Using a combination of CYP2C19 genotype and postoperative time to determine the initial voriconazole dosing regimens followed by therapeutic drug monitoring could help to advance individualized treatment in renal transplantation patients with invasive fungal infections.

Improved survival following organ transplantation has brought to the forefront some long-term complications, among which osteoporosis and associated fractures are the major ones that adversely affect the quality of life in recipients. The pathogenesis of osteoporosis in transplant recipients is complex and multifactorial which may be related to increased bone resorption, decreased bone formation, or both. Studies have shown that the preexisting underlying metabolic bone disorders and the use of immunosuppressive agents are the major risk factors for osteoporosis and fractures after organ transplantation. And rapid bone loss usually occurs in the first 6–12 months with a significant increase in fracture risk. This paper will provide an updated review on the possible pathogenesis of posttransplant osteoporosis and fractures, the natural history, and the current prevention and treatment strategies concerning different types of organ transplantation.

Mitochondrial transcription factor A (TFAM) is required for mitochondrial DNA (mtDNA) replication and transcription. microRNAs (miRNAs) act as key factors in the regulation of gene expression. However, the roles of TFAM and certain miRNAs and their association in cancer development remain unclear. The present study reported that the expression of TFAM was significantly increased in bladder cancer, while the expression of miRNA-590-3p was downregulated. The luciferase assay showed that TFAM was the direct target of miRNA-590-3p. Furthermore, the forced overexpression of miRNA-590-3p significantly inhibited the proliferation, migration and colony-forming ability of 5637 cells, which was in contrast with the results from the forced overexpression of TFAM in the 5637 cells. Furthermore, cell proliferation- and migration-related genes, including phosphoinositide-3-kinase (PI3K), Akt, matrix metalloproteinase (MMP)-2 and MMP9, were significantly downregulated in the miRNA-590-3p-overex-pressing 5637 cells, but upregulated in the TFAM-overexpressing cells. In conclusion, the present study suggested that TFAM, a direct target of miRNA-590-3p, may play a significant role in the tumorigenesis of bladder cancer and thus may be a promising target for cancer therapeutics.

IntroductionRecent studies have demonstrated the critical roles of micro-RNAs in tumorigenesis and tumor progression. Here, we describe the regulation and function of miR-490-5p in bladder cancer.Material and methodsPaired tissue samples were collected from bladder cancer patients (n = 20). Real-time PCR revealed that miR-490-5p expression was significantly down-regulated in human bladder cancer tissues and cells. Also there was an inverse relationship between the expression level of miR-490-5p and the pathological grade of bladder cancer. Western blotting was performed to detect the expression levels of c-FOS and TET1 in 6 matched tumor tissue samples and 4 bladder cell lines. Furthermore, to better understand the underlying mechanisms of miR-490-5p, we conducted gain and loss of function analysis by transfecting bladder cancer T24 cells with chemically synthesized miR-490-5p mimics and inhibitor, respectively.ResultsWe found that overexpression of miR-490-5p in T24 cells could inhibit cell proliferation and invasion and induce cell apoptosis. Conversely, suppression of miR-490-5p expression induced cell proliferation and invasion, while it inhibited cell apoptosis. In addition, our bioinformatics prediction and experimental data showed that c-FOS was a potential target of miR-490-5p. The expression level of c-FOS was significantly decreased after miR-490-5p overexpression and significantly increased after miR-490-5p suppression, indicating that c-FOS was a target of miR-490-5p.ConclusionsThese findings suggest that miR-490-5p is a novel tumor suppressor, contributing to the carcinogenesis of bladder cancer by targeting c-FOS.