RESUMO
There are controversial reports about cardiac differentiation potential of mesenchymal stem cells (MSCs), and there is still no well-defined protocol for the induction of cardiac differentiation. The effects of retinoic acid (RA) and dimethyl sulfoxide (DMSO) on the proliferation and differentiation of human fetal liver-derived MSCs (HFMSCs) as well as the pluripotent state induced by 5-azacytidine (5-aza) in vitro were investigated. MSCs were isolated from fetal livers and cultured in accordance with previous reports. Cells were plated and were treated for 24 h by the combination of 5-aza, RA and DMSO in different doses. Different culture conditions were tested in our study, including temperature, oxygen content and medium. Three weeks later, cells were harvested for the certification of cardiac differentiation as well as the pluripotency, which indicated by cardiac markers and Oct4. It was found that the cardiac differentiation was only induced when HFMSCs were treated in the following conditions: in high-dose combination (5-aza 50 µM + RA 10(-1) µM + DMSO 1 %) in cardiac differentiation medium at 37 °C and 20 % O2. The results of immunohistochemistry and quantitative RT-PCR showed that about 40 % of the cells positively expressed Nkx2.5, desmin and cardiac troponin I, as well as Oct4. No beating cells were observed during the period. The combined treatment with RA, DMSO and 5-aza in high-dose could promote HFMSCs to differentiate into cardiomyocyte-like cells and possibly through the change of their pluripotent state.
Assuntos
Azacitidina/farmacologia , Diferenciação Celular/efeitos dos fármacos , Dimetil Sulfóxido/farmacologia , Feto/citologia , Fígado/embriologia , Células-Tronco Mesenquimais/citologia , Tretinoína/farmacologia , Biomarcadores/metabolismo , Forma Celular/efeitos dos fármacos , Humanos , Imuno-Histoquímica , Células-Tronco Mesenquimais/efeitos dos fármacos , Células-Tronco Mesenquimais/metabolismo , Miocárdio/citologia , Fator 3 de Transcrição de Octâmero/metabolismo , Osteogênese/efeitos dos fármacos , Fenótipo , Reação em Cadeia da Polimerase em Tempo Real , Reprodutibilidade dos TestesRESUMO
The deterioration of fruit could reduce the shelf life, decreased marketability and substantial economic value. Thus, a safe, simple, economical and environmentally friendly preservation technology for fruit is of great significance. Here, the postharvest preservation technology was investigated with zinc-doped carbon quantum dots and chlorogenic acid (Zn-CQDs/CGA) composite. Zn-CQDs/CGA composite were synthesized, which exhibits superior antioxidant and antibacterial activities. The binding mechanism of the Zn-CQDs/CGA composite was investigated, which revealed that the bindings of two components were mainly driven by hydrogen bonding and van der Waals forces to create a novel composite. The Zn-CQDs/CGA composite was applied to longan preservation and was found to significantly reduce the incidence of mildew spot, browning of fruit endocarp and pulp, as well as the degree of degradation of quality indexes. These results suggest that the Zn-CQDs/CGA composite has the potential for inhibiting browning and preserving the quality of longan during storage.
Assuntos
Antioxidantes , Pontos Quânticos , Antioxidantes/farmacologia , Zinco , Ácido Clorogênico/farmacologia , Ácido Clorogênico/química , Carbono/química , Antibacterianos/farmacologia , Pontos Quânticos/químicaRESUMO
OBJECTIVE AND DESIGN: The very late antigen-4 (VLA-4) bound to vascular cell adhesion molecule-1 could provide co-stimulatory signals for the activation of T lymphocytes, and these adhesion molecules play key roles in leukocyte adherence and propagation of inflammatory responses. We examined the levels of VLA-4 in the peripheral blood mononuclear cells (PBMC) of patients with hemorrhagic fever with renal syndrome (HFRS). MATERIALS AND METHODS: The levels of VLA-4 in PBMC samples collected from 53 patients by immunohistochemical staining were detected. RESULTS: The expression of VLA-4 in PBMC of HFRS patients at different stages were significantly higher than those in normal controls (P < 0.05), except recovery stage (P > 0.05). The expression of VLA-4 in PBMC of HFRS patients at different types were significantly higher than those in healthy controls (P < 0.05). The levels of VLA-4 in patients with HFRS were positively correlated with serum levels of blood urea nitrogen (BUN) and creatinine (Cr). CONCLUSIONS: VLA-4 might play an important role in the immunopathological lesions of HFRS. We found that VLA-4 levels were closely correlated to the severity of the HFRS and the degree of kidney damage.
Assuntos
Febre Hemorrágica com Síndrome Renal/imunologia , Integrina alfa4beta1/imunologia , Leucócitos Mononucleares/imunologia , Febre Hemorrágica com Síndrome Renal/patologia , Febre Hemorrágica com Síndrome Renal/fisiopatologia , Humanos , Rim/patologia , Leucócitos Mononucleares/citologiaRESUMO
Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease characterized by endothelial dysfunction. The cellular immune response, especially the virus-specific CD8+ T lymphocytes, is known to attack vascular endothelial cells (VEC) and to contribute to the diffuse damage and penetrability increasing of VEC. Lymphocyte function associated antigen 3 (LFA-3) is expressed on T lymphocytes and VEC, which is contributed to the activation of T lymphocytes. The expression of LFA-3 on the activated T lymphocytes and VEC is highly increased, which can exfoliate into plasma to increase the level of soluble LFA-3 (sLFA-3) in plasma. So the change of sLFA-3 levels is correlated with the activation of T lymphocytes. In this study we detected the levels of sLFA-3 in plasma of patients with HFRS. We examined the levels of sLFA-3 in plasma samples collected from 53 HFRS patients by double antibody sandwich ELISA. We found variable, but persistently elevated levels of sLFA-3 throughout the various phases and types of the HFRS disease, which suggest that sLFA-3 levels have correlation with disease stages. Moreover, elevated sLFA-3 levels are closely correlated to the severity of HFRS and the degree of kidney damage.
Assuntos
Antígenos CD58/sangue , Febre Hemorrágica com Síndrome Renal/sangue , Nitrogênio da Ureia Sanguínea , Creatinina/urina , Células Endoteliais/fisiologia , Febre Hemorrágica com Síndrome Renal/imunologia , HumanosRESUMO
It was previously reported that several kinds of intercellular adhesion molecules are closely related to chronic HBV infection. The complex of CD2 and CD58 plays an important role in enhancing the adhesion of T lymphocytes to target cells, and promoting hyperplasia and activation of T lymphocytes. In this study, we detected the level of CD2 expressed on the surface of PBMC, the expression level of CD2 mRNA in PBMC and the percentage of CD2 positive cells in PBMC of patients with chronic HBV infection and compared them with the expression level of normal controls. We also determined the level of serum HBV DNA from patients with chronic HBV infection and from normal controls. The clinical characteristics of hepatic function were tested as well. The results showed that the expression of CD2 significantly increased with the severity of chronic HBV infection, which suggested that CD2 might contribute to the hepatocyte damage in chronic HBV infection.
Assuntos
Antígenos CD2/metabolismo , Antígenos CD58/metabolismo , Moléculas de Adesão Celular/metabolismo , Leucócitos Mononucleares/imunologia , Adulto , Antígenos CD2/imunologia , Antígenos CD58/imunologia , Moléculas de Adesão Celular/imunologia , DNA Viral/sangue , Feminino , Vírus da Hepatite B/isolamento & purificação , Hepatite B Crônica/imunologia , Hepatite B Crônica/virologia , Humanos , Leucócitos Mononucleares/metabolismo , Ativação Linfocitária , Masculino , RNA Mensageiro/metabolismoRESUMO
BACKGROUND: Several kinds of intercellular adhesion molecules closely relate to hepatitis B. The complex of CD(2) and CD58 plays an important role in enhancing the adhesion of T lymphocytes to target cells, hyperplasia and activation of T lymphocytes. In this study, we explored the relationship between the expression of CD58 in liver tissue and chronic hepatitis B infection. METHODS: We determined the expression of the CD58 molecule on the surface of hepatocytes by using immunohistochemistry and the levels of serum HBV DNA from patients with HBV infection and from normal controls. The biochemical parameters of hepatic function were analyzed as well. RESULTS: CD58 expression in hepatocytes significantly increased with the severity progression of chronic HBV infection. The IOD levels (log10) of CD58 in the control, mild, moderate, and severe chronic HBV infection groups were 0, (7.20+/-4.64) x 10(3), (25.63+/-7.41) x 10(3) and (37.47+/-11.17) x 10(3) respectively (P<0.05 compared with the control group, respectively). CONCLUSION: CD58 probably increases cell mediated immunity to eliminate hepatitis B virus and leads to damage of hepatocytes.
Assuntos
Antígenos CD58/análise , Hepatite B Crônica/imunologia , Fígado/imunologia , DNA Viral/sangue , Humanos , Imuno-Histoquímica , Fígado/fisiopatologia , Linfócitos T/fisiologiaRESUMO
The impact of heart failure (HF) on acute myocardial infarction (AMI) in patients from southwestern China remains unclear. The present study aimed to compare in-hospital cardiovascular events, mortality and clinical therapies in AMI patients with or without HF in southwestern China. In total, 591 patients with AMI hospitalized between February 2009 and December 2012 were examined; those with a history of HF were excluded. The patients were divided into four groups according to AMI type (ST-elevated or non-ST-elevated AMI) and the presence of HF during hospitalization. Clinical characteristics, in-hospital cardiovascular events, mortality, coronary angiography and treatment were compared. Clinical therapies, specifically evidence-based drug use were analyzed in patients with HF during hospitalization, including angiotensin converting enzyme inhibitors (ACEIs) and ß-blockers (BBs). AMI patients with HF had a higher frequency of co-morbidities, lower left ventricular ejection fraction, longer length of hospital stay and a greater risk of in-hospital mortality compared with AMI patients without HF. AMI patients with HF were less likely to be examined by cardiac angiography or treated with reperfusion therapy or recommended medications. AMI patients with HF co-treated with ACEIs and BBs had a significantly higher survival rate (94.4 vs. 67.5%; P<0.001) compared with untreated patients or patients treated with either ACEIs or BBs alone. Logistic regression analysis revealed that HF and cardiogenic shock in patients with AMI were the strongest predictors of in-hospital mortality. AMI patients with HF were at a higher risk of adverse outcomes. Cardiac angiography and timely standard recommended medications were associated with improved clinical outcomes.