RESUMEN
PURPOSE: This study aimed at investigating the efficacy of percutaneous transhepatic biliary stenting (PTBS) combined with 125I seeds intracavitary irradiation in the treatment of extrahepatic cholangiocarcinoma (EHC) and to preliminarily explore the prognostic values of inflammation-based scores in these patients. METHODS: A total of 113 clinically/pathologically diagnosed cases of EHC who received PTBS combined with 125I seeds implantation were retrospectively analyzed. The postoperative changes of clinical symptoms and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total serum bilirubin (TBIL), direct bilirubin (DBIL), and albumin (ALB) were observed. Preoperative clinical data were extracted to calculate inflammation-based scores, including systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), and platelets-to-lymphocyte ratio (PLR). Kaplan-Meier survival curves and Cox regression analyses were used to evaluate the prognostic significance of inflammation-based scores. RESULTS: After operation, clinical symptoms such as jaundice and fever significantly improved in all patients. At 1 month and 3 months postoperatively, serum levels of ALT, AST, ALP, TBIL, and DBIL significantly reduced, and ALB significantly increased, compared with preoperative values. The median survival time of the patients was 12 months and the 1-year survival rate was 56.8%. Univariate analysis revealed that factors related to overall survival were CA19-9, TBIL, ALB, SII, and NLR. Multivariate analysis further identified SII and NLR as independent prognostic models. CONCLUSION: The combination of PTBS and 125I seeds intracavitary irradiation is an effective palliative treatment for advanced EHC. Elevated SII and NLR can be used to predict poor survival.
Asunto(s)
Neoplasias de los Conductos Biliares/mortalidad , Procedimientos Quirúrgicos del Sistema Biliar/mortalidad , Colangiocarcinoma/mortalidad , Mediadores de Inflamación/metabolismo , Inflamación/diagnóstico , Radioisótopos de Yodo/uso terapéutico , Stents , Anciano , Neoplasias de los Conductos Biliares/metabolismo , Neoplasias de los Conductos Biliares/patología , Neoplasias de los Conductos Biliares/terapia , Colangiocarcinoma/metabolismo , Colangiocarcinoma/patología , Colangiocarcinoma/terapia , Terapia Combinada , Femenino , Estudios de Seguimiento , Humanos , Inflamación/inmunología , Inflamación/metabolismo , Masculino , Siembra Neoplásica , Pronóstico , Estudios Retrospectivos , Tasa de SupervivenciaRESUMEN
Myocardial ischemia is a major cause of death and remains a disease with extremely deficient clinical therapies and a major problem worldwide. Cold inducible RNA-binding protein (CIRBP) is reported to be involved in multiple pathological processes, including myocardial ischemia. However, the molecular mechanisms of myocardial ischemia remain elusive. Here, we first overexpressed CIRBP by transfection of pc-CIRBP (pcDNA3.1 containing coding sequenced for CIRBP) and silenced CIRBP by transfection of small interfering RNA targeting CIRBP (siCIRBP). pcDNA3.1 and the negative control of siCIRBP (siNC) were transfected into H9C2 cells to act as controls. We then constructed a cell model of myocardial ischemia through culturing cells in serum-free medium with hypoxia in H9C2 cells. Subsequently, AlamarBlue assay, flow cytometry and western blot analysis were used, respectively, to assess cell viability, reactive oxygen species (ROS) level and apoptosis, and expression levels of IκBα, p65 and Bcl-3. We demonstrated that CIRBP overexpression promoted cell proliferation (P<0.001), inhibited cell apoptosis (P<0.05), reduced ROS level (P<0.001), down-regulated phosphorylated levels of IκBα and p65 (P<0.01 or P<0.001), and up-regulated expression of Bcl-3 (P<0.001) in H9C2 cells with myocardial ischemia. The influence of CIRBP knockdown yielded opposite results. Our study revealed that CIRBP could protect H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.
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Isquemia Miocárdica/metabolismo , Isquemia Miocárdica/prevención & control , FN-kappa B/antagonistas & inhibidores , Sustancias Protectoras/farmacología , Proteínas de Unión al ARN/farmacología , Animales , Apoptosis/efectos de los fármacos , Western Blotting , Proliferación Celular/efectos de los fármacos , Supervivencia Celular , Células Cultivadas , Citometría de Flujo , Regulación de la Expresión Génica , FN-kappa B/metabolismo , ARN Interferente Pequeño , Proteínas de Unión al ARN/genética , Proteínas de Unión al ARN/metabolismo , Ratas , Especies Reactivas de Oxígeno/análisis , Reproducibilidad de los Resultados , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factores de Tiempo , Transfección/métodosRESUMEN
Chronic obstructive pulmonary disease (COPD) is a devastating lung disorder characterized by sustained airway flow restriction that is not fully reversible. The precise pathogenic mechanisms are unknown, but it is clear that cigarette smoking and chronic inflammatory stimulation are the major causes of COPD. Lung inflammation associated with COPD involves multiple cytokines, aggregation, and activation of neutrophils in the airway and lung tissue, and release of proteases and oxygen free radicals. In this study, a rat model of COPD was established by daily cigarette smoke exposure plus endotoxin treatment (the experimental group). Respiratory curves were recorded by the BL-420 biological signal collecting and processing system. Furthermore, the contents of inflammatory mediators, intercellular adhesion molecular (ICAM)-1 and interleukin (IL)-1ß, in bronchoalveolar lavage fluid (BALF) were determined by enzyme linked immunosorbent assay for experimental, smoke-exposed only (control), and untreated (blank) rat groups. Protein expression levels of ICAM-1 and IL-1ß in the lung tissue were also compared among groups by the immunohistochemical streptavidin-peroxidase method. The COPD model rats exhibited severe dyspnea and lung inflammation as evidenced by significantly prolonged expiratory duration, higher respiratory rate, elevated ICAM-1 and IL-1ß in BALF, and higher ICAM-1 and IL-1ß protein expression in lung tissue compared to control and blank group rats. Chronic cigarette smoke exposure plus endotoxin is a feasible and reliable model of COPD that recapitulates many clinical signs and pathogenic responses. ICAM-1 and IL-1ß upregulation are possible early contributors to COPD-associated inflammatory lung injury.
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Molécula 1 de Adhesión Intercelular/metabolismo , Interleucina-1beta/metabolismo , Lesión Pulmonar/metabolismo , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Animales , Líquido del Lavado Bronquioalveolar , Citocinas/metabolismo , Molécula 1 de Adhesión Intercelular/genética , Interleucina-1beta/genética , Lesión Pulmonar/genética , Lesión Pulmonar/patología , Modelos Animales , Enfermedad Pulmonar Obstructiva Crónica/genética , Enfermedad Pulmonar Obstructiva Crónica/patología , Ratas , Ratas Sprague-Dawley , Factor de Necrosis Tumoral alfa/metabolismo , Regulación hacia ArribaRESUMEN
In this study, we identified potential serum biomarkers for the diagnosis of active tuberculosis (TB) and screening for latent TB infections (LTBIs). Peripheral blood samples from 40 healthy individuals, 40 patients with TB, and 40 LTBI individuals were stimulated with the TB-specific antigens ESAT-6 and CFP-10. Human inflammatory cytokine arrays were used to detect the expression of inflammatory cytokines. Cytokines with significant changes were screened to construct a cytokine regulation network. The levels of the cytokines CCL1 (I-309), CXCL9 (MIG), IL-10, IL-6, CSF2, CSF3, IL-8, IL-1α, IL-7, TGF-ß1, CCL2, IL-2, IL-13, and TNFα were significantly upregulated in the active TB group. The levels of CCL3, IL-1ß, CCL8, IFNγ, and CXCL10 were significantly increased in the TB groups compared to those in the healthy control group. sTNF RII was upregulated in the LTBI group. CCL4 and MIP1d were significantly increased in all groups.The upregulated cytokines were mainly found in the IFNγ and IL-1α regulatory networks. Importantly, we found that CXCL10 (IP-10), CCL3, CCL8, and IL-1ß may be more suitable than IFNγ for active or latent TB infection screening. Furthermore, we found that levels of CCL1 (I-309), CXCL9 (MIG), IL-10, IL-6, CSF2, CSF3, IL-8, IL-1α, IL-7, TGF-ß1, CCL2, IL-2, and IL-13 after TB antigen stimulation may help distinguish between active and latent TB.
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Antígenos Bacterianos/inmunología , Citocinas/sangre , Mycobacterium tuberculosis/inmunología , Tuberculosis/sangre , Tuberculosis/inmunología , Adolescente , Adulto , Biomarcadores , Estudios de Casos y Controles , Niño , Femenino , Humanos , Tuberculosis Latente/sangre , Tuberculosis Latente/inmunología , Masculino , Tuberculosis/diagnóstico , Adulto JovenRESUMEN
The aim of this study was to examine the expression of macrophage migration-inhibitory factor (MIF) in duodenal ulcer epithelial cells and its relation to Helicobacter pylori (Hp) infection, and to discuss the pathogenic roles of MIF expression and Hp infection in duodenal ulcer. MIF protein and mRNA expression was examined in samples from patients with duodenal ulcer with and without Hp infection (N = 40 each, experimental group), and in normal duodenal bulb mucosal tissue (N = 40, control group) using immunohistochemistry and in situ hybridization. Patients without Hp infection received routine treatment, and treatment was provided to the patients positive for Hp to eradicate Hp infection. Hp and MIF expression levels before treatment and after the ulcer had been cured were compared. The positive rates of MIF protein and mRNA in patients with Hp infection before treatment were 67.5 and 65%, respectively, and were 18.9 and 21.6% in the 37 patients from whom Hp was eliminated. These were statistically different both before and after treatment compared with controls (P < 0.05). In the patients without Hp infection, the positive rates of MIF protein and mRNA expression before (45 and 47.5%, respectively) and after (32.5 and 30%) treatment were not significantly different (P > 0.05). The results of this study suggested that MIF is related to the development of duodenal ulcer, and that the presence of Hp is closely related with the expression of MIF in the duodenal mucosa and the development of duodenal ulcer.
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Úlcera Duodenal/etiología , Úlcera Duodenal/metabolismo , Infecciones por Helicobacter/complicaciones , Infecciones por Helicobacter/microbiología , Helicobacter pylori , Factores Inhibidores de la Migración de Macrófagos/metabolismo , Adulto , Anciano , Biopsia , Úlcera Duodenal/diagnóstico , Femenino , Expresión Génica , Infecciones por Helicobacter/tratamiento farmacológico , Humanos , Inmunohistoquímica , Hibridación in Situ , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patología , Factores Inhibidores de la Migración de Macrófagos/genética , Masculino , Persona de Mediana Edad , ARN Mensajero/genética , ARN Mensajero/metabolismo , Adulto JovenRESUMEN
We aimed to evaluate the effect of melatonin on myo-cardial cell oncosis in the myocardial ischemia/reperfusion injury rat, and the role of the mitochondrial permeability transition pore (MPTP) therein. Sprague Dawley rats (N = 60) were randomly divided into five groups of 12 rats each: control, ischemia/reperfusion (I/R), melatonin treatment (MT), melatonin treatment + atractyloside (MT+ATR), and atractyloside (ATR). We prepared the myocardial ischemia/reperfusion model by reperfusion after the left anterior descending coronary artery was ligated for 30 min. The MT rats were given a 10 mg/kg MT intra-venous injection immediately thereafter; the MT+ATR rats were also given a 5 mg/kg ATR intravenous injection 15 min before the ischemia; the ATR rats were given the ATR injection only. After 2-h re-perfusion, myocardial tissue was extracted, the infarction size was determined, and myocardial ultrastructures were observed using electron microscopy. The expression level of the preoncosis receptor (porimin), which can induce membrane injury, was determined by western blot; the nicotinamide adenine dinucleotide (NAD(+)) content was determined spectrophotometrically. The four treatment groups showed upregulat-ed expression of myocardial porimin, increased myocardial infarction size, and reduced NAD(+) content (P < 0.05). Compared with the I/R and MT+ATR groups, MT rats showed downregulated expression of myo-cardial porimin, reduced myocardial infarct size, and increased myo-cardial cell NAD(+) content (P < 0.05). The above indices between the ATR and MT+ATR groups were not significantly different (P > 0.05). Thus, MT might protect myocardial ischemia/reperfusion rats by inhibiting MPTP opening and reducing myocardial cell oncosis.
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Melatonina/farmacología , Proteínas de Transporte de Membrana Mitocondrial/metabolismo , Daño por Reperfusión Miocárdica/metabolismo , Daño por Reperfusión Miocárdica/patología , Miocardio/patología , Animales , Masculino , Poro de Transición de la Permeabilidad Mitocondrial , Infarto del Miocardio/metabolismo , Infarto del Miocardio/patología , Miocardio/ultraestructura , NAD/metabolismo , Ratas Sprague-Dawley , Receptores de Superficie Celular/metabolismoRESUMEN
Twenty-four microsatellite markers were isolated from the genomic DNA of Amomum tsaoko Crevost et Lemaire, an important economic plant in China, using the method fast isolation by AFLP of sequences containing repeats (FIASCO). Polymorphism within each locus was assessed in 60 individuals from three populations in Yunnan Province, China, and nine of them were polymorphic. The number of alleles per polymorphic locus was 2, and the expected and observed heterozygosities ranged from 0.224 to 0.513, and from 0.050 to 0.600, respectively. Among nine microsatellite markers with polymorphism, five showed significant deviation from Hardy-Weinberg equilibrium (P < 0.01), probably due to anthropic selection and short-cloning history in cultivation. No significant linkage disequilibrium was detected between loci in our analysis. These polymorphic microsatellite markers will facilitate further studies of gene flow, population structure, identification of cultivated variety, and evaluation of germplasm resources.