Ragıp Ortaç

Dr. Behcet Uz Children's Hospital, Nikfer, Denizli, Turkey

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Publications (17)16.91 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Medullary thyroid carcinoma (MTC) makes up 5–10% of thyroid malignancies. Small cell, squamous, giant cell or melanocytic differentiation can rarely be seen in MTCs. It is important to determine those with the potential to act aggressively such as cases with melanocytic differentiation at the time of diagnosis.Materials and methodA total of 46 MTC cases diagnosed at four different centers between 2002 and 2013 were included in the study. Immunohistochemical (IHC) staining with Melan-A and HMB-45 was performed in all cases.ResultsSix of the 46 MTC cases were medullary microcarcinomas and three were multicentric medullary carcinomas. There were 34 females and 12 males with a mean age at onset of 51.4 years and mean tumor diameter of 23.2 mm. Lymph node metastasis (LNM) was found in 13 of the 38 cases that had data regarding the lymph nodes. Immunohistochemically, Melan A staining was seen in four cases. HMB45 staining was seen in four cases. A statistically significant relationship was found between LNM and diameter, Melan A expression (p = 0.02, p = 0.03 respectively) but there was no significant relationship with HMB45 expression (p = 0.07). General survival data were present for 35 of the 46 cases. All cases without lymph node metastasis survived (21/21) while 8 of 11 cases with lymph node metastasis survived among cases with survival data; one case that was diffuse-strong positive for both HMB45 and Melan A was lost due to distant organ metastasis six months after the diagnosis.DiscussionShould the possibility of melanocytic differentiation be evaluated in cases where melanocytic differentiation is not reflected in the morphology (lack of pigment) in MTCs? We did not come across a study on the subject in the English literature. The effect of melanocytic differentiation on the prognosis in MTCs should be investigated in larger series.
    Pathology - Research and Practice 11/2014; · 1.56 Impact Factor
  • Turkiye Klinikleri Journal of Medical Sciences 01/2013; 33(3):678-684. · 0.10 Impact Factor
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    ABSTRACT: Angiomyxoma is a distinct soft tissue tumor characterized by the presence of prominent myxoid matrix and numerous thin-walled blood vessels. This tumor has a predilection for the trunk, head and neck, extremities, and genitalia. It is a benign tumor and total excision is curative. Recurrence is rare except for aggressive angiomyxomas. A 12-year-old girl with a 10-year history of a subcutaneous mass on the left gluteus measuring 4.5x4x3 cm had been referred. The tumor was encapsulated and was located in the reticular dermis and subcutaneous tissue, composed of stellate cells with mucinous stroma. Thin-walled blood vessels were prominent. Immunohistochemically, tumor cells were immunoreactive for vimentin. No immunoreactivity was present for estrogen receptor, CD34, smooth muscle actin, S-100 protein and desmin. The purpose of this report is to present a classical example of an isolated superficial angiomyxoma and discuss the differential diagnosis, because of its relatively infrequent occurence.
    Turk Patoloji Dergisi 01/2012; 28(2):162-4.
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    ABSTRACT: Objective: We describe the characteristic features of 11 patients (6 men and 5 women) with dysferlinopathies confirmed by muscle biopsies. In addition, we aimed to provide a realistic comprehensive picture of the severe muscle diseases in the Aegean Region of Turkey. Material and Method: We retrospectively reviewed 90 patients who underwent muscle biopsy examinations between 2008 and 2011 in the pathology laboratory of Izmir Dr.Behcet Uz Children's Hospital. Biopsy specimens of all patients clinically diagnosed as muscular dystrophy referred from 4 different centers of neurological disorders were collected. Results: Dystrophinopathy was the most (n=45) and gammasarcoglycanopathy was the second common (n=13) muscular dystrophy in this series. The mean age of all 90 patients was 8.8 years (3 months- 64 years). Only 14 cases (15.5%) were older than 14, and 23 cases were younger than two years. Dysferlinopathy was the most common dystrophy in the older age group. There were statistical significant differences between the types of dystrophy and inflammation (0.021), creatine kinase levels (p= 0.001), age (p=0.001), and gender (p < 0.001) of the patients. Conclusion: The present study revealed that dysferlinopathies is not an uncommon form of muscular dystrophies in western Turkey. We have concluded that if avoidance from unnecessary therapeutic interventions is desired, we must be aware of the relative frequencies of dysferlinopathies.
    Turk Patoloji Dergisi 01/2012; 28(3):259-265.
  • Deri Hastaliklari ve Frengi Arsivi 09/2011; 45(3):137-139. · 0.05 Impact Factor
  • Anadolu kardiyoloji dergisi: AKD = the Anatolian journal of cardiology 05/2011; 11(4):E17-8. · 0.72 Impact Factor
  • Turkiye Klinikleri Journal of Medical Sciences 01/2011; 31(4):809-815. · 0.10 Impact Factor
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    ABSTRACT: Centronuclear myopathies (CNM) describe a group of rare muscle diseases typically presenting an abnormal positioning of nuclei in muscle fibers. To date, three genes are known to be associated to a classical CNM phenotype. The X-linked neonatal form (XLCNM) is due to mutations in MTM1 and involves a severe and generalized muscle weakness at birth. The autosomal dominant form results from DNM2 mutations and has been described with early childhood and adult onset (ADCNM). Autosomal recessive centronuclear myopathy (ARCNM) is less characterized and has recently been associated to mutations in BIN1, encoding amphiphysin 2. Here we present the first clinical description of intrafamilal variability in two first-degree cousins with a novel BIN1 stop mutation. In addition to skeletal muscle defects, both patients have mild mental retardation and the more severely affected male also displays abnormal ventilation and cardiac arrhythmia, thus expanding the phenotypic spectrum of BIN1-related CNM to non skeletal muscle defects. We provide an up-to-date review of all previous cases with ARCNM and BIN1 mutations.
    Orphanet Journal of Rare Diseases 12/2010; 5:35. · 3.96 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: The purpose of the study was to investigate and compare iloprost and levosimendan on spinal cord ischemia in an experimental model. The study was done in two stages. For the 4-hour short survival study, 50 New Zealand white rabbits were randomly allocated into five groups. Spinal cord ischemia was induced by clamping the aorta just below the left renal artery and just proximal to the aortic bifurcation with bulldog artery clamps. The aortic clamps were removed after 40 min and restoration of blood flow was verified visually. The groups were analyzed at 1 and 4 h after reperfusion. For the 48-hour survival study, two different groups (iloprost plus levosimendan, n = 10; saline-treated controls, n = 10) were analyzed at 24 and 48 h after reperfusion. The neurologic status of the animals in the treatment and sham groups was better than that in the control group both at 1 and 4 h after reperfusion. Viability index values in the levosimendan, iloprost and iloprost plus levosimendan groups were statistically higher than in the control group indicating less or no neuronal damage. The results suggest that levosimendan, as well as iloprost, may reduce ischemic damage in transient spinal ischemia and provide better neurologic outcome.
    European Surgical Research 02/2008; 41(1):1-7. · 1.43 Impact Factor
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    ABSTRACT: The neuroprotective effect of trimetazidine (TMZ) was tested prospectively in a rabbit spinal cord ischemia model. Ischemia was induced by clamping the aorta just distal to the left renal artery and proximal aortic bifurcation for 20 min. Twenty-five male New Zealand white rabbits were randomized as follows: TMZ group (n=100) receiving 3 mg/kg trimetazidine intravenously before the occlusion of the aorta; control group undergoing occlusion but receiving no pharmacologic intervention (n=10); sham-operation group (n=5) subjected to operative dissections without aortic occlusion. Physiological parameters and somatosensory evoked potentials (SEP) were monitored in animals before the ischemia, during the ischemia and in the 1st, 15th and 60th min of reperfusion. Neurologic status was assessed 24 and 48 h after the operation. The spinal cord, abdominal aorta, and its branches were processed for histopathologic examinations 48 h after the operation. At the end of the ischemic period, the average N1-P1 amplitude was reduced to 22% of the baseline in all ischemic animals. This was followed by a gradual return to 90+/-2% of the initial amplitude in the TMZ group and 81+/-2% in the control group (P<0.05) after 60 min of reperfusion. The average motor function score was significantly higher in the TMZ group than the control group (3.7+/-0.5 vs 3.1+/-0.6 at 24 and 3.5+/-0.7 vs 2.9+/-0.6 at 48 h; P<0.05). Histologic observations were clearly correlated with the neurologic findings. The results suggest that trimetazidine reduces spinal cord injury during thoracoabdominal aortic operations and may have therapeutic utility during high risk operations.
    Research in Experimental Medicine 12/2000; 200(1):43-51.
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    ABSTRACT: The neuroprotective effect of trimetazidine (TMZ) on ischemic-reperfusion injury was tested by randomized, controlled, prospective study in a rat model of transient global cerebral ischemia. Thirty wistar albino rats were used for study. Animals in TMZ group (n=10) received trimetazidine (3 mg/kg IV bolus) before the occlusion of carotid arteries. A similar volume of saline solution was used in the control group (n=10). The sham group (n=10) were anaesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters, somatosensory evoked potentials (SEP's) were monitored. The neurological outcomes had been clinically evaluated and scored up to 4 days post ischemia. The intergroup differences were compared. Histological observations were clearly correlated with the neurological findings. The percentage of damaged neurons in CA1 and CA3 in subfield of hypochampus 346% and 166% in the TMZ group, whereas it was 445% and 245% in the control group (p
    International Journal of Angiology 01/2000; 9(3):183-187.
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    ABSTRACT: A green alga, Chlorococcum littorale, has a tolerance to extremely high-CO2 conditions (Kodama et al., J. Marine Biotech. 1 (1993) 21–25). In order to elucidate the mechanism underlying the resistance to such high CO2 levels, we compared the changes in excitation energy ditribution between photosystem I (PS 1) and photosystem II (PS II) by 77 K fluorescence in cells of the high CO2-resistant C. littorale and the non-resistant Stichococcus bacillaris. Immediately after the cell are transferred from air to 40% CO2, the F714/F687 ratio derived from 77 K fluorescence increases in C. littorale cells, suggesting an increase of transition from state 1 to state 2. During this period, more than 80% of plastoquinone A is in the reduced form and the activity of PS I increass. Eventually the F714/F687 ratio, the concentration of reduced plastoquinone A and PS I activity decrease. However, no significant increase of F714/F687 ratio is observed after the transfer of S. bacillaris cells from air to 40% CO2. The level of reduced plastoquinone A in S. bacillaris gradually increases and the activity of PS I does not show a large change. During the transient period, the level of the D1 protein is approximately constant in C. littorale cells, but is lowered in S. bacillaris. These results suggest that, under extremely high-CO2 conditions, PS II is protected from photoinhibition by control of the state transition in C. littorale cells, whereas such a protection mechanism does not function in the alga S. bacillaris, non-resistant to CO2.
    Journal of Photochemistry and Photobiology B Biology 07/1998; 44(3). · 2.80 Impact Factor
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    ABSTRACT: Neurological injury due to transient cerebral ischemia is a potential complication of cardiovascular surgery. The neuroprotective effect of magnesium, when given subcutaneously before the ischemia, was assessed in a rat model of transient global cerebral ischemia. Thirty-six male Wistar albino rats were included to this randomized, controlled, prospective study. In 24 animals, ischemia was induced with four-vessel occlusion technique with the duration of 15 min. MgSO4 was given 600 mg/kg subcutaneously 48 h before the procedure in group 1 (n = 12). Similar volume of saline solution was used in animals of control group (group 2, n = 12). The animals in group 3 (sham group, n = 12) were anesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 30 min of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days postischemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 5 +/- 3% of the baseline in all ischemic animals. This was followed by a gradual return to 87 +/- 10% and 83 +/- 8% of the initial amplitude after 30 min of reperfusion in group 1 and group 2, respectively (P > 0.05). The average neurological score was significantly higher in group 1 than in group 2 at 48, 72 and 96 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. The results suggest that subcutaneous MgSO4 reduces cerebral injury and preserves neurologic function when given two days before the transient global ischemia in rats.
    European Journal of Cardio-Thoracic Surgery 07/1998; 14(1):82-8. · 2.81 Impact Factor
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    ABSTRACT: The beneficial effect of pentoxifylline (PTX) on ischaemic-reperfusion injury was assessed in a rat model of transient global cerebral ischaemia. Randomized, controlled, prospective study. University research laboratory. Thirty-six male Wistar albino rats. Ischaemia was induced with a four-vessel occlusion technique in 24 animals with the duration of 15 minutes. Group 1 animals (n = 12) received PTX treatment started 20 minutes before the occlusion of carotid arteries (60 mg/kg bolus followed by infusion at 0.1 mg/kg/min). A similar volume of saline solution was used in animals of the control group (group 2, n = 12). The animals in group 3 (sham group, n = 12) were anaesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters and somatosensory evoked potentials (SEP) were monitored in animals before ischaemia, during ischaemia and in the first 30 minutes of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days post ischaemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of the ischaemic period, the average amplitude was reduced to 4 +/- 3% of the baseline in all ischaemic animals. This was followed by a gradual return to 92 +/- 9% and 82 +/- 8% of the initial amplitude after 30 minutes of reperfusion in group 1 and group 2, respectively (p < 0.05). The average neurological score was significantly higher in group 1 than in group 2 in the post-ischaemia period (p < 0.05). Histological observations were clearly correlated with the neurological findings. The results suggest that PTX reduces cerebral injury and preserves neurologic function in transient global ischaemia in rats.
    Acta cardiologica 01/1998; 53(2):89-95. · 0.56 Impact Factor
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    ABSTRACT: Objective: Neurological injury due to transient cerebral ischemia is a potential complication of cardiovascular surgery. The neuroprotective effect of magnesium, when given subcutaneously before the ischemia, was assessed in a rat model of transient global cerebral ischemia. Methods: Thirty-six male Wistar albino rats were included to this randomized, controlled, prospective study. In 24 animals, ischemia was induced with four-vessel occlusion technique with the duration of 15 min. MgSO4 was given 600 mg/kg subcutaneously 48 h before the procedure in group 1 (n=12). Similar volume of saline solution was used in animals of control group (group 2, n=12). The animals in group 3 (sham group, n=12) were anesthetized and subjected to operative dissections without vascular occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 30 min of reperfusion. Their neurological outcome had been clinically evaluated and scored up to 4 days postischemia. The intergroup differences were compared. Then the animals were sacrificed and their brains were processed for histopathological examination. Results: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 5±3% of the baseline in all ischemic animals. This was followed by a gradual return to 87±10% and 83±8% of the initial amplitude after 30 min of reperfusion in group 1 and group 2, respectively (P>0.05). The average neurological score was significantly higher in group 1 than in group 2 at 48, 72 and 96 h after the ischemic insult (P
    European Journal of Cardio-thoracic Surgery - EUR J CARDIO-THORAC SURG. 01/1998; 14(1):82-88.
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    ABSTRACT: The protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit spinal cord ischemia model. Randomized, controlled, prospective study. University research laboratory. New Zealand white rabbits (36) of both sexes. In 24 animals, ischemia was induced with midline laparotomy and clamping the aorta just distal to left renal artery and proximal to aortic bifurcation for 20 min. Aprotinin was given 30000 KIU as a short intravenous injection after anesthesia, and was followed by 10000 KIU/h by continuous infusion in group 1 (n = 12). Similar volume of saline solution was used in control group of animals (group 2, n = 12). Group 3 of animals (sham group, n = 12) were anesthetized and subjected to laparotomy without aortic occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 60 min of reperfusion. Their neurological outcome was clinically evaluated up to 48 h postischemia. Their motor function was scored, and the intergroup differences were compared. The animals were sacrificed after two days of postischemia. Their spinal cord, abdominal aorta, and its branches were processed for histopathological examination. In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 53+/-7% of the baseline in all ischemic animals. This was followed by a gradual return to 89+/-8 and 81+/-13% of the initial amplitude after 60 min of reperfusion in group 1 and group 2 correspondingly (P > 0.05). The average motor function score was significantly higher in group 1 than group 2 at 24 and 48 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. The results suggest that aprotinin reduces spinal cord injury and preserves neurologic function in transient spinal cord ischemia in rabbits.
    European Journal of Cardio-Thoracic Surgery 12/1997; 12(6):913-8. · 2.81 Impact Factor
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    ABSTRACT: Objective: The protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit spinal cord ischemia model. Design: Randomized, controlled, prospective study. Setting: University research laboratory. Subjects: New Zealand white rabbits (36) of both sexes. Methods: In 24 animals, ischemia was induced with midline laparotomy and clamping the aorta just distal to left renal artery and proximal to aortic bifurcation for 20 min. Aprotinin was given 30 000 KIU as a short intravenous injection after anesthesia, and was followed by 10 000 KIU/h by continuous infusion in group 1 (n=12). Similar volume of saline solution was used in control group of animals (group 2, n=12). Group 3 of animals (sham group, n=12) were anesthetized and subjected to laparotomy without aortic occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 60 min of reperfusion. Their neurological outcome was clinically evaluated up to 48 h postischemia. Their motor function was scored, and the intergroup differences were compared. The animals were sacrificed after two days of postischemia. Their spinal cord, abdominal aorta, and its branches were processed for histopathological examination. Results: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 53±7% of the baseline in all ischemic animals. This was followed by a gradual return to 89±8 and 81±13% of the initial amplitude after 60 min of reperfusion in group 1 and group 2 correspondingly (P>0.05). The average motor function score was significantly higher in group 1 than group 2 at 24 and 48 h after the ischemic insult (P<0.05). Histological observations were clearly correlated with the neurological findings. Conclusion: The results suggest that aprotinin reduces spinal cord injury and preserves neurologic function in transient spinal cord ischemia in rabbits.
    European Journal of Cardio-Thoracic Surgery.