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Lung cancer is the second most common, and the deadliest, disease globally. Because it is often diagnosed late, surgical resection is not a viable treatment option for ∼75 % of patients, often resulting in a poor prognosis. Of the available treatments, radioactive iodine-125 (125-I) seed implantation therapy, or brachytherapy, has emerged as a promising option. In this procedure, small radioactive seeds are implanted inside tumor cells to produce sustained effects. Because of the short radial distance of this radiation, 125-I brachytherapy selectively and efficiently kills cancer cells while minimizing injury to adjacent cells. The present review describes the mechanism of 125-I seed implantation in the treatment of lung cancer, its efficacy and safety, and its combination with other therapies. We conclude that radioactive 125-I seed implantation and its use in combination with other therapies are good options for the management of local tumor growth, pain palliation, and improving the life span of patients suffering from lung cancers. This technique can enhance the clinical efficacy of treatment and improve the overall survival of patients with lung cancers. However, standardized dosage regimens and other procedures are still required to achieve treatment homogeneity and provide guidance for the clinical implementation of this technique., Competing Interests: Declaration of competing interest No relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

PM 2.5 exposure has been found to cause gut dysbiosis and impair glucose homeostasis in human and animals, yet their underlying biological connection remain unclear. In the present study, we aim to investigate the biological significance of gut microbiota in PM 2.5 -induced glucose metabolic abnormalities. Our results showed that microbiota depletion by antibiotics treatment significantly alleviated PM 2.5 -induced glucose intolerance and insulin resistance, as indicated by the intraperitoneal glucose tolerance test, glucose-induced insulin secretion, insulin tolerance test, insulin-induced phosphorylation levels of Akt and GSK-3β in insulin sensitive tissues. In addition, faecal microbiota transplantation (FMT) from PM 2.5 -exposed donor mice successfully remodeled the glucose metabolism abnormalities in recipient mice, while the transplantation of autoclaved faecal materials did not. Faecal microbiota analysis demonstrated that the composition and alpha diversity of the gut bacterial community were altered by PM 2.5 exposure and in FMT recipient mice. Furthermore, short-chain fatty acids levels analysis showed that the circulating acetate was significantly decreased in PM 2.5 -exposed donor and FMT recipient mice, and supplementation of sodium acetate for 3 months successfully improved the glucose metabolism abnormalities induced by PM 2.5 exposure. These results indicate that manipulating gut microbiota or its metabolites could be a potential strategy for preventing the adverse health effects of ambient PM 2.5 ., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Ambient fine particles (PM 2.5 ) are known to cause various reproductive and developmental diseases. However, the potential mechanisms of PM 2.5 exposure induced female reproductive damage remain unclear., Methods: Four weeks old female C57BL/6 J mice were exposed to filtered air (FA, n = 10) or concentrated ambient PM 2.5 (CAP, n = 10) using a versatile aerosol concentration enrichment system. After 9 weeks of the exposure, mice were sacrificed under sevoflurane anesthesia and tissue samples were collected. Immunohistochemical analysis, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, and RNA-sequencing were performed to analyze the effects of PM 2.5 exposure on follicle development and elucidate its potential mechanisms., Results: Chronic PM 2.5 exposure resulted in follicular dysplasia. Compared to the FA-exposed group, follicular atresia in the CAP-exposed mice were significantly increased. Further studies confirmed that CAP induced apoptosis in granulosa cells, accompanied by a distortion of hormone homeostasis. In addition, RNA-sequencing data demonstrated that CAP exposure induced the alteration of ovarian gene expressions and was associated with inflammatory response., Conclusions: Chronic exposure to CAP can induce follicular atresia, which was associated with hormone modulation and inflammation., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Aim: Ambient fine particulate matter (PM 2.5 ) consists of various components, and their respective contributions to the toxicity of PM 2.5 remains to be determined. To provide specific recommendations for preventing adverse effects due to PM 2.5 pollution, we determined whether the induction of pulmonary inflammation, the putative pathogenesis for the morbidity and mortality due to PM 2.5 exposure, was fractioned through solubility-dependent fractioning., Methods: In the present study, the water and heptane solubilities-dependent serial fractioning of diesel exhaust particulate matter (DEP), a prominent source of urban PM 2.5 pollution, was performed. The pro-inflammatory actions of these resultant fractions were then determined using both an intratracheal instillation mouse model and cultured BEAS-2B cells, a human bronchial epithelial cell line., Results: Instillation of the water-insoluble, but not -soluble fraction elicited significant pulmonary inflammatory and acute phase responses, comparable to those induced by instillation of DEP. The water-insoluble fraction was further fractioned using heptane, a polar organic solvent, and instillation of heptane-insoluble, but not -soluble fraction elicited significant pulmonary inflammation and acute phase responses. Furthermore, we showed that DEP and water-insoluble DEP, but not water-soluble DEP, activated pro-inflammatory signaling in cultured BEAS-2B cells, ruling out the possibility that the solubility impacts the in vivo distribution and thus the pulmonary inflammatory response., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Ambient fine particulate matter (PM 2.5 ) exposure correlates with adverse cardiometabolic effects. The underlying mechanisms have not yet been fully understood. Hypothalamic-pituitary-adrenal (HPA) axis, as the central stress response system, regulates cardiometabolic homeostasis and is implicated in the progression of various adverse health effects caused by inhalational airborne pollutant exposure. In this study, we investigated whether ambient PM 2.5 exposure activates HPA axis and its effect mediating PM 2.5 -induced pulmonary inflammation. C57Bl/6 J mice were intratracheally instilled with different concentrations of diesel exhaust PM 2.5 (DEP), and plasma was harvested at different times. Assessments of plasma stress hormones revealed that DEP instillation dose- and time-dependently increased mouse circulating corticosterone and adrenocorticotropic hormone (ACTH) levels, strongly supporting that DEP instillation activates HPA axis. To determine which components of DEP activate HPA axis, C57Bl/6J mice were intratracheally instilled with water-soluble and -insoluble fractions of DEP. Plasma analyses showed that water-insoluble but not -soluble fraction of DEP increased circulating corticosterone and ACTH levels. Consistently, concentrated ambient PM 2.5 (CAP) exposure significantly increased mouse urine and hair corticosterone levels, corroborating the activation of HPA axis by ambient PM 2.5 . Furthermore, deletion of stress hormones by total bilateral adrenalectomy alleviated PM 2.5 -induced pulmonary inflammation, providing insights into the contribution of central neurohormonal mechanisms in modulating adverse health effects caused by exposure to PM 2.5 ., (Copyright © 2020 Elsevier Inc. All rights reserved.)