Lung injuries induced by ozone exposure in female mice: Potential roles of the gut and lung microbes.

Ozone (O3) is one of the most harmful pollutants affecting health. However, the potential effects of O3 exposure on microbes in the gut-lung axis related to lung injuries remain elusive. In this study, female mice were exposed to 0-, 0.5- and 1-ppm O3 for 28 days, followed by routine blood tests, lung function tests and histopathological examination of the colon, nasal cavity and lung. Mouse faeces and lungs were collected for 16s rRNA sequencing to assess the overall microbiological profile and screen for key differential enriched microbes (DEMs). The key DEMs in faecal samples were Butyricimonas, Rikenellaceae RC9 and Escherichia-Shigella, whereas those in lung samples were DNF00809, Fluviicola, Bryobacter, Family XII AD3011 group, Sharpea, MND1 and unclassified Phycisphaeraceae. After a search in microbe-disease databases, these key DEMs were found to be associated with lung diseases such as lung neoplasms, cystic fibrosis, pneumonia, chronic obstructive pulmonary disease, respiratory distress syndrome and bronchiectasis. Subsequently, we used transcriptomic data from Gene Expression Omnibus (GEO) with exposure conditions similar to those in this study to cross-reference with Comparative Toxicogenomic Database (CTD). Il-6 and Ccl2 were identified as the key causative genes and were validated. The findings of this study suggest that exposure to O3 leads to significant changes in the microbial composition of the gut and lungs. These changes are associated with increased levels of inflammatory factors in the lungs and impaired lung function, resulting in an increased risk of lung disease. Altogether, this study provides novel insights into the role of microbes present in the gut-lung axis in O3 exposure-induced lung injury.

Invisible Hand behind Female Reproductive Disorders: Bisphenols, Recent Evidence and Future Perspectives.

Reproductive disorders are considered a global health problem influenced by physiological, genetic, environmental, and lifestyle factors. The increased exposure to bisphenols, a chemical used in large quantities for the production of polycarbonate plastics, has raised concerns regarding health risks in humans, particularly their endocrine-disrupting effects on female reproductive health. To provide a basis for future research on environmental interference and reproductive health, we reviewed relevant studies on the exposure patterns and levels of bisphenols in environmental matrices and humans (including susceptible populations such as pregnant women and children). In addition, we focused on in vivo, in vitro, and epidemiological studies evaluating the effects of bisphenols on the female reproductive system (the uterus, ovaries, fallopian tubes, and vagina). The results indicate that bisphenols cause structural and functional damage to the female reproductive system by interfering with hormones; activating receptors; inducing oxidative stress, DNA damage, and carcinogenesis; and triggering epigenetic changes, with the damaging effects being intergenerational. Epidemiological studies support the association between bisphenols and diseases such as cancer of the female reproductive system, reproductive dysfunction, and miscarriage, which may negatively affect the establishment and maintenance of pregnancy. Altogether, this review provides a reference for assessing the adverse effects of bisphenols on female reproductive health.

Exploration of the damage and mechanisms of BPS exposure on the uterus and ovary of adult female mice.

Bisphenol S (BPS) has been followed with interest for its endocrine disrupting effects, but exploration on the reproductive system of adult females is lack of deep investigation. In the present study, adult female CD-1 mice were treated with BPS for 28 days at 300 µg/kg/day. After that, uteruses and ovaries were harvested for histopathological examination, RNA-seq analysis, and diseases risk prediction. Hematoxylin-eosin (H&E) staining results showed significant histological alterations in the uterus and ovary of the BPS-exposed mice. Bioinformatics analysis of the RNA-seq screened a certain number of differentially expressed genes (DEGs) in both uterus and ovary between BPS group and their corresponding vehicle control groups (Veh), respectively. Functional enrichment analysis of DEGs found that hormone metabolism and immunoinflammatory related pathways were enriched. Disease risk evaluation of the hub genes was performed and the results indicated that diseases associated with uterus and ovary were mainly related to tumors and cancers. Further pan cancer and ovarian cancer survival analysis based on human diseases database pointed out, Foxa1, Gata3, S100a8 and Shh for uterus, Itgam, Dhcr7, Fdps, Hmgcr, Hsd11b1, Hsd3b1, Ptges, F3, Fn1, Ptger4 and Srd5a1 for ovary were significant correlation with cancer. The findings suggest that BPS causes some histopathological changes, alters the expressions of hub genes, enhances uterine and ovarian tumors or even cancer risks.

Inhibition Sequence of miR-205 Hinders the Cell Proliferation and Migration of Lung Cancer Cells by Regulating PETN-Mediated PI3K/AKT Signal Pathway.

The aim of this study was to identify the pro-tumor role of miR-205 in patients with lung cancer (LC) on the cell proliferation and migration through regulating PTEN-mediated PI3K/AKT signal pathway. Paired cancer tissues and adjacent tissues were collected from 107 LC patients who received treatment in Jinan Central hospital. In addition, the purchased LC cell lines were transfected into HCC827 cell line to observe and compare the biological behaviors. Compared with adjacent tissues, miR-205 was statistically higher in LC tissues, while PTEN was notably lower (P < 0.05). Inhibition of miR-205 not only suppressed cell proliferation, migration and invasion, increased apoptosis rate, but regulated epithelial mesenchymal transformation (EMT)-related proteins. Likewise, overexpression of PETN played the same role as that of miR-205 inhibition sequence. Inhibited miR-205 or PTEN overexpression brought dramatically decreased PI3K and p-Akt. The relationship between miR-205 and PTEN was verified through the biological prediction website and luciferase reporter. Co-transfection experiments revealed that after cotransfection of miR-205 inhibitor and si-PETN, the cell proliferation and invasion showed no marked difference between cotransfection group and NC group. MiR-205 is involved in LC cell proliferation and migration by regulating PETN-mediated PI3K/AKT signal pathway, which may be a feasible treatment target for LC in clinical practice.

Self-assembly of L-cysteine-copper(II)/copper(I) multilayer thin films on gold.

Self-assembled multilayer thin films have been prepared on Au substrate by alternate surface derivatization with L-cysteine hydrochloride and cupric perchlorate. The layer-by-layer structure at each step of multilayer formation was investigated by X-ray photoelectron spectroscopy. The measurements indicate that there are two structure modes in the multilayers. One is that Cu(2+) sandwiches between two amino acid groups. The other one is that Cu(+) is bonded through disulfide and thiolate. This process is also confirmed by cyclic voltammetry of Cu ion at different self-assembled multilayers. Steps further on will lead to repeated multilayer films.