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Biomedical subjects

L Miao

Publications and source records attributed to L Miao.

At least 37 records · Page 2Linked to original sources
PubMed1999

Off-lattice model for the phase behavior of lipid-cholesterol bilayers.

Lipid bilayers exhibit a phase behavior that involves two distinct, but coupled, order-disorder processes, one in terms of lipid-chain crystalline packing (translational degrees of freedom) and the other in terms of lipid-chain conformational ordering (internal degrees of freedom). Experiments and previous approximate theories have suggested that cholesterol incorporated into lipid bilayers has different microscopic effects on lipid-chain packing and conformations and that cholesterol thereby leads to decoupling of the two ordering processes, manifested by a special equilibrium phase, "liquid-ordered phase," where bilayers are liquid (with translational disorder) but lipid chains are conformationally ordered. We present in this paper a microscopic model that describes this decoupling phenomena and which yields a phase diagram consistent with experimental observations. The model is an off-lattice model based on a two-dimensional random triangulation algorithm and represents lipid and cholesterol molecules by hard-core particles with internal (spin-type) degrees of freedom that have nearest-neighbor interactions. The phase equilibria described by the model, specifically in terms of phase diagrams and structure factors characterizing different phases, are calculated by using several Monte Carlo simulation techniques, including histogram and thermodynamic reweighting techniques, finite-size scaling as well as non-Boltzmann sampling techniques (in order to overcome severe hysteresis effects associated with strongly first-order phase transitions). The results provide a consistent interpretation of the various phases of phospholipid-cholesterol binary mixtures based on the microscopic dual action of cholesterol on the lipid-chain degrees of freedom. In particular, a distinct small-scale structure of the liquid-ordered phase has been identified and characterized. The generic nature of the model proposed holds a promise for a unifying description for a whole series of different lipid-sterol mixtures.

Journal Article↗
PubMed1999

[Nested polymerase chain reaction in detecting Mycobacterium tuberculosis DNA in bioptic tissue from patients with endobronchial tuberculosis].

OBJECTIVE: To evaluate the nested polymerase chain reaction (NPCR) technique in diagnosing endobronchial tuberculosis. METHODS: NPCR method was used to detect Mycobacterium tuberculosis DNA in bioptic tissue from 67 patients with endobronchial tuberculosis, and the results were compared with pathologic examination, brushing smear, sputum smear and culture for Mycobacterium tuberculosis after bronchoscopy. The controls were 43 patients with lung cancer. RESULTS: The positive rates of detecting Mycobacterium tuberculosis were 13%, 19%, 22%, 15% and 76% respectively by pathologic examination, brushing smear, sputum smear, culture after bronchoscopy and NPCR methods. Significant differences were found between NPCR and the other 4 methods (all Ps < 0.01). No positive result for Mycobacterium tuberculosis was found in 43 controls by NPCR. CONCLUSIONS: NPCR is a useful method for diagnosing patients with endobronchial tuberculosis, especially for those with normal demonstration in X-ray chest film, negative sputum and nonspecific pathologic changes in endobronchial biopsy.

Biopsy↗
PubMed1998

The comparative trial of TCu 380A IUD and progesterone-releasing vaginal ring used by lactating women.

The objective of this paper was to compare the efficacy, acceptability, safety, and bleeding pattern of TCu 380A intrauterine device (IUD) and progesterone-releasing vaginal ring used by breastfeeding women. The study population included 97 breastfeeding women using IUD and 100 women using vaginal ring. Of the IUD users, no insertion failure, perforation, or accidental pregnancy occurred in 12 months. There was one IUD expulsion. There were no discontinuations of IUD due to medical reasons other than expulsion. The total discontinuation rate was 2.3%. In the ring group, no accidental pregnancy occurred. The major reasons for discontinuation were ring use-related problems and vaginal problems. The total discontinuation rate was 65.4% within 1 year. The frequency of any one complaint among the ring users was higher than that among the IUD users. There were no differences in the proportion of women having no sexual activity and in the weight of their babies between the two groups. Compared with the IUD users, the median number of bleeding/spotting (B/S) episodes and B/S days of the vaginal ring users were fewer; consequently, the mean length of B/S-free interval was longer in all four reference periods; the mean length of B/S episode and segment were the same; the occurrence of amenorrhea was more frequent; in contrast, the proportions of normal bleeding patterns were fewer. The frequencies of prolonged bleeding, frequent bleeding, and infrequent bleeding patterns did not differ between the two groups. The percentage of irregular bleeding was fewer only in the first two reference periods. It is concluded that the TCu 380A IUD and progesterone-releasing vaginal ring used by breastfeeding women are safe and effective. The higher discontinuation rate of the ring users was mainly because of use-related problems. Breastfeeding women with TCu 380A IUD had better tolerance and acceptability. The TCu 380A IUD does not, but the progesterone-releasing vaginal ring does, suppress the recovery of ovarian function. However, once return of menstruation occurred, there were no differences in bleeding patterns between the two contraceptive methods.

Administration, Intravaginal↗
PubMed1998

[Study of the liver changes by B-ultrasound and histopathology in severe pregnancy induced hypertension].

OBJECTIVE: To investigate the liver changes in severe pregnancy induced hypertension (PIH) on B-ultrasound and pathological examination and to detect a possible connection with fatty liver of pregnancy. METHODS: From Jan 1992 to Nov 1997, 90 pregnant women in the third trimester were enrolled for study. They were divided into 3 groups: the pregnant women with liver diseases; mild and moderate PIH; and severe PIH (30 cases each). Ultrasonography of the liver was performed on each patient after admission. 15 percutaneous liver biopsies were performed under the guidance of real-time ultrasound scans on 15 severe PIH patients with or without liver dysfunction. Tissues were stained with specific lipid staining (Sudan) and with hematoxylin-eosin. All specimens were analyzed by light microscopy. RESULTS: Fatty liver was observed by B-ultrasound in 2 and 12 cases of the pregnancy with liver diseases group and the severe PIH group, respectively. 14 of the 15 liver biopsy specimens showed fatty infiltration of varying degrees. however, only 8 of the 14 cases were detected fatty liver by B-ultrasound. CONCLUSIONS: These findings suggest that liver involvement in severe PIH is a pathological change. Severe PIH and acute fatty liver in pregnancy could have related pathogenesis components of the same.

Adult↗
PubMed1998

Clinical study on reservation of part of stomach for patients with cardiac cancer of the gastric stump.

OBJECTIVE: To explore the clinical significance of the resection of the cardia and fundus for patients suffering from cardiac cancer of the gastric stump. METHODS: Twenty-five patients suffering from cardiac cancer with a mean period of 13 years and 3 months after subtotal gastrectomy were included in this study. Their average age was 59.1 years. Among them, 19 patients got exploratory thoracotomy. RESULTS: Of the 19 patients, 1 was inoperable, 1 underwent resection of the gastric stump and esophagojejunostomy because of his huge tumor, 17 underwent resection of the cardia and fundus of the gastric stump and accepted gastroesophagostomy (9 were subjected to tunnel gastroesophagostomy and 8 to end-to-end esophagogastrostomy). The largest tumor was 5 cm x 4 cm in size. Except for a death resulting from intestinal obstruction following operation, the others attained a good recovery. The longest period of survival was 4.5 years. CONCLUSIONS: Resection of the cardia and fundus and gastroesophagostomy can be carried out for patients suffering from cardiac cancer of the gastric stump. The method is in line with the principle of the conservation surgery.

Adenocarcinoma↗
PubMed1997

Mechanisms of positive inotropic action of flosequinan, hydralazine, and milrinone on mammalian myocardium.

Flosequinan is an arterial and venous dilator that also has a positive inotropic effect at relatively higher doses. The purpose of this study was to determine the mechanism of this positive inotropic effect in ferret papillary muscles loaded with the Ca2+ indicator, aequorin. Over the range of doses from 10(-6) to 10(-3) M, flosequinan produced a 61 +/- 9% increase in peak tension that was accompanied by a corresponding increase in [Ca2+]i. This positive inotropic effect was not selectively blocked by addition to the perfusate of procaine 0.6 microM, tetrodotoxin 10(-6) M or by verapamil, 5 x 10(-8) M. In contrast, the positive inotropic effect of flosequinan, but not milrinone or hydralazine, was potentiated by prior addition of ouabain 3 nM to enhance intracellular Ca2+ via reduction of the Na+/Ca2+ exchange. Moreover, antagonists of Na+/Ca2+ exchange, including cadmium 10 microM, amiloride 600 microM and choline substitution for 1/3 Na+ in the perfusate, blocked the response to flosequinan but not hydralazine or milrinone. These results indicate that flosequinan produces a positive inotropic effect by reduction of Na+/Ca2+ exchange in mammalian myocardium. Moreover, flosequinan has the potential to interact synergistically with other positive inotropic agents such as digoxin that affect Na+/Ca2+ exchange by direct or indirect actions.

Aequorin↗
PubMed1997

Efficient adenovirus-mediated ectopic gene expression of human lipoprotein lipase in human hepatic (HepG2) cells.

Gene therapy to deliver and express a corrective lipoprotein lipase (LPL) gene may improve the lipid profile and reduce the morbidity and potential atherogenic risk from hypertriglyceridemia and dyslipoproteinemia in patients with complete or partial LPL deficiency. We have used an E1-/E3- adenoviral vector, with an RSV-driven human LPL cDNA expression cassette (Ad-RSV-LPL), to achieve high ectopic LPL gene expression in the human hepatoma cell line HepG2, an accepted hepatocellular model of lipoprotein metabolism. Ad-RSV-LPL transduction of HepG2 cells with a multiplicity of infection (moi) between 12.5 and 100 yielded dose-dependent increments in LPL mass and activity. Peak levels of LPL protein of 2,032.1 +/- 274.5 ng/10(5) cells per ml (mol 100) correlated with increased activity of 92.7 +/- 22.6 mU/10(5) cells per ml relative to negligible LPL levels in Ad-RSV-LacZ (beta-galactosidase) controls. Exogenous LPL expression over a 5-day period peaked at day 3. Susceptibility to inhibition by 1 M NaCl and an anti-LPL monoclonal antibody confirmed that lipase activity was indeed derived from human LPL. Hydrolysis, by LPL-overexpressing HepG2 cells, of TG carried in very-low-density lipoprotein (VLDL) showed that greater than 50% of the triglycerides (TG) disappeared after 4 hr of incubation. These results were compatible with FPLC evidence of a marked reduction in VLDL-TG. These results provide strong in vitro evidence that adenoviral-mediated ectopic expression of the human LPL gene could render hepatic cells capable of VLDL catabolism and thus support the possibility for in vivo adenoviral vector-mediated liver-targeted LPL gene therapy.

Adenoviridae↗
PubMed1997

Cholesterol supplementation prevents necrosis and inflammation but enhances fibrosis in alcoholic liver disease in the rat.

Based on studies that show a role for the low-density lipoprotein (LDL)-receptor in arachidonic acid delivery and eicosanoid synthesis in macrophages, the present study investigated the effect of cholesterol supplementation on pathological changes and thromboxane (TX) synthesis in alcoholic liver injury. Male Wistar rats were intragastrically fed ethanol with either corn oil or fish oil for 1 month. Control rats received isocaloric amounts of dextrose instead of ethanol. An additional group of rats fed either ethanol or dextrose with fish oil or corn oil were supplemented with 1% cholesterol. At the time of killing, all rats had the following evaluated: liver histopathology, lipid peroxidation, liver and plasma thromboxane levels, plasma endotoxin and messenger RNA (mRNA) levels of LDL-receptor, tumor necrosis factor alpha (TNF-alpha), cyclooxygenase (Cox)-1 and -2, and transforming growth factor beta (TGF-beta). Rats fed ethanol with either fish oil or corn oil developed fatty liver, necrosis, inflammation, and central vein collagen deposition. Cholesterol supplementation enhanced the degree of fibrosis but prevented necrosis and inflammation. These alterations in pathological changes by cholesterol were accompanied by absent TNF-alpha and Cox-2 mRNAs, decreased thromboxane levels, decreased lipid peroxidation, and increased TGF-beta mRNA. Cholesterol enrichment of the diet thus decreases proinflammatory components, but enhances fibrosis in ethanol-fed rats.

Animals↗
PubMed1997

Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease in the rat.

We investigated the potential of dietary saturated fatty acids to decrease endotoxemia and suppress expression of cyclooxygenase 2 (Cox-2) and tumor necrosis factor alpha (TNF-alpha) in established alcohol-induced liver injury. Six groups (five rats/group) of male Wistar rats were studied. Rats in group 1 were fed a fish oil-ethanol diet for 6 weeks. Rats in groups 2, 3, and 4 were fed fish oil and ethanol for 6 weeks. Ethanol administration was stopped at this time, and the rats were switched to isocaloric diets containing dextrose with fish oil (group 2), palm oil (group 3), or medium-chain triglycerides (group 4) as the source of fat for an additional 2 weeks. Rats in groups 5 and 6 were fed fish oil-ethanol and fish oil-dextrose, respectively, for 8 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, and levels of messenger RNA (mRNA) for Cox-2 and TNF-alpha. Concentrations of endotoxin were determined in plasma. The most severe inflammation and fibrosis were detected in groups 1 and 5, as were the highest levels of endotoxin, lipid peroxidation, and mRNA for Cox-2 and TNF-alpha. After ethanol was discontinued, there was minimal histological improvement in group 2 but near normalization of the histology, including regression of fibrosis, in groups 3 and 4. Histological improvement was associated with decreased levels of endotoxin, lipid peroxidation, and reduced expression of Cox-2 and TNF-alpha. The data indicate that a diet enriched in saturated fatty acids (groups 3 and 4) effectively reverses alcohol-induced liver injury, including fibrosis. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation, which in turn result in decreased levels of TNF-alpha and Cox-2.

Animals↗
PubMed1997

Thromboxane inhibitors attenuate pathological changes in alcoholic liver disease in the rat.

BACKGROUND & AIMS: Thromboxane levels correlate with severity of liver injury in rats given alcohol. The aim of this study was to evaluate the effect of thromboxane inhibitors on pathological changes in experimental alcoholic liver disease. METHODS: Male Wistar rats were given a liquid diet and ethanol intragastrically for 1 month. The thromboxane inhibitors tested were a thromboxane receptor antagonist (TXRA) and a thromboxane synthase inhibitor (TXSI). Pathological changes, liver and plasma thromboxane levels, 6-ketoprostaglandin F1 alpha levels, lipid peroxidation, and messenger RNA levels for tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF) beta were evaluated. RESULTS: Treatment with thromboxane inhibitors prevented necrosis and inflammation. In the TXSI-treated group, fatty liver was also decreased. Ethanol administration led to a 3-4-fold increase in liver thromboxane levels; a reduction in thromboxane levels and lipid peroxidation was seen in the TXSI group. In all treatment groups, TNF-alpha and TGF-beta messenger RNA levels were decreased. CONCLUSIONS: The prevention of necroinflammatory changes in thromboxane-treated groups is related to a decrease in TNF-alpha levels. Inhibition of TGF-beta expression may also prevent fibrosis in ethanol-treated rats.

Animals↗
PubMed1997

Enhanced cyclooxygenase-2 gene expression in alcoholic liver disease in the rat.

BACKGROUND & AIMS: Inflammatory stimuli and lipid peroxidation up-regulate cyclooxygenase (COX)-2. This study evaluated the relationship between inflammatory mediators, COX expression, and pathological changes in experimental alcoholic liver disease. METHODS: Rats (5 per group) were fed ethanol and a diet containing saturated fat, corn oil, or fish oil by intragastric infusion. Dextrose isocalorically replaced ethanol in controls. In the first set of experiments, whole livers were analyzed. In the second set of experiments, Kupffer cells, endothelial cells, and hepatocytes were isolated from rats in each group. Pathological analyses and measurements of lipid peroxidation, tumor necrosis factor (TNF)-alpha, COX-1 and COX-2 messenger RNA (mRNA), endotoxin, and liver and plasma thromboxane were performed. RESULTS: Increased expression of COX-2 mRNA was detected in the livers of rats showing necroinflammatory changes. The Kupffer cell was the cell primarily responsible for the increase in COX-2 mRNA level. Increased expression of COX-2 was associated with increased levels of endotoxin, TNF-alpha mRNA, lipid peroxidation, and synthesis of thromboxane. COX-1 mRNA was decreased in Kupffer cells in rats with the most severe liver injury. CONCLUSIONS: Up-regulation of COX-2 in alcoholic liver injury occurred in the presence of proinflammatory stimuli and resulted in increased synthesis of inflammatory and vasoactive eicosanoids. Down-regulation of COX-1 may result in decreased synthesis of cytoprotective eicosanoids and additionally exacerbate liver injury.

Animals↗
PubMed1997

Acute and chronic cocaine exposure can produce myocardial ischemia and infarction in Yucatan swine.

The purpose of this study was to determine whether the acute and chronic administration of cocaine could induce myocardial infarction. Twenty-five minipigs were studied before and 4 months after balloon angioplasty of the left anterior descending artery (LAD) and balloon denudation of the left circumflex artery (LCx). Minipigs received cocaine in the initial and in the 4-month study (0.1, 0.5, and 3 mg/kg i.v.). Minipigs were randomized to group I (high-cholesterol diet + daily cocaine; 500 mg i.m.; n = 8), group II (high-cholesterol diet + no i.v. cocaine; n = 5), group III (chow diet + daily cocaine; 500 mg i.m.; n = 6), group IV (chow diet + no i.v. or i.m. cocaine; n = 6). In vivo, coronary flow significantly decreased and vascular resistance significantly increased after the administration of cocaine. Histamine significantly decreased the luminal diameters (LAD and LCx) in groups I, II and III. There were a total of five acute and 16 chronic infarctions among the three groups that received either short- or long-term cocaine; however, no infarct occurred in group IV. The combination of daily cocaine abuse with a cholesterol-rich diet enhanced coronary vasoreactivity in vivo and in vitro. We conclude that long-term or sporadic cocaine abuse can induce myocardial infarction.

Animals↗
PubMed1997

Correction of hypertriglyceridemia and impaired fat tolerance in lipoprotein lipase-deficient mice by adenovirus-mediated expression of human lipoprotein lipase.

Humans homozygous or heterozygous for mutations in the lipoprotein lipase (LPL) gene demonstrate significant disturbances in plasma lipoproteins, including raised triglyceride (TG) and reduced HDL cholesterol levels. In this study we explored the feasibility of adenovirus-mediated gene replacement therapy for LPL deficiency. A total of 5 x 10(9) plaque-forming units (pfu) of an E1/E3-deleted adenovirus expressing either human LPL (Ad-LPL) or the bacterial beta-galactosidase gene (Ad-LacZ) as a control were administered to mice heterozygous for targeted disruption in the LPL gene (n = 57). Peak expression of total postheparin plasma LPL activity was observed at day 7 in Ad-LPL mice versus Ad-LacZ controls (834 +/- 133 vs 313 +/- 89 mU/mL, P < .01), and correlated with human-specific LPL activity (522 +/- 219 mU/mL) and mass (9214 +/- 782 ng/mL), a change that was significant to 14 and 42 days, respectively. At day 7, plasma TGs were significantly reduced relative to Ad-LacZ mice (0.17 +/- 0.07 vs 1.90 +/- 0.89 mmol/L, P < .01) but returned to endogenous levels by day 42. Ectopic liver expression of human LPL was confirmed by in situ hybridization analysis and from raised LPL activity and mass in liver homogenates. Analysis of plasma lipoprotein composition revealed a marked decrease in VLDL-derived TGs. Severely impaired oral and intravenous fat-load tolerance in LPL-deficient mice was subsequently corrected after Ad-LPL administration and closely paralleled that observed in wild-type mice. These findings suggest that liver-targeted adenovirus-mediated LPL gene transfer offers an effective means for transient correction of altered lipoprotein metabolism and impaired fat tolerance due to LPL deficiency.

Adenoviridae↗
PubMed1997

Ethnic variation and in vivo effects of the -93t-->g promoter variant in the lipoprotein lipase gene.

Recently, a (t-->g) transition at nucleotide -93 in the lipoprotein lipase (LPL) gene promoter has been observed in Caucasians. Here, we have compared the frequency of the -93g carriers in three distinct populations (Caucasians, South African Blacks, and Chinese). The carrier frequency in the Caucasian population was 1.7% (4/232), which was in contrast to the South African Black population, which had a frequency for this allele of 76.4% (123/161) of the individuals tested. This transition was not observed in the Chinese population under study. Near complete linkage disequilibrium between the -93g and the previously described D9N mutation was observed in the Caucasian population but not in South African Blacks. To further assess the ancestral origins of these DNA changes, DNA haplotyping using a CA repeat 5' to these substitutions was performed. The -93t allele was associated with only a few specific dinucleotide repeat sizes. In contrast, the -93g allele occurred on chromosomes with many different repeat lengths. The broad distribution of repeats on -93g carrying chromosomes, their high frequency in the South African Black population, and the conservation of the -93g allele among different species may suggest that the -93g allele is the ancestral allele on which a transition to t and the D9N mutations arose. The very high frequency of the -93g allele distinct from the N9 allele in a cohort of Black South Africans allowed us to specifically assess the phenotypic effects of the -93g allele on lipids. Individuals homozygous for the g allele at -93 showed mildly decreased triglycerides compared with individuals homozygous for the t allele (1.14 +/- 0.66 mmol/L versus 0.82 +/- 0.3; P = .04). Thus, the -93g allele in this cohort is associated with low plasma triglyceride levels.

Adult↗
PubMed1997

[Brain dialysis--a new technique for determining the release of neurotransmitters and neuropeptides].

Brain dialysis, also called microdialysis, is a new technique based on the push-pull cannula. It can be used for continuously perfusing and collecting perfusate of certain brain areas in freely moving animals. Coupled with high performance liquid chromatography (HPLC) and radioimmunoassay (RIA), brain dialysis is allowed to determine the extracellular changes of many neurotransmitters in the brain, such as acetylcholine, noradrenaline, dopamine, 5-HT and their metabolites, free amino acids, small peptides, phosphoethanolamine, vitamins, various ions and so on.

Acetylcholine↗
PubMed1997

[Subperiosteal implantation of block coral on the rabbit cavarial bone].

The aim of this study was to evaluate osteoconductive effect of coral implanted on surface of the cortical bone. The 2 mm thick block corals were implanted on the surface of one side of rabbits cavarial bone, the another side were used as blank control. The specimen was examined by light microscopy, histometry and scanning electron microscopy at 2, 4, 8, 12 weeks after operation respectively. The results show that the new bone growth into the pore of the coral at 2 weeks after implantation. The coral was progressively absorbed and replaced by new bone. Up to 12 weeks, most of the coral was absorbed and newly formed bone had been remodeled. The reconstructed height of new bone in coral group was significantly higher than that of blank control and lower than the thickness of block coral. The study demonstrated good osteoconductive property of coral implanted on surface of cortical bone.

Animals↗
PubMed1997

Relationship between lipoprotein lipase and high density lipoprotein cholesterol in mice: modulation by cholesteryl ester transfer protein and dietary status.

Plasma lipoprotein lipase (LPL) activity correlates with high density lipoprotein (HDL) cholesterol levels in humans. However, in several mouse models created either through transgenesis or targeted inactivation of LPL, no significant changes in HDL cholesterol values have been evident. One possible explanation for this species difference could be the absence of plasma cholesteryl ester transfer protein (CETP) activity in mice. To explore this possibility and further investigate interactions between LPL and CETP modulating HDL cholesterol levels in vivo, we examined the relationship between LPL activity and HDL levels in mice expressing the simian CETP transgene, compared with littermates not carrying the CETP gene. On a chow diet, increasing LPL activity was associated with a trend towards increased HDL levels (51 +/- 29 vs. 31 +/- 4 mg/dL highest vs. lowest tertiles of LPL activity, P = 0.07) in mice expressing CETP, while no such effects were seen in the absence of CETP (65 +/- 12 vs. 61 +/- 15 mg/ dL). Furthermore, in the presence of CETP, a significant positive correlation between LPL activity and HDL cholesterol was evident (r = 0.15, P = 0.006), while in the absence of CETP no such correlation was detected (r = 0.15, P = 0.36), highlighting the interactions between LPL and CETP in vivo. When mice were challenged with a high fat, high carbohydrate diet, strong correlations between LPL activity and HDL cholesterol were seen in both the presence (r = 0.45, P = 0.03) and absence (r = 0.73, P < 0.001) of CETP. Therefore, under altered metabolic contexts, such as those induced by dietary challenge, the relation between LPL activity and HDL cholesterol may also become evident. Here we have shown that both genetic and environmental factors may modulate the association between LPL activity and HDL cholesterol, and provide explanations for the absence of any changes in HDL values in mice either transgenic or with targeted disruption of the LPL gene.

Animals↗