ACTH stimulation test and computed tomography are useful for differentiating the subtype of primary aldosteronism.

The diagnostic steps for primary aldosteronism (PA) include case screening tests, confirmatory tests, and localization. The aim of this study was to identify useful confirmatory tests and their cut-off values for differentiating the subtype of primary aldosteronism, especially in unilateral PA, such as aldosterone-producing adenoma, and bilateral PA, such as idiopathic hyperaldosteronism. Seventy-six patients who underwent all four confirmatory tests, the captopril-challenge test (CCT), furosemide upright test (FUT), saline infusion test (SIT), and ACTH stimulation test (AST), and who were confirmed to have an aldosterone excess by adrenal venous sampling (AVS) were recruited. Subjects were diagnosed as having unilateral aldosterone excess (n=17) or bilateral aldosterone excess (n=59) by AVS. The SIT-positive rate was significantly higher in the unilateral group (94.1%) than in the bilateral group (57.6%). Multivariable logistic regression analysis showed that tumor on computed tomography (CT) and plasma aldosterone concentration (PAC)max/cortisol on the AST were useful for differentiating the subtype of PA. Receiver operating characteristic (ROC) curve analysis for distinguishing the subtype of PA showed that a cut-off value of 18.3 PACmax/cortisol on the AST had a sensitivity of 83% and a specificity of 88%. The area under the ROC curve was 0.918 (95% confidence interval 0.7916-0.9708). These data suggest that abdominal CT and AST are useful for differentiating the subtype of PA and the indication for AVS.

A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord.

Axons in the adult mammalian central nervous system (CNS) exhibit little regeneration after injury. It has been suggested that several axonal growth inhibitors prevent CNS axonal regeneration. Recent research has demonstrated that semaphorin3A (Sema3A) is one of the major inhibitors of axonal regeneration. We identified a strong and selective inhibitor of Sema3A, SM-216289, from the fermentation broth of a fungal strain. To examine the effect of SM-216289 in vivo, we transected the spinal cord of adult rats and administered SM-216289 into the lesion site for 4 weeks. Rats treated with SM-216289 showed substantially enhanced regeneration and/or preservation of injured axons, robust Schwann cell-mediated myelination and axonal regeneration in the lesion site, appreciable decreases in apoptotic cell number and marked enhancement of angiogenesis, resulting in considerably better functional recovery. Thus, Sema3A is essential for the inhibition of axonal regeneration and other regenerative responses after spinal cord injury (SCI). These results support the possibility of using Sema3A inhibitors in the treatment of human SCI.

Hzf regulates adipogenesis through translational control of C/EBPalpha.

Adipocyte differentiation requires a well-defined programme of gene expression in which the transcription factor C/EBPalpha (CCAAT/enhancer-binding protein) has a central function. Here, we show that Hzf (haematopoietic zinc-finger), a previously identified p53 transcriptional target, regulates C/EBPalpha expression. Hzf is induced during differentiation of preadipocyte cell lines, and its suppression by short hairpin RNA disrupts adipogenesis. In Hzf's absence, expression of C/EBPalpha is severely impaired because of reduced translation of its mRNA. Hzf physically interacts with the 3' untranslated region of C/EBPalpha mRNA to enhance its translation. Taken together, these findings underscore a critical role of Hzf in the adipogenesis regulatory cascade.

Different pathogenesis of glucose intolerance in two subtypes of primary aldosteronism: Aldosterone-producing adenoma and idiopathic hyperaldosteronism.

AIMS/INTRODUCTION: An increased risk of diabetes mellitus has been reported in primary aldosteronism, but the pathogenesis of glucose intolerance between the primary aldosteronism subtypes remains unclear. This study aimed to evaluate glucose metabolism in oral glucose tolerance test between aldosterone-producing adenoma and idiopathic hyperaldosteronism, and characterize patients with improved glucose intolerance after primary aldosteronism treatment. MATERIALS AND METHODS: Oral glucose tolerance test was carried out in 116 patients who were diagnosed with primary aldosteronism and received adrenal venous sampling for subtyping. Oral glucose tolerance test was re-evaluated after starting the treatment of primary aldosteronism for those who had glucose intolerance before the treatment. RESULTS: A total of 46.4% and 52.3% of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively, were diagnosed with impaired glucose tolerance or diabetes. The insulinogenic index was significantly lower in aldosterone-producing adenoma than in idiopathic hyperaldosteronism (P = 0.045), whereas the Matsuda insulin sensitivity index was significantly higher in aldosterone-producing adenoma than in idiopathic hyperaldosteronism (P = 0.022). After the treatment of primary aldosteronism, glucose intolerance was improved in 66.6% and 45.8% of aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively. The presence of obesity and central obesity were significantly lower in patients who improved glucose intolerance after the treatment of primary aldosteronism as compared with those not improved (P = 0.013 and P = 0.033, respectively). CONCLUSIONS: Insulin secretion impairment and insulin resistance play pathogenic roles for glucose intolerance in aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively. In addition, primary aldosteronism treatments can ameliorate glucose intolerance more effectively in patients without obesity and/or central obesity.

Bioremediation of bisphenol-A polluted soil by Sphingomonas bisphenolicum AO1 and the microbial community existing in the soil.

Bisphenol A (BPA, 2,2'-Bis (4-hydroxyphenyl) propane) is an artificial pollutant that is easily detected in soil and water environments. BPA decomposition and removal from the environment is relatively difficult due to its stability. This study evaluated the BPA decomposition and removal activities of the microbial community existing in the soil with or without Sphingomonas bisphenolicum AO1, and revealed the toxic effects of BPA towards the microbial community. The microbial community in soil was able to degrade BPA at 1.0 mg·g(-1) soil or lower, although its degradation was slow. On the other hand, BPA at more than 10 mg·g(-1) soil was not only degraded by the microbial community but also decreased its diversity, suggesting that BPA is harmful to many microorganisms. PCR-TTGE analysis and the cloned 16S rRNA gene sequence analysis indicated that Sphingomonadales, Xanthomonadales, Burkholderiales and Pseudomonadales in the microbial community might independently or cooperatively degrade BPA. On the other hand, supplementation with strain AO1 was able to significantly improve the BPA decomposition activity of the microbial community in soil even at 10 mg BPA·g(-1) soil, although BPA at 100 mg·g(-1) soil overwhelmed the BPA decomposition activity of strain AO1. Furthermore, it was also concluded that strain AO1 could not inhabit BPA purified soil after decomposition of BPA by strain AO1 and the soil microbial community, suggesting that the application of strain AO1 could be a low-burden method for the decomposition and removal of BPA from the natural environment.