This study focused on prevention and treatment of acute and chronic asthma by oligonucleotides containing unmethylated CpG motifs (CpG-ODNs). Acute and chronic asthma models of mice were made by sensitizing and inhaling ovalbumin (OVA); The number of white blood cells (WBC) and eosnophils (EOS) in bronchoalveolar lavage fluid (BALF) was counted and the concentration of cytokines and vascular endothelial growth factor (VEGF) was examined in BALF by ELISA kit. After that, TLR-9 mRNA was detected in mice spleen cells by reverse transcription polymerase chain reaction (RT-PCR) and TLR-9 protein was determined in mice lung tissues by Western blotting. Compared with acute asthma models of mice, WBC in BALF decreased obviously in the groups of Bordetella pertussis, CpG-ODNs and seq A to seq I which were administrated by both of intragastric (ig) and intraperitoneal (ip) injection group, EOS decreased obviously in Bordetella pertussis, CpG+ and seq A to seq D ig groups, and in all ip administrating groups, although it was not effective in the groups of seq E to seq I. In chronic asthma models of mice, IFN-gamma increased ((1) control: 176.45 +/- 23.46 pg x mL(-1); (2) model: 174.11 +/- 22.71 pg x mL(-1); (3) CpG+ ip: 220.56 +/- 15.42 pg x mL(-1); (4) seq A ip: 225.23 +/- 21.60 pg x mL(-1)) and IL-4 decreased obviously (1) control: 66.91 +/- 5.81 pg x mL(-1); (2) model: 81.02 +/- 11.24 pg x mL(-1); (3) CpG+ ip: 63.99 +/- 6.09 pg x mL(-1); (4) seq A ip: 62.75 +/- 10.03 pg x mL(-1)) in the BALF of CpG+ and seq A ip group, although VEGF was not changed in this research. And also, TLR-9 mRNA in spleen cells (TLR-9/GAPDH: (1) control: 0.62 +/- 0.13; (2) model: 0.66 +/- 0.17; (3) CpG+ ip: 1.46 +/- 0.26; (4) seq A ip: 1.42 +/- 0.34) and TLR-9 protein in lung tissues (TLR-9/beta-actin: (1) control: 0.63 +/- 0.16; (2) model: 0.61 +/- 0.07; (3) CpG+ ip: 1.15 +/- 0.25; (4) seq A ip: 1.03 +/- 0.29) both increased in ip groups, but the change was not significant in ig group. The study confirms that CpG-ODNs and seq A could inhibit airway inflammation remarkably, this mechanism might be related with regulating Th1/Th2 balance and controlling the expression of TLR-9.

This paper introduces the concensus on the relationship between sleep apnea and cardiovascular disease reached by experts with corresponding backgrounds from Chinese Medical Association.The relationship is that of sleep apnea with hypertension,coronary artery disease,arrhythmias,and congestive heart failure,and the relationship can improve the diagnosis and treatment of these two types of diseases.

Objective To investigate the concentration changes of vascular endothelial growth factor(VEGF), nitric oxide(NO) and endothelin (ET) in elderly patients with obstructive sleep apnea syndrome (OSAS) combined with eerebrovascular disease.Methods One hundred and thirty-two subjects were divided into four groups: OSAS with cerebrovaseular disease group (OC group), OSAS without cerebrovascular disease group (O group), cerebrovascular disease without OSAS group (C group) and normal control group (N group).The concentrations of VEGF, NO and ET in the plasma were compared in each subgroup.Results The concentration of VEGF was significantly increased in OC group and O group compared with C group and N group[(195.34±56.7)ng/L, (162.34±48.7)ng/L, (156.4 4±51.8) ng/L, (114.1 ± 54.2) ng/L, F= 21.02, P< 0.05].The concentration of NO was increased gradually in OC group, C group, O group and N group[(62.3±4.9)mmol/L,(64.7±5.1) mmol/L, (66.2± 4.2)retool/L, (77.5 ± 6.8) mmol/L, F= 17.35, P<0.05], and the concentration of ET was decreased gradually in OC group, C group, O group and N group[(59.8±9.6)ng/L, (56.5±4.3)ng/L, (54.7±7.9)ng/L, (37.2±8.5)ng/L, F= 4.27, P<0.05].Conclusions The concentrations of VEGF and ET are increased and the concentration of NO is decreased in patients with OSAS.Patients with OSAS combined with cerebrovascular disease have higher VEGF and ET concentrations and lower NO concentration than in patients with simple OSAS.The results indicate that vascular endothelial dysfunction may play an important role in the development of cerebrovascular disease in patients with OSAS.

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Objective To evaluate CT features of hepatic abscess caused by different etiologies.Methods CT appearances and clinical data of hepatic abscesses were retrospectively studied in 54 cases.Results There appeared low density lesions in hepatic abscess.Target sign,cluster sign and air in the cavity were special CT manifestations of hepatic abscess.Abscess caused by different etiologies had different features,which included infection by blood stream or bile duct abnormalities,amebic liver abscess,and hepatocellular carcinoma complicated with suppurative infection after treated with TAE.Conclusion The CT manifestations of hepatic abscess were characteristic.These manifestations were helpful in diagnosing hepatic abscess not only in location but also in nature and etiology.

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Objective To investigate the expression of endothelin-1 (ET-1 ), nitrogen monoxidium (NO), vascular endothelial growth factor (VEGF) and brain tissue VEGF induced by chronic intermittent hypoxia (CIH) in aged rats. Methods The CIH model of aged rat was established by using intermittent hypoxia. The levels of ET-1, NO and VEGF in the plasma were detected at 3, 6 and 9 weeks after experiment in each group. The expression of VEGF in brain tissues and the pathological changes of the vessels of the cerebra and the ratio between the thickness of vessel wall and external diameter (WT%) were observed. Results In CIH group, the ET-1 and VEGF levels increased, however NO level decreased. The levels of ET-1 and VEGF were higher at 3 weeks in CIH group than in UC group (t=2.47 and 2.38, both P<0.05), however NO level was lower in CIH group than in UC group (t=2.39, P<0.05). VEGF levels increased significantly at 9 weeks in CIH as compared with UC group [(171.1±13.5) pg/ml vs. (109.8±8.6) pg/ml, t = 3.46, P< 0.01]. The levels of VEGF in CIH group increased remarkably at 9 weeks as compared with 3 weeks [(129.3±12.3) pg/ml, t=2.38, P<0.053. VEGF levels in CIH group showed positive correlation with the time of intermittent hypoxia. The changes of cerebral vessels in UC group were not found, while the aged rats in CIH group showed cerebral neuron cells swelling and blood vessel hyperplasia. The WT% of cerebral small artery was more apparent in CIH group than in UC group at 3 weeks (t=2.34,P<0.05). The expression of VEGF in cerebra was higher in CIH group than in UC group in the three stages (r=2.37, P<0.05). There was an aggravated tendency in the change of the expression of brain tissue VEGF and WT% over time. The change was more apparent at 9 weeks than at 3 weeks (t=2.32 and 2.35, both P<0.05). Conclusions CIH can induce an increase in the expression of ET-1 and VEGF, a decrease in the expression of NO in aged rats. The over expression of VEGF and the disbalance of ET-1 and NO levels can cause brain cellular swelling, arteriola vessel wall thickening,lumens stenosis.

Objective To explore the mechanism of severe intermittent hypoxia on oognitive function by evaluatig the effect of chronic intermittent hypoxia on cognitive function,neurons structure,damage,p38MAPK protein expression and neuronal apoptosis in rats hippocampal CA1.Methods Ninety-six mature and male Wistar rats were randomly divided into two groups:control group (UC) and 5％ chronic intermittent hypoxia group (5％CIH).Rats in IH groups were suffered 8 hours intermittent hypoxia everyday,and the duration of experiment was respectively 2,4,6 and 8 weeks.After exposed for 2,4,6,and 8 weeks,the cognitive function of rats was assessed with the Morris water maze (MWM) ; the changes in the morphology of nerve cells in hippocampus CA1 region were observed; the expression of phosphorylated p38MAPK protein in hippocampus was detected by the methods of immunohistochemistry and western blot; the apoptosis of nerve cells was detected by the method of TUNEL.Results Compared with control group,with prolonged hypoxia,the time of escape latency obviously prolonged and the time of across the target quadrant shortened significantly in rats of 5％ CIH group.The time of escape latency at the 8th week was the longest ((71.71 ± 5.49)s,P＜ 0.05) in 5％ CIH group,and the time of across the target quadrant at the 8th week was the shortest ((26.82 ± 4.30) s,P ＜ 0.05) in 5％ CIH group.There appeared neuronal degeneration and necrosis in hippocampus CA1 in 5％ CIH group.Compared with the control group,the density of the nerve cells survival in the region of hippocampal CA1 reduced dramatically at the 2nd,4th,6th and 8th week and was the lowest at the 8th week(14.16 ± 2.07,P ＜ 0.05).By Immunohistochemical method,the expression of phosphorylated p38 MAPK of 5％ CIH group in hippocampal CA1 was more than UC group at the 2nd,4th,6th and 8th week.By western blot,the expression of phosphorylated p38MAPK of 5％ CIH group was more than UC group at the 2nd,4th,6th and 8th week and was the most at the 6th week (2.45 ± 0.14,P＜ 0.05) ;the index of neuronal apoptosis in hippocampal CA1 was increased significantly at the 2nd,4th,6th and 8th week than UC group and reached to the peak at the 6th week (0.608 ± 0.069,P ＜ 0.05) in the 5 ％ CIH group.Conclusion Chronic intermittent hypoxia could cause the activation of p38MAPK/pathway of neuronal apoptosis and was important mechanism of cognitive dysfunction at the early and middle stage.