Bursting activities

Arthur, M.J.P., Kowalski-Saunders, P. and Wright, R. (1986a). C. /Mm -elicited hepatic macrophages demonstrate enhanced respiratory burst activity compared with resident Kupffer ceUs in the rat. Gastroenterology 91, 174-181. 

Baldassano, R.N., Schreiber, S., Johnston, R.B. and MacDermott, KP. (1991). Increased respiratory burst activity from Crohn s disease peripheral blood mononuclear ph o-cytes. Gastroenterology 100, A559. 

Mahida, Y.R., Wu, K.C. and Jewell, D.P. (1989). Respiratory burst activity of intestinal macrophages in normal and inflammatory bowel disease. Gut 30, 1362-1370. 

Stanghellini et al. [122] have carefully defined the most common abnormalities of phase III activity and other abnormal motility patterns that occur in patients with chronic intestinal pseudoobstruction, who often suffer from bacterial overgrowth [113], This concerns phase III with abnormal migration (stationary or retrograde) and with abnormal isotonic component, abnormal burst activity, and a failure of the postprandial pattern. 

Yearlings exposed to 6.4, 16, or 26.9 pg Cu/L for up to 21 days Adverse effects on survival during first 48 h and decrease in respiratory burst activity at all concentrations tested. At high dose, percentage of monocytes increased and lymphocyte percent decreased 168... 

Peterson, P.K., Sharp, B., Gekker, G., and Keane, W.F., Opioid-mediated suppression of cultured peripheral blood mononuclear cell respiratory burst activity, J. Immunol., 138,3907, 1987. 

It is known that protein kinase C can phosphorylate a number of key oxidase components, such as the two cytochrome b subunits and the 47-kDa cytoplasmic factor. This process is prevented by protein kinase C inhibitors such as staurosporine (although it is now recognised that this inhibitor is not specific for protein kinase C), which also inhibits the respiratory burst activated by agonists such as PMA. However, when cells are stimulated by fMet-Leu-Phe, translocation of pAl-phox to the plasma membrane can occur even if protein kinase C activity is blocked - that is, phosphorylation is not essential for the translocation of this component in response to stimulation by this agonist. Similarly, the kinetics of phosphorylation of the cytochrome subunits do not follow the kinetics of oxidase activation, and protein kinase C inhibitors have no effect on oxidase activity elicited by some agonists -for example, on the initiation of the respiratory burst elicited by agonists such as fMet-Leu-Phe (Fig. 6.14). Furthermore, the kinetics of DAG accumulation do not always follow those of oxidase activity. Hence, whilst protein kinase C is undoubtedly involved in oxidase activation by some agonists, oxidase function is not totally dependent upon the activity of this kinase. 

Ca2+ concentration and relation with respiratory burst activation. J. Biol. Chem. 266, 23152-6. 

Koenderman, L., Tool, A., Roos, D., Verhoeven, A. J. (1989). 1,2-Diacylglycerol accumulation in human neutrophils does not correlate with respiratory burst activation. FEBSLett. 243, 399-403. 

In vivo administration of y-interferon to atypical X-CGD patients also led to improvements in monocyte and neutrophil respiratory-burst activity and killing, and in some cases spectroscopically-detectable cytochrome b has been observed (occasionally present at up to 50% of normal levels). This improvement followed two subcutaneous doses (0.1 mg/m2) on consecutive days and lasted for up to a month. Because TNF can act synergisti-cally with y-interferon in increasing the expression of the heavy chain of cytochrome b, perhaps the combined use of y-interferon with TNF or some other cytokine(s) will prove even more beneficial. 

This disease was first observed in the mid- to late-1970s when several patients presented with recurrent bacterial infections, primarily of the skin and subcutaneous tissues, middle ear and oropharyngeal mucosa. When examined in vitro, the neutrophils from these patients had defects in chemo-taxis, phagocytosis, particle-stimulated respiratory-burst activity and granulation. Some patients also had a leukocytosis, and many had a delayed umbilical cord separation. Treatment is by prophylactic antibiotic therapy and aggressive antibiotic therapy during infections, but mortality rates are very high. 

Infection is the most common cause of morbidity and mortality in MDS patients, accounting for 40-60% of deaths in various studies. The common infections are those normally associated with neutropenias, such as Gramnegative septicaemia and bacterial bronchopneumonias. Indeed, most MDS patients are neutropenic at some stage in their disease. Even those who do not have a neutropenia may have a defect in their neutrophil function. Many patients have clearly-defined defects in T- and B-lymphocyte functions, and variable defects in monocyte numbers or function have been described. Disorders of neutrophil function are common. Many reports indicate that phagocytosis, chemotaxis, respiratory-burst activity and degranulation are defective in some MDS patients, and hypogranulation is often observed. 

Indirect mechanisms Nicotine has indirect effects on monoamine systems. A considerable amount of research has examined the relationships between nicotine and dopamine activity in the brain, in light of dopamine s role in reinforcement and nicotine s addictive properties. Nicotine increases dopamine turnover in the striatum and cerebral cortex (Clarke and Reuben 1996 Tani et al. 1997 Nanri et al. 1998). It also increases burst activity in dopamine neurons of the ventral tegmental area (VTA), a primary source of dopamine to the forebrain (Nisell et al. 1995 Fisher et al. 1998). Such a firing pattern in the VTA is associated with processes of reinforcement, learning, and cognitive activity. Nicotine actions on dopaminergic neurons occur at both somatodendritic sites and synaptic terminals. Further, both systemic nicotine and direct administration into the VTA increase dopamine release in the nucleus ac-... 

Excitatory neurotransmitters also may be involved in the appearance of epilepsy, since the bursting activity typically seen during epileptic discharges may be due in part to the action of glutamate acting on A-methyl-o-aspartate (NMDA) receptor channels to produce depolarization. It is likely that a major part of the anticonvulsant activity of felbamate involves blockade of the NMDA receptor. Table 32.2 summarizes the most likely mechanism of action associated with available anticonvulsant drugs. 

Z0218 Sugaya, A., T. Tsuda, E. Sugaya, M. ZO230 Takato, and K. Takamura. Effects of Chinese medicine saiko-keishi-to on the abnormal bursting activity of snail neurons. Planta Med 1978 34 294-298. Z0231... 

Horvitz, J. , T. Stewart, and B. L. Jacobs. 1997. "Burst Activity of Ventral Segmental Dopamine Neuros Is Elicited by Sensory Stimuli in the Awake Cat." Brain Research 759 251-60. 

Nessel CC, Henry WL, Mastrofrancesco B, Reichner JS, Albina JE. Vestigial respiratory burst activity in wound macrophages. American Journal of Physiology 1999, 276, R1587-R1594. 

K., and Braun, H.A. Phasic bursting activity of paraventricular neurons is modu-... 

Jackson ME, Homayoun H, Moghaddam B. 2004. NMDA receptor hypofunction produces concomitant firing rate potentiation and burst activity reduction in the prefrontal cortex. Proc Natl Acad Sci USA 101 8467-8472. 

Horvitz JC, Stewart T, Jacobs BL (1997) Burst activity of ventral tegmental dopamine neurons is elicited by sensory stimuli in the awake cat. Brain Res 759(2) 2518. 

Petersorr PK, Sharp B, Gekker G, Brummitt C, Kearre WE (1987a) Opioid-mediated suppressiorr of cultured peripheral blood morro-rruclear cell respiratory burst activity. J Immurrol 138 3907—3912. 

Chao CC, Gekker G, Sheng WS, Hu S, Tsang M, Peterson PK (1994) Priming effect of morphine on the production of tumor necrosis factor-alpha by microglia Implications in respiratory burst activity and human immunodeficiency virus-1 expression. J Pharmacol Exp Ther 269 198-203. 

Oscillations of [Ca2+][ have been reported following initiation of insulin release by nutrients and sulphonylureas (Heilman etal., 1992). The frequency of these large-amplitude oscillations corresponds to 0.2-0.5 min-1 in mouse B-cells, which is similar to the slow cyclic variations in burst activity recorded with intracellular microelectrodes in intact islets and also the periodicity of insulin release. However, this oscillatory pattern of the electrical and [Ca2+]j responses induced by glucose is not accompanied by, and thus probably not due to, similar oscillations in metabolism (Gilon and Henquin, 1992). However, Longo et al. (1991) reported oscillations with similar periods in insulin secretion, oxygen consumption and [Ca2+]j. Since oscillations appear in vivo as well as in vitro there must be a pacemaker in the islet tissue itself (Goodner et al., 1991). 

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