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Biomedical subjects

Jian-hua Zhu

Publications and source records attributed to Jian-hua Zhu.

At least 19 recordsLinked to original sources

Effects of Astragalus membranaceus and its main components on the acute phase endothelial dysfunction induced by homocysteine.

OBJECTIVE: This study was designed to investigate the effects of Astragalus membranaceus (AM) and its main components, astragalus saponin (ASP), astragalus polysaccharide (APS) and aminobutyric acid (GABA), on homocysteine (Hcy) induced acute impairment of vascular tone and to explore whether the antioxidant mechanism was involved in AM protective effect. METHODS: Inhibitory effects of Hcy and protective effects of AM and its main components on endothelium-dependent relaxation of aortic rings were determined by isometric tension recordings and nitric oxide signaling was assayed with 125I-cGMP RIA Kit. Furthermore, generation of reactive oxygen species (ROS) in endothelial cells was detected using 5-(6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (CM-H2DCF-DA). RESULTS: Hcy significantly inhibited endothelium-dependent relaxation to acetylcholine (ACh) in a dose-dependent manner, and decreased cGMP levels increased by ACh in aorta. Furthermore, superoxide dismutase (SOD), AM, and ASP markedly attenuated inhibition of vasorelaxation and downregulation of cGMP level by Hcy, and APS exerted a tendency to reverse both of the depressive responses, while GABA had no similar effects. Additionally, partially impaired relaxation by Hcy was completely blocked due to the presence of N(omega)-nitro-L-arginine-methyl ester (L-NAME), which could not be further altered by treatment with AM, ASP, APS or GABA. Finally, Hcy significantly increased intracellular ROS levels in endothelial cells as measured by CM-H2DCF-DA fluorescence. SOD, AM, ASP, and APS, but not GABA, inhibited Hcy-stimulated ROS generation. CONCLUSION: This study demonstrated that AM and ASP, potently protected endothelium-dependent relaxation against the acute injury from Hcy through nitric oxide regulatory pathways, in which antioxidation played a key role.

Acetylcholine↗

Characterization of lactoferrin receptor in brain endothelial capillary cells and mouse brain.

We present, herein, the evidence for lactoferrin (Lf) binding sites in brain endothelial capillary cells (BCECs) and mouse brain. The results from confocal microscopy showed the presence of Lf receptors on the surface of BCECs and the receptor-mediated endocytosis for Lf to enter the cells. Saturation binding analyses revealed that Lf receptors exhibited two classes of binding sites in BCECs (high affinity: dissociation constant (K (d)) = 6.77 nM, binding site density (B (max)) = 10.3 fmol bound/mug protein; low affinity: K (d) = 4815 nM, B (max) = 1190 fmol bound/mug protein) and membrane preparations of mouse brain (high affinity: K (d) = 10.61 nM, B (max) = 410 fmol bound/mug protein; low affinity: K (d) = 2228 nM, B (max) = 51641 fmol bound/mug protein). The distribution study indicated the effective uptake of (125)I-Lf in brain after intravenous administration. The present study provides experimental evidence for the application of Lf as a novel ligand for brain targeting.

Animals↗

[Inhibitory effect of antisense oligodeoxynucleotides targeting HER-2 mRNA on growth of breast cancer: experiment in vivo with mice].

OBJECTIVE: To investigate the inhibitory effect of antisense oligodeoxynucleotides targeting HER-2 mRNA on growth of breast cancer. METHODS: Human breast cancer cells of the line SK-BR-3 that overexpresses HER-2 were injected subcutaneously into BALB/c nude mice. Seven to ten days after tumors were collected and made into homogenate. Antisense oligodeoxynucleotide HA6722 targeting HER-2 mRNA and its control sequence Scramble were synthesized. Forty-nine BALB/c nude mice were injected with homogenate of SK-BR-3 cells and then randomly divided into 7 equal groups: Group 1, injected intravenously with docetaxel (TXT) 7.5 mg.kg(-1).d(-1) once a week twice; Group 2, injected intravenously with TXT 15 mg.kg(-1).d(-1) once a week twice; Group 3, injected intravenously with TXT 7.5 mg.kg(-1).d(-1) once a week twice + HA6722 5 mg.kg(-1).d(-1) for 12 days; Group 4, injected intravenously with HA6722 5 mg.kg(-1).d(-1) for 12 days; Group 5, injected intravenously with TXT 7.5 mg.kg(-1).d(-1) once a week twice + Scramble6722 5 mg.kg(-1).d(-1) for 12 days; and Group 7, injected with normal saline. After the drug administration the mice were observed for additional 3-4 weeks to measure the size of tumor every other day. Then the mice were killed and the tumors were taken out to be examined. The inhibition rate was calculated. RESULTS: The inhibition rate of tumor in Group 3 was 88.3%, not significantly different from that in Group 2 (88.7%, P > 0.05). The inhibition rate in Group 4 was 76.3%. The inhibition rates of tumor of Groups 2, 3, and 4 were all significantly higher than that in Group 7. However, the inhibition rate of tumor of Group 6 was not significantly different from that in Group 7. CONCLUSION: Antisense oligodeoxynucleotides targeting HER-2 mRNA inhibits the growth of breast cancer in a sequence specific and dose-dependent manner.

Animals↗

[Experimental pathological study of acute intoxication by Chloranthus serratus Roem. Et Schalt].

OBJECTIVE: To find out the pathological change and the toxic mechanism of Chloranthus serratus Roem. et Schalt in mice. METHODS: Mice were intoxicated by oral administration with extracts of Chloranthus serratus Roem. et Schalt followed by pathological, serum biochemical, and coagulation mechanism examination. RESULTS: The LD50 in mice was 41.12 g/kg; All poisoned mice serum BUN and ALT increased markedly; Thrombocyte decreased and coagulation time increased; The organ index of liver, spleen and kidneys increased significantly; The cells of liver, kidney and heart were degeneration and necrosis, There were extensive hyperemia and hemorrhage in many organs. CONCLUSION: The experiment suggests that the target organs were liver, kidney, heart and blood vessels; The toxic mechanism was the damage on the mitochondrional, endoplasmic reticulum and coagulation system.

Animals↗

[Effects of exogenous ER beta expression on the cell growth properties of MCF-7 breast cancer cell line].

OBJECTIVE: To study the effects of exogenous ER beta on the growth of breast cancer MCF-7 cells under different treatment. METHODS: An eukaryotic expression vector containing 1.6 kb of human entire coding sequence of ER beta (pCDNA3-ER beta) was transfected into human breast cancer MCF-7 cells using lipofectamine 2000. The biological activity of ER beta was detected with the luciferase reporter containing estrogen responsive element (ERE) and the expression of ER beta protein by Western blot. The growth properties of MCF-7, pCDNA 3-transfected MCF-7 and pCDNA 3-ER beta-transfected MCF-7 cells under different treatment, including E2 (17beta-estradiol) and 4-OHT (4-hydroxytamoxifen), were observed. RESULTS: A stronger activation of the reporter by ER beta in the presence of E2 was observed in the pCDNA 3-ER beta-transfected MCF-7 cells than in the pCDNA 3-transfected MCF-7 and in MCF-7 cells. Western blot analysis showed that the protein level of ER beta in the pCDNA 3-ER beta-transfected MCF-7 cells was markedly increased. Exogenous ER beta expression did not change the growth properties and the morphology of MCF-7 cells under normal condition. The pCDNA 3-ER beta-transfected MCF-7 cells proliferated at the same rate as naive cells in the presence of 4-OHT, whereas a strong inhibition of the proliferation of the pCDNA 3-ER beta-transfected MCF-7 cells in the presence of E2 was observed. CONCLUSION: Exogenous ER beta expression does not increase the resistance to 4-OHT, and a strong inhibition of the proliferation may occur in the presence of E2.

Breast Neoplasms↗

[The relationship between endothelin-1 and tumor necrosis factor-alpha and myocardial microcirculation dysfunction].

OBJECTIVE: To investigate the relationship between endothelin-1 (ET-1) and tumor necrosis factor-alpha and myocardial microcircular dysfunction during coronary microembolization (CME). METHODS: CME was induced in 10 miniswine by selective infusion of microspheres (45 microm) into left anterior descending artery (LAD). We measured (1) coronary sinus level of ET-1, TNF-alpha using radioimmunoassay; (2) CFR, a measure of microvascular integrity, using Doppler flow wire in LAD at baseline and different doses of microspheres. RESULTS: CFR decrease significantly with different doses of microspheres (vs. baseline, P < 0.05). Level of ET-1, TNF-alpha increased significantly with doses of 5 x 10(4) and peaked with 10 x 10(4). Interestingly, ET-1 progressively decrease while TNF-alpha persistently elevated from doses of 12 x 10(4) to 15 x 10(4). There are reverse correlations between ET-1 and CFR (r = -0.31, P < 0.05). CONCLUSIONS: The extent of microvascular injury wasn't linearly related to the extent of ME, where, it closely associated with myocardial ET-1.

Animals↗

[Psychologic status comparison in patients treated with transradial or transfermoral approach coronary catheterizations].

OBJECTIVE: We previously showed that factorial score of somatization, which was obtained by the examination of symptom checklist-90 (SCL-90), was higher in patients received transfemoral coronary catheterization than norm. The aim of the present study was to compare the patient's psychologic status between transradial approach and transfemoral approach percutaneous coronary catheterizations. METHODS: A total of 198 inpatients (105 transfemoral, 93 transradial) underwent scheduled first time coronary catheterizations were enrolled. All patients were studied by symptom SCL-90 on present psychologic status 24 hours before and 24-48 hours after coronary catheterizations. RESULTS: Age, sex, weight, smokers, employment, educational background, marriage status, family relations, family history of cardiovascular disease, income and medical insurance status were similar between the two groups. There was also no difference in diabetes, hypertension history as well as coronary heart disease confirmed by coronary catheterization between the 2 groups. Compared with the status before the procedure, factorial scores of somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, global severity index and total positive symptoms were significantly reduced after percutaneous coronary catheterizations (1.50 +/- 0.51 vs. 1.64 +/- 0.53, 1.50 +/- 0.48 vs. 1.67 +/- 0.55, 1.28 +/- 0.41 vs. 1.38 +/- 0.49, 1.42 +/- 0.43 vs. 1.55 +/- 0.53, 1.38 +/- 0.41 vs. 1.58 +/- 0.54, 1.32 +/- 0.35 vs. 1.44 +/- 0.41, 1.38 +/- 0.34 vs. 1.49 +/- 0.42, and 23.08 +/- 17.30 vs. 27.72 +/- 18.79, respectively, P all < 0.05). Scores on somatization, depression and positive symptom severity index were significantly lower in patients received transradial coronary catheterizations than those received transfemoral coronary catheterization approach (1.52 +/- 0.51 vs. 1.62 +/- 0.53, 1.43 +/- 0.54 vs. 1.54 +/- 0.43 and 2.36 +/- 0.66 vs. 2.50 +/- 0.43, respectively, P all < 0.05). CONCLUSION: Patients' psychologic status improved significantly after percutaneous coronary catheterizations. Improvement on psychologic status is significantly better in patients underwent transradial coronary catheterizations than that underwent transfemoral coronary catheterizations.

Aged↗

Statins reduce connexin40 and connexin43 expression in atherosclerotic aorta of rabbits.

BACKGROUND: Gap junction protein connexin43 (Cx43) expression was enhanced in proliferating smooth muscle cells (SMCs) in the neointima of atherosclerotic lesions. HMG-CoA Reductase Inhibitors (statins) can reduce Cx43 expression in vivo and in vitro. Connexin40 (Cx40) is also a very important connexin in SMCs of arterial wall. METHODS: We observed the expression of Cx40 and Cx43 in a rabbit model of a high-cholesterol diet and investigated the effect of lovastatin (10 mg.kg-1.d-1, 2 weeks) or fluvastatin (10 mg.kg-1.d-1, 2 weeks) on these changes by the methods of western blotting, RT-PCR, immunohistochemistry, and transmission electron microscope. RESULTS: There was abundant expression of Cx40 mRNA and protein in SMCs of rabbit aorta. Besides Cx43, Cx40 expression was also obviously upregulated in atherosclerotic plaques. Treatment with statins reduced the over-expression of Cx43 and Cx40 in atherosclerotic lesion. Cx40 and Cx43 gap junction quantity from each of the arteries obtained at the different drug treatment levels revealed no significant difference. Neointimal SMCs had abundant, large gap junctions, whereas normal SMCs had smaller, less frequent junctions. Statins also normalized the enlarged gap junctions. CONCLUSIONS: These results provide novel in vivo evidence for the key role of gap junctions in atherogenesis and the possible mechanism in antiatherogenic effect of statins.

Animals↗

A novel splice mutation of HERG in a Chinese family with long QT syndrome.

Congenital long QT syndrome (LQTS) is a genetically heterogeneous disease in which six ion-channel genes have been identified. The phenotype-genotype relationships of the HERG (human ether-a-go-go-related gene) mutations are not fully understood. The objective of this study is to identify the underlying genetic basis of a Chinese family with LQTS and to characterize the clinical manifestations properties of the mutation. Single strand conformation polymorphism (SSCP) analyses were conducted on DNA fragments amplified by polymerase chain reaction from five LQT-related genes. Aberrant conformers were analyzed by DNA sequencing. A novel splice mutation in C-terminus of HERG was identified in this Chinese LQTS family, leading to the deletion of 11-bp at the acceptor splice site of Exon9 [Exon9 IVS del (-12-->-2)]. The mutation might affect, through deficient splicing, the putative cyclic nucleotide binding domain (CNBD) of the HERG K(+) channel. This mutation resulted in a mildly affected phenotype. Only the proband had a history of syncopes, while the other three individuals with long QT interval had no symptoms. Two other mutation carriers displayed normal phenotype. No sudden death occurred in the family. The 4 affected individuals and the two silent mutation carriers were all heterozygous for the mutation. It is the first splice mutation of HERG reported in Chinese LQTS families. Clinical data suggest that the CNBD mutation may be less malignant than mutations occurring in the pore region and be partially dominant over wild-type function.

Asian People↗

[Cloning, expression and sequence analysis and tissue distribution of angiotensin-converting enzyme 2 (ACE2) gene in adult mice].

OBJECTIVE: o clone angiotensin-converting enzyme 2(ACE2) gene, to analyze its amino acids and nucleotides sequence and to investigate tissue distribution of ACE2 in adult mice. METHODS: The full-length ACE2 encoding sequence was amplified from the RNA of mice kidney tissue by RT-PCR technique, cloned into plasmid pGEM-T easy, then subcloned into plasmid pcDNA3.1+. After identification of DNA sequence, the recombinant plasmid pmACE2 was transfected into Cos7 cells with lipofectin reagent. The transient expression of ACE2 molecule was detected by SDS-PAGE. Sequence analysis was conducted with CLUSTALX program. Tissue distribution of ACE2 in mice was detected by RT-PCR. RESULTS: A fragment about 2.6 kb was amplified and the recombinant plasmid pmACE2 was confirmed by two-enzyme digesting and DNA sequencing. The cloned DNA sequence was consistent with that previously reported, except for 3 variations: A701G, T1102C and T1330C. SDS-PAGE proved that expression of a soluble, truncated products form of ACE2 was a glycoprotein of approximately 80 kD in Cos7 cells. The predicted mice ACE2 sequence contained an N-terminal signal sequence (amino acid residues 1-18), a single HHEMGHIQ zinc-binding domain (amino acid residues 373-380) and C-terminal membrane anchor (amino acid residues 738-765). Mice ACE2 showed 84 % identity with that of human, and 90 % identity with that of rat. Expression of ACE2 was the greatest in lungs, hearts and kidneys, and moderate levels were also detected in testes and livers. CONCLUSION: Mice ACE2 gene has been cloned and successfully expressed in vitro. The tissue-specific expression of ACE2 in different species is not identical.

Amino Acid Sequence↗

[Effect of acute coronary microembolization on microvascular injury and myocardial endothelin-1 levels].

OBJECTIVE: To investigate the effect of coronary microemboliation (CME) on coronary microvascular injury and myocardial endothelin-1 (ET-1) level. METHODS: CME was induced in 10 miniswines by selective infusion of microspheres (45 microm) into left anterior descending artery (LAD). The ET-1 level in coronary sinus was measured with radioimmunoassay. The microvascular integrity indicator CFR was measured by Doppler flow wire in LAD at baseline and after infusion of microspheres. RESULT: Compared to the baseline, CFR decreased significantly with different doses of microspheres. ET-1 level increased significantly with doses of 5 x 10(4) and peaked with 10 x 10(4), and progressively decreased from doses of 12 x 10(4) to 15 x 10(4) microspheres. There was negative correlation between ET-1 and CFR (r=-0.31, P=0.02). CONCLUSION: The extent of microvascular injury is not linearly related to the extent of microembolization, but it is closely associated with myocardial ET-1 level.

Animals↗

[ERK expression and activation in myocardial hypertrophy of spontaneously hypertensive rats with different ages].

OBJECTIVE: To investigate the expression and activation of extracellular signal-regulated kinases (ERK) in myocardial hypertrophy of spontaneously hypertensive rats (SHR) with different ages. METHODS: SHRs and Wistar Kyoto (WKY) rats were divided into 4 groups (5-, 8-,14-, 24-week old) respectively. The ratio of left ventricle weight to body weight (LVW/BW) was measured as the indicator of myocardial hypertrophy. The basal ERK expression (b-ERK) and phosphorylated-ERK (p-ERK) in myocardial tissue were examined by Western blot. RESULT: The blood pressure of SHR was significantly higher than that of age-matched WKY rats from 8-week-old (P<0.001). The ratio of LVW/BW in SHR was increased significantly from 14-week-old (P<0.01). There was no significant difference of b-ERK expression between SHR and age-matched WKY rats. The p-ERK level of 5-week-old SHR was similar to that of 5-week-old WKY rats. The p-ERK level of SHR was significantly higher than that of age-matched WKY rats from 8-week-old to 24-week-old (P<0.01). The ratio of LVW/BW was positively related to p-ERK level but not related to b-ERK. CONCLUSION: The activation of ERK may play an important role in the development of myocardial hypertrophy caused by hypertension.

Age Factors↗

[Comparison of the antithrombotlic effect and safety between intravenous nadroparin and unfractionated heparin in patients undergoing percutaneous coronary intervention].

OBJECTIVE: The study was designed to compare the antithrombotic property and safety between nadroparin and unfractionated heparin during percutaneous coronary intervention (PCI). METHODS: A prospective, single blind, randomized study was performed. A total of 98 patients (aged 65.1 +/- 8.6 years, female, 28.6%, diabetes, 7.1%) undergoing selective PCI were randomized to be administered intravenously either nadroparin (0.075 ml/10 kg) or unfractionated heparin (100U/kg) for procedural anticoagulation, in whom stable angina was 42.9%, unstable angina, 27.6%, myocardial infarction, 29.6%, two or three-vessel disease, 23.5%, stent, 100%. Blood samples for anti-Xa level were assayed in the first 22 patients of the nadroparin group before and after administration at the following intervals: 8 min, 1 h, 2 h and 4 h. Bleeding complications were classified according to Thrombolysis In Myocardial Infarction (TIMI) criteria. The bleeding index (change in hemoglobin) was calculated. All patients were monitored for adverse clinical events (i.e. death, myocardial infarction, need for revascularization) during the period of 30 days after PCI. RESULTS: (1) There were no significant differences in baseline characteristics between the two randomized groups. (2) Plasma anti-Xa activities were 0.10 +/- 0.00 IU/ml at the time just before the administration of nadroparin, 1.89 +/- 0.24 IU/ml, 0.96 +/- 0.24 IU/ml, 0.47 +/- 0.13 IU/ml, and 0.30 +/- 0.12 IU/ml at the time of 8 min, 1 h, 2 h and 4 h after the use of nadroparin (and the rate of > 0.5 IU/ml were 100%, 100%, 45% and 9% patients), respectively. (3) There were no significant differences in the mean bleeding index, post-PCI hemoglobin and hematocrit between nadroparin and unfractionated heparin group [(1.16 +/- 5.80) g/L vs (0.90 +/- 6.50) g/L, P = 0.858; (129.5 +/- 13.6) g/L vs (125.5 +/- 14.9) g/L, P = 0.175; (39.0 +/- 3.9)% vs (37.9 +/- 4.6)%, P = 0.205]. (4) None of the patients in two randomized groups were observed hemorrhagic events, which including TIMI major or minor bleeding complications, gross or microscopic hematuria, melena, positive stool occult blood. There were no blood transfusions and no hematoma at the vascular access site in either of the group. (5) No death, no recurrent angina pectoris, and no urgent revascularization occurred within 30 days in both groups. One patient in nadroparin group was observed "no reflow" phenomenon that was accompanied with an elevated ST segment and a risen serum level of cTnI. This patient was diagnosed as non-Q-wave myocardial infarction. Though no myocardial infarction was found in unfractionated heparin group, there was no significant difference in the rate of myocardial infarction between the two groups of the study (P = 0.970). CONCLUSIONS: The administration of nadroparin before PCI seems effective and safe. Compared with unfractionated heparin, nadroparin was associated with neither an excess of bleeding nor an increase of clinical complications in this study.

Adult↗

[Expression of connexin in atrium of patients with atrial fibrillation and its signal transduction pathway].

OBJECTIVE: To explore the expression of connexin (Cx) and its signal transduction pathway in the atrium of patients with atrial fibrillation (AF). METHODS: Atrial tissue samples of 63 patients undergoing cardiac surgery, including patients with chronic AF or paroxysmal AF (PAF), and those with sinus rhythm, were collected during operation. The mRNA expressions of calcineurin B and mitogen-activated protein kinase-1 (MKP-1) were detected by semi-quantitative RT-PCR. The protein expressions of extracellular-signal regulated kinase 1 (ERK1), phospho-ERK1 (P-ERK1), Cx40 and Cx43 were analyzed by Western blotting. HE staining and immunohistochemistry were used to examine the distribution of Cx40 and Cx 43. RESULTS: Increased amounts of Cx40 protein (left atrium: 2.2 +/- 0.8, 2.2 +/- 0.6; right appendages: 2.1 +/- 0.5, 2.0 +/- 0.8) were found in the left atrium and right appendages of patients with Chronic persistent AF (CAF) or paroxysmal AF (PAF) (P < 0.05). The expression of Cx43 was only increased in the left atrium of patients with CAF and PAF (3.1 +/- 0.6, 2.8 +/- 0.7 vs 1.0 +/- 0.2, both P < 0.05). The amounts of Calcineurin B mRNA, MKP-1 mRNA and P-ERK1 of patients with CAF or PAF were significantly increased compared with patients in sinus rhythm (P < 0.05). Immunohistochemistry revealed that Cx40 and Cx43 of CAF patients and PAF patients acculmated in the intracellular site, and at the lateral member of atrial cells, both connexins redistributed. CONCLUSION: The increased expression and disorderly distribution of Cx 40 and Cx 43 protein in the atrium of AF patients may be related with the abnormal activation and disequilibria of regulation of ERK1, MKP-1 and calcineurin.

Adult↗

[Effect of homocysteine on NF-kappaB activity in cultured rat vascular smooth muscle cells].

OBJECTIVE: To investigate the effect of homocysteine (Hcy) on nuclear factor-kappaB (NF-kappaB) activity in cultured rat vascular smooth muscle cells (VSMCs). METHODS: Rat VSMCs were stimulated with 0.25 mmol/L Hcy. Cells were collected and nuclear protein was extracted at 30 min, 1 h and 2 h following stimulation. NF-kappaB activity was examined by electrophoretic mobility shift assay (EMSA). RESULT: Baseline NF-kappaB nuclear binding in VSMCs increased more than 1.76-fold at 30 min (P<0.01), 1.91-fold at 1h (P<0.01) and 1.84-fold at 2 h (P<0.01) following stimulation of Hcy. CONCLUSION: Hcy can enhance transient mobilization of N-kappaB in VSMCs, which suggests that some regulating effect of Hcy on VSMCs might be exerted through NF-kappaB activation pathway.

Animals↗

[Effects of hypercholesterolemia on the number and activity of endothelial progenitor cells in peripheral blood].

OBJECTIVE: To investigate whether hypercholesterolemia has influences on the number and activity of endothelial progenitor cells (EPCs). METHODS: Mononuclear cells were isolated from patients with hypercholesterolemia (n = 20) and age-matched control subjects (n = 20). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs proliferation and migration were assayed by MTT assay and modified Boyden chamber assay, respectively. EPCs adhesion assay was performed by replating cells on fibronectin-coated dishes, then counting the adherent cells. RESULTS: The number of EPCs was significantly reduced in patients with hypercholesterolemia as compared with that in control subjects [(41.8 +/- 8.7 vs 64.5 +/- 16.6) EPCs/x 200 fields; P < 0.05] and it was inversely correlated with total cholesterol levels (r = -0.659, P < 0.001) and LDL cholesterol levels (r = -0.611, P < 0.001). In addition, EPCs proliferative, migratory and adhesive capacity were also impaired. CONCLUSION: It is suggested that a novel pathophysiological mechanism of hypercholesterolemia may be defined i.e. reduction of EPCs with decreased functional activity.

Aged↗

[Effects of atenolol and diltiazem-SR on quality of life in the hypertensive patients].

OBJECTIVE: To compare the efficacy of atenolol and diltiazem-SR and the effects on the quality of life in hypertensive patients. METHODS: Seventy-three patients with mild to moderate hypertension (DBP 90 - 109 mmHg) were allocated randomly to be administered with atenolol 25 mg/d (group A, n=37) and diltiazem-SR 90 mg/d (group B, n=36) for eight weeks. The changes of heart rate, office blood pressure(OBP), ambulatory blood pressure(ABP) and the quality of life were compared before and after treatment. RESULTS: Heart rate, OBP and ABP decreased after treatment in both groups. The effective rate of blood pressure was 88.2% in group A and 93.8% in group B. Twenty four hour mean daytime and nighttime BP,daytime and nighttime BP loads declined in both groups (P<0.05 - 0.01). The quality of life was significantly increased in group B (P<0.05). Side effects were 21.6% in group A and 11.1% in group B, respectively (P>0.05). CONCLUSION: Atenolol and diltiazem-SR are more effective and tolerant in the treatment of the hypertension. Diltiazem improves the quality of life better than atenolol.

Adult↗