Objective To investigate the independent risk factors of cerebral white matter lesions (WML) of different degrees in the elderly aged 80 years and over,and provide the evidences for forecasting the prognosis of WML.Methods Brain magnetic resonance images (MRI) findings in 151 people aged 74 to 93 years were collected and analyzed.According to the severity of WML in brain MRI using the Fazekas Scale,the persons were divided into non-WML (control) group,mildWML (grade 1 WML) group and moderate-to-severe WML (grade 2 WML) group.The cognitive score,vascular risk factors,cerebral hemodynamic and arteriosclerotic index,and radiological features were compared among the three groups.Subsequent one-way ANOVA and multivariate logistic analysis were performed to determine the statistically significant factors and the independent risk factors among groups.Results The statistically significant factors with one-way ANOVA analysis among the three groups were cognitive performance (F = 48.595,P = 0.000),hypertension (x2 =7.052,P=0.029),cigarette history (x2 = 19.476,P= 0.000),cholesterol (TC) (F= 3.086,P=0.049),Crouse score (F=3.968,P=0.021) and multiple cerebral atrophy indexes.When compared with control group,cigarette history (OR 2.031,95%CI 1.244-1.317),lacunar infarction (LI)numbers (OR 2.031,95%CI 1.316-4.015) and cholesterol (OR 1.610,95%CI 0.972-2.668) were independent risk factors in grade 1 WML group (all P＜0.05).The independent risk factors between grade 1 and 2 WML group were cognitive performance (OR 0.276,95%CI 0.143-0.532),cigarette history (OR 2.262,95% CI 1.260-4.059),and sylvian fissure ratio (SFR) (OR 1.954,95% CI 1.013-3.768) (all P＜0.05).The independent risk factors between the grade 2 WML group and control group were cognitive performance (OR 0.091,95%CI 0.030-0.273),bicoudate ratio (BCR)(OR 2.511,95%CI 1.147-5.499),Crouse score (OR 2.304,95%CI1.127-4.712)and LI numbers (OR 2.200,95%CI 1.028-4.707) (all P＜0.05).Conclusions Mild WML patients have no significant abnormalities in cognition,brain atrophy and cerebral atherosclerosis.Moderate to severe WML patients manifest remarkable cognitive disorder,cerebral atherosclerosis and brain atrophy.Compared with the controls,cognitive performance,BCR,Crouse score,LI numbers were the independent risk factors for moderate-severe WML patients.

Objective To investigate the methods of preparation and quality control for FU FANG QIN KUN Cream. Methods Baicalin, hydroquinone and vitamin E were serving as main raw material to produce O / W cream by adding suitable emulsifier, HPLC method was used to determine content of baicalin in the cream. Results FU FANG QIN KUN Cream is stable without irritation. The assay method was rapid and accurate. When the dosage of Baicalin was controlled in 0.25μg to 2.5 μg, the sample volume and absorption area percentile showed a good linear relationship. The average recovery was 98.9% and the RSD was 0.73% (n=5). This result was accurate and reproducible. Conclusion The formulation and preparation of FU FANG QIN KUN Cream are reasonable and its quality can be well controlled.

Objective To observe the curative effect of continuous airway positive pressure ventilation (CPAP) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and cough syncope. Methods Forty-three hospitalized patients with OSAHS and cough syncope were collected in the Department of Respiration of Tianjin General Hospital, and analyzed the related information. They were given CPAP treatment, and were divided into good compliance group (n=26) and poor compliance group (n=17) according to CPAP compliance after a half-year treatment. The apnea hypoventilation index (AHI) and c-reactive protein (CRP) were compared before and after treatment between two groups. Results The positive correlation was found between the frequency of the cough syncope and indicators of OSAHS, such as AHI, body mass index (BMI), CRP, sleepiness score (ESS) and circumference of abdomen and neck (r=0.612, 0.431, 0.224, 0.654, 0.435 and 0.344,P<0.05). All these patients were cured after the treatment of both CPAP and medication for 1 or 2 weeks. During a half-year follow-up, the cough syncope didn’t occur in those patients of good compliance group, otherwise cough syncope still happened but with less frequency in patitents of poor compliance group. Before the treatment , there was no significant difference in AHI (45.00±15.69 vs. 48.70±16.47) and CRP (3.46± 1.15 vs. 3.38±0.72) between the two groups. After treatment, AHI (26.97±14.06 vs. 48.18±15.96) and CRP (1.56±0.76 vs. 3.18± 0.78) were significantly lower in the good compliance group than those of the poor compliance group (P<0.01). Conclusion Timely and sustained treatment of OSAHS may help reduce the incidence of cough syncope and significantly improve AHI, CRP and cough symptoms.

Objective To establish the rat overlap syndrome (OS) model of intermittent hypoxia (IH) and emphyse-ma, explore the systematic and endothelial inflammation status, and observe the changes of endothelial progenitor cell (EPC) level in peripheral blood. Methods Sixty male Wistar rats were randomly divided into four groups:normal oxygen control group (A), IH group (B), emphysema group (C) and OS group (D). The rat model of emphysema was established by smoke ex-posure for 16 weeks. From the 13-week, pre-programmed intermittent hypoxia/re-oxygenation (IH/ROX) exposure was giv-en in the meantime of smoke exposure. After exposure, ELISA method was used to detect values of tumor necrosis factor al-pha (TNF-α) and interleukin (IL)-6 in plasma and in the endothelium of right common carotid artery. Real-time-PCR assay was used to analyze RhoA mRNA level in the endothelium of right common carotid artery. The percentage of intima-media thickness (IMT) in the all wall of right carotid artery (C-IMT%) was measured. Flow cytometry was used to detect EPC levels. Results The values of TNF-α, IL-6, RhoA mRNA and C-IMT%were significantly higher in D group than those of A, B and C groups (P<0.05). The EPC levels were significantly lower in D group than those of A, B and C groups (P<0.05). Con-clusion OS rats had more serious vascular endothelial injury than that of emphysema or IH rats. Meanwhile, the repair ca-pacity of EPC for endothelium was worse, which increased the risk of cardiovascular diseases.

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.

Objective To investigate an effective method of treating primary hepatic cancer(PHC) with portal venous tumor thrombosis (PVTT). Methods The clinical data Of 23 patients with PHC and PVTT were retrospectivly analysed. Results Of the 23 patieats after hepatoma resection and PVTT extraction, continuous micro dose infusion chemotherapy or perfusion chemotherapy by DDS was adopted. In 8 patients with main portal vein tumor thrombus, 2 died, 4 recured in 6 months. In 8 patients with the first class branch of portal vein tumor thrombus, 2 recurrd in 6 months and 6 recurred in 12 months. In 4 patients with secondary class branch of portal vein tumor thrombus, l recurred in 12 months (P

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.

To study the effect of different levels intermittent hypoxia on inflammatory cytokines and adipokines in a rat model. 160 male Wistar rats were divided into five groups, three groups with intermittent hypoxia (5% O2:IH-1 group;7. 5% O2: IH-2 group;10% O2: IH-3 group), continuous hypoxia group (10% O2, CH group);and the intermittent normal oxygen control group(IN). Before the exposure and at the second, fourth, sixth, and eighth week after the exposure, eight rats in each group were selected randomly with blood samples collected. Blood glucose was measured by glucose oxidase-peroxidase ( GOD-POD ) reagents, double sandwich enzyme-linked immunosorbent assay ( ELISA) was used to detect serum concentration of insulin, tumor necrosis factor alpha( TNF)-α, interleukin ( IL)-6, leptin, and adiponectin and adipocyte nuclear factor kappa B ( NF-κB) levels. In IH-1, IH-2, and IH-3 group, blood glucose, insulin, TNF-α, IL-6, leptin, and nuclear NF-κB in rats showed consecutive increment after exposure to intermittent hypoxia, and those findings in IH-1 group were higher than those in IH-2 and IH-3 group (P<0. 05), but the level of TNF-α dropped slightly on the 8th week. The level of adiponectin showed consecutive decrease from the outset and its level in IH-1 group was significantly lower than that in IH-2 and IH-3 group(P<0. 05). Cytoplasmic NF-κB levels did not have obvious difference in all these groups(P>0. 05). These results demonstrate that intermittent hypoxia could activate NF-κB and result in extensive changes of proinflammatory cytokines and adipokines in the serum of rats. The release of pro-inflammatory cytokines and adipokines keeps pace with the degree of intermittent hypoxia.

Objective To study the effect of different degrees of intermittent hypoxia (IH) on inflammatory cytokines and adipokines in 3T3-L1 adipocytes. Methods An intermittent hypoxia/reoxygenation (IH/ROX) from obstructive sleep apnea (OSA) adipocyte model was established. 3T3-L1 adipocytes were divided into five groups, three IH groups (5% O2, 7.5%O2 and 10%O2, referred to as IH-1, IH-2 and IH-3), sustained hypoxia group (10%O2, CH) and the normal oxygen control group (21%O2, IN). ELISA method was used to detect values of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), leptin and adiponectin in cell supernatant. Western blot analysis was used to detect levels of hypoxia-inducible fac-tor-1α(HIF-1α) and glucose transporter-1 (Glut-1). RT-PCR assay was used to analyze HIF-1α, Glut-1, TNF-α, IL-6, leptin and adiponectin mRNA expression levels in adipocytes. Results The expression levels of TNF-α, IL-6 and leptin were significantly higher in IH and CH groups than those of IN group (P<0.05). The expression levels of TNF-α, IL-6 and leptin protein and leptin mRNA were significantly higher in IH-1 group than those of IH-2 and IH-3 groups (P<0.05). The adiponectin and its mRNA levels were significantly lower in IH and CH groups than those of IN group (P<0.05). The adipo-nectin level was significantly lower in IH-1 group than that of IH-2 and IH-3 groups (P<0.05). Conclusion These results demonstrate that IH is related to the extensive changes in the expression and release of inflammation-related adipokines in cultured adipocytes. IH from OSA may underlie the development of the inflammatory response in adipocytes, which is in-volved in insulin resistance in patients with OSA.