[Removal of bile duct stones by endoscopic papillary balloon dilatation (EPBD) of papilla of Vater].
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Adult↗
Biomedical subjects
S Yamamura
Publications and source records attributed to S Yamamura.
Nucleotide sequence of oat (Avena sativa L.) cDNA encoding an auxin-binding protein (ABP1).
We isolated and determined a nucleotide sequence of a cDNA clone encoding a protein homologous to maize major auxin-binding protein (ABP1) from a cDNA library of oat coleoptiles. The deduced amino acid sequence of this clone contained an N-linked glycosylation signal and an ER-retention signal. Furthermore, two domains that were important to interact with auxins, were conserved in this clone at amino acid level.
Amino Acid Sequence↗
New medicinal treatment for severe gingivostomatitis.
We formulated de novo a poraprezinc-sodium alginate suspension (P-AG) as a specific treatment for severe gingivostomatitis and administered it to 15 patients who had developed such inflammation while on chemotherapy. Very high utility of P-AG was demonstrated and the response was classified as excellent in 10 patients and good in 5 patients. The mechanism of the beneficial effect of P-AG in treatment of severe gingivostomatitis accompanied by hemorrhagic erosion and ulcers is considered to involve the mucosal protective effect, free radical scavenging activity and tissue repair promoting action of poraprezinc together with the hemostatic action of sodium alginate.
Adult↗
Isolation and characterization of an auxin-inducible SAUR gene from radish seedlings.
A gene homologue to the auxin-inducible SAUR (Small Auxin Up RNAs) of soybean was isolated from a cDNA and a genomic library of radish. The cDNA clone was about 470 bp in length and contained a DST (Down STream) element that was involved in mRNA instability in the 3'-untranslated region. The genomic clone contained two short sequences that related to auxin-responsible core sequences (AGTCTC and TATCCCAC) in its promoter region. The radish SAUR transcript was accumulated by auxin and cycloheximide treatments in the same way as that in other plant species. However, the NDE and DUE elements that were reported in all of the other SAUR gene promoters were not conserved in this radish SAUR gene. The results suggest that the promoter activity of the SAUR gene will be regulated by only two short sequences.
Amino Acid Sequence↗
N,N-dimethylsphingosine 1-phosphate activates human platelets.
We recently reported that N,N-dimethylsphingosine 1-phosphate (DMS-1-P) can be formed from N,N-dimethylsphingosine (DMS) in activated platelets [Y. Yatomi et al., Biochem. Biophys. Res. Commun. 231 (1997) 848-851]. In this study, we synthesized, for the first time, DMS-1-P and examined the functional effects of DMS-1-P and its related sphingolipids on platelets. Although exogenous DMS was inactive, its phosphorylated derivative, DMS-1-P, induced platelet intracellular Ca2+ mobilization and shape change, but not aggregation or release reactions. Since sphingosine 1-phosphate (Sph-1-P) is structurally related to DMS-1-P and activates platelets more strongly than DMS-1-P, a competitive binding experiment for [3H]Sph-1-P was performed using DMS-1-P. DMS-1-P reduced the binding of [3H]Sph-1-P to platelets almost as much as unlabeled Sph-1-P did. These results suggest that DMS-1-P activates platelets via an interaction with a platelet surface receptor for Sph-1-P.
Blood Platelets↗
Sphingosine 1-phosphate regulates melanoma cell motility through a receptor-coupled extracellular action and in a pertussis toxin-insensitive manner.
Our previous work showed that sphingosine 1-phosphate (Sph-1-P) inhibits the cell motility of mouse melanoma B16/F10, and other types of cells at 10-100 nM concentrations. In the present paper, we have identified and characterized specific cell surface binding sites for Sph-1-P in F10 cells. Sph-1-P immobilized on controlled pore glass beads inhibited the motility of F10 cells, suggesting that Sph-1-P acts on the cells from the outside. Binding assays with [3H]Sph-1-P revealed the presence of specific cell surface binding sites for Sph-1-P in F10 cells. Scatchard analysis demonstrated a single class of binding sites for Sph-1-P. The binding of [3H]Sph-1-P to F10 cells was inhibited by the addition of excess unlabeled Sph-1-P but not other natural sphingolipids. The specific binding was also sensitive to treatment with a protease. Using Sph-1-P-immobilized affinity chromatography, we, for the first time, identified 41-kDa and 79-kDa Sph-1-P binding proteins on the melanoma cell surface, although the 41-kDa protein was less specific to Sph-1-P. We demonstrated that pertussis toxin (PTX) treatment did not abolish the motility inhibition by Sph-1-P, suggesting that no PTX-sensitive G-protein is involved in the signaling. Furthermore, Sph-1-P was found to be specifically released from mouse BALB/3T3 clone A31 cells and F10 cells. Collectively, these results strongly suggest that Sph-1-P regulates melanoma cell motility through an extracellular action by specific binding to cell surface receptor protein(s), which is independent of PTX-sensitive G-protein.
Animals↗
A close association of GM3 with c-Src and Rho in GM3-enriched microdomains at the B16 melanoma cell surface membrane: a preliminary note.
B16 melanoma is characterized by high content of GM3 ganglioside, which has been recognized as a melanoma-associated antigen defined by specific monoclonal antibodies. We report now that GM3 is present predominantly (>90%) in the 1% Triton X-100-insoluble, low-density microvesicular fraction ("detergent-insoluble glycosphingolipid-enriched microdomain"; DIGEM) separated on sucrose density-gradient centrifugation. Associated with DIGEM, many signal transducer molecules such as c-Src, FAK, and the low-molecular-weight G-proteins Rho A and H-Ras were also found. Rho A and FAK were found in part, and PLC-beta2 and G alphas were found exclusively, in the high-density fraction. Immunoprecipitation of GM3 present in DIGEM by anti-GM3 antibody DH2, followed by Western blotting, revealed co-precipitation of Rho A and c-Src with GM3. These findings suggest (i) a specific organization of GM3 in close association with Rho A and c-Src within DIGEM at the melanoma cell surface; and (ii) such organizational units may be directly involved in signal transduction, in which glycosphingolipids receive signals which are subsequently transduced by associated transducer molecules.
Animals↗
Sphingosine 1-phosphate induces platelet activation through an extracellular action and shares a platelet surface receptor with lysophosphatidic acid.
Sphingosine 1-phosphate (Sph-1-P) has been implicated as an intracellular second messenger in many studies. We investigated the metabolism of Sph-1-P and the mechanism by which Sph-1-P induces activation in enucleated and highly differentiated platelets. Platelets lack Sph-1-P lyase activity, possess persistently active sphingosine (Sph) kinase, and abundantly store Sph-1-P. Although exogenous Sph-1-P activated platelets, intracellular Sph-1-P, formed from exogenously added Sph by cytosolic Sph kinase, failed to do so. To support the notion that exogenous Sph-1-P stimulates platelets from outside, contact of platelet surfaces with immobilized Sph-1-P covalently linked to glass particles resulted in platelet activation. Furthermore, we detected the specific binding sites for radiolabeled Sph-1-P on the platelet surface, suggesting extracellular effects of Sph-1-P on plasma membrane receptors. This specific Sph-1-P binding was inhibited not by other sphingolipids but by lysophosphatidic acid (LPA), and platelet aggregation response to LPA was specifically desensitized by prior addition of Sph-1-P. Finally, internally stored Sph-1-P is released extracellularly upon stimulation, and the release correlated well with protein kinase C activation in intact platelets. These results suggest that Sph-1-P acts not intracellularly but intercellularly, following discharge from activated platelets, and shares a platelet surface receptor with LPA.
Blood Platelets↗
Prostaglandin levels of primary bone tumor tissues correlate with peritumoral edema demonstrated by magnetic resonance imaging.
BACKGROUND: Several reports have shown peritumoral edema accompanying primary bone tumors demonstrated by magnetic resonance imaging (MRI). However, the mechanism of this inflammatory reaction is still unclear. The authors postulated that the reaction was caused by some chemical mediators including prostanoids, because several investigators have observed that some types of bone tumors synthesize prostanoids. Therefore, the authors compared MRI findings and tumor prostaglandin (PG) levels. METHODS: The subjects were 29 patients with primary bone tumor or tumor-like conditions: chondroblastoma (n = 5); chondrosarcoma, including rare variants (n = 8); giant cell tumor (n = 6); osteochondroma (n = 5); osteoblastoma (n = 2); Ewing's sarcoma (n = 2); and eosinophilic granuloma (n = 1). T1- and T2-weighted spin echo images were obtained in all but one patient before surgery. The tumor concentration of prostaglandin E2, 6-keto-PGF1 alpha, and thromboxane B2 were measured by radioimmunoassay. RESULTS: MRI distinctly showed bone marrow edema in 9 and soft tissue edema in 12 of the 28 patients examined. These findings were significantly correlated with the PG levels. Moreover, the PG levels were correlated with the histologic classifications (P < 0.001). In particular, the chondroblastomas showed prominent concentrations of PGs compared with other cartilaginous tumors or giant cell tumors. CONCLUSIONS: Although peritumoral edema accompanying benign and malignant bone tumors is not necessarily related to one single pathophysiologic mechanism, these results suggest that PG production was an important cause of the inflammatory reaction that was revealed by MRI. Recognition of this phenomenon is advantageous not only for strict diagnostic purposes but also for understanding the characteristic features of individual primary bone tumors.
6-Ketoprostaglandin F1 alpha↗
Gorham massive osteolysis.
Gorham syndrome (massive osteolysis) is a very rare tumour-like lesion characterized by progressive osteolysis. The diagnosis must be confirmed by the microscopic finding of intramedullary angioma-like vascular structures. We report a case of a 15-year-old boy with a pathological fracture in his left humerus. Imaging modalities such as magnetic resonance imaging, computed tomography, angiography and bone scintigraphy failed to disclose to tumorous lesion that filled a cavity in the left humerus. After observing the boy's progress for 6 months, a temporary diagnosis of Gorham syndrome was made, and surgical treatment was chosen. After resection of the left humeral head and the proximal one-quarter of the humerus, thorough curettage was performed in the distal humerus and an intramedullary artificial humeral head fixed with adequate success. Pathological examination of the specimen revealed intramedullary haemangioma of the humerus.
Adolescent↗
Use of adriamycin-impregnated methylmethacrylate in the treatment of tumor metastases in the long bones.
Internal fixation or endoprosthetic replacement of a long bone metastatic lesion was performed using adriamycin-containing bone cement (methylmethacrylate) after resection or curettage of the lesion in 25 patients (27 limbs). Survival rate, limb function, and local recurrence rate were retrospectively evaluated in this patient cohort. Survival rate was 53% at 12 months and 30% at 24 months, which was better than in previous reports. One patient showed local recurrence radiographically. Postoperatively, none of the patients developed infection, delayed wound healing, myelo-suppression attributed to adriamycin, and 74% of the patients were able to walk outdoors.
Adolescent↗
Malignant hemangioendothelioma of the left calcaneus associated with fever and hematological abnormalities.
A case of malignant hemangioendothelioma of the left calcaneus associated with unique system manifestations is reported here. The severe toxic manifestations included: high fever, anemia, leukocytosis, coagulation abnormalities, and other signs. Because of poor response to many antibiotic regimens, the confusion of diagnosis, and severe coagulation abnormalities with clinical signs that the life of the patient was endangered, below the knee amputation was performed. Pathological studies revealed a malignant hemangioendothelioma. A review of the case suggests that the signs and symptoms were possibly due to an immune response to the tumor rather than to secondary infection, although the latter possibility cannot be completely excluded.
Adult↗
Activation of pp60c-src is necessary for human vascular smooth muscle cell migration.
BACKGROUND: The most widely distributed nonreceptor tyrosine kinase is pp60c-src (src), yet the role of this intracellular signaling protein in cell migration has not been defined. Given that smooth muscle cell (SMC) migration is essential for the development of intimal hyperplasia, we investigated the importance of src in locomotion of human vascular SMC. METHODS: SMC migration was evaluated using a microchemotaxis chamber assay and videomicroscopy. Src kinase activity was determined by measuring phosphorylation of a synthetic derivative of p34cdc2, a specific substrate for src. Blocking antibodies to src were introduced using a cytoplasmic microinjection technique. RESULTS: Stimulation of SMC with platelet-derived growth factor (PDGF)-BB and AB resulted in an increase in src activation, whereas PDGF-AA did not consistently enhance src activity. These findings correlated with the ability of the PDGF isotypes to stimulate SMC chemotaxis; PDGF-BB and AB produced 7.4 +/- 0.3- and 5.3 +/- 0.5-fold increases in SMC chemotaxis, whereas PDGF-AA inhibited chemotaxis. SMC migration in response to PDGF-BB and serum was significantly inhibited by intracellular injection of a blocking antibody. CONCLUSIONS: Our findings reveal an association between agonist-induced src activation and chemotaxis. Moreover, an antibody that inhibits src activation dramatically inhibits migration of individual SMC. We conclude that activation of src is necessary for SMC migration. Because of its importance in SMC migration, either molecular or pharmacologic inhibitors of src may be useful in the control of intimal hyperplasia.
Becaplermin↗
Platelet-derived growth factor and extracellular matrix proteins provide a synergistic stimulus for human vascular smooth muscle cell migration.
PURPOSE: Smooth muscle cell (SMC) migration contributes significantly to the hyperplastic response that follows arterial injury. In vitro studies have shown that a number of growth factors and extracellular matrix (ECM) proteins individually stimulate vascular SMC migration. However, after arterial injury, SMCs exist in a complex environment in which they are exposed to many of these proteins simultaneously. The response of SMCs to multiple simultaneous stimuli may differ significantly from their response to any single individual stimulus. In this study, we evaluated the chemotactic response of human vascular SMCs to various combinations of growth factors and ECM proteins. METHODS: Human saphenous vein SMCs were used for all experiments. Using a 4-hour modified Boyden-chamber assay, we evaluated the effect on SMC chemotaxis of combinations of one of three growth factors (platelet-derived growth factor [PDGF]-AB, basic fibroblast growth factor [bFGF], or epidermal growth factor [EGF]), and one of four ECM proteins (fibronectin, laminin, or collagen type I or IV). A standard fluorimetric assay was used to assess changes in intracellular calcium ([Ca2+]i) in response to the various combinations of growth factors and ECM proteins. RESULTS: A simple additive effect was seen between ECM proteins and bFGF or EGF. However, when SMCs were simultaneously exposed to PDGF and ECM proteins, we observed a synergistic increase in chemotaxis. This synergy was evident for all concentrations of collagen type I and IV but only with higher concentrations of fibronectin and laminin. We evaluated whether intracellular calcium may be the signaling pathway through which this synergistic effect is mediated. Although ECM proteins alone did not stimulate a rise in [Ca2+]i, ECM proteins enhanced the early peak in [Ca2+]i induced by PDGF. CONCLUSION: These data show that PDGF acts synergistically with the ECM proteins to promote SMC migration; this effect appears to be specific for PDGF and was not observed with other growth factors. The mechanism responsible for this phenomenon may be a synergistic increase in [Ca2+]i in SMCs simultaneously exposed to both proteins.
Calcium↗
Acceleration of impairment of endothelium-dependent responses under poor runoff conditions in canine autogenous vein grafts.
OBJECTIVES: To assess the effects of changes in shear stress on endothelium-dependent responses. MATERIALS AND METHODS: Autologous vein grafts were implanted in poor or normal distal runoff limbs of 10 mongrel dogs. Six weeks after grafting the vein grafts were removed, cut into rings, and suspended in organ chambers for isometric tension recording. RESULTS: The average value of intimal thickening was 110.7 +/- 45.2 microns in poor runoff limbs and 65.5 +/- 27.9 microns in control limbs, respectively. There was a significant difference between the two groups. Acetylcholine caused comparable endothelium-independent contractions in both groups. In the control group, adenosine diphosphate, thrombin and A23187 caused endothelium-dependent relaxations. In the poor runoff group, the endothelium-dependent relaxations caused by adenosine diphosphate and thrombin were impaired, while A23187 caused comparable endothelium-dependent relaxations. Direct relaxations in response to sodium nitroprusside were comparable between the two groups. CONCLUSIONS: This dysfunction of the endothelium under conditions of abnormal flow may accelerate intimal thickening of the vein graft and result in late graft failure.
Animals↗
Surgical strategy of abdominal aortic aneurysm with preoperative renal failure.
OBJECTIVES: To determine the effect of preoperative renal failure on the outcome of patients suffering from infrarenal abdominal aortic aneurysm (AAA). METHOD: During the period from January 1979 to August 1995, 364 patients with AAA were admitted to our hospital and 323 underwent elective repair. The patients were retrospectively analysed in three groups. Group I was composed of 273 patients with a normal renal function who underwent an aneurysm repair. Group II was composed of 50 patients who demonstrated a preoperative renal dysfunction (creatinine above 2.0 mg/dl or creatinine clearance below 40 ml/min) and underwent an operation, including three patients maintained on chronic haemodialysis. Group III was composed of 18 patients with a renal dysfunction who did not undergo repair, including one patients maintained on chronic haemodialysis. RESULTS: The operative mortality rate of groups I and II were 0.4% and 2.0%, respectively, although no significant difference was observed. The incidence of postoperative cardiac and pulmonary complications were also comparable in two groups. No patients required acute haemodialysis. The 5-year survival rate of group II (44%) was significantly higher than that of group III (20%), and seven of the 18 patients (39%) in group III ultimately died of a rupture of the AAA. CONCLUSIONS: Patients with chronic renal failure can undergo an abdominal aortic aneurysm repair based on the same indications as those without renal failure.
Aged↗
Change of the microstructure of microcrystalline cellulose with grinding and compression.
The microstructure of microcrystalline cellulose was investigated by use of a radial distribution function (RDF) based on the intensity of X-ray scattering data. Changes in the microstructure of the cellulose as a result of grinding and compression were detected by use of the RDF. The RDF of intact microcrystalline cellulose had peak maxima corresponding to distances of approximately 1.5, 2.6, 5.0, 8.2, 13.3 and 17.0 A. The first two corresponded to the intramolecular atomic distances; other peaks were attributable to the intermolecular (inter-fibre) atomic distance. Changes in the RDF as a result of grinding indicated that the regular intermolecular atomic arrangement was gradually lost. Compression resulted in formation of long-range (> 20 A) ordering of the intermolecular (inter-fibre) atomic arrangement. These results show that RDF analysis is suitable for monitoring changes in the structure of microcrystalline cellulose which occur as a result of grinding and compression.
Cellulose↗
Effects of serotonin and endothelin on the smooth muscle cells of autogenous vein grafts.
BACKGROUND: The purpose of this study was to compare the effects of vasoconstrictor substances such as 5-hydroxytryptamine (5-HT) and endothelin on the smooth muscle of canine femoral veins and vein grafts. METHODS: The right canine femoral vein was grafted into the right femoral artery. The left femoral vein was used as a control. In other experiments to examine the effects of surgical procedures such as dissection of the adventitia and the effects of grafting (vein-to-vein bypass), the right femoral vein was dissected out but not removed for grafting and an autogenous vein bypass of the right femoral vein was made using the left femoral vein. In all experiments, the veins were removed 4 weeks after operation and suspended in organ chambers for isometric tension recording. RESULTS: Maximum contractions to endothelin were comparable in control vein and vein grafts. In control vein, the maximum contraction to 5-HT was small, and was inhibited by both methiothepin, a 5-HT, and 5-HT2 antagonist, and sarpogrelate hydrochloride, a 5-HT2 antagonist. In vein grafts 5-HT produced significantly larger contractions than in control veins, which were inhibited by methiothepin but not by the 5-HT2 antagonist. In veins with adventitial dissection alone and vein-to-vein grafts, 5-HT produced small contractions which were comparable to those in control vein. CONCLUSION: The larger contraction response to 5-HT in canine vein grafts may be due to an increased responsiveness of the 5-HT1 receptor caused by grafting into the arterial circulation.
Animals↗