Objective of the Study: Fentanyl and atropine are drugs used for analgesia during induction and for premedication, respectively. The aim of this study was to observe the effect of atropine used for premedication on cough developing in association with fentanyl use during anesthesia induction. Methods: This was a single-blind, prospective, multi-arm, parallel, randomized clinical trial involving 120 patients between ages 3 and 15 years undergoing general anesthesia. Patients were randomized into three groups: a control group (Group C), an atropine group (Group A), and a lidocaine group (Group L). Results: Incidence of cough was 45% (n = 16) in Group C, 16% (n = 6) in Group A, and 16% in Group L (n = 6) (p = 0.009). Cough was moderate in two cases in Group A and in two in Group L, and mild in all others in these groups. In Group C, cough was mild in seven cases, moderate in six, and severe in two. Conclusion: We determined that premedication with atropine suppressed the incidence and severity of fentanyl-induced cough during induction of general anesthesia. We think that, due to its antimuscarinic effect, atropine is as effective as lidocaine as a premedication.

It is known that oxidative stress originating from reactive oxygen species plays a role in the pathogenesis of Alzheimer's disease. In this study, the role of antioxidant status associated with oxidative stress in Alzheimer's disease was investigated. Peripheral blood samples were obtained from 28 healthy individuals (as control) and 28 Alzheimer's patients who met the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association criteria. Catalase, glutathione S‐transferase and paraoxonase 1 enzyme activities in blood plasma and glutathione S‐transferase enzyme activities in erythrocytes were determined by spectrophotometer. Catalase, glutathione S‐transferase and presenilin 1 gene expressions in leukocytes were determined using qRT‐PCR. Data were analysed with SPSS one‐way anova, a LSD post hoc test at p < 0.05. The activity of each enzyme was significantly reduced in Alzheimer's patients compared to control. The catalase gene expression level did not change compared to the control. Glutathione S‐transferase and presenilin 1 gene expression levels were increased compared to the control.

Background: Intensive care units (ICUs) have impact on physical and mental health not only for patients but also for health professionals. Post‐traumatic stress disorder that may occur in ICU professionals may negatively affect the treatment and care process by affecting their sleep quality. Aim: This study aims to evaluate the relationship between post‐traumatic stress disorder and sleep quality in intensive care unit professionals. Study Design: The cross‐sectional study conducted with 341 (nurses, physicians and others) professionals working in the ICUs in Turkey. Data were collected with a socio‐demographic form, Posttraumatic Stress Disorder‐Short Scale (PTSD‐SS) and Richard‐Campbell Sleep Questionnaire (RCSQ). Results: The mean PTSD‐SS and RCSQ scale scores of the participants were 15.37 ± 6.72 (min: 0, max: 35) and 46.61 ± 22.46 (min: 0, max: 100). When the cutoff points of the scores obtained from PTSD‐SS was examined, 12.9% ( n = 33) of ICU nurses, 11.3% ( n = 6) of the physicians and 3.4% ( n = 1) of the other health professionals had post‐traumatic stress disorder symptoms, and it was determined that the prevalence of PTSD in all ICU professionals was 12% ( n = 40). In addition, there was a statistically significant negative weak correlation between PTSD‐SS and RCSQ ( r = −0.207) ( p < .05). Conclusions: The results of this study show that increasing the level of PTSD causes sleep quality to deteriorate. Therefore, evaluation and recognition of PTSD symptoms in ICU professionals and interventions to be important in maintaining sleep quality. Additionally, the results of this study can be used in planning to improve the mental health of ICU nurses. Therefore, greater support for ICU nurses to prevent PTSD is recommended. Relevance to Clinical Practice: It is important and necessary to prevent the development of PTSD in ICU nurses and to reduce its negative impact on sleep quality.

Opioids are widely used as an analgesic drug in the surgical setting. Remifentanil is an ultra-short acting opioid with selective affinity to the mu (μ) receptor, and also exhibits GABA agonist effects. The aim of this study was study of the neurotoxic or neuroprotective effect of different doses of remifentanil in glutamate-induced toxicity in olfactory neuron cell culture. Olfactory neurons were obtained from newborn Sprague Dawley rat pups. Glutamate 10^-5 mM was added to all culture dishes, except for the negative control group. Remifentanil was added at three different doses for 24 hours, after which evaluation was performed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), and Annexin V. The highest and lowest viability values were obtained from the low and high remifentanil doses at approximately 91% and 75%, respectively. TAC and TOS were correlated with the MTT results. TAC, TOS and MTT most closely approximated to the sham group values in the remifentanil 0.02 mM group. Our results suggest that remifentanil has the potential to reduce glutamate toxicity and to increase cell viability in cultured neuron from the rat olfactory bulb.