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Biomedical subjects

H Iida

Publications and source records attributed to H Iida.

At least 595 records · Page 33Linked to original sources
PubMed1981

Hepatic glomerulonephritis. Characteristics of hepatic IgA glomerulonephritis as the major part.

Glomerular lesions associated with hepatic disease were evaluated. Among 752 consecutive patients with hepatitis and cirrhosis, nephritic urinary changes appeared in 1.0% of chronic hepatitis and 9.2% of cirrhotics, but none in patients with acute or subacute hepatitis. Kidney tissue was obtained from 141 cases, of which 59 underwent immunofluorescent studies. Except for a few with possibly coincidental glomerulonephritis, the main glomerular pathology was mesangial depositive or proliferative lesions with frequent circumferential mesangial interposition. The highest incidence (up to 69.2%) occurred in liver cirrhosis. The glomerular immunohistology was not necessarily homogeneous. In acute or subacute hepatitis, IgG or IgM, if present, was dominant. The more chronic the course the liver disease followed, the more frequently significant IgA deposition emerged, occurring in 60.5% of cirrhotics. The IgA positive cases often disclosed paramesangial dense deposits, which is one of the characteristics of primary IgA nephritis. Hepatic IgA nephritis exhibited a lower nephritogenicity and a proneness to show mesangial interposition when compared with primary or purpuric IgA nephritis. The possible origin of glomerular IgA associated with liver disease is discussed.

Chronic Disease↗
PubMed1981

Hepatic glomerulonephritis. Role of hepatitis B surface antigen (HBsAg).

A possible role of HBsAg in hepatic glomerulonephritis was evaluated in kidney specimens from 104 patients with various diseases. Huang's method using formalin-fixed and paraffin-embedded sections was applied to the kidney from 65 cases. Only 4 (3.8%) with liver cirrhosis had glomerular HBsAg deposition; 3 on frozen and one on paraffin sections. In one case of crescentic glomerulonephritis, HBsAg appeared to have had a pathogenetic role with glomerular immunofluorescence dominant for IgM, less intense IgG and negative IgA. The glomerular HBsAg in the remaining 3 patients with hepatic IgA glomerulonephritis was likely to be concomitant or superimposed. One of them had a nephrotic syndrome for which corticosteroid treatment was given, resulting in a near-complete remission and disappearance of HBsAg in the glomeruli, but the glomerular immunohistology was unaffected by the treatment. The present findings suggest that HBsAg has only a minor role.

Chronic Disease↗
PubMed1981

Enhancement of vinblastine-induced cytotoxicity by lysolecithin and phosphatidylinositol.

Vinblastine inhibited the growth of cultured KB cells 3 days after drug treatment by 55% and 67% at 2.7 ng/ml and 3.5 ng/ml of the medium, respectively. Lysolecithin and phosphatidylinositol showed only a marginal inhibitory effect on the growth of KB cells at respective concentrations of 35-125 microgram/ml and 50-150 microgram/ml of the medium. Lysolecithin, however, enhanced the cytotoxicity of vinblastine. Depending upon the concentrations of lysolecithin (35-125 microgram/ml), the growth of KB cells was inhibited by 60-91% and 86-98% at respective vinblastine concentrations of 2.7 ng/ml and 3.5 ng/ml. Enhancement of vinblastine-induced cytotoxicity also occurred similarly for phosphatidylinositol. The mechanism could be explained partly by an elevated amount of intracellular vinblastine. Other possible mechanisms can only be speculated.

Cells, Cultured↗
PubMed1981

Recovery of CNV area after nonresponse condition: inverted-U relation with arousal.

The effect of motor-response recovery after a nonresponse condition on the CNV was investigated in relation to the MPI in 53 healthy adults. The control CNV area before the nonresponse condition had an inverted-U relation to the extraversion score. At the recovery condition the inverted-U relation between the CNV area and the extraversion score shifted toward the lower extraversion score in those subjects who showed a shortened reaction time: i.e., the introverts, particularly the dysthymiacs, responded with the larger CNV area at the recovery condition than at the control condition. These results suggest that the dysthymiacs who possibly have obsession and depression are at a high arousal level and compel attention to a repetitive event as habituating.

Adult↗
PubMed1981

Homogeneity and heterogeneity of toxins produced by Clostridium botulinum type C and D strains.

Five Clostridium botulinum strains were used in the present work, two of type C, C-Stockholm (C-ST) and C-CB19, and three of type D, D-South African (D-SA), D-1873, and D-CB16. The toxins, except for those of C-CB19 and D-CB16, were purified, and antisera were prepared in rabbits. To clarify the antigenicity of the toxins, neutralization and agar gel double-diffusion tests were performed. Anti-C-ST toxin serum neutralized two kinds of type C(1) toxin to a similar extent. Antisera against D-SA and D-1873 toxins, however, showed different neutralizing activity toward three type D toxins. Precipitin lines formed between D-SA and D-1873 toxins, and their antisera spurred to each other. From anti-D-SA toxin serum, two neutralizing fractions, one which neutralized D-SA, D-1873, and D-CB16 and one which neutralized only D-SA, were obtained. These results indicate that the antigenicities of D-SA and D-1873 toxins are not identical. Anti-C-ST toxin serum produced cross-neutralization on type D toxins, although the neutralization titer differed depending on the kind of toxin used. A precipitin line was formed with D-SA toxin, but not with D-1873; the developed line spurred to the C-ST toxin precipitin line. Two anti-D toxin sera also caused cross-neutralization on type C(1) toxins. However, the neutralizing activity of each serum to the same type C(1) toxin was different, and only anti-D-SA toxin serum developed a precipitin line with C-ST toxin which spurred to the D-SA toxin precipitin line. From anti-D-SA toxin serum, two different fractions capable of neutralizing C(1) and D toxins were obtained; one neutralized C-ST, C-CB19, and D-SA toxins, but not D-1873 and D-CB16, and the other neutralized all five toxins. There may be at least two common parts among C-ST, C-CB16, and D-SA toxin molecules.

Antigens, Bacterial↗
PubMed1981

Inhibition of lymph node metastasis of P388 leukemia by bestatin in mice.

Bestatin, a chemically defined immunostimulant of low molecular weight, suppressed the gradually-occurring lymph node metastasis of P388 leukemia in CDF1 mice when administered i.p. at the doses of 1 approximately 30 micrograms/mouse. It could not, however, suppress the established large metastasis of P388 leukemia. Lymph node cells isolated from the mice given bestatin i.p. at 1 and 30 microgram/mouse showed cytostatic activity against P388 leukemic cells in vitro than those from the untreated mice.

Animals↗
PubMed1981

In vitro regeneration of resting lymphocytes from stimulated lymphocytes and its inhibition by insulin.

Concanavalin A- (Con A) stimulated mouse lymphocytes were separated from unstimulated cell populations by a bovine serum albumin (BSA) density gradient centrifugation 2 days after the stimulation. The stimulated cells divided, but did not initiate a new round of DNA replication when cultured further in the absence of Con A. The divided cells became similar in various properties to unstimulated lymphocytes during a prolonged incubation, suggesting that they entered the resting state. In the present study, the process toward the resting state of lymphocytes from the proliferating state was manifested by: a) a decrease in a cell volume, b) lowering of protein content, c) a loss of responsiveness to T cell growth factor (Interleukin 2) (TCGF(IL2)) probably as a result of disappearance of TCGF(IL2) receptors, d) disappearance of insulin receptors, and e) a duration of time lag between the addition of Con A and the onset of DNA synthesis. In addition, it was found that insulin was not mitogenic for recently divided lymphocytes, but prevented these cells from entering the resting state. This suggests that there may be an in vivo system that keeps stimulated lymphocytes highly responsive to antigens for at least several days without initiating DNA synthesis and cell division.

Animals↗
PubMed1981

Overcoming of vincristine resistance in P388 leukemia in vivo and in vitro through enhanced cytotoxicity of vincristine and vinblastine by verapamil.

A noncytotoxic dose of verapamil, a coronary vasodilator, enhances the cytotoxicity of vincristine (VCR) and vinblastine in P388 leukemia and its VCR-resistant subline, P388/VCR. When 2.2 to 6.6 microM verapamil was added along the VCR to the P388/VCR culture in vitro, VCR resistance was completely overcome. Verapamil in doses of 50 to 100 mg/kg administered daily for 10 days with VCR also enhances the chemotherapeutic effect of VCR in P388- and, especially, P388/VCR-bearing mice. When approximately 3 times the amount of VCR was given to a P388/VCR bearer as compared to a P388 bearer, VCR resistance was almost completely overcome in vivo with 50 to 100-mg/kg doses of verapamil. The amount of VCR incorporated into P388 cells was larger than that in P388/VCR cells. Verapamil (6.6 microM) enhanced the cellular level of VCR in P388 cells 2-fold and enhanced the level of VCR in P388/VCR cells 10-fold. The amount of VCR in P388/VCR cells reached the same level as that found in P388 cells. The overcoming of VCR resistance in vivo and in vitro could be explained by the effective accumulation of VCR by verapamil in P388/VCR cells mediated by the inhibition of a VCR efflux function of the cells, a mechanism which remains to be solved.

Animals↗
PubMed1981

Membrane affinity and metabolism of N4-palmitoyl-1-beta-D-arabinofuranosylcytosine into cultured KB cells.

N4-Palmitoyl-1-beta-D-arabinofuranosylcytosine (N4-palmitoyl-ara-C), a lipophilic derivative of 1-beta-D-arabinofuranosylcytosine, possessed an affinity for KB cell plasma membrane. Approximately 15 to 25% of the drug incorporated into KB cells was retained in plasma membrane when the cells were treated with the drug for 1 to 32 hr at 10 microM, the concentration required for 50% inhibition of cell growth. Less than 5.3% of the drug was found in the plasma membrane when the cells were treated with 1-beta-D-arabinofuranosylcytosine. N4-Palmitoyl-ara-C in the membrane fraction cosedimented with plasma membrane in a sucrose density gradient at 4 degrees, indicating a close association between the drug and the membrane. The affinity of N4-palmitoyl-ara-C for plasma membrane probably contributes to the efficient uptake rate and the strong cytotoxic effect of N4-palmitoyl-ara-C reported previously. The metabolites of N4-palmitoyl-ara-C in KB cells, treated with the drug for 32 hr at the concentration required for 50% inhibition of cell growth (10 microM), were analyzed by diethylaminoethyl Sepharose CL-6B column chromatography and thin-layer and paper chromatography. This analysis showed that over 98% of the drug present in the KB cell was N4-palmitoyl-ara-C. The active metabolites, 1-beta-D-arabinofuranosylcytosine, 1-beta-D-arabinofuranosylcytosine 5'-monophosphate, N4-palmitoyl-1-beta-D-arabinofuranosylcytosine 5'-monophosphate, and 1-beta-D-arabinofuranosylcytosine 5'-triphosphate, were found in amounts of 0.41, 0.37, 0.17, and 0.05%, respectively, of the total drug found in the cells. Also found were the inactive metabolites 1-beta-D-arabinofuranosyluracil and 1-beta-D-arabinofuranosylcytosine diphosphate choline in amounts of 0.61 and 0.29%, respectively.

Animals↗
PubMed1980

Suppression of Friend leukemia virus by Bacillus Calmette-Guérin and a streptococcal preparation, OK-432.

OK-432, a streptococcal preparation, and BCG effectively inhibited splenomegaly in Friend leukemia virus (FLV)-infected mice. Divided drug dosage resulted in stronger inhibition than single administration. When the second dose was fixed at the 3rd pre-infection day, the best timing for the first dose was approximately 30 days before infection. The optimal dosages were 100--600 KE/kg for OK-432 and 25--100 mg/kg for BCG. Transfer of peritoneal exudate cells (PEC) from immunomodulator-treated mice, but not PEC from untreated mice, conferred resistance against FLV which was highest when PEC were transferred 1 day before FLV infection. The transfer of PEC on the day of or one day after infection had no protective effect. Inactivation also occurred when FLV was incubated in the presence of PEC from immunomodulator-treated mice, however, no significant effect was observed for PEC from untreated mice.

Animals↗
PubMed1980

Inhibition of murine colon adenocarcinomas and Lewis lung carcinoma by 1-hexylcarbamoyl-5-fluorouracil.

1-Hexylcarbamoyl-5-fluorouracil (HCFU) and its parent compound 5-fluorouracil (5-FU) were tested PO for antitumor activity against mouse colon adenocarcinoma 26 (colon 26), colon adenocarcinoma 38 (colon 38), and Lewis lung carcinoma. The drugs were given orally at 2--4 days intervals for a total of ten doses. 5-FU was moderately active against colons 26 and 38 but not against Lewis lung carcinoma. In this treatment regimen the most impressive antitumor activity was obtained with HCFU against colons 26 and 38, especially colon 38 tumor. At 300 mg HCFU/kg, one out of seven mice inoculated with colon 26 and five out of ten mice inoculated with colon 38 became tumor-free. HCFU, however, was marginally effective in the prolongation of survival time of mice bearing Lewis lung carcinoma. 5-FU is approximately twice as active as HCFU against cultured cell lines from colon 26, colon 38, and Lewis lung carcinoma. Lewis lung carcinoma cells were most sensitive against HCFU, which is in contrast to the results obtained in the in vivo experiment. The IC50 value of HCFU against Lewis lung carcinoma cells was approximately half that against colon 26 and colon 38 cells. This higher sensitivity of Lewis lung cells against HCFU could be explained by the higher cellular uptake of the drug.

Adenocarcinoma↗
PubMed1980

Antigenic similarity of toxins produced by Clostridium botulinum type C and D strains.

Antisera against purified type C1 toxin of Clostridium botulinum and its heavy-chain component cross-neutralized type D toxin. Antisera against partially purified type D toxin cross-neutralized type C1 toxin. From the latter serum, a component which neutralized only type D toxin and a component which equally neutralized both C1 and D toxins were obtained. We concluded that the cross-neutralization was not due to the fact that type C and D strains produce both C1 and D toxins but rather to the fact that the toxins have an antigen(s) common to their molecules. The results of the agar gel-double-diffusion test also supported this conclusion.

Antibody Specificity↗
PubMed1980

Antitumor efficacies of aclacinomycin A by oral administration.

For the purpose of seeking a possible base for the oral clinical application of an anthracycline antibiotic, aclacinomycin A (ACM), ACM was given orally to the mice bearing Lewis lung carcinoma, colon adenocarcinomas 26 and 38, and compared with the effect of adriamycin (ADM). Oral administration of ACM at 5 or 10 mg/kg for 10 time suppressed the growth of Lewis lung carcinoma. There was no significant difference in survival times of the tumor-bearing mice given ACM orally at various dosages tested. ADM was not effective orally as long as the antitumor effect was examined at the dose levels tested. However, significant increase in the survival time of the mice implanted s.c. with colon adenocarcinoma 26 or 38 was noted for oral administration of ACM at 5-10 mg/kg for 10 times. Ths is, at 10 mg/kg of ACM, T/C% was 187% against colon 26 and 141% against colon 38, respectively. ADM, was not effective against these mouse tumors when given orally. Clinical application of ACM by oral administration, however, will need further studied including preclinical pharmacology, drug formulation and others.

Aclarubicin↗