Search PubMed⌕ Search

Biomedical subjects

F Koizumi

Publications and source records attributed to F Koizumi.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effective monitoring of concentrations of ofloxacin in saliva of patients with chronic respiratory tract infections.

To ascertain whether monitoring of the concentrations of ofloxacin in saliva during a course of treatment is more suitable and safer than that of its levels in blood, we simultaneously monitored its concentrations in three body fluids (blood, saliva, and expectorated sputum) after a 300-mg administration in 18 patients with chronic respiratory infection. The mean (+/- standard error of the mean) half-lives derived from the three drug level-time relationships were similar: 6.04 +/- 0.58 h for serum, 6.34 +/- 0.63 h for sputum, and 6.61 +/- 0.65 h for saliva. The mean peak concentration (4.06 to 4.53 micrograms/ml) did not differ at the three sites, but the times taken to reach peak concentration in saliva and sputum (3.17 +/- 0.46 h) were significantly longer than that in serum (2.22 +/- 0.28 h). The ratios of the concentrations in saliva and sputum to the concentration in serum increased during the first 2 h and reached 1.0 between 2 and 8 h after administration. They rose above 1.0 16 h after administration: 1.14 +/- 0.11 for saliva and 1.19 +/- 0.10 for sputum. The concentration-time relationship for sputum corresponded closely with the concentration-time relationship for saliva, and an overall significant correlation between the concentrations in sputum and saliva was obtained (P < 0.01). These results suggest that monitoring concentrations in saliva may be more valid, as well as less invasive, than monitoring of the levels in blood for ensuring that the drug concentration reaches its therapeutic level in bronchial secretions.

Adult↗
PubMed1994

Effect of eicosapentaenoic acid ethyl ester on albuminuria in streptozotocin-induced diabetic rats.

Wistar rats (4-week-old) were administered with streptozotocin (45 mg/kg) through tail veins. After 3 months, diabetic rats were divided into 2 groups. One group (EPA group, n = 16) was fed a lipid-free diet (90%, w/w) plus lard (8%) and 90% pure eicosapentaenoic acid ethyl ester (2%) for 6 months. The other group (control group, n = 16) was fed in the same way except that eicosapentaenoic acid ethyl ester was replaced by safflower oil. Twenty-four-hour urine was collected just before starting the experimental diets and during the 6-month experimental period at monthly intervals. There were no differences in food intake and body weight between the two groups throughout the experiment. The mean microalbuminuria of the EPA group became significantly lower than that of the control group after 4 months on the diets through the end of the study (6 months). The mean microalbuminuria levels at the end of the study were 1.38 mg/day in the EPA group (n = 9) and 5.19 mg/day in the control group (n = 6) (p < 0.01). Eicosapentaenoic acid administration might retard the progression of diabetic nephropathy by reducing microalbuminuria.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured vascular smooth-muscle cells.

We studied alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) in vascular smooth-muscle cells from bovine aorta in a culture system. It was found that rhTNF alpha at 10 ng/ml and below significantly increased the incorporation of [35S]sulfate (35S) but conversely decreased that of [3H]glucosamine (3H) into GAGs in the trypsinate fraction of the cell layer after a 24-h incubation. These results suggested that rhTNF alpha reduced the formation and/or the anchorage of sugar chains in the cell layer but enhanced their sulfation in whole GAG synthesis by the cells. In results, the ratio of 35S to 3H in the GAGs was markedly increased. This increase occurred after 24 h and longer when the cells were treated with 1.0 ng/ml rhTNF alpha. The TNF alpha-induced alteration of the incorporation of both 35S and 3H was completely blocked by anti-rhTNF alpha antibody. Other cytokines including recombinant human interleukin-1 beta and -6, and platelet-derived growth factor failed to alter the ratio of 35S to 3H in the GAGs of the trypsinate fraction of the cell layer. In cultured vascular endothelial cells from bovine aorta, however, rhTNF alpha at 1.0 ng/ml significantly decreased the incorporation of both 35S and 3H into GAGs of both the trypsinate fraction and the medium; the ratio of 35S to 3H was not changed. Characterization of GAGs in vascular smooth muscle cell trypsinate fraction revealed that rhTNF alpha at 10 ng/ml induced (i) no change of the incorporation of 3H in the hyaluronate fraction, (ii) a marked increase in the incorporation of 35S and no change of that of 3H in chondroitin sulfates (A plus C) fraction, (iii) a significant decrease in the incorporation of both 35S and 3H in the heparan sulfate fraction, and (iv) no change of the incorporation of 35S and a marked decrease in that of 3H in the dermatan sulfate fraction. In the medium, rhTNF alpha also induced various changes of GAGs. It was therefore concluded that TNF alpha may have a capacity of inducing a qualitative change of vascular smooth-muscle cell GAGs, which may be involved in the vascular pathology such as atherosclerosis.

Animals↗
PubMed1993

Production of cytokines belonging to the interleukin-8 family by human gingival fibroblasts stimulated with interleukin-1 beta in culture.

Three major neutrophil chemotactic peptides belonging to the interleukin-8 (IL-8) family were purified to homogeneity from the conditioned medium of the IL-1 beta-stimulated human gingival fibroblasts culture. On the basis of their molecular masses and NH2-terminal amino acid sequences, these three neutrophil chemotactic factors were identical to melanoma growth stimulatory activity-alpha (MGSA/gro-alpha), MGSA/gro-gamma and Ala-Val-Leu-Pro-Arg-IL-8 (AVLPR-IL-8), each belonging to the IL-8 family. It has been shown by the chemotaxis studies in vitro that the chemotactic activity of MGSA/gro-gamma is similar to that of MGSA/gro-alpha for both human and rat neutrophils, while AVLPR-IL-8 is chemotactic for human neutrophils but not for rat neutrophils. The in vitro findings were supported by the histological studies in vivo on the intradermal injection of either MGSA/gro-alpha or AVLPR-IL-8 into the back of the rats. The results obtained in the present experiment suggest that human gingival fibroblasts play an important role in gingival inflammation through the production of neutrophil chemotactic factors newly characterized as the IL-8 family in response to inflammatory chemical mediators including IL-1 beta.

Amino Acid Sequence↗
PubMed1993

Mechanism of insulin secretion by midaglizole.

Midaglizole was introduced as a hypoglycemic agent, but its insulin releasing mechanism remains unknown. In the present study, the effect of midaglizole upon the B cell function of the pancreas was investigated, using an in situ local circulation of the canine pancreas. The graded doses of midaglizole (0.2, 1.0 and 2.0 mg/kg) revealed a dose-related response of plasma insulin. The administration of yohimbine, a classical alpha 2-antagonist (1.11 mg/kg) revealed a similar increase in plasma insulin to that with midaglizole of equimolar amount. During the clonidine infusion midaglizole did not elicit any significant rise in plasma insulin, whereas yohimbine increased plasma insulin significantly. During glucagon infusion plasma insulin increased following midaglizole infusion but not by yohimbine. The simultaneous administration of diazoxide (K-channel opener) suppressed the midaglizole-induced insulin secretion. These results obtained in the present experiments revealed a different mechanism of insulin releasing action of midaglizole from that of yohimbine. Furthermore, the finding with diazoxide administration suggests that midaglizole stimulates insulin release through an interaction of K(+)-channel of the pancreatic B-cell.

Animals↗
PubMed1993

Large tonsillolith mimicking peritonsillar abscess: a case report.

A case of large tonsillolith is described. A 26-year-old male presented with a history of recurrent throat infections. A diagnosis of peritonsillar abscess was made. A tonsillolith was spontaneously expelled on admission. A tonsillectomy was subsequently performed. The tonsillolith was yellowish-gray, measured 30 x 26 x 16 mm, and weighed 8.5 g, which was the largest reported case in Japan. Chemical analysis revealed the stone to consist of calcium phosphate.

Adult↗
PubMed1993

Protein-losing enteropathy due to secondary amyloidosis of the gastrointestinal tract.

A case of a 71 year old woman who experienced weight loss, diarrhea and edema due to protein-losing enteropathy caused by amyloidosis secondary to rheumatoid arthritis is described. Amyloid deposits were found in the systemic organs, specifically in the bowel. The arterioles were massively involved within the laminae propriae and many were narrowed considerably due to amyloid deposits. Ulcerative lesions, which were accompanied with the ruptured arterioles, were also found. Lymphangiectasia was present in the submucosa, subserosa and mesenterium. The mesenteric lymphatic vessels were deposited markedly with amyloid. The principal cause of the protein loss might be related to the increased capillary permeability to plasma proteins and the exudation through an inflamed mucosa. Functional disruption of the lymphatic flow in the bowel and mesenterium might also participate in the mechanisms of the protein loss. Evidence in this study supports the theory that lymphatic disorders in some patients with gastrointestinal amyloidosis are one of the important factors in the pathogenesis of protein-losing enteropathy.

Aged↗
PubMed1993

Characterization of tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured cells: comparison among vascular smooth-muscle cells, vascular endothelial cells, Chang liver cells and LLC-PK1 cells.

We investigated the alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) using confluent cultures of bovine aortic smooth-muscle cells, bovine aortic endothelial cells, Chang liver cells and porcine kidney LLC-PK1 cells. It was found that the incorporation of both [35S]sulfate and [3H]glucosamine into GAGs in the trypsinate fraction of the cell layer was significantly decreased by rhTNF alpha in vascular smooth-muscle cells and vascular endothelial cells; the incorporation of [35S]sulfate was increased but that of [3H]glucosamine was unchanged in Chang liver cells; the incorporation of both [35S]sulfate and [3H]glucosamine was increased by rhTNF alpha in LLC-PK1 cells. In the conditioned medium, the incorporation of both [35S]sulfate and [3H]glucosamine was not greatly changed by rhTNF alpha in all tested cell types. Characterization of GAGs revealed that each cell type uniquely altered its GAGs after rhTNF alpha treatment; the cytokine-induced alteration of each GAG component was not necessarily the same among different cell types. It was therefore concluded that rhTNF alpha-induced alteration of GAGs is dependent upon cell type.

Animals↗
PubMed1993

Expanded primary T nodules in the palatine tonsils from patients with IgA nephropathy.

We designed a study to investigate the morphological expression of immune responses in the palatine tonsils from patients with IgA nephropathy. To distinguish between the histological characteristics of the tonsils in habitual tonsillitis (47 patients) and IgA nephropathy (11 patients), we studied the T nodules, B-lymphoid follicles, germinal centers, areas of mixed T and B lymphocytes, lacunar epithelium and connective tissues; then we compared patients with habitual tonsillitis and IgA nephropathy. The T nodules in patients with IgA nephropathy were enlarged, and this change was not accompanied by atrophy of B-lymphoid follicles. Morphologically, primary T nodules were predominant. In reactive lymph nodes, T nodules generally play an important role in the extra-follicular maturation of stimulated B lymphocytes into Ig-secreting plasma cells. Therefore the enlarged primary T nodules remind us that this maturation may occur more frequently in the tonsils of patients with IgA nephropathy than in those with habitual tonsillitis. This suggests that some immunoregulatory dysfunction exists in the secretory immune system of mucosa-associated lymphoid tissues in patients with IgA nephropathy.

Adult↗
PubMed1993

[Gastrointestinal hormones: recent developments].

Progress in gastrointestinal hormone research has increased our knowledge in peptide hormone biochemistry and gastrointestinal physiology considerably. However, this knowledge has not yet helped our understanding of common gastrointestinal diseases. More specific and reliable methods are needed to prove or to exclude the participation of gastrointestinal peptides in the pathogenesis of gastrointestinal diseases. Peptide hormones are potentially useful as diagnostic and therapeutic modalities in the practice of gastroenterology.

Diagnosis, Differential↗
PubMed1992

Plasmin stimulates the release of dermatan sulfate from vascular smooth muscle cells in culture.

We investigated the effect of plasmin on the release of sulfated glycosaminoglycans (GAG) from cultured vascular smooth muscle cells. Confluent cultures of vascular smooth muscle cells from bovine aorta were labelled with [35S]sulfate and incubated at 37 degrees C for principally 60 min in a serum-free medium in the presence of plasmin. Plasmin at 10 mU/ml (approximately 2.7 micrograms/ml) and above significantly increased the release of [35S]sulfate-labeled GAG (35S-GAG) from the cell layer after a 60 min incubation. A time course study showed that plasmin at 10 mU/ml significantly increased the 35S-GAG release after 20 min and longer. However, plasminogen at 100 mU/ml and below did not cause a significant change of the 35S-GAG release after a 90 min incubation. A characterization of 35S-GAG revealed that plasmin increased both dermatan sulfate and the other 35S-GAG in the medium. Plasmin at 100 mU/ml enhanced the cell detachment significantly but only slightly. From these results, it was suggested that a endogenous thrombin inhibitor heparin cofactor II may be activated in the liquid phase by dermatan sulfate released from plasmin-stimulated vascular smooth muscle cells when the vascular is disrupted and plasma is exposed to extravessel.

Animals↗
PubMed1992

Effect of cadmium on the monolayer maintenance of vascular endothelial cells in culture.

We investigated the effect of cadmium on the maintenance of the monolayer of vascular endothelial cells to clarify a possible involvement of endothelium injury in cadmium-induced vascular disorders. Endothelial cells from bovine aorta were cultured with cadmium chloride (0.5, 1.0, 2.0 or 5.0 microM) for 24 or 72 h. A histological observation revealed that a de-endothelialized space was formed in the monolayer by cadmium treatment; the number of endothelial cells was significantly decreased by the metal. Cadmium significantly decreased the number of growing endothelial cells with a significant decrease in the [3H]thymidine incorporation, suggesting that cadmium inhibited the cell proliferation. On the other hand, cadmium significantly increased the detachment of [3H]thymidine-labeled endothelial cells from the monolayer with a parallel increase in the lactate dehydrogenase activity in the medium. From these results, it was suggested that cadmium impairs the endothelial cell monolayer; the de-endothelialized space was formed by both an increase in the cell detachment by cadmium cytotoxicity and a retardation of the repair of the space which was due to an inhibition of the cell proliferation caused by the metal.

Animals↗
PubMed1992

Reversibility of the inhibitory effect of rhodamine B on the proliferation of cultured human lip fibroblasts.

To investigate the reversibility of rhodamine B inhibition of cell proliferation, human lip fibroblast KD cells were cultured for 3 days in the presence of 25 or 50 micrograms/ml of the dye and the effect of removal of the dye from the culture medium on cell histology and on incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was investigated. Removal of rhodamine B on the last 1 or 2 days resulted in an increase in cell number, and incorporation of [3H]thymidine was also restored after removal of the dye; [3H]thymidine incorporation by the cells treated with the dye for only the 1st day was the same as that by the control cells cultured without the dye. In conclusion, it was shown that the decrease in KD cell proliferation caused by rhodamine B can be reversed by removal of the dye.

Cell Division↗
PubMed1992

Endothelin modulation of tissue plasminogen activator release from human vascular endothelial cells in culture.

To clarify a possible involvement of the vasoconstrictive peptide endothelin in the regulation of endothelial cell-mediated fibrinolytic system, confluent cultures of vascular endothelial cells from human umbilical vein were incubated in serum-free medium in the presence of endothelin-1 at 100 nM and below, and tissue plasminogen activator antigen (t-PA:Ag) in the medium was determined by enzyme immunoassay. Endothelin-1 at 1 nM and above significantly decreased the release of t-PA:Ag from the endothelial cells after a 24 h incubation. The t-PA:Ag release was also decreased by either endothelin-2 or endothelin-3 at 10 nM. The activity of lactate dehydrogenase in the medium was not changed by endothelin-1 at 100 nM and below, suggesting that the peptide did not cause nonspecific cell damage. The decrease in the t-PA:Ag release induced by endothelin-1 occurred in the presence or absence of 8-bromo cyclic AMP, which is an active congener of cyclic AMP; 3-isobutyl-1-methylxanthine, which is an inhibitor of phosphodiesterase; and forskolin, which is a stimulator of adenylate cyclase. These results strongly indicated that cyclic AMP which is known to down-regulate t-PA:Ag release was not involved in the endothelin-1 effect. However, endothelin-1 failed to decrease the t-PA:Ag release in the presence of either calcium ionophore A23187 or EGTA; the ionophore itself markedly decreased the release. The cytosolic calcium accumulation was significantly increased by endothelin-1. These results suggest that endothelin-1 decreases the release of t-PA:Ag from human endothelial cells through an excess accumulation of intracellular, especially cytosolic which would be mediated by an extracellular, calcium-dependent mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1992

[The first report of human chronic sinusitis by Pasteurella multocida subsp. multocida in Japan].

A 53-year-old male visited our hospital due to nasal obstruction persisting for 6 months and constant rhinorrhea. Pasteurella multocida subsp. multocida was isolated from his nasal discharge and lavage fluid of the maxillary sinus, and also from the oral cavity of the dog he kept. The bacterial strains isolated from the patient and dog were identical in terms of biochemical properties, and drug sensitivity. Although serotype was different, the strain from the patient showed (A:6) and that from his dog showed (A:5). The microorganism is not present in the general environment. The patient had contact with his dog such as he kissed it frequently, gave it food with his chopsticks et al.. From the mouth of the people who kiss one's dog, we detected Pasteurella of the same character of bacteria as from the mouth of the dog. We detected two Pasteurella multocida of different character from only one mouth of a cat. Pasteurella multocida was checked in only one colony for sero type. Sero type A is the popular type for dogs and cats. The above suggest that their was a high possibility that the Pasteurella multocida subsp. multocida found in the patient was from his dog. In Japan, the incidence of Pasteurella multocida subsp. multocida infection has been increasing. In 1969, the Japanese Ministry of Health and Welfare officially communicated this infection as a zoonosis to related institutions. At both medical and surgical departments, wither the patient keeps a pet should be confirmed during interview, and guidance of pet keeping methods is important in some cases from the aspect of clinical bacteriology.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Insulin releasing action of N-terminal peptides of glucagon in dogs.

The relationship between the molecular structure and insulin releasing action of glucagon remains unknown. In order to investigate the direct action of N-terminal peptides of glucagon, glucagon (1-14), and glucagon (1-21) were studied using an in situ local circulation of the canine pancreas. These glucagon fragments as well as glucagon (1-29) were infused into the superior pancreaticoduodenal artery in a dose of 400 pmol for 10 min during the glucose or arginine infusion, and plasma insulin and glucagon in the superior pancreaticoduodenal vein were determined by radioimmunoassay. During the glucose infusion, glucagon (1-14) elicited a slight increase in plasma insulin, whereas glucagon (1-21) and (1-29) revealed significant changes in plasma insulin. In these experiments plasma glucagon did not change significantly following the administration of glucagon (1-14) or (1-21). During the arginine infusion all of the glucagon fragments studied enhanced insulin secretion markedly, whereas glucagon secretion was not affected. Furthermore, graded doses of glucagon (1-14) (50, 150, and 400 pmol) elicited an increase in plasma insulin in a dose-related manner. It is concluded from the present study that the N-terminal peptides of glucagon stimulate insulin release especially during the arginine infusion.

Animals↗