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Journal of Biosciences and Medicines 2019年第8期7卷 42-67页

作者： María Fernanda Izaguirre Carolina Daniela Galetto Lautaro Baró Víctor Hugo Casco laboratorio de microscopía aplicada a estudios moleculares y celulares Facultad de Ingeniería Universidad Nacional de Entre Ríos Oro Verde Entre Ríos República Argentina Instituto de Investigación y desarrollo en Bioingeniería y Bioinformática (IBB) Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET) CABA República Argentina

E-cadherin molecules are cell-cell molecular connectors, but also act attaching cell surface to the cytoskeleton through catenin’s and additional partner proteins. Its main function is to regulate cellular adhesion and motility, and therefore acts as an invasion suppressor system. Its role is crucial in the induction and maintenance of cell polarity and differentiation, and in the organization and maintenance of tissue architecture. Downregulation or loss of its function is associated with an invasive and aggressive phenotype in many types of human cancers. In alterations of animal development, E-cadherin dysfunction influence in premature lethality or epidermal barrier and immunity defects. However, new hypothesis over its promoter role in tissue invasion is on focus. In addition to its tumor suppressor role, E-cadherin is a guiding molecule in collective cell migration increasing the metastasis risk during in vivo tumorigenesis. This E-cadherin function explains the retention of the functional E-cadherin expression, and that the epithelial-mesenchymal transition (EMT) is not required for the metastasis occurrence. However, like a switch, in some tumoral environments E-cadherin post-translational modifications may cause cell cluster migration. Like in development, in certain in vivo tumoral contexts, E-cadherin apparently involves signaling rather than cell contact formation. In this report, we explore the possibility of a novel role of thyroid hormones (THs) in the signal via E-cadherin-catenins, this not only should be involved in development and homeostasis, but also in cancer susceptibility of gastrointestinal tract.

关键词： Cell Adhesion Molecules Complexes E-Cadherin Cancer Thyroid Hormones

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Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis

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World Journal of Gastroenterology 2015年第45期21卷 12742-12756页

作者： Manuel A Valenzuela Jimena Canales Alejandro H Corvalán Andrew FG Quest laboratorio de Comunicaciones celulares Centro de Estudios Moleculares de la Célula Programa de Biología Celular y Molecular ICBM Facultad de Medicina Universidad de Chile Cellular Communication Laboratory Center for Molecular Studies of the Cell Advanced Center for Chronic Diseases School of Medicine Universidad de Chile UC-Centro de Investigación en Oncología Pontificia Universidad Católica de Chile departamento de Hematología-Oncología Facultad de Medicine Pontificia Universidad Católica de Chile

The sequence of events associated with the development of gastric cancer has been described as "the gastric precancerous cascade". This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia. According to this model, Helicobacter pylori(H. pylori) infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis. The presence of virulence factors in the infecting H. pylori drives the carcinogenesis process. Independent epidemiological and animal studies have confirmed the sequential progression of these precancerous lesions. Particularly long-term follow-up studies estimated a risk of 0.1% for atrophic gastritis/intestinal metaplasia and 6% in case of dysplasia for the long-term development of gastric cancer. With this in mind, a better understanding of the genetic and epigenetic changes associated with progression of the cascade is critical in determining the risk of gastric cancer associated with H. pylori infection. In this review, we will summarize some of the mostrelevant mechanisms and focus predominantly but not exclusively on the discussion of gene promoter methylation and mi RNAs in this context.

关键词： Helicobacter pylori Methylation Gastric cancer Epi

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E coli Accumulation behind an Obstacle

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Advances in Microbiology 2018年第6期8卷 451-464页

作者： Gastón L.Mino Magali Baabour Ricardo Chertcoff Gabriel Gutkind Eric Clément Harold Auradou Irene Ippolito Lab. de microscopía aplicada a estudios moleculares y celulares (LAMAE) Fac. de Ingeniería Univ. Nac. de Entre Ríos (FI-UNER) and Inst. de Investigación y Desarrollo en Bioingeniería y Bioinformática IBB-(UNER-CONICET) Oro Verde Argentina Universidad de Buenos Aires Facultad de Ingeniería Grupo de Medios Porosos Buenos Aires Argentina Universidad de Buenos Aires Facultad de Farmacia y Bioquímica Cátedra de Microbiología Buenos Aires Argentina Physique et Mécanique des Milieux Hétérogénes (UMR 7636 ESPCI/CNRS/Univ. P.M. Curie/Univ. Paris-Diderot) Paris France Laboratoire FAST Univ. Paris Sud CNRS Université Paris-Saclay F-91405 Orsay France

This paper describes our findings regarding the accumulation of motile bacteria at the rear of a confined obstacle and the physical description of the mechanisms at play. We found that the modification of flow due to the presence of the obstacle produces vorticity that favor the diffusion of bacteria towards the downstream stagnation point. By testing different flow rates, we determined the range in which bacteria accumulate. More interestingly, we observe that hydrodynamic interaction between the bacteria and the top and bottom surface of the microfluidic chip maintain the bacteria in the region where the flow velocity is lower than their own velocity. In the case of non-motile bacteria, this effect is not observed because bacteria follow the streamlines as passive tracers do.

关键词： E coli Motility Filtration Microfluidic Bacterial Accumulation

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Early detection of White Spot Syndrome Virus(WSSV)in Isolated Hemocytes of Litopenaeus vannamei

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CellBio 2017年第1期6卷 1-12页

作者： Ariadne Hernandez-Perez Rossanna Rodriguez-Canul Edgar Torres-Irineo Fernando Mendoza-Cano Daniel Eduardo Coronado-Molina Jesus Alejandro Zamora-Briseno Jorge Hernandez-Lopez laboratorio de Inmunología y Biología Molecular Centro de Investigación y de Estudios Avanzados del IPN(CINVESTAV-IPN)Unidad MéridaMéridaMéxico laboratorio de Pesquerías Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional-Unidad MéridaMéridaMéxico UMDI-Sisal Facultad de CienciasUniversidad Nacional Autónoma de MéxicoSierra PapacalMéxico Centro de Investigaciones Biológicas del Noroeste HermosilloMéxico

To date, White Spot Syndrome (WSS) produced by the White Spot Syndrome Virus (WSSV) causes one of the most severe diseases infecting penaeid shrimps worldwide. Although a vast amount of studies has elucidated pathogenesis in live infection models, there is still little information about the interaction of WSSV infections using in vitro models in the whiteleg shrimp Litopenaeus vannamei (L. vannamei) hemocytes. In this study, a WSSV infection kinetics was performed using total hemocytes isolated from healthy L. vannamei organisms and maintained in in vitro conditions using isotonic solution for shrimp (ISS). The infected experimental cells received ≈ 30,000 viral copies of WSSV. The viability of the hemocytes (control and infected group) was measured during the kinetics with trypan blue exclusion method and cells were maintained up to 6 hpi (post-infection) with non-significant differences of viability between both groups. WSSV replication was assessed using RT- PCR at the RNA expression level of the early viral gene Ie1 and transcripts were detected as early as 30 min pi. Hemocytes from WSSV group showed disrupted integrity, degranulation and irregular shape. This study provides evidence of the capability of WSSV to infect and replicates in L. vannamei hemocytes using in vitro assays in short times as 30 min.

关键词： WSSV Litopenaeus vannamei Ie1 Gene Hemocytes In Vitro Infection GLS Analysis

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