[Clinical application of ampicillin suppository (KS-Rl) in pedodontic clinic].
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Biomedical subjects
Publications and source records attributed to H Oguchi.
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We examined the effects of atrial natriuretic polypeptide (hANP) on exocrine function in the isolated and blood-perfused dog pancreas in situ. Intra-arterial injection of hANP (1-10 micrograms) resulted in the dose-dependent increases of the pancreatic juice secretion. The secretory activity of 3 micrograms of hANP was approximately equal to one third of the secretory activity of 0.1 units of secretin. The use of hANP increased the concentration of bicarbonate but not that of sodium and protein in the pancreatic juice as compared with the basal values. These secretory responses to hANP were not inhibited by treatment with haloperidol, sulpiride, phentolamine, propranolol, atropine, cimetidine or ethacrynic acid. These results suggest that hANP acts directly on the pancreatic exocrine gland to stimulate pancreatic secretion; without, however, increasing sodium excretion. The mechanism of this effect remains to be elucidated.
A clinicopathological study was made on 65 patients from a small area of Nagano Prefecture, Japan, with hereditary generalized amyloidosis with polyneuropathy to clarify the clinical variety of the disease. Forty-five patients from Ogawa village showed similar clinical features. The age of onset ranged widely from 16 to 62 years. The main neurological manifestations were polyneuropathy starting in the legs and autonomic dysfunction. Lower cranial nerves were also affected in the advanced stages. Severe cardiac and renal involvement was uncommon. All these clinical features are consistent with type I familial amyloid polyneuropathy (FAP). The remaining 20 patients from five unrelated kinships showed unique clinical pictures. Two families from Ogawa village had type I FAP, but 4 out of the 5 affected patients showed marked nephropathy with heavy proteinuria from an early stage. Of the three other families, one, with 10 patients, was notable for the involvement of the central nervous system. Most of the patients showed cerebellar ataxia and pyramidal tract signs in addition to a sensorimotor and autonomic peripheral neuropathy. Another family had 2 siblings who had severe amyloid heart disease from the onset and developed polyneuropathy with autonomic features at an advanced stage. In the third family, onset occurred in the sixth decade in all 3 patients and the course was mild in 2, although the clinical features were those of typical type I FAP. Immunohistochemical study revealed that the amyloid fibril proteins in the patients with all four unusual clinical phenotypes were related to plasma prealbumin. The most common form of hereditary generalized amyloidosis in Japan is type I FAP, but the disease shows considerable variety in the age of onset and involves more systemic organs than previously recognized. The newly recognized clinical forms of hereditary generalized amyloidosis with severe amyloid heart disease or central nervous dysfunction indicate clinical heterogeneity of hereditary amyloidosis with polyneuropathy.
Idiopathic membranous nephropathy has been reported rarely to develop in genetic association with certain HLA antigens. This paper describes two male siblings presenting with nephrotic syndrome with histologically proven membranous nephropathy. The younger brother maintained a normal renal function with slight proteinuria during the 3 years of follow-up, but the older one experienced a rapid decline in renal function and had to be put on maintenance hemodialysis. No clinical evidence of contributory underlying disease such as malignancy or systemic lupus erythematosus could be found. HLA typing was carried out in the two patients and in members of their family. Several HLA antigens were found to be shared by the two patients. However, the HLA antigens which have been reported to be associated with idiopathic membranous nephropathy were not found in either of them.
The Lewis (Le) phenotype of both erythrocytes and sera and serum CA19-9 levels were studied in 49 patients with pancreatic carcinoma, in 37 with gastric cancer, in 22 with colorectal cancer, in 21 with bile duct carcinoma, and in 19 with hepatocellular carcinoma. The Le phenotype was determined in sera with the use of the dot-immunobinding assay and on erythrocytes. The localizations of the Le antigen and CA19-9 were studied in pancreatic tissues from 22 patients with pancreatic carcinoma. The prevalence of Le(a-,b-) on erythrocytes was significantly higher in patients with pancreatic carcinoma than in normal controls. Nineteen of 21 patients with pancreatic carcinoma, whose Le phenotype on erythrocytes was Le(a-,b-), had Le antigen in tissues and sera, and they had a raised serum CA19-9 level. The remaining 2 patients were of the Le(a-,b-) phenotype for both erythrocytes and sera, and their serum CA19-9 levels were below 6 U/ml. Neither Le antigen nor CA19-9 could be localized in tissues of these 2 patients. Two patients with gastric cancer, 6 with colorectal cancer, and 6 with bile duct carcinoma had Le antigen in sera in spite of having Le(a-,b-) on erythrocytes. These results indicate that the Le phenotype on erythrocytes can undergo a change not infrequently in patients with pancreatic carcinoma as well as in patients with other gastrointestinal cancers, but patients with the Le(a-,b-) phenotype in sera cannot synthesize CA19-19.
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Fourteen patients with suspected chronic alcoholic pancreatitis (CAP) and 21 patients who had been shown to have the disease were followed up by the pancreozymin-secretin test in order to clarify the serial changes in exocrine pancreatic function in alcoholic pancreatitis. The initial and final test data for secretory volume, maximal bicarbonate concentration, bicarbonate output (BO), and amylase output (AmO) of exocrine secretion were compared in these two groups. Patients with suspected CAP showed a significant serial decrease only in AmO; definite CAP developed in 3 of them during the follow-up period. In definite CAP, a significantly progressive decrease in BO as well as AMO was observed. It is suggested that in the earlier stage of CAP, AMO is initially affected, whereas decreased secretion of both bicarbonate and enzyme becomes apparent in the later stage.
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In order to elucidate the functional states of the pancreas in the asymptomatic latent stage of chronic alcoholic pancreatitis, 45 chronic alcoholics with no obvious pancreatic structural abnormalities judged by endoscopic pancreatography were studied by pancreozymin-secretin test. We found three patterns of exocrine pancreatic function in alcoholics with or without cirrhosis: normal secretion (40%), hyposecretion (29%) and hypersecretion (31%). In the hyposecretory group, the amylase output proved to be impaired more frequently. In the hypersecretory group increases were observed in one or more of the following parameters, volume, bicarbonate output and amylase output. However, increase in volume was a fundamental condition in this hypersecretion. This study confirmed that exocrine pancreatic hyposecretion and hypersecretion were almost equally frequent in asymptomatic chronic alcoholics with no obvious pancreatographic abnormalities. These results suggest that ongoing exocrine pancreatic dysfunctions exist in the subclinical stage of chronic alcoholic pancreatitis.
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