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A randomized controlled trial of homeopathic treatment of weaned piglets in a commercial swine herd.

Homeopathy. 2008 Oct; 97(4): 202-5Soto FR, Vuaden ER, Coelho C, Benites NR, Bonamin LV, de Azevedo SSAIM: To evaluate the zootechnic performance and occurrence of diarrhea in piglets in the week post-weaning comparing supplementation with sucrose saline which contained or did not contain added homeopathic medicine. METHOD: Animals were randomly divided into three groups of 24 piglets each. The control group did not receive any treatment. Another group received sucrose saline, and the third group received sucrose saline with homeopathic medicine added, in the period of zero to seven days post-weaning. The homeopathic treatment consisted of Echinacea angustifolia, Avena sativa, Ignatia amara, Calcarea carbonica, all 6cH. Piglets were weighed daily for weight gain or loss, and observed for diarrhea and feed intake. RESULTS: Animals receiving sucrose saline alone and sucrose saline with homeopathy had less weight loss than control (p=0.017, p=0.0001 respectively). There was no statistical difference in relation to overall incidence of diarrhea or food consumption. These data suggest that the supplementation with sucrose saline with added homeopathic medicine in the first seven days post-weaning may be an useful option to reduce weight loss in weaned piglets.

Endothelial dysfunction -an obstacle of therapeutic angiogenesis.

Ageing Res Rev. 2009 Apr 20; Sun L, Bai Y, Du GDue to ageing populations and improvements in survival, increasing numbers of patients suffering from ischemic cardiovascular disease are not amenable to revascularization. Hence, interests are currently focused on "therapeutic angiogenesis", which is the clinical use of growth factors to enhance or promote the development of collateral blood vessels in ischemic tissue. Several growth factors (or genes encoding these growth factors) are now available for therapeutic vascular growth in normal and ischemic tissues. However, the successes of angiogenic therapy observed in pre-clinical studies have not been realized in clinical trials. Most animal studies demonstrating the physiologic effectiveness of angiogenic therapies have been performed in normal young animals, while clinical trials typically enroll older patients with various endothelial disruptive risk factors. The promising results of trials using endothelial function-improving strategies support the hypothesis that the decreased effectiveness of growth factor therapy due to endothelial dysfunction could be a principle reason for failure of trials using growth factors. We will have a retrospection of therapeutic angiogenesis trials and discuss the mechanisms that contribute to an impaired angiogenic response in the setting of endothelial dysfunction. We also briefly explore endothelial function-improving procedures that have the potentially therapeutic benefit of enhancing the angiogenic response.

U0126 enhances the cytotoxicity of combretastatin A4 independent of mitogen-activated protein kinase kinase.

J Pharmacol Exp Ther. 2009 Apr 18; Quan H, Liu H, Li C, Lou LCombretastatin A4 (CA4) is a novel vascular-disrupting agent that has shown promising anticancer effects through its inhibition of microtubule assembly and subsequent disruption of tumor blood flow. In this report, we demonstrate that U0126, a selective inhibitor of mitogen-activated protein kinase kinase (MEK), significantly enhances the cytotoxicity of CA4 in BEL-7402 cells, independent of MEK inhibition. This independence is evidenced by the fact that another, more specific MEK inhibitor, PD0325901, does not have the same effect as U0126. The disassembled microtubules are able to reassemble in the later stages of CA4 treatment, due to the inactivating glucuronidation of CA4. U0126, but not PD0325901, inhibits CA4 glucuronidation, thereby blocking microtubule reassembly and enhancing CA4-induced G2/M cell cycle arrest. Consistent with this, U0126 significantly enhances CA4-induced cytotoxicity for cells in which CA4 glucuronidation occurs, but not for cells in which such glucuronidation does not occur. These results suggest that great caution should be exercised when interpreting data obtained using U0126, or when CA4 is combined with inhibitors of glucuronidation in clinical practice. More importantly, these findings indicate that the combination of CA4 with inhibitors of glucuronidation may be a novel and rational strategy for cancer therapy.

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