[Impact of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood thrombogenicity in adults].

Objective: To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults. Methods: A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2'-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders. Results: The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM2.5-bound PAHs was (55.29±74.99) ng/m3. Six sources of PM2.5-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per IQR increase (60.33 ng/m3) in exposure to PAHs were 14.36% (95%CI:6.94%-22.28%), 9.33% (95%CI: 1.71%-17.51%) and 2.07% (95%CI:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Conclusion: Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.

[Pulmonary mucormycosis after lung transplantation:3 cases report with literature review].

Objective: To report the risk factors, clinical characteristics and treatment courses of pulmonary mucormycosis after lung transplantation(LT). Methods: We included 3 cases with pulmonary mucormycosis after LT from March 2017 to July 2020 in the centre for lung transplantation of China-Japan Friendship Hospital. Twelve cases from Chinese and English literature from China National Knowledge Infrastructure (CNKI), China Biomedical Literature Service System and Pubmed Database from March 1980 to July 2020 were added. The risk factors, clinical characteristics and treatment courses of all cases were summarized and analyzed. Results: Pulmonary mucormycosis occurred in 1.06% (3/284) in our centre. A total of 15 cases with 12 cases from literature included 10 males and 5 females with a mean age of(47±20)years. Thirteen cases occurred after LT, and 2 cases occurred after heart-lung transplantation (HLT). Nine probable cases were diagnosed by positive isolation of the pathogen from bronchoalveolar lavage fluid or sputum. Three proven cases were diagnosed by transbronchial lung biopsy. Meanwhile, the other 3 proven cases diagnosed by CT-guided percutaneous lung biopsy, autopsy and surgical operation respectively. Ten cases (66.7%) were diagnosed with pulmonary mucormycosis within 90 days after lung transplantation. The mortality was as high as 46.67% (7/15), but if it occurred within 90 days, the mortality reached 70% (7/10). The average interval between transplantation and positive isolation of the pathogen was 112.3 (5-378) days. Conclusions: The clinical and radiographic features of pulmonary mucormycosis after LT were nonspecific. It had a high mortality, especially in those occurred within 90 days after LT. The combination of antifungal therapy and surgical resection may contribute to a better outcome of the disease.

First Report of Peach Brown Rot Caused by Monilinia fructicola in Central and Western China.

Brown rot of peach (Prunus persica) in China has been reported to be caused by at least three Monilinia species (1). In the present study, peaches with symptoms resembling brown rot caused by Monilinia species were collected from commercial orchards in the northwestern province of Gansu in August 2010, the southwestern province of Yunnan in July 2011, and in the central province of Hubei in July 2012. Affected fruit showed the typical symptoms of brown rot with zones of sporulation. Fungal isolates were single-spored and cultured on potato dextrose agar (PDA). Colonies showed grayness with concentric rings of sporulation after incubation at 25°C in the dark. Mean mycelial growth of isolates YHC11-1a and YHC11-2a from Yunnan, GTC10-1a and GTC10-2a from Gansu, and HWC12-14a and HWC12-23a from Hubei, was 4.6 ± 0.4 and 7.5 ± 0.7 cm after 3 and 5 days incubation, respectively. Conidia were lemon shaped and formed in branched monilioid chains, and the mean size was 9.3 (6.7 to 11.5) × 12.5 (7.9 to 17.8) µm, which was consistent with the characteristics of Monilinia fructicola (1,2). The species identification was confirmed by sequencing of the ribosomal ITS sequences. The ribosomal ITS1-5.8S-ITS2 region was amplified from each of the six isolates using primers ITS1 and ITS4 (3). Results indicated that the ITS sequences of these isolates were identical and showed the highest similarity (100%) with M. fructicola ITS sequences from isolates collected in China (GenBank Accession Nos. HQ893748, FJ515894, and AM887528), Slovenia (GU967379), Italy (FJ411109), and Spain (EF207423). The pathogen was also confirmed to be M. fructicola based on the detection of an M. fructicola- specific band (534 bp) using a PCR-based molecular tool developed for distinguishing Chinese Monilinia species affecting peach (1). Pathogenicity was tested on surface-sterilized, mature peaches (Shui Mi Tao) with representative isolates. Fruits were holed at three equidistant positions to a depth of 5 mm using a sterile cork borer. Mycelial plugs (5 mm in diameter) from the periphery of a 4-day-old colony of each isolate were placed upside down into each hole, control fruits received water agar. After 3 days of incubation at 22°C in a moist chamber, inoculated fruits developed typical brown rot symptoms while control fruits remained healthy. Pathogens from the inoculated fruit were confirmed to be M. fructicola based on morphological characteristics. To our knowledge, this is the first report of occurrence of M. fructicola in Gansu, Yunnan, and Hubei provinces, thousands of kilometers away from eastern China where occurrence of peach brown rot caused by M. fructicola has been confirmed (2,4). The results indicated the further geographical spread of the M. fructicola in China. References: (1) M. J. Hu et al. Plos One 6(9):e24990, 2011. (2) M. J. Hu et al. Plant Dis. 95:225, 2011. (3) T. J. White et al. Amplification and direct sequencing of fungal ribosomal RNA genes for phylogenetics. Academic Press, San Diego, 1990. (4) X. Q. Zhu et al. Plant Pathol. 54:575, 2005.