Assay for equine peripheral blood lymphocytes blastogenic response using ethidium bromide.
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Biomedical subjects
Publications and source records attributed to M Tajima.
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A discontinuous sucrose gradient was employed in the separation of mouse blood platelets using a modified Booyse method. The platelets of male CD-1 mice aged 8 to 12 weeks were divided into five distinct populations (A, B, C, D & E). Distribution of light to heavy platelets patterns in 10 normal CD-1 mice was demonstrable at; A (S.G. 1.188), as 14.8 +/- 5.6%; B (S.G. 1.199), 44.0 +/- 4.6%; C (S.G. 1.207), 24.1 +/- 3.4%; D (S.G. 1.214), 13.0 +/- 3.6%; and E (S.G. 1.221), 4.0 +/- 1.5%.
Chloropolysporins A, B and C, as well as derivatives prepared from this group and alpha- and beta-avoparcins by enzymatic and mild acid hydrolysis, were active against Gram-positive bacteria including clinically isolated methicillin-resistant Staphylococci (MIC 0.39-6.25 micrograms/ml) and anaerobic enterobacteria (MIC 0.10-1.56 micrograms/ml). Derhamnosyl and demannosyl derivatives from both groups of antibiotics showed stronger activities than the parent compounds. The MIC and MBC values against Staphylococci were similar and were not effected by the presence of serum. Moreover, chloropolysporin C exhibited very strong synergistic effects with various beta-lactam antibiotics against methicillin-resistant strains of Staphylococcus aureus. Some of these compounds also protected mice from experimental infection with S. aureus. Acute toxicities of chloropolysporin by intravenous administration ranged from 215-290 mg/kg in mice. Chloropolysporin B as well as other glycopeptide antibiotics, showed distinctive growth promoting activity in broiler chickens.
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The therapeutic effects of alpha-difluoromethylornithine (DFMO) on rats with bladder tumors induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) were examined. Eight-week-old male Wistar rats were given 0.05% BBN in their drinking water for a period of 4 weeks. Therapy (0.1% DFMO in their drinking water) was started at week 4 and all rats were killed at week 60. DFMO was seen to significantly reduce the incidence, the mean number and the total size of tumors. No side-effects of DFMO were noted, except alopecia, which started at month 7 of the therapy.
Ultrasonography in a sector scanner at real time was performed on the normal kidneys of 126 males and 101 females up to 12 years of age including infants. The growth of the kidneys was well correlated with the age, height and body weight, but the following findings of the kidney length were obtained when the male and female kidneys were measured in a comprehensive manner. 1) y (mm) = 2.987 X age + 55.029 with 0.864 correlation coefficient and less than 1% risk rate showed a positive correlation with the age. 2) y (mm) = 0.407 X height + 28.045 with 0.879 correlation coefficient and less than 1% risk rate showed a positive correlation with the height. 3) y (mm) = 0.949 X body weight + 50.904 with 0.878 correlation coefficient and less than 1% risk rate showed a positive correlation with the body weight. No difference was recognized between both sexes and the right and left kidneys of infants and school students in their kidney length and thickness.
Ultrasonography of both kidneys was performed, on 231 male and 220 females normal junior and senior high school age adolescents. 12 and 20 years. Kidneys grew in correlation with the age, height and body weight. 1) Relationship between the kidney length and the age was y (mm) = 1.747x + 67,663 with 0.489 correlation coefficient and less than 1% risk rate in males, and y (mm) = 1.550x + 76,719 with 0.374 correlation coefficient and less than 1% risk rate in females. 2) Relationship between the kidney length and the height was y (mm) V 0.305x + 43.852 with 0.360 correlation coefficient and less than 1% risk rate in males, and y (mm) = 0.589x + 9.042 with 0.367 correlation coefficient and less than 1% risk rate in females. 3) Relationship between the kidney length and the body weight was y (mm) = 0.290x + 78.258 with 0.373 correlation coefficient and less than 1% risk rate in males, and y (mm) = 0.490x + 76,286 with 0.450 correlation coefficient and less than 1% risk rate in females. No difference the right and left kidney length was recognized in either sex. The growth of female kidneys was faster than that of male kidneys between the ages of 14-17. No difference was observed in length of the right or left kidney or sex with the age group of 18 or over.
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In vitro and in vivo antibacterial activities of cefmetazole alone and in combination with fosfomycin against methicillin- and cephem-resistant (MR) strains of Staphylococcus aureus were investigated, and the mechanism of synergistic effect between cefmetazole and fosfomycin was also studied. Cefmetazole inhibited the growth of 71 strains of MR S. aureus at concentrations ranging from 1.56 to 50 micrograms/ml; the antibacterial activity of cefmetazole against these strains was enhanced approximately 4 times with the addition of fosfomycin at a concentration of 1.56 micrograms/ml. The binding affinity of cefmetazole for the penicillin-binding protein 2' fraction specific for MR S. aureus was higher than that of methicillin, cloxacillin, cefazolin, and cefotaxime. A synergy experiment in vitro was performed by checkerboard titration with Mueller-Hinton agar plates containing various concentrations and ratios of cefmetazole and fosfomycin. The fractional inhibitory concentration index ranged from 0.09 to 0.75. Exposure of cefmetazole plus fosfomycin to exponentially growing cultures at a concentration at which both antibiotics had no bactericidal effect when given alone exerted bactericidal action. Combined administration of cefmetazole with fosfomycin at a ratio of 1:1 against systemic MR S. aureus infections with mice showed an excellent therapeutic efficacy as compared with administration of either antibiotic alone. Penicillin-binding protein 2', 2, and 4 fractions were scarcely detectable in MR S. aureus strains grown in the presence of fosfomycin at concentrations of 0.25 MIC and 0.5 MIC, respectively.
We constructed a series of deletions in the 5' noncoding region of the Saccharomyces cerevisiae GAL7 gene, fused them to the Escherichia coli gene lacZ, and introduced them into yeasts by using a multicopy vector. We then studied the effect of the deletions on beta-galactosidase synthesis directed by the gene fusions in media with various carbon sources. This analysis identified a TATA box and two upstream activating sequences as necessary elements for galactose-controlled GAL7 transcription. Two upstream activating sequences exhibiting 71% homology with each other were located 255 and 168 base pairs, respectively, upstream of the GAL7 transcription start point. Each sequence consists of 21 base pairs, displaying an approximate rotational symmetry with a core consensus sequence of GAA--AGCTGCTTC--CGCG. At least one of the two sequences is required for galactose induction and also for glucose repression of the GAL7'-lac'Z gene. Analysis with host regulatory mutants delta gal14 and delta gal180 suggests that these sequences are the site at which the GAL4 product exerts its action to activate the GAL7 gene. We also observed that a deletion lacking both upstream activation sequences allowed the gene fusion to be expressed in the absence of galactose at about 10% of the fully induced level of the intact fusion. This constitutive expression depended on the presence of the TATA box of GAL7 in cis but not on a functional GAL4 gene. The level of the uncontrolled expression was decreased by increasing the distance between the TATA box and the pBR322 sequence in the vector plasmid.
The characterization of acetyl glyceryl ether phosphorylcholine (AGEPC)-induced paw edema in rats was explored. Edema formation was maximum at 45 min after the injection of AGEPC. The dose for maximal response was 1 microgram/site, while edema was suppressed at higher doses. The systemic administration (s.c.) of cyproheptadine (CH, 10 mg/kg) did not inhibit this edema differently from serotonin-induced edema, while the local treatment of CH suppressed AGEPC-induced edema in a dose-dependent manner. The combination of local treatments with pyrilamine and methysergide also suppressed this edema. The s.c. injection of indomethacin (IM, 10 mg/kg) did not inhibit AGEPC edema differently from carrageenin-induced edema, while locally given IM suppressed it partially. The local treatment with caffeic acid and esculetin, lipoxygenase inhibitors, or with FPL 55712, an antagonist of SRS-A, suppressed AGEPC edema slightly. Various combinations of local treatment with IM and lipoxygenase inhibitors gave synergistic suppression of this edema. Dexamethasone strongly suppressed AGEPC edema when given both systemically and locally 3 hr before the injection of AGEPC. However, phospholipase A2 (PLA2) inhibitors, i.e. mepacrine, p-bromophenacyl bromide, chlorpromazine and tetracaine, did not show the same effect as dexamethasone. These results suggest that the edema formation induced by AGEPC may involve not only the combined action of histamine and serotonin but also the synergistic action of cyclooxygenase and lipoxygenase products. Dexamethasone may inhibit this edema by mechanisms other than the inhibitory action of PLA2.
The area of wound holes made in the parietal bone of 4-week-old rats was measured at 1, 2 and 4 weeks after the operation using Alizarin red S staining without the use of histological sections. Dexamethasone and indomethacin were administered s.c. after the operation every day except Sunday. The inhibitory action of dexamethasone on bone wound healing was stronger than that of indomethacin, as was its inhibitory action on skin wound healing. Inhibition of the age-related decrease in radiolucency of femurs and some changes in serum calcium level were also observed by dexamethasone administration, but not by indomethacin. These results suggest that dexamethasone inhibits bone wound healing through its effects on calcium metabolism in addition to its general inhibitory action on wound healing which is shared with indomethacin. Dexamethasone also strongly inhibited the decrease in Alcian blue stainability which occurs with an increase in age, both in the normal portion and in the wound hole portion of the calvaria, whereas indomethacin showed a weak inhibitory effect only in the wound hole portion. This result suggests that one of the mechanisms by which dexamethasone inhibits bone wound healing may be based on the retardation of mineralization caused by the inhibition of removal of acid mucopolysaccharide.
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