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 investigate and analyze the behavioral and pathological differences in early-stage mouse models of epilepsy established by 2 different administration routes for kainic acid(KA),intracerebroventricular(ICV)injection and intraperitoneal(IP)injection.Methods A total of 100 male C57BL/6N wild-type(WT)mice(20～22 g)were randomly divided into ICV+normal saline(NS)control group(n=10),ICV+KA model group(n=40),IP+NS control group(n=10)and IP+KA model group(n=40).The ICV+KA model group was given 600 nL of KA(0.5 mg/mL)via ICV injection,and the IP+KA model group was injected with different dose of KA(25 mg/kg).Two control groups were administered equal volumes of NS via corresponding routes.After 3 d of modeling,the evaluation of behavioristics,molecular biology(including Western blotting),and neuropathological assessments(including FJB staining,TUNEL staining and immunofluorescence staining)were performed.Results No epileptic seizures were observed in both 2 control groups,while exhibited seizures were observed in both model groups.The mortality rates of the IP+KA group and the ICV+KA group were 47.50%and 65.00%respectively,while the success rates of modeling were 80.00%and 60.00%respectively.Compared with the IP+KA group,the ICV+KA group showed a significant increase in success rate and a significant reduction in mortality rate.FJB and TUNEL staining results showed that,compared with the IP+KA group,the severity of neurodegeneration and apoptotic changes in the hippocampus of the ICV+KA group were more significant(P＜0.05).Compared with the IP+KA group,there was also a significant difference in the expression of apoptotic proteins in the hippocampus of the ICV+KA group(P＜0.05).Immunofluorescence results showed that the astrocytes and microglia in the hippocampus and cortex of the ICV+KA and IP+KA groups were significantly activated compared with the control groups(P＜0.05),but the activation of glial cells in the hippocampus and cortex of the ICV+KA group was stronger than that of the IP+KA model group(P＜0.05)and the activation levels in the ICV+KA group were higher than in the IP+KA model group(P＜0.01).Moreover,expression levels of GFAP and Iba-1 proteins in the hippocampus and cortex were higher in the ICV+KA group than the IP+KA group(P＜0.05).Conclusion Two routes of KA administration are effective in construct epilepsy models.The mice with ICV administration route show a higher success rate and lower mortality rate,and more significant neuropathological damage and glial cell activation.