Juan Carlos Rivera

Effects of electronic cigarettes (E-cigs) compared with tobacco cigarettes (T-cigs) in the Western population are largely undetermined. Here, we assessed chronic, intermittent exposures to either E-cigs or T-cigs on cardiovascular parameters in hyperlipidemic mice with similar nicotine levels. Our findings suggest that both E-cigs and T-cigs imposed adverse effects on cardiac function, heart chamber size, and atherosclerotic lesions in diet and sex-dependent manners, suggesting that electronic cigarettes are not a safer alternative to conventional cigarettes.

Ulcerative colitis (UC) is a highly frequent inflammatory bowel disease (IBD), which causes are unknown. We have shown that the offspring gestated under thyroxine (T4) deficiency, condition named hypothyroxinemia (HTX), shows inflammatory features at the intestine. Moreover, the offspring gestated under HTX (HTX-offspring) suffers strong experimental autoimmune disease. Suggesting that gestational HTX could imprint their offspring with a high immune response after an inflammatory challenge. Thus, we think that the HTX-offspring will be more prone to suffer IBD. To analyze this hypothesis C57BL6 pregnant mice were induced with gestational HTX during E10 to E15 by giving them methimazole in the tap-drinking water. Then, UC was induced to the HTX-offspring or control at postnatal P55 by giving them dextran sodium sulphate (DSS) in the tap-drinking water for six days. Body weight, pathological score of IBD and hidden blood in stool were analyzed daily. Then, mice were sacrificed at day 10 to evaluate their inflammatory response. For that histological analysis were performed in the intestine; the content of cytokines in serum and intestine by ELISA and the populations of innate and adaptive immune cells at the intestine and spleen by flow cytometry. Our results shown that the male and female offspring developed an opposite immune response to UC. The female HTX-offspring were more resistant and the male HTX-offspring were more sensitive to UC compared to their respective female and male control groups. Thus, our results suggest that the immune response of an individual can be set up during gestation and that the normal level of maternal T4 during gestation is fundamental for the proper function of the offspring immune system.

Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle‐specific ubiquitin ligases atrogin‐1 and MuRF‐1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet‐induced obesity. Mesenchymal stem cells (MSCs) are a population of self‐renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet‐induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet‐induced obesity and diabetes.