Cubital tunnel syndrome refers to compression neuropathy caused by pressure on the ulnar nerve pathway around the elbow. A 63-year-old male patient visited the clinic complaining of decreased sensation and weakness in his left ring finger and little finger, stating that the symptoms first began 6 months prior. He had undergone surgery to remove a ganglion cyst from his left elbow joint about 5 years prior in Mongolia. Magnetic resonance imaging revealed a cystic mass located at the previous surgical site, which was compressing the ulnar nerve within the cubital tunnel. Ulnar nerve decompression and anterior transposition were performed, and the cystic mass was excised. Upon pathological examination, the mass was diagnosed as a ganglion cyst. The patient’s symptoms including sensory dysfunction and weakness improved over the 1-year follow-up period. This report describes a rare case of ganglion cyst recurrence compressing the ulnar nerve in the cubital tunnel after previous ganglion cyst excision.

BACKGROUND: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. METHODS: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. RESULTS: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. CONCLUSION: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.
Cadmium ; Cytokines ; Environmental Pollutants ; Epithelial Cells* ; Gene Expression ; Gene Expression Profiling ; Humans* ; Immunohistochemistry ; In Situ Hybridization ; Inflammation ; Lung ; Lung Neoplasms ; Pulmonary Disease, Chronic Obstructive ; RNA, Messenger ; Signal Transduction ; Smoke ; Smoking ; Succinate Dehydrogenase