Healthcare students' vaccination status, knowledge, and protective behaviors regarding hepatitis B: a cross-sectional study in Turkey.

AIM: We aimed to determine the vaccination status, knowledge, and protective behaviors of healthcare students related to hepatitis B and to examine the related factors. METHOD: This cross-sectional study was conducted in seven universities from seven geographical regions of Turkey. The study group included 5451 healthcare students. Data were collected with a questionnaire including items on sociodemographic characteristics, vaccination status, knowledge and protective behaviors related to hepatitis B. Data were analyzed with Pearson's chi-square and logistic regression analyses. RESULTS: 86.0% of the students had hepatitis B vaccine while 7.6% did not. Vaccination was higher in nursing and midwifery students (aOR = 1.87, CI 95%: 1.26-2.77; aOR = 3.87, CI 95%: 2.14-7.02, respectively). Vaccination was 1.28 times higher in females (CI 95% 1.03-1.60). The ≥23 age group had 1.79 times higher vaccination rate than those in the ≤19 (CI 95%: 1.26-2.53). Vaccination was higher in students whose family's economic status is middle and high (aOR = 1.53, CI 95%: 1.07-2.19; aOR = 1.47, CI 95%: 1.03-2.19, respectively). Vaccination was higher in those living in towns and cities during childhood (aOR = 1.36, CI 95%: 1.06-1.74; aOR = 1.79, CI 95%: 1.34-2.38, respectively). Females had more knowledge of hepatitis B and protective behaviors. Both knowledge and protective behavior scores of vaccinated participants were significantly higher (p < .05). CONCLUSION: We found that the vaccination rate in healthcare students was high, but lower than the country's targets. The students were sensitive about the protective behaviors from hepatitis B infection and had sufficient knowledge of HBV contamination.

Effects of Dexmedetomidine on Renal Ischaemia Reperfusion Injury in Streptozotocin-Induced Diabetic Rats.

OBJECTIVE: The aim of this study was to investigate the effects of dexmedetomidine before and after ischaemia in diabetic rat kidney ischaemia reperfusion (IR) injury in the experimental diabetic rat model. METHODS: Data belonging to 35 rats weighing between 250 and 300 g were analysed. Diabetes mellitus (DM) was induced using streptozotocin. Groups had bilateral renal vasculature clamped for 45 min ischaemia before clamps were removed, and 4 hours reperfusion was applied. Rats were divided into five groups: Group I or nondiabetic sham group (n=7), Group II or diabetic sham group (n=7), Group III or diabetic IR group (n=7), Group IV or diabetic IR+prophylactic Dex P (before ischaemia) (n=7) and Group V or diabetic IR+therapeutic Dex T (following reperfusion) (n=7). Dexmedetomidine was administered at a dose of 100 µg kg-1 intraperitoneally. Histomorphological and biochemical methods were used to assess the blood and tissue samples. RESULTS: The proximal tubule injury score in the control sham group was significantly lower than in other groups. The proximal tubule and total cell damage scores of the diabetic IR group were significantly higher than the diabetic IR+Dex T group, and no significant difference was detected in the diabetic IR+Dex P group. The biochemical parameters of the IR group were significantly increased compared to Groups I and II; however, there was no significant reduction in these parameters in the groups administered dexmedetomidine. CONCLUSION: Although administration of dexmedetomidine after ischaemia in the diabetic rat renal IR model was found to be more effective on the histopathological injury scores compared to preischaemic administration, this study has not shown that dexmedetomidine provides effective and complete protection in DM.

Evaluation of the Effectiveness of Sugammadex for Digoxin Intoxication: An Experimental Study.

Previous studies have shown that cyclodextrin group medicines bind to various drugs. The hypothesis of our study is to determine whether sugammadex could bind to digoxin and delay the cardiovascular toxicity of that drug. Twenty-eight sedated Wistar rats were infused with digoxin at 3 mg/h (0.25 mg/ml). Five minutes after the start of infusion, animals were treated with a bolus of either 16 mg/kg (Sgdx16), 100 mg/kg (Sgdx100), or 1000 mg/kg (Sgdx1000) sugammadex. The control group infusion did not contain sugammadex. Heart rate, electrocardiography, and respiratory rate were monitored. The primary endpoint was time to asystole. Digoxin infusion continued until the animals arrested. The time to asystole for the Sgdx1000 group was significantly longer compared to that for the control group (p < 0.05). The mean lethal dose of digoxin was 5.35 ± 2.06 mg/kg in the saline-treated rats. On the other hand, the mean lethal dose of digoxin was 8.54 ± 1.51 mg/kg in the sugammadex 1000 group (p < 0.05). The mean lethal dose of digoxin was significantly higher than control group (p < 0.05). We found that the 1000 mg/kg dose of sugammadex delayed digoxin cardiotoxicity in a rat model of digoxin toxicity. We conclude that further research must be conducted on the interaction between digoxin and sugammadex.

The role of resveratrol on full - Thickness uterine wound healing in rats.

OBJECTIVE: Healing of the uterus after cesarean section and myomectomy operation is clinically important. In this study, we aimed to investigate the effects of resveratrol (3,5,4'-o-trihydroxystilbene) on the wound healing process of the uterus in rats treated with resveratrol following full thickness injury of the uterus. MATERIALS AND METHODS: Twenty-one female wistar albino rats were divided randomly into three groups (1) control group with no intervention (2) injury group with uterine full thickness injury (3) resveratrol group with uterine full thickness injury and treated with resveratrol. Resveratrol was injected by oral gavage at the doses of 0.5 mg/kg/day for 30 days following uterine full thickness injury. Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) distributions were assessed using the immunohistochemical methods in tissue and ELISA methods in the tissue homogenate. Glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were evaluated with colorimetric method and malondialdehyde (MDA) levels also were measured using high performance liquid chromatography in the tissue homogenate. The effects of resveratrol on the uterine histology also were evaluated histologically with the light microscopy. RESULTS: Histological evaluation and immunohistochemical evaluations showed that treatment with a resveratrol significantly increased the thickness of the uterine wall and VEGF expression and decreased expression PDGF during wound healing. Biochemically, GPx and SOD activities were increased significantly after treatment with resveratrol. Additionally, resveratrol administration decreased MDA levels. CONCLUSION: These results showed that the antioxidant effects of resveratrol has been shown to have a positive influence on wound healing of the uterus.

The Effect of Insulin Like Growth Factor-1 on Recovery of Facial Nerve Crush Injury.

OBJECTIVES: The aim of this study is to investigate the efficacy of locally applied insulin-like growth factor 1 (IGF-1) on the recovery of facial nerve functions after crush injury in a rabbit model. METHODS: The rabbits were randomly assigned into three groups. Group 1 consisted of the rabbits with crush injury alone; group 2, the animals applied saline solution onto the crushed facial nerve and group 3, IGF-1 implemented to the nerve in the same manner. Facial nerve injury was first electrophysiologically studied on 10th and 42nd days of the procedure. The damage to the facial nerves was then investigated histopathologically, after sacrification of the animals. RESULTS: In the electrophysiological study, compound muscle action potential amplitudes of the crushed nerves in the second group were decreased. In pathological specimens of the first and second groups, the orders of axons were distorted; demyelination and proliferation of Schwann cells were observed. However, in IGF-1 treated group axonal order and myelin were preserved, and Schwann cell proliferation was close to normal (P<0.05). CONCLUSION: Local application of IGF-1 in a slow releasing gel was found efficacious in the recovery of the facial nerve crush injury in rabbits. IGF-1 was considered worthy of being tried in clinical studies in facial nerve injury cases.

Evaluation of the effects of intra-arterial sugammadex and dexmedetomidine: an experimental study.

BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

[Evaluation of the effects of intra-arterial sugammadex and dexmedetomidine: an experimental study]. / Avaliação dos efeitos de sugamadex e dexmedetomidina intra-arterial: estudo experimental.

BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

Intravenous lipid emulsion prolongs survival in rats intoxicated with digoxin.

BACKGROUND: Intravenous lipid emulsion eliminates the toxicity-related symptoms of several drugs. We hypothesized that intravenous lipid emulsion prolongs the survival time in digoxin-intoxicated rats. METHODS: Electrocardiograms of 14 anesthesized Wistar rats were monitored. All of the rats received digoxin infusion at a rate of 12 mL/h (0.25 mg/mL). Five minutes after the start of digoxin infusion, animals were treated either with 12.4 mL/kg intravenous lipid emulsion (group L) or saline (group C). The primary outcome variable was time elapsed until asystole development. Cumulative dose of digoxin required to induce asystole was also recorded. RESULTS: Mean time until asystole development in groups C and L were 21.28 ± 8.61 and 32.00 ± 5.41 minutes, respectively (P< .05). The mean lethal doses of digoxin in the groups C and L were 3.97 ± 1.54 and 6.09 ± 0.96 mg/kg, respectively (P< .05). CONCLUSION: Intravenous lipid emulsion prolonged the time until asystole development and increased cumulative lethal dose in rats intoxicated with digoxin.

Evaluation of the effectiveness of sugammadex for verapamil intoxication.

Previous studies have shown that medications from the cyclodextrin family bind to verapamil. The aim of our study was to determine whether sugammadex could bind to verapamil and prevent the cardiovascular toxicity of that drug. Twenty-eight sedated Wistar rats were infused with verapamil at 37.5 mg/kg/h. Five minutes after the start of infusion, the animals were treated with a bolus of either 16 mg/kg, 100 mg/kg or 1000 mg/kg sugammadex. The control group was treated with an infusion without sugammadex. The heart rate and respiratory rate were monitored, and an electrocardiogram was recorded. The primary end-point was the time to asystole. The verapamil infusion continued until the animals arrested. The asystole time for the S16 group was significantly longer compared to those for the control and S1000 groups (p < 0.05). The asystole time for the S1000 group was significantly shorter than those for all of the other groups (p < 0.05). Reflecting these data, there was a near doubling of the mean lethal dose of verapamil from 13.57 mg/kg (S.D. ±8.1) in the saline-treated rats to 22.42 mg/kg (S.D. ±9.9) in the sugammadex 16 group (p < 0.05). However, for the sugammadex 1000 group, the mean lethal dose was found to be 6.28 ± 1.11 mg/kg. This dose is significantly lower than those for all of the other groups (p < 0.05). We found that treatment with 16 mg/kg sugammadex delayed verapamil cardiotoxicity in rats. However, 1000 mg/kg sugammadex accelerated verapamil cardiotoxicity in rats. Further studies must be conducted to investigate the interaction between verapamil and sugammadex.