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Biomedical subjects

Y Kaneda

Publications and source records attributed to Y Kaneda.

At least 325 records · Page 18Linked to original sources
PubMed1996

[A case of adult chest wall rhabdomyosarcoma].

A 68-year-old woman was admitted to our hospital with a left anterior chest wall tumor. A percutaneous needle biopsy was performed, leading to a pathological diagnosis of pleomorphic rhabdomyosarcoma. A wide en bloc excision of the left anterior chest wall was performed, including the left sixth and seventh ribs. The defect of the chest wall was closed with Marlex mesh. Postoperative adjuvant chemotherapy (CYVADIC) was administered. The patient remained free of local recurrence two years after surgery. We conclude that wide en block excision and close follow-up are important in the management of rhabdomyosarcoma of the chest wall because of a high risk of recurrence.

Aged↗
PubMed1996

Sex differences in visual evoked potential and electroencephalogram of healthy adults.

Sex differences in flash visual evoked potentials (VEPs) and electroencephalograms (EEGs) were studied in 200 healthy adults (100 females and 100 males). Following results were obtained. (1) Waveforms of Group Mean VEPs of each sex had roughly triphasic contour, consisted of components P1 approximately N8, within 500 msec of latency. (2) Latencies of VEP components by t-test, (3) By analysis of covariance, sex differences in peak-to-peak amplitudes were still significant after eliminating effects of body height, body weight or age, but not those in latencies after eliminating the effect of body height. (4) Quantitative analysis of EEGs resulted in significantly smaller absolute amplitudes, and significantly larger theta, larger beta 1 and smaller alpha 2 power % in females. (5) Peak-to-peak amplitudes of later components in VEPs for 5CH (O1-->Cz) were significantly and positively correlated with EEG absolute amplitudes within each sex group. (6) There were few significant differences in VEP components between follicular phase and luteal phase in females. The sex differences in VEPs verified in this study may be attributed to genetically determined sex differences in neuroendocrinological systems.

Adult↗
PubMed1995

The loss of 40-kDa chromosomal protein in tuberous sclerosis lesions.

Tuberous sclerosis is an genetic disease characterized by systemic hamartomas. Some of the cultured cells derived from tuberous sclerosis show the distinct chromosomal disarrangement and abnormal cell division. To detect the proteins responsible for this phenomenon, we investigated many nuclear components related to cell division. 40-kDa protein (p40) recognized by one monoclonal antibody M108, which was present in nucleus, chromosomes and cytoplasm of many vertebrate culture cells, significantly decreased in the tuberous sclerosis cells. Immunoblot analysis revealed that in all the fractions the quantity of p40 of severe tuberous sclerosis cells was approximately 4 times less than p40 in normal fibroblasts.

Antibodies, Monoclonal↗
PubMed1995

Overexpression of prostacyclin synthase inhibits growth of vascular smooth muscle cells.

To define the local effects of prostacyclin (PGI2) on the growth of vascular smooth muscle cells (VSMC), we transfected VSMC with an expression vector harboring the cDNA for PGI2 synthase (PGIS), which catalyzes the rearrangement of prostaglandin H2 to PGI2. Transfection of the human PGIS cDNA into rat VSMC did not affect DNA synthesis under serum-free basal conditions, but it increased PGI2 synthesis and decreased DNA synthesis under serum-stimulated conditions (in the presence of 1 or 5% fetal calf serum). These results demonstrated that locally synthesized PGI2 can exert autocrine and/or paracrine inhibitory effects on VSMC growth. It was also suggested that in vivo transfer of PGIS gene may be useful for the gene therapy for vascular disease such as neointimal hyperplasia.

Animals↗
PubMed1995

Efficiency of in vivo gene transfection into transplanted rat heart by coronary infusion of HVJ liposome.

BACKGROUND: Current methods of in vivo gene transfer into myocardium are limited by low efficiency. To improve in vivo gene transfer, a gene transfer method using hemagglutinating virus of Japan (HVJ) as a viral vector can be an alternative. METHODS AND RESULTS: In vivo gene transfection of FITC-labeled oligonucleotide (F-ODN) and cDNA of beta-galactosidase (beta-gal) was examined with use of the HVJ liposome (H group) or without it (C group). In the H group, F-ODN or cDNA of beta-gal were complexed with liposomes, DNA binding nuclear protein (HMG1), and the viral protein coat of HVJ. After the harvest of donor rat hearts arrested by cardioplegia, the coronary artery was infused with the liposome gene complex. The hearts were transplanted into the abdomens of recipient rats and harvested 3 days after transplantation. Regarding F-ODN, the H group clearly showed FITC staining in the nuclei of the myocytes and endothelial cells in almost all layers of the myocardium as compared with the C group. Regarding the expression of beta-gal, the H group showed a clear expression of beta-gal on myocytes, whereas very low expression of beta-gal was seen in the C group. CONCLUSIONS: The donor hearts were transfected with F-ODN and beta-gal gene in almost all layers of the myocardium as a result of coronary infusion of the HVJ liposome during cardioplegic arrest. Our method is seen as a novel in vivo gene transfer technique for the heart and may provide a new tool for both research and therapy of heart transplantation.

Animals↗
PubMed1995

A histologically distinctive interstitial pneumonia induced by overexpression of the interleukin 6, transforming growth factor beta 1, or platelet-derived growth factor B gene.

Interstitial pneumonia is characterized by alveolitis with resulting fibrosis of the interstitium. To determine the relevance of humoral factors in the pathogenesis of interstitial pneumonia, we introduced expression vectors into Wistar rats via the trachea to locally overexpress humoral factors in the lungs. Human interleukin (IL) 6 and IL-6 receptor genes induced lymphocytic alveolitis without marked fibroblast proliferation. In contrast, overexpression of human transforming growth factor beta 1 or human platelet-derived growth factor B gene induced only mild or apparent cellular infiltration in the alveoli, respectively. However, both factors induced significant proliferation of fibroblasts and deposition of collagen fibrils. These histopathologic changes induced by the transforming growth factor beta 1 and platelet-derived growth factor B gene are partly akin to those changes seen in lung tissues from patients with pulmonary fibrosis and markedly contrast with the changes induced by overexpression of the IL-6 and IL-6 receptor genes that mimics lymphocytic interstitial pneumonia.

Adenoviridae↗
PubMed1995

A gene therapy strategy using a transcription factor decoy of the E2F binding site inhibits smooth muscle proliferation in vivo.

The application of DNA technology to regulate the transcription of disease-related genes in vivo has important therapeutic potentials. The transcription factor E2F plays a pivotal role in the coordinated transactivation of cell cycle-regulatory genes such as c-myc, cdc2, and the gene encoding proliferating-cell nuclear antigen (PCNA) that are involved in lesion formation after vascular injury. We hypothesized that double-stranded DNA with high affinity for E2F may be introduced in vivo as a decoy to bind E2F and block the activation of genes mediating cell cycle progression and intimal hyperplasia after vascular injury. Gel mobility-shift assays showed complete competition for E2F binding protein by the E2F decoy. Transfection with E2F decoy inhibited expression of c-myc, cdc2, and the PCNA gene as well as vascular smooth muscle cell proliferation both in vitro and in the in vivo model of rat carotid injury. Furthermore, 2 weeks after in vivo transfection, neointimal formation was significantly prevented by the E2F decoy, and this inhibition continued up to 8 weeks after a single transfection in a dose-dependent manner. Transfer of an E2F decoy can therefore modulate gene expression and inhibit smooth muscle proliferation and vascular lesion formation in vivo.

Animals↗
PubMed1995

Genetic engineering of vein grafts resistant to atherosclerosis.

Previously, researchers have speculated that genetic engineering can improve the long-term function of vascular grafts which are prone to atherosclerosis and occlusion. In this study, we demonstrated that an intraoperative gene therapy approach using antisense oligodeoxynucleotide blockage of medial smooth muscle cell proliferation can prevent the accelerated atherosclerosis that is responsible for autologous vein graft failure. Selective blockade of the expression of genes for two cell cycle regulatory proteins, proliferating cell nuclear antigen and cell division cycle 2 kinase, was achieved in the smooth muscle cells of rabbit jugular veins grafted into the carotid arteries. This alteration of gene expression successfully redirected vein graft biology away from neointimal hyperplasia and toward medial hypertrophy, yielding conduits that more closely resembled normal arteries. More importantly, these genetically engineered grafts proved resistant to diet-induced atherosclerosis. These findings establish the feasibility of developing genetically engineered bioprostheses that are resistant to failure and better suited to the long-term treatment of occlusive vascular disease.

Animals↗
PubMed1995

A fast, convenient diagnosis of the bovine freemartin syndrome using polymerase chain reaction.

To establish the polymerase chain reaction (PCR) method for detecting the XY cells in cases suspected to have the bovine freemartin syndrome, a PCR reaction test was conducted on blood from a normal bull diluted in blood from a normal cow. From the results obtained, it was shown that the Y-specific sequence was detectable down to a concentration of 0.1%. Various types of the bovine freemartin syndrome, which occurs in heterosexual twins, single-born sterile heifers, and heifers born with Acardius amorphus, were examined by the chromosome analysis and the PCR method. The Y-specific sequence was detected in all 26 cases that showed chromosome chimerism but which was absent in the 5 cases without a chimerism. The PCR method was found to be effective and convenient for quickly diagnosing the various types of bovine freemartin syndrome.

Journal Article↗
PubMed1995

Gene therapy inhibiting neointimal vascular lesion: in vivo transfer of endothelial cell nitric oxide synthase gene.

It is postulated that vascular disease involves a disturbance in the homeostatic balance of factors regulating vascular tone and structure. Recent developments in gene transfer techniques have emerged as an exciting therapeutic option to treat vascular disease. Several studies have established the feasibility of direct in vivo gene transfer into the vasculature by using reporter genes such as beta-galactosidase or luciferase. To date no study has documented therapeutic effects with in vivo gene transfer of a cDNA encoding a functional enzyme. This study tests the hypothesis that endothelium-derived nitric oxide is an endogenous inhibitor of vascular lesion formation. After denudation by balloon injury of the endothelium of rat carotid arteries, we restored endothelial cell nitric oxide synthase (ec-NOS) expression in the vessel wall by using the highly efficient Sendai virus/liposome in vivo gene transfer technique. ec-NOS gene transfection not only restored NO production to levels seen in normal untreated vessels but also increased vascular reactivity of the injured vessels. Neointima formation at day 14 after balloon injury was inhibited by 70%. These findings provide direct evidence that NO is an endogenous inhibitor of vascular lesion formation in vivo (by inhibiting smooth muscle cell proliferation and migration) and suggest the possibility of ec-NOS transfection as a potential therapeutic approach to treat neointimal hyperplasia.

Amino Acid Oxidoreductases↗
PubMed1995

In vivo transfection of genes for renin and angiotensinogen into the glomerular cells induced phenotypic change of the mesangial cells and glomerular sclerosis.

Locally activated renin angiotensin system plays an important role in the progression of the glomerular diseases. In order to understand the local effect of overexpressed angiotensin II in the glomerulus in situ, we introduced human genes for renin and angiotensinogen into the rat kidney by hemagglutinating virus of Japan-liposome procedure. Three days after transfection human renin was detected in the glomeruli by immunohistochemistry. Seven days after transfection, extracellular matrix was expanded in the glomeruli and alpha-smooth muscle actin was expressed in the mesangial cells. These results suggest that locally activated renin angiotensin system induces glomerular sclerosis and a phenotypic change in mesangial cells.

Actins↗
PubMed1995

Uterine atrophy in chronic murine toxoplasmosis due to ovarian dysfunction.

Uterine atrophy is a conspicuous finding in Nya:NYLAR female mice chronically infected with Toxoplasma gondii. Administration of 17B-estradiol to infected mice induced a vigorous uterotropic response, i.e., an increase in uterine weight, in endometrial hypertrophy and proliferation, and in the activity of three estrogen-regulated uterine enzymes. These findings rule out a parasite-induced refractoriness of the uterus to estrogen and point to ovarian dysfunction (hypogonadism) as the immediate cause of the uterine atrophy.

Adenylate Kinase↗
PubMed1995

Etiology of ovarian dysfunction in chronic murine toxoplasmosis.

Ovarian dysfunction develops in Nya:NYLAR mice chronically infected with Toxoplasma gondii. To differentiate between primary ovarian failure and pituitary gonadotropin insufficiency, we (a) monitored ovarian responsiveness to pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) and (b) assessed endogenous pituitary gonadotropin capacity by the degree of ovarian compensatory hypertrophy (OCH) developing after unilateral ovariectomy (ULO). PMSG stimulated vigorous folliculogenesis and estrogen synthesis, but not ovulation. HCG given 3 days after PMSG induced "superovulation" within 16 h. These observations indicate the absence of the critical preovulatory surge of endogenous luteinizing hormone (LH) from the pituitary. In addition, ULO did not result in compensatory hypertrophy of the contralateral ovary, an indication of follicle-stimulating hormone (FSH) insufficiency. We hypothesize that cytokines released peripherally in response to the parasite reached the hypothalamus and initiated a sequence of events that inhibited the pulsatile release of gonadotropin-releasing hormone (GnRH), leading to the subsequent impairment of the pituitary-ovarian axis.

Animals↗
PubMed1995

Abnormal cardiac histology in severe intrauterine growth retardation infants.

Four infants with severe intrauterine growth retardation (IUGR) weighing less than 1000 g at birth developed heart failure and died in our unit, where heart failure of IUGR infants is the main reason of death in extremely low birth-weight infants. The causes of their heart failure are one of the main themes in current neonatal medicine. The subjects of this study were four small for gestational age infants; all died due to heart failure 5 to 10 days after birth. Microscopic specimens of hearts from autopsies were evaluated with respect to the following characteristics: thickness of myocardial fibers, maturation of nuclei, presence of dysgenesis or necrosis in myocardium, and amount of glycogen in the heart. Neither dysgenesis nor infarction of the heart was found but hypoplasia in myocardial fibers and decreased glycogen levels were observed. Maturation delay in myocytes' nuclei did not appear to be severe. We conclude that these infants' hearts failed to adapt to postnatal hemodynamic changes because of inadequate myocardial function and inadequate glycogen reserves.

Fetal Growth Retardation↗