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Biomedical subjects

A Kamiya

Publications and source records attributed to A Kamiya.

At least 127 records · Page 7Linked to original sources

A clinical survey on the compliance of exercise therapy for diabetic outpatients.

To clarify the present state of exercise therapy for diabetes mellitus, we conducted a survey of 570 diabetic outpatients by written questionnaires. The results revealed that approximately 30% of the patients did not implement the prescribed exercise regimen. The principal reasons for low compliance were 'lack of time to do' and 'lack of mind to do'. 'Lack of time to do' was particularly numerous in male patients. Other reasons were 'lack of guidance by physician', 'lack of interest', 'lack of understanding of procedure'. These findings indicated that the patients should be motivated adequately when they are diagnosed as having diabetes and subsequently encouraged to reinforce their intentions by the physician and co-medical staff. Furthermore, they showed that specific approaches suitable for each individual patient and not standardized guidelines should be devised. As regards the daily environment of patients, the cooperation of the patient's family would be effective and the exercise facilities and the exercise guidance personnel should be augmented.

Diabetes Mellitus↗

[Study on the experimental ulcerative colitis (UC) model induced by dextran sulfate sodium (DSS) in rats (2)].

We have confirmed that symptoms in the experimental UC model in rats induced by ingesting 3% DSS were similar to those of the human UC. In this study, we investigated the procedure for assessing the therapeutic effect of SASP and PSL. (1) The UC model was produced by giving rats drinking water containing 3% DSS, and animals were selected when bloody stool was observed in more than 90% of the animals. (2) Procedure for selection of rats: (a) presence of bloody stool for more than two consecutive days, (b) concentration of hemoglobin at more than 10 g/dl and (c) B.W. on the day of selection was not decreased more than 20 g against the B.W. on the day before the selection. (3) After selection, various concentrations of DSS (1-3%) were given to rats for 14 days. SASP and PSL were administered to the UC model once a day for 14 and 7 days, respectively, with the animals given drinking water containing 1% DSS after the selection. SASP (100 mg/kg, p.o.) and PSL (1 mg/kg, i.r.) significantly inhibited the formation of erosion by 56.1 and 47.5%, respectively. In conclusion, this procedure used herein seems to be useful for assessing the therapeutic effect of a drug for human UC.

Animals↗

Bacterial contamination of aerosol solutions containing antibiotics.

In an investigation of microbial contamination of aerosol solutions containing antibiotics (hospital pharmaceutical preparations, no preservatives added), five of six residual solutions after multiple use for 7 days were contaminated at a concentration of 10(6) viable counts/ml. Contaminants were glucose-nonfermenting Gram-negative bacilli such as Pseudomonas cepacia and Flavobacterium meningosepticum. The major contaminant, P. cepacia, multiplied rapidly in the aerosol solution under simulated actual-use conditions. The contamination seemed to have been caused by storage, at room temperature instead of in a refrigerator, of the multiple-dose solutions and by frequent re-use of syringes to measure the solutions. Prompt refrigerator storage after each use of the solutions and abandonment of the syringes within 24 h eliminated bacterial contamination of the solutions. Sufficient attention is not paid to prevent bacterial contamination of aerosol solutions containing antibiotics because of the fact that they contain antibiotics. Thus aerosol solutions containing antibiotics should be handled with great care to prevent bacterial contamination.

Aerosols↗

Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells.

Cultured bovine fatal aortic endothelial cells (BAECs) were stimulated with nitric oxide (NO)-releasing vasodilators and NO gas-saturated solution, and changes in the cell proliferation were examined. Sodium nitroprusside (SNP) and nitroglycerin (NTG) shifted the growth curve downward, and inhibited 3H-thymidine incorporation by the ECs in a dose-dependent manner. Application of NO solution also reduced 3H-thymidine incorporation. SNP, NTG and NO solution increased the intracellular cGMP in BAECs. A cGMP analog, 8-bromo-cGMP, inhibited 3H-thymidine incorporation, and a guanylate cyclase inhibitor, methylene blue, almost completely blocked the inhibitory effect of SNP and NTG on 3H-thymidine incorporation. These findings suggest that exogenous NO inhibits EC proliferation, and that intracellular cGMP is involved in the inhibitory effect of NO.

Animals↗

Laminar flow stimulates ATP- and shear stress-dependent nitric oxide production in cultured bovine endothelial cells.

Based on the fact that nitric oxide (NO) production is associated with changes in intracellular cGMP levels and is selectively inhibited by N omega-methyl L-arginine (L-NME), we investigated the shear stress dependency of NO production in endothelial cells (ECs) from its cGMP responses to various shear stress loads. Cultured fetal bovine aortic ECs treated with a phosphodiesterase inhibitor, isobutylmethylxanthine (IBMX; 1 mM), were exposed to a laminar flow of Krebs buffer solution for 5 minutes in a parallel-plate flow chamber and examined for changes in intracellular cGMP levels by radioimmunoassay using an [125I] cGMP kit. Application of flow increased the cGMP levels. The increase was significant in the presence of extracellular ATP (1 microM)(control, 286.1 +/- 43.6; flow, 506.5 +/- 44.9 fmol/10(7) cells; p < 0.001), but not in its absence (control, 256.6 +/- 60.6; flow, 301.5 +/- 91.4 fmol/10(7) cells; N.S.). The cGMP levels increased significantly as the magnitude of shear stress applied increased. Treatment of ECs with a specific inhibitor of NO production, L-NMA (200 microM), completely inhibited the flow-induced increase in cGMP, and L-arginine reversed the L-NMA-induced inhibition, indicating that the increase in cGMP was due to NO produced by the flow. The flow-induced increase in NO production was markedly suppressed when extracellular Ca++ was chelated by adding EGTA to the perfusate. These findings suggest that flow stimulates NO production to increase cGMP levels shear stress-dependently in ECs and that extracellular Ca++ and ATP modulate the effects of flow.

1-Methyl-3-isobutylxanthine↗

Comparative effectiveness of hand-cleansing agents for removing methicillin-resistant Staphylococcus aureus from experimentally contaminated fingertips.

BACKGROUND: Five subjects participated in a study of optimal conditions for removing methicillin-resistant Staphylococcus aureus from contaminated fingertips. METHODS: Fingertips were contaminated experimentally and cleaned by various methods. Bacterial removal was measured as percentage and is given as mean +/- standard error of the mean. RESULTS: Rinsing the fingertips with tap water for 20 seconds and drying them with paper towels removed 95.2% +/- 1.6% of the contamination. Application of hand-cleansing agents to fingertips for 20 seconds, followed by a 20-second tap-water rinse and towel drying, removed bacteria as follows: povidone-iodine detergent, 99.2% +/- 0.4%; chlorhexidine detergent, 97.2% +/- 0.8%; and liquid soap, 96.1% +/- 1.1%. In a modification of the method, 80% ethyl alcohol applied to the fingertips for 20 seconds, followed by air drying for 40 seconds, removed 99.1% +/- 0.8% of the bacteria. Statistical analyses indicated that povidone-iodine and 80% ethyl alcohol were more effective than the other agents. CONCLUSIONS: Rinsing contaminated fingertips with tap water and towel drying them is sufficient to reduce contamination with methicillin-resistant S. aureus by 95%. Washing with povidone-iodine or 80% ethyl alcohol further reduces contamination by an additional 99%.

Adult↗

Shear stress inhibits adhesion of cultured mouse endothelial cells to lymphocytes by downregulating VCAM-1 expression.

Monolayers of endothelial cells (EC) cultured from mouse lymph nodes were exposed to controlled levels of shear stress (0-7.1 dyn/cm2) in a parallel plate flow chamber, and binding between the flow-loaded EC and mouse lymph node-derived lymphocytes was assayed. A large number of lymphocytes adhered to the stationary control EC, but in EC exposed to a shear stress of 1.5 dyn/cm2 for 6 h, the adhesion decreased to 68.8 +/- 12.8% (SD; n = 19) of control (n = 29, P < 0.001). The decrease in adhesion induced by flow loading was time and shear stress dependent and reversible. Treatment of stationary EC with a monoclonal antibody (MAb) to vascular cell adhesion molecule-1 (VCAM-1) reduced the adhesion to 70.6 +/- 11.5% (n = 19) of control (P < 0.001), whereas MAb to CD44 and to intercellular adhesion molecule-1 had no effect on it. Flow cytometric analysis revealed that the amount of VCAM-1 expressed on the cell surface was decreased to 48.5 +/- 15.8% (n = 6) of control by flow loading (P < 0.001). Flow loading experiments using two perfusates with different viscosities demonstrated that the decrease in VCAM-1 expression due to flow was shear stress rather than shear rate dependent. The detection of mRNA by reverse transcriptase-polymerase chain reaction showed that VCAM-1 mRNA levels were markedly depressed in EC exposed to flow loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Preventive effect of betamipron on nephrotoxicity and uptake of carbapenems in rabbit renal cortex.

The preventive effect of betamipron (N-benzoyl-3-propionic acid: BP) on the renal uptake and nephrotoxicity of carbapenems (panipenem and imipenem) was studied in rabbits. Panipenem, a new carbapenem antibiotic, induced nephrotoxicity at a dose of 200 mg/kg, i.v., but this was less severe than that caused by a single dose of imipenem or cephaloridine. Along with the significant reduction of nephrotoxicity, the uptake of these carbapenems in the renal cortex was remarkably inhibited by simultaneous treatment with BP (200 mg/kg, i.v.). These results suggest that BP reduces the nephrotoxicity of carbapenems through inhibiting the active transport of carbapenems in the renal cortex. Because of the low toxicity of BP (LD50 in the rat, more than 3,000 mg/kg, i.v.), it was concluded that BP might be a good candidate for reducing the nephrotoxicity induced by panipenem or imipenem.

Alanine↗

Effect of 1,6-dihydro-2-[2-(2-methylpropoxy)anilino]-6-oxo-5-pyrimidinecarboxylic acid on gastric mucosal defensive factors and gastric secretion in rats.

1,6-dihydro-2-[2-(2-methylpropoxy)anilino]-6-oxo-5-pyrimidinecarbo xylic acid, (MAR-99, CAS 98772-05-5) (10-30 mg/kg i.g.) improved the reduction of gastric blood flow rate induced by the administration of 99.5% ethanol or acidified-acetylsalicylic acid (ASA). In addition, MAR-99 (3 x 10(-6)-3 x 10(-5) mol/l) protected dose-dependently the damage of epithelial cells induced by ulcerogenic agents such as ethanol or acidified-ASA. MAR-99 (1-10 mg/kg p.o.) prevented dose-dependently the reduction of hexosamine content in glandular stomach. Furthermore, MAR-99 (10-30 mg/kg i.g.) improved the decrease in gastric potential difference induced by 99.5% ethanol and acidified-ASA. MAR-99 (10-30 mg/kg p.o.) significantly inhibited the lesion formation induced by 99.5% ethanol and such effect of this compound was not attenuated by the pretreatment with indomethacin. Furthermore MAR-99 (10 and 30 mg/kg p.o.) had no effect on the prostaglandins (PGE2 and I2) contents in the stomach of normal rats. In pylorus-ligated rats, MAR-99 (3-100 mg/kg i.d.) showed a weak or no effect on acidity and pepsin activity in gastric juice, although this compound decreased dose-dependently the volume of gastric juice. In perfused stomachs, MAR-99 (30-100 mg/kg i.d.) slightly prevented the acid secretion induced by carbachol and pentagastrin. However, MAR-99 did not affect the acid secretion stimulated by histamine. These results indicated that anti-ulcer effect of MAR-99 was mainly due to maintenance of the gastric mucosal resistance.

Animals↗

Efficacy of disinfectants against biofilm cells of Pseudomonas aeruginosa.

The effect of disinfectants on biofilm cells of Pseudomonas aeruginosa were evaluated. Biofilm cells of P. aeruginosa were eradicated by 0.4 to 0.5% chlorhexidine and 2% glutaral within 1 min, by 0.3% chlorhexidine, 0.5% benzalkonium chloride, 0.1% sodium hypochlorite, and 0.1% titratable I2 providone-iodine within 10 min, and by 0.2% chlorhexidine, 0.1% benzalkonium chloride, and 0.01% sodium hypochlorite within 30 min. However, 0.1% chlorhexidine and 0.1 to 0.5% alkyldiaminoethyl glycine were ineffective for eradication even after 1 h. Eradication of biofilm cells of P. aeruginosa by disinfectants required much longer time than that of planktonic cells in suspensions. The bactericidal effect of disinfectants against biofilm cells was found to be considerably enhanced by increasing the concentrations of the disinfectants.

Disinfectants↗

The effect of flow on the expression of vascular adhesion molecule-1 by cultured mouse endothelial cells.

Adherence of leukocytes to vascular endothelial cells (ECs) is known to be sensitive both to blood flow and adhesive proteins on EC surface. To elucidate the effect of blood flow on the surface expression of adhesive proteins, cultured ECs derived from mouse lymph nodes were exposed to different levels of wall shear stress in a flow-loading chamber, and changes in the expression of vascular adhesion molecule-1 (VCAM-1) and CD44 were evaluated by immunostaining with monoclonal antibodies and flow cytometry. Both proteins were expressed on non-activated cultured ECs. When exposed to flow with shear stress of 1.5 dynes/cm2 for 24 hr, VCAM-1 nearly disappeared on fluorescence micrographs, while CD44 showed no change. Flow cytometric analysis showed that the mean channel fluorescence of VCAM-1 was decreased about 75% by application of flow for 24 hr (p < 0.001), but that of CD44 remained unchanged. VCAM-1 expression began to decrease around 1 hr after the initiation of flow and became markedly reduced with time, reaching a minimum after 24 hr. When the cells subjected to flow for 24 hr were returned to stationary state, the reduced VCAM-1 expression was almost completely restored in 72 hr, indicating that the change was reversible. The magnitude of the reduction of VCAM-1 expression was also dependent on the intensity of the wall shear stress applied, ranging from 0 to 7.2 dynes/cm2. These results, demonstrating an explicit down-regulating effect of flow on VCAM-1 expression of cultured ECs, suggested preferential adhesion of leukocytes to ECs at low shear regions at the vascular wall.

Animals↗

Optimality analysis of vascular-tissue system in mammals for oxygen transport.

The efficiency of the vascular-tissue system in mammals for oxygen (O2) transport to tissue was evaluated by employing the following simulation models; (i) the spherical tissue model for assessing the maximum tissue mass for which a certain number of capillaries located in the center of each sphere can deliver sufficient O2; (ii) the minimum volume model of the multi-terminal vascular system for estimating the energy cost of blood flow supply to that number of capillaries; and (iii), the efficiency evaluation of the whole system by the ratio (the maximum O2 uptake)/(the energy cost). The computer simulation was carried out by inputting the physiological estimates of tissue O2 consumption rate and cardiac output of mammals in the resting and exercising states, which were calculated from the statistically determined power functions of body weight (the allometric relationship) in the range of 10 g to 500 kg. The results obtained from the data during exercise revealed that the optimum capillary number attaining the maximum efficiency alters nearly in proportion to the body weight and that the total tissue mass corresponding to the optimum capillary number agrees well with the actual tissue mass for virtually all the mammals, while their maximum efficiency remains constant. From these results, it is concluded that any mammal is provided with an equally efficient mass transport system, which is optimized for O2 transport to tissue under the highest metabolic activity, regardless of body weight variation. This may suggest one of the reasons why so many species of mammals with greatly different sizes can exist on the earth.

Animals↗

Wall shear stress rather than shear rate regulates cytoplasmic Ca++ responses to flow in vascular endothelial cells.

Recent evidence suggests that the vascular endothelial cell (EC) can sense the flow-rate over its surface and according to the information, regulates not only its own morphology and functions but also those of the surrounding smooth muscle and other tissues. There is now a discussion over which of the following mechanisms actually initiates the signal-transacting response of EC against flow: the mechanical shear deformation of the cell due to flow-oriented wall shear stress (tau), or the diffusional accumulation of vasoactive agonists on the cell surface modulated by wall shear rate (gamma) or both. To identify the relative importance of each mechanism, we examined quantitative changes in the cytoplasmic free Ca++ concentration ([Ca++]i) in cultured EC in the presence of the Ca++ mobilizing agonist ATP, i.e., a second messenger response of the internal signalling system, following the perfusion of two buffers with different viscosities (mu), which relates these factors as tau = mu gamma. The results of in vitro fluorescence photometry in EC with Fura-2 showed that the [Ca++]i level was enhanced with increase in the shear rate but to a greater extent with higher viscosity, and that the [Ca++]i levels at the same calculated level of shear stress were virtually identical, regardless of difference in shear rate and viscosity. This quantitative one-to-one relationship between the shear stress and the second messenger response suggests that wall shear stress rather than wall shear rate is the principal physical factor eliciting EC responses to flow.

Animals↗

Microbial contamination of enteral feeding solution and its prevention.

In an investigation of microbial contamination of enteral feeding solutions, all 22 residual solutions obtained immediately after administration were contaminated at concentrations of 10(3) to 10(6) viable counts/ml. Major contaminants were glucose-nonfermenting gram-negative bacilli such as Pseudomonas aeruginosa and Acinetobacter calcoaceticus var anitratus. Contamination seemed to have been caused by frequent reuse of bag-type containers and the infusion tubes connected to the bags, neither of which can be washed or dried. Decontamination methods were evaluated by using polypropylene containers that can be washed and disinfected for administration. Few Serratia marcescens on the inside wall of the container were removed by rinsing with tap water, alone or in combination with detergent scrub. Tap water and detergent plus air-drying at 56 degrees C for 1 hour reduced Serratia marcescens only somewhat. Tap water and detergent plus immersion in 0.01% sodium hypochlorite for 1 hour or in water at 70 degrees C for 3 minutes eliminated all 10(11) cells of Serratia marcescens.

Bacteria↗

Close correlation between cytoplasmic Ca++ levels and release of an endothelium-derived relaxing factor from cultured endothelial cells.

We studied whether there is a quantitative relationship between free cytosolic Ca++ levels and the release of an endothelium-derived relaxing factor (EDRF) from cultured fetal bovine aortic endothelial cells (EC). EC pretreated with indomethacin were stimulated by the agonists adenosine triphosphate (ATP), bradykinin (BKN), acetylcholine (ACh) and calcium ionophore (A23187) in various concentrations (10(-8)-10(-5) M), and the amount of EDRF released was determined on the basis of endothelium-free rabbit aortic ring relaxation and cultured smooth muscle cell cGMP content. Changes in intracellular Ca++ concentration ([Ca++]i) in response to the same stimuli were determined by photometric fluorescence microscopy using the fluorescent calcium indicator Fura-2. EC stimulation by ATP and A23187 induced dose-dependent increases in both [Ca++]i and the amount of EDRF released. BKN increased both [Ca++]i and EDRF release upon initial exposure (10(-8)M), but there were no further changes at higher concentrations. ACh induced no significant changes in either [Ca++]i or EDRF release. There was a close quantitative correlation between agonist-induced changes in [Ca++]i and the amount of EDRF released (relaxation response in aortic rings and cGMP levels.) (p < 0.001) Removal of extracellular Ca++ eliminated continuous elevation in both [Ca++]i and the amount of EDRF induced by ATP (10(-5)M), BKN (10(-8)M) and A23187 (10(-6)M). These findings suggest that intracellular Ca++ levels are directly linked to the amount of EDRF released, and that extracellular Ca++ is essential for EDRF release because its influx is involved in the continuous elevation of [Ca++]i.

Acetylcholine↗

[Study on the experimental ulcerative colitis model induced by dextran sulfate sodium in rats: estimation of mucosal erosions by the alcian blue-staining method].

We have developed a new method that is applicable for a macroscopic and objective evaluation of erosion in the large intestine in the experimental ulcerative colitis model induced by dextran sulfate sodium (DSS) in rats. The large intestine (without cecum) fixed in 10% neutral buffered formalin solution for more than one week was opened and stained with 1% alcian blue solution. The mucosal surface was stained in light and shade-blue. Histopathological examination revealed that the dark blue area on the mucosal surface had no epithelia and that the connective tissues in the lamina propria were stained with alcian blue. Salazosulfapyridine at 15 and 50 mg/kg twice a day inhibited the erosion area (dark blue area) by 29.6% and 50.2%, respectively. Also, prednisolone at 0.5 mg/kg, twice a day inhibited the erosion by 53.3%. Thus, by measuring the dark blue area stained with 1% alcian blue solution, we could estimate macroscopically and objectively the area of erosions. This method seems to be a useful index for assessing the damages produced in the experimental ulcerative colitis model in rats.

Alcian Blue↗

Protective effect of N-acyl amino acids (NAAs) on cephaloridine (CER) nephrotoxicity in rabbits.

The protective effect of N-acyl amino acids (NAAs) against cephaloridine (CER)-induced nephrotoxicity was studied in rabbits. A large single intravenous dose of CER (more than 100 mg/kg) induced severe proximal tubular necrosis. Simultaneous treatment with several NAAs (at dosages of 100, 200 mg/kg, etc., i.v.), such as N-benzoyl-beta-alanine (NBBA), N-benzoyl-6-aminocaproic acid, and N alpha,epsilon-dibenzoyl-D,L-lysine, remarkably suppressed the histopathological damage in the kidney induced by CER. NAAs have generally low toxicity in laboratory animals (e.g., the LD50 of NBBA was more than 3,000 mg/kg, i.v. in rats), and NAAs were suggested to be good candidates for reducing the nephrotoxicity of CER and other beta-lactam antibiotics.

Alanine↗

Blood flow and vascular endothelial cell function.

Vascular endothelial cells (ECs) are not merely a selective permeability barrier between blood and underlying tissue but actively play an important role in maintaining homeostasis of circulation. ECs that have a variety of synthetic, metabolic, secretory and self-adaptive capabilities regulate vascular tonus and interact with other cells such as vascular smooth muscle cells and white cells. Recent evidence suggests that these functions are affected by shear stress on the endothelial wall, which is a rheological force shearing the luminal surface of the blood vessel when a viscous fluid such as blood flows over it. Wall shear stress reportedly regulates adaptive vessel growth and angiogenesis, and might be a local risk factor in the pathogenesis of atherosclerosis. Shear stress also modulates the production of vasoactive substances such as endothelium-derived relaxing factor, prostacyclin, histamine and endothelin, and regulates macromolecule permeability and endocytosis. More recent studies have shown that shear stress exerts an influence on the expression of mRNA such as tissue plasminogen activator mRNA. These facts suggest that ECs serve as mechanoreceptors by which changes in blood flow or shear stress are recognized by the EC and the signal is transmitted to intracellular organelles. It has been indicated so far that intracellular Ca2+ and the membrane potential might be involved in the shear stress-sensing mechanism of ECs. Knowledge of EC biomechanics, i.e. the EC response to shear stress, will help us to understand the mechanism not only of blood flow-dependent vessel growth and remodeling but also atherogenesis.

Animals↗