Febrile seizures (FS) are one of the most common neurological disorders in pediatrics, commonly seen in children from three months to five years of age. Most children with FS have a good prognosis, but some febrile convulsions progress to refractory epilepsy (RE). Epilepsy is a common chronic neurological disorder , and refractory epilepsy accounts for approximately one-third of epilepsies. The etiology of refractory epilepsy is currently complex and diverse, and its mechanisms are not fully understood. There are many pathophysiological changes that occur after febrile convulsions, such as inflammatory responses, changes in the blood-brain barrier, and oxidative stress, which can subsequently potentially lead to refractory epilepsy, and inflammation is always in tandem with all physiological changes as the main response. This article focuses on the pathogenesis of refractory epilepsy resulting from post-febrile convulsions.
Objective To investigate the clinical significance of low dose corticosteroid applied in early period after lung volume reduction surgery（LVRS）. Methods From Apr. 2001 to Mar. 2004, 27 patients with chronic obstructive pulmonary disease were undergone video-assisted unilateral LVRS assisted with mini-incision in our department were retrospectively reviewed. According to whether dispensed with postoperative corticosteroid or not, patients were divided into corticosteroid group and non-corticosteroid group. Corticosteroid group received dexamethasone 10mg iv tid for 3 days and then declined to prednisone 5mg qd for 7 days. Both groups were measured and compared the quantity of thoracic drainage flow, duration of chest tube drainage, the time of air leaks and fever, and so on. At same time, blood gas analysis and blood routine test were performed at 1, 3, 7 and 30 d after operation. Results Corticosteroid and non-corticosteroid groups had no statistically differences in the air leaks time （P 〉 0.05）, but the quantity of thoracic drainage flow of corticosteroid group was lower than that of non-corticosteroid group evidently （700±210ml vs. 950±150ml, P = 0.001）. There was significant difference in average duration of chest tube drainage between both groups （9±3 d vs. 12±2 d, P = 0. 05）. Compared with non-corticosteroidgroup, PaO2 of corticosteroid group was higher at 1, 3d after operation （P〈0.05）. The amount of blood leukocyte of corticosteroid group was lower than that of non-corticosteroid group at 3, 7d after operation, there was no statistically significant in two groups （P 〉 0. 05）. At early period after surgery, both groups had no significant infection and death patient. Conclusion The low dose corticosteroid applied in early period after LVRS for short time（10 days in this research） could shorten the duration of chest tube drainage, decrease the quantity of thoracic drainage flow and the extent of inflammation in pleural cavity. In the mean time, this treatment does not increase the occurrence of significant complications during the early postoperative period, and there is no negative influence to the blood gas analysis.
ObjectiveTo investigate the expression of histone deacetylase 2 (HDAC2) in animal model of benign tracheal stenosis, and explore the mechanism of HDAC2 in development of tracheal stenosis.MethodsEighteen rabbits were randomly divided into a blank control group, a model group, and an erythromycin group, with 6 rats in each group. The model group and the erythromycin group underwent tracheostomy, the inner wall of trachea was brushed back and forth with a nylon brush for more than 20 times to induce benign tracheal stenosis. From 7 days before surgery to 9 days after surgery, the model group received gavage with saline, the erythromycin group received gavage with low-dose erythromycin in dose of 15 mg·kg–1·d–1, and the control group did not receive any treatment. On the 10th day after operation, all the rabbits were sacrificed and the trachea was cut to measure the tracheal stenosis. RNA and protein were extracted from the granulation tissue in the stenosis and the relative mRNA expressions of HDAC2, interleukin (IL)-6 and IL-8 in the granulation tissue were detected by real-time fluorescence quantitative PCR. The relative expression of HDAC2 protein was detected by Western blot.ResultsCompared with the blank control group, the tracheal stenosis in the model group was more obvious [(84.60±1.14)% vs.(27.00±6.44)%], the mRNA and protein expressions of HDAC2 were decreased (0.29±0.07 vs. 1.00±0.00, 0.20±0.02 vs. 0.49±0.04), the mRNA expressions of IL-6 and IL-8 were up-regulated (4.22±0.67 vs. 1.00±0.00, 162.72±23.23 vs.1.00±0.00). Compared with the model group, tracheal stenosis in the erythromycin group was relieved [(64.00±12.25)% vs. (84.60±1.14)%], the mRNA and protein expressions of HDAC2 were increased (0.42±0.14 vs. 0.29±0.07, 0.43±0.01 vs. 0.20±0.02), the mRNA expressions of IL-6 and IL-8 were decreased (0.72±0.24 vs. 4.22±0.67, 130.22±7.93 vs. 162.72±23.23). All the differences were statistically significant (all P<0.05). The Pearson correlation coefficient between tracheal stenosis and HDAC2 mRNA relative expression was –0.96 (P<0.05).ConclusionsThe down-regulation of HDAC2 expression in model of benign tracheal stenosis is related to the occurrence and development of tracheal stenosis. The low dose of erythromycin may be used to treat benign tracheal stenosis by up-regulating expression of HDAC2 and thus inhibiting the inflammatory disorder during tracheal injury repair.
ObjectiveTo summarize the advance of triggering receptor expressed on myeloid cells-1 (TREM-1). MethodsLiteratures about the recent studies on the TREM-1 were reviewed. ResultsTREM1 was a mediator of inflammation. It could amplify the inflammation and lead to overexpression of inflammation in final. ConclusionTREM-1 is very important in development of many diseases and provide a new molecule target to cure.
Objective To investigate the relations between the human beta defensin-2 (HBD-2) and systemic inflammatory responses in patients with lower respiratory tract infection（LRTI）. Methods Eighty-one patients with confirmed LRTI including community-acquired pneumonia，acute exacerbation of chronic obstructive pulmonary disease or concurrent lung infection，and bronchiectasis concurrent infection were enrolled，and twenty healthy volunteers were included as control. Plasma concentrations of HBD-2，IL-1β，and IL-8 were assayed with ELISA method in all patients and controls. Furthermore the patients were divided into three groups according to the onset of disease:,ie.group A （shorter than 7 days），group B （7 to 14 days），and group C （more than 14 days）. The differences between these groups were compared. Correlation between HBD-2 and IL-1β or IL-8 concentrations was analyzed. Results HBD-2，IL-1β，white blood cell （WBC） of the peripheral blood in the patients with LRTI were all significantly higher than those in the healthy controls. HBD-2 and IL-1β increased in group A and group B，and decreased in group C comparing to the control group （Plt;0.05 respectively）. There was no significant difference of IL-8 in group A，B and C. HBD-2 showed a positive linear correlation with IL-1β （r=0.313，P=0.030） and no correlation with IL-8（Pgt;0.05）. Conclusions The plasma HBD-2 concentration is increased in LRTI patients，which may be a biomarker of systemic inflammation in the early or relative early course of LRTI.
Objective To explore the relationship between the structure and function of galectin-3， lipid metabolism disorders， and investigate the expression of galectin-3 in the occurrence and progress of lower limb arteriosclerosis block disease. Methods Related articles were reviewed. Results Galectin-3 participates in inflammatory reaction and lipid metabolism disorders， regulates the cell growth， differentiation， adhesion， apoptosis， and angiogenesis， and palys a role in the occurrence and progress of arteriosclerosis obliterans. Conclusion Galectin-3 is correlation with the occurrence， progress， and the prognosis of arteriosclerosis obliterans.
The hallmark lesions of age-related macular degeneration (AMD) are drusen and basal linear deposit which are lipid substances deposited in Bruch membrane or the compartment on the Bruch membrane. There is a prevailing hypothesis that lipid and its oxidized derivant deposited in retina may have important roles in the pathogenesis of AMD. Lipid oxidation products are toxic, may affect the adjacent cells, induce inflammation, and trigger neovascularization.7-ketocholestoral (7KCh), a naturally occurring oxidized form of cholesterol, had been found to be toxic to retinal cells and able to induce chronic inflammation, which may play a critical role in the development of AMD. However the precise mechanism remains to be elucidated. Thus we will make a brief review of 7KCh and its association with AMD.
ObjectiveTo study on the relationship of serum apelin level with inflammation in patients with atrial fibrillation (AF). MethodsWe recruited 58 patients with valvular heart disease who admitted in our hospital between October 2014 and December 2014 and planned to undergo surgery, including 29 patients with persistent AF (an AF group) and 29 patients with sinus rhythm (a SR group). There were 14 males and 15 females in the AF group at an average age of 57±8 years. There were 20 males and 9 females in the SR group at an average age of 54±10 years. The left atrial diameter (LAD) and ejection fraction (EF) were detected by echocardiography. The levels of serum apelin and interleukin-6 (IL-6) were measured by enzyme linked immuno sorbent assay, and the level of high-sensitivity C-reactive protein (hs-CRP) were determined by turbidimetric inhibition immuno assay. ResultsCompare with the SR group, the serum apelin level (201.94±71.96 pg/ml vs. 286.72±129.33 pg/ml) and EF (54.52%±3.94% vs. 56.41%±2.85%) were significantly lower in the AF group, while the hs-CRP (5.58±12.90 mg/L vs. 1.89±3.55 mg/L), IL-6 (2.59±0.64 pg/ml vs. 2.26±0.55 pg/ml) and LAD (57.10±11.69 mm vs. 43.07±5.31 mm) were significantly higher in the AF group (P<0.05). Correlation analysis showed that the apelin level was negatively correlated with hs-CRP and LAD (r=-0.308, P=0.019; r=-0.313, P=0.017), and were positively correlated with EF (r=0.265, P=0.044). ConclusionSerum apelin level is significantly lower in patients with AF and levels of inflammation makers are significantly higher. Apelin may be closely related to AF and inflammation, and may take part in the occurrence and maintenance of AF through the regulation of inflammatory processes.
Objective To investigate the role of alveolar macrophages ( AMs ) in airway inflammation of smoke-induced COPD rat model and its possible regulating mechanism. Methods Twelve Wistar rats were randomly divided into a COPD group and a control group. The rat model of COPD was established with smoke exposure and LPS intrathacheal instillation. Bronchoalveolar lavage fluid ( BALF)was collected for measurement of total and differential cell counts. Then AMs were isolated and identified byimmunofluorescence. Western blot was employed to analyze the cytoplasmic and nuclear NF-κB p65 expression of AMs. The concentrations of TNF-α,macrophage inflammatory protein 2 ( MIP-2) and IL-10 in cell culture supernatantwere assayed by ELISA.Results The scores of bronchitis and mean liner intercepts in the COPD group were significantly higher than those in the control group [ 4. 33 ±1. 16 vs. 1. 33 ±0. 58,P =0. 016; ( 168. 77 ±11. 35) μm vs. ( 93. 61 ±4. 16) μm, P = 0. 000) ] . The total cell count in BALF of the COPD group was significantly higher than that in the control group ( P lt; 0. 05) , and the AMs and neutrophils were predominant [ ( 72. 00 ±2. 22) % and ( 18. 29 ±8. 34) % ] . The cytoplasmic NF-κB p65 expression of AMs in the COPD group was significantly lower , while the nuclear NF-κB p65 expression was significantly higher ( P lt; 0. 05) compared with the control group. The ELISA results showed that the concentrations of TNF-αand MIP-2 in culture supernatant of AMs in the COPD group were significantly higher than those in the control group ( P lt;0. 05) , while the concentration of IL-10 was not significantly different between the two groups ( P gt;0. 05) . Conclusions COPD rat model was established successfully with smoke exposure and LPS intratracheal instillation with a profile of macrophage-based chronic inflammation and increased secretion of TNF-αand MIP-2. The mechanismis closely related to activation of NF-κB.
Objective To observe the genotype distribution of Haemophilus parainfluenzae from patients with acute exacerbations of chronic obstructive pulmonary disease ( AECOPD) and their effects on A549 cells. Methods 80 hospitalized patients with AECOPD in our hospital were enrolled. Haemophilus parainfluezae were collected by sputum culture and genotyped, then inoculated with cell line A549. IL-6 and IL-8 concentrations in the supernatant were detected and cell morphology was observed at different time points. Results The patients were divided into three groups according to their symptoms. 15 Haemophilus parainfuenzae strains were collected and the positive culture rate between type 1 and type 3 COPD patients were statistically different. The concentrations of IL-6 and IL-8 were both significantly higher than control and increased as time passed. 4 genotypes were got by random amplification of polymorphic DNA ( RAPD) . In RAPD Ⅲ group, the IL-8 concentration was higher at 12h and 24h than others. No morphologic change was found in the cells inoculated with Haemophilus parainfuenzae by microscope after fixing. Conclusions Positive culture rate of Haemophilus parainfuenzae was different in different COPD groups according to symptoms. Haemophilus parainfuenzae can stimulate a cytokine response in A549 cells, maybe one of the pathogens of AECOPD, especially the RAPDⅢ type. Haemophilus parainfuenzae is not an intracellular bacteria.