Fixed drug eruption due to cimetidine.
Explore the source record for details and available documents.
Cimetidine↗
Biomedical subjects
S Taniguchi
Publications and source records attributed to S Taniguchi.
Antiarrhythmic drugs inhibit the G-protein and K+ channels in the cultured thyroid cell line.
We examined the effects of antiarrhythmic drugs on the induction of cAMP by TSH (thyroid-stimulating hormone), using continuously cultured FRTL-5 rat thyroid cells. Group Ia antiarrhythmic drugs had no effect, but Group Ib antiarrhythmic drugs suppressed cAMP induction by TSH. These drugs suppressed cAMP induction in response to cholera toxin but did not inhibit TSH receptor binding or cAMP induction by forskolin. These results indicate that Group Ib antiarrhythmic drugs inhibit thyroid G-protein, resulting in a decrease in cAMP induction by TSH. We also examined the effect of antiarrhythmic drugs on K+ channels. Group Ia antiarrhythmic drugs had no effect on K+ channel activation by TSH and cAMP. On the other hand, Group Ib antiarrhythmic drugs suppressed K+ channel activation by TSH and cAMP. This indicates that the mechanism of suppression is not inhibition of TSH receptors or G-proteins but the direct suppression of K+ channels. Group Ib antiarrhythmic drugs inhibited thyroid Gs-protein and thyroid K+ channels. Considering the close relationship between G-protein and ion channels in the cardiac cell membrane, these different effects of Group Ia and Group Ib antiarrhythmic drugs on G-proteins and K+ channels are of interest. Further investigation is necessary to clarify the relationship between thyroid G-proteins and thyroid K+ channels.
Animals↗
Plasma levels of type II phospholipase A2 and cytokines in patients with sepsis.
Plasma levels of type II phospholipase A2 (type II PLA2), cytokines and endotoxin were determined in patients with sepsis to investigate their interrelations and their role in the patient's prognosis. Type II PLA2 was measured by radioimmunoassay, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and IL-8 were each measured by enzyme-linked immunosorbent assay (ELISA). Endotoxin was determined by a method based on an endotoxin-specific synthetic substrate. Plasma levels of type II PLA2 were significantly higher in the patients who died of sepsis than in those who survived the illness. There was a significant correlation between type II PLA2 and TNF-alpha and IL-6. Type II PLA2, TNF-alpha, IL-6, and IL-8 may be useful as indices of disease severity. The results suggest that TNF-alpha and IL-6 stimulate the production of type II PLA2 in the plasma of patients with sepsis.
Adult↗
Blood levels of endothelin-1 and thrombomodulin in patients with disseminated intravascular coagulation and sepsis.
We evaluated the roles of plasma endothelin-1 and plasma thrombomodulin in the development of disseminated intravascular coagulation (DIC) in patients with sepsis. Plasma endothelin-1 was measured by radioimmunoassay (RIA). Plasma thrombomodulin and tumor necrosis factor-alpha (TNF-alpha) were measured by enzyme-linked immunosorbent assay (ELISA), and serum protein C (protein C) was measured by the synthetic substrate method. Endotoxin was measured by the Endospecy test, a synthetic substrate method. A new perchloric acid method was used for the pretreatment of plasma. Blood levels of endothelin-1 and thrombomodulin were significantly higher in patients with DIC than in those without DIC (p < 0.0001). Endothelin-1 and thrombomodulin levels were positively correlated (r = 0.8645, p = 0.0001), as were endothelin-1 and TNF-alpha levels (r = 0.5441, p = 0.0002). Thrombomodulin and protein C levels were negatively correlated (r = -0.5627, p = 0.0001). Endotoxin was elevated above the normal level 14.3% (6/42) for these patients. TNF-alpha is involved in the production of endothelin-1 and thrombomodulin, which play a role in the pathogenesis of DIC and whose blood levels reflect its severity.
Adult↗
Expression of trkC in a mouse osteoblastic cell line and its response to neurotrophin-3.
In a cultured osteoblastic cell line, MC3T3-E1 derived from newborn mouse calvaria, the mRNA encoding TRKC, which is the receptor molecule of neurotrophin-3 (NT-3), was detected by the polymerase chain reaction (PCR) method. The mRNAs of the normal type and one alternative form (C14) were highly expressed in the exponential growth phase of MC3T3-E1 cells and decreased as the cells reached the differentiation stage. NT-3, but not nerve growth factor (NGF), stimulated the proliferation of MC3T3-E1 cells in a dose-dependent manner. NT-3 also stimulated calcium incorporation through the surface of MC3T3-E1 cells, indicating the association of NT-3 and its receptor on the cell surface.
Animals↗
Metastatic potential of transformed rat 3Y1 cell lines is inversely correlated with lysosomal-type sialidase activity.
We have investigated sialidase activities in transformed rat 3Y1 cells of different metastatic potential. Only lysosome-type sialidase was apparent in the particulate fractions of 3Y1 cells and their transformants. As compared with control 3Y1 cells, src-transformed cells exhibited decreased sialidase activity, and v-fos transfer to these latter induced even more severe decrease in the sialidase activity with acquisition of high lung metastatic ability. Various lysosomal enzymes other than sialidase were hardly affected by the transformation. Sialic acid transfer to N-linked glycoproteins was slightly elevated in the transformants, but not in parallel with their metastatic potential.
Animals↗
Isolation of a yeast tropomyosin-related cDNA clone that encodes a novel transmembrane protein having a C-terminal highly basic region.
A novel cDNA clone was isolated from a yeast Saccharomyces cerevisiae lambda gt11 cDNA library using rabbit anti-rat tropomyosin (TM30nm) polyclonal antibody (RTM8-2). It consists of an open reading frame of 951 bp, encoding 317 amino acid residues. The putative sequence recognized by RTM8-2 was present in Asn-235 to Thr-250. The deduced amino acid sequence and hydropathy plot suggested that this protein has a tropomyosin-homologous sequence, a predicted transmembrane, and a C-terminal basic region. A search of the data bases (EMBL and GenBank) revealed that the 128bp sequence in the 3' untranslated region (3'UTR) is almost identical (96.9%) to the human cDNA clone 54E05 sequence (EMBL accession number Z15978).
Amino Acid Sequence↗
A variant actin (beta m) reduces metastasis of mouse B16 melanoma.
We recently reported an acidic actin co-expressed with beta and gamma actin in mouse B16 melanoma, whose expression was inversely correlated with the metastatic potential. The cDNA for this actin is slightly different from the hitherto recognized mouse beta actin cDNA, and we designated it beta m actin. In order to directly investigate the effects of beta m actin on metastasis, we transfected the beta m actin cDNA into a re-cloned B16-BL6 cell line which is more invasive than the highly metastatic cell line, B16-F10; we have already reported the suppressive effect of beta m actin on the invasiveness of B16-F10. Here we report on the decline in the metastatic ability of beta m-transfected cells. In the beta m-transfected B16-BL6 cell line, we observed an increase in the organization of actin stress fibers, accompanied by a decrease in metastasis to the lung, in the invasion of collagen gels, in in vivo invasiveness, and in cell migration on a glass plate covered with colloidal gold particles. We observed no correlation of beta m actin expression either with cell attachment to Matrigel, or with type-IV collagenase expression. These results suggest that beta m actin can play a role in reducing the invasiveness of mouse B16 melanoma, most probably through decreasing cell motility, which may thus result in suppression of the metastatic ability of cells.
Actins↗
Repression of in vitro transcription of the Escherichia coli fnr and nar X genes by FNR protein.
In facultative anaerobes, the anaerobic expression of respiratory genes is regulated by a transcriptional activator, FNR. Transcription in vitro of the E. coli fnr gene was repressed by its product, FNR. The transcription of the E. coli narX gene encoding the nitrate sensor protein was likewise repressed. DNA truncation experiments for fnr and narX genes indicated that multiple anaero-boxes in each promoter region are essential for repression by the FNR protein, but they also suggest that factor-independent upstream activation signals are operating with these promoters.
Bacterial Proteins↗
Expression of nerve growth factor family neurotrophins in a mouse osteoblastic cell line.
With cultured osteoblastic cells, clone MC3T3-E1 derived from newborn mouse calvaria, the mRNAs encoding three representative neurotrophins, namely, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), were proved in estimation by the polymerase chain reaction (PCR) method. The increase and then subsequent decrease of all three mRNAs within the proliferation phase were followed by their gradual increase in the differentiation phase, with a tendency of enhancement by exogenous TGF-beta as was particularly evident in the case of NGF. These findings were further substantiated by identification of NGF-like neutrophils in the conditioned medium of the osteoblastic cells by an immunoblotting and neurite extension assay.
Animals↗
Extracellular matrix components regulating glandular differentiation and the formation of basal lamina of a human pancreatic cancer cell line in vitro.
The interaction between the extracellular matrix and human tumor-cell clones S2-013 and S2-020, derived from a pancreatic cancer cell line (SUIT-2), was examined in vitro, using various cell differentiation-promoting matrices in two- and three-dimensional cultures. S2-013 cells (well-differentiated tubular adenocarcinoma in xenografts in nude mice) cultured in Matrigel formed glandular structures. Ultrastructural observation revealed a morphological polarity of cells and a distinct basal lamina. On the other hand, S2-020 cells (poorly differentiated tubular adenocarcinoma in xenografts) cultured in Matrigel formed neither glandular structures nor a basal lamina, but only cell aggregates. The morphology of these two sublines cultured in Matrigel expressed the histological degree of differentiation which they presented in nude mice. In contrast, in type I collagen gel, S2-013 cells formed glandular structures without a basal lamina, and in soft agar, they were able to form neither glandular structures nor a basal lamina. S2-020 cells cultured in type I collagen gel or soft agar formed the same simple cell aggregates as in Matrigel. Matrices used in a three-dimensional culture influenced the degree of differentiation in S2-013 cells but had no effect on the morphological differentiation in S2-020 cells. To detect the factors which induce basal lamina formation, S2-013 cells were cultured on a microporous membrane coated with extra-cellular matrix components such as laminin, type IV collagen, and fibronectin. S2-013 cells formed a basal lamina only on the laminin. These cell lines may be useful in investigating the mechanisms regulating the formation of glandular structures and basal lamina.
Adenocarcinoma↗
Expression patterns of two fibroblast growth factor receptor genes during early chick eye development.
The expression patterns of two distinct types of fibroblast growth factor receptor (FGFR) genes, FGFR1 and FGFR2, were compared during early chick eye development. In situ hybridization was performed with riboprobes synthesized from cDNA fragments of FGFRs cloned by the polymerase chain reaction method. FGFR1 was expressed in the prospective lens, neural retina, pigment epithelium and mandibular mesenchyme. In contrast, FGFR2 was expressed predominantly in the periocular mesenchyme of a 2.5 day-old embryo. In the 5.5-day-old embryo, transcripts of FGFR2 were detected in the prospective corneal epithelium. The results suggest that expression patterns of FGFR1 and FGFR2 are complementary and ligands of each FGFR might be involved differentially in early chick eye development. It is concluded that the action of FGFs on pigment epithelium and lens cells reported so far, probably occurs through FGFR1, and both types of FGFR are involved in head mesenchymal development.
Animals↗
Endotoxin causes early changes in glutathione concentrations in rabbit plasma and liver.
The effects of endotoxin on glutathione concentrations in rabbit plasma and liver were investigated. Lipopolysaccharide (2 mg/kg) from Escherichia coli was administered intravenously to seven male Japanese rabbits. In the liver, the concentrations of reduced glutathione (GSH) started to decrease, and those of oxidized glutathione (GSSG) started to increase 1 hr after the endotoxin administration, resulting in a progressive decline in the hepatic GSH/GSSG ratio. In the arterial plasma, the concentrations of both GSH and GSSG started to increase 1 hr after the endotoxin administration. Because the increase in the concentrations of GSSG was greater than that in the concentrations of GSH, the GSH/GSSG ratio in the plasma decreased as did that in the liver. These changes in glutathione concentrations occurred simultaneously with the increase in serum osmolality, but earlier than the decrease in the arterial ketone body ratio, both of which are thought to be useful markers for liver damage. It was concluded that endotoxin induced an increase in the plasma concentrations of GSH as well as GSSG, and that the changes in plasma glutathione status might be useful markers of endotoxin-induced damage in organs, including the liver.
Animals↗
In vitro assay of the invasive potential of malignant bone and soft tissue tumours through basement membranes.
We have used reconstituted basement membrane molecules which have formed into barriers in order to investigate the invasive potential of malignant bone and soft tissue tumour cells in vitro. A number of cell lines established from human malignant tumours demonstrated a high degree of invasiveness, although fibroblasts showed no ability to penetrate the basement membrane barrier. H-ras oncogene transfected cells into the fibroblasts were much more invasive than the parent lines. Primary cultures of malignant tumour cells demonstrated invasiveness, while those of nonmetastatic cells and fibroblasts did not. The binding of tumour cells to laminin in the basement membranes was found to induce secretion of collagenase and motility which are crucial factors for invasion. A synthetic peptide, Tyr-Ile-Gly-Ser-Arg, was able to suppress the invasiveness of HT1080 human fibrosarcoma cells, and also reduced lung colonisation in vitro. The results suggest that the in vitro assay was useful, firstly to determine the invasive potential, secondly to investigate the mechanism of invasion, and finally to development treatment against invasion and metastases.
Basement Membrane↗
Clostridial gas gangrene associated with congenital generalized lipodystrophy: report of a case.
Congenital generalized lipodystrophy (CGL) is a rare disease, the main symptoms of which are a reduction of systemic subcutaneous fat, characteristic facial features, hypertrichosis, and insulin-resistant diabetes. We report herein the unusual case of a 25-year-old man with CGL in whom gas gangrene developed, an association which has never before been encountered.
Adult↗
Heterogeneities of attachment, chemotaxis, and protease production among clones with different metastatic potentials from a human pancreatic cancer cell line.
The present study extends our investigations into the metastatic heterogeneity among four clonal cell lines (S2-007:H, S2-013:M1, S2-020:M2, and S2-028:L) from a human pancreatic cancer cell line (SUIT-2), and extends our discussion the positive correlation between metastatic potential and the type I collagenase activity of the cells, focusing on their interaction with extracellular matrix. Ability to attach to the reconstituted basement membrane (Matrigel) was higher for clone H than clone L during an observation period of 30-60 min, whereas clones M1 and M2 were found to be intermediate in ability. In densitometric and radioactive studies, clone L exhibited the lowest collagenolytic activity against mouse and human type IV collagen, while clone H exhibited the highest activity in the densitometric study and clone M1 was the highest in the radioactive study. The production of urinary-type plasminogen activator was highest in clone L and lowest in clone H. On the other hand, tissue-type plasminogen activator was highest in clone M2 and low in both clones H and L. Clone M2 exhibited the highest chemotactic activity toward diluted Matrigel, whereas clone L had the lowest activity. On the whole, these clones showed heterogenous interactions with an extracellular matrix. It is suggested that the attachment activity to basement membrane and the type IV collagenolytic activity of the cells may be positively correlated with their metastatic potential, whereas the production of urinary-type plasminogen activator was negatively correlated, but confirmation of these findings awaits further study.
Cell Adhesion↗
Toxicity and chemical form of selenium in the liver of mice orally administered selenocystine for 90 days.
The subacute oral toxicity of selenocystine and chemical form of selenium in the liver following exposure to this compound were assessed in ICR male mice. Animals were dosed 6 days/week for 30, 60 or 90 days with 0, 5, 10 or 15 mg/kg per day. Body weight gain decreased with dosage. The activities of aspartate aminotransferase and alanine aminotransferase in plasma were significantly elevated at the highest dose level after 60 days and at the two higher dose levels after 90 days of exposure. However, the level of selenium content in the liver was the same at the two higher dosages at both 60 and 90 days of exposure. The subcellular distribution of selenium in the liver from mice treated with selenocystine showed that the major part of the total selenium content, 68.3-72.1%, existed in the cytosolic fraction. Sephadex G-150 chromatograms of liver cytosol of the animals administered selenocystine revealed three selenium-containing fractions which involve glutathione peroxidase (molecular weight 80,000) high molecular (molecular weight 55,000-60,000) and low molecular (molecular weight < 10,000) substances. Selenium content and acid-volatile selenium content in the high molecular weight fraction increased with exposure time to selenocystine. Thus, in a subacute toxicity study selenocystine given for 90 days caused hepatic damage in mice, depending on the acid-volatile selenium content in the liver cytosol.
Administration, Oral↗