Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
Folia Neuropathol ; 61(3): 249-265, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37818686

RESUMEN

INTRODUCTION: Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) is involved in glioma progression, but the specific molecular mechanism of CDKN2A in glioma cell migration and invasion needs to be further explored. MATERIAL AND METHODS: Data related to CDKN2A expression and glioma overall survival were obtained from The Cancer Genome Atlas (TCGA) database. Then, CDKN2A expression in glioma tissues/cells or paracancer tissues/astrocytes was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blot. Afterwards, Wound healing, Transwell and tube formation assay were performed to identify the invasion, migration and angiogenesis of glioma cells, respectively. TargetScan database predicted the targeted binding between miR-484 and CDKN2A, which was verified by dual luciferase reporter gene assay. Western blot and qRT-PCR were performed to detect the expression of VEGF, E-cadherin, N-cadherin and Vimentin in glioma cells. RESULTS: CDKN2A was low-expressed in glioma tissue/cells as compared to paracancer tissue/astrocytes, and was strongly associated to the poor prognosis of glioma. Further studies found that down-regulation of CDKN2A could promote migration, invasion and angiogenesis of glioma cells. Besides, miR-484 was high-expressed in glioma cells compared to astrocytes. Up-regulation of miR-484 could enhance migration, invasion and angiogenesis of glioma cells. In addition, up-regulated miR-484 suppressed the expression of E-cadherin, and promoted the expression of N-cadherin, Vimentin and VEGF. However, there was negative regulation of miR-484 and CDKN2A, and CDKN2A could partially offset the effect of miR-484. CONCLUSIONS: MiR-484 promoted cell migration, invasion and angiogenesis by inhibiting CDKN2A expression.


Asunto(s)
Glioma , MicroARNs , Humanos , MicroARNs/genética , MicroARNs/metabolismo , Vimentina/genética , Vimentina/metabolismo , Línea Celular Tumoral , Factor A de Crecimiento Endotelial Vascular/genética , Glioma/genética , Glioma/patología , Proliferación Celular/genética , Cadherinas/genética , Cadherinas/metabolismo , Regulación Neoplásica de la Expresión Génica/genética , Inhibidor p16 de la Quinasa Dependiente de Ciclina/genética , Inhibidor p16 de la Quinasa Dependiente de Ciclina/metabolismo
2.
Brain Sci ; 12(12)2022 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-36552106

RESUMEN

Objectives: To determine the short- and medium-term therapeutic effects of subthalamic nucleus (STN) deep brain stimulation (DBS) on restless legs syndrome (RLS) in patients with Parkinson's disease (PD) and to study the optimal position of activated contacts for RLS symptoms. Methods: We preoperatively and postoperatively assessed PD Patients with RLS undergoing STN-DBS. Additionally, we recorded the stimulation parameters that induced RLS or relieved RLS symptoms during a follow-up. Finally, we reconstructed the activated contacts' position that reduced or induced RLS symptoms. Results: 363 PD patients were enrolled. At the 1-year follow-up, we found that the IRLS sum significantly decreased in the RLS group (preoperative 18.758 ± 7.706, postoperative 8.121 ± 7.083, p < 0.05). The results of the CGI score, MOS sleep, and RLS QLQ all showed that the STN-DBS improved RLS symptoms after one year. Furthermore, the activated contacts that relieved RLS were mainly located in the central sensorimotor region of the STN. Activated contacts in the inferior sensorimotor part of the STN or in the substantia nigra might have induced RLS symptoms. Conclusions: STN-DBS improved RLS in patients with PD in one year, which reduced their sleep disorders and increased their quality of life. Furthermore, the central sensorimotor region part of the STN is the optimal stimulation site.

3.
Clin Chim Acta ; 523: 290-296, 2021 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-34655609

RESUMEN

BACKGROUND: Triggering receptor expressed on myeloid cells-1 (TREM-1) participates in neuroinflammation. We intended to ascertain whether serum soluble TREM-1 (sTREM-1) could be utilized as a biomarker of inflammation, severity, early neurologic deterioration (END) and outcome after primary intracerebral hemorrhage (ICH). METHODS: Serum sTREM-1 levels were gauged in 104 ICH patients and 104 healthy controls. END was diagnosed when the National Institutes of Health Stroke Scale (NIHSS) score increased ≥ 4 points or death between admission and 24 h after admission. Patients with a modified Rankin scale score of > 2 at 3 months were considered to have poor outcome. RESULTS: As compared to controls, patients exhibited significantly elevated serum sTREM-1 levels (median: 309.0 vs 67.9 pg/ml). Serum sTREM-1 concentrations were intimately correlated with NIHSS score (r = 0.574), hematoma volume (r = 0.554), blood leukocyte count (r = 0.529) and serum C-reactive protein concentrations (r = 0.509). Serum sTREM-1 concentrations > 309.0 pg/ml independently predicted END and poor outcome with odds ratio values of 4.054 and 4.721 respectively. Serum sTREM-1 concentrations distinguished END and poor outcome with areas under receiver operating characteristic curve of 0.789 and 0.813 respectively. CONCLUSION: Serum sTREM-1 may represent a promising inflammatory biomarker for assessment of severity and prediction of END and poor outcome after ICH.


Asunto(s)
Hemorragia Cerebral , Enfermedades Neuroinflamatorias , Receptor Activador Expresado en Células Mieloides 1/sangre , Biomarcadores/sangre , Hemorragia Cerebral/diagnóstico , Humanos , Enfermedades Neuroinflamatorias/diagnóstico , Pronóstico
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA