Immobilization of alkynyl functionalized manganese phthalocyanine via click electrochemistry for electrocatalytic oxygen evolution reaction.

Peripherally and non-peripherally terminal alkynyl substituted manganese phthalocyanines (MnPc) were synthesized and characterized and then used as functional materials in modified electrodes. MnPcs were substituted with alkynyl groups, which are reactive moieties in click electrochemistry (CEC) reactions. Mn(iii) cations were incorporated into the cavity of the Pc ring in order to increase the redox activity of the complexes. Electrochemical characterizations of the complexes were determined by voltammetric and in situ spectroelectrochemical measurements in order to determine their possible technological applications. MnPc complexes illustrated five redox couples and these redox couples were assigned as [Cl-MnIIIPc2-]/[Cl-MnIIPc2-]1-, [Cl-MnIIPc2-]1-/[Cl-MnIPc2-]2-, [Cl-MnIPc2-]2-/[ Cl-MnIPc3-]3-, and [Cl-MnIIIPc2-]/[Cl-MnIIIPc1-]1+ redox processes. The position of the substituents affected the mechanism of the redox reactions and influenced the tendency to react with the molecular oxygen. Moreover, changing the position of the substituents slightly influenced the peak potentials and reversibility of the redox processes. For the applications, modified electrodes (ITO/PANI-N3-MnPc and GCE/PANI-N3-MnPc) were constructed with CEC reaction between azido functionalized polyaniline (PANI-N3) and terminally alkynyl substituted MnPcs and these electrodes. Voltammetric characterizations of the modified electrodes illustrated suitable redox activity and conductivity for the practical applications. Finally, the GCE/PANI-N3-MnPc electrode was tested as a potential electrocatalyst for water splitting reaction. Although the GCE/PANI-N3-MnPc electrode did not catalyze the hydrogen evolution reaction (HER), it significantly catalyzed the oxygen evolution reaction (OER) in aqueous solution.

Relationship between genuine and pseudohalitosis and social anxiety disorder.

Halitosis is described as offensive breath caused by various factors such as periodontal diseases, bacterial coating of tongue, systemic disorders and different types of foods. Pseudohalitosis is a situation that patients complain of oral malodor even though they do not have offensive odour. The purpose of this study was to compare the relationships between social anxiety estimations and both pseudohalitosis and genuine halitosis cases. Liebowitz Social Anxiety Scale (LSAS) and questionnaire regarding halitosis were applied to 100 participants. Halitosis was determined using organoleptic method, gas chromatography and portable sulphur monitor. anova test and 2-tailed Spearman's rank-order correlation coefficient were used to determine the differences and relations between groups. With reference to LSAS, 62% of participants had anxiety. Among these patients, 98% had genuine halitosis (P < 0·05). The mean measurements of VSC values were 248·65 ppm in halimeter, 298·02 ppm of H2 S, 95·33 ppm of CH3 SH and 47·00 ppm of (CH3 )2 S in gas chromatography. Halitosis was present in 90% of participants, and it was absent in 10% by organoleptic assessment. There was a significant correlation between organoleptic and halimeter measurements. Moreover, statistically significant relationship was detected between anxiety and halitosis. Genuine halitosis patients exhibit social anxiety, so it can be said that there is a causal relationship between halitosis and anxiety. Comparison of the results of objective measurements (sulphur monitor, gas chromatography, organoleptic method) was statistically significant; therefore, it can be said that these methods can be used in diagnosis of halitosis with high accuracy.

Anatomic characteristics and dimensions of the nasopalatine canal: a radiographic study using cone-beam computed tomography.

BACKGROUND: Description of the nasopalatine canal (NPC) is important for planning surgical treatment and comprehension of the morphology and pathogenesis of lesions that occur in the anterior maxilla. The goal of this study was to analyse the dimensions and anatomic characteristics of the NPC on cone-beam computed tomography (CBCT) scans, to determine the incidence of anatomical variation; and to assess the correlations of these variables with age, gender, and dental status. MATERIALS AND METHODS: A total of 320 individual CBCT images were included. Reformatted sagittal, coronal and axial slices were evaluated. Sagittal images were used for measurements of the NPC and to classified shape and direction-course of the NPC. Coronal images were used to analyse the NPC division levels and axial images were used to detect the number of palatal and nasal opening. RESULTS: The mean NPC length was 11.45 ± 2.50 mm; statistically significant differences were detected between males and females (p < 0.05). Mean nasopalatine angle was 76.26 ± 8.12°; significant differences were detected in sagittal and coronal classifications. The most common canal was: funnel-shaped (29%), slanted-curved direction-course (53.1%), middle third division level (43.1%), and one incisive foramen with two Stenson's foramina (1-2) (77.2%). CONCLUSIONS: The current study ensures new findings on the literature concerning the description of the anatomical structure of the canal. Also, the study highlights a significant variability in the anatomy and morphology of the NPC. Therefore, three-dimensional analysis of this structure is important for facilitating surgical management and preventing possible complications in this area.

The relationship between neutrophil/lymphocyte and platelet/lymphocyte ratios with oxidative stress in active Crohn's disease patients.

BACKGROUND: This study investigated the relationship between the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) values with oxidative stress in active Crohn's disease (CD) patients. We investigated whether these parameters were useful for follow-up assessments of CD activity. METHODS: Forty-nine patients with a confirmed diagnosis of CD (24 active and 25 inactive) and 38 control subjects were enrolled in the study. We measured serum activity of superoxide dismutase (SOD) using an enzyme-linked immunosorbent assay (ELISA) and malondialdehyde (MDA) levels using a spectrophotometric method. Neutrophil, lymphocyte and platelet counts were recorded, and the NLR and PLR values were calculated from these parameters. RESULTS: Patients with active CD exhibited significantly higher serum levels of MDA (p =0.007), NLR (p =0.034), and PLR (p =0.026) than inactive CD patients. Receiver operating characteristic (ROC) curve analysis demonstrated that the optimum cut-off values of MDA, NLR, and PLR based on the differences between active and inactive patients were 0.14 µmol/L, 2.58, and 192.26, respectively. The NLR value increased in active patients with elevated MDA levels as a dependent variable (B: 0.422, p =0.029). CONCLUSIONS: We suggest the use of MDA, PLR, and NLR values as a noninvasive test to evaluate disease activity in CD patients. NLR values may also reflect the presence of oxidative stress, and this value may be efficient and useful in determining CD activity. Hippokratia 2016, 20(4): 268-273.

Age related changes in the effect of electroconvulsive shock on the blood brain barrier permeability in rats.

Age-related changes in blood-brain barrier permeability to macromolecules were investigated during electrically induced seizures. Evans-blue was used as the barrier tracer. There was no change in the permeability of the blood brain barrier associated with aging in the rats. However, the extravasation of Evans-blue albumin was most pronounced in the brain after ten repeated electroshocks in old rats. In the adult group that was given a single electroconvulsive shock, there was no coloration of the brain tissue, whereas the group given ten repeated electroconvulsive seizures showed slight staining of the thalamic nuclei, hypothalamus, and midbrain in 5 out of 13 rats. In 30-day-old rats, Evans-blue leakage was similar to that of adults, except that the frequency and intensity of blood-brain barrier breakdown was less after ten repeated electroshocks. In 15-day-old rats, the blood-brain barrier breakdown to Evans-blue albumin was the same after a single and ten electroshocks and the same in control and electroshocked rats. According to our results ten repeated electroshocks have a more pronounced effect on the old animals and have less effect on the young animals in comparison to adult ones.

Intracarotid hypothermic saline infusion: a new method for reversible blood-brain barrier disruption in anesthetized rats.

An animal model for reversible blood-brain barrier disruption has been developed. Retrograde infusion of hypothermic saline solution (8 +/- 1 degree C) into the left external carotid artery of normothermic, Wistar rats reversibly increases cerebrovascular permeability to Evans blue albumin in the left cerebral hemisphere. Isotonic saline solutions at 37 degrees C for Group I and at 8 +/- 1 degree C for Group II were infused for 30 s at a constant rate of 0.12 ml/s into the left external carotid artery. Evans blue, the barrier tracer, was administered intravenously either prior to or at intervals 5, 30, 180, 360 min after the hypothermic saline infusion under pentobarbital anesthesia. All animals receiving hypothermic saline perfusion had disturbed blood-brain barrier permeability. Based on visual inspection, disruption grade in the left hemispheres of 10 of 16 animals was 3+. Mean values for Evans blue dye were found to be 0.32 +/- 0.08 mg% in left the hemisphere after normothermic saline infusion (Group 1), and 2.9 +/- 0.4 mg% in the same hemisphere after hypothermic saline infusion (Group II). The difference was found to be significant between Group I and Group II (P < 0.001). The increase in cerebrovascular permeability was temporary, however, although Evans blue albumin extravasion remained slightly elevated 3 h after infusion, it was normal 6 h after infusion.

Influence of acute arterial hypertension on blood-brain barrier permeability in streptozocin-induced diabetic rats.

The effect of acute arterial hypertension on blood-brain barrier (BBB) permeability was studied in streptozocin-induced diabetic rats using Evans blue as a barrier tracer. Four groups of rats were studied: Group 1, normotensive normoglycemia; Group II, normotensive+diabetes mellitus; Group III, arterial hypertension+diabetes mellitus; Group IV, arterial-hypertension+normoglycemia. During adrenaline-induced acute arterial hypertension the mean arterial blood pressure increased in both non-diabetic and diabetic animals. Changes in BBB permeability were observed in 52% of the non-diabetic rats, and in 72% of the diabetic rats after adrenaline-induced acute arterial hypertension. Mean levels of Evans blue in the whole brain were found to be 0.63 +/- 0.1 mg% in non-diabetic and 0.90 +/- 0.2 mg% in diabetic rats. The difference between the non-diabetic and the diabetic rats was found to be statistically significant (P < 0.01). From these results it was suggested that the extravasation of Evans blue albumin is more pronounced in the brains of diabetic rats in comparison with non-diabetic rats after adrenaline-induced acute hypertension, which is indicative of changes in BBB permeability due to diabetes mellitus.

The effect of profound hypothermia on blood-brain barrier permeability during pentylenetetrazol-induced seizures.

The changes in the permeability of the blood-brain barrier during pentylenetetrazol (PTZ)-induced seizures were investigated in normothermic and hypothermic rats. Six groups of rats were studied: (I) normothermic control; (II) hypothermic control; (III) normothermia plus PTZ (80 mg/kg); (IV) normothermia plus PTZ (160 mg/kg); (V) hypothermia plus PTZ (80 mg/kg); (VI) hypothermia plus PTZ (160 mg/kg). The rats were anesthetized with diethyl ether. In the hypothermic animals, colonic temperature was reduced to 20 +/- 1 degree C by submerging the animals in ice water. In normothermic animals, distinct Evans-blue leakage was observed in the occipital cortex, thalamus, hypothalamus, substantia nigra, corpus striatum, and medulla oblongata in both PTZ groups. However, hypothermic animals which received a high dose of PTZ showed the most severe blood-brain barrier breakdown. Mean levels of Evans blue in the brains of low-dose (80 mg/kg) PTZ-treated animals were 8.7 +/- 2.2 micrograms/g and 5.7 +/- 1.4 micrograms/g in the normothermic and hypothermic groups, respectively. This difference was significant (P < 0.01). The levels in the high dose (160 mg/kg) PTZ-treated animals were 10.2 +/- 3.5 micrograms/g and 15.9 +/- 3.6 micrograms/g in the normothermic and hypothermic groups, respectively (P < 0.02). In conclusion, deep hypothermia prevents the blood-brain barrier disruption induced by 80 mg/kg pentylenetetrazol and aggravates the increase in permeability after 160 mg/kg pentylenetetrazol.

Asymmetrical changes in blood-brain barrier permeability during pentylenetetrazol-induced seizures and in acute hypertension.

The asymmetrical breakdown of the blood-brain barrier to Evans-blue was studied in male and female rats during epileptiform seizures and in acute hypertension. The animals were divided into six groups. Group I: control female; Group II: control male; Group III: female + acute hypertension; Group IV: male + acute hypertension; Group V: female + seizure; Group VI: male + seizure. Asymmetric breakdown of the blood-brain barrier had been seen in female rats treated with pentylenetetrazol. Pentylenetetrazol-induced seizure produces less disruption of the blood-brain barrier in right cerebral hemisphere than in left cerebral hemisphere in female rats. There were no asymmetrical changes of blood-brain barrier permeability between the left and right hemispheres in acute hypertension in both sexes, and male rats treated with pentylenetetrazol.

Blood-brain barrier permeability after electrically induced seizure in normoglycemic, hypoglycemic, and hyperglycemic rats.

The influence of hyperglycemia and moderate hypoglycemia plus electroconvulsive seizure on the permeability of the blood-brain barrier to protein was studied in rats. Evans blue was used as a blood-brain barrier tracer. Following a single electroconvulsive seizure, slight staining of brain tissue was seen. After 10 electroconvulsive stimuli followed by sustained seizure activity, this phenomenon was more pronounced in moderate hypoglycemic animals. In this group, Evans blue albumin extravasation occurred in all regions of the hemispheres, but the most severe protein leakage was seen in the thalamus, hypothalamus, amygdala nuclei, and frontal, parietal, and occipital cortex. Ten repeated electroconvulsive stimuli applied in case of hyperglycemia made no important difference in blood-brain barrier dysfunction according to normoglycemic group. Our results suggest that moderate hypoglycemia provokes the effect of electroconvulsive seizure on the permeability of the blood-brain barrier.

The influence of nifedipine on blood-brain barrier permeability during bicuculline-induced seizures.

The influence of the calcium channel blocker nifedipine plus bicuculline-induced seizures on the permeability of the blood-brain barrier to protein was studied in rats. Evans-blue was used as a blood-brain barrier tracer. Four groups of rats were studied. Group I: control, Group II: Nifedipine, Group III: bicuculline-induced seizure, Group IV: Nifedipine + seizure. The mean value for Evans-blue dye in the brain was found to be 0.23+/-0.03 mg/g in control animals and 0.32+/-0.06 mg/g in the group of all rats during nifedipine-induced hypotension. This difference between control and hypotensive animals was not statistically significant (p < 0.5). Mean value for Evans-blue dye in the brain was found to be 1.4+/-0.3 mg/g in bicuculline-induced seizure, and 0.73+/-40.2 mg/g in the group of nifedipine plus bicuculline-induced seizures. This difference between Group III and Group IV was found statistically significant (p < .01). The calcium channel blocker nifedipine significantly prevents the blood brain barrier disruption during bicuculline-induced seizure.

The effect of acute hypertension on blood-brain barrier permeability to albumin during experimentally induced epileptic seizures.

The present study was to examine the effect on the blood-brain barrier function of a rapid blood pressure elevation and the duration of this pressure during bicuculline and pentylenetetrazol-induced seizures. The experiments were carried out on Wistar rats. Evans blue was used as a blood-brain barrier tracer. Our results showed that the presence of blood pressure increase does not always result in blood-brain barrier leakage during convulsions. Besides the rate of increase in the pressure, the duration of this increased pressure was the important factor in the disruption of blood-brain barrier during bicuculline or pentylenetetrazol-induced seizures.

Hypertension-induced protein leakage in the brain in chronic ethanol administered rats.

The effect of adrenalin on permeability of blood brain barrier in chronic alcohol administered rats was examined by using Evans-blue as a barrier tracer. Chronic alcohol per se did not have remarkable effect on blood-brain barrier permeability. Adrenalin administration to the chronic alcohol group caused minimal disruption in blood brain barrier. The results shown that chronic alcohol protects the blood brain barrier permeability against hypertension due to adrenalin.

Influence of an abrupt increase in blood pressure on the blood-brain barrier permeability during acute hypertension and epileptic seizures.

The interrelationship between the breakdown of the blood-brain barrier according to the Evans-blue passage and an abrupt increase in blood pressure (DeltaP) was studied in rats subjected to adrenaline-induced acute hypertension and also pentylenetetrazol-induced seizures. Arterial blood pressure was increased by adrenaline, then immediately i.v. nifedipine was injected and subsequently decreased to the control value in the acute hypertensive group. Arterial blood pressure was increased by pentylenetetrazol, then immediately GABA (gamma-aminobutiric acid) was injected and the blood pressure was decreased to the control value in the seizure group. The animals were divided into five groups. Group I: control; Group II: acute hypertension; Group III: acute hypertension + nifedipine; Group IV: seizure; Group V: seizure + GABA. The Evans-blue dye content was found to be 0.25 +/- 0.01 mg% in the whole brain in the control animals, and 0.803 +/- 0.1 mg% in the acute hypertensive group. This difference between these groups was found to be significant: P< 0.01. In the nifedipine group (Group III) the Evans-blue content was 0.30 +/- 0.1 mg% in the whole brain; and there was no significant difference between control values and nifedipine-treated animals (P> 0.5). The Evans-blue content was 1.6 +/- 0.2 mg% in the whole brain during seizure, and decreased to 0.36 +/- 0.1 mg% after GABA injection was administered. There was also no significant difference between the control value and the GABA-treated animals (P> 0.5). These results have shown that an abrupt increase in blood pressure (DeltaP) did not change the blood-brain barrier permeability in both acute hypertension and seizures.

Blood-brain barrier permeability during acute and chronic electroconvulsive seizures.

The effect of chronic electroconvulsive seizure on the blood brain barrier permeability to albumin was investigated in the male rats. Evans blue was used as a blood brain barrier tracer. The following situations were studied: Acute electroshock: a. one electroshock stimulus, b. ten electroshock stimuli. Chronic electroshock: a) group of animals were pretreated with electroshock given as one electroshock (ES) every other day (ES x 7); b) chronic electroshock + one electroshock, c) chronic electroshock + ten repeated electroshocks. As a result, chronic electroshock per se does not effect the blood-brain barrier permeability.

Reversible blood-brain barrier dysfunction after intracarotid hyperthermic saline infusion.

An animal model for reversible blood-brain barrier disruption has been developed. Retrograde infusion of hyperthermic saline solution 43 degrees C into the left external carotid artery of normothermic, Wistar rats, reversibly increases cerebrovascular permeability to Evans-blue albumin in the left cerebral hemisphere. Isotonic saline solutions at 37 degrees C for group I and 43 degrees C for group II were infused for 30-s at a constant rate of 0.12 ml/s into the left external carotid artery. Evans-blue, the barrier tracer was administered intravenously either prior to or at intervals of 5, 30, 180, 360 min after the hyperthermic saline infusion under pentobarbital anesthesia. All animals receiving hyperthermic saline perfusion had disturbed blood-brain barrier permeability. Based on visual inspection, disruption grade in the left hemispheres of six of 11 animals was grade 3+. Mean values for Evans-blue dye were found to be 0.28 +/- 0.06 mg/g of tissue in left hemisphere after normothermic saline infusion (group I), and 2.41 +/- 0.5 mg/g of tissue in the same hemisphere after hyperthermic saline infusion (group II). The difference was found to be significant between group I and group II (p < 0.01). The increase in cerebrovascular permeability was temporary, even though Evans-blue albumin extravasation remained slightly elevated 3 h after infusion and was normal 6 h after infusion.

Reversibility of blood-brain barrier dysfunction in acute hypertension induced by angiotensin.

The reversibility of blood-brain barrier (BBB) dysfunction was examined in rats after acute experimental hypertension. A short-lasting (less than or equal to 4 min) acute hypertension was produced by intravenous injection of 20 micrograms/kg angiotensin. Evans blue, the barrier tracer, was administered intravenously either prior to or at intervals of 3, 10, 20, 30, and 60 min after the angiotensin injection. It was observed that the BBB dysfunction showed a peak 30 min after the angiotensin injection. Three of six animals that received Evans blue 60 min after angiotensin administration showed extravasation of the tracer on gross inspection. We concluded that BBB dysfunction may remain even 60 min after an acute hypertensive episode of short duration.

Influence of orchidectomy and ovariectomy on the blood-brain barrier permeability during bicuculline-induced seizures.

The changes in the permeability of the blood-brain barrier (BBB) during bicuculline-induced seizures were investigated in ovariectomized female and orchidectomized male rats. The rats were anesthetized with diethyl ether. Evans blue, which was used as a BBB tracer, was injected into femoral vein 5 min before administering bicuculline to induce grandmal seizures. Ten groups of rats were studied: Group I: control female; Group II: control male; Group IIl: intact female + bicuculline; Group IV: intact male + bicuculline; Group V: ovariectomized female; Group VI: orchidectomized male; Group VII: ovariectomized female + bicuculline; Group VIII: orchidectomized male + bicuculline (1.2 mg/kg, i.v.); Group IX: ovariectomized female + estrogen + bicuculline; Group X: orchidectomized male + estrogen + bicuculline. Adult male and female rats were orchidectomized and ovariectomized 3 weeks before the experiments, or sham operated under general anesthesia. During bicucculline-induced seizures, the mean arterial blood pressure increased significantly in both intact and ovariectomized and orchidectomized rats. BBB lesions were present in 80 percent of intact female rats and 50 percent of ovariectomized rats after bicuculline-induced seizures. This difference between intact and ovariectomized rats was found to be significant (p < 0.01). There was no statistically significant change in the BBB permeability between intact and orchidectomized rats after convulsion. Generating seizures in both ovariectomized and orchidectomised rats, after administrating of estrogen, did not lead to any significant alteration in BBB permeability. Our results suggest that the extravasation of Evans blue albumin was most pronounced in the brain of intact female rats when compared to ovariectomized rats after bicuculline-induced seizures. After administrating estrogen, the decreased BBB permeability values of ovariectomised rats could not reach the values in intact rats.

Influence of pregnancy on blood-brain barrier integrity during seizures in rats.

The effect of pregnancy on blood-brain barrier permeability was investigated during bicuculline-induced seizure in Wistar rats, using Evans-blue as a tracer. The experiments were carried out with two methods to investigate the integrity of the blood-brain barrier, i.e. Evans-blue albumin extravasation was determined as a macroscopical finding. A quantitative estimation with a spectrophotometer using homogenized brain to release the dye was performed to evaluate the macroscopical findings in a separate group of animals. During convulsions the mean arterial blood pressure increased in both pregnant and nonpregnant rats. The extravasation of Evans-blue was more pronounced in the nonpregnant rats. Mean values for Evans-blue dye were found to be 0.29 +/- 0.07 mg% whole brain in nonpregnant control female rats and 0.30 +/- 0.09 mg% whole brain in pregnant rats. This difference was not significant (P > 0.05). Mean values for Evans-blue dye were 1.02 +/- 0.30 mg% whole brain in nonpregnant female rats, and 0.60 +/- 0.12 mg% in the pregnant rats during bicuculline-induced seizures. This difference was significant (P < 0.01). The severe protein leakage was seen in the thalamus, midcaudate, hypothalamus and mesencephalon bilaterally in the nonpregnant rats. However, in pregnant rats, Evans-blue leakage was similar to that of female rats except that the intensity of blood-brain barrier breakdown was less after convulsion.

Influence of profound hypothermia on the blood-brain barrier permeability during acute arterial hypertension.

In hypothermic rats with acute hypertension induced by intravenous injection of adrenalin, regional changes in blood-brain barrier permeability to macromolecules were investigated using Evans blue as indication. Evans blue albumin extravasation was determined as a macroscopic finding and a quantitative estimation with a spectrophotometer using homogenized brain to release the dye was also performed to evaluate the macroscopic findings. Five groups of rats were studied: Group I: normothermia + acute hypertension; Group II: hypothermia + acute hypertension; Group III: control hypothermia; Group IV: normothermia + hypotension; Group V: control normothermia. The rats were anaesthetized with diethyl-ether. Body temperature was lowered by submerging anaesthetized animals in an ice water bath. The colonic temperature was reduced to 20 +/- 1 degrees C. During adrenaline-induced acute hypertension the mean arterial blood pressure increased in both normothermic and hypothermic animals. Blood-brain barrier lesions were present in 40% of normothermic rats, and 60% of hypothermic rats after adrenaline-induced hypertension. Mean value for Evans blue dye in the whole brain was found to be 0.530 +/- 0.202 mg% in the normothermic rats and 0.752 +/- 0.256 mg% in the hypothermic rats during adrenaline-induced hypertension. This difference between normothermic and hypothermic rats was found to be statistically significant (P less than 0.01). Our results showed that the extravasation of Evans blue albumin was most pronounced in the brains of hypothermic rats compared to normothermic rats after adrenaline-induced acute hypertension.