The mammary gland lipase activity of the mouse mammary gland increased to 45-fold of that in unmated gland at 15th day of pregnancy and reached to 65-fold at 20th day of pregnancy. After parturition, the activity abruptly decreased during 3 days to 38% of that at 20th day of preagnancy. On the other hand, only a very small lipoprotein lipase activity was observed in the pregnant gland, but after parturition, that activity increased to 15-fold of that in 20-day-pregnant one at 3rd day of lactation. These facts suggest that the mammary epithelial cells (the mammary gland lipase activity was detected only in epithelial cells) utilizes the fat reserved in the gland in preagnancy, but the lactating mammary epithelial cells utilizes the fat supplied from the blood circulation. The mammary gland lipase activity was decreased by the treatment with epinephrin which increases the fat mobilization in other adipose tissues. In addition, no hormone-sensitive lipase activity was observed in the mammary gland. Thus, the control of fat mobilization must be different in the mammary gland from that in other adipose tissues. Insulin decreased the mammary gland lipase activity in the gland of the unmated mouse. Prolactin increased the enzyme activity and the effect of prolactin was enhanced in the presence of insulin. Hydrocortisone and prolactin decreased the activity in the glands of pregnancy and lactation. The difference in the responsibility to these hormones in the gland of unmated mouse and in those of pregnant and lactating one may due to the fact that the glands in latter two stages already received the hormone actions.

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Dipsogenic effect of α-methyl-p-tyrosine (α-MPT) was reported previousely. This study was carried out to clarify a possible mechanism for the induction of this phenomenon. The effect of α-MPT was observed in intact rats dose-relatedly. The concentration of catecholamines in the hypothalamus was diminished after α-MPT in intact rats, suggesting that the dipsogenic effect might be resulted in central action of α-MPT. However, the dipsogenic effect was found to occur in rats administered angiotensin II (A II) peripherally. The concentration of A II in peripheral blood after administration of α-MPT was significantly higher than that of control rats. Angiotensin I (A I) as well as renin was also increased in peripheral blood by α-MPT administration. Thus, α-MPT induced an activation of peripheral renin-angiotensin system. One possibility was suggested that A I would penetrate into brain, there converted to A H. The dipsogenic effect of α-MPT was enhanced by a simultaneous administration of captopril (CP) . When low dose and moderate dose of CP were pre-administrated, drinking effect of α-MPT was enhanced, whereas higher dose of CP suppressed the drinking behavior. From these experimental results, it is possible to speculate that the dipsogenic effect of α-MPT in rats may closely relate to stimulation of chemical compounds derived from reninangiotensin system in rats. Further experiment, however, will be necessary to clarify an exact mechanism for stimulation of drinking behavior due to peripheral α-MPT adminisation in rats.

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Bacteroides fragilis strain KHM027 isolated from a patient with colitis is resistant to penicillins, cephalosporins and oxyiminocephalosporins and harbors a β-lactam antibiotics resistance plasmid pBFSK1. In the present study the plasmid pBFSK1 was characterized through the molecular genetic and biochemical analyses. Restriction endonuclease cleavage studies were used to construct a physical map of plasmid pBFSK1 for the restriction enzymes Hind III, EcoR I , Pst I , Bam H I, Sma I, Sal I, Pvu II, Dra I, Ara I, Acc I and Hinf I. Based on the sizes of restriction fragments generated in these studies, the molecular size of plasmid pBFSK1 was estimated at 2.62 kilobase pairs (kb). A 0.85-kb region of the plasmid required for resistance to β-lactam antibiotics and a 1.16-kb region essential for replication were mapped by the technique of transposon Tn5 and insertion sequence 73 insertion mutagenesis. The β-lactamase polypeptide expressed from β-lactamase gene on plasmid pBFSK1 was synthesized in minicells derived from Escherichia coli x984 for the determination of molecular weight by SDS-polyacrylamide gel electrophoresis and examination of hydrolysis activity to various β-lactam antibiotics by iodine-colorimetric assay. The present study proved that the β-lactamase was type II oxyiminocephalosporinase with a molecular weight of 29 kilodaltons. The nucleotide sequence of 92 base pair (bp) EcoR I -Pst I fragment in the β-lactamase gene region was determined by dideoxy chain termination sequencing, and the homology of the nucleotide sequences of 92-bp region in TEM β-lactamase gene of transposon Tn3 and β-lactamase gene of Klebsiella pneumoniae LEN-1 chromosome to that of EcoR I-Pst I fragment was examined. The TEM and LEM-1 β-lactamase genes showed 50% and 67% homology to the type II oxyiminocephalosporinase gene on plasmid pBFSK1, respectively. Furthermore, the incompatibility associated with replication of plasmid pBFSK1 was examined, and it was found that pBFSK1 belongs to the C incompatibility group. This seemed to be the first report of a molecular genetic and biochemical analyses for the oxyiminocephalosporinase plasmid in all sorts of bacteria.

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Two serious cases of acute myocarditis in children, were reported. Case 1, 8 year old boy was admitted because of epigastralgia and consciousness disturbance. On admission his electrocardiogram (ECG) showed highgrade atrioventricular (A-V) block with ventricular rate of 41/min. Temporary pacemaker was inserted through his subclabian vein, and the patient responded well to the treatment. Case 2, 10 year old girl was transferred to our hospital with signs of severe congestive heart failure with acute onset. On admission, her ECG showed remarkable ST elevation in V_1-V_3, and ST depression in II, III and _aV_F. These findings are similar to those of acute myocardial infarction, but in the recent literature a few reports can be found of acute myocarditis with myocardial infarction like findings in ECG. During the course, ventricular tachycardia developed, which was treated with lidocaine. This was followed by an onset of respiratory insufficiency, which improved through respiratory control. Signs of congestive heart failure disappeared in about 2 weeks after admission. In myocarditis in children, limited numbers of reports are found in the literature in which temporary transplantation of pacemaker was performed, and also very few cases were reported with myocardial infarction like findings in ECG.

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The case is a 73-year-old male. On radiological examination of the stomach three years previously, a polypoid lesion was noted at the duodenal bulbar region but no treatment was made. This time, an endoscopic examination revealed a nodular lesion of Yamada's IV with hemorrhage and central depression. For a biopsy study Group IV was given and a diagnosis of duodenal bulbar carcinoma was made. A gastrectomy was performed. Histological findings indicated a well differentiated tubular adenocarcinoma with depth of invasion limited to the mucosal layer, with no lymph node metastasis. In the present paper a study was done on endocopic findings and treatments of the 33 cases reported in Japan, including our case with polypoid lesion in the duodenal bulbar region. Endoscopically, irregularity of surface with redness, erosion and hemorrhage were evident in many cases. On reviewing 19 cases with perceivable prognosis, there is no differentiation in their prognosis in spite of different treatments such as endoscopic or surgical polypectomy, gastrectomy or pancreatoduodenectomy. We have suggested that, when a polypoid lesion is found endoscopically in the duodenal bulbar region, an endoscopic polypectomy should be done at first. When histological findings indicate invasion of the submucosal layer, further surgical resection or/and gastrectomy should be done as the second step operation. In this way, a better quality of life can be insured for the patients.

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