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Biomedical subjects

Huai Bai

Publications and source records attributed to Huai Bai.

At least 19 recordsLinked to original sources

Plasma very-low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein oxidative modification induces procoagulant profiles in endogenous hypertriglyceridemia.

This study was to investigate whether oxidatively modified lipoproteins were associated with changes of pro- and anticoagulant profiles in hypertriglyceridemic subjects. Plasma VLDL, LDL, and HDL were isolated with the one-step density gradient ultracentrifugation method. The oxidation of the lipoproteins was identified. Prothrombin time (PT) and activated partial thrombplastin time (APTT), tissue plasminogen activator and plasminogen activator inhibitor-1, and platelet aggregation rate were determined with a reaction system consisting of mixed fresh normal plasma, in endogenous hypertriglyceridemic (HTG) patients, in in vitro modified lipoproteins from a normolipidemic donor, and in experimental rats. The results indicated that oxVLDL, oxLDL, and oxHDL occurred in the plasma of HTG patients. Compared with the control group, PT and APTT, incubated with plasma VLDL, LDL, or HDL from HTG patients, respectively, were significantly reduced, while platelet maximal aggregation rates were significantly higher (P < 0.05-0.01). Similar procoagulant profiles were observed in in vitro modified lipoprotein components and in rats with intrinsic hypertriglyceridemia as well. These results support our previous finding that LDL, VLDL, and HDL were all oxidatively modified in vivo in the subjects with HTG, and suggest that procoagulation state may result from the abnormal plasma lipoprotein oxidative modification in vivo.

Aged↗

[Analysis of cholesterol ester transfer protein gene Taq IB and -629 C/A polymorphisms in patients with endogenous hypertriglyceridemia in Chinese population].

OBJECTIVE: To investigate the variations of cholesterol ester transfer protein (CETP) gene and its relation to endogenous hypertriglyceridemia (HTG) in Chinese population. METHODS: One hundred and thirty-five endogenous hypertriglyceridemics and 214 healthy subjects from a population of Chinese Han nationality in Chengdu area were studied using restriction fragment length polymorphism (RFLPs) amplified by polymerase chain reaction (PCR). The polymorphic sites studied included Taq IB and -629 C/A polymorphism in CETP gene. RESULTS: The frequencies of B(2) allele at Taq IB site in normal group and HTG group were 0.418 and 0.382, respectively. The frequencies of A allele at -629 C/A site in the two groups were 0.479 and 0.489, respectively. No significant difference between normal control and HTG groups were found in both allele frequency of the two polymorphism. Linkage disequilibrium was observed between Taq IB and -629 C/A polymorphic sites (D'=0.881). In the normal control group, subjects with genotype B(2)B(2) of Taq IB site had a higher serum mean concentration of HDL-C and lower LDL-C when compared with that of genotype B(1)B(1) and B(1)B(2), respectively (both P< 0.05), while those with genotype CC of -629 C/A site had a lower LDL-C level and higher Apo A II level when compared with that of genotype AC (P< 0.01 and P< 0.05, respectively). The changes of the lipid and lipoprotein levels were only observed in normal male subjects when male and female groups were further separated. No significant changes of lipid and lipoprotein levels were observed in both polymorphism in HTG group. Combined genotype analysis of the two sites, subjects with genotype B(2)B(2)CC in normal controls had higher HDL-C levels but lower serum triglyceride (TG) when compared with B(1)B(1)CC. CONCLUSION: These results suggest that Taq IB and -629 C/A polymorphisms in CETP gene are associated with healthy control subjects to some extent in Chinese population, but not with endogenous hypertriglyleridemia in the population group.

Adult↗

Identification of a novel gene, HCR2, in aorta of hypercoagulable rats using suppression subtractive hybridization.

Screening and identification of novel genes involved in hypercoagulable state (HCS) is important in understanding the underlying mechanisms of development of atheroslerosis, which implicated in critical vascular diseases such as coronary heart disease and stroke. HCS was induced in rats with high carbohydrate diet. Subtractive hybridization experiments between aorta tissues from hypercoagulable rats and controls showed that a novel cDNA (GenBank Accession No. AY234417), designated as hypercoagulability related gene-2 (HCR2), was highly expressed in aorta tissue. The predicted protein encoded by HCR2 contains 78 amino acids, which has a theoretical isoelectric point (pI) of 8.59 and molecular weight (MW) of 8841.7 based on sequence analysis. Our data suggest that HCR2 may be involved in HCS and identification of the gene may contribute to our understanding of the mechanisms for the production of a hypercoagulable state of several critical clinical disorders.

Amino Acid Sequence↗

Relationship between plasma HDL subclasses distribution and apoA-I gene polymorphisms.

BACKGROUND: It is generally accepted that apolipoprotein (apo) A-I is the dominant structural apolipoprotein of HDL particles and different HDL subclasses have distinct but interrelated metabolic functions. HDL is known to directly affect the atherogenic process hence changes in HDL subclasses distribution may be related to the incidence and prevalence of atherosclerosis. METHODS: The ApoA-I contents (mg/l) of plasma HDL subclasses were determined by 2-dimensional gel electrophoresis coupled with immunodetection and apoA-I genotypes were assayed by PCR-RFLP in 307 Chinese subjects (169 males, 138 females). RESULTS: The G/G and C/C genotypes were the most frequent at -78 bp and +83 bp of apoA-I gene, respectively. There were no significant differences in the frequencies of rare A allele at -78 bp and rare T allele at +83 bp between males and females. Compared with the G/G carriers, G/A and A/A carriers had significantly higher plasma concentrations of TG, apoC-II, apoC-III, apoA-I contents of prebeta(1)-HDL, HDL(3a) and TG/HDL-C ratio. And in addition, A/A carriers had significantly lower apoA-I contents of HDL(2a) and HDL(2b). Females had increased plasma concentrations of apoA-I, HDL-C, apoA-I contents of HDL(2a) and HDL(2b) while decreased apoA-I contents of prebeta(1)-HDL, HDL(3b) and TG/HDL-C ratio as compared to males carrying the same genotype. No significant differences were demonstrated on the concentrations of plasma lipids, lipoproteins, apolipoproteins and apoA-I contents of plasma HDL subclasses between the C/C and C/T subjects. CONCLUSION: The G/A polymorphism at -78 bp of apoA-I gene was associated with changes of HDL subclasses distribution. There was a general shift towards smaller-sized HDL, which, in turn, indicated that reverse cholesterol transport (RCT) might be weakened and HDL maturation might be abnormal in the subjects with G/A mutation.

Adult↗

[Cloning and bioinformatic analysis of a novel gene HCR2 up-regulated in aorta of hypercoagulable rat].

OBJECTIVE: The aim of this study was to clone the full-length cDNA of HCR2 up-regulated in aorta of hypercoagulable rat and make the relevant bioinformatic analysis. METHODS: Rapid amplification of cDNA end (RACE) and nested PCR technique was used to amplify the full-length cDNA of HCR2 from an EST (GenBank accession number BQ901227) which was significantly up-regulated in hypercoagulable rat. RESULTS: The full-length cDNA of HCR2 has been obtained (GenBank accession number AY234417). Semi-quantitative RT-PCR demonstrated that HCR2 is up-regulated in aorta of hypercoagulable rat. Bioinformatic analysis showed that HCR2 gene is located in rat chromosome 4q11. The full-length cDNA of HCR2 is 1275 bp, coding for a 78 amino acids polypeptide with a theoretical molecular weight of 8841.7 and isoelectric point of 8. 59. This protein has no signal peptide and transmembrane sequence. It may be a nuclear protein. It shares no significant homology with any known protein. CONCLUSION: The successful cloning of HCR2 has laid a solid foundation for further study of its function and its possible role in the occurrence and development of hypercoagulability.

Amino Acid Sequence↗

[Construction and preliminary screening of a forward-subtracted cDNA library for differentially expressed genes in rat liver of prothrombotic state].

OBJECTIVE: To construct and preliminarily screen the forward-subtracted cDNA library of differentially expressed genes in rat liver of prothrombotic state (PTS). METHODS: The forward-subtracted cDNA library for differentially expressed genes in rat liver of PTS was constructed by suppression subtractive hybridization using cDNAs synthesized from mRNA of PTS rat as Tester and cDNAs from mRNA of control rat as Driver. The products from the last PCR amplification of suppression subtractive hybridization were inserted into a T/A plasmid vectors to transform the Escherichia coli JM109 cells. To produce the library, the transformed cells were incubated at 37 C overnight on a LB agar plate containing ampicillin (50 microg/ml), IPTG and X-gal. Forward-subtracted cDNA probes and reverse-subtracted cDNA probes were prepared by nested PCR amplification, which were labeled with HRP. Positive clones were selected by differential screening in which forward-subtracted and reverse-subtracted cDNA probes were separately hybridized with the membranes slot-blotted by plasmid DNAs amplified and isolated from the library. Inserts in the positive clones were submitted to DNA sequencing. Nucleic acid sequence homology search was performed against the GenBank DNA database (non-redundant, and non-mouse and non-human EST entries) using the Standard nucleotide-nucleotide BLAST [blastn] program via a network connection to the National Center for Biotechnology information. RESULTS: The forward-subtracted cDNA library for differentially expressed genes in rat liver of PTS was successfully constructed. Two differentially expressed cDNA fragments were found after preliminary screening. CONCLUSION: The forward-subtracted cDNA library for differentially expressed genes in rat liver of PTS was successfully constructed in the present study.

Animals↗

DC electric fields induce distinct preangiogenic responses in microvascular and macrovascular cells.

OBJECTIVE: Electrical stimulation induces significant angiogenesis in vivo. We have shown recently that electrical stimulation induces directional migration, reorientation, and elongation of macrovascular endothelial cells. Because angiogenesis occurs mainly in the microvasculature, we have extended this observation to include human microvascular endothelial cells (HMEC-1s) and compared the responses with that of vascular fibroblasts and smooth muscle cells and human umbilical vein endothelial cells. METHODS AND RESULTS: Four types of vascular cells were cultured in electric fields (EFs). Dynamic cell behaviors were recorded and analyzed with an image analyzer. EFs of 150 to 400 mV/mm induced directed migration, reorientation, and elongation of all the vascular cells. HMEC-1s showed the greatest directional migration (migration rate of 11 microm/h and directedness of 0.35 at 200 mV/mm). Most intriguingly, HMEC-1s migrated toward the cathode, whereas the other cell types migrated toward the anode. CONCLUSIONS: Endothelial cells derived from angiogenic microvascular as opposed to nonangiogenic macrovascular tissues were more responsive to electrical stimulation. This intriguing directional selectivity indicates that a DC electrical signal as a directional cue may be able to play a role in the spatial organization of vascular structure.

Animals↗

Serum high-density lipoprotein-cholesterol levels modify the association between plasma levels of oxidatively modified low-density lipoprotein and coronary artery disease in men.

We investigated the association among plasma levels of oxidatively modified low-density lipoprotein (Ox-LDL), high-density lipoprotein-cholesterol (HDL-C), and the prevalence of coronary artery disease (CAD) in a case-control study. Cases (n = 183, male [M]/female [F]:138/45, age: 64.9 +/- 10.6 years) were defined as patients with angiographically proven coronary atherosclerosis (>/=50% stenosis) and controls were subjects with normal coronary arteries (n = 74, M/F:36/38, age: 57.6 +/- 14.4 years). Plasma Ox-LDL levels were measured by a sensitive detection method using the monoclonal antibody DLH3. In women, both Ox-LDL and lipid variables were similar between cases and controls. In men, cases had significantly lower (P <.05) levels of HDL-C (39.1 +/- 10.3 v 42.8 +/- 10.9 mg/dL) and apolipoprotein (apo) A-I than controls, while the difference in Ox-LDL between cases and controls was not significant (1.05 +/- 0.79 and 0.83 +/- 0.65 ng/10 microg LDL protein, respectively). However, HDL-C levels interacted with the association between Ox-LDL levels and CAD in males: increased Ox-LDL levels were significantly associated with CAD after controlling for age when HDL-C levels were high, but were not associated with CAD when HDL-C levels were low, as assessed by a multiple logistic regression analysis. In addition, the combination of HDL-C and Ox-LDL levels was a better indicator for CAD in males than HDL-C levels alone (-2 log likelihood, 24.1 v 19.4) after controlling for age and conventional risk factors of CAD, while Ox-LDL levels were not significantly associated with CAD. HDL-C levels interact with the association between plasma Ox-LDL levels and CAD in men, and increased Ox-LDL levels are an indicator of CAD in male subjects with high HDL-C levels.

Adult↗

[Effects of hypertriglyceridemia on platelet activities in endogenous hypertriglyceridemic patients].

OBJECTIVE: To explore the effects of hypertriglyceridemia on platelet activities. METHODS: The plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fg), blood platelet count (BPC) and platelet alpha granule membrane protein-140 (GMP-140) levels in endogenous hypertriglyceridemic patients were determined, and the relationship between platelet activities and fasting plasma lipids was assessed. RESULTS: It was found that PT, Fg levels, BPC and plasma GMP-140 concentration showed no statistically significant difference between the control and hypertriglyceridemic subjects (P > 0.05). PT was correlated with the levels of plasma BG and apo E (r = 0.500, P = 0.012), the levels of Fg was positively correlated with BG (r = 0.598, P = 0.000), and BPC of HTG subjects was negatively correlated with TG (r = -0.489, P < 0.05). GMP-140 content was positively correlated with the levels of plasma TC and LDL-C (r = 0.647, 0.833, P < 0.01); in HTG patients it was inversely correlated with age and PT (r = -0.480, -0.490, P < 0.05). CONCLUSION: All of these indicated that increasing of coagulation activity in hypertriglyceridemic patients was correlated with dysfunction of plasma lipids and change of apolipoproteins levels. Plasma GMP-140 was not obviously correlated with plasma TG content, but was positively correlated with plasma TC and LDL-C contents.

Aged↗

[Construction of a reverse-subtracted cDNA library for differentially expressed genes in rat liver of prothrombotic state].

OBJECTIVE: To inquire into the mechanism of prothrombotic state (PTS) and the roles of liver therein by constructing a reverse-subtracted cDNA library for differentially expressed genes in rat liver of PTS. METHODS: The reverse-subtracted cDNA library for differentially expressed genes in rat liver of PTS was constructed by suppression subtractive hybridization. The rat model of PTS was induced by a high-carbohydrate diet. Poly A+ mRNAs were isolated from PTS and control rats, and cDNAs were synthesized from the mRNAs. After digestion by means of Ras I, cDNAs 400-600 bp in size were obtained. For suppression subtractive hybridization, cDNAs from PTS rat were used as Driver and the cDNAs from control rat as Tester. The Tester was divided into two parts and ligated to adaptor 1 and adaptor 2R respectively. After two times of subtractive hybridization and two times of nested PCR, the products of the last PCR amplification were inserted into T/A plasmid vectors to transform the Escherichia coli JM109 cells. The transformed cells were incubated at 37 degrees C overnight on a LB agar plate containing ampicillin (50 micrograms/ml), IPTG and X-gal. The colonies were counted. RESULTS: 78% of the colonies were white and the reverse-subtracted cDNA library for differentially expressed genes in rat liver of prothrombotic state was successfully constructed. CONCLUSION: Prothrombotic state caused by malfunction of homeostasis and fibrinolysis is an important risk factor of cardiovascular disease. Liver plays important roles in the development of PTS, for the majority of the factors in the coagulation as well as fibrinolytic cascades are generated by the liver and secreted into the bloodstream. The reverse-subtracted cDNA library for differentially expressed genes in rat liver of PTS, successfully constructed in the present study, provides an efficient way to further investigate the mechanism of PTS and the relevant liver functions.

Animals↗

[Preliminary screening of a reverse-subtracted cDNA library for differentially expressed genes in rat liver of prothrombotic state].

OBJECTIVE: To identify differentially expressed cDNA sequences for rat liver of prothrombotic state (PTS) by screening a reverse-subtracted cDNA library. METHODS: Forward-subtracted cDNA probes and reverse-subtracted cDNA probes were prepared by nested PCR amplification, which were labeled with HRP. Positive clones were selected by differential screening in which forward-subtracted and reverse-subtracted cDNA probes were separately hybridized with the membranes slot-blotted by plasmid DNAs amplified and isolated from the library. Inserts in the positive clones were submitted to DNA sequencing. Nucleic acid sequence homology search was performed against the GenBank DNA database (non-redundant, and non-mouse and non-human EST entries) using the Standard nucleotide-nucleotide BLAST [blastn] program via a network connection to the National Center for Biotechnology information. RESULTS: Five positive clones were found by differential screening. For 3 of the 5 sequences, known genes of high homology (Score>225 bits) in the GenBank DNA database were found. For the other 2 sequences, only genes of low homology (Score=56) or intermediate homology (Score=151) were found. CONCLUSION: Five cDNA sequences were found PTS related. 3 of them may represent the genes that are either identical or nearly identical to previously reported genes The other 2 sequences are most probably new sequences not existing in GenBank DNA database, which have been registered in the GenBank DNA database as new sequences.

Animals↗

[Inhibitory effect of quercetin, rutin and puerarin on HDL oxidation induced by Cu2+].

OBJECTIVE: To evaluate the inhibitory effect of quercetin, rutin and puerarin on the HDL oxidation induced by Cu2+ and to investigate their action on the prevention and cure of atherosclerosis. METHODS: The serum HDL of healthy human was isolated by the one step density gradient ultracentrifugation. The HDL oxidation was induced by Cu2+ in vitro for different time, quercetin and rutin at 5 micromol/L were added ahead, respectively. HDL was oxidized, then identified by A234, REM, TBARS and protein carbonyls content, and was compared with control group. Inhibition of puerarin was weak. RESULTS: (1) A234, REM, TBARS and protein carbonyls formation increased gradually during HDL oxidation induced by Cu2+ in vitro. (2) During HDL oxidation induced by Cu2+ in vitro and incubation with quercetin and rutin, the kinetic changes of A234, REM, TBARS and protein carbonyls formation showed lag phases of 2 h, 2-4 h, 2-4 h and 4 h respectively, and showed reductions by 24.2%-49.0% (P<0.001) and 9.4%-42.0% (P<0.01); 3.0%-25.0% and 4.0%-20.7% (P<0.05); 7.9%-34.1% and 1.2%-26.8% (P<0.05); 28.3%-50.4% and 18.6%-64.6% (P<0.001) respectively. In the puerarin group, only protein carbonyls formation showed a lag phase of 4 h and a reduction by 14.1%-52.1% (P<0.001) while its A234, REM, TBARS reduced to a small extent. CONCLUSION: The above findings suggested that quercetin and rutin inhibit oxidation of HDL significantly, but puerarin has less antioxidative function.

Antioxidants↗

Electrical stimulation directly induces pre-angiogenic responses in vascular endothelial cells by signaling through VEGF receptors.

Controlling angiogenesis is crucial. Growth factors and cytokines are key regulators but a full understanding remains elusive. Endogenous electrical potential differences exist within and around the vasculature, both in relation to blood flow and in situations where active angiogenesis occurs, such as wound healing, development and tumor growth. Recent work shows that electrical stimulation induces significant angiogenesis in vivo, through enhanced vascular endothelial growth factor (VEGF) production by muscle cells. We report that applied electric fields (EFs) of small physiological magnitude directly stimulate VEGF production by endothelial cells in culture without the presence of any other cell type. EFs as low as 75-100 mV mm-1 (1.5-2.0 mV across an endothelial cell) directed the reorientation, elongation and migration of endothelial cells in culture. These pre-angiogenic responses required VEGF receptor activation and were mediated through PI3K-Akt and Rho-ROCK signaling pathways, resulting in reorganization of the actin cytoskeleton. This indicates that endogenous EFs might play a role in angiogenesis in vivo by stimulating the VEGF receptor signaling pathway, to induce key pre-angiogenic responses. In addition, it raises the feasibility of using applied EFs to initiate and guide angiogenesis through direct effects on endothelial cells.

Acute-Phase Proteins↗

[Screening of hypercoagulability-related genes in aorta of hypertriglyceridemic rats].

OBJECTIVE: The aim of this study was to screen hypercoagulability-related genes in aorta of hypertriglyceridemic rats. METHODS: Suppression subtractive hybridization (SSH) was used to construct hypercoagulable rat cDNA subtractive library. Semi-quantitative RT-PCR was applied to identify differentially expressed genes. RESULTS: Hypercoagulable rat cDNA subtractive library had been successfully constructed. Sequence analysis and homology searching of 20 clones showed that these clones represent 19 genes: 8 are known genes newly found to have a relationship to hypercoagulability and 11 are novel genes (ESTs) that had been deposited to GenBank. Three ESTs (HC002, HC057 and HC067) were confirmed to be over-expressed genes by semi-quantitative RT-PCR. CONCLUSION: The constructed subtractive library is highly efficient and has laid a foundation for screening and cloning hypercoagulability-related novel genes of rat, HC002, HC057 and HC067 are probably related to hypercoagulability induced by hypertriglyceridemia.

Animals↗

[Plasma haemostatic and fibrinolytic activities and their relationship to levels of serum lipids and apolipoproteins in endogenous hypertriglyceridemic patients].

OBJECTIVE: To investigate the changes of plasma haemostatic and fibrinolytic activities and their relationship to serum lipids and apolipoproteins levels in endogenous hypertriglyceridemic patients. METHODS: We determined the plasma prothrombin time(PT), activated partial thromplastin time(APTT), activity of tissue-type plasminogen activator(t-PA), activity of plasminogen activator inhibitor-1 (PAI-1) and fibrinogen(Fg) level of 24 endogenous hyper-triglyceridemic patients and 34 healthy controls, and observed their relationship to serum lipids and apolipoproteins. RESULTS: The PT and APTT of patients with hypertriglyceridemia were obviously shorter than those of control subjects (P < 0.01, P < 0.05); PAI-1 of patients was significant higher than that of control group (P < 0.01); there was no statistically significant difference in t-PAI-1: a between the control subjects and the hypertriglyceridemic patients; the levels of Fg in patients was 27% higher than that in healthy control (P < 0.01). The correlation analysis indicated that PT was significantly associated with the levels of plasma HDL-C (r = 0.445, P < 0.01), and inversely associated with the levels of plasma TG, apoC III, BG and BMI (r = -0.294, -0.320, -0.282, -0.272, P < 0.05); APTT was negatively correlated with serum TG and apoC III levels (r = -0.345, -0.320, P < 0.05); t-PA was negatively correlated with BG levels (r = -0.336, P < 0.01). PAI-1 and Fg levels were strongly correlated with serum TG, apoC II, C III and E levels (r = 0.400, 0.408, 0.497, 0.454, P < 0.01 and r = 0.642, 0.581, 0.673, 0.304, P < 0.01, respectively), and negatively correlated with HDL-C (r = -0.366, -0.524, P < 0.01). CONCLUSION: Increasing of coagulating activity and decreasing of fibrinolytic activity in hypertriglyceridemic patients were significantly associated with serum lipids and apolipoproteins levels.

Apolipoproteins↗

[Polymorphism of insulin receptor substrate-1 gene in patients with coronary heart diseases].

OBJECTIVE: To explore the relationship between the polymorphism of insulin receptor substrate-1 (IRS-1) gene and coronary heart diseases in Chinese population. METHODS: A total of 113 patients with coronary heart diseases and 194 healthy Chengdu residents with less than 82 mmol/L of TG and 6.2 mmol/L of TC in fasting serum testing were selected and compared. The genotype and allele frequency of IRS-1 gene polymorphism was assayed by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). The serum lipids were measured by enzymatic kits. RESULTS: The GG genotype dominated in the IRS-1 gene with frequency of 0.960 and 0.985 for patients and healthy controls respectively. Difference appeared in R allele frequency (0.015 for healthy controls and 0.040 for patients, P = 0.05). Patients with genotype G/R had significantly higher level of serum TC and lower level of plasma glucose than patients with genotype G/G (P < 0.05). CONCLUSION: IRS-1 gene polymorphism is associated with coronary heart disease in Chinese population. The G/R and G/G genotype of IRS-1 gene contributes to the increasing of serum cholesterol and plasma glucose respectively.

Aged↗

[Effects of plasma very low density lipoprotein, low density lipoprotein and high density lipoprotein on platelet aggregation in endogenous hypertriglyceridemia].

OBJECTIVE: To study whether plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) were oxidatively modified in endogenous hypertriglyceridemia (HTG) and to investigate the effects of HTG VLDL, LDL and HDL on platelet aggregation in vitro. METHODS: Blood samples were taken from 21 patients with endogenous triglyceridemia and 21 normal healthy subjects; these two groups were similar in respect to age and sex. Their plasma VLDL, LDL and HDL were isolated by density gradient ultracentrifugation method, and plasma triglycerides (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) were measured by enzyme method. The oxidative modification of LDL, VLDL and HDL was identified by agarose gel relative electrophoretic mobility (REM), absorbance at 234 nm (A234) and fluorescence of thiobarbituric acid reaction substances (TBARS). With the reaction system that consisted of mixed fresh normal plasma, platelet aggregation was induced by adenosine diphosphate (ADP), and the platelet maximal aggregation rate (MAR) was recorded on a 4-channel light aggregometer. RESULTS: The plasma TG, TBARS levels in HTG group were 1.6 and 0.4 times over those of the control group respectively (P < 0.01). The plasma HDLC in HTG group was 32% lower than those of the control group (P < 0.01). REM, A234 and TBARS of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group (P < 0.01). MAR of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group (P < 0.05). The correlation analysis indicated that REM, A234 and TBARS of LDL and HDL in HTG group were positively correlated with MAR (P < 0.01). CONCLUSION: The above data indicated that oxidative modification of plasma VLDL, LDL, HDL did occur in endogenous hypertriglyceridemia in vivo, and VLDL, LDL and HDL enhanced platelet aggregation in vitro.

Aged↗

[Study on lipoprotein lipase gene Hind III polymorphism in Chinese type IIb hyperlipoproteinemia].

OBJECTIVE: To investigate whether lipoprotein lipase (LPL) gene Hind III polymorphism is associated with Chinese type IIb hyperlipoproteinemia. METHODS: Lipoprotein lipase gene Hind III polymorphism was studied using polymerase chain reaction (PCR) and restriction fragment length polymorphisms (RFLP) in 103 type IIb hyperlipoproteinemia patients and 129 healthy subjects from a population of Chinese Hans in Chengdu area. RESULTS: Both in type IIb hyperlipoproteinemia group and control group, the H+H+ homozygote was the major allelotype. The H+ allelic frequency of type IIb hyperlipoproteinemia group was higher than that of control group (0.864 vs 0.705, P<0.01). But the H- allelic frequency of type IIb hyperlipoproteinemia group was significantly lower than that of control group (0.136 vs 0.295, P<0.01). The plasma triglycerides (TG) level of H+H+ genotype was significantly higher than that of H+H- and H-H- genotypes (P<0.05 and P<0.01); the plasma TC level and TG/HDL C ratio were higher than those of H+H- and H-H- genotypes (P<0.05); apoA II levels of H+H+ and H+H- genotypes were significantly lower than that of H-H- genotype (P<0.01 and P<0.05). CONCLUSION: The Hind III RFLP at intron 8 of LPL gene is associated with type II b hyperlipoproteinemia to some extent in Chinese population.

Adult↗