Histologic features of 112 liver biopsy specimens from patients with alcoholic liver injury were studied. Alcoholic hyalin was found in 6 specimens (5.4%). Spherical giant mitochondria were detected in 9 specimens (8.0%). Fatty metamorphosis, infiltration by polymorphonuclear leucocytes, and pericellular fibrosis were observed in manyspecimens. Zonal or submassive necrosis was also found in 20 specimens (1 7.9%). Cholestasis was seen in 32 specimens (28.6%). Histologic changes in interlobular bile ducts were investigated in 103 specimens containing such ducts. Among31 specimens with cholestasis, changes in interlobular bile ducts were detected in 19 specimens (61.3%), whereas biopsy specimens without cholestasis showed the changes in only 4 of 72 (5.6%). Changes observed in interlobular bile ducts included inflammatory cell infiltration and vacuolation of epithelium in most specimens. Swollen or flattened epithelial cells, karyopyknosis and eosinophilic degeneration were observed in many. These results suggest that the changes of interlobular bile ducts may be partially related to cholestasis in alcoholic liver injury.

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Concentrations of plasma 6-keto-prostaglandin F_1α (6-kcto-PGF_1α), a stable metabolite of prostacyclin, were measured by radioimmunoassay before and after 3 min of induced ischemia in 45 diabetics and 23 controls matched for age. In the 45 diabetics, 15 had no vascular complications (group I), 10 had a macroangiopathy (group II), 10 had a microangiopathy (group III) and 10 had both macroangiopathy and microangiopathy (group IV). Plasma levels of 6-keto-PGF_1α; before forearm ischemia were significantly lower in group IV diabetics than in non-diabetic controls (188 ± 17 pg/ml and 245 ± 14 pg/ml, respectively). After 3 min of ischemia, plasma 6-keto-PGF_1α concentrations were increased in control subjects by 34% and by 21% in group I diabetics. In group III diabetics as well as diabetics with atherosclerotic vascular lesions (groups II and IV), no significant change was observed after 3 min of ischemia. These results suggest that impaired vessel wall prostacyclin production may to some extent be responsible for the developmentof diabetic retinopathy and nephropathy as well as atherosclerotic vascular complications.

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An increased incidence of lung cancer and epithelial metaplasia or hyperplasia which is felt to be as a precursor of cancer, has been reported in patients with idiopathic pulmonary fibrosis (IPF). In this study, carcinoembryonic antigen (CEA) in bronchoalveolar lavage (BAL) fluid was measured in 53 control patients, 31 patients with sarcoidosis, 10 patients with hypersensitivity pneumonitis, 16 patients with primary lung cancer and 26 patients with histologically confirmed IPF. High ratio of CEAto albumin (Alb), exceeding mean + 2SD of nonsmoking control patients, were found in 8 (25%) out of 32 smoking control patients, 4 (44%) out of 9 nonsmoking patients with IPF, 8 (62%) out of 13 smoking patients with IPF, 3 (75%) out of 4 smoking patients with IPF and lung cancer and 13 (81%) out of 16 patients with primary lung cancer, although BALwas performed at the noncancerous parts of the lung in the cases of lung cancer. Furthermore, it was confirmed that CEAincreased in BALfluid in these subjects were different from nonspecific cross-reacting antigen (NCA) which was detectable in the normal lung. Thus we consider that the increase of CEA/Albratio in BALfluid is a possible marker of these early histological disorders in the lung, and also suggests a greater risk of malignant change in the clinical course of IPF.

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The amino acids in human gastric juice were measured in the hospital control (n = 9), gastric ulcer (n = 10), duodenal ulcer (n = 12), gastroduodenal ulcer (n = 9), and gastric cancer patients (n = 16) by high performance liquid chromatography, and the total of 15 kinds of amino acids was correlated with value determined by Ninhydrin method. The patients with gastric cancer had elevated levels of all amino acids, especially alanine, leucine, valine and threonine. In all but the gastric cancer disease groups, the aromatic amino acids, phenylalanine and tyrosine as well as leucine were at high levels in 1 5 amino acids. The different patterns of amino acids in these four groups tended to correlate with the variabilities of protein loss from the gastric wall.

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Monoclonal antibodies to small cell lung cancer (SCLC) were produced by fusion of P3X63/AgU1 mouse myeloma cells with spleen cells from BALB/cmice immunized against intact cells of SCLCtumors grownin BALB/c athymic nude mice. The antibody TFS-2 demonstrated "pancarcinoma"reactivity showing binding to non-small cell lung cancer (NSCLC)and carcinomas derived from other organs such as stomach, pancreas, and colon. This antibody failed to react with a variety of normal tissues including lung, bone marrow, spleen, stomach, colon, and pancreas. TFS-2 showed complement-mediated cytolysis of target cells. TFS-2 had no significant effects on hematopoietic stem cells. This antibody will serve as a powerful tool for the in vitro removal of tumor cells from bone marrow, thus facilitating highdose chemotherapy of SCLCwith autologous bone marrow transplantation. In contrast, TFS-4 monoclonal antibody reacted specifically with SCLCbut not with NSCLStumors. This antibody can distinguish SCLCfrom NSCLCtumors in histologic diagnosis at transbronchial biopsy, and in cytological identification of tumor cells in malignant effusion, and in infiltrated bone marrow. Radiolabeled TSF-4 specifically accumulated into SCLCtumors that were implanted subcutaneously into athymic nude mice. Thus, the antibody will be useful not only for diagnosis of lung cancer but also for targeting anti-tumor agents.

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A 42-year-old man was admitted because of episodic attack of general malaise. He was lethargic and had a severe lactic acidosis and hypoglycemia. Blood chemistry and endocrinological data were normal. Glucose administration led to an improvement in the hypoglycemia but not the lactic acidosis. At autopsy, there was a massive infiltration of leukemic cells in both kidneys and in liver. Phosphoenolpyruvate carboxykinase, pyruvate carboxylase and glocose-6-phosphatase activities in patient's liver were muchthe same as in the control liver, but fructose-1, 6-diphosphatase activity was slightly reduced. Since circulatory failure was absent, type B lactic acidosis has to be considered. Since hypoglycemia was associated with acidosis, the severe lactic acidosis in our patient may have been due to an overproduction of lactic acid as well as to an impaired hepatic gluconeogenesis in the presence of leukemic cells.

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Three cases of recurrent generalized muscle spasmswere reported. All three cases are of Chinese descent and show some typical features of recurrent painful muscle cramps, alopecia, diarrhea and abnormalities of bone and endocrine systems. Recurrent generalized muscle spasms or Satoyoshi's disease is recognized as an entity of the disease not only in Japan but also in China. The result that one of the three cases is associated with myasthenia gravis might suggest an immunological abnormality as a mechanism of the disease.

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Reversible hyperkalemia induced by flufenamic acid in an asymptomatic hyporenemic patient with IgA nephropathy is reported. Flufenamic acid, 600 mgdaily, was given for four months to a 64-yearold womanwith biopsy proven IgA-nephropathy. This produced hyperkalemia, hypertension and congestive heart failure with slowly progressive renal impairment. Weconclude that a further suppression of the renin angiotensin system causing selective hypoaldosteronism together with the nephrotoxic effects of this drug mayhave been responsible for hyperkalemia in this patient.

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Wereport a case of neurofibromatosis associated with multiple bullae and fibrosis in the lungs which can be clearly seen with computed tomography.

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