The authors identified individual randomized controlled trials from previous meta-analyses and additional searches, and then performed meta-analyses on cardiovascular disease outcomes and all-cause mortality. The authors assessed publications from 2012, both before and including the U.S. Preventive Service Task Force review. Their systematic reviews and meta-analyses showed generally moderate- or low-quality evidence for preventive benefits (folic acid for total cardiovascular disease, folic acid and B-vitamins for stroke), no effect (multivitamins, vitamins C, D, β-carotene, calcium, and selenium), or increased risk (antioxidant mixtures and niacin [with a statin] for all-cause mortality). Conclusive evidence for the benefit of any supplement across all dietary backgrounds (including deficiency and sufficiency) was not demonstrated; therefore, any benefits seen must be balanced against possible risks.

Abstract-Transgenic mice overexpressing the calcium binding protein, S100A4/Mts1, occasionally develop severe pulmonary vascular obstructive disease. To understand what underlies this propensity, we compared the pulmonary vascular hemodynamic and structural features of S100A4/Mts1 with control C57Bl/6 mice at baseline, following a 2-week exposure to chronic hypoxia, and after 1 and 3 months "recovery" in room air. S100A4/Mts1 mice had greater right ventricular systolic pressure and right ventricular hypertrophy at baseline, which increased further with chronic hypoxia and was sustained after 3 months "recovery" in room air. These findings correlated with a heightened response to acute hypoxia and failure to vasodilate with nitric oxide or oxygen. S100A4/Mts1 mice, when compared with C57Bl/6 mice, also had impaired cardiac function judged by reduced ventricular elastance and decreased cardiac output. Despite higher right ventricular systolic pressures with chronic hypoxia, S100A4/Mts1 mice did not develop more severe PVD, but in contrast to C57Bl/6 mice, these features did not regress on return to room air. Microarray analysis of lung tissue identified a number of genes differentially upregulated in S100A4/Mts1 versus control mice. One of these, fibulin-5, is a matrix component necessary for normal elastin fiber assembly. Fibulin-5 was localized to pulmonary arteries and associated with thickened elastic laminae. This feature could underlie attenuation of pulmonary vascular changes in response to elevated pressure, as well as impaired reversibility. Key Words: elastin Ⅲ fibulin-5 Ⅲ hypoxia Ⅲ mouse Ⅲ pulmonary hypertension Ⅲ smooth muscle cells Ⅲ S100 proteins Ⅲ vascular smooth muscle cells Ⅲ vascular disease F amilial idiopathic pulmonary arterial hypertension (PAH) is associated with mutations in bone morphogenetic receptor II (BMPR-II), but the inheritance pattern is that of a dominant gene with low penetrance, in that only Ϸ20% of affected family members develop the disease. 1,2 This coupled to the fact that genetically engineered mice with abnormalities in BMPR-II have pulmonary hypertension but fail to reproduce the pathology seen in patients with pulmonary vascular obstructive disease (PVD) 3,4 indicates that multiple genetic and environmental cofactors may be necessary for the disease to develop. A potential modifier gene is the calciumbinding protein, S100A4/Mts1, because a small subpopulation (Ϸ5%) of transgenic mice Ͼ1 year of age, that overexpress S100A4/Mts1, develops PVD. 5 Furthermore, heightened expression of S100A4/Mts1 is observed in the neointima and adventitia of occlusive and early plexiform lesions in patients with a congenital heart defect or idiopathic PAH. 5 S100A4/Mts1 is induced in malignant metastatic breast cancer 6 and although its intracellular properties have been implicated in the motility of cancer cells, 7 it is also secreted and can stimulate angiogenesis. 8 Moreover, recombinant S100A4/Mts1 promotes proliferation and migration of cultured pulmonary artery (PA) SMC. 8a Although ...

Previous American Telemedicine Association (ATA) Teledermatology Practice Guidelines were issued in 2007. This updated version reflects new knowledge in the field, new technologies, and the need to incorporate teledermatology practice in a variety of settings, including hospitals, urgent care centers, Federally Qualified Health Centers, school-based clinics, public health facilities, and patient homes.

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