Systems Biology Analyses Show Hyperactivation of Transforming Growth Factor-β and JNK Signaling Pathways in Esophageal Cancer

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香砂六君子汤预防危重病脾胃虚弱型患者胃肠功能障碍的临床观察

胃肠功能障碍(GIDF)是重症监护病房(ICU)患者常见的并发症,是多脏器功能不全综合征的重要组成部分,也是诱发和(或)加剧多脏器功能不全综合征的因素之一。近年来对GIDF的研究较多,但缺乏理想的治疗手段。有学者对危重病GIDF患者进行辨证分析发现,病性证素以气虚最多,血虚其次;病位证素以脾最多,胃其次;证型以脾胃气血两虚证最多[1]。本研究旨在观察香砂六君子汤预防危重病脾胃     

杨少山运用千金苇茎汤临证思路与验案3则

国家级名老中医杨少山对千金苇茎汤的运用有自己独特的见解,不囿于古法,除用于治疗肺痛外,亦用于治疗其他肺系疾病或肠道疾病。     

Induction of phosphorylated c‐Jun in neonatal spinal motoneurons after axonal injury is coincident with both motoneuron death and regeneration

c‐Jun activation has been implicated not only in neuronal degeneration, but also in survival and regeneration. Here, we investigated c‐Jun activation in injured motoneurons by using a nerve crush model in neonatal rats. We identified two distinct subpopulations of motoneurons: about 60% underwent degeneration following injury whereas the remaining 40% survived and induced a regeneration response at 3 weeks post injury. However, all motoneurons examined expressed phosphorylated‐c‐Jun‐immunoreactivity (p‐c‐Jun‐IR) at the early stage of 3 days following injury. These results suggest that active c‐Jun was induced in all neonatal motoneurons following nerve crush injury, regardless of whether they were destined to degenerate or undergo successful regeneration at a later stage. Our findings therefore support the hypothesis that active c‐Jun is involved in both neuronal degeneration and regeneration.     

Activation of c-Jun N-terminal kinase in non-cancerous liver tissue predicts a high risk of recurrence after hepatic resection for hepatocellular carcinoma

Aim: Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer deaths worldwide. Hepatic resection is the mainstay of curative treatment for early stage HCC. Although c‐Jun N‐terminal kinase (JNK) activation contributes to hepatocyte proliferation and HCC development in mice, the extent of involvement of JNK in human HCC development is unknown. The aim of this study is to assess the predictive value of JNK for postoperative recurrence in HCC. Methods: From April 2005 to March 2008, 159 patients underwent curative resection for HCC. From the 159 patients, 20 patients each matched for age, gender and etiology were registered as three groups: (i) without recurrence (no recurrence group), (ii) with recurrence within one year after surgery (early recurrence group), and (iii) with recurrence at one year or more after surgery (late recurrence group) (a cross‐sectional control study). We investigated factors contributing to postoperative early and late phase recurrence. Results: Multivariate analysis using a Logistic regression model showed that JNK activity in non‐cancerous liver tissue was correlated with postoperative late recurrence. (P = 0.02, odds ratio; 5.79, 95% confidence interval [CI]; 1.33–25.36). Conclusions: JNK activity in non‐cancerous liver tissue is considered as a reliable predictive biomarker for post‐operative recurrence in HCC.     

氟氯西林镁颗粒的人体生物等效性研究

目的:比较氟氯西林镁颗粒与氟氯西林钠胶囊的人体生物等效性。方法:24名健康受试者随机分为两组,采用双周期自身交叉方法,单剂量口服受试制剂氟氯西林镁颗粒或参比制剂氟氯西林钠胶囊0.5 g。用液-质联用(LC-MS/MS)法测定氟氯西林的血浆浓度,并计算其药动学参数,比较二者的人体生物等效性。结果:受试制剂与参比制剂的药动学参数分别为:t1/2(1.53±0.29)、(1.55±0.25)h,cmax(34.56±8.13)、(34.67±8.89)mg/L,tmax(0.72±0.25)、(0.74±0.25)h,AUC0-24 h(69.51±15.34)、(70.47±16.19)mg·h/L,受试制剂的相对生物利用度为(99.29±10.34)%。结论:氟氯西林镁颗粒与氟氯西林钠胶囊在吸收程度上具有生物等效性。     

Role of AMPK in pancreatic beta cell function

Pharmacological activation of AMP activated kinase (AMPK) by metformin has proven to be a beneficial therapeutic approach for the treatment of type II diabetes. Despite improved glucose regulation achieved by administration of small molecule activators of AMPK, the potential negative impact of enhanced AMPK activity on insulin secretion by the pancreatic beta cell is an important consideration. In this review, we discuss our current understanding of the role of AMPK in central functions of the pancreatic beta cell, including glucose-stimulated insulin secretion (GSIS), proliferation, and survival. In addition we discuss the controversy surrounding the role of AMPK in insulin secretion, underscoring the merits and caveats of methods used to date.