Search

Pulmonary embolism (PE) is a disease caused by blood clots, tumor embolism, and other emboli within the pulmonary arteries. Various scoring scales are used for PE. One such same is the PESI, but it has 12 variables, making it inconvenient for clinical application.The aim of this study was to develop a new simple nomogram model to assess 30-day survival in PE patients. The new nomogram makes it easier and faster for clinicians to assess the prognosis of patients with PE.We collected data about the patients with PE from the Medical Information Mart for Intensive Care-III (MIMIC-III) database and used the receiver operating characteristic (ROC) curve, area under the ROC curve (AUROC), calibration plot, integrated discrimination improvement (IDI), and decision curve analysis (DCA) to evaluate the predictive power of the new model, and compared these with the PESI.According to the multivariable Cox regression model results, alongside the actual clinical conditions, we included the following seven variables: race, bicarbonate, age, tumor, systolic blood pressure (SBP), body temperature, and oxygen saturation (Spo2). The AUROC of the new model was greater than 0.70. Its IDI exceeded 0, but with P-value0.05.The predictive performance of the new model was not worse than the PESI, but the new model only has seven variables, and is therefore more convenient for clinicians to use.

BACKGROUND At present, large-scale studies on the clinical characteristics of sepsis-induced cardiomyopathy (SIC) are lacking. AIM To investigate the clinical characteristics of SIC. METHODS Based on the analysis of the MIMIC-III public database, we performed a large-scale retrospective study involving sepsis patients who were admitted to the intensive care unit (ICU) and had no concomitant cardiac disease. We used propensity score matching analysis and multivariate logistic regression to ensure the robustness of the results. The primary outcome was hospital mortality, and the secondary outcomes included the number of patients who received mechanical ventilation or renal replacement therapy during their hospital stay, the number of patients administered with vasopressors, the length of ICU stay, and the length of hospital stay. RESULTS In the present study, after screening 38605 patients, 3530 patients with sepsis were included. A total of 997 patients met the SIC diagnostic criteria, and the incidence of SIC was 28.20% (95% confidence interval [CI]: 26.80%-29.70%). Compared to patients in the non-SIC group, patients in the SIC group were of older age and had a higher Simplified Acute Physiology Score (SAPS)-I score, SAPS-II score, and Elixhauser comorbidity index (ECI). A total of 367 (36.8%) of 997 patients in the SIC group and 818 (32.3%) of 2533 patients in the non-SIC group died in the hospital, which resulted in a significant between-group difference (odds ratios = 1.22, 95%CI: 1.05-1.42; P = 0.011). For the secondary outcomes, more patients in the SIC group received mechanical ventilation and vasopressors. Multivariate logistic regression analysis showed that age, male sex, ECI, hemoglobin level, diabetes, and mechanical ventilation use on the first day of ICU admission were risk factors for SIC. CONCLUSION Compared with non-SIC patients, hospital mortality is higher in SIC patients.

To investigate the effects of inhibition of NF-κB activation on left ventricular (LV) remodelling in a rat model of myocardial infarction (MI).The acute MI model was established by ligation of left anterior descending coronary artery. Pyrrolidine dithiocarbamate (PDTC) (20mg/kg, Qd) was administered intraperitoneally to inhibit NF-κB activation. Eight weeks later, the cardiac structure and LV ejection fraction were assessed with echocardiography. The rat body, heart, and LV weights were measured to calculate LV mass indices. Activation of NF-κB in non-infarcted myocardium was detected by a TransAM NF-κB p65 Transcription Factor Assay Kit. Cardiac collagen volume fraction was evaluated by Masson staining.Eight weeks after the MI model was established, the LV posterior wall thickness in PDTC and MI group was 1.75±0.07mm and 1.85±0.07mm respectively (p0.05). The LV mass index in the PDTC group (2.53±0.09) was lower than in the MI group (2.65±0.08, p0.05). The LVEF in the PDTC group (63.89%±4.21%) was higher than in the MI group (42.73%±8.94%, p0.05). The interstitial collagen deposition in the non-infarcted myocardium in the PDTC group was less than in the MI group (7.25%±1.88% vs. 10.09%±2.19%, p0.05).Inhibition of activation of NF-κB may result in improvement of myocardial remodelling after myocardial infarction, which is possibly attributable to reduced collagen deposition in non-infarcted areas.

Cardiac troponin I (cTnI) and creatine kinase MB isoenzyme (CK-MB) were measured in the plasma of 37 patients with acute heart failure. Elevated plasma cTnI concentrations were found in 89% of acute heart failure patients ( P < 0·001) compared with a normal population), while plasma CK-MB showed no significant difference ( P = 0·09). During follow-up, serial measurements of cTnI and CK-MB were performed. In acute heart failure patients, improvement of the clinical profile was associated with declining cTnI concentrations, while deterioration of heart function was closely related to increasing cTnI. Plasma CK-MB activities remained within the normal range throughout the observation period. This preliminary study provides evidence of cardiac damage to functionally overloaded myocytes. cTnI may be a sensitive marker both for early detection of myocyte damage and for monitoring of function in patients with acute heart failure.

To explore the effects of Notch signaling pathway and the vascular endothelial growth factor [VEGF(165)] gene on the functions of endothelial cells derived from rat bone marrow mesenchymal stem cells (MSCs).Isolated and cultivated rat bone marrow MSCs in vitro, then the cells were treated by VEGF165 and basic fibroblast growth factor (bFGF) for 2 weeks to induce them to differentiate into endothelial cells. The gene of VEGF165 was transfected into differentiated endothelial cells to promote the functions of the cells. The receptor Notch1 and the ligand Jagged1 of the Notch signaling were detected by reverse transcription-polymerase chain reaction (RT-PCR) before and after the transfection. γ-secretase inhibitor L-685458 was used to block Notch pathway. Migration ability of cells was detected by scarification test. Cells were inoculated on semisolid gel to study their ability of forming capillary-like structure.After transfection, VEGF165 mRNA could be detected on the differentiated endothelial cells. The expression of Jagged1 mRNA was up regulated(1.08 ± 0.01 vs. 1.01 ± 0.02,P0.01) and there was no change in Notch1 mRNA(0.60 ± 0.02 vs. 0.59 ± 0.01,P0.05). The ability of migration was enhanced (number of cells on the scratched area:46.45 ± 4.46 vs. 41.61 ± 1.42,P0.05), and the ability of forming capillary-like structure on semisolid gel showed no change (cells classification: 3.00 ± 0.89 vs. 2.00 ± 0.89,P0.05). After the transfection, using the γ-secretase inhibitor L-685458 to block the Notch signaling transduction, the ability of migration of the differentiated endothelial cells (number of cells on the scratched area: 51.72 ± 3.47 vs. 46.45 ± 4.46,P0.05), and that of forming capillary--like structure (cells classification: 4.17 ± 0.75 vs. 3.00 ± 0.89, P0.05), was also further enhanced.Transfection of the gene of VEGF165 into the differentiated endothelial cells can reinforce the function of these cells, and when Notch signaling was blocked, this effect can be further amplified.

To research the role of Notch signaling during the differentiation of bone marrow mesenchymal stem cells (MSCs) into endothelial cells and its effect on the functions of the differentiated cells.Rat bone marrow MSCs were isolated and cultured in vitro, then the cells were treated with vascular endothelial growth factor (VEGF165) and basic fibroblast growth factor (bFGF) for 2 weeks to induce it to differentiate into endothelial cells. The differentiated cells were identified by fluorescence immunoassay. The receptors and ligands of the Notch signaling were detected by reverse transcription-polymerase chain reaction (RT-PCR) before and after the differentiation. γ-secretase inhibitor was used to block Notch pathway. Migration ability of cells were assessed by scarification test. Cells were inoculated on semisolid gel to study their ability of forming the capillary-like structure.After inducing MSCs to differentiate into endothelial cells by VEGF165 and bFGF, MSCs gained the characteristics of the endothelial cells with expression of CD31 and Flk1. There were Notch1 mRNA and Jagged1 mRNA expressions in rat bone marrow MSCs. The expression changes in the receptor Notch1 were not statistically significant on the differentiated cells (0.59±0.01 vs. 0.59±0.01, P0.05), but there was a trend towards an increase of Jagged1 mRNA (1.01±0.02 vs. 0.99±0.03, P0.05). When Notch pathway was blocked, the differentiated cells' migration ability was increased (number of cells on the scratched area: 44.61±4.34 vs. 40.06±2.43, P0.05), and the ability of forming capillary-like structure was also increased (cells classification: 3.67±0.82 vs. 2.00±0.89, P0.01).Notch signaling may have an important role during the differentiation of MSCs into endothelial cells. The function of differentiated cells were strengthened when Notch pathway was blocked.

To investigate the relationship between apoptosis of myocardial cell in the rats with sepsis and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) mRNA, and the protective effect of glutamine (Gln) against apoptosis of myocardial cell.Rat model of sepsis was reproduced by peritoneal injection with lipopolysaccharide (LPS), and the animals were divided into control group, LPS group and Gln group. Rats in each group were further divided into four subgroups, 0, 6, 12 and 24 hours ( n =6). Apoptosis of myocardial cells was surveyed, and TLR4, TNF-alpha and IL-6 mRNA expressions were assessed with reverse transcription-polymerase chain reaction (RT-PCR). The pathological changes in myocardial cells were observed.Myocardial apoptosis rate in LPS group was higher. Compared with the control group, expressions of TLR4 mRNA, TNF-alpha mRNA and IL-6 mRNA were significantly higher at all time points after LPS administration in the LPS group and the Gln group (all P0.05). Compared with the LPS group, the rate of myocardial apoptosis in Gln group was lower, and expression of TLR4 mRNA in the Gln group was significantly lower at 12 hours and 24 hours; the expression of TNF-alpha mRNA was obviously lower at 6 hours and 24 hours; the expression of IL-6 mRNA in the Gln group was significantly lower at 12 hours (all P0.05).TLR4, TNF-alpha and IL-6 gene expressions play extremely important role in apoptosis of myocardial cell in the rat with sepsis. Gln can affect apoptosis-related gene expressions, thus alleviating the apoptosis of myocardial cell.

Background To investigate the efficacy of intracoronary tirofiban during primary percutaneous coronary intervention (PCI) for patients with acute coronary syndrome (ACS). Methods and Results The 118 patients aged 70 years and above (average age 75±2) were divided into study (n=58, intracoronary bolus tirofiban) and control (n=57, intravenous tirofiban) groups. The culprit vessels were targeted with primary PCI in all patients. Compared with the control group, the study group showed better Thrombolysis In Myocardial Infarction (TIMI) flow grades and TIMI myocardial perfusion grades (TMPG) immediately after PCI (p=0.016 and 0.026, respectively). The 14-day composite major adverse cardiac events rate was lower in the study group (3.5% vs 17.5%, p=0.030), but was similar between the 2 groups at 30 days following PCI (7.0% vs 1.7%, p=0.350). The left ventricular ejection fraction in the study group was higher than in the control group 30 days following PCI (67.4±6.2% vs 60.7±4.6%, p=0.033). The 14-day bleeding complication (p=0.201) and platelet reduction rates (p=0.984) were similar between the 2 groups. Conclusion In patients with ACS undergoing primary PCI, intracoronary bolus administration of tirofiban is superior to intravenous bolus injection for improving coronary flow, myocardial perfusion and short-term clinical outcomes. (Circ J 2008; 72: 1605 - 1609)

To examine whether urotensinII (UII) induces hypertrophy of neonatal rat cardiomyocytes cultured in vitro.The primary cardiac myocytes cultured for 40 h followed by further culture in serum-free media for another 24 h were subjected to exposure to UII of varied concentrations for 24 h, after which the changes in the size of the cells were analyzed by flow cytometry with (3)H-leucine incorporation also measured.At the concentration of 1x10(-7) mol/L, UIIcould increase the size of the cultured cardiac myocardial cells (P=0.021) and 3H-Leucine incorporation (P=0.015).UII may induce hypertrophy of neonatal rat cardiac myocytes cultured in vitro.