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Objective: To investigate the protective effect of compound Longmaining isoprenaline hydrochloride-induced myocardial infarction model and its effect on Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear transcription factor-kappa B (NF-κB) signaling pathway.Method: Forty-eight male SD rats were randomly divided into 6 groups:normal group,model group,compound salvia miltiorrhiza drop pill group (0.072 9 g·kg-1),and low,medium and high-dose compound Longmaining decoction groups (0.36,0.71,1.43 g·kg-1).The acute myocardial infarction model was induced through subcutaneous injection with isoproterenol.The pathological changes of myocardial tissue were examined by hematoxylin-eosin (HE) staining.The levels of interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),monocyte chemotaxis protein-1(MCP-1) and nitrogen (NO) in serum were measured by enzyme linked immunosorbent assay (ELISA).The expression levels of inhibitors of NF-κB kinase subunit-β(IKKβ),NF-κB inhibitor α(IκBα),TLR4,MyD88 and NF-κB p65 were measured by immunohistochemical staining and Western blot.Result: Compared with normal group,the myocardial injury in model group was obvious.The levels of IL-1β,IL-6,TNF-α,MCP-1 and NO in serum increased significantly (PκBα decreased significantly (Pβ,TLR4,MyD88 and NF-κB p65 increased significantly in myocardial tissue (Pβ,IL-6,TNF-α,MCP-1 and NO levels in the serum (PκBα(Pβ,TLR4,MyD88 and NF-κB p65(PConclusion: Compound Longmaining plays a protective effect on acute myocardial infarction by regulatingthe expressions of TLR4/MyD88/NF-κB p65 signaling pathway and relevant inflammatory factors.
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Objective To assess the dosimetric impact on the target volumes and organs at risk ( OARs) using simultaneous integrated boost ( SIB ) for the hypoxic regions of the pancreatic cancer patients treated with stereotactic body radiotherapy ( SBRT ) , and to predict an optimal way of SIB. Methods The setup corrections guided by 100 sets of CBCT scans of 10 patients previously treated with SBRT were imported to the treatment planning system ( TPS ) to recalculate the dose to the target and OARs. Two tumor control probability ( TCP ) models were applied to calculate the TCP under various hypoxic situations. The correlations between the TCP and target dose were analyzed. Results Without setup corrections, the PTV and ITV were underdosed by 8. 9％ and 9. 2％ on average respectively relative to planed dose. With setup corrections, the mean dose to PTV and ITV coverage were 1. 6％ and 1. 3％lower than planned respectively. The mean deviations of OAR dose were between -0. 11 Gy and 0. 26 Gy for all plans. The predictive values of Dmean on hypoxic regions were 31. 4, 34. 0 and 37. 2 Gy (Niemierko model) or 31. 6, 33. 9 and 37. 2 Gy (Poisson model) when the oxygen enhancement ratios (OERs) were 1, 1. 5 and 3 respectively. Conclusions With CBCT setup corrections, the dosimetric impacts of setup errors on the target and OARs can be neglected. Significant deviations of TCP calculation were observed without accounting for tumor hypoxia. To counteract the impacts of hypoxia, the mean dose to the hypoxic regions should be at least 1. 24 times of prescribed dose.
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Background@#The impact of fasting plasma glucose (FPG) on survival outcomes in patients with acute heart failure (HF) is unclear, and the relationship between intensity of glycemic control of FPG in diabetes mellitus (DM) patients and HF prognosis remains uncertain. This retrospective study aimed to evaluate the prognostic impact of FPG in patients with acute HF.@*Methods@#A total of 624 patients hospitalized with acute HF from October 2000 to April 2014 were enrolled in this study. All patients were stratified by three groups according to their admission FPG levels (i.e., DM, impaired fasting glucose [IFG], and non-DM). All-cause and cardiovascular mortality was the primary end point, and HF re-hospitalization was the secondary end point during follow-up period.@*Results@#A total of 587 patients were included in final analysis. The all-cause mortality rates of patients with DM, IFG, and non-DM were 55.5%, 40.3%, and 39.2%, with significant difference (P = 0.001). Moreover, compared with those with IFG (34.3%) and non-DM (32.6%), patients with DM had significantly higher rate of cardiovascular mortality (45.1%). Multiple Cox regression analysis showed that DM as well as IFG was related to all-cause mortality (DM: hazard ratio [HR] = 1.936, P < 0.001; IFG: HR = 1.672, P = 0.019) and cardiovascular mortality (DM: HR = 1.739, P < 0.001; IFG: HR = 1.817, P = 0.013). However, they were both unrelated to HF re-hospitalization. DM patients with strictly controlled blood glucose (FPG <3.9 mmol/L) had higher all-cause mortality than patients with non-DM, IFG, and DM patients with moderately controlled glucose (3.9 mmol/L≤ FPG <7.0 mmol/L). Likewise, both the primary end point and secondary end point were found to be worse in DM patients with poorly controlled blood glucose (FPG ≥7.0 mmol/L).@*Conclusions@#IFG and DM were associated with higher all-cause mortality and cardiovascular mortality in patients with acute HF. The association between mortality and admission FPG in DM patients with acute HF appeared U-shaped.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Blood Glucose , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Fasting , Heart Failure , Blood , Mortality , Hospitalization , Prognosis , Retrospective StudiesABSTRACT
<p><b>OBJECTIVE</b>It is revealed that circulating fibrocytes are elevated in patients/animals with cardiac fibrosis, and this review aims to provide an introduction to circulating fibrocytes and their role in cardiac fibrosis.</p><p><b>DATA SOURCES</b>This review is based on the data from 1994 to present obtained from PubMed. The search terms were "circulating fibrocytes " and "cardiac fibrosis ".</p><p><b>STUDY SELECTION</b>Articles and critical reviews, which are related to circulating fibrocytes and cardiac fibrosis, were selected.</p><p><b>RESULTS</b>Circulating fibrocytes, which are derived from hematopoietic stem cells, represent a subset of peripheral blood mononuclear cells exhibiting mixed morphological and molecular characteristics of hematopoietic and mesenchymal cells (CD34+/CD45+/collagen I+). They can produce extracellular matrix and many cytokines. It is shown that circulating fibrocytes participate in many fibrotic diseases, including cardiac fibrosis. Evidence accumulated in recent years shows that aging individuals and patients with hypertension, heart failure, coronary heart disease, and atrial fibrillation have more circulating fibrocytes in peripheral blood and/or heart tissue, and this elevation of circulating fibrocytes is correlated with the degree of fibrosis in the hearts.</p><p><b>CONCLUSIONS</b>Circulating fibrocytes are effector cells in cardiac fibrosis.</p>
Subject(s)
Humans , Coronary Disease , Pathology , Fibroblasts , Physiology , Fibrosis , Pathology , Heart Failure , Pathology , Hypertension , Pathology , Myocardium , PathologyABSTRACT
<p><b>BACKGROUND</b>Metabolic syndrome (MS) is a risk factor for stroke and thromboembolism event. Left atrial or LA appendage (LA/LAA) thrombus is a surrogate of potential stroke. The relationship between MS and atrial thrombus remains unclear. In this study, we sought to investigate the effect of MS on risk stratification of LA/LAA thrombus formation in patients with nonvalvular atrial fibrillation (NVAF).</p><p><b>METHODS</b>This cross-sectional study enrolled 294 consecutive NVAF patients without prior anticoagulant and lipid-lowering therapies. LA/LAA thrombus was determined by transesophageal echocardiography. Risk assessment of LA/LAA thrombus was performed using the CHADS2 , CHA2DS2 -VASc, MS, CHADS2 -MS, and CHA2DS2 -VASc-MS scores. Logistic regression analyses were performed to determine which factors were significantly related to LA/LAA thrombus. Odds ratio (OR) including 95% confidence interval was also calculated. The predictive powers of different scores for the risk of LA/LAA thrombus were represented by C-statistics and compared by receiver operating characteristic (ROC) analysis.</p><p><b>RESULTS</b>LA/LAA thrombi were identified in 56 patients (19.0%). Logistic analysis showed that MS was the strongest risk factor for LA/LAA thrombus in NVAF patients (OR = 14.698, P < 0.001). ROC curve analyses revealed that the C-statistics of CHADS2 -MS and CHA2DS2 -VASc-MS was significantly higher than those of CHADS2 and CHA2DS2 -VASc scores (CHADS2 -MS vs. CHADS2 , 0.807 vs. 0.726, P = 0.0019). Furthermore, MS was helpful for identifying individuals with a high risk of LA/LAA thrombus in the population with a low risk of stroke (CHADS2 or CHA2DS2 -VASc score = 0).</p><p><b>CONCLUSIONS</b>MS is associated with LA/LAA thrombus risk in patients with NVAF. In addition to the CHADS2 and CHA2DS2 -VASc scores, the CHADS2 -MS and CHA2DS2 -VASc-MS scores provide additional information on stroke risk assessment.</p>