Arteriovenous (AV) access failure resulting from venous neointimal hyperplasia is a major cause of morbidity in patients with ESRD. To understand the role of chronic kidney disease (CKD) in the development of neointimal hyperplasia, we created AV fistulae (common carotid artery to jugular vein in an end-to-side anastomosis) in mice with or without CKD (renal ablation or sham operation). At 2 and 3 wk after operation, neointimal hyperplasia at the site of the AV anastomosis increased 2-fold in animals with CKD compared with controls, but cellular proliferation in the neointimal hyperplastic lesions did not significantly differ between the groups, suggesting that the enhanced neointimal hyperplasia in the setting of CKD may be secondary to a migratory phenotype of vascular smooth muscle cells (VSMC). In ex vivo migration assays, aortic VSMC harvested from mice with CKD migrated significantly greater than VSMC harvested from control mice. Moreover, animals with CKD had higher serum levels of osteopontin, which stimulates VSMC migration. When we treated animals with bone morphogenic protein-7, which promotes VSMC differentiation, before creation of the AV anastomosis, the effect of CKD on the development of neointimal hyperplasia was eliminated. In summary, CKD accelerates development of neointimal hyperplasia at the anastomotic site of an AV fistula, and administration of bone morphogenic protein-7 neutralizes this effect.

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The clinicopathological significance of amplification was investigated of the gene encoding cyclin E (CCNE1) and we assessed whether CCNE1 was a potential target in endometrioid endometrial carcinomas. CCNE1 amplification and CCNE1 or F-box and WD repeat domain-containing 7 (FBXW7) expression in endometrial endometrioid carcinoma was assessed by immunohistochemistry and fluorescence in situ hybridization. CCNE1 knockdown by small interfering RNA (siRNA) was used to assess the CCNE1 function. The results showed that CCNE1 amplification was present in 9 (8.3%) of 108 endometrial carcinomas. CCNE1 amplification was correlated with high histological grade (Grade 3; P=0.0087) and lymphovascular space invasion (P=0.0258). No significant association was observed between CCNE1 amplification and FIGO stage (P=0.851), lymph node metastasis (P=0.078), body mass index (P=0.265), deep myometrial invasion (P=0.256), menopausal status (P=0.289) or patient age (P=0.0817). CCNE1 amplification was significantly correlated with shorter progression-free and overall survival (P=0.0081 and 0.0073, respectively). CCNE1 protein expression or loss of FBXW7 expression in endometrial endometrioid carcinoma tended to be correlated with shorter progression-free and overall survival; however, this difference was not statistically significant. Multivariate analysis showed that CCNE1 amplification was an independent prognostic factor for overall survival but not for progression-free survival (P=0.0454 and 0.2175, respectively). Profound growth inhibition was observed in siRNA-transfected cancer cells with endogenous CCNE1 overexpression compared with that in cancer cells having low CCNE1 expression. CCNE1 amplification was independent of p53, HER2, MLH1 and ARID1A expression but dependent on PTEN expression in endometrial carcinomas. These findings indicated that CCNE1 amplification was critical for the survival of endometrial endometrioid carcinomas. Furthermore, the effects of CCNE1 knockdown were dependent on the CCNE1 expression status, suggesting that CCNE1-targeted therapy may be beneficial for patients with endometrial endometrioid carcinoma having CCNE1 amplification.

The high tensile and compressive strains found at the base of the pedicle of T10, L1, and L4 indicate that the base of the pedicle is the site of fracture initiation. The higher tensile strain at the superior vertebral rim of L1 and L4 supports the clinical observation of the thoracolumbar burst fractures.

No abstract

Anterior decompression and stabilization for unstable burst fracture without initial neurologic deficits in the thoracolumbar spine has some advantages in the view of anatomical reduction and rigid stability that allows patients an early rehabilitation, return to work, and gainful employment.

There was a weak significant correlation between tumor size and ADC value of clear-cell RCC. Using ROC and regression analysis, ADC was statistically significant index for distinguishing low-grade from high-grade clear-cell RCC more than tumor size and ADC/size ratio.

Study design Retrospective epidemiological study. Objective To investigate the epidemiology of traumatic spinal cord injury (TSCI) in the fastest aging area in Japan. Setting Hospitals in Akita Prefecture, Japan. Akita Prefecture has the highest ratio of people aged 65 or older in Japan (30.4% in 2012 and 34.6% in 2016). Methods Patients with acute TSCI who required hospital treatment between 2012 and 2016 were included. The incidence of TSCI, cause, level, skeletal injury, and Frankel grade were investigated. Results The mean annual incidence of TSCI excluding Frankel E was 86 per million (range 86-104 per million) during the 5-year study period, with a mean age of 65.9 years (male, 75.1%) and patients in their 60s as the largest age group. Cervical injury was seen in 89.8%, and cervical TSCI without skeletal injury was seen in 65.5%. Frankel D was the most common neurological deficit (53.5%). The most common cause was falls on level surfaces (32.1%), followed by low falls (21.6%) and road traffic accidents (15.6%). Conclusions Recent incidence and characteristics of TSCI in the fastest aging society in Japan are presented. The incidence of incomplete cervical TSCI and falls on level surfaces appear to be increasing.