Effect of small bowel transplantation in the congenitally enzyme-deficient Gunn rat.
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Biomedical subjects
Publications and source records attributed to K Ishida.
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Serum activity of adenosine deaminase (ADA) and angiotensin converting enzyme (ACE) was investigated in 32 patients with sarcoidosis, 22 patients with Behçet's disease, 22 patients with Vogt-Koyanagi-Harada's (VKH) disease and 253 healthy controls. In healthy controls, the ADA level was significantly higher in females than in males (p < 0.01). In patients with sarcoidosis, the serum ADA level was significantly higher in both males and females than in the controls (p < 0.01). In patients with Behçet's disease, the serum ADA level was significantly higher than in the controls (p < 0.01) in males only. In VKH disease, the serum ADA level showed no significant difference from the normal controls. Significant elevation of the serum ACE activity was observed only in patients with sarcoidosis (p < 0.01). Serum ACE activity was therefore considered to be more specific to sarcoidosis than serum ADA activity.
The circulatory effects of stellate ganglion block (SGB) on the blood flow through the common carotid artery were determined in 35 patients in acute phase of idiopathic facial palsy (Bell's palsy). SGB was performed by para-tracheal approach with 8 ml of 1% mepivacaine. The blood flow was measured with an ultrasonic blood flowmeter before and 30 minutes after SGB at both sides of the common carotid artery in 20 cases. Measurement was performed continuously for 90 minutes on the palsy side in the other 15 patients. Before SGB, there were no significant differences between the blood flow of the palsy side and the intact side. Thirty minutes after SGB, the blood flow markedly increased to 169.4 +/- 6.2% on the performed side with no change on the non-performed side in 20 cases. In the other 15 patients, the blood flow increased significantly 5 minutes after SGB and reached its peak of 179.7 +/- 11.1% at 20 minutes later. This increase continued for 75 minutes after SGB. It is well known that impaired microcirculation in the facial nerve has an important role in the pathophysiology of Bell's palsy. In view of the fact that the nutrient arteries for the facial nerve are the peripheral branches of the external carotid artery, we believe that SGB which causes significant increase in the blood flow through the common carotid artery is an effective treatment in Bell's palsy.
An isozyme of cytochrome P-450 catalyzing lanosterol 14 alpha-demethylation was purified from human liver using column chromatography, including immunoaffinity chromatography. The purified protein exhibited a single protein band (53 kDa) on sodium dodecylsulfate-polyacrylamide gel electrophoresis. When reconstituted with NADPH-cytochrome P-450 reductase, the purified protein showed an activity of 14 alpha-demethylation of 24,25-dihydrolanosterol (3.20 nmol/min per mg protein). The apparent Km value for 24,25-dihydrolanosterol was found to be 27 microM. This enzyme converted in the reconstituted system, the oxygenated intermediates of 24,25-dihydrolanosterol 14 alpha-demethylation, 32-hydroxy-24,25-dihydrolanosterol and 32-oxo-24,25-dihydrolanosterol, to the 32-nor compound, 4,4-dimethylcholesta-8,14-dien-3 beta-ol.
The enzyme that catalyzed the conversion of human salivary alpha-amylase family A (HSA-A) to family B (HSA-B) was identified. It was partially purified from the precipitate obtained by centrifugation of human saliva at 105,000 x g for 60 min by solubilization with 3[(3-cholamidopropyl)dimethylammonio]-1-propane sulfonate and column chromatographies with Sephacryl S-300-HR and hydroxylapatite. The enzyme preparation was practically free from contaminating exoglycosidases and proteases. The enzyme cleaved the N,N'-diacetylchitobiose moiety of the sugar chain of HSA-A, as shown by the isolation of the protein moiety which contained 1 GlcNAc and 1 Fuc residue and the sugar chain (Gal)2(Fuc)1(GlcNAc)2(Man)3(GlcNAc). This enzyme also cleaved the N,N'-diacetylchitobiose moiety of the sugar chain of human transferrin tetraglycopeptide Asn-Tyr-Asn(GlcNAc)2(Man)3(GlcNAc)2(Gal)2-Lys to yield equimolar amounts of peptide Asn-Tyr-Asn(GlcNAc)Lys and sugar chain (Gal)2(GlcNAc)2(Man)3(GlcNAc). The enzyme was identified as an endo-beta-N-acetylglucosaminidase. The enzyme acted on HSA-A with desialylated and defucosylated outer chain moieties of the sugar chains at a similar rate as that of native HSA-A. The enzyme activity was reduced to 13 and 5% using HSA-A with the sugar chains whose outer chain moieties lacked Gal and GlcNAc, respectively, from the nonreducing end. The enzyme also acted on human transferrin, calf fetuin, and asparagine oligosaccharides of transferrin and fetuin. On the other hand, the enzyme did not act on ovalbumin, RNase B, Taka-amylase, yeast invertase, and ovalbumin asparagine oligosaccharides. These results indicate that human salivary endo-beta-N-acetylglucosaminidase is specific for complex type sugar chains and can release the sugar chains from native glycoproteins and glycopeptides regardless of the existence of a Fuc residue on the proximal GlcNAc of the N,N'-diacetylchitobiose core of their sugar chains. The source of the enzyme was epithelial cells peeling from the oral cavity epithelium into saliva. The enzyme was thought to be integrated on the surface of the epithelial cell membrane. This enzyme was named endo-beta-N-acetylglucosaminidase HS. Thus, these studies indicate that the properties of the enzyme are distinct from those of known endo-beta-N-acetylglucosaminidase and endo-beta-N-acetylglucosaminidase HS is a novel endo-beta-N-acetylglucosaminidase.
A structural study was performed by 13C-n.m.r. spectroscopy and methylation analysis of the O-chain of lipopolysaccharide (LPS) from Vibrio bioserogroup 1875 possessing antigenic factor(s) in common with O1 Vibrio cholerae. It was demonstrated to contain a linear homopolymer of (1-->2)-linked N-3-hydroxypropionyl-alpha-D-perosamine [4-(3-hydroxypropanamido)-4,6-dideoxy-alpha-D-mannopyranose], which is very similar to, but not identical with, both (1-->2)-linked linear N-3-deoxy-L-glycero-tetronyl(S-2,4-dihydroxybutyryl)-alpha-D - perosamine homopolymer and (1-->2)-linked linear N-acetyl-alpha-D-perosamine homopolymer which constitute the O-chains of O1 V. cholerae and non-O1 V. cholerae bioserogroup Hakata LPS respectively.
A chymotrypsin-like protease was purified to homogeneity from human tonsils by a series of chromatographic procedures. The purified enzyme gave a single protein band with an apparent molecular mass of 30 kDa on SDS-PAGE. The sequence of the first 21 amino acids at the N-terminus of the enzyme was determined. A cDNA for the enzyme was cloned by PCR amplification from extracted tonsillar mRNA using a supposed N-terminal oligonucleotide primer and a conserved C-terminal primer of the chymase family. The deduced amino acid sequence of the isolated clone was identical to that of human chymase in connective tissue-type mast cells from heart except for a Ser instead of a Cys at the N-terminal 7th position.
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A new microcrystalline boehmite (tentatively named PT-A) was synthesized as an efficient phosphate adsorbent to replace aluminum hydroxide gel. The characteristic structure of PT-A was examined by nitrogen adsorption/desorption, X-ray diffraction, deviation microscopy, and scanning electron microscopy to establish a pore structural model of PT-A. With this model structure, the details of the mechanism of interaction between PT-A and phosphate in the presence of bovine serum albumin (BSA) are discussed. PT-A is a spherical particle with a diameter of approximately 100 microns and a porous surface structure, and its inside is packed with boehmite microcrystals (crystallite size, 2 nm). PT-A has three types of pores in its structure: a micropore with a narrow size-distribution, a mesopore with a broad size-distribution, and a macropore (radii of pores are 0.7, 1-20, and approximately 300 nm, respectively). When phosphate was incubated with PT-A in human gastric and intestinal juices or in an aqueous solution containing BSA, the amounts of phosphate adsorbed by PT-A were not affected by the presence of proteins. The nitrogen adsorption/desorption isotherms and energy dispersive X-ray analyses demonstrated that phosphate could diffuse to the smaller tunnels freely even if the external surface of PT-A was covered with BSA. It was also demonstrated that the main site of adsorption for phosphate was in micropores of PT-A, whereas BSA was adsorbed only to the external surface and none entered inside smaller tunnels consisting of micro- and mesopores.
In the natural process of the migration of chum salmon from the sea to the river, spermatozoa moved from the testis to the sperm duct, and the pH value of seminal plasma, concentration of cyclic adenosine monophosphate (AMP) in the sperm cells, and potential for sperm motility increased. Cyclic AMP levels and the potential for motility gradually increased when testis spermatozoa with no capacity for movement were incubated in the artificial seminal plasma of which the pH was much the same as, or higher than, the pH of natural seminal plasma from the sperm duct. Such correlation in motility, pH, and cyclic AMP suggests that the increases in seminal pH and intracellular cyclic AMP level during passage of spermatozoa from the testis to the sperm duct cause the acquisition of potential for motility. Motility of testicular spermatozoa demembranated with Triton X-100 was very low in fish caught in the sea, while motility of spermatozoa from the posterior portion of the sperm duct was much higher in fish caught in the river. Furthermore, nondemembranated, intact spermatozoa showed a lag in the timing of the acquisition of potential for motility vs. demembranated spermatozoa: The demembranated sperm exhibited the potential earlier than the nondemembranated sperm. These data suggest that increase in activity of the motile apparatus, the axoneme, is a prerequisite, in part, for the acquisition of sperm motility, whereas the development of some function of the plasma membrane also contributes to this phenomenon.
To examine the ventilatory response at the onset of passive leg movements during sleep in man and the concomitant changes in cardiac output (Qc), five healthy male subjects had their knee joints extended and flexed alternately at a frequency of about 60.min-1 for about 8 s. Minute ventilation (VI), respiratory frequency, tidal volume, end-tidal partial pressure of carbon dioxide and of oxygen, stroke volume (SV), heart rate (fc) and Qc were measured before, during and after passive leg movement during sleep stage III or IV (SLEEP). These values were compared with those of the awake condition (AWAKE). The VI increased significantly (P < 0.05) compared with the mean of five breaths preceding the movement (pre-movement) within one or two breaths at the onset of passive leg movements in both conditions. The difference between the mean of the first and second breaths after the onset of leg movement and pre-movement was 5.2 (SEM 1.9) l.min-1 for SLEEP and 2.7 (SEM 1.1) l.min-1 for AWAKE, respectively. Four of the five subjects showed a larger increase in ventilation during SLEEP compared with AWAKE. The fc increased significantly (P < 0.05) at the beginning of the passive movement in all cases, while SV showed an increase or decrease so that Qc showed no significant change in either condition. These results would suggest that afferent drive from moving limbs could produce an increase in ventilation without any change in Qc.
Two hundred and thirty eight persons were examined to evaluate the interrelations among seven key factors for arteriosclerosis: body mass index (BMI), systolic blood pressure (BPs), plasma glucose (PG), serum cholesterol (CHO), serum triglyceride (TG), serum glutamic-pyruvic transaminase (SGPT), and serum insulin (IRI). BPs showed the significant positive correlation with PG (r = 0.346), BMI (r = 0.318), and IRI (r = 0.200). However, there were no significant correlations between BPs and CHO, between BPs and TG, between BPs and SGPT. SGPT showed the significant positive correlation with IRI (r = 0.367), BMI (r = 0.268), and TG (r = 0.343); but no significant correlations were observed in relations between SGPT and PG, between SGPT and BPs, between SGPT and CHO. IRI showed the significant positive correlations with TG (r = 0.234), and PG (r = 0.427). These data suggest that IRI has an effect on BPs and SGPT. The effect of IRI on BPs relates with PG but does not relate with serum lipid. The effect of IRI on SGPT relates with TG but not with PG.
Clinicopathological and immunohistochemical analyses were performed on ten samples of gastrointestinal carcinoids resected in Ishikawa Prefectural Central Hospital. All samples showed positive reaction to chromogranin A. Serotonin was detected in 8 samples, somatostatin in 4 samples, gastrin in 2 samples. Glucagon/Glicentin in 1 sample, and PYY production in 2 samples. CEA production was detected in 8 samples, and microvascular invasion was observed in 6 of these 8 patients. The PCNA/cyclin labeling index (L.I.) of the cases with metastases was significantly higher than those without metastases. In conclusion, the expression of CEA and the PCNA/cyclin L.I. may be useful markers of the malignant potential of carcinoid tumors.
Male BALB/c mice were infected with Angiostrongylus cantonensis and at various times p.i. treated with cyclosporin A (CsA) either for 5 days continuously or intermittently, or for 12-16 days on alternate days. They were monitored for peripheral blood eosinophilia and at necropsy examined for CSF and bone marrow eosinophilia, and worm recovery. CsA treatment provoked a transient inhibition of peripheral blood eosinophilia in all groups examined, followed by rebounding eosinophilia. There was no significant difference in bone marrow and CSF eosinophilia between CsA- and vehicle-treated groups. Mice treated with CsA on alternate days yielded lower intracranial worm recovery with small-sized worms at days 7, 21 and 30 p.i. than vehicle-treated groups did. No significant reduction in worm recovery was noted in mice treated for 5 days either continuously or intermittently, although worms, especially female ones, harvested from groups treated with CsA from days--1 to 3 or from days 13 to 17 were significantly smaller than those from vehicle-treated groups. CsA-treatment suppressed blastogenic responses of spleen cells against Con A or worm antigen at days 7 and 21 p.i. In vitro treatment of the 3rd stage larvae with CsA did not adversely influence survival of A. cantonensis in mice. These data indicate that CsA exerts anti-parasitic effects against A. cantonensis in mice.