Objective: To observe the effect of oxidative stress on intestinal mucosal barrier dysfunction following traumatic brain injury (TBI). Methods: Seventy-two male Wistar rats were randomly divided into three groups, group B and group C served as TBI models, group A was designated as the normal controlgroup(shame operation). In group C rats were treated with dimethyl sulfoxide(DMSO) prior to TBI, while rats in group A and B were treated with equivalent normal saline. During the experiment period, the morphological changes of intestinal mucosa were observed, and the intestinal mucosal permeability was detected by measuring the level of endotoxin, diamine oxidase(DAO). Superoxide dismutase(SOD), malondiadehycle (MDA), myeloperoxidase(MPO) and xanthine oxidase(XOD) activities were also detected. Results: During the observed period, the intestinal mucosal barrier function was damaged and the intestinal mucosal permeability increased. The content of endotoxin in serum significantly increased(P < 0.05). As early as 3 h after TBI, the DAO activity in the serum began to increase obviously. At 24 hafter TBI it increased to the highest level(P < 0.05).In group TBI the activity of SOD in intestinal mucosal decreased significantly(P < 0.01); however the levels of MDA and the activity of MPO increased significantly (P < 0.01), the activity of XOD increased significantly as well, and then decreased after 6 h. When pr-treatment with DMSO, intestinal mucosal damage was improved, the content of endotoxin in serum was reduced (P < 0.05), and the increased DAO activity in the serum were inhibited (P < 0.05). When compared with group TBI, there was an inhibition in the decreased activity of SOD and the increased level of MDA in group DMSO (P < 0.05), but they were still higher than that of control group(P < 0.05). There were no significant differences in the activity of XOD and MPO between group DMSO and group TBI. Conclusion: The structure and function of intestinal mucosal barrier were damaged following TBI. Oxidative stress played an important role in the intestinal mucosal barrier dysfunction following TBI. Both XOD and activated polymorphonuclear neutrophils(PMN) were the major source of oxygen free radicals.

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Asthma is a serious health problem that involves not only the respiratory system but also the central nervous system. Previous studies identified either regional or network alterations in patients with asthma, but inconsistent results were obtained. A key question remains unclear: are the regional and neural network deficits related or are they two independent characteristics in asthma? Answering this question is the aim of this study. By collecting resting-state functional magnetic resonance imaging from 39 patients with asthma and 40 matched health controls, brain functional measures including regional activity (amplitude of low-frequency fluctuations) and neural network function (degree centrality (DC) and functional connectivity) were calculated to systematically characterize the functional alterations. Patients exhibited regional abnormities in the left angular gyrus, right precuneus, and inferior temporal gyrus within the default mode network. Network abnormalities involved both the sensorimotor network and visual network with key regions including the superior frontal gyrus and occipital lobes. Altered DC in the lingual gyrus was correlated with the degree of airway obstruction. This study elucidated different patterns of regional and network changes, thereby suggesting that the two parameters reflect different brain characteristics of asthma. These findings provide evidence for further understanding the potential cerebral alterations in the pathophysiology of asthma.
Asthma/diagnostic imaging* ; Brain/diagnostic imaging* ; Brain Mapping ; Humans ; Magnetic Resonance Imaging