Investigating the activation of passive metals by a combined in-situ AFM and Raman spectroscopy system: a focus on titanium.

Understanding the main steps involved in the activation of passive metals is an extremely important subject in the mechanical and energy industry and generally in surface science. The titanium-H2SO4 system is particularly useful for this purpose, as the metal can either passivate or corrode depending on potential. Although several studies tried to hypothesise the surface state of the electrode, there is no general consensus about the surface state of Ti in the active-passive transition region. Here by combining in-situ atomic force microscopy (AFM) and Raman spectroscopy, operating in an electrochemical cell, we show that the cathodic electrification of Ti electrodes causes the dissolution of the upper TiO2 portion of the passive film leaving the electrode covered by only a thin layer of titanium monoxide. Fast anodic reactions involved the acidification of the solution and accumulation of sulphur containing anions. This produces a local increase of the solution turbidity, allowing to distinguish favourable regions for the precipitation of TiOSO4·2H2O. These results give a clear answer to the long-stated question of the physical origin behind the formation of negative polarization resistances, sometimes occurring in corroding systems, and a rationale about the proton-induced degradation of passive surfaces in presence of sulphur containing species.

Effect of acid suppressant medications on the laxative action of magnesium preparations in patients with opioid-induced constipation: A pharmacovigilance analysis of the FDA Adverse Event Reporting System.

Objective: Magnesium oxide is widely used for treating opioid-induced constipation, a serious analgesic-associated problem. Opioid analgesic users are often prescribed non-steroidal anti-inflammatory drugs, which are sometimes combined with acid suppressants to prevent gastrointestinal adverse events. Magnesium preparations combined with acid suppressants may diminish magnesium preparations' laxative effect. This study was aimed at evaluating the effect of magnesium preparations combined with acid suppressants on the incidence of opioid-induced constipation by using the Food and Drug Administration Adverse Event Reporting System. Methods: Adverse events were defined per the Medical Dictionary for Regulatory Activities; the term 'constipation (preferred term code: 10010774)' was used for analysis. After adjusting for patient background factors using propensity score matching, acid suppressants' effect on constipation incidence was evaluated in opioid users prescribed magnesium preparations alone as laxatives by using a test for independence. Key Findings: The Food and Drug Administration Adverse Event Reporting System contains 14,475,614 reports for January 2004 to December 2021. Significantly increased constipation incidence was related to magnesium preparations combined with acid suppressants, especially proton pump inhibitors (P < 0.0001, McNemar's test). Conclusion: Magnesium preparations combined with acid suppressants may diminish magnesium preparations' laxative effect; healthcare professionals should pay attention to this issue.

Red ear syndrome presenting with vestibular migraine: case study and review of the literature.

BACKGROUND: Red ear syndrome is a rare disorder in which the colour of the ear suddenly becomes red, with discomfort, pain and a burning sensation. This paper reports a case of primary red ear syndrome presenting with vestibular migraine. CASE REPORT: A 39-year-old woman from Bangladesh reported dizziness and repeated headaches experienced since 18 years of age. She initially attended our hospital with dizziness aged 34 years. When dizzy, the colour of her right ear sometimes became red. Therefore, she was diagnosed with red ear syndrome with vestibular migraine. CONCLUSION: This patient experienced repeated episodes of a red ear with discomfort, leading to the diagnosis of red ear syndrome. In addition, she had repeated dizziness and headaches, and was also diagnosed with vestibular migraine. The diagnosis of red ear syndrome with vestibular migraine should be considered in cases of dizziness and headache with recurrent redness of the ear.

The effect of laryngeal elevation training on swallowing function in patients with dysphagia.

OBJECTIVE: To investigate the effect of laryngeal elevation training without highly loaded head lifting on swallowing function in patients with dysphagia. METHODS: Fifty-seven patients with dysphagia (36 men; mean age, 78.5 ± 11.4 years) were included. All participants performed the swallowing forehead exercise and the chin push-pull manoeuvre for two months. Videoendoscopy to assess swallowing function, the peak expiratory flow test and the hand grip strength test were performed at the initial visit (time 1) and two months after the start of the intervention (time 2). We used the Hyodo score, a scoring method for videoendoscopic assessment, for evaluation of swallowing function. RESULTS: The linear mixed model showed a significant main effect of time (the Hyodo score at time 1 was greater than the score at time 2). The effects of the co-variates were not significant. CONCLUSION: The present study demonstrated the significant effect of laryngeal elevation training without head lifting on the Hyodo score.

The effects of isoflurane on adrenomedullin-induced haemodynamic responses in pithed rats.

BACKGROUND AND OBJECTIVES: Adrenomedullin is a potent vasodilatory peptide. The mechanisms of adrenomedullin-induced responses are via guanine nucleotide guanosine 5'-triphosphate-binding protein (G-protein)-coupled receptor activation and are similar to those of calcitonin gene-related peptide (CGRP). Previously, we reported that sevoflurane and isoflurane inhibit CGRP-induced haemodynamic responses. The effects of volatile anaesthetics on adrenomedullin-induced haemodynamic responses, however, are unclear. We hypothesized that the volatile anaesthetic isoflurane inhibits adrenomedullin-induced haemodynamic responses. We studied the effects of isoflurane on adrenomedullin-induced haemodynamic responses in pithed rats, which enables us to evaluate the direct cardiovascular effects of drugs without interference from centrally mediated circulatory reflexes. METHODS: Male Wistar rats were pithed by inserting a stainless-steel rod into the spinal cord. Following median sternotomy, a flow probe was placed around the ascending aorta to measure aortic blood flow. Mean arterial pressure and cardiac output were maintained at approximately 100 mmHg and 50 mL min-1, respectively, with continuous infusion of norepinephrine. After 30 min inhalation of isoflurane (1%, or 2%) in oxygen, or only oxygen, adrenomedullin (1, 3, 10 or 30 microg kg-1) was administered intravenously. RESULTS: Adrenomedullin administration induced a transient increase followed by a persistent decrease in mean arterial pressure and cardiac output. Isoflurane (2%) significantly inhibited the initial increase in mean arterial pressure and the later decrease in mean arterial pressure and systemic vascular resistance. CONCLUSION: Isoflurane inhibits adrenomedullin-induced vasodilation and positive inotropic effect in pithed rats. Isoflurane might inhibit the adrenomedullin receptor-mediated response, which is a common pathway for both actions.

Percutaneous radio-frequency mandibular nerve rhizotomy guided by CT fluoroscopy.

We describe a new method for radio-frequency mandibular nerve rhizotomy under CT fluoroscopy. A patient with cancer had severe intractable and drug-resistant pain in his left mandibular region. Because he had an anatomic deformity due to cancer invasion and radiation therapy, we planned a mandibular nerve rhizotomy under CT fluoroscopic imaging. The needle was advanced to the mandibular nerve just caudal to the foramen ovale under real-time CT fluoroscopy, avoiding the cancer region. Pain scores of the patient were reduced after the nerve rhizotomy, without any complications.

Changes in the effect of propofol in response to altered plasma protein binding during normothermic cardiopulmonary bypass.

BACKGROUND: During normothermic cardiopulmonary bypass (CPB), the effect on propofol pharmacokinetics of changes in its binding to plasma proteins is consistent with the predictions of the well-stirred model of hepatic elimination for nonrestrictively cleared drug. However, whether changes in binding lead to clinically significant changes in the drug effect remains unclear. The purpose of this study was to assess changes in the drug effect of propofol in response to altered plasma binding using quantitative EEG measurements. METHODS: Thirty patients undergoing cardiac surgery were assigned randomly to receive propofol infusions at 4 (Group P-4) or 6 (Group P-6) mg kg(-1) h(-1) during surgery. The concentration of propofol in blood samples, collected from the radial artery at predetermined intervals, was determined by HPLC. The unbound fraction of drug in plasma was estimated using equilibrium dialysis. Bispectral index (BIS) and burst suppression ratio (BSR) were measured at the time blood samples were collected. RESULTS: The total concentration of propofol in blood was unchanged during CPB relative to the pre-CPB value in both groups. However, the fraction of unbound propofol in blood increased by 2-fold during CPB. While BIS values were unchanged during CPB in Group P-4, there was a slight, but significant, decrease in Group P-6. In both groups, BSR significantly increased during CPB. BIS values showed a weak correlation with the concentration of unbound propofol (r(2)=0.19, P<0.001). BSR showed a moderate correlation with the concentration of unbound propofol (r(2)=0.56, P<0.001). CONCLUSIONS: The anaesthetic effect of propofol significantly increased during CPB without any alteration in the total drug concentration. The enhanced efficacy may be caused by a reduction in plasma binding of the drug.

Changes in apparent systemic clearance of propofol during transplantation of living related donor liver.

BACKGROUND: Propofol is used during living-related donor liver transplantation because its metabolism is not greatly affected by liver failure. However, the pharmacokinetics of propofol during liver transplantation have not been fully defined. The purpose of this study was to evaluate the apparent systemic clearance of propofol during the dissection, anhepatic and reperfusion phases of living-related donor liver transplantation, and to estimate the role of the small intestine and lung as extrahepatic sites for propofol disposition. METHODS: Ten patients scheduled for living-related donor liver transplantation were enrolled in the study. Anaesthesia was induced with vecuronium 0.1 mg kg(-1) and propofol 2 mg kg(-1), and then maintained by 60% air, 0.5-1.5% isoflurane in oxygen and a constant infusion of propofol at 2 mg kg(-1) h(-1). Apparent systemic clearance during the dissection, anhepatic and reperfusion phases was calculated from the pseudo-steady-state concentration for each phase. Disposition in the small intestine was determined by measuring arteriovenous blood concentration in 10 liver transplantation donors. Pulmonary disposition was determined by measuring the arteriovenous blood concentration in 10 recipients during the anhepatic phase. The data are expressed as mean (sd). RESULTS: Apparent systemic clearances in the dissection, anhepatic and reperfusion phases were 1.89 (sd 0.48) litre min(-1), 1.08 (0.25) litre min(-1) and 1.53 (0.51) litre min(-1), respectively. The concentration of propofol in the portal vein was lower than in the radial artery. The intestinal extraction ratio calculated from the concentration in the radial artery and portal vein was 0.24 (0.12). There were no significant differences in propofol concentrations between the radial and pulmonary arteries. CONCLUSION: Apparent systemic clearance was decreased by approximately 42 (10)% during the anhepatic phase compared with the dissection phase. After reperfusion, liver allografts rapidly began to metabolize propofol. The small intestine also participates in the metabolism of propofol.

Effects of AM281, a cannabinoid antagonist, on systemic haemodynamics, internal carotid artery blood flow and mortality in septic shock in rats.

INTRODUCTION: The purpose of this study was to examine the effects of AM281, a cannabinoid receptor antagonist, on systemic haemodynamics, internal carotid artery blood flow and mortality during septic shock in rats. METHODS: The study included three sets of experiments: measurements of changes in systemic haemodynamics and left internal carotid artery flow (30 animals divided into three groups of 10); measurements of biochemical variables (n=30); assessment of mortality (n=30). Male Wistar rats (7 weeks old) were randomly divided into three groups: group 1, control; group 2, lipopolysaccharide (LPS) i.v., Escherichia coli endotoxin 10.0 mg kg(-1) i.v., bolus; group 3, LPS 10.0 mg kg(-1) i.v.+AM281 1 mg kg(-1) i.v. Systemic haemodynamics, carotid artery flow changes and biochemical variables were assessed at pretreatment and 1, 2 and 3 h after the treatment was performed. RESULTS: Administration of AM281 could prevent the haemodynamic changes induced by sepsis. Tumour necrosis factor-alpha and interleukin 1-beta increased in the LPS i.v. and LPS i.v.+AM281 groups at 1, 2 and 3 h after treatment; significant differences were observed in these levels in the two groups at these times. Internal carotid artery blood flow remained fairly constant in the control and LPS i.v.+AM281 groups compared with baseline values. In the LPS i.v. group, it decreased at 2 and 3 h after the treatment compared with baseline values [at 2 h: control 12.7 (SD 0.9) ml min(-1), LPS i.v. 8.7 (1.4) ml min(-1) (P<0.05), LPS i.v.+AM281 11.5 (0.9) ml min(-1); at 3 h: control 12.7 (0.4) ml min(-1), LPS i.v. 7.7 (1.3) ml min(-1) (P<0.05), LPS i.v.+AM281 11.6 (1.0) ml min(-1)]. Significant differences in mortality within 6 and 12 h were found between the LPS i.v. and LPS i.v.+AM281 groups [6 h mortality: LPS i.v. 5/10 (50%), LPS i.v.+AM281 2/10 (20%), P<0.05; 12 h mortality: LPS i.v. group 10/10 (100%), LPS i.v.+AM281 5/10 (50%), P<0.05]. CONCLUSIONS: Administration of AM281 prevented changes in systemic haemodynamic and internal carotid artery blood flow and could improve mortality in experimentally induced septic shock in rats. These findings may have significant therapeutic implications in the treatment of septic shock.

Is the degree of sensitivity to nondepolarizing muscle relaxants related to requirements for postoperative ventilation in patients with myasthenia gravis?

The purpose of this study was to examine whether the degree of sensitivity to nondepolarizing muscle relaxants is related to the requirement for postoperative ventilatory support in patients with myasthenia gravis. Thirty-six patients with myasthenia gravis undergoing trans-sternal thymectomy were monitored by electromyography in order to assess the neuromuscular response to vecuronium. After calibration to 100% of baseline electromyographic response values using an EMG monitor, incremental doses of 5, 10 and 20 microg/kg of vecuronium were administrated to produce 95% neuromuscular blockade and to obtain a cumulative dose-response curve for each patient. A univariable logistic regression with odds ratio was used to examine the predictive variables of prolonged postoperative ventilation. Depending on their postoperative ventilatory needs, patients were divided into an early extubation group and a prolonged ventilatory group. There were no significant differences between the two groups in terms of vecuronium ED95 (prolonged ventilation group: 23.2 +/- 18 microg/kg; early extubation group: 23.2 +/- 18 microg/kg P=0.129) and vecuronium requirement to maintain less than 25% neuromuscular blockade (prolonged ventilation group: 24 +/- 1.7 mg/kg; early extubation group: 3.8 +/- 4.5 mg/kg P=0.249). There were, however, significant differences in the incidence of a history of previous respiratory crises and the presence of bulbar palsy between the early extubation and prolonged ventilation groups. History of previous respiratory crisis (odds ratio (OR), 3.5; 95% confidence interval (CI), 1.0-13; P=0.03) and presence of bulbar palsy (OR, 3.7; 95%CI, 0.9-15; P=0.049) were associated with the need for prolonged postoperative ventilation. However, we failed to demonstrate that the degree of sensitivity to nondepolarizing muscle relaxants was related to an increased requirement for postoperative ventilation in patients with myasthenia gravis.

Correlation and linear regression between blood pressure decreases after a test dose injection of propofol and that following anaesthesia induction.

Propofol reduces systemic vascular resistance and suppresses cardiac function when injected rapidly. In this study we investigated whether blood pressure decrease after a minimal dose (test-dose) injection of propofol correlates with that after an induction-dose injection. Patients were randomly divided into two groups; anaesthesia was induced in group A (n = 60) using 1.5 mg/kg propofol and in group B (n = 61) using 2.0 mg/kg. Blood pressure reduction after a minimal dose injection (0.4 mg/kg) was examined non-invasively prior to anaesthetic induction. Bispectral Index monitoring was measured and sedation level scored to evaluate anaesthetic depth. After the minimal dose injection, 18 of 121 patients showed behaviour suggesting minor disinhibition, five patients were sedated and seven were drowsy. Oxygen saturation was not significantly changed after test-dose injection. Reduction in systolic blood pressure (mean +/- SD) was 17 +/- 11 mmHg after the minimal dose injection, 42 +/- 20 mmHg after a 1.5 mg/kg induction dose injection, and 42 +/- 22 mmHg after a 2.0 mg/kg induction-dose injection. In both groups, blood pressure after induction was significantly lower than the control value (P < 0.05). In both groups, a positive correlation was observed between blood pressure reduction after the minimal dose injection and that after the induction-dose injection [P < 0.01, R value for systolic blood pressure correlation in group A 0.712 (P < 0.01) and in group B 0.758 (P < 0.01)]. We concluded there was a positive correlation between blood pressure reduction after a minimal (test-dose) injection and that after an induction-dose injection.

Slow rewarming improves jugular venous oxygen saturation during rewarming.

BACKGROUND: There have been many studies regarding the etiology of postoperative cognitive dysfunction after coronary artery bypass graft (CABG) surgery. Although its etiology remains unresolved, one possible factor related to postoperative cognitive dysfunction is a reduced internal jugular venous oxygen hemoglobin saturation (SjvO2) during the rewarming period. The purpose of this study was to examine the effect of rewarming rates on SjvO2 during rewarming. METHODS: One-hundred patients scheduled for elective CABG surgery were randomly divided into two groups; control group (0.48 +/- 0.09 degrees C, n = 50), slow rewarming group (0.24 +/- 0.09 degrees C, n = 50). After the induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor SjvO2 continuously. Hemodynamic parameters, arterial and jugular venous blood gases were measured at nine time-points. RESULTS: Cerebral desaturation (defined as a SjvO2 value below 50%) during rewarming was more frequent in the control group than in the slow group. Cerebral desaturation time (duration when SjvO2 was less than 50%) and the ratio of the cerebral desaturation time to the total CPB time in the control group differed significantly from those in the slow group (control group: 17 +/- 11 min, 12 +/- 4%, slow group: 10 +/- 8 min, 7 +/- 4%, respectively, P < 0.05). There was no significant difference in mini-mental state examination on the day before the operation nor at 1 month after the surgery among four values (the day before the operation: control group; 48 +/- 8, slow group; 48 +/- 7, at one month after the surgery: control group; 46 +/- 7, slow group; 45 +/- 9). CONCLUSIONS: A slow rewarming rate could reduce the chance of a decrease in SjvO2 during rewarming.

The comparative effects of propofol versus thiopentone on left ventricular function during electroconvulsive therapy.

The purpose of this study was to compare the effect of propofol versus thiopentone on haemodynamics during electroconvulsive therapy (ECT), as estimated by echocardiography. Twenty-eight ASA 1 or 2 patients scheduled for ECT were randomly divided into two groups, to receive propofol 1 mg/kg (propofol group, n = 14) or thiopentone 2 mg/kg (thiopentone group, n = 14). Bilateral ECT was performed after the administration of propofol or thiopentone, succinylcholine and following assisted mask ventilation with 100% oxygen. Cardiac function was examined by transthoracic echocardiography, prior to induction of anaesthesia and throughout ECT until ten minutes after the seizure. In the propofol group, increased end-systolic area (ESA) and decreased fractional area change (FAC) were observed at one minute after the electrical shock compared with the awake condition. In the thiopentone group, increased ESA and decreased FAC were observed from one to three minutes after the electrical shock compared with the awake condition. There was no statistically significant change in afterload in the propofol group during the study. In contrast, increased afterload was observed from one to three minutes after the electrical shock in the thiopentone group (awake condition, 26 +/- 7 mmHg/cm2 [mean +/- SD]; one minute after ECT, 42 +/- 7*; two minutes after ECT, 44 +/- 6*; three minutes after ECT; 40 +/- 5*, respectively) (*P < 0.05). We concluded that a lesser haemodynamic change occurs after propofol anaesthesia (1 mg/kg) compared with thiopentone anaesthesia (2 mg/kg) during ECT.

Chronic intraperitoneal endotoxin treatment in rats induces resistance to d-tubocurarine, but does not produce up-regulation of acetylcholine receptors.

BACKGROUND: Chronic systemic inflammation resulting from intraperitoneal Eschevichia coli endotoxin administration or Corynebacterium injections induces tolerance to non-depolarizing neuromuscular blockers in rodents. Although this has been explained as up-regulation of muscle acetylcholine receptors (AChR), the numbers of involved receptors have not been documented. The aim of this study was to determine the effects of chronic endotoxin administration on rat muscle AChR. METHODS: One day after one, seven, or 14 daily intraperitoneal doses of lipopolysaccharide endotoxin (0 or 0.5 mg kg(-1)), we studied in vivo dose-response relationships for d-tubocurarine (d-Tc) and AChR binding using [125I]alpha-bungarotoxin as a ligand. RESULTS: One day after seven and 14 daily intraperitoneal doses of endotoxin, the effective dose of d-Tc required to suppress the twitch response to 50% of the control (ED50) was significantly increased compared with that of time-matched control rats (146.5 +/- 38.2 vs. 76.1 +/- 9.0 microg kg(-1) for seven doses; 116.4 +/- 51.3 vs. 74.4 +/- 9.6 micro g kg-1 for 14 doses, P < 0.05). However, this was not associated with an increase in the number of AChR in the anterior tibial muscle or diaphragm. CONCLUSIONS: Mechanisms other than AChR up-regulation might be responsible for the increased d-Tc requirement during chronic intraperitoneal endotoxin administration.

Patterns of canal and otolith afferent input convergence in frog second-order vestibular neurons.

Second-order vestibular neurons (2 degrees VN) were identified in the isolated frog brain by the presence of monosynaptic excitatory postsynaptic potentials (EPSPs) after separate electrical stimulation of individual vestibular nerve branches. Combinations of one macular and the three semicircular canal nerve branches or combinations of two macular nerve branches were stimulated separately in different sets of experiments. Monosynaptic EPSPs evoked from the utricle or from the lagena converged with monosynaptic EPSPs from one of the three semicircular canal organs in ~30% of 2 degrees VN. Utricular afferent signals converged predominantly with horizontal canal afferent signals (74%), and lagenar afferent signals converged with anterior vertical (63%) or posterior vertical (37%) but not with horizontal canal afferent signals. This convergence pattern correlates with the coactivation of particular combinations of canal and otolith organs during natural head movements. A convergence of afferent saccular and canal signals was restricted to very few 2 degrees VN (3%). In contrast to the considerable number of 2 degrees VN that received an afferent input from the utricle or the lagena as well as from one of the three canal nerves (~30%), smaller numbers of 2 degrees VN (14% of each type of 2 degrees otolith or 2 degrees canal neuron) received an afferent input from only one particular otolith organ or from only one particular semicircular canal organ. Even fewer 2 degrees VN received an afferent input from more than one semicircular canal or from more than one otolith nerve (~7% each). Among 2 degrees VN with afferent inputs from more than one otolith nerve, an afferent saccular nerve input was particularly rare (4-5%). The restricted convergence of afferent saccular inputs with other afferent otolith or canal inputs as well as the termination pattern of saccular afferent fibers are compatible with a substrate vibration sensitivity of this otolith organ in frog. The ascending and/or descending projections of identified 2 degrees VN were determined by the presence of antidromic spikes. 2 degrees VN mediating afferent utricular and/or semicircular canal nerve signals had ascending and/or descending axons. 2 degrees VN mediating afferent lagenar or saccular nerve signals had descending but no ascending axons. The latter result is consistent with the absence of short-latency macular signals on extraocular motoneurons during vertical linear acceleration. Comparison of data from frog and cat demonstrated the presence of a similar organization pattern of maculo- and canal-ocular reflexes in both species.

N-methyl-D-aspartate receptor-dependent and -independent cytotoxic effects of Dictyostelium discoideum differentiation-inducing factor-1 on rat cortical neurons.

Differentiation-inducing factor-1 (DIF-1) is a chlorinated alkylphenone (small lipophilic hormone) that induces stalk cell formation in the cellular slime mold Dictyostelium discoideum. Recent studies have revealed that DIF-1 inhibits growth and induces the differentiation of mammalian tumor cells. The present study examines the effects of DIF-1 on rat cortical neurons in primary culture. We found that DIF-1 induced rapid neuronal cell death. The release of lactate dehydrogenase (LDH), as an indicator of cell death, increased dose-dependently with DIF-1. The release of LDH was inhibited by the N-methyl-D-aspartate (NMDA) receptor antagonists MK801 and AP5, suggesting that the NMDA receptor is involved in the induction of cell death by DIF-1. However, glutamate cytotoxicity could not explain the entire action of DIF-1 on neurons because the estimated concentration of glutamate around DIF-1-treated neurons was below 50 microM and DIF-1 caused more severe cell death than 500 microM glutamate. We discovered that another portion of DIF-1 cytotoxicity is independent of the NMDA receptor; that is, coaddition of DIF-1 and MK801 induced dendritic beading and increased expression of the immediate early genes c-fos and zif/268. These results indicate that DIF-1 induces rapid cell death via both NMDA receptor-dependent and -independent pathways in rat cortical neurons.