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Intricate Mechanism (intricate + mechanism)
Selected AbstractsVitamin B2 -sensitized Photo-oxidation of DopaminePHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 5 2008Walter A. Massad Kinetics and mechanism of the photo-oxidation of the natural catecholamine-type neurotransmitter dopamine (DA) has been studied in aqueous solution, under aerobic conditions, in the presence of riboflavin (Rf, vitamin B2) as a photosensitizer. Results indicate the formation of a weak dark complex Rf,DA, with a mean apparent association constant Kass = 30 m,1, only detectable at DA concentrations much higher than those employed in photochemical experiments. An intricate mechanism of competitive reactions operates upon photoirradiation. DA quenches excited singlet and triplet states of Rf, with rate constants of 4.2 × 109 and 2.2 × 109 m,1 s,1, respectively. With the catecholamine in a concentration similar to that of dissolved molecular oxygen in air-saturated water, DA and oxygen competitively quench the triplet excited state of Rf, generating superoxide radical anion (O2,,) and singlet molecular oxygen (O2(1,g)) by processes initiated by electron and energy-transfer mechanisms, respectively. Rate constants values of 1.9 × 108 and 6.6 × 106 m,1 s,1 have been obtained for the overall and reactive (chemical) interaction of DA with O2(1,g). The presence of superoxide dismutase increases both the observed rates of aerobic DA photo-oxidation and oxygen uptake, due to its known catalytic scavenging of O2,,, a species that could revert the overall photo-oxidation effect, according to the proposed reaction mechanism. As in most of the catecholamine oxidative processes described in the literature, aminochrome is the DA oxidation product upon visible light irradiation in the presence of Rf. It is generated with a quantum yield of 0.05. [source] Damage-induced reactivation of cohesin in postreplicative DNA repairBIOESSAYS, Issue 1 2008Alexander R. Ball Jr Cohesin establishes sister-chromatid cohesion during S phase to ensure proper chromosome segregation in mitosis. It also facilitates postreplicative homologous recombination repair of DNA double-strand breaks by promoting local pairing of damaged and intact sister chromatids. In G2 phase, cohesin that is not bound to chromatin is inactivated, but its reactivation can occur in response to DNA damage. Recent papers by Koshland's and Sjögren's groups describe the critical role of the known cohesin cofactor Eco1 (Ctf7) and ATR checkpoint kinase in damage-induced reactivation of cohesin, revealing an intricate mechanism that regulates sister-chromatid pairing to maintain genome integrity.1,2 BioEssays 30:5,9, 2008. © 2007 Wiley Periodicals, Inc. [source] Immune activation and inflammation in HIV-1 infection: causes and consequences,THE JOURNAL OF PATHOLOGY, Issue 2 2008V Appay Abstract Thorough research on HIV is progressively enabling us to understand the intricate mechanisms that link HIV-1 infection to the onset of immunodeficiency. The infection and depletion of CD4+ T cells represent the most fundamental events in HIV-1 infection. However, in recent years, the role played by chronic immune activation and inflammation in HIV pathogenesis has become increasingly apparent: quite paradoxically, immune activation levels are directly associated with HIV-1 disease progression. In addition, HIV-1-infected patients present intriguing similarities with individuals of old age: their immune systems are characterized by a loss of regenerative capacity and an accumulation of ageing T cells. In this review, we discuss the potential reasons for the establishment of sustained immune activation and inflammation from the early stages of HIV-1 infection, as well as the long-term consequences of this process on the host immune system and health. A simplified model of HIV pathogenesis is proposed, which links together the three major facets of HIV-1 infection: the massive depletion of CD4+ T cells, the paradoxical immune activation and the exhaustion of regenerative capacity. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Modelling parasite dissemination: host cell subversion and immune evasion by Toxoplasma gondiiCELLULAR MICROBIOLOGY, Issue 3 2010Henrik Lambert Summary Protozoan parasites belong to the most widespread and devastating human pathogens. Their ability to manipulate host responses and establish infection in their hosts continues to puzzle researchers. Recent developments of experimental model systems are contributing to the discovery of new aspects of the biology of parasite dissemination. Here, we review current knowledge on strategies utilized by the apicomplexan parasite Toxoplasma gondii to disseminate and establish infection in its host. Recent findings have revealed intricate mechanisms by which this obligate intracellular protozoan sequesters cellular functions of the immune system to assure propagation. These mechanisms include the hijacking of migratory leucocytes, modulation of migratory properties of infected cells and rapid transfer of parasites between different leucocyte populations by cytotoxicity-induced parasite egress. Collectively, Toxoplasma strikes a delicate balance, assuring efficient dissemination and establishment of asymptomatic lifelong infection in its host while protecting its intracellular entity and limiting host pathology. [source] | ||||||||||