Elucidation of the therapeutic role of mitochondrial biogenesis transducers NRF-1 in the regulation of renal fibrosis.

Background: Mitochondrial dysfunction is a newly established risk factor for the development of renal fibrosis. Cell survival and injury repair is facilitated by mitochondrial biogenesis. Nuclear respiratory factor 1 (NRF-1) is a transcriptional regulation factor that plays a central role in the regulation of mitochondrial biogenesis.

Treatment with cytokine thymic stromal lymphopoietin short hairpin RNA substantially reduces TGF-β1-induced interstitial cellular fibrosis.

Thymic stromal lymphopoietin (TSLP) has previously been linked to allergic inflammatory diseases, and tissue fibrosis and organ dysfunction may also arise from such inflammation. It remains unclear, however, whether TSLP plays any role in the occurrence of renal fibrosis, so this study investigated that possibility. An in vitro fibrosis model was established by treating normal rat kidney fibroblast (NRK-49F) cells with transforming growth factor-β1 (TGF-β1), after which the levels of various fibrogenic markers (e.

MLN4924, a novel protein neddylation inhibitor, suppresses proliferation and migration of human urothelial carcinoma: In vitro and in vivo studies.

MLN4924, a small molecule inhibitor of NEDD8 activating enzyme (NAE), has been reported to elicit an anti-tumor effect on various malignancies. In this study, we investigated the anti-tumor effect of MLN4924 in human urothelial carcinoma (UC) in vitro and in vivo by using three human UC cell lines of various grading (T24, NTUB1 and RT4). The impact of MLN4924 on UC cells was determined by measuring viability (MTT), proliferation (BrdU incorporation), cell cycle progression (flow cytometry with propidium iodide staining) and apoptosis (flow cytometry with annexin V-FITC labeling).

Persistent monocytosis after intravenous immunoglobulin therapy correlated with the development of coronary artery lesions in patients with Kawasaki disease.

Background And Purpose: This study was conducted to investigate whether changes in the complete blood count (CBC)/differential count (DC) and C-reactive protein (CRP) were correlated to Kawasaki disease (KD) with coronary artery lesions (CALs).

Methods: A retrospective analysis was performed of all children with KD at Chang Gung Memorial Hospital at Kaohsiung from 2001 to 2006. KD patients were divided into those with and without CALs for testing of correlations with changes in CBC/DC and CRP levels.

Childhood macrophage activation syndrome differs from infection-associated hemophagocytosis syndrome in etiology and outcome in Taiwan.

Background And Purpose: Hemophagocytic lymphohistiocytosis (HLH) is a syndrome composed of macrophage activation syndrome (MAS), infection-associated hemophagocytosis syndrome (IAHS), malignancy-associated HLH and genetic HLH. Differentiation of MAS from IAHS and other HLH is important for early appropriate treatment.

Methods: A retrospective analysis was used to differentiate childhood MAS from IAHS and other HLH in Chang Gung Memorial Hospital (CGMH), Kaohsiung.

Methylprednisolone pulse therapy for massive lymphadenopathy in a child with intravenous immunoglobulin-resistant Kawasaki disease.

Kawasaki disease (KD) is an acute febrile multi-system vasculitis of unknown etiology. The diagnosis is based on clinical features. We describe a case of intravenous immunoglobulins (IVIG)-resistant KD presenting with persistent fever and massive cervical lymphadenopathy associated with mild respiratory distress.

An open-label, crossover study of a new phosphate-binding agent in haemodialysis patients: ferric citrate.

Background: Hyperphosphataemia contributes to secondary hyperparathyroidism and renal osteodystrophy in patients with end-stage renal disease (ESRD). Calcium salts are widely employed to bind dietary phosphate (P) but they may promote positive net calcium balance and metastatic calcification. We recently reported that ferric compounds bind intestinal phosphate in studies of normal and azotemic rats.