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Biomedical subjects

H Kawaguchi

Publications and source records attributed to H Kawaguchi.

At least 145 records · Page 8Linked to original sources
PubMed1998

Surgical complications of pediatric kidney transplantation: a single center experience with the extraperitoneal technique.

PURPOSE: The complex nature of pediatric renal transplantation and the often fragile condition of children with end stage renal disease create the potential for a number of complications. To decrease surgical complications we have performed renal transplantation via the extraperitoneal approach at our institution even in children who weigh less than 20 kg. We retrospectively evaluated whether renal transplantation via the extraperitoneal approach decreases surgical complications in pediatric kidney transplant recipients. MATERIALS AND METHODS: From February 1983 to December 1996, 1,115 patients underwent renal transplantation at our institution, including 60 boys and 47 girls with a mean age of 11.9 years who comprise the study group. Mean weight was 30 kg. at transplantation, and 32 and 75 patients weighed less than 20 and 20 or more kg., respectively. All 107 patients were treated with cyclosporine or tacrolimus based immunosuppression, including methylprednisolone and azathioprine or mizoribine. Living related and cadaveric renal transplantation was performed in 92 and 15 cases, respectively. The extraperitoneal technique was performed in all recipients, even in low weight children. The aorta and inferior vena cava, common iliac artery and vein or hypogastric artery and external vein were used for vascular anastomosis depending on recipient size. The ureter was anastomosed to the bladder via a modification of Paquin's method or an extravesical technique. RESULTS: During observation 7 surgical complications (6.5%) developed, including ureteral stricture, ureteral necrosis, renal artery stenosis, lymphocele, subcapsular hematoma, bladder leakage and significant vesicoureteral reflux to the graft in 1 patient each. There were no gastrointestinal complications. One patient with ureteral necrosis and 1 with subcapsular hematoma required surgical repair, and 1 underwent laparoscopic fenestration of a lymphocele. One patient with ureteral stricture and 1 with bladder leakage were treated conservatively, while another underwent ureteroneocystostomy. Overall only 1 graft (1%) was lost to a surgical complication (renal artery stenosis). CONCLUSIONS: The incidence of surgical complications of the extraperitoneal technique in pediatric renal transplant patients was low (6.5%) and seems to be acceptable. The extraperitoneal technique did not cause any gastrointestinal complications, which seems to be its greatest advantage. The extraperitoneal technique may be used safely even in low weight children.

Adolescent↗
PubMed1998

Surgical management of giant schwannoma in the lumbosacral region.

Giant lumbosacral schwannoma is rare and only 11 cases have been reported. We experienced two cases: a 58-year-old woman with recurrent schwannoma from L2 to S3, and a 52-year-old woman with schwannoma from T12 to L5. Total resection was possible in the latter case, which was the patient's first operation. Although she had neurologic deterioration, there was no recurrence during the 4-year follow-up. The recurrent case required a bone graft because of her fragile spine, and she was severely disabled. In the literature, total resection has been confirmed in only two cases of a first operation. Total resection is nonetheless strongly recommended in spite of the risk of leaving a neurologic deficit.

Cauda Equina↗
PubMed1998

[Aortic valvular vegetation in annuloaortic ectasia due to idiopathic cystic medial necrosis: a case report].

Annuloaortic ectasia is often accompanied by Marfan syndrome and associated with infective endocarditis usually involving the mitral valves. We treated a patient with annuloaortic ectasia due to idiopathic cystic medial necrosis who developed congestive heart failure with aortic valvular vegetation. A 56-year-old man had dyspnea on effort since the beginning of January, 1997 and was admitted to our hospital on April 6, 1997 because of orthopnea. The diagnosis was congestive heart failure due to severe aortic regurgitation with annuloaortic ectasia detected by echocardiography. Medication and rest after hospitalization relieved his symptoms but congestive heart failure deteriorated after he had a high fever. At this time, a vegetation attached to the noncoronary cusp of the aortic valve was found which had not been detected on admission. Blood culture yielded Streptococcus sanguis. The diagnosis was infective endocarditis involving the aortic valve. Surgical correction (Bentall method) improved congestive heart failure and he was discharged on August 4, 1997 without recurrence of endocarditis. Infective endocarditis involving the aortic valves is a possible cause of development or deterioration of congestive heart failure in patients with annuloaortic ectasia.

Aortic Diseases↗
PubMed1998

Aorto-atrial fistula associated with recurrent aortic dissection after ascending aorta replacement.

A 70-year-old woman with a bicuspid aortic valve had undergone ascending aorta replacement for acute DeBakey type I dissection. Computed tomography and aortography 2 months after the operation revealed a thrombosed false lumen in the ascending aorta proximal to the prosthetic graft. However, recurrence of dissection was found at the aortic root proximal to the graft 4 years after the initial operation. Significant aortic stenosis was also noted. Despite intensive medical treatment, she had refractory and progressive heart failure. At the second surgery, an aorto-right atrial fistula, which probably was responsible for the severe heart failure was revealed. Closure of the aorto-right atrial fistula, and aortic root replacement were performed using Piehler's method, with a composite graft. The etiology and management of this rare case are discussed.

Aged↗
PubMed1997

A new mechanism of bone destruction in rheumatoid arthritis: synovial fibroblasts induce osteoclastogenesis.

Bone-resorbing multinucleated cells were efficiently formed in primary culture of cells isolated from synovial tissues of patients with rheumatoid arthritis in 2-3 weeks in the presence of 1,25(OH)2vitaminD3 without any additional stromal cells, and that formation was further facilitated by macrophage-colony stimulating factor. Furthermore, we show that osteoclast-like cells are formed in co-culture of peripheral blood mononuclear cells and rheumatoid synovial fibroblasts obtained by continued sub-cultures. The multinucleated cells showed all the phenotypical and functional characteristics of osteoclasts including the expression of tartrate resistant acid phosphatase, vitronectin receptors, receptors for human calcitonin and the ability to resorb bone. These results indicate that synovial macrophages are capable of differentiating into osteoclasts in the presence of rheumatoid synovial fibroblasts which can support differentiation of monocytes/ macrophages, implicating that osteoclasts generated within the synovial membrane are probably involved in bone destruction in rheumatoid arthritis.

Acid Phosphatase↗
PubMed1997

Mutation of the mouse klotho gene leads to a syndrome resembling ageing.

A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes. A defect in klotho gene expression in the mouse results in a syndrome that resembles human ageing, including a short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema. The gene encodes a membrane protein that shares sequence similarity with the beta-glucosidase enzymes. The klotho gene product may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.

Aging↗
PubMed1997

In vivo gene transfection of human endothelial cell nitric oxide synthase in cardiomyocytes causes apoptosis-like cell death. Identification using Sendai virus-coated liposomes.

BACKGROUND: Nitric oxide (NO) has various actions on the cardiovascular system, although its pathophysiological significance in myocardial cells remains obscure. The aim of the present study was to identify direct NO actions on cardiomyocytes by gene transfection in vivo using a newly developed vector under physiological conditions. METHODS AND RESULTS: Liposomes containing the beta-galactosidase (beta-gal) gene alone or with the human endothelial cell nitric oxide synthase (ecNOS) gene were coated with UV-inactivated Sendai virus and injected into the left ventricular wall of rat heart in vivo. Histological examination confirmed that the transfection efficiency was comparable to adenovirus-mediated transfection and that the new vector per se caused no inflammation. beta-Gal expression was confined to cardiomyocytes between two intercalated discs, suggesting that the transfected gene did not permeate the discs. An immunohistochemical study showed that cotransfection of the ecNOS gene induced massive myocardial cell shrinkage in both transfected cells and the adjacent myocytes in a time- and dose-dependent manner. Histochemical findings in shrunk cells coincided with apoptosis as identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling. Electron microscopy of the lesion revealed myofibrillar degradation and accumulation of mitochondria but no apoptotic bodies. Pre-treatment with the NOS inhibitor N omega-nitro-L-arginine methyl ester abolished these morphological alterations. CONCLUSIONS: The efficient expression of the human ecNOS gene in vivo suggests that NO or its toxic metabolite caused myocardial degradation, a part of which was compatible with apoptosis of the transfected cardiomyocytes themselves and the adjacent cells as a paracrine effect. These morphological features mimicked acute myocarditis or ischemic injury.

Animals↗
PubMed1997

Idiopathic low molecular weight proteinuria associated with hypercalciuric nephrocalcinosis in Japanese children is due to mutations of the renal chloride channel (CLCN5).

The annual urinary screening of Japanese children above 3 yr of age has identified a progressive proximal renal tubular disorder characterized by low molecular weight proteinuria, hypercalciuria, and nephrocalcinosis. The disorder, which has a familial predisposition and occurs predominantly in males, has similarities to three X-linked proximal renal tubular disorders that are due to mutations in the renal chloride channel gene, CLCN5. We have investigated four unrelated Japanese kindreds with this tubulopathy and have identified four different CLCN5 mutations (two nonsense, one missense, and one frameshift). These are predicted to lead to a loss of chloride channel function, and heterologous expression of the missense CLCN5 mutation in Xenopus oocytes demonstrated a 70% reduction in channel activity when compared with the wild-type. In addition, single-stranded conformation polymorphism (SSCP) analysis was found to be a sensitive and specific mutational screening method that detected > 75% of CLCN5 mutations. Thus, the results of our study expand the spectrum of clinical phenotypes associated with CLCN5 mutations to include this proximal renal tubular disorder of Japanese children. In addition, the mutational screening of CLCN5 by SSCP will help to supplement the clinical evaluation of the annual urinary screening program for this disorder.

Adolescent↗
PubMed1997

Stimulation of bone formation by intraosseous application of recombinant basic fibroblast growth factor in normal and ovariectomized rabbits.

The effect on intraosseous bone formation of a single local injection of recombinant human basic fibroblast growth factor into the distal femur was examined in normal and ovariectomized rabbits. In normal rabbits, basic fibroblast growth factor increased bone mineral density around the injected site in a dose-dependent manner at 4 weeks, with significant effects at concentrations of 400 micrograms and greater. Doses of 400 and 1,600 micrograms of basic fibroblast growth factor increased bone mineral density by 8 and 9%, respectively, compared with the opposite control femur. Histological examination showed that basic fibroblast growth factor (400 micrograms) induced the proliferation or recruitment of undifferentiated mesenchymal cells around the existing trabeculae at 3 days after the injection. For the first 2 weeks, osteoid formation was strongly stimulated, and this was followed by mineral apposition for another 2 weeks, at which time the femurs were harvested. Consequently, basic fibroblast growth factor stimulated intraosseous bone formation at 4 weeks. We speculate that the direct action of basic fibroblast growth factor on bone formation may be to stimulate proliferation or recruitment of minimally differentiated mesenchymal cells and to initiate the cascade of events in later stages of bone formation. In ovariectomized rabbits, basic fibroblast growth factor (400 micrograms) also increased bone mineral density, histomorphometrical bone formation markers, and trabecular connectivity to levels similar to those in rabbits who had received sham operations.

Animals↗
PubMed1997

Somatic and renal effects of growth hormone in rats with chronic renal failure.

Recombinant human growth hormone (rhGH) has been widely used to improve growth in children with chronic renal failure (CRF). However, there has been great concern that GH may aggravate renal disease and hasten the progression to end-stage renal failure. We therefore investigated the effect of prolonged administration of rhGH at various doses on somatic growth and renal function and structure in rats with CRF, divided into four groups based on rhGH dose (vehicle, 0.4, 2.0, and 10.0 IU/day). rhGH was administered subcutaneously daily for 8 weeks. The mean growth was significantly greater in rats treated with high-dose rhGH (10.0 IU) than those treated with low-dose rhGH (P = 0.0089) or vehicle (P = 0.0011). Body weight gain increased in parallel with body length (Creatinine clearance at the end of the experiment was significantly lower in rats on high or medium-dose rhGH than those on low-dose rhGH and controls (P < 0.05). The glomerular sclerosing index was greater in rats treated with higher doses of rhGH. There were significant differences between rats treated with high-dose rhGH and controls (P = 0.0144) and also between rats on medium-dose rhGH and controls (P = 0.0065). Although there was no significant difference, rats treated with higher doses of rhGH tended to excrete more protein. Renal insulin-like growth factor-I (IGF-I) content and circulating IGF-I and IGF-II levels did not significantly differ among groups. We conclude that: (1) GH improves somatic growth failure in rats with CRF, but prolonged administration of GH dose-dependently induces deterioration in renal function and structure and (2) this effect was induced neither via circulating IGF-I and IGF-II nor by local production of IGF-I, but seems to be direct.

Animals↗
PubMed1997

Angiotensinogen gene polymorphism in Japanese patients with hypertrophic cardiomyopathy.

To examine the contribution of the renin-angiotensin system to hypertrophic cardiomyopathy (HCM), we studied 96 patients with HCM (mean age 50 years, 55% male), 105 of their unaffected siblings and offspring, and 160 healthy subjects without known hypertension and left ventricular hypertrophy (LVH) who were frequency matched to cases by age and sex. Patients were divided into familial or sporadic HCM (FHCM or SHCM) groups with or without affected members of their family. The region of interest in the angiotensinogen (AGT) gene, the missense mutation with methione-to-threonine amino acid substitution at codon 235 in angiotensinogen (M235T), was amplified by polymerase chain reaction with the use of allele-specific oligonucleotide primers flanking the polymorphic region of the AGT gene to amplify template deoxyribonucleic acid prepared from peripheral leukocytes. The T allele frequency was higher in the SHCM group than in unaffected siblings and offspring (88% vs 78%, X2 = 4.6, p < 0.05). The M allele frequency was higher in unaffected siblings and offspring than in patients with SHCM (23% vs 12%, X2 = 4.6, p < 0.05). The T allele frequency among unaffected siblings and offspring was similar to that observed in healthy subjects (78% vs 78%). We conclude that HCM, especially in sporadic cases, is partially determined by genetic disposition. The molecular variant of angiotensinogen T235 seems to be a predisposing factor for cardiac hypertrophy in HCM and carries an approximately twofold increased risk.

Adult↗
PubMed1997

Down-regulation of manganese-superoxide dismutase gene expression in idiopathic nephrotic syndrome.

An oxidant stress has been shown to prevail in experimental and clinical nephrotic syndrome. Such oxidant stress may be induced by a reduced activity of antioxidant systems. We examined the altered expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, in patients with idiopathic nephrotic syndrome, in whom an increased oxidant stress had been demonstrated. The Mn-SOD activities in peripheral blood mononuclear cells obtained from 12 patients with active nephrotic syndrome (6.0 +/- 1.1 years of age, mean +/- SE) and hypoproteinemia were 42% lower (p < 0.05) than in 12 control subjects (5.5 +/- 0.5 years of age) with normal serum total protein concentrations. Reverse-transcriptase polymerase chain reaction also demonstrated that Mn-SOD messenger RNA expression in the patients with nephrotic syndrome was, on average, 59% lower than in control subjects. Because expressions of some genes are sensitive to serum, the serum dependency of Mn-SOD gene transcription was studied in glomerular endothelial cells transfected with a luciferase reporter gene fused with a rat Mn-SOD DNA fragment of -806 to +22 bp of the transcription initiation site (-806:+22). When these cells were exposed to different concentrations of fetal bovine serum (0.5% to 15%), the transcriptional activities determined by luciferase activities were proportional to serum concentrations. This serum-dependent transcriptional activation was also demonstrated by the fragment (-220:+22) but not by the fragment (-220:-20). When glomerular endothelial cells transfected with the fragment (-220:+22) were treated with 5% serum from patients with active nephrotic syndrome, transcriptional activation was more than 80% less than that by 5% serum from control subjects without nephrosis. These results indicate that Mn-SOD gene transcription is regulated at least in part by serum, and that the serum-dependent transcription of the gene is diminished in patients with idiopathic nephrotic syndrome. The regulatory region of serum-dependent gene transcription resides within its early promoter region. Our findings suggest that down-regulation of antioxidant enzyme transcription may contribute increased oxidant stress in idiopathic nephrotic syndrome.

Animals↗
PubMed1997

Predominance of type 2 cytokine-producing CD4+ and CD8+ cells in patients with atopic dermatitis.

BACKGROUND: Recently, increased IL-4 and decreased interferon-gamma (IFN-gamma) production in peripheral blood mononuclear cells (PBMCs) from patients with atopic dermatitis have been reported by several groups. They measured the total amount of each cytokine in culture supernatants in their studies. These studies suggested a predominance of type 2 cytokine-producing cells in atopic dermatitis. However, it is still unclear whether the cytokine imbalance is the result of an imbalance of specific T-cell subsets or of dysregulation of the cytokine-producing ability in T-cell subsets. Here, we examined frequencies of IL-4-, IFN-gamma-, or IL-2-producing CD4+ cells and CD8+ cells in PBMCs from patients with atopic dermatitis at a single cell level by using flow cytometry. METHODS: PBMCs from 45 patients with atopic dermatitis and 24 healthy control subjects were stimulated with immobilized anti-CD3 monoclonal antibody for 6 hours in the presence of monensin. Cells were fixed, made permeable, and stained for intracellular cytokines in combination with staining for cell surface markers CD4 and CD8. RESULTS: The frequency of IL-4-producing CD4+ cells and CD8+ cells from patients with atopic dermatitis was significantly higher (p < 0.001) than that from healthy control subjects. In contrast, the frequency of IFN-gamma-producing CD4+ cells and CD8+ cells was significantly decreased (p < 0.01) in the patients with atopic dermatitis. The frequency of IL-2-producing cells from patients with atopic dermatitis was comparable to that from healthy control subjects. CONCLUSION: Our findings indicate that frequencies of type 2 cytokine-producing cells, not only among CD4+ cells but also among CD8+ cells, were significantly higher in patients with atopic dermatitis than in healthy control subjects.

Adolescent↗
PubMed1997

Cellular immuno-competence of infected root canal contents in pathogenesis of periapical lesions.

The soluble fractions of infected root canal contents (IRCC) were collected from about 300 human extracted teeth and examined for the presence of mononuclear cell (MNC) chemotaxis and cellular immunocompetence. IRCC showed remarkable chemotactic activity for polymorphonuclear leukocytes but a weak activity for MNC. However, generation of intrinsic MNC chemotaxis and induction of cellular immunity were confirmed in rats given repeated injections of IRCC.

Animals↗
PubMed1997

Mesangial phenotypic changes associated with cellular lesions in primary focal segmental glomerulosclerosis.

Injury to glomerular visceral epithelial cells has been proposed as the initial step in glomerular scar formation in primary focal segmental glomerulosclerosis (FSGS); however, the subsequent process that ultimately results in glomerular scar formation remains uncertain. This study examined whether phenotypically altered mesangial cells determine the early progression of primary FSGS. Cellular lesion characterized by proliferative epithelial cell reaction with occasional endocapillary hypercellularity has been considered to be an early morphologic feature in the development of glomerular scar in primary FSGS. We compared the immunohistologic findings of 10 patients with primary FSGS showing cellular lesion, 15 patients with primary FSGS showing only segmental scar, and 10 patients with minimal-change nephrotic syndrome. Histologically normal kidney tissue samples obtained from three patients with renal trauma were used as normal controls. Alpha-smooth muscle actin expression detected by a mouse anti-human monoclonal antibody as well as de novo type III collagen expression determined by a goat polyclonal antibody were prominent in the glomerular tufts with cellular lesions in FSGS patients. A significant increase in the number of glomerular CD68+ (a mouse anti-human monoclonal antibody) macrophages was also observed in association with the cellular lesion. Repeat renal biopsies in six of the 10 FSGS patients with a cellular lesion showed disappearance of the cellular lesion, reduced glomerular alpha-smooth muscle actin expression, decreased number of glomerular CD68+ macrophage, and progression of glomerular scar formation. These results indicate that mesangial cells undergo phenotypic changes to myofibroblasts in association with the cellular lesion in primary FSGS. Thus, the phenotypically altered mesangial cells acquiring features of a myofibroblast may have an important role in the early process of glomerular scar formation in certain types of primary FSGS.

Actins↗