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911.
A. Marçalo J. Araújo P. Pousão‐Ferreira G. J. Pierce Y. Stratoudakis K. Erzini 《Journal of fish biology》2013,83(3):480-500
The behavioural effects of confinement of sardine Sardina pilchardus in a purse seine were evaluated through three laboratory experiments simulating the final stages of purse seining; the process of slipping (deliberately allowing fishes to escape) and subsequent exposure to potential predators. Effects of holding time (the time S. pilchardus were held or entangled in the simulation apparatus) and S. pilchardus density were investigated. Experiment 1 compared the effect of a mild fishing stressor (20 min in the net and low S. pilchardus density) with a control (fishing not simulated) while the second and third experiments compared the mild stressor with a severe stressor (40 min in the net and high S. pilchardus density). In all cases, sea bass Dicentrarchus labrax were used as potential predators. Results indicated a significant effect of crowding time and density on the survival and behaviour of slipped S. pilchardus. After simulated fishing, S. pilchardus showed significant behavioural changes including lower swimming speed, closer approaches to predators and higher nearest‐neighbour distances (wider school area) than controls, regardless of stressor severity. These results suggest that, in addition to the delayed and unobserved mortality caused by factors related to fishing operations, slipped pelagic fishes can suffer behavioural impairments that may increase vulnerability to predation. Possible sub‐lethal effects of behavioural impairment on fitness are discussed, with suggestions on how stock assessment might be modified to account for both unobserved mortality and sub‐lethal effects, and possible approaches to provide better estimates of unobserved mortality in the field are provided. 相似文献
912.
Vascular endothelial growth factor (VEGF), an angiogenic factor induced by hypoxia, also exerts direct effects on neural tissues. VEGF up‐regulation after hypoxia coincides with expression of its two tyrosine kinase receptors Flt‐1(VEGFR‐1) and Flk‐1 (KDR/VEGFR‐2), which are the key mediators of physiological angiogenesis. We have recently shown that hypoxic‐preconditioning (PC) leading to tolerance to hypoxia–ischemia in neonatal piglet brain resulted in increased expression of VEGF. In this study, we used a hypoxic‐preconditioning model of ischemic tolerance to analyze the expression and cellular distribution of VEGF receptors and phosphorylation of cAMP‐response element‐binding protein (CREB) in newborn piglet brain. The response of Flt‐1 and Flk‐1 mRNA to PC alone was biphasic with peaks early (6 h) and late (1 week) after PC. The mRNA expression of Flt‐1 and Flk‐1 in piglets preconditioned 24 h prior to hypoxia–ischemia was significantly higher than non‐preconditioned piglets and remained up‐regulated up to 7 days. Furthermore, PC prior to hypoxia–ischemia significantly increased the protein levels of Flt‐1 and Flk‐1 compared with hypoxia–ischemia in a time‐dependent manner. Double‐immunolabeling indicated that both Flt‐1 and Flk‐1 are expressed in neurons and endothelial cells with a similar time course of expression following PC and that PC leads to the growth of new vessels. Finally, our data demonstrate that PC significantly phosphorylated and activated cAMP‐response element‐binding protein in nucleus. These results suggest that mechanism(s) initiated by PC can induce VEGF receptor up‐regulation in newborn brain and that VEGF–VEGF receptor‐coupled signal transduction pathways could contribute to the establishment of tolerance following hypoxia–ischemia. 相似文献
913.
Thaís Augusto Marinho Carmen Luci Rodrigues Lopes Sheila Araújo Teles Nádia Rúbia Silva Reis Megmar Aparecida dos Santos Carneiro Andreia Alves de Andrade Regina Maria Bringel Martins 《Memórias do Instituto Oswaldo Cruz》2013,108(4):519-522
The prevalence of hepatitis C virus (HCV) in a population of
recyclable waste collectors (n = 431) was assessed using a cross-sectional
survey in all 15 cooperatives in the city of Goiânia, Central-West Brazil. The
HCV prevalence was 1.6% (95% confidence interval: 0.6-3.6) and a history of
sexually transmitted infections was independently associated with this
infection. HCV RNA (corresponding to genotype 1; subtypes 1a and 1b) was
detected in five/seven anti-HCV-positive samples. Although the study population
reported a high rate (47.3%) of sharps and needle accidents, HCV infection was
not more frequent in recyclable waste collectors than in the general Brazilian
population. 相似文献
914.
Andréa Cássia Sim?es Vimieiro Neusa Araújo Naftale Katz John Robert Kusel Paulo Marcos Zech Coelho 《Memórias do Instituto Oswaldo Cruz》2013,108(7):881-886
Mice infected with Schistosoma mansoni were treated with oxamniquine, praziquantel, artesunate at the pre-patent phase, aiming at observing schistogram alterations. Half of the animals were perfused five days post-treatment for counting and classification of immature worms, based on pre-established morphological criteria (schistogram); the remaining animals were evaluated 42 or 100 days after infection and perfusion of the portal-system was performed for collection and counting of adult worms and oogram. It was observed that oxamniquine and artesunate treatment administered at the pre-postural phase causes significant reduction in the number of immature and adult worms. However, there was little reduction with praziquantel when used at the dose of 400 mg/kg for treatments administered 14, 15, 21 or 23 days post-infection. Artesunate was responsible for significant alterations in development of young worms, as well as for a higher number of worms presenting intestinal damages. Immature adult worms were detected in mice treated with artesunate or oxamniquine at the pre-patent phase of infection and recovered by perfusion 100 days after infection. Schistogram proved to be a very useful tool for experimental evaluation of the activity of antischistosomal drugs and a good model to identify the most sensitive stages to drugs. 相似文献
915.
Coexpression Networks Implicate Human Midfetal Deep Cortical Projection Neurons in the Pathogenesis of Autism 总被引:1,自引:0,他引:1
A. Jeremy Willsey Stephan J. Sanders Mingfeng Li Shan Dong Andrew T. Tebbenkamp Rebecca A. Muhle Steven K. Reilly Leon Lin Sofia Fertuzinhos Jeremy A. Miller Michael T. Murtha Candace Bichsel Wei Niu Justin Cotney A. Gulhan Ercan-Sencicek Jake Gockley Abha R. Gupta Wenqi Han Xin He Ellen J. Hoffman Lambertus Klei Jing Lei Wenzhong Liu Li Liu Cong Lu Xuming Xu Ying Zhu Shrikant M. Mane Ed S. Lein Liping Wei James P. Noonan Kathryn Roeder Bernie Devlin Nenad Sestan Matthew W. State 《Cell》2013
916.
Paulo Marco Marco A. Reis Araújo Magda K. Barcelos Mairy Barbosa Loureiro Santos 《Studies on Neotropical Fauna and Environment》2013,48(1):73-80
Quantitative samples of the aquatic invertebrate fauna associated to water-hyacinth (Eichhornia crassipes) vegetation were taken in an eutrophicated reservoir in southeastern Brazil. The assemblage was dominated by detritivores, most frequently oligochaetes, probably due to the large amount of sediment and detritus retained in the roots. Multivariate analysis (PCA and Canonical Correlation) suggested that, while some environmental variables were important to the dynamics of the system, biological interactions with the prosobranchiad snail Melanoides tuberculata could explain abundance patterns between sample sites. 相似文献
917.
918.
?ngela Zanatta Alana Pimentel Moura Anelise Miotti Tonin Lisiane Aur��lio Knebel Mateus Grings Vannessa Ara��jo Lobato C��sar Augusto Jo?o Ribeiro Carlos Severo Dutra-Filho Guilhian Leipnitz Moacir Wajner 《Cellular and molecular neurobiology》2013,33(1):137-146
Isolated 3-methylcrotonyl-CoA carboxylase deficiency (3MCCD) is an autosomal recessive disorder of leucine metabolism biochemically characterized by accumulation of 3-methylcrotonylglycine (3MCG), 3-methylcrotonic acid (3MCA) and 3-hydroxyisovaleric acid. A considerable number of affected individuals present neurological symptoms with or without precedent crises of metabolic decompensation and brain abnormalities whose pathogenesis is poorly known. We investigated the in vitro effects of 3MCG and 3MCA on important parameters of oxidative stress in cerebral cortex of young rats. 3MCG and 3MCA significantly increased TBA-RS and carbonyl formation, indicating that these compounds provoke lipid and protein oxidation, respectively. In contrast, nitric oxide production was not affected by 3MCG and 3MCA. Furthermore, 3MCG- and 3MCA-induced elevation of TBA-RS values was fully prevented by melatonin, trolox and reduced glutathione, but not by the nitric oxide inhibitor N??-nitro-l-arginine methyl ester or the combination of catalase plus superoxide dismutase, indicating that reactive oxygen species were involved in the oxidative damage caused by these compounds. We also found that the activity of the antioxidant enzymes glutathione peroxidase, catalase, superoxide dismutase and glutathione reductase were not altered in vitro by 3MCG and 3MCA. It is therefore presumed that alterations of the cellular redox homeostasis caused by the major metabolites accumulating in 3MCCD may potentially be involved in the pathophysiology of the neurological dysfunction and structural brain alterations found in patients affected by this disorder. 相似文献
919.
Dezső David Bárbara Marques Cristina Ferreira Carlos Araújo Luís Vieira Gabriela Soares Cristina Dias Maximina Pinto 《Human genetics》2013,132(11):1287-1299
Trichorhinophalangeal syndrome type I (TRPS I) is a rare autosomal dominant syndrome caused by haploinsufficiency of TRPS1 due to point mutations or deletions. Here, we report the first familial TRPS I due to a t(8;13)(q23.3;q21.31) translocation breakpoint <100 kb from the 5′ end of TRPS1. Based on the additional abnormalities observed exclusively in the index patient that are mainly compatible with clinical features of TRPS, her phenotype was defined as expanded TRPS I including brain malformations and intellectual disability. Initial analyses did not reveal any genetic defect affecting TRPS1 or any genomic alteration within the breakpoint regions or elsewhere in the genome. The pathogenic chromosome 8q23.3 breakpoint is at position g.116,768,309_116,768,310 within a transposon type I element, 87 kb from the TRPS1 5′ end. The 13q21.31 breakpoint is within a tandem repeat region at position g.65,101,509_65,101,510 (genome assembly GRCh37/hg19). This breakpoint is flanked by protocadherin 9 (PCDH9) and protocadherin 20 (PCDH20). As an outcome of the translocation, an evolutionarily conserved non-coding VISTA enhancer element from 13q21.31 is placed within the TRPS1 5′ region, 1,294 bp from the breakpoint. The increased expression of TRPS1 found by three independent methods is most probably translocation allele derived and driven by the translocated enhancer element. The index patient’s expanded phenotype presumably involves the epithelial-to-mesenchymal transition pathway that may be due to TRPS1 overexpression. Together, these findings support that the reported translocation-associated phenotypes are “cis-ruption” and TRPS1 overexpression related, the latter most probably caused by the novel enhancer element in the TRPS1 5′ region. 相似文献
920.