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Biomedical subjects

S Abe

Publications and source records attributed to S Abe.

At least 1,063 records · Page 59Linked to original sources
PubMed1982

Induction of macrophage-mediated tumor lysis by an animal lectin, Sarcophaga peregrina agglutinin.

Several animal lectins, such as Sarcophaga peregrina agglutinin, Limulus polyhemus agglutinin, Helix pomatia agglutinin and Helix aspersa agglutinin, were tested for induction of tumor lysis mediated by macrophages. Among them, only S. peregrina agglutinin purified from the hemolymph of S. peregrina larvae lysed tumor cells in co-operation with macrophages from the peritoneal cavity of mice. S. peregrina agglutinin alone did not kill target tumor cells. Macrophages in the presence of this lectin could kill other syngeneic tumor cells. This lectin-dependent cytolysis by macrophages was inhibited by galactose, a sugar which is specifically recognized by S. peregrina agglutinin. These findings suggest that the animal lectin S. peregrina agglutinin is a ligand in macrophage-mediated cytolysis, inducing binding of effector macrophages to target cells which in turn triggers off lysis of the target cells.

Agglutinins↗
PubMed1982

Combination therapy of murine tumors with lentinan plus lipopolysaccharide plus cyclophosphamide.

A combination of lentinan and bacterial lipopolysaccharide (LPS), previously reported to have strong antitumor activity against some tumors, was only slightly effective on solid-type MH134 hepatoma and colon 38 adenocarcinoma and was not effective on ascitic L1210 in CDF1 mice. On the other hand, additional combination therapy with cyclophosphamide (CY), that is, lentinan plus LPS plus CY, strongly inhibited the growth of solid-type MH134 and colon 38 adenocarcinoma even when administered from day 12 after tumor inoculation. The antitumor delayed hypersensitivity reaction against MH134 hepatoma, measured by means of the footpad test, was augmented by this combination. The possible role of CY is discussed in relation to the importance of inhibition of immune suppressive mechanisms in this combination therapy.

Adenocarcinoma↗
PubMed1982

Changes of antitumor immunity of hosts with murine mammary tumors regressed by lentinan: potentiation of antitumor delayed hypersensitivity reaction.

From 2 weeks after sc inoculation of MM46 mammary carcinoma cells into C3H/He mice, lentinan caused tumor regression, irrespective of its administration schedule (i.e., various doses and times of treatment, before and after tumor inoculation). The humoral and cellular immune responses of tumor-bearing mice with or without lentinan treatment were studied kinetically. From 2 weeks after tumor inoculation, antitumor antibodies (detected by macrophage-mediated or complement-dependent cytotoxicity assay) and LB (a serum protein) increased in tumor-bearing mice but the delayed-type hypersensitivity reaction against tumor (T-DHR) decreased. Lentinan restored and potentiated the T-DHR. The conditions under which lentinan is effective and the antitumor reactions responsible for tumor regression are discussed on the basis of these results.

Adjuvants, Immunologic↗
PubMed1981

Partial purification and characterization of a neutral protease which cleaves type IV collagen.

A neutral protease has been extracted from the media of cultured metastatic tumor cells and purified approximately 1000 times after sequential ammonium sulfate fractionization, concanavalin A column chromatography, and molecular sieve chromatography. The protease has an apparent molecular weight of 70 000--80 000, is inactive at acid pH, requires trypsin activation, and is inhibited by ethylene-diaminetetraacetic acid but not by phenylmethanesulfonyl fluoride, N-ethylmaleimide, or soybean trypsin inhibitor. The enzyme produces specific cleavage products for both chains of pro type IV collagen isolated without pepsinization and apparently cleaves at one point in a major pepsin-extracted chain of placenta type IV collagen. The partially purified enzyme fails to significantly degrade other collagens or fibronectin under digestion conditions in which specific reaction products are produced for type IV collagen. The existence of this enzyme is significant since previously described animal collagenases fail to degrade type IV collagen. Such a type IV specific collagenase could play a role in tumor invasion and may be secreted by other cells such as endothelial cells, epithelial cells, and immune cells.

Animals↗
PubMed1981

Localization of the human fibronectin (FN) gene on chromosome 8 by a specific enzyme immunoassay.

The fibronectin produced by clonal murine-human hybrid cell lines containing various complements of human chromosomes was measured. Human and murine fibronectins were assayed by specific immunoassay, and the production of human fibronectin was correlated with karyology and isozyme markers for specific human chromosomes. The data show a 100% concordance between the expression of human fibronectin and glutathione reductase, a marker for human chromosome 8, indicating that chromosome 8 codes for the fibronectin polypeptide.

Animals↗
PubMed1981

[Studies on toxicity of hydrocortisone 17-butyrate 21-propionate -1. Acute toxicity of hydrocortisone 17-butyrate 21-propionate and its analogues in mice, rats and dogs (author's transl)].

The acute toxicity of hydrocortisone 17-butyrate 21-propionate (HBP), hydrocortisone 17-butyrate (HB17) and hydrocortisone 21-butyrate (HB21) were investigated by three administration routes (s.c., i. p. and p. o.) in mice, rats and dogs. In the case of HBP, LD50 by oral administration was the highest, and followed by subcutaneous and intraperitoneal administration in mice and rats. And LD50 of HB17 and HB21 were not different from HBP in mice by subcutaneous administration. The depression of spontaneous movement and respiratory rate, ptosis, larcrymation and the collapse were commonly observed in all drugs, and it was independent of administration routes. The autopsy revealed the atrophy of thymus, spleen and adrenal glands, the supprative nodules of heart and liver and the ulcers of alimentary tract in mice and rats. But the changes observed in mice and rats were recognized when 1000 mg/kg of HBP was administered to dogs subcutaneously. Many of these changes were common to glucocorticoids, and the LD50 of HBP was rather high compared with other synthetic steroids; therefore, HBP was among less toxic steroid.

Administration, Oral↗
PubMed1981

[Influence of hydrocortisone 17-butyrate 21-propionate on the visual and the auditory organs (author's transl)].

The visual toxicity and the ototoxicity of hydrocortisone 17-butyrate 21-propionate (HBP), a newly synthesized anti-inflammatory steroid, was investigated using rats and dogs. (1) Electroretinogram (ERG) and visually evoked potential (VEP) in rats were not changed when HBP was administered intravenously and intraperitoneally, even at the semilethal doses. Consequently, it was suggested that HBP had no effect on the visual nervous system. (2) Similar to other corticosteroids, the intra ocular pressure rose in the dogs received HBP. Nevertheless, these dogs showed neither the remarkable changes in ERG, in the fundus of the eye, in the histological examination, nor the turbidity of the cornea and the lens. Based on these facts, it was reasonable to think that the the rise in the intra ocular pressure caused by HBP was not so severe that induce the secondary influence to other visual functions. (3) The rats received HBP did not show any changes in the auditory function by the audiometry. As the result, HBP was thought to be one of the rather safety corticosteroids concerning the visual toxicity and the ototoxicity.

Administration, Topical↗
PubMed1981

[Studies on toxicity of hydrocortisone 17-butyrate 21-propionate -2. Subacute toxicity in rats by subcutaneous administration (author's transl)].

Subacute toxicity of hydrocortisone 17-butyrate 21-propionate (HBP), a new synthetic corticosteroid, was studied in rats, using betamethasone 17-valerate (BV) and hydrocortisone 17-butyrate (HB) as the reference drugs. HBP was subcutaneously injected to rats at the daily doses of 0.08, 0.4, 2.0, 10 and 50 mg/kg for 30 days. BV and HB were also administered at the daily doses of 0.08, 0.4 and 2.0 mg/kg. The recovery test was performed for 4 weeks after administration of HBP, BV and HB. The suppression of body weight gain by HBP was observed at the doses more than 0.08 mg/kg in male and more than 2.0 mg/kg in female rats. In addition, at the doses more than 0.4 mg/kg of HBP induced the dose-dependent symptoms such as decrease in the number of circulating white blood cells, lymphocyte counts and S-ALP level, increase in total cholesterol, GOT and GPT level of serum, and regressive changes in adrenals, lymphatic and hematopoietic tissues. There were fatal cases in rats given 50 mg/kg of HBP. These changes are considered to be common phenomena to other corticosteroids, and less toxic in female than male rats. Changes of symptoms caused by the administration of HBP 2.0 mg/kg were almost recovered after withdrawal. The toxicities of three corticosteroids were in the order of BV greater than HB greater than or equal to HBP in strength. As the result, maximum non-toxic dose of HBP was estimated to be 0.08 mg/kg in female and lower than that in male rats.

Administration, Topical↗
PubMed1981

[Studies on toxicity of hydrocortisone 17-butyrate 21-propionate -3. Subacute toxicity in rats by percutaneous administration (author's transl)].

Subacute toxicity of hydrocortisone 17-butyrate 21-propionate (HBP) was studied in rats. HBP was percutaneously given to rats with 0.1% and 0.5% creame (0.1% HBP-C, 0.5% HBP-C) and ointment (0.1% HBP-O, 0.5% HBP-O) at the daily dose level of 150 mg per 100 g body weight for 1 month. Rats receiving HBP-C and HBP-O showed some dose-dependent symptoms such as the suppression of body weight gain, emaciation, decrease in the number of white blood cells, hemoglobin, hematocrit, and serum total cholesterol level, regressive changes in adrenals, skin, lymphatic and hematopoietic tissues, which are known as toxic effects of synthetic corticosteroids. These symptoms were comparatively high toxic in male rats and in cream groups, and almost disappeared in rats elapsed recovery time of 1 month after withdrawal of HBP.

Administration, Topical↗
PubMed1981

Bronchial cast shadow due to cellular impaction of the bronchi.

The genesis of unusual radiographic shadows by bronchi filled with tumor cells is reported. These shadows, similar to those caused by mucus or pus, are rod-like and indicate the replacement of air by water dense materials. The unifying term, "bronchial cast shadow" is proposed as the radiographic diagnostic sign.

Bronchial Neoplasms↗