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Biomedical subjects

Y Kanazawa

Publications and source records attributed to Y Kanazawa.

At least 127 records · Page 7Linked to original sources
PubMed1989

Electrophysiological demonstration of anterograde concealed conduction in accessory atrioventricular pathways capable only of retrograde conduction.

Anterograde concealed conduction into the concealed accessory atrioventricular (AV) pathway has been postulated to be one of the factors preventing the reciprocating process via the accessory pathway in patients with the concealed Wolff-Parkinson-White(WPW) syndrome but its presence has not been documented. To demonstrate the occurrence of anterograde concealment, 12 patients with the concealed WPW syndrome were selected for study. A pacing protocol was designed in which the retrograde conduction of the ventricular extrastimulus over the accessory pathway was assessed during ventricular pacing alone (conventional method) and during the AV simultaneous pacing (simultaneous method); the results were then compared. When the high right atrium was simultaneously paced, the effective refractory period of the concealed accessory pathway shortened as compared with the conventional method in five of 12 patients (from 341.7 +/- 110.8 to 312.5 +/- 108.2 msec, n = 12), whereas, it decreased in all patients studied when the coronary sinus near the accessory pathway was simultaneously paced (from 375.7 +/- 135.0 to 287.1 +/- 116.1 msec, n = 7). These results demonstrate that the AV simultaneous pacing frequently shortens the refractoriness of the concealed accessory AV pathway and such facilitation seems to be well explained by the probable anterograde concealment in it and peeling back of the refractory barrier.

Atrioventricular Node↗
PubMed1989

[A case of huge duodenal leiomyosarcoma].

A case of duodenal leiomyosarcoma with large central necrosis was reported. Tumor was 15 X 10 X 10 cm in size. Ultrasonography showed a cystic tumor with thick wall in the right upper abdomen. CT scan revealed a gas formation in the central cystic cavity of the tumor. The gas formation was probably caused by bacterial infection. The diagnosis was confirmed histologically.

Aged↗
PubMed1989

Creeping: a new mutant rat with neurological disease.

We describe a new mutant rat, named creeping, that exhibits severe ataxia characterized by a creeping posture due to the inability to stand up. Affected animals can be recognized at 14.8 +/- 1.6 (mean +/- SD) days of age and die within 35 days after birth. There are no sex differences in phenotype. The breeding data suggest that the abnormal locomotion is caused by an autosomal recessive gene. We have tentatively named the gene creeping (cre). The cerebellum of affected rats is much smaller than that of normal littermates. The cerebellar lobes of the mutant are barely formed. The notable histopathological changes are disarrangement of neuronal cells in the cerebellum and cerebral cortices, although the several cell types that are present in the cortices of normal rats are also found in the cortex of the creeping rats. The same type of change is also present in the hippocampus and fascia dentata.

Animals↗
PubMed1988

Studies with antipeptide antibody suggest the presence of at least two types of glucose transporter in rat brain and adipocyte.

Three antipeptide antibodies were prepared by immunizing rabbits with synthesized short peptides corresponding to residues 215-226, 466-479, and 478-492 predicted from the cDNA of both the human hepatoma HepG2 and rat brain glucose transporters. All three antibodies were found to precipitate quantitatively the [3H]cytochalasin B photoaffinity-labeled human erythrocyte glucose transporter. Each antibody also recognized the rat brain protein of Mr 45,000 on immunoblots, and a similar molecular weight protein was labeled with [3H]cytochalasin B in a D-glucose-inhibitable manner, suggesting that this protein is glucose transporter. However, only up to 30% of the labeled rat brain glucose transporters were precipitated, even by repeated rounds of immunoprecipitation. In addition, these antibodies were observed to be unable to immunoprecipitate significantly the [3H]cytochalasin B-labeled rat adipocyte glucose transporter. Further, one-dimensional peptide maps of [3H]cytochalasin B-labeled human erythrocyte and adipocyte glucose transporters generated distinct tryptic fragments. Although Mr 45,000 protein in rat adipocyte low density microsomes was detected on immunoblots and its amount was decreased in insulin-treated cells, the rat adipocyte low density microsomes were much less reactive on immunoblots than the rat brain membranes in spite of the fact that the rat adipocyte low density microsomes contained more [3H]cytochalasin B-labeled glucose transporters. In addition, the ratio of cytochalasin B-labeled glucose transporter per unit HepG2-type glucose transporter mRNA was more than 10-fold higher in rat adipocyte than in rat brain. These results indicate that virtually all the human erythrocyte glucose transporters are of the HepG2 type, whereas this type of glucose transporter constitutes only approximately 30 and 3% of all the glucose transporters present in rat brain and rat adipocyte, respectively; and the rest, of similar molecular weight, is expressed by a different gene.

Adipose Tissue↗
PubMed1988

Alteration of insulin and glucagon secretion from the perfused BB rat pancreas before and after the onset of diabetes.

Secretion of insulin and glucagon from perfused BB rat pancreas was examined in rats (5 weeks old; n = 6) before and 2 weeks after (13 weeks old; n = 5) the onset of diabetes mellitus. The secretion of insulin and glucagon was modified by increasing concentrations of glucose in the perfusate from 2.8 mM to 16.5 mM. In 5-week-old BB rats, glucagon secretion was higher at the low glucose concentration (2.8 mM) and insulin secretion lower at the high glucose concentration (16.5 mM) than the corresponding values in age-matched control rats. In 13-week-old BB rats, insulin secretion was undetectable irrespective of glucose concentration. Glucagon secretion was only moderately suppressed by the perfusion of high glucose (16.5 mM) and was significantly higher than that of age-matched controls. The reduction in insulin secretion observed in 5-week-old rats without insulitis indicated that pancreatic B cells of BB rats of this age are somehow injured by humoral factors rather than cell infiltration. Cell function was apparently modified indirectly by the destruction of neighboring B cells.

Aging↗
PubMed1988

Enhanced synthesis and secretion of apolipoprotein E from sciatic nerves of streptozotocin-induced diabetic rats after injury.

To elucidate the pathogenesis of diabetic neuropathy, synthesis and secretion of apolipoprotein E (apo E) from sciatic nerves after injury was studied in normal and streptozotocin-induced diabetic rats. Seven, 14, 28, 45 and 59 days after making crush injury on sciatic nerves with concomitant administration of streptozotocin (50 mg/kg body weight), the nerves were taken out and incubated with [35S]methionine. The [35S]labeled apo E was precipitated with specific antiserum. The amounts of apo E secreted into medium by nerves of diabetic rats were 7 times greater than those of non-diabetic rats 7 days after injury. This enhanced secretion of apo E was relatively selective for this protein, since the ratio of the immunoprecipitable apo E to the TCA preciptitable protein in the medium increased in diabetic rats. Intriguing possibility deduced from these results is that the secretion of apo E is involved in the development of diabetic neuropathy.

Animals↗
PubMed1988

Cloning of a rabbit brain glucose transporter cDNA and alteration of glucose transporter mRNA during tissue development.

A full-length cDNA clone that codes for glucose transporter protein was isolated from a rabbit brain cDNA library by using synthetic oligonucleotide probe derived from the sequence of human glucose transporter cDNA. The coding region shared 93.2% nucleotide and 97.0% amino-acid similarities with those of human glucose transporter and 89.4% nucleotide and 97.4% amino-acid similarities with those of rat transporter. Northern blot analysis revealed that glucose transporter mRNA is most abundant in the placenta and that it is also abundant in the brain. The fat tissue, heart, liver, and skeletal muscle of adult rats contained a very small amount of mRNA, while heart, liver, skeletal muscle and kidney of fetal rats contained a very high amount of glucose transporter mRNA. These results suggest that this type of glucose transporter might be closely related with cell proliferation and tissue development.

Aging↗
PubMed1988

Long-term comparison of oral hypoglycemic agents in diabetic retinopathy. Gliclazide vs. other sulfonylureas.

Gliclazide has been reported to possess the properties of preventing the progression of diabetic retinopathy and of controlling blood glucose levels. This report describes a long-term comparative clinical trial of this agent to assess its efficacy against diabetic retinopathy. One hundred and fifty-nine NIDDM patients with no retinopathy or with simple retinopathy entered this trial. One hundred and nineteen patients receiving other sulfonylurea agents were randomly allocated to two groups (G: gliclazide, SU: other sulfonylureas). Forty patients continued to be treated with diet alone (D group). Finally a total of 60 patients, that is, 21 patients in the G group, 19 patients in the SU group, and 20 patients in the D group, were followed with funduscopic examinations for more than 4 years. The results are summarized as follows. (1) Distribution of background factors between the two drug therapy groups was balanced, but in the D group more male patients and relatively milder cases were involved than in the drug therapy groups. (2) Fasting blood glucose control in the three groups was not significantly different. (3) Funduscopic deterioration was observed less frequently, though not significantly, in the G group than in the other groups. (4) Progression to preproliferative retinopathy was significantly less frequent in the G group than in the SU group. Thus, gliclazide seems to have additional properties compared with other sulfonylurea drugs in preventing deterioration of diabetic retinopathy, and particularly in preventing progression to proliferative retinopathy.

Diabetes Mellitus, Type 2↗
PubMed1988

Multiple endocrine neoplasia type I with Cushing's disease, primary hyperparathyroidism, and insulin-glucagonoma.

A case of multiple endocrine neoplasia type I (MEN I) consisting of Cushing's disease, primary hyperparathyroidism, and insulin-glucagonoma is described. This condition was treated successfully by transsphenoidal pituitary adenomectomy, subtotal parathyroidectomy, and enucleation of pancreatic tumors. Histologic features showed a basophilic adenoma in the pituitary, chief cell hyperplasia in the parathyroid, and islet cell adenomas in the pancreas. The rarity of multiple endocrine hyperfunctioning states and the pathophysiology created by the combination of these three diseases in this patient are of interest.

Adenoma, Islet Cell↗
PubMed1988

Glucocorticoids increase insulin binding and the amount of insulin-receptor mRNA in human cultured lymphocytes.

The effect of steroid hormones on insulin binding and the amount of insulin-receptor mRNA was examined in IM-9 lymphocytes. Cortisol and cortexolone, but not oestrogen, increased both the binding of insulin and the amount of insulin-receptor mRNA in a time- and dose-dependent manner. Cortisol was most potent, and induced a 2-fold increase in insulin binding and a 4-fold increase in mRNA. The elevation in binding was due to an increased number of insulin receptors at the cell surface. The increase in mRNA involved all four of the insulin-receptor mRNAs and could not be inhibited by cycloheximide. The cortisol-induced increase in mRNA was associated with a 3-4-fold increase in the synthesis of pro-receptor. The relative potency of the three steroids indicated that these effects were mediated by an interaction with the glucocorticoid receptor. The results of this study suggest that cortisol can increase the number of insulin receptors at the cell surface by increasing the amounts of insulin-receptor mRNA and the synthesis de novo of insulin receptors.

17-Hydroxycorticosteroids↗
PubMed1988

[A study on the disc sensitivity test for clavulanic acid/amoxicillin combination].

Susceptibilities of 179 strains of 30 bacterial species or subspecies to clavulanic acid/amoxicillin (CVA/AMPC) combination were determined by the 2-fold agar dilution method as well as by diameters of inhibition zones in the single-disc method, under the experimental conditions established by Kanazawa. The experiments demonstrated significant correlation between MICs by the dilution method and diameters of inhibition zones in each of conventional assays of the over-night (about 16 hours) incubation, the delayed assay (about 24 hours incubation), and the rapid assay (after 3-4 or 5-6 hours incubation), thus confirming applicability of the single-disc assay for activities of CVA/AMPC combination. From an analysis of the data obtained using CVA/AMPC (1:2) combination of disc containing 45 micrograms, the primary regression equations were obtained as follows: D (diameter, mm) = 27.4-10.1 log MIC (micrograms/ml) in the conventional assay; D = 33.7-13.4 log MIC (micrograms/ml) in the delayed assay; D = 20.7-6.6 log MIC (micrograms/ml) in the 5-6 hours rapid assay, and D = 14.5-3.6 log MIC (micrograms/ml) in the 3-4 hours rapid assay. The range of variations in MICs of CVA/AMPC combination estimated from diameters of inhibition zones by the disc test was then calculated in comparison with that in MICs determined by the 2-fold agar dilution method to estimate experimental errors involved in assaying MICs of CVA/AMPC combination by the single-disc assay.

Amoxicillin↗
PubMed1987

Insulin induces chloroquine-sensitive recycling of insulin-like growth factor II receptors but not of glucose transporters in rat adipocytes.

Incubation of insulin-treated rat adipocytes with chloroquine, in a time- and concentration-dependent manner, was observed to inhibit the insulin-stimulated increase in insulin-like growth factor II (IGF-II) binding activity, whereas no significant change in IGF-II binding was observed in the absence of insulin. The incremental increase of insulin-stimulated IGF-II binding was inhibited 50% by 0.2 mM chloroquine within 15 min and was nearly completely abolished by 60 min. Interestingly, IGF-II binding was never observed to decrease below the binding value in cells without insulin treatment even when incubation was extended to 180 min. Scatchard analysis of IGF-II binding as well as the specific binding of an anti-IGF-II receptor antibody demonstrated that the loss of IGF-II binding in the insulin-stimulated chloroquine-treated adipocytes was due to a decrease in the number of cell-surface IGF-II receptors, whereas the total number of cellular IGF-II receptors was unaltered. The effect of chloroquine was observed to be reversible, temperature-dependent, and sensitive to the metabolic poison KCN. Furthermore, NH4Cl was also observed to inhibit insulin-stimulated increase in IGF-II binding. In contrast, chloroquine or NH4Cl did not inhibit the basal or insulin-stimulated glucose transport activity. Photoaffinity labeling of the glucose transporter with [3H]cytochalasin B also demonstrated that the basal and insulin-stimulated subcellular distribution of the glucose transporters was unaltered by chloroquine treatment. These results suggest that 1) insulin induces a constitutive, acidotropic agent-sensitive recycling of IGF-II receptor and 2) the glucose transporter and IGF-II receptor do not share the same insulin-regulated intracellular trafficking pathways.

Adipose Tissue↗