Aims/hypothesis The associations between adiponectin polymorphisms and type 2 diabetes have been studied widely; however, results are inconsistent. Methods We searched electronic literature databases and reference lists of relevant articles. A fixed or random effects model was used on the basis of heterogeneity. Sub-group and meta-regression analyses were conducted to explore the sources of heterogeneity.

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Necroptosis is mediated by signaling complexes called necrosomes, which contain receptor-interacting protein 3 (RIP3) and upstream effectors, such as RIP1. In necrosomes, the RIP homotypic interaction motif (RHIM) of RIP3 and RIP1 forms amyloidal complex. But how the amyloidal necrosomes control RIP3 activation and cell necroptosis has not been determined. Here, we showed that RIP3 amyloid fibrils could further assemble into large fibrillar networks which presents as cellular puncta during necroptosis. A viral RHIM-containing necroptosis inhibitor M45 could form heteroamyloid with RIP3 in cells and prevent RIP3 puncta formation and cell necroptosis. We characterized mutual antagonism between RIP3-RHIM and M45-RHIM in necroptosis regulation, which was caused by distinct inter-filament interactions in RIP3, M45 amyloids revealed with atomic force microscopy. Moreover, double mutations Asn464 and Met468 in RIP3-RHIM to Asp disrupted RIP3 kinase-dependent necroptosis. While the mutant RIP3(N464D/M468D) could form amyloid as wild type upon necroptosis induction. Based on these results, we propose that RIP3 amyloid formation is required but not sufficient in necroptosis signaling, the ordered inter-filament assembly of RIP3 is critical in RIP3 amyloid mediated kinase activation and cell necroptosis.

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Objective: To evaluate computed tomography (CT) and magnetic resonance imaging (MRI) features in patients with diastematomyelia and to investigate clinical characteristics of this lesion. Study design: A retrospectively study. Setting: The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University. Methods: A total of 82 diastematomyelia cases were retrospectively studied. All the patients underwent neurological examinations as well as MRI and CT of the spine. A self-established neurological functional grading system was used, and posterior tibial nerve somatosensory cortical-evoked potential (PTNSCEP) was measured to assess the neurological status of the patients. Imaging features of symmetry of splitting, presence of septum, location of lesion and number of split segments were studied. The neurological functional grading, PTNSCEP, and imaging findings were then analyzed and compared, and the difference was considered to be significant if P-value was lower than 0.05. Results: Neurological functional grading and latency of PTNSCEP were significantly different but related in terms of symmetry of splitting, presence of septum and location of lesion. Although no significant differences were present in the number of split segments, the severity of the neurological functional grading and PTNSCEP impairment were not related to the number of split segments. INTRODUCTIONDiastematomyelia is an uncommon congenital malformation of the vertebral axis where the spinal cord is split longitudinally into two. Each hemicord contains a central canal and a set of dorsal and ventral horns and nerve roots. The precise etiology is not known. The clinical manifestations include cutaneous abnormality overlying the spine, neurologic deficits and orthopedic abnormalities. [1][2][3][4] Clinically, the symptomatology is not specific and does not differ from that seen in other forms of spinal dysraphism. [5][6][7][8] Despite its low incidence, diastematomyelia results in severe neurological dysfunction. The clinical diagnosis and treatment of the lesion are therefore important. Delayed or improper treatment due to incorrect diagnosis may lead to the worsening of neurological symptoms. Conventionally, diagnosis of diastematomyelia is based on its clinical manifestations and radiological examination. Plain radiography and myelography have traditionally been used. With the improvement in imaging technology, computed tomography (CT) and magnetic resonance imaging (MRI) are established as the primary diagnostic strategies for evaluating the symptoms of diastematomyelia. Although CT and MRI findings of diastematomyelia have been discussed in the literature, 9-11 there are few reports concerning the characteristic imaging and the clinical manifestations. 12,13 The relationship between the clinical severity of diastematomyelia and the morphological changes reflect in imaging findings has never been thoroughly investigated.

Abstract. The function of kinesin family member 18A (KIF18A) in human renal cell carcinoma (RCC) is unclear.The purpose of the current study was to determine the expression and prognostic significance of KIF18A in RCC. Specimens from 273 RCC patients undergoing nephrectomies were studied. Expression of KIF18A mRNA was examined by reverse transcription-polymerase chain reaction (RT-PCR) or quantitative PCR, and the expression of KIF18A protein was examined by immunohistochemistry and western blotting. The expression of KIF18A in clear-cell RCC cell lines was decreased using small interfering RNA targeting KIF18A, and increased by transfection with KIF18A cDNA. The proliferative ability of RCC cells in vitro and in vivo was detected by WST-1 assay and an animal xenograft model with BALB/c nude mice, respectively. The association between KIF18A expression and overall survival was calculated using Kaplan-Meier analysis. The results showed that KIF18A expression was significantly increased in RCC tissues compared with normal kidney tissues. The level of KIF18A expression was significantly associated with tumor stage, histological grade, metastasis and tumor size. Moreover, KIF18A increased the proliferation of RCC cells in vitro and in vivo. KIF18A expression was upregulated in RCC and enhanced the proliferation of RCC cells. Therefore, it appears that KIF18A plays a key role in the carcinogenesis and progression of RCC, and is a novel candidate prognostic marker for RCC patients. Furthermore, silencing KIF18A expression may serve as a new therapeutic strategy against RCC.