Lung diseases, such as asthma, chronic obstructive pulmonary diseases (COPD), and cystic fibrosis (CF), are among the leading causes of mortality and morbidity globally. They contribute to substantial economic burdens on society and individuals. Currently, only a few treatments are available to slow the development and progression of these diseases. Thus, there is an urgent unmet need to develop effective therapies to improve quality of life and limit healthcare costs. An increasing body of clinical and experimental evidence suggests that altered zinc and its regulatory protein levels in the systemic circulation and in the lungs are associated with these disease’s development and progression. Zinc plays a crucial role in human enzyme activity, making it an essential trace element. As a cofactor in metalloenzymes and metalloproteins, zinc involves a wide range of biological processes, such as gene transcription, translation, phagocytosis, and immunoglobulin and cytokine production in both health and disease. Zinc has gained considerable interest in these lung diseases because of its anti-inflammatory, antioxidant, immune, and metabolic modulatory properties. Here we highlight the role and mechanisms of zinc in the pathogenesis of asthma, COPD, CF, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, and pulmonary hypertension.
Spatially- and/or temporally-controlled drug release has always been the pursuit of drug delivery systems (DDSs) to achieve the ideal therapeutic effect. The abnormal pathophysiological characteristics of the tumor microenvironment, including acidosis, overexpression of special enzymes, hypoxia, and high levels of ROS, GSH, and ATP, offer the possibility for the design of stimulus-responsive DDSs for controlled drug release to realize more efficient drug delivery and anti-tumor activity. With the help of these stimulus signals, responsive DDSs can realize controlled drug release more precisely within the local tumor site and decrease the injected dose and systemic toxicity. This review first describes the major pathophysiological characteristics of the tumor microenvironment, and highlights the recent cutting-edge advances in DDSs responding to the tumor pathophysiological environment for cancer therapy. Finally, the challenges and future directions of bio-responsive DDSs are discussed.
Introduction. Thoracoscopic minimally invasive surgery is the main method for the treatment of lung cancer. The reduction of surgical trauma can effectively reduce the intraoperative and postoperative inflammatory reaction. The aim of the study is to compare the intraoperative and postoperative inflammatory reactions in patients with non-small-cell lung cancer (NSCLC) treated by single-port thoracoscopic surgery and three-port thoracoscopic surgery. Methods. A total of 68 NSCLC patients (stages I and II) of thoracoscopic surgery were selected and randomly divided into two groups where they received either single-port thoracoscopic surgery or three-port thoracoscopic surgery. Intraoperative and postoperative serum inflammatory markers (C-reactive protein, CRP; serum amyloid A protein, SAA; and interleukin 6, IL-6) were detected using the enzyme-linked immunosorbent assay. Results. The CRP level of the single-port group was significantly lower than that of the three-port group during surgery, the first day after surgery, and third day after surgery ( P < 0.05 ). The level of IL-6 in the single-port group was significantly lower than that in the three-port group during surgery on the first and third days after surgery ( P < 0.05 ). The level of SAA in the single-port group was also significantly lower than that in the three-port group on the first and third days after surgery ( P < 0.05 ). Conclusion. Compared with three-port thoracoscopic surgery, single-port thoracoscopic surgery could reduce the inflammatory response and improve the recovery of NSCLC patients. Single-port thoracoscopic surgery is worthy of further promotion in the current treatment field of NSCLC in terms of reducing intraoperative and postoperative inflammatory reactions.
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