Some studies have reported that temporomandibular joint disorder (TMD) is related to tinnitus. However, there is no study of the relationship and prevalence of dental pain and tinnitus. We evaluated the associations between the prevalence of tinnitus and TMD and dental pain by analysing the Korean national health survey. We analysed totally 11 745 participants. The presence of tinnitus, TMD symptoms and dental pain was surveyed by self-assessment questionnaires from all the participants. Multivariable regression analysis was applied to acquire odds ratios (OR) and 95% confidence intervals (CI). The prevalence of tinnitus was higher in the subjects with dental pain (21.1%), TMD (22.5%) and both symptoms (31.2%) than subjects without those symptoms (19.6%). After adjusting for all covariates, subjects with TMD had tinnitus 1.6 times more than subjects without TMD. In the subanalysis, age group more than 65 years, women, and obese subjects had tinnitus more than men, age group <65, and non-obese subjects, respectively. TMD alone and both dental pain and TMD were associated with tinnitus (OR = 1.389 and 95% CI 1.054-1.832 and 2.206 and 1.637-2.974, respectively). Subjects with TMD had more tinnitus than subjects without TMD. Moreover, subjects with dental pain in addition to TMD had increased prevalence of tinnitus than TMD alone.

The pathogenic role of core promoter (CP) mutations (T1762/A1764) of hepatitis B virus (HBV) in hepatitis B e antigen (HBeAg) seroconversion or disease progression remains unclear. We investigated the clinical relevance of these mutants over a long-term follow-up period of up to 15 years. In this longitudinal cohort study, 29 HBeAg-positive patients with biopsy-proved chronic active hepatitis without cirrhosis were regularly monitored for >10 years. The viral isolates were characterized, using the frozen liver tissue obtained on the day of biopsy. Long-term outcomes were compared between patients with and without CP mutations of HBV at baseline. HBV genotyping showed that 100% of study subjects were infected with genotype C HBV. During a median follow-up period of 12.5 years, patients without double CP mutations of HBV at baseline showed a tendency towards achieving an earlier HBeAg seroconversion than those with (6.9 vs 9.4 years, P = 0.062) double CP mutations. Double CP mutations at baseline were also significantly associated with the eventual development of cirrhosis or hepatocellular carcinoma (P = 0.013), whereas the absence of double CP mutations predicted inactive carrier status at the last follow-up (P = 0.027). At 10 years, liver-related tests were also significantly better in patients without double CP mutations of HBV than in those with these mutations, as reflected by higher platelet counts and albumin levels (P = 0.036 and P = 0.044, respectively). Double T1762/A1764 mutations are significantly related to liver deterioration in HBeAg-positive genotype C active hepatitis patients. A longer period of immune clearance coupled with delayed HBeAg seroconversion appears to contribute to disease progression in patients harbouring these mutations in the CP region of HBV.

Th17 cells that produce interleukin (IL)‐17 play a key role in the pathogenesis of autoimmune inflammation. Among the various cytokines that are involved in the IL‐17 pathway, members of the IL‐1β family, including IL‐18, have recently gained attention. In this study, we stimulated synovial fibroblasts with a combination of IL‐17 and IL‐18 and quantified their stromal cell–derived factor‐1 (SDF‐1) production by enzyme‐linked immunosorbent assay and their transcript levels by reverse transcription–polymerase chain reaction. Both IL‐17 and IL‐18 significantly increased the level of SDF‐1, not only individually but also synergistically (P < 0.05). The synergism was effectively suppressed by anti‐IL‐17 and ‐IL‐18 antibodies, and a PI3K inhibitor. To the best of our knowledge, this is the first report of PI3K‐dependent synergism between IL‐18 and IL‐17, and this work adds a novel perspective of the role of IL‐18 in immune regulation. The individual effects of these two cytokines, and their interactions, suggest an interrelationship between the IL‐1 family and IL‐17.

Histological changes in the brains of Fischer rats at different times after interstitial heating with various thermal doses were studied. The brains, subjected to sham-heating, and heating at 39 and 40 degrees C for 30 min showed mild capillary congestion and minimal vacuolation at 4, 24 and 72 h. In the brains heated to 41, 42 and 43 degrees C for 30 min, there was local vascular congestion, petechiae, vacuolation and cellular shrinkage with nuclear pyknosis at 4 h; enhanced congestion and petechiae, acute cellular necrosis, infiltration of polymorphonuclear leukocytes and marked vacuolation at the margin at 24h; total coagulative necrosis of all parenchymal and vascular elements, early liquefaction necrosis and vascular hyperplasia at the margin at 72 h; enhanced vascular hyperplasia at the margin at 120 h and 168 h. The threshold thermal dose for the histopathological damage in the rat brain was heating at 41 degrees C for 30 min.