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Biomedical subjects

K Joh

Publications and source records attributed to K Joh.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Clinical study of systemic juvenile rheumatoid arthritis (Still)].

Thirty-seven patients with systemic JRA were analyzed. Fifty four per cent of patients had mono-cyclic systemic type. Age at onset ranged from 6.0-6.8 years (median 6.4). Boys were more affected than girls (24/11). Cardiac involvement occurred in 10 patients (27%). Patients with cardiac troubles showed significantly much number of the white blood cell counts at admission and the max white blood cell count than those without cardiac troubles. Duration of positive CRP was shorter in patients with cardiac involvement who were all given cortico-steroid hormone those without cardiac involvement. This means that it is better to use steroid hormone early for patients with cardiac involvement. Patients with chronic arthritis type had higher elevated erythrocyte sedimentation rate and serum C3 level at admission and longer duration of positive CRP. We speculated that these date showed inflammation of joints. The onset subtype, which was determined by manifestations during the first 6 months of disease, was important for predicting clinical course and outcome.

Arthritis, Juvenile↗
PubMed1991

Analysis of upstream regulatory regions required for the activities of two promoters of the rat aldolase A gene.

Rat aldolase A gene has 2 promoters with different tissue specificities (M- and AH promoters). The M promoter is active only in adult skeletal muscle and induced during myogenesis, whereas the AH promoter is active ubiquitously in many tissues, including various cancer cells. Regulatory sequences for these promoters were investigated through assays for transient expression after introduction into myogenic and nonmyogenic cells. When M promoter-CAT fusion genes were transfected into primary cultures of chicken myoblasts, expression of CAT activity was drastically induced during myotube formation. The region comprising 202 to 85 base pairs (bp) upstream from the transcription initiation site was found to be necessary for the induction and an enhancer activity whose region includes the AT-rich recognition sequence (MEF-2 binding site). On the other hand, 2 upstream regions were found to be responsible for AH promoter activity expressed in HepG2 cells. The distal region (-280 to -260) of the promoter includes the AP1 binding sequence, whereas the proximal region (-207 to -180) contains a novel inverted repeat consisting of 22 bp but does not contain known promoter and enhancer sequences.

Animals↗
PubMed1991

Tumor necrosis factor-independent protective effect of recombinant IFN-gamma against acute toxoplasmosis in T cell-deficient mice.

rIFN-gamma conferred remarkable resistance against acute infection with Toxoplasma gondii in T cell-deficient (athymic nude) mice. Mice that received an i.p. injection of rIFN-gamma every other day beginning 24 h before infection for a total of eight doses survived significantly longer than untreated control mice although all of the treated mice died after the lymphokine was discontinued. Mice that received 14 doses of rIFN-gamma survived significantly longer than those that received eight doses of the lymphokine although mice started dying soon after the final (14th) injection of rIFN-gamma and eventually all of the treated mice died. Histologic study revealed that the IFN-gamma treatment prevented proliferation of the organisms in all organs examined, including brain, lung, heart, liver, and spleen. The treatment was effective even when started 1 day after infection. Peritoneal macrophages obtained from mice injected with rIFN-gamma were activated and effectively killed tachyzoites of T. gondii in vitro. TNF activity could not be detected in sera of the infected mice during treatment with rIFN-gamma. Administration of anti-TNF antibody did not affect the protective effect of rIFN-gamma against T. gondii infection. These facts indicate that rIFN-gamma can confer resistance to acute infection with T. gondii without collaboration of lymphokines derived from T cells and TNF. This suggests that rIFN-gamma may be effective for therapy of toxoplasmosis in immunosuppressed patients who have impaired activity of T cell function, especially those with AIDS.

Acute Disease↗
PubMed1991

An additional promoter functions in the human aldolase A gene, but not in rat.

The aldolase A gene was isolated from a human DNA library, mapped and sequenced. This gene comprises 12 exons and spans 6.5 kb. From the genomic DNA sequence and from the previous sequence analysis of the cDNA, it was revealed that the first exon L1 and the second exon encode the 5' non-coding sequence of mRNA L1, while the third and forth exons (corresponding to exons M and L2) encode different mRNA, mRNA M and L2, respectively; the following eight exons (exons 5-12) are shared commonly by all the mRNA species. These results indicate that the mRNA species are generated from a single aldolase A gene from one of exons L1, M or L2, in addition to exons 5-12, and also that the usage of a leader exon is similar but clearly distinct from that of rat aldolase A gene which we analyzed [Joh, K., Arai, Y., Mukai, T. & Hori, K. (1986) J. Mol. Biol. 190, 401-410]. By comparing the promoter regions in the human and rat aldolase A genes, we found similar sequences in the rat genome corresponding to those of the human L1, M and L2 promoter. We could not, however, detect any transcripts starting from sequences corresponding to the human L1 promoter in the rat genome, although the products corresponding to human M and L2 were detected. Thus, we conclude that the L1 promoter was either acquired by the human genome or deleted from the rat genome after human and rat diverged during evolution.

Amino Acid Sequence↗
PubMed1991

The structure of the brain-specific rat aldolase C gene and its regional expression.

The rat aldolase C gene was isolated from a rat genomic DNA library. This gene comprises 9 exons and spans 3590 base pairs. A single copy of the gene occurs per haploid rat genome. The initiation of transcription occurs at two different sites. The cellular localization of aldolase C mRNA was determined in the central nervous system along with aldolase A mRNA by in situ hybridization. The result indicates the predominant expression of this gene in Purkinje cells of the cerebellar cortex, where aldolase A mRNA was rather repressed.

Amino Acid Sequence↗
PubMed1991

Suppression of murine leukemia virus-mediated 3Y1 cell fusion by expression of mouse MHC class I.

Rat 3Y1 fibroblasts transformed by adenovirus type 12 or its E1A gene formed syncytia by cocultivation with Friend murine leukemia virus (MuLV)-producing cells. On the other hand, parental 3Y1 cells and those derivatives induced by other tumor viruses or chemical carcinogen showed no MuLV-mediated syncytium formation [N. Momozaki et al. (1990) Arch. Virol. 115: 123-126]. The expression of major histocompatibility complex (MHC) class I mRNA and antigens was significantly reduced in these Ad12- and E1A-transformed 3Y1 cells. In contrast, other tumor virus-and chemical carcinogen-transformed 3Y1 cells expressed MHC class I almost in normal levels as did parental 3Y1 cells. Furthermore, Ad12-transformed 3Y1 cells which started to express the transfected exogenous MHC class I gene, H-2Ld, showed no more MuLV-mediated 3Y1 cell fusion. These results indicate that the expression of MHC class I on the cell membrane is closely related to the inhibition of 3Y1 cell fusion by MuLV.

Actins↗
PubMed1991

N-myc gene amplification and neuron specific enolase production in immature teratomas.

The primary tumour tissues from 13 teratomas were investigated, 3 cases of immature teratoma (1 of pure type and 2 of mixed type), 5 cases of dermoid cyst, and 5 cases of mature solid teratoma, with special reference to N-myc gene amplification, productivity of neuron specific enolase (NSE), and the presence of double minutes (DMs). The possible relationship between these variables and malignancy of the tumours was also examined. N-myc gene amplification and NSE production were recognized in the primary tumour tissues and the first and the third passage cultured cells of all of the 3 cases of immature teratoma containing immature neural tissues. In 2 cases DMs were recognized. In dermoid cysts and mature teratoma, neither N-myc gene amplification nor NSE production were recognized in either the primary tumour tissues or cultured cells. The chromosomes were normal. Malignancy of teratoma is generally decided by the clinical stage and histological grade, but a more securely based decision is necessary where an immature teratoma contains immature neural tissues. The presence of N-myc gene amplification, NSE productivity and the presence of DMs may be valuable.

Adult↗
PubMed1991

Focal segmental glomerulosclerosis associated with infantile spasms in five mentally retarded children: a morphological analysis on mesangiolysis.

We report five cases of nephrotic syndrome due to focal segmental glomerulosclerosis (FSGS) in mentally retarded children with severe infantile spasms. Four of the five children diagnosed as West syndrome, Lennox syndrome, or petit mal epilepsy also had cerebral palsy and microcephaly. The other patient had petit mal epilepsy without cerebral palsy and microcephaly. All patients first developed infantile spasms, with the time of onset ranging from 1 week to 2 years of age, and subsequently developed proteinuria, followed by the nephrotic syndrome at 3 to 14 years of age. Four of the five developed terminal renal failure between 7 and 11 years of age. Three subsequently died, but the other underwent kidney transplantation and is still living without further complications. The light, electron microscopic, and immunohistochemical studies performed on the renal biopsies from all the patients and on the autopsy specimens from two cases exhibited FSGS-like lesions. Besides segmental hyalinosis, differing degrees of mesangiolysis were seen, which sometimes developed into dissecting microaneurysms of the glomerular capillary loops. The clinical picture described can be differentiated from congenital nephrotic syndrome (CNS) or infantile nephrotic syndrome (INS) with respect to the age of onset, outcome, and morphological appearance. We reviewed the previous literature and extended earlier observations about an unusual association between the nephrotic syndrome due to FSGS-like lesion, mental retardation, infantile spasms, and/or microcephaly in children.

Adolescent↗
PubMed1991

Congenital factor VII abnormality discovered in an infant at a routine checkup.

Congenital coagulation factor VII abnormality in an infant was first discovered because of a decreased normotest value at a routine health checkup at the age of 1 month. No bleeding tendency had been noticed. The normotest value did not respond to an administration of vitamin K. The prothrombin time (PT) was prolonged, and the activated partial thromboplastin time (A-PTT) was in the normal range. Factor VII activity was extremely low, whereas the level of factor VII antigen was relatively low. These data indicate that the propositus is a factor VII reduced variant, a rare variant of congenital factor VII deficiency. The propositus and her brother are homozygotes, and her parents and sister are heterozygotes.

Blood Coagulation Tests↗
PubMed1991

Clinical characterization of drug-induced allergic nephritis.

To elucidate the clinical characterization of drug-induced allergic nephritis (DIAN), we analyzed the cases attending our department. We now report on the 14 cases of DIAN due to administration of penicillin in 2 cases, cephem antibiotics in 6 cases, nonsteroidal anti-inflammatory drugs in 4 cases and new quinolone anticidal drugs in 2 cases. With 1 exception, all these cases reached the stage of acute renal failure after taking these drugs for 2-13 days, followed by characteristic allergic symptoms such as fever, skin eruptions and serum IgE elevation in 5 of the 14 cases. A lymphocyte stimulation test (LST) with the suspected drugs proved to be positive in 10 of the 12 cases examined, and the uptake of 67Ga in the kidneys was extremely positive in all 6 cases examined, reflecting the natural course of this disease. Furthermore, there were some cases where 67Ga accumulated in the kidneys in spite of the negative result of LST examination. In all of these cases, a needle or open renal biopsy was performed, and acute tubulointerstitial nephritis (AIN) was diagnosed. Almost all cases were treated with glucocorticoid for AIN or dialysis for acute uremic symptoms several times. However, 4 of the 14 cases could not return to normal condition in spite of these forms of treatment. We would therefore like to suggest that LST and 67Ga scintigram are useful diagnostic tools for DIAN as an alternative to renal biopsy.

4-Quinolones↗
PubMed1991

[The respiratory function in children with collagen disease].

Respiratory function tests were performed on 60 children with collagen disease. Twenty-seven cases (45%) showed abnormalities in the respiratory function. These abnormalities were restrictive in 14 cases (52%), obstructive in 6 cases (22%), and mixed type in 7 cases (26%). Eight out of 14 SLE patients (57%) showed abnormalities of various types. Abnormalities were seen in 9 out of 25 JRA patients (36%) including 6 cases (67%) with restrictive type changes. Four out of 6 MCTD (67%) and 3 out of 9 DM (33%) patient showed functional abnormalities. Most of patients with these two types of collagen disease showed restrictive changes. Investigations performed by a research group of the Ministry of Health and Welfare showed the incidence of restrictive type changes (% VC less than 80) in adult patients of collagen disease to be in the following descending order: PM/DM greater than PSS greater than MCTD greater than SLE. Though small in number, our investigation revealed that a considerable proportion of MCTD and SLE patients showed restrictive changes in respiratory function. In evaluating the clinical course of the disease, it was thus considered to be important to follow up the progress of respiratory functions in children with collagen disease.

Adolescent↗
PubMed1991

A gene(s) within the H-2D region determines the development of toxoplasmic encephalitis in mice.

Studies were performed in a murine model to determine if there is genetic control of the development of toxoplasmic encephalitis. Ten weeks after infection with the ME49 strain of Toxoplasma gondii, mice with the H-2b haplotype (C57BL/6, C57BL/10) and H-2k haplotype (C3H/He, CBA/J) developed remarkable inflammatory changes in their brains, whereas mice with the H-2a haplotype (A/J) and H-2d haplotype (BALB/c, DBA/2) did not. In the area of acute focal inflammation in mice with the H-2b and H-2k haplotypes, tachyzoites and toxoplasma antigens were demonstrated by immunoperoxidase staining, suggesting that the focal inflammation was induced by toxoplasma organisms. B10 congenic mice were used for further analysis of this genetic regulation. Presence of the encephalitis in B10 and B10.BR but not in B10.A and B10.D2 mice at 10 weeks after infection indicated regulation of the inflammation by a gene(s) within the H-2 complex. The encephalitis developed in B10.A (2R) and B10.A (4R) mice but not in B10.A (3R) and B10.A (18R) during infection. These results clearly indicated that the development of toxoplasmic encephalitis was controlled by a gene(s) in the H-2D region. The Qa and Tla genes did not appear to be critical in determining susceptibility to the encephalitis. There was no correlation between serum toxoplasma antibody titres and occurrence of the encephalitis. Injection of a monoclonal antibody to interferon-gamma (IFN-gamma) remarkably augmented the inflammatory changes in the brains of the infected B10 mice. In contrast, the treatment did not induce any inflammatory response in the brains of the infected BALB/c mice. A similar genetic regulation may be operative in determining development of toxoplasmic encephalitis in AIDS and other immunocompromised patients.

Animals↗
PubMed1990

Transcriptional regulation of an aldolase gene in the regenerating rat liver.

The relative abundance of rat aldolase A, B, C, alpha-fetoprotein, and albumin mRNAs was determined by Northern hybridization during liver regeneration after partial hepatectomy. Aldolase A mRNA increased more than 10-fold on the 3rd day after partial resection compared with that of normal adult rat liver. S1 analysis revealed that three species of aldolase A mRNAs (mRNA I, II & III) reappeared. However, transcriptional rate of aldolase A mRNA did not change at all during the regeneration. In contrast, aldolase B, aldolase C and albumin mRNAs did not change at all. These findings suggest that the differentiated hepatocyte maintains a differentiated state during the liver regeneration as seen in aldolase B, whereas "oncofetal" isozymes such as aldolase A resurge after partial hepatectomy under the control of post-transcriptional mechanism.

Albumins↗