Search

This study aims to explore the factors affecting variation in ozone concentration, using ozone concentration monitoring data from the Beijing–Tianjin–Hebei (Jing–Jin–Ji) region from 2015 to 2022. The characteristics of the spatial and temporal variation in ozone concentration, as well as the impact of meteorological and land-use types on this variation, were investigated. Seasonally, ozone concentrations in the Jing–Jin–Ji region were highest in summer, followed by spring and autumn, and were lowest in winter. Spatially, a characteristic trend of lower concentrations in urban centers and higher concentrations in suburban areas was found. From the results of correlation analysis and a stepwise regression model, temperature and solar radiation were found to be the primary factors affecting seasonal variations in ozone concentration, explaining 67.9% of the variance. Additionally, the results of geographically weighted regression models confirmed the spatial heterogeneity of the impact of temperature and solar radiation on ozone concentration. In urban centers, such as Beijing and Tianjin, temperature and solar radiation more strongly influenced ozone concentration. To determine the factors driving this spatial heterogeneity, a geodetector was employed to analyze the impact of various geographical factors on the spatial distribution of ozone concentration. In winter, the impact of various factors of urbanization, such as lighting index, population density, and construction land, as well as air quality factors (PM2.5 and NO2), on ozone concentration was stronger, with q values greater than 0.2. However, in autumn, the influence of these factors on ozone concentration weakened. Furthermore, the results of the two-factor interaction detection analysis showed that the q values for the interaction between urban and air quality factors ranged between 0.40 and 0.47, which were substantially higher than those for other interactions. This further confirmed the strong influence of urban activities on ozone concentration. [ABSTRACT FROM AUTHOR]

Purpose: Diabetic retinopathy (DR) is a serious complication of diabetes mellitus, which nearly happens to all the diabetic sufferers. This study aims to identify the preliminary molecular regulation involved in the therapeutic efficacy of astragaloside IV (AS- IV) for DR. Methods: Diabetic rat models were established and treated with AS-IV. Optical coherence tomography (OCT) and Hematoxylin-eosin (HE) staining was employed to demonstrate the histopathological changes. The main targets of AS-IV were identified by searching from public databases of traditional Chinese medicine (GeneCards, PharmMapper and Swiss Target Prediction). Besides, disease targets of DR were also obtained by integrated data from GEO datasets and predicted from public databases. Protein-protein interaction (PPI) network was constructed by Cytoscape with overlapping genes and 10 core targets were selected, on which Gene Ontology (GO) along with Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted. The interaction between AS-IV and these crucial genes were analyzed using molecular docking. RT-qPCR and western blot were used to verify the expression variation of core targets. Results: OCT imaging and HE staining demonstrated that AS-IV administration significantly increased retinal thickness in diabetic rats, obviously alleviating DR induced histopathological changes as well as elevated blood glucose levels. 107 common targets of AS-IV and DR were determined after intersection. PPI network analysis filtered 10 hub genes potentially targeted by AS-IV, including VEGFA, CASP3, HIF1α, STAT3, CTNNB1, SRC, AKT1, EGFR, IL1β and IL6. Enrichment analysis indicated that these genes were mainly enriched in biological processes like T cell activation, epithelial cell proliferation and protein kinase B signaling, and involved in oxidative stress, apoptosis and inflammation-related pathways. The molecular docking prediction suggested that AS-IV exhibited stable binding to these core targets. In addition, mRNA levels of core targets in diabetic rats were differentially expressed before and after AS-IV treatment. Western blot further revealed that AS-IV treatment elevated DR-depressed protein levels of PI3K and AKT. Conclusion: Our study elucidated the effect of AS-IV in attenuating retinopathy induced by diabetes in rats and preliminarily unveiled the therapeutic efficacy of AS-IV in the treatment of DR might be attributed to activation of PI3K-AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Aim of the study: To investigate the differences and relevance, and to evaluate the clinical significance of fluorescence in situ hybridisation and immunohistochemistry (IHC) in detecting HER2 in gastric cancer tissues. Material and methods: The expression of HER2 protein and the amplification of the HER2 gene in 118 gastric cancer tissues were detected by immunohistochemistry and fluorescence in situ hybridisation, respectively. Results: Using IHC, we found that in 40 cases (33.9%) the HER2 expression was at level 0, in 33 cases (28.0%) the HER2 expression was at level 1+, in 16 cases (14%) the HER2 expression was at level 2+, and in 29 cases (25.6%) the HER2 expression was at level 3+, respectively. Using the FISH test, 38 of 118 cases (32.2%) were judged as positive results. The concordance rate between the results of IHC and FISH in all cases was 85.6%. The concordance rate of IHC and FISH was high in cases of HER2 expression at level 0, 1+ and 3+ according to IHC, but low in cases of 2+ according to IHC (43.8%). Conclusions: Immunohistochemistry cannot predict HER2 gene amplification accurately. The FISH test should be executed in IHC 2+ cases. [ABSTRACT FROM AUTHOR]

Cryptococcus brain abscess was uncommon and cryptococcal cerebellar abscess and pneumonia were rarely in immunocompetent patients. We report a case of an immunocompetent adult with multiple cerebellarabscess and pneumonia caused by cryptococcus. She gave a history of headache, vomiting, chest pain and bilateral cerebellar signs. Multiple Cerebellar abscess and pneumonia were detected on magneticresonance imaging (MRI). Our patient underwent lung biopsy, resection of the lesion and thecryptococcoma was subsequently diagnosed by histopathologic examination. The patient was treated successfully with debridements and prolonged antifungal medicine therapy. [ABSTRACT FROM AUTHOR]

• HIE exerted tremendous pernicious effects on the development of neonatal brain. • BDNF induces lower expression of Stx1b and higher expression of VDAC1. • BDNF promotes neurite regeneration. • This study provide a theoretical foundation for clinical therapy of HIE. Neonatal hypoxic-ischemic encephalopathy (HIE), is a major cause of neurologic disorders in terms of neonates, with the unclear underlying mechanisms. In the study, triphenyl tetrazolium chloride (TTC) staining and Zea-longa score were performed to examine the neurologic damage in hypoxia and ischemia (HI) rats. The results showed that HI induced obviously infarct and serious neurologic impairment in neonatal rats. Then, protein chip was applied to detect the differential expression genes in cortex and hippocampus and found the brain-derived neurotrophic factor (BDNF) down-regulated both in cortex and hippocampus. Moreover, low expression of BDNF after HI in right cortex and hippocampus was validate by immunohistochemistry (IHC) and Western Blotting (WB). Afterwards, overexpressing and interfering HSV vector were produced, then verified by immunofluorescent staining and real-time quantitative polymerase chain reaction (qRT-PCR). The results of Tuj1 staining indicated that overexpression of BDNF could promote axonal regeneration and inhibit neuron swelling, whereas BDNF interference take an opposite effect after Oxygen glucose deprivation (OGD) injury. Finally, the interaction network among BDNF and associated proteins as examined by Genemania and confirmed by qRT-PCR. We found that the expression of VDAC1 was decreased and Stx1b was increased when BDNF overexpressing, which indicated that BDNF promoted neurite regrowth after OGD might be related to downregulation of VDAC1 and upregulation of Stx1b. Our results might provide novel strategy for the treatment of neurological defects induced by cerebral ischemia and hypoxia. [ABSTRACT FROM AUTHOR]