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1.
Neotrop Entomol ; 48(5): 717-728, 2019 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-31062186

RESUMEN

Pollinators foraging for food resources can be waylaid by mass-flowering plants located in their foraging pathway in landscapes. The waylaying effect of pollinators is often studied at a single spatial scale; to date, little is known about the best spatial extent at which waylaying effect of pollinators can be measured. In this study, we selected a landscape with mass-flowering tufted vetches to determine the spatial scale of waylaying effect of honey bees as well as the consequence of waylaying effect on vetch pollination service. The spatial scale of waylaying effect was determined by the strongest association between honey bee density and distance, selected from a gradient of nested circular buffers centering on apiaries in three different locations. Linear models were used to predict the influence of flower visitor densities on pollination service. For our landscape, honey bee densities were best associated with distances at spatial scales of 500 m, 1150 m, and 1400 m respectively for the three locations of apiaries. Honey bee was the only pollinator whose density displayed a positive relationship with pollination service. At the scales of effect, honey bee density and pollination service declined along the distance. Our findings suggest that the waylaying effect of pollinators needs to be examined at a specific spatial scale and farmers who use honey bees to pollinate their mass-flowering crops need to consider the spatial scale of waylaying effect of pollinators in order to maximize pollination service within agricultural ecosystems.


Asunto(s)
Abejas/fisiología , Flores/fisiología , Polinización , Animales , China , Productos Agrícolas/fisiología , Modelos Lineales , Magnoliopsida/fisiología
2.
Genet Mol Res ; 15(2)2016 May 13.
Artículo en Inglés | MEDLINE | ID: mdl-27323039

RESUMEN

ErbB4 is an oncogene belonging to the epidermal growth factor receptor family and contributes to the occurrence and development of multiple cancers, such as gastric, breast, and colorectal cancers. Therefore, studies of the regulation of ErbB4 in cancerigenic pathway will advance molecular targeted therapy. Advanced bioinformatic analysis softwares, such as ExPASy, Predictprotei, QUARK, and I-TASSER, were used to analyze the regulatory mechanism after ErbB4 gene mutation in terms of amino acid sequence, primary, secondary, and tertiary structure of the protein and upstream-downstream receptor/ligands. Mutation of the 19th and 113th amino acids at the carboxyl terminus of ErbB4 protein did not affect its biological nature, but its secondary structure changed and protein binding sites were near 2 mutational sites; moreover, after mutation introduction, additional binding sites were observed. Tertiary structure modeling indicated that local structure of ErbB4 was changed from an α helical conformation into a ß chain folding structure; the α helical conformation is the functional site of protein, while active sites are typically near junctions between helical regions, thus the helical structures are easily destroyed and change into folding structures or other structures after stretching. Mutable sites of ErbB4 is exact binding sites where dimer formed with other epidermal growth factor family proteins; mutation enabled the ErbB4 receptor to bind to neuregulin 1 ligand without dimer formation, disrupting the signal transduction pathway and affecting ErbB4 function.


Asunto(s)
Modelos Genéticos , Mutación , Receptor ErbB-4/genética , Secuencia de Aminoácidos , Biología Computacional/métodos , Humanos , Modelos Moleculares , Neoplasias/genética , Neoplasias/metabolismo , Fosforilación , Unión Proteica , Estructura Secundaria de Proteína , Receptor ErbB-4/química , Receptor ErbB-4/metabolismo , Transducción de Señal , Relación Estructura-Actividad
3.
Braz J Med Biol Res ; 48(8): 703-10, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-26108098

RESUMEN

Chronic ethanol consumption can produce learning and memory deficits. Brain-derived neurotrophic factor (BDNF) and its receptors affect the pathogenesis of alcoholism. In this study, we examined the expression of BDNF, tropomyosin receptor kinase B (TrkB) and p75 neurotrophin receptor (p75NTR) in the hippocampus of a dog model of chronic alcoholism and abstinence. Twenty domestic dogs (9-10 months old, 15-20 kg; 10 males and 10 females) were obtained from Harbin Medical University. A stable alcoholism model was established through ad libitum feeding, and anti-alcohol drug treatment (Zhong Yao Jie Jiu Ling, the main ingredient was the stems of watermelon; developed in our laboratory), at low- and high-doses, was carried out. The Zhong Yao Jie Jiu Ling was effective for the alcoholism in dogs. The morphology of hippocampal neurons was evaluated using hematoxylin-eosin staining. The number and morphological features of BDNF, TrkB and p75NTR-positive neurons in the dentate gyrus (DG), and the CA1, CA3 and CA4 regions of the hippocampus were observed using immunohistochemistry. One-way ANOVA was used to determine differences in BDNF, TrkB and p75NTR expression. BDNF, TrkB and p75NTR-positive cells were mainly localized in the granular cell layer of the DG and in the pyramidal cell layer of the CA1, CA3 and CA4 regions (DG>CA1>CA3>CA4). Expression levels of both BDNF and TrkB were decreased in chronic alcoholism, and increased after abstinence. The CA4 region appeared to show the greatest differences. Changes in p75NTR expression were the opposite of those of BDNF and TrkB, with the greatest differences observed in the DG and CA4 regions.


Asunto(s)
Abstinencia de Alcohol , Alcoholismo/metabolismo , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Hipocampo/química , Receptor de Factor de Crecimiento Nervioso/metabolismo , Receptor trkB/metabolismo , Animales , Factor Neurotrófico Derivado del Encéfalo/genética , Enfermedad Crónica , Modelos Animales de Enfermedad , Perros , Femenino , Regulación de la Expresión Génica , Hipocampo/metabolismo , Inmunohistoquímica , Masculino , Receptor de Factor de Crecimiento Nervioso/genética , Receptor trkB/genética
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