Association between social class and food consumption in the Italian EPIC population

AIMS AND BACKGROUND: The objectives of the present study were to validate the social stratification variables adopted by the European Prospective Investigation into Cancer and Nutrition (EPIC) by comparing them with data from another independent source and to evaluate the geographic and social distribution of eating habits in the Italian EPIC population. METHODS: The validation of the socioeconomic data collected by the EPIC study was performed with the Turin Longitudinal Study as gold standard and using Cohen's kappa statistics to evaluate the concordance between the studies. We then analyzed food groups based on the consumption of meat and fats, carbohydrates, sweets and alcohol, and on an index of the Mediterranean diet. The standardized scores for each food group were subdivided into quartiles, which were used to compare persons in the extreme quartiles. Analysis of the differences in eating habits by center and by educational level was conducted separately for men and women, calculating the prevalence rate ratios and controlling for age, area of birth and body mass index. RESULTS: Concordance between the two data sources was high for educational level and low for the social-class index based on occupation. Most of the eating habits considered to be potentially harmful (high consumption of meat or fats and alcohol and low consumption of olive oil and fish) were more frequent in Northern than in Southern Italy. These habits were inversely correlated with educational level, especially in the South. CONCLUSIONS: A significant improvement in health could be obtained in the Italian population if culturally and socioeconomically disadvantaged individuals were to abandon their diet rich in meat and fats, as done by more advantaged persons. In the absence of preventive interventions specifically addressed to disadvantaged groups, it is likely that social inequalities in mortality and morbidity will increase.     

Kif1Bbeta isoform is enriched in motor neurons but does not change in a mouse model of amyotrophic lateral sclerosis

The kinesin superfamily motor protein Kif1B is expressed in two isoforms, Kif1Balpha and Kif1Bbeta, with distinct cargo-binding domains. We examined the mRNA distribution of the two isoforms in adjacent sections of brain and spinal cord of adult mice using in situ hybridization analysis. Kif1Bbeta mRNA is enriched in several regions of brain and spinal cord. Its levels are four to five times higher than that of the alpha isoform, which was barely detectable. The highest mRNA levels of Kif1Bbeta were found in the cortex, hippocampus, cerebellum and the grey matter of the spinal cord. At the cellular level the highest signal was found in motor neurons in the motor nuclei of medulla oblongata and the ventral horn of spinal cord. Because expression of other Kif genes is altered in amyotrophic lateral sclerosis (ALS) models, we examined the expression level of Kif1Bbeta mRNA in the spinal cord of transgenic mice carrying the SOD1G93A mutation, a model of familial ALS, at presymptomatic and early stages of the disease. No changes were observed in Kif1Bbeta mRNA in motor neurons or in other regions of the spinal cord. These findings indicate that Kif1Balpha, which modulates the transport of mitochondria, may play a major role in tissues other than the central nervous system. Instead Kif1Bbeta, responsible for the transport of synaptic vesicle precursors, seems to play an important role in the nervous system, particularly in the lower motor neurons. The absence of changes of Kif1Bbeta mRNA in transgenic SOD1G93A mice suggests that other molecular mechanisms may play a role in the disruption of axonal transport occurring in the motor neurons of these mice.     

Beta-endorphin levels in peripheral blood mononuclear cells and long-term naltrexone treatment in autistic children.

We assessed the clinical and biological effects of high-dose, long-term Naltrexone (NTX) treatment in 11 children (3-11 years), who had been diagnosed as autistic. The drug was given following an open design, for 12 weeks. Beta-Endorphin (beta-END) was assayed in peripheral blood mononuclear cells after 1 and 3 months of treatment, and 6 months after the completion of the course. Baseline beta-END levels were higher than in healthy age-matched controls. In seven patients treatment reduced beta-END, whose levels rose in four children. Autistic symptoms were considerably attenuated in all cases, with functional improvements involving several areas. There was a close correlation between the reduction in beta-END levels and the decrease of social withdrawal, and an evident--though weak--correlation between increases in beta-END and decreases in stereotypy and abnormal speech. Both effects persisted after treatment stopped.     

Ultrastructural effects of cadmium on the epididymis of the cryptorchid rat

The short-term (90 min) effect of an intraperitoneal injection of cadmium chloride (3 mumol/100 g body weight) was studied with the electron microscope in the epididymis of mature rats rendered unilaterally cryptorchid 60 days before injection. It was found that the endothelium of the epididymal capillaries of the cryptorchid organ, at this low dose and short time, showed neither separation of cytoplasmic leaflets, nor platelet damage, nor extravasation, which are the lesions previously described by us and which were present in the contralateral, scrotal epididymis. The possible mechanisms for the protective action of cryptorchidism against the effects of cadmium on capillary endothelia are discussed.     

Endogenous opioids and their receptors in stress-induced analgesia

Stress can induce a naloxone reversible and a naloxone non reversible analgesia according to its parameters. We showed that naloxone non reversible analgesia can be reversed by antagonists of the kappa opiate receptor and that naloxone reversible analgesia can be related to mu receptors and beta-endorphin, while the kappa receptor mediated analgesia can be related to dynorphin. We have also shown that the characteristics of the receptors might change in consequence to stress and that the analgesic responses might be modulated by benzodiazepine agonists and antagonists.     

Studies on the effects of antidepressant drugs on the antinociceptive action of morphine and on plasma morphine in rat and man

In the rat we studied the effect of 3 tricyclic antidepressants: chlorimipramine, amitriptyline and nortriptyline, and the atypical antidepressant trazodone on pain thresholds when administered alone or together with morphine. Moreover, we evaluated the effect of the antidepressants on free morphine plasma concentrations both in the rat and in man. We observed that chlorimipramine and amitriptyline, two tricyclic antidepressants active on the serotoninergic system, induce analgesia and potentiate morphine analgesia in a dose-related fashion. The noradrenergic tricyclic nortriptyline and trazodone did not elicit analgesia and inconsistently affected morphine analgesia. In the rat, all drugs tested increased plasma concentrations of morphine with the exception of amitriptyline. In man, only chlorimipramine and amitriptyline increased the plasma concentration of the free opiate.     

Laryngeal motility alteration: A missing link between sleep apnea and vagus nerve stimulation for epilepsy

This study aimed to evaluate the prevalence and the relationship of sleep breathing disorders (SBDs) and laryngeal motility alterations in patients with drug‐resistant epilepsy after vagus nerve stimulator (VNS) implantation. Twenty‐three consecutive patients with medically refractory epilepsy underwent out‐of‐center sleep testing before and after VNS implantation. Eighteen eligible subjects underwent endoscopic laryngeal examination post‐VNS implantation. Statistical analysis was carried out to assess an association between laryngeal motility alterations and the onset/worsening of SBDs. After VNS implantation, 11 patients showed a new‐onset mild/moderate SBD. Half of the patients already affected by obstructive sleep apnea (OSA) showed worsening of SBD. All of the patients with a new‐onset OSA had a laryngeal pattern with left vocal cord adduction (LVCA) during VNS stimulation. The association between VNS‐induced LVCA and SBD was statistically significant. This study suggests an association between VNS and SBD, hinting to a pivotal role of laryngeal motility alterations. The relationship between SBD and VNS‐induced LVCA supports the need to routinely investigate sleep respiratory and laryngeal motility patterns before and after VNS implantation.