Browsing by Author "Owen, Gareth, I"

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    Cancer Research in Latin America, 2014-2019, and its Disease Burden
    (2021) Lewison, Grant; Owen, Gareth, I; Gomez, Henry; Cazap, Eduardo; Murillo, Raul; Unger Saldana, Karla; Dreyer, Marisa; Tsunoda, Audrey; Jimenez De la Jara, Jorge
    There is little available information on cancer research overall in Latin American and Caribbean countries, and on its relationship with the disease burden from cancer, which is increasing as a proportion of the total. We identified cancer research papers in the Web of Science from 2014-19. Outputs of the region on anatomical cancer sites were compared with the relative disease burden from these cancers. Outputs of individual countries were compared with their wealth and their disease burden from cancer. Their usage and impact on other researchers were determined from U2, a new usage indicator, citation counts over three years (C0-2), and the impact factor of the journals in which they were published (JIF). In 2014-19, Brazil, Chile and Uruguay published twice the amounts expected from the Latin American trend-line, but much less than European countries, relative to their Gross Domestic Products (GDPs). Most countries under-researched cancer relative to its burden. Lung, pancreatic and oesophageal cancers were relatively neglected. Less populous countries' research was of high impact, principally due to international collaboration with larger nations. Latin American research funding was dominated by the public sector. Current research orientation and funding is insufficient to combat the growing cancer burden in Latin America. This reflects the lack of research funding overall, relative to the countries' GDPs. The paucity of private-non-profit support needs to be addressed with policies to encourage public donations, and the endowment of foundations. There is also a need to improve the infrastructure for clinical trials.
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    Impact of the Potential Antitumor Agent 2-(4-Hydroxyphenyl) Amino-1,4-Naphthoquinone (Q7) on Vasomotion Is Mediated by the Vascular Endothelium, But Not Vascular Smooth Muscle Cell Metabolism
    (2021) Palacios, Javier; Benites, Julio; Owen, Gareth, I; Morales, Pablo; Chiong, Mario; Nwokocha, Chukwuemeka R.; Paredes, Adrian; Cifuentes, Fredi
    Vasomotion is defined as rhythmic oscillations in arterial diameter that regulate the blood flow and blood pressure. Because antitumor treatment may impair vascular functions and increase the blood pressure, we sought to evaluate whether a new naphthoquinone derivative, postulated as an antitumor agent, manifests adverse effects on vascular function. In this article, we evaluated the toxicity of 2-(4-hydroxyphenyl) amino-1,4-naphthoquinone (Q7) and its effects on vascular vasomotion in 3 models of vascular structure: endothelial cells, aortic ring, and smooth muscle cells. Although showing nontoxic effects, Q7 inhibited the formation of capillary-like structures of the EA.hy926 endothelial cell line grown on Matrigel. In exvivo experiments with aortic rings precontracted with phenylephrine (PE, 10(-6) M), Q7 (10(-5) M) significantly (P < 0.05) reduced vascular rhythmic contractions induced by the acetylcholine (ACh; 10(-7)-10(-5) M), whereas sodium nitroprusside (a nitric oxide donor; 10(-8) M) recovered the vasomotion. Furthermore, Q7 (10(-5) M) did not decrease KCl-induced vascular rhythmic contractions in the aortic rings precontracted with BaCl2 (a nonselective K+ channel blocker; 10(-3) M). Vascular smooth muscle cells (A7r5) preincubated with Q7 (10(-5) M) for 3 hours also demonstrated a reduced glucose uptake. However, the Adenosine Triphosphate content was unaffected, suggesting that the rapid reduction in vasomotion observed in vascular reactivity experiments did not involve cellular metabolism but may be due to faster mechanisms involving endothelial nitric oxide and K+ channels leading to oscillations in intracellular Ca2+. In summary, the naphthoquinone derivative Q7 presents low cytotoxicity yet may alter the endothelial cell response and vasomotion in the absence of changes in smooth muscle cell metabolism.