The aim of this study was to evaluate the value of metagenomic next-generation sequencing (mNGS) in peripheral pulmonary infection management by comparing the diagnostic yield of mNGS and traditional pathogen detection methods on interventional specimens obtained by bronchoscopy. Patients and Methods: This study enrolled patients suspected with pulmonary infection who were admitted to Tianjin Medical University General Hospital from June 2018 to August 2019. Specimens were obtained from bronchoscopy for mNGS analysis and traditional pathogen detection (including bronchoalveolar lavage fluid microbial culture, smear microscopy, and lung biopsy histopathology), and the diagnostic yields were compared between mNGS and traditional methods to evaluate the diagnostic value of mNGS in peripheral pulmonary infection diagnosis. Results: In this study, by comparing mNGS with traditional pathogen detection, the results indicated that, first, mNGS identified at least one microbial species in almost 89% of the patients with pulmonary infection; second, mNGS detected microbes related to human diseases in 94.49% of samples from pulmonary infection patients who had received negative results from traditional pathogen detection; third, the accuracy and sensitivity of mNGS are higher than those of traditional pathogen detection; and, finally, mNGS could simultaneously detect and identify a large variety of pathogens. Conclusion: Metagenomic NGS analysis provided fast and precise pathogen detection and identification, contributing to prompt and accurate treatment of peripheral pulmonary infection.

No abstract

No abstract

The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Results revealed that MPs could damage cardiac structure and function with impaired mitochondria integrity, as well as increased levels of creatine kinase‐MB and cardiac troponinI (cTnI). Moreover, MPs administration triggered oxidative stress as indicated by increased levels of malondialdehyde and decreased activity of superoxide dismutase, glutathione peroxidase and catalase. Treatment with MPs resulted in apoptosis and pyroptosis as evidenced by increasing expressions of interleukin (IL)‐1β, IL‐18. Additionally, MPs were shown to induce the NOD‐like receptor protein 3 inflammasomes activation in cardiac tissue, enabling activation of Caspase‐1‐dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In summary, these results illustrated that pyroptosis played a vital role in polystyrene MPs‐induced cardiotoxicity, which might be helpful to understand the mechanism of cardiac dysfunction and induced by MPs.

Post-transplant IFI was an unfavorable prognostic factor of the SCT recipients, and risk stratification can identify patients with high risk of IFI. Use of steroid played an important role in the pathogenesis as well as prognosis of IFI.

No abstract

No abstract

Objective: Silica nanoparticles (SiO 2 NPs) have been extensively employed in biomedical field. SiO 2 NPs are primarily designed to enter the circulatory system; however, little information is available on potential adverse effects of SiO 2 NPs on the nervous system. Methods: The neurotoxicity of SiO 2 NPs at different concentrations (3, 6, 12 ng/nL) on zebrafish embryos was determined using immunofluorescence and microarray techniques, and subsequently confirmed by qRT-PCR. Results: SiO 2 NPs disrupt the axonal integrity and decrease the length of axons in Tg (NBT: EGFP) transgenic lines. The number of apoptotic cells in the brain and central nervous system of zebrafish embryos was increased in the presence of 12 ng/nL of SiO 2 NPs, but the difference did not reach statistical significance. Screening for changes in the expression of genes involved in the neuroactive ligand-receptor interaction pathway was performed by microarray and confirmed by qRT-PCR. These analyses demonstrated that SiO 2 NPs markedly downregulated genes associated with neural function (grm6a, drd1b, chrnb3b, adrb2a, grin2ab, npffr2.1, npy8br, gabrd, chrma3, gabrg3, gria3a, grm1a, adra2b, and glra3). Conclusion: The obtained results documented that SiO 2 NPs can induce developmental neurotoxicity by affecting the neuroactive ligand-receptor interaction signaling pathway. This new evidence may help to clarify the mechanism of SiO 2 NPs-mediated neurotoxicity.