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Studying of influence of periodontal disease on vitality of pulp, the response thresholds of 421 teeth (250 normal teeth, 171 periodontal diseased teeth) were examined electronically by means of an automatic pulptester. (ANALYTIC TECHNOLOGY CO.) The pulp tester values of three experiments were averaged. The average value of normal teeth was 36.3 and that of periodontal diseased teeth 31.4. The response thresholds of periodontal diseased teeth were lower than those of normal teeth. This indicated that pulp was inflamed by periodontal disease and pulp vitality became weak.

This paper reports an autopsy case of a 78-year-old male with multiple nodules in the liver developed after long-termed administration of phosphate diethylstilbestrol (PDES) for prostatic cancer. Large part of these nodules were suspected to be well differentiated hepatocellular carcinoma with high level of serum alpha-fetoprotein (AFP) up to 3,400 ng/ml, but a part of them was evaluated to be a borderline between hepatocellular carcinoma and adenoma with mild cellular atypism. The liver other than the nodules showed liver fibrosis associated with liver cell dysplasia and peliosis hepatis-like change. This is a unique autopsy case of hepatocellular carcinoma closely related to diethylstilbestrol (DES) therapy for prostatic cancer.

Both granular and multiocular periadrenal brown adipose tissue (BAT) was present in 16 patients with Duchenne's progressive muscular dystrophy (PMD). In 12 cases (75%), diffusely distributed periadrenal BAT was observed. The common cause of death was respiratory failure, and blood gas level showed marked hypoxia. Scattered myocardial fibrosis was seen in all cases of PMD. We suspected that chronic hypoxia and cardiac fibrosis might be largely responsible for BAT transformation in patients with PMD.

A 78-year-old man with primary gastric plasmacytoma showing massive rod-shaped intracytoplasmic inclusions is presented. The patient was initially diagnosed as having a benign gastric ulcer and underwent partial gastrectomy. Around the ulcer of the resected stomach specimen, diffuse proliferation of plasma cells with massive rod-shaped intracytoplasmic inclusions was noticed by light microscopy. Immunohistochemically, these cells were found to contain IgM-kappa-type immunoglobulin upon peroxidase-antiperoxidase (PAP) staining. Electron microscopy showed that the intracytoplasmic inclusions were localized in the rough endoplasmic reticulum and had a lattice structure with a periodicity of about 120 A.

We report an autopsy case of methamphetamine-related intracranial hemorrhage and vasculitis. The possible relationship between drug usage and the occurrence of intracranial bleeding and cerebral vasculitis in such patients is discussed. A 22-year-old woman died after an intravenous injection of unknown dose of methamphetamine. A computed tomography head scan demonstrated massive subarachnoid hemorrhage and hematoma in corpus callosum. Cerebral angiography revealed nonfilling of bilateral intracranial carotid arteries and extravasation of contrast medium from right pericallosal artery which was visualized retrogradely via vertebral artery. Postmortem studies showed cerebral edema, subarachnoid and intracerebral hemorrhage, and intracranial vasculitis in the absence of aneurysm, arteriovenous malformation or chronic hypertension. Histological findings of necrosis of blood vessel walls with destruction of the elastica and smooth muscle layer, and without leukocytotic infiltration of the blood vessel walls were observed in order of anterior cerebral, middle cerebral, vertebral, posterior cerebral and basilar arteries. These angiographic and histological evidence suggests that such hemorrhage results from the development of fibrinonecrosis in the large intracerebral vessels, in addition to a sudden rise in blood pressure.

Ventricular inhibited demand pacemakers (VVI) were implanted in 27 patients with complete A-V block and pacemaker arrhythmias were analyzed by Holter system ambulatory electrocardiograms and conventional electrocardiograms. With Holter ECG, 13 patients showed myopotential inhibition, 5 patients had sensing failure and premature ventricular contractions (PVC) were observed in all patients. On the contrary, myopotential inhibition and sensing failure were not detected by conventional ECG and the detection rate of PVC was only 30%. The transient recovery of A-V conduction was observed in 14 of 27 patients with Holter ECG, but was not detected by conventional ECG. The Holter system ambulatory electrocardiogram clearly demonstrated the complex cardiac arrhythmias. Therefore, it is useful for monitoring arrhythmias caused by VVI pacemakers.

To determine the role of the sympathetic nervous system in the development of stress ulcer, we carried out experiments on spontaneously hypertensive rats (SHR) exposed to restraint and water immersion stress for 7 h. Normotensive Wistar-Kyoto rats (WKY) were used as controls. Catecholamine (CA) contents in gastric tissues, divided into mucosal and muscular layers of both antrum and corpus, were quantitated by high-performance liquid chromatographic electrochemical detection (HPLC-EC). The stress ulcer formation was much less frequently induced in SHR than in WKY. The noradrenaline (NA) contents in all regions of gastric tissues were higher in SHR than in WKY. The contents of adrenaline (A) and dopamine (DA), present in small quantities in gastric tissues showed no difference between SHR and WKY. After exposure to stress, the NA contents in mucosal and muscular layers of the gastric corpus decreased significantly in both SHR and WKY, whereas the value remained higher in the former. On the contrary, a remarkable increase of A contents (probably released from the adrenal medulla by the stress) was observed in all gastric tissues, of both SHR and WKY. Increase of the A contents in the mucosal layer was remarkable in the SHR. The DA contents increased in both strains. These results suggest that the peripheral sympathetic hyperfunction in the stomach in the SHR may have an inhibitory role in stress ulcer formation.

Five cases of chronic neutropenia which developed mainly in infancy were investigated and followed up for 5 to 34 months. Antineutrophil antibody levels were assayed by the direct and indirect immunofluorescence methods using flow cytometry. Selective neutropenia, myeloid hyperplasia and/or maturation arrest of myeloid series cells in the bone marrow, and the demonstration of antineutrophil antibody in the sera and on autologous neutrophils, indicated that the neutropenias involved were autoimmune in nature. Two cases exhibited spontaneous recovery 12 and 14 months respectively after the diagnosis, with concomitant marked decreases in antineutrophil antibody levels. Our study of these five cases supports the view that this disorder may be a clinical entity with a relatively consistent clinical presentation and course. Within this framework of the disorder, however, a clear heterogeneity in clinical presentation and course was also noted in our cases. Clinical severity in this disorder may be enhanced by arrested maturation of myeloid series cell in the bone marrow.