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T Masaki

Publications and source records attributed to T Masaki.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Direct laryngoscopic extirpation and wound suture for hypopharyngeal lipoma: a case report].

We report a case of hypopharyngeal lipoma. An 82-year-old woman referred to our clinic for 10 years of wheezing and intermittent breathlessness developing 1 month before admission was found on laryngoscopic examination to have a mobile mass arising from the hypopharyngeal region intermittently obstructing the laryngeal airway. After emergency tracheotomy, the tumor was removed under direct laryngoscopy, given the patients age and general status. Under general anesthesia, the tumor was extirpated using a laser and electric scalpel under microlaryngoscopy. The operative wound was sutured under direct laryngoscopy using a specially designed probe with a U-shaped tip. The tumor was histologically diagnosed as lipoma. The surgical procedure enabled the operative wound to heal rapidly and oral feeding to start early.

Aged↗
PubMed2001

Colonoscopic treatment of colon cancers.

Recent advances in endoscopic technology have enabled conservative treatment for patients with carcinoma in situ. The treatment of submucosally invasive carcinomas, or malignant polyps, is still controversial, however. The use of widely advocated histologic criteria, such as poorly differentiated histology (Grade III cancer), level 4 invasion or involved margin status, or lymphatic venous invasion as risk factors for adverse outcome, should be examined by multivariate analysis. Unfavorable histology at the invasive margin, PCNA, MUC-1 expression, and chromosomal abnormalities may be new candidates for prognostic indicators in patients with submucosally invasive carcinoma.

Carcinoma in Situ↗
PubMed2001

Ca(2+) influx through nonselective cation channels plays an essential role in noradrenaline-induced arachidonic acid release in Chinese hamster ovary cells expressing alpha(1A)-, alpha(1B)-, or alpha(1D)-adrenergic receptors.

We constructed Chinese hamster ovary (CHO) cells stably expressing alpha(1A)-, alpha(1B)-, or alpha(1D)-adrenergic receptors (CHO-alpha(1A), CHO-alpha(1B), or CHO-alpha(1D), respectively) and compared the Ca(2+) channels activated by noradrenaline (NA) in these cells using whole-cell recordings and monitoring of the intracellular free Ca(2+) concentration ([Ca(2+)](i)). We also investigated the involvement of Ca(2+) channels in the NA-induced arachidonic acid release. In all three cell types, NA at concentrations > or =10 nM induced a sustained increase in [Ca(2+)](i) attributable to extracellular Ca(2+) influx in [Ca(2+)](i) monitoring and an inward current in whole-cell recording. The current-voltage relationships were linear, and their reversal potentials were close to 0 mV. The reversal potential of the currents was not affected by a change in the concentration of Cl(-) in the bath solution. Moreover, a current could be induced in a bath solution containing only Ca(2+) as the movable cation. LOE 908, a receptor-operated Ca(2+) channel blocker, inhibited the sustained increase in [Ca(2+)](i) and inward currents in a concentration-dependent manner, and complete inhibition was observed at concentrations > or = 3 microM. NA induced arachidonic acid release in all three cell types. This release was entirely dependent on extracellular Ca(2+) influx. Moreover, LOE 908 at concentrations > or = 3 microM blocked the NA-induced increase in arachidonic acid release. These results indicate that 1) NA activates LOE 908-sensitive Ca(2+)-permeable nonselective cation channels (NSCCs) in CHO-alpha(1A), CHO-alpha(1B), and CHO-alpha(1D), and 2) the Ca(2+) influx through NSCCs may play an important role in the NA-induced enhancement of arachidonic acid release in these cells.

Acetamides↗
PubMed2000

Enhanced expression and activation of Ca(2+)/calmodulin-dependent protein kinase IV in hepatocellular carcinoma.

BACKGROUND: Ca(2+)/calmodulin-dependent protein kinase IV (CaM-kinase IV) is a multifunctional protein kinase that is expressed abundantly in the central nervous system and, to a lesser degree, in nonneuronal tissues such as the liver. In the current study, the authors demonstrated the expression of CaM-kinase IV in hepatocytes from hepatocellular carcinoma (HCC) in both humans and rats. METHODS: Immunoblotting and immunohistochemical analysis were performed to confirm the expression of CaM-kinase IV and CaM-kinase kinase in HCC occurring in both humans and rats. The kinase activity of CaM-kinase IV in the lysate of each of these liver supernatant fluids was measured using a specific substrate (peptide gamma) for this enzyme before and after phosphorylation by exogenously added CaM-kinase kinase. RESULTS: Marked positive staining of HCC hepatocytes was found and the subcellular staining pattern mainly was cytosolic. One immunoreactive band with a molecular weight of 64 kilodaltons, which was identical to an isoform of rat cerebellum CaM-kinase IV, was demonstrated by immunoblotting. Ca(2+)/calmodulin-dependent CaM-kinase IV activity was high in HCC and showed almost no difference in activity in specimens with and without CaM-kinase kinase phosphorylation. CONCLUSIONS: CaM-kinase IV was found to be expressed in HCC and might have been involved in the development of HCC. CaM-kinase IV that was expressed in cancerous hepatocytes was phosphorylated mainly by CaM-kinase kinase that also was expressed in tumor cells.

Animals↗
PubMed2000

Isolation and characterization of the gene encoding mouse tax-responsive element-binding protein (TREB) 5.

TREB5/hXBP-1/HTF is a basic region leucine zipper protein which binds to a cyclic AMP responsive element (CRE)-like element in both human T-cell leukemia virus type 1 and human major histocompatibility complex (MHC) class II genes. To analyze the structure and transcription regulation of the TREB5 gene, we isolated the mouse TREB5 gene and cDNA. The mouse TREB5 gene contains five exons and four introns and spans approximately 5 kb. The deduced amino acid sequence of mouse TREB5 exhibited 77% and 94% homology to human and rat TREB5, respectively. The b-zip structure is completely conserved in mouse, rat and human. Southern blot analysis of the mouse genomic DNA demonstrated that positive bands exactly coincide with those expected from sequences of the cloned genes, indicating that the mouse TREB5 gene is present as a single copy. The transcription start site of the mouse TREB5 gene was mapped to -15 bp upstream from the ATG initiation codon. Promoter analysis of serial deletion mutants revealed that the -142 bp upstream region is the minimum sequence to promote mouse TREB5 gene expression and that the -1.0 kb upstream region is required for full promoter activity.

3T3 Cells↗
PubMed2000

Pancreatic duct cell carcinomas express high levels of high mobility group I(Y) proteins.

The high mobility group I (HMGI) family of proteins in mammals belongs to a group of nonhistone nuclear proteins known as architectural transcriptional factors. They function in vivo as both structural components of chromatin and auxiliary gene transcription factors. In an earlier study (N. Abe et al, Cancer Res., 59: 1169-1174, 1999), we demonstrated that the expression level of the HMGI(Y) gene/proteins was significantly increased in colorectal adenocarcinoma and colorectal adenoma with severe cellular atypia. In the current study, we analyzed HMGI(Y) expression in several human pancreatic lesions to investigate (a) whether HMGI(Y) overexpression is also observed in pancreatic carcinoma, and (b) the role of HMGI(Y) in the diagnosis of pancreatic neoplasms. To this end, HMGI(Y) expression was determined at the protein level by immunohistochemistry using a HMGI(Y)-specific antibody in 6 surgically resected specimens of nonneoplastic tissue (4 specimens of normal pancreatic tissue and 2 specimens of chronic pancreatitis tissue), 8 pancreatic cystic neoplasms (5 intraductal papillary mucinous adenomas, 1 serous cystadenoma, and 2 solid pseudopapillary tumors), and 15 duct cell carcinomas of the pancreas. Immunohistochemical analysis revealed intense nuclear staining in the pancreatic carcinoma cells, whereas only very faint nuclear staining was seen in the nonneoplastic cells. There was a strong correlation between HMGI(Y) protein overexpression and a diagnosis of carcinoma (P = 0.000018). Thus, an increased expression level of the HMGI(Y) proteins was clearly associated with the malignant phenotype in pancreatic tissue. In addition, a low level of protein expression was also apparent in two of the cystic neoplasms that exhibited cellular atypia, but not in those that did not exhibit cellular atypia. Based on these findings, we propose that the HMGI(Y) proteins could be closely associated with tumorigenesis in the pancreas and that HMGI(Y) could serve as a potential diagnostic molecular marker for distinguishing pancreatic malignancies unambiguously from normal tissue or benign lesions.

Carcinoma↗
PubMed2000

Transforming growth factor-beta(1) increases the expression of lectin-like oxidized low-density lipoprotein receptor-1.

Lectin-like oxidized low-density lipoprotein (Ox-LDL) receptor-1 (LOX-1) is a novel cell-surface receptor for Ox-LDL, which can be expressed by vascular endothelial cells, smooth muscle cells, and macrophages. On the other hand, transforming growth factor (TGF)-beta(1), which plays crucial roles in vascular remodeling and the pathogenesis of atherosclerosis, has been shown to inhibit expression of class A scavenger receptors and CD36 in macrophages. Here we provide the evidence that TGF-beta(1) (0.1-10 ng/mL) induces LOX-1 protein and mRNA expression in both bovine aortic endothelial cells and smooth muscle cells in a dose- and time-dependent fashion, probably at the transcriptional level. TGF-beta(1) also upregulates LOX-1 mRNA expression in murine peritoneal macrophages. Thus TGF-beta(1) can highly induce LOX-1 expression in vascular endothelial cells, smooth muscle cells, and macrophages, suggesting that TGF-beta(1) appears one of the key regulators that modulates expression of scavenger receptors.

Animals↗
PubMed2000

Cholesterol oxidation switches the internalization pathway of endothelin receptor type A from caveolae to clathrin-coated pits in Chinese hamster ovary cells.

We investigated the mechanism of endothelin receptor type A (ETA) internalization in Chinese hamster ovary cells using two assays; flow cytometric quantification of cell surface myc-ETA and in situ localization of Cy5-labeled ET-1. In both assays, agonist-dependent internalization of myc-ETA was inhibited by nystatin and filipin, both of which disrupt internalization via caveolae, whereas it was barely affected by chlorpromazine and hypertonic sucrose, both of which disrupt internalization via clathrin-coated pits. In addition to myc-ETA, ET-1 caused intracellular translocation of caveolin-1 and this translocation was also blocked by nystatin but not by chlorpromazine. These results strongly argue that ETA is internalized via caveolae but not clathrin-coated pits. Treatment of the cells with cholesterol oxidase reduced cellular cholesterol and caused intracellular translocation of caveolin-1 but did not affect cell surface localization of myc-ETA. In cholesterol oxidase-treated cells, however, both chlorpromazine and hypertonic sucrose effectively blocked ET-1-induced myc-ETA internalization and nystatin was less effective than in untreated cells. Accordingly, expression of a dominant negative form of beta-arrestin blocked myc-ETA internalization in cholesterol oxidase-treated cells but not in untreated cells. These results suggest that, in Chinese hamster ovary cells, 1) agonist-occupied ETA can be internalized either via caveolae or clathrin-coated pits; 2) of the two, the former is the default pathway; and 3) the oxidative state of cell surface cholesterol is one of the factors involved in the pathway selection.

Animals↗
PubMed2000

Biosynthesis and post-translational processing of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1). N-linked glycosylation affects cell-surface expression and ligand binding.

LOX-1 (lectin-like oxidized low density lipoprotein receptor-1) is a type II membrane protein belonging to the C-type lectin family that can act as a cell-surface receptor for atherogenic oxidized low density lipoprotein (Ox-LDL) and may play crucial roles in atherogenesis. In this study, we show, by pulse-chase labeling and glycosidase digestion, that LOX-1 is synthesized as a 40-kDa precursor protein with N-linked high mannose carbohydrate chains (pre-LOX-1), which is subsequently further glycosylated and processed into the 48-kDa mature form within 40 min. Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Cell enzyme-linked immunosorbent assay, flow cytometry, and immunofluorescence confocal microscopy demonstrated that the deglycosylated form of LOX-1 is not efficiently transported to the cell surface, but is retained in the endoplasmic reticulum or Golgi apparatus in tumor necrosis factor-alpha-activated bovine aortic endothelial cells, but not in BLOX-1-CHO cells. Radiolabeled Ox-LDL binding studies revealed that the deglycosylated form of LOX-1 expressed on the cell surface of BLOX-1-CHO cells has a reduced affinity for Ox-LDL binding. Taken together, N-linked glycosylation appears to play key roles in the cell-surface expression and ligand binding of LOX-1.

Amidohydrolases↗
PubMed2000

LOX-1 mediates lysophosphatidylcholine-induced oxidized LDL uptake in smooth muscle cells.

A novel receptor for oxidized low-density lipoprotein (OxLDL), lectin-like OxLDL receptor (LOX-1), was cloned from endothelial cells. Since OxLDL is taken up by vascular smooth muscle cells (VSMC) in atheroma, we analyzed the inducible expression of LOX-1 in VSMC in the present study. Incubation of cultured bovine VSMC with lysophosphatidylcholine (LPC), an atherogenic component of OxLDL, increased the level of mRNA for LOX-1 in a dose- and time-dependent manner. Since LPC did not significantly change the half-life of LOX-1 mRNA, the induction seemed to occur at the transcriptional level. The induction accompanied an increase in the protein level of LOX-1 and activity of OxLDL uptake. Blocking antibody against LOX-1 significantly suppressed the enhanced uptake of OxLDL. Thus, LOX-1 is a major receptor for OxLDL in VSMC as in endothelial cells. The enhanced expression of LOX-1 by LPC suggests that OxLDL and LPC would progressively change the function of VSMC and accelerate atherogenesis in vivo.

Animals↗
PubMed2000

A platelet-endothelium interaction mediated by lectin-like oxidized low-density lipoprotein receptor-1.

One crucial role of endothelium is to keep the innermost surface of a blood vessel antithrombotic. However, the endothelium also expresses prothrombotic molecules in response to various stimuli. The balance between the antithrombotic and prothrombotic nature of the endothelium is lost under certain conditions. During atherosclerosis, the attachment of platelets to the vessel surface has been suggested to promote the proliferation of smooth muscle cells and intimal thickening as well as to affect the prognosis of the disease directly through myocardial infarction and stroke. Dysfunctional endothelium, which is often a result of the action of oxidized low-density lipoprotein (OxLDL), tends to be more procoagulant and adhesive to platelets. Herein, we sought the possibility that the endothelial lectin-like OxLDL receptor-1 (LOX-1) is involved in the platelet-endothelium interaction and hence directly in endothelial dysfunction. LOX-1 indeed worked as an adhesion molecule for platelets. The binding of platelets was inhibited by a phosphatidylserine-binding protein, annexin V, and enhanced by agonists for platelets. These results suggest that negative phospholipids exposed on activation on the surface of platelets are the epitopes for LOX-1. Notably, the binding of platelets to LOX-1 enhanced the release of endothelin-1 from endothelial cells, supporting the induction of endothelial dysfunction, which would, in turn, promote the atherogenic process. LOX-1 may initiate and promote atherosclerosis, binding not only OxLDL but also platelets.

Animals↗
PubMed2000

Expression of dystroglycan and laminin-2 in peripheral nerve under axonal degeneration and regeneration.

In Schwann cells, the transmembrane glycoprotein beta-dystroglycan composes the dystroglycan complex, together with the extracellular glycoprotein alpha-dystroglycan which binds laminin-2, a major component of the Schwann cell basal lamina. To provide clues to the biological functions of the interaction of the dystroglycan complex with laminin-2 in peripheral nerve, the expression of beta-dystroglycan and laminin-alpha2 chain was studied in rat sciatic nerves undergoing axonal degeneration and regeneration as well as in normal condition. In normal sciatic nerve, immunoreactivity for the cytoplasmic domain of beta-dystroglycan was consistently and selectively localized in the Schwann cell cytoplasm underlying the outer (abaxonal) membrane apposing the basal lamina. While beta-dystroglycan expression was gradually down-regulated in Schwann cells losing contact with axons during axonal degeneration, it was progressively up-regulated as the regenerating process of ensheathment and myelination proceeded during regeneration. Interestingly, beta-dystroglycan expression, when detectable, was always restricted to the Schwann cell cytoplasm beneath the outer membrane apposing the basal lamina during both axonal degeneration and regeneration. Furthermore, laminin-alpha2 immunoreactivity roughly paralleled that of beta-dystroglycan during both axonal degeneration and regeneration, indicating that the expression of beta-dystroglycan and laminin-alpha2 is induced and maintained by the Schwann cell contact with axons. Our results indicate that the dystroglycan complex is involved in the adhesion of the Schwann cell outer membrane with the basal lamina and suggest that the dystroglycan complex may play a role in the process of Schwann cell ensheathment and myelination through the interaction with laminin-2.

Animals↗
PubMed2000

Predictive value of histology at the invasive margin in the prognosis of early invasive colorectal carcinoma.

To accurately select patients with malignant colorectal polyps who are at high risk of adverse outcome, we examined the predictive value of clinicopathological factors, with special attention paid to the histology at the invasive margin. We examined 75 submucosal carcinomas from 75 patients, initially resected by polypectomy, including endoscopic, trans-anal, trans-sacral, and trans-sphincteric local excision. The associations between clinicopathological features such as sex and age; tumor size, location, shape, depth of submucosal invasion, vascular invasion, histology at the central part, and histology at the invasive margin; and the presence or absence of a residual adenomatous component and adverse outcome were examined by univariate and multivariate logistic regression analyses. Lymph node metastases were found in 2 patients, local recurrence in 4, and distant metastases in 2. Univariate logistic regression analysis showed that unfavorable histology at the invasive margin was significantly associated with lymph node metastasis or local recurrence (P = 0.0373), whereas the association of lymphatic invasion and vascular (lymphatic or venous) invasion with lymph node metastasis or local recurrence had marginal significance (P = 0.0785; P = 0.0990). Multivariate logistic regression analysis, with unfavorable histology at the invasive margin and lymphatic invasion as independent variables, showed that unfavorable histology alone had significance (P = 0.0373) in predicting adverse outcome. Widely accepted criteria such as massive submucosal invasion, positive vascular invasion, and poorly differentiated histology, were less useful in predicting adverse outcome. These results suggest that unfavorable histology at the invasive margin is a useful risk factor for predicting lymph node metastasis or local recurrence in patients with malignant colorectal polyps.

Adult↗
PubMed2000

Psoas abscess complicating Crohn's disease: report of a case.

We describe herein the case of a psoas abscess complicating Crohn's disease, and present a review of the literature on this unusual disease entity. A 22-year-old Japanese man with a 5-year history of Crohn's ileocolitis presented with right lower abdominal and hip pain, and a diagnosis of right psoas abscess was subsequently made by abdominal computed tomography (CT). Following the administration of antibiotics and CT-guided percutaneous drainage of the abscess, the patient's symptoms temporarily improved; however, 2 weeks later, the abscess cavity was found to have extended around the periarticular tissue of the right hip joint. To prevent the development of septic arthritis of the hip joint, surgical drainage of the abscess cavity and ileocecal resection were immediately performed, after which the patient's condition greatly improved. The resected specimen showed Crohn's ileocolitis with an external fistula in the terminal ileum which was considered to have caused the psoas abscess. Since psoas abscess in Crohn's disease can result in serious complications such as septic arthritis of the hip joint if left untreated, aggressive treatment should be initiated without delay.

Adult↗
PubMed2000

A possible novel src-related tyrosine kinase in cancer cells of LEC rats that develop hepatocellular carcinoma.

BACKGROUNDS/AIMS: Src-related protein tyrosine kinase is known to be related to cell transformation. In this study, we report a possible novel src-related tyrosine kinase of 100 kDa specifically expressed in the nuclei of hepatocytes and/or cancer cells in Long-Evans Cinnamon rats, one of the experimental models of hepatocellular carcinoma. METHODS: Src-related protein tyrosine kinase in hepatocytes of Long-Evans Cinnamon rats was analyzed by using immunohistochemistry and Western blot and in vitro tyrosine kinase assay using a specific antibody (src antibody) against a synthetic peptide corresponding to the conserved autophosphorylation site of src family tyrosine kinases. RESULTS: Src-related protein was found to be expressed in the nuclei of hepatocytes and/or cancer cells in Long-Evans Cinnamon rat liver, exhibiting tyrosine kinase activity, and migrated to the position of 100 kDa. The protein quantity and activity of this 100-kDa src-related protein tyrosine kinase significantly increased with the progress of chronic hepatitis to hepatocellular carcinoma, especially in the tumorous portion of the liver. On the other hand, the 100-kDa src-protein tyrosine kinase was not observed in the nuclei of hepatocytes and/or cancer cells in normal age-matched control Wistar rats. CONCLUSIONS: Since the src-family tyrosine kinases have been observed at a molecular weight of 55 to 62 kDa and located in the hepatocellular membrane and/or cytoplasm, the 100-kDa src-related protein tyrosine kinase observed in the present study may be novel, and closely related to the pre-cancerous and cancerous process in Long-Evans Cinnamon rat liver.

Animals↗