Serefden Acikgoz

Effects of dexmedetomidine or methylprednisolone on inflammatory responses in spinal cord injury

Background: The aim of this study was to compare the anti‐inflammatory response of methylprednisolone and the α2‐agonist dexmedetomidine in spinal cord injury (SCI).

Effect of coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats.

BackgroundHead trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out.ResultsIn the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05).ConclusionNeuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

Comparison of angiotensin-converting enzyme, malonaldehyde, zinc, and copper levels in preeclampsia

Preeclampsia is a syndrome of unknown etiopathogenesis. Recent studies carried out on preeclampsia have focused on the increase in free radicals in the feto-placental unit with poor perfusion. It is believed that the renin-angiotensin system (RAS) has a role in the poor perfusion of the placenta. It is uncertain whether there is a pre-existing impairment in RAS in pre-eclamptic pregnant women or not. In the present study, we measured angiotensin-converting enzyme (ACE), malonaldehyde (MDA), zinc, and copper levels in the placental tissue of 16 pre-eclamptic pregnant women and compared them with those in 20 healthy pregnant women.Whereas ACE activity and MDA were found to be high in the placentas of pre-eclamptic patients, zinc and copper levels were low and there was a negative correlation between ACE activity and zinc concentration. These findings suggest that high ACE activity might play a role in the increase in tissue hypoxia and consequent lipid peroxidation through vasoconstriction; zinc deficiency in the placental tissue might cause insufficiency of superoxide dismutase, an antioxidant enzyme. Furthermore, deficiency in placental zinc also plays a role in the biosynthesis of connective tissue, maintaining its integrity, which might have an impact on the structure of the spiral arteries

Inflammatory markers in preeclamptic patients.

Abstract Background: Preeclampsia is characterized by hypertension and proteinuria that begins in the second half of pregnancy. Endothelial dysfunction and trophoblastic hypoperfusion seen in preeclampsia suggested to be part of an increased maternal inflammatory response to pregnancy. In this study, we aimed to evaluate some inflammatory markers in pre-eclamptic and normotensive pregnants. Methods: The study included 36 cases with mild preeclamp-sia, 36 cases with severe preeclampsia and 33 cases of normotensive pregnant. High sensitive C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured by enzyme-linked immunosorbent assays, serum procalcitonin was measured by enzyme-linked fluorescent immunassay. Mean arterial pressure (MAP) was used as an indicator of the severity of the disease. Results: In severe preeclampsia group hsCRP, serum amyloid A and procalcitonin levels were significantly higher than mild preeclamptic and normotensive groups. SAA and hsCRP levels were higher in mild preeclamptic group when compared with normotensive pregnant but no significant difference was found in procalcitonin between these groups. There were significant correlations betweeen hsCRP, SAA, procalcitonin and MAP. Conclusions: The results confirm that inflammatory reactions are closely associated with preeclampsia.

Predictors of atrial fibrillation after coronary artery bypass surgery.

ObjectiveAtrial fibrillation is one of the most common arrhythmias associated with not only increased morbidity after coronary artery bypass grafting but also increased healthcare costs. Many factors are associated with atrial fibrillation onset after coronary artery bypass grafting. We prospectively examined which factors could predict atrial fibrillation after coronary artery bypass grafting. MethodsFifty-seven consecutive patients (37 men, mean age=60.2±12 years) with sinus rhythm before coronary artery bypass grafting are included the study. Clinical, demographic, laboratory and echocardiographic characteristics are all evaluated prospectively. The maximum and minimum P-wave duration (Pmax and Pmin) were measured from the 12-lead surface electrocardiogram. The difference between the Pmax and the Pmin was calculated and defined as P-wave dispersion. Preoperative venous blood samples were taken for N-terminal proBrain natriuretic peptide level analysis. ResultsTen (17%) patients had postoperative atrial fibrillation. Patients with postoperative atrial fibrillation were older (69.4±6 versus 58.2±12 years, P=0.01), had lower ejection fraction (44.1±8.9% versus 54.3±9; P=0.002), higher proBrain natriuretic peptide levels (538±136 pg/ml versus 293±359 pg/ml; P=0.03), longer Pmax (142.2±13.7 ms versus 120.8±21.2 ms; P=0.006) and longer P-wave dispersion (55.0±8.2 ms versus 41.3±14.3 ms; P=0.008) compared with the patients without atrial fibrillation. Univariate analysis showed that increased age (P=0.01), lower ejection fraction (P=0.02), enlargement of left atrium (P=0.02), increased Pmax (P=0.006) and increased P-wave dispersion (P=0.008) and increased level of preoperative proBrain natriuretic peptide (P=0.03) were associated with postoperative atrial fibrillation. Positive correlation was seen between the age and level of proBrain natriuretic peptide (r=0.322 and P=0.015). In multivariate analysis, age (P=0.05), lower ejection fraction (P=0.03), left atrial enlargement (P=0.05), longer Pmax (P=0.01) and P-wave dispersion (P=0.01) were found to be independent predictors of postoperative atrial fibrillation. ConclusionAge, poor left ventricular functions, Pmax and P-wave dispersion are found to be independent predictors of atrial fibrillation after coronary artery bypass grafting.

Oxidized low-density-lipoprotein accumulation is associated with liver fibrosis in experimental cholestasis

OBJECTIVE The aim of the present study was to examine the probable relationship between the accumulation of oxLDL and hepatic fibrogenesis in cholestatic rats. INTRODUCTION There is growing evidence to support the current theories on how oxidative stress that results in lipid peroxidation is involved in the pathogenesis of cholestatic liver injury and fibrogenesis. One of the major and early lipid peroxidation products, OxLDL, is thought to play complex roles in various immuno-inflammatory mechanisms. METHODS A prolonged (21-day) experimental bile duct ligation was performed on Wistar-albino rats. Biochemical analysis of blood, histopathologic evaluation of liver, measurement of the concentration of malondialdehyde (MDA) and superoxide-dismutase (SOD) in liver tissue homogenates, and immunofluorescent staining for oxLDL in liver tissue was conducted in bile-duct ligated (n = 8) and sham-operated rats (n = 8). RESULTS Significantly higher levels of MDA and lower concentrations of SOD were detected in jaundiced rats than in the sham-operated rats. Positive oxLDL staining was also observed in liver tissue sections of jaundiced rats. Histopathological examination demonstrated that neither fibrosis nor other indications of hepatocellular injury were found in the sham-operated group, while features of severe hepatocellular injury, particularly fibrosis, were found in jaundiced rats. CONCLUSION Our results support the finding that either oxLDLs are produced as an intermediate agent during exacerbated oxidative stress or they otherwise contribute to the various pathomechanisms underlying the process of liver fibrosis. Whatever the mechanism, it is clear that an association exists between elevated oxLDL levels and hepatocellular injury, particularly with fibrosis. Further studies are needed to evaluate the potential effects of oxLDLs on the progression of secondary biliary cirrhosis.

The effectiveness of dexmedetomidine in experimental spinal cord injury compared to methylprednisolone in rats.

The present study aimed to investigate the neuroprotective efficacy of dexmedetomidine in a rat experimental spinal cord injury model. The rats (n=40) were equally divided into four groups: G1, G2, G3, and G4. Rats in the G1 group underwent a laminectomy only. For the rats in the G2, G3, and G4 groups, spinal cord injury was induced by placing an aneurysm clip extradurally for 60 s at T10. The rats in G2 did not receive any post-injury treatment. Immediately after trauma was induced, rats in G3 were given methylprednisolone (30 mg/kg) and in G4, dexmedetomidine (10 microg/kg), both intraperitoneally. The rats were sacrificed under anesthesia 24 hours later and 1.5 cm lengths of injured spinal cord were obtained. Malonyldialdehyde values were significantly increased in G2 compared to G1, G3 and G4 (p<0.05). The neuronal cell count in G1 was significantly higher than in G2 and G3 (p=0.0001; p=0.007). G4 had higher cell counts compared to G2 and G3 (p=0.0001; p=0.05). These findings indicated that dexmedetomidine might have neuroprotective effects in spinal cord injury.

Lipid peroxidation and homocysteine levels in Behçet's disease.

Abstract Background: The aim of this study was to investigate serum paraoxonase (PON1) activity in relation to homocysteine, malondialdehyde (MDA) and lipid parameters in active and inactive Behçets disease (BD). Methods: A total of 46 consecutive BD patients and 25 healthy control subjects were included in the present study. Results: Serum PON1 activity in both active and inactive BD was significantly lower compared with healthy subjects (p<0.05). When compared to the control group, serum MDA levels were significantly higher in both active and inactive BD (p<0.05). Serum C-reactive protein (CRP) and homocysteine concentrations were significantly higher in active BD than those in inactive BD and control subjects (p<0.05). In addition, there was significant negative correlation between serum PON1 and MDA levels (r=−0.697, p<0.05) and serum PON1 activity was also negatively correlated with homocysteine levels (r=−0.428, p<0.05) in BD patients. Conclusions: Decreased PON1 could explain the increased lipid peroxidation and oxidative stress observed in BD. Also, according to our results, we suggest that homocysteine may contribute to decreased serum PON1 activity. Clin Chem Lab Med 2006;44:1115–8.

Is direct method of low density lipoprotein cholesterol measurement appropriate for targeting lipid lowering therapy

OBJECTIVES The aim of this study was to compare the Friedewald Formula with direct homogeneous low density lipoprotein cholesterol (LDL-C) assay for the detection of LDL-C levels. METHODS Fasting serum samples were obtained for lipid analysis from 1001 patients. Total cholesterol (TC) and triglyceride (TG) levels were measured with enzymatic methods and the measurements of high density lipoprotein cholesterol (HDL-C) and LDL-C levels were detected using direct methods. RESULTS The mean levels of serum TC, TG, HDL-C and LDL-C were detected with in the reference range. The LDL-C estimated by the Friedewald formula was significantly correlated (P<0.01) with the direct method but there was a negative bias among them. CONCLUSION Laboratories cannot use direct method as a substitute for Friedewald formula because direct method has not been standardized in large populations and increase cholesterol assay costs.

Low-Density Lipoproteins Oxidized After Intestinal Ischemia/Reperfusion in Rats

BACKGROUND Intestinal ischemia/reperfusion (I/R) is a complex phenomenon causing destruction of both local and remote tissues, as well as multiple-organ failure. We investigated the role of lipid peroxidation in damage to intestinal, liver, and lung tissues in this pathology. MATERIALS AND METHODS The superior mesenteric artery was blocked for 30 min followed by 24 h of reperfusion. Tissues were removed and the presence of oxidized LDL, the activities of the superoxide dismutase enzyme, malondialdehyde levels, and inducible nitric oxide synthase expression were each evaluated in the intestinal, liver, and lung tissues. RESULTS While there was no staining in the control group tissues, ischemia/reperfusion resulted in positive oxidized LDL staining in all of the I/R test group tissue samples. Inducible nitric oxide synthase expression was significantly increased in the ischemia/reperfusion group tissues. Compared with those of the control group rats, the ischemia/reperfusion group tissues showed significantly higher malondialdehyde levels and lower superoxide dismutase activities. CONCLUSIONS This study demonstrated for the first time that oxidized LDL accumulated in the terminal ileum, liver, and lung tissues after intestinal ischemia/reperfusion. This occurrence (or the presence of oxidized LDL) may be an indicator of ongoing oxidative stress and enhanced lipid peroxidation. Augmentation of inducible nitric oxide synthase expression may play a role in progression of inflammation and LDL oxidation. These data support the hypothesis that cellular oxidative stress is a critical step in reperfusion-mediated injury in both the intestine and end organs, and that antioxidant strategies may provide organ protection in patients with reperfusion injury, at least through affecting interaction with free radicals, nitric oxide, and oxidized LDL.