Territorial analysis of Aedes aegypti distribution in two Colombian cities: a chorematic and ecosystem approach / Análise territorial da distribuição do Aedes aegypti em duas cidades da Colômbia: aproximação desde a coremática e a abordagem ecossistêmica / Análisis territorial de la distribución de Aedes aegypti en dos ciudades de Colombia: aproximación desde la coremática y el enfoque ecosistémico

A territorial analysis of Aedes aegypti density was conducted in two Colombian cities using an ecosystem and chorematic approach. Entomological and behavioral data (by cluster) and information on the urban context were used to analyze the relationship between territorial structures and dynamics and vector density. The results were represented in graphic (chorematic) models. Arauca showed higher vector density than Armenia. Higher density was related to unplanned urbanization, flood-prone areas, low socioeconomic strata, household water tanks, higher temperature, and recall of control measures for adult mosquitos. Zones with low density indices coincided with diverse socioeconomic, ecological, and behavioral conditions. The study found a relationship between territorial structures and dynamics and vector density in both Arauca and Armenia, where the interaction between ecological and social systems shape areas with high and low A. aegypti density.

Foi realizada uma análise territorial da densidade do Aedes aegypti em duas cidades da Colômbia, desde um enfoque ecossistêmico e da coremática. Com base em informação entomológica e comportamental (por conglomerados) e informação do contexto urbano, foi indagada a relação de estruturas dinâmicas do território com a densidade vetorial. Foram apresentados os resultados com modelos gráficos (coremática). Identificou-se maior densidade vetorial em Arauca do que na Armênia. Maiores densidades foram relacionadas à urbanização não planejada, zonas de alagamento, estratos socioeconômicos baixos, tanques baixos (reservatórios), maior temperatura e relatório de ações contra os mosquitos adultos. Zonas de densidades baixas coincidiram com diversas condições socioeconômicas, ecológicas e comportamentais. Foi encontrada uma relação das estruturas e dinâmicas do território com a densidade vetorial para Arauca e Armênia, onde a interação entre sistemas ecológicos e sociais configura zonas particulares de alta e baixa densidades de A. aegypti.

Se realizó un análisis territorial de la densidad de Aedes aegypti en dos ciudades de Colombia desde un enfoque ecosistémico y la coremática. A partir de información entomológica y comportamental (por conglomerados) e información del contexto urbano, se indagó la relación de estructuras y dinámicas del territorio con la densidad vectorial. Se representaron los resultados con modelos gráficos (coremática). Se identificó mayor densidad vectorial en Arauca que en Armenia. Mayores densidades se relacionaron con urbanización no planeada, zonas de inundación, estratos socioeconómicos bajos, tanques bajos (alberca), mayor temperatura y reporte de acciones hacia los mosquitos adultos. Zonas de densidades bajas coincidieron con diversas condiciones socioeconómicas, ecológicas y comportamentales. Se encontró relación de las estructuras y dinámicas del territorio con la densidad vectorial para Arauca y Armenia, donde la interacción entre sistemas ecológicos y sociales configuran zonas particulares de alta y baja densidad de A. aegypti.

IGF-1 induces expression of zinc-finger protein 143 in colon cancer cells through phosphatidylinositide 3-kinase and reactive oxygen species

Expression of zinc-finger protein 143 (ZNF143), a human homolog of the Xenopus transcriptional activator protein Staf, is induced by various DNA-damaging agents including etoposide, doxorubicin, and gamma-irradiation. ZNF143 binds to cisplatin-modified DNA, and its levels are increased in cancer cells that are resistant to anticancer drugs, including cisplatin, suggesting that it plays a role in carcinogenesis and cancer cell survival. However, the mechanism of ZNF143 induction in cancer cells remains unclear. Both insulin-like growth factor-1 (IGF-1) and its receptor (IGF-1R) have been reported to be overexpressed in cancer cells and to be related to anticancer drug resistance, but the identity of the relevant signaling mediators is still being investigated. In the present study, we observed that IGF-1 was able to induce ZNF143 expression in HCT116 human colon cancer cells and that wortmannin, an inhibitor of phosphatidylinositide 3-kinase (PI3-kinase), inhibited this induction, as did diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, and monodansylcardavarine (MDC), a receptor internalization inhibitor. Treatment with MDC decreased the IGF-1-stimulated generation of reactive oxygen species. Taken together, these data suggest that IGF-1 induces ZNF143 expression in cancer cells via PI3-kinase and reactive oxygen species generation during receptor internalization.

Impaired Delta NP63 Expression is Associated with Poor Tumor Development in Transitional Cell Carcinoma of the Bladder

The oncogenic isoform of the p63 protein, delta NP63, plays an important role in the pathogenesis of many epithelial carcinomas, and emerging evidences suggest that delta NP63 is a promising drug target. However, the functions of delta NP63 in transitional cell carcinoma of bladder (TCCB) are poorly defined. In this study, a delta NP63 shRNA expression vector was transfected into TCCB cell line 5637 and cell cycling, cell proliferation and protein expression were assessed by flow cytometry and 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-dimethyl tetrazolium bromide (MTT) assay, and immunohistochemistry, respectively. The delta NP63 shRNA expression vector was also injected into 5637 cell xenograft tumors in nude mice, and tumor size was measured, tumor tissue morphology was assessed by immunohistopathology and transmission electron microscopy. In the in vitro study, delta NP63 shRNA transfection caused successful delta NP63 gene silencing and resulted in significant arrest of cell cycling and cellular proliferation (p<0.05) as well as cyclin D1 expression. In the nude mouse xenograft model, delta NP63 shRNA greatly inhibited tumor growth, induced tumor cell apoptosis (p<0.05) and resulted in cyclin D1 downregulation. Our data suggest that delta NP63 may play an oncogenic role in TCCB progression through promoting cell survival and proliferation. Intratumoral administration of delta NP63-specific shRNA suppressed tumor delta NP63 expression and cellular proliferation while promoted tumor cellular apoptosis, and therefore inhibited tumor growth and improved survival of xenograft-bearing mice, which was not accompanied by significant signs of systemic toxicity.

PDX-1 expression in pancreatic ductal cells after partial pancreatectomy in adult rats / 华中科技大学学报（医学）（英德文版）

To investigate the protein and mRNA expression of pancreas/duodenal homeobox-1 (PDX-1), a transcription factor as a marker for pancreatic stem cells, in pancreatic ductal cells of rats after partial (90%) pancreatectomy and evaluated the significance of the PDX-1 expression. Western blot and Reverse transcriptase-polymerase chain reaction (RT-PCR) were used to detect the expression of PDX-1 protein and mRNA respectively. PDX-1 protein was only faintly detected in pancreatic ductal cells on the day 1 after partial pancreatectomy. On the day 2 and 3 after operation in operation group, a 2-3 fold increased PDX-1 protein was observed, corresponding to the characteristic 42-kD protein in Western blot. There was significant difference between operation group and sham-operation group (P0.05). RT-PCR revealed the PDX-1 mRNA expression showed no significant difference between operation group at various time points and sham-operation group (P> 0.05). These results indicate that there was overexpression of PDX-1 in the cells of pancreatic epithelium during the regeneration of remnant pancreas after partial pancreatectomy in adult rats, suggesting the pancreatic stem cells in pancreatic ductal epithelial cells are involved in the regeneration of remnant pancreas and the expression of PDX-1 in ductal cells was regulated posttranscription.

Expression and Localization of the Transforming Growth Factor-beta Type I receptor and Smads in Preneoplastic Lesions during Chemical Hepatocarcinogenesis in Rats

Little is known about the involvement of Smad-related molecules in the regulation of the Transforming Growth Factor (TGF)-beta signaling pathway during hepatocarcinogenesis, particularly with respect to preneoplastic lesions of a rat liver. The aims of this study were to investigate the localizations and temporal expressions of TGF-beta Receptor Type 1 (TGR1) and Smads during the promotion stage of chemical hepatocarcinogenesis in rats. We investigated expressions and localizations of TGR1, Smad2, Smad4, and Smad7 by using semi-quantitative RT-PCR and immunohistochemistry in preneoplastic lesions during rat chemical hepatocarcinogenesis induced by Solt and Farber's method. The down-regulation of TGR1, Sma-d2, and Smad4 was evident during the later steps of the promotion stage of chemical hepatocarcinogenesis. In contrast with other Smads, increased Smad7 expression was evident during the later steps of the promotion stage. Also immunohistochemistry revealed that the main site of TGR1, Smad2, Smad4, and Smad7 expression was mainly in hepatocytes of the preneoplastic lesions of a rat liver. Dysregulation of the downstream effectors of TGF-beta such as TGR1, Smad2, Smad4 and, Smad7 might contribute to the progression of preneoplastic lesions during chemical hepatocarcinogenesis in a rat.