10 research outputs found

    Review about mites (Acari) of rubber trees (Hevea spp., Euphorbiaceae) in Brazil

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    Biologia de Agistemus brasiliensis Matioli, Ueckermann & Oliveira (Acari: Stigmaeidae) e sua potencialidade de predação sobre Brevipalpus phoenicis (Geijskes) (Acari: Tenuipalpidae)

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    O presente trabalho objetivou estudar a biologia de Agistemus brasiliensis Matioli, Ueckermann & Oliveira nas temperaturas de 15; 20; 25; 30 e 35°C, alimentada com Brevipalpus phoenicis (Geijskes) e pólen de Thypha sp. em condições de laboratório. Tabelas de vida de fertilidade foram calculadas para determinar os parâmetros biológicos. A temperatura ideal para o desenvolvimento de A. brasiliensis foi 29°C. Os valores de T (ciclo de vida - dias), R0 e r m, na temperatura de 30°C, foram de 13,95; 16,25 e 0,20, respectivamente. A potencialidade de predação de A. brasiliensis foi estudada para as densidades populacionais de 5; 10; 20; 40 e 60 adultos de B. phoenicis a 29°C, em arenas de 3 cm de diâmetro, sobre frutos de laranja-pêra. A densidade de 20 ácaros foi suficiente para que o predador consumisse seu número máximo de presas (7,6 ácaros por dia). Densidades acima de 40 ácaros da leprose proporcionaram 4,7 ovos por dia, em comparação aos 2,5 ovos por dia obtidos na densidade de 20 ácaros da leprose.The present work aimed to study the biology of Agistemus brasiliensis Matioli, Ueckermann & Oliveira at the following temperatures, namely 15, 20, 25, 30 and 35°C, fed with Brevipalpus phoenicis (Geijskes) and Typha pollen, in laboratory conditions. Life tables were calculated to evaluate the biological parameters. The optimal development of A. brasiliensis took place at 29°C. The values of T (time of generation - days), R0 and r m at 30°C were, 13.95, 16.25 and 0.20, respectively. The prey consumption of A. brasiliensis was studied at the densities of 5, 10, 20, 40 and 60 leprosis mite females per cage (3 cm in diameter) on citrus fruits at 29°C. The maximum prey, namely 7.6 B. phoenicis females per day, were consumed at a density of 20 leprosis mites. At densities of above 40 leprosis mites per cage, A. brasiliensis oviposits 4.7 eggs per day, in comparison to 2.5 eggs per day at 20 mites per cage.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

    Nutrientes afetando as mudas de alecrim-pimenta (Lippia sidoides Cham.) e seus artrópodes

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    O objetivo deste trabalho foi avaliar o efeito da omissão de nutrientes nas mudas de Lippia sidoides Cham. (Verbenaceae) e seu possível efeito sobre os seus artrópodes, sendo os tratamentos: 1) testemunha; 2) completo 1 adubado com N, P, K, S, B, Cu, e Zn + calagem (C1); 3) completo 2: C1 sem calagem + Ca e Mg como sulfato (C2); 4) C1 sem calagem; 5) C1 sem N; 6) C1 sem P; 7) C1 sem K; 8) C1 sem S; 9) C1 sem B; 10) C1 sem Cu; 11) C1 sem Zn; 12) C2 sem Ca e 13) C2 sem Mg. O delineamento foi inteiramente casualizado com quatro repetições. O Tetranychus sp. (Acari: Tetranychidae) atacou mais os tratamentos 3, 6, 9 e 13 e os maiores danos nos tratamentos 6 e 13. A maior população de Aphis gossypii Glover (Homoptera: Aphididae) foi encontrada nos tratamentos 5, 6, 7, 8, 11 e 13, colonizando preferencialmente o tratamento 4. O Phenacoccus sp. (Hemiptera: Pseudococcidae) foi encontrado em maior número nos tratamentos 4 e 9 e Insignorthezia insignis (Browne) (Hemiptera: Ortheziidae) em 13. Foram mais notados adultos de Bemisa tabaci (Genn.) (Hemiptera: Aleyrodidae) nos tratamentos 5, 7, 8 e 13 e ninfas nos três últimos tratamentos. Em geral, os tratamentos 1, 5 e 10 são os menos atacados por artrópodes. Dirigir a pulverização, quando necessário, sempre para a face inferior da folha

    Diversity and Phylogeny of Neotropical Electric Fishes (Gymnotiformes)

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    Ácaros de cafeeiro (Coffea spp.) no Estado de São Paulo, Brasil: Parte II. Prostigmata

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    Curr Diabetes Rev

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    BACKGROUND: Type 2 diabetes represents an increasing health burden world-wide and its prevalence in particularly higher in elderly population. Consistent epidemiological evidence suggests an increased risk of dementia associated to type 2 diabetes; the mechanisms underlying these associations, however, remain unclear. OBJECTIVE: The study aims to review epidemiological, clinical and pre-clinical data that weigh on pathophysiological links, mechanisms of disease and associations between type 2 diabetes and dementia to identify areas of opportunity for future research. METHODS: We searched the following electronic bibliographic databases: PUBMED, EMBASE, SCIELO, MEDLINE and OVID for clinical, translational and epidemiological research literature that summarize diabetes-related risk factors for dementia, metabolic and neurological changes associated to T2D, evidence of therapeutic approaches in type 2 diabetes and its pathophysiological implications for dementia. RESULTS: Type 2 diabetes mellitus increases risk for all-cause dementia, vascular dementia and Alzheimer's disease. The most evaluated mechanisms linking both disorders in pre-clinical studies include an increase in neuronal insulin resistance, impaired insulin signaling, pro-inflammatory state, mitochondrial dysfunction and vascular damage which increase deposition of beta-amyloid, tau proteins and GSK3beta, leading to an earlier onset of dementia in individuals with impairment in the glucose metabolism. Neuroimaging and neuropathology evidence linking cerebrovascular lesions, neurodegeneration and particularly small-vessel disease in the onset of dementia is consistent with the increased risk of incident dementia in type 2 diabetes, but consistent evidence of AD-related pathology is scarce. Epidemiological data shows increased risk of dementia related to hypoglycemic episodes, glycemic control, metabolic syndrome, insulin resistance and genetic predisposition, but the evidence is not consistent and statistical analysis might be affected by inconsistent covariate controlling. Therapeutic approaches for T2D have shown inconsistent result in relation to dementia prevention and delay of cognitive decline; lifestyle intervention, particularly physical activity, is a promising alternative to ameliorate the impact of disability and frailty on T2D-related dementia. CONCLUSION: Vascular disease, inflammation and impaired brain insulin signaling might occur in T2D and contribute to dementia risk. Evidence from epidemiological studies has not consistently reported associations that could integrate a unified mechanism of disease in humans. Evaluation of the effect of antidiabetic medications and non-pharmacological interventions in dementia prevention in type 2 diabetes is promising but has thus far offered inconsistent results
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