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1.  Neuroprotective effect of atorvastatin in spinal cord ischemia-reperfusion injury 
Clinics  2015;70(1):52-60.
OBJECTIVES:
Prevention of the development of paraplegia during the repair of the damage caused by descending thoracic and thoracoabdominal aneurysms remains an important issue. Therefore, we investigated the protective effect of atorvastatin on ischemia-induced spinal cord injury in a rabbit model.
METHOD:
Thirty-two rabbits were divided into the following four equally sized groups: group I (control), group II (ischemia-reperfusion), group III (atorvastatin treatment) and group IV (atorvastatin withdrawal). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs of each animal was evaluated according to the Tarlov score. Spinal cord and blood samples were obtained for histopathological and biochemical analyses.
RESULTS:
All of the rabbits in group II exhibited severe neurological deficits. Atorvastatin treatment (groups III and IV) significantly reduced the level of motor dysfunction. No significant differences were observed between the motor function scores of groups III and IV at the evaluated time points. Light microscopic examination of spinal cord tissue samples obtained at the 72nd hour of reperfusion indicated greater tissue preservation in groups III and IV than in group II.
CONCLUSION:
This study demonstrates the considerable neuroprotective effect of atorvastatin on the neurological, biochemical and histopathological status of rabbits with ischemia-induced spinal cord injury. Moreover, the acute withdrawal of atorvastatin therapy following the induction of spinal cord ischemia did not increase the neuronal damage in this rabbit model.
doi:10.6061/clinics/2015(01)10
PMCID: PMC4311118
Atorvastatin; Spinal Cord; Ischemia-Reperfusion Injury
2.  Role of Oxidative Stress on Vaginal Bleeding during The First Trimester of Pregnant Women 
Background:
Reactive oxygen species (ROS) are produced in many metabolic and physiologic processes. Antioxidative mechanisms remove these harmful species. Our aim was to assess whether serum total antioxidant capacity and total oxidant status altered during first trimester pregnancies with vaginal bleeding.
Materials and Methods:
In this cross-sectional study, A group of pregnant women at less than 10 weeks of gestation with vaginal bleeding (n=25) and a control group of healthy pregnancies with similar characteristics (n=25) were included. All of the patients in the two groups were matched for age, gestational age and body mass index. Serum total antioxidant capacity and total oxidant status levels were determined using a Hitachi 912 analyzer and compared between the two groups.
Results:
Characteristics, including maternal age, parity, and gestational age were similar between the two groups. Serum total antioxidant capacity levels were significantly lower in the women with vaginal bleeding than in control women (1.16 ± 0.20 vs. 1.77 ± 0.08 mmol Trolox Equiv./L; p=0.001), whereas higher total oxidant status measurements were found in women with vaginal bleeding compared to the control group (4.01 ± 0.20 vs. 2.57 ± 0.65 µmol H2O2 Equiv./L; p=0.001).
Conclusion:
Increased total oxidant status might be involved in the pathophysiology of vaginal bleeding during early first trimester pregnancies.
PMCID: PMC3901185  PMID: 24520496
Oxidative Stress; Vaginal Bleeding; First Trimester
3.  Uric Acid and Pentraxin-3 Levels Are Independently Associated with Coronary Artery Disease Risk in Patients with Stage 2 and 3 Kidney Disease 
American Journal of Nephrology  2011;33(4):325-331.
Background and Objectives
Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD.
Material and Methods
In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m2, we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score.
Results
The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 ± 1.5 mg/dl, 6.4 ± 3.4 ng/ml and 3.5 ± 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = −0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = −0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score.
Conclusions
SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD.
doi:10.1159/000324916
PMCID: PMC3064941  PMID: 21389698
Chronic kidney disease; Coronary artery disease; Uric acid; Pentraxin-3

Results 1-3 (3)