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Biomedical subjects

Y Osada

Publications and source records attributed to Y Osada.

At least 181 records · Page 10Linked to original sources
PubMed1983

Aarskog syndrome.

A rare case of Aarskog syndrome is presented. The Aarskog syndrome is characterized by short stature with typical facial, digital, and genital anomalies.

Abnormalities, Multiple↗
PubMed1983

Antimycoplasmal activity of ofloxacin (DL-8280).

Ofloxacin (DL-8280; (+/-)-9-fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1- pipera-zinyl)-7-oxo-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxylic acid) showed a broader spectrum and a greater potency of antimycoplasmal activity than did pipemidic acid, norfloxacin, tetracyclines, and lincomycin, but was inferior to erythromycin. Its mycoplasmacidal potency against clinical isolates of Mycoplasma pneumoniae was also greater than that of other quinolones and tetracyclines.

Anti-Bacterial Agents↗
PubMed1983

Stimulation of nonspecific resistance to infection induced by muramyl dipeptide analogs substituted in the gamma-carboxyl group and evaluation of N alpha-muramyl dipeptide-N epsilon-stearoyllysine.

Stimulation of resistance to infection induced by the analogs of muramyl dipeptide (MDP) having substituted functions in the gamma-carboxyl group of D-isoglutamyl residue was examined in experimental Escherichia coli infections in mice. An MDP analog which is an efficient strengthener of resistance to infection, N alpha-MDP-N epsilon-stearoyllysine [MDP-Lys(L18)], was selected through the comparative assessment of a number of compounds in three categories: (i) gamma-alkylamides, (ii) gamma-esters, and (iii) N alpha-MDP-N epsilon-acyllysine derivatives. Furthermore, the antiinfectious activity of MDP-Lys(L18) was evaluated bacteriologically in comparison with that of MDP. The effect of MDP-Lys(L18) on the susceptibility of mice to infections with various species of microorganisms was studied. Protective activity was greatest against E. coli and staphylococcal infections, considerable against Pseudomonas and Candida infections, and least against Klebsiella infection. The effects of bacterial inoculum size and MDP treatment timing, dose, and route of administration on protective activity were studied. The efficacy of MDP-Lys(L18) in protection tests was demonstrated for all administration routes, even the oral. Its high potency was confirmed by the smaller influence of inoculum size and particularly small value of the minimum dosage required for inducing protective activity. A decrease in bacterial survival was observed in the blood and organs of mice treated with the analog and infected with E. coli. The following two useful effects were obtained: the synergistic effect of glycopeptide and chemotherapeutic agents and the stimulation of resistance to infection in animals immunocompromised by cyclophosphamide treatment.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

Stimulation of complement production in mice by N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine.

N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine, a synthetic muramyl dipeptide analog, stimulated the production of the third component of complement (C3) in mice. The serum concentration of C3 was elevated significantly by subcutaneous treatment with a single dose (10 to 100 micrograms per mouse) of the adjuvant 24 h before assay of the serum. Thereafter, the concentration decreased gradually with time and returned to the normal level on day 4 to 5. Immunoelectrophoretic analysis of the serum revealed that the decrease in serum C3 could not be accounted for by the cleavage to C3a and C3b. By intermittent treatment with the adjuvant on every fifth day, a significant increase in serum C3 was repeated. However, no continuous retention of the serum level of C3 was established even during continuous treatment with the adjuvant once a day for 10 consecutive days. Instead, in this case, the level of C3 increased repeatedly at almost 5-day intervals.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1982

Bilateral renal artery stenosis and renovascular hypertension in rabbits.

In 21 rabbits bilateral renal artery stenosis was produced by constriction of the right renal artery with 1 of 3 different clips in size followed by left renal artery constriction with the smallest clip. Five to 6 weeks after left renal artery constriction, 5 ml. of the blood samples for the measurement of plasma renin activity (PRA) was taken from both renal veins and the distal vena cava, and the left nephrectomy was performed. In 17 out of 21 rabbits, PRA was determined in 3 different blood veins: L, left renal vein PRA; R, right renal vein PRA; and P, distal vena cava vein PRA. Three PRA patterns, L greater than P greater than or equal to R (A type), L, R greater than P (B type) and R greater than L not equal to P (C type), were observed. Removal of the left kidney caused a significant decrease in the average blood pressure persisting for 5 weeks in the rabbits with the type A pattern of PRA (p less than 0.05). In all 4 animals with the type B or C pattern of PRA hypertension persisted even after removal of the left kidney. Comparison of the PRA values between the venous blood in 3 different vascular trees seems very useful to predict the depressor response that follows nephrectomy of the severer constricted side.

Animals↗
PubMed1982

Enhancement of non-specific resistance to Pseudomonas pneumonia by a synthetic derivative of muramoyl dipeptide in immunosuppressed guinea pigs.

A synthetic derivative of muramoyl dipeptide, 6-O-stearoyl-N-acetylmuramoyl-L-alanyl-D-isoglutamine [L18-MDP(A)], showed a protective effect against bacteraemic and non-bacteraemic pneumonia caused by Pseudomonas aeruginosa in immunosuppressed guinea pigs. In about half of the animals treated with the compound before infection, death from bacteraemic pneumonia produced by intratracheal inoculation of P. aeruginosa was delayed for 7 d, although all of the animals infected without prior treatment with the compound died within 4 d of infection. Multiplication of the organisms in the lung was also suppressed for at least 10 d by treatment with the compound when the animals inhaled an aerosol of P. aeruginosa. In contrast, in untreated animals the numbers of bacteria in the lung gradually increased from 10(6) to 10(9) c.f.u. g-1, and a few animals in which the organism increased to 10(9) c.f.u. g-1 had died by 6 and 10 d after infection. In both healthy and immunosuppressed animals, the accumulation of polymorphonuclear leukocytes (PMNs) in a subcutaneous air-pouch injected with heat-killed organisms was augmented by subcutaneous treatment with L18-MDP(A) 1 d before bacterial injection. The phagocytic activity of peritoneal PMNs was also increased by treatment with this compound. The augmentation of protective mechanisms against pseudomonas pneumonia by L18-MDP(A) may be attributed at least partly to the increased chemotactic and phagocytic activity of PMNs.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1982

Nonbacteremic pseudomonas pneumonia in immunosuppressed guinea pigs.

An experimental model of nonbacteremic pneumonia with a virulent strain of Pseudomonas aeruginosa was successfully established in guinea pigs immuno-suppressed with cortisone acetate although the organisms were eliminated rapidly from the lungs without cortisone treatment. Using a pocket nebulizer, almost all the animals which received 10(6) organisms/g-lung developed bronchopneumonia without any septic findings as long as 10 days after challenge. The lesions produced in such animals were characterized by dissemination of multiple purulogranulomatous changes. In the early stage of infection, infiltration of polymorphonuclear cells (PMNs) in the bronchiolar and alveolar spaces was diffuse, later showing multifocal accumulation with the formation of central spherical grains enclosing bacterial colonies. In the later stage, granulation tissue consisting of large mononuclear cells, fibroblasts and collagen fibers developed around the PMN accumulation. The animals which received 10(7) organisms/g-lung, on the other hand, developed severe pulmonary hemorrhages and necrosis followed by septic death.

Animals↗
PubMed1982

In vitro and in vivo activity of DL-8280, a new oxazine derivative.

DL-8280, 9-fluoro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H- pyrido-(1,2,3-de)1,4-benzoxazine-6-carboxylic acid, is a new nalidixic acid analog with a broad spectrum of antibacterial activity against gram-negative and gram-positive bacteria, including obligate anaerobes. The activity of DL-8280 against Enterobacteriaceae, Pseudomonas aeruginosa, Haemophilus influenzae, Neisseria gonorrhoeae, and Clostridium perfringens was roughly comparable to that of norfloxacin and far exceeded that of pipemidic acid and nalidixic acid. DL-8280 had greater activity against Staphylococcus spp., Streptococcus spp., Pseudomonas maltophilia, Acinetobacter spp., and Bacteroides fragilis than did norfloxacin, pipemidic acid, and nalidixic acid. Nalidixic acid-resistant Enterobacteriaceae, ampicillin-resistant gonococci, and clindamycin-resistant obligate anaerobes were also susceptible to DL-8280. The activity of DL-8280 was affected very little by inoculum size, and its action was bactericidal at two times the minimal inhibitory concentrations at most. Administered orally to mice experimentally infected with Staphylococcus aureus, Streptococcus pyogenes, Escherichia coli, Proteus mirabilis, Serratia marcescens, or P. aeruginosa, DL-8280 was 2 to 7 times more effective than norfloxacin and 7 to more than 50 times more active than pipemidic acid.

Animals↗
PubMed1982

Effect of L18-MDP(Ala), a synthetic derivative of muramyl dipeptide, on nonspecific resistance of mice to microbial infections.

By subcutaneous treatment with an aqueous solution of 6-O-stearoyl-N-acetylmuramyl-L-alanyl-D-isoglutamine [6-O-CH3-(CH2)16-CO-MurNAc-L-Ala-D-isoGln] [referred to here as L18-MDP(Ala)], an augmentation of the resistance of mice to Escherichia coli, Pseudomonas aeruginosa. Staphylococcus aureus, and Candida albicans infections was observed, but not to infections with Klebsiella pneumoniae and Listeria monocytogenes. Against E. coli infections, L18-MDP(Ala) was highly protective, irrespective of the administration route. Bacteremia occurring at an early phase of such infections was almost completely prevented by subcutaneous treatment 1 day before infection. Single or multiple doses were also effective against C. albicans infection. The phagocytosis of E. coli by mouse peritoneal polymorphonuclear cells was enhanced by treatment with the adjuvant, and the phagocytosis of K. pneumoniae was also enhanced, but only when the mice were treated either with rabbit normal serum or with a specific immune serum. The growth of the fungus in the kidneys was significantly inhibited, and growth was eliminated from the kidneys by treatment with the adjuvant once a day for 4 consecutive days, starting 1 day before infection. However, no growth suppression of L. monocytogenes in the livers or spleens of infected mice was observed when they were treated with a single dose of the adjuvant. This difference may be ascribed to the differences in the effector mechanisms of defense and to the different degree of augmentation of each defense mechanism by L18-MDP(Ala).

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1982

Polymorphonuclear leukocyte activation by a synthetic muramyl dipeptide analog.

N alpha-(N-Acetylmuramyl-L-alanyl-D-isoglutaminyl)-N epsilon -stearoyl-L-lysine, a synthetic derivative of muramyl dipeptide, stimulated the chemotactic mobility, phagocytic activity, and superoxide anion (O2-) productivity of peritoneal polymorphonuclear cells in mice. The chemotactic mobility of both cells preincubated with the adjuvant in vitro and those derived from the mice previously treated with the adjuvant was significantly enhanced. The phagocytic activity of cells preincubated in vitro with the adjuvant was also enhanced transiently, and that of the cells derived from the mice treated subcutaneously with the adjuvant 24 h before intraperitoneal inoculation with Escherichia coli was significantly greater than that of cells from the mice given phosphate-buffered saline instead of the adjuvant. The release of O2- from the cells derived from the adjuvant-treated mice was also greater than that from the cells of untreated control mice. However, the exposure of the cells derived from untreated mice to the adjuvant in vitro did not stimulate O2- generation by the cells.

Acetylmuramyl-Alanyl-Isoglutamine↗