Search

Objective. We sought to analyze the distribution and antibiotic sensitivity of pathogens in hospitalized patients and to provide a scientific reference for the rational application of antibiotics. Methods. From January 2014 to December 2018, urine cultures from patients in our hospital were collected and analyzed retrospectively for the presence, distribution, and drug sensitivity of pathogens. Results. A total of 42,854 midstream urine cultures were collected from which 11,891 (27.75%) pathogens were isolated, including 8101 (68.13%) strains of gram-negative bacteria, 2580 (21.69%) strains of gram-positive bacteria, and 1210 (10.18%) strains of fungi. Escherichia coli and Enterococci were the most common species of gram-negative and gram-positive bacteria, respectively. Drug sensitivity varied among different pathogens. Clear drug resistance was observed in bacteria, while fungus exhibited relatively lower resistance. Conclusion. Pathogens responsible for urinary tract infections in hospitalized patients are diversiform and display resistance to some antibiotics. Drug resistance monitoring should be enhanced to optimize antimicrobial therapy. [ABSTRACT FROM AUTHOR]

Tumor markers are beneficial for the diagnosis and therapy monitoring of lung cancer. However, the value of tumor markers in lung cancer histological diagnosis is unknown. In this study, we analyzed the serum levels of six tumor markers (CEA, CYFRA21-1, SCC, NSE, ProGRP, and CA125) in 2097 suspected patients with lung cancer and determined whether the combination of the tumor markers was useful for histological diagnosis of lung cancer. We found that CYFRA21-1 was the most sensitive marker in NSCLC. ProGRP showed a better clinical performance than that of NSE in discriminating between SCLC and NSCLC. The serum level of CYFRA21-1 or SCC was significantly higher in squamous carcinoma (p<0.05), and the levels of ProGRP and NSE were significantly higher in SCLC (p<0.05). According to the criteria established, SCLC and NSCLC were discriminated with sensitivity of 87.12 and 62.63% and specificity of 64.61 and 99.5%, respectively. The sensitivity and specificity in the differentiation of adenocarcinoma and squamous carcinoma were 68.1 and 81.63% and 70.73 and 65.93%, with NPV of 46.03 and 68.97% and PPV of 85.82 and 79.47%, respectively. Our results suggested the combination of six tumor markers could discriminate the histological types of lung cancer. [ABSTRACT FROM AUTHOR]

• Disulfiram played a protective role to corneal transparency in mouse early fungal keratitis. • Disulfiram impaired IL-1β secretion against A. fumigatus by inhibiting GSDMD pore formation. • Disulfiram combined with antifungal medicine may be a potential therapy for fungal keratitis. Disulfiram, an inhibitor of gasdermin D-induced pore formation, is known to suppress interleukin (IL)-1β secretion and pyroptosis. However, its effects on fungal keratitis remain unknown. Therefore, we investigated the role of disulfiram in Aspergillus fumigatus keratitis. In vitro , Cell Count Kit-8 (CCK8) assay and cell scratch test were performed to determine optimal concentration. In vivo and in vitro experiments were conducted in a mouse model, human neutrophils, and mouse peritoneal macrophages. We pre-treated the mice or cells with disulfiram and infected them with A. fumigatus at specific times. We subsequently evaluated the development of fungal keratitis lesions, the recruitment of inflammatory cells, and the production of inflammatory cytokines using slit lamp microscopy, clinical evaluation, quantitative reverse transcription polymerase chain reaction, immunofluorescence staining, enzyme-linked immunosorbent assay, and western blotting. We also used slit lamp microscopy and clinical evaluation to assess the effect of natamycin with or without disulfiram. Disulfiram at 20 μM has no significant cytotoxic effect and does not affect cell migration. In the mouse model, disulfiram significantly suppressed inflammatory responses, reduced neutrophil and macrophage recruitment, and down-regulated myeloperoxidase and nitric oxide synthase levels at earlier stages of infection. Disulfiram had no effect on IL-1β production and maturation, but it inhibited IL-1β secretion in macrophages. Disulfiram combined with natamycin significantly increased corneal transparency in the mice model. Overall, disulfiram reduced the host immune response in fungal keratitis by attenuating neutrophil and macrophage recruitment and inhibiting IL-1β secretion in macrophages. Disulfiram in combination with antifungal agents may serve as a novel therapeutic method for reducing corneal opacity in fungal keratitis. [ABSTRACT FROM AUTHOR]