电针对APP/PS1转基因小鼠海马低密度脂蛋白受体相关蛋白-1及其mRNA表达的影响

目的:研究电针是否是通过影响LRP1mRNA水平、提高LRP1的表达,从而促进脑内Aβ清除。方法:将4月龄APP/PS1转基因鼠,随机分为模型组、电针治疗组,以同窝同背景转基因阴性小鼠为正常对照组。电针干预"涌泉"、"百会"0.1 m A,15 min/次,隔日1次,治疗6周。治疗后,以免疫组化法观察脑组织LRP1阳性表达,以Western blotting法检测海马LRP1表达,以Real-time PCR法检测海马LRP1mRNA表达。结果:LRP1表达于脑微血管内皮细胞、胶质细胞、神经元等处。模型组海马LRP1蛋白、LRP1mRNA相对表达量低于正常对照组(P<0.05),电针治疗组海马LRP1及LRP1mRNA比模型组有上升趋势,但差异无统计学意义(P>0.05)。结论:电针干预可能影响5月龄APP/PS1转基因小鼠海马内所有细胞LRP1及LRP1mRNA表达,可能是电针干预AD发病的潜在靶点,但实验方案还需进一步完善。

低密度脂蛋白受体基因全长cDNA序列分析法检测1例家族性高胆固醇血症患儿基因突变

目的建立低密度脂蛋白受体(LDLR)基因全长cDNA序列分析方法并对1例家族性高胆固醇血症(FH)患儿进行基因检测。方法设计7对LDLR基因cDNA引物并验证;对1例临床诊断为FH的患儿进行家系调查和临床体检,提取外周血DNA和RNA,DNA扩增结合测序分析LDLR基因并找出其突变位点;RNA经PCR反转录为cDNA后扩增LDLR基因,将扩增产物进行正、反双向核苷酸序列分析,并与GenBank中LDLR基因的正常序列对比找出突变位点后与传统DNA测序方法结果比对。结果 LDLR基因全长cDNA序列分析方法检测LDLR基因为2 583个碱基,与标准序列完全一致;本例患儿确诊为"FH纯合子",cDNA测序结果与传统DNA测序结果相符,均为第2外显子终止突变和第6外显子点突变及框移突变。结论 LDLR基因全长cDNA序列分析法检测FH患儿突变,与传统DNA方法检测结果相符,可为FH的基因诊断提供新的方法依据。

脂肪代谢障碍

9731764 家族性血胆固醇过多800例的临床所见[日]/筱宫正树∥动脉硬化.-1995,23(3).-169 冀医情 9731765 摄取大豆蛋白食品可减轻脂肪负荷后残余脂蛋白血症[日]/繁英树∥动脉硬化.-1995,23(3).-176

宽胸丹胶囊对动脉粥样硬化兔血清TC、TG、HDL、LDL影响的研究

目的 :探讨宽胸丹胶囊 (药物 :瓜蒌、陈皮、枳实、川芎、水蛭、苍术等 )对动脉粥样硬化兔血清总胆固醇 (TC)、甘油三脂(TG)、高密度脂蛋白 (HDL)、低密度脂蛋白 (LDL)的影响。方法 :取健康新西兰纯种大耳白兔 4 0只 ,随机分为 5组 ,即空白组、模型组、宽胸丹大剂量组、宽胸丹小剂量组、多烯康组 ,每日喂养相应的正常、造模或含药饲料 ,4 0d后 ,测定血清TC、TG、HDL、LDL的含量。结果 :模型组与正常组有显著差异 (P <0 .0 5 ) ,宽胸丹大、小剂量组均能明显降低TC、TG、LDL ,较模型组有显著差异 (P <0 .0 5 ) ,大剂量组能明显升高HDL(P <0 .0 5 ) ,且在改善TC、TG、LDL方面 ,优于多烯康组 (P <0 .0 5 )。提示宽胸丹胶囊具有减轻动脉粥样硬化程度、防治冠心病的作用 ,此作用可能与其升高HDL、降低TC、TG、LDL有关。

The Effects of Apolipoprotein E Polymorphism on Serum Lipids, Lipoproteins and Apolipoproteins Variation

Objective: To study the effects of Apolipoprotein E (ApoE) polymorphism onserum levels of lipids, lipoproteins and apolipoproteins. Methods: Fragments of ApoE gene forthex-on containing codon 112 and 158 polymorphic locus were amplified by PCR, and then digested untilCfo I endonuclease. Genotypes and alleles frequencies of 168 healthy persons in Jiangsu area werecalculated. The effects of ApoE genotypes and alleles on serum lipids, lipoproteins andapolipoproteins variation were analyzed. Results: The effects of ApoE alleles on total cholesterol(TC), law density lipoprotein-cholesterol (LDL-C), ApoB was: along a decreasing gradientε_4>ε_3>ε_2. The effect of ε_4 allele was to increase serum levels of TC, LDL-C and ApoB, andthe ε_2 allele had an effect opposite to that of ε_4 allele. Conclusion: ApoE polymorphism is anindependent genetic factor on individual serum levels of lipids and apolipoproteins.

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Berberine is identified to lower the serum cholesterol level in human and hamster through the induction of low density lipoproteins （LDL） receptor in hepatic cells. To evaluate its potential in preventing atherosclerosis, the effect of berberine on atherosclerosis development in apolipoprotcin E-deficient （apoE^-/-） mice was investigated. In apoE^-/- mice, berberine induced in rivo foam cell formation and promoted atheroselerosis development. The foam cell formation induced by berberinc was also observed in mouse RAW264.7 cells, as well as in mouse and human primary macrophages. By inducing scavenger receptor A （SR-A） expression in macrophages, berberine increased the uptake of modified LDL （DiO-Ac-LDL）. Bcrberine-induced SR-A expression was also observed in macrophage foam cells in vivo and in the cells at atherosclerotic lesion. Analysis in RAW264.7 cells indicated that berberine induced SR-A expression by suppressing PTEN expression, which led to sustained Akt activation. Our results suggest that to evaluate the potential of a cholesterol-reducing compound in alleviating atherosclerosis, its effect on the ceils involved in atherosclerosis development, such as macrophages, should also be considered. Promotion of foam cell formation could counter-balance the beneficial effect of lowering serum cholesterol.

Hyperhomocysteinemia independently causes and promotes atherosclerosis in LDL receptor-deficient mice

Background Hyperhomocysteine is an independent risk factor of coronary heart disease （CHD）. However, whether hyperhomocys teine affects the progression of atherosclerosis is unclear. In the present study, we examined the effect of hyperhomocysteine on the forma tion of atherosclerosis in low-density lipoprotein receptor-deficient （LDLr ） mice. Methods Forty-eight 7-week-old LDLr/ mice were assigned to the following groups： mice fed a standard rodent diet （control group）, mice fed a high-methionine diet （high-methionine group）, mice fed a high-fat diet （high-fat group）, and mice fed a diet high in both methionine and fat （high-methionine and high-fat group）. At the age of 19, 23, and 27 weeks, four mice at each interval in every group were sacrificed. Results At the end of the study, mice did not show atherosclerotic lesions in the aortic sinus and aortic surface until 27 weeks old in the control group. However, atherosclerotic lesions developed in the other three groups at 19 weeks. The amount of atherosclerotic lesions on the aortic surface was lower in the high-methionine group than in the high-fat group （P 〈 0.001）. Atherosclerotic lesions on the aortic surface in the high-methionine and high-fat group were the most severe. The mean area of atherosclerotic lesions in the aortic sinus compared with atherosclerotic lesions on the aortic surface was lower in the high-methionine group than in the high-fat group （P 〈 0.001）. Atherosclerotic lesions in the aortic sinus in the high-methionine and high-fat group were the most severe. Conclusions Homocysteinemia accelerates atherosclerotic lesions and induces early atherosclerosis independently in LDLrmice. Reducing the level of homocysteinemia may be beneficial for prevention and treatment of CHD.

Metabolic syndrome and gallstone disease

AIM： To investigate the association between metabolic syndrome （NetS） and the development of gallstone disease （GSD）. METHODS： A cross-sectional study was conducted in 7570 subjects （4978 men aged 45.0：1：8.8 years, and 2592 women aged 45.3：1：9.5 years） enrolled from the physical check-up center of the hospital. The subjects included 918 patients with gallstones （653 men and 265 women） and 6652 healthy controls （4325 men and 2327 women） without gallstones. Body mass index （BII）, waist circumference, blood pressure, fasting plasma glucose （FPG） and serum lipids and lipoproteins levels were measured. Colorimetric method was used to measure cholesterol, high-density lipoprotein cho- lesterol （HDL-C） and low-density lipoprotein cholesterol （LDL-C）. Dextrose oxidizing enzyme method was used to measure FPG. Subjects were asked to complete a questionnaire that enquired about the information on demographic data, age, gender, histories of diabetes mellitus, hypertension, and chronic liver disease and so on. Metabolic syndrome was diagnosed according to the Adult Treatment Panel HI （ATP ]3） criteria. Gall- stones were defined by the presence of strong intralu- minal echoes that were gravity-dependent or attenu- ated ultrasound transmission. RESULTS： Among the 7570 subjects, the prevalence of the gallstone disease was 12.1% （13.1% in men and 10.2% in women）. BMI, waist circumference, systolic blood pressure, diastolic blood pressure, fasting blood glucose and serum triglyceride （TG） in cases group were higher than in controls, while serum high-density lipid was lower than in controls. There were significant differences in the waist circumference, blood pressure, FPG and TG between cases and controls. In an age- adjusted logistic regression model, metabolic syndrome was associated with gallstone disease. The age-adjust- ed odds ratio of MetS for GSD in men was 1.29 [95% confidence interval （CI）, 1.09-1.52; P = 0.0030], and 1.68 （95% CI, 1.26-2.25; P = 0.0004） in women; the overall age-adjusted odds ratio of NetS for GSD was 1.42 （95% CI, 1.23-1.64; P 〈 0.0001）. The men with more metabolic disorders had a higher prevalence of gallstone disease, the trend had statistical significance （P 〈 0.0001）. The presence of 5 components of the MetS increased the risk of gallstone disease by 3.4 times （P 〈 0.0001）. The prevalence of GSD in women who had 5 components of NetS was 5 times higher than in those without Nets component. The more the components of Mets, the higher the prevalence of GSD （P 〈 0.0001）. The presence of 5 components of the Mets increased the risk of gallstone disease by 4.0 times. CONCLUSION： GSD appears to be strongly associated with MetS, and the more the components of NetS, the higher the prevalence of GSD.

Inhibitory Effect of Isorhapontigenin on Copper-Mediated Peroxidation of Human Low-Density Lipoprotein in vitro

Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from sera df normal lipidemic donors was separated bysequential ultracentrifugation. The separated human IDL 1 mg·mL^(-1) in phosphate buffer saline, pH7.4, was incubated with cupric sulfate (10 μmol·L^(-1) ) at 37℃ for 10 h in the presence orabsence of various concentrations of Iso. Malondialdehyde (MDA) formation, vitamin E consumption,electrophoretic mobility of LDL, mitochondria] membrane potential of mouse peritoneal macrophages,phagocytosis of neutral red, and release of nitric oxide (NO) from macrophages were determined byvarious methods. Results Iso 1 - 100 μmol·L^(-1) significantly inhibited the increase of MDAformation, vitamin E consumption and electrophoretic mobility of LDL induced by Cu^(2+) in aconcentration-dependent manner. The injury of the mitochondrial membrane potential of mouseperitoneal macrophages due to incubation with ox-LDL (0.1 mg·mL^(-1)) at 37℃ for 12 h was markedlyprotected by 10 μmol·L^(-1) Iso. After pretreat-ment of the macrophages with 10 μmol · L^(-1)of Iso and then exposure to ox-LDL for 4 h, the reduction of phagocytosis of neutral red and releaseof NO in response to lipopolysaccharide (IPS) stimulation were significantly prevented. ConclusionIso has protective action against Cu^(2+) - mediated LDL peroxidation and ox-LDL induced toxicity tomacrophages in vitro.

Yi-Qi-Zeng-Min-Tang,a Chinese medicine,ameliorates insulin resistance in type 2 diabetic rats

AIM:To investigate the effects of the Chinese herbal decoction,Yi-Qi-Zeng-Min-Tang(YQZMT),on insulin resistance in type 2 diabetic rats.METHODS:Sprague-Dawley rats were divided into two dietary regiments by feeding either normal pellet diet(NPD) or high fat diet(HFD).Four weeks later,the HFD-fed rats were injected intraperitoneally with lowdose streptozotocin(STZ).Rats with non-fasting blood glucose level ≥ 16.67 mmol/L were considered type 2 diabetic and further divided into five subgroups:the type 2 diabetes model group,low-dose,medium-doseand high-dose YQZMT groups,and rosiglitazone group.Age-matched NPD-fed rats served as controls.YQZMT or rosiglitazone were administered for 8 wk.Intraperitoneal glucose and insulin tolerance tests were performed before and after the treatment to measure the glucose tolerance and insulin sensitivity.Serum levels of biochemical parameters,adipocytokines,such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),as well as free fatty acids(FFAs),were also analyzed.RESULTS:There was significant elevation of insulin resistance and serum levels of fasting glucose(12.82 ± 1.08 mmol/L vs 3.60 ± 0.31 mmol/L,P < 0.01),insulin(7197.36 ± 253.89 pg/mL vs 4820.49 ± 326.89 pg/mL,P < 0.01),total cholesterol(TC)(8.40 ± 0.49 mmol/L vs 2.14 ± 0.06 mmol/L,P < 0.01),triglyceride(2.24 ± 0.12 mmol/L vs 0.78 ± 0.05 mmol/L,P < 0.01),low-density lipoprotein cholesterol(LDL-c)(7.84 ± 0.51 mmol/L vs 0.72 ± 0.04 mmol/L,P < 0.01) and decrease in high-density lipoprotein cholesterol(HDL-c)(0.57 ± 0.03 mmol/L vs 1.27 ± 0.03 mmol/L,P < 0.01) in the low-dose STZ and high-fat diet induced type 2 diabetic group when compared with the control group.Administration of YQZMT induced dose-and timedependent changes in insulin resistance,glucose and lipid profile,and reduced levels of FFA,TNF-α and IL-6 in the type 2 diabetic rats.After the treatment,compared with the diabetic group,the insulin resistance was ameliorated in the high-dose YQZMT(2.82 g/100 g per day) group,with a significant reduction in serum glucose(12.16 ± 1.00 mmol/L vs 17.65 ± 2.22 mmol/L,P < 0.01),homeostasis model assessment of basal insulin resistance(22.68 ± 2.37 vs 38.79 ± 9.02,P < 0.05),triglyceride(0.87 ± 0.15 mmol/L vs 1.99 ± 0.26 mmol/L,P < 0.01),TC(3.31 ± 0.52 mmol/L vs 6.50 ± 1.04 mmol/L,P < 0.01) and LDL-c(2.47 ± 0.50 mmol/L vs 6.00 ± 1.07 mmol/L,P < 0.01),and a signif icant increase in HDL-c(0.84 ± 0.08 mmol/L vs 0.50 ± 0.03 mmol/L,P < 0.01).But the body weight was not changed signif icantly.CONCLUSION:YQZMT,which ameliorates insulin resistance and does not cause increase in body weight,may be a suitable therapeutic adjunct for the treatment of type 2 diabetes.

Liraglutide reduces oxidized LDL-induced oxidative stress and fatty degen- eration in Raw 264.7 cells involving the AMPK/SREBP1 pathway

Baekgound Recent studies have suggested a potential role for liraglutide in the prevention and stabilization ofatherosclerotic vascular disease. However, the molecular mechanisms underlying the effect of liraglutide on atherosclerosis have not been well elucidated. The pur- pose of this study was to examine whether liraglutide protects against oxidative stress and fatty degeneration via modulation of AMP-activated protein kinase （AMPK）/sterol regulatory element binding transcription factor 1 （SREBP1） signaling pathway in foam ceils. Methods Mouse macrophages Raw264.7 cells were exposed to oxidized low density lipoprotein （oxLDL） to induce the formation of foam cells. The cells were incubated with oxLDL （50 μg/mL）, liraglutide （0.1, 0.5, 1 and 2 nmol/L） or exendin-3 （9-39） （1, 10 and 100 nmol/L） alone, or in combination. Oil Red O staining was used to detect intracellular lipid droplets. The levels of TG and cholesterol were measured using the commercial kits. Oxidative stress was determined by measuring intracellular reactive oxygen species （ROS）, malondialdehyde （MDA） and superoxide dismutase 1 （SOD）. Western blot analysis was used to examine the expression of AMPKal, SREBP1, phosphory- lated AMPKal, phosphorylated SREBP1, glucagon-like peptide-1 （GLP-1） and GLP-1 receptor （GLP-1R）. Results Oil Red O staining showed that the cytoplasmic lipid droplet accumulation was visibly decreased in foam cells by treatment with liraglutide. The TG and cholesterol content in the liraglutide-treated foam cells was significantly decreased. In addition, foam ceils manifested an impaired oxidative stress following liraglutide treatment, as evidenced by increased SOD, and decreased ROS and MDA. However, these effects of liraglutide on foam cells were attenuated by the use of GLP-IR antagonist exendin-3 （9-39）. Furthermore, we found that the expression level of AMPKa 1 and phosphorylated AMPKct 1 was significantly increased while the expression level of SREBP 1 and phosphorylated SREBP 1 was significantly decreased in foam cells following treatment with liraglutide. Conclusions This study for the first time demonstrated that the effect of liraglutide on reducing oxidative stress and fatty degeneration in oxLDL-induced Raw264.7 cells is accompanied by the alteration of AMPK/SREBP1 pathway. This study provided a potential molecular mechanism for the effect of liraglutide on reducing oxidative stress and fatty degeneration.

Characterization of lipid parameters in diabetic and non-diabetic atherosclerotic patients

Background ＆ Objective The relationship between lipid profile perturbation and diabetes associated complications has long been an area of interest. Dyslipidemia is a potent predictor of cardiovascular morbidity and mortality in diabetic patients. The aim of present study was to investigate relationship between aging and lipid profiles in diabetic and non-diabetic atherosclerotie patients. Methods Five hundred and seventy six individuals （45-75 year age） participated in this study. Among these, 192 were having history of diabetes mellitus and atherosclerosis. Individuals are categorized on the base of health （normal, non-diabetic atheroselerosis, diabetic atherosclerosis） and age （45-55 years, 56~55 years, and 66-75 years）. All the participants were subjected to the procedures like a detailed history, biochemical analysis for fasting blood sugar, hemoglobin Alc, total cholesterol （TC）, triglycerides （TG）, low-density lipoprotein-（LDL）, very low-density lipoprotein （VLDL） and high-density lipoprotein （HDL）. All these parameters were compared between diabetic and non-diabetic atherosclerotic patients of all three age groups. TC/HDL and LDL/HDL were also calculated. Results Diabetic atherosclerotic individuals （both males and females） had high level of TC, TG, LDL, VLDL and low level of HDL in comparison to non-diabetic atherosclerotie and normal control individuals. Among all three age groups, lipoprotein abnormality was observed to be more frequent in females than males. There was a significant increase in TC/HDL and LDL/HDL ratio in diabetic atherosclerotic subjects compared to age and sex matched non-diabetic atherosclerotic and normal control. Conclusions Degree of dyslipidemia increases with increase in age in both genders. Female are more prone to diabetic dyslipidemia and hence have more risk of developing atherosclerosis with increasing age.

ASSOCIATION BETWEEN LOW- DENSITY LIPOPROTEIN RECEPTOR- RELATED PROTEIN GENE, BUTYRYLCHOLINESTERASE GENE AND ALZHEIMER'S DISEASE IN CHINESE

Objective. To research the relations between low- density lipoprotein receptor- related protein gene (LRP) polymorphism, butyrylcholinesterase gene (BchE) polymorphism and Alzheimer’s disease (AD) in Chinese. Methods. The gene polymorphisms of LRP and BchE were genotyped in 38 AD cases and 40 controls with polymerase chain reaction- restriction fragment length polymorphism (PCR- RFLP) methods. AD groups were classified according to the LRP C/C genotype and compared with matched controls. Results. AD group had higher frequencies of C/C homozygote (81.6％ vs 60.0％ , P< 0.05) and of C allele (89.5％ vs 76.3％ , P< 0.05),with no significant difference between any of these LRP genotypes classified AD groups and their respective control groups. Conclusions. A positive correlation was found between LRP gene polymorphism and AD, but not between BchE gene polymorphism and AD in Chinese AD cases.

Attainment of multifactorial treatment targets among the elderly in a lipid clinic

Objective To examine target attainment of lipid-lowering, antihypenensive and antidiabetic treatment in the elderly in a specialist set- ting of a University Hospital in Greece. Methods This was a retrospective study including consecutive subjects 〉 65 years old （n = 465） with a follow-up 〉 3 years. Low-density lipoprotein cholesterol （LDL-C）, blood pressure （BP） and glycated hemoglobin （HbAlc） goal achievement were recorded according to European Society of Cardiology/European Atherosclerosis Society （ESC/EAS）, European Society of Hypertension （ESH）/ESC and European Association for the Study of Diabetes （EASD） guidelines. Results The LDL-C targets were attained by 27~,4, 48% and 62% of very high, high and moderate risk patients, respectively. Those receiving statin ＋ ezetimibe achieved higher rates of LDL-C goal achievement compared with those receiving statin monotherapy （48% vs. 33%, P 〈 0.05）. Of the diabetic sub- jects, 71% had BP 〈 140/85 mmHg, while 78% of those without diabetes had BP 〈 140/90 mmHg. A higher proportion of the non-diabetic individuals （86%） had BP 〈 150/90 mmHg. Also, a higher proportion of those with diabetes had HbAlc 〈 8% rather than 〈 7% （88% and 47%, respectively）. Of note, almost one out of three non-diabetic individuals and one out of ten diabetic individuals had achieved all three treatment targets. Conclusions Even in a specialist setting of a University Hospital, a high proportion of the elderly remain at suboptimal LDL-C, BP and HbAlc levels. The use of drug combinations could improve multifactorial treatment target attainment, while less strict tar- gets could be more easily achieved in this population.

Baicalin and geniposide inhibit the development of atherosclerosis by increasing Wntl and inhibiting dickkopf-related protein-1 expression

Background Our previous study showed that the combined Chinese herbs containing scutellaria baicalensis georgi and gardenia jasminoids ellis inhibited atherosclerosis. In this study, we sought to determine if baicalin and geniposide could inhibit atherosclerosis through Wntl and dickkopf-related protein-1 （DKK1）. Methods The wild-type and ApoE-/- mice were treated with baicalin, geniposide, and baicalin plus geniposide daily by gavage for 12 weeks. Blood lipid levels were measured with an automatic biochemistry analyzer. Aortic atherosclerotic lesion areas were analyzed with Image-ProPlus software. The mRNA and protein expression of DKK1, Wntt and nuclear factor-r,B （NF-κB） were measured with RT-PCR and Westem Blot. Serum levels of interleukin-12 （IL-12） were quantified with ELISA. Results The baicalin or geniposide monotherapy as well as combination therapy inhibited the development of atherosclerotic lesions, increased Wntl and decreased DKKI expression and elevated the ratio of Wntl/DKK1 compared with high-lipid diet group. However, only baicalin or geniposide monotherapy decreased NF-κB expression. Moreover, baicalin and geniposide monoor combination therapy lowered IL-12 levels. Geniposide reduced both serum total cholesterol and low density lipoprotein levels, while baicalin either alone or in combination with geniposide did not affect serum lipid levels. In human, umbilical vein endothelial ceils stimulated by oxidized low density lipoprotein, baicalin and geniposide also increased Wntl and decreased DKK1 expression and elevated the ratio of Wntl/DKK1. Condusions Baicalin and geniposide exert inflammation-regulatory effects and may prevent atherosclerotic lesions through enhancing Wntl and inhibit- ing DKK1 expression.

Variations of very low-density lipoprotein receptor subtype expression in gastrointestinal adenocarcinoma cells with various differentiations

AIM: This study is aimed at investigating the expression and possible significances of very low-density lipoprotein receptor (VLDLR) subtypes in gastroenteric adenocarcinoma tissues and cells with various differentiations. METHODS: Thirty-one cases of gastroenteric carcinoma/ adjacent normal tissues were enrolled in the study, which were diagnosed and classified by the clinicopathological diagnosis. The expression of VLDLR subtypes was detected in gastroenteric carcinoma/adjacent normal tissues and three various differentiated human gastric adenocarcinoma cell lines (MKN28, SGC7901 and MKN45) by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.RE,SULTS: Two VLDLR subtypes, namely, type Ⅱ VLDLR and type Ⅰ VLDLR, were found to express changes in gastroenteric carcinoma tissues, their adjacent normal tissue, and gastric adenocarcinoma cell lines as well. Type Ⅱ VLDLR is predominantly expressed in poorly- or moderately-differentiated gastroenteric carcinoma tissues and gastric adenocarcinoma cell lines, whereas type ⅠVLDLR is mainly detected in well-differentiated intestinal carcinoma tissues and gastric adenocarcinoma cells compared with the adjacent normal tissues. CONCLUSION: The results suggested that the variations of the VLDLR subtype expression might be correlated with the progress and differentiation of gastroenteric carcinoma.

Atherosclerosis： from biology to pharmacological treatment

A recent explosion in the amount of cardiovascular risk has swept across the globe. Primary prevention is the preferred method to lower cardiovascular risk. Lowering the prevalence of obesity is the most urgent matter, and is pleiotropic since it affects blood pressure, lipid profiles, glucose metabolism, inflammation, and atherothrombotic disease progression. Given the current obstacles, success of primary prevention remains uncertain. At the same time, the consequences of delay and inaction will inevitably be disastrous, and the sense of urgency mounts. Pathological and epidemiological data confirm that atherosclerosis begins in early childhood, and advances seamlessly and inexorably throughout life. Risk factors in childhood are similar to those in adults, and track between stages of life. When indicated, aggressive treatment should begin at the earliest indication, and be continued for many years. For those patients at intermediate risk according to global risk scores, C-reactive protein, coronary artery calcium, and carotid intima-media thickness are available for further stratification. Using statins for primary prevention is recommended by guidelines, is prevalent, but remains under prescribed. Statin drugs are unrivaled, evidence-based, major weapons to lower cardiovascular risk. Even when low density lipoprotein cholesterol targets are attained, over half of patients continue to have disease progression and clinical events. Though clinical evidence is incomplete, altering or raising the blood high density lipoprotein cholesterol level continues to be pursued. The aim of this review is to point out the attention of key aspects of vulnerable plaques regarding their pathogenesis and treatment.

Dyslipidemia： evidence of efficacy of the pharmacological and non-pharmacological treatment in the elderly

The clinical decision to control risk factors for cardiovascular disease （CVD） in the elderly takes the followings into consideration： （1） the elderly life expectancy; （2） the elderly biological age and functional capacity; （3） the role of cardiovascular disease in the elderly group; （4） the prevalence of risk factors in the elderly; and （5） The effectiveness of treatment of risk factors in the elderly. A large number of studies showed the efficacy of secondary and primary prevention of dyslipidemia in the elderly. However, the only trial that included patients over 80 years was the Heart Protection Study （HPS）. Statins are considered the first line therapy for lowering low-density lipoprotein cholesterol （LDL-C）. Because lifestyle changes are very difficult to achieve, doctors in general tend to prescribe many drugs to control cardiovascular risk factors. However, healthy food consumption remains a cornerstone in primary and secondary cardiovascular prevention and should be implemented by everyone.