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Hyper-reactivity

Thorin E, Pham-Dang M, Clement R, Mercier I, Calderone A (2003) Hyper-reactivity of cerebral arteries from ovariectomized rats therapeutic benefit of tamoxifen. Br J Pharmacol 140 1187-1192... [Pg.246]

Landgraf R, Wigger A, Holsboer F, Neumann ID (1999) Hyper-reactive hypothalamo-pituitary adrenocortical axis in rats bred for high anxiety-related behaviour. J Neu-roendocrinol 11 405-407... [Pg.66]

Further studies are needed to characterize the mechanisms underlying AVP over-expression and over-release in more detail. The same holds true for the hyper- and hypo-emotional Roman low- and high-avoidance rats, originally selected and bred for poor versus rapid acquisition of two-way active avoidance response (Steimer and Driscoll 2003). In the former, more ACTH and corticosterone were secreted upon a mild stressor, again indicating a hyper-reactive HPA axis. This was shown to be associated with higher AVP mRNA levels in the PVN, whereas CRH mRNA did not differ between the hnes (Aubry et al. 1995). [Pg.351]

As stated above in entry 36, my problems began in the early 1990s with a severe sinus infection. The hyper-reactivity that followed has remained. Despite repeated visits to the general practitioner and the ear, nose and throat specialist due to my nose and sinus problems, little really changed I was prescribed some inhalers, pills and antibiotics. For years I had a slightly high body temperature (99.3—100.4 degrees Fahrenheit)... [Pg.55]

Using the isoTOP-ABPP method, the soluble proteome of the breast cancer cell line MCF7 was interrogated and, of the 800 probe-labeled cysteines, 10% were found to be hyper-reactive (/ io i < 2). A database search further revealed that hyper-reactive cysteines were over-represented in functional residues (active site... [Pg.33]

Another factor to consider is that patients with endogenous skin disease are frequently more susceptible to cosmetic reactions. One reason is that patients with preexisting skin disease may have skin barrier dysfunction, with consequent increased permeability. Skin hyper-reactivity in atopic patients, particularly, has been gathering interest in recent years. Epidemiologic associations between atopic dermatitis and irritant dermatitis are now supported by skin bioengineering data.25... [Pg.492]

There also are case reports of reactive airways dysfunction syndrome (RADS) associated with chlorine exposure (Alberts and do Pico 1996 Donnelly and FitzGerald 1990 Schonhofer et al. 1996). RADS is persistent hyper-reactivity of the airways that occurs after a single exposure to a high concentration of an irritant gas (Brooks et al. 1985). All reported RADS cases have resulted from accidental exposures in which exposure concentrations can be presumed to have been high. [Pg.123]

Jackson, D.M., and R.P.Eady. 1988. Acute transient S02-induced airway hyper reactivity Effects of nedocromil sodium. J. Appl. Physiol. 65(3) 1119—1124. [Pg.306]

The NAC/AEGL Committee estimates the range in variability of response to specific chemical exposures primarily on the basis of quantitative human data. Acceptable experimental data are more likely to be available for AEGL-1 and AEGL-2 endpoints than for AEGL-3 endpoints. For example, numerous studies have considered induction of bronchospasm after controlled exposmes to sulfur dioxide (SO2) in asthmatic and nonasthmatic individuals (see references below). There is marked individual variability in the severity of reaction to inhalation of low concentrations of SO2. Asthmatics, individuals with hyper-reactive airways, smokers, and those with chronic respiratory or cardiac disease respond at relatively lower concentrations (Aleksieva 1983 Simon 1986). Susceptibility may also be increased in people over 60 years of age, but reports have not been consistent (Rondinelli et al. 1987 Koenig et al. 1993). By contrast, comparable human data for AEGL-3 tier concentrations are limited to anecdotal case reports. [Pg.109]

The hyper-reactivity of the HPA axis that occurs with chronic stress is also often observed in depressed patients. (Owens and Nemeroff, 1991)... [Pg.482]

Recently a hyperactivity model induced by a combination of D-amphetamine and chlordiazepoxide was studied. Lamotrig-ine, valproate, and carbamazepine, all used to treat bipolar disorder, were all found to decrease this hyperactivity (Arban et al., 2005). Interestingly, while most mania models assume an increase in dopamine, an early model used dopamine depletion with in tracerebr oven trie ular injection of 6-hydroxydopa-mine, which induces hyper-reactivity to environmental stimuli, but not hyperactivity per se (Petty and Sherman, 1981). This model was responsive to chronic lithium and to chronic electroconvulsive shock, and also to acute chloiq romazine, while imipramine w orsened the behavior. [Pg.503]

The role of the HPA axis in coordinating responses to stressors, and the role of the immune system in mediating the sickness response, underscore this reciprocal relationship between the CNS and the immune system. However, the relationship is complex, and it should be clear that we are in the early stages of understanding how immune tissue can contribute to psychiatric disorders. In spite of this nascent state of knowledge, the evidence for hyper-reactivity of the HPA axis and the alterations in cytokine levels observed in both MDD and schizophrenia serve as a foundation for further research establishing a causative relationship between alterations in immune system function and these debilitating CNS disorders. [Pg.490]

In a blind, randomized study, 29 children aged under 2 years, with moderate to severe acute exacerbations of hyper-reactive airways disease, were treated with either a standard dose of nebulized salbutamol (0.15 mg/kg) or a low dose of nebulized salbutamol (0.075 mg/kg) plus nebulized ipratropium bromide 250 micrograms (4). Standard and low-dose nebulized salbutamol was given three times at intervals of 20 minutes and nebulized ipratropium bromide was given once. Clinical improvement, measured as O2 saturation and relief of respiratory distress, was similar in both groups. QT dispersion was measured at baseline and after treatment and was... [Pg.448]

Regular exposure to a racemate, especially during or after an allergic reaction, will cause hyper-reactivity to spasmogens, and this could be due to an effect of the 5-isomer. This effect is not seen immediately, because of beta2-adrenoceptor-mediated bronchodilatation by the R-isomer. [Pg.451]

The pressure response to endothelin-1 in the canine circulation has been investigated in isolated perfused dog lung (74). Acute treatment of the isolated lobes with fenfluramine increased pulmonary arterial pressure. Chronic treatment with fenfluramine potentiated the pulmonary vasoconstrictor response to endothelin-1. Based on these findings, the authors proposed that the pulmonary vasculature becomes hyper-reactive to vasoactive substances, such as serotonin and endothelin-1, possibly leading to pulmonary hjrpertension. [Pg.1339]

The symptoms of overexposnre to glutaral vapor inclnde watery and/or burning eyes, nose and throat irritation, and some respiratory discomfort. Glutaral also causes asthma-hke sjmptoms in a few hypersensitive individuals. However, in none of these cases was there evidence that an immune-mediated process was present these cases probably represent bronchial hyper-reactivity rather than respiratory sensitization (6). [Pg.1514]

Vitamin D3 has been reported to cause hyper-reactivity of skin with pseudoxanthoma elasticum (39). [Pg.3673]

Zager RA, Johnson AC, Lund S, Endotoxin tolerance TNF-a hyper-reactivity and tubular cytoresistance in a renal cholesterol loading state. Kidney Int, 2007, 71 496-503. [Pg.291]

The dopamine theory holds that the basic physiological pathology involves primarily overactive or hyper-reactive dopamine neurons. The excessive dopamine activity can lead to behavioral agitation, a failure to adequately screen stimuli, and disorganization of perception and thought. This theory is supported by two observations The first is that the potency of antipsychotic drugs has correlated closely with their ability to bind to and block the postsynaptic dopamine (D2) receptors in the mesolimbic system (see figure 9-A). [Pg.111]

Blease K, Lukacs NW, Hogaboam CM, Kundel SL. Chemokines and their role in airway hyper-reactivity. Respir Res 2000 1 54-61. [Pg.725]


See other pages where Hyper-reactivity is mentioned: [Pg.307]    [Pg.800]    [Pg.480]    [Pg.575]    [Pg.578]    [Pg.161]    [Pg.278]    [Pg.66]    [Pg.638]    [Pg.349]    [Pg.186]    [Pg.336]    [Pg.33]    [Pg.227]    [Pg.487]    [Pg.488]    [Pg.155]    [Pg.276]    [Pg.2327]    [Pg.342]    [Pg.3923]    [Pg.23]    [Pg.107]    [Pg.228]    [Pg.1952]    [Pg.3093]    [Pg.276]    [Pg.216]   
See also in sourсe #XX -- [ Pg.42 ]




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Skin hyper-reactivity

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