Publications (83) View all
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Article: Endothelial Progenitor Cell Dysfunction in Cardiovascular Diseases: Role of Reactive Oxygen Species and Inflammation.
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ABSTRACT: Endothelial progenitor cells (EPCs) move towards injured endothelium or inflamed tissues and incorporate into foci of neovascularisation, thereby improving blood flow and tissue repair. Patients with cardiovascular diseases have been shown to exhibit reduced EPC number and function. It has become increasingly apparent that these changes may be effected in response to enhanced oxidative stress, possibly as a result of systemic and localised inflammatory responses. The interplay between inflammation and oxidative stress affects the initiation, progression, and complications of cardiovascular diseases. Recent studies suggest that inflammation and oxidative stress modulate EPC bioactivity. Clinical medications with anti-inflammatory and antioxidant properties, such as statins, thiazolidinediones, angiotensin II receptor 1 blockers, and angiotensin-converting enzyme inhibitors, are currently administered to patients with cardiovascular diseases. These medications appear to exert beneficial effects on EPC biology. This review focuses on EPC biology and explores the links between oxidative stress, inflammation, and development of cardiovascular diseases.BioMed research international. 01/2013; 2013:845037. -
Article: Reduced number and impaired function of circulating endothelial progenitor cells in patients with abdominal aortic aneurysm.
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ABSTRACT: AIM: Circulating endothelial progenitor cells (EPCs) are associated with coronary artery disease (CAD) and predict its outcome. Although the pathophysiology of abdominal aortic aneurysm (AAA) is different, it shares some risk factors with CAD. Therefore, the correlation between EPCs and AAA was investigated. METHODS AND RESULTS: Seventy-eight subjects (age 77.2±7.8years) with suspected AAA were prospectively enrolled. Cut-off values (men, 3.5-5.5cm; women, 3-5cm) were used to define normal aorta, small AAA, and large AAA on thoraco-abdominal computer tomography. Endothelial function was measured by flow-mediated vasodilation (FMD). Flow cytometry and colony-forming units (CFUs) were used to evaluate circulating EPC numbers. Circulating EPCs were defined as mononuclear cells with low CD45 staining and double-positive staining for KDR, CD34, or CD133. Late out-growth EPCs were cultured from six patients with large AAAs and six age- and sex-matched controls to evaluate proliferation, adhesion, migration, tube formation, and senescence. FMD was significantly lower with large (5.26%±3.11%) and small AAAs (6.31%±3.66%) than in controls (8.88%±4.83%, P=0.008). Both CFUs (normal 38.39±12.99, small AAA 21.22±7.14, large AAA 6.98±1.97; P=0.026) and circulating EPCs (CD34(+)/KDR(+) and CD133(+)/KDR(+)) were significantly fewer in AAA patients than in controls. On multivariate analysis, CFUs and circulating EPCs (CD34(+)/KDR(+)) were independently, inversely correlated to AAA diameter. Proliferation, adhesion, migration, tube formation, and senescence of late EPCs were significantly impaired in AAA patients. CONCLUSION: The number and function of EPCs were impaired in AAA patients, suggesting their potential role in AAA.International journal of cardiology 11/2012; · 7.08 Impact Factor -
Article: Functional preservation of deep brain stimulation electrodes after brain shift induced by traumatic subdural haematoma - case report.
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ABSTRACT: A Parkinson's disease patient with deep brain stimulation (DBS) implantation experienced an acute subdural haematoma (SDH) after a fall. The DBS electrodes and brain parenchyma were shifted. Fortunately, the patient recovered after craniectomy and removal of SDH, and the DBS was re-activated with the same parameters. Patients with DBS implants who suffer a traumatic brain injury do not necessarily incur permanent implant failure; there is every chance that the DBS may continue to work as reported here.British Journal of Neurosurgery 11/2012; · 0.88 Impact Factor -
Article: High expression of heme oxygenase-1 is associated with tumor invasiveness and poor clinical outcome in non-small cell lung cancer patients.
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ABSTRACT: BACKGROUND: Heme oxygenase-1 (HO-1), a rate-limiting enzyme in heme catabolism, is known to play a role in the protection of cells against oxidative stress, inflammation, anomalous proliferation and apoptosis. As yet, the role of HO-1 expression in non-small cell lung cancer (NSCLC) development and metastasis remains unclear and insufficient data are available regarding its impact on the prognosis of NSCLC patients. METHODS: Seventy NSCLC patients who underwent surgical resection were included in this HO-1 expression study and, concomitantly, clinical parameters were collected. Two lung adenocarcinoma cell lines (A549 and H441) were used to assess both invasive and migratory parameters in vitro. RESULTS: NSCLC patients with a high HO-1 expression ratio (tumor tissue/normal tissue) (> 1) exhibited a significantly poorer prognosis and a higher metastatic rate compared to those with a low HO-1 expression ratio (p < 0.05). The invasive and migratory abilities of A549 and H441 cells significantly increased after exogenous HO-1 over-expression and significantly decreased after siRNA-mediated HO-1 expression silencing. HO-1 up- and down-regulation also positively correlated with the expression of metastasis-associated proteins EGFR, CD147 and MMP-9. In addition, we found that HO-1 expression can be inhibited by PI3K and AKT inhibitors, but not by MAPK inhibitors. CONCLUSIONS: HO-1 is a poor prognostic NSCLC predictor and its over-expression may increase the metastatic potential of NSCLC. Based on our findings and those of others, HO-1 may be considered as a novel NSCLC therapeutic target.Cellular oncology (Dordrecht). 10/2012; -
Article: Stress urinary incontinence following vaginal trauma involves remodeling of urethral connective tissue in female mice.
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ABSTRACT: The molecular mechanisms underlying stress urinary incontinence (SUI) are not clear. This study was conducted to evaluate molecular alterations in the urethras of mice with experimentally induced SUI. Eighteen virgin female mice were equally distributed into three groups as follows: two groups undergoing vaginal distension (VD) for 1 h with 3 mm and 8 mm dilators each, and a non-instrumented control group. Changes in leak point pressure (LPP), morphology, lysyl oxidase (LOX) expression and the metabolism of urethral connective tissue were assessed. The LPP was significantly decreased in the 3 mm and 8 mm VD groups compared with that in the control group. Collagen and elastin expression in the urethra was significantly decreased in the 8 mm VD group compared with that in the control group, while LOX expression was significantly enhanced. SUI following vaginal trauma involves over-expression of LOX and decreased synthesis of extracellular matrix components or increased proteolysis in the urethra.European journal of obstetrics, gynecology, and reproductive biology 05/2012; 163(2):224-9. · 1.97 Impact Factor
