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Biomedical subjects

K Joh

Publications and source records attributed to K Joh.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Estimation of probiotics by infection model of infant rabbit with enterohemorrhagic Escherichia coli O157:H7].

We examined the preventative effect against enterohemorrhagic Escherichia coli O157:H7 (EHEC) infection in rabbits on administration of probiotics contained in Streptococcus faecalis, Clostridium butyricum and Bacillus mesentericus. The probiotics were administered to 5 days old Japanese white rabbits throughout the experiment. Inoculation of 10(6) colony forming units (CFUs) of EHEC per rabbit was tried 8 days after birth. Three days after EHEC inoculation, in the control group (not administered probiotics), diarrhea was observed in approximately 80% of the rabbits, on the other hand, in the group administered probiotics, rabbits showed diarrhea in 15%. In necropsy, the number of EHEC in the contents of the cecum and the number of attaching and effacing (AE) lesions were fewer in the probiotics group than in the control group. These results suggest that infant rabbits are useful as a colitis model for EHEC, and the probiotics are effective for the prevention of the growth of EHEC in the intestine and for diarrhea.

Animals↗
PubMed1998

Nephrotic syndrome associated with diffuse mesangial hypercellularity: is it a heterogeneous disease entity?

Diffuse mesangial hypercellularity (DMH) is a rare primary mesangial proliferative glomerulonephritis associated with idiopathic nephrotic syndrome (INS). We conducted this study on 15 patients, including 5 patients with repeated specimens, with a follow-up of 0.9-17.5 years and evaluated the clinical course and pathological findings. Seven patients were male. Ten patients were under 14 years of age. All specimens had INS and were diagnosed morphologically with primary diffuse mesangial proliferative glomerulonephritis at initial biopsy; 4 were diagnosed with focal segmental glomerulosclerosis (FSGS) within 3 years by the second biopsy. The remaining 11 patients included 8 initial responders and 3 initial nonresponders to 8 weeks' steroid therapy and had the histologic variant of the minimal-change nephrotic syndrome (MCNS). Ten of the 11 patients had normal renal function during the investigation period. One patient with the MCNS variant who was refractory to steroid therapy developed end-stage renal disease (ESRD) within 6 years. Four patient with the histologic variant of FSGS included 1 initial responder, 2 late responders, and 1 steroid-refractory case. One patient with the FSGS variant developed ESRD within 4 years. The follow-up biopsies documented that the severity of mesangial hypercellularity was associated with the severity of proteinuria or hematuria. We conclude that DMH may be divided into heterogeneous disease entities, whereas morphologic changes in initial biopsies were similar. Each variant as well as the degree of DMH should be recognized routinely by follow-up biopsy, because they are prognostic indicators.

Adolescent↗
PubMed1998

Isolation and characterization of tubular basement membrane antigen common to humans and rats.

Using Brown Norway (BN) rats, we isolated and characterized the tubular basement membrane (TBM) antigens that are immunologically common to humans. The renal basement membrane (RBM) of BN rat, as an antigen source, was solubilized with 8 M urea instead of collagenase followed by extraction with 0.5 M NaCl. On frozen section-immunohistochemistry, the autoantibody obtained from BN rats, which had been immunized with human RBM and showed tubulointerstitial nephritis, bound to the TBM, the basement membrane of the Bowman's capsule, and the brush border of the proximal tubules, but not to the GBM of the normal BN rat kidney. Nephritogenic antigens were isolated by immunoaffinity chromatography using Sepharose-bound purified autoantibody. By Western blot analysis of the eluate, bands with molecular weight of 200 kDa and 180 kDa were positively reacted to anti-FX1A (brush border antigen) antibody and were apparently different from the major bands with molecular weight of 145 kDa and 130 kDa. The bands with molecular weight of 145 and 130 kDa showed major cross reactivity with antibodies to fibronectin and laminin. In contrast with these high molecular weight (HMW) bands, the major 60 kDa band with three minor bands showed no reactivity with any type of antibody tested. These results indicated that the non-enzymatic solubilization of RBM is one of the possible procedures for isolating the HMW form of antigens. These antigens may be epitopically modified pre-existing constitutions of the basement membrane and may play a role in the induction of tubulointerstitial nephritis.

Animals↗
PubMed1998

[Twelve cases of systemic lupus erythematosus in boys].

We compared clinical findings in 12 cases of systemic lupus erythematosus (SLE) in boys with those in 49 cases in girls. The age at which SLE developed in boys was consistent with that of infantile SLE and there was no age specificity. Momy cases in boys were diagnosed earlier as compared with cases in girls. Symptoms of infantile SLE, such as fever, arthalgia, butterfly rash, and urinary abnormalities, did not differ between boys and girls. However, a higher percentage of boys (58.3%) had central nervous system complications at onset than did girls (30.6%). Platelet counts tended to be higher in boys than in girls, a finding that suggests SLE tends to be more severe in boys than in girls. The incidence in the appiarance of LE cells, anti-Sm antibodies and immune complexes was higher in boys than in girls. Type IV or V renal pathologic changes (World Health Organization Histologic Classification) were present in 70% of boys. Our findings suggest that SLE in boys is more severe than that in girls and is more likely to be associated with central nervous system complications and severe renal complications.

Adolescent↗
PubMed1997

Caenorhabditis elegans has two isozymic forms, CE-1 and CE-2, of fructose-1,6-bisphosphate aldolase which are encoded by different genes.

Two distinct types of cDNAs for fructose-1,6-bisphosphate (FBP) aldolase, Ce-1 and Ce-2, have been isolated from nematode Caenorhabditis elegans, and the respective recombinant aldolase isozymes, CE-1 and CE-2, have been purified and characterized. The Ce-1 and Ce-2 are 1282 and 1248 bp in total length, respectively, and both have an open reading frame of 1098 bp, which encodes 366 amino acid residues. The entire amino acid sequences deduced from Ce-1 and Ce-2 show a high degree of identity to one another and to those of vertebrate and invertebrate aldolases. The highest sequence diversity was found in the carboxyl-terminal region that corresponds to one of the isozyme group-specific sequences of vertebrate aldolase isozymes that play a role in determining isozyme-specific functions. Southern blot analysis suggests that CE-1 and CE-2 are encoded by different genes. Concerning general or kinetic properties, CE-2 is quite different from CE-1. CE-1 exhibits unique characteristics which are not identical to any aldolase isozymes previously reported, whereas CE-2 is similar to vertebrate aldolase C. These results suggest that CE-2 might preserve the properties of a progenitor aldolase with a moderate preference for FBP over fructose 1-phosphate (F1P) as a substrate, whereas CE-1 evolved to act as an intrinsic enzyme that exhibits a much broader substrate specificity than dose CE-2.

Amino Acid Sequence↗
PubMed1997

Purification and characterization of human nephritogenic antigen that induces anti-GBM nephritis in rats.

Human nephritogenic antigen induces anti-glomerular basement membrane antibody glomerulonephritis in rats. This antigen was purified from collagenase-solubilized renal basement membrane by means of gel filtration and affinity chromatography using a rabbit antibody. Western blots of the purified nephritogenic antigen using epitope-defined monoclonal antibodies showed that it contains the NC1 domains of the a1 to a6 chains of type IV collagen. Nephritogenicity was thought to be a feature of the NC1 domains of the a3 to a5 chains, because the a6 chain is not located in the glomerular basement membrane, and because an NC1 fraction consisting of the NC1 domains of the a1 and a2 chains was poorly nephritogenic. Autoantibodies in the sera of patients with Goodpasture's syndrome were detected by ELISA using the purified nephritogenic antigen. These results indicate that the nephritogenic antigen contains the Goodpasture antigen, defined as the antigen reactive with sera from patients with Goodpasture's syndrome.

Animals↗
PubMed1997

Diffuse mesangial sclerosis associated with Kawasaki disease: an analysis of alpha chains (alpha 1-alpha 6) of human type IV collagen in the renal basement membrane.

A case of diffuse mesangial sclerosis (DMS) associated with Kawasaki disease is reported. A previously healthy Japanese girl, aged 4 months, presented with clinical features of Kawasaki disease. At week 10 of the illness, she developed the nephrotic syndrome, which was refractory to steroid therapy. Renal biopsy demonstrated a diffuse mesangial proliferative glomerulonephritis with microcystic tubular dilatation and, ultrastructurally, marked thinning of the lamina densa in the glomerular basement membrane (GBM) and the tubular basement membrane (TBM) of the proximal tubule. She went into chronic renal failure and died at the age of 11 months. At autopsy, the kidney revealed DMS. Histologically, we found Finnish microcystic disease in its early stages in the biopsy. Using a newly developed monoclonal antibody, we analysed the alpha chains (alpha 1-alpha 6) of type IV collagen in the GBM and TBM. There was no defective constitution of alpha chains on the thin GBM, but the thin TBM of the microcystic proximal tubule showed a weak or discontinuous reactivity for alpha 1 and alpha 2 chains, suggesting faulty formation of the basement membrane. The sclerosing glomeruli of the DMS did not depend on collapse of the GBM, which was positive for alpha 3-alpha 5 chains, but mainly on the proliferation of mesangial matrix, which was positive for alpha 1 and alpha 2 chains.

Basement Membrane↗
PubMed1997

Normal distribution of collagen IV in renal basement membranes in Epstein's syndrome.

BACKGROUND: Epstein's syndrome is defined as a subtype of Alport's syndrome, and is distinguished from the other subtypes by accompanying macrothrombocytopenia. Mutations in collagen IV genes are known to be involved in the pathogenesis of typical Alport's syndrome. However, the presence of an underlying genetic defect has not been demonstrated in Epstein's syndrome. AIM: To clarify the involvement of collagen IV in Epstein's syndrome. METHODS: The distribution of the alpha(IV) chain was studied in renal specimens obtained from three patients with Epstein's syndrome using chain specific monoclonal antibodies and an antigen retrieval procedure. RESULTS: The patients showed a normal distribution of alpha(IV) chains: alpha 1(IV) and alpha 2(IV) were expressed ubiquitously, whereas expression of alpha 3(IV) through to alpha 6(IV) chains was limited to the glomerular basement membrane, Bowman's capsular basement membrane, and/or a portion of the tubular basement membrane. CONCLUSIONS: These results suggest that genes other than those encoding alpha(IV) chains are responsible for the pathogenesis of Epstein's syndrome.

Basement Membrane↗
PubMed1997

A case of renal amyloidosis associated with hepatic adenoma: the pathogenetic role of tumor necrosis factor-alpha.

We report a case of a 35-year-old man with secondary amyloidosis chiefly involving the kidney and heart. The patient showed severe proteinuria and ischemic heart damage and had hepatic adenoma at the age of 33. Biopsy specimens from the kidney, heart, stomach and rectum showed extensive deposition of amyloid. After the surgical resection of a 300-gram hepatic adenoma, highly elevated c-reactive protein (CRP) levels decreased and the serum amyloid A (SAA) level was completely normalized. Normal liver cells were immunostained with rabbit anti-SAA antibody, but the cells in adenoma tissue and kidney were not. Electron microscopic examination revealed extracellular deposition of amyloid fibrils in the hepatic adenoma and kidney tissue. The concentration of tumor necrosis factor-alpha (TNF-alpha) (312 pg/mg tissue protein) was 7-fold higher in adenoma tissue than in normal liver tissue. Moreover, SAA (2.8 ng/mg tissue protein) was 2-fold higher in normal liver tissue than in adenoma tissue. Since TNF-alpha has been known to induce SAA production in target cells, the present results suggest that the hepatic adenoma produced TNF-alpha, which then caused mainly secondary amyloidosis in the kidney and heart. Currently, 2 years after surgical resection, urinary excretion of protein has been markedly reduced (from 3.5 to 0.8 g/day) and renal and cardiac functions are normal without specific medical treatment.

Adenoma↗
PubMed1997

[Predictive indicators for progression to severe complications(hemolytic-uremic syndrome and encephalopathy) and their prevention in enterohemorrhagic Escherichia coli infection].

The treatment of infection with enterohemorrhagic Escherichia coli(EHEC) aims for early prediction and prevention of severe complications such as hemolytic-uremic syndrome, encephalopathy and/or thrombotic thrombocytopenic purpura. Factors related to the complications are divided into three categories; risk factors or predisposition, predictors, and indicators of severity and outcome. Risk factors for complications include two extreme ages, infection with verotoxin 2 producing E. coli, positive stool culture for EHEC, use of antimotility drug, use of trimethoprim-sulfamethoxazole. Predictors for complications include severe abdominal pain and bloody diarrhea development of high fever, change of consciousness, urinal protein and/or occult blood, abrupt increase of white blood cell count, urinal NAG, alpha 1 microglobulin, beta 2 microglobulin, low osmolar urine, high thrombomodulin level, marked thickening of intestinal wall, increased brightness of kidney in ultrasound sonography. No preventive treatment for these complications is proven except SYNSORB-pk which is expected to effectively aborb verotoxin in the intestine.

Bacterial Toxins↗
PubMed1997

Massive uncomplicated vascular immune complex deposits in the kidney of a patient with systemic lupus erythematosus.

The case of a patient with systemic lupus erythematosus (SLE) is reported which was accompanied by renal dysfunction and massive vascular immune deposits in the kidney without active glomerular lesions. The renal biopsy showed arterioles and small arteries with circumferential periodic acid-Schiff (PAS) and Masson trichrome-positive homogenous material in the subendothelial area in the absence of thrombotic, necrotizing or inflammatory lesions. Immunofluorescence and electron microscopy examination demonstrated immune deposits in the vascular walls. Glomeruli showed only minor abnormalities with a trend to collapse. There was no improvement in renal dysfunction over a 4-year period until the patient's death, despite steroid therapy producing a decrease in disease activity. The autopsy showed similar vascular changes to those seen in the biopsy, however; glomeruli were either sclerotic or showed a trend to collapse. Massive uncomplicated vascular immune complex deposition without active glomerular lesions is rare. The present case indicates that this type of lupus vasculopathy may be a prognostic factor for the loss of renal function in SLE mediated by hemodynamic glomerular injury.

Aged↗
PubMed1996

Development of nephrotic syndrome in a patient with acute myeloblastic leukemia after treatment with macrophage-colony-stimulating factor.

We describe a patient with acute myeloblastic leukemia (AML) who developed nephrotic syndrome after receiving several courses of chemotherapy, including macrophage-colony-stimulating factor (M-CSF). At the onset of nephrotic syndrome, the patient remained in a hematological remission. A renal biopsy showed diffuse mesangial proliferation with marked glomerular infiltration of macrophages and massive subendothelial and mesangial deposits. After the institution of the combined therapy with corticosteroid, anticoagulant, and dipyridamole, urinary protein excretion was attenuated to less than 1.0 g/day. It should be emphasized that the recurrence of nephrotic syndrome was observed after the following chemotherapy, including M-CSF, whereas the bone marrow still remained completely remitted. In contrast, after the last course of chemotherapy, which did not include M-CSF, urinary protein excretion was not enhanced. Of note is that the renal histology at autopsy showed a remarkable improvement of mesangial hypercellularity with concomitant reduction in the number of glomerular macrophages. These evolutional changes in both proteinuria and glomerular histology suggest a close linkage between the M-CSF treatment and macrophage-related glomerular injury. The possibility can be raised that M-CSF accelerated the underlying renal disease in this case through enhancing macrophage accumulation into the glomerulus, leading to the development of nephrotic syndrome.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

Nucleotide sequence of ribosomal protein L3 cDNA and the exon-intron structure of L3 gene in the nematode, Caenorhabditis elegans.

A cDNA and a gene encoding the nematode (C. elegans) ribosomal protein L3 have been cloned and sequenced. The nearly full-length cDNA is 1255 bp in size except for the poly (A) tail. The encoded protein consists of 401 amino acids and has calculated molecular weight of 45,657 daltons. The gene sequence determined is 1649 bp and consists of four exons. The sequence of the nematode protein shows high homology to other eukaryotic proteins.

Amino Acid Sequence↗
PubMed1996

[A quantitative analysis of the cells infected with Epstein-Barr virus in the peripheral blood mononuclear cells derived from the patients with infectious mononucleosis].

The quantitative analysis of the cells infected with Epstein-Barr virus was performed on the peripheral blood mononuclear cells from the patients with infectious mononucleosis, by using in situ hybridization with Epstein-Barr virus encoded small nuclear RNA1 (EBER1). An alkaline-phosphatase conjugated oligonucleotide probe complementary to EBER1 was used as an antisense probe, while oligonucleotide DNA probe compatible with the sequence of EBER1 was used as a sense probe, control probe. The EBER1 positive cells on the slide-glass were enumerated microscopically. In situ hybridization revealed that 50,000 peripheral blood mononuclear cells from the patients in the acute phase of infectious mononucleosis contained 35 +/- 36 cells infected with Epstein-Barr virus (n = 11). The cells infected with Epstein-Barr virus apparently decreased in the convalescence of all the patients with infectious mononucleosis and the mean of the cells infected with Epstein-Barr virus was 3 +/- 4 in the convalescence (n = 6) (p < 0.02). On the other hand, no positive cells were detected in healthy individuals with past-infection of Epstein-Barr virus (n = 10) or without any previous Epstein-Barr virus infection (n = 11). The striking increase of the cells with Epstein-Barr virus genome was clearly demonstrated in the peripheral blood mononuclear cells from the patients with infectious mononucleosis.

Child↗
PubMed1996

Mitochondrial encephalomyopathies preceded by de-Toni-Debré-Fanconi syndrome or focal segmental glomerulosclerosis.

We report two rare cases of mitochondrial encephalomyopathies which were preceded by renal diseases. One occurred in an 11-year-old girl diagnosed with Kearns-Sayre syndrome, which was preceded by de-Toni-Debré-Fanconi syndrome 8 years previously. The other occurred in a 14-year-old girl diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, who developed focal segmental glomerulosclerosis 3 years prior to confirmation of the diagnosis. Tissue from both patient demonstrated morphological abnormalities of the mitochondria in the distal renal tubular epithelium and leiomyocytes of the small renal artery. The present cases illustrate various clinical and morphologic evidence of renal diseases which may further our understanding of mitochondrial encephalomyopathies.

Adolescent↗
PubMed1995

Monoclonal antibody, Mab 12C3, is a sensitive immunohistochemical marker of early malignant change in epithelial ovarian tumors.

A murine monoclonal antibody (MAb 12C3) that is specific to human ovarian carcinomas was generated by immunizing mice with a human ovarian germinoma cell line (JOHYC-2). The antigen distribution that was defined by MAb 12C3 in normal and malignant human tissues was analyzed by immunohistochemistry on paraffin-embedded and frozen sections. The antibody reacted with 67.7% (21 of 31 cases) of epithelial ovarian carcinomas (6 of 12 cases of serous cystadenocarcinoma, 5 of 7 cases of mucinous cystadenocarcinoma, 7 of 9 cases of clear cell carcinoma, 3 of 3 cases of endometrioid adenocarcinoma), but did not react with any of the benign epithelial ovarian adenomas tested. Partial regions of borderline ovarian malignancies that exhibited marked papillary projection of the lining cells with cellular atypia reacted positively with MAb 12C3 in 14 of 25 cases (56.0%). The histologic features of regional early malignant change corresponded to the expression of the MAb 12C3 epitope in the borderline malignant tumor cells. There was a low frequency of reaction (4.3%) between the antibody and other gynecologic and nongynecologic malignancies (46 cases of 12 tissues). In normal tissues, the antibody reacted positively with only three tissues, including corpora lutein cells, excretory ducts in the submandibular gland, and basal cells of the sebaceous glands. The antigen epitope defined by MAb 12C3 was present on a glycoprotein with a molecular mass of 200 kDa and did not exhibit any cross-reactivity with other well-known tumor markers. These data suggest that MAb 12C3 may be a useful tool for the immunohistologic detection of early malignant changes in epithelial ovarian tumors. In addition, MAb 12C3 also may facilitate a differential diagnosis between benign and borderline malignancies.

Adenocarcinoma, Clear Cell↗
PubMed1995

Copy-dependent and position-independent expression of rat aldolase A gene.

In order to understand the molecular mechanisms of the temporal and spatial differences of gene expression in higher organisms, rat aldolase A gene carrying two distinct promoters was introduced into fertilized eggs and the resulting transgenic mice were analyzed. The transgene expression is tissue-specific and is developmentally regulated. In addition, the expression is regulated in a copy-dependent manner irrespective of where the transgene is integrated, suggesting that a mechanism excluding the effect of the integration site exists within the transgene itself. To explore the conformational change of this gene in the genome, the DNase I hypersensitive sites of the gene were examined. Three sites (DHS-1,2, and 3) were identified upstream and downstream of the gene and these sites were retained in the transgene as well as in the gene observed endogenously.

Animals↗