The effect of health belief model based initiatives in preventing school injuries

Okul çağı çocukları, dış etkenlerle oluşabilecek zararlara karşı kendini korumada savunmasız gruplardandır. Bu nedenle yaralanmalara sıklıkla maruz kalmaktadırlar. Kaza sonucu meydana gelen yaralanmalar çoğunlukla bu gruplarda, özellikle çocuk ve adölesanlarda görülmektedir. Ancak bu konuda alınan önlemlerin çoğu zaman yetersiz olduğu ve göz ardı edildiği bilinmektedir. Ülkemizde özellikle öğrencilere sunulan okul sağlığı hizmetlerinin oldukça sınırlı olduğu bir gerçektir; oysaki okul kazalarına yönelik basit kişisel ve çevresel tedbirlerle istenmeyen yaralanmaların önlenebileceği bildirilmektedir. Okullarda geliştirilecek programların çevre değişimi, davranış değişimi, denetim ve politikaların geliştirilmesi konularını kapsaması, ders müfredatına entegre edilmesi önerilmektedir. Programların etkililiğini artırmada modeller her zaman yol gösterici olmuştur. Sağlığı geliştirme modellerinden biri olan Sağlık İnanç Modeli (SİM), kişilerin sağlığını; bireysel özellikler (sosyo-demografik özellikler), algılar (duyarlılık, durumun ciddiyeti, yarar, engeller, öz-etkililiği) ve eyleme geçiriciler (hazır oluşluk) ile etkilendiğini belirtmektedir. Bu derleme makalede amaç, okul sağlığı hemşireleri olarak; yaralanma riski yüksek olan öğrenci toplumunda okul yaralanmalarını önlemede bir rehber olan Sağlık İnanç Modelini tanıtmak; modelin okul yaralanmalarını önlemedeki etkisini yapılmış araştırmalarla ortaya koymak ve bu model ile yapılacak çalışmalara yol göstermek amaçlanmıştır

Polietilen glikol hidrojel dural bariyer nörotoksisitesinin değerlendirilmesi

AIm: Although polyethylene glycol (PEG) is a neutral, biocompatible hydrophilic polymer recognized for its lack of interaction with biological barrier, its neurotoxicity has not been clearly identified in neurosurgery. This study is constructed to evaluate the possible neurotoxicity of a PEG hydrogel dural sealant. Ma terIal and Methods: After a burrhole was opened in the left parietal bone of the twenty five Wistar albino rats, the dura mater and cerebral cortex were incised and the experimental material (activated polyethylene glycol and polyethylene imine) was sprayed into the burrhole. Then brain tissues were harvested for histopathological and biochemical studies at 72 hours to investigate the acute stage changes and on 15th day to evaluate the chronic stage changes. Results: There were statistically significant differences among the groups regarding the comparison of the values of the PMNL cell infiltration grades, gliosis and congestion in both acute and chronic stages. However, the values of the MNL cell infiltration grades, edema and fibrin formation, lipid peroxidation levels of harvested brain tissues were similar in all groups. ConclusIon: Although this study did not present the detailed histopathological and biochemical evaluation results, it indicated that the application of the PEG-based hydrogel sealant was not associated with neurotoxicity, delayed healing, or degenerative changes

HEMOGLOBİN VE NİTRİT BAĞIMLI TİROZİN NİTRASYONU

Nitric oxide (NO) reacts with oxyhemoglobin or oxymyoglobin resulting in the generation of nitrate and metHb or metMb. Unlike the case of nitrate, nitrite is not an innocuous end product of NO oxidation. Hemoproteins including several peroxidases are shown to cause nitrite oxidation in the presence of H2O2. Reactive nitrogen oxides generated in hemoprotein-catalyzed nitrite oxidation are held responsible for bactericidal and cytotoxic actions of nitrite. In this study with Griess method the oxidation of nitrite to nitrate in the presence of H2O2 by hemoglobin were searched. No nitrite oxidation was observed either in the absence of H2O2 or hemoglobin, showing that the reactive species causing nitrite oxidation is a oxoferryl complex (compound I) formed from the reaction of H2O2 with hemoglobin. In this study, similar to peroxidase enzymes, we found that hemoglobin causes the nitration of tyrosine. Hemoglobin-catalyzed tyrosine nitration was pH-dependent with the optimum pH of 6,0. Hemoglobin and H2O2 were essential components for tyrosine nitration. We have not observed any tyrosine nitration without hemoglobin even at the lowest pH studied. However during hemoglobin-catalyzed nitrite oxidation in the presence of H2O2, nitrating species are produced. We conclude that, by the series of reactions between hemoglobin, H2O2 and nitrite, nitrogen dioxide radical (NO2 - ) and/or peroxynitrite like reactive species are produced, and these species are responsible for tyrosine nitration

Hemoglobin And Nitrite Dependent Tyrosine Nitration

Nitric oxide (NO) reacts with oxyhemoglobin or oxymyoglobin resulting in the generation of nitrate and metHb or metMb. Unlike the case of nitrate, nitrite is not an innocuous end product of NO oxidation. Hemoproteins including several peroxidases are shown to cause nitrite oxidation in the presence of H2O2. Reactive nitrogen oxides generated in hemoprotein-catalyzed nitrite oxidation are held responsible for bactericidal and cytotoxic actions of nitrite. In this study with Griess method the oxidation of nitrite to nitrate in the presence of H2O2 by hemoglobin were searched. No nitrite oxidation was observed either in the absence of H2O2 or hemoglobin, showing that the reactive species causing nitrite oxidation is a oxoferryl complex (compound I) formed from the reaction of H2O2 with hemoglobin. In this study, similar to peroxidase enzymes, we found that hemoglobin causes the nitration of tyrosine. Hemoglobin-catalyzed tyrosine nitration was pH-dependent with the optimum pH of 6,0. Hemoglobin and H2O2 were essential components for tyrosine nitration. We have not observed any tyrosine nitration without hemoglobin even at the lowest pH studied. However during hemoglobin-catalyzed nitrite oxidation in the presence of H2O2, nitrating species are produced. We conclude that, by the series of reactions between hemoglobin, H2O2 and nitrite, nitrogen dioxide radical (NO2 - ) and/or peroxynitrite like reactive species are produced, and these species are responsible for tyrosine nitration.Nitrik oksit (NO) oksihemoglobin ve oksimiyoglobin ile tepkimeye girmesi nitrat ve metHb veya metMb'nin meydana gelmesine neden olmaktadır. Nitratin tersine, nitrit NO oksidasyonunun zararsız bir son ürünü değildir. Hemoproteinlerden peroksidazların H2O2 varlığında nitrit oksidasyonuna neden oldukları gösterilmiştir. Hemoproteinlerin katalizlediği nitrit oksidasyonunda meydana gelen reaktif nitrojen oksitler, nitritin bakterisid ve sitotoksik etkilerinin sorumlusudurlar. Bu çalışmada Griess metodu ile hemoglobin tarafından H2O2 varlığında nitritin nitrata oksidasyonu araştırıldı. Hem H2O2 hem de hemoglobin yokluğunda nitrit oksidasyonu gözlenmedi, bu da göstermektedir ki nitrit oksidasyonuna neden olan reaktif tür H2O2 ile hemoglobinin reaksiyonundan meydana gelen oksoferril kompleksidir (bileşik I). Bu çalışmada, peroksidaz enzimlerine benzer şekilde, hemoglobinin tirozin nitrasyonuna neden olduğu bulundu. Hemoglobinin katalizlediği tirozin nitrasyonu pH bağımlı olup, nitrasyonun optimum pH'si 6,0 dır. Hemoglobin ve H2O2 tirozin nitrasyonu için gerekli bileşenlerdir. Hemoglobin yokluğunda, çalışılan en düşük pH'de bile tirozin nitrasyonu gözlenmedi. Bununla beraber H2O2 varlığında hemoglobinin katalizlediği nitrit oksidasyonu esnasında, nitratlayıcı türler meydana getirilmektedir. Sonuç olarak hemoglobin, H2O2 ve nitrit arasındaki reaksiyon serileri tarafından nitrojen dioksit radikali (NO2 - ) ve/veya peroksinitrit benzeri reaktif türler meydana getirilmektedir ve bu türler tirozin nitrasyonundan sorumludurlar

Serum lipid peroxidation levels in small-for-gestational-age babies

The levels of lipid peroxidation in sera of asymmetric small-for-gestational-age (SGA) babies at the second hour of life were investigated. Lipid peroxidation levels, measured as malondialdehyde (MDA), were 3.3 ± 1.1 and 3.9 ± 1.2 mmol/L in SGA and appropriate-for-gestational age (AGA) groups, respectively. The difference was not significant (p>0.05). This result may indicate that free radical scavengers are sufficient in SGA babies

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

Using Salivary Nitrite and Nitrate Levels as a Biomarker for Drug-Induced Gingival Overgrowth

Aim: Drug-induced gingival overgrowth has a multifactorial nature and the pathogenesis is still uncertain. It has been suggested that Nitric Oxide (NO) might play a role in the pathogenesis of drug induced gingival overgrowth due to the contribution of NO to immune response and matrix degradation. NO levels in biological fluids have been used as a diagnostic biomarker in many diseases. The aim of this study is to determine whether NO levels in plasma, saliva, and gingival crevicular fluid (GCF) can serve as a potential biomarker for the evaluation of drug induced gingival overgrowth risk. Materials and Methods: A total of 104 patients, receiving cyclosporine A (p = 35), phenytoin (n = 25), nifedipine (n = 26), or diltiazem (n = 18) participated in the study. The amount of gingival overgrowth was evaluated with two indices and was given as percentage. Periodontal clinical parameters including plaque index (PI), gingival index (GI), gingival bleeding time index (GBTI), and probing depth (PD) were also assessed. Saliva, GCF, and plasma samples were obtained from each participants. Nitrite and nitrate levels in saliva, GCF, and plasma were analyzed by Griess reagent. Results: Salivary nitrite and nitrate levels in responders were significantly higher than those in non responders in only phenytoin group (p 0.05). Nitrite and nitrate levels of gingival crevicular fluid and plasma did not significantly differ between responders and non-responders in all study groups (p > 0.05). Salivary nitrite levels exhibited a significant correlation with PD, GBTI, severity of gingival overgrowth (%G0), and GCF volume (p 0.05). Conclusion: Salivary nitrite and nitrate levels could be used as periodontal disease biomarkers in phenytoin induced gingival overgrowth, and that saliva seems to have a better diagnostic potential than GCF and plasma for the evaluation of drug-induced gingival overgrowth risk. However, when all drug groups were considered, saliva nitrite and nitrate levels could not be used as a biomarker for drug induced gingival overgrowth

The effect of HDL-bound and free PON1 on copper-induced LDL oxidation

Oxidative modification of LDL plays an important role in the development of atherosclerosis. High density lipoprotein (HDL) confers protection against atherosclerosis and the antioxidative properties of paraoxonase 1 (PON1) has been suggested to contribute to this effect of HDL. The PON1 exist in two major polymorphic forms (Q and R), which regulate the concentration and activity of the enzyme and alter its ability to prevent lipid oxidation. However, the association of Q192R polymorphism with PON1's capacity to protect against LDL lipoperoxidation is controversial. The aim of this study was to evaluate the effects of the purified PON1 Q192R and the partially purified HDL-bound PON1 Q192R isoenzymes (HDL-PON1 Q192R) on LDL oxidation, with respect to their arylesterase/homocysteine thiolactonase (HTLase) activities. Cupric ion-induced LDL oxidation was reduced up to 48% by purified PON1 Q192, but only 33% by an equivalent activity of PON1 R192. HDL-PON1 Q192 isoenzyme caused a 65% reduction, whereas HDL-PON1 R192 isoenzyme caused only 46% reduction in copper ion-induced LDL oxidation. These findings reflect the fact that PON1 Q and PON1 R allozymes may have different protective characteristics against LDL oxidation. The protection against LDL oxidation provided by HDL-PON1 Q192R isoenzymes is more prominent than the purified soluble enzymes. Inhibition of the Ca+2-dependent PON1 Q192R arylesterase/HTLase by the metal chelator EDTA, did not alter PON1's ability to inhibit LDL oxidation. These studies indicate that the active site involvement of the purified enzyme is not similar to the HDL-bound one, in terms of both PON1 arylesterase/HTLase activity and the protection of LDL from copper ion-induced oxidation. Moreover, PON1's ability to protect LDL from oxidation does not seem to require calcium. (C) 2016 Elsevier Ireland Ltd. All rights reserved

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

Kanser Tedavisi Gören Çocuklarda Uzun Süre Sonra Görülen Diş Anomalileri

Objective: the aim of this study is to determine the frequency of dental anomalies (DAs) (microdontia, hypodontia, hyperdontia, enamel defect, root malformation) in pediatric cancer patients at the ages <5 years and between 5 and 7 years, and understand their relationship with the received therapy. Materials and Methods: Pediatric patients who were diagnosed with cancer and treated before the age of 7 years were investigated in a case- control design. the study included 93 pediatric patients whose ages at diagnosis were between 9 months and 7 years and whose treatments were completed before 5-8 years. Group A consisted of patients in the age range of 9 months to 4 years and Group B consisted of patients in the age range of 5-7 years. Seventy-two siblings with compatible dental age ranges were included in the control group. For both groups, intraoral examinations were performed and panoramic radiographs were taken. Results: Among the 93 pediatric patients, the mean age was 9.54±1.25 (range: 8-13 years) and 48 (51.6%) patients were male. the most common diagnosis was hematologic malignancy with a rate of 65.5%. At least one DA was detected in 7 (9.7%) individuals of the control group and in 78 (83.9%) of the patient group. While the patients in the study group had all kinds of DAs, those in the control group had only enamel defects. the rates of microdontia (p=0.077) and hypodontia (p=0.058) were detected to be significantly higher in Group A than in Group B. Root malformation was more common in patients receiving chemotherapy and radiotherapy than in those receiving only chemotherapy (p=0.006). Conclusion: in this study it was found that the pediatric patients who received cancer treatment before the age of 7 years constituted a high-risk group for DAs. the frequencies of microdontia and hypodontia were increased even more when the patient was treated for cancer before 5 years of age.Amaç: Çalışmanın amacı <5 ve 5-7 yaş arası kanser tanısı alıp tedavi görmüş hastalarda diş anomalileri (DA) (mikrodonti, hipodonti, hiperdonti, mine kusuru, kök şekil bozukluğu) sıklığını belirlemek ve alınan tedavi ile ilişkini saptamaktır. Gereç ve Yöntemler: Kanser tanısı alıp 7 yaş öncesi tedavi görmüş çocuk hastalar olgu kontrol yöntemiyle araştırıldı. Kanser tedavisinin üzerinden en az 5-8 yıl geçmiş, tanı yaşı 9 ay ile 7 yıl arasında değişen, 93 hasta çalışmaya dahil edildi. Grup A 9 ay-4 yaş arasındaki hastalardan, Grup B 5-7 yaş arasındaki hastalardan oluşuyordu. Kontrol grubu olarak hastaların yaş aralığı uygun 72 kardeşi alındı. Hasta ve kontrol grubunun ağız içi muayeneleri yapıldı ve panoramik radyografileri alındı. Bulgular: Doksan üç hastanın yaş ortalaması 9,54±1,25 (dağılım 8-13 yıl) ve 48’i (%51,6) erkekti. En sık rastlanan tanı, %65,5 oranında hematolojik malignitelerdir. En az bir tane DA, hasta grubunun 78’inde (%83,9) ve kontrol grubunun 7’sinde (%9,7) saptandı. Çalışma grubundaki hastalarda her çeşit DA görülürken, kontrol grubunda sadece mine kusuru vardı. Grup A’da mikrodonti (p=0,077), hipodonti (p=0,058) oranlarının, Grup B’ye göre daha yüksek olduğu saptandı. Kök şekil bozukluğu kemoterapi ve radyoterapi alan hastalarda sadece kemoterapi alanlara göre daha fazla görüldü (p=0,006). Sonuç: Bu çalışmada 7 yaşından önce kanser tedavisi gören hastaların DA’lar yönünden yüksek riskli grup oluşturduğu saptanmıştır. Hastalar 5 yaşından önce kanser tedavisi gördüğünde mikrodontia ve hipodontinin sıklığı daha da artmıştır