• Sonuç bulunamadı

ÖZELLİKLERİ

3.3. Fiziksel Kısıtlamanın Nörovasküler Etkiler

Fiziksel olarak kısıtlanan bölgenin birinci günden, beşinci güne kadar nörovasküler özelliklerindeki değişime ilişkin bulgular Tablo 3’te sunuldu. Bulgulara göre; fiziksel

58 24-27 April 2019 Burdur/TURKEY kısıtlama altındaki bölgedeki ödemin, renk değişikliğinin beş günlük izlem sürecinde istatistiksel olarak anlamlı farkla arttığı, nabız gücünün ise azaldığı saptandı (p<0.05). Kısıtlanan bölgenin ısısı ve kapiller geri dolum süresi gibi özelliklerin ise beş günlük izlem süresince anlamlı bir değişiklik göstermediği belirlendi (p>0.05).

Ödem ve nabız gücü özellikleri bakımından tespit materyalleri arasında istatistiksel bakımdan anlamlı bir farklılık olmadığı belirlenirken, renk değişikliği, kapiller geri dolum süresi, ikinci ve üçüncü günlerdeki kısıtlanan bölenin ısısı parametreleri bakımından kısıtlama materyallerinin anlamlı farklılık gösterdiği saptandı (p<0.05).

Ödem bulguları bakımından kısıtlama materyal türleri arasında anlamlı bir farklılık olmadığı görülse de, beş günlük gözlem süresince gazlı bez ve yeşil bağ kullanılarak kısıtlanan hastalarda, ödem görülen hasta sayısında artış olduğu, hasta güvenlik kemeri ile kısıtlanan hastalarda ödem görülen hasta sayısının gözlem günlerine göre daha az değişim gösterdiği saptandı.

Hasta güvenlik kemeri kullanılarak kısıtlanan hastalarda, bölgede renk değişimi gözlemlenen hasta oranının beş günlük gözlem süresince azaldığı belirlenirken, yeşil kumaş bağ kullanılan hastalarda bu oranın artış gösterdiği, gazlı bez ile kısıtlanan hastalarda ise renk değişikliği gözlenen ve gözlenmeyen hasta oranlarının gözlem süresince birbirine benzer olduğu saptandı. Yeşil kumaş bağ ile kısıtlanan hastalarda kapiller geri dolum süresi iki sn'nin üzerinde olan hasta oranının beş günlük gözlem sürecinde artış gösterdiği belirlenirken, hasta güvenlik kemeri ile kısıtlanan hastalarda, azalma yönünde değişim gösterdiği saptandı.

4.SONUÇ

Yapılan bu çalışma, YBÜ'deki kısıtlama uygulamalarının önemli bir bölümünü FK'nin oluşturduğunu, yoğun bakım hemşirelerinin kısıtlama uygulamalarında aktif rol aldığını ve karar verici bir pozisyonda olduklarını göstermekle birlikte, mevcut yasal düzenlemelere rağmen kısıtlama uygulamasına karar verme ve gerekliliğini order etme hususunda sağlık ekibi üyeleri arasında işbirliğinin yetersiz olduğunu göstermiştir. Bununla birlikte, YBÜ'de hastanın güvenliğini sağlamada bir öncelik olarak tercih edilen FK'nin uygulama süresindeki artışın, nörovasküler komplikasyon görülme olasılığını arttırdığı, özel kısıtlama ekipmanı kullanımının, nörovasküler komplikasyonların görülme olasılığını azaltabileceği söylenebilir.

59 KAYNAKÇA

1. Azizpour M, Moosazadeh M, Esmaeili R. (2017). Use of physical restraints in intensive care unit: a systematic review study. Acta Medica Mediterr 33: 129-36.

2. Dolan J, Dolan Looby SE. (2017). Determinants of nurses' use of physical restraints in surgical intensive care unit patients. Am J Crit Care 26: 373-9.

3. Mitchell DA, Panchisin T, Seckel MA.(2018). Reducing use of restraints in ıntensive care units: A quality

ımprovement project. Crit Care Nurse 38: e8-e16.

4. Krüger C, Mayer H, Haastert B, et al. (2013). Use of physical restraints in acute hospitals in Germany: a multi-centre cross-sectional study. Int J Nurs Stud 50: 1599-6.

5. Springer G. (2015). When and how to use restraints. American Nurse Today 10: 26-32.

6. Ahmadi M, Bagheri-Saweh MI, Nouri B. et al. (2019). Effect of interventional educational programs on intensive care nurses' perception, knowledge, attitude, and practice about physical restraints: A pre- /postclinical trial. Crit Care Nurs Q 42: 106-16.

7. Li X, Fawcett NT. (2014). Clinical decision making on the use of physical restraint in intensive care units. Int J Nurs Stud 1: 4446-50.

8. Eskandari F, Abdullah KL, Zainal NZ. et al. (2017). Use of physical restraint: Nurses’ knowledge, attitude, intention and practice and influencing factors. J Clin Nurs 26: 4479-88.

9. Cunha M, André S, Bica I. et al. (2016). Chemical and physical restraint of patients. Procedia - Social and Behavioral Sciences 217: 389-99.

10. Huang HC, Huang YT, Lin KC. et al. (2014). Risk factors associated with physical restraints in residential aged care facilities: a community-based epidemiological survey in Taiwan. J Adv Nurs 70: 130-43.

11. Benbenbishty J, Adam S, Endacott R. (2010). Physical restraint use in intensive care units across Europe: the PRICE study. Intensive Crit Care Nurs 26: 241-45.

12. Langley G, Schmollgruber S, Egan A. (2011). Restraints in intensive care units-a mixed method study. Intensive Crit. Care Nurs 27: 67-75.

13. Luk E, Sneyers B, Rose L. et al. (2014). Predictors of physical restraint use in Canadian intensive care units. Crit Care 18: R46.

14. Johnson K, Curry V, Steubing AS, et al. (2016). A non-pharmacologic approach to decrease restraint use. Intensive Crit Care Nurs 34: 12-9.

15. Moradimajd P, Noghabi AA, Zolfaghari M, Mehran A. (2015). Physical restraint use in intensive care units. Iran J Crit Care Nurs 8: 173-8.

16. Al-Khaled TH, Zahran EM, El-Soussi AH. (2011). Nurses’ related factors influencing the use of physical restraint in critical care units. J Am Sci 7: 13-22.

17. Suliman M. (2018). Prevalence of physical restraint among ventilated intensive care unit patients. J Clin Nurs 27: 3490-6.

18. Azab SMS, Negm LA. (2013). Use of physical restraint in intensive care units (ICUs) at Ain Shams University Hospitals, Cairo. J Am Sci 9: 230-40.

19. Nasrate H, Shamlawi A, Darawad MW. (2017). Improving ICU nurses’ practices of physical restraints in Jordan: Effect of an educational program. Health 9: 1632-43.

60 24-27 April 2019 Burdur/TURKEY 20. Taha MN, Ali HZ. (2013). Physical restraints in critical care units: impact of a training program on nurses’

knowledge and practice and on patients’ outcomes. J Nurs Care 2: 135.

21. Demir A. (2007). Nurses’ use of physical restraints in four Turkish hospitals. J Nurs Scholarship 39: 38-45. 22. Eşer İ, Khorshid L, Hakverdioğlu G. (2007). The characteristics of physically restrained patients in intensive

care units. Int J Human Sci 4: 1-10.

23. Kandeel NA, Attia AK. (2013). Physical restraints practice in adult intensive care units in Egypt. Nurs Health Sci 15: 79-85.

61 INVESTIGATION OF THE BDNF GENE EXPRESSION IN EPILEPSY PATIENTS

Suat Cakına1,*, Selma Yucel2, Cemre Cagan Polat2 , Tulay Tan2, Samil Ozturk1

1Canakkale Onsekiz Mart University, Health Service Vocational College, Çanakkale, Turkey,

suatcakina@comu.edu.tr, samilozturk16@hotmail.com

2Canakkale Onsekiz Mart University, Faculty of Medicine, Department of Neurology, Çanakkale, Turkey,

selmayucel@comu.edu.tr, caganpolat@comu.edu.tr, tantulay@comu.edu.tr

ABSTRACT

Brain-induced neurotrophic factor (BDNF) is a neurotrophin which involved in a central and peripheral nervous system, growth and function of neurons, neurotrophin life. In recent years, studies on BDNF have accelerated due to the importance of neuronal survival and function in the nervous system. The aim of this study was to compare BDNF gene expression in epilepsy patients with control group. In this study, blood samples were taken from 30 epilepsy patients and 30 healthy individuals. Expression of the BDNF gene was measured using a method based on real-time PCR. The results of our study showed that BDNF gene expression was significantly upregulated in the patient group compared to the control group. (p<0.05). BDNF gene expression may be effective in the pathogenesis of epilepsy disease. Further studies are needed to determine the role of BDNF in the treatment of epilepsy and the pathogenesis of epilepsy.

Key words: Epilepsy, Brain-induced neurotrophic factor, gene expression.

1. Introduction

Epilepsy is a common chronic neurological disease that affects people's quality of life and is a complex genetic disease (1, 2). Brain-induced neurotrophic factor (BDNF) is a neurotrophic factor that affects neural survival and it is highly present in brain areas such as the hypothalamus, amygdala, hippocampus, and neocortex (3, 4). BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates intracellular signaling cascades, leading to neural plasticity, neurogenesis, stress resistance and survival of the cell (4, 5). The levels of BDNF are decreased in many neurodegenerative diseases such as Parkinson's disease (PD), multiple sclerosis (MS) and Huntington's disease (6-8). This study aims to evaluate the gene expression levels of BDNF between the patient and the control group.

62 24-27 April 2019 Burdur/TURKEY This study was approved by Çanakkale Onsekiz Mart University Ethics Committee (2011- KAEK-27/2018-E.1800189100) and informed written consent was obtained from all participants. Totally, 60 individuals including 30 unrelated epilepsy patients diagnosed with epilepsy according to International League Against Epilepsy (ILAE) 1989 criteria and 30 age- and sex matched controls were selected in the current case-control study. Exclusion criteria included ischemic cerebrovascular accident, aneurysm, arteriovenous malformation, intracranial mass, alcohol use, antidepressant-antipsychotic use, metabolic disorders, prolonged postictal confusion, syndromic seizures, and hypersomnia or insomnia. Blood samples were collected epilepsy patients who were treated at the Faculty of Medicine, Department of Neurology and healthy volunteers.into EDTA tubes and stored at -80 oC. Total RNA was extracted from blood samples with a commercial kit (Bioneer) and the quantity of RNA was assessed using the NanoDrop ND-1000 spectrophotometer. cDNA was synthesized from the total RNA using the commercial kit (Bioneer). Real-time RT-PCR was performed using GreenStar qPCR Master Mix and Bioneer system. Real-time PCR amplification for BDNFwas performed using a total volume of 20 μL that contained 10 µl qPCR mix, 5 µl of each primer, 2µ cDNA and distile water. The PCR conditions were as follows: 94 °C for 3 min, and then 35 cycles of 94 °C for 60 s, 55 °C for 45 s, and 72 °C for 1.5 min, and finally 72 °C for 2 min. Target gene expression levels were compared using Ct values in the patient and control groups.

Statistical analysis

Statistical analysis was performed using SPSS, version 19.0. (SPSS, IBM Company). Normality of the variables was evaluated by the Kolmogorov-Smirnov test. Parametric variables were compared using the Mann–Whitney U test and independent samples t-test. p- values ≤0.05 are taken as statistical significant.

3. Results

The epileptic group comprised 30 patients (20 males, 10 females) and the control group comprised 30 healthy individuals (20 males, 10 females). The mean age of the epileptic patients and the control group was 42.1±11.1 and 41.9±8.2 years, respectively. The patient and control groups were similar given the age and sex ( p >0.05). BDNF gen expression levels were 35.62±1.27 in the epileptic group and 31.50±1.33 in the control group. The BDNF was significantly upregulated in epilepsy patients compared with healthy subjects (p<0.05).

63 4. Discussion

Epilepsy is one of the most common neurological conditions triggered by the disruption of the abnormal electrochemical activities of the brain’s neurological system. Epilepsy affects approximately 0.5% to 1% of the general population (9). BDNF is one of the crucial nerve growth factors in the family of neurotrophins and plays an important role in the maintenance, regulation, and differentiation of peripheral and central nervous system neurons (10). A large amount of research has indicated that abnormal expression of BDNF plays a critical role in the pathological process of epilepsy development. Martínez-Levy et al and de Souza Bernardino et al found an increased expression of BDNF transcription in patients with epilepsy (11, 12).

We demonstrated significant upregulation of BDNF in people with epilepsy compared with controls. BDNF has been shown to strengthen excitatory (glutamatergic) synapses while weakening inhibitory (GABAergic) ones and contribute to activity-dependent synaptic plasticity.

5. Conclusion

BDNF gene expression may enhance the susceptibility of epilepsy and useful as genetic biomarker and further studies with large sample sizes are needed.

References

1. Gholami A, Salarilak S, Lotfabadi P, Kiani F, Rajabi A, Mansori K, et al. Quality of life in epileptic patients compared with healthy people. Medical journal of the Islamic Republic of Iran. 2016;30:388-.

2. Mirza N, Appleton R, Burn S, du Plessis D, Duncan R, Farah JO, et al. Genetic regulation of gene expression in the epileptic human hippocampus. Human molecular genetics. 2017;26(9):1759-69.

3. Bathina S, Das UN. Brain-derived neurotrophic factor and its clinical implications. Archives of medical science : AMS. 2015;11(6):1164-78.

4. Binder DK, Scharfman HE. Brain-derived neurotrophic factor. Growth factors (Chur, Switzerland). 2004;22(3):123-31.

5. Phillips C. Brain-Derived Neurotrophic Factor, Depression, and Physical Activity: Making the Neuroplastic Connection. Neural plasticity. 2017;2017:7260130.

6. Mughal MR, Baharani A, Chigurupati S, Son TG, Chen E, Yang P, et al. Electroconvulsive shock ameliorates disease processes and extends survival in huntingtin mutant mice. Human molecular genetics. 2011;20(4):659-69.

7. Scalzo P, Kummer A, Bretas TL, Cardoso F, Teixeira AL. Serum levels of brain-derived neurotrophic factor correlate with motor impairment in Parkinson's disease. Journal of neurology. 2010;257(4):540-5.

64 24-27 April 2019 Burdur/TURKEY 8. Sohrabji F, Lewis DK. Estrogen-BDNF interactions: implications for neurodegenerative diseases. Frontiers in neuroendocrinology. 2006;27(4):404-14.

9. Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005;46(4):470-2.

10. Yogeetha BS, Haupt LM, McKenzie K, Sutherland HG, Okolicsyani RK, Lea RA, et al. BDNF and TNF-alpha polymorphisms in memory. Molecular biology reports. 2013;40(9):5483-90.

11. de Souza Bernardino TC, Teixeira AL, Miranda AS, Guidine PM, Rezende G, Doretto MC, et al. Wistar Audiogenic Rats (WAR) exhibit altered levels of cytokines and brain-derived neurotrophic factor following audiogenic seizures. Neuroscience letters. 2015;597:154-8.

12. Martinez-Levy GA, Rocha L, Rodriguez-Pineda F, Alonso-Vanegas MA, Nani A, Buentello-Garcia RM, et al. Increased Expression of Brain-Derived Neurotrophic Factor Transcripts I and VI, cAMP Response Element Binding, and Glucocorticoid Receptor in the Cortex of Patients with Temporal Lobe Epilepsy. Molecular neurobiology. 2018;55(5):3698-708.

65 DETERMINATION OF ALPHA-SYNUCLEIN ENZYME ACTIVITY: RESTLESS

LEG SYNDROME IN MULTIPLE SCLEROSIS PATIENTS