In vivo dual targeting of the oncogenic Ether-à-go-go-1 potassium channel by calcitriol and astemizole results in enhanced antineoplastic effects in breast tumors.

Background: The oncogenic ether-à-go-go-1 potassium channel (EAG1) activity and expression are necessary for cell cycle progression and tumorigenesis. The active vitamin D metabolite, calcitriol, and astemizole, a promising antineoplastic drug, target EAG1 by inhibiting its expression and blocking ion currents, respectively. We have previously shown a synergistic antiproliferative effect of calcitriol and astemizole in breast cancer cells in vitro, but the effect of this dual therapy in vivo has not been studied.

Calcitriol reduces thrombospondin-1 and increases vascular endothelial growth factor in breast cancer cells: implications for tumor angiogenesis.

Calcitriol, a potent antineoplastic vitamin D metabolite, inhibits proliferation, induces apoptosis and slows the growth of tumors. Calcitriol also may exert either antiangiogenic or proangiogenic effects depending on the tissue. Vascular endothelial growth factor (VEGF) and thrombospondin-1 (Tsp-1) are key factors involved in promoting and inhibiting angiogenesis, respectively.

Learning curve in a Western training center of the circumferential en bloc esophageal endoscopic submucosal dissection in an in vivo animal model.

Aim. Evaluate the feasibility to overcome the learning curve in a western training center of the en bloc circumferential esophageal (ECE-) ESD in an in vivo animal model. Methods.

Endoscopic submucosal dissection in dogs in a World Gastroenterology Organisation training center.

Aim: To evaluate if canine models are appropriate for teaching endoscopy fellows the techniques of endoscopic submucosal dissection (ESD).

Methods: ESD was performed in 10 canine models under general anesthesia, on artificial lesions of the esophagus or stomach marked with coagulation points. After ESD, each canine model was euthanized and surgical resection of the esophagus or stomach was carried out according to "The Principles of Humane Experimental Technique, Russel and Burch".

Zinc-induced survival of Leydig cells in Fischer rats (Rattus norvegicus) treated with cadmium chloride.

Zinc is known to prevent cadmium-induced carcinogenesis and Leydig cell destruction in rat testes; however, the mechanism of action is not known, although it has been suggested that pituitary feedback increases the production of luteinizing hormone (LH) in response to low circulating androgen. We therefore examined the biological role of zinc in reducing cadmium toxicity in the Leydig cells of Fischer rats. Two groups of eleven 6-month-old rats were injected subcutaneously with 20 micromol CdCl2/kg weekly for 5 weeks; one of these groups also received 1 mmol/kg zinc acetate weekly for the same 5 weeks.