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Biomedical subjects

Hao Pan

Publications and source records attributed to Hao Pan.

12 recordsLinked to original sources

Relationship between hs-CRP, proMMP-1, TIMP-1 and coronary plaque morphology: intravascular ultrasound study.

BACKGROUND: Rupture of unstable plaque with subsequent thrombus formation is the common pathophysiological substrate of the acute coronary syndrome (ACS). It is of potential significance to explore the blood indexes predicting plaque characteristics. Little studies have focused on this field. Therefore we investigated the relationship between hypersensitive C-reactive protein (hs-CRP), pro-matrix metalloproteinase-1 (proMMP-1), tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) and coronary plaque morphology. METHODS: Intravascular ultrasound (IVUS) examination was done in 152 patients with confirmed coronary heart disease before percutaneous coronary intervention from February 2003 to July 2005. Plasma samples of arterial blood were collected prior to the procedure. The level of hs-CRP, proMMP-1 and TIMP-1 were respectively measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Unstable and ruptured plaque were found more frequently in patients with acute myocardial infarction and unstable angina. External elastic membrane cross-sectional area (EEM CSA), plaque area, lipid pool area and plaque burden were significantly larger in ruptured and unstable plaque group. Positive remolding, thinner fabric-cap, smaller minimal lumen cross-sectional area (MLA), dissection and thrombus were significantly more frequent in ruptured and unstable plaque group. The levels of plasma hs-CRP, proMMP-1 and TIMP-1 were higher in ruptured plaque group. hs-CRP > 8.94 mg/L was used to predict ruptured plaque with a ROC curve area of 0.76 [95% confidence interval (CI), 67.0% - 85.8%], sensitivity of 71.8%, specificity of 77.0% and accuracy of 69.2% (P < 0.01), similarly for proMMP-1 > 0.12 ng/ml with a ROC curve area of 0.69 [95% CI, 58.2% - 80.2%], sensitivity of 69.2%, specificity of 75.2% and accuracy of 66.2% (P < 0.01), and TIMP-1 > 83.45 ng/ml with a ROC curve area of 0.67 [95% CI, 56.2% - 78.3%], sensitivity of 66.7%, specificity of 61.9% and accuracy of 66.2% (P < 0.01). CONCLUSION: The plaque characteristics correlate with the clinical presentation. The elevation of hs-CRP, proMMP-1 and TIMP-1 are related to the plaque instability and rupture.

Aged↗

A simple parallel analytical method of prenatal screening.

Protein microarray has progressed rapidly in the past few years, but it is still hard to popularize it in many developing countries or small hospitals owing to the technical expertise required in practice. We developed a cheap and easy-to-use protein microarray based on dot immunogold filtration assay for parallel analysis of ToRCH-related antibodies including Toxoplasma gondii, rubella virus, cytomegalovirus and herpes simplex virus type 1 and 2 in sera of pregnant women. It does not require any expensive instruments and the assay results can be clearly recognized by the naked eye. We analyzed 186 random sera of outpatients at the gynecological department with our microarray and commercial ELISA kit, and the results showed there was no significant difference between the two detection methods. Validated by clinical application, the microarray is easy to use and has a unique advantage in cost and time. It is more suitable for mass prenatal screening or epidemiological screening than the ELISA format.

Dose-Response Relationship, Drug↗

Pulmonary complications in patients with chronic obstructive pulmonary disease following transthoracic esophagectomy.

AIM: To investigate the incidence of various types of postoperative pulmonary complications (POPCs) and to evaluate the significance of perioperative arterial blood gases in patients with esophageal cancer accompanied with chronic obstructive pulmonary disease (COPD) after esophagectomy. METHODS: Three hundred and fifty-eight patients were divided into POPC group and COPD group. We performed a retrospective review of the 358 consecutive patients after esophagectomy for esophageal cancer with or without COPD to assess the possible influence of COPD on postoperative pulmonary complications. We classified COPD into four grades according to percent-predicted forced expiratory volume in 1 s (FEV1) and analyzed the incidence rate of complications among the four grades. Perioperative arterial blood gases were tested in patients with or without pulmonary complications in COPD group and compared with POPC group. RESULTS: Patients with COPD (29/86, 33.7%) had more pulmonary complications than those without COPD (36/272, 13.2%) (P < 0.001). Pneumonia (15/29, 51.7%), atelectasis (13/29, 44.8%), prolonged O(2) supplement (10/29, 34.5%), and prolonged mechanical ventilation (8/29, 27.6%) were the major complications in COPD group. Moreover, patients with severe COPD (gradeIIB, FEV1<50% of predicted) had more POPCs than those with moderate(gradeIIA, 50%-80% of predicted) and mild (gradeI> or =80% of predicted) COPD (P < 0.05). PaO(2) was decreased and PaCO(2) was increased in patients with pulmonary complications in COPD group in the first postoperative week. CONCLUSION: The criteria of COPD are the critical predictor for pulmonary complications in esophageal cancer patients undergoing esophagectomy. Severity of COPD affects the incidence rate of the pulmonary complication, and percent-predicted FEV1 is a good predictive variable for pulmonary complication in patients with COPD. Arterial blood gases are helpful in directing perioperative management.

Aged↗

Effects of VEGFR-1, VEGFR-2, and IGF-IR hammerhead ribozymes on glucose-mediated tight junction expression in cultured human retinal endothelial cells.

PURPOSE: To evaluate whether transfection of human retinal endothelial cells (HRECs) with plasmids expressing ribozymes designed to specifically cleave the mRNA and reduce expression of either vascular endothelial growth factor (VEGF) receptor-1 (VEGFR-1), or VEGF receptor-2 (VEGFR-2), or insulin-like growth factor-I receptor (IGF-IR) modulates occludin expression in high glucose-treated cells. METHODS: Hammerhead ribozymes that specifically cleave the human VEGFR-1, VEGFR-2, and IGF-IR mRNAs were developed and tested in vitro to determine ribozyme kinetics and cleavage specificity. HRECs grown in normal (5.5 mM) and high (25 mM) glucose medium were transfected with plasmids expressing VEGFR-1, VEGFR-2, or IGF-IR hammerhead ribozymes. VEGF and IGF-I levels were measured in conditioned medium of HREC exposed to high glucose conditions, and the effect of varying glucose concentration on VEGFR-1 and VEGFR-2 phosphorylation was examined. The amount of the tight junction protein occludin was determined by western analysis, and the protein was localized by immunohistochemistry. RESULTS: Exposure of HRECs to high glucose resulted in increased VEGF and IGF-I expression as well as VEGFR-2 but not VEGFR-1 phosphorylation. Immunocytochemistry and western analysis revealed that HRECs exposed to high glucose had reduced occludin staining and protein expression, respectively. Transfection of HRECs exposed to high glucose with either VEGFR-1, VEGFR-2, or IGF-IR hammerhead ribozymes prevented the downregulation of occludin protein expression. CONCLUSIONS: Our studies support that activation of VEGFR-1, VEGFR-2, and IGF-IR by high glucose contributes to disruption of tight junctions by decreasing occludin expression and may be important in the pathogenesis of blood-retinal barrier dysfunction in diabetic retinopathy.

Animals↗

The dipeptide Arg-Gln inhibits retinal neovascularization in the mouse model of oxygen-induced retinopathy.

PURPOSE: Premature infants undergoing intensive care are highly vulnerable to amino acid deprivation. Supplementation of glutamine or arginine has resulted in beneficial effects in human neonates. This study was conducted to examine the effect of the dipeptide arginyl-glutamine (Arg-Gln) on vascular endothelial cell growth factor (VEGF) levels in primary human retinal pigment epithelial (hRPE) cell cultures and on inhibition of neovascularization in the oxygen-induced retinopathy (OIR) model. METHODS: The effects of Arg-Gln on VEGF levels were measured in supernates from hRPE cells by using ELISAs. For in vivo studies, mouse pups received twice-daily intraperitoneal injections of Arg-Gln, a control dipeptide (Ala-Gly) or were not injected. Retinal flatmounts from one cohort were prepared and retinal vessel morphology examined. The contralateral eyes were embedded, sectioned, and stained to count preretinal neovascular nuclei. RNA was isolated from retinas of selected animals and was used to quantify VEGF mRNA by real-time RT-PCR. RESULTS: Treatment of hRPE cells with Arg-Gln decreased VEGF levels in a dose-dependent manner. In the OIR model, Arg-Gln at 5 g/kg per day reduced preretinal neovascularization by 82%+/-7% (P<0.005), when compared with the control dipeptide Ala-Gly, and reduced VEGF mRNA by 64%+/-9% (P<0.001). CONCLUSIONS: Arg-Gln dramatically inhibited retinal neovascularization in the OIR model. This effect was associated with a reduction in retinal VEGF mRNA levels. Similarly the dipeptide reduced VEGF expression in hRPE cells, a cell type likely to respond to retinal hypoxia by expressing VEGF. Arg-Gln appears to be safe and, with future studies in human infants, may prove beneficial in the prevention of ROP.

Angiogenesis Inhibitors↗

Expression of protein kinase CK2 in astroglial cells of normal and neovascularized retina.

We previously documented protein kinase CK2 involvement in retinal neovascularization. Here we describe retinal CK2 expression and combined effects of CK2 inhibitors with the somatostatin analog octreotide in a mouse model of oxygen-induced retinopathy (OIR). CK2 expression in human and rodent retinas with and without retinopathy and in astrocytic and endothelial cultures was examined by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction. A combination of CK2 inhibitors, emodin or 4,5,6,7-tetrabromobenzotriazole, with octreotide was injected intraperitoneally from postnatal (P) day P11 to P17 to block mouse OIR. All CK2 subunits (alpha, alpha', beta) were expressed in retina, and a novel CK2alpha splice variant was detected by reverse transcriptase-polymerase chain reaction. CK2 antibodies primarily reacted with retinal astrocytes, and staining was increased around new intraretinal vessels in mouse OIR and rat retinopathy of prematurity, whereas preretinal vessels were negative. Cultured astrocytes showed increased perinuclear CK2 staining compared to endothelial cells. In the OIR model, CK2 mRNA expression increased modestly on P13 but not on P17. Octreotide combined with emodin or 4,5,6,7-tetrabromobenzotriazole blocked mouse retinal neovascularization more efficiently than either compound alone. Based on its retinal localization, CK2 may be considered a new immunohistochemical astrocytic marker, and combination of CK2 inhibitors and octreotide may be a promising future treatment for proliferative retinopathies.

Angiogenesis Inhibitors↗

[C-reactive protein induced human endothelium cells apoptosis is associated with Bcl-2/Bax gene expression changes].

OBJECTIVE: In the present study, we examined the expression changes of Bcl-2/Bax in C-reactive protein (CRP) treated human endothelium cells in vitro. METHODS: The human umbilical vein endothelial cells (HUVEC) were cultured by digest method for 2 - 3 posterities and incubated with human CRP (0, 1, 5, 25 mg/L for 24 hours) and analyzed by flow cytometer for apoptosis ratio. The effects of CRP in various concentrations on Bcl-2/Bax mRNA and protein expression were examined by RT-PCR and Western Blotting. RESULTS: Apoptosis ratio increased, downregulated Bcl-2 (gene promoting cell survival) and upregulated Bax (gene promoting apoptosis) at mRNA and protein levels in proportion to increased CRP concentrations. CONCLUSION: These results demonstrate that Bcl-2/Bax could be regulated by CRP in human HUVECs and might play a causal role in CRP-induced apoptosis.

Apoptosis↗

[The evaluation on stent implantation efficacy of myocardial bridge and severe atherosclerosis lesions in the segments proximal to the myocardial bridge].

OBJECTIVE: To assess long term stent implantation efficacy of myocardial bridge and severe atherosclerosis lesions in the segments proximal to the myocardial bridge. METHODS: The study population consisted of 3 groups (103 patients). Group A included 28 patients with severe atherosclerosis lesion of luminal narrowing of > or = 70% in the segments proximal to the myocardial bridge. Group B included 16 patients with symptomatic myocardial bridge lesion of systolic luminal narrowing of > or = 95%. Group C included 59 patients with severe atherosclerotic lesion of luminal narrowing of > or = 70%. All lesions were successfully treated with stent by standard interventional techniques. Quantitative coronary angiography was performed before and immediately after stent deployment. Follow-up Quantitative coronary angiography was performed at six months or later. Clinical evaluation was done at 20 months after PCI. RESULTS: There was no significant difference in luminal diameter and stent diameter among 3 groups immediately after stent implantation (P > 0.05). At six months, restenosis occurred in 4 patients in Group A (14.3%), in 7 patients in Group B (43.7%), and in 8 patients in Group C (14.8%), respectively. The rate of restenosis was significantly lower in group A and C than in group B (P < 0.05). No significant difference was found between group A and C. Additional balloon dilating of stent were performed in all restenosis patients. Clinical evaluation at 20 months showed that all patients remained free of angina and cardiac events. CONCLUSION: The efficacy of intracoronary stent implantation in treating severe atherosclerosis lesion in the segments proximal to the myocardial bridge is not affected by abnormal haemodynamic changes of myocardial bridges. The rate of restenosis in intracoronary stent implantation of myocardial bridges is higher than that of atherosclerotic lesions in the segments proximal to myocardial bridge.

Adult↗

Molecular targeting of antiangiogenic factor 16K hPRL inhibits oxygen-induced retinopathy in mice.

PURPOSE: To examine the ability and mechanism of the 16 kDa N-terminal fragment of human prolactin (16K hPRL) in the inhibition of abnormal retinal neovascularization. METHODS: The 16K hPRL-encoding sequence was inserted into an adenoviral vector (16K-Ad). Western blot analysis verified the expression of 16K hPRL and inhibition of proliferation, confirming functional activity of the 16K hPRL in virus-infected adult bovine aortic endothelial (ABAE) cells. 16K hPRL inhibited retinal neovascularization in a mouse model of oxygen-induced retinopathy. The ability of recombinant 16K hPRL expressed in E. coli (r16K hPRL) was compared to that of endostatin in inducing apoptosis of cultured human retinal endothelial cells (HREC). RESULTS: 16K was expressed in virus-infected ABAE cells and resulted in a dose-dependent inhibition of cell proliferation. Eyes injected with 16K-Ad showed a reduction in preretinal neovascularization of 82.3 +/- 9.3% (P < 0.00001) when compared to uninjected controls. r16K hPRL was 100 times more potent than endostatin in inducing apoptosis in HRECs. CONCLUSIONS: Intravitreal administration of 16K hPRL inhibited neovascularization in the mouse model of oxygen-induced retinopathy. 16K hPRL stimulated apoptosis in HRECs and inhibited cell proliferation in ABAE cells. These results suggested a potential therapeutic role for 16K hPRL in the treatment of proliferative retinopathies.

Adenoviridae↗

The role of growth factors in the pathogenesis of diabetic retinopathy.

Diabetic retinopathy (DR) is the most severe of several ocular complications of diabetes. The earliest clinical signs of DR are microaneurysms and haemorrhages. Later signs include dilated, tortuous irregular veins and retinal non-profusion, leading to retinal ischaemia that ultimately results in neovascularisation. Diabetic macular oedema, which involves the breakdown of the blood-retinal barrier, also occurs and is responsible for a major part of vision loss, particularly in Type 2 diabetes. The pathogenesis of DR is very complex. Many biochemical mechanisms have been proposed as explanations for the development and progression of DR. Chronic hyperglycaemia leads to oxidative injury, microthrombi formation, cell adhesion molecule activation, leukostasis and cytokine activation. Next, ischaemia-mediated overexpression of growth factors and cytokines occurs. These factors include vascular endothelial growth factor, insulin-like growth factor-1, angiopoetin-1 and -2, stromal-derived factor-1, fibroblast growth factor-2 and tumour necrosis factor. Because of the complex interplay between these factors, targeting a single growth factor will be unlikely to result in therapeutic inhibition of angiogenesis. These growth factors no doubt act in synergy to mediate the steps of angiogenesis, including protease production, endothelial cell proliferation, migration and tube formation. This review attempts to provide an overview of perspectives regarding the pathogenesis of this disease. The focus, however, is on describing the unique features of selected relevant factors and how each growth factor may act in a synergistic manner with other factors.

Animals↗

Further analysis of interpolation effects in mutual information-based image registration.

This paper presents an analysis of the mutual information (MI) metric in rigid-body registration of two digital images, in particular, local fluctuations of the MI value due to interpolation. In contrast to existing work in this area, this paper starts with two hypothetical continuous images, based on which both sampling and interpolation effects are analyzed. This analysis indicates that an "ideal" interpolator may not be able to completely suppress the undesirable local minima of the MI metric if the sampling effect is not negligible. Several preprocessing methods are discussed for reducing the interpolation effects.

Algorithms↗

[Surveillance of Escherichia coli O157:H7 among animals in Jiangsu province in 1999].

OBJECTIVE: To understand the Escherichia coli O157:H7 carrier rate of host animals and the toxic gene of the strains in different areas in Jiangsu province. METHODS: Surveillance spots were set up in different areas, to collect feces of pigs, chickens, sheep, cattle to culture for O157:H7 with immunomagnetic separation as well as detection of toxic gene of the strain with MPCR were both carried out. RESULTS: One hundred and seventy strains of O157:H7 were separated from 1 767 feces of different animals in six spots, with a overall positive rate 9.62%. The positive rates of cattle and sheep were 19.05% and 12.01% respectively. Among 85 strains SLT1, SLT2, eaeA and hly toxic genes were detected. In which, 56.47% of the strains were positive curturely while 79.17% of them carried SLT2, eaeA and hly gene simultaneously. CONCLUSION: The positive rate of O157:H7 in animals and the positive rates of strains were correlated to the incidence of the area. The highest rates were seen in areas where there had been O157:H7 epidemic, followed by the areas where there were only scattered cases identified while the lowest was in areas with no patients. Data indicated that it was important to enforce the surveillance of O157:H7 in animals to better predict and control of the disease.

Animals↗