RESUMEN
As strategic assets for organizations, information systems (IS) have been adopted to enhance organizational knowledge performance. Based on the absorptive capacity perspective, we investigated intertwined relationships among IS adoption, organizational capabilities, IS-enabled absorptive capacity, and organizational knowledge performance. We empirically examined our model with survey data from 417 IS employees of 21 different state governments in the United States. We find that: (1) IS adoption does not directly generate IS-enabled absorptive capacity; (2) organizational capabilities positively affect IS-enabled absorptive capacity; (3) synergies arising from complementarity between IS adoption and organizational capabilities have a positive impact on IS-enabled absorptive capacity; and (4) IS-enabled absorptive capacity significantly drives manager and employee knowledge performance. This research enriches the understanding of the relationships among IS adoption, organizational capabilities, and organizational knowledge performance in U.S. public sectors.
RESUMEN
DESIGN: From July 2016 to June 2018, 36 women with symptomatic early pregnancy around 4-8 weeks of gestation were recruited into the study. Among them, there were 16 women with viable intrauterine pregnancy (VIP), 9 women with spontaneous abortion (SA), and 11 women of EP. Serum exosomal miRNAs were extracted and measured at the first prenatal visit. Statistical analysis was performed to determine the clinical utility of these biomarkers as single markers and as multimarker panels for EP. RESULTS: Concentrations of miR-378d in serum exosomes were significantly higher in EP than in VIP and also SA group. As a single marker, miR-378d had the highest specificity of 64% at the sensitivity of 89.1%. Comparatively, both combined panels of hCG, progesterone, miR-100-5p and hCG, progesterone, and miR-215-5P yielded the specificity of 96%. Panels for all markers achieved the highest specificity of 80% at the sensitivity of 91%. CONCLUSIONS: Although further validation in large-scale prospective studies is necessary, our results suggest that serum exosomal miR-378d, miR-100-5p, and miR-215-5P are promising biomarkers for early EP.
Asunto(s)
Exosomas/química , MicroARNs/sangre , Embarazo Ectópico/diagnóstico , Adulto , Biomarcadores/sangre , Femenino , Humanos , MicroARNs/genética , Embarazo , Embarazo Ectópico/sangre , Curva ROC , Reacción en Cadena en Tiempo Real de la PolimerasaRESUMEN
OBJECTIVE: Genistein obviously inhibits the migration and invasion of various tumor cells. However, its effects on cervical cancer cells have seldom been referred. We aimed to evaluate the effects of genistein on the proliferation, migration and invasion of cervical cancer HeLa cells, the expressions and phosphorylations of proteins related with FAK-paxillin and MAPKs signaling pathways, as well as the expressions of related key genes. MATERIALS AND METHODS: HeLa cells were stimulated with genistein for 24 h and 48 h respectively. After adherence for 2 h, 0 µM, 12.5 µM, 25 µM, 50 µM and 100 µM genistein solutions were added in DMEM. Cell proliferation was tested by the CCK-8 assay. After treatment with 100 µM genistein, the migration ability was detected by the scratch assay. Transwell assay was used to detect cell migration and invasion abilities. Western blot and qRT-PCR were used to detect the expressions of proteins and mRNAs related with FAK-paxillin and MAPKs signaling pathways respectively. RESULTS: The effect of genistein on the proliferation of HeLa cells was proportional to treatment time and drug dose, and the proliferation was inhibited after 24 h and 48 h at 100 µM. After treatment with 100 µM genistein, the scratch migration rate was significantly lower than that of the control group at 24 h and 48 h (P < 0.05). Genistein also inhibited the invasion of tumor cells through the upper chamber and Matrigel. The number of invasive cells was significantly lower than that of the control group (P < 0.05). Genistein significantly inhibited the phosphorylations of FAK, paxillin, p38 and p42/44. Compared to the control group, 100 µM genistein significantly suppressed the mRNA expressions of FAK, paxillin, Snail and twist. CONCLUSION: Genistein inhibited the migration and invasion of cervical cancer HeLa cells by regulating FAK-paxillin and MAPK signaling pathways in dose-dependent manners.
Asunto(s)
Anticarcinógenos/farmacología , Quinasa 1 de Adhesión Focal/metabolismo , Genisteína/farmacología , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Paxillin/metabolismo , Neoplasias del Cuello Uterino/tratamiento farmacológico , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Femenino , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Células HeLa , Humanos , Invasividad Neoplásica , FosforilaciónRESUMEN
Non-coding RNAs (ncRNAs) have received significant attention over the last few years. Malat1, as one of the most extensively studied ncRNAs, is believed to be not only a potential biomarker for disease diagnosis and prognosis, but also a candidate drug target for gynecological cancers. This potential is supported by a growing body of experimental evidence demonstrating that Malat1 participates in the occurrence, progression, and metastasis of tumors. Research has also shown that Malat1 can influence patient survival by regulating a range of target genes and signaling pathways. However, previous review articles have generally failed to consider the role of Malat1 in gynecological cancer in detail. In the present review, we summarize recent progress in research relating to the clinical relevance of Malat1 and the molecular mechanisms underlying the action of this ncRNA. Besides, we put forward some action points for further research after taking into consideration the sub-location and other essential properties of Malat1, which might enable us to have a better understanding of the potential of this molecule regarding clinical diagnosis and treatment.