An Experimental Biomimetic Platform for Artificial Olfaction

Artificial olfactory systems have been studied for the last two decades mainly from the point of view of the features of olfactory neuron receptor fields. Other fundamental olfaction properties have only been episodically considered in artificial systems. As a result, current artificial olfactory systems are mostly intended as instruments and are of poor benefit for biologists who may need tools to model and test olfactory models. Herewith, we show how a simple experimental approach can be used to account for several phenomena observed in olfaction.     

The use of physical restraints in an acute care hospital

To fill the knownledge gap on the extension and quality of physical restraints in acute care hospitals a survey aiming at evaluating knowledge, opinions and behaviours of nurses in this area of care was performed. A questionnaire administered to the nurses of a large Italian hospital obtained a response rate of 66.2% (227 nurses) and the situation of 77 patients (15.8% of admitted patients) hospitalised and constrained in the target wards was reported. The physical restraints were widely used in intensive care and medical specialty wards (bed rails and limbs constraints). The main reasons for restraining the patients were: disorientation, agitation, aggressiveness, and balance disturbances. The application of constraints is an autonomous of the nurses decision in 60.8% of cases and the information is seldom reported in clinical or nursing records. Fifty-two per cent of nurses feel uneasy in constraining patients because of the relational implications with relatives. Lack of knowledge on ethical and legal implications and on the possible negative effects of constraining patients, on the different forms of constriction and on alternative strategies warrant an educational intervention to control and improve the implementation of physical measures of containment.     

Rapid determination of brain natriuretic peptide in patients with acute myocardial infarction.

We evaluated a rapid brain natriuretic peptide (BNP) assay (Triage BNP, Biosite Diagnostics) as indicator of infarct size, left ventricular (LV) dysfunction, and longterm survival in patients with acute myocardial infarction (AMI) during the coronary care unit stay. We studied 64 AMI patients in whom infarct size was estimated by creatine kinase isoenzyme MB (CK-MB) peak concentrations and single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi, and LV function by gated SPECT imaging. Measurements of BNP and SPECT were performed approximately 3 days after admission. SPECT was also repeated 3 months later. We found a significant correlation between BNP and both the peak CK-MB concentrations (r = 0.40, p = 0.001) and the perfusion defect size at SPECT (r = 0.38, p = 0.002). BNP was weakly related to LV ejection fraction (LVEF) assessed both early and 3 months after AMI (r = -0.29, p = 0.02; and r = -0.27, p = 0.04, respectively). The sensitivity and specificity of BNP for predicting survival of patients over 1 year of follow-up was 100% and 43%, respectively, with a negative predictive value of 100%. The positive predictive power of BNP was very modest (12%). Considering our results, the measurement of BNP did not look nearly as promising when tested in the setting of our cardiological intensive care.     

Risk factors in multiple sclerosis: a population-based case–control study in Sicily. Background and methods

Incidence of multiple sclerosis (MS) has steeply increased over time during the last 30 years in the city of Catania. We carried out a population-based case–control study to evaluate the possible role of both environmental and genetic factors. From 1975 to 2004 in Catania, 367 MS patients diagnosed according to the Poser’s criteria had the onset of disease. A sample of MS patients was randomly selected from this incident cohort. Three controls matched by age and sex were randomly selected from the rosters of 14 GPs. Controls were proportionally selected according to the distribution by municipality of the target population using a multistage sampling methods. All cases and controls underwent a face-to-face interview to record information concerning environmental factors and a blood sample was taken for serological and genetic analysis. 164 MS patients (64 % women; mean age of 46.4 ± 10.7) and 481 controls (69 % women; mean age of 47.7 ± 14.8) were enrolled in the study. The distribution of the whole population and the selected controls by municipalities was similar. A blood sample was taken from 150 MS cases and from 337 controls. At the end of the enrolment, we obtained a representative sample of the MS cases and population controls avoiding possible selection bias. Participation rate was very high also concerning the collection of biological specimens.     

Cholesterol hydroperoxides generate singlet molecular oxygen [O(2) ((1)Δ(g))]: near-IR emission, (18)O-labeled hydroperoxides, and mass spectrometry

In mammalian membranes, cholesterol is concentrated in lipid rafts. The generation of cholesterol hydroperoxides (ChOOHs) and their decomposition products induces various types of cell damage. The decomposition of some organic hydroperoxides into peroxyl radicals is known to be a potential source of singlet molecular oxygen [O(2) ((1)Δ(g))] in biological systems. We report herein on evidence of the generation of O(2) ((1)Δ(g)) from ChOOH isomers in solution or in liposomes containing ChOOHs, which involves a cyclic mechanism from a linear tetraoxide intermediate originally proposed by Russell. Characteristic light emission at 1270 nm, corresponding to O(2) ((1)Δ(g)) monomolecular decay, was observed for each ChOOH isomer or in liposomes containing ChOOHs. Moreover, the presence of O(2) ((1)Δ(g)) was unequivocally demonstrated using the direct spectral characterization of near-infrared light emission. Using (18)O-labeled cholesterol hydroperoxide (Ch(18)O(18)OH), we observed the formation of (18)O-labeled O(2) ((1)Δ(g)) [(18)O(2) ((1)Δ(g))] by the chemical trapping of (18)O(2) ((1)Δ(g)) with 9,10-diphenylanthracene (DPA) and detected the corresponding (18)O-labeled DPA endoperoxide (DPA(18)O(18)O) and the (18)O-labeled products of the Russell mechanism using high-performance liquid chromatography coupled to tandem mass spectrometry. Photoemission properties and chemical trapping clearly demonstrate that the decomposition of Ch(18)O(18)OH generates (18)O(2) ((1)Δ(g)), which is consistent with the Russell mechanism and points to the involvement of O(2) ((1)Δ(g)) in cholesterol hydroperoxide-mediated cytotoxicity.     

Role of quercetin in preventing thioacetamide-induced liver injury in rats

In hepatic toxicity induced in rats by two injections of thioacetamide (TAA, 350 mg/kg with an interval of 8 hr), the action of quercetin was investigated. After 96 hr, TAA administration resulted in hepatic necrosis, significant increases in serum transaminase activity, and increases in hepatic lipoperoxidation. Thioacetamide-induced hepatotoxicity also showed changes in antioxidant enzymes in the liver of rats, with alterations in p-ERK 1/2 (phosphorylated extracellular-signal related kinase 1/2) as well as an imbalance between proapototic protein Bax and anti-apoptotic protein Bcl-2 expression. With administration of the flavonoid quercetin (50 mg/Kg i.p.) for four consecutive days following TAA, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity were close to normal values in rats. Histological findings suggested that quercetin had a preventive effect on TAA-induced hepatic necrosis. Quercetin treatment caused significant decreases in lipid peroxide levels in the TAA-treated rats, with some changes in antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Quercetin also inhibited the change of the p-ERK1/2 by TAA and significantly prevented the increase in Bax/Bcl-2 ratio, thus preventing apoptosis. Findings indicate that quercetin may have a preventive effect on TAA-induced hepatotoxicity by modulating the oxidative stress parameters and apoptosis pathway.     

Rosmarinic acid as a protective agent against genotoxicity of ethanol in mice

The aim of the present work was to study the protective effects of rosmarinic acid against ethanol-induced DNA damage in mice. The antigenotoxic capacity of rosmarinic acid (100 mg/kg) was tested using pre-, co- and post-treatment with ethanol (5 g/kg). Peripheral blood (1 and 24 h) and brain cells (24 h) were evaluated using the comet assay and bone marrow was analyzed using the micronucleus assay (24 h). The results were compared to data of TBARS, enzymes with antioxidant activity, and DCFH-DA test. Peripheral blood and brain cells show that mean damage index (DI) and damage frequency (DF) values of ethanol with pre-treatment with rosmarinic acid group were significantly lower than in the ethanol group. In brain cells all different treatments with ethanol and rosmarinic acid showed significant decrease in DI and DF mean values when compared to ethanol group and negative control. No significant differences were observed in micronucleus frequency, activity of antioxidant enzymes and TBARS between groups. The DCFH-DA test show a reduction of 18% of fluorescence intensity when compare with ethanol group. The results show that rosmarinic acid could decrease the levels of DNA damage induced by ethanol, for both tissues and treatment periods.     

Longitudinal evaluation of mycophenolic acid pharmacokinetics in pediatric kidney transplant recipients. The role of post-transplant clinical and therapeutic variables

Abstract:  This longitudinal study assessed the influence of post-transplant clinical and therapeutic variables in 50 kidney transplant recipients aged 2–19 yr receiving a triple immunosuppressive regimen consisting of cyclosporine microemulsion (CsA), steroids and MMF (300–400 mg/m² body surface area twice daily), the full pharmacokinetic profile (10 points) of which was investigated on post-transplant days 6, 30, 180 and 360. Total plasma MPA was measured by Enzyme Multiplied Immunoassay Technique. CsA therapeutic drug monitoring (TDM) was performed via C2 blood monitoring, while MPA TDM via C0. MPA Cmax, tmax, AUC0-12 and AUC0-4 pharmacokinetic profile changed significantly during the first post-transplant year. C0 was a poor predictor of the total MPA exposure [as measured by the area under the concentration-time curve AUC)], while a truncated AUC was a good surrogate of the 12-h profile (r = 0.91; p < 0.001) Graft function and cyclosporine therapy influenced MPA pharmacokinetics, as shown by the univariate and multivariate analyses. We conclude that because after transplantation MPA exposure varied over time, a strict TDM is advisable in the pediatric population.     

Optical coherence tomography accurately identifies intermediate atherosclerotic lesions--an in vivo evaluation in the rabbit carotid artery

OBJECTIVE: We tested the ability of optical coherence tomography (OCT) to identify very early stages of atherosclerosis in vivo. METHODS: Twelve New Zealand white male rabbits (weight 3.5-4.0 kg) underwent perivascular electrical injury of the common carotid arteries, and were then fed a cholesterol-rich diet. At 43+/-16 (range 27-63) days after injury, arteries were imaged by OCT, then rabbits were euthanized and vessels processed for histology. RESULTS: A total of 14 carotid arteries were imaged by OCT and histology; 22 atherosclerotic lesions were identified, 16 (73%) occurring at the site of the electrical injury. At histology, 4 lesions were defined as Stary type I (isolated macrophages), 8 as type II (intracellular lipid accumulations), and 10 as type III (small extracellular lipid pools). No advanced (> or =type IV) lesions were documented. OCT failed to detect any type I lesions, but correctly defined a minority (2/8, 25%) of type II lesions and the majority (8/10, 80%) of type III lesions. For type III lesions, sensitivity, specificity and diagnostic accuracy of OCT were 80%, 95%, and 95%, respectively. CONCLUSIONS: OCT can accurately detect intermediate (type-III) atherosclerotic lesions in vivo, but still fails to identify earlier stages of atherosclerosis.