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Biomedical subjects

M Nose

Publications and source records attributed to M Nose.

At least 163 records · Page 9Linked to original sources
PubMed1990

The effect of high-energy underwater shock waves on implanted urinary bladder cancer in rabbits.

We have examined the effects of high-energy shock waves (HESW) on implanted urinary bladder cancer in rabbits. The bladder cancer was exposed to 2000 to 6000 shots of focused HESW under ultrasound guidance. Although only focal necrosis of the tumor was seen in the one-day HESW exposure (2000 shots), wider and deeper necrosis was observed in the tumors following serial HESW (4000 or 6000 shots; 2 or 3 days). These results indicate that serial HESW exposure has destructive effects on implanted bladder cancer in rabbits.

Animals↗
PubMed1990

Radioligand binding characteristics of beta 2-adrenoceptors of cultured melanoma cells.

The existence of beta-adrenoceptors on intact cells of the human malignant melanoma cell line A-375 was investigated using the binding properties of the tritiated radioligand (-)-[3H]CGP-12177, a hydrophilic non-selective beta-adrenoceptor antagonist. Displacement experiments of the radioligand from its binding site were performed with antagonists and agonists to determine the beta-adrenoceptor subtype selectivity. The binding of (-)-[3H]CGP-12177 was saturable, of high affinity (KD = 0.025 nmol/l, n = 12) and was rapid and readily reversible. The maximal number of binding sites (Bmax) was 33.5 +/- 1.9 fmol/10(7) cells or 2018 +/- 114 receptors per cell. beta-adrenoceptor antagonists inhibited binding of the radioligand with monophasic displacement curves. IC50 values were (nmol/l): propranolol (non-selective) 2.82, alprenolol (non-selective) 2.0, ICI 118,551 (beta 2-selective) 3.5 and bisoprolol (beta 1-selective) 2200. Agonists inhibited binding in the order of potency of isoprenaline greater than adrenaline greater than noradrenaline. It is concluded that cells of the melanoma cell line A-375 contain a homogeneous population of beta 2-adrenoceptors.

4-Chloro-7-nitrobenzofurazan↗
PubMed1990

[Allergen skin tests to insects, chironomid, caddis fly and silkworm moth, in patients with nasal allergy].

The present study was undertaken to assess the importance of insects as allergens causing nasal allergy. We performed intradermal skin tests with extracts from three insects, chironomid, caddis fly, and silkworm moth, on patients with nasal allergy and on volunteers among medical students. Twenty-two (27.5%) of 80 nasal allergic patients showed positive reactions to chironomid allergen and 9 (11.3%) had positive reactions to caddis fly allergen and 18 (22.5%) to silkworm moth allergen. These positive rates were as frequent as those to Candida or ragweed. Medical students were divided into two groups, symptomatic and asymptomatic, according to the presence or the absence of nasal allergy. Three (11.5%) of 26 symptomatic group showed positive reactions to chironomid and one (3.8%) to caddis fly and 5 (19.2%) to silkworm moth. While even 4 (8.3%) of 48 asymptomatic group showed positive reactions to chironomid, 2 (4.8%) to caddis fly, and 6 (12.5%) to silkworm moth. These results suggested that these insects, chironomid, caddis fly, and silkworm moth, are relatively common than we expected and suspected as important allergens in nasal allergy.

Adolescent↗
PubMed1990

Tissue distribution of HRF20, a novel factor preventing the membrane attack of homologous complement, and its predominant expression on endothelial cells in vivo.

A 20,000 molecular weight (MW) homologous restriction factor (HRF20), detected by 1F5 monoclonal antibody (mAb), is present on blood cell surfaces and inhibits the terminal stage of the formation of membrane attack complexes by homologous complement activation. The tissue distribution of HRF20 was studied by immunohistochemical analysis using 1F5. HRF20 was predominantly expressed on endothelial cells of systemic arteries, veins and capillaries, as well as on the surface of cultured human umbilical vein endothelial cells. HRF20 was also detected, to a lesser extent, on the Schwann sheath of peripheral nerve fibres, ependymal cells and certain epithelial cells such as acinar cells of the salivary gland, bronchial epithelium, renal tubules and squamous epithelium. The distribution pattern of HRF20 differed somewhat from that of decay-accelerating factor (DAF), which is another membrane inhibitor of homologous complement activation.

Antibodies, Monoclonal↗
PubMed1990

Recognition of N-glycosidic carbohydrates on esophageal carcinoma cells by macrophage cell line THP-1.

Cell-to-cell contact between macrophages and tumor cells is an important initial reaction in a host defense mechanism against tumor cells. The authors have studied cell surface components of human esophageal carcinoma cells recognized by macrophages. Superoxide release from THP-1 cells, a human macrophage cell line, was analyzed in their interaction with a battery of human squamous cell carcinoma cell lines (TE) originated from esophageal cancer patients. The macrophage-triggering ability of TE 1 cell line, a high stimulant, was reduced after treatment with trypsin or tunicamycin, an inhibitor of N-glycosidic glycosylation. Addition of monosaccharides was efficient in competitive inhibition of these cellular interaction. Moreover, con-A-resistant mutation of TE 1 cells was found to reduce their macrophage-triggering ability, associated with increase of L-PHA-binding capacity, suggesting substitution to the GlcNAc beta(1----6)-linked lactosamine antenna in N-glycosidic carbohydrates. These findings suggest that terminal residues of N-glycosidic carbohydrates on some esophageal carcinoma cells may contribute to the recognition sites of macrophages.

Carcinoma, Squamous Cell↗
PubMed1990

Increase of beta 1-6-branched oligosaccharides in human esophageal carcinomas invasive against surrounding tissue in vivo and in vitro.

The -GlcNAc beta 1-6Man- (beta 1-6) branched N-glycosidic oligosaccharides expressed on tumor cells have been found to contribute to malignant and metastatic potential in experimental tumor models. Phaseolus vulgaris leukoagglutinin (L-PHA) requires the beta 1-6-linked lactosamine antenna for high-affinity binding and was used histochemically to characterize the distribution of these sugar structures in human esophageal squamous cell carcinomas from 42 patients. Leukoagglutinin-reactive carcinoma cells in the invasive tumors were distributed predominantly on the outer surface of the tumor adjacent to the surrounding tissue. Furthermore, when TE 1 cells, a human esophageal squamous cell carcinoma line, were cultured in a collagen gel matrix to obtain colonies in a three-dimensional form, these colonies exhibited high affinity for L-PHA binding only in the outer cell layer facing the collagen matrix, unrelated to the cell growth cycle. These findings suggest that the increase in beta 1-6-branched oligosaccharides in esophageal carcinomas is an important trait of the tumor in the invasion into the surrounding tissue.

Acetylglucosamine↗
PubMed1990

[Molecular and immunological approach to hematological disease: detection and analysis of intracellular modified nucleosides by flow cytometry].

Modified nucleosides are components of ribosomal RNA (rRNA), transfer RNA (tRNA) and messenger RNA (mRNA). 1-methyladenosine and pseudouridine are members of those modified nucleosides. The urinary concentration of 1-methyladenosine and pseudouridine of cancer patients are higher than that of healthy controls, and those compounds were reduced after effective chemotherapy. Thus those compounds might be expected to use as tumor markers. In this study cellular origin of 1-methyladenosine and pseudouridine were analysed about two tumor cell lines (HUT-102, THP-1), peripheral blood lymphocytes (PBL) from healthy adult and PBL under the phytohemagglutinin stimulation, by flow cytometric analysis and immunofluorescent staining of cellular RNA using monoclonal antibodies specific for 1-methyladenosine (AMA) and pseudouridine (APU). Both 1-methyladenosine and pseudouridine were detected in more than 90% of tumor cells above the thresholds of flow cytometric detection (Spectrum III, Ortho). The PBL under the PHA stimulation also tended to take the same way of the tumor cell lines, whereas few of the PBL contained 1-methyladenosine above the thresholds. According to the DNA analysis of those cell lines, high contents of the modified nucleosides in the cell might follow DNA synthesis, this leads to one reason for high levels of the urinary excretion of the modified nucleosides in cancer patient.

Adenosine↗
PubMed1989

Substitution of asparagine324 with aspartic acid in the Fc portion of mouse antibodies reduces their capacity for C1q binding.

The sequence of the heavy chain C region of mouse mutant IgG2a antibodies with reduced capacity for C1q binding but with retained ability for Fc receptor-mediated functions was determined by cDNA cloning and by mRNA sequencing. The specific mutation was found to be the substitution of asparagine324 with aspartic acid. Asparagine324 represents a new residue relating to the C1q-binding sites previously described.

Amino Acid Sequence↗
PubMed1989

Establishment and characterization of mouse leukemia cell lines L615K and L7212K derived from transplantable murine leukemias maintained in China.

Two culture cell lines L615K and L7212K were established from transplanted murine leukemias L615 and L7212, which had been established and maintained in China for years. Based on morphological, immunological and gene rearrangement analyses, L7212K cells are considered to be of T-cell origin while L615K cells might be immature T-cells. Immunofluorescence assays of viable leukemia cells and fluorescence focus assays of their culture supernate for infectious viruses suggested that recombinant mink cell focus-inducing viruses were significantly involved in both leukemic cell lines. Chromosome analysis of the L615K cells revealed a translocation t(12;17) which probably involved the c-fos locus on chromosome 12, since the DNA rearrangement of c-fos was demonstrated by Southern blot analysis with Hind III, and c-fos has been assigned to this chromosome. Although the expression of this gene was not detected by RNA Northern blot analysis, c-myc was slightly expressed in both L615K and L7212K cells.

Animals↗
PubMed1989

Time course and extent of alpha 1-adrenoceptor density changes in rat heart after beta-adrenoceptor blockade.

1. It has been suggested that impaired beta-adrenoceptor stimulation is a condition under which the functional role of cardiac alpha 1-adrenoceptors is enhanced. We therefore investigated the extent and time course of changes in alpha 1-adrenoceptor characteristics after chronic treatment with the beta-adrenoceptor blocker propranolol in rat heart. For comparison beta-adrenoceptors were also studied. The mechanism of the changes in adrenoceptor density was investigated with cycloheximide, an inhibitor of protein synthesis. The functional significance of an increased alpha 1-adrenoceptor density was tested by measuring isometric force of contraction in the presence of phenylephrine or isoprenaline in right ventricular papillary muscles. 2. Rats were treated with propranolol (9.9 mg kg-1 daily) or 0.9% NaCl, applied with osmotic minipumps for 1, 2, 3 or 7 days. Propranolol treatment resulted in a maximally 28% increase of alpha 1-adrenoceptor density after 3 days (NaCl 95.9 +/- 3.5 vs. propranolol 123.0 +/- 1.6 fmol mg-1 protein, n = 6, P less than 0.01). This up regulation reached significant levels after 2 days of treatment and was reversible after cessation of treatment within two days. KD-values were the same for NaCl- and propranolol-treated rats. Changes of Bmax and KD in beta-adrenoceptor binding assays did not reach significant levels. 3. Cycloheximide (1.5 mg kg-1 i.p. daily for 3 days) inhibited the propranolol-induced increase in Bmax of alpha 1-adrenoceptors completely. In addition, cycloheximide also decreased the density of alpha 1- and beta-adrenoceptors also under control conditions. 4. pD2-values for the positive inotropic effect of phenylephrine and isoprenaline in isolated electrically driven papillary muscle were similar in NaCl- and propranolol-treated rats (phenylephrine: 5.41 + 0.11 vs. 5.41 + 0.19, n = 7; isoprenaline: 6.31 + 0.18 vs. 6.65 + 0.19, n = 7). The observed increase in alpha-adrenoceptor density in healthy rat heart may therefore not be high enough to enhance the phenylephrine-induced increase in force of contraction. 5. In conclusion, time course and effects of cycloheximide indicate that the increase in B,,,, of myocardial alpha 1-adrenoceptors is due to de novo synthesis of receptors. However, at least for the rat heart model, a functional significance of this increase could not be demonstrated.

Adrenergic beta-Antagonists↗
PubMed1989

Corticosterone secretion-inducing activity of saikosaponin metabolites formed in the alimentary tract.

The corticosterone secretion-inducing activities of saikosaponin a, saikosaponin c and saikosaponin d, isolated from the root of Bupleurum falcatum L., and 27 metabolites formed in the murine alimentary tract were studied in mice. Serum corticosterone was determined by high-performance liquid chromatography (HPLC). Intraperitoneal administration of saikosaponin a and its intestinal metabolite, prosaikogenin F, showed corticosterone secretion-inducing activity at a dose of 0.1 mmol/kg, and maximally increased it at a dose of 0.4 mmol/kg. On the other hand, the genuine sapogenin, saikogenin F, was inactive. Saikosaponin b1 and saikosaponin g, gastric metabolites of saikosaponin a, and their intestinal metabolites, prosaikogenin A, prosaikogenin H, saikogenin A and saikogenin H, were also inactive. Serum corticosterone was increased by the administration of saikosaponin d and its intestinal metabolite, prosaikogenin G, at a dose of 0.04 mmol/kg, and it reached the maximal level at the dose of 0.1 mmol/kg. Saikogenin G also showed a slight activity. A gastric metabolite of saikosaponin d, saikosaponin b2, and its intestinal metabolites, prosaikogenin D and saikogenin D, were inactive. In the experiments on saikosaponin c and its metabolites, saikosaponin c was inactive but its intestinal metabolites, especially prosaikogenin E-2, showed activity almost equal to that of saikosaponin a. Saikosaponin h and saikosaponin i, gastric metabolites of saikosaponin c, were also inactive, but their prosaikogenins showed slight activities. When these compounds were orally administered, their corticosterone secretion-inducing activities were similar to those obtained in the intraperitoneal experiment. These results suggest that a proper polar balance between the sugar moiety and the aglycone is important for the corticosterone secretion-inducing activity of saikosaponins and their metabolites.

Animals↗
PubMed1989

Effects of saikosaponin metabolites on the hemolysis of red blood cells and their adsorbability on the cell membrane.

The hemolytic properties and the adsorbability on red blood cells of saikosaponin a, saikosaponin d and 13 metabolites formed in the alimentary tract were investigated. Among these compounds, saikosaponin d and its intestinal product, prosaikogenin G, which possess an alpha-hydroxyl function at C16, showed the strongest hemolytic activity at the dose range of 1.0 to 5.0 micrograms/ml. Saikosaponin a and its intestinal product, prosaikogenin F, which possess a beta-hydroxyl function at C16, showed activity above 10 micrograms/ml. In this case, the monoglycoside, prosaikogenin F, showed the stronger activity than the diglycoside, saikosaponin a. Among the gastric products whose ether ring was cleaved to produce a carbinol, the monoglycosides, prosaikogenin A and prosaikogenin H, showed a slight activity above 25 micrograms/ml, and the saikogenins except saikogenin A were inactive. Saikogenin A, however, had hemolytic activity at a dose of 15 micrograms/ml. The adsorbabilities of these compounds on red blood cell membranes closely paralleled their degrees of hemolytic activity.

Adsorption↗
PubMed1989

[Clinical study on mandibular condylar fracture. 1. Retrospective study in 100 patients with 130 temporomandibular joint fractures with special consideration in the treatment for the various locations and forms of the fractures].

Clinical retrospective investigation was conducted on mandibular condylar fractures of 100 hospitalized cases at the Department of Oral Surgery, Kyoto University Hospital during the period from 1973 to 1983. The following results were obtained, 1. There were 74 males and 26 females. The age of the patients at the time of injury ranged from 4 to 78 years old. The average age was 28.1 years old. 2. Twenty-six patients were treated within a week of injury, 22 cases within 2-weeks and 33 cases were treated after more tham 3 weeks. 3. Of the 100 cases, 70 were unilateral fractures and 30 were bilateral. The incidence of the concomitant fractures of the mandible were higher in bilateral than in unilateral condylar fractures. 4. On fracture level and form 130-site in 100 patients were divided according to the classification of Maclennan and Kubo. Dislocated and high condylar fractures were most frequently observed. 5. Surgical reduction was mainly achieved in low neck fracture, and the contrary conservative treatment was observed in the higher level fracture. On the other hand condylectomy was infrequently indicated in the dislocated head fracture.

Adolescent↗
PubMed1989

[Clinical study on mandibular condylar fracture. 2. Long-term follow-up study in 48 patients with 66 joints].

Sixty-six joints in 49 patients with mandibular condylar fracture were investigated by means of long-term follow-up observation. The group of patients consisted of 39 males and 10 females with ages from 15 to 75 years. The classification of the fractures was follows: MacLennan type 1; four, type 2; four, type 3; 39, and type 4; 39 joints respectively. Treatment was as follows: 25 joints were by conservative therapy, 31 joints were by surgical fixation, and 10 joints condylectomy. The follow-up period of observation ranged from 18 months to 10 years and one month an average of five years and seven months. Clinical assessment was based upon Nakatomi's dysfunction index on mandibular condylar fracture, of which the criteria are as follows; Excellent (No clinical dysfunction sign on the TMJ), Fair (Slight pain, noise, and limited range of motion of the mandible, but clinically no affected mastication), Poor (Moderate dysfunctioned jaw), and Failure (Severe dysfunctioned jaw). 23 joints in 18 patients were ranked as having excellent results. 31 joints in 22 patients were assessed as fair. Ten joints in seven patients were defined as poor, and the remaining two joints in two patients were failures. The overall success rate was 81.7%. There are no statistical differences between patient's groups based on age, sex, uni/bilateral modality, with/without other concomitant fracture, surgical/conservative procedure, location and form of fractures, and duration of period from injury. These results indicated that the conservative procedure would be the first choice as a reasonable and less invasive procedure for functional repair of mandibular condylar fracture. On the other hand, as most patients had some dysfunction sign on the TMJ after mandibular condylar fracture, a more appropriate treatment, surgical or otherwise, should be found.

Adolescent↗
PubMed1989

Analysis of granulomatous arteritis in MRL/Mp autoimmune disease mice bearing lymphoproliferative genes. The use of mouse genetics to dissociate the development of arteritis and glomerulonephritis.

MRL/Mp mice bearing the lymphoproliferation gene (lpr) spontaneously develop systemic granulomatous arteritis coincident with glomerulonephritis (GNP). Although the association of lpr-dependent lymphoproliferation in these mice seems to be a prerequisite for the development of granulomatous arteritis, the genetic basis is poorly understood. The first approach to this problem was to study the ability of another, nonallelic, lymphoproliferative gene, gld (generalized lymphoproliferative disease), inducing arteritis in MRL/Mp mice. The gld gene was placed on an MRL/Mp background by producing reciprocal (MRL/Mp-+/+ X C3H/Hej-gld/gld)F2 hybrid mice. Seventeen percent of these mice with lymphoproliferation had arteritis and GNP, suggesting that more than one lymphoproliferative gene could induce GNP and arteritis in an MRL/Mp background. Next, the effect of rearrangements in the genetic background of MRL/Mp-lpr/lpr mice by hybridization with non-autoimmune lpr-bearing mice was examined. This was done by making MRL/Mp-lpr/lpr X reciprocal (MRL/Mp-lpr/lpr X C57BL/6-lpr/lpr)F1 mice. Thirty-three percent of these mice developed arteritis, but one third of these did not get GNP, thus showing that susceptibility to arteritis was separate from GNP. The histopathologic features of the arteritis in both the F2 hybrids and the backcross mice were granulomatous and were identical to those seen in MRL/Mp-lpr/lpr mice. These findings suggested that it might be possible to dissociated two components (arteritis and GNP) of a severe autoimmune disease of MRL/Mp mice and to study their pathogenesis separately.

Animals↗
PubMed1989

Lectin histochemistry in adrenocortical hyperplasia and neoplasms with emphasis on carcinoma.

Lectin binding analysis of Con A, SBA, PNA, WGA, HPA, RCA-I, DBA, and UEA-I was performed in two cases of normal human adrenal gland, four cases of adrenocortical hyperplasia, six cases of adrenocortical adenoma, and seven cases of adrenocortical carcinoma to examine the differences of lectin binding properties. No lectins were bound specifically to adrenocortical cells. Binding of RCA-I was observed in some carcinoma cells focally but not in benign counterparts. With WGA and Con A, the cytoplasmic binding became apparent in the cells manifesting hypercorticism. In adrenocortical carcinoma, various WGA and Con A binding patterns were intermingled, but no specific patterns were identified. The focal nature of RCA-I binding, and no specific WGA and Con A binding properties in carcinoma, suggest that diagnosis of malignant neoplasm must still largely rely on clinical, hormonal, and structural criteria in adrenocortical neoplasms.

Adenoma↗
PubMed1988

Mutant monoclonal antibodies with select alteration in complement activation ability. Impact on immune complex functions in vivo.

Mutagenesis of mAb is a useful means for studying the biologic and pathologic functions of immune complexes. Treatment of the Hy-1.2 hybridoma-producing IgG2a-anti-TNP antibodies with ethylmethanesulfonate provided us with a mutant clone, producing antibodies with reduced capacity for C activation. The antibodies retained normal Ag-binding capacity, staphylococcal protein A reactivity, and association to FcR for IgG on murine macrophages. No significant polypeptide deletion or class-switch was observed, but a significant change in clonotype was revealed by IEF. Intravenous injection of the mutant antibodies in immune complex form induced different tissue distributions of Ag in mice; i.e., more in kidneys and less in spleen, and developed more mesangial deposits in renal glomeruli compared with those of the wild type. Moreover, the production of granulomatous lesions in vivo caused by immune complexes of TNP-Sepharose was augmented by using mutant antibodies. These lesions demonstrated an enhanced accumulation of macrophages with multinucleated giant cells. Availability of this kind of mutant mAb is thus helpful in the elucidation of the biologic functions and consequences of immune complexes.

Animals↗