Analysis of Changes of Ang-2 and TNF-α Levels in Patients with AMI Complicated with Pulmonary Infection and Drug Resistance of Infectious Pathogens.

Objective: This study aimed to investigate the changes in angiopoietin-2 and tumor necrosis factor α levels in patients with acute myocardial infarction complicated with pulmonary infection. Methods: Retrospective selection was conducted on 61 patients with acute myocardial infarction complicated with pulmonary infection and 122 patients with simple acute myocardial infarction. A comparison was made between the two groups regarding general information and serum myocs. The distribution and drug resistance of pathogenic bacteria were also explored. Results: The study showed significant differences in the duration of alcohol consumption, the proportion of diabetes mellitus, and levels of certain markers (serum cardiac troponin T, creatine kinase isoenzyme, myoglobin, angiopoietin-2, tumor necrosis factor α) between the two groups (P < .05). Logistic regression analysis identified elevated levels of serum angiopoietin-2 and tumor necrosis factor α, along with diabetes mellitus, as independent risk factors for acute myocardial infarction complicated with pulmonary infection (P < .05). Pearson correlation analysis demonstrated a positive correlation between serum angiopoietin-2 and tumor necrosis factor α levels and CPI scores in patients (P < .05). ROC curve analysis indicated that combined diagnosis of serum angiopoietin-2 and tumor necrosis factor α had an AUC of 0.867, with a sensitivity of 85.25% and specificity of 77.87% for detecting acute myocardial infarction complicated with pulmonary infection. Among the sputum culture specimens, gram-negative bacteria accounted for 55.34%, gram-positive bacteria for 39.81%, and fungi for 4.85%. Gram-negative bacteria like Klebsiella pneumoniae and Escherichia coli showed high resistance to various antibiotics, while gram-positive bacteria like Streptococcus pneumoniae and Staphylococcus aureus had relatively low resistance to specific antibiotics. Conclusion: Gram-negative bacteria were the main pathogens and exhibited resistance to several antibiotics. Increased levels of angiopoietin-2 and tumor necrosis factor α were observed. Early detection of these markers can assist in the clinical diagnosis and guide the appropriate use of antibiotics.

PI3K/Akt/uncoupling protein 2 signaling pathway may be involved in cell senescence and apoptosis induced by angiotensin II in human vascular endothelial cells.

Oxidative DNA damage contributes to replicative senescence. We explored the mechanism by which angiotensin II (Ang II) induces senescence in human vascular endothelial cells (HUVECs). Following weeklong incubation with Ang II, cell senescence, apoptosis, reactive oxygen species (ROS) content and mitochondrial membrane potential (MMP) were measured by ß-galactosidase, annexin V/propidium iodide, DCFH-DA and rhodamine 123 staining, respectively. The protein levels of telomerase reverse transcriptase (TERT), UCP2, Akt, phosphor (p)-Akt, c-myc, and p53 were assessed by immunoblot. LY294002 was applied to inhibit PI3K/Akt signaling. Ang II induced HUVEC senescence and apoptosis, and increased ROS content and depolarization of MMP in a dose-dependent manner. Ang II further elevated protein levels of TERT from 0.006 ± 0.041 at baseline, to 0.480 ± 00.031 in the presence of 10 µM Ang II, UCP2 from 0.297 ± 0.051 to 2.512 ± 0.024, p-Akt from 0.012 ± 0.024 to 0.874 ± 0.015, c-myc from 0.521 ± 0.015 to 1.064 ± 0.025, and p53 from 0.035 ± 0.047 to 1.195 ± 0.029 (all P < 0.01, vs. baseline). LY294002 pre-treatment significantly alleviated Ang II-induced HUVEC senescence, and partly reversed the elevation of TERT, UCP2, p-Akt, c-myc and p53 protein levels. PI3K/Akt/UCP2 signaling may be involved in cell senescence and apoptosis induced by Ang II in HUVECs.