The Communicative-Relational Operating Model of the Italian National Institute of Health for an Effective Telephone Intervention in Public Health, Structured on Basic Counselling Skills.

Introduction: Communication has a crucial role in public health, because it becomes an essential component of prevention; it is also a proactive tool in health promotion. From a planning perspective, it is appropriate to use communication means that can help the bidirectional communication process, such as face-to-face communication and telephone communication. Materials and methods: In relation to this, the Italian National Institute of Health has developed the "Modello Operativo Comunicativo-Relazionale" (the "Communicative-Relational Operating Model"). It is based on the fundamental skills of the counselling, this gives a protocol to the health professionals that is replicable and organized and it allows health professionals to carry out a telephone communication that is efficient with the user through technical-scientific and communication-relational skills. The goal is to answer in a customized way to the various users' health needs. The Operating Model was created by experts of the National AIDS and Sexually Transmitted Infections Helpline of the Operational Unit of Psycho-Socio-Behavioural Research, Communication, Training, of the Infectious Diseases Department. Later, the Operating Model was proposed to the experts of the Helplines in the National Centre on Addictions and Doping and the National Helpline of the National Centre for Rare Diseases in the National Institute of Health that integrated this method into their telephone approach. Results: The Operating Model illustrated above was applied to several helplines of the National Institute of Health as an example of correct scientific information, updated and customized on sexual transmitted infections, addictions and rare diseases. Conclusions: This article aims to illustrate the Operating Model, the theoretical prerequisites that subtend it and its possible application in the different public health structures that use the telephone for a profes-sional relationship with their users.

Which group of smokers is more vulnerable to the economic crisis?

OBJECTIVES: Studies investigating whether smoking increases or decreases during economic downturn provided contrasting results. For the first time, we used direct questions to analyse changes in smoking behaviour due to the 2008 financial crisis, comparing socio-economic characteristics of smokers who changed with those who kept their smoking intensity. STUDY DESIGN: Cross-sectional survey. METHODS: We used data from three annual surveys conducted in Italy in 2012-2014 on representative samples of the Italian general population aged ≥15 years. RESULTS: A total of 1919 current smokers were asked specific questions on the influence of the economic crisis that started in 2008 on their smoking behaviour. Overall, 77.4% of 1919 current smokers reported not to have changed their smoking behaviour, 19.1% to have reduced, and 3.5% to have increased their smoking intensity as a consequence of the economic crisis. The reduction in cigarette smoking increased with age: compared to the respondents aged <25 years, the multivariate odds ratio (OR) for those aged 25-44, 45-64 and ≥65 years were 0.65, 0.46 and 0.33, respectively (P for trend<0.001). Reduction was significantly lower among intermediate (OR = 0.68 compared to low) and high education levels (OR = 0.28; P for trend<0.001). A significant inverse trend for increasing consumption was observed with age (P = 0.022), education (P = 0.003) and family income (P < 0.001). CONCLUSIONS: The large majority of current smokers did not change their smoking habit following the economic crisis. However, there are specific vulnerable subgroups of smokers, constituted by the young and subjects with low socio-economic status, that were reactive to the global economic crisis. These groups are more prone to change their smoking behaviours, either for better or -, in a smaller proportion -, for worse.

Osteoimmunology and its implications for transplantation.

Osteoimmunology is a field of research dedicated to the study of the interactions between the immune system, the hemopoietic system and bone. Among the cells of the immune system that regulate bone cells and the hemopoietic function are T lymphocytes. These cells secrete inflammatory cytokines that promote bone resorption, as well as Wnt ligands that stimulate bone formation. In addition, T cells regulate bone homeostasis by cross talking with BM stromal cells and osteoblastic cells via CD40 ligand (CD40L) and other costimulatory molecules. This article describes the immune cells relevant to bone and the hemopoietic function, reviews the role of lymphocytes as mediators of the effects of PTH and estrogen in bone and the hemopoietic system and discusses the implication of osteoimmunology for transplant medicine.

A survey of Italian and Spanish neonatologists and paediatricians regarding awareness of the diagnosis of FAS and FASD and maternal ethanol use during pregnancy.

BACKGROUND: Ethanol is the most widely used drug in the world and a human teratogen whose consumption among women of childbearing age has been steadily increasing. There are no Italian or Spanish statistics on ethanol consumption during pregnancy nor any information regarding prevalence of fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD). There is also a reasonable suspicion that these two diseases are underdiagnosed by professionals from the above-reported countries. The objectives of this study were: 1) to evaluate the experience, knowledge and confidence of Italian and Spanish neonatologists and paediatricians with respect to the diagnosis of FAS and FASD, and 2) to evaluate professionals awareness of maternal drinking patterns during pregnancy. METHODS: A multiple-choice anonymous questionnaire was e-mailed to Italian neonatologists registered in the mailing list of the corresponding Society and administered to Italian and Spanish paediatricians during their National Congress. RESULTS: The response rate was 16% (63/400) for the Italian neonatologists of the National Society while a total of 152 Spanish and 41 Italian paediatricians agreed to complete the questionnaire during National Congress. Over 90% of the surveyed physicians declared that FAS is an identifiable syndrome and over 60% of them identified at least one of the most important features of FAS. Although over 60% Italian responders and around 80% Spanish responders were aware that ethanol use in pregnancy is dangerous, approximately 50% Italian responders and 40% Spanish ones allowed women to drink sometimes a glass of wine or beer during pregnancy.Neonatologists and paediatricians rated confidence in the ability to diagnosis FAS and FASD as low, with over 50% responders feeling they needed more information regarding FAS and FASD identification in newborn and child. CONCLUSIONS: Italian and Spanish neonatologists and paediatricians do not feel confident about diagnosing FAS and FASD. More training is needed in order to accurately diagnose ethanol use during pregnancy and correctly inform pregnant women on the consequences on the newborn.

Commentary - Heroin purity and adulteration: an updated snapshot from the Italian Early Warning System.

Not Available.

[Prenatal exposure to drugs of abuse using meconium analysis in a low socioeconomic population in Barcelona]. / Exposición prenatal a drogas de abuso a través del análisis de meconio en una población de bajo nivel socioeconómico en Barcelona.

INTRODUCTION: For the first time in Europe, the <> aimed to estimate the prevalence of drug use by pregnant women and the subsequent foetal exposure to illicit drugs. PATIENTS AND METHOD: Between October 2002 and February 2004, 1209 mother-infant dyads from the Hospital del Mar, Barcelona, Spain met eligibility criteria and agreed to participate in the study. Data on socio-economic and demographic characteristics and on drug habits during pregnancy were collected using a structured questionnaire. Neonatal meconium was collected within 24h after birth and analyzed by standardized chromatographic techniques for the presence of opiates, cocaine, cannabinoids and amphetamines. RESULTS: Meconium analysis showed an overall 10.9% positivity for drugs of abuse, with a specific prevalence of heroin, cocaine and cannabis with foetal exposure of 4.7, 2.6 and 5.3%, respectively. Structured interviews also revealed that 0.3, 1.2 and 1.5% of mothers used heroin, cocaine and cannabis, respectively, while only one mother declared ecstasy consumption, confirmed by meconium analysis. Parental ethnicity and working class was not associated with drug use. Drug consuming mothers were shown to have a higher number of previous abortions when compared to non-consumer mothers, which was probably due to a lack of family planning. Significantly lower birth weight and length was found in newborns from mothers exposed to cocaine alone or in combination with other drugs. CONCLUSIONS: This study, although developed in a low socio-economic-status cohort, may serve as an eye opener for any hidden non-negligible drug consumption during pregnancy. In this sense, meconium analysis can be important to identify neonates with a high suspicion of exposure to drugs of abuse in utero, and provides the basis for appropriate treatment and adequate medical and social follow-up.

Cognitive performance in recreational ecstasy polydrug users: a two-year follow-up study.

There is important preclinical evidence of long lasting neurotoxic and selective effects of ecstasy MDMA on serotonin systems in non-human primates. In humans long-term recreational use of ecstasy has been mainly associated with learning and memory impairments. The aim of the present study was to investigate the neuropsychological profile associated with ecstasy use within recreational polydrug users, and describe the cognitive changes related to maintained or variable ecstasy use along a two years period. We administered cognitive measures of attention, executive functions, memory and learning to three groups of participants: 37 current polydrug users with regular consumption of ecstasy and cannabis, 23 current cannabis users and 34 non-users free of illicit drugs. Four cognitive assessments were conducted during two years. At baseline, ecstasy polydrug users showed significantly poorer performance than cannabis users and non-drug using controls in a measure of semantic word fluency. When ecstasy users were classified according to lifetime use of ecstasy, the more severe users (more than 100 tablets) showed additional deficits on episodic memory. After two years ecstasy users showed persistent deficits on verbal fluency, working memory and processing speed. These findings should be interpreted with caution, since the possibility of premorbid group differences cannot be entirely excluded. Our findings support that ecstasy use, or ecstasy/cannabis synergic effects, are responsible for the sub-clinical deficits observed in ecstasy polydrug users, and provides additional evidence for long-term cognitive impairment owing to ecstasy consumption in the context of polydrug use.

On-site screening and GC-MS analysis of cocaine and heroin metabolites in body-packers urine.

The illicit transportation of cocaine and heroin either swallowed or inserted into the rectum and/or vagina of individuals, defined as "body-packers", is becoming increasingly common. Assessment of smuggling by urinalysis from body-packers has been sparsely reported and on-site rapid screening methods are essentially lacking. We screened the presence of cocaine and heroin metabolites in urine from suspected body-packers by an on-site immunochromatographic test and confirmed the obtained results by gas chromatography-mass spectrometry and X-ray examination. Samples were collected from 64 individuals (45 men, 19 women) stopped at Fiumicino and Ciampino airports of Rome (Italy) for suspicion of internal concealment of cocaine and heroin between October 2006 and July 2007. Urine was immediately screened on-site by Cozart rapid urine test. Irrespective of test results, individuals underwent X-ray examination and urine samples were analyzed by gas chromatography-mass spectrometry (GC-MS). In 48 out of 64 cases (24 positives and 24 negatives) screening results were confirmed by GC-MS assay and X-ray examination. In 5 cases, positive to the on-site test and GC-MS analysis, abdominal radiography was negative and individuals resulted to be drug users. In 11 cases, negative to the on-site test and radiological investigation, GC-MS analysis found benzoylecgonine in 10 cases and morphine in one case. Concentration of both substances was in all cases lower than 50ng/ml and compatible with personal drug use. From obtained results, on-site detection of cocaine and heroin metabolites in the urine of suspected body-packers appears to be a reliable screening test to disclose internally concealed drugs and justify subsequent radiological investigations.

Interleukin-1 receptor antagonist and tumor necrosis factor binding protein decrease osteoclast formation and bone resorption in ovariectomized mice.

To investigate the contribution of IL-1, IL-6, and TNF to the increased osteoclastogenesis induced by estrogen deficiency, ovariectomized (ovx) mice were treated with either IL-1 receptor antagonist (IL-1ra), a competitive inhibitor of IL-1, TNF binding protein (TNFbp), an inhibitor of TNF, or the anti-IL-6 antibody (Ab) 20F3 for the first 2 wk after surgery. ovx increased the bone marrow cells secretion of IL-1 and TNF, but not IL-6, and the formation of TRAP-positive osteoclast-like multinucleated cells (MNCs) in bone marrow cultures treated with 1,25(OH)2D3. The increase in MNC formation induced by ovx was prevented by in vivo treatment with either 17 beta estradiol, IL-1ra, TNFbp, or anti-IL-6 Ab. However, the percent change in MNC formation induced by the anti-IL-6 Ab was similar in ovx and sham-operated animals, whereas IL-1ra and TNFbp were effective only in ovx mice. MNC formation was also decreased by in vitro treatment of bone marrow cultures with IL-1ra and TNFbp, but not with anti-IL-6 Ab. Ovx also increased bone resorption in vivo and in vitro, as assessed by the urinary excretion of pyridinoline cross links and the formation of resorption pits, respectively. IL-1ra, TNFbp and estrogen decreased bone resorption in vivo and in vitro whereas the anti-IL-6 Ab inhibited bone resorption in vitro but not in vivo. In conclusion, these data indicate that IL-1 and TNF play a direct role in mediating the effects of ovx on osteoclastogenesis and bone resorption. The data also suggest that IL-6 is not essential for increasing bone resorption in the early postovariectomy period.

M-CSF neutralization and egr-1 deficiency prevent ovariectomy-induced bone loss.

Increased stromal cell production of M-CSF, an event caused by enhanced phosphorylation of the nuclear protein Egr-1, is central to the mechanism by which estrogen (E2) deficiency upregulates osteoclast (OC) formation. However, the contribution of enhanced M-CSF production to the bone loss induced by E2 deficiency remains to be determined. We found that treatment with an Ab that neutralizes M-CSF in vivo completely prevents the rise in OC number, the increase in bone resorption, and the resulting bone loss induced by ovariectomy (ovx). We also found that adult, intact Egr-1-deficient mice, a strain characterized by maximally stimulated stromal cell production of M-CSF, exhibit increased bone resorption and decreased bone mass. In these mice, treatment with anti-M-CSF Ab restored normal levels of bone resorption, thus confirming that increased M-CSF production accounts for the remodeling abnormalities of Egr-1-deficient mice. Consistent with the failure of ovx to further increase M-CSF production in Egr-1-deficient mice, ovx neither increased bone resorption further, nor caused bone loss in these animals. In summary, the data demonstrate that E2 deficiency induces M-CSF production via an Egr-1-dependent mechanism that is central to the pathogenesis of ovx-induced bone loss. Thus, Egr-1 and M-CSF are critical mediators of the bone sparing effects of E2 in vivo.

IL-1-induced murine osteoblast IL-6 production is mediated by the type 1 IL-1 receptor and is increased by 1,25 dihydroxyvitamin D3.

IL-1-induced osteoblast IL-6 production represents one possible mechanism by which IL-1 augments bone resorption. In this report, we show that the murine osteoblastic cell line (MC3T3-E1) expresses type 1 IL-1 receptors based on 125I-HrIL1 alpha binding, blocked by type 1 IL-1R antibodies (35F5), and analysis of MC3T3 RNA by reverse transcription (RT)-DNA amplification and Northern analysis. MC3T3 cells do not express detectable type 2 IL-1R mRNA by RT-DNA amplification. IL-1 induces (IL-1 ED50, 0.1 pM) IL-6 production through the type 1 IL-1R as 35F5 antibodies block IL-1-stimulated IL-6 production. Vitamin D3 increases IL-1R expression dose- and metabolite-dependently, with 1,25-(OH)2D3 having the greatest potency, and also enhances IL-1's capacity to stimulate IL-6 production at low IL-1 levels. Both IL-1 and 1,25-(OH)2D3 induce type 1 IL-1R and not type 2 IL-1R upregulation based on ligand binding and RT-DNA amplification. Increased IL-1R expression requires a 5-7-h treatment and is protein/RNA synthesis dependent. These observations imply that IL-1-induced IL-6 production in osteoblasts is mediated by type 1 IL-1Rs and that increased IL-1R expression could play a role in mediating IL-1-induced skeletal responses.

Collagen-induced release of interleukin 1 from human blood mononuclear cells. Potentiation by fibronectin binding to the alpha 5 beta 1 integrin.

PBMC express cell surface receptors for extracellular matrix components known as integrins. We have recently shown that ligand binding to one PBMC integrin, the collagen receptor alpha 2 beta 1, stimulates the secretion of interleukin 1 (IL-1). We have now investigated the role of fibronectin (Fn), an adherence protein that has binding sites for both PBMC and collagen, in the generation of the IL-1 response to collagen. In contrast to collagen, Fn did not stimulate IL-1 release but Fn-depleted serum decreased the release of IL-1 induced by collagen. A polyclonal antiserum directed against Fn also decreased the collagen-induced IL-1 secretion. The IL-1 response to collagen from cells incubated in Fn-depleted serum was restored by the addition of either purified Fn or the 120-kD cell-binding fragment of Fn, which contains the cell-binding site but not the collagen-binding domain. Smaller Arg-Gly-Asp (RGD) peptides failed to enhance the PBMC response to collagen but inhibited in a concentration-dependent fashion the potentiating effect Fn. As expected, a MAb against the alpha 2 beta 1 collagen receptor decreased collagen-induced IL-1 release. However collagen-induced IL-1 release was also inhibited by a MAb against the alpha 5 beta 1 Fn receptor. The effect of the two MAbs was not additive, suggesting that the occupancy of both receptors by ligands is required in order for collagen to induce an maximal response from PBMC. The mechanism by which Fn exerts its effect remains unknown. However, flow-cytometric analysis revealed that Fn does not alter expression of the alpha2beta1 receptor on PBMC. These data demonstrate a potentiating effect of Fn on the collagen-induced secretion of IL-1 from human PBMC and suggest that this effect is mediated via the integrin alpha5beta1. These findings indicate a complex interactive role for specific integrin receptors in the regulation of the mononuclear cell immune response.

Estrogen blocks M-CSF gene expression and osteoclast formation by regulating phosphorylation of Egr-1 and its interaction with Sp-1.

Central to the pathogenesis of osteoporosis is the ability of estrogen deficiency to increase osteoclast formation by enhancing stromal cell production of the osteoclastogenic cytokine macrophage colony-stimulating factor (M-CSF). We report that stromal cells from ovariectomized mice exhibit increased casein kinase II-dependent phosphorylation of the nuclear protein Egr-1. Phosphorylated Egr-1 binds less avidly to the transcriptional activator Sp-1 and the resulting higher levels of free Sp-1 stimulate transactivation of the M-CSF gene. Estrogen replacement fails to block M-CSF mRNA expression and osteoclast formation in ovariectomized mice lacking Egr-1, confirming the critical role played by this transcription factor in mediating the antiosteoclastogenic effects of estrogen. Thus, by downregulating formation of a novel Egr-1/Sp-1 complex in stromal cells, estrogen deficiency results in enhanced levels of free Sp-1 and increased M-CSF gene expression and osteoclast formation.

Estrogen decreases TNF gene expression by blocking JNK activity and the resulting production of c-Jun and JunD.

Central to the bone-sparing effect of estrogen (E(2)) is its ability to block the monocytic production of the osteoclastogenic cytokine TNF-alpha (TNF). However, the mechanism by which E(2) downregulates TNF production is presently unknown. Transient transfection studies in HeLa cells, an E(2) receptor-negative line, suggest that E(2) inhibits TNF gene expression through an effect mediated by estrogen receptor beta (ERbeta). We also report that in RAW 264.7 cells, an E(2) receptor-positive murine monocytic line, E(2) downregulates cytokine-induced TNF gene expression by decreasing the activity of the Jun NH(2)-terminal kinase (JNK). The resulting diminished phosphorylation of c-Jun and JunD at their NH(2)-termini decreases the ability of these nuclear proteins to autostimulate the expression of the c-Jun and JunD genes, thus leading to lower production of c-Jun and JunD. The consequent decrease in the nuclear levels of c-Jun and JunD leads to diminished binding of c-Jun/c-Fos and JunD/c-Fos heterodimers to the AP-1 consensus sequence in the TNF promoter and, thus, to decreased transactivation of the TNF gene.

Estrogen deficiency induces bone loss by enhancing T-cell production of TNF-alpha.

Estrogen deficiency induces bone loss by upregulating osteoclastogenesis by mechanisms not completely defined. We found that ovariectomy-enhanced T-cell production of TNF-alpha, which, acting through the TNF-alpha receptor p55, augments macrophage colony-stimulating factor-induced (M-CSF-induced) and RANKL-induced osteoclastogenesis. Ovariectomy failed to induce bone loss, stimulate bone resorption, or increase M-CSF- and RANKL-dependent osteoclastogenesis in T-cell deficient mice, establishing T cells as essential mediators of the bone-wasting effects of estrogen deficiency in vivo. These findings demonstrate that the ability of estrogen to target T cells, suppressing their production of TNF-alpha, is a key mechanism by which estrogen prevents osteoclastic bone resorption and bone loss.

Bone matrix constituents stimulate interleukin-1 release from human blood mononuclear cells.

To test the hypothesis that mononuclear cells are stimulated to release interleukin 1 (IL-1) by bone fragments released in the bone microenvironment during the remodeling cycle, we have investigated the effects of bone matrix and some of its constituents on IL-1 secretin from peripheral blood mononuclear cells (PBMC). Increases in IL-1 activity were observed when either PBMC or adherent monocytes, but not lymphocytes depleted of monocytes, were co-cultured with either human or rat bone particles but not with latex particles of similar size. Co-culture of PBMC with bone particles in a transwell system where the cells were physically separated from the bone particles, or with osteoblast- or osteoclast-covered bone particles, did not stimulate IL-1 release, indicating that a physical contact between PBMC and the bone surface is required for eliciting IL-1 release. This was confirmed by the finding of a lower stimulatory effect of bone particles pretreated with etidronate, a bisphosphonate which decreases the bone binding capacity of PBMC. Constituents of bone matrix, such as collagen fragments, hydroxyproline, and, to a lesser extent, transforming growth factor-beta, but not osteocalcin, alpha 2HS glycoprotein, fragments of either bone sialoprotein or osteopontin, and fibronectin, stimulated PBMC IL-1 release in a dose-dependent fashion. Collagen-stimulated IL-1 release was partially and specifically inhibited by a monoclonal antibody directed against the alpha 2 beta 1-integrin cell surface collagen receptor. These data demonstrate that products of bone resorption, known to be chemotactic for mononuclear cells, stimulate PBMC IL-1 activity. These findings may help explain previous documentation of increased IL-1 secretion by circulating monocytes obtained from patients with high turnover osteoporosis.

Interleukin-1 receptor antagonist decreases bone loss and bone resorption in ovariectomized rats.

Interleukin-1 (IL-1), a cytokine produced by bone marrow cells and bone cells, has been implicated in the pathogenesis of postmenopausal osteoporosis because of its potent stimulatory effects on bone resorption in vitro and in vivo. To investigate whether IL-1 plays a direct causal role in post ovariectomy bone loss, 6-mo-old ovariectomized rats were treated with subcutaneous infusions of IL-1 receptor antagonist (IL-1ra), a specific competitor of IL-1, for 4 wk, beginning either at the time of surgery or 4 wk after ovariectomy. The bone density of the distal femur was measured non invasively by dual-energy X-ray absorptiometry. Bone turnover was assessed by bone histomorphometry and by measuring serum osteocalcin, a marker of bone formation, and the urinary excretion of pyridinoline cross-links, a marker of bone resorption. Ovariectomy caused a rapid increase in bone turnover and a marked decrease in bone density which were blocked by treatment with 17 beta estradiol. Ovariectomy also increased the production of IL-1 from cultured bone marrow cells. Ovariectomy induced-bone loss was significantly decreased by IL-1ra treatment started at the time of ovariectomy and completely blocked by IL-1ra treatment begun 4 wk after ovariectomy. In both studies IL-1ra also decreased bone resorption in a manner similar to estrogen, while it had no effect on bone formation. In contrast, treatment with IL-1ra had no effect on the bone density and the bone turnover of sham-operated rats, indicating that IL-1ra specifically blocked estrogen-dependent bone loss. In conclusion, these data indicate that IL-1, or mediators induced by IL-1, play an important causal role in the mechanism by which ovariectomy induces bone loss in rats, especially following the immediate post ovariectomy period.

Hepatotoxicity associated with illicit use of anabolic androgenic steroids in doping.

Anabolic Androgenic Steroids (AAS) abuse and misuse is nowadays a harmful habit involving both professional or recreational athletes, as well as general population. AAS are also frequently present in over-the-counter dietary supplements without being declared in the list of ingredients, leaving consumers unaware of the risks of adverse effects. Indeed, health risks of AAS consumption in pharmaceutical preparations or dietary complements seem still underestimated and under-reported. The variety of complications due to AAS misuse involves cardiovascular, central nervous, musculoskeletal and genitourinary systems of both males and females; psychiatric and behavioral effects, damages to metabolic system, skin and mainly liver. For instance, relevant concern has been raised by the AAS hepatotoxicity including adenoma, hepatocellular carcinoma, cholestasis, and peliosis hepatis. The present review reports the information available on the hepatotoxic effects of AAS use in professional and amateur athletes.