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Biomedical subjects

M Takagi

Publications and source records attributed to M Takagi.

At least 631 records · Page 35Linked to original sources
PubMed1991

[Laboratory and clinical studies of cefpirome in pediatric field].

We have carried out laboratory and clinical studies on cefpirome (CPR, HR 810). The results are summarized as follows. CPR was given by 30-minute drip infusion to 3 children at a single dose of 20 mg/kg. After the 30-minute drip infusion, the mean peak serum level of CPR was 65.7 +/- 2.2 micrograms/ml at the end of infusion, and the mean half-life was 1.49 +/- 0.046 hours. The mean urinary excretion rate of CPR was 57.0 +/- 25.8% in the first 8 hours after the 30-minute drip infusion of 20 mg/kg. Treatment with CPR was made in 9 cases of pediatric bacterial infections; 1 case each of tonsillitis, pharyngitis, and bronchopneumonia, 4 cases of pneumonia, 2 cases of urinary tract infection. Results obtained were excellent in 6 cases, good in 3 cases. No significant side effects due to the drug were observed except one case of elevated GOT and GPT, and 3 cases of eosinophilia.

Adolescent↗
PubMed1991

A projection of the lens accommodation-related area to the pupillo-constrictor area in the posteromedial lateral suprasylvian area in cats.

The fiber connection between areas related to lens accommodation and to pupillary constriction was studied in the posteromedial lateral suprasylvian area (PMLS) in the extrastriate cortex of the cat. The accommodation-related area was located in the PMLS by microstimulation, and the anterograde tracer Phaseolus vulgaris leucoagglutinin was injected into this area. Anterogradely-labeled fibers and terminals were found in the upper part of the medial bank of the middle suprasylvian sulcus, the area corresponding to the pupillo-constrictor area in the PMLS. The labeling was also found in the fundus of the middle suprasylvian sulcus, the medial bank of the lateral sulcus and the superficial layers of the superior colliculus. It is concluded that the area related to lens accommodation projects to the area related to pupillary constriction in the PMLS.

Accommodation, Ocular↗
PubMed1991

[Elevated plasma interleukin-6 in patient with idiopathic thrombocytopenic purpura].

Plasma Interleukin-6 (IL-6) level was measured in patients with idiopathic thrombocytopenic purpura (ITP), systemic lupus erythematosus (SLE), rheumatoid arthritis and aplastic anemia. Increase in the plasma level of IL-6 was observed in patients with ITP and SLE. The plasma IL-6 level decreased with progression of the treatment for ITP, and it showed weak negative correlations with the platelet count at the onset of ITP. The increases in the plasma IL-6 level suggest the involvement of activation of the immune system in the pathogenesis of ITP.

Adolescent↗
PubMed1990

Sse8387I, a new type-II restriction endonuclease that recognizes the octanucleotide sequence 5'-CCTGCAGG-3'.

A type II restriction endonuclease designated Sse8387I was partially purified from Streptomyces sp. 8387. This enzyme cleaved adenovirus 2 DNA at three sites, lambda phage DNA at five sites, and pUC18 and M13mp18 RF DNA at one site each, but did not cleave the DNAs from pBR322, SV40, or phi X174. Sse8387I recognized the octanucleotide sequence 5'-CCTGCA decreases GG-3', cleaving where shown by the arrow. Sse8387I is the first restriction endonuclease to be reported that recognizes an octanucleotide sequence consisting of all four nucleotides, G, A, T, and C. The frequency of occurrence of Sse8387I sites within sequenced regions of primate genomes was 2.4 times that of NotI sites.

Adenoviruses, Human↗
PubMed1990

Induction of mixed erythroid-megakaryocyte colonies and bipotential blast cell colonies by recombinant human erythropoietin in serum-free culture.

The effects of recombinant human erythropoietin (rEp) on murine hematopoietic progenitors were studied using a serum-free culture. A high concentration of rEp stimulated the formation of mixed erythroid-megakaryocyte colonies (EM colonies) and blast cell colonies, as well as erythroid colonies, erythroid bursts, and megakaryocyte colonies from normal mouse bone marrow cells. Direct effects of rEp on EM colony, megakaryocyte colony, and erythroid burst formation were confirmed by depletion of accessory cells such as T cells, B cells, and macrophages from crude bone marrow cells, and inhibition of the colonies by the addition of rabbit anti-rEp antibody to the culture in a dose-dependent fashion. Replating experiments were performed to confirm the differentiating ability of blast cell colonies grown in the presence of rEp. Most of the blast cell colonies yielded not only secondary erythroid colonies but also megakaryocyte colonies in the presence of 2 IU/mL rEp. Some of the blast cell colonies produced secondary EM colonies in the presence of 16 IU/ml rEp of 2 IU/mL rEp plus interleukin-3, although no granulocyte-macrophage colonies were found in the secondary culture. These results suggest that Ep acts not only as a late-acting factor that is specific for erythroid progenitors, but also as a bipotential EM-stimulating factor for murine hematopoietic cells.

Animals↗
PubMed1990

Antiproliferative effect of IFN-gamma on proliferation of mouse connective tissue-type mast cells.

Mouse rIFN-gamma suppressed clonal growth of tissue-type mast cells (CTMC) separated from mouse peritoneal cells (greater than or equal to 98% purity) in methylcellulose culture containing IL-3 + IL-4 in a dose-dependent fashion. The IFN-gamma-mediated suppression was also observed both in serum-free culture and in single-cell culture. In addition, mAb to mouse IFN-gamma neutralized the suppressive effect of IFN-gamma on CTMC proliferation supported by the combination of IL-3 + IL-4. These observations suggest a direct antiproliferative effect of IFN-gamma on CTMC. No suppression of CTMC proliferation was observed when CTMC were washed with alpha-medium after 24 h of preincubation with IL-3 + IFN-gamma and then cultured in methylcellulose medium containing IL-3 + IL-4. IFN-gamma had suppressive effects on CTMC after preincubation with IL-3 + IL-4. These preincubation studies suggest that IFN-gamma exerts a reversible inhibitory effect on CTMC which have entered into a proliferative state by IL-3 + IL-4, and has neither cytotoxic nor irreversible suppressive effects on resting CTMC in cultures containing IL-3 alone. CTMC proliferation after stimulation with the cross-linking of cell-bound IgE by specific Ag in the presence of IL-3 was also suppressed by IFN-gamma. By contrast, proliferation of CTMC induced by the combination of 12-O-tetradecanoyl phorbol-13-acetate + IL-3 was not affected by the addition of IFN-gamma to the culture. Based on these observations, we suggest that IFN-gamma antagonizes the colony inducing effect of IL-4 and IgE-Ag stimulation which act synergistically with IL-3 on CTMC.

Animals↗
PubMed1990

Role of adenosine A1 and A2 receptors in the regulation of aldosterone production in rat adrenal glands.

To investigate the roles of adenosine A1 and A2 receptors in the regulation of aldosterone production, we examined the effects of adenosine and adenosine agonists (N6-cyclohexyl adenosine; selective adenosine A1 receptor agonist and 5'-N-ethylcarboxamine adenosine; selective adenosine A2 receptor agonist) on aldosterone and cyclic AMP production in rat adrenal capsular cells. Neither adenosine nor 5'-N-ethylcarboxamine adenosine caused significant effects on basal aldosterone or cyclic AMP production. Also, adenosine (10(-3) M) showed no consistent effects on aldosterone and cyclic AMP production induced by ACTH. On the other hand, N6-cyclohexyl adenosine exhibited a significant inhibition of basal aldosterone and cyclic AMP production at doses of 10(-4) M and 10(-3) M; furthermore, 10(-3) M N6-cyclohexyl adenosine inhibited aldosterone and cyclic AMP production stimulated by ACTH. These results suggest that adenosine A1 receptors are coupled to and inhibit adenylate cyclase and may be involved in the inhibition of aldosterone production.

Adenosine↗
PubMed1990

Interleukin-6 enhances murine megakaryocytopoiesis in serum-free culture.

We investigated the effect of interleukin-6 (IL-6) on murine megakaryocytopoiesis in a serum-free culture system. The addition of IL-6 to a culture containing interleukin-3 (IL-3) resulted in a significant increase in the number of megakaryocyte colonies by bone marrow cells of normal mice. The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Polyclonal anti-IL-6 antibody neutralized the stimulatory effect of IL-6 on megakaryocyte colony growth supported by IL-3. Delayed addition experiments and replating experiments of blast cell colonies showed that megakaryocytic progenitors are supported by IL-3 in the early stage of the development but require IL-6 for their subsequent proliferation and differentiation. In addition, IL-6 increased the size of megakaryocytes in granulocyte-macrophage-megakaryocyte colonies. The combination of granulocyte colony-stimulating factor or granulocyte-macrophage colony stimulating factor with IL-3 resulted in an increase in the granulocyte-macrophage colony growth of bone marrow cells of 5-FU-treated mice or normal mice, respectively, but had little effect on the enhancement of pure and mixed megakaryocyte colony growth. These results suggest that IL-6 plays an important role in murine megakaryocytopoiesis.

Animals↗
PubMed1990

Effects of interleukin-3 and interleukin-4 on the development of "connective tissue-type" mast cells: interleukin-3 supports their survival and interleukin-4 triggers and supports their proliferation synergistically with interleukin-3.

We examined the effects of interleukin-3 (IL-3) and interleukin-4 (IL-4) on connective tissue-type mast cells (CTMC) purified from murine peritoneal cells. Although both factors failed to induce extensive proliferation of CTMC, they stimulated CTMC proliferation synergistically in a dose-dependent manner. Pretreatment of CTMC with IL-3 and/or IL-4 indicated that the sustained presence of both factors was required for the development of type 1 mast cell colonies. The delayed addition of IL-3 to cultures of purified CTMC with IL-4 induced no colony formation, while the delayed addition of IL-4 to cultures with IL-3, even on day 28 of culture, induced type 1 colony formation. In replating type 1 colonies induced by IL-3 and IL-4 to secondary cultures with IL-3 alone, few secondary colonies developed. However, the delayed addition of IL-4 to the secondary culture induced many type 1 colonies. The purified CTMC cultured with IL-3 retained the morphological and cytochemical characteristics of CTMC, as well as proliferative ability. These observations indicate that IL-3 supports the survival of CTMC in methylcellulose culture and that IL-4 triggers and supports CTMC proliferation synergistically with IL-3. The serum-free culture of purified CTMC and the culture of single CTMC demonstrated that the synergistic effect of IL-3 and IL-4 on colony growth and the surviving effect of IL-3 on CTMC require no influence from accessory cells or other humoral factors.

Animals↗
PubMed1990

Synergistic action of phorbol ester and IL-3 in the induction of "connective tissue-type" mast cell proliferation.

12-O-Tetradecanoylphorbol-13-acetate (TPA), a tumor-promoting phorbol ester, induced the proliferation of connective tissue-type mast cells (CTMC) synergistically with IL-3 in a methylcellulose culture, as well as with IL-4. The culture of single CTMC and the serum-free culture of CTMC fractionated by Percoll density gradient centrifugation showed that this synergistic action of IL-3 and TPA required no effects of accessory cells or other humoral factors. Although the populations of CTMC acted on by TPA and IL-4 seemed to be close to each other, the velocity of colony growth induced by the simultaneous stimulation of the combination of TPA and IL-4 was faster than that induced by either TPA or IL-4 in the presence of IL-3. In addition, the addition of anti-IL-4 antibody did not neutralize the effect of TPA on the proliferation of CTMC. These results suggest that TPA and IL-4 act on the proliferation of CTMC synergistically with IL-3 via a different pathway. Beside TPA, other phorbol derivatives capable of activating protein kinase C (PKC) induced the proliferation of CTMC synergistically with IL-3, but phorbol derivatives which were unable to activate PKC did not. These results indicate that the activation of PKC is involved in the process of TPA action on the proliferation of CTMC. Furthermore, the facts that 1-oleoyl-2-acetylglycerol, which activated membrane PKC transiently, and staurosporine, which has been reported to inhibit PKC, did not induce the proliferation of CTMC in the presence of IL-3 and that the effect of TPA was exhibited by the sustained stimulation suggest that the action of TPA on the proliferation of CTMC requires at least two steps. The first one is the primary activation of membrane PKC and the second one is the disappearance of PKC from the cells, "down-regulation."

Alkaloids↗
PubMed1990

Ultrastructural and cytochemical study of elastic fibers in the ventral aorta of a teleost, Anguilla japonica.

Previous studies have revealed that amorphous elastin and microfibrils are structural entities of mammalian elastic fibers. Elastin shows a wide phylogenetic distribution, but the presence of elastin-associated microfibrils has not been demonstrated in teleost aorta. Thus, we have ultrastructurally and cytochemically examined elastic fibers in the ventral aorta of eel, a teleost, by utilizing routine uranyl acetate and lead double staining, the tannic acid (pH 7.0)-uranyl acetate (TA-UA) method, elastase en bloc digestion, Thiéry's periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) method, and the horseradish-peroxidase-labeled concanavalin A (Con A) method. In the ventral aorta of eel, a little ultrastructural difference between elastic fibers in the intima and media and those in the adventitia was noticed, but in either tunic each elastic fiber was basically composed of a "fibrillar core" and surrounding microfibrils. The fibrillar core was a collection of fibrils which showed a tendency to coalesce with each other, and these constituent fibrils were TA-UA positive and elastase-sensitive, representing their nature of elastin. By contrast, microfibrils associated with the fibrillar core were TA-UA negative and elastase-resistant, and their glycoproteinaceous nature was demonstrated by PA-TCH-SP and Con A methods. Thus, this study provides evidence for the presence of elastin-associated microfibrils in teleost aorta. These results are discussed in relation to the topographical difference of elastic fibers in eel aortic wall.

Anguilla↗
PubMed1990

Cleavage of double helical DNA by Cu2+ ion in the presence of bisintercalator containing penta(ethylene glycol) connector chain.

In designing new DNA recognizing and cleaving reagents, we introduce herein a bisacridine derivative (referred to as bisacridine) in which two acridine heterocycles are connected by a penta(ethylene glycol) bridging chain. This compound offers two possible functions: 1, stabilization of DNA bisacridine intercalator complex by metal ion. The penta(ethylene glycol) chain stabilizes metal ions binding to the phosphate site of DNA, where the penta(ethylene glycol) chain constitutes a part of a pseudomacrocyclic ligand for metal binding; and 2, enhancement of metal-assisted hydrolytic cleavage of DNA by means of a metal concentration effect by the pseudomacrocyclic ethereal chain. The binding isotherms of bisacridine with DNA in the presence of metal ions showed that the binding was mainly governed by the cation exchange reaction on the anionic DNA polymer chain, i.e., the exchange between metal ions and the cationic bisacridine. The bisacridine showed an increase DNA binding ability compared to quinacrine, the monoacridine counterpart, and caused an enhancement of DNA cleavage in the presence of Cu2+ ions. Additional experiments which included DNase 1 footprinting in the presence of bisacridine and the DNA cleavage by Cu2+/bisacridine using a 32P end-labelled DNA fragment, suggested that the Cu2(+)-assisted DNA cleavage sites in the presence of bisacridine were in reasonable overlap with the DNA binding sites of bisacridine.

Acridines↗
PubMed1990

Correct splicing of modified introns of a Rhizopus proteinase gene in Saccharomyces cerevisiae.

The intron of the Rhizopus aspartic proteinase gene (RNAP-I) was modified by in vitro mutagenesis and examined for its splicing efficiency in Saccharomyces cerevisiae. The wild-type intron of the RNAP-I gene was not spliced at all in spite of its structural similarity to introns of S. cerevisiae. The primary transcript of the RNAP-I gene was converted to correctly translatable mRNA only when the complete consensus sequence of S. cerevisiae introns (i.e. 5'-GTATGT-----TACTAAC-----TAG-3') was introduced into its intron, although the efficiency of splicing was low. It is also shown that transformants carrying the RNAP-I gene with the complete consensus sequence of S. cerevisiae introns produce active RNAP-I protein.

Aspartic Acid Endopeptidases↗
PubMed1990

Immunohistochemical study of vascular lesions in severe hypertension induced by DOCA and salt administration to spontaneously hypertensive rats.

In order to evaluate whether immunoglobulin deposition in vessels plays some role in the development of vascular lesions in severe hypertension, an immunohistochemical study was performed in spontaneously hypertensive rats (SHRs), to which deoxycorticosterone acetate (DOCA) and salt were administered. DOCA and salt rapidly induced severe hypertensive vascular lesions, including necrotizing arteriolitis and productive endarteritis. In these rats, considerable deposits of IgG and IgM were found in the small arteries and arterioles of the kidneys. These deposits were accompanied by complement (C3), and could be eluted by acid incubation. They were localized in periodic acid-Schiff-positive insudative lesions, which were thought to be an early phase of the hypertensive vascular lesions. These results suggest that the immunoglobulins might be bound to an unknown antigen in the vascular lesions and that some immunological mechanism mediated by the immunoglobulins is involved in the development of vascular lesions in severe hypertension.

Animals↗
PubMed1990

Effects of magnesium on changes in blood pressure and plasma aldosterone induced by angiotensin II.

This study examined the effects of magnesium on changes in blood pressure and plasma aldosterone concentration (PAC) elicited by angiotensin II in rats. The infusion of angiotensin II (0.1 nmol/kg/min) for 30 min increased mean arterial pressure (MAP) and PAC. Simultaneous infusion of magnesium sulphate (5 mumols/kg/min) attenuated the MAP elevation (157.0 +/- 5.2 (SE) v 141.6 +/- 3.5 mm Hg, P less than .01) and the increase in PAC (447 +/- 70 v 233 +/- 50 pg/mL, P less than .01) brought about by angiotensin II. These effects of magnesium were abolished when endogenous angiotensin II was suppressed by the administration of captopril, an angiotensin converting enzyme inhibitor. The results suggest that magensium may attenuate the biological actions of angiotensin II.

Aldosterone↗
PubMed1990

Carcinosarcoma of the submandibular gland. An autopsy case.

We present a rare case of submandibular gland carcinosarcoma occurring in a 45-year-old male patient. His clinical history revealed that the carcinosarcoma had developed from a carcinoma ex mixed tumor in three years. In spite of repeated resection, intensive chemotherapy and irradiation, the tumor recurred and grew rapidly, and the patient died of hemothorax caused by rupture of a pulmonary metastatic tumor. The fourth recurrent tumor and autopsy specimens showed features of carcinosarcoma consisting of three tumor components, i.e., undifferentiated carcinoma, and chondrosarcomatous and osteosarcomatous growth. The metastatic nodules in both lungs and pulmonary hilar lymph nodes showed the same pattern. Immunohistochemically, the chondrosarcomatous cells were positive for vimentin and S-100 protein, and for epithelial markers such as epithelial membrane antigen (EMA) and cytokeratin (MA-902). Undifferentiated carcinoma cells, on the other hand, were partially positive for muscle actin other than cytokeratin (KL 1). Ultrastructurally, desmosome-like structures were seen in the chondrosarcomatous cells. These findings suggest that the sarcomatous lesions might have originated from epithelial cells.

Actins↗