A clinicopathological analysis was carried out on 16 cases of lung cancer complicated by silicosis, which were diagnosed from April 1975 to March 1983, and the results were discussed with a review of the literature. All of the patients were male, and a smoking habit with a Brinkman index of more than 500 was found in 14 of them (87.5%). Twelve cases (75.0%) had advanced tumors of clinical stages III and IV, suggesting that the early detection of lung cancer complicated by silicosis is difficult. Tumors were uniformly found in all lobes of the lung. Histological types were mainly epidermoid or undifferentiated carcinoma, with very few adenocarcinomas. Carcinogens from smoking seemed to be responsible for the carcinogenesis. Twocases were thought to be scar carcinomas.

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A unique amyloid fibril protein (Nis) was extracted from a patient with medullary carcinoma of the thyroid (MCT). This amyloid protein has a molecular weight of approximately 1 7, 000 daltons, and has different amino acid composition from AA, AL or AF type amyloid fibril proteins. Immunochemical analysis using antiserum raised against Nis-DAMand Nis-GAMproteins disclosed that positive reactions were obtained only with degraded amyloids of MCTand with sera from patients with MCT.In contrast, there were negative reactions for other type of amyloid proteins, sera from other type of amyloid, normal sera or urinary proteins. Therefore Nis-amyloid fibril protein has some antigenic determinants characteristic of MCT-related amyloid fibril protein.

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Riboflavin-2', 3', 4', 5'-tetrabutyrate (B₂-But) inhibited, in vitro, ADP (4 μg/ml)-induced platelet aggregation whenadded at the concentration of more than 1 jug/ml and arachidonic acid (Aa) (1 mM)- induced platelet aggregation when given at the concentration of more than 0.1 jug/ml. These inhibitions were dose-dependent. Both cyclic AMPand prostaglandin metabolites in the platelets, however, remained unchanged when the amount of B₂-But added was between 0.1-10 μg/ml. In a volunteer study, 80 mg of B₂-But taken in one bolus inhibited both ADP-and Aa-induced platelet aggregation 4 hr after oral administration. The administration of B₂-Butat this dose was associated with a significant decrease in malondialdehyde formation in plasma. The oral administration of 40 mg (t.i.d.) of B²-But daily did not result in significant changes in ADP-and Aa-induced platelet aggregation. B₂ -But showed no significant effects on either platelet adhesiveness or collagen-induced platelet aggregation, in vitro or in vivo. Our data suggest that a decrease of lipoperoxide in plasma, not in platelets, influences platelet aggregation induced by ADP and Aa.

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Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. Fromthese results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences maypartly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanismof plasma prolactin increment.

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Serial estimation of plasma nor-epinephrine (PNE), 24 hours urinary vanilmandelic acid (VMA) and plasma cortisol was made in 25 adult patients of Guillain-Barré syndrome. Healthy adult age and sex matched volunteers served as controls. The mean level of PNE, VMA and plasma cortisol in controls was 1.07 ± 0.50 ng/ml, 2.81 ± 1.18 mg/24 hours and 12.9 ± 3.10 μg/100ml, respectively. Incases of Guillain-Barrésyndrome with autonomic dysfunction the mean level of PNE, VMAand plasma cortisol was 3.34 ± 2.47 ng/ml, 7.98 ±5.71 mg/24 hours and 27.25 ± 4.94 μg/100 ml on the day of admission while in cases of Guillain-Barré syndrome without autonomic dysfunction it was 1.09 ± 0.32 ng/ml, 3.04 ± 2.22 mg/24 hours and ll.8 ± 4.2 Mg/100 ml, respectively. An increase in circulating PNE, VMA and plasma cortisol was demonstrated in patients of Guillain-Barré syndrome with autonomic dysfunction presenting as hypertension and tachycardia. The maximum rise of 284% (PNE) and 253% (VMA) occurred at the height of paralysis. The elevated levels fell to near control values at the time of significant recovery, and glucose tolerance tests improved. It is suggested that increased levels of catecholamines and cortisol contributed to the development of dysautonomia as these levels were within normal limits in patients of Guillain-Barrésyndromewithout autonomicdysfunction.

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Changes in plasma ADH levels were investigated in human male subjects whose blood volume was altered under isotonic circumstances. Blood volume was reduced by ambulation and increased by isotonic saline infusion in an overnight dehydrated state, and determinations were made on plasma ADH levels, plasma osmolality and hematocrit values. Plasma ADH levels were clearly affected by the small changes in blood volume, and significantly negative correlation was found between plasma ADH levels and the percent changes in blood volume under isotonic circumstances. From these findings, it was concluded that ADH release in human subjects is also controlled by the changes of the blood volume factor in addition to osmotic stimuli.

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To clarify the protein metabolism in peptic ulcer disease, the amino acid content was determined in gastric juice of gastric ulcer patients (n = 30), duodenal ulcer patients (n = 16), gastroduodenal ulcer patients (n = 8), and hospital controls (n = 8). The amino acid output in the gastric ulcer group was greater than that of the hospital control both in basal and maximal secretion. In the duodenal ulcer group of patients who were high secretors of gastric juice, the amino acid concentration was low, so the amino acid output was also lower than that of the hospital control group. Tetragastrin did not increase the amino acid output in the gastric juice. The amino acid amount maybe decided also by the architecture of the gastric mucosa and not only by the ulcer lesion itself. The protein loss from gastric mucosa maywell result in hypoproteinemiain peptic ulcer disease of the stomach.

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Out of 1, 124 cases of diverticular disease of the colon seen during the past 15 years, 27 cases (2.4%) of diverticulitis and 44 cases (3.9%) of diverticular hemorrhage were found. The incidence of diverticulitis was more frequent in the both-sides colon type, and also in the multiple form having 10 or more diverticula. The average age was higher in diverticulitis of the sigmoid colon (57.8 years) than in diverticulitis of the right-side colon (47.9 years). Twenty-two cases (81%) of these patients were recovered by medical treatment, and in 5 cases (19%) of these, elective colectomy was carried out. On the other hand, the incidence of diverticular hemorrhage was more frequent in patients over 70 years old, and also in the multiple form having 10 or more diverticula. Though anemia was seen in 1 1 (25%) of 44 cases, all patients were recovered by medical management.Namely, diverticulitis of the right-side colon is more frequent in middle age, and both diverticulitis of the sigmoid colon and diverticular hemorrhageare morefrequent in old age.

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A patient with unilateral ureteral obstruction by urolithiasis at the ureteropelvic junction was accompanied by hypertension. Plasma renin activity (PRA) was high in peripheral veins and was significantly higher in the renal vein drained from the affected kidney than the contralateral. Infusion of angiotensin II antagonist or an oral administration of captopril, an angiotensin converting enzyme (ACE) inhibitor, resulted in a prompt drop of blood pressure. After pyrlolithotomy was successfully performed, both the blood pressure and peripheral PRAcompletely normalized. It is suggested that the renin-angiotensin systemmight have played a major role in the mechanismof the accompaniedhypertension. Hyperreninemia could have been caused by both renal ischemic vasoconstriction, which might be due to uretero-renal reflex, and increased synthesis of prostaglandins resulting from ureteropelvic obstruction.

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Patients with partial lipodystrophy frequently show hypocomplementemia but rarely have associated autoimmunediseases. Wereport here a patient of myasthenia gravis associated with limb lipodystrophy, a variant form of partial lipodystrophy, and hypocomplementemia.

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Hypoparathyroidism is known to exhibit various neurological manifestations, but most of the neurological disorders seen in this condition are motor ones, and involuntary movementis rarely encountered. Basal ganglion calcification is a commonfeature in hypoparathyroidism. But calcification of the cerebral cortex is, to our knowledge, extremely rare with only nine previously documented cases reported. Wereport a case of both involuntary movementand extensive cortical calcification with some reference to the literature. Furthermore, we discuss the relationship between neurological disorders and intracranial calcificaion.

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A 58-year-old man with essential thrombocythemia terminating in myelofibrosis and myeloblastic transformation is described. He was treated with busulfan and lived for 6 years and 6 months. At autopsy, significant osteomyelofibrosis was noted. Moreover, myeloblastic infiltration with proliferation of megakaryocytes and erythroblasts was seen in the bone marrow and spleen. In the lymph nodes, myeloid metaplasia was noted. The past reports on this disease terminating in myelofibrosis and/or blast transformation have been reviewed.

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