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Interactive Role (interactive + role)
Selected AbstractsInteractive roles of fibroblast growth factor 2 and neurotrophin 3 in the sequence of migration, process outgrowth, and axonal differentiation of mouse cochlear ganglion cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2008Waheeda A. Hossain Abstract A growth factor may have different actions depending on developmental stage. We investigated this phenomenon in the interactions of fibroblast growth factor 2 (FGF2) and neurotrophins on cochlear ganglion (CG) development. The portions of the otocyst fated to form the CG and cochlear epithelium were cocultured at embryonic day 11 (E11). Cultures were divided into groups fed with defined medium, with or without FGF2 and neurotrophin supplements, alone or in combination, for 7 days. We measured the number of migrating neuroblasts and distances migrated, neurite outgrowth, and axonlike processes. We used immunohistochemistry to locate neurotrophin 3 (NT3) and its high-affinity receptor (TrkC) in the auditory system, along with FGF2 and its R1 receptor, at comparable developmental stages in vitro and in situ from E11 until birth (P1) in the precursors of hair cells, support cells, and CG cells. Potential sites for interaction were localized to the nucleus, perikaryal cytoplasm, and cell surfaces, including processes and growth cones. Time-lapse imaging and quantitative measures support the hypothesis that FGF2 alone or combined with neurotrophins promotes migration and neurite outgrowth. Synergism or antagonism between NT3 and other factors suggest interactions at the receptor level. Formation of axons, endings, and synaptic vesicle protein 2 were increased by interactions of NT3 and FGF2. Similar experiments with a mutant overexpressor for FGF2 suggest that endogenous FGF2 supports migration and neurite outgrowth of CG neuroblasts as well as proliferation, leading to accelerated development. The findings suggest interactive and sequential roles for FGF2 and NT3. © 2008 Wiley-Liss, Inc. [source] Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000K. Takeuchi Summary Background: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or NG -nitro- l -arginine methyl ester (L-NAME). Results: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. Conclusions: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine. [source] Glutamate-Dopamine Cotransmission and Reward Processing in AddictionALCOHOLISM, Issue 9 2006Christopher C. Lapish While Dale's principle of "one neuron, one neurotransmitter" has undergone revisions to incorporate evidence of the corelease of atypical neurotransmitters such as neuropeptides, the corelease of classical neurotransmitters has only recently been realized. Surprisingly, numerous studies now indicate that the corelease of neurotransmitters in the mammalian central nervous system is not an obscure and rare phenomenon but is widespread and involves most classical neurotransmitters systems. However, the suggestion that glutamate can be coreleased with dopamine (DA) has remained controversial. Furthermore, glutamate-DA cotransmission has not yet been seriously considered in the context of the neurocircuitry of addiction. If glutamate is in fact coreleased with DA as some evidence now suggests, this may have significant implications for advancing our understanding of the interactive role that these 2 neurotransmitters play in cognitive and reward processes. In this commentary, we review the evidence for and against glutamate as a cotransmitter and discuss the potential role of glutamate-DA corelease in addiction. In particular, we describe a recently proposed model in which coreleased glutamate transmits a temporally precise prediction error signal of reward described by Schultz et al., whereas the function of coreleased DA is to exert prolonged modulatory influences on neuronal activity. In addition, we suggest that as alcohol consumption transitions from recreational use to addiction, there is a corresponding transition in the reward valence signal from better than predicted to worse than predicted. [source] High prevalence of parkinsonian disorders associated to manganese exposure in the vicinities of ferroalloy industriesAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 11 2007Roberto G. Lucchini MD Abstract Objective To assess the prevalence of Parkinsonian disturbances in relationship to environmental exposure to manganese due to ferroalloy industries in the province of Brescia, Northern Italy. Methods Manganese concentrations were measured in settled dust collected in each of the 206 municipalities. Parkinsonian patients were identified using two sources: (1) clinical registers from local hospitals, specialized neurologists, and exemption from prescription payment; (2) L-Dopa prescriptions. Standardized prevalence rates and raw and full Bayesian-smoothed standardized morbidity ratios (SMRs) were calculated for the entire province and for each municipality. Results Manganese concentrations in settled dust were significantly higher in the surroundings and downwind from the industrial plants. A total number of 2,677 Parkinsonian cases were identified among 903,997 residents (crude prevalence, 296/100,000; 95% CI: 284.80,307.20; standardized prevalence, 407/100,000; 95% CI: 393.87,420.12). Significantly higher SMRs (Kruskal,Wallis ,2 1 df,=,17.55, P,<,0.001) were observed in 37 municipalities in the vicinities of ferromanganese plants (324 cases among 77,708 residents; standardized prevalence 492/100,000; 95% CI: 442.80,541.20), compared to the other 169 municipalities of the province (2,353 cases among 826,289 residents, standardized prevalence 321/100,000; 95% CI 308.80,333.20). Row and Bayesian SMRs were associated with the concentrations of manganese in settled dust. Conclusion Study results suggest that environmental exposure to manganese is associated with an increased prevalence of Parkinsonian disturbances. Since the highest prevalence rates were observed in a closed community of the pre-Alps where the industries are located, further research should address a possible interactive role of genetic factors. Am. J. Ind. Med. 50:788,800, 2007. © 2007 Wiley-Liss, Inc. [source] Placental macrophage contact induces complete replicative cycle of human immunodeficiency virus in latently infected syncytiotrophoblast cells: role of interleukine-6 and tumor necrosis factor-,AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2002Ferenc D. Tóth The phenotypic mixing between human immunodeficiency virus type 1 (HIV-1) and vesicular stomatitis virus (VSV) has been exploited to assay the susceptibility of human term syncytiotrophoblast cells to penetration by various strains of HIV-1. VSV (HIV-1IIIB) and VSV (HIV-1Ba-L) pseudotypes were found to enter syncytiotrophoblasts. Infection of syncytiotrophoblasts was mediated by envelope glycoproteins of IIIB and Ba-L strains of HIV-1. Although certain strains of HIV-1 could enter syncytiotrophoblasts, the cells did not exhibit permissiveness for HIV-1. The next studies tested the possibility that placental macrophages might induce replication of HIV-1 carried in syncytiotrophoblast cells and that infected syncytiotrophoblasts would be capable of transmitting virus into neighbouring macrophages. For this purpose, the macrophage-tropic Ba-L strain of HIV-1 was used. Interactions between syncytiotrophoblasts and macrophages activated HIV-1 from latency in syncytiotrophoblast cells, which delivered HIV-1 to cocultured macrophages. The stimulatory effect of coculture on HIV-1 gene expression was mediated by marked tumor necrosis factor-, and interleukin-6 release from macrophages, an effect caused by contact between the different placental cells. Results suggest an interactive role for the syncytiotrophoblast layer and placental macrophages in the dissemination of HIV-1 among placental tissue. [source] Folate deficiency followed by ionizing radiation perturbs hepatic dihydrofolate reducatse activityBIOFACTORS, Issue 4 2008Vipen Batra Abstract There is lot of interest in the folate metabolism because of the essential role of folate coenzymes in nucleic acid synthesis. Gamma (,) radiation is well known for inducing damage in the DNA. To counteract these damage, a variety of DNA repair pathways have evolved that require regular supply of DNA bases whose biosynthesis in turn depends on sufficient pools of folate dependent enzymes like dihydrofolate reductase (DHFR). In the present study, we examined the ionizing radiation mediated perturbation of DHFR activity in folate deficient and folate sufficient conditions. In folate deficient animals a potent inhibition of liver DHFR activity was observed. Our results showed that combination of folate starvation and ionizing radiation might adversely affect the DHFR activity, compared to their individual treatments. Measurement of apurinic/apyrimidinic sites (AP sites), a major type of DNA damage generated by radiation induced loss of purine and/or pyrimidine base, indicated a dose dependent DNA damage in folate deficient animals. In conclusion our data suggest an interactive role of folate deficiency and radiation injury in inhibiting DHFR activity. [source] | |||||||||||||