Impact of Work Motivation on Occupational Health in Healthcare Workers.

OBJECTIVES: The present cross-sectional study investigated, in a group of Italian healthcare workers (HCWs), the association between work motivation and occupational health and the impact of socio-demographic and job-related variables on this association. METHODS: A total of 656 subjects (nurses, technicians, midwives and physiotherapists) completed the survey. Linear regression models were used to correlate motivation types (by Scale of Motivation At Work) with health indicators (general health, depression, professional exhaustion, satisfaction and turnover intention) and burnout's subscales (emotional exhaustion, depersonalization and reduced professional achievement). FINDINGS: Autonomous motivation correlated positively with general health and work satisfaction and negatively with depression, exhaustion and turnover intention. Scoring high on intrinsic/integrated regulation was associated with better health and job satisfaction and with turnover intention, depression and emotional exhaustion. Controlled motivation, demotivation and external regulation nourished burnout's indicators, while autonomous motivation was protective. Operating in intensive care or surgical areas negatively affected general health; working as a nurse manager or midwife increased one's depressive risk and reduced satisfaction; being older than 60 increased emotional exhaustion and turnover intention; having a master's degree protected from exhaustion and depression. IMPLICATIONS: Collectively, our findings extend evidence on the role of work motivation in shaping occupational health and underline the importance for healthcare organizations of promoting actions to reinforce autonomous motivation at work.

The biased hand. Mouse-tracking metrics to examine the conflict processing in a race-implicit association test.

In this study, we adapted a race-Implicit Association Test (race-IAT) to mouse-tracking (MT) technique to identify the more representative target observed MT-metrics and explore the temporal unfolding of the cognitive conflict emerging during the categorisation task. Participants of Western European descent performed a standard keyboard-response race-IAT (RT-race-IAT) and an MT-race-IAT with the same structure. From a behavioural point of view, our sample showed a typical Congruency Effect, thus a pro-White implicit bias, in the RT-race-IAT. In addition, in the MT-race-IAT, the MT-metrics showed a similar Congruency Effect mirroring the higher attraction of the averaged-trajectories towards the incorrect response button in incongruent than congruent trials. Moreover, these MT-metrics were positively associated with RT-race-IAT scores, strengthening the MT approach's validity in characterising the implicit bias. Furthermore, the distributional analyses showed that mouse trajectories displayed a smooth profile both in congruent and incongruent trials to indicate that the unfolding of the decision process and the raised conflict is guided by dynamical cognitive processing. This latter continuous competition process was studied using a novel phase-based approach which allowed to temporally dissect an Early, a Mid and a Late phase, each of which may differently reflect the decision conflict between automatic and controlled responses in the evolution of the mouse movement towards the target response. Our results show that the MT approach provides an accurate and finer-grained characterisation of the implicit racial attitude than classical RT-IAT. Finally, our novel phase-based approach can be an effective tool to shed light on the implicit conflict processing emerging in a categorisation task with a promising transferable value in different cognitive and neuropsychological fields.

A proposal for the reference intervals of the Italian microbiota "scaffold" in healthy adults.

Numerous factors, ranging from genetics, age, lifestyle, and dietary habits to local environments, contribute to the heterogeneity of the microbiota in humans. Understanding the variability of a "healthy microbiota" is a major challenge in scientific research. The gut microbiota profiles of 148 healthy Italian volunteers were examined by 16S rRNA gene sequencing to determine the range and diversity of taxonomic compositions in the gut microbiota of healthy populations. Possible driving factors were evaluated through a detailed anamnestic questionnaire. Microbiota reference intervals were also calculated. A "scaffold" of a healthy Italian gut microbiota composition was identified. Differences in relative quantitative ratios of microbiota composition were detected in two clusters: a bigger cluster (C2), which included 124 subjects, was characterized by more people from the northern Italian regions, who habitually practised more physical activity and with fewer dietary restrictions. Species richness and diversity were significantly higher in this cluster (C2) than in the other one (C1) (C1: 146.67 ± 43.67; C2: 198.17 ± 48.47; F = 23.40; P < 0.001 and C1: 16.88 ± 8.66; C2: 35.01 ± 13.40; F = 40.50; P < 0.001, respectively). The main contribution of the present study was the identification of the existence of a primary healthy microbiological framework that is only marginally affected by variations. Taken together, our data help to contextualize studies on population-specific variations, including marginal aspects, in human microbiota composition. Such variations must be related to the primary framework of a healthy microbiota and providing this perspective could help scientists to better design experimental plans and develop strategies for precision tailored microbiota modulation.

Cortisol, chronotype, and coping styles as determinants of tolerance of nursing staff to rotating shift work.

Hypothalamo-pituitary-adrenal axis activity and cortisol patterns are likely to play a role in shift work tolerance, i.e., ability to adapt to shift work without suffering stress-related consequences. Yet, the evidence is scanty. Here, salivary cortisol output during night shifts and leisure days was assessed in fast-forward rotating shift work nursing staff (N = 30), and possible links with a series of variables - gender (30% male), age (M = 39.6, SEM = 1.57 y), years of service (M = 12.43, SEM = 1.48 y), BMI (M = 23.29, SEM = 0.66 Kg/m2), self-rated chronotype, sleep quality, and psycho-behavioral factors - were investigated. Main results show that cortisol output during night shifts: i) is larger in morning-oriented chronotypes, thus affected by the circadian misalignment between biological and working rhythms; ii) associates with dysfunctional coping styles at work; iii) positively correlates with diurnal cortisol secretion on leisure days, i.e., individuals with larger cortisol output during shifts display higher cortisol secretion on non-working days. Chronotype and psycho-behavioral factors explain most of the correlational weight linking cortisol output during the night shift and off-days. In conclusion, we confirm salivary cortisol testing as a suitable objective marker of occupational stress and propose it as a valuable index for monitoring shift work tolerance, in combination with chronotype. Moreover, we emphasize the importance of evaluating psycho-behavioral factors in professional settings, because these modifiable variables can be addressed with tailored psychological interventions to ameliorate poor job satisfaction, reduce work-related distress, and avoid chronic cortisol excess experienced by shift workers.

Excitotoxicity, neuroinflammation and oxidant stress as molecular bases of epileptogenesis and epilepsy-derived neurodegeneration: The role of vitamin E.

Glutamate-mediated excitotoxicity, neuroinflammation, and oxidative stress are common underlying events in neurodegeneration. This pathogenic "triad" characterizes the neurobiology of epilepsy, leading to seizure-induced cell death, increased susceptibility to neuronal synchronization and network alterations. Along with other maladaptive changes, these events pave the way to spontaneous recurrent seizures and progressive degeneration of the interested brain areas. In vivo models of epilepsy are available to explore such epileptogenic mechanisms, also assessing the efficacy of chemoprevention and therapy strategies at the pre-clinical level. The kainic acid model of pharmacological excitotoxicity and epileptogenesis is one of the most investigated mimicking the chronicization profile of temporal lobe epilepsy in humans. Its pathogenic cues include inflammatory and neuronal death pathway activation, mitochondrial disturbances and lipid peroxidation of several regions of the brain, the most vulnerable being the hippocampus. The importance of neuroinflammation and lipid peroxidation as underlying molecular events of brain damage was demonstrated in this model by the possibility to counteract the related maladaptive morphological and functional changes of this organ with vitamin E, the main fat-soluble cellular antioxidant and "conditional" co-factor of enzymatic pathways involved in polyunsaturated lipid metabolism and inflammatory signaling. The present review paper provides an overview of the literature supporting the potential for a timely intervention with vitamin E therapy in clinical management of seizures and epileptogenic processes associated with excitotoxicity, neuroinflammation and lipid peroxidation, i.e. the pathogenic "triad".

Stress and the psyche-brain-immune network in psychiatric diseases based on psychoneuroendocrineimmunology: a concise review.

In the last decades, psychoneuroendocrineimmunology research has made relevant contributions to the fields of neuroscience, psychobiology, epigenetics, molecular biology, and clinical research by studying the effect of stress on human health and highlighting the close interrelations between psyche, brain, and bodily systems. It is now well recognized that chronic stress can alter the physiological cross-talk between brain and biological systems, leading to long-lasting maladaptive effects (allostatic overload) on the nervous, immune, endocrine, and metabolic systems, which compromises stress resiliency and health. Stressful conditions in early life have been associated with profound alterations in cortical and subcortical brain regions involved in emotion regulation and the salience network, showing relevant overlap with different psychiatric conditions. This paper provides a summary of the available literature concerning the notable effects of stress on the brain and immune system. We highlight the role of epigenetics as a mechanistic pathway mediating the influences of the social and physical environment on brain structure and connectivity, the immune system, and psycho-physical health in psychiatric diseases. We also summarize the evidence regarding the effects of stress management techniques (mainly psychotherapy and meditation practice) on clinical outcomes, brain neurocircuitry, and immune-inflammatory network in major psychiatric diseases.

Neurobiological Correlates of Alpha-Tocopherol Antiepileptogenic Effects and MicroRNA Expression Modulation in a Rat Model of Kainate-Induced Seizures.

Seizure-triggered maladaptive neural plasticity and neuroinflammation occur during the latent period as a key underlying event in epilepsy chronicization. Previously, we showed that α-tocopherol (α-T) reduces hippocampal neuroglial activation and neurodegeneration in the rat model of kainic acid (KA)-induced status epilepticus (SE). These findings allowed us to postulate an antiepileptogenic potential for α-T in hippocampal excitotoxicity, in line with clinical evidence showing that α-T improves seizure control in drug-resistant patients. To explore neurobiological correlates of the α-T antiepileptogenic role, rats were injected with such vitamin during the latent period starting right after KA-induced SE, and the effects on circuitry excitability, neuroinflammation, neuronal death, and microRNA (miRNA) expression were investigated in the hippocampus. Results show that in α-T-treated epileptic rats, (1) the number of population spikes elicited by pyramidal neurons, as well as the latency to the onset of epileptiform-like network activity recover to control levels; (2) neuronal death is almost prevented; (3) down-regulation of claudin, a blood-brain barrier protein, is fully reversed; (4) neuroinflammation processes are quenched (as indicated by the decrease of TNF-α, IL-1ß, GFAP, IBA-1, and increase of IL-6); (5) miR-146a, miR-124, and miR-126 expression is coherently modulated in hippocampus and serum by α-T. These findings support the potential of a timely intervention with α-T in clinical management of SE to reduce epileptogenesis, thus preventing chronic epilepsy development. In addition, we suggest that the analysis of miRNA levels in serum could provide clinicians with a tool to evaluate disease evolution and the efficacy of α-T therapy in SE.

α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions.

Neuroplasticity is an "umbrella term" referring to the complex, multifaceted physiological processes that mediate the ongoing structural and functional modifications occurring, at various time- and size-scales, in the ever-changing immature and adult brain, and that represent the basis for fundamental neurocognitive behavioral functions; in addition, maladaptive neuroplasticity plays a role in the pathophysiology of neuropsychiatric dysfunctions. Experiential cues and several endogenous and exogenous factors can regulate neuroplasticity; among these, vitamin E, and in particular α-tocopherol (α-T), the isoform with highest bioactivity, exerts potent effects on many plasticity-related events in both the physiological and pathological brain. In this review, the role of vitamin E/α-T in regulating diverse aspects of neuroplasticity is analyzed and discussed, focusing on the hippocampus, a brain structure that remains highly plastic throughout the lifespan and is involved in cognitive functions. Vitamin E-mediated influences on hippocampal synaptic plasticity and related cognitive behavior, on post-natal development and adult hippocampal neurogenesis, as well as on cellular and molecular disruptions in kainate-induced temporal seizures are described. Besides underscoring the relevance of its antioxidant properties, non-antioxidant functions of vitamin E/α-T, mainly involving regulation of cell signaling molecules and their target proteins, have been highlighted to help interpret the possible mechanisms underlying the effects on neuroplasticity.

High Cardiorespiratory Fitness Is Negatively Associated with Daily Cortisol Output in Healthy Aging Men.

Physical fitness has salutary psychological and physical effects in older adults by promoting neuroplasticity and adaptation to stress. In aging, however, the effects of fitness on the hypothalamic-pituitary-adrenal (HPA) axis are mixed. We investigated the association between cardiorespiratory fitness and HPA activity in healthy elderly men (n = 22, mean age 68 y; smokers, obese subjects, those taking drugs or reporting recent stressful events were excluded), by measuring in saliva: i) daily pattern of cortisol secretion (6 samples: 30' post-awakening, and at 12.00, 15.00, 18.00, 21.00, 24.00 h); and ii) the cortisol response to a mental challenge. Cardiorespiratory fitness (VO2max) was estimated using the Rockport Walking Test and the participants were assigned to high-fit (HF, ≥60°, n = 10) and low-fit (LF, ≤35°, n = 12) groups according to age-specific percentiles of VO2max distribution in the general population. At all daytimes, basal cortisol levels were lower in the HF than the LF group, most notably in the evening and midnight samples, with a significant main effect of physical fitness for cortisol levels overall; the area-under-the-curve for total daily cortisol output was significantly smaller in the HF group. Among the subjects who responded to mental stress (baseline-to-peak increment >1.5 nmol/L; n = 13, 5 LF, 8 HF), the amplitude of cortisol response and the steepness of recovery decline displayed an increasing trend in the HF subjects, although between-group differences failed to reach the threshold for significance. In conclusion, cardiorespiratory fitness in healthy aging men is negatively correlated with daily cortisol output and contributes to buffering the HPA dysregulation that occurs with advancing age, thus possibly playing a beneficial role in contrasting age-related cognitive and physical decline.

Brief training of psychoneuroendocrinoimmunology-based meditation (PNEIMED) reduces stress symptom ratings and improves control on salivary cortisol secretion under basal and stimulated conditions.

CONTEXT: Meditation is proposed as an anti-stress practice lowering allostatic load and promoting well-being, with brief formats providing some of the benefits of longer interventions. OBJECTIVES: PsychoNeuroEndocrinoImmunology-based meditation (PNEIMED) combines the teaching of philosophy and practice of Buddhist meditation with a grounding in human physiology from a systemic and integrative perspective. We evaluated the effects of four-day PNEIMED training (30 h) on subjective and objective indices of stress in healthy adults. DESIGN: A non-randomized, controlled, before-and-after study was conducted. Participants (n = 125, mostly health practitioners) answered a questionnaire rating stress symptom before (T0) and after (Tf) a PNEIMED course. In an additional sample (n = 40; smokers, overweight persons, women taking contraceptives, and subjects with oral pathologies were excluded), divided into PNEIMED-attending (intervention, n = 21) and non-meditating (control, n = 19) groups, salivary cortisol was measured upon awakening and during a challenging mental task. RESULTS: Self-rated distress scores were highly reduced after the PNEIMED course. In the intervention group, improvement of psychological well-being was accompanied by decrease in cortisol levels at awakening. No T0-vs-Tf changes in distress scores and morning cortisol were found in controls. Based on baseline-to-peak increment of cortisol response at T0, 26 subjects (n = 13 for each group) were classified as task-responders. The amplitude and duration of the cortisol response decreased after PNEIMED, whereas no effects were found in controls. CONCLUSIONS: Brief PNEIMED training yields immediate benefits, reducing distress symptoms and adrenocortical activity under basal and stimulated conditions. PNEIMED may represent an effective practice to manage stress and anxiety, particularly among subjects facing a multitude of job-related stressors, such as healthcare workers.

Post-seizure α-tocopherol treatment decreases neuroinflammation and neuronal degeneration induced by status epilepticus in rat hippocampus.

Vitamin E (as α-tocopherol, α-T) was shown to have beneficial effects in epilepsy, mainly ascribed to its antioxidant properties. Besides radical-induced neurotoxicity, neuroinflammation is also involved in the pathophysiology of epilepsy, since neuroglial activation and cytokine production exacerbate seizure-induced neurotoxicity and contribute to epileptogenesis. We previously showed that α-T oral supplementation before inducing status epilepticus, markedly reduces astrocytic and microglial activation, neuronal cell death and oxidative stress in the hippocampus, as observed 4 days after seizure. In order to evaluate the possibility that such a neuroprotective and anti-inflammatory effect may also provide a strategy for an acute intervention in epilepsy, in this study, seizures were induced by single intaperitoneal injection of kainic acid and, starting from 3 h after status epilepticus, rats were treated with an intraperitoneal bolus of α-T (250 mg/kg b.w.; once a day) for 4 days, that was the time after which morphological and biochemical analyses were performed on hippocampus. Post-seizure α-T administration significantly reduced astrocytosis and microglia activation, and decreased neuron degeneration and spine loss; these effects were associated with the presence of a lowered lipid peroxidation in hippocampus. These results confirm and further emphasize the anti-inflammatory and neuroprotective role of α-T in kainic acid-induced epilepsy. Moreover, the findings show that post-seizure treatment with α-T provides an effective secondary prevention against post-seizure inflammation-induced brain damages and possibly against their epileptogenic effects.

Rotating shift-work as an independent risk factor for overweight Italian workers: a cross-sectional study.

BACKGROUND: A job-related factor is attracting a growing interest as a possible determinant of body weight gain in shift-workers. OBJECTIVE: The aim of the study was to reinvestigate the issue of overweight between rotating shift workers and daytime workers, taking into consideration possible confounding covariate factors. METHODS: This is a cross-sectional study, conducted by reviewing data from subjects participating in an occupational surveillance program in 2008. Participants answered a self-administered questionnaire to retrieve information about socio-demographic factors and working conditions (job schedule type, job-related physical activity, time in job), subjective health status, health care visits during the previous year, and lifestyle factors (dietary habits, leisure time physical activity, alcohol consumption). Participants underwent a medical examination for measurement of BMI, and acquisition of medical history. RESULTS: Compared to daytime workers (N = 229), rotating shift workers (N = 110) displayed higher BMI (mean BMI was 27.6±3.9 and 26.7±3.6 for shift workers, and daytime workers, respectively; p<0.05). Logistic regression analysis allowed to highlight the role of rotating shift-work as an independent risk factor for increased body weight (OR 1.93, 95%CI 1.01-3.71), being aged between 35 and 54 years was a major determinant of increased BMI (OR 2.39, 95%CI 1.14-5.00). In addition, family history of obesity was the strongest determinant of overweight/obesity (OR 9.79, 95%CI 1.28-74.74). Interestingly, no significant association was found between overweight and other potentially relevant factors, such as diet quality and food choices, alcohol consumption, levels of occupational and leisure-time physical activity. CONCLUSIONS: Present findings seem to support the notion that rotating shift work is an independent risk factor for overweight, regardless of workers' dietary habits and physical activity levels.

Fish oil supplementation reduces cortisol basal levels and perceived stress: a randomized, placebo-controlled trial in abstinent alcoholics.

Behavioral distress and dysfunctions of hypothalamic-pituitary-adrenocortical (HPA) axis play a central role in alcohol abuse. Omega-3 fatty acids are proposed as having antistress, regulatory effects on HPA responsiveness, but a possible protective role in ethanol addiction is unexplored.A randomized, doubleblind, placebo-controlled trial was performed in male alcoholics undergoing residential rehabilitation program, to evaluate the effects of 3-week supplementation with fish-oil providing eicosapentaenoic (60 mg/day) and docosahexaenoic acid (252 mg/day) on perceived stress/anxiety and HPA activity, assessed by measuring saliva basal cortisol levels at various daytimes (0730 h, 1130 h, 1600 h, 2000 h, and 2400 h) and the acute cortisol response to Trier Social Stress Test.Results showed that in supplemented subjects, before versus after decrease of stress/anxiety ratings was accompanied by reduction of cortisol basal levels throughout the day; no changes were observed in placebo group. At the end of intervention, amplitude, and duration of stress-evoked cortisol response did not differ between groups; however, the peak of cortisol response was temporally anticipated in supplemented subjects. In conclusion, an elevated omega-3 intake may reduce distress symptoms and basal cortisol secretion in abstinent alcoholics, thus providing a valid subsidiary measure to increase the efficacy of rehabilitation programs in ethanol addicts.

Maternal dietary loads of α-tocopherol differentially influence fear conditioning and spatial learning in adult offspring.

α-Tocopherol, the main component of vitamin E, is well known to be a radical scavenger, so an increased intake of vitamin E is recommended in complicated pregnancy, to prevent possible fetus damage by free radical. In a previous work, we found that maternal α-tocopherol supplementation affects PKC-mediated cellular signaling and hippocampal synaptic plasticity in developing brain; the latter effect persists in adulthood. Here, adult rats maternally exposed to supranutritional doses of α-tocopherol were evaluated for Contextual Fear Conditioning and spatial learning in Morris Water Maze, two different hippocampus-dependent learning tasks. Moreover, anxiety, spontaneous activity, and explorative drive were also evaluated as factors potentially affecting learning performance. Treated rats showed a different behavior with respect to controls: performance in Contextual Fear Conditioning was improved, while spatial learning tested in Morris Water Maze, was impaired. The improvement of fear response was not ascribable to differences in anxiety level and/or spontaneous activity; thus it appears to be a specific effect of α-tocopherol overloading during brain development. On the contrary, the impaired performance in Morris Water Maze exhibited by treated rats can be in part explained by their enhanced explorative drive. Although extrapolation from rats to humans is difficult, a caveat in assuming supranutritional doses of vitamin E in pregnancy arises from this study.

Dietary supplementation with α-tocopherol reduces neuroinflammation and neuronal degeneration in the rat brain after kainic acid-induced status epilepticus.

Vitamin E (as α-tocopherol, α-T) is proposed to alleviate glia-mediated inflammation in neurological diseases, but such a role in epilepsy is still elusive. This study investigated the effect of α-T supplementation on glial activation, neuronal cell death and oxidative stress of rat brain exposed to kainate-induced seizures. Animals were fed for 2 weeks with a α-T-enriched diet (estimated intake of 750 mg/kg/day) before undergoing status epilepticus. Compliance to supplementation was demonstrated by the remarkable increase in brain α-T. Four days after seizure, brain α-T returned to baseline and lipid peroxidation markers decreased as compared to non-supplemented rats. Status epilepticus induced a lower up-regulation of astrocytic and microglial antigens (GFAP and MHC II, respectively) and production of pro-inflammatory cytokines (IL-1ß and TNF-α) in supplemented than in non-supplemented animals. This anti-inflammatory effect was associated with a lower neuronal cell death. In conclusion, α-T dietary supplementation prevents oxidative stress, neuroglial over-activation and cell death occurring after kainate-induced seizures. This evidence paves the way to an anti-inflammatory and neuroprotective role of α-T interventions in epilepsy.

Maternal dietary loads of α-tocopherol depress protein kinase C signaling and synaptic plasticity in rat postnatal developing hippocampus and promote permanent deficits in adult offspring.

Vitamin E (α-tocopherol) supplementation has been tested as prophylaxis against gestational disorders associated with oxidative damage. However, recent evidence showing that high maternal α-tocopherol intake can adversely affect offspring development raises concerns on the safety of vitamin E extradosages during pregnancy. Besides acting as an antioxidant, α-tocopherol depresses cell proliferation and modulates cell signaling through inhibiting protein kinase C (PKC), a kinase that is deeply involved in neural maturation and plasticity. Possible effects of α-tocopherol loads in the maturing brain, where PKC dysregulation is associated to developmental dysfunctions, are poorly known. Here, supranutritional doses of α-tocopherol were fed to pregnant and lactating dams to evaluate the effects on PKC signaling and morphofunctional maturation in offspring hippocampus. Results showed that maternal supplementation potentiates hippocampal α-tocopherol incorporation in offspring and leads to marked decrease of PKC phosphorylation throughout postnatal maturation, accompanied by reduced phosphorylation of growth-associated protein-43 and myristoylated alanine-rich C kinase substrate, two PKC substrates involved in neural development and plasticity. Although processes of neuronal maturation, synapse formation and targeting appeared unaffected, offspring of supplemented mothers displayed a marked reduction of long-term synaptic plasticity in juvenile hippocampus. Interestingly, this impairment persisted in adulthood, when a deficit in hippocampus-dependent, long-lasting spatial memory was also revealed. In conclusion, maternal supplementation with elevated doses of α-tocopherol can influence cell signaling and synaptic plasticity in developing hippocampus and promotes permanent adverse effects in adult offspring. The present results emphasize the need to evaluate the safety of supranutritional maternal intake of α-tocopherol in humans.

The effects of educational intervention on nutritional behaviour in alcohol-dependent patients.

AIMS: To evaluate the nutritional status and the impact of an educational intervention on nutritional behaviour in alcohol-dependent patients. METHODS: A pre-and post-intervention questionnaire and a follow-up interview were administered to 58 patients of a residential alcohol treatment service. RESULTS: Females were at lower risk of being overweight than males, even after adjusting for amount and preferred type of alcohol beverage. Before intervention, 19% consumed 3 meals/day. Following the educational intervention, 22.2% of participants improved their knowledge. After 6 months, when 45 patients agreed to a telephone interview of whom 80% reported continued abstinence, 70.7% reported eating more than 3 meals/day. CONCLUSIONS: Nutritional behaviour of alcohol patients after residential treatments improved during follow-up, and it is possible that an educational intervention to increase knowledge on healthy nutrition style may have contributed.

GABAergic miniature spontaneous activity is increased in the CA1 hippocampal region of dystrophic mdx mice.

Duchenne muscular dystrophy (DMD), a genetic disease due to dystrophin gene mutation and characterised by skeletal muscle failure, is associated with non-progressive cognitive deficits. In human and mouse brain, full-length dystrophin is localised postsynaptically in neocortical, hippocampal and cerebellar neurons. Evidence obtained in the CNS of dystrophic mice (mdx) suggested alterations of the GABAergic system. However, a direct functional evaluation of GABAergic synaptic transmission in mdx mice has not been conducted in the hippocampus, which is involved in cognitive processes and is rich in full-length dystrophin. Here, we investigated evoked and miniature inhibitory postsynaptic currents (IPSCs) in CA1 pyramidal neurons of mdx mice with patch clamp recording techniques. Results showed an increased frequency of miniature spontaneous IPSCs in mdx mice compared with controls, whereas evoked IPSCs did not show significant variations. Paired-pulse facilitation (PPF) analysis showed lack of facilitation at short intervals in mdx mice compared with that in wild-type mice. Analysis of density of synapses that innervate CA1 pyramidal cell bodies did not indicate significant differences between mdx mice and controls. Therefore, we suggest that increased miniature spontaneous IPSC frequency is due to altered pre-synaptic release probability. The present findings are discussed in the light of the accrued evidence for alterations of inhibitory synaptic transmission in the brain of dystrophic mice.

Mitochondrial localization of Na+/Ca2+ exchangers NCX1-3 in neurons and astrocytes of adult rat brain in situ.

In neural cells, Na+/Ca2+ exchanger (NCX) participates in Ca2+ recycling across mitochondrial membranes, thus contributing to shape Ca2+ responses. NCX exchanger isoform proteins, NCX1-3, are widely distributed in mammalian brain, where they localize to neuronal, glial and endothelial cells, but anatomical data on their mitochondrial expression are scanty. In the present work, mitochondrial localization of NCX1-3 was investigated in rat neocortex and hippocampus by means of western blotting analysis and in situ electron microscopy immunocytochemistry. Results showed that a conspicuous population of neuronal and astrocytic mitochondria express NCX1-3, with distinct isoforms exhibiting differential patterns of mitochondrial expression. In neurons, percentages of NCXs-labelled mitochondria varied significantly between diverse subcellular regions: the majority of NCXs-expressing mitochondria were found in dendrites, often located beneath the plasmalemma and near postsynaptic sites. In astrocytes, most NCXs-labelled mitochondria were situated close to the cellular surface. Present quantitative and qualitative immunocytochemical data suggest that all NCX isoforms contribute to mitochondrial Ca2+ homeostasis in neurons and glial cells in vivo, and that NCXs may be particularly involved in handling Ca2+ in dendritic, subplasmalemmal mitochondria, thus emphasizing the role of mitochondrial NCX1-3 in shaping postsynaptic calcium transients.

Cellular and subcellular localization of Na+-Ca2+ exchanger protein isoforms, NCX1, NCX2, and NCX3 in cerebral cortex and hippocampus of adult rat.

Na(+)-Ca(2+) exchanger (NCX) controls cytosolic Ca(2+) and Na(+) concentrations ([Ca(2+)](i) and [Na(+)](i)) in eukaryotic cells. Here we investigated by immunocytochemistry the cellular and subcellular localization of the three known NCX isoforms, NCX1, NCX2 and NCX3, in adult rat neocortex and hippocampus. NCX1-3 were widely expressed in both brain areas: NCX1 immunoreactivity (ir) was exclusively associated to neuropilar puncta, while NCX2-3 were also detected in neuronal somata and dendrites. NCX1-3 ir was often identified around blood vessels. In both neocortex and hippocampus, all NCX isoforms were prominently expressed in dendrites and dendritic spines contacted by asymmetric axon terminals, whereas they were poorly expressed in presynaptic boutons. In addition, NCX1-3 ir was detected in astrocytes, notably in distal processes ensheathing excitatory synapses. All NCXs were expressed in perivascular astrocytic endfeet and endothelial cells. The robust expression of NCX1-3 in heterogeneous cell types in the brain in situ emphasizes their role in handling Ca(2+) and Na(+) in both excitable and non-excitable cells. Perisynaptic localization of NCX1-3 in dendrites and spines indicates that all isoforms are favourably located for buffering [Ca(2+)](i) in excitatory postsynaptic sites. NCX1-3 expressed in perisynaptic glial processes may participate in shaping astrocytic [Ca(2+)](i) transients evoked by ongoing synaptic activity.