Search

Your search keyword '"Gokten, Murat"' showing total 13 results
Start Over Author "Gokten, Murat" Publication Year Range Last 10 years
13 results on '"Gokten, Murat"'

3. Pruritus: An Overlooked Symptom of Spinal Tumors.

Author

Gökten, Dilara Bulut, Gokten, Murat, and Mercan, Rıdvan

Subjects
*PERIPHERAL nervous system, *THYROID gland function tests, *BLOOD cell count, *BLOOD sedimentation, *KIDNEY function tests, *ITCHING
Abstract

A 65-year-old female patient, with no known diseases and no regular medication usage, presented with a complaint of itching that had been ongoing for the past two years. Itching initially started in approximately five cm areas on the bilateral below-knee flexor surfaces. The patient, whose complaints persisted, was referred to the internal medicine outpatient clinic by dermatology. On physical examination, erythematous excoriated papules were observed in the areas affected by itching. The patient's blood sugar, liver and kidney function tests, complete blood count, erythrocyte sedimentation rate, thyroid function tests, urinalysis, stool parasitology were all normal or negative. The patient reported a sensation of coldness in the same area, was referred to neurosurgery to investigate the etiology of possible neuropathic itching. The patient's spinal imaging, revealed a spinal mass. She underwent surgery performed by a neurosurgeon, during which the spinal mass was completely removed. She reported that her itching had completely disappeared post-operatively. The concept of itching as a variant of pain is not very new. Any damage occurring in the central nervous system or peripheral nervous system that affects the neurons responsible for transmitting and processing itch can lead to neuropathic itching. Focusing on spinal cord pathologies, any condition that damages the spinal cord may cause itching, depending on the level of damage. In cases of itching with dermatomal localization, where pain, hot or cold sensations, and paroxysmal itching are present, additional imaging methods or investigations for etiology should be performed. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

5. Neuroprotective Effects of Milrinone on Acute Traumatic Brain Injury

Author

Açıkalın, Ridvan, Zırh, Selim, Sezer, Can, Gokten, Murat, Sezer, Aykut, Bilgin, Emre, Zirh, Elham Bahador, Açıkalın, Ridvan, Zırh, Selim, Sezer, Can, Gokten, Murat, Sezer, Aykut, Bilgin, Emre, and Zirh, Elham Bahador

Abstract

BACKGROUND: Traumatic brain injury is still an important health problem worldwide. Traumatic brain injury not only causes direct mechanical damage to the brain but also induces biochemical changes that lead to secondary nerve cell loss. In this study, we investigated the neuroprotective effect of milrinone after traumatic brain injury (TBI) in a rat model. METHODS: Forty male Wistar albino rats, were used. Rats were divided into 4 groups: 1) sham, 2) TBI, 3) TBI + Ringers, and 4) TBI + Milrinone. In group 1 (sham), only craniotomy was performed. In group 2 (TBI), TBI was performed after craniotomy. In group 3 (TBI + Ringer), TBI was performed after craniotomy and intraperitoneal Ringers solution was given immediately afterward. Group 4 (TBI + Milrinone), TBI was performed after craniotomy, and milrinone was given 1.0 mg/kg milrinone intraperito-neally directly (0.5 mg/kg milrinone intraperitoneally again 24 hours, 48 hours, and 72 hours after trauma). Tests were performed for neurological and neurobehavioral functions. Immunohistochemistry and histopathology studies were performed. RESULTS: In group 4 compared with group 2 and group 3 groups, tests for neurological functions and neuro-behavioral functions were significantly better. In the mil-rinone treatment used in group 4, plasma and brain tissue tumor necrosis factor, 8-OH 2-deoxyguanosine , and inter-leukin 6 levels were significantly decreased, and increased plasma and tissue IL-10 levels were detected. Histopathological spinal cord injury and apoptotic index increased in groups 2 and 3, while significantly decreasing in group 4. CONCLUSIONS: This study shows for the first time that the anti-inflammatory, antioxidant and antiapoptotic prop-erties of milrinone may be neuroprotective after TBI.

Published
2023

6. Neuroprotective Effects of Milrinone on Acute Traumatic Brain Injury

Author

Zırh, Selim, Zirh, Elham Bahador, Gokten, Murat, Sezer, Aykut, Sezer, Can, Açıkalın, Ridvan, Bilgin, Emre, Zırh, Selim, Zirh, Elham Bahador, Gokten, Murat, Sezer, Aykut, Sezer, Can, Açıkalın, Ridvan, and Bilgin, Emre

Abstract

BACKGROUND: Traumatic brain injury is still an important health problem worldwide. Traumatic brain injury not only causes direct mechanical damage to the brain but also induces biochemical changes that lead to secondary nerve cell loss. In this study, we investigated the neuroprotective effect of milrinone after traumatic brain injury (TBI) in a rat model. METHODS: Forty male Wistar albino rats, were used. Rats were divided into 4 groups: 1) sham, 2) TBI, 3) TBI + Ringers, and 4) TBI + Milrinone. In group 1 (sham), only craniotomy was performed. In group 2 (TBI), TBI was performed after craniotomy. In group 3 (TBI + Ringer), TBI was performed after craniotomy and intraperitoneal Ringers solution was given immediately afterward. Group 4 (TBI + Milrinone), TBI was performed after craniotomy, and milrinone was given 1.0 mg/kg milrinone intraperito-neally directly (0.5 mg/kg milrinone intraperitoneally again 24 hours, 48 hours, and 72 hours after trauma). Tests were performed for neurological and neurobehavioral functions. Immunohistochemistry and histopathology studies were performed. RESULTS: In group 4 compared with group 2 and group 3 groups, tests for neurological functions and neuro-behavioral functions were significantly better. In the mil-rinone treatment used in group 4, plasma and brain tissue tumor necrosis factor, 8-OH 2-deoxyguanosine , and inter-leukin 6 levels were significantly decreased, and increased plasma and tissue IL-10 levels were detected. Histopathological spinal cord injury and apoptotic index increased in groups 2 and 3, while significantly decreasing in group 4. CONCLUSIONS: This study shows for the first time that the anti-inflammatory, antioxidant and antiapoptotic prop-erties of milrinone may be neuroprotective after TBI.

Published
2023

13. The Effect of Intravenous L-Carnitine on the Vasospasm Process in the Experimental Subarachnoid Hemorrhage Model.

Author

Soyer A, Gokten M, Oge K, and Soylemezoglu F

Subjects
Animals, Carnitine therapeutic use, Disease Models, Animal, Male, Rabbits, Vasospasm, Intracranial drug therapy, Basilar Artery drug effects, Carnitine administration & dosage, Subarachnoid Hemorrhage complications, Vasospasm, Intracranial etiology
Abstract

Aim: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is an important cause of morbidity and mortality. In this study, we examined the effects of L-carnitine on the cerebral vasospasm process., Material and Methods: Twenty male New Zealand white rabbits were randomly divided into 4 groups. Group 1 served as control; group 2 was not subjected to SAH and received intravenous L-carnitine 3 times; group 3 was subjected to SAH and group 4 was subjected to SAH and treated with 100 mg/kg intravenous L-carnitine at 0, 24, and 48 hours after SAH. All animals were euthanized by perfusion-fixation 72 hours after SAH induction. The brains were then removed and stored in fixative +4°C overnight. The subjects" basilar arteries were sectioned from four separate zones. Basilar artery cross-sectional areas and thicknesses of vessels were measured by using the SPOT for Windows Version 4.1 computer programme. Statistical comparisons were performed by using the Kruskal-Wallis and Mann-Whitney U tests., Results: Basilar artery wall thicknesses in group 4 were significantly lower than in group 3 (p=0.009). Basilar artery cross-sectional areas in group 4 were higher than in group 3 and the difference was statistically significant (p=0.008)., Conclusion: L-carnitine was shown to be potentially beneficial on the resolution of cerebral vasospasm following SAH.

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results