Influence of Qingdai Compound Capsule on the expression of c-myc in psoriatic keratinocytes) on the expression of c-myc in psoriatic keratinocytes

In this immunohistochemical study, the authors detected the expression of c-myc in keratinocytes (ECK) from 30 psoriatics before and after Qingdai Compound Capsule (QDCC) treatment and 12 normal subjects for control. The results showed that the ECK of patients before treatment was significantly higher than that in the normal control group, and its level was correlated with histopathological changes of affected skin. After treatment the ECK was normalized. It is believed that QDCC could decrease the ECK in psoriatics and this effect was probably mediated by inhibiting c-myc expression. This study provided an experimental evidence for the application of QDCC in treating psoriasis.     

改良超滤对婴幼儿心脏手术输血的影响

目的　观察改良超滤技术在婴幼儿体外循环心血管手术中对输血及术后出血的影响。方法　 6 0例接受体外循环下心血管手术的先天性心脏病患儿 ,均分为对照组 (不接受任何超滤 )、常规超滤组 (CUF组 )和改良超滤组 (MUF组 )。观察术中库血用量、血浆用量、血球压积的变化及术后2 4h出血量 ,并用SSPS/PC进行统计学处理。结果　MUF组库血用量、血浆用量、术后 2 4h出血量显著低于对照组和CUF组 (P <0 0 1) ,且滤出水量明显多于CUF组 (P <0 0 1)。结论　在婴幼儿心血管手术中 ,改良超滤可有效排出体内水分 ,提高血球压积 ,明显减少输血及术后出血 ,是节约用血的重要手段之一。     

纸质病案保存期限的思考

本文作者比较了不同时期的纸质病案的使用率,讨论了旧病案的缺点,如难于保存,占用空间及实用价值不大.作者提出了改进保存病案的办法.     

王霞芳治疗小儿泄泻的经验

小儿泄泻的病因病机因其自身稚阴稚阳的生理特点而较成人为多发,泄泻久甚,易耗伤气液,甚至出现伤阴伤阳的重证、变证。故要重视及时正确地治疗,以防产生危候。王霞芳老师治疗小儿泄泻首先注重审证求因,在精确辨证基础上立法选方而施治,并在病变过程中法随症变,灵活化裁,刻刻护卫脾气胃津,斡旋脾胃气机,重视清浊升降枢机作用。尝用葛根、扁豆衣、荷叶等轻灵升清之品,宣发清阳,泄泻自和。对屡治不愈、迁延日久者,王师认为应辨证细致,选药精到,且又及时而适当地参入止涩药物。固肠止涩法之运用,必须具备苔净,腹软,溲通,无表证和里积等条件,方为合宜。     

Conditional estimation of sensitivity and specificity from a phase 2 biomarker study allowing early termination for futility

Development of a disease screening biomarker involves several phases. In phase 2 its sensitivity and specificity is compared with established thresholds for minimally acceptable performance. Since we anticipate that most candidate markers will not prove to be useful and availability of specimens and funding is limited, early termination of a study is appropriate, if accumulating data indicate that the marker is inadequate. Yet, for markers that complete phase 2, we seek estimates of sensitivity and specificity to proceed with the design of subsequent phase 3 studies. We suggest early stopping criteria and estimation procedures that adjust for bias caused by the early termination option. An important aspect of our approach is to focus on properties of estimates conditional on reaching full study enrollment. We propose the conditional‐UMVUE and contrast it with other estimates, including naïve estimators, the well‐studied unconditional‐UMVUE and the mean and median Whitehead‐adjusted estimators. The conditional‐UMVUE appears to be a very good choice. Copyright © 2008 John Wiley & Sons, Ltd.     

BKV in Simultaneous Pancreas-Kidney Transplant Recipients: A Leading Cause of Renal Graft Loss in First 2 Years Post-Transplant

With the introduction of more potent immunosuppressive agents, rejection has decreased in simultaneous pancreas/kidney transplant (SPK) recipients. However, as a consequence, opportunistic infections have increased. The purpose of this report is to outline the course of SPK patients who developed polyomavirus-associated nephropathy (PVAN). A retrospective review of 146 consecutive SPK recipients from January 1, 1996 to December 31, 2002 was performed. Immunosuppression, rejection and development of PVAN were reviewed. Nine patients were identified. All received induction with either OKT3 or thymoglobulin. Immunosuppression included tacrolimus/cyclosporine, MMF/azathioprine and sirolimus/prednisone. Two patients were treated for kidney rejection prior to the diagnosis of PVAN. Time to diagnosis was an average of 359.3 days post-transplantation. Immunosuppression was decreased but five ultimately lost function. However, none developed pancreatic abnormalities as demonstrated by normal glucose and amylase. Two underwent renal retransplantation after PVAN diagnosis and both have normal kidney function. PVAN was the leading cause of renal loss in SPK patients in the first 2 years after transplantation and is a serious concern for SPK recipients. The pancreas, however, is spared from evidence of infection, and no pancreatic rejection occurred when immunosuppression was decreased.     

Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke.

Bone marrow stromal cells (MSCs) increase vascular endothelial growth factor (VEGF) expression and promote angiogenesis after stroke. Angiopoietin-1 (Ang1) and its receptor Tie2 mediate vascular integrity and angiogenesis as does VEGF and its receptors. In this study, we tested whether MSC treatment of stroke increases Ang1/Tie2 expression, and whether Ang1/Tie2 with VEGF/ vascular endothelial growth factor receptor 2 (VEGFR2) (Flk1), in combination, induced by MSCs enhances angiogenesis and vascular integrity. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAo) and treated with or without MSCs. Marrow stromal cell treatment significantly decreased blood-brain barrier (BBB) leakage and increased Ang1, Tie2, and occludin (a tight junction protein) expression in the ischemic border compared with MCAo control. To further test the mechanisms of MSC-induced angiogenesis and vascular stabilization, cocultures of MSCs with mouse brain endothelial cells (MBECs) or astrocytes were performed. Supernatant derived from MSCs cocultured with MBECs significantly increased MBEC expression of Ang1/Tie2 and Flk1 compared with MBEC alone. Marrow stromal cells cocultured with astrocytes also significantly increased astrocyte VEGF and Ang1/Tie2 expression compared with astrocyte culture alone. Conditioned media from MSCs alone, and media from cocultures of MSCs with astrocytes or MBECs, all significantly increased capillary tube-like formation of MBEC compared with control Dulbecco's modified Eagle's medium media. Inhibition of Flk1 and/or Ang1 significantly decreased MSC-induced MBEC tube formation. Knockdown of Tie2 expression in MBECs significantly inhibited MSC-induced tube formation. Our data indicate MSC treatment of stroke promotes angiogenesis and vascular stabilization, which is at least partially mediated by VEGF/Flk1 and Ang1/Tie2.