Exploring the influencing factors of academic doctoral students' academic innovation behavior in the context of generative artificial intelligence: Self-determination theory and motivation-opportunity

Sudden sensorineural hearing loss (SSNHL) is an otologic emergency characterized by a hearing loss of at least 30 dB across three consecutive frequencies occurring within 72 hours []. It may present with accompanying symptoms such as tinnitus, aural fullness, and vertigo, significantly affecting patients’ quality of life []. The incidence of SSNHL ranges from 5 to 27 cases per 100,000 individuals annually, and approximately 90% of cases are classified as idiopathic []. Although multiple etiological hypotheses have been proposed, including viral infections, autoimmune mechanisms, and vascular dysfunction, the exact pathophysiology remains incompletely understood []. Among these, vascular dysfunction has emerged as one of the most widely accepted mechanisms. The cochlea is particularly vulnerable to ischemic injury due to its lack of collateral blood supply, rendering inner ear perfusion highly sensitive to hemodynamic changes []. Consequently, even minor disturbances in cochlear microcirculation, such as endothelial damage or microthrombosis, may trigger sudden hearing loss [,]. The abrupt onset of SSNHL resembles clinical events such as transient ischemic attacks, acute myocardial infarction, or retinal vascular occlusion, further supporting the critical role of vascular factors in its pathogenesis []. Homocysteine (HCY) is a sulfur-containing amino acid involved in methionine metabolism and plays a key role in biochemical pathways mediated by folic acid and vitamin B12 []. Elevated homocysteine levels have been recognized as an independent risk factor for vascular disease due to their association with endothelial dysfunction, increased oxidative stress, platelet activation, and structural alterations of the vascular wall [,]. Numerous studies have demonstrated a relationship between hyperhomocysteinemia and peripheral vascular disease, cerebrovascular events, and coronary artery disease [,]. In addition to its vascular effects, homocysteine has been implicated in neuronal toxicity through mechanisms such as excitotoxicity, calcium imbalance, DNA damage, and apoptosis [,]. Given the delicate microvascular and neural structure of the cochlea, these effects suggest that elevated homocysteine levels may contribute to the development of SSNHL.