Intermittent hypoxia induces tumor immune escape in murine S180 solid tumors via the upregulation of TGF-β in mice.

Purpose: Studies have shown that intermittent hypoxia (IH) alters host immune functions and promotes tumor growth. However, the relevant mechanisms of these effects have not been completely elucidated. We hypothesized that IH promotes the growth of tumors by changing cytokine levels in the tumor microenvironment and inducing immune escape.

Niclosamide attenuates inflammatory cytokines via the autophagy pathway leading to improved outcomes in renal ischemia/reperfusion injury.

Renal ischemia/reperfusion (I/R) injury is a debilitating condition that leads to loss renal function and damage to kidney tissue in the majority of patients with acute kidney disease. Previous studies have indicated that autophagy serves a protective function in renal I/R injury. In the present study, the effect of the anthelmintic niclosamide in the regulation of inflammatory responses in kidney I/R was investigated.

[Effects of 1, 25(OH)(2);D(3); on parathyroid hormone induced transdifferentiation and TGF-β(1); expression in cultured human renal tubular epithelial cells].

Aim: To explore the effects of 1, 25(OH)(2);D(3); on parathyroid hormone (PTH) induced transdifferentiation and TGF-β(1); expression in cultured human renal tubular epithelial cells.

Methods: HK-2 cells were cultured in DMEM/F12 medium supplemented with 50 mL/L FBS. Cells were divided into three groups.