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Background To investigate changes of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in the acute phase of cardiogenic stroke in patients with atrial fibrillation (AF). Methods A total of 152 patients with nonvalvular persistent AF, 103 cardiogenic stroke patients with nonvalvular persistent AF, and 126 cases with noncardiogenic stroke were enrolled. Non-AF patients (n = 138) without stroke served as controls. The clinical data, biochemical indicators, and plasma levels of von Willebrand factor (vWF), TF, and TFPI were determined. Results Compared with controls, the plasma levels of vWF and TF were significantly higher, while TFPI and TFPI/TF ratio were lower in noncardiogenic stroke patients (all P < 0.05). Compared with cardiogenic stroke patients, noncardiogenic stroke subjects showed significantly higher plasma vWF and TF levels while TFPI levels and TFPI/TF ratio were significantly lower (all P < 0.05). Compared with AF patients, plasma levels of vWF, TF, and TFPI were higher while TFPI/TF ratios were decreased in the cardiogenic ischemic stroke subjects (all P < 0.05). Logistic regression analysis showed that a lower TFPI/TF ratio was an independent predictor of cardiogenic stroke in patients with nonvalvular AF (odds ratio = 3.78, 95% confidence interval: 1.86–7.31). Conclusions During the acute stage of stroke, TFPI/TF ratio is decreased in both cardiogenic and noncardiogenic stroke patients while plasma TFPI levels show divergent changes.

BACKGROUND Acute lung injury in children is a complicated disease linked to the inflammation response. MicroRNA (miRNA) plays a vital role in acute lung injury. However, the role of miR-30b-5p in the pathogenesis of acute lung injury is not clear. The purpose of our study was to investigate the alteration of miR-30b-5p, suppressor of cytokine signaling 3 (SOCS3), in children with acute lung injury, and also in a mouse model of acute lung injury induced by the endotoxin lipopolysaccharide (LPS). MATERIAL AND METHODS The levels of miR-30b-5p, SOCS3, FKN (fractalkine), tumor necrosis factor (TNF)-α, NF-κB (nuclear factor kappa-light-chain-enhancer of activated B), interleukin-6 (IL-6), and IL-8 were detected by ELISA (enzyme-linked immunosorbent assay), western blot, and qRT-PCR (quantitative reverse transcription polymerase chain reaction) assay. The alveolar permeability index and the ratio of wet weight/dry weight (W/D) were measured. Then, we examined the inflammation and apoptosis using hematoxylin and eosin (H&E) staining and TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay. Additionally, SOCS3 was investigated as a direct target of miR-30a-5p in RAW264.7 cells by dual-luciferase reporter assays. RESULTS Our study indicated that the level of miR-30b-5p was decreased and the levels of SOCS3, FKN, TNF-α, NF-κB, IL-6, and IL-8 were increased in lung tissue, serum, and bronchoalveolar lavage fluid of mice with acute lung injury induced by LPS. In addition, LPS increased alveolar permeability index and the ratio of W/D and induced inflammatory responses, including the activation of the NF-kB pathway in a mouse model. Furthermore, SOCS3 was confirmed to be a target of miR-30a-5p in RAW264.7 cells. CONCLUSIONS Our data demonstrated an important role for miR-30b-5p in acute lung injury inflammation and suggested that miR-30b-5p might be an important therapy target in children with acute lung injury.

To test the relationship not yet explored before among earthquake and related environmental factors, low-density lipoprotein receptor (LDLR) and posttraumatic stress disorder (PTSD), the genetic variation of LDLR rs5925 was selected and PTSD was examined by PTSD Checklist-Civilian Version (PCL C) in adolescents with different genotypes of LDLR rs5925 longitudinally at 6, 12 and 18 months after the 2008 Wenchuan earthquake. The C allele carriers were observed to have higher PTSD prevalence than the TT homozygotes in the male subjects, and higher PTSD prevalence and PCL-C scores in the female subjects only at 6 months. When compared to that at 12 months, decreased PTSD prevalence was observed at 18 months only in the female C allele carriers, but not in the female TT homozygotes or the male subjects. The potential risk factors of PTSD and predictors of PCL-C scores were different during the follow-up. LDLR rs5925 was one of the predictors for PCL-C scores at 6 and 12 months, and one of the potential factors for PTSD prevalence at 6 months. These results suggest that interactions may occur between earthquakes and other related environmental factors, which could affect the relationship of LDLR rs5925 with PTSD and be considered for individualized treatment.

Background:Rheumatoid arthritis (RA) is a chronic systemic and autoimmune inflammatory disease ending with the destruction of joints. Current therapies can relieve RA symptoms, but some also bring severe adverse events. Therefore, an effective and safe therapeutic strategy remains to be crea

Doxorubicin (DOX) is a highly effective chemotherapeutic agent related to dose-dependent cardiomyopathy. Recent evidence suggests that erythropoietin (EPO) can play a protective role in cardiovascular diseases by non-erythropoietic effects. In the present study, we tested the hypothesis that EPO may protect against DOX-induced cardiomyopathy through anti-apoptotic mechanisms both in vitro and in vivo.Isolated neonatal Wistar rat cardiomyocytes were treated with vehicle, DOX with or without EPO, or EPO. Twenty-four hours later, the cells were used to determine cardiomyocyte apoptosis (TUNEL assay). Cardiomyopathy was induced in Wistar rats by intraperitoneal injections (IP) of DOX (2.5 mg/kg, six times for 2 weeks). EPO (2,500 U/kg, six times for 2 weeks) was administered simultaneously in the DOX+EPO group and the EPO group. Two weeks after the last administration, cardiac function was evaluated by echocardiography and invasive haemodynamic measurements. Rats were then sacrificed for histological and TUNEL analyses, with immunological detection for cardiac Troponin-T (cTnT), alpha-actinin, Bax and Bcl-2.EPO significantly ameliorated DOX-induced apoptosis of cultured cardiomyocytes as demonstrated by TUNEL assay. In the rat model, cardiac function significantly decreased in the DOX group. In contrast, the DOX+EPO group showed considerable improvement in cardiac function, inhibition of cardiomyocyte apoptosis, reduction of fibrosis, as well as up-regulation of Bcl-2 protein expression.Our results suggest that EPO exerts preventive cardioprotective effects on DOX-induced cardiomyopathy via anti-apoptotic pathways. The up-regulation of Bcl-2 protein expression may contribute to this.

Double tachycardia is a relatively uncommon type of tachycardia. In this report, we discuss a 68-year-old woman with history of frequent palpitations. Electrophysiologic study revealed that narrow QRS tachycardias from 2 origins and 1 wide QRS tachycardia were induced and each of the tachycardias was induced by the other. We found that 2 focal atrial tachycardias and 1 ventricular tachycardia originated from right ventricular outflow tract. All of these tachycardias were successfully ablated during one session, and no recurrence appeared during 10 months of follow-up.

Excision repair cross-complementation group 1 (ERCC1) is important in repairing DNA damage and genomic instability, and polymorphisms in ERCC1 may play a role in human tumors. In this study, the relationship of two ERCC1 polymorphisms, 8092C > A and 19007G > A, with susceptibility to acute lymphoblastic leukemia (ALL) was investigated in 183 childhood patients. For the ERCC1 8092C > A polymorphism, individuals carrying the ERCC1 8092CC genotype had a significantly higher risk when compared with those carrying at least one A allele gene (AA/AC). Analysis after stratification for sex showed that the males carrying ERCC1 8092CC genotype were associated with highly significant increased risk of ALL (1.94-fold) but not females. There was no association between ERCC1 19007G > A polymorphism and ALL risk when all patients as a group were analyzed. However, the males carrying ERCC119007A allele were associated with highly significant increased risk of ALL (2.36-fold). For the ERCC1 8092C > A polymorphism, individuals under 8 years old (median age) carrying CC genotype had significantly higher risk. However, the 19007G > A polymorphism was not associated with such age-related ALL risk. These results suggest that the ERCC1 8092C > A polymorphism may be related to the occurrence of childhood ALL in a Chinese population.

BACKGROUND: Tissue factor (TF) is the initiation factor of the extrinsic coagulation pathway, and plays a critical role in the process of thrombosis. This study aimed to investigate the expression of TF and to explore their clinical effect on the pulmonary artery after acute pulmonary thromboembolism. METHODS: Thirty-four Japanese white rabbits (Level II animals) supplied by Tianjin Medical University were randomly assigned into: group A, specimens of the pulmonary artery taken 3 hours after pulmonary embolism ( n=8); group B, specimens of the pulmonary artery taken 8 hours after pulmonary embolism ( n=8); group C, specimens of the pulmonary artery taken 24 hours after pulmonary embolism ( n=8); and control group, pseudo-operations performed without injection of autologous blood clots ( n=10). The animal model of pulmonary thrombo-embolism was established by injection of autologous blood clots into the jugular vein through a 5F catheter, and was confi rmed by digital subtraction angiography. The mRNA expression of TF in different parts of the pulmonary artery was accessed by RT-PCR. The q test was used if there was a signifi cant difference in a given continuous variable among the three groups assessed by ANOVA. The experiment equipment was supplied by the State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, the Chinese Academy of Medical Sciences and Peking Union Medical College. RESULTS: The TF expression in the specimen adjacent to emboli was stable at 3, 8 or 24 hours after embolism. The mRNA expression of TF at 3 and 8 hours after embolism was lower in the specimens taken from the distal end of the morbid pulmonary artery than those adjacent to emboli. While at 24 hours after embolism, there were similar mRNA levels in specimens either adjacent or distal to emboli. CONCLUSION: The high level of TF expression in pulmonary artery tissue adjacent to emboli could lead to locally increased coagulation activity, indicating the necessity of initiating anticoagulation treatment as soon as possible after acute pulmonary embolism.