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Biomedical subjects

S Kondo

Publications and source records attributed to S Kondo.

At least 1,009 records · Page 56Linked to original sources
PubMed1987

In vitro and in vivo evaluations of BMY-28100, a new oral cephalosporin.

A new semisynthetic oral cephalosporin, BMY-28100, was evaluated for in vitro and in vivo antibacterial activities in comparison with cefaclor and cephalexin. BMY-28100 showed in vitro activity 3- and 10-fold more potent than that of cefaclor against Staphylococcus aureus and Streptococcus pneumoniae, respectively. BMY-28100 was slightly better than cefaclor and about 4 times more active than cephalexin against Haemophilus influenzae and Neisseria gonorrhoeae. Escherichia coli, Klebsiella pneumoniae and Proteus mirabilis were comparably susceptible to BMY-28100 and cefaclor. The bactericidal activity of BMY-28100 against S. aureus, E. coli and P. mirabilis was equal to or twice as high as MIC value, which was similar to that of cefaclor. The stability of BMY-28100 against penicillinases was nearly comparable to that of cefaclor, whereas cefaclor was somewhat unstable to cephalosporinases. BMY-28100 was about twice as active as cefaclor against three Gram-positive bacterial infections. BMY-28100 was also more potent against infections of H. influenzae and P. mirabilis, but slightly less active against E. coli Juhl than cefaclor. Blood level parameters of BMY-28100 were significantly superior to those of cefaclor and slightly better than cephalexin in mice and rats. The urinary recovery of BMY-28100 was somewhat higher and comparable to that of cefaclor and cephalexin, respectively. BMY-28100 was more stable than cefaclor in human and calf sera at 37 degrees C.

Animals↗
PubMed1987

Evidence that plasma lipoproteins inhibit the factor VIIa-tissue factor complex by a different mechanism that extrinsic pathway inhibitor.

Factor VIIa participates in blood clotting by activating factor X and/or factor IX by limited proteolysis. The proteolytic activity of factor VIIa is absolutely dependent on a lipoprotein cofactor designated tissue factor. We have examined the ability of purified preparations of human plasma high density, low density and very low density lipoproteins, as well as apolipoproteins A-I and A-II, to inhibit the factor VIIa-tissue factor mediated activation of either factor X or factor IX before and after treatment of the lipoprotein preparation with polyclonal antibody directed against partially-purified human plasma extrinsic pathway inhibitor (EPI). In the absence of anti-EPI IgG, HDL, LDL, VLDL, and apolipoprotein A-II noncompetitively inhibited factor X activation by factor VIIa-tissue factor with apparent Ki values of 3.39 mumol/L, 124 nmol/L, 33 nmol/L, and 10.5 mumol/L, respectively. Apolipoprotein A-I had no effect on this reaction. The inhibitory activity of HDL, LDL, VLDL, and apolipoprotein A-II in this reaction was unaffected by the presence of high levels of anti-EPI IgG. In the absence of exogenous factor Xa, none of the lipoproteins studied inhibited the activation of factor IX using the tritiated peptide release assay. In the presence of added factor Xa (1 nmol/L), LDL and VLDL, but not HDL and apolipoprotein A-II, inhibited the activation of factor IX by factor VIIa-tissue factor. This inhibition was completely blocked by prior incubation of the lipoprotein with anti-EPI IgG indicating association of EPI with these particles. Taken collectively, our data indicate that HDL, LDL, and VLDL, at or below their plasma concentration, each selectively inhibits the factor VIIa-tissue factor mediated activation of factor X by a mechanism that appears to be distinct from extrinsic pathway inhibitor. These lipoproteins may not only play a role in the regulation of extrinsic blood coagulation, but may also selectively promote the activation of factor IX by factor VIIa-tissue factor in vivo at low tissue factor concentrations.

Apolipoproteins↗
PubMed1987

[A case of colonic carcinoma associated with intestinal tuberculosis, and an analysis of 26 cases reported in Japan].

A case of tuberculosis and adenocarcinoma co-existing in the ileocecal region in a 61-yr-old woman is described. The Japanese literature is reviewed and several points discussed regarding the epidemiological and morphological features in a colon carcinoma associated with tuberculosis. (1) Females predominate by a ratio of 17:9 in such cases. (2) The tumor has been found in the right side of the colon in 17 out of 26 cases. (3) The most characteristic histological finding is that of the cancer, which shows a well differentiated adenocarcinoma with a tendency to produce a mucin. These unique findings are consistent with those in our case. It is of interest that these unique findings may support the possibility that the cancer originated from a tuberculous lesion.

Adenocarcinoma↗
PubMed1986

Studies on the effect of PEG-modified urokinase on coagulation-fibrinolysis using beagles.

Urokinase (UK), a human urinary plasminogen activator, was modified by the covalent attachment of methoxypolyethylene glycol (PEG) of 5,000 daltons. There were observed changes in substrate specificity and an increase in molecular weight in PEG-modified UK (PEG-UK). We evaluated PEG-UK by ex vivo study using beagles, and found that UK activity in the blood was well maintained over hours after intravenous injection, and that fibrinolysis was more activated compared with native UK by coagulation-fibrinolysis studies.

Animals↗
PubMed1986

Purification and characterization of cytotoxic factors in the venom of the Okinawa habu (Trimeresurus flavoviridis).

Two cytotoxic factors in the venom of Okinawa habu (Trimeresurus flavoviridis), a crotalid, have been purified and characterized. They had cell monolayer-disrupting activity against cells cultivated in vitro, but no proteolytic, hemorrhagic or direct hemolytic activity nor lethal toxicity. They were heat labile acidic proteins (isoelectric points 5.2 and 5.4) having similar molecular weights (approx. 14,000) and amino acid compositions. They were indistinguishable immunologically.

Amino Acids↗
PubMed1986

Effect of calyceal resection on pelviureteral peristalsis in isolated pig kidney.

Pelviureteral peristalsis in the isolated pig kidney with calyceal resection was studied by electromyography. Ureteral peristalsis normally remained under control of calyceal pacemakers while at least one of the upper, middle and lower major calyces of the isolated pig kidney was intact. After resection of all these calyces, uncontrolled spontaneous contractions began to arise from the renal pelvis, pelviureteral junction (PUJ) and stump of the ureter. In such kidneys, the PUJ and cut end of the ureter showed discharge potentials with irregular intervals while the potential recorded from the center of the pelvis had virtually constant intervals of discharge. The spontaneous contractions arising in the pelvis were rarely propagated to the PUJ and ureter, and there was irregular antiperistalsis of the ureter generating at the cut end and also irregular ureteral normoperistalsis originating at the PUJ and propagating to the ureter. With increased intrapelvic fluid infusion, the discharge interval of the renal pelvis shortened whereas that of the PUJ and ureter was prolonged. These facts suggest the importance of the calyceal pacemaker both as an origin of ureteral peristalsis and as a supervisor for maintaining normal ureteral peristalsis.

Action Potentials↗
PubMed1986

Photoreactivation rescue and hypermutability of ultraviolet-irradiated excisionless Drosophila melanogaster larvae.

There is accumulating evidence suggesting that expression of genes for repair of UV damage to DNA in mammals and fish is regulated developmentally. Therefore, the activity of excision repair and photoreactivation in vivo in young larvae of Drosophila melanogaster was examined in a strain carrying the mutation mus201 that was unable to carry out excision repair. The photoreactivation activity in first-instar larvae was so high that UV-induced lethality in excision-less larvae was almost completely rescued by posttreatment with fluorescent light. Excision repair activity in first-instar repair-proficient larvae was so high that UV irradiation was scarcely able to produce somatic eye-color mutations. In contrast, excisionless larvae showed a high incidence of somatic eye-color mutation after UV-irradiation, and this incidence was reduced to the spontaneous level by posttreatment with fluorescent light. Incorporation of a postreplication repair-defective mutation into the excisionless strain decreased the incidence of UV-induced somatic mutations by a factor of 3. The analogous repair dependence of UV mutagenesis in Drosophila and Escherichia coli is discussed. It is proposed that UV-induced somatic mutations in excisionless Drosophila larvae are caused primarily by pyrimidine dimers and that a constitutive, error-prone pathway for filling daughter-strand gaps opposite dimers is, at least partly, responsible for the fixation of mutations.

Age Factors↗
PubMed1986

Molecular basis for two different affinity states of the interleukin 2 receptor: affinity conversion model.

Two affinity species of the interleukin 2 (IL-2) receptor are different states of a single receptor molecule. We assumed that a binary complex between the IL-2 receptor and another lymphocyte-specific protein would constitute the high-affinity receptor. To test this assumption, we counted the numbers of IL-2 receptors with high and low affinity in a murine T-cell line CT/hR-1 that expresses not only murine but also human receptors by cDNA transfection. We found that human high-affinity receptors disappeared when the murine high-affinity receptors were already occupied by the ligand. The results were incompatible with a fixed number of human and murine receptors with high affinity in CT/hR-1 cells. We suggest that the high-affinity state of the IL-2 receptor is a ternary complex of IL-2, the IL-2 receptor, and a postulated "converter" protein, which is fewer in number than the receptors. The converter would be unable to form a complex with the IL-2 receptor unless IL-2 was already bound to it. The ligand binding to the receptor would cause a conformational change in the receptor, increasing its affinity to the converter. Ternary complex formation would, in turn, change the apparent affinity of the receptor to the ligand from low to high by reduction of the dissociation constant.

Allosteric Regulation↗
PubMed1986

DNA repair dependence of somatic mutagenesis of transposon-caused white alleles in Drosophila melanogaster after treatment with alkylating agents.

DNA repair-defective alleles of the mei-9, mei-41, mus-104 and mus-101 loci of Drosophila melanogaster were introduced into stocks bearing the UZ and SZ marker sets. Males with the UZ marker set, z1 (zeste allele) and w+(TE) (genetically unstable white allele presumably caused by a transposable element), or the SZ marker set, z1 and w+R (semistable white allele caused by partial duplication of the w+ locus plus transposon insert), were exposed to EMS at the first instar. After emergence, adult males bearing red spots on lemon-yellow eyes were scored as flies with somatic reversions of w+(TE) or w+R. The relative mutabilities (relative values of reversion frequency at an equal EMS dose) of either w+(TE) or w+R in a repair-proficient strain and in mei-9, mei-41, mus-104 and mus-101 strains were 1: approximately 1.2:0.3:0.3:0.7, despite the fact that w+(TE) reverted two to three times as frequently as w+R under both the repair-proficient and repair-deficient genetic conditions. Similarly, after treatment with MMS, MNNG and ENNG, w+(TE) was somatically more mutable in the mei-9 strain and less mutable in the mei-41 and mus-104 strains than in the repair-proficient strain. From these results, we propose that mutagenic lesions produced in DNA by treatment with these chemicals are converted to mutant DNA sequences via the error-prone repair mechanisms dependent on the products of the genes mei-41+ (mei-41 and mus-104 being alleles of the same locus) and mus-101+, whereas they are eliminated by mei-9+-dependent excision repair. In contrast to the approximately linear responses of induced reversions of w+(TE) with ENNG in the repair-proficient, mei-9, and mei-41 strains, seemingly there were dosage insensitive ranges for induced reversion with MNNG in the repair-proficient and mei-41 strains, but not for reversion in the mei-9 strain; w+(TE) in the mus-104 strain was virtually nonmutable with MNNG and ENNG. These results suggest that O6-methylguanine (O6MeG) produced in DNA with MNNG, but not O6-ethylguanine produced with ENNG, is almost completely repaired in a low dose range by constitutive activity of DNA O6MeG transmethylase. From the distribution of clone sizes of spontaneous revertant spots and other data, we propose that both w+(TE) and w+R have a similar tendency to spontaneously revert more frequently at early rather than at later developmental stages probably reflecting a common property of their inserted transposons.

Alkylating Agents↗