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Samples of ambient volatile organic compounds （VOCs） were collected using SUMMA canisters at three Country Control Sites in Shijiazhuang during the spring of 2019, 2021, and 2022, which were detected using gas chromatography/mass spectrometry （GC/MS）. To investigate the characteristics and temporal variations of VOCs mass concentration levels, the online monitoring data of ozone （O3） and PM2.5 at the same site were also collected. Subsequently, the ozone formation potential （OFP） and secondary organic aerosol formation potential （SOAFP） were utilized to assess the chemical activity of VOCs. Additionally, the potential source areas of VOCs in spring in Shijiazhuang were further identified using the potential source contribution factor （PSCF） method and concentration weight trajectory analysis （CWT）. Hence, the major VOCs sources were evaluated with the VOCs initial mixing ratio. The results demonstrated that the averaged concentration of VOCs during the polluted period and clean period of spring in Shijiazhuang were 191.17 µg·m-3 and 122.18 µg·m-3, respectively. Meanwhile, the OFP was 361.23 µg·m-3 during the polluted period and 266.96 µg·m-3 during the clean period, whereas the SOAFP was 1.98 µg·m-3 and 1.61 µg·m-3, respectively. Therefore, effective control of benzene, toluene, ethylbenzene, and xylene （BTEX） is crucial for reducing PM2.5 and O3 pollution. Based on the results obtained from weight PSCF and CWT, the potential source areas of VOCs were further identified to be primarily located in the eastern Yuhua District, the high-tech district, and the northern Luancheng District of Shijiazhuang. These areas were influenced not only by local emissions but also by transport from neighboring regions, in which consistency between the CWT and PSCF results further supported these findings. Furthermore, the results obtained from the benzene/toluene/ethylbenzene （B/T/E） and xylene/benzene （X/B） ratios indicated that the main sources of VOCs in Shijiazhuang in spring were vehicle exhaust sources and burning sources, leading to a more serious air mass aging phenomenon. Hence, controlling vehicle emissions and implementing regional cooperative measures are the effective strategies for optimizing the air quality of Shijiazhuang.

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The "14th Five-Year Plan" period is the key stage for southern Hebei cities (Shijiazhuang, Xingtai, and Handan) to be removed from the bottom ten of the Air Quality Composite Index. The hourly ozone (O3) data of 15 country-controlled monitoring stations in the southern cities of Hebei Province from April to October 2020, hourly data of three volatile organic compound (VOCs) supersites, and the meteorological data of the same period were used for analysis, combined with the spatiotemporal succession, O3 formation potential (OFP), backward trajectory modeling, and spatial statistical modeling. The results showed the following:firstly, the temporal variations in O3 in southern cities of Hebei Province from April to October presented an inverted "U" shape, and the spatial distribution was high in the south and low in the north. O3 pollution was the most serious in June, with Xingtai (233.8 µg·m-3)>Handan (225.2 µg·m-3)>Shijiazhuang (224.8 µg·m-3). O3 was positively correlated with temperature and wind speed and negatively correlated with humidity and VOCs; furthermore, the ρ(TVOC) from April to October followed the order of Xingtai (274 µg·m-3)>Shijiazhuang (266 µg·m-3)>Handan (218 µg·m-3). The total OFP of alkenes and aromatics accounted for more than half; moreover, the trajectory of O3 pollution in southern cities of Hebei Province showed spatial directionality and relevance. The highest mass concentration of O3 (198.92 µg·m-3) was in the trajectory from Shijiazhuang to Xingtai, and the highest frequency of O3 pollution was in the trajectory from Handan to Xingtai. Moreover, the transmission contributions of O3from Xingtai to Shijiazhuang agglomerations were high (27.39%), and Handan played a significant role in the transmission contribution of O3 to Xingtai (32.76%).

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In order to systematically study the transmission characteristics of seasonal and typical pollutants in Shijiazhuang, hourly data of ground-level pollutants(PM2.5, PM10, O3, NO2, SO2, and CO) from 46 state-and provincial-controlled stations, and meteorological(temperature, humidity, and wind speed) data from 17 counties in Shijiazhuang City from December 2018 to November 2019 was analyzed. The interpolation(IDW) and correlation analysis were applied to seasonal and temporal spatial patterns of pollutant concentration. The backward trajectories analysis was performed to explore the seasonal transmission pattern and potential source areas of pollution in Shijiazhuang by combining with the global data assimilation system(GDAS). The results indicate that the different seasons have characteristic pollutants, as follows:spring(PM10, 48.91%), summer(O3, 81.97%), autumn(PM10 and PM2.5, 47.54% and 32.79%), and winter(PM2.5, 74.44%), which are related to the variation of meteorological conditions. Furthermore, the PM10(spring) concentration correlated negatively with the wind speed, presenting a high distribution in the northwest and low in the southeast, with a southerly transmission direction(53.32%). Central and southern Hebei, central and northern Henan, and central Shanxi are the potential sources of pollution(WPCWTij ≥ 160 µg·m-3), impacting western Shandong and northwest Shanxi(WPSCFij ≥ 0.3) with PM10. Moreover, the O3(summer) concentration correlated positively with temperature, and negatively with humidity. The southeast-south(54.24%) is the source direction of the transmission, and the potential source of O3 pollution is an arc area with Shijiazhuang in the center and Cangzhou and Heze as the double wings. Lastly, the PM2.5(autumn and winter) concentration correlated positively with humidity, and the winter concentration shows an increasing gradient from west to east. The trajectories of PM2.5 clustered the source directions:autumn(northeast-southeast, 74.75%), winter(northwest, 55.47%); central and southern Hebei, central and western Shanxi and northern Henan are the concentrated sources of potential pollution(WPCWTij ≥ 180 µg·m-3).

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In order to study the seasonal variations and pollution sources of carbonaceous species in PM2.5 in Chengde, the concentration of these components was determined in atmospheric PM2.5 samples collected in January, April, July, and October 2019. The change in carbonaceous species were analyzed based on the estimation of the ratio of organic carbon(OC) to elemental carbon(EC), total carbonaceous aerosol(TCA), and secondary organic carbon(SOC). The source of these pollutants was determined by means of the backward trajectory and principal component analysis(PCA). The results showed that the mean mass concentrations of PM2.5, OC, and EC during the sampling period were(31.26±21.39) µg·m-3,(13.27±8.68) µg·m-3, and(2.80±1.95) µg·m-3, respectively. The seasonal variations of PM2.5 were:winter[(47.68±30.37) µg·m-3]>autumn[(28.72±17.12) µg·m-3]>spring[(26.59±15.32) µg·m-3]>summer[(23.17±8.38) µg·m-3], consistent with the trend of total carbon(TC), OC, and EC. The source of OC and EC during winter(R2=0.85) was similar. Based on the ratio of OC/EC, all four seasons were affected by traffic and coal-burning source emissions, and the most affected season by bituminous coal emissions was winter. The average concentration of TCA was(21.38±13.68) µg·m-3, which accounted for 68.39% of PM2.5. The order of secondary conversion rate(SOC/OC) was:spring(54.09%) >autumn(37.64%) >summer(32.91%) >winter(25.43%). The results of the backward trajectory simulation show that the pollutant concentrations carried by air masses are relatively low in spring and summer, and the transport channels of pollutants are southwest in autumn and northwest in winter. The results of the PCA showed that the key to reducing PM2.5 in Chengde is to control emissions from vehicle exhausts, and coal and biomass combustion sources.

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Ground-level O3, NO2, and meteorological (temperature, humidity, wind speed, precipitation, and sunshine duration) data from 18 counties in Shijiazhuang City from 2014 to 2017, and volatile organic compounds (VOCs) data for Summer 2017, were analyzed to explore the spatial patterns, evolution, influencing factors, and source apportionment of O3 and NO2 in Shijiazhuang City. Network analysis and inverse distance weighted (IDW) spatial autocorrelation and backward trajectories analyses were performed. The results indicate that O3 concentrations increased between 2014 and 2017, and monthly variations showed a unimodal trend. The typical period of peak O3 pollution (O3 ≥ 160 µg·m-3) was from May to September, characterized by high temperatures, low humidity, weak winds, and strong solar radiation. The O3 concentrations were negatively correlated with the NO2. Furthermore, O3 concentrations increased year-on-year since 2015 in main urban area, and the dominant pollutant type had changed from NO2 (2014 to 2016) to VOCs (2016 and 2017). However, the O3 concentration of county-areas limited by the VOCs. The main factors affecting O3 concentrations were industry, agriculture, economy, and population, and centers of O3 pollution associated with secondary industry appeared in the main urban areas of Shijiazhuang and Luancheng. Moreover, VOCs trajectories during the summer monitoring period were clustered in three source directions:(A) East-northeast, 26.67%; (B) Northwest-west, 43.33%; and (C) Southeast-south, 30%). Trajectories (A) and (C) were the dominant directions of VOC transmission (east-southeast).

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OBJECTIVE: To investigate the role of liver X receptors (LXRs) on endothelin-1 (ET-1) induced murine HL-1 cardiomyocytes hypertrophy. METHODS: Cultured murine HL-1 cardiomyocytes were divided into four experiment groups: (1) CONTROL GROUP:treated with DMSO; (2) T0901317 group:treated with LXRs agonist T0901317 (1 µmol/L); (3) ET-1 group:treated with ET-1 (1 nmol/L); (4) T0901317 + ET-1 group:treated with T0901317 (1 µmol/L) for 8 hours, then treated with ET-1 (1 nmol/L). Twenty-four hours later, immunofluorescent staining was performed on HL-1 cells, the surface area of HL-1 cells was analyzed with NIH Image J software, and the synthetic rate of protein in HL-1 cells was detected by (3)H-leucine incorporation. The mRNA level of atrial natriuretic peptide (ANP) and ß-myosin heavy chain (ß-MyHC) was measured by quantitative realtime PCR. The effect of T0901317 on mRNA expression of ANP was also detected after LXRs gene silencing. RESULTS: The surface area of HL-1 cells, mRNA expression of ANP and ß-MyHC, and (3)H-leucine incorporation in ET-1 group were 2.00 ± 0.29, 1.98 ± 0.47, 2.13 ± 0.39 and 1.79 ± 0.17, respectively, which were significantly higher than those of control group (1.00 ± 0.26, 1.00 ± 0.21, 1.00 ± 0.31 and 1.00 ± 0.03, respectively, all P < 0.05). Compared with ET-1 group, the surface area of HL-1 cells, mRNA expression of ANP and ß-MyHC, and (3)H-leucine incorporation were significantly decreased in T0901317 + ET-1 group (1.24 ± 0.25, 1.19 ± 0.21, 1.48 ± 0.27 and 1.15 ± 0.11, respectively, all P < 0.05). After inhibition of LXRα/ß expression in HL-1 cardiomyocytes using the specific siRNAs, the mRNA expression of ANP in T0901317 + ET-1 group was 1.78 ± 0.05, which was similar as that in ET-1 group (1.94 ± 0.17, P > 0.05). CONCLUSION: T0901317, an agonist of LXRs, could inhibit ET-1 induced cardiac hypertrophy in vitro, and LXR ligand-mediated inhibition on ANP mRNA expression by T0901317 is receptor dependent.

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Curcumin affects the functions of adipocytes. But it is not known whether curcumin has some effect on the cholesterol efflux process of adipocytes. Rabbit subcutaneous adipocytes were incubated with 5, 10 and 20 µg/ml curcumin for 24 h. The cholesterol efflux onto apoAI was assessed, and the peroxisome proliferators-activated receptor (PPAR) γ, liver X receptor (LXR) α and ATP-binding cassette transporter A1 (ABCA1) mRNA expression in adipocytes were quantified by reverse-transcription polymerase chain reaction (RT-PCR). Curcumin increased the cholesterol efflux from adipocytes in dose-dependent manner. The increased expression of PPARγ, LXRα and ABCA1 caused by curcumin were parallel. When the adipocytes were pre-treated by GW9662, the increased expression of PPARγ induced by curcumin was partially prevented, subsequent to the down-regulation of LXRα and ABCA1. Curcumin can affect the cholesterol efflux from adipocytes by regulating the PPARγ-LXR-ABCA1 passway.

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OBJECTIVE: To explore the relationship of apolipoprotein E (ApoE) genotype with hypertriglyceridemia-associated recurrent acute pancreatitis. METHODS: Taking the fasting serum triglyceride (TG) level > or = 2.3 mmol/L as hypertriglyceridemia, ApoE genotypes in 115 patients with hypertriglyceridemia-associated recurrent acute pancreatitis were assessed by polymerase chain reaction. According to the fasting serum TG level, all patients were divided into 3 groups: TG mild elevation group (2.3 mmol/L < or = TG < 5.5 mmol/L, Group A), TG moderate elevation group (5.5 mmol/L < or = TG < 11.3 mmol/L, Group B), and TG severe elevation group (TG > or = 11.3 mmol/L, Group C). RESULTS: Group C had significantly fewer patients with biliary tract disease, improper diet and heavy alcohol consumption, and significantly more patients with passed history of moderate-severe hypertriglyceridemia than Group A and B (P < 0.05). The proportion of patients with E3/4, E3/2, E2/4 and E2/2 genotypes and gene frequency for epsilon 2 and epsilon 4 alleles are significantly higher in Group C than in Group A and B(P < 0.05). Group B had significantly more patients with E3/2 genotype and higher gene frequency for epsilon 2 allele than Group A (P < 0.05). CONCLUSIONS: Apo epsilon 2 and epsilon 4 alleles are closely related to moderate-severe hypertriglyceridemia-associated recurrent acute pancreatitis.

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BACKGROUND: Human hepatic lipase (HL) is a glycoprotein that catalyzes the hydrolysis of triglycerides and phospholipids in all major classes of lipoproteins. We studied whether the hepatic lipase gene -250G(guanine)-->A(adenine) polymorphism affect blood lipids level and the coronary heart disease. METHODS: Two hundred and thirty subjects were included. Among them there were 122 patients with coronary heart disease and 108 subjects without coronary heart disease. Polymerase chain reaction-restricted fragments length polymorphism was used to determine HL genotype. RESULTS: The serum HDL-C level of HL-250A heterozygote (carriers of GA genotype) and homozygote (carriers of AA genotype) [(1.32+/-0.35) mmol/l] was significantly higher than wild type [carriers of GG genotype, (1.19+/-0.30) mmol/l, P<0.005]. This effect to blood lipids appears more evident in women (P<0.005). But the distribution of the 3 genotypes of HL-250 among the patients with coronary heart disease (GG54.1%, GA37.7%, AA8.2%) were similar with those of the control (GG54.6%, GA37.0%, AA8.4%, P>0.05). Both the male and the female had similar ratio for 3 HL genotypes. CONCLUSIONS: HL-250G-->A variation affects blood lipids profile and results in the increasing of the serum HDL-C level. This beneficial effect to blood lipids profile is more obviously seen in the female.

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OBJECTIVE: To observe the effects of different doses of atorvastatin on the plasma hypersensitive C-reactive protein (hsCRP) and interleukin-6 (IL-6) in patients with acute cerebral infarction. METHODS: 131 patients with acute cerebral infarction, 73 males and 58 females, aged 63 +/- 11, were randomly divided into 3 groups: Group A (n = 47), with basal treatment; Group B (n = 42), atorvastatin 10 mg was added every night; and Group C (n = 42), atorvastatin 20 mg was added every night. Before the treatment and 7 and 14 days after the treatment the plasma levels of hsCRP and IL-6, fasting plasma levels of lipid, such as total cholesterol (TC) and low density lipoprotein-C (LDL-C), liver functions, such as aspartate aminotransferase (ALT) and alanine transaminase (ALT), creatine kinase (CK), urea nitrogen, were detected. Neurological function deficit was determined. The survival condition was surveyed 6 months after. RESULTS: (1) The TC and LDL-C decreased after treatment in the 3 groups with significant differences between Group A and Group C, Group B and Group C, and Group B and Group C (all P < 0.05). (2) The plasma level of hsCRP decreased by 9.1%, 33.9%, and 30.1% respectively 7 days after treatment in Groups A, B, and C with significant differences between Groups A and B and between Groups A and C (both P < 0.05), however, without significant difference between Group B and Group C. The level of hsCRP decreased by 34.3%, 56.0%, and 52.9% respectively 14 days after treatment in the 3 groups with significant differences between Groups A and B and between Groups A and C (both P < 0.05), however, without significant difference between Group B and Group C. (3) The level of IL-6 decreased 7 and 14 days after treatment in all 3 groups, however, without significant differences between any 2 groups (all P > 0.05). (4) The decrease of hsCRP and decrease of IL-6 were not correlated with the percentage of TC decrease (both P > 0.05) in Group B. The decrease of hsCRP was not correlated with the changes of blood lipids in Group C. (5) Both the plasma hsCRP and IL-6 before treatment were positively correlated with the infection volume and neurological function score (all P < 0.01). CONCLUSION: Atorvastatin has an anti-inflammatory action benefiting the alleviation of secondary inflammatory damaged in acute cerebral infarction that is independent of lipid lowering.

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OBJECTIVE: To investigate the relationship between apolipoprotein E (ApoE) gene polymorphism and serum lipid profile. METHODS: Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine ApoE genotype on 1452 subjects including 1101 cases with cardio cerebrovascular disease including 379 cases with cerebral infarction, 313 cases with cerebral hemorrhage, 257 cases with coronary heart disease, and 152 cases with other types and on 351 healthy controls. RESULTS: After adjusting for age, sex and BMI, the subjects with ApoE4 carriers had significantly higher levels of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) and ApoB than those with ApoE2 carriers and ApoE3/3 (P < 0.05), and higher level of triglyceride(TG) than those with ApoE3/3 (P < 0.05), while the subjects with ApoE2 carriers had significantly higher levels of high density lipoprotein-cholesterol (HDL-C) than those with ApoE4 (P < 0.05). The effects of ApoE polymorphism exhibited similarity in different sex and age of subjects. Linear regression analysis showed that unlike ApoE3/3, the HDL-C level in ApoE2 carriers tend upward with age (beta = 0.178, P = 0.015), significantly higher than ApoE4 carriers and ApoE3/3 in the cohort of 65-74 years (P < 0.05). The level of TC and TG in ApoE4 carriers had a tendency of downward with age (p = -0.179, P = 0.009; beta = -0.147, P = 0.032). CONCLUSION: ApoE gene polymorphism affected profile of blood lipids and the effects were found in different sex and age. The degrees of effects related to ApoE2 carriers and ApoE4 carriers to blood lipid level seemed to be related to age.

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OBJECTIVE: To investigate the effect of interaction between paranoxonase 1 (PON1)gene polymorphism and ATP-binding cassette transporter 1 (ABCA1) genetic variation on serum lipid level. METHODS: Polymerase chain reaction-restricted fragments length polymorphism was used to determine PON1 A/B192 and ABCA1R219K genotype of 1019 subjects, including 680 patients with strokes and 339 healthy individuals as controls. RESULTS: No significant association between A/B192 genotype and any of the lipid measurements was detected. The levels of HDL-C in the subjects with RR, RK and KK genotypes showed a significant upward tendency respectively (P < 0.05); the levels of their triglyceride (TG) tended downward respectively, but there were no significant differences between them. The relationship between R219K genotype and serum lipid level was modified by A/B192 genotype. The levels of HDL-C in the subjects with AA/RR genotype and BB/KK genotype [(1.41 +/- 0.40) mmol/L, (1.41 +/- 0.39) mmol/L] were significantly different from that in the subjects with BB/RR genotype [(1.28 +/- 0.36) mmol/L] (P < 0.05). CONCLUSION: The result exhibited an interaction of PON1 A/B192 and ABCA1 R219K on serum lipid level.

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OBJECTIVE: To measure the effect of atorvastatin on COX-2 expression in monocytes in patients with acute myocardial infarction (AMI). METHODS: Forty patients with AMI (AMI group) and 18 patients with stable coronary heart disease (control group) were enrolled, and patients with AMI were randomly given routine therapy (n = 20) and routine therapy plus atorvastatin (20 mg/day, n = 20) for a week. Peripheral blood monocytes for each participant including patients with AMI were isolated and cultured for 24 hours. During the culture, monocytes in patients with pretreatment AMI were incubated with celecoxib in different concentration (0, 0.1, 1 and 10 micromol/L). COX-2 mRNA expression in monocytes was measured by reverse transcription polymerase chain reaction (RT-PCR); concentrations of interleukin-6 (IL-6) in supernatant from monocytes and plasma hs-CRP levels were measured by using enzyme-linked immunosorbent assay (ELISA). RESULTS: COX-2 expression in monocytes in patients with AMI (0.92 +/- 0.13) was significantly higher than that in the control subjects (0.19 +/- 0.08), and decreased by 66% after atorvastatin (compared with that on routine therapy, P < 0.05); IL-6 secretions of monocytes in the AMI group (204.8 +/- 45.6 ng/L) increased dramatically compared with those in the control group (40.9 +/- 1.2 ng/L, P < 0.05), and reduced dramatically by 58% when incubated with 10 micromol/L celecoxib (P < 0.05) in a concentration-dependent manner; plasma levels of CRP in the AMI group (43.3 +/- 14.9 mg/L) significantly increased compared with those in the control group (1.7 +/- 0.8 mg/L), and reduced by 62% after atorvastatin (compared with those in the routine therapy group, P < 0.05). COX-2 expression in monocytes in the AMI group was positively correlated with both secretions of IL-6 and plasma level of CRP (r = 0.636 and 0.662, respectively, both P < 0.05). CONCLUSIONS: There is an inflammatory activation in peripheral blood monocytes in patients with early AMI, and the monocytes-derived COX-2 may play an important role in promoting early inflammatory process. Atorvastatin may decrease COX-2 expression in peripheral blood monocytes in patients with AMI and cyclooxygenase-dependent pathway might be correlated with the anti-inflammation mechanism of statin.

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OBJECTIVE: To investigate whether ATP-binding cassette transporter 1 (ABCA1) R219K genetic variation is correlated with blood lipids. METHOD: Specimens of peripheral blood were collected from 692 patients with cerebral apoplexy, aged 62 +/- aged 12, and 352 sex- and age-matched persons without cardio-cerebro-vascular disease. Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine the ABCA1 genotype: RR type (177 bp), RK type (177 bp, 107 bp, and 70 bp); and KK type (107 bp and 70 bp). The RR and KK type products were sequenced. RESULTS: The level of HDL-C showed an upward trend in the sequence of RR, RK, and KK genotypes with a significant difference between RR genotype (1.3 mmol/L +/- 0.4 mmol/L) and KK genotype (1.4 mmol/L +/- 0.4 mmol/L), especially in the males. The levels of TG tended downward in the sequence of RR, RK, and KK genotypes, however, without a significant difference between any 2 genotypes. Linear regression analysis showed that the HDL-C level was positively correlated with age in the noncarriers of ABCA1R219K genetic variation (RR genotype), and the TC level was negatively correlated with age in the carriers (RK + KK genotype). In the cohort aged

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BACKGROUND: Apolipoprotein epsilon4 has been proposed as a genetic predictor for CHD. Peroxisome proliferator-activated receptors (PPAR), a recent identified nuclear transcription factor, is involved in regulation of many target genes and plays an important role in lipid metabolism, insulin sensitivity, obesity and atherosclerosis. PPARgamma gene polymorphisms may affect the profile of CHD-related risk factors. HYPOTHESIS: Interaction between PPARgamma gene polymorphism and apoE polymorphisms affect the presence of CHD. METHOD: This is a case-control study, which enrolled 150 cases with CHD and 157 controls without CHD. Polymerase chain reaction-restricted fragments length polymorphism was used to determine the apoE genotype and PPARgamma C161-->T substitution. RESULTS: ApoE epsilon4 allele was significantly more prevalent in CHD patients than in controls (13.05 vs. 7.35%, P<0.05). The apoE epsilon4 carries had significant higher LDL-C levels than other apoE carriers and this tendency could be modified by PPARgamma CT genotype. ApoE genotype epsilon4 was an independent risk factor for CHD (OR=4.29, 95%CI: 1.6-11.48, P=0.004). A significant interaction between apoE epsilon4 and PPARgamma CT genotype was detected with respect to the effect on CHD (P=0.045). CONCLUSION: This is the first study to explore the effect of interaction between PPARgamma C161-->T variant and apoE epsilon4 genotype. The result exhibited an interaction effect of two genes on serum cholesterol level. The association of CHD to apoE genotype was subjected to the attenuation effect of PPARgamma CT genotype.

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BACKGROUND: The monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 may play critical roles in plaque instability. Anti-inflammation may be one benefit of statin drugs in acute coronary syndrome (ACS). We investigated the effects of atorvastatin therapy on plasma MCP-1 concentrations and production of MCP-1 released by peripheral blood monocytes from ACS patients. METHODS: Forty patients with ACS were randomly separated into two groups, those receiving conventional therapy (Group A, n=20), and conventional therapy+atorvastatin (10 mg/day, Group B, n=20). The study the effects of atorvastatin on secretion and expression of MCP-1, human peripheral blood monocytes from healthy donors were incubated with atorvastatin (0.1-10 micromol/l) for up to 24 h in vitro. MCP-1 concentrations in plasma and monocytes culture supernatants were measured by enzyme-linked immunosorbent assays (ELISA). MCP-1 expression was measured by RT-PCR. RESULTS: Plasma concentrations of MCP-1 were significantly lower after 4 weeks therapy in both groups of patients [Group A from 97.4 (50.1-164) to 72.6 (36.3-156) pg/ml, Group B from 101 (60-178) to 45 (29-91) pg/ml, (P<0.05, respectively)]. Compared with conventional therapy alone, atorvastatin significantly further reduced plasma MCP-1 concentrations. There was no significant correlation between the degree of changes in plasma MCP-1 and LDL-C. In vitro, atorvastatin inhibits production of MCP-1 up to 73%, in a concentration-dependent manner, and suppressed MCP-1 expression in peripheral blood monocytes. CONCLUSIONS: Atorvastatin reduced plasma MCP-1 concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.

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BACKGROUND: Inflammatory process plays an important role in the pathogenesis of coronary heart disease (CHD). With the growing use of gemfibrozil and other fibrates, their anti-inflammatory effects have been noted. But little is known about the effect of gemfibrozil on tumor necrosis factor (TNF)-alpha secretion in peripheral blood mononuclear cells (PBMC) from patients with coronary heart disease. METHODS: PBMC were obtained from CHD patients (n=16) and healthy controls (n=13). PBMC (2x10(6) cells/ml) were cultured in 24-well plates with or without Ang II (10(-8), 10(-7), 10(-6) mol/l), or Ang II (10(-6) mol/l) plus gemfibrozil (10(-6), 10(-5), 10(-4) mol/l). After 24-h incubation, the supernatants were separated, and TNF-alpha was measured by an enzyme-linked immunosorbent assay (ELISA). RESULTS: Spontaneous release of TNF-alpha was 299.2+/-110.7 pg/ml in PBMC from CHD patients and 179.3+/-78.2 pg/ml in PBMC from control subjects (P<0.05). Incubated with Ang II (10(-8), 10(-7), 10(-6) mol/l), TNF-alpha secretion was 307.7+/-141.8, 318.9+/-135.6, 328.6+/-123.9 pg/ml in PBMC from CHD patients, and 225.3+/-135.4, 224.1+/-141.0,218.7+/-134.8 pg/ml in PBMC from control subjects, respectively. Ang II did not significantly trigger TNF-alpha secretion in both groups. Compared with that incubated with Ang II (10(-6) mol/l) alone, release of TNF-alpha intervened by gemfibrozil (10(-6),10(-5),10(-4) mol/l) decreased to 279.4+/-132.2, 268.0+/-132.7, 226.6+/-102.7 pg/ml in PBMC from CHD patients, and 177.6+/-94.4, 156.1+/-69.4, 105.3+/-52.7 pg/ml in the control group, respectively. Gemfibrozil (10(-5),10(-4) mol/l) significantly inhibited TNF-alpha secretion in both groups (P<0.05). CONCLUSIONS: Our data demonstrated that gemfibrozil reduced release of TNF-alpha in PBMC both from CHD patients and controls. This effect may partially be relevant to the clinical benefits of gemfibrozil in the treatment of dyslipidemia and atherosclerosis.

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OBJECTIVE: Coronary heart disease (CHD) is one of the most common causes of death in the world. Some studies suggested that CHD begins in childhood. Obesity and dyslipidemia are important risk factors of coronary heart disease. Apolipoprotein (apo)E gene associated with dyslipidemia and coronary heart disease. The present study was designed to investigate the expression status of apoE gene in peripheral blood monocyte and association of apoE gene expression with lipids in children with obesity. METHODS: Among 32 children with obesity and 32 healthy children without obesity or overweight, ApoE gene expressions were determined by competitive reverse transcription-polymerase chain reaction in peripheral blood monocyte. The concentrations of plasma triglyceride, total cholesterol, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol, lipoprotein(a), apoA I, apoB(100) and apoE were measured. RESULTS: Expression of apoE gene was detected in peripheral blood monocyte. Expression of apoE gene was significantly reduced in children with obesity as compared with control group (0.29 +/- 0.14 moles/mole GAPDH mRNA vs. 0.36 +/- 0.10 moles/mole GAPDH mRNA, t = 2.15, P < 0.05). The more severe was the degree of obesity, the more significantly reduced the expression of apoE gene; the degree of obesity was negatively correlated with the levels of expression of apoE gene (correlation coefficient = -0.40, P < 0.05). Compared with control group, the levels of triglyceride, total cholesterol, low density lipoprotein-cholesterol, and apoB(100) were higher, and those of high density lipoprotein-cholesterol, apoA I and apoE were lower in children with obesity [(1.68 +/- 0.50) mmol/L vs. (0.99 +/- 0.54) mmol/L, (4.47 +/- 0.91) mmol/L vs. (3.33 +/- 0.90) mmol/L, (2.23 +/- 0.71) mmol/L vs. (1.13 +/- 0.96) mmol/L, (94.48 +/- 9.97) mg/dl vs. (83.81 +/- 15.64) mg/dl, (1.47 +/- 0.39) mmol/L vs. (1.73 +/- 0.36) mmol/L, (112.71 +/- 27.86) mg/dl vs. (134.80 +/- 45.36) mg/dl, (24.50 +/- 10.92) mg/L vs.(35.07 +/- 9.79) mg/L, respectively, P < 0.05]. ApoE gene expression was associated with plasma lipids metabolism in children with obesity. The quantity of apoE gene expression was inversely associated with low density lipoprotein-cholesterol, positively correlated with apoE (correlation coefficient = -0.33, 0.35, respectively, P < 0.05). The quantity of apoE gene expression was not associated with total cholesterol, triglyceride, high density lipoprotein-cholesterol, lipoprotein(a), apoA I, and apoB(100) (correlation coefficient = -0.19, -0.11, 0.16, 0.09, 0.18, 0.22, P > 0.05). CONCLUSION: Expression of apoE gene was significantly reduced in peripheral blood monocyte in children with obesity. The quantity of apoE gene expression was associated with degree of obesity and abnormality of blood lipids.

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