Urate-lowering therapy may mitigate the risks of hospitalized stroke and mortality in patients with gout.

Objectives: Although studies have demonstrated the association of hyperuricemia with cardiovascular (CV) diseases, few have explored the effect of urate-lowering therapy (ULT) on the incidence of CV diseases. Therefore, we compared the risks of hospitalized coronary artery disease (CAD), stroke, heart failure (HF), and all-cause mortality between ULT users and nonusers among patients with gout.

Methods: We performed this retrospective cohort study using Taiwan's population-based National Health Insurance Research Database.

Urate-lowering therapy exerts protective effects against hypertension development in patients with gout.

Many studies have demonstrated that hyperuricemia is associated with hypertension (HTN) development, but few studies have explored whether urate-lowering therapy (ULT), which reverses hyperuricemia, decreases the risk of incident HTN. In this retrospective cohort study, we compared the risk of incident HTN of gout patients between those undergoing and not undergoing ULT. Risks of new-onset diabetes mellitus (DM) and chronic kidney disease (CKD) were also examined.

Urate-Lowering Therapy May Prevent the Development of Coronary Artery Disease in Patients With Gout.

Substantial evidence has demonstrated a close relationship between hyperuricemia and cardiovascular (CV) diseases, but few studies have explored the possibility of using urate-lowering therapy (ULT) to attenuate the development of CV diseases. To compare the risks of incident coronary artery disease (CAD), stroke, and heart failure (HF) between ULT users and non-users in patients with gout, we conducted a retrospective cohort study from the population-based National Health Insurance Research Database in Taiwan. In total, 4,072 patients with gout were included between 2000 and 2012.

Nanog expression is negatively regulated by protein kinase C activities in human cancer cell lines.

Nanog is a transcription factor that is essential for the maintenance of pluripotency of the embryonic stem cells. Nanog has been shown to be expressed in various kinds of human tumors, suggesting a role in tumorigenesis. In this study, we found that Nanog expression was upregulated by inhibition of protein kinase C (PKC) activity in six human cancer cell lines examined.

Glycogen synthase kinase-3beta regulates DeltaNp63 gene transcription through the beta-catenin signaling pathway.

Overexpression of DeltaNp63 has been observed in a number of human cancers, suggesting a role for DeltaNp63 in carcinogenesis. In the present study, we show that inhibition of glycogen synthase kinase-3beta (GSK-3beta) by lithium chloride (LiCl) elicited a stimulatory effect on DeltaNp63 promoter activity in HEK 293T cells. Exposure to LiCl induced DeltaNp63 promoter activation as well as DeltaNp63 protein expression in the cells.

Transcriptional activity of the DeltaNp63 promoter is regulated by STAT3.

The N terminus-truncated splicing variant of TAp63 is known as DeltaNp63. DeltaNp63 lacks transactivation function and is thought to antagonize the transcriptional regulation of the p53 and TAp63 target genes. Overexpression of DeltaNp63 has been observed in a number of human cancers, suggesting a role in carcinogenesis.