36 research outputs found
POPULAÇÃO MICROBIANA, DISPONIBILIDADE DE NUTRIENTES E CRESCIMENTO DE UMBUZEIRO EM SUBSTRATOS CONTENDO RESÍDUOS ORGÂNICOS
Produção de mudas de meloeiro amarelo, sob cultivo protegido, em diferentes substratos
Goiabeiras Paluma, Pedro Sato e Cortibel 6 propagadas por miniestaquia e miniestaquia seriada
Do genetic factors protect for early onset lung cancer? A case control study before the age of 50 years
<p>Abstract</p> <p>Background</p> <p>Early onset lung cancer shows some familial aggregation, pointing to a genetic predisposition. This study was set up to investigate the role of candidate genes in the susceptibility to lung cancer patients younger than 51 years at diagnosis.</p> <p>Methods</p> <p>246 patients with a primary, histologically or cytologically confirmed neoplasm, recruited from 2000 to 2003 in major lung clinics across Germany, were matched to 223 unrelated healthy controls. 11 single nucleotide polymorphisms of genes with reported associations to lung cancer have been genotyped.</p> <p>Results</p> <p>Genetic associations or gene-smoking interactions was found for <it>GPX1(Pro200Leu) </it>and <it>EPHX1(His113Tyr)</it>. Carriers of the Leu-allele of <it>GPX1(Pro200Leu) </it>showed a significant risk reduction of OR = 0.6 (95% CI: 0.4–0.8, p = 0.002) in general and of OR = 0.3 (95% CI:0.1–0.8, p = 0.012) within heavy smokers. We could also find a risk decreasing genetic effect for His-carriers of <it>EPHX1(His113Tyr) </it>for moderate smokers (OR = 0.2, 95% CI:0.1–0.7, p = 0.012). Considered both variants together, a monotone decrease of the OR was found for smokers (OR of 0.20; 95% CI: 0.07–0.60) for each protective allele.</p> <p>Conclusion</p> <p>Smoking is the most important risk factor for young lung cancer patients. However, this study provides some support for the T-Allel of <it>GPX1(Pro200Leu) </it>and the C-Allele of <it>EPHX1(His113Tyr) </it>to play a protective role in early onset lung cancer susceptibility.</p
METACOHORTS for the study of vascular disease and its contribution to cognitive decline and neurodegeneration: an initiative of the Joint Programme for Neurodegenerative Disease Research
Dementia is a global problem and major target for health care providers. Although up to 45% of cases are primarily or partly due to cerebrovascular disease, little is known of these mechanisms or treatments because most dementia research still focuses on pure Alzheimer's disease. An improved understanding of the vascular contributions to neurodegeneration and dementia, particularly by small vessel disease, is hampered by imprecise data, including the incidence and prevalence of symptomatic and clinically “silent” cerebrovascular disease, long-term outcomes (cognitive, stroke, or functional), and risk factors. New large collaborative studies with long follow-up are expensive and time consuming, yet substantial data to advance the field are available. In an initiative funded by the Joint Programme for Neurodegenerative Disease Research, 55 international experts surveyed and assessed available data, starting with European cohorts, to promote data sharing to advance understanding of how vascular disease affects brain structure and function, optimize methods for cerebrovascular disease in neurodegeneration research, and focus future research on gaps in knowledge. Here, we summarize the results and recommendations from this initiative. We identified data from over 90 studies, including over 660,000 participants, many being additional to neurodegeneration data initiatives. The enthusiastic response means that cohorts from North America, Australasia, and the Asia Pacific Region are included, creating a truly global, collaborative, data sharing platform, linked to major national dementia initiatives. Furthermore, the revised World Health Organization International Classification of Diseases version 11 should facilitate recognition of vascular-related brain damage by creating one category for all cerebrovascular disease presentations and thus accelerate identification of targets for dementia prevention
Fontes e proporções de materiais orgânicos na germinação de sementes e crescimento de plantas jovens de goiabeira
O comércio internacional de peles silvestres na Amazônia brasileira no século XX
Durante o século XX, o comércio internacional de peles foi responsável pelo abate de milhões de mamíferos e répteis na Amazônia. Negociadas no regime de comércio fluvial e aviamento, as peles seguiam dos portos e seringais, localizados no interior, para as casas aviadoras e exportadoras de Manaus e Belém, de onde eram exportadas principalmente para os Estados Unidos, a Europa e o sul brasileiro. Neste artigo, analisamos documentos fiscais inéditos liberados pelo extinto império econômico do aviamento - a empresa J. G. Araujo -, bem como periódicos da Associação Comercial do Amazonas e os registros portuários da Manáos Harbour Ltd. O comércio internacional de peles silvestres intensificou-se imediatamente após a crise da borracha (1912) e atingiu seu auge entre 1935 e 1946, com o pico durante a Segunda Guerra Mundial. O segundo pico ocorreu na década de 1960, principal e ironicamente logo após a publicação da Lei de Proteção à Fauna (1967). Ao longo do período que antecedeu a aprovação da Convenção sobre o Comércio Internacional de Espécies Ameaçadas (CITES), em 1973-1975, não houve depreciação significativa no preço ou na demanda internacional por peles silvestres, sugerindo um esforço de caça constante e intenso por quase meio século