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Acta Microbiologica et Immunologica Hungarica
Authors: Elena Nikolaevna Filatova, Elena Viktorovna Anisenkova, Nataliya Borisovna Presnyakova and Oleg Vladimirovich Utkin

herpesvirus type 6. They are lymphotropic viruses that can affect the functional state of the cells of the immune system. In particular, they cause anergy of T-lymphocytes and regulate proliferation and apoptosis of immunocompetent cells [2] . It is

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Perner, F.: A veseátültetés eredményét befolyásoló tényezők. Doktori értekezés, Budapest. 1988. Salahudeen, A. K., Joshi, M., Jenkins, J. K.: Apoptosis

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. , Musarrat , J. and Al-Khedhairy , A. A. ( 2012 ): Apoptosis induction by silica nanoparticles mediated through reactive oxygen species in human liver cell line HepG2 . Toxicol. Appl. Pharm. 259 , 160 – 168

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Communal C, Colucci WS: The control of cardiomyocyte apoptosis via the beta-adrenergic signaling pathways. Arch. Mal. Coeur. Vaiss. 98, 236–241 (2005) Colucci WS The control of cardiomyocyte apoptosis via the beta

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Interventional Medicine and Applied Science
Authors: Balázs Nemes, P. Sótonyi, G. Lotz, A. Heratizadeh, F. Gelley, C. Doege, M. Hubay, Zs. Schaff and B. Nashan

1972 Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics Br J Cancer 26 239 257 . 2

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Bannerman, D. D., Tupper, J. C., Rickets, W. A., Bennet, C. F., Winn, R. K. and Harlan, J. M. (2001): A constitutive pathway protects endothelial cells from lipopolysaccharide-induced apoptosis. J. Biol. Chem. 276 , 14924

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Acta Biologica Hungarica
Authors: C. Pekcetin, Muge Kiray, B. Ergur, K. Tugyan, H. Bagriyanik, G. Erbil, Basak Baykara and U. Camsari

., Kim, C. J. (2003) Acupuncture suppresses ischemia-induced increase in c-Fos expression and apoptosis in the hippocampal CA1 region in gerbils. Neurosci. Lett. 347 , 5–8. Kim C. J

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Leptin (L) is recognised as an important regulator of puberty and a factor which controls reproduction. Whole pig ovarian follicles were incubated with different doses of leptin (2, 20 and 200 ng/ml) added alone or in combination with 100 ng/ml of GH or 50 ng/ml of IGF-I. The expression of the functional long form leptin receptor (Ob-Rb) mRNA was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) in follicular cells cultured with GH or IGF-I. Both GH and IGF-I increased leptin receptor expression in prepubertal pig ovaries. In separate experiments, the action of leptin on ovarian follicular steroidogenesis and cell apoptosis was examined. After 24 h of incubation with leptin alone or in combination with GH or IGF-I, oestradiol (E2) levels were determined in the culture medium while follicular tissue was used for the estimation of caspase-3 activity. Leptin increased E2 secretion and significantly diminished caspase-3 activity at all doses used. Both GH and IGF-I stimulated oestradiol secretion and decreased caspase-3 activity. No differences were demonstrable in oestradiol secretion and caspase-3 activity between cells treated with GH plus leptin and GH alone or cells treated with IGF-I plus leptin as compared to cultures treated with GH or IGF-I alone. However, GH diminished leptin-stimulated oestradiol secretion while IGF-I was without effect on it. Both GH and IGF-I reversed the anti-apoptotic action of leptin. In conclusion, we infer that (1) leptin directly affects ovarian function in prepubertal animals by its action on oestradiol secretion and cell apoptosis, (2) GH and IGF-I modulate the action of leptin, and (3) at least in part, the direct effect of GH/IGF-I on leptin production is due to an action on leptin receptor expression.

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Increased levels of the matrix metalloproteinases-2 and -9 (also referred to gelatinase-A and -B, respectively) can be detected in intestinal inflammation. We have recently shown that selective gelatinase blockage by the synthetic compound RO28-2653 ameliorates acute murine ileitis and colitis. We here investigated whether RO28-2653 exerts anti-inflammatory effects in acute Campylobacter jejuni-induced enterocolitis of gnotobiotic IL-10−/− mice generated following antibiotic treatment. Mice were perorally infected with C. jejuni (day 0) and either treated with RO28-2653 (75 mg/kg body weight/day) or placebo from day 1 until day 6 post infection (p.i.) by gavage. Irrespective of the treatment, infected mice displayed comparable pathogen loads within the gastrointestinal tract. Following RO28-2653 administration, however, infected mice exhibited less severe symptoms such as bloody diarrhea as compared to placebo controls. Furthermore, less distinct apoptosis but higher numbers of proliferating cells could be detected in the colon of RO28-2653-treated as compared to placebo-treated mice at day 7 p.i. Remarkably, gelatinase blockage resulted in lower numbers of T- and B-lymphocytes as well as macrophages and monocytes in the colonic mucosa of C. jejuni-infected gnotobiotic IL-10−/− mice. Taken together, synthetic gelatinase inhibition exerts anti-inflammatory effects in experimental campylobacteriosis.

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Physiology International
Authors: P. Kovács, József Gábor Joó, V. Tamás, Z. Molnár, D. Burik-Hajas, J. Bódis and L. Kornya

Introduction Programmed cell death (apoptosis) plays an important role during the development of the placenta and in the regulation of its ageing during pregnancy [ 35 ]. The regulation of programmed cell death is complex; both proapoptotic

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