Objective:To explore the postprandial plasma low-density lipoprotein cholesterol (LDL-C) changes by various detection methods.Methods:A total of 85 subjects admitted to the Second Xiangya Hospital of Central South University from November 2017 to May 2019 were included. Serum samples were collected from fasting and the 2 nd hour and the 4 th hour after breakfast. Serum lipid levels were measured with enzymatic assays and nuclear magnetic resonance spectroscopy (NMRS), and proprotein invertase subtilisin/kexin type 9 (PCSK9) levels were measured with enzyme-linked immunosorbent assays. The differences of blood lipid components at different time points were compared by Friedman two-way rank analysis of variance and Wilcoxon signed rank test, and the correlation between PCSK9 level and lipoprotein particles was analyzed by Spearman correlation. Results:Measured by enzymatic assays, compared with the fasting state, LDL-C decreased at the 2 nd hour and the 4 th hour after the meal (2.58[2.09, 3.12], 2.47[1.92, 3.02], 2.37[1.82, 2.80] mmol/L, P<0.001). Measured by NMRS, the concentration of LDL particles (1 086[830, 1 239], 1 083[848, 1 213], 1 061[814, 1 213] nmol/L, P=0.417) did not change significantly, and cholesterol in LDL particles were 2.13 (1.56, 2.54), 2.16 (1.68, 2.50), 2.06 (1.58, 2.50) mmol/L, respectively ( P=0.047)，and postprandial cholesterol in LDL particles in the 2 nd hour and in the 4 th hour did not change significantly compared with fasting ( P>0.05). while the concentration of large LDL particles (185.2[150.6,221.6], 173.0[144.8,220.3], 178.1[144.0,233.6] nmol/L, P=0.001), and the cholesterol level in large LDL particles (0.49[0.39, 0.57], 0.47[0.38, 0.57], 0.46[0.37, 0.58]mmol/L, P<0.001) decreased after the meal. The PCSK9 level also decreased significantly after the meal (299[233, 397], 257[208, 342], 251[215, 340] ng/ml, P<0.001). There was an independent positive correlation between the decrease of PCSK9 levels and the increase of remnant cholesterol detected by MNRS after the meal ( r=0.232, P=0.035). Conclusions:The postprandial LDL-C level measured by NMRS and enzymatic assays is not consistent. The decrease of LDL-C measured by enzymatic assays is not caused by the clearance of LDL particles, but by the redistribution of cholesterol in each LDL subfraction.

Diabetes is the most important comorbidity of cardiovascular disease, and cardiovascular disease is the main cause of mortality and disability of patients with type 2 diabetes. In order to standardize the diagnosis and treatment of patients with diabetes and cardiovascular disease, the National Health Commission Capacity Building and Continuing Education Center organized the experts from the field of cardiology and endocrinology systematically reviewing the research progresses and expert experiences of relevant disciplines from home and abroad, and formulated this consensus. This consensus covers the diagnosis, drug treatment, and risk factor management for patients with diabetes and cardiovascular disease (including atherosclerotic cardiovascular disease and heart failure) from the perspective of cardiovascular disease and diabetes management aiming to strengthen the comprehensive management of patients and ultimately to improve the prognosis of patients. The management of cardiovascular diseases mainly includes the management of blood pressure, blood lipids, anti-thrombosis, anti-myocardial ischemia, anti-ventricular remodeling and so on. Diabetes management mainly includes lifestyle intervention (including diet, exercise, weight loss, etc.), anti-hyperglycemia therapy (including drugs and insulin), blood glucose monitoring, and hypoglycemic prevention. In addition, specific clinical recommendations are given to patients with special health care needs such as diabetic nephropathy, elderly (>75 years), and cardiovascular critical illness.

Low-density lipoprotein cholesterol (LDL-C) has been recommended as the primary treatment target on lipid management in coronary heart disease (CHD) patients for several decades. However, even by aggressive LDL-C lowering treatment, patients still present a significant residual risk of major adverse cardiovascular events. Non-high-density lipoprotein cholesterol (non-HDL-C) contained all the atherogenic lipoproteins. Non-HDL-C is superior to LDL-C for the prediction of cardiovascular events and has many other compelling advantages over LDL-C and other traditional lipid parameters. This review mainly discusses the definition and test advantages of non-HDL-C, the predictive value of non-HDL-C, recommended value of non-HDL-C goals, and related guideline recommendations of non-HDL-C.

Objective To observe the effects of apolipoprotein AⅠ (apoAⅠ) on autophagy,lipid retention,and apoptosis in foam cells, and to explore the anti-atherosclerotic mechanism of apoAⅠ. Methods Macrophages derived from THP-1 cells were randomly divided into the control group,the 3-MA+apoAⅠ group,and the apoAⅠ group. Each group was administered oxidized low-density lipoprotein for 36 hours,then lipid droplets and autophagosomes were observed and cellular cholesterol content was quantified. LC3 and Beclin-1 expression was examined by western blot and the apoptotic ratio determined using flow cytometry. Results Compared with the results of the control group,apoAⅠ treatment inhibited lipid retention and apoptosis in foam cells,decreased cellular cholesterol content,and up-regulated the expression of LC3 and Beclin-1 (P < 0.01). Administration of 3-MA abrogated the effects of apoAⅠ (P < 0.05). Conclusion apoAⅠ inhibits lipid retention and apoptosis in foam cells by inducing autophagy.

Objective: To investigate the effect and related mechanism of apolipoprotein A5 (ApoA5) on adipogenic differentiation of human adipose-derived mesenchymal stem cells (AMSC). Methods: Subcutaneous adipose tissue was obtained from 40 patients undergoing abdominal surgery at our hospital from February to July 2015. After induction of human AMSC by collagenase digestion, the adipose tissue was induced to differentiate into mature adipocytes and treated with ApoA5 at 600 and 1 200 ng/ml, respectively (ApoA5 intervention groups). Cells treated without ApoA5 protein were used as control group. The cells were harvested on the 7th and 14th day of differentiation, and the following assays were performed: (1) the effect of ApoA5 on TG content was measured by a TG assay kit; (2) RT-qPCR assay was used to detect the effect of ApoA5 on aP2 and FAS mRNA expression; (3) the effect of ApoA5 on the expression of CIDEC mRNA and protein was detected by RT-qPCR and Western blot; (4) the effect of ApoA5 on the expression of C/EBPβ mRNA and protein was detected by RT-qPCR and Western blot; (5) using lentiviral transfection technique, we overexpressed the gene of CIDEC in AMSC and cells were divided into lentiviral negative control group, lentiviral over-expressed CIDEC group and lentiviral over-expressed CIDEC+ApoA5 intervention group (the ApoA5 intervention concentration was 1 200 ng/ml). Thereby, we examined the effect of ApoA5 on the above indicators in adipogenic differentiation of AMSC in the case of CIDEC overexpression. Results: (1) Effect of ApoA5 on TG content in AMSC: on the 7th and 14th day after the intervention, the TG levels were lower in ApoA5 600 and 1 200 ng/ml group AMSC than those in the control group (all P<0.05). (2) The effect of ApoA5 on the expression of aP2 and FAS mRNA in AMSC: on the 7th day after intervention, the expression levels of aP2 and FAS mRNA were significantly lower in ApoA5 600 and 1 200 ng/ml group than those in the control group (all P<0.05). On the 14th day after intervention, the expression levels of aP2 and FAS mRNA were lower in ApoA5 600 and 1 200 ng/ml group than those in the control group (all P<0.05). (3) The effect of ApoA5 on the mRNA and protein expression of CIDEC in AMSC: on the 7th day after intervention, the mRNA and relative protein expression levels of CIDEC were significantly lower in AMSC of ApoA5 600 and 1 200 ng/ml group than those of the control group (all P<0.05). On the 14th day after intervention, the mRNA and relative protein levels of CIDEC were further reduced in ApoA5 600 and 1 200 ng/ml AMSC groups than those in the control group (all P<0.05). (4) The effect of ApoA5 on C/EBPβ mRNA and protein expression in AMSC: on the 7th day after intervention, C/EBPβ mRNA and relative protein expression levels were significantly lower in ApoA5 600 and 1 200 ng/ml group than those in the control group (all P<0.05). On the 14th day after intervention, the levels of C/EBPβ mRNA and relative protein were lower in ApoA5 600 and 1 200 ng/ml group than those in the control group (all P<0.05). (5) The effect of ApoA5 on the content of TG in AMSC after CIDEC overexpression: on the 7th and 14th day after intervention, the TG contents in AMSC were higher in the lentivirus over-expressed CIDEC group than in the lentivirus negative control group (both P<0.05). However, TG contents in AMSC were similar between the over-expressed CIDEC group and the CIDEC+ApoA5 over-expression group (both P>0.05). (6) The effect of ApoA5 on the expression of aP2 and FAS mRNA in AMSC after CIDEC overexpression: on the 7th day after intervention, the expression levels of aP2 and FAS mRNA in AMSC were higher in the lentivirus over-expressed CIDEC group than in the lentivirus negative control group (both P<0.05). On the 14th day after intervention, the expression level of aP2 mRNA in the AMSC was higher in the lentivirus over-expressed CIDEC group than in the lentivirus negative control group (P<0.05). On the 7th and 14th day after intervention, the expression levels of aP2 and FAS mRNA in AMSC were similar between the lentivirus over-expressed CIDEC group and the lentivirus over-expressed CIDEC+ApoA5 group (all P>0.05). (7) The effect of ApoA5 on the expression of C/EBPβ mRNA and protein in AMSC after CIDEC overexpression: on the 7th day after intervention, the mRNA and relative protein expressions of C/EBPβ in AMSC were higher in lentivirus-overexpressed CIDEC group than in lentivirus negative control group (both P <0.05). On the 14th day after intervention, C/EBPβ mRNA and protein expression levels in AMSC were higher in the lentivirus over-expressed CIDEC group than in the lentivirus negative control group (both P<0.05). On the 7th and 14th day after intervention, the expressions of C/EBPβ mRNA and protein in AMSC were similar between lentivirus over-expressed CIDEC group and lentivirus over-expression CIDEC+ApoA5 intervention group (all P>0.05). Conclusions ApoA5 can inhibit the adipogenic differentiation of AMSC,and this effect may be mediated by down-regulating the expression of CIDEC. Furthermore, our results indicate that CIDEC could be considered as a key factor in adipogenic differentiation.

Objective: To verify whether Apo A5 could inhibit the adipogenic differentiation of adipose mesenchymal stem cells (AMSCs). Methods: We isolated AMSCs by collagenase digestion method from the adipocyte tissue of patients underwent abdominal surgery in our hospital from February to July 2015. AMSCs were differentiated into mature adipocytes and incubated with Apo A5 (600 and 1 200 ng/ml) for 7, 14 and 21 days. Morphological changes, TG content, and gene expression levels of adipogenic differentiation markers were determined. Results: (1) The results of detecting the oil red O absorbance by spectrophotometer are as follows: At the 7th, 14th and 21st days after intervention, the absorbance of oil red O with 600 and 1 200 ng/ml Apo A5 intervention was lower than that of the control group (Day 7: 145.6±21.1, 110.5±31.5 vs. 195.4±35.7; Day 14: 289.2±24.2, 250.4±45.2 vs. 341.6±34.5; Day 21: 431.9±33.2, 374.7±26.4 vs. 488.2±22.5, all P<0.05). (2) The intracellular TG content after Apo A5 intervention were detected by TG quantitative detection kit detection. At the 7th, 14th and 21st days, intracellular TG contents in 600 and 1 200 ng/ml Apo A5 groups were lower than that in the control group (Day 7:(203.1±22.6), (174.2±25.8)nmol/mg protein in Apo A5 intervention group vs. (266.25±23.7)nmol/mg protein in control group; Day 14: (332.5±23.2), (231.1±22.2)nmol/mg protein in Apo A5 intervention group vs. (452.2±16.4)nmol/mg protein in control group; Day 21: (482.8±21.2), (294.2±29.9)nmol/mg protein vs. (597.2±22.1)nmol/mg protein in control group, P<0.05). (3) aP2 gene expression detected by real-time PCR and intracellular fatty acid synthase and lipid droplets coated protein gene expression levels determined by Western blot on day 7, 14 and 21 were significantly lower in Apo A5 groups than in control group (all P<0.05). Conclusions Apo A5 significantly reduced intracellular TG content and modulated the gene expression levels of adipogenic differentiation marker, thus, Apo A5 treatment can inhibit the adipogenic differentiation of adipose mesenchymal stem cells.

Objective To study the effect of epigallocatechin-3 gallate (EGCG) on cholesterol efflux in foam cells and its mechanism.Methods THP-1 cells were induced to differentiate into macrophages which were then transformed to foam cells.Foam cells were divided into 0 μmol/L EGCG group,10 μmol/L EGCG group,30 μmol/L EGCG group,and 100 μmol/L EGCG group (1.5 × 106 in each group).Their cholesterol content was measured with a cholesterol test kit,apoA-I-mediated cholesterol efflux was assayed with a liquid scintillation counter,expression of ATP-binding cassette A1 (ABCA1) was detected by RT-PCR and Western blot respectively.Results The ABCA1 mRNA and protein expression levels and cholesterol efflux were significantly higher while the cholesterol content was significantly lower in 10 μmol/L EGCG group,30 μmol/L EGCG group,and 100 μmol/L EGCG group than in 0 μmol/L EGCG group (7.04％ ±0.21％,7.75％±0.17％ and 8.53％±0.18％ vs 3.37％±0.16％,P＜0.01;419.33±19.75 mg/g,352.58± 14.23 mg/g and 312.62±17.45 mg/g vs 520.51 ±20.62 mg/g,P＜0.01),and in 30 μmol/L EGCG group,100μmol/L EGCG group than in 10μmol/L EGCG group (P＜0.05).Conclusion EGCG increases cholesterol efflux and decreases cholesterol content in foam cells by upregulating the transcription and expression of ABCA1.

Objective To explore effects of apoAI on MCP?1 levels in the plasma and the Ly6Chi monocyte proportion in the blood and spleen of atherosclerotic mice,as well as on CCR2 expression in vitro. Methods Sixteen male apoE?/?mice were fed with high cholesterol diet for 12 weeks. Mice were randomly divided into control and apoAI groups and were administered with PBS or apoAI(40 mg/kg),respectively,via tail vein on the 1st and 3rd day before sacrifice. Mice in both groups were administered LPS(25μg/mouse)via intraperitoneal injection 12 h before sacrifice. Plas?ma levels of MCP?1 were determined using ELISA,and the Ly6Chi monocyte proportion was analyzed using flow cytometry. In addition,human monocytic THP?1 cells were randomly divided into control and apoAI(10 mg/L)?treated groups,pretreated with corresponding intervention,and incubated with LPS(10μg/L). CCR2 expression levels were measured by Western blotting. Results Compared with the control treatment, apoAI treatment remarkably reduced MCP?1 levels in plasma and Ly6Chi monocyte proportion in the blood and spleen(P<0.01). Furthermore, apoAI treatment inhibited CCR2 expression in monocytes in vitro(P<0.05). Conclusion apoAI can reduce MCP?1 levels in plasma and the Ly6Chi monocyte proportion in the blood and spleen and can inhibit CCR2 expression in monocytes in vitro.

Familial amyloid cardiomyopathy is a challenging condition that mimics many other diseases,particularly in patients with pronounced neurological presentations and unexplained or equivocal cardiac abnormalities.In this case,a 57-year-old man was admitted for outpatient cardiological evaluation of progressive right heart failure and limb paraesthesias.The patient presented with hypertension,chronic Guillain-Barre syndrome,and sick sinus syndrome.Transthoracic echocardiograms showed a thickened ventricular wall and enlarged atrium.Tissue Doppler showed a restrictive filling pattern.Transthyretin (TTR)-associated amyloidosis,which was revealed by abdominal fat-pad biopsy and DNA analysis,explained the concurrence of independent pathological features,including neuropathy and cardiac involvement.Genetic testing identified a G ＞ T mutation in exon 4 of the transthyretin (TTR) gene.This mutation resulted in the alanine-to-serine substitution at amino acid position 117.Moreover,genetic testing confirmed that the patient's asymptomatic son carried the same amyioidogenic TTR mutation.Given these findings,the diagnosis of familial amyloid cardiomyopathy,which was misdiagnosed as chronic Guillain-Barre syndrome,was proposed.

A case of portopulmonary hypertension characterized by repeated syncope was retrospectively analyzed. Intrahepatic or extrahepatic factor-induced portal hypertension complicated with metabolic disorder of vasoactive substances, vascular pressure, inflammation, etc. may result in systolic and diastolic dysfunction of pulmonary arteries and systemic hyperdynamic circulation, the long-term effect of which can induce vascular remodeling and consequently, pulmonary hypertension. The pathogenic process is rather insidious. Pulmonary hypertension is clinically characterized by the raised average pulmonary artery pressure, normal pulmonary capillary wedge pressure and high pulmonary vascular resistance. Currently available therapeutic approaches include drug therapy targeting on pulmonary hypertension and liver transplantation.
Blood Pressure ; Humans ; Hypertension, Portal ; complications ; diagnosis ; Hypertension, Pulmonary ; complications ; diagnosis ; Liver Transplantation ; Syncope ; complications ; diagnosis