RESUMEN

SUMMARY: Overexpression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in various tumor tissues and cell lines was found to promote tumor cell proliferation, migration, and invasion. However, the role of MALAT1 in gastric cancer (GC) is still unclear. We aimed to investigate the correlation between long-chain non-coding RNAs (lncRNAs), MALAT1, MicroRNAs (miRNA) and vascular endothelial growth factor A (VEGFA) in gastric cancer and to disclose underlying mechanism. The correlation between MALAT1 levels and clinical features was analyzed by bioinformatics data and human samples. The expression of MALAT1 was down regulated in AGS cells to detect the cell proliferation, migration, and invasion characteristics, as well as the effects on signal pathways. Furthermore, we validated the role of MALAT1/miR-330-3p axis in GC by dual luciferase reporter gene assays. Expression of MALAT1 was higher in cancer tissues than in para-cancerous tissues. The high MALAT1 level predicted malignancy and worse prognosis. Down-regulation of MALAT1 expression in AGS cells inhibited cell proliferation, migration, and invasion by targeting VEGFA. By dual luciferase reporter gene assay and miR-330-3p inhibitor treatment, we demonstrate that MALAT1 sponged miR-330-3p in GC, leading to VEGFA upregulation and activation of the mTOR signaling pathway. The MALAT1/miR-330-3p axis regulates VEGFA through the mTOR signaling pathway and promotes the growth and metastasis of gastric cancer.

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Se descubrió que la sobreexpresión del transcrito 1 de adenocarcinoma de pulmón asociado a metástasis (MALAT1) en varios tejidos tumorales y líneas celulares promueve la proliferación, migración e invasión de células tumorales. Sin embargo, el papel de MALAT1 en el cáncer gástrico (CG) aún no está claro. Nuestro objetivo fue investigar la correlación entre los ARN no codificantes de cadena larga (lncRNA), MALAT1, los microARN (miARN) y el factor de crecimiento endotelial vascular A (VEGFA) en el cáncer gástrico y revelar el mecanismo subyacente. La correlación entre los niveles de MALAT1 y las características clínicas se analizó mediante datos bioinformáticos y muestras humanas. La expresión de MALAT1 se reguló negativamente en las células AGS para detectar las características de proliferación, migración e invasión celular, así como los efectos sobre las vías de señales. Además, validamos el papel del eje MALAT1/miR- 330-3p en GC mediante ensayos de genes indicadores de luciferasa dual. La expresión de MALAT1 fue mayor en tejidos cancerosos que en tejidos paracancerosos. El alto nivel de MALAT1 predijo malignidad y peor pronóstico. La regulación negativa de la expresión de MALAT1 en células AGS inhibió la proliferación, migración e invasión celular al apuntar a VEGFA. Mediante un ensayo de gen indicador de luciferasa dual y un tratamiento con inhibidor de miR-330-3p, demostramos que MALAT1 esponjaba miR-330-3p en GC, lo que lleva a la regulación positiva de VEGFA y la activación de la vía de señalización mTOR. El eje MALAT1/miR-330-3p regula VEGFA a través de la vía de señalización mTOR y promueve el crecimiento y la metástasis del cáncer gástrico.

Asunto(s)

Humanos , Neoplasias Gástricas/genética , Neoplasias Gástricas/patología , Factor A de Crecimiento Endotelial Vascular , Serina-Treonina Quinasas TOR , ARN Largo no Codificante , ARN/genética , Transducción de Señal , Regulación Neoplásica de la Expresión Génica , Movimiento Celular , Western Blotting , Apoptosis , Genes Reporteros , Proliferación Celular , Reacción en Cadena en Tiempo Real de la Polimerasa , Invasividad Neoplásica

RESUMEN

OBJECTIVE: The purpose of this study is to investigate the pathogenic role of PPARα in periodontal antigen treated gingival cells in vitro and in experimental periodontitis in vivo . METHODOLOGY: Gingival fibroblasts, gingival epithelial cells and splenocytes were isolated from C57BL/6J wild type (WT) mice and treated with fixed P. gingivalis at for 48 hours. The mRNA levels of PPARs, TNFα, IL-1ß and IL-10 were detected by Real-time quantitative PCR. Silk ligatures after being soaked in the P.gingivalis suspension were tied around both maxillary second molars of WT mice or PPARα knock-out (KO) mice for two weeks. PPARα agonist fenofibrate and vehicle control were injected into the different side of the palatal gingiva on days 3, 6, and 9. At day 14, bone resorption and gingival mRNA expression levels of PPARs, TNFα, IL-1ß and IL-10 were measured by micro-computed tomography and RT-qPCR respectively. RESULTS: P. gingivalis treatment downregulated the expression of PPARα, but not PPARß or PPARγ, and increased the expression of TNF-α and IL-1ß in Gingival fibroblasts, gingival epithelial cells and splenocytes from WT mice. Gingival mRNA levels of PPARα were significantly decreased in experimental periodontitis in WT mice. The bone loss of PPARα KO mice in experimental periodontitis was significantly higher than WT mice and was not reduced by fenofibrate treatment. Gingival TNFα protein expressions were significantly increased by P. gingivalis associated ligation and decreased by fenofibrate treatment in WT mice but not in PPARα KO mice. CONCLUSION: This study suggests that PPARα plays an essential role in periodontitis.

Asunto(s)

Pérdida de Hueso Alveolar , Fenofibrato , PPAR alfa , Periodontitis , Pérdida de Hueso Alveolar/patología , Animales , Fenofibrato/farmacología , Encía/patología , Interleucina-10/metabolismo , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , PPAR alfa/metabolismo , Periodontitis/metabolismo , Periodontitis/patología , Porphyromonas gingivalis/metabolismo , ARN Mensajero/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Microtomografía por Rayos X

RESUMEN

OBJECTIVE: Inflammation-related immune responses and bone metabolism lead to extensive tooth loss in periodontitis.. This study aims to investigate the effect of peroxisome proliferator-activated receptor (PPAR) alpha agonist anti-inflammatory treatment in vitro and in ligature-induced experimental periodontitis in vivo . METHODOLOGY: Splenocytes were isolated from C57BL/6J mice and cultured for 48 hours under the following conditions: control, P. gingivalis lipopolysaccharide (LPS) (1 µg/ml); experimental, LPS (1 µg/ml) + PPARα agonist (fenofibrate) at 1, 10, 50, 100 µM. MRNA and secreted protein levels of TNF-α expression were detected by RT-qPCR and ELISA, respectively. Silk ligatures (7-0) were tied around maxillary second molars of C57BL/6J mice for two weeks. Optimized doses of fenofibrate (50 µM) and vehicle control were injected into the contralateral side of the palatal gingiva on days three, six, and nine. At day 14, bone resorption, osteoclastogenesis, and gingival mRNA expression levels of TNF-α, IL-1ß, IL-6, and RANKL/OPG were measured by micro-computed tomography, Tartrate-resistant acid phosphatase (TRAP) staining, and Real-time quantitative PCR, respectively. RESULTS: TNF-α expression in cultured spleen cells were significantly increased in the presence of LPS, when compared with the control group, and significantly reduced by fenofibrate treatment in a dose-dependent manner from 1-100 µM (p<0.05). Gingival mRNA levels of TNF-α, IL-1ß, IL-6, and the ratio of RANKL/OPG, were significantly decreased after injection of fenofibrate, when compared to the control side (p<0.05). Periodontal bone loss and TRAP positive cell formation were significantly decreased on the side with an injection of fenofibrate, as compared to the control side (p<0.05). CONCLUSIONS: An anti-inflammatory treatment, PPARα agonist, inhibited inflammation and periodontal bone loss in ligature-induced experimental periodontitis.

Asunto(s)

Pérdida de Hueso Alveolar , Periodontitis , Pérdida de Hueso Alveolar/tratamiento farmacológico , Pérdida de Hueso Alveolar/prevención & control , Animales , Ratones , Ratones Endogámicos C57BL , PPAR alfa/uso terapéutico , Periodontitis/tratamiento farmacológico , Periodontitis/metabolismo , Microtomografía por Rayos X

RESUMEN

Pseudomonas aeruginosa (P. aeruginosa), a ubiquitous opportunistic pathogen, can frequently cause chronic obstructive pulmonary disease, cystic fibrosis and chronic wounds, and potentially lead to severe morbidity and mortality. Timely and adequate treatment of nosocomial infection in clinic depends on rapid detection and accurate identification of P. aeruginosa and its early-stage antibiotic susceptibility test. Traditional methods like plating culture, polymerase chain reaction, and enzyme-linked immune sorbent assays are time-consuming and require expensive equipment, limiting the rapid diagnostic application. Advanced sensing strategy capable of fast, sensitive and simple detection with low cost has therefore become highly desired in point of care testing (POCT) of nosocomial pathogens. Within this review, advanced detection and sensing strategies for P. aeruginosa cells along with associated quorum sensing (QS) molecules over the last ten years are discussed and summarized. Firstly, the principles of four commonly used sensing strategies including localized surface plasmon resonance (LSPR), surface-enhanced Raman spectroscopy (SERS), electrochemistry, and fluorescence are briefly overviewed. Then, the advancement of the above sensing techniques for P. aeruginosa cells and its QS biomarkers detection are introduced, respectively. In addition, the integration with novel compatible platforms towards clinical application is highlighted in each section. Finally, the current achievements are summarized along with proposed challenges and prospects.

Asunto(s)

Infecciones por Pseudomonas , Pseudomonas aeruginosa , Antibacterianos , Proteínas Bacterianas , Biomarcadores , Humanos , Infecciones por Pseudomonas/diagnóstico , Percepción de Quorum

RESUMEN

To investigate the cross-linking degree on the in vitro gastrointestinal digestion and absorption properties of surimi gel, three types of surimi gels with low, moderate, and high cross-linking degrees were prepared, and then in vitro digestion models (static and dynamic) and a Caco-2 cell monolayer model combined with LC-MS/MS were used to do peptidomic analysis of digestive and absorbed juices. The results showed that an increase in cross-linking degree promoted the release of peptides after gastrointestinal digestion. These peptides originated from the myosin head and rod, the rod was the main digestion region. More potential bioactive peptides from intestinal digestive juice could be transported through the intestinal epithelium. Compared with static digestion, dynamic digestion digested surimi gels more thoroughly, especially during gastric digestion. This study provides a theoretical basis and guidance for the production of surimi products with higher nutritional value and the in vitro digestion methods of gelatinous foods.

Asunto(s)

Productos Pesqueros , Espectrometría de Masas en Tándem , Células CACO-2 , Cromatografía Liquida , Digestión , Productos Pesqueros/análisis , Geles , Humanos

RESUMEN

Abstract Inflammation-related immune responses and bone metabolism lead to extensive tooth loss in periodontitis. Objective: This study aims to investigate the effect of peroxisome proliferator-activated receptor (PPAR) alpha agonist anti-inflammatory treatment in vitro and in ligature-induced experimental periodontitis in vivo . Methodology: Splenocytes were isolated from C57BL/6J mice and cultured for 48 hours under the following conditions: control, P. gingivalis lipopolysaccharide (LPS) (1 µg/ml); experimental, LPS (1 µg/ml) + PPARα agonist (fenofibrate) at 1, 10, 50, 100 µM. MRNA and secreted protein levels of TNF-α expression were detected by RT-qPCR and ELISA, respectively. Silk ligatures (7-0) were tied around maxillary second molars of C57BL/6J mice for two weeks. Optimized doses of fenofibrate (50 µM) and vehicle control were injected into the contralateral side of the palatal gingiva on days three, six, and nine. At day 14, bone resorption, osteoclastogenesis, and gingival mRNA expression levels of TNF-α, IL-1β, IL-6, and RANKL/OPG were measured by micro-computed tomography, Tartrate-resistant acid phosphatase (TRAP) staining, and Real-time quantitative PCR, respectively. Results: TNF-α expression in cultured spleen cells were significantly increased in the presence of LPS, when compared with the control group, and significantly reduced by fenofibrate treatment in a dose-dependent manner from 1-100 µM (p<0.05). Gingival mRNA levels of TNF-α, IL-1β, IL-6, and the ratio of RANKL/OPG, were significantly decreased after injection of fenofibrate, when compared to the control side (p<0.05). Periodontal bone loss and TRAP positive cell formation were significantly decreased on the side with an injection of fenofibrate, as compared to the control side (p<0.05). Conclusions: An anti-inflammatory treatment, PPARα agonist, inhibited inflammation and periodontal bone loss in ligature-induced experimental periodontitis.

RESUMEN

Abstract Objective The purpose of this study is to investigate the pathogenic role of PPARα in periodontal antigen treated gingival cells in vitro and in experimental periodontitis in vivo . Methodology Gingival fibroblasts, gingival epithelial cells and splenocytes were isolated from C57BL/6J wild type (WT) mice and treated with fixed P. gingivalis at for 48 hours. The mRNA levels of PPARs, TNFα, IL-1β and IL-10 were detected by Real-time quantitative PCR. Silk ligatures after being soaked in the P.gingivalis suspension were tied around both maxillary second molars of WT mice or PPARα knock-out (KO) mice for two weeks. PPARα agonist fenofibrate and vehicle control were injected into the different side of the palatal gingiva on days 3, 6, and 9. At day 14, bone resorption and gingival mRNA expression levels of PPARs, TNFα, IL-1β and IL-10 were measured by micro-computed tomography and RT-qPCR respectively. Results P. gingivalis treatment downregulated the expression of PPARα, but not PPARβ or PPARγ, and increased the expression of TNF-α and IL-1β in Gingival fibroblasts, gingival epithelial cells and splenocytes from WT mice. Gingival mRNA levels of PPARα were significantly decreased in experimental periodontitis in WT mice. The bone loss of PPARα KO mice in experimental periodontitis was significantly higher than WT mice and was not reduced by fenofibrate treatment. Gingival TNFα protein expressions were significantly increased by P. gingivalis associated ligation and decreased by fenofibrate treatment in WT mice but not in PPARα KO mice. Conclusion This study suggests that PPARα plays an essential role in periodontitis.

RESUMEN

Small-bowel bleeding is a relatively uncommon event of gastrointestinal bleeding. Some causes of small-bowel bleeding, such as vascular lesions, are still challenging to confirm, despite the use of various diagnostic modalities (e.g., capsule endoscopy, deep enteroscopy, and radiographic imaging). Vascular lesion-induced bleeding tends to be insidious and intermittent, but sometimes it can be massive and fatal, so that the timing of an endoscopy is critical. We describe herein the case of an elderly female patient with Dieulafoy's lesion-induced small-bowel bleeding presenting with recurrent melena. In this article, we describe how the cause of her bleeding was found and how the bleeding was stopped endoscopically. Finally, we discuss the characteristics of a small-bowel Dieulafoy's lesion and its endoscopic treatment.

Asunto(s)

Endoscopía Capsular , Hemorragia Gastrointestinal/etiología , Mucosa Intestinal/irrigación sanguínea , Anciano , Arterias/anomalías , Endoscopía Gastrointestinal , Femenino , Hemorragia Gastrointestinal/cirugía , Hemostasis Endoscópica , Humanos , Mucosa Intestinal/cirugía , Melena/etiología , Recurrencia

RESUMEN

OBJECTIVE: To investigate the risk factors for orthostatic hypertension in children. STUDY DESIGN: Eighty children with orthostatic hypertension were enrolled in the group with orthostatic hypertension, and 51 healthy children served as the control group. Demographic characteristics, clinical history, daily water intake, nightly sleep duration, the results of the standing test, and complete blood count were recorded and compared between the 2 groups. The risk factors for pediatric orthostatic hypertension were determined by logistic regression analysis. RESULTS: Body mass index and red blood cell distribution width were higher in the group with orthostatic hypertension than in healthy children, whereas daily water intake and sleep duration were lower. Logistic regression analyses showed that, if a child suffered from overweight, suffered from obesity, had a daily water intake of less than 800 mL, or had a red blood cell distribution width that was increased by 1%, the risk of orthostatic hypertension would be increased by 6.069 times (95% CI, 1.375-26.783; P < .05), 7.482 times (95% CI, 1.835-30.515; P < .01), 4.027 times (95% CI, 1.443-11.241; P < .01), or 4.008 times (95% CI, 1.698-9.461; P < .01), respectively. However, if the sleep duration was increased by 1 hour, the risk of developing orthostatic hypertension would be decreased by 74.3% (95% CI, 54.6%-85.4%, P < .01). CONCLUSIONS: Increased body mass index, inadequate water intake and sleep duration, and elevated red blood cell distribution width were identified as risk factors for pediatric orthostatic hypertension.

Asunto(s)

Hipertensión/epidemiología , Hipertensión/etiología , Adolescente , Niño , Femenino , Humanos , Masculino , Factores de Riesgo , Posición de Pie

RESUMEN

Local administration of toll-like receptor 9 (TLR9), agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG ODNs), and CD40 ligand (CD40L) can decrease ligature-induced periodontal inflammation and bone loss in wild type (WT) mouse. OBJECTIVE: This study aimed to explore whether such effect is dependent on TLR9 signaling. MATERIAL AND METHODS: Purified spleen B cells isolated from WT C57BL/6J mice and TLR9 knockout (KO) mice were cultured for 48 hours under the following conditions: CD40L, CpG+CD40L, CpG at low, medium and high doses. We determined B cell numbers using a hemocytometer at 24 h and 48 h. Percentages of CD1dhiCD5+ B cells were detected by flow cytometry. Interleukin-10 (IL-10) mRNA expression and protein secretion were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and by ELISA, respectively. The silk ligature was tied around the maxillary second molars for 14 days, during which the CpG+CD40L mixture or PBS was injected into palatal gingiva on days 3, 6, and 9. RESULTS: For both WT and TLR9 KO mice, CpG significantly induced B cell proliferation, increased IL-10 mRNA expression and protein secretion of IL-10 but reduced CD1dhiCD5+ B cells population; local injection of CpG+CD40L mixture significantly decreased alveolar bone loss and the number of TRAP-positive cells adjacent to the alveolar bone surface, and significantly increased the gingival mRNA expression of IL-10 and decreased RANKL and IFN-γ mRNA expression. CONCLUSIONS: These results indicated that CpG plus CD40L decreased periodontal inflammation and alveolar bone loss in a TLR9-independent manner in ligature-induced experimental periodontitis.

Asunto(s)

Pérdida de Hueso Alveolar/tratamiento farmacológico , Ligando de CD40/farmacología , Citidina/farmacología , Nucleótidos de Guanina/farmacología , Oligodesoxirribonucleótidos/farmacología , Periodontitis/tratamiento farmacológico , Receptor Toll-Like 9/efectos de los fármacos , Adyuvantes Inmunológicos/farmacología , Animales , Linfocitos B/efectos de los fármacos , Células Cultivadas , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Citometría de Flujo , Encía/efectos de los fármacos , Encía/patología , Interleucina-10/análisis , Ratones Endogámicos C57BL , Reacción en Cadena en Tiempo Real de la Polimerasa , Valores de Referencia , Reproducibilidad de los Resultados , Factores de Tiempo , Receptor Toll-Like 9/análisis

RESUMEN

Abstract Local administration of toll-like receptor 9 (TLR9), agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG ODNs), and CD40 ligand (CD40L) can decrease ligature-induced periodontal inflammation and bone loss in wild type (WT) mouse. Objective: This study aimed to explore whether such effect is dependent on TLR9 signaling. Material and Methods: Purified spleen B cells isolated from WT C57BL/6J mice and TLR9 knockout (KO) mice were cultured for 48 hours under the following conditions: CD40L, CpG+CD40L, CpG at low, medium and high doses. We determined B cell numbers using a hemocytometer at 24 h and 48 h. Percentages of CD1dhiCD5+ B cells were detected by flow cytometry. Interleukin-10 (IL-10) mRNA expression and protein secretion were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and by ELISA, respectively. The silk ligature was tied around the maxillary second molars for 14 days, during which the CpG+CD40L mixture or PBS was injected into palatal gingiva on days 3, 6, and 9. Results: For both WT and TLR9 KO mice, CpG significantly induced B cell proliferation, increased IL-10 mRNA expression and protein secretion of IL-10 but reduced CD1dhiCD5+ B cells population; local injection of CpG+CD40L mixture significantly decreased alveolar bone loss and the number of TRAP-positive cells adjacent to the alveolar bone surface, and significantly increased the gingival mRNA expression of IL-10 and decreased RANKL and IFN-γ mRNA expression. Conclusions: These results indicated that CpG plus CD40L decreased periodontal inflammation and alveolar bone loss in a TLR9-independent manner in ligature-induced experimental periodontitis.

Asunto(s)

Animales , Oligodesoxirribonucleótidos/farmacología , Periodontitis/tratamiento farmacológico , Pérdida de Hueso Alveolar/tratamiento farmacológico , Ligando de CD40/farmacología , Citidina/farmacología , Receptor Toll-Like 9/efectos de los fármacos , Nucleótidos de Guanina/farmacología , Valores de Referencia , Factores de Tiempo , Ensayo de Inmunoadsorción Enzimática , Linfocitos B/efectos de los fármacos , Células Cultivadas , Adyuvantes Inmunológicos/farmacología , Reproducibilidad de los Resultados , Interleucina-10/análisis , Modelos Animales de Enfermedad , Receptor Toll-Like 9/análisis , Reacción en Cadena en Tiempo Real de la Polimerasa , Citometría de Flujo , Encía/efectos de los fármacos , Encía/patología , Ratones Endogámicos C57BL

RESUMEN

This study was conducted to investigate the roles of different Toll-like receptor (TLR) signaling in Porphyromonas gingivalis (P. gingivalis)-induced and ligature-induced experimental periodontal bone resorption in mice. Wild-type (WT), TLR2 knockout (KO), TLR4KO, and TLR2&4 KO mice with C57/BL6 background were divided into three groups: control, P. gingivalis infection, and ligation. Live P. gingivalis or silk ligatures were placed in the sulcus around maxillary second molars over a 2-week period. Images were captured by digital stereomicroscopy, and the bone resorption area was measured with ImageJ software. The protein expression level of gingival RANKL was measured by ELISA. The gingival mRNA levels of RANKL, IL-1ß, TNF-α, and IL-10 were detected by RT-qPCR. The results showed that P. gingivalis induced significant periodontal bone resorption in WT mice and TLR2 KO mice but not in TLR4 KO mice or TLR2&4 KO mice. For all four types of mice, ligation induced significant bone loss compared with that in control groups, and this bone loss was significantly higher than that in the P. gingivalis infection group. RANKL protein expression was significantly increased in the ligation group compared with that in the control group for all four types of mice, and in the P. gingivalis infection group of WT, TLR2 KO, and TLR4 KO mice. Expression patterns of RANKL, IL-1ß, TNF-α, and IL-10 mRNA were different in the P. gingivalis infection group and the ligation group in different types of mice. In summary, P. gingivalis-induced periodontal bone resorption is TLR4-dependent, whereas ligation-induced periodontal bone resorption is neither TLR2- nor TLR4-dependent.

Asunto(s)

Pérdida de Hueso Alveolar/etiología , Modelos Animales de Enfermedad , Periodontitis/microbiología , Porphyromonas gingivalis/patogenicidad , Receptor Toll-Like 2/fisiología , Receptor Toll-Like 4/fisiología , Pérdida de Hueso Alveolar/microbiología , Animales , Ensayo de Inmunoadsorción Enzimática , Interleucina-10/metabolismo , Interleucina-1beta/metabolismo , Ligadura , Ratones Endogámicos C57BL , Ratones Noqueados , Reacción en Cadena en Tiempo Real de la Polimerasa , Receptor Activador del Factor Nuclear kappa-B/metabolismo , Reproducibilidad de los Resultados , Factores de Tiempo , Receptor Toll-Like 2/análisis , Receptor Toll-Like 2/genética , Receptor Toll-Like 4/análisis , Receptor Toll-Like 4/genética , Factor de Necrosis Tumoral alfa/metabolismo

RESUMEN

OBJECTIVES:: To investigate the association between diastolic function and the different beneficial effects of cardiac resynchronization therapy in patients with heart failure due to different causes. METHODS:: The 104 enrolled patients were divided into an ischemic cardiomyopathy group (n=27) and a non-ischemic cardiomyopathy group (n=77) according to the cause of heart failure. Before implantation, left ventricular diastolic function was evaluated in all patients using echocardiography. After six months of follow-up, the beneficial effects of cardiac resynchronization therapy were evaluated using a combination of clinical symptoms and echocardiography parameters. RESULTS:: The ischemic cardiomyopathy group included significantly more patients with restrictive filling than the non-ischemic cardiomyopathy group. The response rate after the implantation procedure was significantly higher in the non-ischemic cardiomyopathy group than in the ischemic cardiomyopathy group. Degrees of improvement in echocardiography parameters were significantly greater in the non-ischemic cardiomyopathy group than in the ischemic cardiomyopathy group. Multivariate regression analysis showed that a restrictive filling pattern was an independent factor that influenced responses to cardiac resynchronization therapy. CONCLUSIONS:: This study again confirmed that the etiology of heart failure affects the beneficial effects of cardiac resynchronization therapy and a lower degree of improvement in ventricular systolic function and remodelling was observed in ischemic cardiomyopathy patients than in non-ischemic cardiomyopathy patients. In addition, systolic heart failure patients with severe diastolic dysfunction had poor responses to cardiac resynchronization therapy. Ischemic cardiomyopathy patients exhibited more severe diastolic dysfunction than non-ischemic cardiomyopathy patients, which may be a reason for the reduced beneficial effect of cardiac resynchronization therapy.

Asunto(s)

Terapia de Resincronización Cardíaca , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/terapia , Isquemia Miocárdica/fisiopatología , Isquemia Miocárdica/terapia , Diástole/fisiología , Femenino , Insuficiencia Cardíaca/etiología , Humanos , Masculino , Persona de Mediana Edad , Isquemia Miocárdica/complicaciones

RESUMEN

OBJECTIVES: To investigate the association between diastolic function and the different beneficial effects of cardiac resynchronization therapy in patients with heart failure due to different causes. METHODS: The 104 enrolled patients were divided into an ischemic cardiomyopathy group (n=27) and a non-ischemic cardiomyopathy group (n=77) according to the cause of heart failure. Before implantation, left ventricular diastolic function was evaluated in all patients using echocardiography. After six months of follow-up, the beneficial effects of cardiac resynchronization therapy were evaluated using a combination of clinical symptoms and echocardiography parameters. RESULTS: The ischemic cardiomyopathy group included significantly more patients with restrictive filling than the non-ischemic cardiomyopathy group. The response rate after the implantation procedure was significantly higher in the non-ischemic cardiomyopathy group than in the ischemic cardiomyopathy group. Degrees of improvement in echocardiography parameters were significantly greater in the non-ischemic cardiomyopathy group than in the ischemic cardiomyopathy group. Multivariate regression analysis showed that a restrictive filling pattern was an independent factor that influenced responses to cardiac resynchronization therapy. CONCLUSIONS: This study again confirmed that the etiology of heart failure affects the beneficial effects of cardiac resynchronization therapy and a lower degree of improvement in ventricular systolic function and remodelling was observed in ischemic cardiomyopathy patients than in non-ischemic cardiomyopathy patients. In addition, systolic heart failure patients with severe diastolic dysfunction had poor responses to cardiac resynchronization therapy. Ischemic cardiomyopathy patients exhibited more severe diastolic dysfunction than non-ischemic cardiomyopathy patients, which may be a reason for the reduced beneficial effect of cardiac resynchronization therapy.

Asunto(s)

Humanos , Masculino , Femenino , Persona de Mediana Edad , Terapia de Resincronización Cardíaca , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/terapia , Isquemia Miocárdica/fisiopatología , Isquemia Miocárdica/terapia , Diástole/fisiología , Insuficiencia Cardíaca/etiología , Isquemia Miocárdica/complicaciones

RESUMEN

OBJECTIVE: This study is to determine the effects of P. gingivalis LPS and CpG on B10 cell expansion and IL-10 competency in vitro. MATERIAL AND METHODS: Spleen B cells were isolated from C57BL/6J mice with or without formalin-fixed P. gingivalis immunization. B cells were cultured for 48 hours under the following conditions: CD40L, CD40L+LPS, CD40L+CpG, and CD40L+LPS+CpG in the presence or absence of fixed P. gingivalis. Percentages of CD1dhiCD5+ B cells were measured by flow cytometry. IL-10 mRNA expression and secreted IL-10 were measured by real-time quantitative PCR and by ELISA respectively. RESULTS: P. gingivalis LPS plus CD40L significantly increased CD1dhiCD5+ B cell percentages and secreted IL-10 levels in both immunized and non-immunized mice B cells in the presence or absence of P. gingivalis, compared with control group. Secreted IL-10 levels were significantly increased in CD40L+LPS treated group compared with CD40L treatment group in the absence of P. gingivalis. CpG plus CD40L significantly decreased CD1dhiCD5+ B cell percentages, but greatly elevated secreted IL-10 levels in immunized and non-immunized mice B cells in the absence of P. gingivalis, compared with CD40L treatment group. CONCLUSIONS: P. gingivalis LPS and CpG differentially enhance IL-10 secretion and expansion of mouse B10 cells during innate and adaptive immune responses.

Asunto(s)

Linfocitos B Reguladores/inmunología , Ligando de CD40/fisiología , Interleucina-10/inmunología , Lipopolisacáridos/fisiología , Porphyromonas gingivalis/fisiología , Receptor Toll-Like 4/agonistas , Receptor Toll-Like 9/agonistas , Animales , Células Cultivadas , Ensayo de Inmunoadsorción Enzimática , Inmunidad Innata , Interleucina-10/análisis , Interleucina-10/metabolismo , Ratones Endogámicos C57BL , ARN Mensajero/análisis , Distribución Aleatoria , Reacción en Cadena en Tiempo Real de la Polimerasa , Bazo/citología , Factores de Tiempo , Receptor Toll-Like 4/fisiología , Receptor Toll-Like 9/fisiología

RESUMEN

Abstract IL-10 expressing regulatory B cells (B10) play a key role in immune system balance by limiting excessive inflammatory responses. Effects of toll-like receptor signaling and co-stimulatory molecules on B10 activity during innate and adaptive immune responses are not fully understood. Objective This study is to determine the effects of P. gingivalis LPS and CpG on B10 cell expansion and IL-10 competency in vitro. Material and Methods Spleen B cells were isolated from C57BL/6J mice with or without formalin-fixed P. gingivalis immunization. B cells were cultured for 48 hours under the following conditions: CD40L, CD40L+LPS, CD40L+CpG, and CD40L+LPS+CpG in the presence or absence of fixed P. gingivalis. Percentages of CD1dhiCD5+ B cells were measured by flow cytometry. IL-10 mRNA expression and secreted IL-10 were measured by real-time quantitative PCR and by ELISA respectively. Results P. gingivalis LPS plus CD40L significantly increased CD1dhiCD5+ B cell percentages and secreted IL-10 levels in both immunized and non-immunized mice B cells in the presence or absence of P. gingivalis, compared with control group. Secreted IL-10 levels were significantly increased in CD40L+LPS treated group compared with CD40L treatment group in the absence of P. gingivalis. CpG plus CD40L significantly decreased CD1dhiCD5+ B cell percentages, but greatly elevated secreted IL-10 levels in immunized and non-immunized mice B cells in the absence of P. gingivalis, compared with CD40L treatment group. Conclusions P. gingivalis LPS and CpG differentially enhance IL-10 secretion and expansion of mouse B10 cells during innate and adaptive immune responses.

Asunto(s)

Animales , Lipopolisacáridos/fisiología , Interleucina-10/inmunología , Porphyromonas gingivalis/fisiología , Ligando de CD40/fisiología , Receptor Toll-Like 9/agonistas , Receptor Toll-Like 4/agonistas , Linfocitos B Reguladores/inmunología , Bazo/citología , Factores de Tiempo , ARN Mensajero/análisis , Ensayo de Inmunoadsorción Enzimática , Distribución Aleatoria , Células Cultivadas , Interleucina-10/análisis , Interleucina-10 , Receptor Toll-Like 9/fisiología , Receptor Toll-Like 4/fisiología , Reacción en Cadena en Tiempo Real de la Polimerasa , Inmunidad Innata , Ratones Endogámicos C57BL

RESUMEN

Abstract This study was conducted to investigate the roles of different Toll-like receptor (TLR) signaling in Porphyromonas gingivalis (P. gingivalis)-induced and ligature-induced experimental periodontal bone resorption in mice. Wild-type (WT), TLR2 knockout (KO), TLR4KO, and TLR2&4 KO mice with C57/BL6 background were divided into three groups: control, P. gingivalis infection, and ligation. Live P. gingivalis or silk ligatures were placed in the sulcus around maxillary second molars over a 2-week period. Images were captured by digital stereomicroscopy, and the bone resorption area was measured with ImageJ software. The protein expression level of gingival RANKL was measured by ELISA. The gingival mRNA levels of RANKL, IL-1β, TNF-α, and IL-10 were detected by RT-qPCR. The results showed that P. gingivalis induced significant periodontal bone resorption in WT mice and TLR2 KO mice but not in TLR4 KO mice or TLR2&4 KO mice. For all four types of mice, ligation induced significant bone loss compared with that in control groups, and this bone loss was significantly higher than that in the P. gingivalis infection group. RANKL protein expression was significantly increased in the ligation group compared with that in the control group for all four types of mice, and in the P. gingivalis infection group of WT, TLR2 KO, and TLR4 KO mice. Expression patterns of RANKL, IL-1β, TNF-α, and IL-10 mRNA were different in the P. gingivalis infection group and the ligation group in different types of mice. In summary, P. gingivalis-induced periodontal bone resorption is TLR4-dependent, whereas ligation-induced periodontal bone resorption is neither TLR2- nor TLR4-dependent.

Asunto(s)

Animales , Periodontitis/microbiología , Pérdida de Hueso Alveolar/etiología , Porphyromonas gingivalis/patogenicidad , Modelos Animales de Enfermedad , Receptor Toll-Like 2/fisiología , Receptor Toll-Like 2/genética , Receptor Toll-Like 4/fisiología , Factores de Tiempo , Ensayo de Inmunoadsorción Enzimática , Reproducibilidad de los Resultados , Pérdida de Hueso Alveolar/microbiología , Factor de Necrosis Tumoral alfa/metabolismo , Interleucina-10/metabolismo , Ratones Noqueados , Receptor Toll-Like 2/análisis , Receptor Toll-Like 4/análisis , Receptor Toll-Like 4/genética , Interleucina-1beta/metabolismo , Receptor Activador del Factor Nuclear kappa-B/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Ligadura , Metabolismo , Ratones Endogámicos C57BL

RESUMEN

The relationship between the defects of reduced graphene oxide (RGO) and the oxidation degree of graphite in the preparation of graphene with chemical conversion method has been studied in this work. This study was performed on an artificial graphite through the measurements of X ray diffraction, Raman spectroscopy and particle size analysis. The experimental results have shown that there indeed was a close relationship between the defects and the oxidation degree, which appeared in the form of S-type curve. Also, it was found that a low KMnO4 addition would lead to a partial oxidation of graphite, leaving defects mainly on the edges of RGO; with a high KMnO4 addition, the defects on RGO mostly appeared on the surfaces.