Biomedical subjects
Publications and source records attributed to T Ichikawa.
Reports on aseptic meningitis caused by human parvovirus B19 are extremely rare. A case of aseptic meningitis is described in which human parvovirus B19 DNA was detected in the acute phase in cerebrospinal fluid by the polymerase chain reaction.
We investigated the ability of 25 patients with left unilateral spatial neglect to make a clock face by putting numbers inside a printed circle. Impairment seen in this clock-drawing test did not parallel neglect severity as judged by results of the line-cancellation and line-bisection tests, as well as the copying of a daisy. The score for clock drawing correlated highly with the verbal WAIS score. Most neglect patients with a verbal IQ of 87 or more could draw a clock face fairly well and used planning in placing the numbers 12, 3, 6, and 9 before the others. In clock drawing, verbal intelligence may compensate for left unilateral spatial neglect. We therefore recommend use of the line-cancellation and line-bisection tests, as well as the copying test, but do not recommend use of the clock-drawing test in the diagnosis of left unilateral spatial neglect.
The mechanism of uptake of glycyrrhizin (GLZ) by isolated rat liver cells was studied. The uptake rate was dependent on the unbound GLZ concentration. The initial uptake rate with respect to the unbound GLZ concentration reflected the operation of both saturable and nonsaturable processes, which followed Michaelis-Menten type kinetics; the process involves a Km of 11.3 microM, Vmax of 0.112 nmol/min/10(6) cells, and a first-order rate constant (Kd) of 0.195 nmol/min/10(6) cells/mM. GLZ adsorption on the cell membrane occurs at two types of binding sites with a linear adsorption coefficient = 2.81 nmol/10(6) cells/mM and a dissociation constant = 18.3 microM and its adsorption capacity = 0.12 nmol/10(6) cells describing specific adsorption. GLZ uptake did not require the presence of Na+ in the incubation medium and was not significantly inhibited by ouabain. The Arrhenius plot of uptake of 10 microM GLZ presented a single straight line in the range of 4-37 degrees C, with an activation energy of 15.9 kcal/mol. An energy requirement was also demonstrated, as all metabolic inhibitors studied (rotenone, antimycin A, 2,4-dinitrophenol, and KCN) significantly reduced the uptake of 10 microM GLZ (p < 0.01). The uptake was competitively inhibited by glycyrrhetinic acid (GLA), taurocholate (TCA), and probenecid (PBC) with inhibition constants, Ki, of 13.7, 48.5, and 115.9 microM, respectively, and it was noncompetitively inhibited by bromosulfophthalein (Ki 9.2 microM) and indocyanine green (Ki 13.5 microM) only at low GLZ concentrations (5 and 10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
An inhibitory effect of TZP-4238, a newly synthesized antiandrogen, on the growth of Dunning R3327 rat prostatic tumor was studied and compared with that of chlormadinone acetate (CMA). TZP-4238 markedly suppressed the growth of R3327 tumor. The inhibitory effect of TZP-4238 on the tumor was more potent than that on the prostate. While the inhibitory effect of TZP-4238 on the weight of the ventral prostate was about 6 times as great as that of CMA, the suppressive effect of TZP-4238 on tumor weight was about 40 times as great as that of CMA. Serum levels of testosterone and dihydrotestosterone showed no obvious changes after the administration of either TZP-4238 or CMA. The inhibitory effect of TZP-4238 on the growth of R3327 tumor indicated the application of the compound to human prostatic cancer.
Glycerol has an action to enhance pulmonary tumorigenesis in mice treated with 4-nitroquinoline 1-oxide (4NQO). In order to evaluate factors contributing to enhancing effect of glycerol on 4NQO-induced pulmonary tumorigenesis, we selected alveolar macrophage (AM) as a source of active oxygen formation in the lung and investigated the effect of glycerol on active oxygen formation in AMs of mice treated with 4NQO in this study. AMs were stimulated with opsonized zymosan, and active oxygen formation in AMs after stimulation was examined. Continuous glycerol treatment within 4 weeks after 4NQO injection has no influence on the capacity of active oxygen generation in AMs (expressed as maximum count of chemiluminescence) and total amount of active oxygen generation in AMs (expressed as total count of chemiluminescence). These results suggest that active oxygen formation in AMs don't contribute to enhance 4NQO-induced pulmonary tumorigenesis in mice treated with glycerol.
We examined the effect of a single STZ administration on subsequent islet isograft and allograft survival in NOD mice. Young prediabetic NOD mice were rendered diabetic by STZ administration and transplanted with islet isografts 8-11 days later. The earliest loss of islet function occurred on postgraft day 49. In sharp contrast, 15 of 16 isografts in spontaneously diabetic mice were destroyed within 17 days postgrafting. A comparison of the age of islet isograft destruction in STZ-induced diabetic NOD mice with the course of diabetes development in the NOD mouse colony clearly showed that STZ administration at the prediabetic stage led to a significant delay of diabetes onset in isografts. When STZ was given to overtly diabetic NOD mice, both islet isografts and allografts survived significantly longer than those in untreated, spontaneously diabetic NOD mice. However, the degree of prolongation induced by STZ was much smaller compared with that induced by ALS, a potent immunosuppressive reagent. In vitro mixed lymphocyte culture experiments showed that spleen cells of mice given STZ exhibited time-dependent reduction of their alloantigen reactivities. These results demonstrate that STZ, which is commonly used to induce diabetes in various experimental animals, also possesses an immunosuppressive property, although it is relatively weak compared with ALS.
To investigate the effect of restricted feeding (RF) on the absorption, metabolism, and accumulation of pentachlorobenzene (PECB), rats were fed either ad libitum (AD) or a restricted diet (at 25 or 50% of AD) for 15 days. On the 7th day (day 0), PECB (15 mg/rat) was orally administered. Daily fecal weight and the total amount of PECB excreted into feces were decreased by RF, indicating an increase in PECB absorption due to its prolonged retention in the gastrointestinal tract. However, the amount of PECB excreted was only 4.8% of the dose given to the AD group, and 2.1 and 2.4% of that given to the 50 and 25% restricted diet groups, respectively. The concentrations of PECB and pentachlorophenol, and major metabolite, in blood of the restricted diet groups were higher on day 2 and day 4, while lower on day 6 and day 8 than those of the AD group. On day 8, PECB in liver, kidney, brain, and fat tissue were also lower in the restricted diet groups; the PECB levels in such tissue in the 25 and 50% restricted diet groups were 10-40 and 5-11% of that in the AD group, respectively. These results indicate that PECB metabolism was increased by RF. As PECB is lipophilic, it is most likely that the fat tissue mass, which was markedly decreased by RF, contributed to the enhancement of PECB metabolism. The mechanism seemed to be as follows: as fat tissue mass accumulating PECB decreased, the concentration of PECB in the liver increased, thus the amount of PECB metabolites formed was increased.
Rats were fed either a low vitamin E (VE) diet (-VE), a basal VE diet (+VE, 4.5 mg%), or a high VE diet (+VE, 45 mg%) for 7 weeks. VE content, oxidative DNA damage and lipid peroxide levels in their livers were measured. When purified lard was used as a dietary fat, VE content decreased in the low VE group to one-thirtieth of that in the basal VE group; in the high VE group it increased to 4.5-fold that in the basal VE group. Corresponding to the VE levels, lipid peroxide levels increased to 2.7-fold in the low VE group and decreased to two-thirds in the high VE group. The level of 8-hydroxydeoxyguanosine (8-OHdG) in DNA, a marker of oxidative DNA damage, was about 0.6 per 10(5) deoxyguanosine in the basal VE group and comparable values were found in the low VE and the high VE groups. When either soybean oil or safflower oil was used as a dietary fat, VE content and lipid peroxide levels in the liver were also markedly changed in both the low VE group and the high VE group. 8-OHdG levels in DNA of the low VE with safflower oil group tended to be higher than that of the basal and high VE groups. However, no significant difference was observed among them. These results suggest that the change in VE has little influence on the level of oxidative DNA damage in the liver.
Changes in platelet aggregability patterns and lipid peroxide levels and their relationship were examined in DOCA-salt hypertensive rats during the development of hypertension. In addition, the effect of vitamin E treatment on those changes was also investigated. The blood pressure of the hypertensive rats was 188, 201, 212 mmHg on day 11, 17, and 23, respectively. In the hypertensive rats, both aggregability and granule content in platelet decreased on day 12, 18, 24, and marked decreases were observed on day 24. These data suggested the appearance of exhausted platelets, which had been already activated in vivo due to the hypertension. Marked increases in lipid peroxide levels in serum, the heart and the kidney were observed on day 24 in the hypertensive rats. Increase in serum urea nitrogen was also observed in the hypertensive rats on day 24, suggesting the dysfunction of the kidney. Vitamin E treatment did not prevent in vivo platelet activation due to hypertension, but greatly prevented the elevations of lipid peroxides in serum, the heart and the kidney, and serum urea nitrogen. These results suggested that in vivo platelet activation, an increase of lipid peroxides, and renal dysfunction occur in this order due to hypertension, and that the latter two are significantly prevented by vitamin E treatment.
This work was carried out to estimate the preventive effect of vitamin E on oxy radical-enhanced lung tumorigenesis in ddY mice. We have reported that oxy radicals could be an important factor contributing to the promotive effect of glycerol on 4-nitroquinoline 1-oxide (4NQO)-induced lung tumorigenesis (1). The glycerol-promoted lung tumorigenesis of mice treated with 4NQO was reduced in mice feeding on excessive vitamin E in this study. The levels of nuclear thiobarbituric acid reactive substances (TBARS) and oxidative damage of DNA estimated as DNA single strand breaks (DNA-SSB) were significantly higher in the lungs of mice treated with 4NQO + glycerol than in those treated with 4NQO at 4 weeks after 4NQO administration, This increase was suppressed by the feeding of excessive vitamin E for 4 weeks after 4NQO injection. At 23 weeks after 4NQO injection, the feeding of excessive vitamin E for 4 and 23 weeks after 4NQO injection could cancel the promotive effect of glycerol on lung tumorigenesis. Additionally, the alpha-tocopherol level in serum was related with the degree of lung tumorigenesis at 23 weeks after 4NQO injection. These findings suggest that vitamin E can act as a useful agent to protect mice from oxy radical-promoted lung tumorigenesis.
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The effect of ManducaFLRFamide, a neuropeptide originally isolated from the central nervous system of a sphingid moth, Manduca sexta, was examined on the midgut motility of another sphingid moth, Agrius convolvuli. The peptide was shown to suppress the spontaneous contractions of the isolated gut in adult Agrius at low concentrations (> or = 10(-10) M). Immunoreactivity against anti-FMRFamide antiserum was also detected in the brain-suboesophageal ganglion and the retrocerebral neurohaemal organs of the moth. These observations suggest that ManducaFLRFamide, or its closely-related analog, is a neuropeptide which regulates the activity of the digestive tract in Agrius.
We have isolated a cDNA clone, designated GTI, by screening a tobacco genetic tumor cDNA library with a tumor-specific "subtracted" cDNA probe. The cDNA contained the entire coding sequence for a 94-amino-acid polypeptide that exhibited significant homology to members of the proteinase inhibitor I family from tomato and potato. The predicted protein has a pre-sequence of 22 amino acids but lacks a pro-sequence, unlike genes for proteinase inhibitor I isolated to date. Furthermore, the protein encoded by GTI cDNA has a novel reactive site, having glutamine as the P1 reactive residue. These results suggest that the GTI protein is a novel member of the proteinase inhibitor I family. The mRNA for GTI accumulated at a high level but only transiently after the wounding of tobacco plants. Thus, it appears that the GTI protein has a function that is related to the protection of tissues against damage due to wounding.
1. Glycerol treatment enhanced NADH- and NADPH-driven active oxygen formation and thiobarbituric acid reactive substances (TBARS) in the lungs of ddY mice treated with 4-nitroquinoline 1-oxide (4NQO). 2. A glycerol-associated effect on active oxygen formation and TBARS was not observed in the lungs of A/J mice treated with 4NQO. 3. The differences in the changes of active oxygen formation and TBARS by glycerol treatment between two strains was in agreement with the difference in the enhancing effect of glycerol on 4NQO-induced pulmonary tumorigenesis in mice. This indicates that the alteration in the levels of NADH- and NADPH-driven active oxygen formation and TBARS in the lungs could play a significant role in the enhancement of tumorigenesis associated with glycerol.
Vitamin E had an enhancing effect on active oxygen generation in concanavalin A (Con A)-stimulated alveolar macrophages (AMs) of rats. An inhibitor against protein kinase C (PKC) 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) suppressed a large part of this vitamin E-related effect, but a calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) did not inhibit the increase of active oxygen formation by vitamin E treatment. These results suggest that the activation of PKC presumably relates to the enhancing effect of vitamin E on active oxygen formation in Con A-stimulated AMs.
Glycerol enhances pulmonary tumorigenesis in mice treated with 4-nitroquinoline 1-oxide (4NQO). In order to evaluate factors that contribute to the enhancing effect of glycerol on 4NQO-induced pulmonary tumorigenesis, we selected alveolar macrophage (AM) as a source of active oxygen formation in the lung and investigated the effects of glycerol on active oxygen formation in AMs treated with 4NQO. AMs were stimulated with opsonized zymosan, and active oxygen formation in AMs was examined after stimulation. Continuous glycerol treatment within 4 weeks after 4NQO injection has no influence on the capacity of active oxygen generation in AMs (expressed as maximum count of chemiluminescence) and the total amount of active oxygen generation in AMs (expressed as total count of chemiluminescence). These results suggest that active oxygen formation in AMs does not contribute to enhance 4NQO-induced pulmonary tumorigenesis in mice treated with glycerol.