BACKGROUNDAntibiotic resistance has become a global threat for human health, calling for rational use of antibiotics.AIMTo analyze the distribution and drug resistance of the bacteria, providing the prerequisite for use of antibiotics in emergency patients.METHODSA total of 2048 emergency patients from 2013 to 2017 were enrolled. Their clinical examination specimens were collected, followed by isolation of bacteria. The bacterial identification and drug susceptibility testing were carried out.RESULTSA total of 3387 pathogens were isolated. The top six pathogens were Acinetobacter baumannii (660 strains), Staphylococcus aureus (436 strains), Klebsiella pneumoniae (347 strains), Pseudomonas aeruginosa (338 strains), Escherichia coli (237 strains), and Candida albicans (207 strains). The isolation rates of these pathogens decreased year by year except Klebsiella pneumoniae, which increased from 7.1% to 12.1%. Acinetobacter baumannii is a widely-resistant strain, with multiple resistances to imipenem, ciprofloxacin, minocycline and tigecycline. The Staphylococcus aureus had high resistance rates to levofloxacin, penicillin G, and tetracycline. But the susceptibility of it to vancomycin and tigecycline were 100%. Klebsiella pneumoniae had high resistance rates to imipenem, cefoperazone/sulbactam, amikacin, and ciprofloxacin, with the lowest resistance rate to tigecycline. The resistance rates of Pseudomonas aeruginosa to cefoperazone/sulbactam and imipenem were higher, with the resistance rate to amikacin below 10%. Besides, Escherichia coli had high resistance rates to ciprofloxacin and cefoperazone/sulbactam and low resistance rates to imipenem, amikacin, and tigecycline.CONCLUSIONThe pathogenic bacteria isolated from the emergency patients were mainly Acinetobacter baumannii, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, Escherichia coli, and Candida albicans. The detection rates of drug-resistant bacteria were high, with different bacteria having multiple drug resistances to commonly used antimicrobial agents, guiding the rational use of drugs and reducing the production of multidrug-resistant bacteria.
Aims Whether changes in endothelial tight junctions (TJs) lead to the formation of thoracic aortic aneurysm and dissection (TAAD) and serve as an early indicator and therapeutic target remains elusive. Methods and results Single-cell RNA sequencing analysis showed aberrant endothelial TJ expressions in the thoracic aortas of patients with TAAD. In a β-aminopropionitrile (BAPN)-induced TAAD mouse model, endothelial TJ function was disrupted in the thoracic aortas at an early stage (5 and 10 days) as observed by a vascular permeability assay, while the intercellular distribution of crucial TJ components was significantly decreased by en face staining. For the non-invasive detection of endothelial TJ function, two dextrans of molecular weights 4 and 70 kDa were conjugated with the magnetic resonance imaging (MRI) contrast agent Gd-DOTA to synthesize FITC-dextran-DOTA-Gd and rhodamine B-dextran-DOTA-Gd. MRI images showed that both probes accumulated in the thoracic aortas of the BAPN-fed mice. Particularly, the mice with increased accumulated signals from 5 to 10 days developed TAAD at 14 days, whereas the mice with similar signals between the two time points did not. Furthermore, the protease-activated receptor 2 inhibitor AT-1001, which seals TJs, alleviated the BAPN-induced impairment of endothelial TJ function and expression and subsequently reduced TAAD incidence. Notably, endothelial-targeted ZO-1 conditional knockout increased TAAD incidence. Mechanistically, vascular inflammation and edema were observed in the thoracic aortas of the BAPN-fed mice, whereas these phenomena were attenuated by AT-1001. Conclusion The disruption of endothelial TJ function is an early event prior to TAAD formation, herein serving as a potential indicator and a promising target for TAAD.
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