Alcohol-related behaviour in freshmen university students in Sardinia, Italy

This study aims to provide a picture of University of Cagliari students’ alcohol-related behaviour and to explore factors associated with it. Data were collected by administering a questionnaire to 992 freshmen university students from different programs consisting of twelve closed questions, including three questions from the Alcohol Use Disorders Identification Test for Consumption (AUDIT-C short form). Three subgroups of alcohol-related behaviour were distinguished (risky drinkers, social drinkers and abstainers). In order to explore factors associated with patterns of alcohol consumption, a multivariate logistic regression was performed. The prevalence of risky drinkers was 35%. A binge-drinking behaviour at least once in the last twelve months was declared by 65% (more widespread in men and in students living away from their parents). Risky consumption is significantly associated with age of onset of alcohol use, living away from parents’ home, drinking outside meals and attending health courses. Regarding the levels of daily alcohol consumption perceived as a health risk, 66% of men and 88% of women indicate values higher than those recommended. The results underline the need for tailored prevention measures. University could be a promising setting to implement actions according to a health promotion perspective, to empower students to control their alcohol consumption

Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons

The development of abnormal primary sensory neuron excitability and neuropathic pain symptoms after peripheral nerve injury is associated with altered expression of voltage-gated sodium channels (VGSCs) and a modification of sodium currents. To investigate whether the beta2 subunit of VGSCs participates in the generation of neuropathic pain, we used the spared nerve injury (SNI) model in rats to examine beta2 subunit expression in selectively injured (tibial and common peroneal nerves) and uninjured (sural nerve) afferents. Three days after SNI, immunohistochemistry and Western blot analysis reveal an increase in the beta2 subunit in both the cell body and peripheral axons of injured neurons. The increase persists for >4 weeks, although beta2 subunit mRNA measured by real-time reverse transcription-PCR and in situ hybridization remains unchanged. Although injured neurons show the most marked upregulation,beta2 subunit expression is also increased in neighboring non-injured neurons and a similar pattern of changes appears in the spinal nerve ligation model of neuropathic pain. That increased beta2 subunit expression in sensory neurons after nerve injury is functionally significant, as demonstrated by our finding that the development of mechanical allodynia-like behavior in the SNI model is attenuated in beta2 subunit null mutant mice. Through its role in regulating the density of mature VGSC complexes in the plasma membrane and modulating channel gating, the beta2 subunit may play a key role in the development of ectopic activity in injured and non-injured sensory afferents and, thereby, neuropathic pain

A trial platform to develop a tailored theory-based intervention to improve professional practice in the disclosure of a diagnosis of dementia: Study protocol [ISRCTN15871014]

BACKGROUND: For people with dementia, care should include an explanation of the diagnosis to individuals and their carers, and information about the likely prognosis and possible packages of care. However, this is neither routine nor inevitable, and there is wide variation in the practice of disclosure. The aim of this study is to develop a tailored theory-based intervention to promote appropriate disclosure of diagnosis of dementia. METHODS: There are three objectives. Objective 1 is to define and develop an appropriate model of disclosure; this will be addressed using a multidisciplinary consensus development process. Objective 2 is to identify factors that influence disclosure of diagnosis; a questionnaire based upon theoretical constructs from a range of behavioural theories will be developed and members of old age mental health teams will be surveyed. The analysis will identify those factors that best predict intention to disclose a diagnosis to a person with dementia. Objective 3 is to develop and pilot test a theory-based intervention to promote disclosure of diagnosis that targets attitudes, beliefs and actions most amenable to change. Objective 3 will use the results of Objectives 1&2 to design and pilot test an intervention to improve the process of and increase the proportion of individuals receiving a diagnosis of dementia, for members of old age mental health teams. This work will lead to a proposal for a randomised controlled trial of the intervention

Ultrastructural changes of the intracellular surfactant pool in a rat model of lung transplantation-related events

<p>Abstract</p> <p>Background</p> <p>Ischemia/reperfusion (I/R) injury, involved in primary graft dysfunction following lung transplantation, leads to inactivation of intra-alveolar surfactant which facilitates injury of the blood-air barrier. The alveolar epithelial type II cells (AE2 cells) synthesize, store and secrete surfactant; thus, an intracellular surfactant pool stored in lamellar bodies (Lb) can be distinguished from the intra-alveolar surfactant pool. The aim of this study was to investigate ultrastructural alterations of the intracellular surfactant pool in a model, mimicking transplantation-related procedures including flush perfusion, cold ischemia and reperfusion combined with mechanical ventilation.</p> <p>Methods</p> <p>Using design-based stereology at the light and electron microscopic level, number, surface area and mean volume of AE2 cells as well as number, size and total volume of Lb were determined in a group subjected to transplantation-related procedures including both I/R injury and mechanical ventilation (I/R group) and a control group.</p> <p>Results</p> <p>After I/R injury, the mean number of Lb per AE2 cell was significantly reduced compared to the control group, accompanied by a significant increase in the luminal surface area per AE2 cell in the I/R group. This increase in the luminal surface area correlated with the decrease in surface area of Lb per AE2. The number-weighted mean volume of Lb in the I/R group showed a tendency to increase.</p> <p>Conclusion</p> <p>We suggest that in this animal model the reduction of the number of Lb per AE2 cell is most likely due to stimulated exocytosis of Lb into the alveolar space. The loss of Lb is partly compensated by an increased size of Lb thus maintaining total volume of Lb per AE2 cell and lung. This mechanism counteracts at least in part the inactivation of the intra-alveolar surfactant.</p

Activation of N-heterocyclic carbenes by {BeH₂} and {Be(H)(Me)} fragments

A stable three-coordinate dimethylberyllium species coordinated by the 1,3-bis­(2,4,6-trimethylphenyl)­imidazol-2-ylidene (IMes) ligand is readily converted to the corresponding methylhydrido derivative through metathetical reaction with phenylsilane. Attempts to synthesize the corresponding molecular dihydrides are, however, unsuccessful and result in ring opening of an IMes ligand through hydride transfer to the donor carbon atom and the consequent formation of a heterocyclic beryllium organoamide. In agreement with previous calculations, we suggest that this process occurs via a Schlenk-type equilibration process and formation of a four-coordinate bis-NHC beryllium dihydride. These species are not observed, however, as the steric pressure exerted by coordination of the two sterically demanding IMes ligands is sufficient to induce hydride transfer. The latter deduction is supported by the observation that a similar ring-opened product, but derived from methyl and hydride transfer, is available through the introduction of a further equivalent of IMes to the isolated beryllium methyl hydride species. In the latter case the ring-opening process is more facile, which we ascribe to the increased steric pressure achieved upon the formation of four-coordinate beryllium. In a further striking reaction under more forcing thermal conditions, the carbene carbon center of an IMes ligand is observed to be completely eliminated with selective formation of a three-coordinate diamidoberyllium species

Assessment and analysis of mechanical allodynia-like behavior induced by spared nerve injury (SNI) in the mouse

Experimental models of peripheral nerve injury have been developed to study mechanisms of neuropathic pain. In the spared nerve injury (SNI) model in rats, the common peroneal and tibial nerves are injured, producing consistent and reproducible pain hypersensitivity in the territory of the spared sural nerve. In this study, we investigated whether SNI in mice is also a valid model system for neuropathic pain. SNI results in a significant decrease in withdrawal threshold in SNI-operated mice. The effect is very consistent between animals and persists for the four weeks of the study. We also determined the relative frequency of paw withdrawal for each of a series of 11 von Frey hairs. Analysis of response frequency using a mixed-effects model that integrates all variables (nerve injury, paw, gender, and time) shows a very stable effect of SNI over time and also reveals subtle divergences between variables, including gender-based differences in mechanical sensitivity. We tested two variants of the SNI model and found that injuring the tibial nerve alone induces mechanical hypersensitivity, while injuring the common peroneal and sural nerves together does not induce any significant increase in mechanical sensitivity in the territory of the spared tibial nerve. SNI induces a mechanical allodynia-like response in mice and we believe that our improved method of assessment and data analysis will reveal additional internal and external variability factors in models of persistent pain. Use of this model in genetically altered mice should be very effective for determining the mechanisms involved in neuropathic pain

Effects of inorganic nitrate and vitamin C co-supplementation on blood pressure and vascular function in younger and older healthy adults: A randomised double-blind crossover trial

Background: Vitamin C and inorganic nitrate have been linked to enhanced nitric oxide (NO) production and reduced oxidative stress. Vitamin C may also enhance the conversion of nitrite into NO. Aims: We investigated the potential acute effects of vitamin C and inorganic nitrate co-supplementation on blood pressure (BP) and peripheral vascular function. The secondary aim was to investigate whether age modified the effects of vitamin C and inorganic nitrate on these vascular outcomes. Methods: Ten younger (age 18–40 y) and ten older (age 55–70 y) healthy participants were enrolled in a randomised double-blind crossover clinical trial. Participants ingested a solution of potassium nitrate (7 mg/kg body weight) and/or vitamin C (20 mg/kg body weight) or their placebos. Acute changes in resting BP and vascular function (post-occlusion reactive hyperemia [PORH], peripheral pulse wave velocity [PWV]) were monitored over a 3-h period. Results: Vitamin C supplementation reduced PWV significantly (vitamin C: −0.70 ± 0.31 m/s; vitamin C placebo: +0.43 ± 0.30 m/s; P = 0.007). There were significant interactions between age and vitamin C for systolic, diastolic, and mean arterial BP (P = 0.02, P = 0.03, P = 0.02, respectively), with systolic, diastolic and mean BP decreasing in older participants and diastolic BP increasing in younger participants following vitamin C administration. Nitrate supplementation did not influence BP (systolic: P = 0.81; diastolic: P = 0.24; mean BP: P = 0.87) or vascular function (PORH: P = 0.05; PWV: P = 0.44) significantly in both younger and older participants. However, combined supplementation with nitrate and vitamin C reduced mean arterial BP (−2.6 mmHg, P = 0.03) and decreased PWV in older participants (PWV: −2.0 m/s, P = 0.02). Conclusions: The co-administration of a single dose of inorganic nitrate and vitamin C lowered diastolic BP and improved PVW in older participants. Vitamin C supplementation improved PWV in both age groups but decreased systolic and mean BP in older participants only. Clinical trial registration: Current Controlled Trials (ISRCTN98942199)