Thyroid cancer is caused by multiple factors, including genetics, environment, metabolism, and the immune microenvironment, among which ionizing radiation exposure is an important risk factor for thyroid cancer. As one of the most sensitive target organs of ionizing radiation, the thyroid gland may have different risks of thyroid cancer caused by different types of ionizing radiation exposures, such as medical exposure, occupational exposure, and emergency exposure. The sensitivity of children and adolescents are higher than that of adults. The dose-response relationship still needs to be further explored. The molecular mechanism between ionizing radiation and the increased risk of thyroid cancer is complex, which may involve DNA damage and repair abnormalities, gene mutations, non-coding RNA regulation, DNA methylation, cell cycle regulation imbalance, and immune microenvironment changes. This article reviews the risk and molecular mechanisms associated with different types of ionizing radiation exposure in thyroid cancer, based on literature retrieved from CNKI and PubMed databases. It aims to provide a theoretical basis for the early monitoring, prevention, and intervention of thyroid cancer related to ionizing radiation exposure.

The increasing prevalence of food allergies significantly affects both the physical and mental health of patients, while concurrently imposing a substantial economic burden on a global scale. Immunoglobulin E (IgE)-mediated food allergies typically manifest as acute reactions and may lead to severe allergic responses. Previous treatment strategies have been predominantly centered on allergen avoidance and oral immunotherapy (OIT), resulting in augmented economic and psychological burdens. In recent years, omalizumab, the anti-IgE monoclonal antibody, has emerged as a treatment option, either as monotherapy or in combination with OIT, for patients with IgE-mediated food allergies. Omalizumab holds promise in augmenting allergen tolerance, accelerating desensitization processes, and mitigating adverse effects associated with OIT. Nonetheless, a multitude of unresolved inquiries persist concerning the practical applications of omalizumab, necessitating additional real world studies for clarification.

Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy- and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.
Pulmonary Disease, Chronic Obstructive/physiopathology* ; Autophagy/physiology* ; Humans ; Muscle, Skeletal/pathology* ; Mitophagy ; Animals ; Mitochondria/metabolism* ; Lysosomes

Polycystic ovary syndrome (PCOS) is the predominant cause of subfertility in reproductive-aged women; however, its pathophysiology remains unknown. Neurotensin (NTS) is a member of the gut-brain peptide family and is involved in ovulation; its relationship with PCOS is unclear. Here, we found that NTS expression in ovarian granulosa cells and follicular fluids was markedly decreased in patients with PCOS. In the in vitro culture of cumulus-oocyte complexes, the neurotensin receptor 1 (NTSR1) antagonist SR48692 blocked cumulus expansion and oocyte meiotic maturation by inhibiting metabolic cooperation and damaging the mitochondrial structure in oocytes and surrounding cumulus cells. Furthermore, the ERK1/2-early growth response 1 pathway was found to be a key downstream mediator of NTS/NTSR1 in the ovulatory process. Animal studies showed that in vivo injection of SR48692 in mice reduced ovulation efficiency and contributed to irregular estrus cycles and polycystic ovary morphology. By contrast, NTS partially ameliorated the ovarian abnormalities in mice with dehydroepiandrosterone-induced PCOS. Our findings highlighted the critical role of NTS reduction and consequent abnormal NTSR1 signaling in the ovulatory dysfunction of PCOS, suggesting a potential strategy for PCOS treatment.
Polycystic Ovary Syndrome/physiopathology* ; Female ; Animals ; Neurotensin/metabolism* ; Receptors, Neurotensin/antagonists & inhibitors* ; Mice ; Ovulation/drug effects* ; Humans ; Granulosa Cells/metabolism* ; Adult ; Oocytes/metabolism* ; MAP Kinase Signaling System ; Signal Transduction ; Follicular Fluid/metabolism* ; Disease Models, Animal ; Gonadotropin-Releasing Hormone/analogs & derivatives*

Objective:To summarize the best evidence for the management of ovarian hyperstimulation syndrome in patients undergoing assisted reproductive therapy.Methods:Evidence related to the management of ovarian hyperstimulation syndrome in patients undergoing assisted reproductive therapy,including guidelines,clinical decision,best clinical practice,systematic evaluation,expert consensus and evidence summary and related original research were systematically searched in UpToDate,BMJ Best Practice,World Health Organization(WHO)website,Guidelines International Network(GIN),National Institute for Health and Clinical Excellence(NICE)website,National Guidelines website,American Society for Reproductive Medicine(ASRM)website,New York Academy of Sciences(NYAS)website,Joanna Briggs Institute(JBI)database,Cochrane Library,CINAHL,PubMed,Wanfang database,CNKI,and China Biomedical Literature Database from inception to May 31,2024.Two researchers independently evaluated the quality of the literature,and a senior researcher made the final decision for literature inclusion.Results:A total of 15 articles were included in the study.Following quality assessment,one article was excluded.The remaining 14 articles included 5 practice guidelines,3 systematic reviews,2 expert consensuses,1 evidence summary,and 3 from UpToDate.Ultimately,27 pieces of evidence were identified across five key aspects:risk assessment,disease monitoring,early prevention,institutional management and health education.Conclusion:The updated evidence indicates that the monitoring and prevention of ovarian hyperstimulation syndrome should start early,personalized treatment plans should be provided for patients,and the rational allocation of treatment resources needs to be promoted to enhance effective management of ovarian hyper-stimulation syndrome.