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Biomedical subjects

K Joh

Publications and source records attributed to K Joh.

At least 55 records · Page 3Linked to original sources
PubMed1995

Case report of a malignant Brenner tumor with hyperestrogenism.

A rare malignant Brenner tumor of the ovary presenting with hyperestrogenism in a 79 year old woman was examined immunohistochemically and by light and electron microscopy. High pre-operative serum and urinary estrogen concentrations, low serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels, and histologically confirmed atypical endometrial hyperplasia suggested the presence of hyperestrogenism. The reduction in serum and urinary estrogen and the increase in serum LH and FSH concentrations after tumor removal confirmed that the tumor was synthesizing estrogen. Histologically, the malignant element was predominantly a squamous cell carcinoma. Transitional cell carcinoma was partially found on the cyst wall. There was a spectrum of morphologic changes between benign and malignant elements with an intermediate area with a proliferating Brenner tumor. Immunohistochemically, only the carcinoembryonic antigen was positive exclusively on the malignant element as well as in the microcyst in the benign epithelial cord, whereas all of the markers for germ cell tumors were negative. The ultrastructural features of the stromal cells were of two types: fibroblasts and steroid-producing cells. The latter type of cells might correspond morphologically to estrogen-producing cells. The present case is the fourth report showing a malignant Brenner tumor combined with apparent hyperestrogenism.

Aged↗
PubMed1995

Antigenicities of enteropathogenic Escherichia coli, lysozyme, and alpha-1-antichymotrypsin on macrophages of genitourinary malacoplakia.

Seven cases of genito-urinary malacoplakia were analyzed histologically, ultrastructurally and immunohistochemically in a comparison with two cases of xanthogranulomatous pyelonephritis. Immunohistochemically, von Hansemann cells and Michaelis-Guttmann bodies, both hallmarks for the diagnosis of malacoplakia, showed a common antigenicity for enteropathogenic Escherichia coli as cytoplasmic granules of varying sizes. These microscopic manifestations corresponded ultrastructurally to a series of phagolysosomal degradations of coliform bacilli. Serogroups against E. coli OK antigens, which were positive for malacoplakic cells, were not confined to a particular group. Macrophages of xanthogranulomatous pyelonephritis did not show the E. coli antigenicity. Antigenicity of lysozyme and alpha-1-antichymotrypsin on the von Hansemann cells was equivocal, but these enzymes were strongly positive on macrophages of xanthogranulomatous pyelonephritis. The macrophages of both malacoplakia and xanthogranulomatous pyelonephritis were positive for antihuman macrophage antibody. These results indicate that malacoplakia depends mainly on infection by a non-specific strain of enteropathogenic E. coli and may arise from defective digestive enzyme activity of infiltrating macrophages. Immunohistochemical analysis using antisera against E. coli OK antigens, lysozyme and alpha-1-antichymotrypsin was useful in identifying the prediagnostic stage of malacoplakia and in differentiating the lesion from xanthogranulomatous pyelonephritis.

Adult↗
PubMed1995

Newly discovered familial juvenile gouty nephropathy in a Japanese family.

Our attention was initially called to 2 young Japanese sisters with gout and renal insufficiency, which led to an investigation of members of their family with similar conditions. One sister, a 26-year-old woman who had suffered from polyuria since infancy, suffered from gout and renal insufficiency. Her younger sister also had a history of polyuria, hyperuricemia, and moderately reduced renal function. Their urinary uric acid levels were reduced but purine enzyme activities in the erythrocytes were normal. A renal biopsy specimen from the younger sister showed severe interstitial fibrosis with tubular atrophy. An investigation of the family revealed an autosomal dominant transmission pattern. We believe these are new familial cases of juvenile gouty nephropathy found in a Japanese family.

Adult↗
PubMed1995

[A case report of Epstein syndrome].

Epstein's triad which is a syndrome with the combination of macrothrombocytopenia, deafness and nephritis, is similar to Alport's syndrome. We report on a case of Epstein syndrome and describe the results of morphological examination of a renal biopsy, specimen. The patient was a 14-year-old girl with the diagnosis of chronic idiopathic thrombocytopenic purpura that had preseated from the age of 3 years. She was referred to Daisan Hospital of the Jikei University School of Medicine on April 1, 1991 for refractory thrombocytopenia. She had shown sensorineural hearing loss since the age of 6 years and her peripheral blood smear revealed giant platelets on admission. She was treated with interferon, prednisolone, and high-dose gamma-globulin (400 mg/day x 5 days). However, the platelet count did not increase, but hypermenorrhea continued. She subsequently showed proteinuria and hematuria. She underwent splenectomy and renal biopsy on August 12, 1992. The glomeruli appeared to be almost normal under light microscopy. The interstitium showed regional fibrosis containing foam cells and the renal tubuli showed mild atrophy. Under electronmicroscopy, the basement membrane of the glomeruli was associated with mesangial interposition and the lamina densa was split into several layers. These ultrastructural findings were compatible with those of Alport's syndrome.

Adolescent↗
PubMed1994

MHC class I gene(s) in the D/L region but not the TNF-alpha gene determines development of toxoplasmic encephalitis in mice.

Previous studies revealed that mice with the b or k allele at the H-2D region are susceptible to toxoplasmic encephalitis (TE); those with the d allele are resistant. To determine whether the b or d allele is dominant, F1 hybrids between susceptible C57BL/6 (H-2b) and resistant BALB/c (H-2d) mice were infected with T. gondii. TE was not observed in the F1 hybrids, indicating that the d allele is dominant for protection against development of TE. Mice with a mutation in the D/L region were used to determine whether the D gene or the L gene of MHC class I Ags of the H-2D region is most critical for resistance against development of TE. B10.D2-H2dm1 (dm1) mice that have the mutant D/L hybrid gene formed by fusion of the 5' part of the Dd gene and the 3' part of the Ld gene developed TE in contrast to their background B10.D2 mice. BALB/c-H-2dm2 (dm2) mice, which have a complete deletion of the Ld gene, had significantly more T. gondii cysts in their brains than did dm1 mice and developed large areas of necrosis in their brains that were not observed in dm1 mice. These results indicate that a gene(s) in the D/L region determines whether TE will occur and that the Ld gene plays a critical role in the resistance against development of TE. Polymorphisms in the TNF-alpha gene (located in the H-2D region) have been reported to correlate with resistance against the development of TE. When development of TE was studied in BALB/c and dm2 mice that have the same TNF-alpha gene, only dm2 mice developed TE. This indicates that the TNF-alpha gene is not a determining factor for the development of TE. Transcripts for TNF-alpha were detected in brains of infected dm2 mice but not in BALB/c mice. Injection of neutralizing Abs against TNF-alpha resulted in worsening of the TE in infected dm2 mice but did not induce TE in infected BALB/c mice. Thus, TNF-alpha appears to be produced in the brain after TE has developed and is responsible for preventing the progression of TE.

Animals↗
PubMed1994

Selective planting of cationized, haptenized ovalbumin on the rat tubular basement membrane.

We developed an experimental protocol for planting exogenous antigens with different molecular weights and charges on the constituents of the renal tubulointerstitium. The cationized antigens were injected selectively into the left renal arteries of Wistar rats. Antigen localization was documented by immunohistochemistry on frozen sections. Cationized bovine serum albumin (BSA; 68 kDa, isoelectric point = 9.5) localized almost exclusively along the glomerular capillary wall. After application of highly cationic polyethyleneimine, cationized BSA given subsequently was found in a linear distribution along the glomerular capillary wall and along the peritubular capillaries. The fate of highly cationized ovalbumin conjugated with trinitrophenol (TNP-OA), subjected to gel filtration to obtain monomers (42 kDa, isoelectric point > 10) differed; it was deposited in a linear pattern on the tubular basement membrane (TBM) and Bowman's capsule, and remained up to 36 h after injection. Noncationized, monomeric TNP-OA (42 kDa, isolectnic point = 4.6) showed fine granular deposition in the tubular epithelium exclusively. These findings indicate that the barrier of the glomerular BM acts selectively on antigens with different molecular weights. They either settle on the peritubular capillaries, after passing the glomerular, or reach the urinary space, after which they are reabsorbed by the tubular epithelial cells to reach the TBM.

Animals↗
PubMed1994

Effect of the strain of Toxoplasma gondii on the development of toxoplasmic encephalitis in mice treated with antibody to interferon-gamma.

To examine whether differences observed in the development of toxoplasmic encephalitis between strains of Toxoplasma gondii are determined by the numbers of cysts occurring in the brain, C57BL/10 mice were infected with ten cysts of the ME49, Beverley, or C56 strain of the parasite. At 10 weeks after infection, the numbers of cysts and inflammatory changes in the brains of the mice were examined in each of the experimental groups. The ME49 strain formed significantly more cysts than did the other two strains, with no difference in the number of cysts being noted between the Beverley and C56 strains. Mice infected with the ME49 strain showed infiltration of inflammatory mononuclear cells in both the meninges and the parenchyma of their brains, whereas mice infected with the Beverley or C56 strain showed no inflammatory changes in their brains. Treatment of mice with a monoclonal antibody to interferon-gamma (IFN-gamma) once weekly for 3 weeks beginning at 10 weeks after infection augmented the inflammatory changes in the brains of mice infected with each strain. However, the intensity of the inflammatory changes differed significantly between the mice, depending on the strain of T. gondii with which they were infected. Mice infected with the ME49 strain showed the most remarkable inflammatory changes in their brains. Mice infected with the Beverley strain developed foci of acute inflammation in their brains after treatment with an antibody to IFN-gamma.(ABSTRACT TRUNCATED AT 250 WORDS)

Agglutination Tests↗
PubMed1994

Pyridoxal kinase immunoreactivity in rabbit brain.

Murine polyclonal antibody against purified bovine brain pyridoxal kinase (EC 2.7.1.35) was generated and showed cross-reactivity with rabbit brain pyridoxal kinase. This antibody was used to immunohistochemically examine the distribution of pyridoxal kinase in the rabbit brain. The cytoplasm of neuronal cells and neuroglial cells in the cerebral cortex, hippocampal region, brain nuclei and cerebellar cortex showed positive staining with various degrees of intensity. The neuronal cells and surrounding fibers in some brain nuclei, such as the area tegmentalis ventralis or the substantia nigra, showed intense staining. The neuronal cells of the hippocampal region showed somewhat weak reactivity, but some with intense reactivity were found sparsely distributed and positive staining fiber networks of a very low density were also observed.

Animals↗
PubMed1994

A severe outbreak of haemorrhagic colitis and haemolytic uraemic syndrome associated with Escherichia coli O157:H7 in Japan.

UNLABELLED: In 1990, an outbreak of Escherichia coli O157:H7 infection occurred in 174 children in a nursery school in Saitama, Japan. The organism was isolated from tap water supplied from the well in the school. Clinical manifestations varied from asymptomatic infection to non-bloody diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome (HUS) and death. Among culture-confirmed 42 cases of E. coli O157:H7, 7 children were asymptomatic, 21 children had only diarrhoea, and 14 children developed HUS. Bloody diarrhoea with abdominal pain following initial frequent diarrhoea appeared to be associated with subsequent HUS. In patients with HUS, both leucocyte count and lactate dehydrogenase activity continued to increase in the early phase of the disease, and on day 3 of illness attained markedly higher levels than in patients without HUS. These two parameters seemed to be important as predictors of the development of HUS. CONCLUSION: E. coli O157:H7 is a common pathogen causing colitis. It should be kept in mind in paediatric practice and public health.

Child↗
PubMed1994

Crystalline inclusions in the glomerular podocytes in a patient with benign monoclonal gammopathy and focal segmental glomerulosclerosis.

We report a case of a 40-year-old woman with benign monoclonal gammopathy who developed focal segmental glomerulosclerosis associated with widespread deposition of large crystalline inclusions in the glomerular podocytes. Electron microscopy showed that the crystalline structures were electron dense and needle shaped or polygonal. At a higher magnification, they were seen to be surrounded by unit membranes and to feature a longitudinal filamentous substructure. These inclusions showed positive immunohistochemical staining for kappa light chain. Clinically, the patient had shown nephrotic syndrome on the first medical examination, and later revealed chronic renal failure and monoclonal gammopathy of the immunoglobulin G kappa type, but no evidence of multiple myeloma or other lymphoproliferative diseases. This patient seems to have had a rare form of glomerular involvement associated with benign monoclonal gammopathy.

Adult↗
PubMed1993

Bovine serum albumin-doxorubicin conjugate overcomes multidrug resistance in a rat hepatoma.

A bovine serum albumin-conjugated doxorubicin via the glutaraldehyde bridge (BSA-DXR conjugate) showed potent dose-dependent inhibition of cell growth against daunorubicin-resistant AH66 (AH66DR) cells as well as parental AH66 (AH66P) cells in vitro as compared to treatment with DXR or BSA-glutaraldehyde conjugate without DXR (BSA-GA). In the culture of AH66DR with BSA-DXR conjugate, drug accumulation in the AH66DR cells increased as a function of time up to 24 h reaching approximately the same drug level as AH66P cells treated with DXR. The intracellular accumulation of the BSA-DXR conjugate was inhibited by the addition of ammonium chloride, while that of DXR alone was not inhibited. Intracellular DXR was effluxed rapidly from AH66DR cells, but BSA-DXR conjugate or pharmacologically active DXR adduct remained in the cells at a relatively high concentration over a 36-h time period. The life-prolonging effect of the conjugate was assessed using rats inoculated i.p. with AH66P or AH66DR. The rats were treated with the BSA-DXR conjugate, DXR, a mixture of DXR with BSA, or BSA-GA by either the i.p. or i.v. route. Treatment with DXR had no significant surviving effect as compared to that with saline in AH66P-bearing rats. By contrast, BSA-DXR conjugate showed a significant life-prolonging effect as compared with DXR alone in the same degree both in AH66P- and AH66DR-bearing rats. BSA-GA did not show any toxicity in vivo as well as in vitro. These results indicate that the BSA-DXR conjugate allows DXR to escape from the multidrug resistance mechanism.

Animals↗
PubMed1993

Morphologic variations of dense deposit disease: light and electron microscopic, immunohistochemical and clinical findings in 10 patients.

Twenty-one renal biopsy specimens obtained from 10 patients with dense deposit disease (DDD) were investigated using light microscopy, electron microscopy and immunohistochemistry. The patients included four females and six males aged 6 to 35 years (mean 16.1 years). A morphological diagnosis of DDD was made following the ultrastructural detection of continuous intramembranous dense deposits (CIMDD) in some capillary loops of at least one of the series of the repeated biopsies from each patient. With light microscopy, six patients showed membranoproliferative glomerulonephritis (MPGN). The other four patients showed diffuse proliferative glomerulonephritis (DPGN) with acute lesions showing intraglomerular neutrophilic infiltration, hump formation and endothelial swelling in three and minor glomerular abnormalities in one. Follow-up biopsies were obtained in six patients. Two patients progressed from DPGN to MPGN within 7 months, whereas three patients with MPGN showed morphologic improvement that featured increased capillary patency and regional disappearance of dense deposits along with the reduction of proteinuria. Dense deposit disease did not always feature typical amorphous and osmiophilic CIMDD spreading across the whole width of the lamina densa. This classical ultrastructural manifestation was mainly found in the patients with histologic non-MPGN and a linear peripheral pattern of complement component (C3) deposition. The MPGN patients with a granular peripheral pattern of C3 deposition also had CIMDD, but also additionally featured less dense subepithelial deposits superimposed on the CIMDD to produce an appearance simulating membranous transformation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Neurological manifestations of hemorrhagic colitis in the outbreak of Escherichia coli O157:H7 infection in Japan.

An outbreak of hemorrhagic colitis associated with Escherichia coli O157:H7 occurred in a kindergarten in Saitama, Japan from September to November, 1990. Seven patients admitted to our hospital showed neurological manifestations: generalized seizures, impaired consciousness, urinary incontinence, gaze nystagmus, phrenic nerve palsy, action tremor and vertigo. Two patients died. On the basis of the clinical courses and laboratory findings of the seven patients and postmortem findings of one case, these neurological symptoms were suspected to be induced by the verotoxin elaborated by Escherichia coli O157:H7.

Bacterial Toxins↗
PubMed1993

Augmented production of interleukin-8 in cerebrospinal fluid in bacterial meningitis.

Interleukin-8 (IL-8) elaborated by monocytes and endothelial cells is a cytokine which is responsible for adhesion of leucocytes to vascular endothelium and migration of neutrophils into the cerebrospinal fluid (CSF) from the intravascular space. The inflammation in meningitis is elicited by the cytokine release from leucocytes which encounter micro-organisms in the arachnoid or subarachnoid space. In bacterial meningitis, tumour necrosis factor (TNF), IL-1 and IL-6 are produced vigorously, and initiate and augment the inflammation in the central nervous system. In this study, utilizing a quantitative immunometric sandwich enzyme immunoassay, the concentration of IL-8 was investigated in the CSF of patients with bacterial meningitis, patients with aseptic meningitis, and patients with gastroenteritis who served as controls. The IL-8 concentration was markedly higher in the CSF of patients with bacterial meningitis (224 +/- 2.57 pg/ml; mean +/- SD) than in the CSF of patients with aseptic meningitis (less than 30 pg/ml). The IL-8 level in the CSF of patients with aseptic meningitis did not differ from that in the CSF of the patients with gastroenteritis (less than 30 pg/ml). The augmented production of IL-8 in CSF may account for the inflammation in bacterial meningitis being more severe than that in aseptic meningitis.

Acute Disease↗
PubMed1992

Hyper-response of serum IgG1 to Staphylococcus aureus peptidoglycan in patients with hyper-IgE syndrome.

The hyper-IgE (HIE) syndrome is characterized by high IgE serum levels, chronic dermatitis and recurrent infections. To determine whether an impairment of the antibody response to Staphylococcus aureus contributes to infections in this syndrome we measured total serum IgG subclass, specific IgG1 and IgG2 levels against peptidoglycan (PG), the immunodominant cell wall component of S. aureus and serum opsonic activity to PG. Of the 14 patients with HIE syndrome, nine had increased level of serum IgG1 and six had IgG2 subclass deficiency. In regard to specific response of IgG1 and IgG2 antibodies to PG, patients were divided into five groups related to ages and compared with 10 control subjects for each age cohort. Patients with HIE syndrome had significant high levels of serum-specific IgG1 to PG and significant decreased levels of serum-specific IgG2 to PG in all five groups. Additionally, serum opsonic activity in patients was significantly higher than that in normal control subjects. It is concluded that IgG2 deficiency or poor IgG2 antibody response to S. aureus is not the explanation of the abnormal susceptibility to S. aureus infections of HIE patients.

Adolescent↗
PubMed1992

Interstitial nephritis associated with glomerulonephritis in a patient with Hashimoto's disease and idiopathic portal hypertension.

A middle-aged women with hypothyroidism, idiopathic portal hypertension and nephrotic syndrome is presented. This unusual clinical appearance could not be explained as SLE by serological examinations. Pathohistological examinations showed "Banti's liver", Hashimoto's thyroiditis and diffuse proliferative glomerulonephritis with severe tubulo-interstitial nephritis. Immunohistochemical studies revealed IgA deposits in glomeruli. Electron microscopic study disclosed peculiar lucent areas of rarefaction with osmiophilic particles in tubular basement membranes. This tubulointerstitial nephritis was considered to be related to the immunological mechanism involving thyroid gland, liver and kidney disorders. This case thus had a clinically rare combination of these three.

Female↗