慢性心衰患者电话干预的随机试验：DIAL试验

目的:明确集中的电话干预能否降低慢性心衰门诊患者死亡或因心衰加重而住院的发生率。设计:多中心、随机对照试验。地点:阿根廷的51个中心(包括公立、私立的医院及流动设施)。参与者:1518例患有稳定的慢性心衰且已接受最佳药物治疗方案治疗的门诊患者,由心脏科主治医师分层后随机分为电话干预组和常规治疗组。干预:在常规治疗的基础上,由一个中心通过护士频繁的电话随访对患者进行教育、辅导和监督。主要观察指标:全因死亡或由于心衰加重而住院。结果:99.5%的患者完成了全部随访。常规治疗组758例患者中由于心衰加重而住院或死亡的比例(235…     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.     

Modeling mechanisms of skull base injury for drivers in motor vehicle collisions.

OBJECTIVE: To develop biomechanical variable models for driver skull base injury mechanisms in motor vehicle collisions. STUDY DESIGN: Retrospective database review. METHODS: Biomechanical collision variables and safety restraint data were analyzed for Crash Injury Research and Engineering Network skull base trauma subjects enrolled during the recruitment period between 1996 and 2005. RESULTS: For drivers satisfying inclusion criteria (n = 26), injury resulted from contact with rigid vehicle structural elements in 82%, and occurred in 50% despite both seatbelt and air bags. Eight percent used neither seatbelts nor air bags. Seventy-two percent involved vector velocity changes greater than 30 mph. The relative morbidity of skull base injuries was also detailed. CONCLUSION: The majority of driver skull base injuries resulted from contact with rigid vehicle structural elements in high velocity crashes. Seatbelt and air bag use could not be definitively correlated with skull base injury. CLINICAL SIGNIFICANCE: Injury mechanism models can be developed that facilitate further investigations to determine impact and scope on a national scale.     

Otolaryngologic approach to the diagnosis and management of otitis media

Otitis media is a common childhood disease caused by multiple factors. Understanding the pathogenesis of otitis media is important in the diagnosis and management of it. The mode of therapy should be chosen depending on the type and stage of the disease. Treatment options available to an otolaryngologist include antibiotics, tympanocentesis, myringotomy and tympanostomy tube insertions, adenoidectomy with or without tonsillectomy, exploratory tympanotomy, atympanoplasty, and mastoidectomy.     

Cyclin E, p27 and mutant p53 do not predict the prognosis in AJCC stage II colorectal carcinomas.

BACKGROUND/AIMS: Carcinogenesis is characterized by the abnormal regulation of cell cycle. The abnormal expression of the regulators of cell cycle may be related to the prognosis. Since the clinical significance of the expression of the three proteins in colorectal carcinomas is still controversial, we evaluated the prognostic value of the expression of cyclin E, p27 and mutant p53 in stage II colorectal cancer. METHODS: The expression levels of cyclin E, p27 and mutant p53 proteins in 41 patients with stage II colorectal carcinomas were analyzed by immunohistochemistry. RESULTS: In the univariate analysis, the level of CEA at diagnosis was associated with disease relapse. In the multivariate analysis, the clinicopathological variables such as age, gender, site of primary tumor, tumor size, state of tumor differentiation and preoperative plasma CEA level were not associated with disease relapse. When Kaplan-Meier survival curves were constructed to determine the prognosis, cyclin E, p27 and mutant p53 expressions did not predict poor prognosis. CONCLUSIONS: Our results suggested that the expression of cyclin E, p27 and mutant p53 proteins did not predict the clinical outcome in the stage II colorectal carcinomas.     

Regulation of phospholipase C-β isozymes by G-proteins

Phospholipase C (PLC) isozymes are known to be regulated, in part, by heterotrimeric GTP-binding protein (G-protein) subunits, including Gα subunits of the G_q family and Gβγ subunits. New data show that PLC can also be regulated by a high molecular weight G-protein that doubles as a cellular transglutaminase. Furthermore, a soluble phosphatidylinositol transfer protein (PITP) has been implicated in sustaining the activity of PLC by delivering substrate to the plasma membrane. Such diverse regulatory mechanisms imply that the PLC isozymes are precisely controlled and have specific roles in generating second messengers in response to various external stimuli.