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Biomedical subjects

S Nishi

Publications and source records attributed to S Nishi.

At least 91 records · Page 5Linked to original sources
PubMed1997

Crush syndrome sustained in the 1995 Kobe, Japan, earthquake; treatment and outcome.

STUDY OBJECTIVE: To assess the treatment and outcome of patients with crush syndrome sustained in an earthquake disaster. METHODS: We conducted a retrospective analysis of eight patients with crush syndrome and subsequent acute kidney failure who were treated in the ICU of a university hospital. All eight patients had been extricated from buildings that collapsed in the 1995 Kobe, Japan, earthquake. Crush injury involved the upper extremities in one patient and the lower extremities in seven. Each patient received intravenous fluid infusion and diuretic drugs and underwent hemodialysis. Emergency fasciotomy was performed in some patients, 17 to 100 hours after extrication. RESULTS: All patients were conscious and lucid on admission, and blood pressure and heart rate were normal. All the patients demonstrated kidney failure with increased concentrations of serum creatinine (1.9 to 9.6 mg/dL [169 to 852 mumol/L]). Six patients were oliguric. Hyperkalemia (5.6 to 8.8 mEq/L) was present in six patients. We found close correlations between the serum potassium and creatine kinase concentrations, between the serum myoglobin and potassium concentrations, and between the serum myoglobin and creatine kinase concentrations. All the patients were weaned from hemodialysis. The serum creatinine concentration decreased to a normal level within 20 to 52 days of admission in all patients. No patients underwent amputation. Muscle weakness and sensory deficits persisted in all patients 6 months after the earthquake. CONCLUSION: Our findings support current therapeutic strategies for crush syndrome, despite the long delay to initiation of intensive therapy. All the patients recovered kidney function and were weaned from hemodialysis; none required amputation.

Acute Kidney Injury↗
PubMed1997

Switch from conventional to high-flux membrane reduces the risk of carpal tunnel syndrome and mortality of hemodialysis patients.

The use of a high-flux membrane, which eliminates larger molecular weight solutes with better biocompatibility, has steadily increased since the discovery of beta-2 microglobulin (beta 2m) amyloidosis in 1985. The long-term effects of a dialyzer membrane on morbidity and mortality are not completely understood. To examine the membrane effect as a factor of carpal tunnel syndrome onset and mortality, multivariate Cox regression analysis with time-dependent covariate was conducted on 819 patients from March 1968 to November 1994 at a single center. Two hundred and forty-eight of the patients were either switched from the conventional to high-flux membrane or treated only with a high-flux membrane. Fifty-one patients underwent a CTS operation and 206 died. Membrane status (on high-flux or on conventional) was considered as time-dependent covariate and risk was adjusted for age, gender, type of renal disease and calendar year of dialysis initiation. The relative risk of CTS was reduced to 0.503 (P < 0.05) and mortality 0.613 (P < 0.05) by dialysis on the high-flux membrane, compared to the conventional membrane. Serial measurements of beta 2m indicated significantly lower beta 2m to persist in patients on the high-flux membrane. The high-flux membrane decreased the risk of morbidity and mortality substantially. Larger molecule elimination was shown important not only for preventing beta 2m amyloidosis, but for prolonging survival of dialysis patients as well.

Adult↗
PubMed1997

Involvement of beta 2-glycoprotein I and anticardiolipin antibodies in oxidatively modified low-density lipoprotein uptake by macrophages.

Anticardiolipin antibodies (aCL) in the sera of patients with antiphospholipid syndrome (APS) recognize an altered structure of beta 2-glycoprotein I (beta 2-GPI) interacting with solid-phase negatively charged phospholipids. beta 2-GPI bound to Cu2+-oxidized plasma lipoproteins, i.e. oxidized very low-density lipoprotein (oxVLDL), oxidized low-density lipoprotein (oxLDL), or oxidized high-density lipoprotein (oxHDL). beta 2-GPI inhibited in vitro uptake, i.e. cell surface binding, cellular association, and proteolytic degradation of oxLDL by murine macrophage J774A.1 cells. The binding of oxLDL to the macrophages was inhibited by the addition of polyinosinic acid (poly (I)), a competitor of the scavenger receptor, but not by another polyanionic acid, polycytidylic acid (poly (C)). Conversely, the binding of oxLDL was significantly increased by the simultaneous addition of human beta 2-GPI and monoclonal aCL derived from NZW x BXSB F1 (WB F1) mice, an animal model of APS, or anti-beta 2-GPI antibodies from BALB/c mice immunized with human beta 2-GPI. These findings indicate that beta 2-GPI may be an antiatherogenic protein and that the autoimmune response against beta 2-GPI may have a role in the development of atherosclerosis in APS.

Animals↗
PubMed1997

Lectin affinity electrophoresis in a yolk sac tumour in the vagina with yolk sac tumour-type glycoform of alpha fetoprotein.

AIMS: To investigate a potential diagnostic use of alpha fetoprotein (alpha FP) isoform analysis by lectin affinity electrophoresis to distinguish between endodermal sinus tumours arising in the vagina in infants from those at other sites. METHODS: alpha FP in the serum of a patient with a vaginal endodermal sinus tumour was analysed for its isoforms by lectin affinity electrophoresis. The isoforms were compared with that of cord serum, sera of hepatoid adenocarcinoma of the uterus, and endodermal sinus tumour of the ovary. RESULTS: The isoforms of alpha FP obtained by lectin affinity electrophoresis in the serum of the patient with vaginal endodermal sinus tumour differed from the isoforms of alpha FP in the cord serum of normal neonates, and sera of patients with hepatoid adenocarcinoma of the uterus or endodermal sinus tumour of the ovary. CONCLUSIONS: Endodermal sinus tumour arising in the vagina could be distinguished from that in the ovary by the lectin affinity electrophoresis, and a potential diagnostic use of alpha FP isoform analysis by the lectin affinity electrophoresis for the detection of the endodermal sinus tumour in infants was demonstrated.

Diagnosis, Differential↗
PubMed1997

Early increase of chondroitin sulfate glycosaminoglycan in the glomerular basement membrane of rats with diabetic glomerulopathy.

A decrease in anionic change and the loss of heparan sulfate proteoglycan have previously been observed in the glomerular basement membrane (GBM) during diabetic glomerulosclerosis. We studied the chronological changes in the anionic character and the glycosaminoglycan content in the GBM of WBN/ Kob rats with spontaneous diabetes. Two types of cationic probes were used: polyethyleneimine (PEI) and cationic colloidal gold (CCG). Immunogold labeling was performed with anti-monoclonal-heparan-sulfate-glycosaminoglycan (HS-GAG) and anti-chondroitin-sulfate-glycosaminoglycan (CS-GAG) antibodies. The GBM width, the anionic sites and the GAG sites were investigated in diabetic WBN/Kob rats at 2, 10 and 19 months, compared with control rats. Diabetes was confirmed in WBN/Kob rats after 8 months in this study. The GBM width gradually thickened with age. The PEI anionic sites significantly decreased in the lamina rara externa (LRE) at 19 months (vs. 2 and 10 months). The HS-GAG sites also significantly decreased in the LRE at 10 and 19 months (vs. 2 months). However, the CCG anionic sites and the CS-GAG sites significantly increased in the LRE and the lamina densa at 10 months (vs. 2 months) and, after 19 months, returned to the level seen at 2 months. Results indicate that there is an early transient increase in CS-GAG in the GBM while HS-GAG decreases. We noticed a transient increase in the CCG anionic sites at this early stage of diabetic glomerulosclerosis as well. The increase in CS-GAG may provide a marker for early diabetic changes in the GBM.

Animals↗
PubMed1997

Histological localization of advanced glycosylation end products in the progression of diabetic nephropathy.

We studied the immunohistochemical localization of advanced glycosylation end products (AGEs) in the progression of diabetic nephropathy. Fourteen NIDDM patients with diabetic nephropathy were evaluated: 2 patients with normoalbuminuria, 4 with microalbuminuria (MA) and 8 with overt proteinuria (OP). Three patients with minor glomerular abnormalities were used as nondiabetic controls. Immunoreactivity to a monoclonal anti-AGE antibody (6D12) was recognized on the internal elastic membranes of arterial walls in every diabetic group. Hyaline lesions of arterioles of the MA and OP groups demonstrated strong reactions with 6D12. A portion of the nodular and exudative lesions in glomeruli of OP group patients also revealed immunoreactivity to 6D12. No immunoreactivity to 6D12 was observed in nondiabetic control specimens. We confirm that the accumulation of AGEs began in arterial walls of the early stage and presented in glomerular lesions of the late stage of the progression of diabetic nephropathy.

Adult↗
PubMed1997

Pathophysiological significance of the obese gene product, leptin, in ventromedial hypothalamus (VMH)-lesioned rats: evidence for loss of its satiety effect in VMH-lesioned rats.

To explore the pathophysiological significance of the obese (ob) gene product, leptin, in ventromedial hypothalamus (VMH)-lesioned rats, we examined the synthesis and secretion of leptin and its satiety effect in VMH-lesioned rats compared with those in sham-operated rats. Northern blot analysis revealed that ob gene expression is markedly augmented in the mesenteric and sc white adipose tissue, but remained unchanged in the epididymal white adipose tissue during the development of obesity in VMH-lesioned rats. Plasma leptin levels were relatively constant in sham-operated rats, but were elevated during the development of obesity in VMH-lesioned rats. In sham-operated rats, a single i.v. (1.0 mg/rat) or intracerebroventricular (2.0 micrograms/rat) injection of recombinant human leptin reduced food intake and body weight gain in sham-operated rats. By contrast, no significant effect on food intake or body weight gain was observed in VMH-lesioned rats. The present study provides evidence that VMH-lesioned rats overproduce leptin and increase its release but cannot respond to it and suggests that the loss of its satiety effect contributes to the development of obesity and the obesity-related phenotypes in VMH-lesioned rats.

Animals↗
PubMed1997

Glucocorticoid regulation of leptin synthesis and secretion in humans: elevated plasma leptin levels in Cushing's syndrome.

Leptin, the obese (ob) gene product, is an adipocyte-derived satiety factor that is involved in the regulation of food ingestion and body weight. To investigate glucocorticoid regulation of leptin synthesis and secretion in humans, we measured plasma leptin levels in patients with Cushing's syndrome with adrenal or pituitary adenoma and in patients with iatrogenic Cushing's syndrome. Plasma leptin levels in patients with Cushing's syndrome were significantly elevated compared to those in nonobese healthy subjects and obese subjects without any metabolic or endocrine diseases at a given percentage of body fat by analysis of covariance. In patients with adrenal or pituitary adenoma, after the tumor resection, plasma leptin levels were reduced, with a concurrent decrease in plasma cortisol levels. With no significant changes in body weight, plasma leptin levels were also elevated significantly in lean healthy volunteers 24 h after the administration of 1 mg dexamethasone. Dexamethasone potently induced ob gene expression and leptin secretion in the organ culture of human adipose tissue. The data demonstrate that glucocorticoids act, at least in part, directly on the adipose tissue and increase leptin synthesis and secretion in humans.

Adenoma↗
PubMed1997

Molecular screening of both the promoter and the protein coding regions in the human ob gene in Japanese obese subjects with non-insulin-dependent diabetes mellitus.

OBJECTIVE: Although the molecular mechanism of obesity has been poorly understood, recent studies indicate that leptin plays a critical role in regulating both food intake and body weight. Because obesity decreases the sensitivity to insulin, the human ob gene is presumed to be one of the candidate genes for non-insulin-dependent diabetes mellitus (NIDDM) associated with obesity. Although the protein coding region in the ob gene has been screened for mutations, the promoter region and the non-coding first exon have not yet been studied. We investigated the involvement of the human ob gene, especially mutations at the promoter region and the non-coding first exon, in the development of NIDDM associated with obesity. SUBJECTS: The study group comprised 60 Japanese obese subjects with NIDDM (body mass index (BMI) 43.6 > or = BMI > or = 26.4, 29.0+/-0.41 (mean+/-S.E.M.)) and 24 obese individuals with impaired glucose tolerance (IGT) (30 > or = BMI > or = 26.4, 27.1+/-0.22). METHODS: Mutations at both the promoter region and all three exons in the human ob gene were screened by the single-stranded conformational polymorphism analysis. When aberrantly migrated bands were recognized, the PCR-amplified DNA fragment was directly sequenced. RESULTS: In the protein coding region a silent mutation in the second exon was detected. The non-coding first exon and the about 100 bp 5'-flanking region of the gene which contains a proximal CCAAT/enhancer-binding protein site were screened, but no mutations were found. CONCLUSION: These results suggest that no mutations in either the promoter region at the about 100 bp 5'-flanking region of the gene, or in any of the three exons, are involved in the development of NIDDM or IGT associated with obesity.

Asian People↗
PubMed1997

Hemodynamic and metabolic disturbances in patients with intracranial dural arteriovenous fistulas: positron emission tomography evaluation before and after treatment.

In patients with intracranial dural arteriovenous fistulas (AVFs), clinical symptoms and angiographic findings vary. The relevance of disturbed venous drainage to clinical symptoms and prognosis has been recognized. However, the roles of cerebral hemodynamics and metabolism, which are impaired by shunt flow or disturbed venous drainage, have not been fully evaluated. The authors studied the cerebral hemodynamic and metabolic status in 10 patients with intracranial dural AVFs using positron emission tomography (PET) scanning. Ten patients with dural AVFs underwent a PET study before treatment. The regional cerebral blood flow (rCBF), regional oxygen extraction fraction (rOEF), regional cerebral metabolic rate of oxygen (rCMRO2), and regional cerebral blood volume (rCBV) were measured using the 15O-labeled gas inhalation steady-state method The PET parameters that were obtained were analyzed and compared with the patients' neurological and angiographic findings. In six of the 10 patients, a PET study was also performed after treatment. Before treatments, all four patients with cerebral symptoms showed a severe reduction in rCBF and a mild elevation in the rOEF. The areas showing reduced rCBF corresponded with areas in which retrograde venous drainage into the cortical veins and delayed parenchymal circulation were seen on angiograms. In another two patients with occlusion of the affected sinus and/or retrograde drainage into the cortical veins, mild abnormalities were demonstrated in rCBF mapping. In the remaining four patients, all PET parameters except rCBV were within normal limits and venous flow was not impaired on the angiograms. In four patients who underwent surgical excision or transvenous embolization of the affected sinus, the cerebral hemodynamics and metabolism were improved, as were the clinical symptoms. In two patients who underwent transarterial embolization of the feeding vessels only or craniotomy, no hemodynamic improvement was achieved. Our results indicate that hemodynamic insufficiency detected by the PET study corresponded well with cerebral symptoms and angiographic findings of retrograde venous drainage into the cortical veins and delayed parenchymal circulation, but not with sinus occlusion or arterial blood supply. Eradication or prevention of retrograde venous drainage from the affected sinus into the cortical veins should be a treatment goal in patients with dural AVFs.

Aged↗
PubMed1997

[The effects of vasoconstrictors on distribution of ischemic tissue flow in isolated perfused rat liver].

We studied the effects of ATP and epinephrine on distribution of ischemic hepatic tissue flow in the isolated perfused rat liver. Five minutes after clamping both the portal vein and hepatic artery, perfusion was started. Lidocaine was infused into the portal vein, and the concentration of lidocaine in hepatic outflow was measured with FPIA. The oxygen extraction ratio was also measured. Tissue surface blood flow was measured with laser-Doppler flowmetry. We measured the tissue flow at 2 points: one where flow was more than 10 ml.min-1.100 gm liver weight-1 (R), and the other where flow was less than 10 ml.min-1.100 gm liver weight-1 (P). After perfusion pressure had become stable, ATP or epinephrine was infused for 15 minutes. Perfusion pressure increased, and tissue flow of R decreased significantly, while that of P increased (not significantly). The extraction ratio of lidocaine decreased significantly by epinephrine, and that of oxygen decreased (not significantly). We conclude that in the ischemic liver, vasoconstriction results in changes in the distribution of tissue blood flow and alters drug metabolism.

Adenosine Triphosphate↗
PubMed1997

Detection of embolic signals during and after percutaneous transluminal angioplasty of subclavian and vertebral arteries using transcranial Doppler ultrasonography.

OBJECTIVE: Percutaneous transluminal angioplasty (PTA) is accepted as a safe and effective procedure for the treatment of stenotic arterial lesions of various sites. However, distal embolism may cause serious complications in the PTA of cephalic arteries. By monitoring embolic signals using transcranial Doppler (TCD) ultrasonography, we speculated regarding the safety and/or risk of PTA for vertebral and subclavian artery stenosis. METHODS: Twelve consecutive patients undergoing PTA for subclavian and vertebral artery stenosis of atherosclerotic origin were studied. All patients were refractory to initial medical treatment and were considered for PTA. During the PTA procedure, all patients were heparinized. Before, during, and after PTA, TCD monitoring was performed to detect embolic signals for 30 minutes at each time. After PTA, anticoagulant and antiplatelet therapies were continued in all patients. RESULTS: Before, during, and after PTA, a steady flow signal could be obtained from each vertebral artery monitored using TCD ultrasonography. No embolic signals were detected in any patient before angioplasty. During angioplasty, one embolic signal was detected immediately after balloon deflation in 1 of 12 patients. Several embolic signals were detected after the procedure in 6 of 12 patients, but thereafter embolic signals became less frequent in number. Three days after angioplasty, embolic signals were not detected in any patient. There were no serious complications caused by the PTA procedure. CONCLUSION: TCD monitoring may be a useful modality for detection of microemboli during and after PTA in the posterior circulation. We suspected that subclinical microemboli are released from the dilated vessels for 3 days after vertebral and subclavian PTA and that anticoagulant or antiplatelet therapies may prevent embolic complications after the procedure.

Aged↗
PubMed1997

Differential expression of maf-1 and maf-2 genes in the developing rat lens.

PURPOSE: To examine the expression of maf-1 and maf-2 protocogenes in the developing rat lens. METHODS: Maf-1 and maf-2 transcripts were assayed in rat lenses on embryonic days 13 and 16 (E13 and E16) by in situ hybridization using single-stranded RNA probes. Proteins encoded by the maf-2 gene were assayed immunocytochemically in embryonic (E12, 13, 16, 19) and postnatal day 14 and 90 (P14 and P90) lenses. RESULTS: In embryonic lenses, we detected maf-1 messenger RNA (mRNA) in the lens epithelium and maf-2 mRNA diffusely distributed in the lens fiber cells. By immunocytochemistry, Maf-2 was detected on E12 in the nuclei of almost all lens pit cells. On days E13, E16, and E19, however, lens epithelial cells showed no immunoreactivity, but nuclei of fiber cells reacted strongly. On P14, nuclei containing Maf-2 protein were confined to the equator of the lens, but at 3 months of age, no Maf-2 could be detected in the rat lens. Western blotting showed that the anti-Maf-2 antiserum reacted with a single protein, of molecular weight approximately 39 kDa, in rat lens. CONCLUSIONS: Results showed the spatial and temporal regulation of maf gene expression and suggest that these genes participate in transcriptional regulation during the development of the lens in the rat.

Animals↗