[Measurement of pancreatic main ductal pressure and myoelectrical study of papillary sphincter in monkeys].
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Biomedical subjects
Publications and source records attributed to T Tamura.
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The effect of vitamin K(V.K) administration to the mother on the value of the Hepaplastin test (HPT) was studied in 1,000 neonates. The mean value for HPT on 4th day in the breast feeding group (BF) was 42.2%, which was significantly lower than that in the breast formula feeding group (BFF). 1.6% of BF, and 0.5% of BFF showed an HPT value below 20%. Administration of V.K2 to the mother resulted in a significant increase in the HPT value (BF; 58.9%, BFF; 59.1%). None of the cases showed a HPT value below 20% after the V.K administration. 203 neonates who showed a HPT value below 40% were treated with daily doses of 4 mg V.K2. The HPT value improved to over 40% in all cases within 3 days. V.K1 and K2 concentrations in maternal serum and milk were measured by the method using high performance liquid chromatography. Mean concentrations of V.K1 and K2 on the 4th postpartum day in serum were 0.7 and 0.4 ng/ml and those in the milk were 1.4 and 0.9 ng/ml, respectively. V.K1 administration to the mother after delivery significantly increased V.K1 in serum. V.K2 administration also increased serum V.K2 levels. When V.K1 was given to the mother, both V.K1 and K2 levels in the milk increased. Administration of V.K2 resulted only in an increase in V.K2 in the milk. These results indicated that the administration of V.K to the mother improves the HPT value of the neonate and may be useful in preventing V.K deficiency in the neonate.
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We have studied the effects of tunicamycin and inhibitors of the processing of N-linked glycans including N-methyl-1-deoxynojirimycin, castanospermine, mannodeoxynojirimycin, and swainsonine on the transport of glycoprotein E2 and the intracellular maturation of the coronavirus mouse hepatitis virus A59. Indirect immunofluorescence staining with monoclonal antibodies revealed that glycoprotein E2 exhibits different antigenic properties depending on the presence and on the structure of the N-linked oligosaccharides and that efficient transport of glycoprotein E2 to the plasma membrane requires the removal of glucose residues. In the presence of tunicamycin in the nonglycosylated E2 apoprotein was synthesized in normal amounts and readily acylated throughout the infectious cycle. This E2-species could not be detected on the surface of mouse hepatitis virus A59-infected cells with indirect immunofluorescence staining or lactoperoxidase labeling. N-Methyl-1-deoxynojirimycin and castanospermine, both of which selectively inhibited the processing glucosidases, caused a drop in virion formation by two log steps and a drastic delay in the surface expression of glycoprotein E2. The E2 species synthesized under such conditions was acylated but accumulated intracellularly in a compartment distinct from the Golgi. Concomitantly, synthesis of the matrix glycoprotein E1 of mouse hepatitis virus A59 was drastically impaired. Mannodeoxynojirimycin and swainsonine, which block later stages of the processing pathway, had less or no effect on the transport of glycoprotein E2 and the formation of virus particles.
Histidine decarboxylase (HDC) activity increased 13-, 7-, and 2-fold in the spleen, lung and liver, respectively, but not in other tissues of C57BL/6 mice injected i.v. with 50 micrograms/kg of Staphylococcal enterotoxin A (SEA). But even in the spleen, increase in the histamine level was only 1.5 times that of untreated mice. In genetically mast cell-deficient WBB6F1 - W/Wv mice HDC activity in the spleen increased to the same extent as in wild type WBB6F1 - +/+ mice on SEA treatment, but the histamine level in the spleen also increased 20-fold, whereas it increased only 1.4-fold in +/+ mice. These results suggest that the increases in HDC and histamine resulted from interaction of SEA with non-mast cells in tissues.
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Histochemical and immunohistochemical studies on 47 consecutive specimens excised for choledochal cyst were performed to clarify possible metaplastic changes of the biliary duct in relation to carcinogenesis. An anomalous arrangement of the pancreaticobiliary ductal system was observed in all 39 cases examined. Among the 47 patients, 5 (10.6 per cent) had biliary carcinoma. 27.3 per cent mucous gland, 13.0 per cent goblet cell and 9.5 per cent argyrophil cell in 23 children. On the other hand, 81.8 per cent exhibited mucous gland, 41.7 per cent goblet cell and 27.3 per cent argyrophil cell in 24 adults. These metaplastic changes seemed to be an intestinal metaplasia and increased with age. Immunoreactive-gastrin or -somatostatin were evident immunohistochemically in 4 adults. These findings confirmed that intestinal metaplasia may develop in the biliary duct in cases of choledochal cyst. Although direct evidence between intestinal metaplasia and the development of biliary carcinoma was not found, reflux and stasis of pancreatic enzymes in the biliary duct may relate to the development of intestinal metaplasia and be an important factor related to the carcinogenesis of choledochal cyst.
Eighty-one patients who underwent the extraction of impacted mandibular third molars in the nonfasting state were given a single oral dose of talampicillin (500 mg) preoperatively. Specimens of venous blood (n = 132), gingiva (n = 70), mandibular bone (n = 78), dental follicle (n = 63), and dental pulp (n = 59) were obtained during the operation and assayed for ampicillin content. The mean peak concentrations in serum (9.64 micrograms/ml), gingiva (4.72 micrograms/mg), mandibular bone (1.77 micrograms/ml), dental follicle (3.46 micrograms/ml), and dental pulp (5.53 micrograms/mg) all occurred at approximately 150 minutes after administration of talampicillin. The ratios of the corresponding serum concentration to the peak concentrations in the various oral tissues when both were plotted as drug concentration curves were: gingiva, 0.50; mandibular bone, 0.16; dental follicle, 0.34; and dental pulp, 0.52. Talampicillin was absorbed well by the intestine, and sufficient concentrations of the resulting metabolite, ampicillin, were found in oral tissues.
Ampicillin (ABPC) concentrations in human serum, gingiva, the mandibular bone, and dental follicle after a single oral administration of ampicillin (500 mg) were assayed by the agar diffusion (paper disc) method. The peak times of all specimens were identical, being 120 min after administration. The peak concentrations of the respective specimens were 2.01 micrograms/ml, 1.03, 0.34, and 0.72 micrograms/g, respectively. The concentration ratios of gingiva, the mandibular bone, and dental follicle to their corresponding serum at the peak time were 0.51, 0.16, and 0.35, respectively.
The concentrations of ampicillin (ABPC) from talampicillin (TAPC) and cefadroxil (CDX) in serum and mixed saliva were assayed by the thin layer disc plate method. Talampicillin and cefadroxil (500 mg) were given by a single oral administration. The relationships between serum and mixed saliva ampicillin and cefadroxil concentrations were evaluated in the paired specimens collected from 10 different persons, respectively. The means of concentration ratios of mixed saliva to serum ampicillin and cefadroxil were 0.006 +/- 0.003 and 0.025 +/- 0.010 (mean +/- SD), respectively. Significant correlation coefficients between mixed saliva and serum concentrations were found for both ampicillin and cefadroxil, which were r = 0.78, P less than 0.001, and r = 0.67, P less than 0.001, respectively.
To find whether cis-acting regulatory sequences necessary for sex- and cell-specific expression of two yolk polypeptide genes (Yps) reside near the structural genes themselves, we introduced a 5.0-kilobase genomic DNA segment containing a 3' truncated Yp1 and a complete Yp2 into five different autosomal locations by P-element-mediated gene transfer. Transcripts from the introduced Yp1 were not found in male flies but appeared on a normal developmental schedule in adult females, accumulating in their body walls and ovarian follicles but not in guts or malpighian tubules. Protein from the introduced Yp2 allele was present in female hemolymph and vitellogenic ovaries but was lacking from male hemolymph. We conclude that sequences necessary for the correct stage-, cell-, and sex-specific expression of the Yp1 and Yp2 genes are included in this genomic fragment. These results combined with published work suggest that two tissue-specific, cis-acting, bidirectional, positive regulatory elements placed on either side of a centrally located HindIII site govern expression of both Yp genes--one element specific for fat body and the other specific for ovarian follicle cells.
The hepatic concentrations of copper, zinc and manganese, the activity of the mitochondrial enzyme manganese-superoxide dismutase (MnSOD), and the activity of the cytosolic enzyme copper-zinc SOD (CuZnSOD) were measured in control and ethanol-fed monkeys. In the ethanol-fed group, liver Zn levels were decreased while the Mn concentration was increased. The activity of MnSOD was higher in the ethanol-fed group while the activity of CuZnSOD tended to be lower. The finding of increased activity of MnSOD is consistent with the finding of enlarged mitochondria and increased liver Mn in the ethanol-fed group. Increased MnSOD may reflect substrate induction, since superoxide anions are generated by ethanol metabolism. On the other hand, insufficient CuZnSOD activity may contribute to increased ethanol-induced lipid peroxidation with resultant mitochondrial damage. Thus, the chronic consumption of ethanol results in altered levels of trace minerals and SOD activities in the liver which in turn may contribute to hepatic injury.
We previously reported significant decreases in plasma, whole blood, urinary, seminal and fecal zinc in six young men consuming a semipurified formula diet providing 0.28 mg zinc and 0.8/kg protein per day for 4-9 weeks. During a one-week baseline period, 15.7 mg of zinc (as ZnSO4) were fed; three of the men were repleted with 6.0, 23.2 or 46.3 mg zinc for 2-5 weeks. Biochemical and functional measures of zinc status other than tissue zinc levels were also monitored. No one parameter appeared to parallel dietary zinc status in all subjects, although significant mean changes were seen in serum and leukocyte alkaline phosphatases. Inconsistent changes were noted in erythrocyte delta-amino levulinic acid dehydratase, plasma alkaline ribonuclease and the serum alkaline phosphatase isoenzymes. Nitrogen balance was unaffected by zinc nutritional status. However, alterations in hair root growth phase and morphology, decreases in lymphocyte counts and in transferrin levels during depletion suggest impairment in protein synthesis. Impaired leukocyte chemotaxis and clinical signs indicative of decreased resistance to infection were also noted.
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