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1.
Clin Hemorheol Microcirc ; 82(3): 255-263, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35848014

RESUMEN

AIM: Carotid ultrasound is a key tool for the diagnosis and evaluation of cardio disease, and the measurement of carotid intima-media thickness (CIMT) and hemodynamic parameters is of paramount importance for the imaging method. The aim of this study was to evaluate the feasibility and accuracy of handheld ultrasound devices for measuring carotid parameters. METHODS: We performed a carotid ultrasound on 25 participants using a handheld ultrasound device and a conventional ultrasound machine. For each participant, max and mean CIMT of common carotid artery (CCA) and peak systolic velocity (PSV), end diastolic velocity (EDV) and resistive index (RI) of CCA, bilateral external carotid artery (ECA), internal carotid artery (ICA) and the vertebral artery were measured. Agreement and repeatability were evaluated by linear regression and Bland-Altman analysis. RESULTS: We found a good repeatability and consistent of handheld ultrasound device in measuring mean CIMT (r = 0.68, P < 0.01). Furthermore, there was a moderate to good agreement between handheld and conventional ultrasound systems in measuring max IMT, mean IMT, PSV, EDV and RI of CCA (0.73, 0.79, 0.52, 0.58 and 0.84, respectively). CONCLUSION: Handheld ultrasound devices were able to provide carotid IMT and hemodynamic parameters measurements similar to those of conventional ultrasound. Such capabilities of handheld ultrasound devices might be useful for the primary assessment of carotid in clinical work.


Asunto(s)
Arteria Carótida Común , Grosor Intima-Media Carotídeo , Humanos , Arteria Carótida Común/diagnóstico por imagen , Arteria Carótida Interna/diagnóstico por imagen , Arterias Carótidas/diagnóstico por imagen , Ultrasonografía , Velocidad del Flujo Sanguíneo
2.
Talanta ; 212: 120795, 2020 May 15.
Artículo en Inglés | MEDLINE | ID: mdl-32113557

RESUMEN

In the present study, a kind of Eu(III) post-functionalized Zr(IV)-based metal-organic framework (UiO-66(COOH)2, Zr-MOF: Eu3+) was synthesized and utilized as an independently luminescent probe for sensing bilirubin (BR) in human serum, a biomarker of jaundice hepatitis. It can be served as a turn-off fluorescent switch for BR because its red emission from Eu3+ can be easily quenched by BR through a fluorescent resonant energy transfer (FRET) process between BR and its ligands, and as a result, BR is recognized successfully. Particularly, Zr-MOF: Eu3+ has shown many appealing properties, such as high sensitivity, quick response (less than 1 min), broad response window (0-15 µM), and excellent selectivity. Most importantly, a kind of portable test paper based on Zr-MOF: Eu3+ probe has been developed for directly assessing the level of BR in real human serum and further diagnosing bilirubin-related diseases via visually observing the luminescent color variation.


Asunto(s)
Bilirrubina/sangre , Colorantes Fluorescentes/química , Estructuras Metalorgánicas/química , Colorimetría/instrumentación , Colorimetría/métodos , Europio/química , Transferencia Resonante de Energía de Fluorescencia , Humanos , Circonio/química
3.
J Cell Biochem ; 112(10): 2882-90, 2011 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-21618590

RESUMEN

Hepassocin (HPS) is a specific mitogenic active factor for hepatocytes, and inhibits growth by overexpression in hepatocellular carcinoma (HCC) cells. However, the mechanism of HPS regulation on growth of liver-derived cells still remains largely unknown. In this study, we found that HPS was expressed and secreted into the extracellular medium in cultured L02 human hepatic cells; conditional medium of L02 cells promoted proliferation of L02 cells and this activity could be blocked by anti-HPS antibody. Moreover, we identified the presence of receptor for HPS on L02 cells and HepG2 human hepatoma cells. Overproduction of truncated HPS, which signal peptide was deleted, significantly inhibited the proliferation of HCC cells and induced cell cycle arrest. These findings suggest that HPS promotes hepatic cell line L02 cells proliferation via an autocrine mechanism and inhibits HCC cells proliferation by an intracrine pathway.


Asunto(s)
Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas de Neoplasias/metabolismo , Anticuerpos Neutralizantes/farmacología , Western Blotting , Ciclo Celular/genética , Ciclo Celular/fisiología , Línea Celular Tumoral , Proliferación Celular , Ensayo de Inmunoadsorción Enzimática , Fibrinógeno , Células Hep G2 , Hepatocitos/metabolismo , Humanos , Proteínas de Neoplasias/antagonistas & inhibidores , Transducción de Señal/genética , Transducción de Señal/fisiología
4.
J Agric Food Chem ; 59(5): 1594-7, 2011 Mar 09.
Artículo en Inglés | MEDLINE | ID: mdl-21299253

RESUMEN

An indirect competitive enzyme-linked immunosorbent assay (ic-ELISA) based on monoclonal antibodies (MoAbs) for imidaclothiz was developed. The hapten of imidaclothiz was synthesized and conjugated to bovine serum albumin (BSA) and ovalbumin (OVA) to form the artificial antigens. MoAbs were obtained by immunizing BALB/c mice. Under the optimized conditions (10% methanol, 0.14 M Na(+), and pH 7.4), the half-maximal inhibition concentration (IC(50)) was 0.0875 ± 0.0034 mg/L and the limit of detection (IC(20)) was 0.0178 ± 0.0018 mg/L for imidaclothiz. There were no obvious cross-reactivities with most of the structural analogues of neonicotinoid insecticides, except imidacloprid. The recoveries of imidaclothiz in environmental and agricultural samples, including tap water, paddy water, soil, and cabbage, ranged from 80.43 to 113.83%, well within the requirements of residue detection. These results showed that this immunoassay could be used for the determination of imidaclothiz in environmental and agricultural samples.


Asunto(s)
Anticuerpos Monoclonales , Ensayo de Inmunoadsorción Enzimática/métodos , Residuos de Plaguicidas/análisis , Tiazoles/análisis , Animales , Femenino , Ratones , Ratones Endogámicos BALB C , Suelo/análisis , Verduras/química , Agua/química
5.
Gut ; 59(6): 817-26, 2010 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19880967

RESUMEN

BACKGROUND: Human hepassocin (HPS) was originally detected by subtractive and differential cDNA cloning as a liver-specific gene that was markedly upregulated during liver regeneration. Previous studies suggested that HPS showed mitogenic activity on isolated hepatocytes in vitro. However, its in vivo functions remained largely unknown. Therefore, the function of recombinant human HPS during liver regeneration and chemically induced liver injury was investigated. METHODS: The proliferation of primary hepatocytes was examined by [(3)H]thymidine incorporation and immunohistological staining of proliferating cell nuclear antigen (PCNA). RNA interference was performed to knock down the endogenous expression of HPS. The proliferation of L02 cells was examined by MTS assay. The phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2) was investigated by western blotting analysis. Assessment of liver injury (histology, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels) and of apoptosis, by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay, was performed. RESULTS: Purified recombinant human HPS showed specific mitogenic activity on primary hepatocytes and normal liver cell lines in a mitogen-activated protein kinase (MAPK)-dependent manner and stimulated the proliferation of hepatocytes in rats with 70% partial hepatectomy. Administration of HPS to rats after d-galactose and carbon tetrachloride (CCl(4)) treatment protected against liver injury (minimal liver necrosis, depressed ALT and AST levels, and decreased lethality), reduced apoptosis and enhanced proliferation. Knock-down of endogenous HPS in vivo enhanced the liver injury induced by d-galactose by increasing the apoptosis and elevating ALT and AST levels. CONCLUSIONS: HPS is a hepatic growth factor which can accelerate hepatocyte proliferation in vivo and protect against liver injury. These data point to the potential interest of HPS in the treatment of fulminant hepatic failure.


Asunto(s)
Hepatocitos/efectos de los fármacos , Fallo Hepático Agudo/tratamiento farmacológico , Proteínas de Neoplasias/uso terapéutico , Animales , Apoptosis/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Células Cultivadas , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Modelos Animales de Enfermedad , Fibrinógeno , Hepatocitos/patología , Humanos , Fallo Hepático Agudo/patología , Regeneración Hepática/efectos de los fármacos , Masculino , Proteína Quinasa 1 Activada por Mitógenos/fisiología , Proteína Quinasa 3 Activada por Mitógenos/fisiología , Proteínas de Neoplasias/farmacología , Interferencia de ARN , Ratas , Ratas Wistar , Proteínas Recombinantes/farmacología , Proteínas Recombinantes/uso terapéutico
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