Objective To explore the relation of high sensitive C-reactive protein (hs-CRP) and blood pressure variability(BPV) in primary hypertension. Methods Sixty-four patients with primary hypertension were divided into target organ damaged (TOD)group and no TOD group. Ambulatory blood pressure monitoring (ABPM) was performed and BPV was assessed by coefficient of variation (CV) . Sixty-four patients were divided into higher CV group and lower CV group. Thirty controls were admitted into control group. The level of hs-CRP was measured. Results The systolic CV and the levels of hs-CRP was significandy different in TOD group [(16.12±2.17)%, (7.11±1.04)mg/L]and no TOD group [(13.30±2.64)%, (4.67±1.24)mg/L) ],compared with that in control group [(10.68±2.19)%, (1.68±1.49)mg/L]. The levels of hs-CRP were significantly different in higher CV group (n=32), and lower CV group(n = 32), compared with that in control group. Conclusion Inflammation may be involved in the occurrence and development of BPV.

Objective:To investigate the growth inhibition of nasopharyngeal carcinoma cell strain and effect on its tumorigenic ability by AS-ODN targeting telomerase RNA.Methods:Telomerase activity was analysed by PCR-ELISA technique.Proliferation of HNE-1 cells was examined by MTT test and clone formation test.Ultrastructure changes were examined by electron microscope.AS-ODN treated HNE-1 cells were implanted subcutaneously into nude mice to observe tumor growths.Results:When HNE-1 cells were incubated with the AS-ODN targeting telomerase RNA,telomerase activities of HNE-1 cells were significantly inhibited;proliferation of HNE-1 cells was significantly inhibited,which showed a dose-dependent and time-dependent correlation and was sequential specific;swelling or necrosis was found in a small proportion of HNE-1 cells by electron microscopy but no apoptosis and large necrosis area could be found.AS-ODN reduced the tumorigenic ability of HNE-1 cell strain.The tumor formation time was prolonged and tumor growth was slowed down.Conclusion:Through inhibiting the telomerase activity of HNE-1 cell strain,the AS-ODN targeting telomerase RNA can inhibit its growth and reduce its tumorigenic ability.

Diagnostic Techniques, Respiratory System ; Female ; Follow-Up Studies ; Homeodomain Proteins ; analysis ; therapeutic use ; Humans ; Hypoventilation ; physiopathology ; Male ; Sleep Apnea Syndromes ; diagnosis ; drug therapy ; therapy

Objective To investigate the protective effects of isoflurane preconditioning plus mild hypothermia on isolated rat hearts against ischemia-reperfusion (I/R) injury. Methods Fifty male SD rats weighing 250-300 g were randomly divided into 5 groups ( n = 10 each): group Ⅰ control (group C); group Ⅱ I/R; group Ⅲ isoflurane preconditioning (group P); group Ⅳ mild hypothermia (group M) and group Ⅴ isoflurane preconditioning + mild hypothermia (group PM). The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. The hearts were immediately removed and perfused with Krebs-Hensleit (K-H) solution aerated with 95% O2 and 5% CO2 at 10 kPa via aorta at 37℃ in a Langendorff apparatus. The hearts were made globally ischemic for 30 min followed by 60 min reperfusion in group Ⅱ-Ⅴ. In group P and PM the hearts were perfused with K-H solution saturated with 1.0% isoflurane for 15 min followed by 15 min washout before ischemia.In group M and PM the hearts were made ischemic at 31 ℃ and perfused at 37℃. LVEDP, LVSP, dp/dtmax,dp/dtmm and HR were measured after equilibration (baseline), immediately before ischemia, and at 30 and 60 min reperfusion. The infarct size and cytochrome C level in cytoplasm and mitochondria of myocytes were measured.Motochondrial ultrastructure was examined using electron microscope. Results Cardiac function was significantly better, the infarct size significantly smaller, the cytochrome C level in cytoplasm significantly lower, while the cytochrome C level in mitochondria of myocytes significantly higher in group Ⅲ-Ⅴ than in group Ⅱ and in group Ⅴ than in group Ⅲ. The cytochrome C level in cytoplasm was significantly lower, while the cytochrome C level in mitochondria of myocytes significantly higher in group Ⅴ than in group Ⅳ. Less damage to mitochondria was observed in group PM than in group I/R, P and M. Conclusion Isoflurane preconditioning combined with mild hypothermia provides better protection against myocardial I/R injury by attenuating the release of cytochrome C from mitochrondria.

Asthma,a chronic inflammatory airway disease,is influenced by both genetic and environmental factors.It is a complex disease that involves the interplay among multiple physiological processes.Currently,it has been identified that 17q21 loci genes especially orosomucoid like 3 (ORMDL3) and gasdermin B (GSMDB) are strongly linked with the susceptibility and severity of childhood asthma by using of the Genome-Wide Association Study (GWAS).Furthermore,a better understanding of the molecular mechanism contributes to the asthma target therapeutics and precision medicine.This review summarizes the 17q21 loci genes associated with the susceptibility,severity,and race specificities of childhood asthma.

Objective:This study aimed to analyze and compare the prognosis and the prognostic factors of combined small cell lung cancer (CSCLC) and pure small cell lung cancer (PSCLC) retrospectively. Methods:The clinicopathological characteristics of the 343 small cell lung cancer patients who were diagnosed in Tianjin Medical University Cancer Institute and Hospital between January 2006 and December 2012 were collected and reviewed. Survival analysis was performed and prognostic factors were assessed. Results:The median OS (overall survival) and PFS (progression free survival) of CSCLC were 31 and 21 months, respectively, and the median OS and PFS of PSCLC were 15 and 9 months, respectively. The Kaplan-Meier survival curves revealed that the prognosis of CSCLC was significantly better compared with that of PSCLC. COX analysis showed that disease stage, pathology, and therapy were indepen-dent prognostic factors of small cell lung cancer. Univariate analysis indicated that the small cell lung cancer group benefited from the surgery, particularly the CSCLC. NLR , therapy, and disease stage influenced the prognosis of PSCLC, and disease stage and therapy in-fluenced the prognosis of CSCLC. Multivariate analysis revealed that disease stage and therapy were independent risk factors of CSCLC in regard to OS. Conclusion:The prognosis of CSCLC was better compared with that of PSCLC. Limited-stage small cell lung cancer should undergo surgery, particularly the CSCLC.

A novel solid-phase extraction (SPE) adsorbent for simultaneous extraction of atrazine (ATZ) and its metabolites, deisopropylatrazine (DIA) and deethylatrazine (DEA) from environmental water samples was prepared. Polyacrylonitrile nanofibers (PAN NFs) mat was prepared via electrospinning, and was further functionalized to obtain polypyrrole modified polyacrylonitrile nanofibers (PPy-PAN NFs) mat, hydrazine modified polyacrylonitrile nanofibers (NH2-PAN NFs) mat and carboxyl modified polyacrylonitrile (COOH-PAN NFs) mat. The results showed that the adsorption capacity of COOH-PAN NFs mat was better than other three NFs mats in both static (2.0 mg/g) and dynamic (0.19 mg/g) experiments. Meanwhile, the runoff ratios of COOH-PAN NFs mat were the lowest (less than 30.0％) in the adsorption of three analytes, especially for high polar analytes, which showed that the hydrogen bond between carboxyl groups and analytes was the main interactive force. A combination of mat-based SPE and high performance liquid chromatography-diode array detection was further established for determination of 3 analytes in environmental water samples. The recoveries were 81.4％-120.3％ and the limits of detection were 0.12 ng/mL for DIA, 0.09 ng/mL for DEA and ATZ, respectively.

Objective To investigate the localization coexpression in situ of matrix metalloproteinase(MMP)-2,-8 and vascular endothelial growth factor(VEGF)in human atherosclerotic unstable plaques with monocytes,smooth muscle cells(SMCs)and endothelial cells(ECs).Methods The histopathologic changes of unstable human atherosclerotic plaques were observed by hematoxylin and eosin(HE)staining,and the localization coexpression of MMP-2,MMP-8 and VEGF in the unstable human atherosclerotic plaques were observed by double fluorescent immunochemistry technology and confocal microscopy.Results The human atherosclerotic plaques in 6 cases had typical histopathologic instability,which was classified as super-Ⅳ type unstable plaques.The MMP-2 coexpression was the most obvious in the smooth muscle cells of fibrous cap infiltrated by monocyts,and in the monocytes of shoulder of plaques,and more expression of MMP-2 in the microvascular endothelial cells at the edge of shoulder and lipid necrosis;MMP-8 coexpressed obviously with the monocytes in the fibrous cap and lipid cores of plaques,and next to coexpressing in the smooth muscle cells of fibrous cap,while coexpression in endothelial cells was very little;VEGF coexpression was significant in the proliferative microvascular endothelial cells of plaques;The fibrous cap,which consisted of the smooth muscle cells mainly,and the edge of lipid necrosis infiltrated by more monocyts,were over-expression areas of VEGF.Conclnsions MMP-2,-8 and VEGF can coexpress with monocytes,SMCs and ECs in unstable plaques,and the major expression areas are in the fibrous cap,shoulder and micro-vessel at the edge of lipid necrosis,which are infiltrated by monocytes.Moreover,the outer membrane of vessel is involved in the pathogenesis of atherosclerosis.

BACKGROUND: Cardiac fibrosis, which results from the loss of balance between synthesis and degradation of cardiac matrix component, is the structural foundation of the stiffness of damaged myocardial tissues. Astragalus membranaceus, a traditional Chinese herb, has multiple functions such as exerting a tonic effect on the heart to induce diuresis. However,the effect of astragaloside Ⅳ on cardiac collagen is poorly known in practice.OBJECTIVE: To observe the effects of astragaloside Ⅳ on myocardial collagen and cardiac function in ischemic rats and to investigate the dosage and time effects of astragaloside Ⅳ.DESIGN: A completely randomized grouping design and randomized controlled trial.SETTING: Department of Pediatrics, the Affiliated Hospital of Medical College of Qingdao University.MATERIALS: The study was conducted in the Encephalopathy Research Institute, Medical College of Qingdao University, from July 2003 to February 2004. Totally 132 Wistar rats of cleaning grade were randomized into three groups: control group (n=11), ischemic group (n=10) and astragaloside Ⅳ group (n=121).METHODS: Rats in control group had thoracotomy, but did not have their left anterior descending coronary artery ligated; rats in ischemic group had thoracotomy and had their left anterior descending coronary artery ligated to establish acute myocardial infarction model; rats in astragaloside Ⅳ group were given astragaloside Ⅳ after surgical ligature of left anterior descending coronary artery. The changes in hemodynamic parameters, cardiac function and myocardial collagen were determined. The dosage and time effects of astragaloside Ⅳ on myocardial collagen and cardiac function were observed.MAIN OUTCOME MEASURES: ① The dosage and time effect of astragaloside Ⅳ on the content of myocardial collagen in the left ventricle of rats with myocardial infarction; ② The dosage and time effects of astragaloside Ⅳ on hemodynamics and cardiac function of rats with myocardial infarction.RESULTS: One hundred rats entered the results analysis. There were 10 in control group and ischemic group, respectively, and 80 in astragaloside Ⅳ group. The five dosage groups of astragaloside Ⅳ [2.5, 5.0, 10.0, 15.0 and 20.0 mg/(kg·d)] and the five postoperative time points (3, 7, 14, 21 and 28 days) had eight rats for each. Astragaloside Ⅳ at a dose of 15.0 mg/kg per day was found to have the most marked effect on ischemic myocardium, so this dose was chosen for observing time effect. ① After administration of astragaloside Ⅳ, the content of collagen in myocardial tissues of the infarcted area of left ventricle, the serum concentration of carboxyterminal procollagen type Ⅰ propeptide and aminoterminal procollagen type Ⅲ propeptide decreased gradually with the increased dose of astragaloside Ⅳ and with the prolonged action time of astragaloside Ⅳ [15 mg/(kg·d)] (P ＜ 0.05-0.01). The serum concentration of carboxyterminal procollagen type 1 propeptide and aminoterminal procollagen type Ⅲ propeptide returned to the level of control at a dose of 10 mg·kg-1per day and at 21 days after astragaloside Ⅳ administration, respectively. The content of collagen in myocardial tissues of the infarcted area of left ventricle was higher than that of non-infarcted area (P＜ 0.01); there were no significant changes in the content of cardiac collagen of right ventricle and non-infarcted area of left ventricle before and after astragaloside Ⅳ administration. ② The cardiac function of ischemic rats significantly improved after astragaloside Ⅳ administration (P ＜ 0.05-0.01); cardiac output, heart rate, stroke volume,mean aortic pressure, systolic aortic pressure, and the stroke work of left ventricle gradually returned to the level of control with the increased dose of astragaloside Ⅳ and with the prolonged action time of astragaloside Ⅳ.CONCLUSION: Astragaloside Ⅳ can inhibit the proliferation of cardiac collagen and improve cardiac function in rats with myocardial infarction.The content of myocardial collagen gradually decreases and cardiac function gradually improves with the increased dose of astragaloside Ⅳ and the prolonged action time of astragaloside Ⅳ.

BACKGROUND: Chronic obstructive pulmonary disease(COPD) is characterized of chronic inflammation in airway, pulmonary parenchyma and pulmonary vessels. The mechanism of the increment and activity changes of these inflammatory cells is unclear at present.OBJECTIVE: To study the apoptotic character of peripheral blood polymorphonuclear neutrophils(PMNs) and its relationship with COPD to provide a reference for early intervention and function surveillance for COPD patients.DESIGN: An observatory comparative study based on COPD patients and healthy population as controls.SETTING: Department of pulmonary medicine in a military medical university of Chinese PLA affiliated hospital.PARTICIPANTS: Totally 98 COPD patients were admitted by the Department of Pulmonary Medicine, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between February 2003 and December 2003 due to COPD acute attack. Eighteen patients including 12 males and 6 females aged between 48 and 70 years old [mean of(56 ± 7) years old]were randomly selected into COPD group according to random number table.Totally 14 healthy adults including 10 males and 4 females aged between 50 and 70 years old [mean of (59 ± 8) years old] who were individuals came for physical check up in our hospital were selected in control group.METHODS: PMNs were separated from peripheral blood by density gradient centrifugation. The dynamic changes of PMNs apoptosis in peripheral blood was observed by flow cytometer and TUNEL method.MAIN OUTCOME MEASURES: Comparison of PMNs apoptotic rate in peripheral blood among groupsRESULTS: As indicated by flow cytometric analysis, PMNs apoptotic rate at early apoptotic phase in COPD patients at paracmasis was(8.5 ± 1.3)%,which was significantly lower than(12.5 ± 1.8)% of normal control group( t=6.25, P ＜ 0. 01); PMNs apoptotic rate was(5.1 ±0.6)% at acute aggravation stage, which was significantly lower than that of paracmasis group ( t =5.66, P ＜001). As indicated by TUNEL analysis, PMNs apoptotic rate at paracmasis was(12.42 ±2.7)% , which was significantly lower than (21.5±4.8)% of normal control group(t=5.76, P ＜ 0.01); PMNs apoptotic rate was(4. 9 ±0.4)% at acute aggravation stage, which was significantly lower than that of paracmasis group( t = 6. 12, P ＜ 0. 01 ) . PMNs changes at the late phase of apoptosis/necrosis had a contrary tendency, i. e.,PMNs rate at late apoptotic phase/necrosis was(2. 8 ± 0.5)% in COPD patients at paracmasis, which was significantly higher than(1. 3 ±0.4)% of normal control group ( t= 6. 37, P ＜ 0. 01 ); PMNs rate was (3.7 ± 0. 3) % at acute aggravation stage, which was significantly higher than that of paracmasis group(t=5.81, P ＜0.01).CONCLUSION: PMNs abnormal apoptosis might be an important reason that induces PMNs aggregation in airway and lung tissues in COPD. This process might have an important significance in the generation and development of chronic airway inflammation, which provides an etiologic basis for the primary rehabilitative intervention of COPD.