RESUMEN
SUMMARY: This study aimed to compare the clinical value of carotid ultrasound and digital subtraction angiography (DSA) for carotid artery stenosis in patients with cerebral infarction. Sixty patients with cerebral infarction underwent carotid ultrasound and DSA. Carotid artery stenosis, degree of stenosis (mild, moderate, severe, and occlusion), and carotid artery plaques were recorded and compared. Carotid stenosis rate was 96.67 % (58/60) and 91.67 % (55/60) on DSA and carotid ultrasound, respectively, and the difference was not statistically significant. Mild, moderate, and severe carotid artery stenosis and occlusion were diagnosed in 35, 28, 20, and 17 arteries, respectively, with DSA, and in 39, 25, 10, and 9 arteries, respectively, with carotid ultrasound. There was a statistically significant difference in the degree of carotid stenosis between the two methods (p<0.05). The kappa value of carotid plaques detected by carotid ultrasound and DSA was 0.776, indicating good consistency. Both carotid ultrasound and DSA are effective for screening carotid artery stenosis and carotid atherosclerotic plaques. While carotid ultrasound is faster and more convenient, DSA can more accurately detect the degree of stenosis and presence of occlusion. Thus, our recommendation is a combination of carotid ultrasound and DSA in clinical settings to improve the convenience and accuracy of diagnosis.
Este estudio tuvo como objetivo comparar el valor clínico de la ecografía carotídea y la angiografía por sustracción digital (DSA) para la estenosis de la arteria carótida en pacientes con infarto cerebral. Sesenta pacientes con infarto cerebral fueron sometidos a ecografía carotídea y DSA. Se registraron y compararon la estenosis de la arteria carótida, el grado de estenosis (leve, moderada, grave y oclusión) y las placas de la arteria carótida. La tasa de estenosis carotídea fue del 96,67 % (58/60) y del 91,67 % (55/60) en DSA y ecografía carotídea, respectivamente, y la diferencia no fue estadísticamente significativa. Se diagnosticaron estenosis y oclusión de la arteria carótida leve, moderada y grave en 35, 28, 20 y 17 arterias, respectivamente, con DSA, y en 39, 25, 10 y 9 arterias, respectivamente, con ecografía carotídea. Hubo una diferencia estadísticamente significativa en el grado de estenosis carotídea entre los dos métodos (p<0,05). El valor kappa de las placas carotídeas detectadas por ecografía carotídea y DSA fue de 0,776, lo que indica una buena consistencia. Tanto la ecografía carotídea como la DSA son eficaces para detectar la estenosis de la arteria carótida y las placas ateroscleróticas carotídeas. Si bien la ecografía carotídea es más rápida y conveniente, la DSA puede detectar con mayor precisión el grado de estenosis y la presencia de oclusión. Por lo tanto, nuestra recomendación es una combinación de ecografía carotídea y DSA en entornos clínicos para mejorar la conveniencia y precisión del diagnóstico.
Asunto(s)
Humanos , Masculino , Femenino , Ultrasonido , Angiografía de Substracción Digital , Infarto Cerebral/complicaciones , Estenosis Carotídea/diagnóstico por imagen , Estudios Retrospectivos , Estenosis Carotídea/etiologíaRESUMEN
Golgi protein 73 (also known as GP73 or GOLPH2) is a transmembrane glycoprotein present in the Golgi apparatus. In diseased states, GP73 is expressed by hepatocytes rather than by bile duct epithelial cells. Many studies have reported that serum GP73 (sGP73) is a marker for hepatocellular carcinoma (HCC). For HCC diagnosis, the sensitivities of sGP73 were higher than that of other markers but the specificities were lower. Considering that the concentration of GP73 is consistent with the stage of liver fibrosis and cirrhosis, some studies have implied that GP73 may be a marker for liver fibrosis and cirrhosis. Increased sGP73 levels may result from hepatic inflammatory activity. During liver inflammation, GP73 facilitates liver tissue regeneration. By summarizing the studies on GP73 in liver diseases, we wish to focus on the mechanism of GP73 in diseases.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Biomarcadores de Tumor , Carcinoma Hepatocelular/patología , Humanos , Cirrosis Hepática/diagnóstico , Neoplasias Hepáticas/patología , Proteínas de la MembranaRESUMEN
SUMMARY: Intracranial artery stenosis (ICAS) was one of the main causes of ischemic stroke onset and recurrence. About 30 % of strokes were caused by intracranial artery stenosis. Intracranial artery stenosis had a high incidence in China and faced a high risk of recurrence for a long time. It affected patient safety and quality of life seriously. At the same time, it caused a heavy financial burden for the patient´s family. Therefore, early detection and accuracy of intracranial artery stenosis evaluation were extremely important. High-resolution magnetic resonance imaging (HR-MRI) had been widely used in clinical examinations, making up for the shortcomings of traditional vascular imaging methods that could only show the degree of luminal stenosis, making it possible to perform lumens, tube wall and plaque features of atherosclerotic intracranial arteries at the same time. There were still some controversies about the credibility of this technique in assessing the intracranial artery lumen stenosis. This article reviewed the application efficacy of HR-MRI technology in evaluating the degree of intracranial atherosclerotic stenosis.
RESUMEN: La estenosis de arterias intracraneales (ICAS) es una de las principales causas del ictus isquémico, como así también de su recurrencia. Alrededor del 30 % de los ataques cerebrovasculares son causados por estenosis de la arteria intracraneal. La estenosis de arterias intracraneales tiene una alta incidencia en China y enfrenta un alto riesgo de recurrencia, afectando gravemente la seguridad y la calidad de vida de los pacientes. Al mismo tiempo, supone una importante carga financiera para la familia de los pacientes. Por lo tanto, la detección temprana y la precisión de la evaluación de la estenosis de arterias intracraneales es extremadamente importante. La resonancia magnética de alta resolución (HR-MRI, por sus siglas en inglés) es utilizada ampliamente en los exámenes clínicos, compensando las deficiencias de los métodos tradicionales de imágenes vasculares que solo pueden mostrar el grado de estenosis luminal, haciendo posible el estudio de las características del lumen, pared vascular y la placa ateroesclerótica, de las arterias intracraneales afectadas, al mismo tiempo. Aún existen algunas controversias sobre la credibilidad de esta técnica en la evaluación de la estenosis del lumen de arterias intracraneales. En este artículo se revisó la eficacia de la aplicación de la tecnología HR-MRI para evaluar el grado de estenosis aterosclerótica intracraneal.
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Humanos , Imagen por Resonancia Magnética/métodos , Arteriosclerosis Intracraneal/diagnóstico por imagen , Imagenología Tridimensional/métodos , Constricción Patológica/diagnóstico por imagen , Accidente Cerebrovascular/prevención & controlRESUMEN
This study focused on investigating reactor performance, simultaneous methanogeneis and denitrifiction (SMD) process for treatment of a sulfate plus organic sulfur - rich 3,4,5-Triethoxybenzaldehyde (TMBA) manufacturing wastewater with variable COD/TSO42- (total sulfate) ratio by micro-electric field- zero-valent-iron (ZVI) UASB for 390 days. The initial COD/TSO42- was set as 1.42, 0.9 and 0.5, respectively by manually introducing sulfate. The experimental results indicated that micro-electric field- zero-valent-iron UASB was an attractive integrated option for satisfactory COD removal, nitrate reduction and a reasonable methane yield rate even at COD/TSO42- as low as 0.9. Further declining the COD/TSO42- to 0.5 can result in a moderate inhibition of SMD process. The behavior of organic S release was not inhibited over the entire experimental period. Thus, surprisingly, sulfate concentration in the effluent was always higher than that in the influent. In comparison with sludge sample at Day-1, sludge at Day-390 was characterized with high abundant Tissierella Soehngenia, Anaerolinaceae and Brevundimonas diminuta, which played critical role in promising performance in COD abatement. The relatively low abundance of sulfate reducing bacteria (SRB) such as Desulfobulbus and Desulfomicrobium can explain the lower sulfate reduction efficiency in term of high concentration of sulfate plus released from organic S-rich compounds.
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Reactores Biológicos/microbiología , Técnicas Electroquímicas/métodos , Hierro/química , Metano/biosíntesis , Sulfatos/análisis , Aguas Residuales , Contaminantes Químicos del Agua/análisis , Purificación del Agua/métodos , Anaerobiosis , Benzaldehídos/química , Análisis de la Demanda Biológica de Oxígeno , Desnitrificación , Aguas Residuales/química , Aguas Residuales/microbiologíaRESUMEN
Although the effects of low-intensity pulsed ultrasound (LIPUS) on diverse cell types have been fully studied, the functional role of LIPUS in keratinocytes remains poorly understood. This study aimed to investigate the effects of LIPUS on proliferation and migration of HaCaT cells as well as the regulatory mechanisms associated with signaling pathways. Human HaCaT cells were exposed or not to LIPUS, and cell proliferation and migration were measured by BrdU incorporation assay and Transwell assay, respectively. Expression of proteins associated with proliferation and migration was evaluated by western blot analysis. Expression of key kinases in the PI3K/AKT and JNK pathways was also evaluated by western blot analysis. Effects of LIPUS on the PI3K/AKT and JNK pathways, and whether LIPUS affected HaCaT cells via these two pathways were finally explored. When the parameter of LIPUS (number of cycles) was set at 300, cell viability was the highest after LIPUS stimulation. We then found that the percentage of BrdU positive cells was enhanced by LIPUS, along with up-regulation of cyclinD1, CDK6, CDK4, and VEGF. LIPUS promoted migration, as well as up-regulation of MMP-2 and MMP-9. Phosphorylation levels of key kinases in the PI3K/AKT and JNK pathways were increased by LIPUS. Inhibition of either PI3K/AKT pathway or JNK pathway attenuated effects of LIPUS on HaCaT cells, and co-inhibition of these two pathways showed augmented effects. LIPUS promoted proliferation and migration of HaCaT cells through activating the PI3K/AKT and JNK pathways.
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Movimiento Celular/efectos de la radiación , Proliferación Celular/efectos de la radiación , Queratinocitos/efectos de la radiación , Sistema de Señalización de MAP Quinasas/efectos de la radiación , Fosfatidilinositol 3-Quinasas/efectos de la radiación , Proteínas Proto-Oncogénicas c-akt/efectos de la radiación , Ondas Ultrasónicas , Análisis de Varianza , Western Blotting , Bromodesoxiuridina , Línea Celular Transformada , Supervivencia Celular/efectos de la radiación , Humanos , Queratinocitos/metabolismo , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Reproducibilidad de los Resultados , Transducción de Señal/efectos de la radiación , Regulación hacia ArribaRESUMEN
Although the effects of low-intensity pulsed ultrasound (LIPUS) on diverse cell types have been fully studied, the functional role of LIPUS in keratinocytes remains poorly understood. This study aimed to investigate the effects of LIPUS on proliferation and migration of HaCaT cells as well as the regulatory mechanisms associated with signaling pathways. Human HaCaT cells were exposed or not to LIPUS, and cell proliferation and migration were measured by BrdU incorporation assay and Transwell assay, respectively. Expression of proteins associated with proliferation and migration was evaluated by western blot analysis. Expression of key kinases in the PI3K/AKT and JNK pathways was also evaluated by western blot analysis. Effects of LIPUS on the PI3K/AKT and JNK pathways, and whether LIPUS affected HaCaT cells via these two pathways were finally explored. When the parameter of LIPUS (number of cycles) was set at 300, cell viability was the highest after LIPUS stimulation. We then found that the percentage of BrdU positive cells was enhanced by LIPUS, along with up-regulation of cyclinD1, CDK6, CDK4, and VEGF. LIPUS promoted migration, as well as up-regulation of MMP-2 and MMP-9. Phosphorylation levels of key kinases in the PI3K/AKT and JNK pathways were increased by LIPUS. Inhibition of either PI3K/AKT pathway or JNK pathway attenuated effects of LIPUS on HaCaT cells, and co-inhibition of these two pathways showed augmented effects. LIPUS promoted proliferation and migration of HaCaT cells through activating the PI3K/AKT and JNK pathways.
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Queratinocitos/efectos de la radiación , Movimiento Celular/efectos de la radiación , Fosfatidilinositol 3-Quinasas/efectos de la radiación , Sistema de Señalización de MAP Quinasas/efectos de la radiación , Proliferación Celular/efectos de la radiación , Ondas Ultrasónicas , Bromodesoxiuridina , Línea Celular Transformada , Transducción de Señal/efectos de la radiación , Queratinocitos/metabolismo , Regulación hacia Arriba , Supervivencia Celular/efectos de la radiación , Western Blotting , Reproducibilidad de los Resultados , Análisis de Varianza , Fosfatidilinositol 3-Quinasas/metabolismo , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/metabolismoRESUMEN
In order to explore the change rule of myoblast stem cells (satellite cells, SCs) in the denervated and re-innervated muscle and to investigate the cellular mechanism of the morphological and functional changes of the muscle, denervated muscle atrophy and nerve regeneration models were established in one-month-old rats. Postoperative indexes such as muscle wet weight, cell section areas, content of collagen fibers and DNA, electrophysiology, numbers of SCs in the triceps muscle of calf were dynamically tested. After denervation, the muscle wet weight and cell area reduced rapidly, and the collagen fiber content increased slowly. The number of SCs increased at first, and then declined suddenly two months later. From 4 to 5 weeks after re-neuralization, muscle action potentials could be evoked, but the best innervation effect was found in the groups, which received re-neuralization at 2 months and 3 months after denervation. Denervation causes a progressive progress of muscle atrophy. SCs proliferate within 3 months after denervation, and then atrophy becomes irreversible from 4 months. At 4 or 5 weeks after re-neuralization, muscle action potentials can be evoked. Re-neuralization at 2 months and 3 months after denervation can achieve a good effect on the functional recovery of the atrophic muscle.
Con el fin de explorar la regla de cambio de las células precursoras mioblásticas (células satélite, CSs) en el músculo denervado y re-inervado e investigar el mecanismo celular de los cambios morfológicos y funcionales del músculo, se establecieron, en ratas de un mes de edad, modelos de atrofia del músculo denervado y regeneración del nervio. Fueron examinados de manera dinámica índices postoperatorios tales como, el peso húmedo del músculo, áreas celulares de la sección, contenido de fibras de colágeno y ADN, electrofisiología, número de CSs en el músculo tríceps de las crías. Luego de la denervación, el peso del músculo húmedo y el área celular se redujeron rápidamente, mientras que el contenido de fibras colágenas aumentó lentamente. El número de CSs aumentó al inicio, pero más tarde, a los dos meses, disminuyó repentinamente. Entre las 4 a 5 semanas después de la reneuralización, los potenciales de acción muscular pudieron ser evocados, pero el mejor efecto de inervación se encontró en los grupos que recibieron reneuralización a los 2 y 3 meses después de la denervación. La denervación causó un avance progresivo de la atrofia muscular. Las CSs proliferaron dentro de los primeros 3 meses post-denervación, y luego de los 4 meses la atrofia fue irreversible. A las 4 o 5 semanas después de la reneuralizacón, los potenciales de acción muscular pueden ser evocados. La reneuralización a los 2 y 3 meses después de la denervación puede lograr un buen efecto en la recuperación funcional del músculo atrófico.