We have previously shown impaired ventricular function in asymptomatic middle-aged type 1 (insulin-dependent) diabetic patients who had no evidence of coronary artery disease. The diabetic patients had normal coronary angiograms but reduced ventricular ejection fraction on exercise. To examine the possible contribution of small vessel disease to this functional abnormality, we compared endomyocardial biopsies from seven symptom-free type 1 diabetic patients with biopsies from seven age- and sex-matched non-diabetic subjects. Interstitial fibrosis was present in three diabetic patients, arteriolar hyalinization in three patients and arteriolar thickening was observed in five patients. Morphometry performed on electron micrographs showed no significant difference in the thickness of the capillary basal lamina between diabetics and controls. While the functional significance of the abnormalities on light microscopy is unclear, our findings indicate that the abnormality of cardiac function described in diabetes is not associated with thickening of the myocardial capillary basal lamina.

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SUMMARY The expression ofimmunoreactive a interferon was examined in 78 liver biopsy specimens using an indirect immunoperoxidase technique. Biopsy specimens included cases of acute viral hepatitis, chronic active hepatitis, primary biliary cirrhosis, alcoholic hepatitis, large bile duct obstruction and normal liver. Kupffer cells were positive for a interferon in all cases. Hepatocytes were negative for a interferon in normal liver but in acute viral hepatitis were positive in perivenular and necrotic areas. Hepatocytes were positive in periportal areas, associated with piecemeal necrosis, in chronic active hepatitis and primary biliary cirrhosis, and were positive in perivenular areas in alcoholic hepatitis and large bile duct obstruction.The unexpected finding of a interferon in hepatocytes in non-viral liver disease indicates that the presence of this substance in liver cells cannot be taken as a specific marker of viral infection.Hepatitis B (HBV) virus is not directly cytopathic and T cell mediated cytolysis is considered to be the means of viral elimination in HBV infection. The recognition of infected cells by cytotoxic T lymphocytes depends on the association between viral determinants and class I major histocompatibility complex (MHC) molecules. The interferons are known to induce an increase of synthesis and display of MHC class I molecules, and it has been proposed that during acute HBV infection, interferon promotes hepatocyte MHC class I display, which increases the possibility of immune attack by cytotoxic T cells. There is indirect evidence to support this hypothesis. In uncomplicated acute HBV infection plasma interferon concentrations rise,' and increased hepatocyte expression of (2 microglobulin (a subunit of HLA class I antigen) has been shown.2 Recently a technique for the detection of immunoreactive a interferon (IFN-a) in formalin fixed, paraffin wax embedded tissue has been developed.3 We used this technique on a series of liver biopsy specimens to investigate the expression of a interferon in viral hepatitis and in other liver diseases to ascertain ifits expression by hepatocytes is a specific indicator of viral infection. Material and methodsSeventy eight percutaneous and wedge liver biopsy specimens from nine cases of acute viral hepatitis, 14

the study. Group 1 included 30 "normal" temporal bones from 22 cases (mean age, 70 years; range, 50 -82) having no histopathologic findings of otologic disease. Group 2 included 34 temporal bones from 22 cases (mean age, 74 years; range, 53-89) with cochlear otosclerosis. In the lateral and posterior semicircular canal, the crista ampullaris was cut perpendicular to its axis. Dark cells within 100 microns of the transitional epithelium that had identifiable nuclei were counted.Results: The mean number of dark cells for group 1 was 13.3 (SD Ϯ 2.3) and for group 2, 12.1 (SD Ϯ 3.0). No difference was observed between the groups (P Ͻ 0.05). Conclusion:Our study suggests that cochlear otosclerosis does not injure dark cells of the crista ampullaris.Significance: It has been well established that dark cells show several enzyme activities and are involved in the regulation of the endolymph. Although several studies have reported degeneration of vestibular nerve and Scarpa ganglion cells in otosclerosis, no investigation was performed to evaluate histopathologic changes in dark cells of crista ampullaris in otosclerosis in an effort to understand their role in vestibular symptoms.