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Biomedical subjects

M Gao

Publications and source records attributed to M Gao.

At least 55 records · Page 3Linked to original sources
PubMed2001

Root mucilage from pea and its utilization by rhizosphere bacteria as a sole carbon source.

Plant roots secrete a complex polysaccharide mucilage that may provide a significant source of carbon for microbes that colonize the rhizosphere. High molecular weight mucilage was separated by high-pressure liquid chromatography gel filtration from low molecular weight components of pea root exudate. Purified pea root mucilage generally was similar in sugar and glycosidic linkage composition to mucilage from cowpea, wheat, rice, and maize, but appeared to contain an unusually high amount of material that was similar to arabinogalactan protein. Purified pea mucilage was used as the sole carbon source for growth of several pea rhizosphere bacteria, including Rhizobium leguminosarum 8401 and 4292, Burkholderia cepacia AMMD, and Pseudomonas fluorescens PRA25. These species grew on mucilage to cell densities of three- to 25-fold higher than controls with no added carbon source, with cell densities of 1 to 15% of those obtained on an equal weight of glucose. Micromolar concentrations of nod gene-inducing flavonoids specifically stimulated mucilage-dependent growth of R. leguminosarum 8401 to levels almost equaling the glucose controls. R. leguminosarum 8401 was able to hydrolyze p-nitrophenyl glycosides of various sugars and partially utilize a number of purified plant polysaccharides as sole carbon sources, indicating that R. leguminosarum 8401 can make an unexpected variety of carbohydrases, in accordance with its ability to extensively utilize pea root mucilage.

Amino Acids↗
PubMed2001

Knockout of an azorhizobial dTDP-L-rhamnose synthase affects lipopolysaccharide and extracellular polysaccharide production and disables symbiosis with Sesbania rostrata.

A nonpolar mutation was made in the oac2 gene of Azorhizobium caulinodans. oac2 is an ortholog of the Salmonella typhimurium rfbD gene that encodes a dTDP-L-rhamnose synthase. The knockout of oac2 changed the lipopolysaccharide (LPS) pattern and affected the extracellular polysaccharide production but had no effect on bacterial hydrophobicity. Upon hot phenol extraction, the wild-type LPS partitioned in the phenol phase. The LPS fraction of ORS571-oac2 partitioned in the water phase and had a reduced rhamnose content and truncated LPS molecules on the basis of faster migration in detergent gel electrophoresis. Strain ORS571-oac2 induced ineffective nodule-like structures on Sesbania rostrata. There was no clear demarcation between central and peripheral tissues, and neither leghemoglobin nor bacteroids were present. Light and electron microscopy revealed that the mutant bacteria were retained in enlarged, thick-walled infection threads. Infection centers emitted a blue autofluorescence under UV light. The data indicate that rhamnose synthesis is important for the production of surface carbohydrates that are required to sustain the compatible interaction between A. caulinodans and S. rostrata.

Azorhizobium caulinodans↗
PubMed2001

Impairment of endothelial function after a high-fat meal in patients with coronary artery disease.

OBJECTIVE: To determine the effect of postprandial lipid changes on endothelial function in patients with coronary artery disease (CAD) after a high-fat meal. METHODS: We studied 50 CAD patients and 25 control participants, who were all normocholesterolemic. Flow-mediated vasodilatation of the brachial artery was evaluated by the high-resolution ultrasound technique before and after a single high-fat meal (800 calories; 50 g fat). RESULTS: Postprandial serum triglyceride level increased significantly at 2-7 h and mean flow-mediated vasodilatation was impaired significantly (from 4.22 +/- 0.44 to 2.75 +/- 0.33%, P < 0.01) for 75 subjects. The increment in 2 h serum triglyceride level correlated positively with the decrement in postprandial flow-mediated vasodilatation (r = 0.459, P < 0.01). Postprandial triglyceride level was significantly higher in CAD patients than in control participants. Flow-mediated vasodilatation was significantly impaired in CAD patients (from 3.04 +/- 0.39 to 1.69 +/- 0.23%, P < 0.01) and control participants (from 6.58 +/- 0.52 to 4.87 +/- 0.19%, P < 0.05) after a high-fat meal. The impairment of flow-mediated dilatation was more severe in CAD patients (44.41%) than in control participants (25.99%, P < 0.01). CONCLUSION: Postprandial endothelium-dependent vasodilatation after a single high-fat meal was severely impaired in normocholesterolemic CAD patients and control participants. The disordered postprandial metabolism of triglyceride-rich lipoproteins may play an atherogenic role by inducing endothelial dysfunction.

Adult↗
PubMed2001

Herpes simplex virus DNA cleavage and packaging proteins associate with the procapsid prior to its maturation.

Packaging of DNA into preformed capsids is a fundamental early event in the assembly of herpes simplex virus type 1 (HSV-1) virions. Replicated viral DNA genomes, in the form of complex branched concatemers, and unstable spherical precursor capsids termed procapsids are thought to be the substrates for the DNA-packaging reaction. In addition, seven viral proteins are required for packaging, although their individual functions are undefined. By analogy to well-characterized bacteriophage systems, the association of these proteins with various forms of capsids, including procapsids, might be expected to clarify their roles in the packaging process. While the HSV-1 UL6, UL15, UL25, and UL28 packaging proteins are known to associate with different forms of stable capsids, their association with procapsids has not been tested. Therefore, we isolated HSV-1 procapsids from infected cells and used Western blotting to identify the packaging proteins present. Procapsids contained UL15 and UL28 proteins; the levels of both proteins are diminished in more mature DNA-containing C-capsids. In contrast, UL6 protein levels were approximately the same in procapsids, B-capsids, and C-capsids. The amount of UL25 protein was reduced in procapsids relative to that in more mature B-capsids. Moreover, C-capsids contained the highest level of UL25 protein, 15-fold higher than that in procapsids. Our results support current hypotheses on HSV DNA packaging: (i) transient association of UL15 and UL28 proteins with maturing capsids is consistent with their proposed involvement in site-specific cleavage of the viral DNA (terminase activity); (ii) the UL6 protein may be an integral component of the capsid shell; and (iii) the UL25 protein may associate with capsids after scaffold loss and DNA packaging, sealing the DNA within capsids.

Animals↗
PubMed2001

The multisubstrate adapter Gab1 regulates hepatocyte growth factor (scatter factor)-c-Met signaling for cell survival and DNA repair.

Hepatocyte growth factor (scatter factor) (HGF/SF) is a pleiotrophic mediator of epithelial cell motility, morphogenesis, angiogenesis, and tumorigenesis. HGF/SF protects cells against DNA damage by a pathway from its receptor c-Met to phosphatidylinositol 3-kinase (PI3K) to c-Akt, resulting in enhanced DNA repair and decreased apoptosis. We now show that protection against the DNA-damaging agent adriamycin (ADR; topoisomerase IIalpha inhibitor) requires the Grb2-binding site of c-Met, and overexpression of the Grb2-associated binder Gab1 (a multisubstrate adapter required for epithelial morphogenesis) inhibits the ability of HGF/SF to protect MDCK epithelial cells against ADR. In contrast to Gab1 and its homolog Gab2, overexpression of c-Cb1, another multisubstrate adapter that associates with c-Met, did not affect protection. Gab1 blocked the ability of HGF/SF to cause the sustained activation of c-Akt and c-Akt signaling (FKHR phosphorylation). The Gab1 inhibition of sustained c-Akt activation and of cell protection did not require the Gab1 pleckstrin homology or SHP2 phosphatase-binding domain but did require the PI3K-binding domain. HGF/SF protection of parental MDCK cells was blocked by wortmannin, expression of PTEN, and dominant negative mutants of p85 (regulatory subunit of PI3K), Akt, and Pak1; the protection of cells overexpressing Gab1 was restored by wild-type or activated mutants of p85, Akt, and Pak1. These findings suggest that the adapter Gab1 may redirect c-Met signaling through PI3K away from a c-Akt/Pak1 cell survival pathway.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Tumor necrosis factor-related apoptosis-inducing ligand and chemotherapy cooperate to induce apoptosis in mesothelioma cell lines.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in certain tumor cells. In addition, TRAIL and chemotherapy can act cooperatively, possibly as a result of chemotherapy-induced increases in expression of a TRAIL receptor, DR5. We used cell lines derived from a highly chemoresistant tumor, malignant mesothelioma, to learn whether TRAIL was effective alone or together with chemotherapy and whether cooperativity depended on increases in DR5 expression. TRAIL (codons 95-285) was expressed in a bacterial expression vector and purified by nickel affinity chromatography. TRAIL alone (25 to 500 ng/ml) had little effect on mesothelioma cells. TRAIL plus chemotherapy (doxorubicin, cis-platinum, etoposide, or gemcitabine) acted cooperatively to induce apoptosis in mesothelioma cells (M28, REN, VAMT, and MS-1). For example, in M28 cells treated for 18 h, apoptosis from TRAIL (100 ng/ml) plus doxorubicin (0.6 microg/ml; 71 +/- 11%) greatly exceeded that from TRAIL alone (21 +/- 8%) or from doxorubicin alone (6 +/- 2%) (means +/- standard deviation; P < 0.03). Mesothelioma cells treated with chemotherapy showed no change in DR5 protein by Western analysis or by immunocytochemistry. TRAIL plus chemotherapy was associated with an increase in mitochondrial cytochrome c release and mitochondrial depolarization. We conclude that TRAIL and chemotherapy act cooperatively to kill mesothelioma cell lines, not by increases in DR5 receptor but in association with mitochondrial amplification of apoptotic signals.

Antineoplastic Agents↗
PubMed2001

Electric field directed layer-by-layer assembly of highly fluorescent CdTe nanoparticles.

An electric field directed layer-by-layer assembly technique has been developed by combining electrophoretic deposition and the layer-by-layer self-assembly method. This technique is employed to realize spatially selective deposition of CdTe nanoparticles on electrodes of indium-tin oxide (ITO). The fluorescence measurements prove that the selectivity of the film deposition increases against applied voltage and reaches 99% when the voltage is 1.4 V. Upon further increase of the voltage, the selectivity slightly decreases. This decrease occurs because high voltage leads to a degradation of CdTe particles and thus reduces fluorescence intensity of the resultant CdTe film. However, fluorescence investigation indicates that a spacer layer of polyelectrolyte complex between the ITO electrode and the CdTe film is useful to protect the CdTe from being destroyed under high voltages.

Ammonium Chloride↗
PubMed2001

Poly(A)-binding proteins regulate both mRNA deadenylation and decapping in yeast cytoplasmic extracts.

The pathway of mRNA degradation has been extensively studied in the yeast, Saccharomyces cerevisiae, and it is now clear that many mRNAs decay by a deadenylation-dependent mechanism. Although several of the factors required for mRNA decay have been identified, the regulation and precise roles of many of the proteins involved remains unclear. We have developed an in vitro system that recapitulates both the deadenylation and the decapping steps of mRNA decay. Furthermore, both deadenylation and decapping are inhibited by poly(A) binding proteins in our assay. Our system has allowed us to separate the decay process from translation and we have shown that the poly(A) tail is capable of inhibiting decapping in an eIF4E-independent manner. Our in vitro system should prove invaluable in dissecting the mechanisms of mRNA turnover.

Adenine↗
PubMed2001

Interaction of hypertension and diabetes on impairment of endothelial function.

OBJECTIVE: To investigate whether the interaction of hypertension and diabetes aggravates endothelial dysfunction and leads to smooth muscle dysfunction. METHODS: Noninvasive methods were used to the investigated patients with type 2 diabetes mellitus (2-DM) (Group 1), patients with hypertension (Group 2) and patients with both 2-DM and hypertension (Group 3), as well as a normal control group (Group 4) by studying a brachial artery without evidence of atherosclerotic plaque formation. RESULTS: Results showed that endothelium-dependent vasodilation decreased significantly in Group 1 (5.74% +/- 3.32%, P < 0.05), Group 2 (4.14% +/- 2.93%, P < 0.01), and Group 3 (2.78% +/- 2.08%, P < 0.001) as compared to the control (9.45% +/- 3.88%). The nitroglycerin-induced vasodilation (smooth muscle function) in Group 3 was significantly decreased as compared to the control group (14.11% +/- 4.63% vs 23.53% +/- 6.77%, P < 0.001), but there were no differences in nitroglycerin-induced vasodilation between Group 1, Group 2 and Group 4. On univariate analysis, a reduced vasodilator response to nitroglycerin was associated with endothelium-dependent vasodilation (r = 0.54, P < 0.001). CONCLUSION: Our results indicate that the interaction of 2-DM and hypertension aggravates endothelial dysfunction and further impairs the smooth muscle function.

Aged↗
PubMed2001

[A study of the correlation between p16 protein expression and DNA quantitative analysis in human gastric carcinoma cells].

OBJECTIVE: To investigate p16 protein expression and its correlation with DNA quantity in gastric carcinoma (GC) cells. METHODS: p16 protein expression was quantitatively determined by flow cytometry (FCM) in 41 cases of GC and 10 cases of normal gastric tissues. DNA quantitative analysis of 41 cases of GC was performed by image cytometry (ICM). RESULTS: p16 protein expression in GC was significantly lower than that in normal gastric tissues (respective FI: 0.81 plus minus 0.09 and 1.00 plus minus 0.11, P < 0.01). The expression of p16 protein did not show correlation with such factors as sex and age in GC, but it was significantly stronger in well differentiated GC than that in poorly differentiated GC (P < 0.05). The mean of DNA relative ploid (U value) in GC was from 1.14 to 2.98. U value becomes higher with the increase in grading (P < 0.01). There was significant negative linear correlation between p16 protein expression and U value in GC (P < 0.01). CONCLUSION: Abnormal expression of p16 protein is closely correlated to the occurrence, development and malignancy degree of GC. The level of p16 protein expression implies important clinical significance for GC treatment and may serve as an indicator to predict the prognosis of patients.

Adenocarcinoma↗
PubMed2000

Nanomechanics of individual carbon nanotubes from pyrolytically grown arrays.

The bending modulus of individual carbon nanotubes from aligned arrays grown by pyrolysis was measured by in situ electromechanical resonance in transmission electron microscopy (TEM). The bending modulus of nanotubes with point defects was approximately 30 GPa and that of nanotubes with volume defect was 2-3 GPa. The time-decay constant of nanotube resonance in a vacuum of 10(-4) Torr was approximately 85 micros. A femtogram nanobalance was demonstrated based on nanotube resonance; it has the potential for measuring the mass of chain-structured large molecules. The in situ TEM provides a powerful approach towards nanomechanics of fiberlike nanomaterials with well-characterized defect structures.

Journal Article↗
PubMed2000

Protective effect of high density lipoprotein on endothelium-dependent vasodilatation.

Low concentrations of high-density lipoprotein cholesterol (HDL-C) have been associated with increased risk of coronary heart disease (CHD) even when the total cholesterol (TC) and triglyceride (TG) levels are not elevated. The mechanism by which HDL confers protection against atherosclerosis remains speculative. Using high-resolution ultrasound, we measured the dilatation changes of brachial arteries during reactive hyperemia and after sublingual glyceryl trinitrate (GTN) in 63 patients with established (CHD) and 45 controls, in which the serum TC level was normal. The results showed that both flow-mediated dilatation (FMD) and GTN-induced dilatation of brachial arteries in patients with CHD were much reduced compared with control group (2.31+/-2.46% vs. 7.43+/-4.10% and 16.41+/-6.15% vs. 22.44+/-8.63%, respectively, P<0.001 for all). Univariate analysis indicated that FMD of brachial arteries was inversely related to age (r=-0.226, P<0.05), hypertension (r=-0.229, P<0.05), baseline diameter (r=-0.299, P<0.01) and LDL-C (r=-0.237, P<0.05) and positively related to HDL-C (r=0.491, P<0.01). GTN induced vasodilatation was inversely related to age (r=-0.216, P<0. 05) and baseline diameter (-0.476, P<0.01). Multiple stepwise regression analyses in two groups taken together showed that HDL-C and age were the independent predictors of the FMD of brachial arteries (beta=0.466, P=0.000 and beta=-0.184, P=0.020, respectively). Baseline diameter was significant predictor of GTN-induced vasodilatation (beta=-0.390, P=0.000). The analysis in the group of CHD patients showed that only HDL-C was significantly relate to the FMD of brachial arteries (beta=0.295, P=0.018 ) and in controls that hypertension and HDL-C were significantly relate to the FMD of brachial arteries (beta=-0.395, P=0.004 and beta=0.344, P=0.011, respectively). These finding suggest that endothelium-dependent and endothelium-independent vasodilatation are impaired in the patients with CHD. HDL exerts a protective effect on endothelium-dependent vasodilatation in TC being relatively normal population.

Adult↗
PubMed2000

Comparison of the functional characteristics of the nucleotide binding domains of multidrug resistance protein 1.

Multidrug Resistance Protein 1 (MRP1) transports diverse organic anionic conjugates and confers resistance to cytotoxic xenobiotics. The protein contains two nucleotide binding domains (NBDs) with features characteristic of members of the ATP-binding cassette superfamily and exhibits basal ATPase activity that can be stimulated by certain substrates. It is not known whether the two NBDs of MRP1 are functionally equivalent. To investigate this question, we have used a baculovirus dual expression vector encoding both halves of MRP1 to reconstitute an active transporter and have compared the ability of each NBD to be photoaffinity-labeled with 8-azido-[(32)P]ATP and to trap 8-azido-[(32)P]ADP in the presence of orthovanadate. We found that NBD1 was preferentially labeled with 8-azido-[(32)P]ATP, while trapping of 8-azido-[(32)P]ADP occurred predominantly at NBD2. Although trapping at NBD2 was dependent on co-expression of both halves of MRP1, binding of 8-azido-ATP by NBD1 remained detectable when the NH(2)-proximal half of MRP1 was expressed alone and when NBD1 was expressed as a soluble polypeptide. Mutation of the conserved Walker A lysine 684 or creation of an insertion mutation between Walker A and B motifs eliminated binding by NBD1 and all detectable trapping of 8-azido-ADP at NBD2. Both mutations decreased leukotriene C(4) (LTC(4)) transport by approximately 70%. Mutation of the NBD2 Walker A lysine 1333 eliminated trapping of 8-azido-ADP by NBD2 but, in contrast to the mutations in NBD1, essentially eliminated LTC(4) transport activity without affecting labeling of NBD1 with 8-azido-[(32)P]ATP.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Endothelial dysfunction associated with left ventricular diastolic dysfunction in patients with coronary heart disease.

OBJECTIVE: We sought to assess the correlation between endothelial vasodilation and left ventricular diastolic function. BACKGROUND: Previous studies have demonstrated that similar neurohumoral factors are involved in myocardial and vascular endothelial impairment. The degree of endothelial dysfunction is related to the clinical severity of the heart failure. However, it is not clear whether endothelial dysfunction develops with the progression of left ventricular diastolic dysfunction. We hypothesize that the endothelial dysfunction is associated with left ventricular diastolic dysfunction. METHODS: Using high-resolution ultrasound, we measured the dilator response of the brachial artery to hyperemia (endothelium-dependent vasodilation) and to 0.5 mg nitroglycerin (endothelium-independent vasodilation), and measured peak velocities of the early wave (Evmax) and the atrial wave (Avmax) in 40 coronary heart disease (CHD) patients and 20 normal subjects. We analyzed the relationship between the Evmax/Avmax ratio and endothelium-dependent vasodilation. RESULTS: The results showed that endothelium-dependent and endothelium-independent vasodilation as well as the Evmax/Avmax ratio were lower in the CHD group than those in the control group (4.29%+/-1.42%, 17.58%+/-2.99%, 0.81+/-0.24 vs. 9.62%+/-2.34%, 24.18%+/-3.15%, 1.07+/-0.29, respectively, P<0.01). The Evmax/Avmax ratio was related to endothelium-dependent vasodilation (r=0.45, P<0.01). CONCLUSIONS: Our results showed that the development of endothelial dysfunction was associated with the progression of myocardial diastolic dysfunction, which suggests that the same mechanisms may be involved in the impairment of endothelium and myocardium.

Brachial Artery↗
PubMed2000

Requirement for BMP and FGF signaling during cardiogenic induction in non-precardiac mesoderm is specific, transient, and cooperative.

We previously reported that combined treatment with bone morphogenetic protein-2 (BMP-2) and fibroblast growth factor-4 (FGF-4) induces cardiogenic events culminating in full cardiac differentiation of non-precardiac mesoderm explanted from stage 6 avian embryos (Lough et al. [1996] Dev. Biol. 178:198-202.). To elucidate the respective functions of BMP and FGF in initiating and maintaining the cardiogenic process, we have used these ectopic cells as a cardiac specification model to ascertain requirements for growth factor specificity and extent of application, as well as induction of cardiac transcription factors. The inability of some BMP isoforms to replace the inductive activity of BMPs-2/4 indicated a specific requirement for this signaling pathway; moreover, neither activin-A nor insulin, which support terminal differentiation of precardiac mesoderm, nor leukocyte inhibitory factor (LIF), which promotes hypertrophy in cardiac myocytes, could replace BMP's cardiogenic activity. A similarly specific requirement for FGF-2/4 signaling was revealed since neither FGF-7, activin-A nor insulin could replace this activity. The effect of both factors was concentration-dependent; maximal incidence of explant differentiation for each occurred at 50 ng/ml. Surprisingly, the majority of explants treated with high BMP levels (250 ng/ml) exhibited a non-cardiac phenotype that was characterized by intense expression of alkaline phosphatase, suggesting differentiation toward an alternative mesodermal phenotype. Experiments to assess the duration of exposure to each factor that was required revealed that while exposure to BMP and FGF during only the initial 30 min of a 48-hr culture period was sufficient to induce cardiogenesis in a significant percentage of explants, 100% incidence of explant differentiation was obtained only when FGF treatment was restricted to the first 30 min and BMP was continuously present during the 48-hr culture period. Treatment with both growth factors was required to induce the cardiac transcription factors cNkx-2.5 and SRF; neither mRNA was induced by BMP or FGF alone. These findings indicate that: (1) specific members of the BMP and FGF families are required to induce cardiogenesis in non-precardiac mesoderm; (2) BMPs-2/4 may function as a morphogen; (3) brief application of both factors can induce cardiogenesis in a modest number of explants whereas (4) 100% incidence of explant differentiation can only be attained by brief FGF treatment combined with continuous BMP treatment and (5) both factors are necessary to induce downstream cardiac transcription factors. These findings are interpreted in terms of these factors' possible roles during cardiac specification and differentiation.

Bone Morphogenetic Protein 2↗
PubMed2000

Immunolocalization of LeAGP-1, a modular arabinogalactan-protein, reveals its developmentally regulated expression in tomato.

Arabinogalactan-proteins (AGPs) are highly glycosylated cell surface proteins that are thought to function in plant growth and development. The developmentally regulated expression of LeAGP-1, a novel and major AGP in tomato, was examined in different organs and tissues of tomato (Lycopersicon esculentum Mill. cv. UC82B) plants with an anti-peptide antibody (i.e. the PAP antibody) directed specifically against the lysine-rich subdomain of the LeAGP-1 core protein. During cell differentiation in tomato plants, LeAGP-1 was associated with cell wall thickening and lignification of particular cell types. Specifically, LeAGP-1 was detected in secondary wall thickenings of maturing metaxylem and secondary xylem tracheary elements in roots and stems, and in thickened cell walls of phloem sieve elements. However, LeAGP-1 was also present in thin-walled, cortical parenchyma cells of seedling roots as well as thick-walled collenchyma cells in young stems, both of which are not lignified. Based on these observed patterns, possible roles for LeAGP-1 in plant growth and development are discussed.

Blotting, Western↗
PubMed2000

Endothelium-dependent and -independent functions are impaired in patients with coronary heart disease.

Endothelium plays a pivotal role in the development of atherosclerosis. Endothelial dysfunction participates in the course of acute coronary event. Using high-resolution ultrasound technique, endothelial dysfunction has been demonstrated in patients with atherosclerosis and risk factors for coronary disease, such as hypertension, diabetes mellitus, hypercholesterolemia and being smokers. In the present study, using this non-invasive method, the endothelial function of the brachial artery of patients with coronary heart disease (CHD) (n = 71) and control subjects (n = 34) was investigated. The results showed that endothelium-dependent and -independent vasodilatation were impaired in patients with CHD (2.61+/-2.91 vs. 8.10+/-7.81%, 17.20+/-7.93 vs. 23.19+/-8.89%, respectively) (P<0.001). Flow-mediated dilation (FMD) was significantly positively correlated with nitroglycerine-induced dilation (P<0.001). On univariate and multivariate analysis, the extent of FMD was significantly correlated with serum HDL-C levels (P<0.01). In conclusion, our study indicates both endothelial and underlying smooth muscle functions were impaired in patients with CHD. Decreased HDL-C levels may impair endothelial function.

Adult↗