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Biomedical subjects

M Tajima

Publications and source records attributed to M Tajima.

At least 361 records · Page 20Linked to original sources
PubMedDate not supplied

Enhancement of lipid phagocytosis by cloned cells derived from rat malignant fibrous histiocytoma under hyperlipemic conditions.

The histogenesis of malignant fibrous histiocytoma (MFH) was studied by observing the influence of hyperlipemic (HL) conditions on the behavior of cloned MT-8 cells with an undifferentiated mesenchymal character and MT-9 cells with histiocytic and fibroblastic features, both derived from a spontaneous rat MFH. The cells were grown in medium containing 10% normal rat serum (CSM) or 10% HL rat serum (HSM) for 1, 3, 8 and 24 h. The cells grown in HSM showed a time-dependent, significant increase in numbers of cytoplasmic lipid droplets per cell and cells positive for acid phosphatase (ACP) and non-specific esterase (NSE) compared with cells grown in CSM. The number of cells positive for two different anti-rat monocyte/macrophage monoclonal antibodies (ED-1 and ED-2) also increased significantly in HSM. This histiocytic nature was confirmed by electron microscopy. Tumors were induced by inoculating MT-8 and MT-9 cells into rats on a standard diet and rats on a HL diet. MT-8 and MT-9 tumor cells in HL rats phagocytized lipid droplets and showed stronger positive reactions for ACP and NSE compared with tumors in control rats. These results imply that xanthomatous cells in MFH may be a phenotype of MFH cells expressing an enhanced histiocytic nature. MFH cells seem to alter their behavior depending on cultural or microenvironmental conditions.

Animals↗
PubMedDate not supplied

In vivo effects of apoptosis in asthma examined by a murine model.

BACKGROUND: One of the characteristic features of bronchial asthma is the accumulation of various inflammatory cells, predominantly eosinophils, at the subepithelial region beneath the basement membrane of the airway. Apoptosis is a form of physiological cell death, through which the cellular contents including biologically active substances are kept in the cell membrane and are removed without their harmful effects. So, attempts were made to clarify whether the induction of apoptosis is beneficial in asthma by using a murine model with ovalbumin (OA) as responsible allergen. METHODS: A/J mice, which are genetically predisposed to be hyperresponsive to acetylcholine, were immunized with OA and alum, accompanied by OA inhalation for 2 weeks, during which some of the mice were also treated with either anti-Fas monoclonal antibody or sham control hamster IgG intranasally. Airway responsiveness to acetylcholine was then analyzed by measuring airway resistance with a body plethysmograph box. Apoptosis was assessed by propidium iodide and TUNEL staining. RESULTS: Inhalation of OA increased both airway responsiveness to acetylcholine and the number of cells, mostly eosinophils, infiltrated into the airway. Administration of anti-Fas antibody induced apoptosis in the infiltrated eosinophils and abolished augmentation of airway hyperresponsiveness caused by OA inhalation. CONCLUSION: Induction of apoptosis in proinflammatory cells including eosinophils at the airway may have a beneficial effect on suppressing airway hyperresponsiveness.

Acetylcholine↗
PubMedDate not supplied

Treatment with growth hormone enhances contractile reserve and intracellular calcium transients in myocytes from rats with postinfarction heart failure.

BACKGROUND: Recombinant human growth hormone (GH) improves in vivo cardiac function in rats with postinfarction heart failure (MI). We examined the effects of growth hormone (14 days of 3.5 mg. kg-1. d-1 begun 4 weeks after MI) on contractile reserve in left ventricular myocytes from rats with chronic postinfarction heart failure. METHODS AND RESULTS: Cell shortening and [Ca2+]i were measured with the indicator fluo 3 in myocytes from MI, MI+GH, control, and normal animals treated with GH (C+GH) under stimulation at 0.5 Hz at 37 degrees C. Cell length was similar in MI and MI+GH rats (150+/-5 and 157+/-5 microm) and was greater in these groups than in the control and C+GH groups (140+/-4 and 139+/-4 microm, P<0.05). At baseline perfusate calcium of 1.2 mmol/L, myocyte fractional shortening and [Ca2+]i transients were similar among the 4 groups. We then assessed contractile reserve by measuring the increase in myocyte fractional shortening in the presence of high-perfusate calcium of 3.5 mmol/L. In the control and C+GH groups, myocyte fractional shortening and peak systolic [Ca2+]i were similarly increased in the presence of high-perfusate calcium. In the presence of high-perfusate calcium, both myocyte fractional shortening and peak systolic [Ca2+]i were depressed in the MI compared with the control groups. In contrast, myocyte fractional shortening (14.1+/-.9% versus 11.1+/-.9%, P<0.05) and peak systolic [Ca2+]i (647+/-43 versus 509+/-37 nmol/L, P<0.05) were significantly higher in MI+GH than in MI rats and were comparable to controls. Left ventricular myocyte expression of sarcoplasmic reticulum Ca2+ ATPase 2 (SERCA-2) and left ventricular SERCA-2 protein levels were increased in MI+GH compared with MI rats. CONCLUSIONS: Calcium-dependent contractile reserve is depressed in myocytes from rats with postinfarction heart failure. Long-term growth hormone therapy increases contractile reserve by restoring normal augmentation of systolic [Ca2+]i in myocytes from rats with postinfarction heart failure.

Analysis of Variance↗
PubMedDate not supplied

Angiotensin II type 2 receptor blockade amplifies the early signals of cardiac growth response to angiotensin II in hypertrophied hearts.

BACKGROUND: We have previously shown that the acute molecular growth response of new protein synthesis and protein kinase C activation in response to angiotensin II (Ang II) is altered in left ventricular (LV) hypertrophy compared with normal hearts. We have also shown an upregulation of Ang II type 2 (AT2) receptors in hypertrophied hearts relative to controls. Activation of AT2 receptors is proposed to counteract growth effects of AT1 receptor in response to Ang II. Thus, we tested the hypothesis that in hypertrophied hearts, the AT2 receptor mediates inhibitory effects on the new cardiac protein synthesis in response to acute Ang II stimulation. METHODS AND RESULTS: Flaccid buffer-perfused adult normal and hypertrophied rat hearts were perfused with Ang II 10(-8) mol/L plus prazosin 10(-7) mol/L or Ang II plus the AT2 blocker PD 123319 5x10(-7) mol/L. New protein synthesis was measured by the rate of [3H]phenylalanine incorporation into the LV proteins. In normal hearts, Ang II (n=8) increased the rate of [3H]phenylalanine incorporation by 74+/-27% (P<0.05 versus no drug). Treatment with PD123319 (n=8) did not increase protein synthesis compared with Ang II alone (32+/-11% versus Ang II alone, P=NS). In hypertrophied hearts, Ang II alone (n=6) increased the rate of [3H]phenylalanine incorporation only by 23+/-13% (P=NS versus no drug). In contrast, treatment with PD123319 (n=7) induced a 76+/-21% increase in new LV protein synthesis compared with Ang II alone (P<0.05). AT2 receptor blockade in Ang II-stimulated hypertrophied hearts was associated with enhanced membrane protein kinase C translocation and reduced LV cGMP content. CONCLUSIONS: These data support the hypothesis that in adult hypertrophied rat hearts, inhibition of cardiac AT2 receptors, which are upregulated in chronic LV hypertrophy, amplifies the immediate LV growth response to Ang II. This appears to be related to augmented Ang II-stimulated PKC activation and suppression of cGMP signaling.

Angiotensin II↗
PubMedDate not supplied

Suppressive effect of beta-carotene on the development of pulmonary foam cells in rats with hyper beta-lipoproteinemia.

The effect of beta-carotene (BC) on the development of pulmonary foam cells (PFCs) was studied in rats with diet-induced hyper beta-lipoproteinemia. Rats were fed a standard diet; a hyper-beta-lipoproteinemia diet (HB) consisting of the standard diet, 4% cholesterol, and 1% cholic acid; or the standard diet plus 0.1% BC; or the HB diet plus 0.1% BC diet (HBC). Rats in the HB and HBC groups developed hyper-beta-lipoproteinemia, but no significant differences were observed in serum levels of total cholesterol, phospholipid, and beta- lipoprotein (B-LP) between both groups. The percentages of foamy, lipid-ingested monocytes (FMs) to the number of blood monocytes (BMs), the number and size of lipid droplets in FMs, the percentages of PFCs to the number of alveolar macrophages from bronchopulmonary lavage fluid, and the score of PFC development in the lungs of rats in the HBC group were reduced compared to those of rats in the HB group. There were no differences in latex-phagocytotic activity of BMs among rats in the control, HB, BC, and HBC groups. BC suppressed the foamy transformation of BMs and development of PFCs deriving from the influx of FMs into the alveoli of hyper-beta-lipoproteinemic rats. Based on the present results, it is presumed that the antioxidative property of BC may prevent an oxidative modification of B-LP under the hyper-beta-lipoproteinemic condition, leading to a decrease in the uptake of oxidatively modified B-LP by BMs.

Animals↗
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Olfactory undifferentiated carcinoma with endocranial extension in a Fischer-344 rat.

A spontaneous tumor in the nasal cavity, extending through the cribriform plate to the cranial cavity, was detected in a 103-wk-old female Fischer-344/DuCrj rat. The tumor appeared to arise from the olfactory epithelium and was composed of round to polygonal, undifferentiated cells arranged in solid sheet-like and lobular patterns with scant fibrovascular stroma. Ultrastructurally, the tumor cells often formed desmosomes between contiguous cells and had no neurosecretory granules. Immunohistochemically, the tumor cells did not react with any antibodies specific for intermediate filaments, neuronal, muscular, and endothelial elements. Based on these results, the tumor was diagnosed as undifferentiated olfactory epithelial carcinoma.

Animals↗
PubMedDate not supplied

Carbon tetrachloride-induced hepatotoxicity enhances the development of pulmonary foam cells in rats fed a cholesterol-cholic acid diet.

The effect of CCl4-hepatotoxicity on the development of pulmonary foam cells (PFCs) was studied using 4 groups of rats. Rats in the control group were fed a standard diet; rats in the second group were fed a hyper beta-lipoproteinemic (HB) diet consisting of the standard diet, 4% cholesterol, and 1% cholic acid; rats in the third group were fed the standard diet and administered with CCl4 (1.0 ml/kg, i.p., fortnightly) (CT); and rats in the fourth group were fed the HB diet and administered with CCl4 (HT). At feeding week 10, rats in the HB and HT groups developed hyper beta-lipoproteinemia. The ratios of foamy, lipid-ingested monocytes (FMs) to blood monocytes (BMs) and the histologic scores of PFC development were significantly greater in the HB and HT groups than in the control and CT groups, respectively. The ratio of PFCs to alveolar macrophages from bronchopulmonary lavage fluid was significantly higher in the HT group than in the CT group. At feeding week 20, rats in the CT and HT groups suffered hepatic injury and hypo beta-lipoproteinemia. Despite hypo beta-lipoproteinemia, the FM and PFC development, the ratio of BMs in differential leukocyte counts, and latex-phagocytotic activity of BMs were enhanced in the HT group. Furthermore, markedly enlarged FMs, described here as giant-FMs, that contained numerous lipid droplets in their abundant cytoplasm appeared in the peripheral blood from rats in the HT group. Histologically, embolism caused by giant-FMs in the pulmonary blood vessels and intraalveolar accumulation of PFCs were detected with a high incidence in the HT group. The present study suggests that CCl4-hepatotoxicity may affect lipoprotein synthesis in the liver of hyper beta-lipoproteinemic rats and defective or modified lipoproteins can be phagocytosed actively by BMs, and then BMs transform into FMs or giant-FMs, resulting in the PFC development and pulmonary embolism by giant-FMs.

Animals↗
PubMedDate not supplied

Gene defect of dermatan sulfate proteoglycan of cattle affected with a variant form of Ehlers-Danlos syndrome.

A defect of the core protein of dermatan sulfate proteoglycan was suspected in a Holstein calf affected with a variant form of Ehlers-Danlos syndrome. The mutation was a guanine-to-adenine transition at nucleotide position 254, which resulted in a serine-to-asparagine substitution of the bovine proteoglycan core protein. This substitution occurred in the serine-glycine dipeptide repeat that was suspected to be the binding portion of dermatan sulfate. This point mutation in the genome was also detected by the use of restriction fragment length polymorphism (RFLP) and polymerase chain reaction (PCR) methods. The results of the RFLP and PCR indicated that the calf was a heterozygote of an abnormal gene and a normal gene of the core protein. The interpretation of these data revealed that the functional abnormality in cutaneous tissues of the calf was caused by an abnormal gene of the proteoglycan core protein, which induced a substitution of amino acid.

Amino Acid Sequence↗
PubMedDate not supplied

Relation between cell composition of pleural effusions in patients with pulmonary carcinomas and their clinical courses.

1) Cancer cells of the effusions were decreased by chemotherapy, but this did not always indicate a good clinical course. 2) When the clinical condition was fairly good, the percentage of lymphocytes predominated in the pleural effusion. 3) When the clinical conditions became rather critical, there was an increase in the number of macrophage. 4) The cytologic findings were observed prior to the time the clinical symptoms became manifest. 5) The percentage of lymphocytes and macrophages in pleural effusions was not related to the percentage of lymphocytes and monocytes in peripheral blood.

Adenocarcinoma↗
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Role of carbohydrate moiety in granulocyte colony stimulating factor.

Biological activities of two granulocyte-colony stimulating factor (G-CSF) preparations with (Lenograstim) or without (Filgrastim) sugar moiety were compared. Both G-CSF preparations similarly enhanced the N-Formyl-Met-Leu-Phe-induced-migration of human peripheral blood polymorphonuclear cells, but did not significantly affect the proliferation of human oral tumor cell lines (HSC-2, HSG). However, Lenograstim induced cytotoxicity (accompanied by the production of cytoplasmic vacuoles and large DNA fragments) in human promyelocytic leukemic cells HL-60, more potently than Filgrastim. Lenograstim, but not Filgrastim, enhanced the cytotoxic activity of sodium ascorbate. In contrast to Lenograstim, Filgrastim was degraded gradually, but too slowly to explain its lower biological activity. These data suggest that the carbohydrate moiety in G-CSF might confer unique biological activities.

Ascorbic Acid↗
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Radical modulating activity and cytotoxic activity of synthesized eugenol-related compounds.

The ability of nine synthetic eugenol-related compounds to scavenge O2- (generated by the hypoxanthine-xanthine oxidase reaction) was compared with their radical generation and cytotoxic activity. ESR spectroscopy showed that eugenol (4-allyl-2-methoxyphenol), 2-allyl-4-methoxyphenol, 2-allyl-4-t-butylphenol and 2,4-dimethoxyphenol efficiently scavenged O2- and produced radicals under alkaline conditions. 2-allyl-4-t-butylphenol showed the highest cytotoxic activity and DNA-synthesis inhibitory activity, possibly due to the hydrophobic radical reactivity. 2-allyl-4-methoxyphenol and 2,4-dimethoxyphenol showed higher antioxidant activity than 3-t-butyl-4-hydroxyanisol (BHA), but all these compounds showed comparable cytotoxic activity with each other. These findings suggest a possible link between the cytotoxic activity and radical generation/scavenging activity in eugenol-related compounds.

Antineoplastic Agents↗
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Effect of immune complexes in serum from patients with rheumatoid vasculitis on the expression of cell adhesion molecules on polymorphonuclear cells.

OBJECTIVE: Immune complexes (IC) are frequently detected in patients with rheumatoid vasculitis (RV). To explore the pathogenic role of IC in the development of vasculitis among patients with rheumatoid arthritis (RA), we examined the effect of IC on the expression of cell adhesion molecules (CAM) on polymorphonuclear cells (PMN). METHODS: PMN from healthy volunteers were incubated with the sera from 26 patients with RA including 9 patients with RV, and the expression of CAM on the PMN was assessed by flow cytometry. RESULTS: We found that 67% (6/9) of the serum samples from RV patients and 18% (3/17) of the samples from RA patients without RV revealed up-regulated CD11b expression. On the other hand, 89% (8/9) of the samples from RV patients and 12% (2/17) of the samples from RA patients without RV revealed up-regulated CD18 expression. However, the expression of CD11a was not affected. Up-regulation of CD11b and CD18 on PMN was also induced by the immunoglobulin G (IgG) fraction of the sera of RV patients. Moreover, L-selectin expression on PMN was down-regulated by the sera or IgG of some patients with RV. These changes in CAM expression on PMN induced by IgG of RV patients were not observed when PMN were incubated with the IgG of RV patients from which the IC formed by IgG had been removed. CONCLUSION: These results suggest that IC formed by IgG in patients with RA are involved in the development of vasculitis by affecting the expression of CAM on PMN.

Adult↗
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Occurrence of acute infectious bursal disease with high mortality in Japan and pathogenicity of field isolates in specific-pathogen-free chickens.

Highly virulent infectious bursal disease virus (IBDV) was isolated from field cases, and the pathogenicity of the isolates was examined in specific-pathogen-free chickens. Chickens inoculated with the isolates developed severe clinical disease with a high mortality rate. Histopathologically, infectious bursal disease was characterized by bursal and thymic necrosis, aplastic anemia, acute hepatitis with fatty change, and systemic inflammatory response. In addition to functional abnormalities in the liver, a hypoxic state was induced by aplastic anemia and severe inflammation in the pulmonary air capillary walls. These pathological changes appeared to be closely related to the cause of death.

Animals↗
PubMedDate not supplied

Comparison of immunity induced with a Mycoplasma gallisepticum bacterin between high- and low-responder lines of chickens.

Chickens of the high-responder line GSP and low-responder line BM-C, which had been known to have different antibody responses to Mycoplasma gallisepticum (MG) antigen, were immunized by intramuscular injection and by subsequent intratracheal instillation of MG bacterin. They were then challenged with the pathogenic strain SAS of MG. The preventive effects of local antibodies detectable in the trachea, saliva, and lacrima were compared between the two lines of chickens. The local antibody responses, as determined by an enzyme-linked immunosorbent assay, were higher in line GSP than in line BM-C before and after challenge. Following challenge, chickens of both lines were protected from colonization by MG and the development of respiratory lesions. The degree of protection in line GSP was higher than that of line BM-C. The results suggest that local antibodies may play an important role in the host defense mechanism to respiratory MG infection.

Animals↗
PubMedDate not supplied

Pathogenesis of abnormal feathers in chickens inoculated with reticuloendotheliosis virus.

Abnormal feathers, characterized by thinness and increased transparency of the calamus and rachis, and loss of barbs, were induced at a high frequency by inoculating day-old chicks with reticuloendotheliosis virus (REV) propagated in chicken-embryo fibroblast (CEF) cultures. The few birds that survived inoculation with oncogenic stock of REV derived from liver tissue of an infected chick developed similar abnormalities. Lesions of an inflammatory-degenerative type were observed in close association with the presence of viral antigen and numerous c-type virus particles, characteristic of REV, in the intermediate and cylindrical cell layers of all abnormal feathers examined. These findings, first detected in the intermediate and cylindrical cell layers of developing feathers 6--9 days after infection, suggest that degeneration and necrosis of feather-forming cells result from productive infection of REV, resulting in the development of the abnormal feathers.

Animals↗
PubMedDate not supplied

Immunity induced with an aluminum hydroxide-adsorbed Mycoplasma gallisepticum bacterin in chickens.

The protective effect of an inactivated Mycoplasma gallisepticum (MG) bacterin was evaluated in chickens subsequently challenged intratracheally (IT) with the homologous strain. Antibody responses in sera and tracheal washings (TWs) from these chickens were determined by an enzyme-linked immunosorbent assay. A group of chickens was vaccinated intramuscularly (IM) with two doses of the bacterin containing aluminum hydroxide gel (IM + IM). Another group was vaccinated IM with the same bacterin followed by IT with bacterin lacking the adjuvant (IM + IT). Chickens of both vaccinated groups had similar levels of antibody in TWs at the time of challenge. MG was eliminated from the trachea at higher rates and inflammatory lesions in the trachea were less severe in vaccinated chickens than in unvaccinated controls. The protective effect in chickens vaccinated IM + IT was greater than that in chickens vaccinated IM + IM. Perhaps vaccinal immunity is mediated by local rather than systemic antibody responses, or perhaps resistance provided by vaccination IM + IT is conferred partly by another immune mechanism such as cell-mediated immunity.

Adsorption↗
PubMedDate not supplied

Antibody responses in sera and respiratory secretions from chickens infected with Mycoplasma gallisepticum.

Antibodies in sera and respiratory secretions from chickens infected with Mycoplasma gallisepticum (MG) were measured by an enzyme-linked immunosorbent assay (ELISA). Chickens intratracheally inoculated with 10(5) cells of MG showed a correlation between severity of tracheal lesions and extent of MG colonization in the tracheas in the first 3 weeks postinoculation. Antibody titers in tracheal washings (TWs) of the infected chickens increased during this phase. Thereafter, isolation of MG from the trachea decreased sharply, and there was a concomitant decrease in tracheal lesion scores. At 5 weeks postinfection, the chickens that recovered from the infection exhibited a consistent presence of antibodies in TWs. Chickens reexposed had a faster rate of MG elimination and substantially less severe inflammatory lesions in the tracheas than chickens observed after the first exposure. These findings suggest a possible role of antibodies of the respiratory secretions in resistance to MG. The ELISA was a sensitive and reliable test to detect a minute amount of antibodies in the secretions.

Animals↗