Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Más filtros

Base de datos
Tipo del documento
Asunto de la revista
País de afiliación
Intervalo de año de publicación
1.
Front Microbiol ; 14: 1158659, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37649630

RESUMEN

Extended-spectrum beta-lactamase-producing Gram-negative bacteria are common in the community and hospitals. To monitor ESBLs mediated by the CTX-M genotype, we collected clinical ESBL pathogenic strains from a hospital in central China and observed a strain of Escherichia coli, namely Ec15103 carrying blaCTX-M-14, blaCTX-M-64 and blaTEM-1, isolated from the blood of a 7-day-old infant in 2015. Strain Ec15103 contains two drug resistance plasmids: pEc15103A, an IncFI-type plasmid that cannot be conjugatively transferred and carries the drug resistance genes blaTEM-1, aacC2, aadA5, sul1, mph(A), sul2, strAB, and tetA(A); and pEc15103B, an IncK2/Z-type plasmid that carries the conjugation transfer gene and blaCTX-M-14. In addition, blaCTX-M-64 is located on the chromosome of Ec15103, and it is the first report of pathogen with blaCTX-M-64 located on its chromosome (the search terms used "blaCTX-M-64" and "chromosome"). blaCTX-M-14 and blaCTX-M-64 are carried by ISEcp1-mediated transposon Tn6503a and Tn6502, respectively. The conjugation transfer ability of pEc15103B was significantly inhibited by zidovudine (AZT) and linoleic acid (LA) and that expression of blaCTX-M-14, blaCTX-M-64 and blaTEM-1 at the mRNA level did not change based on the concentration of cefotaxime or ampicillin. Co-occurrence of blaCTX-M-14 and blaCTX-M-64 in a single isolate will enhance the drug resistance of bacteria, and the presence of blaCTX-M-64 in the chromosome may make the resistance more maintain. This fact will facilitate its dissemination and persistence under different antimicrobial selection pressures. It is essential to prevent these strains from further spreading in a hospital environment.

2.
3.
Int J Biol Sci ; 15(1): 169-182, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-30662357

RESUMEN

Polypeptide N-acetylgalactosaminyl transferase-6 (GALNT6), a member of the N-acetyl-D-galactosamine transferase family, was shown to be over-expression in mammary cancer and could be used as a biomarker. However, its roles and underlying mechanisms in the pathogenesis of breast cancer are still unclear. In this study, we reported that GALNT6 was up-expression in breast cancer, and it was not associated with tumor stage. The expression level of GALNT6 and menopause status was associated with patient survival. Biological function results illustrated that knockdown of GALNT6 inhibited proliferation, migration and invasion of MDA-MB-231 cells, and increased cell apoptosis. Knockdown of GALNT6 in breast cancer cell attenuated the protein expression of PCNA, cyclin D1, C-myc and ß-catenin, and increased the expression of E-cadherin, caspase 3 and cleaved PARP1. Cell fractionation assay showed that knockdown of GALNT6 reduced the levels of ß-catenin and MUC1-C in nucleus. Simultaneously knockdown of GALNT6 and ß-catenin significantly reduced the level of C-myc. Co-IP experiments indicated that GALNT6 interacted with MUC1-N, ß-catenin interacting with MUC1-C in breast cancer cells. Together, our study reveals that GALNT6 promotes tumorigenicity and metastasis through ß-catenin/MUC1-C signaling pathway.


Asunto(s)
Apoptosis/fisiología , Neoplasias de la Mama/metabolismo , Proliferación Celular/fisiología , N-Acetilgalactosaminiltransferasas/metabolismo , beta Catenina/metabolismo , Animales , Apoptosis/genética , Western Blotting , Neoplasias de la Mama/genética , Línea Celular Tumoral , Movimiento Celular/genética , Movimiento Celular/fisiología , Proliferación Celular/genética , Femenino , Regulación Neoplásica de la Expresión Génica/genética , Regulación Neoplásica de la Expresión Génica/fisiología , Humanos , Inmunoprecipitación , Células MCF-7 , Ratones , Ratones Desnudos , N-Acetilgalactosaminiltransferasas/genética , Reacción en Cadena en Tiempo Real de la Polimerasa , Cicatrización de Heridas/genética , Cicatrización de Heridas/fisiología , beta Catenina/genética , Polipéptido N-Acetilgalactosaminiltransferasa
4.
Int J Biol Macromol ; 82: 505-13, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-26434529

RESUMEN

Ophiopogon japonicus (Thunb.) Ker-Gawl is a well known traditional Chinese medicine used to treat cardiovascular and chronic inflammatory diseases for thousands of years. The present study was set up to investigate the protective effects of O. japonicus polysaccharide (OJP1) on cardiovascular injuries in diabetic rats. Results showed that OJP1 significantly reduced the MDA concentration and increased the activities of GPx, CAT and SOD in heart of diabetic rats. The levels of AGE, hs-CRP, sICAM-1, NO and ET-1 in diabetic rats were significantly reversed by OJP1 treatment. In addition, the level of ET-1 mRNA was decreased significantly, whereas eNOS mRNA level was increased after administration of OJP1. Meanwhile, the histopathological analysis showed that OJP1 alleviates the heart injury in diabetic rats. Together, these results suggest that OJP1 maintains the antioxidant enzyme levels and improves cardiovascular performance in diabetic rats.


Asunto(s)
Fármacos Cardiovasculares , Ophiopogon/química , Extractos Vegetales/química , Extractos Vegetales/farmacología , Polisacáridos/química , Polisacáridos/farmacología , Sustancias Protectoras , Animales , Glucemia , Catalasa/metabolismo , Diabetes Mellitus Experimental , Modelos Animales de Enfermedad , Endotelina-1/genética , Endotelina-1/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Glutatión Peroxidasa/metabolismo , Corazón/efectos de los fármacos , Riñón/efectos de los fármacos , Hígado/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo III/genética , Óxido Nítrico Sintasa de Tipo III/metabolismo , Oxidación-Reducción/efectos de los fármacos , Ratas , Receptor para Productos Finales de Glicación Avanzada/metabolismo , Superóxido Dismutasa/metabolismo
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA