18 research outputs found
Open Discectomy vs. Microdiscectomy: Results from 519 Patients Operated for Lumbar Disc Herniation
Histopathological Investigation of the Effectiveness of Collagen Matrix in the Repair of Experimental Spinal Dura Mater Defects
Progesterone Treatment After Experimental Spinal Cord Injury
Objective/Background:A growing list of studies gives evidence for the efficacy of progesterone in the nervous systems. Neuroprotective effects of progesterone are well documented for the injured brain models in the literature. However, the effects of progesterone on spinal cord injury (SCI) should be investigated.Methods:Twenty adult male Wistar-Albino rats were included in the study. The rats were randomly allocated into two groups (Control and Progesterone). Progesterone was administered in five days at a dose of 4 mg/kg via intraperitoneal route. Each group underwent motor examination in sixth weeks using Basso, Beattie and Bresnehan (BBB) locomotor test.Results:The score mean values of the control and study groups receiving progesterone treatment after six weeks were 11.40.427 and 14.1 +/- 0.526, respectively (P<0.05). While the improvement process showed a nearly parallel course between the two groups until the end of the third week, the progesterone treated group exhibited a significant difference in BBB scores relative to the control starting from the fourth week (P<0.05). On the examined histological sections, it was determined that progesterone had clear neuroprotective effects.Conclusions:The results supported the fact that progesterone could be a potentially effective therapeutic strategy to treat SCI
Effect of Pregabalin in Preventing Secondary Damage in Traumatic Brain Injury: An Experimental Study
Background: In this study we aimed to explore the effects of pregabalin on a traumatic brain injury model in rats. Material/Methods: This study included 40 adult male Sprague-Dawley rats randomized into 4 groups, each of which contained equal numbers of animals. The control group had no head trauma and thus was not treated. The trauma group had head trauma but was not treated. The pregabalin group had no head trauma but was treated by pregabalin. The trauma + pregabalin group had head trauma treated with pregabalin. The biopsy samples taken from the study animals were histopathologically examined for the presence of edema, inflammation, and neuronal damage. Results: All animals in the trauma group had edema, inflammation, and neuronal damage. Four subjects in the control group, 6 in the pregabalin group, and 4 in the trauma + pregabalin group had edema; inflammation was present in 1 subject in the control group, 3 subjects in the pregabalin group, and 3 subjects in the trauma + pregabalin group; neuronal damage existed in 1 subject in the control group, 1 subject in the pregabalin group, and 6 subjects in the trauma + pregabalin group. The trauma group had significantly higher edema and neuronal damage scores than the other groups. Similarly, inflammation was significantly more prevalent in the trauma group than the control and trauma + pregabalin groups. Conclusions: The results of the present study indicated anti-edema, anti-inflammatory, and neuroprotective effects of pregabalin in an experimental head trauma model in rats. Pregabalin may thus be beneficial in humans with acute TBI by relieving concomitant edema and inflammation
A new described mechanisms of intestinal glandular atrophy induced by vagal nerve/Auerbach network degeneration following subarachnoid hemorrhage: The first experimental study
Stress ulcers is a trouble complication of subarachnoid hemorrhage (SAH). Although gastrointestinal ulcerations may be attributed to increased HCL secretion in SAH; the exact mechanism of that complication has not been investigated definitively. We studied if vagal network degeneration may cause intestinal atrophy following SAH. Study was conducted on 25 rabbits, with 5 control group (Group-A), 5 SHAM group (Group-B), and 15 SAH group via injection of autologue blood to cisterna magna. Seven animals followed for seven days (Early Decapitated-Group-C) and eight animals followed 21 days (Late Decapitated-Group-D). The vagal nodosal ganglia (NGs), Auerbach plexuses and goblet cells of duodenums were examined by current stereological methods and compared statistically. The mean numbers of degenerated axon density/mm(2) of gastric branches of vagal nerves was 8 +/- 2, 34 +/- 11, 189 +/- 49 and 322 +/- 81 in the Group A, B, C, and D respectively. The mean numbers of degenerated neuron density/mm(3) of NGs was 5 +/- 2, 54 +/- 7, 691 +/- 87 and 2930 +/- 410 in the Group A, B, C, and D respectively. The mean numbers of degenerated Auerbach neurons 2 +/- 1, 4 +/- 1, 12 +/- 3 and 27 +/- 5/mm(3) in the Group A, B, C, and D respectively. The mean numbers of degenerated goblet cells/mm(3) were 4.3 +/- 1.02, 11.5 +/- 0.26, 143 +/- 26 and 937 +/- 65 Group A, B, C, and D respectively. Statistical analysis showed that vagal network ischemia could cause intestinal bleeding and so atrophy in SAH progression. Statistical analyses of groups were; Group-D/Group-A < 0.001, Group-D/Group-B < 0.005, Group-C/Group-A < 0.005. Undiscovered effect of ischemic vagal network injuries should be regarded as a major cause of stress ulcerations following SAH which has not been mentioned in the literature. (C) 2018 Elsevier Ltd. All rights reserved
Protective effects of alpha-lipoic acid on experimental sciatic nerve crush injury in rats: assessed with functional, molecular and electromicroscopic analyses
Aim: The present study aimed to demonstrate protective effects of alpha lipoic acid on experimental sciatic nerve crush injury model assessed with functional and electronmicroscopy analyses. Methods: In this study, groups were; Group 1; sham operated, Group 2; applied only sciatic nerve crush (Control), Group 3; Sciatic nerve crush + treated ALA 25 mg/kg (received orally) and Group 4; Sciatic nerve crush + treated ALA 50 mg/kg. Subsequently, sciatic nerves crush injury induced by forceps. At the second and fourth week, all animals were evaluated for sciatic functional index (SFI) and histomorphometric analyses with electronmicroscopy. Results: The SFI was significantly increased for both ALA-treated groups 30 days post-injury compared with control groups. The elecronmicroscopy results demonstrated that the axon diameter, the myelin diameter, the area of regenerating axon and miyelin were better in the treatment group than in the control group. Also ALA decreased IL-1 beta and Caspase 3 levels that increased in SNC group. Conclusions: These results suggest that ALA neuroprotective agent for peripheral nerve injury (PNI) and promoted peripheral nerve regeneration via its anti-inflammatory and antiapoptotic effects
Correction to:Investigating recurrence in pilonidal sinus disease: results of a nationwide, multicenter study in Turkey (PISI TURKEY)
The collaborative Author names are missing in the published proof. The Supplementary material is updated with 2 additional names in the collaborative Author’s list. Ali Yalcinkaya, Ahmet Yalcinkaya, Sezai Leventoglu, Bengi Balci, Alp Ozgun Borcek, Elif Ozeller, Ece Ozturk, Gulsum Sueda Kayacan, Berkay Enes Karaca, Ahmet Faruk Oyanik, Omer Faruk Gul, Basak Bolukbasi, Huseyin Gobut, Cagri Buyukkasap, Aydin Yavuz, Dara Aydin, Zeynep Akdagcik, Alina Pataeva, Douigou Hasan, Omar Hussein, Arda Ozgur Ozturk, Cem Arda Elumar, Ali Derman Dere, Asra Zeynep Balci, Rasim Ozturk, Yasar Copelci, Murat Kartal, Serkan Tayar, Mustafa Yeni, Tolga Kalayci, Ramazan Yavuz, Bulent Calik, Semra Demirli Atici, Selen Ozturk, Gizem Kilinc, Korhan Tuncer, Cengiz Aydin, Mustafa Yener Uzunoglu, Alp Yildiz, Aybala Yildiz, Can Sahin, Mehmet Caglikulekci, Elbrus Zarbaliyev, Murat Sevmis, Baris Sevinc, Nurullah Damburaci, Omer Karahan, Ozgen Isik, Said Kural, Xhenet Hysejni, Ahmet Aktas, Baris Yildiz, Gultekin Ozan Kucuk, Ahmet Can Sari, Mert Candan, Mehmet Mahir Ozmen, Cem Emir Guldogan, Emre Gundogdu, Munevver Moran, Mevlut Recep Pekcici, Saygin Altiner, Enes Cebeci, Tugba Yigit, Bedri Burak Sucu, Mert Col, Omer Faruk, Ozkan Hanife, Seyda Ulgur, Murat Kalin, Emre Furkan Kirkan, Abdullah Yildiz, Sema Yukseksag, Cagri Buyukkasap, Erdinc Kamer, Mesut Ozogul, Nihan Acar, Melek Gokova Bekler, Arif Atay, Halis Bag, Server Sezgin Uludag, Ahmet Necati Sanli, Sefa Ergun, Ergin Erginoz, Veysi Basbayandur, Mehmet Faik Ozcelik, Ahmet Askar, Yuksel Altinel, Adnan Hacim, Serhat Meric, Merve Tokocin, Talar Aktokmakyan, Yunus Aktimur, Kamil Ozdogan, Fikret Calikoglu, Tugba Koc Calikoglu, Ahmet Barcin, Ahmed Salhat, Guray Durmaz, Volkan Ozben, Erman Aytac, Zumrud Aliyeva, Arda Ulas Mutlu, Mert Tanal, Mustafa Fevzi Celayir, Aydin Eray, Tufan Ali Yuksel, Elif Baran, Banu Yigit, Erhan Eroz, Aykhan Abbasov, Hakan Yanar, Huseyin Onur Aydin, Murathan Erkent, Tugan Tezcaner, Tevfik Avci, Murat Kus, Mehmet Abdussamet Bozkurt, Adem Ozcan, Nezihe Berrin Dodur Onalan, Serhan Yilmaz, Yasin Kara, Ali Kocatas, Fatih Yanar, Ali Fuat Kaan Gok, Irem Karatas, Berke Sengun, Ilknur Erenler Bayraktar, Onur Bayraktar, Zulal Emsal, Irem Dalkilic, Cengiz Dibekoglu, Sami Acar, Erman Ciftci, Yunus Yapalak, Cihad Tatar, Mert Mahsuni Sevinc, Ali Emre Nayci, Egemen Saygili, Yavuz Selim Komek, Bayram Kaymak, Fatih Altintoprak, Emrah Akin, Necattin Firat, Emre Gonullu, Ugur Can Dulger, Atilla Kurt, Sinan Soylu, Musa Serin, Omer Topcu, Ali Cihat Yildirim, Mehmet Fatih Ekici, Sezgin Zeren, Ismail Ahmet Bilgin, Tayfun Karahasanoglu, Ismail Hamzaoglu, Afag Aghayeva, Bilgi Baca, Inci Sahin, Osman Bozbiyik, Mustafa Ozgur Kilincarslan, Mustafa Ali Korkut, Erhan Akgun, Cemil Caliskan, Tayfun Yoldas, Timucin Erol, Hilmi Anil Dincer, Omer Cennet, Muhammed Salih Suer, Muhammet Bunyamin Dalkilic, Ibrahim Alkan, Busenur Kirimtay, Emre Balik, Emre Ozoran, Ibrahim Halil Ozata, Derya Salim Uymaz, Tutku Tufekci, Salih Nafiz Karahan, Orhan Agcaoglu, Naciye Cigdem Arslan, Mehmet Yilmaz, Orhan Ureyen, Can Murat Kale, Enver Ilhan, Eray Kara, Semra Tutcu Sahin, Onur Haspolat, Alperen Dalkiran, Ergun Yuksel, Mehmet Kocaoglu, Omer Tasan, Cevdet Tokat, Cihan Ozen, Alptug Mertcan Koc The Original article has been corrected.</p
