclusion:In this study,we found that Salvia miltiorrhizae improved myocardial pathological changes,reduced the content of PLA2 in blood,and decreased the mortality rates of SAP and OJ rats,exerting protective effects on the hearts of the rats.

解脲脲原体脂质相关膜蛋白经Toll样受体2信号通路调控人羊膜上皮细胞诱导IL-6、IL-8和TNF-α的产生（英文）

目的:探讨解脲脲原体(Ureaplasma urealyticum)及其脂质相关膜蛋白(LAMPs)作用于人羊膜上皮细胞(HAECs)过程中白介素6(IL-6)、IL-8和肿瘤坏死因子α(TNF-α)的变化情况,阐明Toll样受体2(TLR2)的调控机制,明确解脲脲原体潜在的致病性。创新点:从解脲脲原体诱导炎症反应的分子机制入手,提出TLR2信号通路在其中的关键作用。方法:经TX-114处理萃取解脲脲原体获得LAMPs,将LAMPs和解脲脲原体分别感染HAECs,用酶联免疫吸附试验(ELISA)测定炎症细胞因子(IL-6、IL-8和TNF-α);采用实时聚合酶链反应(real-time PCR)测定TLR2 mRNA水平,用蛋白质印迹(Western blot)检测TLR2的表达量;经TLR2阻断剂(anti-h TLR2-IgA)处理后,测定相应炎症细胞因子。结论:解脲脲原体LAMPs能诱导HAECs的TLR2表达上调和炎症因子增加,从而发生炎症反应;TLR2受阻断后,炎症因子表达减少,炎症水平下降。TLR2在解脲脲原体LAMPs感染HAECs过程起关键作用。