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S Maeda

Publications and source records attributed to S Maeda.

At least 91 records · Page 5Linked to original sources
PubMed2001

Use of electron microscopic evaluation for the diagnosis of adrenal cortical carcinoma in fine needle aspiration cytology: a case report and review of the literature.

Bilateral adrenal tumors were detected in a 72-year-old man who had a history of hepatic inflammatory pseudotumor. Computet tomography (CT)-guided fine needle aspiration cytology (FNAC) of the adrenal glands was performed. The cytologic findings were similar to the previous diagnosis of "inflammatory pseudotumor" in the liver. However, the origin of some aggregated large atypical cells observed in the adrenal FNAC specimens was not known. Immunocytochemically, these large atypical cells were positive for vimentin and negative for cytokeratin and chromogranin A. An electron-microscopic study showed that these large atypical cells contained mitochondria with tubulovesicular cristae and smooth endoplasmic reticulum arranged in whorled and laminated patterns, and these findings confirmed diagnosis of primary adrenal cortical carcinoma. The histopathological diagnosis of the resected bilateral adrenal tumor was adrenal cortical carcinoma. The patient died 7 months after surgery, with recurrence of the bilateral adrenal cortical carcinoma and extensive metastases. A diagnosis of primary adrenal cortical carcinoma with extensive metastases was finally demonstrated by autopsy. Retrospectively, the previous liver tumor was determined to be a metastatic lesion.

Adrenal Cortex Neoplasms↗
PubMed2001

Establishment of an optimized set of 406 microsatellite markers covering the whole genome for the Japanese population.

Microsatellites, an essential tool for genetic linkage analyses, are selected in genetic studies on the basis of both informativeness and their positions with respect to one another on the genetic map. In order to establish a microsatellite marker set useful for linkage studies in the Japanese population, we first genotyped 64 unrelated Japanese subjects, using 400 microsatellite markers from a commercially available set (ABI PRISM Linkage Mapping Set-MD10) and then determined the allelic frequencies and heterozygosities for these marker loci in the population. In order to optimize the set, we replaced 41 markers having a heterozygosity lower than 0.6 with as many informative markers in the corresponding loci, and newly added six markers in the set to minimize the several gaps found at intervals of over 20 cM. We finally established a set comprising 406 microsatellites with average intervals of 9cM (maximum, 17 cM) and minimum heterozygosities of over 0.6 (mean, 0.76). All data generated in this study, including the specific polymerase chain reaction (PCR) primer sequences of the newly added markers, are freely available to all researchers at our web site. The genetic tool established here should facilitate genetic linkage studies of various hereditary diseases, especially in the Japanese.

Alleles↗
PubMed2001

Gender-specific haplotype association of collagen alpha2 (XI) gene in ossification of the posterior longitudinal ligament of the spine.

Among Japanese, ossification of the posterior longitudinal ligament of the spine (OPLL) is a leading cause of myelopathy, showing ectopic bone formation in the paravertebral ligament. We have provided genetic evidence that the collagen alpha2 (XI) (COL11A2) locus of chromosome 6 constitutes susceptibility for OPLL. Five distinct single nucleotide polymorphisms (SNPs), identified in COL11A2, were combined to construct possible haplotypes by the use of a maximum likelihood program. Estimated haplotype frequency was compared in OPLL patients and non-OPLL controls. We report a gender-specific association of the COL11AA2 haplotvpe with OPLL. The frequency of the most commonly observed haplotype was significantly higher in male patients (P = 0.0003) compared with controls, but not in female patients (P = 0.21). OPLL is predominantly observed in males. with a prevalence ratio of 2:1, and our gender-specific associations indicate that genetic factors involving COL11A2 play a specific role in the etiology of OPLL exclusively in males.

Aged↗
PubMed2001

Subnuclear distribution of afferents from the oral, pharyngeal and laryngeal regions in the nucleus tractus solitarii of the rat: a study using transganglionic transport of cholera toxin.

The central distributions of afferents from the oral cavity, the pharynx, the larynx and the esophagus to the nucleus tractus solitarii (NTS) were examined by using transganglionic anterograde transport of the cholera toxin B subunit (CT-b). Injections of CT-b into the body of the tongue and the hard palate resulted in heavy labeling of the lateral subnucleus (l-NTS) of the NTS rostral to the area postrema. Injection into the root of the tongue resulted in heavy labeling of the l-NTS, the dorsal half of the medial (m-NTS), the intermediate (im-NTS) and the interstitial (is-NTS) subnuclei rostral to the area postrema. Injections into the soft palate and the pharynx resulted in a similar labeling pattern in the is-NTS, im-NTS and m-NTS to that in the case of the root of the tongue, but this labeling extended rostrocaudally. Heavy labeling of the medial aspect of the l-NTS was found in the case of the soft palate, but the labeling was sparse in the case of the pharynx. Moderate labeling was also found in the commissural subnucleus (co-NTS). Injection into the larynx resulted in labeling of the is-NTS throughout the NTS, and of the rostral half of im-NTS. Injection into the esophagus resulted in heavy labeling of the central subnucleus, and moderate labeling of the co-NTS and the caudal half of im-NTS. A few but consistent anterogradely labeled terminals were found to appose retrogradely labeled small neurons in the rostral tip of the dorsal motor nucleus of vagus in the cases of injections into the root of the tongue, the soft palate, the pharynx, and the larynx. These results have characterized the viscerotopic representation of afferent projections from the oral and the cervical visceral organs to the subnuclei of the NTS.

Afferent Pathways↗
PubMed2001

Enhancement of glomerular heme oxygenase-1 expression in diabetic rats.

An increase in oxidative stress in diabetic subjects is implicated to play a pivotal role in diabetic vascular complications. In response to oxidative stress, antioxidant enzymes are considered to be induced and protect cellular functions to keep in vivo homeostasis. However, it remains to be clarified whether antioxidant enzymes are induced against oxidative stress especially in renal glomeruli at an early stage of diabetes. To answer this question, we examined the gene expression of a variety of antioxidant enzymes in glomeruli isolated from streptozotocin-induced diabetic rats. The mRNA expression of antioxidant enzymes such as catalase, glutathione peroxidase, and CuZn-superoxide dismutase, was unaltered in glomeruli of diabetic rats and was comparable to control rats. In contrast, the mRNA expression of heme oxygenase-1 (HO-1) was enhanced in glomeruli of diabetic rats as compared with control rats. A treatment with insulin as well as with vitamin E (40 mg/kg body weight every other day, intra-peritoneal injection) normalized the mRNA expression of HO-1 in the glomeruli of diabetic rats. Immunohistochemical analysis revealed that the up-regulated expression of HO-1 protein was localized in glomerular cells of diabetic rats. In conclusion, these results provide the first evidence that among antioxidant enzymes HO-1 expression is preferentially increased in diabetic glomeruli.

Animals↗
PubMed2001

Metalloproteinase activity in growth plate chondrocyte cultures is regulated by 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) and mediated through protein kinase C.

During endochondral development, growth plate chondrocytes must remodel their matrix in a number of ways as they differentiate and mature. In previous studies, we have shown that matrix metalloproteinases (MMPs) extracted from matrix vesicles can extensively degrade aggrecan and that this is modulated by vitamin D metabolites in a manner involving protein kinase C (PKC). Matrix vesicles represent only a small component of the extracellular matrix, however, and it is unknown if the total metalloproteinase complement, including the MMPs and aggrecanases in the culture, is also regulated in a similar way. This study tested the hypothesis that vitamin D metabolites regulate the level of metalloproteinase activity in growth plate chondrocytes via a PKC-dependent mechanism and play a role in partitioning this proteinase activity between the media and cell layer (cells+matrix) in these cultures. To do this, resting zone cells (RC) were treated with 10(-9)-10(-7) M 24R,25-(OH)(2)D(3), while growth zone cells (GC) were treated with 10(-10)-10(-8) M 1alpha,25-(OH)(2)D(3). Cultures of both cell types were also treated with the PKC inhibitor chelerythrine in the presence and absence of vitamin D metabolites. At harvest, the media were either left untreated or treated to destroy metalloproteinase inhibitors, while enzyme activity in the cell layers was extracted with buffered guanidine and then treated like the media to destroy metalloproteinase inhibitors. Neutral metalloproteinase (aggrecan-degrading activity) activity was assayed on aggrecan-containing polyacrylamide gel beads and collagenase activity was measured on telopeptide-free type I collagen. Neutral metalloproteinase activity was found primarily in the cell layer of both cell types; however, activity was greater in extracts of GC cell layers. No collagenase activity could be detected in RC extracts until the metalloproteinase inhibitors were destroyed. In contrast, extracts of GC cell layers contained measurable activity without removing the inhibitors, and destroying the inhibitors resulted in a greater than two-fold increase in activity. No collagenase activity was found in the media of either cell type. 24,25-(OH)(2)D(3) caused a dose-dependent increase in neutral metalloproteinase activity in extracts of RC cells, but had no effect on collagenase activity. In contrast, 1,25-(OH)(2)D(3) caused a dose-dependent decrease in collagenase activity in extracts of GC cells, but had no effect on neutral metalloproteinase activity. In both cases, the effect of the vitamin D metabolite was mediated through the activation of PKC. These results support the hypothesis that metalloproteinases are involved in regulating the bulk turnover of collagen and aggrecan in growth plate chondrocytes and that the amount of metalloproteinase activity found is a function of the cell maturation state. Furthermore, 83-93% of neutral metalloproteinase activity and 100% of collagenase activity is localized to the cell layer. Moreover, the regulation of metalloproteinase activity by 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) involves a PKC-dependent pathway that is controlled by the target cell-specific vitamin D metabolite.

24,25-Dihydroxyvitamin D 3↗
PubMed2001

Glut1 expression in T1 and T2 stage colorectal carcinomas: its relationship to clinicopathological features.

Glucose uptake is mediated by glucose transporter (Glut) proteins, which exhibit altered expression in a variety of malignant neoplasms. Glut1 expression is thought to be a potential marker for malignant transformation. The aim of the present study was to investigate the expression of Glut1 protein in colorectal adenomas, T1 and T2 stage carcinomas. Immunohistochemical detection of Glut1 protein was examined in 141 formalin-fixed and paraffin-embedded colorectal tumour specimens (57 adenomas, 84 carcinomas). The degree of Glut1 immunostaining of a specimen was graded according to the proportion of Glut1-positive cells in it; absent (positive cells are 0%), weakly positive (less than 10%), moderately positive (10-50%), and strongly positive (more than 50%). Glut1 expression was present in 18% of the adenomas with low-grade dysplasia, and in 63% of the adenomas with high-grade dysplasia. The positivity in such lesions was usually weak, but was moderate in 8% of the adenomas with high grade dysplasia. For the carcinomas, there were significant correlations between Glut1-positivity and depth of invasion (T1 45% versus T2 74%, P<0.01), histological differentiation (well 49% versus moderately to poorly 74%, P< 0.05) and morphological type (polypoid 42% versus depressed 73%, P< 0.05), if the cut-off value was set at 10% of cells. In conclusion, we clarified the relationship between Glut1 expression and clinicopathological features in T1 and T2 stage colorectal carcinomas, and our results suggested a high malignant potential of the depressed-type carcinoma.

Adenocarcinoma↗
PubMed2001

The problems of medical malpractice litigation in Japan: the significant factors responsible for the tendency of patients to avoid litigation.

The present research has demonstrated that the Japanese tendency to avoid medical malpractice litigation can be ascribed to Japan's medical malpractice litigation system, and not the Japanese legal consciousness. From this standpoint, the present research has made clear the specific problem areas of the litigation system by looking at all cases from the last 10 years in the main district courts. The total average time taken for medical malpractice litigation is 3.0 years - much longer than the average time for normal litigation. Furthermore, the average amount of money needed to bring a medical malpractice complaint was 2,200,000 yen, far too much for the patient's family to bear. We have also demonstrated to what extent the amount is inversely related to the patient's age. Naturally, it is possible to bring a case without reliance on a lawyer, but in 90.0% of cases a lawyer was employed, and the success rate of litigants that had not employed a lawyer was 0%. Through the above discussion, we have show the present situation regarding time and costs in medical malpractice litigation, and it is suggested that these are the important reasons why medical malpractice disputants demonstrate a tendency to avoid litigation.

Journal Article↗
PubMed2001

Isolated unilateral absence of a pulmonary artery: influence of systemic circulation on alveolar capillary vessels.

We report a case of isolated unilateral absence of a pulmonary artery. The first clinical symptom that was manifested in the patient was recurrent hemoptysis, and subsequent angiography revealed that the main pulmonary artery was absent in the right lung, which was being fed only from the systemic circulation. Right pneumonectomy was performed, and neither the main pulmonary artery nor its remnant was detected in the resected right lung. Histologically, there were many muscular vessels in the resected lung, with intimal proliferation, or with plexiform-like lesions. The alveolar septum was moderately thickened and alveolar capillary vessels were dilated. We examined the alveolar capillary endothelial cells of the resected lung for immunoreactivity to thrombomodulin (TM) and von Willebrand factor (vWF). The endothelial cells were negative for TM and positive for vWF, while in the normal lung control group, these cells were positive for TM and negative for vWF. We considered that the hemodynamics of the systemic circulation in the resected lung caused the alteration of immunohistochemical characteristics in alveolar capillary endothelial cells.

Adult↗
PubMed2001

Dinucleotide repeat polymorphism of matrix metalloproteinase-9 gene is associated with diabetic nephropathy.

BACKGROUND: Although genetic susceptibility has been proposed as an important factor for the development and progression of diabetic nephropathy, the definitive gene has not been identified. To identify the genetic marker for diabetic nephropathy, we examined the association between the (A-C)n dinucleotide repeat polymorphism upstream of the matrix metalloproteinase-9 (MMP-9) gene and diabetic nephropathy in a group of Japanese patients with type 2 diabetes. METHODS: Patients were divided into three groups based on their urinary albumin excretion rate (AER) and the stage of diabetic retinopathy as follows: uncomplicated group (U), normal albuminuria (AER <20 microg/min) without proliferative retinopathy and with the duration of diabetes more than 20 years (N = 32); microalbuminuria group (M), 20 < or = AER < 200 microg/min (N = 155); overt nephropathy group (O), AER > or = 200 microg/min (N = 63). The region containing the dinucleotide repeat upstream of MMP-9 gene was amplified by polymerase chain reaction (PCR). The amplified products were analyzed with 7% formamide/urea acrylamide gel electrophoresis. The promoter constructs of the MMP-9 gene were transfected with the CMV-beta-galactosidase construct into 293 cells using the liposome method. Twenty-four hours after transfection, cells were harvested, and luciferase and beta-galactosidase activities were measured. RESULTS: Nine alleles of the dinucleotide repeat polymorphism (17 to 25 repeats) were identified, and the frequency of each allele in diabetic subjects was not different from that in nondiabetic controls. The frequency of the allele containing 21 repeats (A21) was most abundant (42.4% in control and 45.6% in diabetic subjects), followed by the allele with 23 repeats (A23; 35.4% in control and 27.6% in diabetic subjects). The A21 allele was less frequent in M and O than U (O, 38.9%; M, 45.5%; U, 59.3%, chi2 = 7.18; P < 0.05, O vs. U), while the frequency of the alleles other than A21 was not different among each group. The calculated odds ratio for nephropathy in the noncarrier, heterozygote, or homozygote of A21 allele was 3.38, 1.97, and 0.2, respectively. Furthermore, the promoter assay for the MMP-9 gene revealed that the A21 allele had a higher promoter activity compared with other alleles. No significant correlation was observed between serum MMP-9 concentrations and the MMP-9 gene polymorphism. CONCLUSION: These results indicate that the patients with A21 allele of the MMP-9 gene may be protected from the development and progression of diabetic nephropathy. Thus, the microsatellite polymorphism upstream of the MMP-9 gene could be a useful genetic marker for diabetic nephropathy.

Aged↗
PubMed2001

Clarithromycin-based triple therapy for non-resistant Helicobacter pylori infection. How long should it be given?

BACKGROUND: We have previously reported mixed infection with wild-type (sensitive) and mutant (resistant) Helicobacter pylori strains using a PCR-based preferential homo-duplex formation assay (PCR-PHFA) to detect gene mutations associated with clarithromycin resistance. Half of the cases with mixed infection were determined as sensitive by conventional MIC assessment and yet failed to respond to clarithromycin-based therapy. The aim of this study is to assess the efficacy of clarithromycin-based triple therapy in patients infected exclusively with wild-type strains as determined by PCR-PHFA. METHODS: Ninety patients who had pure wild-type H. pylori infection were randomly assigned to receive clarithromycin (200 mg b.i.d.), amoxicillin (500 mg q.i.d.) and lansoprazole (30 mg b.i.d.) for either 5 days or 7 days (n = 48 and n = 42, respectively). The outcome of eradication was assessed by [13C] urea breath test. RESULTS: Eradication was achieved in 36/48 (75%) versus 39/42 (93%) by intention-to-treat analysis (P = 0.02), and in 36/45 (80%) versus 39/40 (98%) by per protocol analysis (P = 0.01), for the 5-day and 7-day protocols, respectively. Compliance and the incidence of untoward effects were similar in both groups. CONCLUSIONS: Seven-day administration is necessary and sufficient for the triple therapy with clarithromycin, amoxicillin and lansoprazole in patients with pure wild-type H. pylori infection.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Age-related changes in cortical and trabecular bone mineral status. A quantitative CT study in lumbar vertebrae.

PURPOSE: To investigate the age and sex dependence of the bone mineral status of human lumbar vertebrae with special regard to differences between cortical and trabecular bone. MATERIAL AND METHODS: The study group comprised 125 normal Japanese healthy volunteers (54 males and 71 females), and was subdivided into adult male and female groups (subjects younger than 40 years), intermediate male and female groups (ages ranging between 41 and 64 years) and old male and female groups (subjects older than 65 years). The cortical bone mineral status was estimated using a single-energy quantitative CT (SE-QCT) technique, whereas trabecular bone mineral density (BMD) was estimated using a dual-energy (DE-QCT) technique. RESULTS: A considerable gender difference in the age-related cortical bone status was found. There was a significant reduction of the mean values of the cortical volume and BMD in the old female group compared with those obtained in the old male group. CONCLUSION: The results suggest that in men, cortical and trabecular bone volume decrease very little with age. In women, cortical volume and BMD and trabecular BMD decrease with age while trabecular bone volume does not. The study showed that all variables had higher values in men than in women and that the difference increased with age.

Adult↗
PubMed2001

A trigeminal neuralgia-like paroxysmal pain condition presumably due to buccal nerve compression in the temporalis muscle.

We encountered three patients with trigeminal neuralgia-like paroxysmal pain in the buccal nerve region. In all cases, paroxysmal pain was felt spreading to the receptive field of the ipsilateral buccal nerve, and clear tenderness was observed during intraoral palpation at the inner side of the mandibular ramus where the temporalis muscle runs and attaches. It was assumed that the paroxysmal pain might be caused by nerve compression related to temporalis muscle hyperactivity. To lend support to this hypothesis, we also studied the anatomical relationship between the buccal nerve and the masticatory muscles. In this autopsy study, the buccal nerve pierced the temporalis muscle in six (12%) of 52 specimens from 26 cadavers. These findings support the hypothesis that peripheral buccal nerve compression could be an etiology of paroxysmal neuropathic pain in the unilateral orofacial region.

Aged↗
PubMed2001

Thyroid stimulating hormone downregulates vascular endothelial growth factor expression in FRTL-5 cells.

We studied the regulation of the expression of vascular endothelial growth factor (VEGF) by TSH in monolayer cultures of rat thyroid FRTL-5 cell lines. The VEGF mRNA synthesis was significantly inhibited by TSH as well as dibutyryl cyclic adenosine monophosphate (cAMP) in a dose-dependent manner in FRTL-5 cells. This observation is contrary to previously published results using the thyroid follicular culture system. Our results suggest that the direct effect of TSH/cAMP is to inhibit the VEGF synthesis in monolayer cells.

Animals↗
PubMed2001

Transient activation of c-Jun NH2-terminal kinase by growth factors influences survival but not apoptosis of human thyrocytes.

Activation of c-Jun NH2-terminal kinase (JNK), a member of the mitogen-activated protein kinase (MAPK) family, is involved in apoptosis or cell proliferation. We have previously demonstrated that ionizing radiation or thyroid-stimulating hormone activated JNK without linking to thyroid cell apoptosis. To clarify the involvement of JNK activation in thyroid cell survival, we investigated the effects of various growth factors on induction of JNK activation in cultured human thyroid cells. JNK activation was observed at 30 minutes after fetal bovine serum (FBS) stimulation and returned to basal level at 240 minutes. Epidermal growth factor (EGF), transforming growth factor-beta (TGF-beta) and hepatocyte growth factor (HGF) also induced JNK activation, but did not trigger apoptotic cell death. Furthermore, we observed high basal activation of JNK in four of five human thyroid cancer cell lines. Overexpression of c-Met, an HGF receptor, was observed in two of the four cell lines with high basal JNK activity. Our results suggest that JNK activation does not induce apoptosis but is associated with survival or transformation of human thyroid cells.

Animals↗
PubMed2001

Endothelin-1 production is enhanced by rotenone, a mitochondrial complex I inhibitor, in cultured rat cardiomyocytes.

In chronic heart failure and acute myocardial infarction, the tissue level of endothelin (ET)-1 in the heart, as well as its plasma level, has been reported to increase markedly. There is, however, little information about what in these pathologic conditions leads to increased production of ET-1, and which type of cell in the heart produces ET-1. We examined the mRNA and peptide expression of ET-1 using cultured rat neonatal cardiomyocytes, in which mitochondrial dysfunction was induced by rotenone, a mitochondrial respiratory chain complex I inhibitor, because one of the common features in failing or ischemic hearts is an alteration in energy metabolism due to mitochondrial dysfunction. Rotenone increased glucose use by the culture cells within 12 h of addition without affecting cell viability, and depressed the mitochondrial membrane potential after 72 h, indicating the induction of mitochondrial dysfunction in cardiomyocytes. Rotenone induced significant increase in the expression level of mRNA for ET-1 within 1 h of addition. In accordance with this finding, immunoreactive ET-1 in culture medium increased 3 times after 24 h of incubation, suggesting active secretion of ET-1 from cultured cells treated with rotenone. Immunocytochemical analysis verified significant increase of ET-1 peptide in cardiomyocytes, confirming the production of ET-1 by cardiomyocytes. These results suggest that derangement of mitochondrial function in cardiomyocytes itself could lead to the increased production of ET-1 in cardiomyocytes, and that this mechanism may contribute to the increased production of ET-1 in failing and ischemic hearts.

Animals↗