The occurrence and development mechanisms of esophageal stricture: state of the art review.

BACKGROUND: Esophageal strictures significantly impair patient quality of life and present a therapeutic challenge, particularly due to the high recurrence post-ESD/EMR. Current treatments manage symptoms rather than addressing the disease's etiology. This review concentrates on the mechanisms of esophageal stricture formation and recurrence, seeking to highlight areas for potential therapeutic intervention. METHODS: A literature search was conducted through PUBMED using search terms: esophageal stricture, mucosal resection, submucosal dissection. Relevant articles were identified through manual review with reference lists reviewed for additional articles. RESULTS: Preclinical studies and data from animal studies suggest that the mechanisms that may lead to esophageal stricture include overdifferentiation of fibroblasts, inflammatory response that is not healed in time, impaired epithelial barrier function, and multimethod factors leading to it. Dysfunction of the epithelial barrier may be the initiating mechanism for esophageal stricture. Achieving perfect in-epithelialization by tissue-engineered fabrication of cell patches has been shown to be effective in the treatment and prevention of esophageal strictures. CONCLUSION: The development of esophageal stricture involves three stages: structural damage to the esophageal epithelial barrier (EEB), chronic inflammation, and severe fibrosis, in which dysfunction or damage to the EEB is the initiating mechanism leading to esophageal stricture. Re-epithelialization is essential for the treatment and prevention of esophageal stricture. This information will help clinicians or scientists to develop effective techniques to treat esophageal stricture in the future.

Biologic Mechanisms of Macrophage Phenotypes Responding to Infection and the Novel Therapies to Moderate Inflammation.

Pro-inflammatory and anti-inflammatory types are the main phenotypes of the macrophage, which are commonly notified as M1 and M2, respectively. The alteration of macrophage phenotypes and the progression of inflammation are intimately associated; both phenotypes usually coexist throughout the whole inflammation stage, involving the transduction of intracellular signals and the secretion of extracellular cytokines. This paper aims to address the interaction of macrophages and surrounding cells and tissues with inflammation-related diseases and clarify the crosstalk of signal pathways relevant to the phenotypic metamorphosis of macrophages. On these bases, some novel therapeutic methods are proposed for regulating inflammation through monitoring the transition of macrophage phenotypes so as to prevent the negative effects of antibiotic drugs utilized in the long term in the clinic. This information will be quite beneficial for the diagnosis and treatment of inflammation-related diseases like pneumonia and other disorders involving macrophages.

Optimizing Flexible Microelectrode Designs for Enhanced Efficacy in Electrical Stimulation Therapy.

To investigate the impact of electrode structure on Electrical Stimulation Therapy (EST) for chronic wound healing, this study designed three variants of flexible microelectrodes (FMs) with Ag-Cu coverings (ACCs), each exhibiting distinct geometrical configurations: hexagonal, cross-shaped, and serpentine. These were integrated with PPY/PDA/PANI (3/6) (full name: polypyrrole/polydopamine/polyaniline 3/6). Hydrogel dressing comprehensive animal studies, coupled with detailed electrical and mechanical modeling and simulations, were conducted to assess their performance. Results indicated that the serpentine-shaped FM outperformed its counterparts in terms of flexibility and safety, exhibiting minimal thermal effects and a reduced risk of burns. Notably, FMs with metal coverings under 3% demonstrated promising potential for optoelectronic self-powering capabilities. Additionally, simulation data highlighted the significant influence of hydrogel non-uniformity on the distribution of electrical properties across the skin surface, providing critical insights for optimizing EST protocols when employing hydrogel dressings.

Enhanced heterogeneous interface to construct intelligent conductive hydrogel gas sensor for individualized treatment of infected wounds.

In this study, we developed an enhanced heterogeneous interface intelligent conductive hydrogel NH3 sensor for individualized treatment of infected wounds. The sensor achieved monitoring, self-diagnosis, and adaptive gear adjustment functions. The PPY@PDA/PANI(3/6) sensor had a minimum NH3 detection concentration of 50 ppb and a response value of 2.94 %. It also had a theoretical detection limit of 49 ppt for infected wound gas. The sensor exhibited a fast response time of 23.2 s and a recovery time of 42.9 s. Tobramycin (TOB) was encapsulated in a self-healing QCS/OD hydrogel formed by quaternized chitosan (QCS) and oxidized dextran (OD), followed by the addition of polydopamine-coated polypyrrole nanowires (PPY@PDA) and polyaniline (PANI) to prepare electrically conductive drug-loaded PPY@PDA/PANI hydrogels. The drug-loaded PPY@PDA/PANI hydrogel was combined with a PANI/PVDF membrane to form an enhanced heterogeneous interfacial PPY@PDA/PANI/PVDF-based sensor, which could adaptively learn the individual wound ammonia response and adjust the speed of drug release from the PPY@PDA/PANI hydrogel with electrical stimulation. Drug release and animal studies demonstrated the efficacy of the PPY@PDA/PANI hydrogel in inhibiting infection and accelerating wound healing. In conclusion, the gas-sensitive conductive hydrogel sensing system is expected to enable intelligent drug delivery and provide personalized treatment for complex wound management.