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A suggestion was made in order to alter the terminology of an inflammatory process from the Latin term of inflammatio or the Greek term of phlogosis to stromatitis (stroma - connective tissue sub-layer). The new term reflects the morphological base of the process and indicates that inflammation develops not in the parenchyma or in cells of tissues and organs but in their stroma. The suggested substitution has been supported by scientific and etymological arguments as well as by numerous examples.
Overtraining is a maladaptive state of athlete’s body related to the physical, behavioral and emotional condition, occurring when exercise training exceeds the recoverability. The cytokine hypothesis of overtraining promoted in recent years is seen as the prevailing theory explaining the understanding of the overtraining phenomenon. The high level of pro-inflammatory cytokines (IL-6, TNFα, IL-1β) involved in the inflammatory response may strongly influence not only the central nervous system but also the endocrine and immune systems. Moreover, there is a range of factors in athlete’s life that appear to increase the risk of depression development, such as psychological and emotional stress associated with sports competition. The aim of this review was to reveal the role of high level of proinflammatory cytokines observed in OTS with the possible occurrence of depression symptoms in athletes. Latest findings have shown an important role of the same pro-inflammatory cytokines in the development of depression. The study discusses a potential mechanism responsible for the development of depression in athletes, which may be helpful in the quick diagnosis of depression basis in athletes. Due to the low number of studies concerning depression and inflammation in athletes further research should be conducted.
In the present study, the pattern of cyclooxygenase-2 (COX-2) expression in health and inflamed porcine uteri was analyzed using real-time reverse transcriptase-polymerase chain reaction (RT-PCR),Western blot and immunohistochemistry. On day 3 of the estrous cycle, 50 ml of saline or 50 ml of Escherichia coli (E. coli) suspension containing 10⁹ colony-forming units/ml, were injected into each uterine horn of the control (n=6) and experimental gilts (n=7), respectively. This latter procedure lead to a moderately (n=3) or severely intense (n=4) acute endometritis after eight days. Expression of both the COX-2 mRNA and protein was increased in the endometrium (ENDO) of animals suffering from the moderate (P<0.05, P<0.01, respectively) and severe (P<0.01) acute endometritis, as compared to the control tissues. Moreover, COX-2 mRNA level and protein content were higher (P<0.05) in the ENDO of animals with severe than with a moderately acute endometritis. An elevation in the COX-2 gene (P<0.05) and protein (P<0.001) expression was also observed in the myometrium (MYO) of animals suffering from severe endometritis, when compared with the levels observed in MYO of both the health and moderate intensely inflamed uteri. However, both the COX-2 mRNA and protein levels were similar in MYO of the control and moderately inflamed organs. The luminal epithelium, some of uterine glands and circular layer of the MYO were more intensely stained for COX-2 in animals with severe endometritis, than in animals with healthy or moderately inflamed uteri. Nonetheless, stronger COX-2 reaction was found in some of the uterine glands in latter group, when compared to that observed in uteri of the control animals. While positive COX-2-labeling was observed in the muscular layer of all arteries supplying the health and inflamed uteri, such staining was exclusively present in the endothelium of some arteries in inflamed organs. Likewise, some arteries in uteri of the animals with severe endometritis displayed immunoreaction stronger than that found in uteri of the animals with moderate inflammation. The present study revealed an up-regulation of COX-2 mRNA and protein in the inflamed porcine uterus, which was directly related to the intensity of the organ inflammation. An increase in the COX-2 expression in the uterus challenged by E. coli-induced inflammation indicates that this enzyme is crucial for elevated prostaglandins production in the inflamed organ.
 Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report.
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Inflammatory bowel diseases and brain-gut axis

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The influence of stress on inflammation in inflammatory bowel disease (IBD) is reviewed. In experimental forms of colitis in rats, stress reactivated the disease. A study of stable IBD patients who were followed for over five years explored the influence of stress on exacerbating the disease. Those patients with high prolonged stressful life events were found to have a 90% recurrence rate of their colitis as compared to only 40% recurrence in low stress patients. Some of the mediators of stress include VIP, TNFalpha, heat shock proteins, glucocorticoid and catecholamines. Stress was shown to increase intestinal permeability to markers such as Cr-EDTA, HRP and dextran 10,000 in rats. In addition, stress increases the permeability of intestinal M-cells. Finally, stress increased the permeability of Paneth cells to HRP. Since Paneth cells synthesize NOD2 mRNA and protein, stress may play a role in the genesis or reactivation of Crohn's disease involving the terminal ileum. Brain-gut interactions via neural, hormonal and cytokine signals can diminish the mucosal protective factors and increase the permeability of luminal antigens into the intestinal epithelial and immune cells. Stress appears to play a key role in exacerbating and accentuating the intestinal inflammation in IBD through brain-gut interactions.
Inhaled corticosteroids (ICS) are widely used for the treatment of COPD despite of controversial statements concerning their efficacy. The use of N-acetylcysteine (NAC), a mucolytic drug with antioxidant properties, is less clear, but it may counteract the oxidant-antioxidant imbalance in COPD. The aim of this study was to evaluate whether treatment of COPD patients with ICS or NAC is able to improve inflammatory indices and to enhance lung function. ICS treatment enhanced protective markers for oxidative stress such as glutathione peroxidase (GPx) (51.2 ±5.8 vs. 62.2 ±8.6 U/g Hb, P<0.02) and trolox-equivalent antioxidant capacity (TEAC) (1.44 ±0.05 vs. 1.52 ±0.06 mM, P<0.05). NAC decreased sputum eosinophil cationic protein (318 ±73 vs. 163 ±30 ng/ml, P<0.01) and sputum IL-8 (429 ±80 vs. 347 ±70 ng/ml, P<0.05). The increased antioxidant capacity prevented an up-regulation of adhesion molecules, since the levels of intracellular adhesion molecule 1 (ICAM-1) correlated negatively with GPx (P<0.0001) and TEAC (P<0.0001). On the other hand, expression of adhesion molecules was promoted by inflammation, reflected by a positive correlation between the levels of IL-8 and ICAM-1 (P<0.0001). The effects of treatment on lung function were only reflected in the FEV1 values. The absolute value of FEV1, both before and after salbutamol inhalation, increased from 1690 ±98 to 1764 ±110 ml, and 1818 ±106 to 1906 ±116 ml, respectively, after ICS (P<0.05) . Ten weeks after treatment, FEV1 values dropped to 1716 ±120 ml post-salbutamol (P<0.05). When followed by treatment with NAC, these values decreased even further to 1666 ±84 ml. These results suggest that ICS improved lung function in COPD patients with moderate airflow obstruction, beside a minor improvement in the oxidant-antioxidant imbalance leading to a lesser expression of ICAM-1. Treatment with NAC decreased some inflammatory parameters and had indirectly an inhibitory effect on the expression of adhesion molecules.
The objective of this investigation was to evaluate the pro- or anti-inflammatory properties of nanoparticles of Ag, Au, and Ag/Cu alloy by examining the expression of NF-κB mRNA. The experiment was performed in ovo, on the chicken embryos' model. The nanoparticles had no effect on embryos' survival; the embryos from all groups were properly developed, without any abnormalities. Contrary to Ag and Au, nanoparticles of Ag/Cu increased NF-κB mRNA expression in embryo liver, indicating a proinflammatory effect. After treatment with LPS there was a significant decrease in NF-κB mRNA expression in the liver of embryos treated with Ag, compared to the placebo, Au, and Ag/Cu groups, indicating that Ag nanoparticles act as a potential anti-inflammatory factor. The results indicate the lack of influence of Ag and Au nanoparticles on NF-κB mRNA expression in chicken embryo liver. Contrary to Ag and Au, nanoparticles of Ag/Cu alloy may be considered as a pro-inflammatory factor. Nanoparticles of Ag, but not Au and Ag/Cu, can prevent over-expression of NF-κB mRNA after LPS stimulation.
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