Targeting novel antigens in the arterial wall in thromboangiitis obliterans.

Thromboangiitis obliterans is an inflammatory disease possibly resulting from cigarette smoking as a primary etiologic factor, perhaps as a delayed type of hypersensitivity or toxic angiitis. As little is known about the pathogenesis of the disease, we aimed to determine novel antigens that might be responsible from the local inflammatory reactions and structural changes observed in this disease. An indirect immunoperoxidase technique is used to examine the tissue samples obtained from the dorsalis pedis artery of affected individuals with twenty monoclonal antibodies. Among these several antigens which are not previously reported in TAO like CD34, CD44 and CD90 were determined in the tissue samples examined. On the other hand, many other antigens like cytokine/chemokine receptors, several enzymes and leukocyte/lymphocyte antigens were lacking giving some clues about the local pathological reactions. We briefly discussed our findings for several critical antigens those first described in the present work, possibly having roles in the development of the disease. Expression of the CD90/CD11c receptor/ligand pair seems to play an important role in mononuclear cell recruitment to the damage site. Vascular invasion of not only tunica intima but also the tunica media in affected vessels is clearly demonstrated using endothelial cell specific antigens

Ratlarda beyin hipoksi-reperfüzyon modelinde glutaminin etkilerinin araştırılması özet

Background: The aim of this study was to explore the effects of glutamine in brain ischemia/reperfusion model in rat. Methods: Right common carotid arteries of 24 Wistar albino rats were clamped for a duration of 30 minutes. Two hours later, except CONTROL group, glutamine was infused into left femoral vein of rats in GLIV group; and glutamine and normal saline was administered into cisterna magna of rats in GLIS and SFIS groups, respectively. After 7 days, all animals were decapitated and each brain was divided into two hemispheres for histopathological and biochemical evaluation. The right hemisphere was called “Hypoxia/Reperfusion side (HRS)” and the left hemisphere was called “Toxicity side (TS)”. Results: In TS and HRS, degenerated neuron counts of GLIV groups were significantly higher than other groups' values. Degenerated neuron count values of TS were significantly lower than HRS values for GLIS, and SFIS groups, but the results of GLIV group in TS did not different from the GLIV group in HRS. LPO levels of TS and HRS of the groups was not statistically significant. Conclusion: This study results showed that glutamine had no beneficial effect to the hypoxia/reperfusion injury in rat model.Amaç: Bu çalışmada glutamin adlı maddenin ratlardaki deneysel serebral hipoksi/reperfüzyon hasarlanması üzerine etkileri araştırılmaya çalışıldı. Yöntem ve Gereç: Yirmi dört adet Wistar albino ratın sağ ana karotis arterleri geçici anevrizma klibi kullanılarak 30 dakika süre ile kapatıldı. İki saat sonra CONTROL grubundaki hayvanlar hariç glutamin adlı materyal GLIV grubundaki ratlara femoral venden; GLIS grubundakilere ise sisterna magnadan enjekte edildi. SFIS grubundaki ratlara sisterna magnadan serum fizyolojik verildi. Yedi gün sonra tüm hayvanların beyinleri çıkarılıp santral sulkustan ikiye bölündü; sağ hemisfere “hipoksi/reperfüzyon tarafı (HRS)”; karşı hemisfere “toksisite tarafı (TS)” ismi verildi ve dokular histopatolojik ve biyokimyasal analize tabi tutuldu. Bulgular: TS ve HRS için GLIV grubunun dejenere nöron sayım sonuçları diğer gruplara göre yüksek bulundu. Her bir grup için TS sayım sonuçları ile HRS sonuçları karşılaştırıldı ve toksisite tarafı SFIS ile GLIS gruplarının sayım sonuçlarının hipoksi/reperfüzyon tarafı gruplarınkine göre anlamlı derecede düşük olduğu görüldü, ancak her iki tarafın GLIV gruplarının sonuçları arasında anlamlı fark saptanmadı. Her iki taraf doku lipid peroksidasyon (LPO) düzeyi sonuçları arasında istatistiksel anlamlı fark yoktu. Sonuç: Bu çalışma sonunda glutamin adlı maddenin ratlarda oluşturulan hipoksi/reperfüzyon yaralanması üzerinde yararlı etkilerinin bulunmadığı sonucuna ulaşıldı

Long-Term Simvastatin Attenuates Lung Injury and Oxidative Stress in Murine Acute Lung Injury Models Induced by Oleic Acid and Endotoxin

BACKGROUND: 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors have several pleiotropic effects, including anti-inflammatory properties, and are reported to improve endothelial functions. Pathophysiologically, acute lung injury (ALI) is caused by a severe inflammatory response and endothelial dysfunction. OBJECTIVE: To investigate the effects of simvastatin (an HMG-CoA reductase inhibitor) on oxidative stress and lung histopathology in 2 murine models of ALI, induced by oleic acid and endotoxin. METHODS: The mice were randomly divided into 2 groups: one received 2 mg/kg/d intraperitoneal simvastatin for 15 days. Then the groups were further divided into 3, which received saline, oleic acid, or endotoxin. Four hours after inducing ALI we obtained lung samples for histopathology analysis, myeloperoxidase, glutathione, and malondialdehyde measurement, and blood samples for malondialdehyde measurement. RESULTS: Endotoxin and oleic acid lung injury increased tissue myeloperoxidase (P = .009 for both), decreased tissue glutathione (P = .02 and P = .009, respectively), and increased tissue malondialdehyde (P = .009 for both), compared to the control group. Simvastatin decreased myeloperoxidase only in the oleic acid group (P = .01). Simvastatin increased glutathione (P = .005 and P = .003, respectively) and lowered malondialdehyde in both the endotoxin and oleic acid groups (P = .003 for both). Histopathology revealed that simvastatin protected the lung tissue in both ALI models, but the protection was greater in the endotoxin group. CONCLUSIONS: Pretreatment with simvastatin decreased the severity of ALI in oleic acid and endotoxin ALI models, by decreasing inflammation and oxidative stress.WoSScopu

Impaired Implantation and Hereditary Thrombophila; Expression of LIF (Leukemia Inhibitory Factor) on Extravillous Trophoblasts

OBJECTIVE: LIF (Leukemia İnhibitory Factor) was shown to have an important role in implantation. The aim of this study is to investigate the expression of LIF on extravillous trophoblasts in normal pregnancies and pregnancies with MTHFR (methylenetetrahydrofolate reductase) mutations. This study was also designed to demonstrate the “impaired implantation based” perinatal complications such as early pregnancy losses in pregnancies with hereditary thrombophilia (MTHFR 677 & 1298 mutations; homocystinemia and impaired folat/vitamin B12 metabolisms). STUDY DESIGN: Abortus material until 10th gestational-week were used in this study. The patients were divided into 2 groups as: Group 1; control group (unwanted induced abortions), Group 2; abortus material from pregnancies with hereditary thrombophilia. Hereditary thrombophilia cases were consisted of only MTHFR homozygote mutations (MTHFR 677 & 1298). Indirect ABC (avidin-biotin-peroxidase complex) was applied to all of the abortus material to investigate the expression of LIF. RESULTS: Expression of LIF in extravillous trophoblasts was immünohistochemically stronger (+++) in MTHFR group than the extravillous trophoblasts of the control group (++). This finding was also found to be statistically significant (p≤ 0.05). CONCLUSION: The impaired LIF expression of extravillous trophoblastic cells in MTHFR patients can be one of the reasons of early fetal losses due to impaired implantation. Direct affect of homocystinemia, cell degragates of maternal endothelial cells due to injury and thrombosis and activation of complement system may be the reasons of defective LIF synthesis. Defective LIF expression on extravillous (interstitial) trophoblasts may result in insufficient activation of the LIF receptors in the decidua and limiting their migration during placentation. On the other hand, number of the extravillous trophoblasts developing from cytotrophoblasts may also be negatively affected by the disturbed LIF expression resulting in a shallow placenta

Effects of the Glutamine on the Neuronal Cell Death in rat Ischemia-reperfusion Model

ATILLA, PERGIN/0000-0001-5132-0002WOS: 000347120800005Background: The aim of this study was to explore the effects of glutamine in brain ischemia/reperfusion model in rat. Methods: Right common carotid arteries of 24 Wistar albino rats were clamped for a duration of 30 minutes. Two hours later, except CONTROL group, glutamine was infused into left femoral vein of rats in GLIV group; and glutamine and normal saline was administered into cisterna magna of rats in GLIS and SFIS groups, respectively. After 7 days, all animals were decapitated and each brain was divided into two hemispheres for histopathological and biochemical evaluation. The right hemisphere was called "Hypoxia/Reperfusion side (HRS)" and the left hemisphere was called " Toxicity side (TS)". Results: In TS and HRS, degenerated neuron counts of GLIV groups were significantly higher than other groups' values. Degenerated neuron count values of TS were significantly lower than HRS values for GLIS, and SFIS groups, but the results of GLIV group in TS did not different from the GLIV group in HRS. LPO levels of TS and HRS of the groups was not statistically significant. Conclusion: This study results showed that glutamine had no beneficial effect to the hypoxia/reperfusion injury in rat model

Targeting novel antigens in the arterial wall in thromboangiitis obliterans

Thromboangiitis obliterans is an inflammatory disease possibly resulting from cigarette smoking as a primary etiologic factor, perhaps as a delayed type of hypersensitivity or toxic angiitis. As little is known about the pathogenesis of the disease, we aimed to determine novel antigens that might be responsible from the local inflammatory reactions and structural changes observed in this disease. An indirect immunoperoxidase technique is used to examine the tissue samples obtained from the dorsalis pedis artery of affected individuals with twenty monoclonal antibodies. Among these several antigens which are not previously reported in TAO like CD34, CD44 and CD90 were determined in the tissue samples examined. On the other hand, many other antigens like cytokine/chemokine receptors, several enzymes and leukocyte/lymphocyte antigens were lacking giving some clues about the local pathological reactions. We briefly discussed our findings for several critical antigens those first described in the present work, possibly having roles in the development of the disease. Expression of the CD90/CD11c receptor/ligand pair seems to play an important role in mononuclear cell recruitment to the damage site. Vascular invasion of not only tunica intima but also the tunica media in affected vessels is clearly demonstrated using endothelial cell specific antigens

Targeting Novel Antigens in the Arterial Wall in Thromboangiitis Obliterans

Thromboangiitis obliterans is an inflammatory disease possibly resulting from cigarette smoking as a primary etiologic factor, perhaps as a delayed type of hypersensitivity or toxic angiitis. As little is known about the pathogenesis of the disease, we aimed to determine novel antigens that might be responsible from the local inflammatory reactions and structural changes observed in this disease. An indirect immunoperoxidase technique is used to examine the tissue samples obtained from the dorsalis pedis artery of affected individuals with twenty monoclonal antibodies. Among these several antigens which are not previously reported in TAO like CD34, CD44 and CD90 were determined in the tissue samples examined. On the other hand, many other antigens like cytokine/chemokine receptors, several enzymes and leukocyte/lymphocyte antigens were lacking giving some clues about the local pathological reactions. We briefly discussed our findings for several critical antigens those first described in the present work, possibly having roles in the development of the disease. Expression of the CD90/CD11c receptor/ligand pair seems to play an important role in mononuclear cell recruitment to the damage site. Vascular invasion of not only tunica intima but also the tunica media in affected vessels is clearly demonstrated using endothelial cell specific antigens.WoSScopu

Ratlarda Beyin Hipoksi-reperfüzyon Modelinde Glutaminin Etkilerinin Araştırılması

Amaç: Bu çalışmada glutamin adlı maddenin ratlardaki deneysel serebral hipoksi/reperfüzyon hasarlanması üzerine etkileri araştırılmaya çalışıldı. Yöntem ve Gereç: Yirmi dört adet Wistar albino ratın sağ ana karotis arterleri geçici anevrizma klibi kullanılarak 30 dakika süre ile kapatıldı. İki saat sonra CONTROL grubundaki hayvanlar hariç glutamin adlı materyal GLIV grubundaki ratlara femoral venden; GLIS grubundakilere ise sisterna magnadan enjekte edildi. SFIS grubundaki ratlara sisterna magnadan serum fizyolojik verildi. Yedi gün sonra tüm hayvanların beyinleri çıkarılıp santral sulkustan ikiye bölündü; sağ hemisfere “hipoksi/reperfüzyon tarafı (HRS)”; karşı hemisfere “toksisite tarafı (TS)” ismi verildi ve dokular histopatolojik ve biyokimyasal analize tabi tutuldu. Bulgular: TS ve HRS için GLIV grubunun dejenere nöron sayım sonuçları diğer gruplara göre yüksek bulundu. Her bir grup için TS sayım sonuçları ile HRS sonuçları karşılaştırıldı ve toksisite tarafı SFIS ile GLIS gruplarının sayım sonuçlarının hipoksi/reperfüzyon tarafı gruplarınkine göre anlamlı derecede düşük olduğu görüldü, ancak her iki tarafın GLIV gruplarının sonuçları arasında anlamlı fark saptanmadı. Her iki taraf doku lipid peroksidasyon (LPO) düzeyi sonuçları arasında istatistiksel anlamlı fark yoktu. Sonuç: Bu çalışma sonunda glutamin adlı maddenin ratlarda oluşturulan hipoksi/reperfüzyon yaralanması üzerinde yararlı etkilerinin bulunmadığı sonucuna ulaşıldı.Background: The aim of this study was to explore the effects of glutamine in brain ischemia/reperfusion model in rat. Methods: Right common carotid arteries of 24 Wistar albino rats were clamped for a duration of 30 minutes. Two hours later, except CONTROL group, glutamine was infused into left femoral vein of rats in GLIV group; and glutamine and normal saline was administered into cisterna magna of rats in GLIS and SFIS groups, respectively. After 7 days, all animals were decapitated and each brain was divided into two hemispheres for histopathological and biochemical evaluation. The right hemisphere was called “Hypoxia/Reperfusion side (HRS)” and the left hemisphere was called “Toxicity side (TS)”. Results: In TS and HRS, degenerated neuron counts of GLIV groups were significantly higher than other groups' values. Degenerated neuron count values of TS were significantly lower than HRS values for GLIS, and SFIS groups, but the results of GLIV group in TS did not different from the GLIV group in HRS. LPO levels of TS and HRS of the groups was not statistically significant. Conclusion: This study results showed that glutamine had no beneficial effect to the hypoxia/reperfusion injury in rat model

Targeting novel antigens in the arterial wall in thromboangiitis obliterans.

Thromboangiitis obliterans is an inflammatory disease possibly resulting from cigarette smoking as a primary etiologic factor, perhaps as a delayed type of hypersensitivity or toxic angiitis. As little is known about the pathogenesis of the disease, we aimed to determine novel antigens that might be responsible from the local inflammatory reactions and structural changes observed in this disease. An indirect immunoperoxidase technique is used to examine the tissue samples obtained from the dorsalis pedis artery of affected individuals with twenty monoclonal antibodies. Among these several antigens which are not previously reported in TAO like CD34, CD44 and CD90 were determined in the tissue samples examined. On the other hand, many other antigens like cytokine/chemokine receptors, several enzymes and leukocyte/lymphocyte antigens were lacking giving some clues about the local pathological reactions. We briefly discussed our findings for several critical antigens those first described in the present work, possibly having roles in the development of the disease. Expression of the CD90/CD11c receptor/ligand pair seems to play an important role in mononuclear cell recruitment to the damage site. Vascular invasion of not only tunica intima but also the tunica media in affected vessels is clearly demonstrated using endothelial cell specific antigens