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1.
Clin Hemorheol Microcirc ; 82(3): 255-263, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35848014

RESUMO

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.


Assuntos
Artéria Carótida Primitiva , Espessura Intima-Media Carotídea , Humanos , Artéria Carótida Primitiva/diagnóstico por imagem , Artéria Carótida Interna/diagnóstico por imagem , Artérias Carótidas/diagnóstico por imagem , Ultrassonografia , Velocidade do Fluxo Sanguíneo
2.
Talanta ; 212: 120795, 2020 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-32113557

RESUMO

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.


Assuntos
Bilirrubina/sangue , Corantes Fluorescentes/química , Estruturas Metalorgânicas/química , Colorimetria/instrumentação , Colorimetria/métodos , Európio/química , Transferência Ressonante de Energia de Fluorescência , Humanos , Zircônio/química
3.
J Cell Biochem ; 112(10): 2882-90, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21618590

RESUMO

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.


Assuntos
Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas de Neoplasias/metabolismo , Anticorpos Neutralizantes/farmacologia , Western Blotting , Ciclo Celular/genética , Ciclo Celular/fisiologia , Linhagem Celular Tumoral , Proliferação de Células , Ensaio de Imunoadsorção Enzimática , Fibrinogênio , Células Hep G2 , Hepatócitos/metabolismo , Humanos , Proteínas de Neoplasias/antagonistas & inibidores , Transdução de Sinais/genética , Transdução de Sinais/fisiologia
4.
J Agric Food Chem ; 59(5): 1594-7, 2011 Mar 09.
Artigo em Inglês | MEDLINE | ID: mdl-21299253

RESUMO

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.


Assuntos
Anticorpos Monoclonais , Ensaio de Imunoadsorção Enzimática/métodos , Resíduos de Praguicidas/análise , Tiazóis/análise , Animais , Feminino , Camundongos , Camundongos Endogâmicos BALB C , Solo/análise , Verduras/química , Água/química
5.
Gut ; 59(6): 817-26, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-19880967

RESUMO

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.


Assuntos
Hepatócitos/efeitos dos fármacos , Falência Hepática Aguda/tratamento farmacológico , Proteínas de Neoplasias/uso terapêutico , Animais , Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/patologia , Modelos Animais de Doenças , Fibrinogênio , Hepatócitos/patologia , Humanos , Falência Hepática Aguda/patologia , Regeneração Hepática/efeitos dos fármacos , Masculino , Proteína Quinase 1 Ativada por Mitógeno/fisiologia , Proteína Quinase 3 Ativada por Mitógeno/fisiologia , Proteínas de Neoplasias/farmacologia , Interferência de RNA , Ratos , Ratos Wistar , Proteínas Recombinantes/farmacologia , Proteínas Recombinantes/uso terapêutico
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