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Biomedical subjects

K Joh

Publications and source records attributed to K Joh.

At least 91 records · Page 5Linked to original sources
PubMed1990

Aldolase DNA polymorphism in subterranean mole-rats: genetic differentiation and environmental correlates.

We analysed the genetic diversity and environmental correlates of the aldolase A and B genes by means of restriction endonucleases (DNA RFLP analysis), in the four chromosomal species (2n = 52, 54, 58 and 60) of the actively speciating subterranean mole-rats of the Spalax ehrenbergi superspecies in Israel. The results indicated that: (i) both aldolase genes are highly polymorphic; (ii) fragment frequencies and fragment profiles display geographical patterns and significant ecological correlates; (iii) discriminant analysis largely succeeded in separating the four chromosomal species on the basis of variation of aldolase RFLPs.

Animals↗
PubMed1990

Microlamellar structures in lobular glomerulonephritis associated with monoclonal IgG lambda paraproteinemia. A case report and review of the literature.

We report a 49-year-old woman who developed lobular glomerulonephritis with prevalent deposition of material positive for IgG, C1q and lambda light chain, but which was not stained by Congo red. Glomeruli revealed massive electron-dense deposits with a microlamellar structure in the mesangial matrix and peripheral capillary loops. Clinically, the patient had nephrotic syndrome, microhematuria and hypertension. No Bence-Jones protein or cryoglobulin was found in the urine or serum. Anti-DNA antibody was positive, but systemic lupus erythematosus (SLE) was ruled out by repeated serological examinations. Immunoelectrophoresis of blood and urine revealed increased IgG-lambda paraprotein, but no free light chains were found. We reviewed 54 cases reported in the literature, which showed organized crystalline structures on ultrastructural examination, but were unassociated with amyloidosis, SLE, cryoglobulinemia or multiple myeloma. The present patient is the first reported to have exhibited a combination of glomerulonephritis with organized deposits, monoclonal IgG lambda paraproteinemia, and the presence of anti-DNA antibody.

Female↗
PubMed1990

Drug-induced hypersensitivity nephritis: lymphocyte stimulation testing and renal biopsy in 10 cases.

The pathomorphological and clinical findings were investigated in 10 cases of drug-induced hypersensitivity nephritis. Hypersensitivity due to drugs was strongly suggested by the lymphocyte stimulation test in all patients. The offending drugs included penicillin, cephem derivatives, nonsteroidal anti-inflammatory drugs, and minocycline. All patients developed acute renal failure shortly after administration of regular doses of the drugs. Allergic symptoms plus a raised level of serum IgE or eosinophilia were seen in 7 patients. The remaining 3 patients receiving nonsteroidal anti-inflammatory drugs had no allergic symptoms, but developed severe proteinuria. Eight patients without severe glomerular damage recovered after withdrawal of the offending drugs and temporal dialysis and/or steroid therapy. Renal biopsies revealed tubulitis and tubular epithelial degeneration with interstitial edema as the common characteristic findings. Granulomatous lesions were occasionally observed. Multinucleated giant cells found in the granulomas were positive for LN-3 which is compatible with HLA-DR antigen. The glomeruli appeared normal, except in 2 cases in whom crescentic glomerulonephritis and thrombotic microangiopathy were seen. Our study suggests that the lymphocyte stimulation test and renal biopsy are the most useful means to confirm the diagnosis and provides further evidence for the participation of cell-mediated immunity in the pathogenesis of drug-induced hypersensitivity nephritis.

Acute Kidney Injury↗
PubMed1990

Regulation of IgE and IgG4 synthesis in patients with hyper IgE syndrome.

In order to investigate the imbalance of IgG subclasses and its relationship to IgE level, 14 patients with hyper IgE syndrome (HIE syndrome) were examined for serum IgG subclasses and IgE levels and five of these patients were studied for in vitro IgE and IgG subclass production by peripheral blood lymphocytes (PBL) in response to interleukin-4 (IL-4)/interferon-gamma (IFN-gamma). Serum IgE levels were highly correlative with serum IgG4 levels (r = 0.75, P less than 0.005), but not with IgG1, IgG2 or IgG3 levels (r = 0.21, 0.43 and 0.41, respectively). In an in vitro study, recombinant IL-4 enhanced not only spontaneous IgE synthesis but also IgG4 synthesis in cultures of PBL from patients with HIE syndrome as well as in healthy donors (P less than 0.01), and the effect of recombinant IL-4 on both IgE and IgG4 synthesis was inhibited by low concentrations of recombinant IFN-gamma (P less than 0.01). The disturbed regulation of IgE and IgG4 seen in patients with hyper IgE syndrome may be caused mainly by the disturbed regulation of both cytokines.

Adolescent↗
PubMed1990

The effect of prostaglandins on experimental storage disease in rats.

The aim of this study was to investigate the effect of prostaglandins (PGs) on the release of lysosomes into the extracellular space in experimentally-induced storage disease in rats. The generalized phospholipidosis was induced by oral administration of chlorphentermine to Wistar rats. PG-E2 or PG-F2 alpha (50 micrograms/100 g) was injected intravenously into rats with phospholipidosis. Control rats were injected with the same amount of saline. Twenty-four hours later, extracellular and intracellular lysosomes were analysed morphometrically in electromicrographs of the liver, kidney, myocardium, skeletal muscle, aorta and cervix uteri, having been stained with acid-phosphatase. The morphometric parameters used were the numerical density of lysosomes per unit volume and the volume density of lysosomes per unit volume. The results show that, in comparison with the controls, a volumetric increase of extracellular lysosomes and a volumetric decrease of intracellular lysosomes were achieved by PG-E2 or PG-F2 alpha administration in several organs, but not in the myocardium or skeletal muscles. The effect of PG-F2 alpha was greater than that of PG-E2 in the liver and kidney, while the effect of PG-E2 was greater than that of PG-F2 alpha in the aorta and cervix uteri. These results indicate that PGs influence the discharge of storage lysosomes in bipolar epithelial cells in the liver and kidney, and also influence the release of non-storing lysosomes in apolar mesenchymal cells in the aorta and cervix uteri.

Animals↗
PubMed1989

Induction of interstitial nephritis in rats by basement membrane of human origin.

A study was conducted to investigate nephritogenic tubular basement membrane antigens common to human and rat kidneys. Brown Norway (BN) rats were immunized with human renal basement membrane in complete Freund's adjuvant simultaneously with Bordetella pertussis vaccine. The immunized rats developed polyuria and increased levels of serum creatinine one week after the second immunization. Renal histology at this time revealed marked, acute tubulointerstitial nephritis with linear deposition of IgG and C3 along the tubular basement membrane and Bowman's capsule, but not along the glomerular basement membrane. Rats with this tubulointerstitial nephritis rapidly developed antibodies against renal antigens from normal BN rats such as tubular basement membrane and proximal tubule brush border, however antibodies to glomerular basement membrane appeared later. Western blotting using the same rat sera detected a 145-kDa antigen from 8 M urea-solubilized human renal basement membrane and 120-kDa, 135-kDa and 145-kDa antigens from 8 M urea-solubilized BN rat renal basement membrane. This suggests that renal basement membranes of human and rat origin have common antigens involved in the pathogenesis of tubulointerstitial nephritis.

Animals↗
PubMed1989

Experimental drug-induced allergic nephritis mediated by antihapten antibody.

Experimental drug-induced allergic nephritis (DIAN) was mediated by an antihapten antibody. It has been postulated that DIAN is induced by cellular and humoral mechanisms. We tried to induce DIAN in mice, where the mechanism depends on humoral immunity. The first attempt was made in mice actively producing antibodies against cephem antibiotics, i.e. cephalothin (CET). Acute interstitial nephritis (AIN), morphologically similar to human disease, was obtained by injection of a CET-protein conjugate into the renal cortex in mice producing anti-CET-IgE and IgG antibodies. AIN could also be induced when normal mice, passively given anti-CET IgG antibody, received a subsequent intrarenal challenge with CET-protein conjugate. These preliminary results indicate that IgG antibody has an important role in the genesis of DIAN. Further experiments were performed with monoclonal antibodies directed against haptens instead of antibiotics in order to clarify the Ig isotype concerned. In mice passively given anti-Dansyl-IgG2a or anti-NP-IgG2a monoclonal antibodies, a challenge with an appropriate hapten-protein conjugate into the renal cortex resulted in AIN. However, transfer of anti-Dansyl-IgE or anti-DNP-IgE monoclonal antibodies, followed by challenge, did not induce AIN. In the experimental systems described, the involvement of a cellular immune mechanism is excluded. The results suggest that IgG, but not IgE antibody, is essential for the induction of DIAN by humoral immune mechanism.

Animals↗
PubMed1989

Fc-epsilon-receptor-bearing lymphocytes in patients with clonorchiasis.

Expression of Fc-epsilon-receptors (Fc epsilon R) on peripheral blood lymphocytes was examined in patients with clonorchiasis. Mean serum IgE levels in these patients was 2,518 IU/ml. Fc epsilon R was detected by flow cytometry analysis with monoclonal antibody. The frequency of Fc epsilon R+ lymphocytes and the density of Fc epsilon R on the cells in the patients were similar to those in normal subjects. Most of the Fc epsilon R+ lymphocytes were B cells. The number of Fc epsilon R+ cells decreased after incubation in serum-free medium at 37 degrees C for 3 h. The amount of regulatory molecules of IgE production, IgE binding factor, was not significantly different between the patients and normal subjects. The number of Fc gamma R bearing T or B cells in the patients was also similar to that of normal subjects. These results indicate that the mechanisms of elevated serum IgE in patients with clonorchiasis might be different from other diseases with hyperglobulinemia E.

Adolescent↗
PubMed1989

Detection and characterization of IgE-producing cells in patients with clonorchiasis.

The ability of peripheral B cells of patients with Clonorchis sinensis infections to secrete IgE spontaneously was investigated in vitro. The de novo synthesis of IgE was observed in unstimulated B-cell cultures of patients. There was a significant relationship between the serum IgE level and the amount of IgE spontaneously secreted by B cells. Pretreatment of patients' B cells with 10 micrograms/ml of rabbit anti-human IgE resulted in the clear suppression of spontaneous IgE synthesis without affecting the IgG synthesis. Their B cells capable of spontaneously secreting IgE were partially sensitive to irradiation with 1,000 rad. The results obtained suggest that such IgE-forming cells may be responsible for at least part of the persistent IgE formation in patients with helminthic infections as well as in those with atopic disease.

Animals↗
PubMed1988

[Pharmacokinetic and clinical studies on imipenem/cilastatin sodium in neonates and premature infants].

Imipenem/cilastatin sodium (IPM/CS) was administered in a dose of 10 mg/10 mg/kg or 20 mg/20 mg/kg by a 1-hour intravenous drip infusion to 19 mature and premature neonates with ages from 1 to 12 days with various bacterial infections, and plasma concentrations and urinary recovery rates in these subjects were measured. Because of the small number of patients recruited, neonates were not divided into mature and premature groups, but into 3 groups based on their day-ages: 0-3 days, 4-7 days and 8 days or older. A clinical evaluation of IPM/CS was carried out in 10 male and 3 female neonates with ages 0-28 days. These patients included 6 with pneumonia, 4 with urinary tract infection and 1 each with septicemia, suspected septicemia and maxillary sinusitis. 1. Plasma concentrations and urinary recovery rates (1) The 1-hour intravenous drip infusion at 10 mg/10 mg/kg of IPM/CS IPM: Its peak plasma concentrations were obtained at the end of drip infusion of the test drug in all 3 groups, their values ranged from 18.18 to 19.90 micrograms/ml with no statistically significant variations. The plasma concentrations rapidly decreased to 0.32-0.98 microgram/ml at 8 hours after administration of IPM/CS. The half-lives tended to be shorter in older neonates, with mean half-lives being 1.87, 1.55 and 1.40 hours, respectively. CS: Its peak plasma concentrations were obtained for all 3 groups at the end of drip infusion and were ranging from 28.23 to 30.00 micrograms/ml with no significant variations. Plasma concentrations in the 0-3 day-age group and the 4-7 day-age group slowly decreased to 6.30 micrograms/ml and 4.58 micrograms/ml at 8 hours after administration of IPM/CS, respectively. Half-lives were 4.10 hours and 3.08 hours, respectively. On the other hand, those of the 8-day or older group rapidly decreased to below the detection limit in 8 hours after administration with a half-life of 1.6 hours. (2) The 1-hour intravenous drip infusion at 20 mg/20 mg/kg of IPM/CS IPM: Peak plasma concentrations were obtained in all 3 groups at the end of drip infusion and were ranging from 31.1 to 38.24 micrograms/ml. Plasma concentrations rapidly decreased, and were 0.95-2.08 micrograms/ml at 8 hours after administration with half-lives of 1.5-1.88 hours. CS: Peak plasma concentrations were obtained in all 3 groups at the end of drip infusion and were ranging from 47.0 to 55.82 micrograms/ml.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1988

[Bacteriological, pharmacokinetic and clinical studies on a rokitamycin dry syrup in the pediatric field].

Bacteriological, pharmacokinetic and clinical studies were done on the effect of rokitamycin (RKM, TMS-19-Q) in the field of pediatrics. The results are summarized below. 1. Antibacterial activities Antibacterial activities of RKM against Staphylococcus aureus (including 50 methicillin-sensitive and 50 methicillin-resistant strains), 18 strains of Haemophilus influenzae and 50 strains of Campylobacter jejuni were studied comparatively with activities of josamycin (JM), midecamycin (MDM), erythromycin (EM) and cefaclor (CCL) or ampicillin. Minimum inhibitory concentrations (MICs) of the 5 antibiotics against methicillin-sensitive S. aureus showed a wide variation but RKM was somewhat superior among them. MIC80 of those antibiotics tested against methicillin-sensitive S. aureus were as follows; RKM 1.56, JM 12.5, MDM 12.5, EM 6.25, and CCL 3.13 micrograms/ml. Among methicillin-resistant S. aureus (MRSA), ratios of strains highly resistant to these antibiotics (MIC greater than or equal to 100 micrograms/ml) to total number of strains tested were: 18% to RKM, and 26%, 34% and 48% to JM, MDM and EM, respectively, again showing the superiority of RKM and the proliferation of resistant organisms to EM. MICs of RKM against H. influenzae were distributed in a range between 0.78 and 12.5 micrograms/ml, which were similar to MIC range of CCL, and approximately twice as high as that of EM, but 4 folds lower than those of JM and MDM. Against C. jejuni, the MIC range of RKM was quite broad, 0.10-12.5 micrograms/ml, with a peak value of 0.20 micrograms/ml. The cumulative number of strains vs. MIC curve was similar to that of EM, and RKM was approximately 4 to 8 folds more effective than the other 3 antibiotics. 2. Absorption and excretion The absorption and the excretion of RKM were studied with its dry syrup preparations. Dose levels examined were 5 mg/kg in 2 cases, 10 mg/kg in 7 cases, 15 mg/kg in 2 cases and 20 mg/kg in 1 case. Peak concentrations of RKM in blood were not dose-dependent and were 0.16-0.23, 0.29-0.91, 0.35-0.46 microgram/ml and 0.53 microgram/ml, respectively, for the 4 dose levels. Most of drug levels dropped below the detection limit in 4 hours after the administration when dose levels up to 10 mg/kg were used, and when dose levels were at or above 15 mg/kg, 0.07-0.09 microgram/ml of RKM was detected in blood at 6 hours after the administration. Urinary recovery rates in 6 hours were between 0.19 and 3.31%.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1987

Molecular gene mapping of human aldolase A (ALDOA) gene to chromosome 16.

Mapping of human aldolase A (ALDOA) gene was performed by molecular hybridization techniques using a panel of human-mouse cell hybrids and sorted fractions of human metaphase chromosomes besides in situ hybridization. For the purpose, three kinds of DNA probes derived from the coding region (probe-1), the 3' noncoding region (probe-2), and the coding and 3' noncoding regions (probe-3) of human aldolase A cDNA clone, pHAAL116-3, were selectively employed. The results of RNA and DNA blot analyses indicated that the human ALDOA gene is located on chromosome 16. The in situ hybridization experiment also indicated that the ALDOA gene was localized to 16q22-q24.

Animals↗
PubMed1987

Macrophage-mediated suppression of immune responses in Toxoplasma-infected mice. III. Suppression of antibody responses to parasite itself.

In acute Toxoplasma infection, anti-sheep erythrocytes (SRBC) antibody responses were strongly suppressed in the infected C57BL/6 mice, and the mice produced low titers of only 2-mercaptoethanol (2-ME)-sensitive antibodies but not 2-ME-resistant antibodies. By contrast, the infected BALB/c mice produced much higher titers of both 2-ME-sensitive and -resistant anti-SRBC antibodies than the infected C57BL/6 mice. In anti-Toxoplasma antibody responses, the 2-ME-resistant antibody titers were significantly lower in the infected C57BL/6 mice than in the BALB/c mice in the early phase of infection, suggesting that the suppressive effect of Toxoplasma infection affects antibody responses to Toxoplasma itself as well as to the unrelated antigen, SRBC. A histological study revealed that in the infected C57BL/6 mice, a large number of acid phosphatase-positive, macrophage-like cells infiltrated into the follicles of their spleens, and an involution of follicles occurred in the acute phase of infection. This histological change was not observed in the infected BALB/c mice. The infected C57BL/6 mice, which had the suppressed anti-Toxoplasma antibody responses, made five times as many as cysts in their brains as compared with the BALB/c mice at the fifth week of infection.

Animals↗
PubMed1987

Human aldolase B gene: characterization of the genomic aldolase B gene and analysis of sequences required for multiple polyadenylations.

The chromosomal gene encoding human aldolase B was isolated. The gene is composed of nine exons interrupted by eight introns and spans 15 kb, and a single copy of it occurs per haploid human genome. The initiation of transcription occurs at three different sites. Two minor sites, m1 and m2, start at 49 and 21 nucleotides, respectively, upstream from the major site, M. The gene also carries poly(A) addition signals at two different sites, thereby another two distinct mRNA species are produced. We examined the sequences required for mRNA 3'-end formation in this gene carrying multiple poly(A) addition sites. By constructing deletion mutants as to the region distal to the poly(A) addition site and then assaying through transfection into COS-1 cells, we demonstrated that 8 nucleotides distal to the site of poly(A) addition is sufficient for proximal polyadenylation, but is not sufficient for distal polyadenylation.

Animals↗