We aimed to investigate the pathophysiology of diabetes-associated hearing impairment in type 1 diabetes using mice with streptozotocin-induced diabetes (C57BL/6J; male). Hearing function was evaluated 1, 3, and 5 months after induction of diabetes (five diabetic and five control animals per time point) using auditory-evoked brain stem responses (ABRs). Mice (four diabetic and four control) were exposed to loud noise (105 dB) 5 months after induction of diabetes. ABRs were measured before and after noise exposure. Cochlear blood flows were measured by laser-Doppler flowmeter. Spiral ganglion cells (SGCs) were counted. Vessel endothelial cells were observed by CD31 immunostaining. Chronologic changes in the ABR threshold shift were not significantly different between the diabetic and control groups. However, vessel walls in the modiolus of the cochleae were significantly thicker in the diabetic group than the control group. Additionally, recovery from noise-induced injury was significantly impaired in diabetic mice. Reduced cochlea blood flows and SGC loss were observed in diabetic mice cochleae after noise exposure. Our data suggest that diabetic cochleae are more susceptible than controls to loud noise exposure, and decreased cochlear blood flow due to sclerosis of the vessels and consequent loss of SGCs are possible mechanisms of hearing impairment in diabetic patients.

Vestibular schwannoma (VS) is an intracranial tumor arising from neoplastic Schwann cells and typically presenting with hearing loss. The traditional belief that hearing deficit is caused by physical expansion of the VS, compressing the auditory nerve, does not explain the common clinical finding that patients with small tumors can have profound hearing loss, suggesting that tumor-secreted factors could influence hearing ability in VS patients. We conducted profiling of patients’ plasma for 66 immune-related factors in patients with sporadic VS ( N > 170) and identified and validated candidate biomarkers associated with tumor size (S100B) and hearing (MCP-3). We further identified a nine-biomarker panel (TNR-R2, MIF, CD30, MCP-3, IL-2R, BLC, TWEAK, eotaxin, and S100B) with outstanding discriminatory ability for VS. These findings revealed possible therapeutic targets for VS, providing a unique diagnostic tool that may predict hearing change and tumor growth in VS patients, and may inform the timing of tumor resection to preserve hearing.

In the arterial phase of dynamic contrast-enhanced MR images, we observed areas of increased contrast enhancement adjacent to hepatocellular carcinomas treated by percutaneous ethanol injection. The purpose of this study was to assess the frequency, appearance, and location of this hyperperfusion abnormality. It is important not to mistake this finding for other pathologic conditions. Multisection dynamic MR images obtained in 33 consecutive patients with hepatocellular carcinoma treated with percutaneous ethanol injection were reviewed. Hepatic parenchymal hyperperfusion abnormalities were diagnosed when areas of early enhancement were seen in the hepatic parenchyma adjacent to the treated tumor. The location, appearance, and frequency of the findings were recorded. Hepatic parenchymal hyperperfusion abnormalities were observed in 15 (45%) of the 33 patients on arterial-dominant-phase images. Of these 15 patients, 10 (67%) had MR imaging within 1 month after percutaneous ethanol injection. Hyperperfusion abnormalities were located in liver parenchyma adjacent to the lesion with wedge-shaped appearances. In two patients, early opacification of the peripheral portal branch was seen within the area of hyperperfusion abnormalities. Hepatic hyperperfusion abnormalities are commonly seen adjacent to a treated hepatocellular carcinoma on contrast-enhanced MR images. Awareness of this hyperperfusion abnormality, which is caused by increased blood flow after percutaneous ethanol injection, is important because such a finding may be misinterpreted as another pathologic condition such as tumor progression or tumor thrombosis of the portal vein branches.

A 12-week, double-blind controlled study comparing low dose α-interferon (5×10⁵ iu, twice a week) and placebo was carried out to determine whether this drug has an immunomodulatory effect in rheumatoid arthritis. There were statistically significant improvements in the patients' joint score, C-reactive protein value and platelet count, without any side effects. Interferon-a caused an increase of serum calcium and a decrease of alkaline phosphatase. Thus, α-interferon requires further investigation as a possible additional useful treatment for rheumatoid arthritis