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Biomedical subjects

A Horii

Publications and source records attributed to A Horii.

At least 109 records · Page 6Linked to original sources
PubMed1997

Warthin's tumor of the parotid gland with extension into the parapharyngeal space.

A case of Warthin's tumor of the parotid gland which extensively extended into the parapharyngeal space is presented. The tumor border against the parotid gland was ill-defined but the border towards the parapharyngeal structures was clear. Solid portions of the tumor appeared hypointense relative to the gland on both unenhanced T1- and T2-weighted MR images without fat suppression, whereas cystic portions appeared hypointense on T2-weighted images and hyperintense on unenhanced T1-weighted images. Pathologic study showed that the ill-defined margin was caused by inflammation and cystic material consisted of highly proteinaceous material. We concluded that the atypical extension into the parapharyngeal space of the tumor was caused by its location in the deep lobe of the parotid gland and its bulky size.

Adenolymphoma↗
PubMed1997

Assessment of parotid masses: which MR pulse sequences are optimal?

The objective of this paper is to determine which MR pulse sequences are optimal for delineation of lesion and predicting pathologic nature of lesion with signal intensity. A prospective study was performed in 53 parotid masses (39 benign and 14 malignant lesions) in 53 patients. Signal intensity of lesion was visually assessed and lesion/parotid contrast-to-noise ratios were measured. On visual assessment, detection sensitivity was 100% for nonenhanced nonfat-suppressed T1-weighted images, 91% for nonfat-suppressed fast spin-echo (FSE) T2-weighted images, 83% for gadolinium-enhanced fat-suppressed T1-weighted images, and 75% for fat-suppressed FSE T2-weighted images. The highest contrast-to-noise ratios were obtained with nonenhanced T1-weighted images. Hypointensity of lesion relative to the parotid gland on nonfat-suppressed FSE T2-weighted images was seen in 11 of 14 malignancies, 12 of 15 Warthin tumors, and two of 18 pleomorphic adenomas. Cystic portion of hyperintensity on nonenhanced T1-weighted images was solely seen in benign tumors (n = 11). Thus, the highest accuracy (81%) (79% sensitivity and 82% specificity) for predicting malignancy was obtained with a criterion of hypointensity on nonfat-suppressed FSE T2-weighted images plus absence of cystic portion of hyperintensity on nonenhanced T1-weighted images. Nonenhanced T1-weighted images combined with nonfat-suppressed FSE T2-weighted images is optimal for delineation of lesion and prediction of pathologic nature of parotid masses.

Adolescent↗
PubMed1997

Analysis of the p53 gene mutations in patients with multiple primary cancers of the oesophagus.

We investigated genetic alterations of the p53 gene in two patients with multiple primary oesophageal squamous cell carcinomas (ESCs). We found that each primary tumour could be distinguished by mutation of p53. Moreover, mutations detected in the p53 gene in metastatic lymph nodes were the same as those detected in at least one of the primary tumours. Our results presented the possibility of: (1) discrimination of primary and metastatic legions in patients with multiple primary ESCs; (2) determination of metastatic pathway to regional lymph nodes; and (3) application for the development of a better clinical management of patients with multiple primary ESCs.

Aged↗
PubMed1997

Infrequent genetic alterations of the PTEN/MMAC1 gene in Japanese patients with primary cancers of the breast, lung, pancreas, kidney, and ovary.

In the present study, we searched for genetic alterations of the entire coding region of PTEN/MMAC1, a recently isolated candidate tumor suppressor gene, in 178 specimens from Japanese patients with various malignant tumors by the polymerase chain reaction-single strand conformation polymorphism method. The samples consisted of 11 glioblastoma multiformes (GBMs), 14 astrocytomas, 47 breast cancers, 25 non-small cell lung cancers, 9 small cell lung cancers, 8 pancreatic cancers, 24 renal cell carcinomas, 20 ovarian cancers, and 20 metastatic lung tumors from various organs. Only one somatic frameshift mutation at codon 319 was observed in one (9%) of eleven GBMs. Our results suggest that mutation of the PTEN/MMAC1 gene does not play a major role in carcinogenesis, at least in the tumor types from Japanese patients analyzed in this study.

Base Sequence↗
PubMed1997

Evidence for involvement of IgA1 hinge glycopeptide in the IgA1-IgA1 interaction in IgA nephropathy.

The study was performed to investigate the role of the IgA1 hinge region in the IgA1-IgA1 interaction, which was observed previously in IgA nephropathy. The competitive inhibition assays of the IgA1-IgA1 binding were performed using the following candidates for inhibitors: native IgA1 hinge glycopeptide (nHGP), IgA1, IgA2, and IgG. The IgA1-IgA1 binding was definitely inhibited by the nHGP and the IgA1 (maximum of percent inhibition: 66.1 and 60.5%, respectively). There was no obvious inhibition in the IgA2 and the IgG. The inhibition curves of the nHGP and the IgA1 were significantly different from that of the IgG (P < 0.01, respectively). Furthermore, to reveal the detailed binding sites in the interaction, the same inhibition assays were performed using the following substances composing the IgA1 hinge glycopeptide: galactose (Gal), N-acetyl-galactosamine (GalNAc), Gal beta 1-3GalNAc, sialic acid, tetrapeptide PTPS, and synthesized hinge proline-rich peptide PVPSTPPTPSPSTPPTPSPS (sHP). sHP, Gal beta 1-3GalNAc, Gal, and GalNAc inhibited the binding (69.3, 34.1, 14.9, 14.6%, respectively). No obvious inhibition was observed in sialic acid and tetrapeptide PTPS. The inhibition curve of sHP was significantly different from that of the PTPS (P < 0.05). Those of Gal beta 1-3GalNAc, Gal, and GalNAc were also significantly different from that of sialic acid (P < 0.05, respectively). These results suggested that the IgA1-IgA1 interaction could be mediated by the core structure including the peptide and the sugars, except for sialic acid in the hinge region, resulting in the formation of the circulating macromolecular IgA1 in IgA nephropathy.

Adult↗
PubMed1997

HMB-45 and tuberin in hamartomas associated with tuberous sclerosis.

Tuberous sclerosis (TSC) is an autosomal dominant condition characterized by various hamartomas. To assess whether these hamartomas have common features, we immunohistochemically analyzed an autopsy case of TSC with subependymal giant cell astrocytoma, hamartomatous lymphangioleiomyomatosis in the lungs and uterus, and angiomyolipomas in the liver, bilateral kidneys, parametrium, and a lymph node, using the specific antibodies for tuberin (the gene product of TSC2) and HMB-45 (a monoclonal antibody specific for human melanoma). Tuberin was ubiquitously expressed in the normal organs. It was negative or very weakly expressed in the hamartomas. In contrast, HMB-45 was commonly observed in the hamartomas except for the lesions in the brain. The subependymal giant cell astrocytoma was composed of cells immunoreactive for synaptophysin, neurofilament protein, glial fibrillary acidic protein, and S-100 protein but negative for HMB-45 and tuberin. The suppression of tuberin in the brain tumor and visceral hamartomas and an abnormal expression of HMB-45 in the visceral hamartomas were observed. We conclude that the hamartomas associated with TSC have common phenotypic and etiologic expressions and that the genes responsible for both tuberin and the antigen recognized by HMB-45 have important roles in the pathogenesis of these hamartomas.

Angiofibroma↗
PubMed1996

Detailed deletion mapping on chromosome arm 12q in human pancreatic adenocarcinoma: identification of a I-cM region of common allelic loss.

As a first step toward understanding molecular mechanisms in human pancreatic carcinogenesis, we searched for the location of tumor suppressor genes by examining loss of heterozygosity (LOH) in 44 pancreatic cancer specimens. We used 46 microsatellite markers that spanned all of the autosomes. Frequent LOH was observed in six chromosomal regions: in chromosome arms lp (32%), 6q (37%), 9p (50%), 12q (30%), 17p (59%), and 18q (35%). Because chromosome arm 12q is a reported target for allelic loss in some other cancers, we focused on this region with 66 primary specimens and identified the minimal common region of allelic loss within a I-cM interval in 12q22-q23.l. Microsatellite instability (MI) was also examined in this study, and the incidence of MI(+) cases, in which MI of two or more microsatellite loci was detected, was 61% (27 of 44 informative cases). In pancreatic tumors with MI(+), mutations of the transforming growth factor beta receptor II (RII) gene were not detected.

Adenocarcinoma↗
PubMed1996

The somatic mutation frequency of the transforming growth factor beta receptor type II gene varies widely among different cancers with microsatellite instability.

Disruption of the DNA mismatch repair system, characterized by microsatellite instability (MSI), plays an important role in the course of human carcinogenesis. Frequent somatic mutations in a polyadenine (poly(A)) tract and two GT repeats within the coding region of the transforming growth factor beta (TGFbeta) receptor II (RII) gene were reported in colorectal cancers with MSI. We examined mutations of RII in cancers of various organs with MSI and found deletions at the poly(A) tract in eight of nine (89%) gastric cancers and four of five (80%) colorectal cancers. In contrast, no mutations were found in cancers of the pancreas, endometrium, or lungs. These results suggest that TGFbeta-mediated growth control plays a very important role in the stomach and colorectum.

Adult↗
PubMed1996

Deletion mapping on chromosome 10q25-q26 in human endometrial cancer.

To understand genetic events which play a role in the development and/or progression of human endometrial cancer, we studied allelotypes on all autosomal chromosomes, as well as chromosome X, with 42 microsatellite markers and 56 endometrial cancers. The most frequent loss of heterozygosity (LOH) was observed on the long arm of chromosome 10 (14 of 30, 47%), which was commonly detected in grade 1 cancer. We constructed a detailed deletion map and defined two commonly deleted regions in 10q25-q26; one was the 8 cM region between D10S209 and D10S216, the other was the 12 cM region between D10S217 and D10S590. Replication errors at two or more loci were observed in 24 of 56 tumours (43%), suggesting that disruption of the DNA mismatch repair system also plays an important role in the course of endometrial carcinogenesis.

Adenocarcinoma, Clear Cell↗
PubMed1996

Deletion mapping on chromosome 1p in well-differentiated gastric cancer.

To define the region on the short arm of chromosome 1 that is thought to include one or more tumour-suppressor genes for gastric cancers, we carried out loss of heterozygosity (LOH) studies in 26 gastric adenocarcinomas, using three restriction fragment length polymorphism (RFLP) markers and nine microsatellite markers. All tumours were informative with at least one locus; three revealed replication errors (RERs) at multiple microsatellite loci, and interstitial or telomeric allelic deletions were observed in 12 cases. Deletion mapping of these tumours defined a commonly deleted region between two loci, D1S201 and D1S197, that are 13 cM apart. As two loci within the commonly deleted region, D1S57 (pYNZ2) and D1S62 (pTHI54), were mapped respectively to 1p35 and 1p34.3 by fluorescence in situ hybridisation, we conclude that a locus likely to contain a tumour-suppressor gene for gastric cancer is located within a 13 cM region encompassing two chromosomal bands.

Chromosome Deletion↗
PubMed1996

Endogenous GABA modulates histamine release from the anterior hypothalamus of the rat.

Using a microdialysis method, we investigated the effects of the nipecotic acid-induced increase in content of endogenous GABA on in vivo release of histamine from the anterior hypothalamus (AHy) of urethane-anesthetized rats. Nipecotic acid (0.5 mM), an inhibitor of GABA uptake, decreased histamine release to approximately 60% of the basal level. This effect was partially antagonized by picrotoxin (0.1 mM), an antagonist of GABAA receptors, or phaclofen (0.1 mM), an antagonist of GABAB receptors. These results suggest that histamine release is modulated by endogenous GABA through both GABAA and GABAB receptors. When the tuberomammillary nucleus, where the cell bodies of the histaminergic neurons are localized, was stimulated electrically, the evoked release of histamine from the nerve terminals in the AHy was significantly enhanced by phaclofen, suggesting that GABAB receptors may be located on the histaminergic nerve terminals and modulate histamine release presynaptically. On the other hand, picrotoxin caused an increase in histamine release to approximately 170% of the basal level, and this increase was diminished by coinfusion with D(-)-2-amino-5-phosphonopentanoic acid (0.1 mM), an antagonist of NMDA receptors. Previously, we demonstrated tonic control of histamine release by glutamate mediated through NMDA receptors located on the histaminergic terminals in the AHy. These results suggest the possible localization of GABAA receptors on glutamatergic nerve terminals and that the receptors may regulate the basal release of histamine indirectly.

2-Amino-5-phosphonovalerate↗
PubMed1996

Steroid therapy during the early stage of progressive IgA nephropathy. A 10-year follow-up study.

This study was undertaken to clarify the effect of corticosteroids on the long-term clinical course of the early stage of progressive IgA nephropathy. The early stage of progressive IgA nephropathy was defined as having moderate proteinuria between 1 and 2 g/day, creatinine clearance values of 70 ml/min or more, and a histological severity score of 7 or more. The number of patients who fulfilled these three conditions during 12 years from 1972 and then were continuously followed up for 10 years or more in our renal unit was 46. Twenty of them received steroid treatment for an average period of 18 months, and the remaining 26 patients had no steroid treatment. The initial data of proteinuria, creatinine clearance values, frequency of hypertensive cases, and histological scores of 7 or more were not different between the two groups: 1.4 +/- 0.4 vs. 1.3 +/- 0.3 g/day, 85 +/- 14 vs. 88 +/- 13 ml/min, 25 vs. 38%, and 10.7 +/- 2.5 vs. 11.0 +/- 3.0, respectively. During the follow-up period of 10 years, the renal survival rate was significantly different between the two groups (100 vs. 84% 5 years after starting therapy and 80 vs. 34% 10 years later; p < 0.001). The final creatinine clearance values were significantly different between the two groups (54 +/- 35 vs. 20 +/- 29 ml/min; p < 0.005). On the other hand, the patient groups with mild histological changes or decreased renal function due to moderate proteinuria showed no significant differences in the final outcome. These results indicate that corticosteroids are beneficial in stabilizing the renal function for a long time during the early stage of progressive IgA nephropathy, although this study was not a randomized one.

Adult↗
PubMed1996

Reactivity of glomerular and serum IgA1 to jacalin in IgA nephropathy.

To analyze O-linked oligosaccharides (O-glycans) in the hinge region of IgA1 in IgA nephropathy (IgAN), the reactivity of IgA1 to jacalin, which specifically binds to O-glycans, was investigated. Initially, renal biopsy specimens from 5 patients with IgAN and 3 patients with other renal diseases were investigated in an immunofluorescence study with jacalin, monoclonal antihuman IgA1 and IgA2 antibodies. All of the renal biopsy specimens of IgAN and none of other renal diseases were positively stained by both FITC-labeled jacalin and monoclonal anti-IgA1 antibody. The glomerular staining patterns of FITC-jacalin were similar to those of the monoclonal anti-IgA1 antibody. IgA2 was negative in all specimens. Based on the positive reactivity of deposited IgA1 to jacalin, the binding ability of serum IgA1 to jacalin was evaluated by inhibition assay using D-galactose in patients with IgAN (n = 58), other primary glomerulonephritides (PGN) (n = 41), and healthy controls (n = 52). The frequencies of the patients with serum IgA1 having a high affinity for jacalin were significantly greater in IgAN (19/58, 32.8%) compared with the healthy controls (2/52, 3.8%) and other PGN (4/41, 9.8%). These results suggested that the increased reactivity of O-glycan(s) in the IgA1 hinge region to jacalin is due to an unusual glycosylation of serum IgA1 in IgAN.

Adult↗
PubMed1996

Lipoprotein derangement during steroid treatment in minimal-change nephrotic syndrome.

To study the pathophysiology of hyperlipidemia in nephrotic syndrome, we compared lipid metabolism in the nephrotic stage (stage 1) and in stage 2, when albuminuria had subsided, in 11 patients with minimal-change disease treated with corticosteroid. High-density lipoprotein (HDL) levels were decreased and HDL contained more cholesterol and triglyceride per unit of protein in stage 1 in the patients than in age-matched healthy controls. The urinary protein level was positively correlated only with low-density lipoprotein (LDL) levels, suggesting that the increased albumin clearance stimulated LDL production. Serum cholesterol levels were positively correlated with apolipoprotein E levels and were negatively correlated with lecithin-cholesterol acyltransferase activity in the nephrotic stage; the opposite correlations were seen in controls. Although triglycerides in HDL had normalized at stage 2, triglycerides in LDL and very-low-density lipoprotein did not return toward normal until stage 3, when serum cholesterol levels were normalized.

Adult↗