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N Sakamoto

Publications and source records attributed to N Sakamoto.

At least 271 records · Page 15Linked to original sources
PubMed1991

Prognostic factors and value of adjunctive nephrectomy in patients with stage IV renal cell carcinoma.

We reviewed 57 cases of Stage IV renal cell carcinoma to clarify the factors influencing prognosis and to evaluate the value of nephrectomy. Cumulative survival from the initial diagnosis was analyzed with respect to the patients' age, sex, side of primary tumor, initial performance status (PS), site of metastasis, and nephrectomy. Overall survival for the patients was 51 percent at one year, 22 percent at three years, and 11 percent at five years. Age, sex, and side of primary tumor had no influence on survival. Improved survival was correlated with good PS, metastases limited to single organ, and removal of the primary tumor. With regard to histopathologic features in nephrectomized patients, low grade and stage were correlated with longer survival. These factors should be considered in the analysis of results of future clinical trials of metastatic renal cell carcinoma.

Aged↗
PubMed1991

Dissociation of hyperthermic and hyperglycemic effects of central prostaglandin F2 alpha.

We previously reported that intraventricular prostaglandins (PGs) produced hyperthermia and hyperglycemia in anesthetized rats. However, the relationship of them is little known. We examined the relationship between hyperthermia and hyperglycemia induced by intraventricular PGF2 alpha using curarized and adrenal demedullated rats. Iv curare completely prevented the PGF2 alpha-induced hyperthermia, but enhanced the hyperglycemic effect of PGF2 alpha. Adrenal demedullation completely prevented the hyperglycemia, but did not affect the hyperthermic effect of PGF2 alpha. To further assess the site of action concerned with PGF2 alpha-induced thermoregulation and glucoregulation in the central nervous system (CNS), we injected saline or PGF2 alpha into the preoptic area of the anterior hypothalamus (POA) in intact rats. After microinjection of PGF2 alpha into the POA, the rectal temperature rose, but the plasma glucose level did not increase significantly, as compared with saline-treated control rats. These results suggest that PGF2 alpha causes the central nervous system to produce hyperthermia via shivering, stimulated the somatic motor system, and to produce hyperglycemia by stimulating central sympathetic outflow to the adrenal medulla, but these operate independently under different neural regulation, and these sensitive sites are organically dissociated in the CNS.

Adrenal Medulla↗
PubMed1991

In vitro retinal and erythrocyte polyol pathway regulation by hormones and an aldose reductase inhibitor.

The effects of a high-glucose medium, insulin, and an aldose reductase inhibitor (ONO-2235) on sorbitol accumulation were compared in the human erythrocyte and the rabbit retina, while the effects of epinephrine on in vitro sorbitol accumulation were investigated in the human and rabbit retina. In both erythrocytes and the retina, linear increments of sorbitol accumulation were observed in a dose-dependent manner with 5 to 50 mM glucose. These increments were markedly inhibited by 100 microM ONO-2235 but not by insulin (400 microU/ml). In the presence of 5 mM glucose, a dose-dependent increase of the sorbitol content of the rabbit retina was seen following epinephrine stimulation (0.4-4.0 microM and this was markedly reduced by 100 microM ONO-2235. Moreover, both 50 mM glucose and 4.0 microM epinephrine increased the sorbitol content of the retina from a diabetic patient, and the glucose-induced increment in sorbitol was significantly reduced by 100 microM ONO-2235. Our data suggested that aldose reductase inhibitors might be useful for the treatment of diabetic retinopathy, since the polyol pathway appears to be an important factor in its pathogenesis, and that catecholamines might have some role in the activation of the retinal polyol pathway.

Aged↗
PubMed1991

Preparation and properties of a lysozyme derivative in which two domains are cross-linked intramolecularly between Trp62 and Asp101.

A lysozyme derivative in which two domains were cross-linked intramolecularly was newly prepared by means of a two-step reaction. First, the beta-carboxyl group of Asp101 in lysozyme was selectively modified with 2-(2-pyridyldithio)ethylamine in the presence of 1-ethyl-3-[3-(dimethylamino)propyl]carbodiimide hydrochloride. After reduction of the pyridyldithio moiety of Asp101 modified lysozyme at pH 4.5 with dithiothreitol, the derivative was allowed to cross-link intramolecularly by reaction with 1,3-dichloroacetone at pH 7. Intramolecularly cross-linked lysozyme thus formed was purified by gel chromatography followed by ion-exchange chromatography. Based on the results of 1H-NMR and peptide analyses, it was concluded that Asp101 was cross-linked to Trp62 with a -CH2COCH2SCH2CH2NH-bridge in this derivative. The derivative showed minor but distinct activity against Micrococcus lysodeikticus and glycol chitin. Its melting temperature for thermal denaturation was higher by 7.3 degrees than that of native lysozyme at pH 3.

Amino Acid Sequence↗
PubMed1991

Sclerosing adenosis of the prostate. Histopathologic and immunohistochemical analysis.

A prostatic lesion, histologically identical to sclerosing adenosis of the breast, was found in five (1.9%) of 263 patients who underwent transurethral resection, open prostatic adenectomy, radical prostatectomy, or total cystoprostatectomy. This uncommon lesion was a localized proliferation of crowded small glands, small solid nests, and individual cells embedded in a cellular stroma, mimicking a small acinar prostatic adenocarcinoma. The proliferating glands were lined by a single layer of secretory cells surrounded by an eosinophilic membranous structure. Basal cells were disclosed in individual glands or as small nests and even individual cells with immunostainability for basal cell-specific cytokeratin (EAB903), S-100 protein, and muscle-specific actin (HHF35). These findings indicate the benign nature of the lesion with myoepithelial differentiation of the basal cells. In contrast, all 25 small acinar adenocarcinomas examined as controls lacked positive stains for the above three antibodies, verifying the usefulness of these antibodies to distinguish between this benign lesion from adenocarcinoma.

Acid Phosphatase↗
PubMed1991

Formation of subepithelial dense deposits in rats induced by a monoclonal antibody against the glomerular cell surface antigen.

We developed a monoclonal antibody, H5H3, of IgG1 subclass by hybridization technique using spleen cells of mice immunized with plasma membrane fraction of isolated rat glomeruli. H5H3 recognized main bands at about 220 kD by immuno-overlay technique and bound to the glomerulus as well as brush border of proximal tubules by indirect immunofluorescence (IF) microscopy on normal rat kidney frozen sections. By immunoelectron microscopy (IEM) it bound to the surface of mainly glomerular epithelial cell and weakly to the endothelial cell. After injection to Wistar rats it remained granularly in the glomerulus for more than 2 weeks seen by IF. When rats were preimmunized with murine IgG 4 days before the injection of H5H3, mouse IgG, rat IgG and C3 were strongly visible granularly in the glomerulus in 14 days by IF. Numerous dense deposits were formed at subepithelial area seen by transmission electron microscopy. Perfusion experiment of H5H3 into rat left kidney showed granular distribution of mouse IgG in 48 h, indicating that the reaction occurred in situ. H5H3 bound diffusely in fine granular pattern on the surface of cultured glomerular epithelial cells (GEC) studied by IF and IEM. Antigenic redistribution occurred on GEC after incubation of H5H3 at 37 C. These results suggested the required conditions to form subepithelial immune dense deposits, namely that H5H3 after reaction with antigen could stay for long time in the glomerulus; that H5H3 became an antigen in autologous phase to induce large immune complexes; and H5H3 could induce antigenic modulation.

Animals↗
PubMed1991

Localization of 20-kD homologous restriction factor (HRF20) in diseased human glomeruli. An immunofluorescence study.

The 20-kD homologous restriction factor (HRF20), which is identical to CD59, is a membrane-associated protein which inhibits the reaction of C9 to form membrane attack complex (MAC) of homologous complements. In various human glomerular diseases deposition of complement components is frequently seen and MAC is reported to associate with immune deposits. Using a specific monoclonal antibody, 1F5, against HRF20, we attempted to study the localization of HRF20 in human glomerulonephritides and to compare the localization of HRF20 with those of immune deposits and MAC. The frozen sections of kidney specimens were fixed in acetone at room temperature before staining. In normal kidneys and kidney specimens from the patients with minimal change nephrotic syndrome, membranous nephropathy, and IgA nephropathy, HRF20 was strongly localized in the peritubular capillaries and along Bowman's capsules. A weaker but well-defined staining was obtained in the mesangial area and faint staining was seen along the glomerular capillary walls. In contrast, glomerular capillary walls were rather strongly stained in the cases with diffuse lupus nephritis which had subendothelial dense deposits. These data suggest that HRF20 (CD59) is present in the human glomeruli and its expression is enhanced under certain conditions such as lupus nephritis.

Antigens, Differentiation↗
PubMed1991

CNS stimulation does not affect hepatic venous glucose concentration in severely diabetic rats.

To assess the role of the central nervous system (CNS) in carbohydrate metabolism in diabetes, neostigmine was injected into the third cerebral ventricle in fed rats with streptozotocin (STZ; 80 mg/kg)-induced diabetes under pentobarbital sodium anesthesia. Changes in hepatic venous plasma glucose concentrations were monitored. Neostigmine injection caused no significant changes in the hepatic venous plasma glucose concentration in untreated diabetic rats, whereas the glucose level increased significantly in insulin-treated diabetic rats similarly to the changes in normal control animals. In diabetic rats, the plasma levels of glucagon, epinephrine, and norepinephrine were increased significantly by neostigmine. After various doses (35-80 mg/kg) were given to rats, it was found that the higher the STZ dose, the lower was the hepatic glycogen content and the smaller was the glycemic response to neostigmine. Our results indicate that, in severe diabetes, CNS stimulation with neostigmine fails to increase hepatic glucose output, because glycogen stores are nearly exhausted and gluconeogenesis is already maximal.

Animals↗
PubMed1991

Relative contribution of nervous system and hormones to hyperglycemia induced by thyrotropin-releasing hormone in fed rats.

In a continuation of our studies on the mechanism of central nervous system induced hyperglycemia in the rat, we evaluated the relative contribution of a direct neural effect on the liver and of certain hormones to the hyperglycemia induced by administration of thyrotropin-releasing hormone (TRH). The findings were compared with those of a previous investigation using neostigmine or 2-deoxy-D-glucose. In the present study TRH was injected into the third cerebral ventricle of rats, and the concentrations of hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine, were measured. Four groups of animals were evaluated: (1) intact rats; (2) rats receiving an infusion of somatostatin with insulin via the femoral vein to inhibit glucagon secretion and to maintain the basal insulin level; (3) rats bilaterally adrenalectomized (ADX) to prevent epinephrine secretion, and (4) ADX rats administered an infusion of somatostatin and insulin. Evaluation of the areas under the glucose curves for the rats receiving somatostatin with insulin, ADX rats, and ADX rats receiving somatostatin with insulin showed values 202, 50, and 79% of those observed in intact animals. These observations suggest that TRH-induced hyperglycemia results from at least two effects: a direct neural effect on the liver including a suppressive effect of epinephrine on insulin secretion (contributing about 79% to the total hyperglycemic effect) and a direct effect of epinephrine on the liver (contributing about 21% to the total hyperglycemic effect).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1991

Unique glomerular lesion with spontaneous lipid deposition in glomerular capillary lumina in the NON strain of mice.

We found a strain of nonobese, nondiabetic (NON) mice which has spontaneous lipid deposition in glomerular capillary lumina. This strain was developed together with a diabetic strain of nonobese diabetic (NOD) mice for the generation of mouse models of diabetes mellitus. In the NON strain, contrary to the name, impaired glucose tolerance (IGT) was observed in about half of the mice. Meanwhile, peculiar glomerular abnormalities which remotely resemble those of diabetic nephropathy were observed in the NON strain. The lesions were characterized by massive lipid accumulation with proteinaceous material within the glomerular capillary lumina. In addition, positive staining for immunoglobulins, especially IgM, was observed by immunofluorescence microscopy. The overall frequency of this lesion was 91%. Mesangiolysis, capillary ballooning with many small lipid vesicles were the striking features by electron microscopy. Histochemical analysis revealed the presence of various lipids in these lesions. However, as far as we examined, these lesions did not correlate with hyperlipidemia or IGT. Lymphoid follicle-like structures were seen around the renal arterioles. The cellular components of these lymphoid follicles reacted with monoclonal antibodies to L3T4. High levels of serum immunoglobulins were observed in this strain. We suppose that the immunological disorders may have some bearing in the evolution of this lesion in NON mice. We believe that this model may be of use in studying the role of lipid derangements in renal diseases.

Animals↗
PubMed1991

Recurrence of bladder tumors following surgery for transitional cell carcinoma of the upper urinary tract.

A retrospective analysis of 53 patients with an upper urinary tract (UUT) transitional cell carcinoma, which was treated surgically, was performed in relation to the development of a subsequent bladder tumor. In 19 of the 53 patients (35.8%) bladder tumors developed following surgery of a UUT tumor. The simultaneous occurrence of a bladder tumor and more than two tumors in the UUT had a significant influence on the rate of bladder tumor recurrence. On the other hand, location, mode of growth, grade, stage and vascular invasion of the UUT tumor, and history of bladder tumors did not seem to be related to the frequency of subsequent bladder tumors. These findings suggest that the diversity of UUT tumors at the time of diagnosis is an important factor in bladder tumor recurrence. Therefore, clinical and pathological examinations should be carefully performed in patients with UUT tumors.

Aged↗
PubMed1991

Ischemic myocardial mitochondrial function and ultrastructural change--influence of regional myocardial blood flow.

Myocardial blood flow (MBF), tissue ATP content, mitochondrial respiratory function and mitochondrial ultrastructure were examined in 62 adult mongrel dogs weighing 6-14 kg in which acute myocardial ischemia had been produced under anesthesia. The left anterior descending coronary artery was dissected free for ligation before the first diagonal branch. MBF was measured before coronary ligation and 60 min following ligation. Then, samples of myocardium were taken and subjected to tissue ATP content assay, mitochondrial respiratory function measurement respiratory control index (RCI) and rate of oxygen consumption in state III (QO2III); and electron microscopic examination. Mitochondrial morphologic injury was evaluated quantitatively according to Schaper's criteria. MBF was significantly correlated with tissue ATP content, mitochondrial respiratory function and mitochondrial ultrastructural change. When MBF was less than 20 ml/min/100g, tissue ATP content (1.86 +/- 1.21 mumol/g wet weight) and mitochondrial respiratory function (RCI 2.51 +/- 0.59) were significantly lower than in the non-ischemic area (ATP 4.52 +/- 1.11, RCI 3.82 +/- 0.37), and mitochondrial ultrastructural injury had deteriorated significantly at an MBF below 40 ml/min/100 g. In conclusion, our findings show that when MBF is reduced, mitochondrial ultrastructural changes precede the depression in mitochondrial oxidative phosphorylation.

Adenosine Triphosphate↗
PubMed1991

Exonic point mutations in NADH-cytochrome B5 reductase genes of homozygotes for hereditary methemoglobinemia, types I and III: putative mechanisms of tissue-dependent enzyme deficiency.

We analyzed the NADH-cytochrome b5 reductase gene of hereditary methemoglobinemia type I and type III, by using PCR-related techniques. The mutation in type I is a guanine-to-adenine substitution in codon 57 of exon 3 of the NADH-cytochrome b5 reductase gene, and the sense of this codon is changed from arginine to glutamine. In type III the mutation is a thymine-to-cytosine transition in codon 148 of exon 5, causing leucine-to-proline replacement in type III. The former mutation abolishes the MspI recognition site. Homozygosity for the former mutation in a patient with type I was confirmed by restriction analysis of PCR-amplified fragments and by dot blot hybridization of amplified products with allele-specific oligonucleotide probes. The latter mutation generates a recognition site for MspI. Amplification of exon 5 by PCR followed by digestion with MspI revealed homozygosity for this mutation in patients with type-III. Putative mechanisms of tissue-dependent enzyme defects in hereditary methemoglobinemia are discussed.

Adult↗
PubMed1991

Distribution of interleukin-6 in normal and diseased human kidney.

Distribution of interleukin 6 (IL-6) in normal and diseased kidneys was examined by an immunohistochemical method. Four specimens of normal kidney tissue and 47 specimens obtained from diseased kidneys by biopsy were studied by indirect immunofluorescence microscopy using specific monoclonal antibody to human IL-6. In the normal kidney, IL-6 was distributed in the glomerular mesangial area and in vascular walls. In the diseased kidneys, IL-6 was observed in the glomerulus in various patterns. The extent of the distribution of IL-6 correlated with the average number of glomerular cells. When sclerosis appeared, the expression of IL-6 decreased. Occasionally, IL-6 was found in the area of synechiae or crescents as well as in the parietal epithelial cells of the glomerulus with synechiae and/or crescents. In the interstitium, IL-6 was seen in atrophic tubules, and the distribution correlated with the extent of tubular atrophy. The binding of anti-IL-6 monoclonal antibody to the renal sections was completely inhibited by preincubation of the antibody with recombinant IL-6. These results suggests that IL-6 expression is a good marker for glomerular cell proliferation and that IL-6 may be involved in the formation of synechiae or crescents and in tubulointerstitial injury.

Antibodies, Monoclonal↗
PubMed1991

Histochemical and immunohistochemical studies of diseased human glomeruli.

In order to study the localization of Lentil lectin (LCH)-binding glycoresidues in glomeruli from patients with a variety of glomerulopathies, and to elucidate the relationship between LCH-binding sugars and the components of the extracellular matrix, laminin and type IV collagen, investigations of formalin-fixed, paraffin-embedded kidney tissues digested with trypsin were carried out by the direct and indirect immunofluorescence microscopy techniques. The glomerular basement membrane (GBM) and the mesangium reacted well with LCH, whereas areas with sclerotic lesions exhibited a decreased reactivity. The pattern of LCH binding to the GBM in various glomerulopathies was similar to that of laminin but different from that of type IV collagen. The pattern of localization of LCH-reacting sites and of laminin in the GBM included the double linear lines in diabetic nephropathy, inner linear line with outer projections (spikes) in membranous nephropathy, and reduplicated basement membrane in membranoproliferative glomerulonephritis. The results obtained by enzyme-linked immunoadsorbent assay showed that LCH had a stronger reactivity for laminin than for type IV collagen or fibronectin. These findings suggest that LCH is more reactive with laminin than with other components of the glomerular extracellular matrix.

Carbohydrates↗