Yurdal Serarslan

Caffeic acid phenethyl ester protects rabbit brains against permanent focal ischemia by antioxidant action: A biochemical and planimetric study

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on brain injury after focal permanent cerebral ischemia, and to determine the possible antioxidant mechanisms. Cerebral infarction in adult male New Zealand rabbits was induced by microsurgical procedures producing right focal permanent middle cerebral artery occlusion (pMCAO). CAPE was administered to the treatment group after pMCAO at a dose of 10 micromol kg(-1) once a day intraperitoneally for 7 days. Neurological deficits were evaluated, using a modified six-point scale. Spectrophotometric assay was used to determine the contents of malondialdehyde (MDA), glutathione (GSH), catalase (CAT), nitric oxide (NO) and xanthine oxidase (XO). In the ipsilateral hemisphere, the infarct volume of the brain was assessed in brain slices stained with heamatoxylen and eosin. The results showed that treatment with CAPE significantly reduced the percentage of infarction in the ipsilateral hemisphere compared with the ischemia group. CAPE treatment significantly attenuated the elevation of plasma MDA, CAT and XO content (p<0.05), whereas it significantly increased the levels of plasma GSH and NO (p<0.05). Therefore, subacute CAPE administration plays a protective role in focal pMCAO due to attenuation of lipid peroxidation and its antioxidant activity. All of these findings suggest that CAPE provides neuroprotection against cerebral ischemia injury through its antioxidant action.

Protective effects of tadalafil on experimental spinal cord injury in rats

Tadalafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Nitric oxide (NO) functions as a retrograde neurotransmitter in the spinal cord, and postsynaptic structures respond to NO by producing cGMP. The concentrations of cGMP in the spinal cord are controlled by the actions of PDE. The aim of the study was to evaluate and compare the effects of the use of both methylprednisolone and tadalafil on serum and tissue concentrations of NO, malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and tissue glutathione peroxidase (GSH-Px) activity in rats with spinal cord injury (SCI). SCI was induced in Wistar albino rats by dropping a 10 g rod from a 5.0 cm height at T8-10. The 28 rats were randomly divided into four equal groups: tadalafil, methylprednisolone, non-treatment and sham groups. Rats were neurologically tested at 24 hours after trauma. At the end of the experiment, blood samples were collected and spinal cord tissue samples were harvested for biochemical evaluation. The tissue level of NO was increased in the tadalafil group compared with the non-treatment and methylprednisolone groups (p<0.05). The tissue levels of SOD and GSH-Px did not differ between the groups. Serum levels of NO were higher in the tadalafil group than in the non-treatment group (p<0.05). The increase in serum SOD levels was greater in the tadalafil group than the methylprednisolone group. Serum MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group (p>0.05). Tissue MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group and sham groups (p>0.05). Although there was no difference in neurological outcome scores between the tadalafil, methylprednisolone and non-treatment groups (p>0.05), the animals in the tadalafil and methylprednisolone groups tended to have better scores than the non-treatment group. Thus, tadalafil appears to be beneficial in reducing the effects of injury to the spinal cord by increasing tissue levels of NO and serum activity of SOD.

Morphometry of the thoracolumbar vertebrae in sickle cell disease

Patients with sickle cell disease (SCD) who have deformities and vertebral fractures due to osteoporosis may require surgery. Spinal surgeons must become familiar with the vertebral morphometry of patients with SCD and to that aim we have examined the morphometry of the thoracolumbar spine in these patients. A cohort of 100 patients with SCD was examined using plain thoraco lumbar anteroposterior/lateral radiographs and dual energy X-ray absorptiometry (DEXA). Vertebral morphometry (vertebral body diameters, pedicle, spinal canal and deformity) was assessed for different age groups. Results were compared to published studies of healthy subjects. The vertebral dimensions for the 16-20-year and the 21+-year-old groups were significantly smaller for females than males at most spinal levels, while measurements in the 6-10 years and 11-15 years age groups were similar across both sexes at most levels. No significant statistical difference was found between the diameters of the right and left pedicles. With the exception of the sagittal diameter, most of the dimensions of the vertebral bodies measured in SCD patients were less than those of healthy individuals; multiple deformities were also observed. Low bone density was noted in 32 patients. Our data highlight the differences in vertebral bone mineral density, anatomy and deformities in patients with SCD compared to healthy individuals. When considering surgical intervention for patients with SCD, it is important that pre-operative radiography and planning is undertaken, and that the surgeon is familiar with the geometry of the pedicles of the thoracolumbar vertebrae necessary for the safe insertion of pedicle screws. Osteoporosis must be considered when planning surgical interventions in these patients.

Bowel Perforation and Transanal Protrusion of a Ventriculoperitoneal Shunt Catheter

148 mg/dl. CSF was clear and colorless. On CSF examination, protein level was 42 mg/dl, glucose 72 mg/dl and leukocytes were not seen. Abdominal X-ray demonstrated the VP shunt placed inside the transverse and descending colon ( fi g. 2 ). At laparotomy we detected that the peritoneal catheter perforated the middle of the transverse colon and was wrapped with omentum and fi brous tissue. There were adhesions among the bowel loops and a focal abscess at the perforation area. The VP shunt was removed and perforation repaired primarily. The patient was discharged on the 10th postoperative day. Introduction

Being a neighbor to Syria: A retrospective analysis of patients brought to our clinic for cranial gunshot wounds in the Syrian civil war

OBJECTIVE Toward the end of 2010, the Arab spring, the waves of revolutionary demonstrations and protests influenced also Syria, where violent clashes turned into a civil war. Hundreds of thousands of people became refugees. The use of excessive force unfortunately culminated in numerous deaths and injuries in many cities. Being the closest city to Aleppo, Damascus and Homs, the biggest cities of Syria, Antioch/Hatay has been the city where initial emergency treatments were performed. For this reason, we examined and retrospectively analyzed the medical records of the patients treated in the clinics of our hospital due to cranial gunshot wounds during the war. MATERIAL AND METHODS The medical records of 186 patients who were injured in the Syrian War and brought to, followed up and treated in the Neurosurgery Clinic of Mustafa Kemal University, Faculty of Medicine in Hatay, a Turkish city on the Syrian border, between April 2011 and June 2013. RESULTS A total of 186 patients were evaluated in a period of more than 2 years. Of all 91.4% of the patients were adults (male/female: 152/18) and 8.6% of them were pediatric patients (male/female: 14/2). The average age of the patients was 31 years, with an age range of between 2 months and 67 years. According to Glasgow coma score (GCS) of the patients at the time of admission, GCS was 3 in 32 patients (17.2%), between 4 and 7 in 70 patients (37.6%), and between 8 and 15 in 84 patients (45.1%). We observed that the patients with GCS of 4-7 had a significantly lower mortality among the 56 patients treated surgically compared with the 14 patients treated medically. DISCUSSION Cranial gunshot wounds are responsible for high mortality and morbidity. A multiplicity of factors plays a role on morbidity and mortality. These are the duration of transport, the injury pattern, the velocities of the weapons used, and the Glasgow Coma Scales of the patients at the time of admission. CONCLUSION The authors recommend that the patients with cranial gunshot wounds who has GCS of 4-7 should be aggressively treated including surgery as well. We do not recommend surgical treatment for patients with GCS of 3. All our experiences show that treatment of gunshot wounds will continue to be a matter of debate, about which there is more to learn. The data presented in this study will once again demonstrate the seriousness of the event, and will, perhaps, contribute to the peace negotiations to end the war.

Protective Effects of Edaravone on Experimental Spinal Cord Injury in Rats

Background: Spinal cord injury (SCI) is a leading cause of morbidity and mortality among youth and adults. Secondary injury mechanisms within the spinal cord (SC) are well known to cause deterioration after an acute impact. Free radical scavengers are among the most studied agents in animal models of SCI. Edaravone is a scavenger of hydroxyl radicals. Methods: We aimed to measure and compare the effects of both methylprednisolone and edaravone on tissue and on serum concentrations of nitric oxide (NO), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and tissue total antioxidant capacity (TAC) in rats with SCI. SCI was induced in four groups of Wistar albino rats by a weight-drop method. The neurological function of the rats was periodically tested. At the end of the experiment, blood samples were collected, and SC tissue samples were harvested for biochemical evaluation. Results: The tissue level of NO was decreased in the edaravone-treated group compared with the no-treatment group (p < 0.05). The tissue levels of SOD and GSH-Px were higher in the edaravone-treated group than in the no-treatment group (p < 0.05). The serum levels of NO were lower in the edaravone-treated and methylprednisolone-treated groups than in the no-treatment group (p < 0.05). The serum levels of SOD in the edaravone-treated group did not differ from those of any other group. The serum levels of MDA in the edaravone-treated and no-treatment groups were higher than in the two other groups (p < 0.05). Tissue levels of MDA in the edaravone-treated group were lower than in the no-treatment group (p < 0.05). Tissue levels of TAC in the edaravone-treated group were higher than in the no-treatment and methylprednisolone-treated groups (p < 0.05). The neurological outcome scores of the animals in treatment groups did not depict any statistically significant improvement in motor functions. However, edaravone seemed to prevent further worsening of the immediate post-SCI neurological status. Conclusion: Our biochemical analyses indicate that edaravone is capable of blunting the increased oxidative stress that follows SCI. We show, for the first time, that edaravone enhances the TAC in SC tissue. This beneficial effect of edaravone on antioxidant status may act to minimize the secondary neurological damage that occurs during the acute phase after SCI.

Effects of trimetazidine on crush injury of the sciatic nerve in rats: A biochemical and stereological study

Trimetazidine (TMZ) is an anti-ischemic agent which has been used for years as an effective anti-anginal agent in cardiac patients. The aim of the study was to investigate the effect of TMZ on the level of malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), catalase (CAT), histopathological changes and the number of myelinated axons in a crush injury model of sciatic nerve in rats. In this study, 50 Wistar albino rats were used and the right sciatic nerves of all animals were injured. They were randomly divided into two groups equal in number, called treatment and non-treatment groups. The animals were subdivided into four subgroups, non-injury/non-treatment (left sciatic nerves of non-treatment animals, NI-NT) and non-injury/treatment (left sciatic nerves of treatment animals, NI-T) and injury/non-treatment (right sciatic nerves of non-treatment animals, I-NT) and injury/treatment (right sciatic nerves of treatment animals, I-T). At the end of the experiment, the bilateral sciatic nerves and blood samples collected from these animals were analyzed using histological, stereological and biochemical methods. There was a progressive increase in the serum level of GSH and progressive decrease in serum MDA levels in the treatment group. Progressive decrease in serum NO levels was observed in the treatment groups and it was statistically significant on day 14 (p<0.05) compared to the non-treatment group. The activities of CAT were low in the treatment groups on days 21 (p<0.05) and 42 (p<0.05). In the NI-NT group, some unimportant degenerative changes such as irregularity in myelin sheets were observed. Many pathologic changes in the I-NT group and some minimal degeneration in the I-T group were observed. TMZ treatment resulted in increases in the myelinated axon numbers by a range of 223 to 604 in the I-NT group compared to the I-T. In conclusion, TMZ appears to be beneficial for induction of axonal regeneration and myelination in healthy nerves as well as injured nerves.

Effects of ebselen on ischemia/reperfusion injury in rat brain

Aim: Interruption of blood flow may result in considerable tissue damage via ischemia/reperfusion (I/R) injury-induced oxidative stress in brain tissues. The aim of the present study was to investigate the effects of Ebselen treatment in short-term global brain I/R injury in rats. Material and Methods: The study was carried out on 27 Wistar-albino rats, divided into three groups including Sham group (n = 11), I/R group (n = 8) and I/R+Ebselen group (n = 8). Results: Malondialdehyde (MDA) levels were significantly increased in I/R group in comparison with the Sham group and I/R+Ebselen group (p < 0.001 and p < 0.01). Superoxide dismutase (SOD) activity was significantly lower in I/R group in comparison to both Sham (p < 0.001) and I/R+Ebselen (p < 0.01) groups. Similarly, SOD activity was decreased in I/R+Ebselen group when compared with Sham group (p < 0.001). Sham and I/R groups were similar in terms of nitric oxide (NO) levels. In contrast, the NO level was lower in I/R+Ebselen group when compared with Sham (p < 0.001) and I/R (p < 0.01) groups. There was no significant difference among the groups in terms of glutathione peroxidase and catalase activities. In histopathological examination, the brain tissues of rats that received Ebselen showed morphological improvement. Conclusion: Ebselen has neuron-protective effects due to its antioxidant properties as shown by the decrease in MDA overproduction, increase in SOD activity and the histological improvement after administration of Ebselen to I/R in brain tissue.

The relationship between the neuron density of the trigeminal ganglion and the posterior communicating artery vasospasm in subarachnoid hemorrhage an experimental study

ObjectivePosterior communicating arteries (PComAs) are innervated by vasodilatatory fibers of the trigeminal ganglion (TGG). We examined whether there is a relationship between the neuron density of the TGG and the severity of PComA vasospasm in a subarachnoid hemorrhage (SAH). MethodsThis study was conducted on 20 rabbits. Five were used as a baseline control group. Five were used as a sham group by injecting 1 mL of serum physiologic, and experimental SAH was applied to 10 animals by injecting homologous blood into the cisterna magna. After 10 days, PComAs and TGGs were examined histopathologically. PComA volumes and the neuron density of TGGs were estimated stereologically, and the results were analyzed statistically. ResultsIn control group, the mean volume of the PComAs was 66,500±8500 &mgr;m3, and the mean neuronal density of the TGGs was 8650±950/mm3. In the serum physiologic group, the mean volume of the PComAs was 65,000±6550 &mgr;m3, and the mean neuronal density of the TGGs was 8600±800/mm3. In the SAH group, the mean volume of the PComAs was 46,500±5500 &mgr;m3, and the mean neuronal density of the TGGs was 4200±500/mm3. The results reveal an inverse relationship between the neuronal density in the TGG and the severity of the PComA vasospasm. ConclusionsThe neuron density of the TGG may be an important factor in the regulation of PComA volume and in the continuation of cerebral blood flow. Low neuron density in the TGG may play an important role in the pathogenesis of PComA vasospasm in SAH.

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

The aim of this study was to assess the effects of minocycline on cerebral ischemia-reperfusion (I/R) injury in rats. The study was carried out on 24 male Wistar albino rats, weighing 200-250 g, which were divided into three groups: (i) control (n = 8), (ii) I/R (n = 8) and (iii) I/R + minocycline (n = 8). Minocycline was administrated at a dose of 90 mg/kg p.o. to the I/R group 48, 24 and 1 h before ischemia. Following bilateral exposure of the common carotid arteries by anterior cervical dissection and separation of the vagus nerve, I/R injury was performed by occlusion. Following reperfusion, malondialdehyde (MDA), superoxide dismutase, glutathione peroxidase and catalase levels in the blood and brain tissue, and creatine kinase (CK), CK-BB, lactate dehydrogenase (LDH), neuron-specific enolase (NSE) and protein S100β levels in the blood were measured and the histopathological changes were monitored. Regarding histopathological evaluation, symptoms of degeneration were significantly improved in the I/R + minocycline group compared to the I/R-only group. Statistical analysis of the biochemical parameters revealed significant differences in MDA (p < 0.001), nitric oxide (p < 0.05), CK (p < 0.05) and CK-MB (p < 0.05) levels between the I/R + minocycline group and the I/R group. According to the literature, the effect of minocycline is firstly assessed by LDH, CK-MB, NSE and S-100β analysis in addition to antioxidant status and histopathological analysis.