Overall, 183 patients underwent a combined 229 bandings with technical success achieved in 225. Complete symptomatic relief (clinical success) was attained in 109 Steal patients and in all high-flow patients. The average follow-up time was 11 months with a 6-month primary

band patency of 75 and 85% for Steal and high-flow patients, respectively. At 24 months the secondary access patency was 90% and the thrombotic event rates for upper-arm fistulas, forearm fistulas, and grafts were 0.21, 0.10, and 0.92 per access-year, respectively. Hence, the minimally invasive MILLER procedure appears to be an effective and durable option for treating Selleck LDN-193189 dialysis access-related steal syndrome and high-flow-associated symptoms.

Kidney International (2010) 77, 359-366; doi: 10.1038/ki.2009.461; published online 9 December 2009″
“MicroRNAs (miRNAs) are a class of endogenous small noncoding RNAs that regulate gene expression after transcription. Aberrant expression of miRNAs has been shown to be involved in tumorigenesis. We showed that miR-21 was one of the most frequently overexpressed miRNA in human glioblastoma (GBM) cell lines. To explore whether miR-21 can serve as a therapeutic target for glioblastoma, we downregulated miR-21 ATR inhibitor with a specific antisense oligonucleotide and found that apoptosis was induced and cell-cycle progression was inhibited in vitro in U251 (PTEN mutant) and LN229 (PTEN wildtype) GBM cells; xenograft tumors from antisense-treated U251 cells were suppressed in vivo. Antisense-miR-21-treated cells showed a decreased expression of EGFR, activated Akt, cyclin D, and Bcl-2. Although miR-21

is known to regulate PTEN and downregulation of miR-21 led to increased PTEN expression both endogenously and in a reporter gene assay, the GBM suppressor effect of antisense-miR-21 is most likely independent of PTEN regulation because U251 has mutant PTEN. Microarray analysis showed that the knockdown of miR-21 significantly altered expression of 169 genes involved in nine cell-cycle and signaling pathways. Taken together, our studies provide evidence that miR-21 may serve as a novel therapeutic target for malignant gliomas Etofibrate independent of PTEN status. Laboratory Investigation (2010) 90, 144-155; doi:10.1038/labinvest.2009.126; published online 4 January 2010″
“Increasing evidence suggests that apoptosis may be the mechanism underlying cell death in selective loss of nigral dopaminergic neurons in Parkinson’s disease (PD). Previous studies strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway has a critical role in the animal model with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. In this study, we report the inhibitory effect of a peptide designated as Tat-JBD on JNKs activation.